Volume 12, Issue 5

Idda ML, McClusky WG, Lodde V, Munk R, Abdelmohsen K, Rossi M, Gorospe M, . Survey of senescent cell markers with age in human tissues. Aging (Albany NY). 2020 Mar 1112:4052-4066. https://doi.org/10.18632/aging.102903

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                TY  - JOUR
                AU  - Idda, M. Laura 
                AU  - McClusky, Waverly G. 
                AU  - Lodde, Valeria 
                AU  - Munk, Rachel 
                AU  - Abdelmohsen, Kotb 
                AU  - Rossi, Martina 
                AU  - Gorospe, Myriam 
                TI  - Survey of senescent cell markers with age in human tissues
                JO  - 
                JA  - Aging (Albany NY)
                VL  - 12
                IS  - 5
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102903
                DO  - 10.18632/aging.102903
                SP  - 4052
                EP  - 4066
                PY  - 
                AB  - Cellular senescence, triggered by sublethal damage, is characterized by indefinite growth arrest, altered gene expression patterns, and a senescence-associated secretory phenotype. While the accumulation of senescent cells during aging decreases tissue function and promotes many age-related diseases, at present there is no universal marker to detect senescent cells in tissues. Cyclin-dependent kinase inhibitors 2A (p16/CDKN2A) and 1A (p21/CDKN1A) can identify senescent cells, but few studies have examined the numbers of cells expressing these markers in different organs as a function of age. Here, we investigated systematically p16- and p21-positive cells in tissue arrays designed to include normal organs from persons across a broad spectrum of ages. Increased numbers of p21-positive and p16-positive cells with donor age were found in skin (epidermis), pancreas, and kidney, while p16-expressing cells increased in brain cortex, liver, spleen and intestine (colon), and p21-expressing cells increased in skin (dermis). The numbers of cells expressing p16 or p21 in lung did not change with age, and muscle did not appear to have p21- or p16-positive cells. In summary, different organs display different levels of the senescent proteins p16 and p21 as a function of age across the human life span.
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HIF-1α/microRNA-128-3p axis protects hippocampal neurons from apoptosis via the Axin1-mediated Wnt/β-catenin signaling pathway in Parkinson’s disease models

Guangping Zhang, Luzhu Chen, Jing Liu, Yan Jin, Zaihong Lin, Shu Du, Zenghui Fu, Tuantuan Chen, Yinghui Qin, Fenghu Sui, Yan Jiang,

https://doi.org/10.18632/aging.102636 pp 4067—4081

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Zhang G, Chen L, Liu J, Jin Y, Lin Z, Du S, Fu Z, Chen T, Qin Y, Sui F, Jiang Y, . HIF-1α/microRNA-128-3p axis protects hippocampal neurons from apoptosis via the Axin1-mediated Wnt/β-catenin signaling pathway in Parkinson’s disease models. Aging (Albany NY). 2020 Mar 1212:4067-4081. https://doi.org/10.18632/aging.102636

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 TY - JOUR
 AU - Zhang, Guangping 
 AU - Chen, Luzhu 
 AU - Liu, Jing 
 AU - Jin, Yan 
 AU - Lin, Zaihong 
 AU - Du, Shu 
 AU - Fu, Zenghui 
 AU - Chen, Tuantuan 
 AU - Qin, Yinghui 
 AU - Sui, Fenghu 
 AU - Jiang, Yan 
 TI - HIF-1α/microRNA-128-3p axis protects hippocampal neurons from apoptosis via the Axin1-mediated Wnt/β-catenin signaling pathway in Parkinson’s disease models
 JO - 
 JA - Aging (Albany NY)
 VL - 12
 IS - 5
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.102636
 DO - 10.18632/aging.102636
 SP - 4067
 EP - 4081
 PY - 
 AB - Parkinson&apos;s disease (PD) is a progressive neurodegenerative disorder. A common and disabling disease of the elderly, the standard dopamine replacement therapies do not arrest the ongoing neurodegeneration, thus calling for new treatment strategies. The present study aimed to clarify the functional relevance of the hypoxia inducible factor-1&#x3B1; (HIF-1&#x3B1;)/microRNA-128-3p (miR-128-3p) axis in hippocampal neurodegeneration in a PD mouse model obtained by intraperitoneal injection of MPTP. Targeting relationship between miR-128-3p and Axin1 was verified, so we probed the roles of Hif1a, miR-128-3p, and Axin1 in apoptosis of hippocampal neurons with gain- and loss-of function experiments using flow cytometry and TUNEL staining. We found that Axin1 was upregulated in hippocampal tissues and cells of the MPTP-lesioned mouse model of PD, while Hif1a and miR-128-3p were downregulated. Elevation of HIF-1&#x3B1;/miR-128-3p inhibited apoptosis of hippocampal neurons via Wnt/&#x3B2;-catenin signaling pathway activation due to the suppression of Axin1 in PD. In addition, forced overexpression of Hif1a could ameliorate motor dysfunction and pathological changes in the model. Collectively, activation of the HIF-1&#x3B1;/miR-128-3p axis could repress hippocampal neurodegeneration in MPTP-lesioned mice through an activated Wnt/&#x3B2;-catenin pathway due to Axin1 downregulation.
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Obstructive sleep apnea syndrome and causal relationship with female breast cancer: a mendelian randomization study

Xiao-Ling Gao, Zhi-Mei Jia, Fang-Fang Zhao, Dong-Dong An, Bei Wang, Er-Jing Cheng, Yan Chen, Jian-Nan Gong, Dai Liu, Ya-Qiong Huang, Jiao-Jiao Yang, Shu-Juan Wang,

https://doi.org/10.18632/aging.102725 pp 4082—4092

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Gao X, Jia Z, Zhao F, An D, Wang B, Cheng E, Chen Y, Gong J, Liu D, Huang Y, Yang J, Wang S, . Obstructive sleep apnea syndrome and causal relationship with female breast cancer: a mendelian randomization study. Aging (Albany NY). 2020 Feb 2912:4082-4092. https://doi.org/10.18632/aging.102725

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                TY  - JOUR
                AU  - Gao, Xiao-Ling 
                AU  - Jia, Zhi-Mei 
                AU  - Zhao, Fang-Fang 
                AU  - An, Dong-Dong 
                AU  - Wang, Bei 
                AU  - Cheng, Er-Jing 
                AU  - Chen, Yan 
                AU  - Gong, Jian-Nan 
                AU  - Liu, Dai 
                AU  - Huang, Ya-Qiong 
                AU  - Yang, Jiao-Jiao 
                AU  - Wang, Shu-Juan 
                TI  - Obstructive sleep apnea syndrome and causal relationship with female breast cancer: a mendelian randomization study
                JO  - 
                JA  - Aging (Albany NY)
                VL  - 12
                IS  - 5
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102725
                DO  - 10.18632/aging.102725
                SP  - 4082
                EP  - 4092
                PY  - 
                AB  - Although observational studies have reported a positive association between obstructive sleep apnea syndrome (OSAS) and breast cancer (BC) risk, causality remains inconclusive. We aim to explore whether OSAS is associated with etiology of BC by conducting a two-sample Mendelian randomization (MR) study in a Chinese population and Asian population from the Breast Cancer Association Consortium (BCAC). We found a detrimental causal effect of OSAS on BC risk in the primary analysis of our samples (IVW OR, 2.47 for BC risk per log-odds increment in OSAS risk, 95% CI = 1.86-3.27; P = 3.6&#xD7;10-10). This was very similar to results of the direct observational case-control study between OSAS and BC risk (OR = 2.80; 95% CI = 2.24-3.50; P =1.4&#xD7;10-19). Replication in the Asian population of the BCAC study also supported our results (IVW OR, 1.33 for BC risk per log-odds increment in OSAS risk, 95% CI = 1.13-1.56; P = 0.0006). Sensitivity analyses confirmed the robustness of our findings. We provide novel evidence that genetically determined higher risk of OSAS has a causal effect on higher risk of BC. Further studies focused on the mechanisms of the relationship between OSAS and breast carcinogenesis are needed.
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Exosomal miR-19a from adipose-derived stem cells suppresses differentiation of corneal keratocytes into myofibroblasts

Ting Shen, Qingqing Zheng, Hongbo Luo, Xin Li, Zhuo Chen, Zeyu Song, Guanfang Zhou, Chaoyang Hong,

https://doi.org/10.18632/aging.102802 pp 4093—4110

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Shen T, Zheng Q, Luo H, Li X, Chen Z, Song Z, Zhou G, Hong C, . Exosomal miR-19a from adipose-derived stem cells suppresses differentiation of corneal keratocytes into myofibroblasts. Aging (Albany NY). 2020 Feb 2912:4093-4110. https://doi.org/10.18632/aging.102802

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                TY  - JOUR
                AU  - Shen, Ting 
                AU  - Zheng, Qingqing 
                AU  - Luo, Hongbo 
                AU  - Li, Xin 
                AU  - Chen, Zhuo 
                AU  - Song, Zeyu 
                AU  - Zhou, Guanfang 
                AU  - Hong, Chaoyang 
                TI  - Exosomal miR-19a from adipose-derived stem cells suppresses differentiation of corneal keratocytes into myofibroblasts
                JO  - 
                JA  - Aging (Albany NY)
                VL  - 12
                IS  - 5
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102802
                DO  - 10.18632/aging.102802
                SP  - 4093
                EP  - 4110
                PY  - 
                AB  - In this study, we investigated the effects of exosomal microRNAs (miRNAs) from adipose-derived stem cells (ADSCs) on the differentiation of rabbit corneal keratocytes. Keratocytes grown in 10% FBS differentiated into myofibroblasts by increasing HIPK2 kinase levels and activity. HIPK2 enhanced p53 and Smad3 pathways in FBS-induced keratocytes. Keratocytes grown in 10% FBS also showed increased levels of pro-fibrotic proteins, including collagen III, MMP9, fibronectin, and &#x3B1;-SMA. These effects were reversed by knocking down HIPK2. Moreover, ADSCs and exosomes derived from ADSCs (ADSCs-Exo) suppressed FBS-induced differentiation of keratocytes into myofibroblasts by inhibiting HIPK2. Quantitative RT-PCR analysis showed that ADSCs-Exos were significantly enriched in miRNA-19a as compared to ADSCs. Targetscan and dual luciferase reporter assays confirmed that the HIPK2 3&#x2019;UTR is a direct binding target of miR-19a. Keratocytes treated with 10% FBS and ADSCs-Exo-miR-19a-agomir or ADSCs-Exo-NC-antagomir showed significantly lower levels of HIPK2, phospho-Smad3, phospho-p53, collagen III, MMP9, fibronectin and &#x3B1;-SMA than those treated with 10% FBS plus ADSCs-Exo-NC-agomir or ADSCs-Exo-miR-19a-antagomir. Thus, exosomal miR-19a derived from the ADSCs suppresses FBS-induced differentiation of rabbit corneal keratocytes into myofibroblasts by inhibiting HIPK2 expression. This suggests their potential use in the treatment of corneal fibrosis.
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Long noncoding RNA LINC00461 induced osteoarthritis progression by inhibiting miR-30a-5p

Yuanmin Zhang, Longfei Ma, Chengqun Wang, Lina Wang, Yanxia Guo, Guodong Wang,

https://doi.org/10.18632/aging.102839 pp 4111—4123

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Zhang Y, Ma L, Wang C, Wang L, Guo Y, Wang G, . Long noncoding RNA LINC00461 induced osteoarthritis progression by inhibiting miR-30a-5p. Aging (Albany NY). 2020 Mar 1012:4111-4123. https://doi.org/10.18632/aging.102839

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                TY  - JOUR
                AU  - Zhang, Yuanmin 
                AU  - Ma, Longfei 
                AU  - Wang, Chengqun 
                AU  - Wang, Lina 
                AU  - Guo, Yanxia 
                AU  - Wang, Guodong 
                TI  - Long noncoding RNA LINC00461 induced osteoarthritis progression by inhibiting miR-30a-5p
                JO  - 
                JA  - Aging (Albany NY)
                VL  - 12
                IS  - 5
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102839
                DO  - 10.18632/aging.102839
                SP  - 4111
                EP  - 4123
                PY  - 
                AB  - Mounting studies have shown that long noncoding RNAs (lncRNAs) play important roles in the development and occurrence of several human diseases. However, the role of LINC00461 in osteoarthritis (OA) remains obscure. A CCK-8 assay was performed to detect cell viability, and qRT-PCR analysis was used to measure mRNA expression. The targeting by miR-30a-5p of the LINC00461 3&#x2019;UTR was detected using a luciferase reporter assay. Our data indicated that the inflammatory mediators IL-6 and TNF-&#x3B1; induced LINC00461 expression in chondrocytes and that the expression of LINC00461 was upregulated in OA tissues. Furthermore, we showed that TNF-&#x3B1; and IL-6 suppressed the expression of miR-30a-5p and that miR-30a-5p expression was lower in OA tissues than in normal samples. The expression level of miR-30a-5p in OA tissues was negatively related to LINC00461 expression. In addition, we showed that LINC00461 directly interacted with miR-30a-5p in chondrocytes. Elevated expression of LINC00461 induced chondrocyte proliferation, cell cycle progression, inflammation, and extracellular matrix (ECM) degradation. However, we demonstrated that ectopic expression of miR-30a-5p suppressed cell growth, cell cycle progression, inflammation and ECM degradation. Finally, we found that overexpression of LINC00461 enhanced chondrocyte proliferation, cell cycle progression, inflammation, and ECM degradation by downregulating miR-30a-5p. These data demonstrated that LINC00461 may modulate the development of OA by suppressing miR-30a-5p expression in chondrocytes. We propose that LINC00461 and miR-30a-5p may be potential therapeutic and diagnostic targets for OA.
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ESHRD: deconvolution of brain homogenate RNA expression data to identify cell-type-specific alterations in Alzheimer’s disease

Ignazio S. Piras, Christiane Bleul, Joshua S. Talboom, Matthew D. De Both, Isabelle Schrauwen, Glenda Halliday, Amanda J. Myers, Geidy E. Serrano, Thomas G. Beach, Matthew J. Huentelman,

https://doi.org/10.18632/aging.102840 pp 4124—4162

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Piras IS, Bleul C, Talboom JS, De Both MD, Schrauwen I, Halliday G, Myers AJ, Serrano GE, Beach TG, Huentelman MJ, . ESHRD: deconvolution of brain homogenate RNA expression data to identify cell-type-specific alterations in Alzheimer’s disease. Aging (Albany NY). 2020 Mar 212:4124-4162. https://doi.org/10.18632/aging.102840

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                TY  - JOUR
                AU  - Piras, Ignazio S. 
                AU  - Bleul, Christiane 
                AU  - Talboom, Joshua S. 
                AU  - De Both, Matthew D. 
                AU  - Schrauwen, Isabelle 
                AU  - Halliday, Glenda 
                AU  - Myers, Amanda J. 
                AU  - Serrano, Geidy E. 
                AU  - Beach, Thomas G. 
                AU  - Huentelman, Matthew J. 
                TI  - ESHRD: deconvolution of brain homogenate RNA expression data to identify cell-type-specific alterations in Alzheimer’s disease
                JO  - 
                JA  - Aging (Albany NY)
                VL  - 12
                IS  - 5
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102840
                DO  - 10.18632/aging.102840
                SP  - 4124
                EP  - 4162
                PY  - 
                AB  - Objective: We describe herein a bioinformatics approach that leverages gene expression data from brain homogenates to derive cell-type specific differential expression results.Results: We found that differentially expressed (DE) cell-specific genes were mostly identified as neuronal, microglial, or endothelial in origin. However, a large proportion (75.7%) was not attributable to specific cells due to the heterogeneity in expression among brain cell types. Neuronal DE genes were consistently downregulated and associated with synaptic and neuronal processes as described previously in the field thereby validating this approach. We detected several DE genes related to angiogenesis (endothelial cells) and proteoglycans (oligodendrocytes).Conclusions: We present a cost- and time-effective method exploiting brain homogenate DE data to obtain insights about cell-specific expression. Using this approach we identify novel findings in AD in endothelial cells and oligodendrocytes that were previously not reported.Methods: We derived an enrichment score for each gene using a publicly available RNA profiling database generated from seven different cell types isolated from mouse cerebral cortex. We then classified the differential expression results from 3 publicly accessible Late-Onset Alzheimer&#x2019;s disease (AD) studies including seven different brain regions.
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Reduced Ca²⁺ spark activity contributes to detrusor overactivity of rats with partial bladder outlet obstruction

Ji Zheng, Hao Zhou, Mengjun Yang, Siji Song, Qiang Dai, Guangju Ji, Zhansong Zhou,

https://doi.org/10.18632/aging.102855 pp 4163—4177

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Zheng J, Zhou H, Yang M, Song S, Dai Q, Ji G, Zhou Z, . Reduced Ca²⁺ spark activity contributes to detrusor overactivity of rats with partial bladder outlet obstruction. Aging (Albany NY). 2020 Feb 2912:4163-4177. https://doi.org/10.18632/aging.102855

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 TY - JOUR
 AU - Zheng, Ji 
 AU - Zhou, Hao 
 AU - Yang, Mengjun 
 AU - Song, Siji 
 AU - Dai, Qiang 
 AU - Ji, Guangju 
 AU - Zhou, Zhansong 
 TI - Reduced Ca2+ spark activity contributes to detrusor overactivity of rats with partial bladder outlet obstruction
 JO - 
 JA - Aging (Albany NY)
 VL - 12
 IS - 5
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.102855
 DO - 10.18632/aging.102855
 SP - 4163
 EP - 4177
 PY - 
 AB - We tested whether or not altered Ca2+ spark activity accounted for detrusor overactivity (DO) of Wistar rats after partial bladder outlet obstruction (PBOO). We constructed a DO model through PBOO and studied the Ca2+ spark activity of detrusor. By way of using confocal microscopy and the patch-clamp technique, Ca2+ sparks and spontaneous transient outward currents (STOCs) in detrusor myocytes were measured respectively. Our results indicated that Ca2+ spark activity and STOCs were significantly reduced in the DO detrusor myocytes compared to unafflicted control cells, and both of these had levels that were remarkably increased by applications of caffeine (10 &#x3BC;M), a RyR agonist, in DO myocytes. In addition, measures of detrusor contractions were also recorded by using freshly isolated detrusor strips. These results indicated that the spontaneous contraction of DO detrusor was significantly enhanced, and that the effect of caffeine (10 &#x3BC;M) upon detrusor contractions was reversed by applications of iberiotoxin (100 nM) which is a BK channel blocker. Western blotting (WB) analyses indicated that the levels of expression of ryanodine receptor type 2 (RyR2) and FK506 binding protein 12.6 (FKBP12.6) in bladder muscle were respectively decreased and increased in the samples from DO rats. Thus, we considered in the rat DO model wherein PBOO, the reduced Ca2+ spark activity in detrusor myocytes partly contributed to overactive detrusor contractions. The impaired Ca2+ spark activity may have resulted from decreased RyR2 expression and increased FKBP12.6 expression. Such novel findings in our research might help to provide means for better treatment outcomes for patients afflicted by bladder dysfunction.
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SIRT3 inhibits cardiac hypertrophy by regulating PARP-1 activity

Xiaojun Feng, Yanan Wang, Wenxu Chen, Suowen Xu, Lingli Li, Yadi Geng, Aizong Shen, Hui Gao, Lei Zhang, Sheng Liu,

https://doi.org/10.18632/aging.102862 pp 4178—4192

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Feng X, Wang Y, Chen W, Xu S, Li L, Geng Y, Shen A, Gao H, Zhang L, Liu S, . SIRT3 inhibits cardiac hypertrophy by regulating PARP-1 activity. Aging (Albany NY). 2020 Mar 412:4178-4192. https://doi.org/10.18632/aging.102862

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                TY  - JOUR
                AU  - Feng, Xiaojun 
                AU  - Wang, Yanan 
                AU  - Chen, Wenxu 
                AU  - Xu, Suowen 
                AU  - Li, Lingli 
                AU  - Geng, Yadi 
                AU  - Shen, Aizong 
                AU  - Gao, Hui 
                AU  - Zhang, Lei 
                AU  - Liu, Sheng 
                TI  - SIRT3 inhibits cardiac hypertrophy by regulating PARP-1 activity
                JO  - 
                JA  - Aging (Albany NY)
                VL  - 12
                IS  - 5
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102862
                DO  - 10.18632/aging.102862
                SP  - 4178
                EP  - 4192
                PY  - 
                AB  - Sirtuin 3 (SIRT3) is a type III histone deacetylase that inhibits cardiac hypertrophy. It is mainly localized in the mitochondria and is thus implicated in mitochondrial metabolism. Recent studies have shown that SIRT3 can also accumulate in the nuclear under stressed conditions, and participated in histone deacetylation of target proteins. Poly [ADP-ribose] polymerase 1 (PARP-1) functions as an important PARP isoform that was involved in cardiac hypertrophy. Our experiments showed that SIRT3 accumulated in the nuclear of cardiomyocytes treated with isoproterenol or SIRT3 overexpression. Moreover, overexpression of SIRT3 by adenovirus inhibited the expression of cardiac hypertrophic genes-ANF and BNP, as well as abrogating PARP-1 activation induced by isoproterenol or phenylephrine. In addition, co-immunoprecipitation experiments revealed that SIRT3 could interact with PARP-1, and overexpression of SIRT3 could decrease the acetylation level of PARP-1. Our results indicate that SIRT3 exerts protective effects against cardiac hypertrophy by reducing the level of acetylation and activity of PARP-1, thus providing novel mechanistic insights into SIRT3-mediated cardiprotective actions.
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Levels of serum S100B are associated with cognitive dysfunction in patients with type 2 diabetes

Huan Yu, Hui Li, Xiaoqian Liu, Xiaoli Du, Binbin Deng,

https://doi.org/10.18632/aging.102873 pp 4193—4203

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Yu H, Li H, Liu X, Du X, Deng B, . Levels of serum S100B are associated with cognitive dysfunction in patients with type 2 diabetes. Aging (Albany NY). 2020 Feb 2912:4193-4203. https://doi.org/10.18632/aging.102873

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                TY  - JOUR
                AU  - Yu, Huan 
                AU  - Li, Hui 
                AU  - Liu, Xiaoqian 
                AU  - Du, Xiaoli 
                AU  - Deng, Binbin 
                TI  - Levels of serum S100B are associated with cognitive dysfunction in patients with type 2 diabetes
                JO  - 
                JA  - Aging (Albany NY)
                VL  - 12
                IS  - 5
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102873
                DO  - 10.18632/aging.102873
                SP  - 4193
                EP  - 4203
                PY  - 
                AB  - Objective: Previous studies have provided robust evidence that cognitive impairment exists in patients with type 2 diabetes. The predictive role of S100B in a variety of neurodegenerative diseases such as Alzheimer&#x2019;s disease, has been shown to be closely related to cognitive function. The purpose of this study was to investigate the correlation between serum S100B levels and cognitive function in type 2 diabetes patients.Results: The type 2 diabetes group scored lower than the healthy control group in all domains of cognitive function except language and attention, and the former group also had lower serum levels of S100B. Besides, serum S100B levels were lower in the type 2 diabetes patients with impaired cognition than in those with normal cognition. In addition, the moderate to severe cognitive impairment group had significantly lower levels than that in mild cognitive impairment group. After adjusting for confounding factors, serum S100B levels were positively correlated with cognitive function in type 2 diabetes patients.Conclusions: Serum S100B levels were positively correlated with cognitive function in type 2 diabetes patients with cognitive impairment. It is suggested that S100B may be involved in the occurrence and development of cognitive dysfunction in type 2 diabetes patients and play a protective role.Methods: The clinical data and biochemical indexes of ninety-six patients with type 2 diabetes and sixty-eight healthy subjects were collected. The levels of serum S100B were detected by enzyme-linked immunosorbent assay. Ninety-six type 2 diabetes patients were divided into a cognitive dysfunction group and a normal cognition group according to Mini-mental State Examination scores. To better understand the differences in various aspects of cognition, we used the Repeatable Battery for the Assessment of Neuropsychological Status scale for further evaluation. To study the relationship between serum S100B levels and cognitive impairment, the cognitive dysfunction group was divided into a mild cognitive impairment group and a moderate to severe cognitive impairment group for further study.
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Comprehensive characterization of endometrial competing endogenous RNA network in infertile women of childbearing age

Meihua Zhang, Junxia Li, Shuyin Duan, Zhenya Fang, Jiaqi Tian, Haoyu Yin, Qingfeng Zhai, Xietong Wang, Lin Zhang,

https://doi.org/10.18632/aging.102874 pp 4204—4221

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Zhang M, Li J, Duan S, Fang Z, Tian J, Yin H, Zhai Q, Wang X, Zhang L, . Comprehensive characterization of endometrial competing endogenous RNA network in infertile women of childbearing age. Aging (Albany NY). 2020 Feb 2912:4204-4221. https://doi.org/10.18632/aging.102874

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                TY  - JOUR
                AU  - Zhang, Meihua 
                AU  - Li, Junxia 
                AU  - Duan, Shuyin 
                AU  - Fang, Zhenya 
                AU  - Tian, Jiaqi 
                AU  - Yin, Haoyu 
                AU  - Zhai, Qingfeng 
                AU  - Wang, Xietong 
                AU  - Zhang, Lin 
                TI  - Comprehensive characterization of endometrial competing endogenous RNA network in infertile women of childbearing age
                JO  - 
                JA  - Aging (Albany NY)
                VL  - 12
                IS  - 5
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102874
                DO  - 10.18632/aging.102874
                SP  - 4204
                EP  - 4221
                PY  - 
                AB  - Endometriosis is widely associated with infertility in women of childbearing age, for which there have been no effective treatments. Recent studies suggest that the dysregulation of RNAs contributes to the pathogenesis of endometriosis, so we conduct the case-control genetic analysis to characterize the expression and interaction of different subtypes of RNAs in infertile women with endometriosis. The ectopic and eutopic endometrium of patients undergoing infertility treatment were collected and subjected to high throughput sequencing, and bioinformatics analysis was conducted to construct the competing endogenous RNA (ceRNA) network. As a result, the RNA interactive network was constructed in endometriosis, and a set of mRNAs such as cyclin-dependent kinase 1 (CDK1) and proliferating cell nuclear antigen (PCNA) along with their corresponding miRNAs and lncRNAs were found to promote the growth and death of endometrial stromal cells, which was essential for the pathogenesis of endometriosis. These data suggest that RNA crosstalk is a crucial segment in the development of endometriosis, where CDK1 and PCNA may serve as emerging targets for the treatment of endometriosis-related infertility in women of childbearing age.
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Identification of frailty-associated genes by coordination analysis of gene expression

Youwen Zhang, Ioulia Chatzistamou, Hippokratis Kiaris,

https://doi.org/10.18632/aging.102875 pp 4222—4229

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Zhang Y, Chatzistamou I, Kiaris H, . Identification of frailty-associated genes by coordination analysis of gene expression. Aging (Albany NY). 2020 Feb 2912:4222-4229. https://doi.org/10.18632/aging.102875

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                TY  - JOUR
                AU  - Zhang, Youwen 
                AU  - Chatzistamou, Ioulia 
                AU  - Kiaris, Hippokratis 
                TI  - Identification of frailty-associated genes by coordination analysis of gene expression
                JO  - 
                JA  - Aging (Albany NY)
                VL  - 12
                IS  - 5
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102875
                DO  - 10.18632/aging.102875
                SP  - 4222
                EP  - 4229
                PY  - 
                AB  - Differential expression analyses provide powerful tools for the identification of genes playing a role in disease pathogenesis. Yet, such approaches are usually restricted by the high variation in expression profiles when primary specimens are analyzed. It is conceivable that with the assessment of the degree of coordination in gene expression as opposed to the magnitude of differential expression, we may obtain hints underscoring different biological and pathological states. Here we have analyzed a publicly available dataset related to frailty, a syndrome characterized by reduced responsiveness to stressors and exhibiting increased prevalence in the elderly. We evaluated the transcriptome that loses its coordination between the frailty and control groups and assessed the biological functions that are acquired in the former group. Among the top genes exhibiting the lowest correlation, at the whole transcriptome level, between the control and frailty groups were TSIX, BEST1 and ADAMTSL4. Processes related to immune response and regulation of cellular metabolism and the metabolism of macromolecules emerged in the frailty group. The proposed strategy confirms and extends earlier findings regarding the pathogenesis of frailty and provides a paradigm on how the diversity in expression profiles of primary specimens could be leveraged for target discovery.
                ER  -

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Development, validation and clinical impact of a prediction model for 6-month mortality in older cancer patients: the GRADE

Eurydice Angeli, Kader Chouahnia, Florence Canoui-Poitrine, Boris Duchemann, Thomas Aparicio, Elena Paillaud, Laurent Zelek, Guilhem Bousquet, Frédéric Pamoukdjian,

https://doi.org/10.18632/aging.102876 pp 4230—4246

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Angeli E, Chouahnia K, Canoui-Poitrine F, Duchemann B, Aparicio T, Paillaud E, Zelek L, Bousquet G, Pamoukdjian F, . Development, validation and clinical impact of a prediction model for 6-month mortality in older cancer patients: the GRADE. Aging (Albany NY). 2020 Mar 1012:4230-4246. https://doi.org/10.18632/aging.102876

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                TY  - JOUR
                AU  - Angeli, Eurydice 
                AU  - Chouahnia, Kader 
                AU  - Canoui-Poitrine, Florence 
                AU  - Duchemann, Boris 
                AU  - Aparicio, Thomas 
                AU  - Paillaud, Elena 
                AU  - Zelek, Laurent 
                AU  - Bousquet, Guilhem 
                AU  - Pamoukdjian, Frédéric 
                TI  - Development, validation and clinical impact of a prediction model for 6-month mortality in older cancer patients: the GRADE
                JO  - 
                JA  - Aging (Albany NY)
                VL  - 12
                IS  - 5
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102876
                DO  - 10.18632/aging.102876
                SP  - 4230
                EP  - 4246
                PY  - 
                AB  - Background: To develop, validate, and assess the clinical impact of a clinical score to predict a 6-month mortality risk among older cancer patients.Results: The mean age was 81.2 &#xB1; 6.1 years (women: 54%, various cancers, metastatic cancer: 45%). The score, namely the GRADE, included two geriatric variables (unintentional weight loss, impaired mobility), two oncological variables (cancer site, cancer extension), and exclusively supportive care. Up to a 14% risk of early death, the decision curves suggest that cancer treatment should be instated.Conclusion: We have developed and validated a simple score, easy to implement in daily oncological practice, to predict early death among older cancer patients which could guide oncologists in their treatment decisions.Methods: 603 outpatients prospectively included in the Physical Frailty in Elderly Cancer patients cohort study. We created a multivariate prediction model by evaluating the strength of the individual components of the Geriatric Assessment regarding risk of death at 6 months. Each component was evaluated by univariate analysis and the significant variables (P &#x2264; 0.20) were carried on as covariates in the multivariate cox proportion hazard analysis. The beta coefficients from the model were used to build a point-based scoring system. Clinical impact was assessed using decision curves.
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Downregulation of lung miR-203a-3p expression by high-altitude hypoxia enhances VEGF/Notch signaling

Wei Cai, Sanli Liu, Ziquan Liu, Shike Hou, Qi Lv, Huanhuan Cui, Xue Wang, Yuxin Zhang, Haojun Fan, Hui Ding,

https://doi.org/10.18632/aging.102878 pp 4247—4267

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Cai W, Liu S, Liu Z, Hou S, Lv Q, Cui H, Wang X, Zhang Y, Fan H, Ding H, . Downregulation of lung miR-203a-3p expression by high-altitude hypoxia enhances VEGF/Notch signaling. Aging (Albany NY). 2020 Feb 2912:4247-4267. https://doi.org/10.18632/aging.102878

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                TY  - JOUR
                AU  - Cai, Wei 
                AU  - Liu, Sanli 
                AU  - Liu, Ziquan 
                AU  - Hou, Shike 
                AU  - Lv, Qi 
                AU  - Cui, Huanhuan 
                AU  - Wang, Xue 
                AU  - Zhang, Yuxin 
                AU  - Fan, Haojun 
                AU  - Ding, Hui 
                TI  - Downregulation of lung miR-203a-3p expression by high-altitude hypoxia enhances VEGF/Notch signaling
                JO  - 
                JA  - Aging (Albany NY)
                VL  - 12
                IS  - 5
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102878
                DO  - 10.18632/aging.102878
                SP  - 4247
                EP  - 4267
                PY  - 
                AB  - Hypoxia-related microRNAs (miRNAs) are involved in the pathogenesis of various diseases. Because potential variations in miRNA expression mediated by hypoxic lung injury at high altitude remain incompletely characterized, we used a rat model to investigate the biochemical and miRNA changes induced by high-altitude hypoxia. After 24, 48, or 72 h of hypoxic exposure, expression of VEGF/Notch pathway-related proteins were increased in rat lung tissues. Microarray screening of hypoxic lung samples revealed 57 differentially expressed miRNAs, 19 of which were related to the VEGF/Notch signaling pathway. We verified that the top downregulated miRNA (miR-203a-3p) suppresses VEGF-A translation through direct binding and also indirectly reduces Notch1, VEGFR2, and Hes1 levels, which restricts the angiogenic capacity of pulmonary microvascular endothelial cells in vitro. These findings may aid in the development of new therapeutic strategies for the prevention and treatment of hypoxic lung injury at high altitude.
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GAA compound heterozygous mutations associated with autophagic impairment cause cerebral infarction in Pompe disease

Xiaodong Jia, Libin Shao, Chengcheng Liu, Tuanzhi Chen, Ling Peng, Yinguang Cao, Chuanchen Zhang, Xiafeng Yang, Guifeng Zhang, Jianlu Gao, Guangyi Fan, Mingliang Gu, Hongli Du, Zhangyong Xia,

https://doi.org/10.18632/aging.102879 pp 4268—4282

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Jia X, Shao L, Liu C, Chen T, Peng L, Cao Y, Zhang C, Yang X, Zhang G, Gao J, Fan G, Gu M, Du H, et al, . GAA compound heterozygous mutations associated with autophagic impairment cause cerebral infarction in Pompe disease. Aging (Albany NY). 2020 Mar 312:4268-4282. https://doi.org/10.18632/aging.102879

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Provider: 
 TY - JOUR
 AU - Jia, Xiaodong 
 AU - Shao, Libin 
 AU - Liu, Chengcheng 
 AU - Chen, Tuanzhi 
 AU - Peng, Ling 
 AU - Cao, Yinguang 
 AU - Zhang, Chuanchen 
 AU - Yang, Xiafeng 
 AU - Zhang, Guifeng 
 AU - Gao, Jianlu 
 AU - Fan, Guangyi 
 AU - Gu, Mingliang 
 AU - Du, Hongli 
 AU - Xia, Zhangyong 
 TI - GAA compound heterozygous mutations associated with autophagic impairment cause cerebral infarction in Pompe disease
 JO - 
 JA - Aging (Albany NY)
 VL - 12
 IS - 5
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.102879
 DO - 10.18632/aging.102879
 SP - 4268
 EP - 4282
 PY - 
 ER -

Provider: 
 TY - JOUR
 AU - Jia, Xiaodong 
 AU - Shao, Libin 
 AU - Liu, Chengcheng 
 AU - Chen, Tuanzhi 
 AU - Peng, Ling 
 AU - Cao, Yinguang 
 AU - Zhang, Chuanchen 
 AU - Yang, Xiafeng 
 AU - Zhang, Guifeng 
 AU - Gao, Jianlu 
 AU - Fan, Guangyi 
 AU - Gu, Mingliang 
 AU - Du, Hongli 
 AU - Xia, Zhangyong 
 TI - GAA compound heterozygous mutations associated with autophagic impairment cause cerebral infarction in Pompe disease
 JO - 
 JA - Aging (Albany NY)
 VL - 12
 IS - 5
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.102879
 DO - 10.18632/aging.102879
 SP - 4268
 EP - 4282
 PY - 
 AB - Clinical manifestations of the late-onset adult Pompe disease (glycogen storage disease type II) are heterogeneous. To identify genetic defects of a special patient population with cerebrovascular involvement as the main symptom, we performed whole-genome sequencing (WGS) analysis on a consanguineous Chinese family of total eight members including two Pompe siblings both had cerebral infarction. Two novel compound heterozygous variants were found in GAA gene: c.2238G&gt;C in exon 16 and c.1388_1406del19 in exon 9 in the two patients. We verified the function of the two mutations in leading to defects in GAA protein expression and enzyme activity that are associated with autophagic impairment. We further performed a gut microbiome metagenomics analysis, found that the child&#x2019;s gut microbiome metagenome is very similar to his mother. Our finding enriches the gene mutation spectrum of Pompe disease, and identified the association of the two new mutations with autophagy impairment. Our data also indicates that gut microbiome could be shared within Pompe patient and cohabiting family members, and the abnormal microbiome may affect the blood biochemical index. Our study also highlights the importance of deep DNA sequencing in potential clinical applications.
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Secondary injury to distal regions after intracerebral hemorrhage influence neurological functional outcome

Kangping Song, Xiaojie Liu, Qiuyue Zheng, Lingling Zhang, Hongying Zhang, Hailong Yu, Yan Zhu, Li-An Huang, Yingzhu Chen,

https://doi.org/10.18632/aging.102880 pp 4283—4298

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Song K, Liu X, Zheng Q, Zhang L, Zhang H, Yu H, Zhu Y, Huang L, Chen Y, . Secondary injury to distal regions after intracerebral hemorrhage influence neurological functional outcome. Aging (Albany NY). 2020 Mar 812:4283-4298. https://doi.org/10.18632/aging.102880

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                TY  - JOUR
                AU  - Song, Kangping 
                AU  - Liu, Xiaojie 
                AU  - Zheng, Qiuyue 
                AU  - Zhang, Lingling 
                AU  - Zhang, Hongying 
                AU  - Yu, Hailong 
                AU  - Zhu, Yan 
                AU  - Huang, Li-An 
                AU  - Chen, Yingzhu 
                TI  - Secondary injury to distal regions after intracerebral hemorrhage influence neurological functional outcome
                JO  - 
                JA  - Aging (Albany NY)
                VL  - 12
                IS  - 5
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102880
                DO  - 10.18632/aging.102880
                SP  - 4283
                EP  - 4298
                PY  - 
                AB  - Although many studies have focused on functional impairment after intracerebral hemorrhage, little is known about the relationship between secondary injuries to distal regions and neurological function. Our study aimed to evaluate the secondary injuries after intracerebral hemorrhage and explore their relationship to neurological functional outcome. Twenty-one patients with hemorrhages in supratentorial, deep locations and 10 healthy subjects were recruited. Longitudinal examinations of diffusion tensor imaging, hydrogen proton magnetic resonance spectroscopy imaging and neuropsychological assessment were performed after weeks 1 and 12 to elucidate the relationship between magnetic resonance imaging parameters and neurologic outcomes. By week 12, motor function had significantly improved, but cognitive function had deteriorated compared to week 1. Fractional anisotropy values for the ipsilateral cerebral peduncle correlated with motor function at week 1. No significant correlation between fractional anisotropy for the ipsilateral cerebral peduncle and the Fugl-Meyer Motor Scale was found at week 12. Fractional anisotropy values for the ipsilateral hippocampus were related to the Montreal Cognitive Assessment and Mini-Mental State Examination at weeks 1 and 12. Deep supratentorial hemorrhage may result in injury to distal regions, which correlate with impaired motor and cognitive function.
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Transient ischemia-reperfusion induces cortical hyperactivity and AMPAR trafficking in the somatosensory cortex

Yuanyuan Li, Ran Ding, Feifei Wang, Cuiping Guo, Aili Liu, Liangpeng Wei, Shiyang Yuan, Feng Chen, Shaowei Hou, Zengguang Ma, Yan Zhang, Robert H. Cudmore, Xiaochuan Wang, Hui Shen,

https://doi.org/10.18632/aging.102881 pp 4299—4321

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Li Y, Ding R, Wang F, Guo C, Liu A, Wei L, Yuan S, Chen F, Hou S, Ma Z, Zhang Y, Cudmore RH, Wang X, et al, . Transient ischemia-reperfusion induces cortical hyperactivity and AMPAR trafficking in the somatosensory cortex. Aging (Albany NY). 2020 Mar 912:4299-4321. https://doi.org/10.18632/aging.102881

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                TY  - JOUR
                AU  - Li, Yuanyuan 
                AU  - Ding, Ran 
                AU  - Wang, Feifei 
                AU  - Guo, Cuiping 
                AU  - Liu, Aili 
                AU  - Wei, Liangpeng 
                AU  - Yuan, Shiyang 
                AU  - Chen, Feng 
                AU  - Hou, Shaowei 
                AU  - Ma, Zengguang 
                AU  - Zhang, Yan 
                AU  - Cudmore, Robert H. 
                AU  - Wang, Xiaochuan 
                AU  - Shen, Hui 
                TI  - Transient ischemia-reperfusion induces cortical hyperactivity and AMPAR trafficking in the somatosensory cortex
                JO  - 
                JA  - Aging (Albany NY)
                VL  - 12
                IS  - 5
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102881
                DO  - 10.18632/aging.102881
                SP  - 4299
                EP  - 4321
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Li, Yuanyuan 
                AU  - Ding, Ran 
                AU  - Wang, Feifei 
                AU  - Guo, Cuiping 
                AU  - Liu, Aili 
                AU  - Wei, Liangpeng 
                AU  - Yuan, Shiyang 
                AU  - Chen, Feng 
                AU  - Hou, Shaowei 
                AU  - Ma, Zengguang 
                AU  - Zhang, Yan 
                AU  - Cudmore, Robert H. 
                AU  - Wang, Xiaochuan 
                AU  - Shen, Hui 
                TI  - Transient ischemia-reperfusion induces cortical hyperactivity and AMPAR trafficking in the somatosensory cortex
                JO  - 
                JA  - Aging (Albany NY)
                VL  - 12
                IS  - 5
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102881
                DO  - 10.18632/aging.102881
                SP  - 4299
                EP  - 4321
                PY  - 
                AB  - Brain ischemia results from cardiac arrest, stroke or head trauma. The structural basis of rescuing the synaptic impairment and cortical dysfunctions induced in the stage of ischemic-reperfusion can occur if therapeutic interventions are applied in time, but the functional basis for this resilience remains elusive. Here, we explore the changes in cortical activity and a-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptor (AMPAR) GluA1 subunit in spine (sGluA1) after transient ischemia-reperfusion in vivo for 28 days. Using in vivo two-photon microscopy in the mouse somatosensory cortex, we found that the average frequency of Ca2+ transients in the spine (there was an unusual synchrony) was higher after 15 min of ischemia-reperfusion. In addition, the transient ischemia-reperfusion caused a reflective enhancement of AMPARs, which eventually restored to normal. The cortical hyperactivity (Ca2+ transients) and the increase in AMPARs were successfully blocked by an NMDA receptor antagonist. Thus, the increase of AMPARs, cortical hyperactivity and the unusual synchrony might be the reason for reperfusion injury after short-term transient ischemia.
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Sirt1 antisense long non-coding RNA attenuates pulmonary fibrosis through sirt1-mediated epithelial-mesenchymal transition

Weibin Qian, Xinrui Cai, Qiuhai Qian,

https://doi.org/10.18632/aging.102882 pp 4322—4336

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Qian W, Cai X, Qian Q, . Sirt1 antisense long non-coding RNA attenuates pulmonary fibrosis through sirt1-mediated epithelial-mesenchymal transition. Aging (Albany NY). 2020 Mar 612:4322-4336. https://doi.org/10.18632/aging.102882

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                TY  - JOUR
                AU  - Qian, Weibin 
                AU  - Cai, Xinrui 
                AU  - Qian, Qiuhai 
                TI  - Sirt1 antisense long non-coding RNA attenuates pulmonary fibrosis through sirt1-mediated epithelial-mesenchymal transition
                JO  - 
                JA  - Aging (Albany NY)
                VL  - 12
                IS  - 5
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102882
                DO  - 10.18632/aging.102882
                SP  - 4322
                EP  - 4336
                PY  - 
                AB  - Long noncoding RNAs sirt1 antisense (sirt1 AS) was reported to play crucial roles in the progression of organ fibrosis. However, the roles of sirt1 AS in idiopathic pulmonary fibrosis (IPF) are still unknown. In addition, we have previously demonstrated that astragaloside IV (ASV), a bioactive saponin extract of the Astragalus root, significantly alleviates IPF by inhibiting transforming growth factor &#x3B2;1 (TGF-&#x3B2;1) induced epithelial-mesenchymal transition (EMT). Further investigations into the influence of ASV on lncRNAs expression will be helpful to delineate the complex regulatory networks underlying the biological function of ASV. Here, we found sirt1 AS expression was significantly decreased in BLM-induced pulmonary fibrosis. We further found that sirt1 AS effectively inhibited TGF-&#x3B2;1-meidated EMT in vitro and alleviated the progression of IPF in vivo. Mechanistically, sirt1 AS was validate to enhance the stability of sirt1 and increased sirt1 expression, thereby to inhibit EMT in IPF. Furthermore, we demonstrated that ASV treatment increased sirt1 AS expression and silencing of sirt1 AS impaired anti-fibrosis effects of ASV on IPF. Collectively, sirt1 AS was critical for ASV-mediated inhibition of IPF progression and targeting of sirt1 AS by ASV could be a potential therapeutic approach for IPF.
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Surgical blood loss during holmium laser enucleation of the prostate (HoLEP) is not affected by short-term pretreatment with dutasteride: a double-blind placebo-controlled trial on prostate vascularity

Gian Maria Busetto, Francesco Del Giudice, Martina Maggi, Gabriele Antonini, Daniele D’Agostino, Daniele Romagnoli, Alessandro Del Rosso, Marco Giampaoli, Paolo Corsi, Katie Palmer, Matteo Ferro, Giuseppe Lucarelli, Daniela Terracciano, Ottavio De Cobelli, Alessandro Sciarra, Ettore De Berardinis, Angelo Porreca,

https://doi.org/10.18632/aging.102883 pp 4337—4347

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Busetto GM, Del Giudice F, Maggi M, Antonini G, D’Agostino D, Romagnoli D, Del Rosso A, Giampaoli M, Corsi P, Palmer K, Ferro M, Lucarelli G, Terracciano D, et al, . Surgical blood loss during holmium laser enucleation of the prostate (HoLEP) is not affected by short-term pretreatment with dutasteride: a double-blind placebo-controlled trial on prostate vascularity. Aging (Albany NY). 2020 Mar 1112:4337-4347. https://doi.org/10.18632/aging.102883

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                TY  - JOUR
                AU  - Busetto, Gian Maria 
                AU  - Del Giudice, Francesco 
                AU  - Maggi, Martina 
                AU  - Antonini, Gabriele 
                AU  - D’Agostino, Daniele 
                AU  - Romagnoli, Daniele 
                AU  - Del Rosso, Alessandro 
                AU  - Giampaoli, Marco 
                AU  - Corsi, Paolo 
                AU  - Palmer, Katie 
                AU  - Ferro, Matteo 
                AU  - Lucarelli, Giuseppe 
                AU  - Terracciano, Daniela 
                AU  - De Cobelli, Ottavio 
                AU  - Sciarra, Alessandro 
                AU  - De Berardinis, Ettore 
                AU  - Porreca, Angelo 
                TI  - Surgical blood loss during holmium laser enucleation of the prostate (HoLEP) is not affected by short-term pretreatment with dutasteride: a double-blind placebo-controlled trial on prostate vascularity
                JO  - 
                JA  - Aging (Albany NY)
                VL  - 12
                IS  - 5
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102883
                DO  - 10.18632/aging.102883
                SP  - 4337
                EP  - 4347
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Busetto, Gian Maria 
                AU  - Del Giudice, Francesco 
                AU  - Maggi, Martina 
                AU  - Antonini, Gabriele 
                AU  - D’Agostino, Daniele 
                AU  - Romagnoli, Daniele 
                AU  - Del Rosso, Alessandro 
                AU  - Giampaoli, Marco 
                AU  - Corsi, Paolo 
                AU  - Palmer, Katie 
                AU  - Ferro, Matteo 
                AU  - Lucarelli, Giuseppe 
                AU  - Terracciano, Daniela 
                AU  - De Cobelli, Ottavio 
                AU  - Sciarra, Alessandro 
                AU  - De Berardinis, Ettore 
                AU  - Porreca, Angelo 
                TI  - Surgical blood loss during holmium laser enucleation of the prostate (HoLEP) is not affected by short-term pretreatment with dutasteride: a double-blind placebo-controlled trial on prostate vascularity
                JO  - 
                JA  - Aging (Albany NY)
                VL  - 12
                IS  - 5
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102883
                DO  - 10.18632/aging.102883
                SP  - 4337
                EP  - 4347
                PY  - 
                AB  - Five &#x3B1;-reductase inhibitors (5ARIs) are able to reduce prostate volume and are a useful treatment for reducing perioperative bleeding during prostate surgery. Holmium laser enucleation of the prostate (HoLEP) is an effective surgical technique for the definitive cure of benign prostate enlargement.We investigated whether pretreatment with dutasteride before HoLEP could reduce intraoperative bleeding. A total of 402 patients were included in this double-blind placebo-controlled trial to receive daily 0.5 mg of dutasteride or placebo over 8 weeks before HoLEP. Vascular endothelial growth factor (VEGF) and microvascular density (MVD) were evaluated. Analysis was also stratified according to prostate volume (&lt;70 mL vs &#x2265;70 mL).Hemoglobin and hematocrit values before and after surgery were not statistically different between the two groups. MVD and VEGF index in smaller prostates were 23.35&#xB1;1.96 and 4.06&#xB1;0.76 in the treatment group and 19.04&#xB1;0.96 and 2.55&#xB1;0.55 in placebo (p&lt;0.05); in patients with larger prostates MVD and VEGF were 26.83&#xB1;2.812 and 8.54&#xB1;1.18 in the treatment group and 20.76&#xB1;0.79 and 3.21&#xB1;0.54 in placebo (p&lt;0.05).Vascularization of the prostate was affected by 5ARIs therapy. HoLEP is less burdened in perioperative bleeding and for this reason we did not find any difference in hemoglobin/hematocrit values pre- and post- surgery.
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Brain hemodynamic changes in amnestic mild cognitive impairment measured by pulsed arterial spin labeling

Xiangbin Wang, Ding Ding, Qianhua Zhao, Xiaoniu Liang, Ling Peng, Xiaohu Zhao, Qian Xi, Zhang Min, Wei Wang, Xiaowen Xu, Qihao Guo, Pei-Jun Wang,

https://doi.org/10.18632/aging.102888 pp 4348—4356

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Wang X, Ding D, Zhao Q, Liang X, Peng L, Zhao X, Xi Q, Min Z, Wang W, Xu X, Guo Q, Wang P, . Brain hemodynamic changes in amnestic mild cognitive impairment measured by pulsed arterial spin labeling. Aging (Albany NY). 2020 Mar 1212:4348-4356. https://doi.org/10.18632/aging.102888

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                TY  - JOUR
                AU  - Wang, Xiangbin 
                AU  - Ding, Ding 
                AU  - Zhao, Qianhua 
                AU  - Liang, Xiaoniu 
                AU  - Peng, Ling 
                AU  - Zhao, Xiaohu 
                AU  - Xi, Qian 
                AU  - Min, Zhang 
                AU  - Wang, Wei 
                AU  - Xu, Xiaowen 
                AU  - Guo, Qihao 
                AU  - Wang, Pei-Jun 
                TI  - Brain hemodynamic changes in amnestic mild cognitive impairment measured by pulsed arterial spin labeling
                JO  - 
                JA  - Aging (Albany NY)
                VL  - 12
                IS  - 5
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102888
                DO  - 10.18632/aging.102888
                SP  - 4348
                EP  - 4356
                PY  - 
                AB  - We used pulsed arterial spin labeling (PASL) to investigate differences in cerebral blood flow (CBF) between 26 patients with amnestic mild cognitive impairment (aMCI) and 27 controls with normal cognition (NC). Hypoperfusion was observed in the right temporal pole of the middle temporal gyrus and the right inferior temporal gyrus in the aMCI compared with NC group. Interestingly, hyperperfusion was observed in the left temporal pole of the middle temporal gyrus, left superior temporal gyrus, bilateral precuneus, postcentral gyrus, right inferior parietal lobule, and right angular gyrus in the aMCI group, which likely resulted from a compensatory mechanism to maintain advanced neural activities. We found that mean CBF in the right inferior temporal gyrus, precuneus, and postcentral gyrus was positively correlated with cognitive ability in the aMCI but not NC group. Collectively, our data indicate that PASL is a useful noninvasive technique for monitoring changes in CBF and predicting cognitive decline in aMCI.
                ER  -

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Elevated systemic inflammatory responses, factors associated with physical and mental quality of life, and prognosis of hepatocellular carcinoma

Yang Deng, Jian Zhu, Ziyi Liu, Maosheng Huang, David W. Chang, Jian Gu,

https://doi.org/10.18632/aging.102889 pp 4357—4370

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Deng Y, Zhu J, Liu Z, Huang M, Chang DW, Gu J, . Elevated systemic inflammatory responses, factors associated with physical and mental quality of life, and prognosis of hepatocellular carcinoma. Aging (Albany NY). 2020 Mar 712:4357-4370. https://doi.org/10.18632/aging.102889

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                TY  - JOUR
                AU  - Deng, Yang 
                AU  - Zhu, Jian 
                AU  - Liu, Ziyi 
                AU  - Huang, Maosheng 
                AU  - Chang, David W. 
                AU  - Gu, Jian 
                TI  - Elevated systemic inflammatory responses, factors associated with physical and mental quality of life, and prognosis of hepatocellular carcinoma
                JO  - 
                JA  - Aging (Albany NY)
                VL  - 12
                IS  - 5
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102889
                DO  - 10.18632/aging.102889
                SP  - 4357
                EP  - 4370
                PY  - 
                AB  - Impaired quality of life (QOL) is common in hepatocellular carcinoma (HCC) patients. In this study, we used a large hospital-based multiethnic HCC patient cohort to systematically identify factors associated with QOL and investigate the prognostic value of QOL.The Short Form-12 questionnaire was used to assess QOL. The Physical Component Summary (PCS) and Mental Component Summary (MCS) scores were categorized into three groups (low, medium, and high) and ordered logistic regression analysis was used to analyze the association of PCS and MCS scores with patient characteristics. The association of PCS and MCS scores with mortality was assessed by Cox regression analysis.Notably, a panel of elevated systemic inflammatory response markers was associated with poor QOL. Other significant factors associated with QOL included age, liver function, sex, smoking, HCC etiology, and major clinical features. Patients with low (hazard ratio [95% CI], 1.72 [1.36-2.17]) and medium (1.52 [1.23-1.89]) PCS scores exhibited higher risks of death compared to patients with high PCS score. The association of MCS with the risk of death was not significant. These observations were consistent across all the different ethnicities.The identified factors associated with QOL may help clinicians formulate interventions to improve QOL and outcomes in HCC patients.
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Vitamin D levels are prognostic factors for connective tissue disease associated interstitial lung disease (CTD-ILD)

Yujuan Gao, Qi Zhao, Xiaohua Qiu, Yi Zhuang, Min Yu, Jinghong Dai, Hourong Cai, Xin Yan,

https://doi.org/10.18632/aging.102890 pp 4371—4378

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Gao Y, Zhao Q, Qiu X, Zhuang Y, Yu M, Dai J, Cai H, Yan X, . Vitamin D levels are prognostic factors for connective tissue disease associated interstitial lung disease (CTD-ILD). Aging (Albany NY). 2020 Mar 1212:4371-4378. https://doi.org/10.18632/aging.102890

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                TY  - JOUR
                AU  - Gao, Yujuan 
                AU  - Zhao, Qi 
                AU  - Qiu, Xiaohua 
                AU  - Zhuang, Yi 
                AU  - Yu, Min 
                AU  - Dai, Jinghong 
                AU  - Cai, Hourong 
                AU  - Yan, Xin 
                TI  - Vitamin D levels are prognostic factors for connective tissue disease associated interstitial lung disease (CTD-ILD)
                JO  - 
                JA  - Aging (Albany NY)
                VL  - 12
                IS  - 5
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102890
                DO  - 10.18632/aging.102890
                SP  - 4371
                EP  - 4378
                PY  - 
                AB  - Objective: Vitamin D deficiency was associated with CTD-ILD and reduced lung function. We sought to confirm that lower Vitamin D level would be related to shorter survival times.Results: The CTD-ILD patients had lower Vitamin D level(P&lt;0.05). Among patients with CTD-ILD who have improved lung function after treatment, elevation of Vitamin D level was positively associated with &#x394;FVC (%), &#x394;FEV1(%) and &#x394;DLCO-SB (%). The median survival time of patients with high serum 25(OH)D level was significantly longer than the patients with low 25(OH)D level group (16.5 months vs14.0 months, P=0.007). The Vitamin D was identified as an independent prognostic factor with a hazard ratio of 0.869 (95% CI 0.772-0.977, P =0.019).Conclusions: Vitamin D level was lower in patients with CTD-ILD and associated with poor prognosis. Continuous levels of Vitamin D may be an important serum biomarker of prognosis.Methods: 85 CTD-ILD patients, 71 Idiopathic pulmonary fibrosis (IPF) patients and 78 healthy control patients were included in the study. In the subgroup analysis, the CTD-ILD patients were divided into anti-MDA5 antibody-positive group and anti-MDA5 antibody-negative group according to the serum autoantibodies results. The survival analysis evaluated effect of Vitamin D level on disease prognosis.
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Genetic variants in RET, ARHGEF3 and CTNNAL1, and relevant interaction networks, contribute to the risk of Hirschsprung disease

Yang Wang, Qian Jiang, Hao Cai, Ze Xu, Wenjie Wu, Beilin Gu, Long Li, Wei Cai,

https://doi.org/10.18632/aging.102891 pp 4379—4393

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Wang Y, Jiang Q, Cai H, Xu Z, Wu W, Gu B, Li L, Cai W, . Genetic variants in RET, ARHGEF3 and CTNNAL1, and relevant interaction networks, contribute to the risk of Hirschsprung disease. Aging (Albany NY). 2020 Mar 612:4379-4393. https://doi.org/10.18632/aging.102891

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 TY - JOUR
 AU - Wang, Yang 
 AU - Jiang, Qian 
 AU - Cai, Hao 
 AU - Xu, Ze 
 AU - Wu, Wenjie 
 AU - Gu, Beilin 
 AU - Li, Long 
 AU - Cai, Wei 
 TI - Genetic variants in RET, ARHGEF3 and CTNNAL1, and relevant interaction networks, contribute to the risk of Hirschsprung disease
 JO - 
 JA - Aging (Albany NY)
 VL - 12
 IS - 5
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.102891
 DO - 10.18632/aging.102891
 SP - 4379
 EP - 4393
 PY - 
 AB - Hirschsprung disease (HSCR), the most common enteric neuropathy, stands as a model for complex genetic disorders. It has recently been demonstrated that both ARHGEF3 and CTNNAL1 map to the RET-dependent HSCR susceptibility loci. We therefore sought to explore whether genetic variants within RET, ARHGEF3 and CTNNAL1, and their genetic interaction networks are associated with HSCR. Taking advantage of a strategy that combined the MassArray system and gene-gene interaction analysis with case-control study, we interrogated 38 polymorphisms within RET, ARHGEF3 and CTNNAL1 in 1015 subjects (502 HSCR cases and 513 controls) of Han Chinese origin. There were statistically significant associations between 20 genetic variants in these three genes and HSCR. Haplotype analysis also revealed some significant global P values, i.e. RET_ rs2435357-rs752978-rs74400468-rs2435353-rs2075913-rs17028-rs2435355 (P = 3.79&#xD7;10-58). Using the MDR and GeneMANIA platforms, we found strong genetic interactions among RET, ARHGEF3, and CTNNAL1 and our previously studied GAL, GAP43, NRSN1, PTCH1, GABRG2 and RELN genes. These results offer the first indication that genetic markers of RET, ARHGEF3 and CTNNAL1 and relevant genetic interaction networks confer the altered risk to HSCR in the Han Chinese population.
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DNA methylation clocks as a predictor for ageing and age estimation in naked mole-rats, Heterocephalus glaber

Robert Lowe, Amy F. Danson, Vardhman K. Rakyan, Selin Yildizoglu, Frédéric Saldmann, Melanie Viltard, Gérard Friedlander, Chris G. Faulkes,

https://doi.org/10.18632/aging.102892 pp 4394—4406

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Lowe R, Danson AF, Rakyan VK, Yildizoglu S, Saldmann F, Viltard M, Friedlander G, Faulkes CG, . DNA methylation clocks as a predictor for ageing and age estimation in naked mole-rats, Heterocephalus glaber. Aging (Albany NY). 2020 Mar 312:4394-4406. https://doi.org/10.18632/aging.102892

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Provider: 
 TY - JOUR
 AU - Lowe, Robert 
 AU - Danson, Amy F. 
 AU - Rakyan, Vardhman K. 
 AU - Yildizoglu, Selin 
 AU - Saldmann, Frédéric 
 AU - Viltard, Melanie 
 AU - Friedlander, Gérard 
 AU - Faulkes, Chris G. 
 TI - DNA methylation clocks as a predictor for ageing and age estimation in naked mole-rats, Heterocephalus glaber
 JO - 
 JA - Aging (Albany NY)
 VL - 12
 IS - 5
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.102892
 DO - 10.18632/aging.102892
 SP - 4394
 EP - 4406
 PY - 
 AB - The naked mole-rat, Heterocephalus glaber (NMR), the longest-lived rodent, is of significance and interest in the study of biomarkers for ageing. Recent breakthroughs in this field have revealed &#x2018;epigenetic clocks&#x2019; that are based on the temporal accumulation of DNA methylation at specific genomic sites. Here, we validate the hypothesis of an epigenetic clock in NMRs based on changes in methylation of targeted CpG sites. We initially analysed 51 CpGs in NMR livers spanning an age range of 39-1,144 weeks and found 23 to be significantly associated with age (p&lt;0.05). We then built a predictor of age using these sites. To test the accuracy of this model, we analysed an additional set of liver samples, and were successfully able to predict their age with a root mean squared error of 166 weeks. We also profiled skin samples with the same age range, finding a striking correlation between their predicted age versus their actual age (R=0.93), but which was lower when compared to the liver, suggesting that skin ages slower than the liver in NMRs. Our model will enable the prediction of age in wild-caught and captive NMRs of unknown age, and will be invaluable for further mechanistic studies of mammalian ageing.
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Telomere shortening reflecting physical aging is associated with cognitive decline and dementia conversion in mild cognitive impairment due to Alzheimer’s disease

Seong-Ho Koh, Seong Hye Choi, Jee Hyang Jeong, Jae-Won Jang, Kyung Won Park, Eun-Joo Kim, Hee Jin Kim, Jin Yong Hong, Soo Jin Yoon, Bora Yoon, Ju-Hee Kang, Jong-Min Lee, Hyun-Hee Park, Jungsoon Ha, Young Ju Suh, Suyeon Kang,

https://doi.org/10.18632/aging.102893 pp 4407—4423

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Koh S, Choi SH, Jeong JH, Jang J, Park KW, Kim E, Kim HJ, Hong JY, Yoon SJ, Yoon B, Kang J, Lee J, Park H, et al, . Telomere shortening reflecting physical aging is associated with cognitive decline and dementia conversion in mild cognitive impairment due to Alzheimer’s disease. Aging (Albany NY). 2020 Mar 312:4407-4423. https://doi.org/10.18632/aging.102893

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                TY  - JOUR
                AU  - Koh, Seong-Ho 
                AU  - Choi, Seong Hye 
                AU  - Jeong, Jee Hyang 
                AU  - Jang, Jae-Won 
                AU  - Park, Kyung Won 
                AU  - Kim, Eun-Joo 
                AU  - Kim, Hee Jin 
                AU  - Hong, Jin Yong 
                AU  - Yoon, Soo Jin 
                AU  - Yoon, Bora 
                AU  - Kang, Ju-Hee 
                AU  - Lee, Jong-Min 
                AU  - Park, Hyun-Hee 
                AU  - Ha, Jungsoon 
                AU  - Suh, Young Ju 
                AU  - Kang, Suyeon 
                TI  - Telomere shortening reflecting physical aging is associated with cognitive decline and dementia conversion in mild cognitive impairment due to Alzheimer’s disease
                JO  - 
                JA  - Aging (Albany NY)
                VL  - 12
                IS  - 5
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102893
                DO  - 10.18632/aging.102893
                SP  - 4407
                EP  - 4423
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Koh, Seong-Ho 
                AU  - Choi, Seong Hye 
                AU  - Jeong, Jee Hyang 
                AU  - Jang, Jae-Won 
                AU  - Park, Kyung Won 
                AU  - Kim, Eun-Joo 
                AU  - Kim, Hee Jin 
                AU  - Hong, Jin Yong 
                AU  - Yoon, Soo Jin 
                AU  - Yoon, Bora 
                AU  - Kang, Ju-Hee 
                AU  - Lee, Jong-Min 
                AU  - Park, Hyun-Hee 
                AU  - Ha, Jungsoon 
                AU  - Suh, Young Ju 
                AU  - Kang, Suyeon 
                TI  - Telomere shortening reflecting physical aging is associated with cognitive decline and dementia conversion in mild cognitive impairment due to Alzheimer’s disease
                JO  - 
                JA  - Aging (Albany NY)
                VL  - 12
                IS  - 5
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102893
                DO  - 10.18632/aging.102893
                SP  - 4407
                EP  - 4423
                PY  - 
                AB  - We investigated whether telomere length (TL) reflecting physical rather than chronological aging is associated with disease progression in the different cognitive stages of Alzheimer&#x2019;s disease (AD). Study participants included 89 subjects with amyloid pathology (A+), determined through amyloid PET or cerebrospinal fluid analysis, including 26 cognitively unimpaired (CU A+) individuals, 28 subjects with mild cognitive impairment (MCI A+), and 35 subjects with AD dementia (ADD A+). As controls, 104 CU A- individuals were selected. The participants were evaluated annually over two years from baseline. Compared to the highest TL quartile group of MCI A+ participants, the lowest TL quartile group yielded 2-year differences of -9.438 (95% confidence interval [CI] = -14.567 ~ -4.309), -26.708 (-41.576 ~ -11.839), 3.198 (1.323 ~ 5.056), and 2.549 (0.527 ~ 4.571) on the Mini-Mental State Examination, Consortium to Establish a Registry for AD, Clinical Dementia Rating-Sum of Boxes, and Blessed Dementia Scale-Activities of Daily Living, respectively. With this group, the lowest TL quartile group had a significantly greater probability of progressing to ADD than the highest TL quartile group (hazard ratio = 13.16, 95% CI = 1.11 ~ 156.61). Telomere shortening may be associated with rapid cognitive decline and conversion to dementia in MCI A+.
                ER  -

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Discovery and validation of the prognostic value of the lncRNAs encoding snoRNAs in patients with clear cell renal cell carcinoma

Wuping Yang, Kenan Zhang, Lei Li, Kaifang Ma, Baoan Hong, Yanqing Gong, Kan Gong,

https://doi.org/10.18632/aging.102894 pp 4424—4444

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Yang W, Zhang K, Li L, Ma K, Hong B, Gong Y, Gong K, . Discovery and validation of the prognostic value of the lncRNAs encoding snoRNAs in patients with clear cell renal cell carcinoma. Aging (Albany NY). 2020 Mar 312:4424-4444. https://doi.org/10.18632/aging.102894

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                TY  - JOUR
                AU  - Yang, Wuping 
                AU  - Zhang, Kenan 
                AU  - Li, Lei 
                AU  - Ma, Kaifang 
                AU  - Hong, Baoan 
                AU  - Gong, Yanqing 
                AU  - Gong, Kan 
                TI  - Discovery and validation of the prognostic value of the lncRNAs encoding snoRNAs in patients with clear cell renal cell carcinoma
                JO  - 
                JA  - Aging (Albany NY)
                VL  - 12
                IS  - 5
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102894
                DO  - 10.18632/aging.102894
                SP  - 4424
                EP  - 4444
                PY  - 
                AB  - Some lncRNAs can encode small nucleolar RNAs (snoRNAs), called small nucleolar RNA host genes (SNHGs), which have exerted certain predictive values for the prognosis of some cancer patients. In this study, using RNA-seq and survival data in TCGA-KIRC, we examined the expression profile of 20 SNHGs and explored their prognostic values in ccRCC. Results showed that SNHG1, GAS5, SNHG3-8, SNHG11, SNHG12, SNHG15-17, SNHG20, SNHG22 and SNHG25 were significantly upregulated in ccRCC tissues compared with adjacent normal tissues. After adjustment for confounding factors, the multivariate analysis confirmed that increased SNHG3 expression was independently associated with shorter OS, while increased SNHG15 expression was an independent predictor of shorter RFS. Using the methylation data, the methylation status of 2 CpG sites (cg07807470 and cg15161854) and 2 CpG sites (cg00953154 and cg16459265) were negatively correlated with SNHG3 and SNHG15 expression, respectively. Moreover, low methylation levels of the 4 CpG sites were significantly associated with shorter OS. Furthermore, we validated the expression patterns, methylation status and prognostic value of SNHG3 and SNHG15 using clinical ccRCC samples. Taken together, SNHG3 and SNHG15 might be valuable prognostic markers in ccRCC, and DNA hypomethylation might play an important role in elevated SNHG3 and SNHG15 transcription in ccRCC.
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Distribution patterns of microsatellites and development of its marker in different genomic regions of forest musk deer genome based on high throughput sequencing

Wen-Hua Qi, Ting Lu, Cheng-Li Zheng, Xue-Mei Jiang, Hang Jie, Xiu-Yue Zhang, Bi-Song Yue, Gui-Jun Zhao,

https://doi.org/10.18632/aging.102895 pp 4445—4462

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Qi W, Lu T, Zheng C, Jiang X, Jie H, Zhang X, Yue B, Zhao G, . Distribution patterns of microsatellites and development of its marker in different genomic regions of forest musk deer genome based on high throughput sequencing. Aging (Albany NY). 2020 Mar 1012:4445-4462. https://doi.org/10.18632/aging.102895

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                TY  - JOUR
                AU  - Qi, Wen-Hua 
                AU  - Lu, Ting 
                AU  - Zheng, Cheng-Li 
                AU  - Jiang, Xue-Mei 
                AU  - Jie, Hang 
                AU  - Zhang, Xiu-Yue 
                AU  - Yue, Bi-Song 
                AU  - Zhao, Gui-Jun 
                TI  - Distribution patterns of microsatellites and development of its marker in different genomic regions of forest musk deer genome based on high throughput sequencing
                JO  - 
                JA  - Aging (Albany NY)
                VL  - 12
                IS  - 5
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102895
                DO  - 10.18632/aging.102895
                SP  - 4445
                EP  - 4462
                PY  - 
                AB  - Forest musk deer (Moschus berezovskii, FMD) is an endangered artiodactyl species, male FMD produce musk. We have sequenced the whole genome of FMD, completed the genomic assembly and annotation, and performed bioinformatic analyses. Our results showed that microsatellites (SSRs) displayed nonrandomly distribution in genomic regions, and SSR abundances were much higher in the intronic and intergenic regions compared to other genomic regions. Tri- and hexanucleotide perfect (P) SSRs predominated in coding regions (CDSs), whereas, tetra- and pentanucleotide P-SSRs were less abundant. Trifold P-SSRs had more GC-contents in the 5&#x2032;-untranslated regions (5&apos;UTRs) and CDSs than other genomic regions, whereas mononucleotide P-SSRs had the least GC-contents. The repeat copy numbers (RCN) of the same mono- to hexanucleotide P-SSRs had different distributions in different genomic regions. The RCN of trinucleotide P-SSRs had increased significantly in the CDSs compared to the transposable elements (TEs), intronic and intergenic regions. The analysis of coefficient of variability (CV) of P-SSRs showed that the RCN of mononucleotide P-SSRs had relative higher variation in different genomic regions, followed by the CV pattern of RCN: dinucleotide P-SSRs &gt; trinucleotide P-SSRs &gt; tetranucleotide P-SSRs &gt; pentanucleotide P-SSRs &gt; hexanucleotide P-SSRs. The CV variations of RCN of the same mono- to hexanucleotide P-SSRs were relative higher in the intron and intergenic regions, followed by that in the TEs, and the relative lower was in the 5&apos;UTR, CDSs and 3&apos;UTRs. 58 novel polymorphic SSR loci were detected based on genotyping DNA from 36 captive FMD and 22 SSR markers finally showed polymorphism, stability, and repetition.
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Role of eotaxin-1/CCL11 in sepsis-induced myocardial injury in elderly patients

Ying Li, Youguang Zhao, Chenming Qiu, Yuanrui Yang, Guihua Liao, Xi Wu, Xiaowan Zhang, Qian Zhang, Ru Zhang, Zhang Wang,

https://doi.org/10.18632/aging.102896 pp 4463—4473

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Li Y, Zhao Y, Qiu C, Yang Y, Liao G, Wu X, Zhang X, Zhang Q, Zhang R, Wang Z, . Role of eotaxin-1/CCL11 in sepsis-induced myocardial injury in elderly patients. Aging (Albany NY). 2020 Mar 912:4463-4473. https://doi.org/10.18632/aging.102896

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                TY  - JOUR
                AU  - Li, Ying 
                AU  - Zhao, Youguang 
                AU  - Qiu, Chenming 
                AU  - Yang, Yuanrui 
                AU  - Liao, Guihua 
                AU  - Wu, Xi 
                AU  - Zhang, Xiaowan 
                AU  - Zhang, Qian 
                AU  - Zhang, Ru 
                AU  - Wang, Zhang 
                TI  - Role of eotaxin-1/CCL11 in sepsis-induced myocardial injury in elderly patients
                JO  - 
                JA  - Aging (Albany NY)
                VL  - 12
                IS  - 5
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102896
                DO  - 10.18632/aging.102896
                SP  - 4463
                EP  - 4473
                PY  - 
                AB  - Myocardial injury is a serious complication of sepsis. The present study aimed to identify potential biomarkers of sepsis-induced myocardial injury. Differentially expressed genes (DEGs) in patients and mice with sepsis-induced myocardial injury were identified via bioinformatic analysis. The identified DEG was tested in elderly patients with sepsis-induced myocardial injury. We identified 19 co-expressed DEGs. The most significant DEG was eotaxin-1/CCL11. We enrolled 25 controls without infections and 28 patients with sepsis-induced myocardial injury. Six of patients died within 30 days. Circulating eotaxin-1/CCL11 levels were significantly higher in patients with sepsis-induced myocardial injury than controls and were higher in non-survivors than survivors (both P &lt; 0.01). Eotaxin-1/CCL11 was positively correlated with troponin I (r=0.48, P=0.01), B-type natriuretic peptide (BNP, r=0.44, P=0.02), and white blood cell (WBC) count (r=0.41, P=0.03). For the prediction of 30-day mortality, eotaxin-1/CCL11 had the greatest discriminatory ability (AUC 0.97) compared with troponin I (AUC 0.89), BNP (AUC 0.80), and WBC count (AUC 0.86). Taken together, eotaxin-1/CCL11 was upregulated in sepsis-injured myocardium and circulating eotaxin-1/CCL11 was a biomarker for predicting severity and mortality of elderly patients with sepsis-induced myocardial injury. These results suggest that eotaxin-1/CCL11 may become a useful biomarkers and potential therapeutic target for sepsis-induced myocardial injury.
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Irisin activates Opa1-induced mitophagy to protect cardiomyocytes against apoptosis following myocardial infarction

Ting Xin, Chengzhi Lu,

https://doi.org/10.18632/aging.102899 pp 4474—4488

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Xin T, Lu C, . Irisin activates Opa1-induced mitophagy to protect cardiomyocytes against apoptosis following myocardial infarction. Aging (Albany NY). 2020 Mar 1012:4474-4488. https://doi.org/10.18632/aging.102899

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                TY  - JOUR
                AU  - Xin, Ting 
                AU  - Lu, Chengzhi 
                TI  - Irisin activates Opa1-induced mitophagy to protect cardiomyocytes against apoptosis following myocardial infarction
                JO  - 
                JA  - Aging (Albany NY)
                VL  - 12
                IS  - 5
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102899
                DO  - 10.18632/aging.102899
                SP  - 4474
                EP  - 4488
                PY  - 
                AB  - Myocardial infarction is characterized by sudden ischemia and cardiomyocyte death. Mitochondria have critical roles in regulating cardiomyocyte viability and can sustain damage under ischemic conditions. Mitophagy is a mechanism by which damaged mitochondria are removed by autophagy to maintain mitochondrial structure and function. We investigated the role of the dynamin-like GTPase optic atrophy 1 (Opa1) in mitophagy following myocardial infarction. Opa1 expression was downregulated in infarcted hearts in vivo and in hypoxia-treated cardiomyocytes in vitro. We found that Opa1 overexpression protected cardiomyocytes against hypoxia-induced damage and enhanced cell viability by inducing mitophagy. Opa1-induced mitophagy was activated by treatment with irisin, which protected cardiomyocytes from further damage following myocardial infarction. Opa1 knockdown abolished the cardioprotective effects of irisin resulting in an enhanced inflammatory response, increased oxidative stress, and mitochondrial dysfunction in cardiomyocytes. Our data indicate that Opa1 plays an important role in maintaining cardiomyocyte viability and mitochondrial function following myocardial infarction by inducing mitophagy. Irisin can activate Opa1-induced mitophagy and protect against cardiomyocyte injury following myocardial infarction.
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Methionine abrogates the renoprotective effect of a low-protein diet against diabetic kidney disease in obese rats with type 2 diabetes

Munehiro Kitada, Yoshio Ogura, Itaru Monno, Jing Xu, Daisuke Koya,

https://doi.org/10.18632/aging.102902 pp 4489—4505

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Kitada M, Ogura Y, Monno I, Xu J, Koya D, . Methionine abrogates the renoprotective effect of a low-protein diet against diabetic kidney disease in obese rats with type 2 diabetes. Aging (Albany NY). 2020 Mar 612:4489-4505. https://doi.org/10.18632/aging.102902

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                TY  - JOUR
                AU  - Kitada, Munehiro 
                AU  - Ogura, Yoshio 
                AU  - Monno, Itaru 
                AU  - Xu, Jing 
                AU  - Koya, Daisuke 
                TI  - Methionine abrogates the renoprotective effect of a low-protein diet against diabetic kidney disease in obese rats with type 2 diabetes
                JO  - 
                JA  - Aging (Albany NY)
                VL  - 12
                IS  - 5
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102902
                DO  - 10.18632/aging.102902
                SP  - 4489
                EP  - 4505
                PY  - 
                AB  - Dietary interventions, including a low-protein diet (LPD) and methionine (Met) restriction, have shown longevity, anti-aging and metabolic health effects. We previously reported that the LPD has a renoprotective effect against diabetic kidney disease (DKD) in rats with type 2 diabetes and obesity. However, it is unclear whether the beneficial effect of the LPD is mediated by low-Met intake or how Met is related to the pathogenesis for DKD. We herein show that the addition of Met with the LPD abrogates the beneficial effects induced by the LPD such as anti-oxidative stress, anti-inflammation and anti-fibrosis, in diabetic kidney. Additionally, the increased levels of S-adenosylmethionine (SAM) in renal tubular cells, which are associated with the reduced expression of glycine N-methyltransferase (Gnmt) and non-restricted Met intake, contributes to the activation of mechanistic target of rapamycin complex 1 (mTORC1) and impaired autophagy, in diabetic kidney. Moreover, starvation-induced autophagy was suppressed in renal cortex of Gnmt null mice and amino acid free-induced autophagy was also suppressed by administration of SAM in cultured HK-2 cells. A LPD could exert a renoprotective effect through the suppression of mTORC1 and restoration of autophagy, which is associated with reduced levels of SAM due to low-Met intake, in diabetic kidney.
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LncRNA GUSBP5-AS promotes EPC migration and angiogenesis and deep vein thrombosis resolution by regulating FGF2 and MMP2/9 through the miR-223-3p/FOXO1/Akt pathway

Li-Li Sun, Feng-Rui Lei, Xu-Dong Jiang, Xiao-Long Du, Lun Xiao, Wen-Dong Li, Xiao-Qiang Li,

https://doi.org/10.18632/aging.102904 pp 4506—4526

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Sun L, Lei F, Jiang X, Du X, Xiao L, Li W, Li X, . LncRNA GUSBP5-AS promotes EPC migration and angiogenesis and deep vein thrombosis resolution by regulating FGF2 and MMP2/9 through the miR-223-3p/FOXO1/Akt pathway. Aging (Albany NY). 2020 Mar 1012:4506-4526. https://doi.org/10.18632/aging.102904

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                TY  - JOUR
                AU  - Sun, Li-Li 
                AU  - Lei, Feng-Rui 
                AU  - Jiang, Xu-Dong 
                AU  - Du, Xiao-Long 
                AU  - Xiao, Lun 
                AU  - Li, Wen-Dong 
                AU  - Li, Xiao-Qiang 
                TI  - LncRNA GUSBP5-AS promotes EPC migration and angiogenesis and deep vein thrombosis resolution by regulating FGF2 and MMP2/9 through the miR-223-3p/FOXO1/Akt pathway
                JO  - 
                JA  - Aging (Albany NY)
                VL  - 12
                IS  - 5
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102904
                DO  - 10.18632/aging.102904
                SP  - 4506
                EP  - 4526
                PY  - 
                AB  - Long non-coding RNAs (lncRNAs) play an essential role in multitudinous physiological and pathological processes, including vascular disease. We previously showed that lncRNA GUSBP5-AS (enst00000511042) is upregulated in endothelial progenitor cells (EPCs) of deep veni thrombosis (DVT) patients. Here, we investigate the role and mechanism of GUSBP5-AS in EPCs and DVT. Using the DVT model, we found that GUSBP5-AS significantly reduced the thrombus size and weight and enhanced the homing ability of EPC to DVT sites to promote resolution and recanalization of thrombus. GUSBP5-AS promoted cell cycle progression, proliferation, migration and invasion in EPCs, enhanced EPC angiogenesis in vitro and in vivo, and inhibited apoptosis. Strikingly, this study showed that GUSBP5-AS was unbalanced and modulated Forkhead Box Protein O1 (FOXO1) in EPCs in patients with DVT by interacting with miR-223-3p. Mechanistically, GUSBP5-AS functions as a sponge of miR-223-3p, which targets FOXO1. Both GUSBP5-AS knockdown and miR-223-3p overexpression remarkably inhibited angiogenesis, migration and invasion in EPCs. Additionally, our data suggested that GUSBP-AS activated the Akt pathway and enhanced fibroblast growth factor 2 (FGF2), matrix metalloproteinase-2/9 (MMP2/9) and F-actin expression. Taken together, this study indicates that GUSBP5-AS modulates angiogenesis, proliferation and homing ability of EPCs via regulating FGF2 and MMP2/9 expression through the miR-223-3p/FOXO1/Akt pathway, which may provide a new direction for the development of DVT therapeutics.
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LncRNA-LALR1 upregulates small nucleolar RNA SNORD72 to promote growth and invasion of hepatocellular carcinoma

Lin-Hong Mao, Si-Yuan Chen, Xiao-Qin Li, Feng Xu, Jing Lei, Qing-Liang Wang, Li-Yang Luo, Hai-Yan Cao, Xin Ge, Tao Ran, Xue Li, Min Zou, Zhi-Hang Zhou, Xiao-Ling Wu, Song He,

https://doi.org/10.18632/aging.102907 pp 4527—4546

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Mao L, Chen S, Li X, Xu F, Lei J, Wang Q, Luo L, Cao H, Ge X, Ran T, Li X, Zou M, Zhou Z, et al, . LncRNA-LALR1 upregulates small nucleolar RNA SNORD72 to promote growth and invasion of hepatocellular carcinoma. Aging (Albany NY). 2020 Mar 1112:4527-4546. https://doi.org/10.18632/aging.102907

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                TY  - JOUR
                AU  - Mao, Lin-Hong 
                AU  - Chen, Si-Yuan 
                AU  - Li, Xiao-Qin 
                AU  - Xu, Feng 
                AU  - Lei, Jing 
                AU  - Wang, Qing-Liang 
                AU  - Luo, Li-Yang 
                AU  - Cao, Hai-Yan 
                AU  - Ge, Xin 
                AU  - Ran, Tao 
                AU  - Li, Xue 
                AU  - Zou, Min 
                AU  - Zhou, Zhi-Hang 
                AU  - Wu, Xiao-Ling 
                AU  - He, Song 
                TI  - LncRNA-LALR1 upregulates small nucleolar RNA SNORD72 to promote growth and invasion of hepatocellular carcinoma
                JO  - 
                JA  - Aging (Albany NY)
                VL  - 12
                IS  - 5
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102907
                DO  - 10.18632/aging.102907
                SP  - 4527
                EP  - 4546
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Mao, Lin-Hong 
                AU  - Chen, Si-Yuan 
                AU  - Li, Xiao-Qin 
                AU  - Xu, Feng 
                AU  - Lei, Jing 
                AU  - Wang, Qing-Liang 
                AU  - Luo, Li-Yang 
                AU  - Cao, Hai-Yan 
                AU  - Ge, Xin 
                AU  - Ran, Tao 
                AU  - Li, Xue 
                AU  - Zou, Min 
                AU  - Zhou, Zhi-Hang 
                AU  - Wu, Xiao-Ling 
                AU  - He, Song 
                TI  - LncRNA-LALR1 upregulates small nucleolar RNA SNORD72 to promote growth and invasion of hepatocellular carcinoma
                JO  - 
                JA  - Aging (Albany NY)
                VL  - 12
                IS  - 5
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102907
                DO  - 10.18632/aging.102907
                SP  - 4527
                EP  - 4546
                PY  - 
                AB  - Hepatocellular carcinoma (HCC) is one of the most prevalent cancers and currently the second leading cause of cancer-related mortality worldwide. One recent study reported that lncRNA-LALR1 promotes liver regeneration, the role and underlying mechanisms of lncRNA-LALR1 in HCC remain largely unknown. In this study, we demonstrated that lncRNA-LALR1 was significantly upregulated in HCC tissues compared with adjacent tissues and high expression of lncRNA-LALR1 was associated with advanced TNM stage, poor differentiation, and distant metastasis. RNA Fluorescence in situ hybridization analysis showed lncRNA-LALR1 was expressed not only in cytoplasm but also in nucleolus. Knockdown of lncRNA-LALR1 obviously inhibited HCC cells growth and invasion in vivo and in vitro. Besides, transcriptomic analysis and subsequent confirmation revealed that lncRNA-LALR1 upregulated small nucleolar RNA SNORD72 via binding with SNORD72 and stabilized ID2 mRNA. SNORD72 was overexpressed in HCC tissues and enhanced HCC cells proliferation, colony formation and invasion. Overexpression of SNORD72 could also stabilize ID2 mRNA and rescue the inhibitory effect of silencing lncRNA-LALR1. In conclusion, lncRNA-LALR1 is highly expressed in HCC and promotes tumor growth and invasion by upregulating SNORD72 to stabilize ID2 mRNA, implying that lncRNA-LALR1 might be a novel target for intervention of HCC.
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ARV-825-induced BRD4 protein degradation as a therapy for thyroid carcinoma

Ling He, Chen Chen, Guoyu Gao, Kun Xu, Zhaoqun Ma,

https://doi.org/10.18632/aging.102910 pp 4547—4557

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He L, Chen C, Gao G, Xu K, Ma Z, . ARV-825-induced BRD4 protein degradation as a therapy for thyroid carcinoma. Aging (Albany NY). 2020 Mar 1212:4547-4557. https://doi.org/10.18632/aging.102910

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                TY  - JOUR
                AU  - He, Ling 
                AU  - Chen, Chen 
                AU  - Gao, Guoyu 
                AU  - Xu, Kun 
                AU  - Ma, Zhaoqun 
                TI  - ARV-825-induced BRD4 protein degradation as a therapy for thyroid carcinoma
                JO  - 
                JA  - Aging (Albany NY)
                VL  - 12
                IS  - 5
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102910
                DO  - 10.18632/aging.102910
                SP  - 4547
                EP  - 4557
                PY  - 
                AB  - Bromodomain-containing protein 4 (BRD4) is overexpressed in thyroid carcinoma, represents as an important therapeutic target. ARV-825 is a novel cereblon-based PROTAC (Proteolysis Targeting Chsimera) compound. It can induce fast and sustained BRD4 protein degradation. Its potential effect in human thyroid carcinoma cells was studied here. In TPC-1 cells and primary human thyroid carcinoma cells, ARV-825 potently inhibited cell viability, proliferation and migration. Furthermore, ARV-825 induced robust apoptosis activation in the thyroid carcinoma cells. ARV-825 induced BRD4 protein degradation and downregulation of its targets, including c-Myc, Bcl-xL and cyclin D1 in thyroid carcinoma cells. It was significantly more potent in inhibiting thyroid carcinoma cells than the known small molecule BRD4 inhibitors. In vivo studies demonstrated that ARV-825 oral administration potently suppressed TPC-1 xenograft tumor growth in severe combined immunodeficient mice. BRD4 protein degradation as well as c-Myc, Bcl-xL and cyclin D1 downregulation were detected in ARV-825-treated TPC-1 tumor tissues. Taken together, ARV-825 induces BRD4 protein degradation and inhibits thyroid carcinoma cell growth in vitro and in vivo.
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Long non-coding RNA RHPN1-AS1 promotes tumorigenesis and metastasis of ovarian cancer by acting as a ceRNA against miR-596 and upregulating LETM1

Junrong Wang, Weimin Ding, Yingke Xu, Enfu Tao, Miaojun Mo, Wei Xu, Xu Cai, Xiaomin Chen, Junhui Yuan, Xiuying Wu,

https://doi.org/10.18632/aging.102911 pp 4558—4572

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Wang J, Ding W, Xu Y, Tao E, Mo M, Xu W, Cai X, Chen X, Yuan J, Wu X, . Long non-coding RNA RHPN1-AS1 promotes tumorigenesis and metastasis of ovarian cancer by acting as a ceRNA against miR-596 and upregulating LETM1. Aging (Albany NY). 2020 Mar 1212:4558-4572. https://doi.org/10.18632/aging.102911

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                TY  - JOUR
                AU  - Wang, Junrong 
                AU  - Ding, Weimin 
                AU  - Xu, Yingke 
                AU  - Tao, Enfu 
                AU  - Mo, Miaojun 
                AU  - Xu, Wei 
                AU  - Cai, Xu 
                AU  - Chen, Xiaomin 
                AU  - Yuan, Junhui 
                AU  - Wu, Xiuying 
                TI  - Long non-coding RNA RHPN1-AS1 promotes tumorigenesis and metastasis of ovarian cancer by acting as a ceRNA against miR-596 and upregulating LETM1
                JO  - 
                JA  - Aging (Albany NY)
                VL  - 12
                IS  - 5
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102911
                DO  - 10.18632/aging.102911
                SP  - 4558
                EP  - 4572
                PY  - 
                AB  - Background: In recent decades, long non-coding RNAs (lncRNAs) have been reported as crucial functional regulators involved in ovarian cancer. In the present study, we explored how lncRNA RHPN1-AS1 influences the progression of epithelial ovarian cancer (EOC) through tumor cell-dependent mechanisms.Results: The expression of RHPN1-AS1 in EOC tissues was higher than that in para-cancerous control tissues. High expression of RHPN1-AS1 was closely associated with poor prognosis in EOC patients. N6-methyladenosine (m6A) improved the stability of RHPN1-AS1 methylation transcript by reducing RNA degradation, which resulted in upregulation of RHPN1-AS1 in EOC. In vitro and in vivo functional experiments showed that RHPN1-AS1 promoted EOC cell proliferation and metastasis. RHPN1-AS1 acted as a ceRNA to sponge miR-596, consequently increasing LETM1 expression and activating the FAK/PI3K/Akt signaling pathway.Conclusion: RHPN1-AS1-miR-596-LETM1 axis plays a crucial role in EOC progression. Our findings may provide promising drug targets for EOC treatment.Methods: We determined the aberrantly expressed lncRNAs in EOC via microarray analysis and validated RHPN1-AS1 expression by qRT-PCR. The RHPN1-AS1-miR-596-LETM1 axis was examined by dual-luciferase reporter assay and RIP assay. The mechanism of RHPN1-AS1 was investigated through gain- and loss-of-function studies both in vivo and in vitro.
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APEX1 is a novel diagnostic and prognostic biomarker for hepatocellular carcinoma

Lei Cao, Hongwei Cheng, Qiuxia Jiang, Hui Li, Zhixian Wu,

https://doi.org/10.18632/aging.102913 pp 4573—4591

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Cao L, Cheng H, Jiang Q, Li H, Wu Z, . APEX1 is a novel diagnostic and prognostic biomarker for hepatocellular carcinoma. Aging (Albany NY). 2020 Mar 1312:4573-4591. https://doi.org/10.18632/aging.102913

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                TY  - JOUR
                AU  - Cao, Lei 
                AU  - Cheng, Hongwei 
                AU  - Jiang, Qiuxia 
                AU  - Li, Hui 
                AU  - Wu, Zhixian 
                TI  - APEX1 is a novel diagnostic and prognostic biomarker for hepatocellular carcinoma
                JO  - 
                JA  - Aging (Albany NY)
                VL  - 12
                IS  - 5
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102913
                DO  - 10.18632/aging.102913
                SP  - 4573
                EP  - 4591
                PY  - 
                AB  - In this study, we analyzed the expression and clinical significance of apyrimidinic endodeoxyribonuclease 1 (APEX1) in hepatocellular carcinoma (HCC). The APEX1 mRNA and protein levels were significantly higher in HCC than adjacent normal liver tissues in multiple datasets from the Oncomine, GEO and TCGA databases. APEX1 levels were significantly higher in early-stage HCC patients with low alpha-fetoprotein expression. The positive predictive value (PPV) for APEX1 was significantly higher than the PPV for alpha-fetoprotein (67.91% vs. 55.22%) in HCC patients. High APEX1 expression correlated with resistance to sorafenib and anti-programmed death 1 (PD-1) therapies in HCC patients, and it associated with poorer overall survival, disease-specific survival, progression-free survival, and relapse-free survival in early- and advanced-stage HCC patients. High APEX1 expression also associated with poor prognosis in non-alcoholic, vascular invasion-negative, and hepatitis virus-negative HCC patients. These data suggest that APEX1 is a better diagnostic and prognostic biomarker than alpha-fetoprotein in HCC. Gene set enrichment analysis (GSEA) showed that APEX1 expression correlated with the DNA damage repair pathway in HCC tissues. These findings demonstrate that APEX1 is a potential diagnostic and prognostic biomarker in HCC.
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Leisure-time physical activity volume, intensity, and duration from mid- to late-life in U.S. subpopulations by race and sex. The Atherosclerosis Risk In Communities (ARIC) Study

Dmitry Kats, Kelly R. Evenson, Donglin Zeng, Christy L. Avery, Priya Palta, Stephen B. Kritchevsky, Gerardo Heiss,

https://doi.org/10.18632/aging.102916 pp 4592—4602

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Kats D, Evenson KR, Zeng D, Avery CL, Palta P, Kritchevsky SB, Heiss G, . Leisure-time physical activity volume, intensity, and duration from mid- to late-life in U.S. subpopulations by race and sex. The Atherosclerosis Risk In Communities (ARIC) Study. Aging (Albany NY). 2020 Mar 1312:4592-4602. https://doi.org/10.18632/aging.102916

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                TY  - JOUR
                AU  - Kats, Dmitry 
                AU  - Evenson, Kelly R. 
                AU  - Zeng, Donglin 
                AU  - Avery, Christy L. 
                AU  - Palta, Priya 
                AU  - Kritchevsky, Stephen B. 
                AU  - Heiss, Gerardo 
                TI  - Leisure-time physical activity volume, intensity, and duration from mid- to late-life in U.S. subpopulations by race and sex. The Atherosclerosis Risk In Communities (ARIC) Study
                JO  - 
                JA  - Aging (Albany NY)
                VL  - 12
                IS  - 5
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102916
                DO  - 10.18632/aging.102916
                SP  - 4592
                EP  - 4602
                PY  - 
                AB  - Mitigating age-related disease and disability presents challenges. Physical activity (PA) may be influential for prolonging health and functioning, warranting characterization of its patterns over the life course in population-based data. With the availability of up to three self-reported assessments of past year leisure-time PA (LTPA) over multiple decades in 15,036 participants (26% African American; 55% women; mean baseline age=54; median follow-up=23 years) from the Atherosclerosis Risk in Communities (ARIC) Study sampled from four U.S. communities, race-sex-stratified trajectories of average weekly intensity (metabolic equivalent of task (MET)), duration (hours), and energy expenditure or volume (MET-h) of LTPA were developed from age 45 to 90 using joint models to accommodate expected non-ignorable attrition. Declines in weekly LTPA intensity, duration, and volume from age 70 to 90 were observed in white women (2.9 to 1.2 MET; 2.5 to 0.6 h; 11.1 to 2.6 MET-h), white men (2.5 to 1.0 MET; 3.5 to 1.8 h; 15.5 to 6.4 MET-h), African American women (2.5 to 2.4 MET; 0.8 to 0.1 h; 6.7 to 6.0 MET-h), and African American men (2.3 to 1.4 MET; 1.5 to 0.6 h; 8.0 to 2.3 MET-h). These data reveal population-wide shifts towards less active lifestyles in older adulthood.
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The prognostic value of tumor mutational burden and immune cell infiltration in esophageal cancer patients with or without radiotherapy

Cheng Yuan, Liyang Xiang, Kuo Cao, Jianguo Zhang, Yuan Luo, Wenjie Sun, Nannan Zhang, Jiangbo Ren, Junhong Zhang, Yan Gong, Conghua Xie,

https://doi.org/10.18632/aging.102917 pp 4603—4616

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Yuan C, Xiang L, Cao K, Zhang J, Luo Y, Sun W, Zhang N, Ren J, Zhang J, Gong Y, Xie C, . The prognostic value of tumor mutational burden and immune cell infiltration in esophageal cancer patients with or without radiotherapy. Aging (Albany NY). 2020 Mar 1212:4603-4616. https://doi.org/10.18632/aging.102917

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                TY  - JOUR
                AU  - Yuan, Cheng 
                AU  - Xiang, Liyang 
                AU  - Cao, Kuo 
                AU  - Zhang, Jianguo 
                AU  - Luo, Yuan 
                AU  - Sun, Wenjie 
                AU  - Zhang, Nannan 
                AU  - Ren, Jiangbo 
                AU  - Zhang, Junhong 
                AU  - Gong, Yan 
                AU  - Xie, Conghua 
                TI  - The prognostic value of tumor mutational burden and immune cell infiltration in esophageal cancer patients with or without radiotherapy
                JO  - 
                JA  - Aging (Albany NY)
                VL  - 12
                IS  - 5
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102917
                DO  - 10.18632/aging.102917
                SP  - 4603
                EP  - 4616
                PY  - 
                AB  - Growing evidence highlighted the tumor mutational burden (TMB) as an important feature of carcinogenesis and therapeutic efficacy in esophageal cancer (EC). Our study aimed to explore the genomic landscape and the correlation between TMB and immune cell infiltration in EC patients with or without radiotherapy. The EC patients were categorized into high TMB (TMB-H) and low TMB (TMB-L) groups by the ESTIMATE algorithm, and subgroup analysis was performed based on receiving radiotherapy or not. Univariate regression analysis indicated TMB and TNM stages as high-risk prognostic factors (Hazard ratio &gt; 1 and P &lt; 0.05). Multivariate regression analysis suggested TMB as an independent prognostic factor (Hazard ratio = 1.051, P = 0.003). Kaplan-Meier analysis showed no significant difference of the overall survival (OS) between TMB-H and TMB-L groups (P = 0.082). However, EC patients without radiotherapy in the TMB-H group had significantly decreased OS (P = 0.038) and increased Tregs cell infiltration (P = 0.033). These results suggested TMB as a prognostic marker for EC patients. Especially for patients who did not receive radiotherapy, the prognosis of TMB-H patients was significantly poorer than that of TMB-L patients, which might result from the different regulatory T cell infiltration.
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Alterations of hand sensorimotor function and cortical motor representations over the adult lifespan

Melina Hehl, Stephan P. Swinnen, Koen Cuypers,

https://doi.org/10.18632/aging.102925 pp 4617—4640

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Hehl M, Swinnen SP, Cuypers K, . Alterations of hand sensorimotor function and cortical motor representations over the adult lifespan. Aging (Albany NY). 2020 Mar 1112:4617-4640. https://doi.org/10.18632/aging.102925

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                TY  - JOUR
                AU  - Hehl, Melina 
                AU  - Swinnen, Stephan P. 
                AU  - Cuypers, Koen 
                TI  - Alterations of hand sensorimotor function and cortical motor representations over the adult lifespan
                JO  - 
                JA  - Aging (Albany NY)
                VL  - 12
                IS  - 5
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102925
                DO  - 10.18632/aging.102925
                SP  - 4617
                EP  - 4640
                PY  - 
                AB  - Using a cross sectional design, we aimed to identify the effect of aging on sensorimotor function and cortical motor representations of two intrinsic hand muscles, as well as the course and timing of those changes. Furthermore, the link between cortical motor representations, sensorimotor function, and intracortical inhibition and facilitation was investigated. Seventy-seven participants over the full adult lifespan were enrolled. For the first dorsal interosseus (FDI) and abductor digiti minimi (ADM) muscle, cortical motor representations, GABAA-mediated short-interval intracortical inhibition (SICI), and glutamate-mediated intracortical facilitation (ICF) were assessed using transcranial magnetic stimulation over the dominant primary motor cortex. Additionally, participants&#x2019; dexterity and force were measured. Linear, polynomial, and piecewise linear regression analyses were conducted to identify the course and timing of age-related differences. Our results demonstrated variation in sensorimotor function over the lifespan, with a marked decline starting around the mid-thirties. Furthermore, an age-related reduction in cortical motor representation volume and maximal MEP of the FDI, but not for ADM, was observed, occurring mainly until the mid-forties. Area of the cortical motor representation did not change with advancing age. Furthermore, cortical motor representations, sensorimotor function, and measures of intracortical inhibition and facilitation were not interrelated.
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Effects of the probiotic formulation SLAB51 in in vitro and in vivo Parkinson’s disease models

Vanessa Castelli, Michele d’Angelo, Francesca Lombardi, Margherita Alfonsetti, Andrea Antonosante, Mariano Catanesi, Elisabetta Benedetti, Paola Palumbo, Maria Grazia Cifone, Antonio Giordano, Giovambattista Desideri, Annamaria Cimini,

https://doi.org/10.18632/aging.102927 pp 4641—4659

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Castelli V, d’Angelo M, Lombardi F, Alfonsetti M, Antonosante A, Catanesi M, Benedetti E, Palumbo P, Cifone MG, Giordano A, Desideri G, Cimini A, . Effects of the probiotic formulation SLAB51 in in vitro and in vivo Parkinson’s disease models. Aging (Albany NY). 2020 Mar 912:4641-4659. https://doi.org/10.18632/aging.102927

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 TY - JOUR
 AU - Castelli, Vanessa 
 AU - d’Angelo, Michele 
 AU - Lombardi, Francesca 
 AU - Alfonsetti, Margherita 
 AU - Antonosante, Andrea 
 AU - Catanesi, Mariano 
 AU - Benedetti, Elisabetta 
 AU - Palumbo, Paola 
 AU - Cifone, Maria Grazia 
 AU - Giordano, Antonio 
 AU - Desideri, Giovambattista 
 AU - Cimini, Annamaria 
 TI - Effects of the probiotic formulation SLAB51 in in vitro and in vivo Parkinson’s disease models
 JO - 
 JA - Aging (Albany NY)
 VL - 12
 IS - 5
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.102927
 DO - 10.18632/aging.102927
 SP - 4641
 EP - 4659
 PY - 
 ER -

Provider: 
 TY - JOUR
 AU - Castelli, Vanessa 
 AU - d’Angelo, Michele 
 AU - Lombardi, Francesca 
 AU - Alfonsetti, Margherita 
 AU - Antonosante, Andrea 
 AU - Catanesi, Mariano 
 AU - Benedetti, Elisabetta 
 AU - Palumbo, Paola 
 AU - Cifone, Maria Grazia 
 AU - Giordano, Antonio 
 AU - Desideri, Giovambattista 
 AU - Cimini, Annamaria 
 TI - Effects of the probiotic formulation SLAB51 in in vitro and in vivo Parkinson’s disease models
 JO - 
 JA - Aging (Albany NY)
 VL - 12
 IS - 5
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.102927
 DO - 10.18632/aging.102927
 SP - 4641
 EP - 4659
 PY - 
 AB - Parkinson is a common neurodegenerative disorder, characterized by motor and non-motor symptoms, including abnormalities in the gut function, which may appear before the motor sign. To date, there are treatments that can help relieve Parkinson&#x2019; disease (PD)-associated symptoms, but there is no cure to control the onset and progression of this disorder. Altered components of the gut could represent a key role in gut-brain axis, which is a bidirectional system between the central nervous system and the enteric nervous system. Diet can alter the microbiota composition, affecting gut-brain axis function. Gut microbiome restoration through selected probiotics&#x2019; administration has been reported. In this study, we investigated the effects of the novel formulation SLAB51 in PD. Our findings indicate that this probiotic formulation can counteract the detrimental effect of 6-OHDA in vitro and in vivo models of PD. The results suggest that SLAB51 can be a promising candidate for the prevention or as coadjuvant treatment of PD.
 ER -

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Adiponectin in renal fibrosis

Huan Jing, Simin Tang, Sen Lin, Meijuan Liao, Hongtao Chen, Youling Fan, Jun Zhou,

https://doi.org/10.18632/aging.102811 pp 4660—4672

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Jing H, Tang S, Lin S, Liao M, Chen H, Fan Y, Zhou J, . Adiponectin in renal fibrosis. Aging (Albany NY). 2020 Feb 1712:4660-4672. https://doi.org/10.18632/aging.102811

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                TY  - JOUR
                AU  - Jing, Huan 
                AU  - Tang, Simin 
                AU  - Lin, Sen 
                AU  - Liao, Meijuan 
                AU  - Chen, Hongtao 
                AU  - Fan, Youling 
                AU  - Zhou, Jun 
                TI  - Adiponectin in renal fibrosis
                JO  - 
                JA  - Aging (Albany NY)
                VL  - 12
                IS  - 5
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102811
                DO  - 10.18632/aging.102811
                SP  - 4660
                EP  - 4672
                PY  - 
                AB  - Renal fibrosis is an inevitable consequence of parenchymal scarring and is the common final pathway that mediates almost all progressive renal diseases. Adiponectin, a hormone produced by adipose tissue, possesses potent anti-insulin, anti-inflammatory, and anti-fibrotic properties. Reportedly, adiponectin serves as an important messenger that facilitates complex interactions between adipose tissue and other metabolically related organs. In recent years, a growing body of evidence supports adiponectin involvement in renal fibrosis. These studies provide a deeper understanding of the molecular mechanism of action of adiponectin in renal fibrosis and also offer a potential preventive and therapeutic target for renal fibrosis. In this review, the physiological role of adiponectin is briefly introduced, and then the mechanism of adiponectin-mediated renal fibrosis and the related signaling pathways are described. Finally, we summarize the findings regarding the clinical value of adiponectin in renal fibrotic diseases and prospected its application potential.
                ER  -

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The flip side of sirtuins: the emerging roles of protein acetyltransferases in aging

Prabakaran Nagarajan, Mark R. Parthun,

https://doi.org/10.18632/aging.102949 pp 4673—4677

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Nagarajan P, Parthun MR, . The flip side of sirtuins: the emerging roles of protein acetyltransferases in aging. Aging (Albany NY). 2020 Mar 1312:4673-4677. https://doi.org/10.18632/aging.102949

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Provider: 
                TY  - JOUR
                AU  - Nagarajan, Prabakaran 
                AU  - Parthun, Mark R. 
                TI  - The flip side of sirtuins: the emerging roles of protein acetyltransferases in aging
                JO  - 
                JA  - Aging (Albany NY)
                VL  - 12
                IS  - 5
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102949
                DO  - 10.18632/aging.102949
                SP  - 4673
                EP  - 4677
                PY  - 
                AB  - Protein N-&#x3B5;-lysine acetylation is is an important post-translational modification that plays critical roles in the regulation of many cellular processes. A role for this modification in the process of aging goes back two decades to the discovery that the yeast NAD+-dependent histone deacetylase Sir2 regulates lifespan in yeast. While the Sirtuin family of protein deacetylases has been intensively studied in many model systems and is definitively linked to aging, the enzymes responsible for protein acetylation, protein acetyltransferases (KATs), have not received a similar level of attention. However, a series of recent studies have directly explored the role of specific KATs in aging. These studies have shown that modulation of KAT activity can influence cellular pathways important for aging and directly effect organismal lifespan.
                ER  -

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Correction for: ciRs-6 upregulates March1 to suppress bladder cancer growth by sponging miR-653

Yinjie Su, Weilian Feng, Guanglei Zhong, Yiyao Ya, Zehu Du, Juanyi Shi, Luping Chen, Wen Dong, Tianxin Lin,

https://doi.org/10.18632/aging.102885 pp 4678—4679

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Su Y, Feng W, Zhong G, Ya Y, Du Z, Shi J, Chen L, Dong W, Lin T, . Correction for: ciRs-6 upregulates March1 to suppress bladder cancer growth by sponging miR-653. Aging (Albany NY). 2020 Mar 212:4678-4679. https://doi.org/10.18632/aging.102885

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Correction for: A novel rhamnoside derivative PL402 up-regulates matrix metalloproteinase 3/9 to promote Aβ degradation and alleviates Alzheimer’s-like pathology

Tingting Hu, Yue Zhou, Jing Lu, Peng Xia, Yue Chen, Xin Cao, Gang Pei,

https://doi.org/10.18632/aging.102898 pp 4680—4681

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Hu T, Zhou Y, Lu J, Xia P, Chen Y, Cao X, Pei G, . Correction for: A novel rhamnoside derivative PL402 up-regulates matrix metalloproteinase 3/9 to promote Aβ degradation and alleviates Alzheimer’s-like pathology. Aging (Albany NY). 2020 Mar 412:4680-4681. https://doi.org/10.18632/aging.102898

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Volume 12, Issue 5

About the Cover

Editorials

Pawel Bieniasz-Krzywiec, Massimiliano Mazzone,

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Cristina González-Estévez, Ignacio Flores,

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Ellen K. Quarles, Peter S. Rabinovitch,

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Priority Research Paper

M. Laura Idda, Waverly G. McClusky, Valeria Lodde, Rachel Munk, Kotb Abdelmohsen, Martina Rossi, Myriam Gorospe,

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Research Papers

Guangping Zhang, Luzhu Chen, Jing Liu, Yan Jin, Zaihong Lin, Shu Du, Zenghui Fu, Tuantuan Chen, Yinghui Qin, Fenghu Sui, Yan Jiang,

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Xiao-Ling Gao, Zhi-Mei Jia, Fang-Fang Zhao, Dong-Dong An, Bei Wang, Er-Jing Cheng, Yan Chen, Jian-Nan Gong, Dai Liu, Ya-Qiong Huang, Jiao-Jiao Yang, Shu-Juan Wang,

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Ting Shen, Qingqing Zheng, Hongbo Luo, Xin Li, Zhuo Chen, Zeyu Song, Guanfang Zhou, Chaoyang Hong,

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Yuanmin Zhang, Longfei Ma, Chengqun Wang, Lina Wang, Yanxia Guo, Guodong Wang,

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Ignazio S. Piras, Christiane Bleul, Joshua S. Talboom, Matthew D. De Both, Isabelle Schrauwen, Glenda Halliday, Amanda J. Myers, Geidy E. Serrano, Thomas G. Beach, Matthew J. Huentelman,

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Ji Zheng, Hao Zhou, Mengjun Yang, Siji Song, Qiang Dai, Guangju Ji, Zhansong Zhou,

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Xiaojun Feng, Yanan Wang, Wenxu Chen, Suowen Xu, Lingli Li, Yadi Geng, Aizong Shen, Hui Gao, Lei Zhang, Sheng Liu,

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Huan Yu, Hui Li, Xiaoqian Liu, Xiaoli Du, Binbin Deng,

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Meihua Zhang, Junxia Li, Shuyin Duan, Zhenya Fang, Jiaqi Tian, Haoyu Yin, Qingfeng Zhai, Xietong Wang, Lin Zhang,

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Youwen Zhang, Ioulia Chatzistamou, Hippokratis Kiaris,

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Eurydice Angeli, Kader Chouahnia, Florence Canoui-Poitrine, Boris Duchemann, Thomas Aparicio, Elena Paillaud, Laurent Zelek, Guilhem Bousquet, Frédéric Pamoukdjian,

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Wei Cai, Sanli Liu, Ziquan Liu, Shike Hou, Qi Lv, Huanhuan Cui, Xue Wang, Yuxin Zhang, Haojun Fan, Hui Ding,

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Xiaodong Jia, Libin Shao, Chengcheng Liu, Tuanzhi Chen, Ling Peng, Yinguang Cao, Chuanchen Zhang, Xiafeng Yang, Guifeng Zhang, Jianlu Gao, Guangyi Fan, Mingliang Gu, Hongli Du, Zhangyong Xia,

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Kangping Song, Xiaojie Liu, Qiuyue Zheng, Lingling Zhang, Hongying Zhang, Hailong Yu, Yan Zhu, Li-An Huang, Yingzhu Chen,

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Yuanyuan Li, Ran Ding, Feifei Wang, Cuiping Guo, Aili Liu, Liangpeng Wei, Shiyang Yuan, Feng Chen, Shaowei Hou, Zengguang Ma, Yan Zhang, Robert H. Cudmore, Xiaochuan Wang, Hui Shen,

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