Volume 11, Issue 14

Viltard M, Durand S, Pérez-Lanzón M, Aprahamian F, Lefevre D, Leroy C, Madeo F, Kroemer G, Friedlander G, . The metabolomic signature of extreme longevity: naked mole rats versus mice. . 11:4783-4800. https://doi.org/10.18632/aging.102116

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                TY  - JOUR
                AU  - Viltard, Mélanie 
                AU  - Durand, Sylvère 
                AU  - Pérez-Lanzón, Maria 
                AU  - Aprahamian, Fanny 
                AU  - Lefevre, Deborah 
                AU  - Leroy, Christine 
                AU  - Madeo, Frank 
                AU  - Kroemer, Guido 
                AU  - Friedlander, Gérard 
                TI  - The metabolomic signature of extreme longevity: naked mole rats <i>versus</i> mice
                JO  - 
                JA  - 
                VL  - 11
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102116
                DO  - 10.18632/aging.102116
                SP  - 4783
                EP  - 4800
                PY  - 
                AB  - The naked mole-rat (Heterocephalus glaber) is characterized by a more than tenfold higher life expectancy compared to another rodent species of the same size, namely, the laboratory mouse (Mus musculus). We used mass spectrometric metabolomics to analyze circulating plasma metabolites in both species at different ages. Interspecies differences were much more pronounced than age-associated alterations in the metabolome. Such interspecies divergences affected multiple metabolic pathways involving amino, bile and fatty acids as well as monosaccharides and nucleotides. The most intriguing metabolites were those that had previously been linked to pro-health and antiaging effects in mice and that were significantly increased in the long-lived rodent compared to its short-lived counterpart. This pattern applies to &#x3B1;-tocopherol (also known as vitamin E) and polyamines (in particular cadaverine, N8-acetylspermidine and N1,N8-diacetylspermidine), all of which were more abundant in naked mole-rats than in mice. Moreover, the age-associated decline in spermidine and N1-acetylspermidine levels observed in mice did not occur, or is even reversed (in the case of N1-acetylspermidine) in naked mole-rats. In short, the present metabolomics analysis provides a series of testable hypotheses to explain the exceptional longevity of naked mole-rats.
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Mitochondrial and ribosomal biogenesis are new hallmarks of stemness, oncometabolism and biomass accumulation in cancer: Mito‐stemness and ribo‐stemness features

Maria Peiris‐Pagès, Béla Ozsvári, Federica Sotgia, Michael P. Lisanti,

https://doi.org/10.18632/aging.102054 pp 4801—4835

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Peiris‐Pagès M, Ozsvári B, Sotgia F, Lisanti MP, . Mitochondrial and ribosomal biogenesis are new hallmarks of stemness, oncometabolism and biomass accumulation in cancer: Mito‐stemness and ribo‐stemness features. . 11:4801-4835. https://doi.org/10.18632/aging.102054

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                TY  - JOUR
                AU  - Peiris‐Pagès, Maria 
                AU  - Ozsvári, Béla 
                AU  - Sotgia, Federica 
                AU  - Lisanti, Michael P. 
                TI  - Mitochondrial and ribosomal biogenesis are new hallmarks of stemness, oncometabolism and biomass accumulation in cancer: Mito‐stemness and ribo‐stemness features
                JO  - 
                JA  - 
                VL  - 11
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102054
                DO  - 10.18632/aging.102054
                SP  - 4801
                EP  - 4835
                PY  - 
                AB  - Using proteomics analysis, we previously compared MCF7 breast cancer cells grown as 3D tumor spheres, with the same cell line grown as monolayers. Our results indicated that during 3D anchorage&#x2010;independent growth, the cellular machinery associated with i) mitochondrial biogenesis and ii) ribosomal biogenesis, were both significantly increased. Here, for simplicity, we refer to these two new oncogenic hallmarks as &#x201C;mito&#x2010;stemness&#x201D; and &#x201C;ribo&#x2010;stemness&#x201D; features. We have now applied this same type of strategy to begin to understand how fibroblasts and MCF7 breast cancer cells change their molecular phenotype, when they are co&#x2010;cultured together. We have previously shown that MCF7&#x2010;fibroblast co&#x2010;cultures are a valuable model of resistance to apoptosis induced by hormonal therapies, such as Tamoxifen and Fulvestrant. Here, we directly show that these mixed co&#x2010;cultures demonstrate the induction of mito&#x2010;stemness and ribo&#x2010;stemness features, likely reflecting a mechanism for cancer cells to increase their capacity for accumulating biomass. In accordance with the onset of a stem&#x2010;like phenotype, KRT19 (keratin 19) was induced by ~6&#x2010;fold during co&#x2010;culture. KRT19 is a well&#x2010;established epithelial CSC marker that is used clinically to identify metastatic breast cancer cells in sentinel lymph node biopsies. The potential molecular therapeutic targets that we identified by label&#x2010;free proteomics of MCF7&#x2010;fibroblast co&#x2010;cultures were then independently validated using a bioinformatics approach. More specifically, we employed publically&#x2010;available transcriptional profiling data derived from primary tumor samples from breast cancer patients, which were previously subjected to laser&#x2010;capture micro&#x2010;dissection, to physically separate breast cancer cells from adjacent tumor stroma. This allowed us to directly validate that the proteins up&#x2010;regulated in this co&#x2010;culture model were also transcriptionally elevated in patient&#x2010;derived breast cancer cells in vivo. This powerful approach for target identification and translational validation, including the use of patient outcome data, can now be applied to other tumor types as well, to validate new therapeutic targets that are more clinically relevant, for patient benefit. Moreover, we discuss the therapeutic implications of these findings for new drug development, drug repurposing and Tamoxifen&#x2010;resistance, to effectively target mito&#x2010;stemness and ribo&#x2010;stemness features in breast cancer patients. We also discuss the broad implications of this &#x201C;organelle biogenesis&#x201D; approach to cancer therapy.
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Effects of transcutaneous vagus nerve stimulation in individuals aged 55 years or above: potential benefits of daily stimulation

Beatrice Bretherton, Lucy Atkinson, Aaron Murray, Jennifer Clancy, Susan Deuchars, Jim Deuchars,

https://doi.org/10.18632/aging.102074 pp 4836—4857

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Bretherton B, Atkinson L, Murray A, Clancy J, Deuchars S, Deuchars J, . Effects of transcutaneous vagus nerve stimulation in individuals aged 55 years or above: potential benefits of daily stimulation. . 11:4836-4857. https://doi.org/10.18632/aging.102074

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                TY  - JOUR
                AU  - Bretherton, Beatrice 
                AU  - Atkinson, Lucy 
                AU  - Murray, Aaron 
                AU  - Clancy, Jennifer 
                AU  - Deuchars, Susan 
                AU  - Deuchars, Jim 
                TI  - Effects of transcutaneous vagus nerve stimulation in individuals aged 55 years or above: potential benefits of daily stimulation
                JO  - 
                JA  - 
                VL  - 11
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102074
                DO  - 10.18632/aging.102074
                SP  - 4836
                EP  - 4857
                PY  - 
                AB  - Ageing is associated with attenuated autonomic function. Transcutaneous vagal nerve stimulation (tVNS) improved autonomic function in healthy young participants. We therefore investigated the effects of a single session of tVNS (studies 1 and 2) and tVNS administered daily for two weeks (study 3) in volunteers aged &#x2265; 55 years. tVNS was performed using modified surface electrodes on the tragus and connected to a transcutaneous electrical nerve stimulation (TENS) machine. Study 1: participants (n=14) received a single session of tVNS and sham. Study 2: all participants (n=51) underwent a single session of tVNS. Study 3: participants (n=29) received daily tVNS for two weeks. Heart rate variability and baroreflex sensitivity were derived. Quality of life (QoL), mood and sleep were assessed in study 3. tVNS promoted increases in measures of vagal tone and was associated with greater increases in baroreflex sensitivity than sham. Two weeks of daily tVNS improved measures of autonomic function, and some aspects of QoL, mood and sleep. Importantly, findings showed that improvements in measures of autonomic balance were more pronounced in participants with greater baseline sympathetic prevalence. This suggests it may be possible to identify individuals who are likely to encounter significant benefits from tVNS.
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CCAT1 promotes triple-negative breast cancer progression by suppressing miR-218/ZFX signaling

Chunyong Han, Xuebiao Li, Qian Fan, Guangshu Liu, Jian Yin,

https://doi.org/10.18632/aging.102080 pp 4858—4875

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Han C, Li X, Fan Q, Liu G, Yin J, . CCAT1 promotes triple-negative breast cancer progression by suppressing miR-218/ZFX signaling. . 11:4858-4875. https://doi.org/10.18632/aging.102080

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                TY  - JOUR
                AU  - Han, Chunyong 
                AU  - Li, Xuebiao 
                AU  - Fan, Qian 
                AU  - Liu, Guangshu 
                AU  - Yin, Jian 
                TI  - CCAT1 promotes triple-negative breast cancer progression by suppressing miR-218/ZFX signaling
                JO  - 
                JA  - 
                VL  - 11
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102080
                DO  - 10.18632/aging.102080
                SP  - 4858
                EP  - 4875
                PY  - 
                AB  - Long non-coding RNAs (lncRNAs) regulate cancer development and progression. Here, we investigated the role of the lncRNA CCAT1 in triple-negative breast cancer (TNBC). CCAT1 expression was higher in TNBC cells than normal breast epithelial cells. Additionally, CCAT1 expression was higher in TNBC patient tumor tissue than adjacent normal breast tissue. Silencing CCAT1 inhibited TNBC cell proliferation, migration, and invasion in vitro, and tumor growth and progression in vivo. Bioinformatics analysis revealed that microRNA-218 (miR-218) is a potential target of CCAT1. Silencing CCAT1 resulted in an increase in miR-218 expression and inhibited TNBC cell proliferation, migration, and invasion. Silencing miR-218 reversed the effects of CCAT1 knockdown on cell proliferation, migration, and invasion, suggesting that CCAT1 promotes TNBC progression by downregulating miR-218 expression. We identified the zinc finger protein ZFX as a putative downstream target of miR-218 through bioinformatics analysis. ZFX expression was higher in TNBC than normal breast cell lines and higher in TNBC tumor tissue than adjacent normal breast tissue. Overexpression of ZFX reversed the tumor-suppressive effects of miR-218 on TNBC cell proliferation, migration, and invasion. Our data indicate that CCAT1 promotes TNBC progression by targeting the miR-218/ZFX axis.
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LncRNA SLCO4A1-AS1 promotes colorectal cancer cell proliferation by enhancing autophagy via miR-508-3p/PARD3 axis

Zhaozhi Wang, Jianjun Jin,

https://doi.org/10.18632/aging.102081 pp 4876—4889

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Wang Z, Jin J, . LncRNA SLCO4A1-AS1 promotes colorectal cancer cell proliferation by enhancing autophagy via miR-508-3p/PARD3 axis. . 11:4876-4889. https://doi.org/10.18632/aging.102081

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                TY  - JOUR
                AU  - Wang, Zhaozhi 
                AU  - Jin, Jianjun 
                TI  - LncRNA SLCO4A1-AS1 promotes colorectal cancer cell proliferation by enhancing autophagy via miR-508-3p/PARD3 axis
                JO  - 
                JA  - 
                VL  - 11
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102081
                DO  - 10.18632/aging.102081
                SP  - 4876
                EP  - 4889
                PY  - 
                AB  - Aberrant expressions of various long non-coding RNAs (lncRNAs) have been involved in the progression and pathogenesis of various carcinomas. However, the expression and biological function of SLCO4A1-AS1 in colorectal cancer (CRC) remain poorly understood. Gain- and loss-of-function assays were applied to determine the roles of SLCO4A1-AS1 in autophagy and CRC progression. qRT-PCR and in situ hybridization (ISH) results showed that SLCO4A1-AS1 was positively associated with PARD3 expression in CRC tissues. In vitro and in vivo studies revealed that SLCO4A1-AS1 knockdown repressed cytoprotective autophagy as assayed by transmission electron microscopy (TEM), and inhibited cell proliferation by directly targeting partition-defective 3 (PARD3). Mechanistically, SLCO4A1-AS1 acted as a sponge of miR-508-3p, leading to upregulation of PARD3 and promotion of CRC cell proliferation. The current study demonstrates that the SLCO4A1-AS1/miR-508-3p/PARD3/autophagy pathway play a critical role in CRC cell proliferation, and might provide novel targets for developing therapeutic strategies for CRC.
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GCN-5/PGC-1α signaling is activated and associated with metabolism in cyclin E1-driven ovarian cancer

Ting Guo, Bin Li, Chao Gu, Xiuying Chen, Mengxin Han, Xiaocheng Liu, Congjian Xu,

https://doi.org/10.18632/aging.102082 pp 4890—4899

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Guo T, Li B, Gu C, Chen X, Han M, Liu X, Xu C, . GCN-5/PGC-1α signaling is activated and associated with metabolism in cyclin E1-driven ovarian cancer. . 11:4890-4899. https://doi.org/10.18632/aging.102082

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                TY  - JOUR
                AU  - Guo, Ting 
                AU  - Li, Bin 
                AU  - Gu, Chao 
                AU  - Chen, Xiuying 
                AU  - Han, Mengxin 
                AU  - Liu, Xiaocheng 
                AU  - Xu, Congjian 
                TI  - GCN-5/PGC-1α signaling is activated and associated with metabolism in cyclin E1-driven ovarian cancer
                JO  - 
                JA  - 
                VL  - 11
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102082
                DO  - 10.18632/aging.102082
                SP  - 4890
                EP  - 4899
                PY  - 
                AB  - Aim: We previously found Cyclin E1-driven high grade serous ovarian cancer (HGSOC) showed metabolic shift. In this study, we aimed to elucidate signaling pathway therein.Methods: In silico reproduction of TCGA ovarian cancer dataset and pathway analysis were performed. Candidate metabolic pathway was validated using in vitro and in vivo assays.Results: We found CCNE1-amplified HGSOC showed significant metabolic alteration besides canonical cell cycle control. Using CCNE1-amplified OVCAR-3 and A2780 OvCa cells, we found that knockdown of CDK2 and GCN5 resulted in decreased G6PC and increased PGC-1&#x3B1; level, and that both genetic and pharmaceutical (MB-3) inhibition of GCN5 resulted in significant decrease in acetylation of PGC-1&#x3B1;. Silencing of CDK2 also resulted in significant decrease in acetylation of both PGC-1&#x3B1; and Rb. GCN5-KD significantly decreased glucose uptake, increased lactate production and decreased SDH activity. Western blots showed hierarchy of the elements indicating Cyclin E1-CDK2/GCN5/PGC-1&#x3B1; regulatory axis from up- to down- stream. Inhibitory effect of Dinaciclib was similar to that of GCN5 silencing, whereas combination therapy further inhibited cell proliferation significantly. Similar findings were noted also in cell cycle arrest, apoptosis, invasion, migration and colony formation assays. Xenograft experiments showed that GCN5-KD alone did not alter tumor growth yet combination therapy of Dinaciclib and GCN5-KD conferred significant inhibition of tumor growth compared with either therapy alone with no toxicity observed.Conclusion: GCN-5/PGC-1&#x3B1; signaling is activated and associated with metabolism in Cyclin E1-driven HGSOC. Targeting GCN5 hold promise to augment current CDK2-targeting strategy and further studies are warranted for clinical translation.
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Osteoprotegerin as a biomarker of geriatric frailty syndrome

Alessia Valentini, Maria Assunta Cianfarani, Umberto Tarantino, Nicola Di Daniele, Aldo Bertoli,

https://doi.org/10.18632/aging.102083 pp 4900—4909

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Valentini A, Cianfarani MA, Tarantino U, Di Daniele N, Bertoli A, . Osteoprotegerin as a biomarker of geriatric frailty syndrome. . 11:4900-4909. https://doi.org/10.18632/aging.102083

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                TY  - JOUR
                AU  - Valentini, Alessia 
                AU  - Cianfarani, Maria Assunta 
                AU  - Tarantino, Umberto 
                AU  - Di Daniele, Nicola 
                AU  - Bertoli, Aldo 
                TI  - Osteoprotegerin as a biomarker of geriatric frailty syndrome
                JO  - 
                JA  - 
                VL  - 11
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102083
                DO  - 10.18632/aging.102083
                SP  - 4900
                EP  - 4909
                PY  - 
                AB  - The lack of a univocal definition of frailty, a condition frequently found in the elderly population which is correlated with an increased risk of mortality, has prompted the search for clinical and laboratory parameters associated with this condition. Whereas OPG is a protein involved in different pathophysiological conditions including bone, vascular, immune and tumor disease and studies found a positive linear correlation between OPG and age we hypothesized that it may represent a frailty marker in the elderly.We conducted an observational study of 172 elderly subjects, with and without hip fracture, including a multidimensional geriatric evaluation and a laboratory evaluation, aimed to evaluate the association between OPG and frailty.Frailty Score was associated with FT3 and osteoprotegerin (OPG), regardless of fracture event. Excluding subjects with hip fracture, in whom the acute event had a direct effect on bone production of OPG, the Frailty Score showed a linear correlation with circulating levels of osteoprotegerin.In the elderly, an increase in osteoprotegerin levels may reflect a progressive accumulation of organ damage leading to the development of frailty. The correlation between OPG and Frailty Score found in our study points to its potential use as a biomarker for geriatric frailty syndrome.
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Blood autophagy defect causes accelerated non-hematopoietic organ aging

Yixuan Fang, Lingjiang Zhu, Ni An, Gaoyue Jiang, Jiawei Qian, Ruijin Zhao, Na Yuan, Suping Zhang, Jianrong Wang,

https://doi.org/10.18632/aging.102086 pp 4910—4922

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Fang Y, Zhu L, An N, Jiang G, Qian J, Zhao R, Yuan N, Zhang S, Wang J, . Blood autophagy defect causes accelerated non-hematopoietic organ aging. . 11:4910-4922. https://doi.org/10.18632/aging.102086

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                TY  - JOUR
                AU  - Fang, Yixuan 
                AU  - Zhu, Lingjiang 
                AU  - An, Ni 
                AU  - Jiang, Gaoyue 
                AU  - Qian, Jiawei 
                AU  - Zhao, Ruijin 
                AU  - Yuan, Na 
                AU  - Zhang, Suping 
                AU  - Wang, Jianrong 
                TI  - Blood autophagy defect causes accelerated non-hematopoietic organ aging
                JO  - 
                JA  - 
                VL  - 11
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102086
                DO  - 10.18632/aging.102086
                SP  - 4910
                EP  - 4922
                PY  - 
                AB  - Autophagy has been well studied in regulating aging; however, the impact of autophagy in one organ on the aging of other organs has not been documented. In this study, we used a mouse model with deletion of an autophagy-essential gene Atg7 in hematopoietic system to evaluate the intrinsic role of hematopoietic autophagy on the aging of non-hematopoietic organs. We found that autophagy defect in hematopoietic system causes growth retardation and shortened lifespan, along with aging-like phenotypes including hypertrophic heart, lung and spleen, but atrophic thymus and reduced bone mineral density at organismal level. Hematopoietic autophagy defect also causes increased oxidative stress and mitochondrial mass or aging gene expression at cellular level in multiple non-hematopoietic organs. The organ aging in the Atg7-deleted mice was reversed by anatomic connection to wild-type mice with intact blood autophagy via parabiosis, but not by injection of blood cell-free plasma. Our finding thus highlights an essential role of hematopoietic autophagy for decelerating aging in non-hematopoietic organs.
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The positive impacts of early-life education on cognition, leisure activity, and brain structure in healthy aging

Yaojing Chen, Chenlong Lv, Xin Li, Junying Zhang, Kewei Chen, Zhongwan Liu, He Li, Jialing Fan, Ting Qin, Liang Luo, Zhanjun Zhang,

https://doi.org/10.18632/aging.102088 pp 4923—4942

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Chen Y, Lv C, Li X, Zhang J, Chen K, Liu Z, Li H, Fan J, Qin T, Luo L, Zhang Z, . The positive impacts of early-life education on cognition, leisure activity, and brain structure in healthy aging. . 11:4923-4942. https://doi.org/10.18632/aging.102088

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                TY  - JOUR
                AU  - Chen, Yaojing 
                AU  - Lv, Chenlong 
                AU  - Li, Xin 
                AU  - Zhang, Junying 
                AU  - Chen, Kewei 
                AU  - Liu, Zhongwan 
                AU  - Li, He 
                AU  - Fan, Jialing 
                AU  - Qin, Ting 
                AU  - Luo, Liang 
                AU  - Zhang, Zhanjun 
                TI  - The positive impacts of early-life education on cognition, leisure activity, and brain structure in healthy aging
                JO  - 
                JA  - 
                VL  - 11
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102088
                DO  - 10.18632/aging.102088
                SP  - 4923
                EP  - 4942
                PY  - 
                AB  - Education in people&#x2019;s early lives are positively related to their cognitive function, but its modulating effects on detailed cognition domains, its interaction with leisure activities and the associated brain changes have yet to be investigated. This report used data from 659 cognitively normal community dwelling elderly who completed neuropsychological tests, leisure activities measurement, and 78 of them underwent structural and diffusion MRI scans. We found that: (i) the highly educated elderly had a better cognitive functioning in multi-domains, higher frequencies of participation in knowledge-related leisure activities, and slower age-related reductions of executive function; (ii) the intellectual and social types of leisure activities mediated the association between education and multiple cognitive domains, including memory, language, attention and executive function; (iii) there was a significant age by education interaction on the gray matter volume of the anterior brain regions and white matter integrity; and (iv) the interaction between age and education affected cognition indirectly through white matter integrity analyzed using structural equation model. Overall, our results revealed that high education in early life served as a protective factor in aging that may help to postpone cognitive and brain reserve decline in cognitively normal aging.
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D-ribose is elevated in T1DM patients and can be involved in the onset of encephalopathy

Lexiang Yu, Yao Chen, Yong Xu, Tao He, Yan Wei, Rongqiao He,

https://doi.org/10.18632/aging.102089 pp 4943—4969

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Yu L, Chen Y, Xu Y, He T, Wei Y, He R, . D-ribose is elevated in T1DM patients and can be involved in the onset of encephalopathy. . 11:4943-4969. https://doi.org/10.18632/aging.102089

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                TY  - JOUR
                AU  - Yu, Lexiang 
                AU  - Chen, Yao 
                AU  - Xu, Yong 
                AU  - He, Tao 
                AU  - Wei, Yan 
                AU  - He, Rongqiao 
                TI  - D-ribose is elevated in T1DM patients and can be involved in the onset of encephalopathy
                JO  - 
                JA  - 
                VL  - 11
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102089
                DO  - 10.18632/aging.102089
                SP  - 4943
                EP  - 4969
                PY  - 
                AB  - Although many mechanisms have been proposed for diabetic encephalopathy in type 2 diabetes mellitus (T2DM), the risk factors for cognitive impairment in type 1 diabetes mellitus (T1DM) are less clear. Here, we show that streptozotocin (STZ)-induced T1DM rats showed cognitive impairment in both Y maze and Morris water maze assays, accompanied with D-ribose was significantly increased in blood and urine, in addition to D-glucose. Furthermore, advanced glycation end products (AGE), Tau hyperphosphorylation and neuronal death in the hippocampal CA4/DG region were detected in T1DM rats. The expression and activity of transketolase (TKT), an important enzyme in the pentose shunt, were decreased in the brain, indicating that TKT may be involved in D-ribose metabolism in T1DM. Support for these change was demonstrated by the activation of TKT with benfotiamine (BTMP) treatment. Decreased D-ribose levels but not D-glucose levels; markedly reduced AGE accumulation, Tau hyperphosphorylation, and neuronal death; and improved cognitive ability in T1DM rats were shown after BTMP administration. In clinical investigation, T1DM patients had high D-ribose levels in both urine and serum. Our work suggests that D-ribose is involved in the cognitive impairment in T1DM and may provide a potentially novel target for treating diabetic encephalopathy.
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Optimism is not associated with two indicators of DNA methylation aging

Eric S. Kim, Kelvin Fong, Lewina Lee, Avron Spiro, Joel Schwartz, Eric Whitsel, Steve Horvath, Cuicui Wang, Lifang Hou, Andrea A. Baccarelli, Yun Li, James Stewart, JoAnn E. Manson, Francine Grodstein, Dawn L. DeMeo, Laura D. Kubzansky,

https://doi.org/10.18632/aging.102090 pp 4970—4989

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Kim ES, Fong K, Lee L, Spiro A, Schwartz J, Whitsel E, Horvath S, Wang C, Hou L, Baccarelli AA, Li Y, Stewart J, Manson JE, et al, . Optimism is not associated with two indicators of DNA methylation aging. . 11:4970-4989. https://doi.org/10.18632/aging.102090

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                TY  - JOUR
                AU  - Kim, Eric S. 
                AU  - Fong, Kelvin 
                AU  - Lee, Lewina 
                AU  - Spiro, Avron 
                AU  - Schwartz, Joel 
                AU  - Whitsel, Eric 
                AU  - Horvath, Steve 
                AU  - Wang, Cuicui 
                AU  - Hou, Lifang 
                AU  - Baccarelli, Andrea A. 
                AU  - Li, Yun 
                AU  - Stewart, James 
                AU  - Manson, JoAnn E. 
                AU  - Grodstein, Francine 
                AU  - DeMeo, Dawn L. 
                AU  - Kubzansky, Laura D. 
                TI  - Optimism is not associated with two indicators of DNA methylation aging
                JO  - 
                JA  - 
                VL  - 11
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102090
                DO  - 10.18632/aging.102090
                SP  - 4970
                EP  - 4989
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Kim, Eric S. 
                AU  - Fong, Kelvin 
                AU  - Lee, Lewina 
                AU  - Spiro, Avron 
                AU  - Schwartz, Joel 
                AU  - Whitsel, Eric 
                AU  - Horvath, Steve 
                AU  - Wang, Cuicui 
                AU  - Hou, Lifang 
                AU  - Baccarelli, Andrea A. 
                AU  - Li, Yun 
                AU  - Stewart, James 
                AU  - Manson, JoAnn E. 
                AU  - Grodstein, Francine 
                AU  - DeMeo, Dawn L. 
                AU  - Kubzansky, Laura D. 
                TI  - Optimism is not associated with two indicators of DNA methylation aging
                JO  - 
                JA  - 
                VL  - 11
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102090
                DO  - 10.18632/aging.102090
                SP  - 4970
                EP  - 4989
                PY  - 
                AB  - Evidence indicates associations between higher optimism and reduced risk of age-related conditions and premature mortality. This suggests optimism is a positive health asset, but research identifying potential biological mechanisms underlying these associations remains limited. One potential pathway is slower cellular aging, which may delay age-related deterioration in health. Data were from the Women&#x2019;s Health Initiative (WHI) (N=3,298) and the Veterans Affairs Normative Aging Study (NAS) (N=514), and included dispositional and explanatory style optimism measures. We evaluated whether higher optimism was associated with metrics suggestive of less cellular aging, as indicated by two DNA methylation algorithms, intrinsic (IEAA) and extrinsic epigenetic age acceleration (EEAA); these algorithms represent accelerated biologic aging that exceeds chronological age. We used linear regression models to test our hypothesis while considering several covariates (sociodemographics, depressive symptoms, health behaviors). In both cohorts, we found consistently null associations of all measures of optimism with both measures of DNA methylation aging, regardless of covariates considered. For example, in fully-adjusted models, dispositional optimism was not associated with either IEAA (WHI:&#x3B2;=0.02; 95% Confidence Interval [CI]:-0.15-0.20; NAS:&#x3B2;=-0.06; 95% CI:-0.56-0.44) or EEAA (WHI:&#x3B2;=-0.04; 95% CI: -0.26-0.17; NAS:&#x3B2;=-0.17; 95% CI: -0.80-0.46). Higher optimism was not associated with reduced cellular aging as measured in this study.
                ER  -

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Long noncoding RNA FALEC inhibits proliferation and metastasis of tongue squamous cell carcinoma by epigenetically silencing ECM1 through EZH2

Bo Jia, Tao Xie, Xiaoling Qiu, Xiang Sun, Jun Chen, Zhijie Huang, Xianghuai Zheng, Zhiping Wang, Jianjiang Zhao,

https://doi.org/10.18632/aging.102094 pp 4990—5007

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Jia B, Xie T, Qiu X, Sun X, Chen J, Huang Z, Zheng X, Wang Z, Zhao J, . Long noncoding RNA FALEC inhibits proliferation and metastasis of tongue squamous cell carcinoma by epigenetically silencing ECM1 through EZH2. . 11:4990-5007. https://doi.org/10.18632/aging.102094

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                TY  - JOUR
                AU  - Jia, Bo 
                AU  - Xie, Tao 
                AU  - Qiu, Xiaoling 
                AU  - Sun, Xiang 
                AU  - Chen, Jun 
                AU  - Huang, Zhijie 
                AU  - Zheng, Xianghuai 
                AU  - Wang, Zhiping 
                AU  - Zhao, Jianjiang 
                TI  - Long noncoding RNA FALEC inhibits proliferation and metastasis of tongue squamous cell carcinoma by epigenetically silencing ECM1 through EZH2
                JO  - 
                JA  - 
                VL  - 11
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102094
                DO  - 10.18632/aging.102094
                SP  - 4990
                EP  - 5007
                PY  - 
                AB  - Tongue squamous cell carcinoma (TSCC), the most common epithelial cancer identified in the oral cavity, has become one of the most common malignancies across the developing countries. Increasing evidence indicates that long non-coding RNAs (lncRNAs) serve as important regulators in cancer biology. The focally amplified long non-coding RNA in epithelial cancer (FALEC) was found downregulated in the tissues of tongue squamous cell carcinoma (TSCC) and was predicted to present a good prognosis by bioinformatics analysis. Experiments indicated that FALEC knockdown significantly increased the proliferation and migration of TSCC cells both in vitro and in vivo; however, FALEC overexpression repressed these malignant behaviors. RNA pull-down and RNA immunoprecipitation demonstrated that FALEC could recruit enhancer of zeste homolog 2 (EZH2) at the promoter regions of extracellular matrix protein 1 (ECM1), epigenetically repressing ECM1 expression. The data revealed that FALEC acted as a tumor suppressor in TSCC and may aid in developing a novel potential therapeutic strategy against TSCC.
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Ginsenoside Rb1 regulates prefrontal cortical GABAergic transmission in MPTP-treated mice

Yan Liu, Xiaodan Zong, Jie Huang, Yanfei Guan, Yuanquan Li, Ting Du, Keyin Liu, Xinpan Kang, Chunyan Dou, Xiangdong Sun, Renhua Wu, Lei Wen, Yunlong Zhang,

https://doi.org/10.18632/aging.102095 pp 5008—5034

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Liu Y, Zong X, Huang J, Guan Y, Li Y, Du T, Liu K, Kang X, Dou C, Sun X, Wu R, Wen L, Zhang Y, . Ginsenoside Rb1 regulates prefrontal cortical GABAergic transmission in MPTP-treated mice. . 11:5008-5034. https://doi.org/10.18632/aging.102095

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                TY  - JOUR
                AU  - Liu, Yan 
                AU  - Zong, Xiaodan 
                AU  - Huang, Jie 
                AU  - Guan, Yanfei 
                AU  - Li, Yuanquan 
                AU  - Du, Ting 
                AU  - Liu, Keyin 
                AU  - Kang, Xinpan 
                AU  - Dou, Chunyan 
                AU  - Sun, Xiangdong 
                AU  - Wu, Renhua 
                AU  - Wen, Lei 
                AU  - Zhang, Yunlong 
                TI  - Ginsenoside Rb1 regulates prefrontal cortical GABAergic transmission in MPTP-treated mice
                JO  - 
                JA  - 
                VL  - 11
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102095
                DO  - 10.18632/aging.102095
                SP  - 5008
                EP  - 5034
                PY  - 
                AB  - Parkinson&#x2019;s disease (PD) is a common neurodegenerative disease, featured by motor deficits and non-motor symptoms such as cognitive impairment, and malfunction of gamma-aminobutyric acid (GABA) mediated inhibitory transmission plays an important role in PD pathogenesis. The ginsenoside Rb1 molecule, a major constituent of the extract from the Ginseng root, has been demonstrated to ameliorate motor deficits and prevent dopaminergic neuron death in PD. However, whether Rb1 can regulate GABAergic transmission in PD-associated deficits and its underlying mechanisms are still unclear. In this study, we explored the effects of Rb1 on the GABAergic synaptic transmission in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of PD. We demonstrated that Rb1 can bind with GABAAR&#x3B1;1 and increase its expression in the SH-SY5Y cells and in the prefrontal cortex (PFC) of MPTP model in vitro and in vivo. Furthermore, Rb1 can promote prefrontal cortical GABA level and GABAergic transmission in MPTP-treated mice. We also revealed that Rb1 may suppress presynaptic GABABR1 to enhance GABA release and GABAA receptor-mediated inhibitory transmission. In addition, Rb1 attenuated MPTP-induced dysfunctional gait dynamic and cognitive impairment, and this neuroprotective mechanism possibly involved regulating prefrontal cortical GABAergic transmission. Thus, Rb1 may serve as a potential drug candidate for the treatment of PD.
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Overexpression of KLF5 is associated with poor survival and G1/S progression in pancreatic cancer

Yilong Li, Rui Kong, Hongze Chen, Zhongjie Zhao, Le Li, Jiating Li, Jisheng Hu, Guangquan Zhang, Shangha Pan, Yongwei Wang, Gang Wang, Hua Chen, Bei Sun,

https://doi.org/10.18632/aging.102096 pp 5035—5057

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Li Y, Kong R, Chen H, Zhao Z, Li L, Li J, Hu J, Zhang G, Pan S, Wang Y, Wang G, Chen H, Sun B, . Overexpression of KLF5 is associated with poor survival and G1/S progression in pancreatic cancer. . 11:5035-5057. https://doi.org/10.18632/aging.102096

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                TY  - JOUR
                AU  - Li, Yilong 
                AU  - Kong, Rui 
                AU  - Chen, Hongze 
                AU  - Zhao, Zhongjie 
                AU  - Li, Le 
                AU  - Li, Jiating 
                AU  - Hu, Jisheng 
                AU  - Zhang, Guangquan 
                AU  - Pan, Shangha 
                AU  - Wang, Yongwei 
                AU  - Wang, Gang 
                AU  - Chen, Hua 
                AU  - Sun, Bei 
                TI  - Overexpression of KLF5 is associated with poor survival and G1/S progression in pancreatic cancer
                JO  - 
                JA  - 
                VL  - 11
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102096
                DO  - 10.18632/aging.102096
                SP  - 5035
                EP  - 5057
                PY  - 
                AB  - Despite improvements in surgical procedures and comprehensive therapies, pancreatic cancer remains one of the most aggressive and deadly human malignancies. It is therefore necessary to determine which cellular mediators associate with prognosis in pancreatic cancer so as to improve the treatment of this disease. In the present study, mRNA array and immunohistochemical analyses showed that KLF5 is highly expressed in tissue samples from three short-surviving patients with pancreatic cancer. Survival analysis using data from The Cancer Genome Atlas showed that patients highly expressing KLF5 exhibited shorter overall and tumor-free survival times. Mechanistically, KLF5 promoted expression of E2F1, cyclin D1 and Rad51, while inhibiting expression of p16 in pancreatic cancer cells. Finally, flow cytometric analyses verified that KLF5 promotes G1/S progression of the cell cycle in pancreatic cancer cells. Collectively, these findings demonstrate that KLF5 is an important prognostic biomarker in pancreatic cancer patients, and they shed light on the molecular mechanism by which KLF5 stimulates cell cycle progression in pancreatic cancer.
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miR-548d-3p inhibits osteosarcoma by downregulating KRAS

Jianhua Chen, Chongnan Yan, Honghao Yu, Shihan Zhen, Quan Yuan,

https://doi.org/10.18632/aging.102097 pp 5058—5069

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Chen J, Yan C, Yu H, Zhen S, Yuan Q, . miR-548d-3p inhibits osteosarcoma by downregulating KRAS. . 11:5058-5069. https://doi.org/10.18632/aging.102097

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                TY  - JOUR
                AU  - Chen, Jianhua 
                AU  - Yan, Chongnan 
                AU  - Yu, Honghao 
                AU  - Zhen, Shihan 
                AU  - Yuan, Quan 
                TI  - miR-548d-3p inhibits osteosarcoma by downregulating <i>KRAS</i>
                JO  - 
                JA  - 
                VL  - 11
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102097
                DO  - 10.18632/aging.102097
                SP  - 5058
                EP  - 5069
                PY  - 
                AB  - MicroRNAs (miRNAs) are known to be associated with certain cancers, including osteosarcoma. We examined osteosarcoma tissues and cell lines, and found that most expressed lower levels of miR-548d-3p than adjacent tissues and normal cell lines. KRAS was identified as a potential target gene of miR-548d-3p. In osteosarcoma cells, miR-548d-3p exerted tumor-suppressive effects by downregulating KRAS. Functional assays revealed that miR-548d-3p mimics dramatically reduced cell growth and migration in vitro. These results suggest that miR-548d-3p mimics could be applied for osteosarcoma treatment.
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Shortening telomere is associated with subclinical atherosclerosis biomarker in omnivorous but not in vegetarian healthy men

Naiara Cinegaglia, Luiza Antoniazzi, Daniela Rosa, Debora Miranda, Julio Acosta-Navarro, Luiz Bortolotto, Valeria Hong, Valeria Sandrim,

https://doi.org/10.18632/aging.102098 pp 5070—5080

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Cinegaglia N, Antoniazzi L, Rosa D, Miranda D, Acosta-Navarro J, Bortolotto L, Hong V, Sandrim V, . Shortening telomere is associated with subclinical atherosclerosis biomarker in omnivorous but not in vegetarian healthy men. . 11:5070-5080. https://doi.org/10.18632/aging.102098

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                TY  - JOUR
                AU  - Cinegaglia, Naiara 
                AU  - Antoniazzi, Luiza 
                AU  - Rosa, Daniela 
                AU  - Miranda, Debora 
                AU  - Acosta-Navarro, Julio 
                AU  - Bortolotto, Luiz 
                AU  - Hong, Valeria 
                AU  - Sandrim, Valeria 
                TI  - Shortening telomere is associated with subclinical atherosclerosis biomarker in omnivorous but not in vegetarian healthy men
                JO  - 
                JA  - 
                VL  - 11
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102098
                DO  - 10.18632/aging.102098
                SP  - 5070
                EP  - 5080
                PY  - 
                AB  - Telomere length is considered to be a biomarker of biological aging and age-related disease. There are few studies that have evaluated the association between telomere length and diet, and none of them have evaluated the impact of a vegetarian diet on telomere length and its correlation with cardiovascular biomarkers in apparently healthy subjects. Therefore, our objectives were to evaluate leukocyte telomere length (LTL) in vegetarians and omnivorous subjects and its association with classical cardiovascular risk biomarkers. From the total of 745 participants initially recruited, 44 omnivorous and 44 vegetarian men apparently healthy were selected for this study and LTL was measured in 39 omnivorous and 41 vegetarians by Real-Time Quantitative PCR reaction. Although telomere length was not different between omnivorous and vegetarians, we found a strong negative correlation between LTL and IMT (intima-media thickness) in omnivorous, but not in vegetarian group. In addition, omnivorous who were classified with short telomere length had higher carotid IMT compared to vegetarians. Our data suggest that telomere length can be a marker of subclinical atherosclerosis in the omnivorous group.
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Better prognostic determination and feature characterization of cutaneous melanoma through integrative genomic analysis

Xia Li, Yunpeng Cai,

https://doi.org/10.18632/aging.102099 pp 5081—5107

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Li X, Cai Y, . Better prognostic determination and feature characterization of cutaneous melanoma through integrative genomic analysis. . 11:5081-5107. https://doi.org/10.18632/aging.102099

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                TY  - JOUR
                AU  - Li, Xia 
                AU  - Cai, Yunpeng 
                TI  - Better prognostic determination and feature characterization of cutaneous melanoma through integrative genomic analysis
                JO  - 
                JA  - 
                VL  - 11
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102099
                DO  - 10.18632/aging.102099
                SP  - 5081
                EP  - 5107
                PY  - 
                AB  - Melanoma is the most dangerous type of skin cancer and has highly heterogeneous features. Despite progress in melanoma classification, interpatient heterogeneity remains difficult to predict, especially in terms of long-term survival. Here, based on mRNA-seq, miRNA-seq and DNA methylation data from 447 cutaneous melanoma patients in the Cancer Genome Atlas, we performed integrative and single-dataset clustering analyses. A novel group of patients was identified, including 301 with better, 55 with poorer and 91 with intermediate prognoses. Immune genes were upregulated in the better prognostic group, and higher immune scores (representing a greater extent of immune cell infiltration into tumor tissues) were associated with better prognoses. Higher expression of 115 genes was determined to predict better outcomes. The better prognostic group also exhibited DNA hypomethylation, and immune pathways were enriched among the hypomethylated genes. Using exome-seq data from the same patients, we observed that the better prognostic group harbored the highest number of mutations. The mutational signature in the better prognostic group was associated with ultraviolet light exposure. These integrated investigations have potential therapeutic significance, as they clarify the molecular heterogeneity of cutaneous melanoma and enhance its classification.
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Activation of AK005401 aggravates acute ischemia/reperfusion mediated hippocampal injury by directly targeting YY1/FGF21

Hongzhi Wan, Ying Yang, Miao Li, Xin Liu, Yeying Sun, Kexin Wang, Chunxiang Zhang, Qingyin Zheng, Chaoyun Wang,

https://doi.org/10.18632/aging.102106 pp 5108—5123

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Wan H, Yang Y, Li M, Liu X, Sun Y, Wang K, Zhang C, Zheng Q, Wang C, . Activation of AK005401 aggravates acute ischemia/reperfusion mediated hippocampal injury by directly targeting YY1/FGF21. . 11:5108-5123. https://doi.org/10.18632/aging.102106

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                TY  - JOUR
                AU  - Wan, Hongzhi 
                AU  - Yang, Ying 
                AU  - Li, Miao 
                AU  - Liu, Xin 
                AU  - Sun, Yeying 
                AU  - Wang, Kexin 
                AU  - Zhang, Chunxiang 
                AU  - Zheng, Qingyin 
                AU  - Wang, Chaoyun 
                TI  - Activation of AK005401 aggravates acute ischemia/reperfusion mediated hippocampal injury by directly targeting YY1/FGF21
                JO  - 
                JA  - 
                VL  - 11
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102106
                DO  - 10.18632/aging.102106
                SP  - 5108
                EP  - 5123
                PY  - 
                AB  - Ischemia exerts a negative impact on mitochondrial function, which ultimately results in neuronal damage via alterations in gene transcription and protein expression. Long non- coding RNAs (LncRNAs) play pivotal roles in the regulation of target protein expression and gene transcription. In the present study, we observed the effect of an unclassical LncRNA AK005401on ischemia/reperfusion (I/R) ischemia-mediated hippocampal injury and investigated the regulatory role of fibroblast growth factor 21 (FGF21) and Yin Yang 1 (YY1). C57Black/6 mice were subjected to I/R using the bilateral common carotid clip reperfusion method, and AK005401 siRNA oligos were administered via intracerebroventricular injection. HT22 cells were used to establish a model of oxygen-glucose deprivation/reoxygenation (OGD/R). We observed pathological morphology and mitochondrial structure. Neuronal apoptosis was evident. Cell activity, cell respiration, FGF21, YY1, and antioxidant capacity were evaluated. I/R or OGD/R significantly increased the expressions of AK005401and YY1 and decreased FGF21expression, which further attenuated the activation of PI3K/Akt, promoted reactive oxygen species (ROS) generation, and then caused mitochondria dysfunction and cell apoptosis, which were reversed by AK005401 siRNA oligos and were aggravated by overexpression of AK005401 and YY1. We conclude that AK005401/YY1/FGF21 signaling pathway has an important role in I/R-mediated hippocampal injury.
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Novel serum metabolites associate with cognition phenotypes among Bogalusa Heart Study participants

Mengyao Shi, Lydia A. Bazzano, Jiang He, Xiaoying Gu, Changwei Li, Shengxu Li, Kristine Yaffe, Jason M. Kinchen, Patrick Stuchlik, Xuenan Mi, Jovia L. Nierenberg, Alexander C. Razavi, Tanika N. Kelly,

https://doi.org/10.18632/aging.102107 pp 5124—5139

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Shi M, Bazzano LA, He J, Gu X, Li C, Li S, Yaffe K, Kinchen JM, Stuchlik P, Mi X, Nierenberg JL, Razavi AC, Kelly TN, . Novel serum metabolites associate with cognition phenotypes among Bogalusa Heart Study participants. . 11:5124-5139. https://doi.org/10.18632/aging.102107

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                TY  - JOUR
                AU  - Shi, Mengyao 
                AU  - Bazzano, Lydia A. 
                AU  - He, Jiang 
                AU  - Gu, Xiaoying 
                AU  - Li, Changwei 
                AU  - Li, Shengxu 
                AU  - Yaffe, Kristine 
                AU  - Kinchen, Jason M. 
                AU  - Stuchlik, Patrick 
                AU  - Mi, Xuenan 
                AU  - Nierenberg, Jovia L. 
                AU  - Razavi, Alexander C. 
                AU  - Kelly, Tanika N. 
                TI  - Novel serum metabolites associate with cognition phenotypes among Bogalusa Heart Study participants
                JO  - 
                JA  - 
                VL  - 11
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102107
                DO  - 10.18632/aging.102107
                SP  - 5124
                EP  - 5139
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Shi, Mengyao 
                AU  - Bazzano, Lydia A. 
                AU  - He, Jiang 
                AU  - Gu, Xiaoying 
                AU  - Li, Changwei 
                AU  - Li, Shengxu 
                AU  - Yaffe, Kristine 
                AU  - Kinchen, Jason M. 
                AU  - Stuchlik, Patrick 
                AU  - Mi, Xuenan 
                AU  - Nierenberg, Jovia L. 
                AU  - Razavi, Alexander C. 
                AU  - Kelly, Tanika N. 
                TI  - Novel serum metabolites associate with cognition phenotypes among Bogalusa Heart Study participants
                JO  - 
                JA  - 
                VL  - 11
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102107
                DO  - 10.18632/aging.102107
                SP  - 5124
                EP  - 5139
                PY  - 
                AB  - Background: Metabolomics study provides an opportunity to identify novel molecular determinants of altered cognitive function.Methods: During 2013 to 2016 Bogalusa Heart Study (BHS) visit, 1,177 participants underwent untargeted, ultrahigh performance liquid chromatography-tandem mass spectroscopy metabolomics profiling. Global cognition and five cognition domains were also assessed. The cross-sectional associations of single metabolites with cognition were tested using multiple linear regression models. Weighted correlation network analysis was used to examine the covariable-adjusted correlations of modules of co-abundant metabolites with cognition. Analyses were conducted in the overall sample and according to both ethnicity and sex.Results: Five known metabolites and two metabolite modules robustly associated with cognition across overall and stratified analyses. Two metabolites were from lipid sub-pathways including fatty acid metabolism [9-hydroxystearate; minimum P-value (min-P)=1.11&#xD7;10-5], and primary bile acid metabolism (glyco-alpha-muricholate; min-P=4.10&#xD7;10-5). One metabolite from the glycogen metabolism sub-pathway (maltose; min-P=9.77&#xD7;10-6), one from the polyamine metabolism sub-pathway (N-acetyl-isoputreanine; min-P=1.03&#xD7;10-5), and one from the purine metabolism sub-pathway (7-methylguanine; min-P=1.19&#xD7;10-5) were also identified. Two metabolite modules reflecting bile acid metabolism and androgenic steroids correlated with cognition (min-P=5.00&#xD7;10-4 and 3.00&#xD7;10-3, respectively).Conclusion: The novel associations of 5 known metabolites and 2 metabolite modules with cognition provide insights into the physiological mechanisms regulating cognitive function.
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Subunit contribution to NMDA receptor hypofunction and redox sensitivity of hippocampal synaptic transmission during aging

Ashok Kumar, Jeffrey S. Thinschmidt, Thomas C. Foster,

https://doi.org/10.18632/aging.102108 pp 5140—5157

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Kumar A, Thinschmidt JS, Foster TC, . Subunit contribution to NMDA receptor hypofunction and redox sensitivity of hippocampal synaptic transmission during aging. . 11:5140-5157. https://doi.org/10.18632/aging.102108

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                TY  - JOUR
                AU  - Kumar, Ashok 
                AU  - Thinschmidt, Jeffrey S. 
                AU  - Foster, Thomas C. 
                TI  - Subunit contribution to NMDA receptor hypofunction and redox sensitivity of hippocampal synaptic transmission during aging
                JO  - 
                JA  - 
                VL  - 11
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102108
                DO  - 10.18632/aging.102108
                SP  - 5140
                EP  - 5157
                PY  - 
                AB  - We examined the contribution of N-methyl-D-aspartate receptor (NMDAR) subunits in the redox-mediated decline in NMDAR function during aging. GluN2A and GluN2B selective antagonists decreased peak NMDAR currents to a similar extent in young and aged animals, indicating that a shift in diheteromeric GluN2 subunits does not underlie the age-related decrease in the NMDAR synaptic function. Application of dithiothreitol (DTT) in aged animals, increased peak NMDAR synaptic currents, prolonged the decay time, and increased the sensitivity of the synaptic response to the GluN2B antagonist, ifenprodil, indicating that DTT increased the contribution of GluN2B subunits to the synaptic response. The DTT-mediated increase in NMDAR function was inhibited by partial blockade of NMDARs, and this inhibition was rescued by increasing Ca2+ concentration in the recording medium. The results indicate that DTT-mediated potentiation requires Ca2+ influx through NMDAR activity. Finally, redox regulation of NMDAR function depends on the activity of Ca2+/calmodulin-dependent protein kinase II (CaMKII). The results indicate that activity-dependent NMDAR synaptic plasticity is suppressed by redox-mediated inhibition of CaMKII activation during aging. The redox regulation of NMDARs represents a suppression of a metaplasticity mechanism, which can disrupt synaptic plasticity and cognition associated with neurological or psychiatric diseases, and aging.
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The diagnostic and prognostic role of RhoA in hepatocellular carcinoma

Yi Bai, Fucun Xie, Fei Miao, Junyu Long, Shan Huang, Hanchun Huang, Jianzhen Lin, Dongxu Wang, Xu Yang, Jin Bian, Jinzhu Mao, Xi Wang, Yilei Mao, Xinting Sang, Haitao Zhao,

https://doi.org/10.18632/aging.102110 pp 5158—5172

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Bai Y, Xie F, Miao F, Long J, Huang S, Huang H, Lin J, Wang D, Yang X, Bian J, Mao J, Wang X, Mao Y, et al, . The diagnostic and prognostic role of RhoA in hepatocellular carcinoma. . 11:5158-5172. https://doi.org/10.18632/aging.102110

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                TY  - JOUR
                AU  - Bai, Yi 
                AU  - Xie, Fucun 
                AU  - Miao, Fei 
                AU  - Long, Junyu 
                AU  - Huang, Shan 
                AU  - Huang, Hanchun 
                AU  - Lin, Jianzhen 
                AU  - Wang, Dongxu 
                AU  - Yang, Xu 
                AU  - Bian, Jin 
                AU  - Mao, Jinzhu 
                AU  - Wang, Xi 
                AU  - Mao, Yilei 
                AU  - Sang, Xinting 
                AU  - Zhao, Haitao 
                TI  - The diagnostic and prognostic role of RhoA in hepatocellular carcinoma
                JO  - 
                JA  - 
                VL  - 11
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102110
                DO  - 10.18632/aging.102110
                SP  - 5158
                EP  - 5172
                PY  - 
                AB  - The aim of this study was to investigate the expression level of Ras homolog gene family, member A (RhoA) in patients with hepatocellular carcinoma (HCC) and to investigate the prognostic and diagnostic value of RhoA. Data mining from various data bases and wet experiments on samples from Peking Union Medical College Hospital showed that RhoA mRNA and protein expression were significantly higher in the HCC tissues than in the normal tissues. Higher expression at both the mRNA and protein levels was associated with a poorer prognosis. High sensitivity (92.5%) and specificity (90.0%) were observed in the diagnostic model based on protein level rather than mRNA level. RhoA expression was modulated by genetic amplification. The lysosome, pathogenic Escherichia coli infection, purine metabolism and pyrimidine metabolism pathways were mainly enriched in the high RhoA level group, while the hedgehog signaling, linoleic acid metabolism, olfactory transduction and taste transduction pathways were enriched in the low RhoA level group. RhoA is commonly upregulated in HCC tissues, and its expression at both the mRNA and protein levels is associated with poor prognosis. Notably, RhoA protein levels serve as a diagnostic biomarker for HCC.
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Genetic polymorphisms and transcription profiles associated with intracranial aneurysm: a key role for NOTCH3

Mengqi Li, Xinlong Dong, Shi Chen, Weihan Wang, Chao Yang, Bochuan Li, Degang Liang, Weidong Yang, Xiaozhi Liu, Xinyu Yang,

https://doi.org/10.18632/aging.102111 pp 5173—5191

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Li M, Dong X, Chen S, Wang W, Yang C, Li B, Liang D, Yang W, Liu X, Yang X, . Genetic polymorphisms and transcription profiles associated with intracranial aneurysm: a key role for NOTCH3. . 11:5173-5191. https://doi.org/10.18632/aging.102111

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                TY  - JOUR
                AU  - Li, Mengqi 
                AU  - Dong, Xinlong 
                AU  - Chen, Shi 
                AU  - Wang, Weihan 
                AU  - Yang, Chao 
                AU  - Li, Bochuan 
                AU  - Liang, Degang 
                AU  - Yang, Weidong 
                AU  - Liu, Xiaozhi 
                AU  - Yang, Xinyu 
                TI  - Genetic polymorphisms and transcription profiles associated with intracranial aneurysm: a key role for NOTCH3
                JO  - 
                JA  - 
                VL  - 11
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102111
                DO  - 10.18632/aging.102111
                SP  - 5173
                EP  - 5191
                PY  - 
                AB  - Intracranial aneurysm (IA) incidence is about 1~2%. However, the specific mechanisms of IA onset and development need further study. Our objective was to discover novel IA-related genes to determine possible etiologies further. We performed next-generation sequencing on nineteen Chinese patients with familial IA and one patient with sporadic IA. We obtained mRNA expression data of 129 samples from Gene Expression Omnibus (GEO) and made statistical computing to discover differentially expressed genes (DEGs). The screened IA-related gene NOTCH3 was determined by bioinformatic data mining. We verified the IA-related indicators of NOTCH3. Association was found between IA and the NOTCH3 SNPs rs779314594, rs200504060 and rs2285981. Levels of NOTCH3 mRNA were lower in IA tissue than in control tissue, but higher in peripheral blood neutrophils from IA patients than in neutrophils from controls. Levels of NOTCH3 protein were lower in IA tissue than in cerebral artery tissue. NOTCH3 also decreased the expression of angiogenesis factors in human umbilical vein endothelial cells. Variation in NOTCH3 and alteration of its expression in cerebral artery or neutrophils may contribute to IA. Our findings also describe a bioinformatic-experimental approach that may prove useful for probing the pathophysiology of other complex diseases.
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Down-regulation of lncRNA MALAT1 alleviates vascular lesion and vascular remodeling of rats with hypertension

Yu-Zeng Xue, Zhi-Juan Li, Wei-Tao Liu, Jin-Jiao Shan, Lei Wang, Qian Su,

https://doi.org/10.18632/aging.102113 pp 5192—5205

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Xue Y, Li Z, Liu W, Shan J, Wang L, Su Q, . Down-regulation of lncRNA MALAT1 alleviates vascular lesion and vascular remodeling of rats with hypertension. . 11:5192-5205. https://doi.org/10.18632/aging.102113

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                TY  - JOUR
                AU  - Xue, Yu-Zeng 
                AU  - Li, Zhi-Juan 
                AU  - Liu, Wei-Tao 
                AU  - Shan, Jin-Jiao 
                AU  - Wang, Lei 
                AU  - Su, Qian 
                TI  - Down-regulation of lncRNA MALAT1 alleviates vascular lesion and vascular remodeling of rats with hypertension
                JO  - 
                JA  - 
                VL  - 11
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102113
                DO  - 10.18632/aging.102113
                SP  - 5192
                EP  - 5205
                PY  - 
                AB  - Objective: Recently, the effect of long non-coding RNAs (lncRNAs) in hypertension (HTN) has been identified. This study aims to explore the expression of lncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) in HTN and its role in vascular lesion and remodeling of HTN rats.Results: LncRNA MALAT1 expression was up-regulated in HTN patients, and lncRNA MALAT1 could be an effective index of HTN diagnosis. Down-regulated MALAT1 and inhibited Notch-1 could reduce relative factor expression, including inflammation-related factors, endothelial function-related factors and oxidative stress-related factors, and inhibit apoptosis of aortic endothelial cells of HTN rats.Methods: LncRNA MALAT1 expression in HTN patients and healthy controls was detected by reverse transcription quantitative polymerase chain reaction (RT-qPCR). Angiotensin II (Ang II)-induced HTN rat models were injected with MALAT1-siRNA, empty lentivirus vector, Notch pathway inhibitor (DAPT) and dimethyl sulphoxide (DMSO) via caudal vein. After three-week treatment, changes of blood pressure, inflammatory factor levels, endothelial function-related factors, oxidative stress indices and apoptosis of vascular endothelial cells were determined by a series of assays.Conclusion: This study revealed that down-regulated lncRNA MALAT1 could alleviate the vascular lesion and remodeling of HTN rats, the mechanism may be related to the inhibited activation of Notch signaling pathway.
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Sex-specific components of frailty in C57BL/6 mice

Cory W. Baumann, Dongmin Kwak, LaDora V. Thompson,

https://doi.org/10.18632/aging.102114 pp 5206—5214

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Baumann CW, Kwak D, Thompson LV, . Sex-specific components of frailty in C57BL/6 mice. . 11:5206-5214. https://doi.org/10.18632/aging.102114

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                TY  - JOUR
                AU  - Baumann, Cory W. 
                AU  - Kwak, Dongmin 
                AU  - Thompson, LaDora V. 
                TI  - Sex-specific components of frailty in C57BL/6 mice
                JO  - 
                JA  - 
                VL  - 11
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102114
                DO  - 10.18632/aging.102114
                SP  - 5206
                EP  - 5214
                PY  - 
                AB  - Many age-related biochemical, physiological and behavioral changes are known to be sex-specific. However, how sex influences frailty status and mortality risk in frail rodents has yet to be established. The purpose of this study was therefore to characterize sex differences in frail mice across the lifespan. Male (n=29) and female (n=27) mice starting at 17 months of age were assessed using a frailty phenotype adjusted according to sex, which included body weight, walking speed, strength, endurance and physical activity. Regardless of sex, frail mice were phenotypically dysfunctional compared to age-matched non-frail mice, while non-frail females generally possessed a higher body fat percentage and were more physically active than non-frail males (p&#x2264;0.05). The prevalence of frailty was greater in female mice at 26 months of age (p=0.05), but if normalized to mean lifespan, no sex differences remained. No differences were detected in the rate of death or mean lifespan between frail male and female mice (p&#x2265;0.12). In closing, these data indicate that sexual differences exist in aging C57BL/6 mice and if the frailty criteria are adjusted according to sex, the prevalence of frailty increases across age with frail mice dying early in life, regardless of sex.
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Profiling of mRNA of interstitial fibrosis and tubular atrophy with subclinical inflammation in recipients after kidney transplantation

Qiang Fu, Minxue Liao, Cheng Feng, Jichao Tang, Rui Liao, Liang Wei, Hongji Yang, James F. Markmann, Kai Chen, Shaoping Deng,

https://doi.org/10.18632/aging.102115 pp 5215—5231

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Fu Q, Liao M, Feng C, Tang J, Liao R, Wei L, Yang H, Markmann JF, Chen K, Deng S, . Profiling of mRNA of interstitial fibrosis and tubular atrophy with subclinical inflammation in recipients after kidney transplantation. . 11:5215-5231. https://doi.org/10.18632/aging.102115

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                TY  - JOUR
                AU  - Fu, Qiang 
                AU  - Liao, Minxue 
                AU  - Feng, Cheng 
                AU  - Tang, Jichao 
                AU  - Liao, Rui 
                AU  - Wei, Liang 
                AU  - Yang, Hongji 
                AU  - Markmann, James F. 
                AU  - Chen, Kai 
                AU  - Deng, Shaoping 
                TI  - Profiling of mRNA of interstitial fibrosis and tubular atrophy with subclinical inflammation in recipients after kidney transplantation
                JO  - 
                JA  - 
                VL  - 11
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102115
                DO  - 10.18632/aging.102115
                SP  - 5215
                EP  - 5231
                PY  - 
                AB  - Interstitial fibrosis and tubular atrophy (IFTA) with inflammation (IFTA-I) is strongly correlated with kidney allograft failure. Diagnosis of IFTA-I accurately and early is critical to prevent graft failure and improve graft survival. In the current study, through analyzing the renal allograft biopsy in patients with stable function after kidney transplantation (STA), IFTA and IFTA-I group with semi-supervised principal components methods, we found that CD2, IL7R, CCL5 based signature could not only distinguish STA and IFTA-I well, but predict IFTA-I with a high degree of accuracy with an area under the curve (AUC) of 0.91 (P = 0.00023). Additionally, IRF8 demonstrated significant differences among STA, IFTA and IFTA-I groups, suggesting that IRF8 had the capacity to discriminate the different classifications of graft biopsies well. Also, with Kaplan-Meier and log-rank methods, we found that IRF8 could serve as the prognostic marker for renal graft failure in those biopsies without rejection (AUC = 0.75) and the recipients expressing high had a higher risk for renal graft loss (P &lt; 0.0001). This research may provide new targets for therapeutic prevention and intervention for post-transplantation IFTA with or with inflammation.
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Aberrant DNA methylation of synaptophysin is involved in adrenal cortisol-producing adenoma

Jia-Yu Zhong, Rong-Rong Cui, Xiao Lin, Feng Xu, Ting Zhu, Fuxingzi Li, Feng Wu, En Zhou, Lu Yi, Ling-Qing Yuan,

https://doi.org/10.18632/aging.102119 pp 5232—5245

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Zhong J, Cui R, Lin X, Xu F, Zhu T, Li F, Wu F, Zhou E, Yi L, Yuan L, . Aberrant DNA methylation of synaptophysin is involved in adrenal cortisol-producing adenoma. . 11:5232-5245. https://doi.org/10.18632/aging.102119

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                TY  - JOUR
                AU  - Zhong, Jia-Yu 
                AU  - Cui, Rong-Rong 
                AU  - Lin, Xiao 
                AU  - Xu, Feng 
                AU  - Zhu, Ting 
                AU  - Li, Fuxingzi 
                AU  - Wu, Feng 
                AU  - Zhou, En 
                AU  - Yi, Lu 
                AU  - Yuan, Ling-Qing 
                TI  - Aberrant DNA methylation of synaptophysin is involved in adrenal cortisol-producing adenoma
                JO  - 
                JA  - 
                VL  - 11
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102119
                DO  - 10.18632/aging.102119
                SP  - 5232
                EP  - 5245
                PY  - 
                AB  - Cortisol-producing adenoma (CPA) is the main cause of Adrenal Cushing syndrome. However, its molecular mechanism is not fully understood. Previous study revealed Synaptophysin (SYP) is ubiquitously expressed in adrenocortical tumors, but its function in CPA still need to be discovered. In the present study we determine the molecular mechanism involved in SYP dysregulation in CPA and how SYP affects the secretion of cortisol in CPA. Our results showed that aberrant DNA methylation of SYP is involved in CPA progress. Using a miRNA microarray and qRT-PCR, we found decreased expression of miR-27a-5p in CPA compared with normal adrenal tissue. Moreover, the expression of TET3, the target gene of miR-27a-5p, increased in CPA compared with normal adrenal tissue. Knock-down of TET3 resulted in hypermethylation of SYP which reducing the expression level of SYP in H295R cells. The miR-27a-5p-TET3-SYP signalling pathway may regulate proliferation and cortisol secretion in H295R cells and, thus, play a key role in CPA development.
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Immune system development and age-dependent maintenance in Klotho-hypomorphic mice

Wandi Sandra Zhu, Lynette Naler, Robert W. Maul, Michelle A. Sallin, Jyoti Misra Sen,

https://doi.org/10.18632/aging.102121 pp 5246—5257

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Zhu WS, Naler L, Maul RW, Sallin MA, Sen JM, . Immune system development and age-dependent maintenance in Klotho-hypomorphic mice. . 11:5246-5257. https://doi.org/10.18632/aging.102121

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                TY  - JOUR
                AU  - Zhu, Wandi Sandra 
                AU  - Naler, Lynette 
                AU  - Maul, Robert W. 
                AU  - Sallin, Michelle A. 
                AU  - Sen, Jyoti Misra 
                TI  - Immune system development and age-dependent maintenance in Klotho-hypomorphic mice
                JO  - 
                JA  - 
                VL  - 11
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102121
                DO  - 10.18632/aging.102121
                SP  - 5246
                EP  - 5257
                PY  - 
                AB  - Circulating Klotho peptide hormone has anti-aging activity and affects tissue maintenance. Hypomorphic mutant Klotho [kl/kl] mice on C57BL/6xC3H, BALB/c and 129 genetic backgrounds, show decreased Klotho expression that correlate with accelerated aging including pre-mature death due to abnormally high levels of serum vitamin D. These mice also show multiple impairments in the immune system. However, it remains unresolved if the defects in the immune system stem from decreased Klotho expression or high vitamin D levels in the serum. Transfer of the kl/kl allele to pure C57BL/6 genetic background [B6-kl/kl] significantly reduced expression of Klotho at all ages. Surprisingly, B6-kl/kl mice showed normalized serum vitamin D levels, amelioration of severe aging-related phenotypes and normal lifespan. This paper reports a detailed analysis of the immune system in B6-kl/kl mice in the absence of detrimental levels of serum vitamin D. Remarkably, the data reveal that in the absence of overt systemic stress, such as abnormally high vitamin D levels, reduced expression of Klotho does not have a major effect on the generation and maintenance of the immune system.
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Glycation of macrophages induces expression of pro-inflammatory cytokines and reduces phagocytic efficiency

Veronika Bezold, Philip Rosenstock, Jonas Scheffler, Henriette Geyer, Rüdiger Horstkorte, Kaya Bork,

https://doi.org/10.18632/aging.102123 pp 5258—5275

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Bezold V, Rosenstock P, Scheffler J, Geyer H, Horstkorte R, Bork K, . Glycation of macrophages induces expression of pro-inflammatory cytokines and reduces phagocytic efficiency. . 11:5258-5275. https://doi.org/10.18632/aging.102123

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                TY  - JOUR
                AU  - Bezold, Veronika 
                AU  - Rosenstock, Philip 
                AU  - Scheffler, Jonas 
                AU  - Geyer, Henriette 
                AU  - Horstkorte, Rüdiger 
                AU  - Bork, Kaya 
                TI  - Glycation of macrophages induces expression of pro-inflammatory cytokines and reduces phagocytic efficiency
                JO  - 
                JA  - 
                VL  - 11
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102123
                DO  - 10.18632/aging.102123
                SP  - 5258
                EP  - 5275
                PY  - 
                AB  - Glycation and the accumulation of advanced glycation end products (AGEs) are known to occur during normal aging but also in the progression of several diseases, such as diabetes. Diabetes type II and aging both lead to impaired wound healing. It has been demonstrated that macrophages play an important role in impaired wound healing, however, the underlying causes remain unknown. Elevated blood glucose levels as well as elevated methylglyoxal (MGO) levels in diabetic patients result in glycation and increase of AGEs. We used MGO to investigate the influence of glycation and AGEs on macrophages. We could show that glycation, but not treatment with AGE-modified serum proteins, increased expression of pro-inflammatory cytokines interleukin 1&#x3B2; (IL-1&#x3B2;) and IL-8 but also affected IL-10 and TNF-&#x3B1; expression, resulting in increased inflammation. At the same time, glycation reduced phagocytic efficiency and led to impaired clearance rates of invading microbes and cellular debris. Our data suggest that glycation contributes to changes of macrophage activity and cytokine expression and therefore could support the understanding of disturbed wound healing during aging and diabetes.
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Aging induces a step-like change in the motor ability structure of athletes

Siddhartha Bikram Panday, Prabhat Pathak, Jeongin Moon, Jooeun Ahn,

https://doi.org/10.18632/aging.102126 pp 5276—5286

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Panday SB, Pathak P, Moon J, Ahn J, . Aging induces a step-like change in the motor ability structure of athletes. . 11:5276-5286. https://doi.org/10.18632/aging.102126

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                TY  - JOUR
                AU  - Panday, Siddhartha Bikram 
                AU  - Pathak, Prabhat 
                AU  - Moon, Jeongin 
                AU  - Ahn, Jooeun 
                TI  - Aging induces a step-like change in the motor ability structure of athletes
                JO  - 
                JA  - 
                VL  - 11
                IS  - 14
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102126
                DO  - 10.18632/aging.102126
                SP  - 5276
                EP  - 5286
                PY  - 
                AB  - Many studies have investigated how aging decreases human strength and endurance. However, understanding the effect of aging on human motor ability requires more than knowledge of the separate temporal profile of individual motor function because the structure of human motor ability is multi-dimensional. We address the effect of aging on the multi-dimensional structure of human motor ability by investigating the performance records of athletes in track events across various age groups. We collected the performance records of 446 top-level decathletes whose ages ranged from 20 to 74, and performed a principal component analysis of the records in 100m, 1500m, and 400m races, which require strength, endurance, and the mixture of both, respectively. Our analysis shows that aging results in a substantial and sudden change in the motor ability structure, contrasting sharply with the gradual decrease in performance in each track event. The rapid structural change develops around the age of 50, which is much earlier than the &#x201C;breakpoint&#x201D; of 70 years suggested in multiple previous studies. Our findings indicate that the structural change in motor ability can significantly precede the failure in the overall motor performance.
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Volume 11, Issue 14

About the Cover

Editorials

Shuai Jiang,

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Saarwaani Vallabhajosyula, Gregory W. Barsness, Saraschandra Vallabhajosyula,

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Jyoti Misra Sen,

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Madalena Esteves, Nuno Sousa, Hugo Leite-Almeida,

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Colwyn Headley, Joanne Turner, Murugesan VS Rajaram,

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Priority Research Paper

Mélanie Viltard, Sylvère Durand, Maria Pérez-Lanzón, Fanny Aprahamian, Deborah Lefevre, Christine Leroy, Frank Madeo, Guido Kroemer, Gérard Friedlander,

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Research Papers

Maria Peiris‐Pagès, Béla Ozsvári, Federica Sotgia, Michael P. Lisanti,

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Beatrice Bretherton, Lucy Atkinson, Aaron Murray, Jennifer Clancy, Susan Deuchars, Jim Deuchars,

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Chunyong Han, Xuebiao Li, Qian Fan, Guangshu Liu, Jian Yin,

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Zhaozhi Wang, Jianjun Jin,

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Ting Guo, Bin Li, Chao Gu, Xiuying Chen, Mengxin Han, Xiaocheng Liu, Congjian Xu,

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Alessia Valentini, Maria Assunta Cianfarani, Umberto Tarantino, Nicola Di Daniele, Aldo Bertoli,

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Yixuan Fang, Lingjiang Zhu, Ni An, Gaoyue Jiang, Jiawei Qian, Ruijin Zhao, Na Yuan, Suping Zhang, Jianrong Wang,

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Yaojing Chen, Chenlong Lv, Xin Li, Junying Zhang, Kewei Chen, Zhongwan Liu, He Li, Jialing Fan, Ting Qin, Liang Luo, Zhanjun Zhang,

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Lexiang Yu, Yao Chen, Yong Xu, Tao He, Yan Wei, Rongqiao He,

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Eric S. Kim, Kelvin Fong, Lewina Lee, Avron Spiro, Joel Schwartz, Eric Whitsel, Steve Horvath, Cuicui Wang, Lifang Hou, Andrea A. Baccarelli, Yun Li, James Stewart, JoAnn E. Manson, Francine Grodstein, Dawn L. DeMeo, Laura D. Kubzansky,

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Bo Jia, Tao Xie, Xiaoling Qiu, Xiang Sun, Jun Chen, Zhijie Huang, Xianghuai Zheng, Zhiping Wang, Jianjiang Zhao,

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Yan Liu, Xiaodan Zong, Jie Huang, Yanfei Guan, Yuanquan Li, Ting Du, Keyin Liu, Xinpan Kang, Chunyan Dou, Xiangdong Sun, Renhua Wu, Lei Wen, Yunlong Zhang,

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Yilong Li, Rui Kong, Hongze Chen, Zhongjie Zhao, Le Li, Jiating Li, Jisheng Hu, Guangquan Zhang, Shangha Pan, Yongwei Wang, Gang Wang, Hua Chen, Bei Sun,

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