Volume 7, Issue 10

Conboy IM, Conboy MJ, Rebo J, . Systemic Problems: A perspective on stem cell aging and rejuvenation. . 7:754-765. https://doi.org/10.18632/aging.100819

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                TY  - JOUR
                AU  - Conboy, Irina M. 
                AU  - Conboy, Michael J. 
                AU  - Rebo, Justin 
                TI  - Systemic Problems: A perspective on stem cell aging and rejuvenation
                JO  - 
                JA  - 
                VL  - 7
                IS  - 10
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                UR  - https://doi.org/10.18632/aging.100819
                DO  - 10.18632/aging.100819
                SP  - 754
                EP  - 765
                PY  - 
                AB  - This review provides balanced analysis of the advances in systemic regulation of young and old tissue stem cells and suggests strategies for accelerating development of therapies to broadly combat age-related tissue degenerative pathologies. Many highlighted recent reports on systemic tissue rejuvenation combine parabiosis with a “silver bullet” putatively responsible for the positive effects. Attempts to unify these papers reflect the excitement about this experimental approach and add value in reproducing previous work. At the same time, defined molecular approaches, which are “beyond parabiosis” for the rejuvenation of multiple old organs represent progress toward attenuating or even reversing human tissue aging.
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Telomere length, cardiovascular risk and arteriosclerosis in human kidneys: an observational cohort study

Katrien De Vusser, Nicky Pieters, Bram Janssen, Evelyne Lerut, Dirk Kuypers, Ina Jochmans, Diethard Monbaliu, Jacques Pirenne, Tim Nawrot, Maarten Naesens,

https://doi.org/10.18632/aging.100814 pp 766—775

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De Vusser K, Pieters N, Janssen B, Lerut E, Kuypers D, Jochmans I, Monbaliu D, Pirenne J, Nawrot T, Naesens M, . Telomere length, cardiovascular risk and arteriosclerosis in human kidneys: an observational cohort study. . 7:766-775. https://doi.org/10.18632/aging.100814

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                TY  - JOUR
                AU  - De Vusser, Katrien 
                AU  - Pieters, Nicky 
                AU  - Janssen, Bram 
                AU  - Lerut, Evelyne 
                AU  - Kuypers, Dirk 
                AU  - Jochmans, Ina 
                AU  - Monbaliu, Diethard 
                AU  - Pirenne, Jacques 
                AU  - Nawrot, Tim 
                AU  - Naesens, Maarten 
                TI  - Telomere length, cardiovascular risk and arteriosclerosis in human kidneys: an observational cohort study
                JO  - 
                JA  - 
                VL  - 7
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100814
                DO  - 10.18632/aging.100814
                SP  - 766
                EP  - 775
                PY  - 
                AB  -           Background          Replicative senescence, associated with telomere shortening, plays an important role in aging and cardiovascular disease. The relation between telomere length, cardiovascular risk, and renal disease is unknown.                          Methods          Our study consisted of a cohort of 257 kidney donors for transplantation, divided into a test and a validation cohort. We used quantitative RT‐PCR to measure relative telomere length (log T/S ratio) in peripheral blood leucocytes, and in kidney biopsies performed prior to implantation. The association between leucocyte and intrarenal telomere length, cardiovascular risk factors, and renal histology, was studied using multiple regression models, adjusted for calendar age, gender and other donor demographics.                          Results          Subjects with intrarenal arteriosclerosis had significantly shorter leucocyte telomere length compared with patients without arteriosclerosis (log T/S ratio ‐0.3 ± 0.4 vs. 0.1 ± 0.2 with vs. without arteriosclerosis; p = 0.0008). Intrarenal arteriosclerosis was associated with shorter telomere length, independent of gender, calendar age, history of hypertension and history of cardiovascular events. For each increase of one standard deviation of the log T/S ratio, the odds for intrarenal arteriosclerosis decreased with 64% (Odds ratio 0.36; 95% CI 0.17‐0.77; p = 0.02). In accordance with leucocyte telomere length, shorter intrarenal telomere length associated significantly with the presence of renal arteriosclerosis (log T/S ratio ‐0.04 ± 0.06 vs. 0.08 ± 0.01 with vs. without arteriosclerosis, p = 0.007), and not with other histological lesions.                          Interpretation          We demonstrate that arteriosclerosis in smaller intrarenal arteries is associated with shorter telomere length. Our study suggests a central role of replicative senescence in the progression of renovascular disease, independent of calendar age.        
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Proteasome function is not impaired in healthy aging of the lung

Anne Caniard, Korbinian Ballweg, Christina Lukas, Ali Ö. Yildirim, Oliver Eickelberg, Silke Meiners,

https://doi.org/10.18632/aging.100820 pp 776—787

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Caniard A, Ballweg K, Lukas C, Yildirim AÖ, Eickelberg O, Meiners S, . Proteasome function is not impaired in healthy aging of the lung. . 7:776-787. https://doi.org/10.18632/aging.100820

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                TY  - JOUR
                AU  - Caniard, Anne 
                AU  - Ballweg, Korbinian 
                AU  - Lukas, Christina 
                AU  - Yildirim, Ali Ö. 
                AU  - Eickelberg, Oliver 
                AU  - Meiners, Silke 
                TI  - Proteasome function is not impaired in healthy aging of the lung
                JO  - 
                JA  - 
                VL  - 7
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100820
                DO  - 10.18632/aging.100820
                SP  - 776
                EP  - 787
                PY  - 
                AB  - Aging is the progressive loss of cellular function which inevitably leads to death. Failure of proteostasis including the decrease in proteasome function is one hallmark of aging. In the lung, proteasome activity was shown to be impaired in age‐related diseases such as chronic obstructive pulmonary disease. However, little is known on proteasome function during healthy aging. Here, we comprehensively analyzed healthy lung aging and proteasome function in wildtype, proteasome reporter and immunoproteasome knockout mice. Wildtype mice spontaneously developed senile lung emphysema while expression and activity of proteasome complexes and turnover of ubiquitinated substrates was not grossly altered in lungs of aged mice. Immunoproteasome subunits were specifically upregulated in the aged lung and the caspase‐like proteasome activity concomitantly decreased. Aged knockout mice for the LMP2 or LMP7 immunoproteasome subunits showed no alteration in proteasome activities but exhibited typical lung aging phenotypes suggesting that immunoproteasome function is dispensable for physiological lung aging in mice. Our results indicate that healthy aging of the lung does not involve impairment of proteasome function. Apparently, the reserve capacity of the proteostasis systems in the lung is sufficient to avoid severe proteostasis imbalance during healthy aging.
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Defective mitochondrial respiration, altered dNTP pools and reduced AP endonuclease 1 activity in peripheral blood mononuclear cells of Alzheimer's disease patients

Scott Maynard, Anne-Mette Hejl, Thuan-Son T. Dinh, Guido Keijzers, Åse M. Hansen, Claus Desler, Maria Moreno-Villanueva, Alexander Bürkle, Lene J. Rasmussen, Gunhild Waldemar, Vilhelm A. Bohr,

https://doi.org/10.18632/aging.100810 pp 793—810

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Maynard S, Hejl A, Dinh TT, Keijzers G, Hansen ÅM, Desler C, Moreno-Villanueva M, Bürkle A, Rasmussen LJ, Waldemar G, Bohr VA, . Defective mitochondrial respiration, altered dNTP pools and reduced AP endonuclease 1 activity in peripheral blood mononuclear cells of Alzheimer's disease patients. . 7:793-810. https://doi.org/10.18632/aging.100810

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                TY  - JOUR
                AU  - Maynard, Scott 
                AU  - Hejl, Anne-Mette 
                AU  - Dinh, Thuan-Son T. 
                AU  - Keijzers, Guido 
                AU  - Hansen, Åse M. 
                AU  - Desler, Claus 
                AU  - Moreno-Villanueva, Maria 
                AU  - Bürkle, Alexander 
                AU  - Rasmussen, Lene J. 
                AU  - Waldemar, Gunhild 
                AU  - Bohr, Vilhelm A. 
                TI  - Defective mitochondrial respiration, altered dNTP pools and reduced AP endonuclease 1 activity in peripheral blood mononuclear cells of Alzheimer's disease patients
                JO  - 
                JA  - 
                VL  - 7
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100810
                DO  - 10.18632/aging.100810
                SP  - 793
                EP  - 810
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Maynard, Scott 
                AU  - Hejl, Anne-Mette 
                AU  - Dinh, Thuan-Son T. 
                AU  - Keijzers, Guido 
                AU  - Hansen, Åse M. 
                AU  - Desler, Claus 
                AU  - Moreno-Villanueva, Maria 
                AU  - Bürkle, Alexander 
                AU  - Rasmussen, Lene J. 
                AU  - Waldemar, Gunhild 
                AU  - Bohr, Vilhelm A. 
                TI  - Defective mitochondrial respiration, altered dNTP pools and reduced AP endonuclease 1 activity in peripheral blood mononuclear cells of Alzheimer's disease patients
                JO  - 
                JA  - 
                VL  - 7
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100810
                DO  - 10.18632/aging.100810
                SP  - 793
                EP  - 810
                PY  - 
                AB  - AIMS Accurate biomarkers for early diagnosis of Alzheimer's disease (AD) are badly needed. Recent reports suggest that dysfunctional mitochondria and DNA damage are associated with AD development. In this report, we measured various cellular parameters, related to mitochondrial bioenergetics and DNA damage, in peripheral blood mononuclear cells (PBMCs) of AD and control participants, for biomarker discovery. METHODS PBMCs were isolated from 53 patients with AD of mild to moderate degree and 30 age-matched healthy controls. Tests were performed on the PBMCs from as many of these participants as possible. We measured glycolysis and mitochondrial respiration fluxes using the Seahorse Bioscience flux analyzer, mitochondrial ROS production using flow cytometry, dNTP levels by way of a DNA polymerization assay, DNA strand breaks using the Fluorometric detection of Alkaline DNA Unwinding (FADU) assay, and APE1 incision activity (in cell lysates) on a DNA substrate containing an AP site (to estimate DNA repair efficiency). RESULTS In the PBMCs of AD patients, we found reduced basal mitochondrial oxygen consumption, reduced proton leak, higher dATP level, and lower AP endonuclease 1 activity, depending on adjustments for gender and/or age. CONCLUSIONS: This study reveals impaired mitochondrial respiration, altered dNTP pools and reduced DNA repair activity in PBMCs of AD patients, thus suggesting that these biochemical activities may be useful as biomarkers for AD.
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Proteomic identification of prognostic tumour biomarkers, using chemotherapy-induced cancer-associated fibroblasts

Maria Peiris-Pagès, Duncan L. Smith, Balázs Győrffy, Federica Sotgia, Michael P. Lisanti,

https://doi.org/10.18632/aging.100808 pp 816—838

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Peiris-Pagès M, Smith DL, Győrffy B, Sotgia F, Lisanti MP, . Proteomic identification of prognostic tumour biomarkers, using chemotherapy-induced cancer-associated fibroblasts. . 7:816-838. https://doi.org/10.18632/aging.100808

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                TY  - JOUR
                AU  - Peiris-Pagès, Maria 
                AU  - Smith, Duncan L. 
                AU  - Győrffy, Balázs 
                AU  - Sotgia, Federica 
                AU  - Lisanti, Michael P. 
                TI  - Proteomic identification of prognostic tumour biomarkers, using chemotherapy-induced cancer-associated fibroblasts
                JO  - 
                JA  - 
                VL  - 7
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100808
                DO  - 10.18632/aging.100808
                SP  - 816
                EP  - 838
                PY  - 
                AB  - Cancer cells grow in highly complex stromal microenvironments, which through metabolic remodelling, catabolism, autophagy and inflammation nurture them and are able to facilitate metastasis and resistance to therapy. However, these changes in the metabolic profile of stromal cancer-associated fibroblasts and their impact on cancer initiation, progression and metastasis are not well-known. This is the first study to provide a comprehensive proteomic portrait of the azathioprine and taxol-induced catabolic state on human stromal fibroblasts, which comprises changes in the expression of metabolic enzymes, myofibroblastic differentiation markers, antioxidants, proteins involved in autophagy, senescence, vesicle trafficking and protein degradation, and inducers of inflammation. Interestingly, many of these features are major contributors to the aging process. A catabolic stroma signature, generated with proteins found differentially up-regulated in taxol-treated fibroblasts, strikingly correlates with recurrence, metastasis and poor patient survival in several solid malignancies. We therefore suggest the inhibition of the catabolic state in healthy cells as a novel approach to improve current chemotherapy efficacies and possibly avoid future carcinogenic processes.
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Blocking the association of HDAC4 with MAP1S accelerates autophagy clearance of mutant Huntingtin

Fei Yue, Wenjiao Li, Jing Zou, Qi Chen, Guibin Xu, Hai Huang, Zhen Xu, Sheng Zhang, Paola Gallinari, Fen Wang, Wallace L. McKeehan, Leyuan Liu,

https://doi.org/10.18632/aging.100818 pp 839—853

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Yue F, Li W, Zou J, Chen Q, Xu G, Huang H, Xu Z, Zhang S, Gallinari P, Wang F, McKeehan WL, Liu L, . Blocking the association of HDAC4 with MAP1S accelerates autophagy clearance of mutant Huntingtin. . 7:839-853. https://doi.org/10.18632/aging.100818

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                TY  - JOUR
                AU  - Yue, Fei 
                AU  - Li, Wenjiao 
                AU  - Zou, Jing 
                AU  - Chen, Qi 
                AU  - Xu, Guibin 
                AU  - Huang, Hai 
                AU  - Xu, Zhen 
                AU  - Zhang, Sheng 
                AU  - Gallinari, Paola 
                AU  - Wang, Fen 
                AU  - McKeehan, Wallace L. 
                AU  - Liu, Leyuan 
                TI  - Blocking the association of HDAC4 with MAP1S accelerates autophagy clearance of mutant Huntingtin
                JO  - 
                JA  - 
                VL  - 7
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100818
                DO  - 10.18632/aging.100818
                SP  - 839
                EP  - 853
                PY  - 
                AB  - Autophagy controls and executes the turnover of abnormally aggregated proteins. MAP1S interacts with the autophagy marker LC3 and positively regulates autophagy flux. HDAC4 associates with the aggregation-prone mutant huntingtin protein (mHTT) that causes Huntington's disease, and colocalizes with it in cytosolic inclusions. It was suggested HDAC4 interacts with MAP1S in a yeast two-hybrid screening. Here, we found that MAP1S interacts with HDAC4 via a HDAC4-binding domain (HBD). HDAC4 destabilizes MAP1S, suppresses autophagy flux and promotes the accumulation of mHTT aggregates. This occurs by an increase in the deacetylation of the acetylated MAP1S. Either suppression of HDAC4 with siRNA or overexpression of the MAP1S HBD leads to stabilization of MAP1S, activation of autophagy flux and clearance of mHTT aggregates. Therefore, specific interruption of the HDAC4-MAP1S interaction with short peptides or small molecules to enhance autophagy flux may relieve the toxicity of mHTT associated with Huntington's disease and improve symptoms of HD patients.
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The p53 tumor suppressor protein protects against chemotherapeutic stress and apoptosis in human medulloblastoma cells

Sarah Waye, Aisha Naeem, Muhammad Umer Choudhry, Erika Parasido, Lucas Tricoli, Angiela Sivakumar, John P. Mikhaiel, Venkata Yenugonda, Olga C. Rodriguez, Sana D. Karam, Brian R. Rood, Maria Laura Avantaggiati, Chris Albanese,

https://doi.org/10.18632/aging.100831 pp 854—867

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Waye S, Naeem A, Choudhry MU, Parasido E, Tricoli L, Sivakumar A, Mikhaiel JP, Yenugonda V, Rodriguez OC, Karam SD, Rood BR, Avantaggiati ML, Albanese C, . The p53 tumor suppressor protein protects against chemotherapeutic stress and apoptosis in human medulloblastoma cells. . 7:854-867. https://doi.org/10.18632/aging.100831

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                TY  - JOUR
                AU  - Waye, Sarah 
                AU  - Naeem, Aisha 
                AU  - Choudhry, Muhammad Umer 
                AU  - Parasido, Erika 
                AU  - Tricoli, Lucas 
                AU  - Sivakumar, Angiela 
                AU  - Mikhaiel, John P. 
                AU  - Yenugonda, Venkata 
                AU  - Rodriguez, Olga C. 
                AU  - Karam, Sana D. 
                AU  - Rood, Brian R. 
                AU  - Avantaggiati, Maria Laura 
                AU  - Albanese, Chris 
                TI  - The p53 tumor suppressor protein protects against chemotherapeutic stress and apoptosis in human medulloblastoma cells
                JO  - 
                JA  - 
                VL  - 7
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100831
                DO  - 10.18632/aging.100831
                SP  - 854
                EP  - 867
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Waye, Sarah 
                AU  - Naeem, Aisha 
                AU  - Choudhry, Muhammad Umer 
                AU  - Parasido, Erika 
                AU  - Tricoli, Lucas 
                AU  - Sivakumar, Angiela 
                AU  - Mikhaiel, John P. 
                AU  - Yenugonda, Venkata 
                AU  - Rodriguez, Olga C. 
                AU  - Karam, Sana D. 
                AU  - Rood, Brian R. 
                AU  - Avantaggiati, Maria Laura 
                AU  - Albanese, Chris 
                TI  - The p53 tumor suppressor protein protects against chemotherapeutic stress and apoptosis in human medulloblastoma cells
                JO  - 
                JA  - 
                VL  - 7
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100831
                DO  - 10.18632/aging.100831
                SP  - 854
                EP  - 867
                PY  - 
                AB  - Medulloblastoma (MB), a primitive neuroectodermal tumor, is the most common malignant childhood brain tumor and remains incurable in about a third of patients. Currently, survivors carry a significant burden of late treatment effects. The p53 tumor suppressor protein plays a crucial role in influencing cell survival in response to cellular stress and while the p53 pathway is considered a key determinant of anti-tumor responses in many tumors, its role in cell survival in MB is much less well defined. Herein, we report that the experimental drug VMY-1-103 acts through induction of a partial DNA damage-like response as well induction of non-survival autophagy. Surprisingly, the genetic or chemical silencing of p53 significantly enhanced the cytotoxic effects of both VMY and the DNA damaging drug, doxorubicin. The inhibition of p53 in the presence of VMY revealed increased late stage apoptosis, increased DNA fragmentation and increased expression of genes involved in apoptosis, including CAPN12 and TRPM8, p63, p73, BIK, EndoG, CIDEB, P27Kip1 and P21cip1. These data provide the groundwork for additional studies on VMY as a therapeutic drug and support further investigations into the intriguing possibility that targeting p53 function may be an effective means of enhancing clinical outcomes in MB.
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Mitochondrial Hormesis links nutrient restriction to improved metabolism in fat cell

Daniele Lettieri Barbato, Giuseppe Tatulli, Katia Aquilano, Maria R. Ciriolo,

https://doi.org/10.18632/aging.100832 pp 869—881

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Barbato DL, Tatulli G, Aquilano K, Ciriolo MR, . Mitochondrial Hormesis links nutrient restriction to improved metabolism in fat cell. . 7:869-881. https://doi.org/10.18632/aging.100832

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                TY  - JOUR
                AU  - Barbato, Daniele Lettieri 
                AU  - Tatulli, Giuseppe 
                AU  - Aquilano, Katia 
                AU  - Ciriolo, Maria R. 
                TI  - Mitochondrial Hormesis links nutrient restriction to improved metabolism in fat cell
                JO  - 
                JA  - 
                VL  - 7
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100832
                DO  - 10.18632/aging.100832
                SP  - 869
                EP  - 881
                PY  - 
                AB  - Fasting promotes longevity by reprogramming metabolic and stress resistance pathways. However, although the impact on adipose tissue physiology through hormonal inputs is well established, the direct role of fasting on adipose cells is poorly understood. Herein we show that white and beige adipocytes, as well as mouse epididymal and subcutaneous adipose depots, respond to nutrient scarcity by acquiring a brown-like phenotype. Indeed, they improve oxidative metabolism through modulating the expression of mitochondrial-and nuclear-encoded oxidative phosphorylation genes as well as mitochondrial stress defensive proteins (UCP1, SOD2). Such adaptation is placed in a canonical mitohormetic response that proceeds via mitochondrial reactive oxygen species (mtROS) production and redistribution of FoxO1 transcription factor into nucleus. Nuclear FoxO1 (nFoxO1) mediates retrograde communication by inducing the expression of mitochondrial oxidative and stress defensive genes. Collectively, our findings describe an unusual white/beige fat cell response to nutrient availability highlighting another health-promoting mechanism of fasting.
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Excess body weight increases the burden of age-associated chronic diseases and their associated health care expenditures

Vincenzo Atella, Joanna Kopinska, Gerardo Medea, Federico Belotti, Valeria Tosti, Andrea Piano Mortari, Claudio Cricelli, Luigi Fontana,

https://doi.org/10.18632/aging.100833 pp 882—892

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Atella V, Kopinska J, Medea G, Belotti F, Tosti V, Mortari AP, Cricelli C, Fontana L, . Excess body weight increases the burden of age-associated chronic diseases and their associated health care expenditures. . 7:882-892. https://doi.org/10.18632/aging.100833

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                TY  - JOUR
                AU  - Atella, Vincenzo 
                AU  - Kopinska, Joanna 
                AU  - Medea, Gerardo 
                AU  - Belotti, Federico 
                AU  - Tosti, Valeria 
                AU  - Mortari, Andrea Piano 
                AU  - Cricelli, Claudio 
                AU  - Fontana, Luigi 
                TI  - Excess body weight increases the burden of age-associated chronic diseases and their associated health care expenditures
                JO  - 
                JA  - 
                VL  - 7
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100833
                DO  - 10.18632/aging.100833
                SP  - 882
                EP  - 892
                PY  - 
                AB  - Aging and excessive adiposity are both associated with an increased risk of developing multiple chronic diseases, which drive ever increasing health costs. The main aim of this study was to determine the net (non‐estimated) health costs of excessive adiposity and associated age‐related chronic diseases. We used a prevalence‐based approach that combines accurate data from the Health Search CSD‐LPD, an observational dataset with patient records collected by Italian general practitioners and up‐to‐date health care expenditures data from the SiSSI Project. In this very large study, 557,145 men and women older than 18 years were observed at different points in time between 2004 and 2010. The proportion of younger and older adults reporting no chronic disease decreased with increasing BMI. After adjustment for age, sex, geographic residence, and GPs heterogeneity, a strong J‐shaped association was found between BMI and total health care costs, more pronounced in middle‐aged and older adults. Relative to normal weight, in the 45‐64 age group, the per‐capita total cost was 10% higher in overweight individuals, and 27 to 68% greater in patients with obesity and very severe obesity, respectively. The association between BMI and diabetes, hypertension and cardiovascular disease largely explained these elevated costs.
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Volume 7, Issue 10

Editorials

Daniel Elias, Henrik J. Ditzel,

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Kaushik N. Thakkar, Sabrina A. Stratton, Michelle Craig Barton,

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Sara G.M. Piccirillo, Andrea Sottoriva, Colin Watts,

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Eric Roth, Jian Cao,

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Gianluca Bossi,

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Boris Bardot, Franck Toledo,

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Giovanni Lavorgna, Francesco Montorsi, Andrea Salonia,

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Tamara Vervloessem, Rita La Rovere, Geert Bultynck,

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Vinay Murtadak, Christoph Becker, Michael Stürzl,

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Amit Dipak Amin, Soumya S. Rajan, Jonathan H. Schatz,

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Review

Irina M. Conboy, Michael J. Conboy, Justin Rebo,

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Research Papers

Katrien De Vusser, Nicky Pieters, Bram Janssen, Evelyne Lerut, Dirk Kuypers, Ina Jochmans, Diethard Monbaliu, Jacques Pirenne, Tim Nawrot, Maarten Naesens,

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Anne Caniard, Korbinian Ballweg, Christina Lukas, Ali Ö. Yildirim, Oliver Eickelberg, Silke Meiners,

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Scott Maynard, Anne-Mette Hejl, Thuan-Son T. Dinh, Guido Keijzers, Åse M. Hansen, Claus Desler, Maria Moreno-Villanueva, Alexander Bürkle, Lene J. Rasmussen, Gunhild Waldemar, Vilhelm A. Bohr,

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Maria Peiris-Pagès, Duncan L. Smith, Balázs Győrffy, Federica Sotgia, Michael P. Lisanti,

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Fei Yue, Wenjiao Li, Jing Zou, Qi Chen, Guibin Xu, Hai Huang, Zhen Xu, Sheng Zhang, Paola Gallinari, Fen Wang, Wallace L. McKeehan, Leyuan Liu,

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Sarah Waye, Aisha Naeem, Muhammad Umer Choudhry, Erika Parasido, Lucas Tricoli, Angiela Sivakumar, John P. Mikhaiel, Venkata Yenugonda, Olga C. Rodriguez, Sana D. Karam, Brian R. Rood, Maria Laura Avantaggiati, Chris Albanese,

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Daniele Lettieri Barbato, Giuseppe Tatulli, Katia Aquilano, Maria R. Ciriolo,

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Vincenzo Atella, Joanna Kopinska, Gerardo Medea, Federico Belotti, Valeria Tosti, Andrea Piano Mortari, Claudio Cricelli, Luigi Fontana,

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