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Cardiovascular diseases such as myocardial ischaemia have a high fatality rate in patients with diabetes. This study was designed to expose the crosstalk between oxidative stress and AMPK, a vital molecule that controls biological energy metabolism, in myocardial ischaemia reperfusion injury (I/RI) in diabetic rats. Diabetes was stimulated in rats using streptozotocin injection. Rats were separated on random into control, control + I/R, Diabetes, Diabetes + I/R, Diabetes + I/R + N-acetylcysteine and Diabetes + I/R + Vas2870 groups. Myocardial infarct size was determined, and the predominant Nox family isoforms were analysed. In vitro, the H9C2 cells were administered excess glucose and exposed to hypoxia/reoxygenation to mimic diabetes and I/R. The AMPK siRNA or AICAR was used to inhibit or activate AMPK expression in H9C2 cells, respectively. Then, myocardial oxidative stress and programmed cell death were measured. Diabetes or high glucose levels were found to aggravate myocardial I/RI or hypoxia/reoxygenation in H9C2 cells, as demonstrated by an increase in myocardial infarct size or lactate dehydrogenase levels, oxidative stress generation and induction of programmed cell death. In diabetic rat hearts, cardiac Nox1, Nox2 and Nox4 were all heightened. The suppression of Nox2 expression using Vas2870 or Nox2-siRNA treatment in vivo or in vitro, respectively, protected diabetic rats from myocardial I/RI. Epigenetic screening AMPK gene knockout increased Nox2 protein expression while AMPK agonist decreased Nox2 expression. Therefore, diabetes aggravates myocardial I/RI by generating of Nox2-associated oxidative stress in an AMPK-dependent manner, which led to the induction of programmed cell death such as apoptosis, pyroptosis and ferroptosis. © 2020 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.We examined the association between household food insecurity and early child development and whether or not maternal depression and anxiety modifies this association. The cross-sectional study included 468 mother-infant pairs recruited at primary health centers of the Federal District, Brazil. Mothers answered a questionnaire that evaluated early child development (outcome), household food insecurity (independent variable), maternal depression and trait anxiety (effect modifiers). Variables were collected with validated questionnaires for the Brazilian population. Pearson's χ2 test and logistic regression analyses were conducted. Infants who lived in a moderate or severe food insecure household had 2.52 times (95% confidence interval [CI] [1.13, 5.65]) the odds of having early child development delays compared with infants in secure households. Maternal depression and anxiety modified the strength of association between household food insecurity and early child development, which is an innovative finding. Among infants with depressed mothers, those experiencing mild (adjusted odds ratio [aOR] 3.33, 95% CI [1.17, 9.46]) and moderate/severe household food insecurity (aOR 10.13, 95% CI [2.18, 47.10]) had higher odds of having early child development delays, compared with infants in food secure households. Among infants with both anxious and depressed mothers, these associations were even stronger for mild (aOR 4.69, 95% CI [1.41, 15.59]) and moderate/severe household food insecurity (aOR 16.07, 95% CI [2.70, 95.66]). In conclusion, household food insecurity is a risk factor for early child development delays, and this association is modified by maternal depression and anxiety. Future studies should evaluate the impact of intervention packages that address maternal depression and anxiety and household food insecurity on preventing early child development delays. © 2020 The Authors. Maternal & Child Nutrition published by John Wiley & Sons Ltd.BACKGROUND In male prepubertal cancer patients, radiation and chemotherapy impact future fertility by eradication of spermatogonial stem cells (SSCs). In macaques spermatogenesis could be regenerated by intratesticular transplantation of SSCs but only a small percentage of spermatozoa produced were of donor origin. Transient hormone suppression with a GnRH antagonist (GnRH-ant) enhanced spermatogenic recovery from transplanted SSCs. OBJECTIVES To evaluate donor-derived and endogenous spermatogenic recovery after SSC transplantation into irradiated monkeys and to test whether hormone suppression around the time of transplantation facilitates spermatogenic recovery. MATERIALS AND METHODS Testes of 15 adult rhesus monkeys were irradiated with 7 Gy and 4 months later transplanted, to one of the testes, with cryopreserved testicular cells containing SSCs from unrelated monkeys. Monkeys were either treated with GnRH-ant for 8 weeks before transplantation, GnRH-ant from 4 weeks before to 4 weeks after transplantatio to the level of colonization by transplanted cells. This article is protected by copyright. Epigenetic screening All rights reserved.Progerin accumulation disrupts nuclear lamina integrity and causes nuclear structure abnormalities, leading to premature aging, that is, Hutchinson-Gilford progeria syndrome (HGPS). The roles of nuclear subcompartments, such as PML nuclear bodies (PML NBs), in HGPS pathogenesis, are unclear. Here, we show that classical dot-like PML NBs are reorganized into thread-like structures in HGPS patient fibroblasts and their presence is associated with late stage of senescence. By co-immunoprecipitation analysis, we show that farnesylated Progerin interacts with human PML2, which accounts for the formation of thread-like PML NBs. Specifically, human PML2 but not PML1 overexpression in HGPS cells promotes PML thread development and accelerates senescence. Further immunofluorescence microscopy, immuno-TRAP, and deep sequencing data suggest that these irregular PML NBs might promote senescence by perturbing NB-associated DNA repair and gene expression in HGPS cells. These data identify irregular structures of PML NBs in senescent HGPS cells and support that the thread-like PML NBs might be a novel, morphological, and functional biomarker of late senescence. © 2020 The Authors. Aging Cell published by the Anatomical Society and John Wiley & Sons Ltd.
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