One of the most compelling features of dry eye disease (DED) is that it occurs more frequently in women than men. In fact, the female sex is a significant risk factor for the development of DED. This sex-related difference in DED prevalence is attributed in large part to the effects of sex steroids (e.g. androgens, estrogens), hypothalamic-pituitary hormones, glucocorticoids, insulin, insulin-like growth factor 1 and thyroid hormones, as well as to the sex chromosome complement, sex-specific autosomal factors and epigenetics (e.g. microRNAs). In addition to sex, gender also appears to be a risk factor for DED. "Gender" and "sex" are words that are often used interchangeably, but they have distinct meanings. "Gender" refers to a person's self-representation as a man or woman, whereas "sex" distinguishes males and females based on their biological characteristics. Both gender and sex affect DED risk, presentation of the disease, immune responses, pain, care-seeking behaviors, service utilization, and myriad other facets of eye health. Overall, sex, gender and hormones play a major role in the regulation of ocular surface and adnexal tissues, and in the difference in DED prevalence between women and men. The purpose of this Subcommittee report is to review and critique the nature of this role, as well as to recommend areas for future research to advance our understanding of the interrelationships between sex, gender, hormones and DED.

TFOS DEWS II Sex, Gender, and Hormones Report

Dry eye affects millions of people worldwide and causes eye well recognized risk factors for dry eye. Anatomical and inflammation-induced age-related changes affect all components of the lacrimal gland functional unit, inclusive of lacrimal gland, conjunctiva, meibomian gland and compromise ocular surface health. There is increased evidence that inflammation plays a role in dry eye. This review will summarize the current knowledge about aging and dry eye, inclusive of lessons learned from animal models and promising therapies.

/pdf/effects-of-aging-in-dry-eye-5ye20woaxp.pdf

Effects of Aging in Dry Eye.

Senescence restricts the development of applications involving mesenchymal stem cells (MSCs) in research fields, such as tissue engineering, and stem cell therapeutic strategies. Understanding the mechanisms underlying natural aging processes may contribute to the development of novel approaches to preventing age-related diseases or slowing individual aging processes. Nampt is a rate-limiting NAD biosynthetic enzyme that plays critical roles in energy metabolism, cell senescence and maintaining life spans. However, it remains unknown whether Nampt influences stem cell senescence. In this study, the function of Nampt was investigated using a rat model of natural aging. Our data show that Nampt expression was significantly lower in MSCs obtained from aged rats than in those obtained from young rats during physiological aging. Reducing the level of Nampt in aged MSCs resulted in lower intracellular concentrations of NAD+ and downregulated Sirt1 expression and activity. After the Nampt inhibitor FK866 was added, young MSCs were induced to become aged cells. The enhanced senescence was correlated with NAD+ depletion and Sirt1 activity attenuation. In addition, Nampt overexpression attenuated cell senescence in aged MSCs. Our findings provide a new explanation for the mechanisms underlying stem cell senescence and a novel target for delaying stem cell senescence and preventing and treating age-related diseases.

/pdf/nampt-expression-decreases-age-related-senescence-in-rat-1nkr0xl6en.pdf

Nampt Expression Decreases Age-Related Senescence in Rat Bone Marrow Mesenchymal Stem Cells by Targeting Sirt1.

Bone is a dynamic organ that undergoes constant remodeling, an energetically costly process by which old bone is replaced and localized bone defects are repaired to renew the skeleton over time, thereby maintaining skeletal health. This review provides a general overview of bone’s main players (bone lining cells, osteocytes, osteoclasts, reversal cells, and osteoblasts) that participate in bone remodeling. Placing emphasis on the family of extracellular matrix metalloproteinases (MMPs), we describe how: (i) Convergence of multiple protease families (including MMPs and cysteine proteinases) ensures complexity and robustness of the bone remodeling process, (ii) Enzymatic activity of MMPs affects bone physiology at the molecular and cellular levels and (iii) Either overexpression or deficiency/insufficiency of individual MMPs impairs healthy bone remodeling and systemic metabolism. Today, it is generally accepted that proteolytic activity is required for the degradation of bone tissue in osteoarthritis and osteoporosis. However, it is increasingly evident that inactivating mutations in MMP genes can also lead to bone pathology including osteolysis and metabolic abnormalities such as delayed growth. We argue that there remains a need to rethink the role played by proteases in bone physiology and pathology.

Destroy to Rebuild: The Connection Between Bone Tissue Remodeling and Matrix Metalloproteinases.

Morphological mutations in bacterial cell make them the most miscellaneous microscopic group. Their non-flagellated species known as gliding bacteria exhibit self-powered motion and leave an adhesi...

A mathematical model of the locomotion of bacteria near an inclined solid substrate: effects of different waveforms and rheological properties of couple-stress slime

Background: Valproic acid (VPA), one of the most important antiepileptic drugs, proved to be inevitable for epileptic pregnant women to limit the hazards of convulsions on the foetuses and mothers. Periconceptional folic acid supple­mentation was investigated to protect against several birth defects. However, its role against VPA cerebellar toxicity was not properly investigated. The present study was conducted to evaluate the protective effect of folic acid against VPA cerebellar neurotoxicity. Materials and methods: Twenty-four pregnant female albino rats were divided into three groups; group I (control group, did not receive any drugs), group II (given VPA at a dose of 50 mg/kg body weight once daily) and group III (given the same dose of VPA and 400 μg/kg of body weight folic acid once daily). Ten male offspring from each group were sacrificed at two ages: at 2 and 12 weeks after birth. Samples of cerebellar cortex were taken and prepared for light, electron microscopic examination, glial fibrillary acidic protein (GFAP) immunohistochemical study and histomorphometric analysis. Results: The present study confirmed the neurotoxic effect of prenatal VPA on the cerebellar cortex, especially on Purkinje cells. The cells appeared shrunken, reduced in density, disorganised and surrounded by empty haloes. Nuclear damage and axon degeneration in the form of vacuolation, loss of organelles and absence of neurofilaments with myelin sheath depletion were detected. Concomitant supply of folic acid was shown to retain the normal architecture of Purkinje cells with their axons and nuclei. In many animals receiving folic acid, the thickness of all layers of the cortex increased up to that of the control groups, after being markedly reduced in VPA-treated groups. GFAP immunoreaction was also improved against the strong positive gliosis detected in VPA-treated groups. Conclusions: The present study confirmed the protective role of folic acid against the cerebellar neurotoxic effects of VPA prenatal exposure. It is recommended that folic acid supplements should be given to every epileptic pregnant mother treated with VPA. (Folia Morphol 2018; 77, 2: 201–209)

/pdf/effect-of-valproic-acid-administration-during-pregnancy-on-5eh9cm53s5.pdf

Effect of valproic acid administration during pregnancy on postnatal development of cerebellar cortex and the possible protective role of folic acid.

Acute renal failure complicates renal ischemia–reperfusion (I/R) owing to reactive oxygen species production. Atorvastatin (ATO) has anti-inflammatory and antioxidant properties. The current study ...

Preconditioning with atorvastatin against renal ischemia-reperfusion injury in nondiabetic versus diabetic rats.

Aims
Although once a common antibiotic, polymyxin E fell out of favor after reports of its nephrotoxicity. However, recent concerns with gram-negative bacteria, which are resistant to multiple antibiotics, have resulted in increased interest in polymyxin E. Silybin is a known antihepatotoxic drug and may have potential for protecting the kidney from polymyxin E. Therefore, the aim of the current study was to evaluate whether silybin affected the damages produced by polymyxin E on the rat kidney.

Methods
Four groups of rats with 10 rats per group were included in the study: control (no treatment, group I), vehicle (control vehicle treatment, group II), polymyxin E treatment (group III), and polymyxin E and silybin treatment (group IV). Groups II-IV received intravenous treatment twice a day for 7 days. All rats were euthanized after 7 days. Histological, ultrastructural, and morphometric analyses were performed on the rats’ kidney tissues.

Results
Analysis of tissues from group III showed differences from groups I and II, such as glomerular and tubular affection and changes in morphometric measures. Results for group IV were more similar to those of groups I and II than those of group III.

Conclusions
Our results suggested that administering silybin with polymyxin E alleviated polymyxin E-induced nephrotoxicity in the rat kidney. Future biochemical studies should investigate whether silybin could ameliorate the nephrotoxicity caused by polymyxin E in rats and whether concomitant administration of silybin could be an effective clinical pharmacological strategy to protect against polymyxin E-induced insult in human kidneys.

Does silybin protect against toxicity induced by polymyxin E in rat kidney

Background: Studies on sperm maturation, epididymal histology, or epididymal tubule physiology are significant parts in reproductive researches. The present study was aimed to evaluate the effect of induced hypercholesterolaemia on the epididymis of adult albino rats and to clarify the possible protective role of selenium. Materials and methods: Forty adult albino Wistar rats were divided into four groups; untreated control group (group I), sham control (group II), group with induced hypercholesterolaemia (group III), group with induced hypercholesterolaemia treated with selenium 0.25 mg/kg/day (group IV). Results: Histological and ultrastructural examination of the epididymal epithelial cells of hypercholesterolaemic rats (group III) showed loss of cilia with many vacuolations, fatty degenerative changes and increased collagen fibres. Morphometrically significant increase (p 0.05). Selenium treated group (group IV) produced marked improvement in histological, ultrastructural and morphometric results as compared with group III. Conclusions: It could be concluded that hypercholesterolaemia produced deleterious effects to the epididymis and selenium could attenuate these effects.

/pdf/efficiency-of-selenium-in-attenuating-epididymal-50ugo3im9f.pdf

Efficiency of selenium in attenuating epididymal histopathological changes in hypercholesterolaemic adult rat.

Background Ethanol has a destructive effect on the pancreas by inducing oxidative damage on pancreatic cells. This injurious effect could be ameliorated by the administration of vitamin E. Aim The aim of the study was to investigate the possible protective role of vitamin E on ethanol-induced alterations in the pancreas in adult male albino rats and also the effect of ethanol withdrawal. Materials and methods Forty adult male albino rats were divided into four equal groups (10 rats each): group I (control group), group II (ethanol-treated group), group III (ethanol and vitamin E-treated group), and group IV (recovery group). At the end of the experiment, the rats were sacrificed by cervical dislocation and their pancreas were excised and prepared for light microscopic and histochemical study. Detection of interleukin (IL)-1B and IL-6 by real-time PCR and proliferating cell nuclear antigen immunoexpression in the pancreatic tissue was carried out. Results Group II showed loss of acinar tissue, distorted degenerated pancreatic acini, dilated distorted interlobular ducts, distorted islets of Langerhans, and dilatation and congestion of the blood vessels. Interlobular inflammatory cellular infiltration was also detected. There was an increased collagen fiber deposition and diminution of the proliferating stem cells. There was a marked increase in IL-1B and IL-6 levels. Group III showed an obvious improvement in the structure of the pancreas. The recovery group showed improvement in the structure of the pancreas and minimal collagen deposition. Conclusion Vitamin E could protect the pancreas against ethanol-induced alteration in adult male albino rats.

Can vitamin E protect the pancreas against ethanol-induced alterations in adult male albino rats? A histomorphometric and immunohistochemical study

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