Gut microbiome is a community of microorganisms in the gastrointestinal tract. These bacteria have a tremendous impact on the human physiology in healthy individuals and during an illness. Intestinal microbiome can influence one's health either directly by secreting biologically active substances such as vitamins, essential amino acids, lipids et cetera or indirectly by modulating metabolic processes and the immune system. In recent years considerable information has been accumulated on the relationship between gut microbiome and brain functions. Moreover, significant quantitative and qualitative changes of gut microbiome have been reported in patients with Alzheimer's disease. On the other hand, gut microbiome is highly sensitive to negative external lifestyle aspects, such as diet, sleep deprivation, circadian rhythm disturbance, chronic noise, and sedentary behavior, which are also considered as important risk factors for the development of sporadic Alzheimer's disease. In this regard, this review is focused on analyzing the links between gut microbiome, modern lifestyle, aging, and Alzheimer's disease.

Controversial, sensational and often contradictory scientific reports have triggered active debates over the biological effects of electromagnetic fields (EMFs) in literature and mass media the last few decades. This could lead to confusion and distraction, subsequently hampering the development of a univocal conclusion on the real hazards caused by EMFs on humans. For example, there are lots of publications indicating that EMF can induce apoptosis and DNA strand-breaks in cells. On the other hand, these effects could rather be beneficial, in that they could be effectively harnessed for treatment of various disorders, including cancer. This review discusses and analyzes the results of various in vitro, in vivo and epidemiological studies on the effects of non-ionizing EMFs on cells and organs, including the consequences of exposure to the low and high frequencies EM spectrum. Emphasis is laid on the analysis of recent data on the role of EMF in the induction of oxidative stress and DNA damage. Additionally, the impact of EMF on the reproductive system has been discussed, as well as the relationship between EM radiation and blood cancer. Apart from adverse effects, the therapeutic potential of EMFs for clinical use in different pathologies is also highlighted.

It has been thought that caloric restriction favors longevity and healthy aging where autophagy plays a vital role. However, autophagy decreases during aging and that can lead to the development of aging-associated diseases such as cancer, diabetes, neurodegeneration, etc. It was shown that autophagy can be induced by mechanical or chemical stress. In this regard, various pharmacological compounds were proposed, including natural polyphenols. Apart from the ability to induce autophagy, polyphenols, such as resveratrol, are capable of modulating the expression of pro- and anti-apoptotic factors, neutralizing free radical species, affecting mitochondrial functions, chelating redox-active transition metal ions, and preventing protein aggregation. Moreover, polyphenols have advantages compared to chemical inducers of autophagy due to their intrinsic natural bio-compatibility and safety. In this context, polyphenols can be considered as a potential therapeutic tool for healthy aging either as a part of a diet or as separate compounds (supplements). This review discusses the epigenetic aspect and the underlying molecular mechanism of polyphenols as an anti-aging remedy. In addition, the recent advances of studies on NAD-dependent deacetylase sirtuin-1 (SIRT1) regulation of autophagy, the role of senescence-associated secretory phenotype (SASP) in cells senescence and their regulation by polyphenols have been highlighted as well. Apart from that, the review also revised the latest information on how polyphenols can help to improve mitochondrial function and modulate apoptosis (programmed cell death).

Skin aging has been associated with a higher dietary intake of carbohydrates, particularly glucose and galactose. In fact, the carbohydrates are capable of damaging the skin’s vital components through nonenzymatic glycation, the covalent attachment of sugar to a protein, and subsequent production of advanced glycation end products (AGEs). This review is focused on the role of D-galactose in the development of skin aging and its relation to oxidative stress. The interest in this problem was dictated by recent findings that used in vitro and in vivo models. The review highlights the recent advances in the underlying molecular mechanisms of D-galactose-mediated cell senescence and cytotoxicity. We have also proposed the possible impact of galactosemia on skin aging and its clinical relevance. The understanding of molecular mechanisms of skin aging mediated by D-galactose can help dermatologists optimize methods for prevention and treatment of skin senescence and aging-related skin diseases.

Mesenchymal stem cells (MSCs) represent a promising cell source for cellular therapy and tissue engineering and are currently being tested in a number of clinical trials for various diseases. However, like other somatic cells, MSCs age, and this senescence is accompanied by a progressive decline in stem cell function. Several lines of evidence suggest a role for the Rho family GTPase Cdc42 activity in cellular senescence processes. In the present study, we have examined aging-associated Cdc42 activity in rat adipose-derived mesenchymal stem cells (ADMSCs) and the consequences of pharmacological inhibition of Cdc42 in ADMSCs from aged rats. We demonstrate that ADMSCs show a decreased rate of cell growth and a decreased ability to differentiate into chrodrogenic, osteogenic and adipogenic cell lineages as a function of rat age. This is accompanied with an increased staining for SA-β-Gal activity and increased levels of Cdc42 bound to GTP. Treatment of ADMSCs from 24-month old rats with three Cdc42 inhibitors significantly increased proliferation rates, decreased SA-β-Gal staining, and reduced Cdc42-GTP. The Cdc42 inhibitor CASIN increased adipogenic and osteogenic differentiation potential in ADMSCs from 24-month old rats, and decreased the levels of radical oxygen species (ROS), p16 levels, F-actin, and the activity of the ERK1/2 and JNK signaling pathways that were all elevated in these cells. These data suggest that ADMSCs show increased rates of senescence as rats age that appear to be due to elevated Cdc42 activity. Thus, Cdc42 plays important roles in MSC senescence and differentiation potential, and pharmacological reduction of Cdc42 activity can, at least partially, rejuvenate aged MSCs.

Background:Air pollution in Kazakhstan is caused by many factors and poses serious threats to public health. Ambient air in the cities of Kazakhstan is polluted due to mining and processing of mineral resources, oil and gas production, gasoline and diesel fuel motor vehicles, industrial enterprises.Objective:The study aim is to assess the air pollution degree in most significant settlements of Kazakhstan and define risk levels for the population health. Ambient air monitoring was conducted in 26 cities. Air pollution severity was assessed by the analysis results and processing of air samples taken at the stationary observation posts. Health risk assessment due to chemical factors was calculated according to the approved risk assessment methodology.Findings:There is high risk of acute adverse effects risk from suspended particles, oxides and dioxides of nitrogen and sulfur in almost all of the studied cities. The most unfavorable situation is in Ust-Kamenogorsk. Also, there is the adverse chronic effects risk caused by suspended particles exposure in majority of the studied cities. Extremely high chronic effects risk as a result of heavy metals exposure was detected in Ust-Kamenogorsk, Shymkent, Almaty, Taraz and Balkhash. Unacceptable carcinogenic risk levels have been determined for professional groups and the whole population with respect to cadmium in Shymkent, Almaty, Balkhash; arsenic in Shymkent, Almaty, Balkhash; lead in Taraz; chromium – in Shymkent, Aktobe, Almaty and Balkhash. Thus, the values of the hazard quotients and indices for acute and chronic exposure in most of the studied cities of Kazakhstan exceed the permissible level equal to 1.0.Conclusion:Due to the unacceptable risk levels in the cities it is strongly recommended to conduct a detailed study of the health status of the population depending on the air pollution.

Background The role of adiponectin (ADIPOQ) in Alzheimer’s disease (AD) has been documented, however, demonstrating controversial results. In this study, we investigated blood serum ADIPOQ levels, methylation of the adiponectin gene promoter, and adiponectin receptors (AdipoR1 and AdipoR2) expression in blood samples isolated from AD patients and healthy controls. Methods We performed a case–control study including 248 subjects (98 AD patients and 150 healthy controls); ADIPOQ serum levels, AdipoR1, and AdipoR2 levels in PBMC were measured by ELISA Kits, and ADIPOQ gene methylation was analyzed using methyl-specific PCR. Results Serum adiponectin levels were threefold higher in the AD group compared to the controls. We have also found a positive correlation between adiponectin and MMSE scores and high-density lipoprotein cholesterol (HDL-C) in AD patients. A significant difference in the proportion of methylation of the CpG sites at − 74 nt of the ADIPOQ gene promoter was detected in AD cases, and the levels of adiponectin in blood serum were significantly higher in methylated samples in the AD group compared to controls. The amount of AdipoR1 was significantly higher among AD subjects, while the expression of AdipoR2 did not vary between AD patients and controls. Conclusion These findings may contribute to a deeper understanding of the etiological factors leading to the development of dementia and may serve as a basis for the development of predictive biomarkers of AD.

Human tissues and disease models require well-defined biomimetic microenvironments. During the past decade, innovative developments in materials science, microfabrication, and polymer science have provided us with the ability to manipulate cellular microenvironments for regenerative medicine and tissue engineering applications. Solution blow spinning is a facile fiber fabricating method that requires a simple apparatus, a concentrated polymer solution within a volatile solvent, and a high-pressure gas source. Commercially available airbrushes, typically used for painting and cosmetic makeup, have successfully generated a range of nanofibers and films. Applications under investigation are similar to electrospinning and include enzyme immobilization, drug delivery, filtration, infection protection, tissue engineering, and wound healing. This review will discuss fiber fabrication methods before a more detailed discussion of the potential of blow-spinning in biomedical applications.