Minimal information for studies of extracellular vesicles 2018 (MISEV2018):a position statement of the International Society for Extracellular Vesicles and update of the MISEV2014 guidelines

The last decade has seen a sharp increase in the number of scientific publications describing physiological and pathological functions of extracellular vesicles (EVs), a collective term covering various subtypes of cell-released, membranous structures, called exosomes, microvesicles, microparticles, ectosomes, oncosomes, apoptotic bodies, and many other names. However, specific issues arise when working with these entities, whose size and amount often make them difficult to obtain as relatively pure preparations, and to characterize properly. The International Society for Extracellular Vesicles (ISEV) proposed Minimal Information for Studies of Extracellular Vesicles (“MISEV”) guidelines for the field in 2014. We now update these “MISEV2014” guidelines based on evolution of the collective knowledge in the last four years. An important point to consider is that ascribing a specific function to EVs in general, or to subtypes of EVs, requires reporting of specific information beyond mere description of function in a crude, potentially contaminated, and heterogeneous preparation. For example, claims that exosomes are endowed with exquisite and specific activities remain difficult to support experimentally, given our still limited knowledge of their specific molecular machineries of biogenesis and release, as compared with other biophysically similar EVs. The MISEV2018 guidelines include tables and outlines of suggested protocols and steps to follow to document specific EV-associated functional activities. Finally, a checklist is provided with summaries of key points

Association of ACE I/D and MMP-3 5A/6A gene polymorphisms with hypertension in men from Serbia

The ACE and MMP-3 loci are involved in the vascular remodeling, increased intima media thickness and arterial stiffness associated with hypertension. We determined ACE I/D and MMP-3 5A/6A gene polymorphisms in 231 Caucasian males (126/105, hypertensive/normotensive). Owing to age-related differences hypertension, the sample was truncated with respect to age (the cut-off point was the age of 40). Our results indicate that ACE I/D and MMP-3 5A/6A polymorphisms are likely to be risk factors for hypertension in men from Serbia = 40 years of age. In the same group, the combined effect of DD/6A+ genotypes on hypertension was more pronounced than their separate effect.ACE и MMP-3 су укључени у процесе ремоделовања зида крвних судова, задебљања интима-медије и губитка еластичности артерија који су повезани са хипертензијом. Утврђивање генотипова полиморфизама I/D и 5A/6A у генима за ACE и MMP-3 је урађено на узорку од 231 мушкарца, Кавказоида (126/105, хипертензивни/нормотензивни). Обзиром на повезаност настанка хипертензије са годинама старости испитивана популација је подељена у две старосне групе (до и преко 40-е године старости). Наши резултати указују да су полиморфизми у генима за ACE (I/D) и MMP-3 (5A/6A) могући фактори ризика за настанак хипертензије код мушкараца = 40 година старости у популацији Србије. У истој старосној групи заједнички утицај генотипова DD/6A+ на настанак хипертензије је био већи од њиховог појединачног утицаја

Comparison of blood pro/antioxidant levels before and afer acute exercise in athletes and non-athletes

The aims of our study were to assess the redox state of adolescent athletes and non-athletes both at rest and afer acute exposure to physical load and to find relations between parametersof redox state and morphofunctional characteristics of subjects. 58 young handball players and 37 non-athletes were subjected to body composition analysis, measuring of maximal oxygen consumption and blood sampling immediately before and afer a maximal progressive exercise test. At rest, athletes had significantly higher superoxide dismutase (SOD) and catalase (CAT) activity, higher levels of reduced glutathione (GSH) and nitric oxide (NO) and lower levels of lipid peroxidation (TBARS) compared with non-athletes. A maximal exercise test induced statistically significant rise of superoxide anion radical (O 2-), hydrogen peroxide (H 2O 2) and NO levels in non-athletes, while TBARS levels decreased. Athletes experienced the fall in NO levels and the fall in CAT activity. Afer exercise, athletes had significantly lower levels of O 2- compared with non-athletes. Two way repeated measures ANOVA showed that the response of O 2-, NO and TBARS to the exercise test was dependent on the sports engagement (training experience) of subjects. Significant correlations between morphofunctional and redox parameters were found. These results suggest that physical fitness affects redox homeostasis

Alien Registration- Smith, George E. (Westbrook, Cumberland County)

https://digitalmaine.com/alien_docs/20281/thumbnail.jp

Pro12Ala gene polymorphism in the peroxisome proliferator-activated receptor gamma as a risk factor for the onset of type 2 diabetes mellitus in the Serbian population

The peroxisome proliferator-activated receptor gamma (PPAR gamma) is a gene candidate for the onset of type 2 diabetes mellitus (T2DM). We investigated the association of the PPAR gamma Pro12Ala gene with the onset of T2DM for the first time in the Serbian population. The study population consisted of 197 controls and 163 T2DM patients. The 12Ala allele tended to be more frequent in the group of T2DM patients (0.11) compared to the control subjects (0.09). The results from this study indicate that the PPAR gamma(2) 12Ala allele presents a non-significant risk factor for T2DM development in the Serbian population

Acute effects of nandrolone decanoate on cardiodynamic parameters in isolated rat heart

Despite worldwide use of anabolic steroids in last decades, there are still contradictory informations about their acute influence on myocardium. The aim of this study was to examine the acute effects of nandrolone decanoate (ND) on cardiodynamics and coronary flow in isolated rat heart. The hearts of male Wistar albino rats (n=48, 12 per group, age 8 weeks, body mass 180–200 g) were excised and perfused according to Langendorff technique at gradually increased coronary perfusion pressures (40–120 cmH2O). After control sets of experiments, the hearts were perfused with ND in dose of 1 μM, 10 μM and 100 μM, successively. Using sensor placed in the left ventricle, we registered: maximum and minimum rate of pressure development in the left ventricle (dp/dt max and dp/dt min), systolic and diastolic left ventricular pressure (SLVP and DLVP) and heart rate (HR). Coronary flow (CF) was measured flowmetrically. The results clearly show the depression in cardiac function caused by higher doses of ND. The highest concentration of ND (100μM) induced most deleterious impact on the myocardial function and perfusion of the heart (coronary circulation), which could be of clinical significance.The accepted manuscript in pdf format is listed with the files at the bottom of this page. The presentation of the authors' names and (or) special characters in the title of the manuscript may differ slightly between what is listed on this page and what is listed in the pdf file of the accepted manuscript; that in the pdf file of the accepted manuscript is what was submitted by the author

De novo pathogenic DNM1L variant in a patient diagnosed with atypical hereditary sensory and autonomic neuropathy

Background: Profiling the entire genome at base pair resolution in a single test offers novel insights into disease by means of dissection of genetic contributors to phenotypic features. Methods: We performed genome sequencing for a patient who presented with atypical hereditary sensory and autonomic neuropathy, severe epileptic encephalopathy, global developmental delay, and growth hormone deficiency. Results: Assessment of the variants detected by mapped sequencing reads followed by Sanger confirmation revealed that the proband is a compound heterozygote for rare variants within RETREG1 (FAM134B), a gene associated with a recessive form of hereditary sensory and autonomic neuropathy, but not with epileptic encephalopathy or global developmental delay. Further analysis of the data also revealed a heterozygous missense variant in DNM1L, a gene previously implicated in an autosomal dominant encephalopathy, epilepsy, and global developmental delay and confirmed by Sanger sequencing to be a de novo variant not present in parental genomes. Conclusions: Our findings emphasize the importance of genome-wide sequencing in patients with a well-characterized genetic disease with atypical presentation. This approach reduces the potential for misdiagnoses