Dysfunction of Neuromuscular Synapses in the Genetic Model of Alzheimer’s Disease

© 2018, Springer Science+Business Media, LLC, part of Springer Nature. The function of synaptic transmission and presynaptic vesicular cycle in the neuromuscular synapses of the diaphragm was studied in transgenic APP/PS1 mice (Alzheimer’s disease model). The decrease in the quantal content of end-plate potential, intense depression of the amplitude of terminal plate potentials under conditions of lasting high frequency stimulation (50 Hz), a drastic prolongation of the synaptic vesicle recycling time in APP/PS1 mice in comparison with wild type mice were detected. Manifest dysfunction of the neuromuscular synapses, caused by disordered neurosecretion and recycling of the synaptic vesicles in the presynaptic nerve endings, was detected in the Alzheimer’s disease model on transgenic APP/PS1 mice. The study supplemented the notions on the pathogenesis of Alzheimer’s disease as a systemic disease, while the detected phenomena could just partially explain the development of motor disorders in this disease

Non-ST-segment elevation acute coronary syndrome in elderly patients and long-livers. Features of treatment. Literature review and case report

Despite the growing population of elderly people and long-livers every year, the treatment of acute coronary syndrome in these groups is not fully developed and is not regulated in clinical guidelines due to the lack of large randomized clinical trials. The article presents a literature review covering the following issues arising during clinical decision-making in the treatment of non-ST-segment elevation acute coronary syndrome in this group of patients: selection of invasive treatment strategy, scope of myocardial revascularization, appointment of dual antiplatelet therapy taking into account the bleeding risk, decreased renal function and senile asthenia. In addition, a case report of successful treatment of a 101-year-old female patient with non-ST-segment elevation myocardial infarction, who underwent percutaneous coronary intervention with stenting of infarct-related artery, was presented

Dysfunction of Neuromuscular Synapses in the Genetic Model of Alzheimer’s Disease

© 2018, Springer Science+Business Media, LLC, part of Springer Nature. The function of synaptic transmission and presynaptic vesicular cycle in the neuromuscular synapses of the diaphragm was studied in transgenic APP/PS1 mice (Alzheimer’s disease model). The decrease in the quantal content of end-plate potential, intense depression of the amplitude of terminal plate potentials under conditions of lasting high frequency stimulation (50 Hz), a drastic prolongation of the synaptic vesicle recycling time in APP/PS1 mice in comparison with wild type mice were detected. Manifest dysfunction of the neuromuscular synapses, caused by disordered neurosecretion and recycling of the synaptic vesicles in the presynaptic nerve endings, was detected in the Alzheimer’s disease model on transgenic APP/PS1 mice. The study supplemented the notions on the pathogenesis of Alzheimer’s disease as a systemic disease, while the detected phenomena could just partially explain the development of motor disorders in this disease

Russia-wide epidemiological survey of congenital and nosocomial infections in newborns

High prevalence and great socio-economic impact of nosocomial infections is documented in obstetric hospitals. Objective: to uncover Russia-wide epidemiological features for congenital and nosocomial infections in newborns. Material and Methods: the data covering 2008–2016 period were retrieved from the Federal Statistical Monitoring Form No. 2 “Report on Infectious and Parasitic Diseases”, via the Unified Interdepartmental Information Statistical System. During 2008–2016, incidence of congenital and nosocomial infections in newborns was analyzed in various constituents of the Russian Federation, which were divided into quartile groups including confidence interval. Results: It was found that the increased/decreased/unchanged incidence of congenital infections in newborns was shown in 30, 31 and 13 subjects, respectively. In case of nosocomial infections in newborns, its incidence was increased/decreased/unchanged in 7, 41 and 26 subjects, respectively. Moreover, a congenital/nosocomial infection ratio in newborns was increased/decreased/ unchanged in 40, 15 and 19 subjects, respectively. Based on the morbidity pattern, 9 major groups might be distinguished. In particular, the most abundant (16 subjects) was the group with increased incidence of congenital infections, decreased incidence of nosocomial infections and increased congenital/nosocomial infection ratio in newborns. However, it is worth mentioning that recording of nosocomial infection cases is incomplete in the vast majority of the subjects of the Russian Federation: as few as seven subjects may be highlighted providing a proper registration of nosocomial and congenital infections in newborns such as: Vologda Region, Trans-Baikal Territory, Nizhny Novgorod Region, Omsk Region, Orenburg Region, Penza Region, and Sverdlovsk Region. Conclusion: to fully assess an objective status on nosocomial and congenital infections in newborns, it is necessary that a hospital epidemiologist investigates every single case; ensure applying a standard approach to determine a case of healthcare-associated infection, congenital infections; official recording of all cases; responsibility of all staff members involved in recording healthcare-associated infection cases; regularly reviewed data by using science-based methods. Key words: congenital infections, nosocomial infections, healthcare associated infections, registration, incidence, mortality

Dysfunction of Neuromuscular Synaptic Transmission and Synaptic Vesicle Recycling in Motor Nerve Terminals of mSOD1 Transgenic Mice with Model of Amyotrophic Lateral Sclerosis

© 2019, Springer Science+Business Media, LLC, part of Springer Nature. Amyotrophic lateral sclerosis (ALS) is a progressive incurable neurodegenerative disease with selective loss of lower and upper motoneurons. Dysfunction and destruction of neuromuscular synapses leading to skeletal muscle denervation is one of the early and major events in ALS pathogenesis. Despite of the presence of studies devoted to investigation of neuromuscular transmission in ALS mouse models, no detailed information about molecular mechanisms underlying synaptic dysfunction in ALS and their temporal dynamics during ALS progression is provided. The goal of present work was to study the processes of neurotransmitter release and presynaptic vesicle recycling in neuromuscular synapses of mutated SOD1 (mSOD1) transgenic mice at different clinical stages of disease. Utilizing combination of electrophysiological recording and FM 1–43 (N-(3-triethylammoniumpropyl)-4-(4-(dibutylamino) styryl) pyridinium dibromide) fluorescent imaging, we found that mSOD1 mice at symptomatic and terminal stages of disease showed decreased baseline quantal content of end-plate potentials and prolonged synaptic vesicle recycling time comparing to wild-type mice. Despite the decrease of end-plate potential (EPP) quantal content, studied mSOD1 mice groups showed unchanged dynamics of EPP relative amplitude comparing to WT mice. We also found an increase of miniature end-plate potential amplitude in mSOD1 mice at symptomatic stage, which may reflect compensatory mechanism that alleviates reduction of EPP amplitude. Thus, we provided one of the first detailed characteristics of presynaptic dysfunction at neuromuscular junction in ALS model. Obtained data expand our understanding of the ALS pathogenesis and contribute to stage- and localization-specific description of ALS pathogenetic mechanisms