[Plasma acid reproduces oxidative and nitrosative stress in bladder tissue in vitro: experimental study].

Aim: To analyze some effects of plasma acid in vitro on the bladder tissue obtained from laboratory animals and to evaluate the possibility of its application for in vitro modeling of IC/BPS.

Materials And Methods: The tissue samples of the bladder wall were obtained from female Wistar rats aged 3 months (n=16, weighing 180-200 g). The tissues were processed for 1 hour in the plasma acid prepared by spark discharge of water for injection in air.

Permissive hypercapnia and hypercapnic hypoxia inhibit signaling pathways of neuronal apoptosis in ischemic/hypoxic rats.

Introduction: In the present study, we aimed to test the hypothesis that hypercapnia, independently and/or in combination with hypoxia, can activate signaling pathways related to the inhibition of proapoptotic (caspase-dependent and caspase-independent) factors and the induction of antiapoptotic factors in facilitating adaptation to hypoxia/ischemia.

Materials And Methods: Following exposure to permissive hypercapnia and/or normobaric hypoxia, the degree of apoptosis was evaluated in experimental ischemia models in vivo and in vitro. The percentages of caspase-3, apoptosis-inducing factor (AIF), Bax, and Bcl-2 in astrocytes and neurons derived from male Wistar rats were also calculated.

Ozone improved the wound healing in type 2 diabetics via down-regulation of IL- 8, 10 and induction of FGFR expression.

Background And Aim: We aimed to investigate the effect of ozonated autohaemotherapy (OA) on the wound  healing, serum values of interleukin (IL) - 6, 8, 10, tumor necrosis factor-alpha (TNF-α), basic fibroblast growth factor (bFGF) and local expression of fibroblast growth factor receptors (FGFR) in type 2 diabetics with the acute soft-tissue infections.

Methods: Patients in the first cohort (n-30) received a basic comprehensive treatment (BCT-group), and the second (n=28) also received OA (OA-group). Blood samples for ELISA and tissue specimens for the immunohistochemical examinations were collected at admission (day 0) and at the 9th day of inpatient treatment.

Reproducibility of developmental neuroplasticity in brain tissue models.

The current prevalence of neurodevelopmental, neurodegenerative diseases, stroke and brain injury stimulates studies aimed to identify new molecular targets, to select the drug candidates, to complete the whole set of preclinical and clinical trials, and to implement new drugs into routine neurological practice. Establishment of protocols based on microfluidics, blood-brain barrier- or neurovascular unit-on-chip, and microphysiological systems allowed improving the barrier characteristics and analyzing the regulation of local microcirculation, angiogenesis, and neurogenesis. Reconstruction of key mechanisms of brain development and even some aspects of experience-driven brain plasticity would be helpful in the establishment of brain models with the highest degree of reliability.

Early Life Stress and Metabolic Plasticity of Brain Cells: Impact on Neurogenesis and Angiogenesis.

Early life stress (ELS) causes long-lasting changes in brain plasticity induced by the exposure to stress factors acting prenatally or in the early postnatal ontogenesis due to hyperactivation of hypothalamic-pituitary-adrenal axis and sympathetic nervous system, development of neuroinflammation, aberrant neurogenesis and angiogenesis, and significant alterations in brain metabolism that lead to neurological deficits and higher susceptibility to development of brain disorders later in the life. As a key component of complex pathogenesis, ELS-mediated changes in brain metabolism associate with development of mitochondrial dysfunction, loss of appropriate mitochondria quality control and mitochondrial dynamics, deregulation of metabolic reprogramming. These mechanisms are particularly critical for maintaining the pool and development of brain cells within neurogenic and angiogenic niches.