Влияние низкотемпературного консервирования без криопротектора и под защитой Me₂SO на активность окислительно-восстановительных ферментов в ткани плаценты

Методами количественной гистохимии и количественного фотометрического анализа проведено исследование изменения активности СДГ, ЛДГ, α-ГФДГ, НАД.Н² і НАДФ.Н² в ткани плаценты после ее низкотемпературного консервирования без криопротектора и после обработки раствором криопротектора Me₂SO.Методами кількісної гістохімії і кількісного фотометричного аналізу проведено дослідження змін активності СДГ, ЛДГ, α-ГФДГ, НАД.Н² і НАДФ.Н² у тканині плаценти після ії низькотемпературного консервування без кріопротектора і після обробки розчином кріопротектора Me₂SO.Using the methods of quantitative histochemistry and quantitative photometric analysis there was carried-out the investigation of change in SDG, LDG, α-GPhDG, NAD.H² and NADP.H² activity in placenta tissue after its low temperature preservation without cryoprotectant and after treatment with Me₂SO cryoprotectant solution

Histochemical markers of myelin damage and impaired remyelination in the aging rhesus monkey brain: relationship to cognitive performance

Myelin damage is known to increase in the normal aging brain and to correlate with age-related cognitive decline. While the causes of increased myelin damage are unknown, here we consider whether the brain’s innate capacity for remyelination diminishes with age and hence could contribute to myelin damage through slow accumulation of myelin defects. Maintenance and repair of myelin depends upon oligodendroglia precursor cells (OPCs), which must differentiate into a sufficient number of healthy mature oligodendroglia (oligos), the myelinating cell of the brain. The extracellular matrix molecule hyaluronic acid (HA) has been shown to inhibit maturation of OPCs into mature myelinating oligos. The present study examined aging changes in myelination using four markers: the damaged myelin basic protein (dMBP) antibody, a histochemical reaction to stain HA, and immunohistochemistry for OPCs and mature oligos. These markers were quantified using cell density (oligos and OPCs), percent area stained (HA and dMBP), and fluorescence intensity (HA and dMBP). Relationships between these markers, age, and behavioral measures of cognitive function were investigated using single and multiple regression analyses. Results showed that in the corpus callosum and cingulum bundle of the rhesus monkey, staining for dMBP as a marker of myelin damage strongly correlated with increases in HA. The increase in HA in the cingulum bundle correlated positively with age. OPC density increased with age in both the cingulum bundle and corpus callosum. Mature oligo density did not change significantly with age, but approached a significant increase in the cingulum and approached a significant decrease in the corpus callosum. The increase in OPC density correlated positively with both HA and dMBP in the cingulum bundle. These data are consistent with the hypothesis that HA accumulation contributes to myelin damage by inhibiting the differentiation of OPCs into mature oligodendrocytes, diminishing the brain’s innate capacity for remyelination with age

Effect of Me2SO Cryoprotectant on the Activity of Reductive-Oxidative Enzymes in Placenta Tissue

Методами количественной гистохимии и количественного фотометрического анализа проведено исследование изменения активности СДГ, ЛДГ, α-ГФДГ, НАД.Н2 и НАДФ.Н2 в ткани плаценты после ее инкубации с раствором криопротектора Me2SO; Методами кількісної гістохімії і кількісного фотометричного аналізу проведено дослідження змін активності СДГ, ЛДГ, α-ГФДГ, НАД.Н2 і НАДФ.Н2 у тканині плаценти після ії інкубації з розчином кріопротектора Me2SO;Using the methods of quantitative histochemistry and quantitative photometric analysis there was performed the investigation of the change in SDG, LDG, α-GPhDG, NAD.H2 and NADP.H2 activity in placenta tissue after its incubation with Me2SO cryoprotectant solution

Nonhuman Primate Models of Respiratory Disease: Past, Present, and Future.

The respiratory system consists of an integrated network of organs and structures that primarily function for gas exchange. In mammals, oxygen and carbon dioxide are transmitted through a complex respiratory tract, consisting of the nasal passages, pharynx, larynx, and lung. Exposure to ambient air throughout the lifespan imposes vulnerability of the respiratory system to environmental challenges that can contribute toward development of disease. The importance of the respiratory system to human health is supported by statistics from the Centers for Disease Control and Prevention; in 2015, chronic lower respiratory diseases were the third leading cause of death in the United States. In light of the significant mortality associated with respiratory conditions that afflict all ages of the human population, this review will focus on basic and preclinical research conducted in nonhuman primate models of respiratory disease. In comparison with other laboratory animals, the nonhuman primate lung most closely resembles the human lung in structure, physiology, and mucosal immune mechanisms. Studies defining the influence of inhaled microbes, pollutants, or allergens on the nonhuman primate lung have provided insight on disease pathogenesis, with the potential for elucidation of molecular targets leading to new treatment modalities. Vaccine trials in nonhuman primates have been crucial for confirmation of safety and protective efficacy against infectious diseases of the lung in a laboratory animal model that recapitulates pathology observed in humans. In looking to the future, nonhuman primate models of respiratory diseases will continue to be instrumental for translating biomedical research for improvement of human health