Phytaspase Does Not Require Proteolytic Activity for Its Stress-Induced Internalization.

Phytaspases differ from other members of the plant subtilisin-like protease family by having rare aspartate cleavage specificity and unusual localization dynamics. Phytaspases are secreted from healthy plant cells but are re-internalized upon perception of death-inducing stresses. Although proteolytic activity is required for the secretion of plant subtilases, its requirement for the retrograde transportation of phytaspases is currently unknown.

Impact of war on HIV-related healthcare services and health workers in eastern Ukraine: a qualitative study.

The 2022 Russian invasion of Ukraine has caused serious challenges for healthcare workers (HCWs) and HIV-related healthcare services. This study assessed the effects of the invasion on HCWs wellbeing and on continuity of HIV services, using in-depth interviews with HCWs from facilities offering HIV antiretroviral therapy (ART) and pre-exposure prophylaxis (PrEP) services in the Donetsk region of Eastern Ukraine. A directed content analysis, with both inductive and deductive approaches, was conducted.

[Somatic embryogenesis in in vitro culture of three larch species].

Embryogenic callus formation in different larch species from Siberia (Larix sibirica, L. gmelinii, and L. sukaczewii) was carried out on MSGm medium supplemented with growth regulators (2.

Focal increases of axoplasmic Ca2+, aggregation of sodium-calcium exchanger, N-type Ca2+ channel, and actin define the sites of spheroids in axons undergoing oxidative stress.

Axonal spheroids occur as part of the pathology of a variety of neurologic diseases. Reactive oxygen species (ROS) trigger formation of spheroids, axonal severing, and Ca(2+) overload. The mechanisms by which ROS lead to the spheroid formation at specific axonal sites remain elusive.

Mitochondrial calcium and its regulation in neurodegeneration induced by oxidative stress.

A proposed mechanism of neuronal death associated with a variety of neurodegenerative diseases is the response of neurons to oxidative stress and consequent cytosolic Ca(2+) overload. One hypothesis is that cytosolic Ca(2+) overload leads to mitochondrial Ca(2+) overload and prolonged opening of the permeability transition pore (PTP), resulting in mitochondrial dysfunction. Elimination of cyclophilin D (CyPD), a key regulator of the PTP, results in neuroprotection in a number of murine models of neurodegeneration in which oxidative stress and high cytosolic Ca(2+) have been implicated.

Activation of the mitochondrial permeability transition pore modulates Ca2+ responses to physiological stimuli in adult neurons.

The participation of mitochondria in cellular and neuronal Ca(2+) homeostatic networks is now well accepted. Yet, critical tests of specific mitochondrial pathways in neuronal Ca(2+) responses have been hampered because the identity of mitochondrial proteins that must be integrated within this dynamic system remain uncertain. One putative pathway for Ca(2+) efflux from mitochondria exists through the formation of the permeability transition pore (PTP) that is often associated with cellular and neuronal death.

[Spectrophotometric determination of cefazolin in mixed saliva of practically healthy subjects and patients with infective somatic pathology].

The behaviour of cefazolin in aqueous and biological media with varying the antibiotic concentration was studied by UV-spectroscopy. Range of the contents and the detection limits of cefazolin were determined. The procedure of UV-spectroscopy of cefazolin in mixed saliva of patients with urinary tract infection was developed.

Effect of roscovitine, a selective cyclin B-dependent kinase 1 inhibitor, on assembly of the nucleolus in mitosis.

It is well known that at the beginning of mitosis the nucleolus disassembles but then reassembles at the end of mitosis. However, the mechanisms of these processes are still unclear. In the present work, we show for the first time that selective inhibition of cyclin B-dependent kinase 1 (CDK1) by roscovitine induces premature assembly of the nucleolus in mammalian cells in metaphase.

Estrogen facilitates neurite extension via apolipoprotein E in cultured adult mouse cortical neurons.

Literature review suggests a close relationship between estrogen and apolipoprotein E (ApoE) in the central nervous system. Epidemiology studies show that estrogen replacement therapy (ERT) decreases the morbidity from several chronic neurological diseases. Alleles of ApoE modify the risk for and progression of the same diseases.

[Activation of transcription of ribosome genes following human embryo fibroblast infection with cytomegalovirus in vitro].

Cytomegalovirus (CMV) infection of human diploid embryo fibroblasts in vitro causes a massive cell death on the 3-4th day of infection with a high primary infection coefficient (1-5 U/cell). Cytopathological effects of viral infection on the 3-4th day includes diminishes of the cell size, changes in their form, compaction of the nuclear chromatin, and disorganization and inactivation of the nucleolus. However, the early stages of the viral infection progression (the 1st-2nd day) are accompanied by unequivocal activation of rDNA (ribosomal gene) and the bulk of chromatin transcription.

[Stability of spatial interactions between chromocenters and pre-kinetochores in the interphase murine cells].

It is known that in mice the centromeric heterochromatin remains compact during the whole cell cycle and at interphase is referred to as "chromocentres". In the current study, by the use of antibodies against prekinetochores and DNA polymerase (a PCNA antigen), we showed that in murine L929 cells chromocentres remain spatially associated with prekinetochores during the entire interphase, including the late S-period, when DNA chromocentres replicate. Augmentation of prekinetochore fluorescence increases concomitantly with the heterochromation replication, but the prekinetochore duplication occurs only in G2 period.

[Effect of cytomegalovirus on cell cycle progression and formation of pathological mitoses in cultured human diploid fibroblasts].

The effect of cytomegalovirus on the cell cycle was studied autoradiographically in an asynchronous culture of human diploid fibroblasts. The analysis of labeled mitosis showed that some cells infected in the S phase ceased to progress through the cell cycle at one of its phases (S, G2, or M); at the same time, at least part of infected cells remained capable of entering mitosis. Beginning from day 2 after infection by cytomegalovirus, the accumulation of pathological mitotic cells blocked at metaphase was observed in the culture.