Effects of Multicide, Antibacterial Drug, on Staphylococcus Biomembranes.

Drug penetration into bacterial biomembranes is one of the most important factors determining the efficiency of antibacterial therapy. Multicide, antibacterial drug, is a nanomolecule 1.3-2.

[ENTRY OF FACULTATIVE PATHOGEN SERRATIA GRIMESII INTO HELA CELLS. ELECTRON MICROSCOPIC ANALYSIS].

Facultative pathogens Serratia grimesii are able to invade eukaryotic cells where they have been found in vacuoles and free in the cytoplasm (Efremova et al., 2001; Bozhokina et al., 2011).

[FUNCTIONAL LINK BETWEEN TRANSPORT PARAMETERS OF MDCK1 CELLS MONOLAYER AND THEIR ACTIN CYTOSKELETON ORGANIZATION].

On MDCK1 cell monolayer, dynamics of the spatial organization of actin cytoskeleton and dynamics of trans-epithelial electrical resistance (TEER) have been studied upon exposure of arginine-vasopressin (AVP) and protein-kinase A (PKA) activator forskolin. It has been found that exposure to these physiologically active compounds causes fibrillary actin depolymerization (both in apical and in basal cytoplasm) and, simultaneously, significant decrease in the cell monolayer trans-epithelial electrical resistance. TEER decrease indicates the stimulation of ions and water flow across the cell monolayer.

Probing for actinase activity of protealysin.

The ability of protealysin, a thermolysin-like metallopeptidase from Serratia proteamaculans 94, to cleave actin and matrix metalloprotease MMP2 is reported. In globular actin, protealysin and S. proteamaculans 94 cell extracts are shown to hydrolyze the Gly42-Val43 peptide bond within the DNase-binding loop and the Gly63-Ile64 and Thr66-Ile67 peptide bonds within the nucleotide cleft of the molecule.

Decreased sensitivity of transformed 3T3-SV40 cells treated with N-acetylcysteine to bacterial invasion.

Long-term treatment of transformed 3T3-SV40 mouse fibroblasts with antioxidant N-acetylcysteine decreased cell level of ROS and increased the concentration of reduced glutathione. Removal of N-acetylcysteine from the medium led to the appearance of well-expressed stress fibrils, virtually absent in control cells. In contrast to control cells, these cells were not invaded by apathogenic Escherichia coli A2 strain producing ECP32 protease specifically cleaving actin.

Giant vacuoles arising during ADH-induced transcellular bulk water flow across the epithelium of the frog urinary bladder.

Structural changes of the cytoplasm of urinary bladder granular cells after an antidiuretic hormone (ADH) stimulation of water transport were studied using standard and cryogenic methods of electron microscopy. Numerous changes occurred in these cells, the cytoplasm of the granular cells becoming swollen, and the intercellular spaces enlarged. Most granules become fused with the apical membrane.