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Biomedical subjects

I Polacheck

Publications and source records attributed to I Polacheck.

59 records · Page 4Linked to original sources
PubMed1978

Distribution of autolysins in hyphae of Aspergillus nidulans: evidence for a lipid-mediated attachment to hyphal walls.

Preparations of broken Aspergillus nidulans hyphae contained both free and wall-bound autolysins. The bound enzymes were not solubilized by 8 M LiCl or neutral or anionic detergents; they were readily detached from walls by a cationic detergent or by autodigestion. Once detached, the enzymes did not reassociate with wall to give salt-resistant complexes. Six enzymes hydrolyzing wall polymers were bound to the envelope, and the same activities were also detected among soluble proteins in the cytoplasmic fraction. It is suggested that cytoplasmic vesicles, containing autolysins, are inserted into or trapped by newly formed wall in the growing hypha; these constitute the wall-bound autolysin fraction. Starvation for a carbon source derepressed the synthesis of five out of the six autolysins, and the amounts of both soluble and wall-bound activities increased by one to two orders of magnitude.

Aspergillus nidulans↗
PubMed1977

Aspergillus nidulans mutant lacking alpha-(1,3)-glucan, melanin, and cleistothecia.

A mutation in Aspergillus nidulans led to a loss of both melanin and alpha-(1,3)-glucan, a major wall polysaccharide. In addition, the mutation prevented the formation of cleistothecia. Mutant walls contained increased amounts of beta-(1,3)-glucan and galactose polymers, and electron micrographs indicated that they had lost the outermost wall layer. Such walls were more readily digested by lytic enzymes, and this increased susceptibility to hydrolysis was due to the absence of alpha-(1,3)-glucan and not of melanin. The pleiotropic effects of the mutation are discussed, with particular reference to the hypothesis that alpha-(1,3)-glucan acts as the endogenous carbon source for biosynthetic processes in the stationary phase of growth. In this view, glucan synthesis would be the primary target of the mutation, and the absence of glucan would result in the lack of melanin and cleistothecia, formed after nutrients are exhausted. Two other mutations that lowered themycelial alpha-(1,3)-glucan content also inhibited melanin and cleistothecia production.

Amino Acids↗
PubMedDate not supplied

Altered gut barrier function to Candida during parenteral nutrition.

We hypothesize that catheter-related sepsis with Candida during total parenteral nutrition (TPN) is caused by Candida translocation from the gut. Fifty male Sabra rats weighing 330 +/- 40 g were randomized into four groups and put into metabolic cages: group 1 (n = 16), nonoperated free-feeding controls; group 2 (n = 10), infused with normal saline and free feeding; group 3 (n = 14), infused with TPN solution for a total of 36 kcal and 1.5 g g protein.100 g-1 body wt.day-1;group 4 (n = 10), same TPN regimen as group 3 but also receiving oral and intravenous antibiotics. On day 7, all animals received 1.5 x 10(10) viable Candida albicans CBS 562 cells by gavage, and 24 h later, the number of Candida colony-forming units in blood, mesenteric lymph nodes, and kidneys was determined. No growth of Candida was detected in group 1 or group 2. Positive Candida cultures were found in the blood, mesenteric lymph nodes, and kidneys of groups 3 and 4, although levels reached statistical significance only for mesenteric lymph nodes in group 3. Because Candida growth occurred exclusively in groups receiving TPN and bowel rest, we conclude that altered gut-barrier function to Candida occurs during TPN and speculate that Candida sepsis during TPN might be the result of Candida translocation from the gut due to the combination of high-density Candida colonization and favorable local conditions in the gut induced by TPN and bowel rest.

Animals↗