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Biomedical subjects

L Morelli

Publications and source records attributed to L Morelli.

At least 145 records · Page 8Linked to original sources

Experimental rat vaginal infection with Candida parapsilosis.

The experimental vaginopathic potential of Candida parapsilosis was determined in ovariectomized rats maintained under pseudoestrus by estrogen administrations. Of the 3 strains of C. parapsilosis tested, that isolated from the vagina of a woman affected by vulvovaginal candidosis gave a prolonged and sustained experimental vaginitis, not different in extent and duration from that caused by a vaginal isolate of C. albicans from a vaginitis patient. The other two isolates of C. parapsilosis (one from the vagina of an asymptomatic subject and another from soil) were unable to infect rat vagina. Microscopic observations of PAS-stained vaginal smears from rats infected with the vaginopathic isolate of C. parapsilosis showed pronounced adherence of yeasts to exfoliated cells. In addition, this isolate of C. parapsilosis produced an elevated quantity of acid proteinase in vitro.

Animals↗

In vivo transfer of pAM beta 1 from Lactobacillus reuteri to Enterococcus faecalis.

Trials were conducted to determine the in vivo transferability of plasmid-mediated antibiotic resistance between two strains of enteric Gram-positive bacteria. Germ-free mice were associated with the donor Lactobacillus reuteri DSM 20016 strain, carrying the broad host range pAM beta 1 plasmid, and with the Enterococcus faecalis JH2SS recipient strain. Analysis of faecal content of associated mice demonstrated that the in vivo transfer of this plasmid did occur and that frequencies of conjugation were affected by the presence of subtherapeutic levels of antibiotic in the diet.

Animals↗

Sequence and functional analysis of a divergent promoter from a cryptic plasmid of Lactobacillus acidophilus 168 S.

We have characterized three of at least five plasmids borne by Lactobacillus acidophilus 168 S. Restriction mapping indicates extensive sequence homology between at least two of them (p1 and p3). We have cloned them in Escherichia coli, and for the smallest (p1) we present the sequence of a region with two divergently arranged promoters which probably share a symmetrical (TTTAAA)-35 box and function efficiently in E. coli cells; an open reading frame contiguous to the promoter, which codes for a 120 amino acid protein of unknown function, and is transcribed in E. coli; and a transcription termination sequence next to this open reading frame. The promoter region contains an AT cluster which is similar to that of the ori2 region of the E. coli F plasmid, and is probably involved in the control of the replication of p1.

Base Sequence↗

Lactobacillus protoplast transformation.

A method for the transformation of Lactobacillus protoplasts by plasmid DNA is reported. The procedure involves polyethylene glycol treatment of protoplasts to induce DNA uptake. A transformation efficiency ranging from 5 to 1000 transformants per microgram of DNA is achieved; the efficiency of protoplast regeneration ranged from 10 to 20%.

DNA, Bacterial↗

Fast and slow milk-coagulating variants of Lactobacillus helveticus HLM 1.

Slow milk-coagulating variants were isolated from Lactobacillus helveticus HLM 1, a fast strain which coagulates milk in 16 h at 42 degrees C. Variants were isolated after subculturing in reconstituted skim milk or complex broth media. Analysis of plasmid content revealed that in slow variants a 3.5-megadalton plasmid was missing.

Animals↗

[Experimental pathogenicity of Cryptococcus cereanus in mice].

Pathogenicity studies in mice with Cryptococcus cereanus. Cr.cereanus, a yeast which showing a characteristic ability to grow above 40 degrees C, was found to induce pathogenicity when i.p. inoculated into mice after 6-7 repeated inoculations. Infected mice were sacrificed after 4, 8, 24 h and 3, 7, 14, 21 days following i.v. inoculation (5 X 10(7) cells); and microbiological, histopathological and blood-clinical tests were performed. The time course of C.F.U. in kidneys and brains (Fig.1) the yeasts colonization in heart and kidney tissues (Fig.5-3) and the characteristic "soap's balls" in brains (Fig.4) were confirmed by the modified serum levels of CPK, LDH, GOT, urea and creatinine. For the first time experimental pathogenicity of Cr. cereanus has been demonstrated.

Animals↗

Plasma glucose and protein concentrations in rat fetuses and neonates exposed to cataractogenic doses of mirex.

Mirex was administered to rats during gestation or the early postnatal period and the effects on blood chemistry were studied, especially with regard to changes which might play a role in the known cataractogenicity of mirex. In the prenatal study dams were intubated with 6 mg/kg/day mirex on Days 8 through 15 of gestation, and fetal blood samples were obtained on Days 18 and 20. For postnatal studies, litters were culled to eight pups at birth. Dams were intubated with 10 mg/kg/day mirex on Days 1 through 4 postpartum, and blood was drawn from pups at ages 6 through 14 days. Glucose determinations were done on a Beckman ASTRA 8 autoanalyzer. Protein determinations were done by the method of Lowry et al. (O.H. Lowry, N. J. Rosebrough , A. L. Farr, and R. J. Randall (1951). J. Biol. Chem. 193, 165-175.) Plasma glucose levels were decreased by over 40% in mirex-treated fetuses which developed cataracts. Postnatal exposure to mirex did not alter plasma glucose. Mean plasma protein concentrations were significantly lower in treated litters on Days 12 and 14 postpartum, and treated pups with cataracts on Day 14 were hypoproteinemic compared to treated pups without cataracts. Hypoproteinemia is a common factor related to cataractogenesis induced by either prenatal or postnatal mirex exposure, and may possibly be a causative factor. Although hypoglycemia may be a contributing factor in prenatal cataractogenesis, it does not seem to be implicated in postnatal cataractogenesis.

Animals↗

The vascular protection of ditazole and its effect on arachidonic acid metabolism.

Ditazole (4,5-diphenyl-2-bis-(2-hydroxyethyl)-aminoxazol) is a weak anti-inflammatory drug and has been shown to inhibit thrombus formation following electrically stimulated vascular damage in the microcirculation of the hamster cheek pouch. The drug was found to inhibit thromboxane A2 (TXA2) production ex vivo as determined by radioimmunoassay (RIA) and to reversibly antagonise the effect of TXA2 on smooth vascular tissue. However, in contrast to acetylsalicylic acid (ASA), it does not inhibit vessel cyclooxygenase. The apparent vascular protective effect of ditazole could not be ascribed to an enhanced production of vascular prostacyclin (PGI2) since the latter, when estimated ex vivo by RIA, was not enhanced following oral treatment with the drug. It is suggested that the mode-of-action of ditazole may be different from the cyclo-oxygenase/PG synthetase blocking action of most other non-steroidal anti-inflammatory drugs.

Animals↗

"In vitro" activity of urokinase on platelet function and on ADP degradation by vascular tissue.

The effects of urokinase on ADP breakdown by vessel-wall, platelet aggregation and the related prostaglandin system "in vitro" were investigated. It is confirmed that urokinase does not induce platelet aggregation both in humans and rabbits "in vitro". Conversely, in high concentrations, urokinase inhibits ADP-induced platelet aggregation in human and rabbit platelet-rich plasma. No effects were observed on rabbit platelet thromboxane A2 release and on rat vascular prostacyclin production, both measured by radioimmunoassay of thromboxane B2 and 6-keto-F1 alpha prostaglandin, respectively. Moreover, the incubation of urokinase with vascular endothelium resulted in an increased disappearance rate.

Adenosine Diphosphate↗

Drug resistance plasmids in Lactobacillus acidophilus and Lactobacillus reuteri.

Sixteen strains of Lactobacillus reuteri and 20 strains of Lactobacillus acidophilus were tested for resistance to 22 antibiotics by using commercially available sensitivity disks. Evidence suggesting linkage of these resistances to plasmids was obtained by "curing" experiments with acridine dyes and high growth temperatures. Examination of plasmid patterns of agarose gel electrophoresis provided further evidence of loss in plasmid DNA under curing conditions in some of the strains examined.

Anti-Bacterial Agents↗

[Experimental pathogenicity of Candida lusitaniae in mice].

Experimental pathogenicity was for the first time demonstrated in a strain of C. lusitaniae of clinical origin by the use of concentrated inocula (5.10(7) Y-shaped cells) and the administration of 4 mg of methylprednisolone acetate i.m. injected 4 days before and 3 days after the inoculation. Counts on malt-agar (fig. 1) in kidney and brain showed a decrease during the first 12 hours, followed by a definite increment in cell number between the first and second day. Clinical tests showed a strong proteinuria, high levels of blood urea and creatinine, and a low GOT increase. Glycemia, GPT, and total serum protein values were normal. Histological examinations of kidney showed a delayed penetration with discrete clumps of Y-shaped cells, inflammatory focuses, and compromised tubules and glomerula (Fig. 2). After 2 weeks of study accumulations of cells followed by degenerative phenomena were seen in the various structures examined. Reparation processes were seldom observed (Fig. 3-4).

Animals↗

Evidence of morphological and physiological transformation of mammalian cells by strong magnetic fields.

Cultures of L-929 and WI-38 cells, frozen to 4.2 degrees K and exposed for 4 to 8 hours to 5000-oersted magnetic fields, were markedly inhibited in their growth as compared to controls. In cultures grown on cover slips, approximately 7 days after exposure, morphologically distinct cells emerged and were propagated from generation to generation; 3 weeks later, in flask cultures, contact inhibition was abolished. It is concluded that under certain experimental conditions, strong magnetic fields induce morphological and physiological transformations of target cells.

Cell Division↗