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Biomedical subjects

M Osman

Publications and source records attributed to M Osman.

At least 73 records · Page 4Linked to original sources

Effect of UV-irradiation on some aspects of metabolic activities in Aspergillus flavus and Penicillium notatum.

Near-UV (NUV) irradiation was found to stimulate protein synthesis in Penicillium notatum and Aspergillus flavus. DNA was also induced by short periods of NUV (10 and 20 min) in P. notatum. Synthesis of DNA in A. flavus decreased under the same treatment and then increased when irradiation was for long periods. The reverse of this observation was seen in the case of RNA synthesis, while RNA synthesis was significantly inhibited by NUV in P. notatum. Induction of RNA synthesis was observed in A. flavus. Far-UV (FUV) irradiation induced protein synthesis in P. notatum and A. flavus; the increase was more pronounced in A. flavus. FUV slightly inhibited DNA synthesis in P. notatum, but the synthesis in A. flavus was fairly constant. RNA synthesis was reversed to a certain extent by FUV in both fungi. UV irradiation produced no effect on the process of lipid synthesis. Total soluble carbohydrates were decreased by NUV in P. notatum and increased markedly in A. flavus (240 min NUV). FUV irradiation resulted in an increase in total soluble carbohydrates in both fungi.

Aspergillus flavus↗

The fibronectin content of canine lungs is increased in bleomycin-induced fibrosis.

Fibronectin (Fn), a high molecular weight glycoprotein, was found to constitute 0.43% of the normal adult beagle dog lung. The tissue Fn (TFn) was solubilized by sequential chemical extractions and quantified by ELISA (enzyme-linked immunoabsorbent assay). Subsequent plasmin digestion did not appear to solubilize significantly more Fn. Since 70% of the lung tissue was solubilized by the extractions and plasmin digestions, the TFn quantified represented the bulk of lung Fn. The TFn was identical to plasma fibronectin in the ELISA and one can infer that the Fn molecule is not significantly altered as it is incorporated into the lung connective tissue matrix. Lungs from beagles in which fibrosis had been induced with bleomycin contained 0.99% Fn, more than a twofold increase over normal. In the ELISA TFn from fibrotic lungs gave an inhibition curve of the same shape as did TFn from normal lungs. Thus, Fn from fibrotic lungs is not different qualitatively from Fn from normal lungs in any way detectable with this antiserum. The TFn content of plasmin digests of intact lung was less than that of extracts, which was the converse of results obtained on placenta (B. A. Bray (1985) Biochem. J. 226, 811-815). This difference between lung TFn and placental TFn may be due to differences in degree of glycosylation, which determines susceptibility to proteases.

Animals↗

Stimulation of lung lysyl oxidase activity in hamsters with elastase-induced emphysema.

Lysyl oxidase activity was measured in lung extracts of hamsters with elastase-induced emphysema 8 days after administration of the enzyme and again after 2, 3, and 4 wk. Levels of activity rose rapidly to 7 times the base values determined in the lungs of saline-injected control animals. In parallel with the increase in lysyl oxidase activity, the rate of 14C-lysine incorporation into desmosine and isodesmosine was at its maximum 1 wk after elastase administration, reflecting the lysyl-oxidase-mediated cross-link formation, which is the final step in the resynthesis of the pulmonary elastin destroyed by the elastolytic insult.

Amino Acid Oxidoreductases↗

Cigarette smoke impairs elastin resynthesis in lungs of hamsters with elastase-induced emphysema.

The severity of pulmonary emphysema can be affected by exposure to cigarette smoke in several ways. Inactivation of alpha-1-antitrypsin and recruitment of leukocytes to lung airways shifts the protease-antiprotease balance towards increased elastolytic activity. The present study demonstrates an additional effect of cigarette smoke inhalation and retardation of the repair process and of the neosynthesis of cross-linked elastin. Hamsters with elastase-induced emphysema, exposed to cigarette smoke for 1 wk immediately after elastase administration, showed a 40% reduction of 14C-lysine incorporation into the elastin-specific cross-links, desmosine, and isodesmosine. Concomitantly, there was a decrease in the level of lung lysyl oxidase to that observed in uninjured control animals, in sharp contrast to the sevenfold increase in lysyl oxidase activity in hamsters with elastase-induced emphysema recovering under atmospheric conditions. These findings suggest that impairment of the production of lysyl oxidase and the resynthesis of cross-linked elastin by smoke inhalation exacerbates alveolar destruction.

Animals↗

Impairment of elastin resynthesis in the lungs of hamsters with experimental emphysema induced by sequential administration of elastase and trypsin.

The nonelastolytic proteases trypsin and chymotrypsin were administered to hamsters 24 hours after intratracheal injection of elastase. Severity of the disease, extent of degradation and resynthesis, new cross-link formation, and the levels of the enzyme lysyl oxidase, which mediates the cross-link formation, were compared with the same parameters measured in hamsters with experimental emphysema induced by elastase alone. Increases in mean linear intercept indicated that a more severe form of the disease was produced. Although elastin degradation after 1 week was similar in both groups, resynthesis of the elastin destroyed by the elastolytic insult was significantly impaired in the animals injected sequentially with elastase and trypsin or chymotrypsin. Formation of new elastin as monitored by 14C-lysine incorporation into the elastin specific cross-links desmosine and isodesmosine was reduced approximately 40%, although there was no significant difference in the levels of lysyl oxidase activity. It is suggested that the most likely mechanism compatible with the recorded observations involves destruction of the microfibrillar component of the elastic fiber by trypsin or chymotrypsin, resulting in the absence of the requisite template for resynthesis of the pulmonary elastin.

Animals↗

Effect of near-UV (366 nm) on the activity of certain nucleic acid enzymes in Verticillium agaricinum.

Verticillium agaricinum when grown for 60 min under near-UV irradiation (366 nm) followed by 24 h in darkness produced maximal activity of a number of nucleic acid enzymes (DNase I, endonuclease, nuclease, RNase A, and RNase T1). Total protein and nucleic acid on the other hand showed a decrease under the same conditions. The nucleic acid enzymes which are involved in reversible reactions seem to favour nucleic acid degradation in this study.

Carotenoids↗

Effect of aspirin on the luteal phase of human menstrual cycle.

The effect of aspirin (acetylsalicylic acid) on the luteal phase length and function was studied in ten normal cycling women. They received three grams daily for twenty days starting from the fifth day of the cycle. Urinary pregnanediol-3 alpha-glucuronide (Pg-diol- 3G ) and luteinising hormone (LH) were assayed in daily early morning urine samples together with daily vaginal smear for cytohormonal evaluation. The excretion profile of Pg-diol- 3G and LH of another group of ten normal women were taken as controls. Aspirin caused shortening of both cycle length and luteal phase duration. Available evidence suggests the presence of corpus luteum deficiency in the treated cycles.

Adult↗

Norfloxacin: activity against urinary tract pathogens and factors influencing the emergence of resistance.

The activity of norfloxacin was investigated in vitro in conventional minimum inhibitory concentration tests, by continuous turbidimetry and in a mechanical model simulating the hydrokinetic conditions that exist in the treatment of bacterial cystitis. The high activity of norfloxacin against virtually all bacterial pathogens isolated from infected urine was confirmed. However, in urine agar (pH 6 X 5) and in DST agar adjusted to pH 5 X 5, the activity was substantially reduced. Turbidimetric experiments indicated that increases in resistance to norfloxacin could be induced easily by sequential subculture, but results obtained in the bladder model, where conditions of exposure more closely resemble those that exist during the treatment of infection, suggest that such resistance is unlikely to arise commonly during treatment.

Anti-Bacterial Agents↗

Amiodarone-induced pulmonary fibrosis in hamsters.

Amiodarone, a cardiac antiarrhythmic agent, has been associated with the development of interstitial pulmonary fibrosis in patients receiving prolonged therapy with the drug. To further assess the toxic effects of amiodarone on lung tissue, Syrian hamsters were given a single intratracheal insufflation of the agent and evaluated for histologic evidence of lung injury. Control animals received intratracheal insufflations of the vehicle in which amiodarone was dissolved. After an initial, transient alveolitis in both experimental and control animals, the amiodarone-treated lungs developed increased interstitial thickening due to fibrinous exudates, alveolar epithelial hyperplasia, inflammatory cell infiltrates, and marked deposition of collagen manifested on trichrome staining. Controls, in contrast, showed nearly complete resolution of the initial alveolitis. An unusual feature of the amiodarone-induced lung injury was reemergence of the alveolitis between 5 and 14 days, which included a marked influx of eosinophils into the lung. Although the precise mechanism of the lung injury is not known, the persistence of the acute inflammatory cells as well as the presence of eosinophils suggests a hypersensitivity-type reaction. Furthermore, the progression of lung injury to fibrosis after a single insult with the drug suggests that mere discontinuation of amiodarone therapy in humans may not reverse the disease process, but that corticosteroid therapy may also be required. Amiodarone appears to be a useful agent to induce diffuse fibrotic reactions in the lung that morphologically resemble idiopathic pulmonary fibrosis in humans.

Amiodarone↗

Measurement of cross-linked elastin synthesis in bleomycin-induced pulmonary fibrosis using a highly sensitive assay for desmosine and isodesmosine.

Cross-linked elastin synthesis was measured in the intratracheal bleomycin model of interstitial pulmonary fibrosis by incorporation of 14C-lysine into the elastin-specific crosslinks, desmosine and isodesmosine. Detection of the labeled crosslinks was facilitated by development of a highly sensitive assay utilizing thin-layer electrophoresis. The results indicate that crosslinked elastin synthesis is significantly elevated from controls (p less than 0.05) at 1 to 3 weeks after exposure to bleomycin and returns to normal by 5 weeks. The increases in labeled elastin synthesis are not directly related to changes in either total lung protein synthesis or the pool size of the 14C-lysine. In comparison with collagen and glycosaminoglycan synthesis in this model of lung injury, maximal increases in cross-linked elastin formation occur later, but overlap with the elevated synthesis of these other connective tissue components. The marked increase from normal in cross-linked elastin synthesis in this model suggests that this tissue component is an important part of the fibrotic response of the pulmonary parenchyma and may play a role in the observed alterations in lung structure and function.

Amino Acids↗

Glycosaminoglycan synthesis in explants derived from bleomycin-treated fibrotic hamster lungs.

Glycosaminoglycan synthesis was studied in explant cultures of hamster lungs 15 and 45 days following intratracheal administration of Bleomycin. At both time points, a statistically significant increase in 35S-sulfate incorporation into glycosaminoglycans was seen in the Bleomycin-treated explants compared with that of the controls. Furthermore, the percentage of label associated with dermatan sulfate was significantly higher in the treated explants than in controls at both 15 and 45 days. Conversely, the percentage of labeled heparin and/or heparan sulfate was significantly lower for the treated explants compared to controls at these times. These results indicate that glycosaminoglycan synthesis is altered from normal in this model of interstitial lung disease. Comparison of these data with previous measurements of glycosaminoglycan synthesis in another model of interstitial lung disease, induced by N-nitroso-N-methylurethane, reveals marked similarity in the changes from normal in 35S-labeling.

Animals↗

Glycosaminoglycan synthesis in bleomycin-induced pulmonary fibrosis: biochemistry and autoradiography.

At 5, 15, and 45 days following induction of interstitial pulmonary fibrosis by intratracheal administration of bleomycin in hamsters, glycosaminoglycan synthesis was measured, using [35S]sulfate. Total labeled sulfate incorporation into lung glycosaminoglycans was maximally increased over that of saline-instilled controls at 5 days (P less than or equal to 0.05), declined markedly at 15 days, and returned to control values at 45 days. Separation of the various labeled glycosaminoglycans by chondroitinase digestion and chromatography revealed a transient rise from controls (P less than or equal to 0.05) in the proportion of labeled chondroitin 4-sulfate at 5 days, followed by an increase from controls (P less than or equal to 0.05) in proportionate labeling of dermatan sulfate at 15 and 45 days postbleomycin. Autoradiography, using [35S]sulfate, performed at 21 days postbleomycin, revealed an increase from controls in film grain formation in areas of interstitial reaction. Grain formation was greatly reduced by pretreatment of the slide sections with hyaluronidase and chondroitinase, demonstrating the specificity of the label for glycosaminoglycans. The results indicate that glycosaminoglycan synthesis is significantly altered from normal in this model of interstitial lung disease and that dermatan sulfate is preferentially synthesized during the fibrotic phase of the lung reaction.

Animals↗

[35S]autoradiographic study of sulfated GAG accumulation and turnover in embryonic mouse tooth germs.

The accumulation of sulfated GAG in embryonic mouse molars before, during, and after terminal differentiation of odontoblasts was localized by [35S]autoradiography combined with the use of chondroitin ABC lyase. Much more sulfated GAG were accumulated in the dental papilla than in the dental epithelium. High incorporation of [35S]sulfate occurred at the epithelio-mesenchymal junction, which is the site of dental basement membrane and predentin. Before terminal differentiation of odontoblasts, the distribution of sulfated GAG was uniform at the basement membrane. After the onset of terminal differentiation of odontoblasts, much more sulfated GAG accumulated at the tip of principal cusps than at the apical (inferior) parts of cusps, and sulfated GAG were then found to be degraded more rapidly at the epithelio-mesenchymal junction than at other parts of the tooth germ. Thus regional variation in the rate of degradation of GAG exists in the tooth germs. Trypsin-isolated dental epithelia cultured in vitro synthesized a new basement membrane that could be labeled with [3H]glucosamine but not with 35SO4(-2). The epithelial-derived basal lamina contains little or no sulfatated GAG.

Animals↗

Neutrophil chemotaxis in infants of diabetic mothers and in preterms at birth.

The chemotaxis of polymorphonuclear leukocytes of infants of diabetic mothers and of preterms was found lower than that of full term newborns when cells were incubated in autologous serum. When leukocytes from full terms were incubated in preterm serum, chemotaxis was significantly reduced. When leukocytes from either infants of diabetic mothers or preterms were incubated with full term serum, chemotaxis was significantly increased. No difference was found between infants of diabetic mothers and preterms. These results suggest that both groups of patients have a deficiency in serum factors playing a part in chemotaxis.

Chemotaxis, Leukocyte↗