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Biomedical subjects

H Smaoui

Publications and source records attributed to H Smaoui.

6 recordsLinked to original sources
PubMed2006

[Study of Haemophilus influenzae strains isolated at the Tunis children's hospital in the prevaccination era (1999-2002)].

OBJECTIVE: This study had for aim to define the pattern of Haemophilus influenzae infections in a Tunisian hospital during the prevaccination era. We determined serotypes, biotypes, and antibiotic susceptibility of H. influenzae strains. DESIGN: 187 H. influenzae strains were identified in various samples between 1999 and 2002. RESULTS: Strains were isolated essentially from respiratory samples in 63.7% and cerebrospinal fluid in 21.4 %. The mean age of children with invasive infections was 16 months. All invasive strains belong to serotype b. Biotypes I, II and III were the most frequent (84.7%). Ampicillin resistance with betalactamase producing mechanism occurred in 26,7% of isolates, this type of resistance was more frequent among invasive strains (37.2%) than in non-invasive ones (22.8%). All betalactamase producing strains had amoxicillin MICs above 1 mg/l, these strains were susceptible to amoxicillin+clavulanate. Three strains were betalactamase negative ampicillin resistant with ampicillin MICs: 1.5, 3, and 4 mg/l. All strains were susceptible to cefotaxim with MICs < 0.19 mg/l. Antibiotic resistance concerned: chloramphenicol: 7.5%, tetracycline: 6.9% and trimethoprime-sulfamethoxazole: 13.9%. 8.1% of the strains were kanamicin resistant but concerned only betalactamase producing strains. CONCLUSION: Before the introduction of a conjugate vaccine, all invasive infections in young children were caused by H. influenzae b strains.

Anti-Bacterial Agents↗
PubMed1996

Protection of rat lung from elastase-induced elastic fiber degradation in vitro and from emphysema in vivo by a trifluoroacetylpeptide anilide inhibitor.

Trifluoroacetylpeptide anilides are powerful reversible inhibitors of human neutrophil elastase (HNE), a serine protease implicated in the pathogenesis of pulmonary emphysema. The in vitro effectiveness of three inhibitors, CF3CO-Phe-Ala-NH-p-C6H4-CF3 (1), CF3CO-Val-Ala-NH-p-C6H4-CF3 (2) and CF3CO-Lys-Ala-NH-p-C6H4-CH(CH3)2 (3) was analyzed. The protection of lung tissue sections of rats from the degradation induced by HNE has been evaluated quantitatively by automated image analysis. Inhibitor 1 (22 microM), 2 (50 microM) or 3 (35 and 70 microM) significantly reduced the HNE-induced degradation of the elastin network by 75, 42, 54 and 44%, respectively. Inhibitor 3 was tested intratracheally on an experimental model of pulmonary emphysema. Rats that received the elastase inhibitor 1 h before instillation of HNE were significantly protected by 40% from experimental emphysema. Reduced protections were observed with the treatment by the inhibitor 1 or 4 h after challenge with the enzyme.

Anilides↗
PubMed1994

Transplacental effects of gentamicin on endocytosis in rat renal proximal tubule cells.

Changes in kidney maturation in utero have been reported after gentamicin administration to pregnant rats. While the proteinuria commonly observed could be related to modifications of the glomerular basement membrane, perturbed renal protein handling could be accounted for by changes in the proximal tubular cells. Therefore, we studied the effect of gentamicin on the renal handling and transport of proteins in proximal tubular cells using the horseradish peroxidase, a fluid-phase marker, as a probe. Gentamicin was administered intraperitoneally to pregnant Wistar rats (75 mg/kg body weight per day) and neonatal kidneys were studied 1 day after birth. In proximal tubular cells of the deep cortical area, containing the fully matured nephrons of neonates, the transport and digestion of reabsorbed peroxidase was considerably reduced compared with controls where peroxidase reached lysosomes after endocytosis. Urinary protein excretion increased in treated animals. We conclude that gentamicin, entering the proximal tubular cells via the endocytic pathway, decreases the tubular reabsorption of proteins, thus increasing urinary protein excretion.

Animals↗
PubMed1993

Gentamicin administered during gestation alters glomerular basement membrane development.

Gentamicin during gestation alters glomerular basement membrane development. A drug-induced nephrotoxicity was described for neonates after gentamicin was given intraperitoneally to pregnant Wistar rats; glomerular alterations and changes in permselectivity were important. We investigated the ultrastructure of the glomerular basement membrane (GBM), the arrangement of anionic sites, and the urinary proteins at two ages, with 1-day- and 12-month-old control and prenatally exposed animals. For neonates, the pattern of glomerular differentiation was similar, anionic sites were made of heparan sulfate proteoglycans, and the GBM had the same total thickness in both groups. After transplacental gentamicin exposure, the lamina densa was larger; the laminae rarae were thinner; the density of anionic sites was increased; the levels of hydroxyproline, sulfate, and hexuronic acid in the kidney were increased; and the immunoelectrophoresis of urinary proteins was abnormal. For adults, prenatal exposure to gentamicin led to altered juxta-medullary glomeruli with a larger GBM and abundant anionic sites, especially in the lamina densa, and to a protein excretion different from that of controls. Thus, gentamicin administered during pregnancy leads to permanent alterations of the GBM with modifications of both the layers and the anionic sites, possibly because of a perturbed protein metabolism. These altered glomeruli are at risk during life and could be the starting point for a kidney disease.

Animals↗
PubMed1991

Glomerular alterations in rat neonates after transplacental exposure to gentamicin.

Alterations of tubules and glomerules have been reported previously in kidneys of rat neonates after aminoglycosides were given to the mother during gestation. Here, we have studied the effects of gentamicin on the development of the glomerular basement membrane (GBM). Pregnant Wistar female rates were treated with gentamicin. Deliveries occurred normally. Using electron microscopy, we looked at the deepest glomerules of the kidneys of 1-day-old neonates: myeloid bodies were found in podocytes, and the GBM appeared thicker and denser than in controls. Anionic ferritin, injected intravenously crossed the GBM in prenatally gentamicin-exposed animals, but not in controls. Furthermore, urine electrophoresis showed the presence of proteins normally found only in the urine of fetuses 2 days before birth. We suggest then, that in utero exposure to gentamicin leads to a delay of renal maturation and that the GBM is altered in juxtamedullary nephrons while it is normally differentiated and functioning in controls. Thus exposure to drugs before birth could be harmful to the GBM.

Abnormalities, Drug-Induced↗