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Biomedical subjects

A Ahmed

Publications and source records attributed to A Ahmed.

At least 127 records · Page 7Linked to original sources
PubMed2000

Midproject findings from a study of the National Collegiate Athletic Association's policy on smokeless tobacco use.

In this paper we present midproject findings from a longitudinal survey of 5,000 male athletes at 56 randomly selected American colleges and universities. The study monitors athletes' compliance with and perceptions of the effects of an organizational policy that restricts smokeless tobacco (ST) use. In 1996 and 1997, 77% of users reported that they complied with the policy during competition. During the same period there was a significant increase in the number of users who complied with policy during practices and of those who credited the policy with contributing to a decline in their overall tobacco consumption (14% vs 68%, p < .001; 17% vs 23%, p < .01: respectively). The findings suggest that organizational policies that regulate ST use can have an impact on young adult ST use.

Adolescent↗
PubMed2000

Quinolizidine alkaloids from Sophora alopecuroides.

A new matrine-type alkaloid, 7alpha-hydroxysophoramine (1), was isolated from the aerial parts of Sophora alopecuroides together with eight known alkaloids, 12beta-hydroxysophocarpine (2), sophoramine (3), 14beta-hydroxymatrine, matrine, sophoridine, sophocarpine, adenocarpine, and baptifoline. The structures of compounds 1-3 were confirmed through single-crystal X-ray diffraction analysis.

Alkaloids↗
PubMed2000

Differential diagnosis of gallstone-induced complications.

Early recognition and prompt intervention are the most crucial steps in the management of gallstone-induced biliary disease. Many conditions can mimic the presentation of gallstone-induced complications. Therefore, participation of a clinically astute physician is essential in evaluating symptoms and interpreting diagnostic data in patients with symptomatic gallstones.

Acute Disease↗
PubMed2000

Ras/mitogen-activated protein kinase mediates norepinephrine-induced phospholipase D activation in rabbit aortic smooth muscle cells by a phosphorylation-dependent mechanism.

Phospholipase D (PLD) activity is regulated by phosphatidylinositol 4,5-biphosphate, protein kinase C (PKC), ADP-ribosylation factor, and Rho. The present study was designed to investigate the mechanism of norepinephrine (NE)-mediated PLD activation in rabbit aortic vascular smooth muscle cells (VSMC). NE (10 microM) caused activation of PLD, as measured by the production of phosphatidylethanol in [(3)H]oleic acid-labeled cells. NE also increased PKC activity in VSMC. However, treatment of cells with bisindolylmaleimide, a PKC inhibitor, or long-term treatment with phorbol-12-myristate-13-acetate that depletes PKC did not decrease NE-induced activation of PLD. NE-stimulated PLD activity was attenuated by farnesyl transferase inhibitors (FPT III and SCH-56582), which reduce activation of both Ras and mitogen-activated protein (MAP) kinase. Moreover, transfection of VSMC with a dominant negative Ras resulted in inhibition of NE-stimulated MAP kinase and PLD activities. Treatment of cells with PD-98059, a MAP kinase kinase inhibitor, also reduced NE-stimulated PLD activity. These data suggest that NE-stimulated PLD activity is mediated via activation of Ras and MAP kinase in rabbit VSMC. To study the mechanism of activation of PLD by Ras/MAP kinase, NE-induced phosphorylation of PLD was examined. In VSMC, PLD of molecular mass 120 kDa was identified with polyclonal PLD antibody. Phosphorylation of PLD by NE, measured as (32)P incorporation into PLD, was inhibited by PD-98059. Moreover, PLD immunoprecipitated from VSMC lysates was phosphorylated in vitro by MAP kinase. Collectively, these results show a novel pathway for activation of PLD that appears to be mediated through Ras/MAP kinase pathway by a mechanism involving phosphorylation.

Adrenergic alpha-Agonists↗
PubMed2000

Activation of platelet-activating factor (PAF) receptor stimulates nitric oxide (NO) release via protein kinase C-alpha in HEC-1B human endometrial epithelial cell line.

BACKGROUND: Impairment of the fertility in the platelet-activating factor (PAF) receptor transgenic female mice suggests changes in PAF functions can influence uterine receptivity. We hypothesized that vasodilatory actions of PAF in the uterus was exerted by PAF-mediated nitric oxide (NO) release via activation of isoenzyme-specific protein kinase C (PKC). MATERIALS AND METHODS: Inducible and endothelial NOS was shown by Reverse transcription polymerase chain reaction RT-PCR in cDNA synthesized from RNA extract of proliferative and secretory endometrium as well endometrial epithelial cell lines HEC-1B. The effect of WEB2170, N(G)-monomethyl-L-arginine (L-NMMA) and Ro31-8220 on PAF mediated NO release by HEC-1B cell was determined. PAF induced translocation of PKCalpha in HEC-1B cell and its antagonist effect by Ro 31-8220 was studied by Western immunoblot analysis. PKC isoenzyme regulated by PAF was determined in HEC-1B cell lysate by immunoprecipitation. RESULTS: PAF-evoked a rapid and concentration-dependent biphasic increase in total NO in human HEC-1B endometrial epithelial cell line [as measured by a Sievers NOA 280A NO Chemiluminescent Analyser.] This increase in NO release was attenuated by the PAF receptor antagonist, WEB2170. Inhibition of NO synthesis by N(G)-monomethyl-L-arginine produced marked dose-dependent attenuation of PAF-mediated NO release, indicating nitric oxide synthase (NOS) activation. PAF-mediated NO release was also inhibited by the PKC inhibitor Ro 31-8220 and by the removal of extracellular calcium, suggesting a dependency on PKC and calcium, respectively. RT-PCR analysis showed expression of inducible NOS and endothelial NOS in human endometrium, myometrium and HEC-1B cells. Western immunoblot analysis showed PKCalpha, betaII and iota were the principal isozymes present in the HEC-1B cell line and normal endometrium, suggesting that both HEC-1B cells and normal endometrium have similar PKC isozymes. PAF induced the translocation of both PKCalpha and PKCiota within the time frame of NO release. The translocation of PKCalpha, but not PKCiota, was susceptible to inhibition by Ro 31-8220 that also inhibited PAF-evoked NO release, suggesting that PKCalpha is the principal isozyme involved in this process and that eNOS may be a substrate for PKCalpha. Kinase assays performed using immunoprecipitated PKCalpha showed that PAF (1 nM) activated PKCalpha that was inhibited by co-incubation with Ro31-8220 and Ca(2+)-free medium. CONCLUSIONS: This study demonstrates that PAF-stimulated NO release via PKCalpha in epithelial cells might regulate endometrial functions such as implantation and menstruation.

Azepines↗
PubMed2000

Extracranial neurilemmoma: a case report and review of the literature.

A 14-year-old male presented with a several month history of an asymptomatic right cervical swelling. An ultrasound scan showed a solid lesion superficial and superior to the thyroid gland. Surgical excision of the lesion was carried out and histological examination revealed a neurilemmoma. Neurilemmomas are relatively rare tumours and even rarer in children. The incidence of such tumours and the management of our patient are discussed.

Adolescent↗
PubMed2000

Induction of placental heme oxygenase-1 is protective against TNFalpha-induced cytotoxicity and promotes vessel relaxation.

BACKGROUND: Pregnancy is characterized by an inflammatory-like process and this may be exacerbated in preeclampsia. The heme oxygenase (HO) enzymes generate carbon monoxide (CO) that induces blood vessel relaxation and biliverdin that acts as an endogenous antioxidant. MATERIALS AND METHODS: We examined the expression and localization of HO-1 and HO-2 in normal and preeclamptic placenta using reverse transcription polymerase chain reaction (RT-PCR), RNase protection assay, immunoblotting and immunohistochemistry. In addition, the effect of HO activation on tumor necrosis factor-alpha (TNFalpha) induced placental damage and on feto-placental circulation was studied. RESULTS: We provide the first evidence for the role of HO as an endogenous placental factor involved with cytoprotection and placental blood vessel relaxation. HO-1 was significantly higher at term, compared with first trimester placentae indicating its role in placental vascular development and regulation. HO-1 predominantly localized in the extravascular connective tissue that forms the perivascular contractile sheath around the developing blood vessels. HO-2 was localized in the capillaries, as well as the villous stroma, with weak staining of trophoblast. Induction of HO-1 caused a significant attenuation of TNFalpha-mediated cellular damage in placental villous explants, as assessed by lactate dehydrogenase leakage (p < 0.01). HO-1 protein was significantly reduced in placentae from pregnancies complicated with preeclampsia, compared with gestationally matched normal pregnancies. This suggests that the impairment of HO-1 activation may compromise the compensatory mechanism and predispose the placenta to cellular injury and subsequent maternal endothelial cell activation. Isometric contractility studies showed that hemin reduced vascular tension by 61% in U46619-preconstricted placental arteries. Hemin-induced vessel relaxation and CO production was inhibited by HO inhibitor, tin protoporphyrin IX. CONCLUSIONS: Our findings establish HO-1 as an endogenous system that offers protection against cytotoxic damage in the placenta, identifies the HO-CO pathway to regulate feto-placental circulation and provides a new approach to study the disease of preeclampsia.

Capillaries↗
PubMed2000

In-vitro antimicrobial activity of Cefpirome: a new fourth-generation cephalosporin against clinically significant bacteria.

OBJECTIVE: To study the in-vitro antimicrobial activity of Cefpirome: A new fourth generation Cephalosporin in comparison with other agents against clinically significant Gram-negative and Gram-positive bacteria. SETTING: A multi-center in-vitro study was conducted in 13 centers. MATERIALS AND METHODS: Bacterial isolates--A total of 1300 isolates were collected from different clinical laboratories and hospitals at 13 centers. Organisms were identified by the API identification systems (API systems, SA Vericeu, France). The age and sex of each patient, type of hospital unit, source of the isolate and genus and species of the bacteria were recorded on standardized report forms. The sensitivity testing was carried out by the "NCCLS (modified Kirby-Bauer) method"--using Mueller-Hinton agar. RESULTS: The results suggest that Cefpirome has a potential clinical advantage against gram-positive and gram-negative bacteria resistant to other third generation cephalosporins. CONCLUSION: Cefpirome was active against both gram-negative and gram-positive organisms. Cefpirome was more active than ceftazidime, cefoperazone, ceftizoxime and ceftriaxone against E. coli, Klebsiella spp, Enterobacter spp, Proteus spp, Salmonella typhi, Enterococci, methicillin sensitive Staphylococci and Betahemolytic Streptococci. The activity of Cefpirome was comparable with ceftazidime against pseudomonas aeruginosa. Cefpirome had the smallest numbers of resistant isolates. Cefpirome was more active than other third generation cephalosporins compared in this study against E. coli (87% vs 61%), Klebsiella spp (84% vs 56%), Enterobacter spp (88% vs 59%), Proteus spp (97% vs 92%), Salmonella typhi (98% vs 96%), methicillin sensitive Staphylococci (86% vs 59%) and Enterococci spp (82% vs 72%).

Bacteria↗
PubMed2000

Culture and sensitivity of Salmonella species: analysis of a two year data.

OBJECTIVE: To determine the proportion and culture/sensitivity (C/S), pattern of different species of Salmonella in blood sent for C/S in a laboratory at a tertiary care hospital. MATERIAL AND METHODS: A retrospective analysis was done on all blood samples sent for C/S to the laboratory of Ziauddin Medical University Hospital during two years period (Jan 1, 1998 to Dec 31, 1999). 9035 blood samples were received for C/S. All blood cultures were inoculated in thioglycolate broth and incubated at 37 degrees for 7 days. Positive blood cultures were processed, colonies were identified using standard biochemical tests and antibiotic susceptibility was checked by Kirby-Bauer disc diffusion method. RESULTS: Three hundred and four (3.4%), out of 9035 blood cultures were positive for Salmonella, among them 220 (72%) were S. typhi, 82 (27%) paratyphi A or B and remaining were other species. Salmonella infection was more common in male (58%) and more prevalent in children under 10 years of age (58%). Ampicillin, chloramphenicol, cotrimoxazole resistance was (46.5%), (39.3%) and (44.8%) respectively. CONCLUSION: Ampicillin chloramphenicol and cotrimoxazole, the first line of drugs for the treatment of infection are losing their efficacy and most of the organisms have developed resistance against these drugs.

Child↗
PubMed2000

Dissolution rate studies on Acetaminophen tablets.

The effect of disintegrants on the dissolution rate of Acetaminophen tablets at different hardness has been investigated. It was determined that the dissolution rate is influenced by disintegrants as well as hardness for all formulations except in tablets containing Veegum as the disintegrant.

Journal Article↗
PubMed1999

Genomic structure and ecdysone regulation of the prophenoloxidase 1 gene in the malaria vector Anopheles gambiae.

Prophenoloxidase, a melanin-synthesizing enzyme, is considered to be an important arthropod immune protein. In mosquitoes, prophenoloxidase has been shown to be involved in refractory mechanisms against malaria parasites. In our study we used Anopheles gambiae, the most important human malaria vector, to characterize the first arthropod prophenoloxidase gene at the genomic level. The complete nucleotide sequence, including the immediate 5' flanking sequence (-855 bp) of the prophenoloxidase 1 gene, was determined. The gene spans 10 kb and is composed of five exons and four introns coding for a 2.5-kb mRNA. In the 5' flanking sequence, we found several putative regulatory motifs, two of which were identified as ecdysteroid regulatory elements. Electrophoretic mobility gel-shift assays and supershift assays demonstrated that the Aedes aegypti ecdysone receptor/Ultraspiracle nuclear receptor complex, and, seemingly, the endogenous Anopheles gambiae nuclear receptor complex, was able to bind one of the ecdysteroid response elements. Furthermore, 20-hydroxyecdysone stimulation was shown to up-regulate the transcription of the prophenoloxidase 1 gene in an A. gambiae cell line.

Animals↗
PubMed1999

Evidence that high-density lipoprotein cholesterol is an independent predictor of acute platelet-dependent thrombus formation.

Plasma total and low-density lipoprotein (LDL) cholesterol are established risk factors for atherosclerotic vascular disease and may also contribute to a prothrombotic risk via enhanced platelet reactivity. This study examines whether high-density lipoprotein (HDL) cholesterol, which is inversely correlated with coronary artery disease, is associated with a reduced thrombogenic potential. Platelet thrombus formation was evaluated by exposing porcine aortic media placed in Badimon perfusion chambers to flowing nonanticoagulated venous blood for 5 minutes at a shear rate of 1,000 s(-1). Forty-five subjects, 23 normal (LDL 104 +/- 31, HDL 50 +/- 15 mg/dl) and 22 hypercholesterolemic (LDL 181 +/- 45, HDL 41 +/- 10 mg/dl) patients without coronary artery disease were studied. Platelet aggregation and CD62 antigen expression, and assay for circulating prothrombotic factors were also performed. In univariate analysis platelet thrombus formation correlated with weight (r = 0.33, p = 0.03), diastolic blood pressure (r = 0.39, p = 0.01), HDL cholesterol (r = -0.45, p = 0.003), total/HDL cholesterol (r = 0.43, p = 0.004) and LDL/HDL (r = 0.38, p = 0.01) ratios, and platelet CD62 expression (r = 0.41, p = 0.02). In multiple regression analysis only HDL cholesterol showed significant correlation with platelet thrombus formation (p = 0.03). Platelet aggregation and circulating prothrombotic factors did not correlate with platelet thrombus formation. A comparison between normal and hypercholesterolemic subjects revealed enhanced thrombus area (0.026 +/- 0.20 vs 0.045 +/- 0.039 mm2/mm; p = 0.04), resting CD62 expression (6 +/- 7% vs 15 +/- 10% positive platelets, p = 0.02), and platelet aggregation (16.7 +/- 5.2 vs 21.7 +/- 6.7 ohms, p = 0.04) in hypercholesterolemic subjects. Our results demonstrate that HDL cholesterol is a significant independent predictor of ex vivo platelet thrombus formation.

Adult↗
PubMed1999

A molecular target for viral killer toxin: TOK1 potassium channels.

Killer strains of S. cerevisiae harbor double-stranded RNA viruses and secrete protein toxins that kill virus-free cells. The K1 killer toxin acts on sensitive yeast cells to perturb potassium homeostasis and cause cell death. Here, the toxin is shown to activate the plasma membrane potassium channel of S. cerevisiae, TOK1. Genetic deletion of TOK1 confers toxin resistance; overexpression increases susceptibility. Cells expressing TOK1 exhibit toxin-induced potassium flux; those without the gene do not. K1 toxin acts in the absence of other viral or yeast products: toxin synthesized from a cDNA increases open probability of single TOK1 channels (via reversible destabilization of closed states) whether channels are studied in yeast cells or X. laevis oocytes.

Animals↗
PubMed1999

Mutator phenotype of BCR--ABL transfected Ba/F3 cell lines and its association with enhanced expression of DNA polymerase beta.

Chronic myelogenous leukemia (CML) is characterized by the Philadelphia chromosome resulting from the translocation t(9-22) producing the chimeric 190 and 210 kDa BCR-ABL fusion proteins. Evolution of the CML to the more agressive acute myelogenous leukemia (AML) is accompanied by increased cellular proliferation and genomic instability at the cytogenetic level. We hypothezised that genomic instability at the nucleotide level and spontaneous error in DNA replication may also contribute to the evolution of CML to AML. Murine Ba/F3 cell line was transfected with the p190 and p210-encoding BCR-ABL oncogenes, and spontaneous mutation frequency at the Na-K-ATPase and the hypoxanthine guanine phosphoribosyl transferase (HPRT) loci were measured. A significant 3-5-fold increase in mutation frequency for the transfected cells relative to the untransfected control cells was found. Furthermore, we observed that BCR-ABL transfection induced an overexpression of DNA polymerase beta, the most inaccurate of the mammalian DNA polymerases, as well as an increase in its activity, suggesting that inaccuracy of DNA replication may account for the observed mutator phenotype. These data suggest that the Philadelphia abnormality confers a mutator phenotype and may have implications for the potential role of DNA polymerase beta in this process.

Animals↗
PubMed1999

Autoantibodies in human chronic graft-versus-host disease after hematopoietic cell transplantation.

Primary biliary cirrhosis (PBC) and graft-versus-host disease (GVHD) are thought to have common immunopathologic features and previous studies have reported that 5.2 to 81% of patients with chronic GVHD after allogeneic hematopoietic cell transplant have antimitochondrial antibodies (AMA). We studied a total of 89 patients with chronic GVHD and 60 controls for AMA reactivity by ELISA and immunoblotting using recombinant PDC-E2, BCOADC-E2, and OGDC-E2, immunoblotting of beef heart mitochondrial proteins, and reactivity to nuclei, smooth muscle (ASMA), ribonucleoprotein JO-1, extractable nuclear antigen, nuclear proteins SSA/ SSB, ribonucleic P proteinase III, cardiolipin (ACA), liver kidney microsomal, thyroid microsomal, myeloperoxidase, and the reactivity of rheumatoid factor. A subset of 60 chronic GVHD sera were tested for reactivity to gp210 and LBR. Finally, liver tissue from patients with chronic GVHD and PBC was studied by immunohistochemistry to determine whether there was comparable abnormal apical staining of biliary epithelial cells using PDC-E2-specific monoclonal antibodies. Surprisingly, there were no AMA found in the sera from the 89 patients with chronic GVHD. Review of published data on AMA in GVHD suggests that previous results were primarily false positives. In contrast, sera from the patients with GVHD did have a variety of other autoantibodies and, in particular, 20/89 (22.4%) positive ANA, 23/89 (25.8%) positive ASMA, and 9/89 (10.1%) positive ACA. The other autoantibodies assayed were not statistically different from controls. Finally, abnormal biliary epithelial luminal staining of bile ducts was found, as expected, in liver tissue of patients with PBC but was absent in chronic GVHD.

Adult↗