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Biomedical subjects

Z Mirza

Publications and source records attributed to Z Mirza.

12 recordsLinked to original sources
PubMed2005

Butane encephalopathy.

Volatile solvent abuse (VSA) is defined at the "intentional inhalation of a volatile substance for the purpose of achieving a euphoric state". The lifetime prevalence of VSA in the UK remains steady at around 15%, the fourth highest rate in Europe, and VSA is the most common form of drug abuse in the 11-15 year age group in England and Wales. A 13 year old girl presented to the accident and emergency unit following inhalation of butane based deodorant, which resulted in a prolonged semiconscious state with encephalopathic symptoms.

Adolescent↗
PubMed2005

Management of suspected scaphoid fractures in accident and emergency departments--time for new guidelines.

INTRODUCTION: The objectives of this work were to assess the clinical knowledge of clinicians in the accident and emergency (A&E) departments in England & Wales and evaluate the current trend for the acute management of radiologically normal, but clinically suspected, fractures of the scaphoid. SUBJECTS AND METHODS: We conducted a telephone survey on 146 A&E senior house officers (SHOs) in 50 different hospitals. This survey assessed the clinicians' experience, their clinical and radiological diagnostic methods, and their initial treatment of suspected scaphoid fractures. RESULTS: The majority (55.8%) of SHOs performed only one clinical test to diagnose suspected scaphoid fractures. Overall, 41% were unable to cite the number of the radiographic views taken and only 10% of departments have direct access to further radiological investigation. There is wide variation in the early treatment of this injury, with the scaphoid cast used most commonly (46%). The majority of SHOs (89%) were unable to describe the features of immobilisation. The mean follow-up period was 10 days, and 53% of cases were followed-up by the senior staff in A&E. Of SHOs, 54% were not aware of any local guidelines for the management of suspected scaphoid fractures in their departments, and 92% were not aware of the existence of the 1992 British Association for Accident and Emergency Medicine (BAEM) guidelines. CONCLUSIONS: The clinical knowledge and the management of suspected scaphoid fractures in A&E are unsatisfactory. We, therefore, suggest that the dissemination of up-to-date guidelines could help to educate clinicians to provide better care to the patients.

Clinical Competence↗
PubMed2004

Prescription and dispensing practices in public sector health facilities in Pakistan: survey report.

OBJECTIVES: To gather information on existing prescription practices, dispensing practices and patient satisfaction in government health services of the NWFP, Baluchistan and Punjab province. METHODS: A cross sectional study design was used for this purpose. Ten health care facilities were selected from each province keeping appropriate representation from first level health facilities, district health facilities and tertiary care hospital. Analysis of selected indicators was carried out on the basis of provinces, health facilities, gender and different age groups. RESULTS: Documentation of 914 responses was completed from three provinces. Almost equal distribution of encounters was maintained representing different health facilities. Forty seven percent of encounters involved children under 15 years of age. Female patients comprised of 56% and the mean age of the entire sample was 26 years. The mean dispensing time was only 38 seconds, the mean consultation time was 1.79 minutes and the average number of drugs per prescription turned out to be 2.7 out of which only 1.6 drugs were being dispensed from the facility. More than half of the prescriptions contained antibiotics and 15% of patients were prescribed with injectables. Only half of the patients expressed satisfaction with their visit to health facility. CONCLUSIONS: Like many other developing countries, prescription and dispensing practices are not satisfactory in public sector health facilities of Pakistan. Appropriate and workable solutions need to be developed and implemented in the country to improve systems. Regular audits and qualitative studies should become part of the effort.

Adolescent↗
PubMed1995

Regulation of Ca(2+)-dependent nitric oxide synthase in bovine aortic endothelial cells.

Vascular endothelium responds to Ca(2+)-mobilizing agonists by producing nitric oxide (NO), a potent vasodilator and inhibitor of platelet aggregation. Regulation of constitutively expressed endothelial NO synthase (eNOS) in intact cells is not well understood. We investigated the kinetics of NO formation in response to Ca(2+)-mobilizing agonists, the requirement for extracellular L-arginine, and the role of NO in regulating eNOS activity. When endothelial cells were stimulated with bradykinin and ATP in the presence of 100 microM L-arginine, we observed a rapid and transient rise in intracellular Ca2+ concentration ([Ca2+]i) from 50 +/- 8 nM to 698 +/- 74 and 637 +/- 53 nM, respectively, and a rapid and transient rise in NO production from a basal level of 37 pmol.min-1.mg protein-1 to 256 and 275 pmol.min-1.mg protein-1, respectively. When cells were stimulated with A-23187 or thapsigargin in the presence of 100 microM L-arginine, we observed a sustained increase in [Ca2+]i and a sustained increase in NO production. The rate of NO synthesis was linear over 30 min, rising above control levels of 7 pmol/min to 53 pmol/min for A-23187 and 62 pmol/min for thapsigargin. Thapsigargin stimulated NO production and [Ca2+]i with 50% effective concentration values of 0.01 and 0.05 microM, respectively. Ca(2+)-stimulated NO production was attenuated by the NO synthase inhibitor NG-monomethyl-L-arginine, the removal of extracellular L-arginine, and the Ca(2+)-chelator ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid. When we exposed cells to NO gas (3.1 mM for 15 min) and S-nitrosoglutathione (10 mM for 1 h) thapsigargin-stimulated NO production was decreased by 50%.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Effect of temperature on bradykinin-induced arachidonate release and calcium mobilization in vascular endothelial cells.

The effect of decreased temperature on Ca(2+)-dependent arachidonic acid release was studied in vascular endothelial cells by investigating bradykinin (BK)-stimulated Ca2+ mobilization, inositol phosphate formation and arachidonic acid release. At both 37 degrees C and 22 degrees C, BK efficiently increased cytosolic Ca2+ concn. ([Ca2+]i). At 22 degrees C, peak [Ca2+]i was higher and returned to basal levels more slowly. Although this response was preceded by rapid formation of Ins(1,4,5)P3, the activity of phospholipase C was significantly impaired at 22 degrees C. To determine if Ins(1,4,5)P3 effectively mobilized intracellular Ca2+, we used saponin-permeabilized cells. Ins(1,4,5)P3, mobilized sequestered Ca2+ to a similar degree at 37 degrees C and 22 degrees C, although Ca2+ release was prolonged at 22 degrees C. In intact cells, BK mobilized intracellular Ca2+ stores and activated Ca2+ entry. The rate of 45Ca2+ entry was approx. 2-fold slower at 22 degrees C, even though the peak and duration of the rise in [Ca2+]i were higher and sustained at the lower temperature. TG mobilized intracellular Ca2+, activated Ca2+ entry and elevated [Ca2+]i at both temperatures. As with BK, the peak [Ca2+]i reached after thapsigargin treatment was higher at 22 degrees C. This effect of lower temperature on [Ca2+]i was most probably due to decreased Ca2+ efflux after a decrease in activity of the Ca(2+)-ATPase on the plasma membrane. Both A23187 and BK were shown to stimulate phospholipase A2 and arachidonic acid release at 22 degrees C. In each case, the rate and extent of release were decreased compared with that at 37 degrees C. Among several effects, lowering the temperature decreases the activity of phospholipase C, Ca(2+)-ATPase(s), Ca(2+)-entry mechanisms and phospholipase A2. Together, these effects lead to a higher and more prolonged elevation of [Ca2+]i, but a decrease in arachidonate release in response to BK.

Arachidonic Acid↗
PubMed1993

Modulation of hydrogen peroxide release from vascular endothelial cells by oxygen.

We have investigated factors that regulate hydrogen peroxide (H2O2) release from vascular endothelial cells. Endothelial cells produce H2O2 at an intracellular site in the vicinity of peroxisomes and at a second site near the cell surface that is inaccessible to intracellular catalase or glutathione peroxidase. Regulation of H2O2 generation at the intracellular site was studied using aminotriazole, which inactivates catalase in the presence of H2O2. Regulation of H2O2 generation at the second site was studied by measuring H2O2 release into the medium. The rate of H2O2 release was constant over 2 h when cells were incubated in room air. Changing O2 levels in the atmosphere from 0% to 10% O2 resulted in a threefold increase in the rate of H2O2 release. Elevation of O2 levels from 10% to 95% O2 produced no further enhancement in the rate of release. Preincubation of cells under hypoxic conditions did not lead to an exaggerated rate of H2O2 release when cells were returned to room air. Pretreatment of cells with exogenous H2O2 inhibited subsequent H2O2 release while pretreatment with catalase enhanced H2O2 release. Although arachidonic acid transiently enhanced the rate of H2O2 release through a mechanism dependent on PGH synthase, basal H2O2 release was independent of this enzyme. Neither hypoxia, hyperoxia, or hypoxia followed by reoxygenation altered H2O2 generation at the intracellular site accessible to peroxisomal catalase. These data demonstrate that H2O2 release from endothelial cells is responsive to changes in O2 concentrations over a narrow range. The mechanisms involved are subject to product inhibition and appear to be saturated at 10% O2 in the atmosphere.

Animals↗
PubMed1992

Regulation of extracellular calcium entry in endothelial cells: role of intracellular calcium pool.

We have investigated the role of the intracellular Ca2+ pool in regulating Ca2+ entry into vascular endothelial cells. The intracellular Ca2+ pool was mobilized using either thapsigargin (TG) or 2',5'-di(tert-butyl)-1,4-benzohydroquinone (BHQ), inhibitors of the endoplasmic reticulum Ca(2+)-adenosinetriphosphatase (ATPase). Mobilization of intracellular Ca2+ stores with either inhibitor depleted intracellular Ca2+ and greatly reduced subsequent mobilization of the inositol 1,4,5-trisphosphate (IP3)-sensitive intracellular Ca2+ pool by bradykinin. However, bradykinin-induced mobilization of the IP3-sensitive intracellular Ca2+ pool only partially reduced the subsequent response of cells to TG and BHQ. Mobilization of the intracellular Ca2+ pool by either TG or BHQ led to a concentration-dependent elevation of cytosolic Ca2+ concentrations ([Ca2+]i) without initiating inositol polyphosphate formation. In contrast to the rapidly developing, transient rise in Ca2+ concentration initiated by bradykinin, maximal concentrations of TG and BHQ stimulated a slowly developing, prolonged elevation of [Ca2+]i that required extracellular Ca2+ and could be blocked by extracellular Ni2+. Extracellular Ca2+ entered the cell through an activated cation entry pathway, since bradykinin, TG, and BHQ stimulated Mn2+ and 45Ca2+ entry. Bradykinin-stimulated 45Ca2+ uptake reached a peak within 2 min, whereas 45Ca2+ influx initiated by TG or BHQ continued for at least 8 min. Importantly, the [Ca2+]i response after low concentrations of BHQ was more transient than that seen after TG. The return of [Ca2+]i to basal values after low concentrations of BHQ was associated with reversal of Ca(2+)-ATPase inhibition and refilling of the IP3-sensitive Ca2+ pool. The continued elevation of [Ca2+]i and prolonged Ca2+ entry seen with TG was associated with continued Ca(2+)-ATPase inhibition and an empty IP3-sensitive Ca2+ pool. We conclude that mobilization of intracellular Ca2+ stores induces Ca2+ entry in endothelial cells which continues until the intracellular Ca2+ pool is refilled.

Animals↗
PubMed1985

Free radical damage to cultured porcine aortic endothelial cells and lung fibroblasts: modulation by culture conditions.

Culture conditions modulating cell damage from xanthine plus xanthine oxidase-derived partially reduced oxygen species were studied. Porcine thoracic aorta endothelial cells and porcine lung fibroblasts were maintained in monolayer culture. Cells were prelabeled with 51Cr before xanthine plus xanthine oxidase exposure. Endothelial cells showed 30 to 100% more lysis than fibroblasts and thus seemed more sensitive to this oxidant stress. The effect of cell culture age, as indicated by population doubling level (PDL), was examined. Response of low PDL endothelial cells and fibroblasts subjected to oxidant stress was compared with the response of PDL 15 cells. Both low PDL endothelial cells and fibroblasts responded differently to the lytic effect of xanthine oxidase-derived free radicals than did higher PDL cells. Specific activities of the antioxidant enzymes catalase, manganese superoxide dismutase, copper-zinc superoxide dismutase, glutathione peroxidase, and glucose-6-phosphate dehydrogenase were measured in both low and high PDL fibroblasts and endothelial cells. Antioxidant enzyme specific activities could only partially explain the differences in response to oxidant stress between fibroblasts and endothelial cells and between low and high PDL cells. Cell culture medium composition modulated the rate of production, and relative proportions of xanthine plus xanthine oxidase-derived partially reduced species of oxygen, i.e. superoxide, hydrogen peroxide, and hydroxyl radical. Serum content of medium was important in modulating free radical generation; superoxide production rates decreased 32%, H2O2 became undetectable, and hydroxyl radical generation decreased 54% in the presence of 10% serum. The medium protein and iron content also modulated free radical generation. The data suggest that cell culture media constituents, cell type, and cell culture age greatly affect in vitro response of cells subjected to oxidant stress.

Animals↗
PubMed1985

Modulation of oxidant lung injury by using liposome-entrapped superoxide dismutase and catalase.

Increased cellular generation of partially reduced species of oxygen mediates the toxicity of hyperoxia to cultured endothelial cells and rats exposed to 95-100% oxygen. Liposomal entrapment and intracellular delivery of superoxide dismutase (SOD) to cultured porcine aortic endothelial cells increased the specific activity of cellular SOD up to 15-fold. The liposome-mediated augmentation of SOD activity persisted in cell monolayers and rendered these cells resistant to oxygen-induced injury in a cell SOD activity-dependent manner. Addition of free SOD to culture medium had no effect on cell SOD activity or resistance to oxygen toxicity. SOD and catalase-containing liposomes injected i.v. into rats increased lung-associated enzyme specific activities two- to fourfold. Liposome entrapment of both SOD and catalase significantly increased the circulating half-lives of these enzymes and was critical for prevention of in vivo oxygen toxicity. Free SOD and catalase injected i.v. in the absence or presence of control liposomes did not increase corresponding lung enzyme activities or survival time in 100% oxygen. These studies show that O2- and H2O2 are important mediators of oxygen toxicity and that intracellular delivery of oxygen protective enzymes can reduce tissue injury owing to overproduction of partially reduced oxygen species.

Animals↗