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Biomedical subjects

A Sheikh

Publications and source records attributed to A Sheikh.

At least 55 records · Page 3Linked to original sources
PubMed1998

Phosphate poisoning by ingestion of clothes washing liquid and fabric conditioner.

A case of deliberate ingestion of clothes washing liquid and fabric conditioner is described. Tracheal intubation and controlled ventilation became necessary because of respiratory muscle dysfunction associated with hypocalcaemia. We suggest that the phosphate component of the clothes washing liquid was responsible for the dramatic metabolic upset and subsequent need for admission to the Intensive Care Unit.

Adult↗
PubMed1997

Cholera in a developing megacity; Karachi, Pakistan.

Despite rapid urbanization and increasing affluence in Karachi, cases of cholera are frequent. We analysed computerized isolation data from the AKUH Clinical Microbiology Laboratory, Karachi, from 1990-6 to examine microbiological, temporal and demographic trends in Vibrio cholerae infections. During this period 888 strains of V. cholerae (566 V. cholerae serogroup O1, and 204 V. cholerae serogroup O139) were isolated from specimens from 886 patients; 214/464 were adult inpatients, and 250/464 paediatric inpatients, the remaining 422 outpatients. Isolations peaked between June and August. Overlapping epidemics occurred in 1993 and 1994 of serogroup O1 (May to August), and serogroup O139 (August to October). All ages and social and economic strata were affected. Forty-four percent of all isolates were from children under the age of 5 years. The mean age of all patients with serogroup O1 infections was 19.6 years (+/-0.9) compared with 367 (+/-1.7) for serogroup O139 infections (P < 0.0001, t test). More than a quarter (27%) of all serogroup O1 isolates were from babies under 2 years of age. One patient had a serogroup O1 infection followed by a serogroup O139 infection 1 year later. Another patient was infected with serogroup O1 strains 5 years apart. Emergence of resistant strains was observed, but by 1996 serogroup O139 had disappeared. An aquatic organism, cholera nevertheless continues to take its toll in this city of 11 million situated in a desert.

Adolescent↗
PubMed1997

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Equipment Failure↗
PubMed1996

Epidemiology of adults hospitalized with burns in Karachi, Pakistan.

Burns are a leading cause of adult death in Karachi slums, therefore we reviewed 1 year's logged experience (November 1992 to October 1993) at Karachi's two adult burn units for patient age, sex, burn severity and outcome. Also 47 inpatients were interviewed regarding their circumstances of injury. We grouped these using Haddon's Matrix. The log identified 832 patients. Females (57 per cent) outnumbered males and were younger on average (25.1 vs 27.6 years, P = 0.002). Females had more severe burns than males (57 per cent vs 50 per cent total body surface area (TBSA) burn, P = 0.002). At the unit with outcome data (n = 556), the case fatality was 56 per cent. The estimated adult mortality due to burns in Karachi was 10.2/100 000, 6.8/100 000 and 14.1/100 000 for men and women, respectively. Burns of interviewed patients were most often associated with flames (33/47), but stove bursts caused the most severe injury (52 per cent TBSA). These patients were predominantly young uneducated female houseworkers, clothed in loose attire who were injured during daylight at home around a floor-level stove, unaware of fire safety, and who received no first aid. It was concluded that the high burn severity and case fatality rates demand: (1) preventive measures, such as kitchen sand buckets, safer stove design and placement and education on fire safety and first aid, and (2) risk factor analysis to refine interventions.

Accidents, Home↗
PubMed1996

A study of the incorrect use of ventilator disconnection alarms.

Pressure-sensitive ventilator disconnection alarms may fail to function correctly when used with discharging compliance ventilators such as the Manley Blease. The increase in gas flow on disconnection generates raised pressure owing to the resistance provided by components of the breathing system. Thirty-four anaesthetists, who were unaware of the nature of the survey, were observed to see if previous recommendations for the correct adjustment of the ventilator alarm were being followed. It was found that 77% of alarms were incorrectly adjusted and would not have alarmed in the event of a true disconnection occurring.

Anesthesia, General↗
PubMed1994

In vitro and in vivo response of hepatocytes from hepatic nodules to the mitoinhibitory effects of phenobarbital.

One of the proposed mechanisms by which phenobarbital (PB) promotes hepatocarcinogenesis in the rat is by differential mitoinhibition. However, our earlier studies indicated that PB inhibited DNA synthesis in vitro in hepatocytes isolated from both surrounding non-nodular liver and hepatic nodules promoted by orotic acid (OA). Since nodules generated by one promoter need not necessarily be resistant to another promoter, the present study was undertaken to determine whether foci/nodules promoted by PB itself are resistant to the mitoinhibitory effects of PB. Accordingly, rats were initiated with diethylnitrosamine (DENA, 200 mg/kg i.p) and promoted with PB (0.07% of PB as its sodium salt) in their drinking water for 16 or 33 weeks. In vitro studies indicated that PB (3-5 mM) inhibited DNA synthesis induced by epidermal growth factor (EGF) in hepatocytes from surrounding non-nodular liver as well as from nodules promoted by PB for 33 weeks. In another experiment, initiated rats exposed to PB for 33 weeks were subjected to either two-thirds partial hepatectomy (PH) or sham hepatectomy. Hepatocytes were labelled with tritiated thymidine in vivo for 48 h. Autoradiographic analysis indicated that in the presence of PB, the hepatocytes from both foci/nodules and the surrounding non-nodular liver responded to PH to the same extent. In addition, they both responded to PH less efficiently as compared to the corresponding controls. Further, initiated rats exposed to PB for 16 weeks when subjected to PH and killed 4 weeks thereafter, the percentage area occupied by gamma-glutamyltranspeptidase-positive foci/nodules in the PB group increased, but to the same extent as in initiated control rats not exposed to PB. The above results raised an interesting possibility that the lack of resistance of the PB-promoted nodules to the mitoinhibitory effects of PB may be because the PB-promoted nodule does not express a resistant phenotype. To examine this aspect, the response of hepatocytes from 33 week PB-promoted nodules to the mitoinhibitory effects of OA was examined. The results indicated that OA (60-120 microM) inhibited EGF-induced DNA synthesis in hepatocytes isolated from both nodules as well as from surrounding non-nodular liver. These results suggest that PB is a mitoinhibitor but may not provide a strong differential growth advantage to foci/nodules in response to a proliferative stimulus. Further, the nodules promoted by PB do not appear to express the resistant phenotype, defined as being resistant to the mitoinhibitory effects of OA and PB.

Animals↗
PubMed1994

Outcome and cost of open- and closed-chest cardiopulmonary resuscitation in pediatric cardiac arrests.

OBJECTIVE: The dismal survival rates of cardiac arrest in children managed with conventional closed-chest cardiopulmonary resuscitation (CC-CPR) have renewed interest in the use of open-chest CPR (OC-CPR). We determined the efficacy of the early use of OC-CPR in children after cardiac arrest. METHODS: A retrospective review of emergency medical services (EMS) and hospital records revealed 27 children who were brought to the emergency department under CPR after blunt trauma. RESULTS: Twelve children had CC-CPR and 15 children underwent OC-CPR. Prehospital resuscitation and transport of both groups of children was excellent by current standards, and OC-CPR was performed within 5 minutes of arrival in the emergency department. CPR was successful with restoration of spontaneous circulation in 17% of children after CC-CPR, whereas 20% of children had restoration of spontaneous circulation after OC-CPR. This difference was not statistically significant. None of the children regained consciousness or survived to discharge. The hospital charges for patients who underwent OC-CPR were significantly higher (P = .005). Less than 30% of the hospital charges were reimbursed in both groups. CONCLUSIONS: OC-CPR does not improve survival in children who sustain cardiac arrest and receive CPR for more than 20 minutes in the field. Under these circumstances OC-CPR is an expensive and futile procedure to undertake.

California↗
PubMed1994

A view of HIV-I infection in Karachi.

A prospective study on the prevalence of HIV-I infection in Karachi, Pakistan was conducted over a period of six years (1986-1992). Over 15,000 individual samples and more than 32,000 donor units of individuals residing in Karachi at the time of sample collection were tested for HIV-I infection by our screening test EIA which revealed a positivity rate of 0.23% and 0.003% in individual and donor units respectively by Western Blot. We divided patients into four groups A, B, C and D based on the most plausible cause of transmission. The largest number of positive patients belonged to group B, who were of either foreign origin or expatriates or Pakistanis settled abroad. They comprised approximately 67% of the total positive cases and were subjected to testing on strong clinical grounds. In individuals of other groups like group A and D, there was history of travel abroad from time to time. The only positive donor unit (group C) belonged to a person who had been living in Middle East for the last 10-12 years. The last group D comprised of samples that were directly sent to us without complete history, except for the fact that they had been travelling back and forth. The large majority of patients fell in 20-50 years age group. Despite the limitations of this study, we conclude that the prevalence of HIV is steadily increasing in our population and so far, we have not been able to find an indigenous case of AIDS in our series.

Adolescent↗
PubMed1993

On the biosynthesis of bovine pancreatic trypsin inhibitor (BPTI). Structure, processing, folding and disulphide bond formation of the precursor in vitro and in microsomes.

The natural gene for bovine pancreatic trypsin inhibitor (BPTI) was expressed by in vitro transcription/translation systems as the 100-residue pre-proBPTI, with a signal peptide for translocation into the endoplasmic reticulum. Expression in the presence of microsomes defined the site of co-translational cleavage of the signal peptide. The resulting proBPTI in the microsomes consists of the 58 residues of mature BPTI, plus an additional 13 residues at the N terminus, including a cysteine residue at position -10, and seven residues at the C terminus. ProBPTI remained in the unfolded, reduced form within microsomes when synthesized under reducing conditions, but folded and formed disulphide bonds rapidly when the disulphide form of glutathione was added. Complete folding could occur within about one minute, even when residue Cys10 was replaced by Ser. The structure of proBPTI was determined by circular dichroism and two-dimensional NMR and found to be that of mature BPTI with flexible extensions on both termini. Its inhibition of the activity of alpha-chymotrypsin was indistinguishable from that of the mature protein. The extensions of the precursor appeared to play only very minor roles in refolding in vitro under conditions where folding and disulphide bond formation are coupled. Under pH and redox conditions thought to reflect those in vivo, complete folding and disulphide bond formation required several hours. Addition of protein disulphide isomerase to in vitro folding experiments caused substantial and similar increases in the rate of formation of the fully folded state for both mature BPTI and proBPTI; the half time for folding to the native state was reduced to approximately two minutes, which is comparable to that occurring in microsomes. The absence of substantial effects of the N and C-terminal extensions on the protein structure, inhibitor activity and refolding leaves their functional roles to be discovered.

Amino Acid Sequence↗
PubMed1993

Effect of orotic acid on in vivo DNA synthesis in hepatocytes of normal rat liver and in hepatic foci/nodules.

One of the proposed mechanisms by which orotic acid (OA) promotes liver carcinogenesis is by differentially mito-inhibiting the normal hepatocytes while permitting the initiated ones to respond to growth stimuli to form foci/nodules. In an attempt to examine this hypothesis, the present study was designed to determine (i) whether OA inhibits DNA synthesis in normal hepatocytes in vivo, and (ii) whether hepatocytes from hepatic foci/nodules are relatively resistant to the mito-inhibitory effects of OA. The results of this study indicate that OA given i.p. as a tablet of 300 mg at the time of partial hepatectomy (PH) almost completely inhibited liver DNA synthesis. Three days later--a time period by which the implanted tablet disappeared--the hepatocytes resumed DNA synthesis. Exposure to OA results in an accumulation of uridine nucleotides and a decrease in adenosine nucleotides. Creation of such an imbalance in nucleotide pools appears to be important for OA to inhibit DNA synthesis. Adenine (a tablet of 300 mg), an agent that inhibits the metabolism of OA to uridine nucleotides, counteracted the mito-inhibitory effects of OA. To determine whether the hepatocytes in foci/nodules are resistant to the mito-inhibitory effects of OA, rats were initiated with diethylnitrosamine (DENA; 150 mg/kg) and promoted by the resistant-hepatocyte model. Fourteen weeks after the administration of DENA, the rats were subjected to PH in the presence of absence of OA (300 mg tablet). The results indicated that, in contrast to hepatocytes in normal or surrounding non-nodular liver, a subpopulation of hepatocyte foci/nodules appear to be relatively resistant to the mito-inhibitory effects of OA. These findings support the hypothesis that differential mito-inhibition is a possible component in the promoting effect of OA. However, whether this is the mechanism by which OA promotes liver carcinogenesis needs to be further investigated.

Adenine↗