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Biomedical subjects

T Hussain

Publications and source records attributed to T Hussain.

At least 19 recordsLinked to original sources

The incidence and immediate respiratory consequences of pulmonary aspiration of enteral feed as detected using a modified glucose oxidase test.

Pulmonary micro-aspiration of enteral feed in intubated critically ill patients has been reported to occur commonly. In this prospective observational study the incidence of micro-aspiration, diagnosed by a modified glucose oxidase test, is reported in 25 enterally fed critically ill and tracheally intubated patients on a general intensive care unit. Episodes of microaspiration were correlated with changes in PaO2/FiO2 ratio as an index of changes in degree of lung injury. The modified glucose oxidase test differs from the traditional glucose oxidase test because of the enrichment of the feed with glucose (10 g glucose added to 500 ml enteral feed resulting in a tenfold increase in glucose concentration). Pulmonary aspiration of feed was detected by exposing a glucose oxidase strip to tracheal secretions. The feed was enriched with glucose to improve the ability of the reagent strip to detect the feed. The incidence of aspiration of feed was 44% with a prevalence of 6.9% per day of intubation. Only 43% of these episodes of aspiration were detected by the feed being seen in the tracheal secretions. Aspiration was associated with a mean fall in the PaO2/FiO2 ratio of 5.6 kPa from 27.1 kPa to 21.5 kPa (P = 0.002). Aspiration of enteral feed is common and causes a demonstrable morbidity. Detection using this simple bedside test may alert the clinician to institute measures to minimize further aspiration.

Enteral Nutrition↗

Hepatitis B and C single and co-infection in chronic liver disease and their effect on the disease pattern.

OBJECTIVE: To find the frequency of hepatitis B and C virus (HBV and HCV) infection and their coinfection in chronic liver disease and any differences in the clinical features of single and coinfections. METHODOLGY: All clinically recognisable adult CLD patients admitted to Military Hospital, Rawalpindi in years 1999-2000, were included in the study. Their history and clinical features were recorded. Seromarkers for HBV (HBsAg, anti-HBc) and HCV (anti-HCV) were done. RESULTS: A total of 97 (52 male, 45 female) patients were included in the study. Mean age was 51.6 years (range 16-75 years). Cirrhosis was present in 74.2%, chronic hepatitis (Ch Hep) in 18.6% and hepatocellular carcinoma (HCC) in 7.2%. Among the 74.1% patients with cirrhosis 28.5% were HBsAg positive, 55.5% anti-HBc positive and 68.1% anti HCV positive. In the chronic hepatitis cases 27.8% were HBsAg positive, 23.6% anti-HBc positive and 61.1% anti HCV positive. Among the patients of HCC 59.7% were HBsAg positive, 71.4% anti-HBc positive and 42% anti HCV positive. Regarding coinfection 7.2% were anti-HCV and HBsAg positive while 35.1% were anti-HCV and anti-HBc positive. CONCLUSION: Ninety percent of patients with CLD had evidence of HBV, HCV or coinfection. Disease was more severe in patients with coinfection. Anti-HBc was found to be a sensitive indicator of past HBV.

Adolescent↗

Intestinal dopaminergic activity in obese and lean Zucker rats: response to high salt intake.

The present study examined intestinal dopaminergic activity and its response to high salt (HS, 1% NaCl over a period of 24 hours) intake in obese (OZR) and lean Zucker rats (LZR). The basal Na+,K+-ATPase activity (nmol Pi/mg protein/min) in the jejunum of OZR was higher than in LZR on normal salt (NS) (OZR-NS = 111.3 +/- 6.0 vs. LZR-NS = 88.0 +/- 8.3). With the increase in salt intake, the basal Na+,K+-ATPase activity significantly increased in both animals (OZR-HS = 145.9 +/- 11.8; LZR-HS = 108.8 +/- 6.7). SKF 38393 (10 nM), a specific D1-like dopamine receptor agonist, inhibited the jejunal Na+,K+-ATPase activity in OZR on HS intake, but failed to inhibit enzyme activity in OZR on NS intake and LZR on NS and HS intakes. The aromatic L-amino acid decarboxylase (AADC) activity in OZR was lower than in LZR on NS intake. The HS intake increased AADC activity in OZR, but not in LZR. During the NS intake the jejunal monoamine oxidase (MAO) activity in OZR was similar to that in LZR. The HS intake significantly decreased MAO activity in both OZR and LZR. The jejunal COMT activity in OZR was higher than in LZR on NS intake. The HS intake reduced COMT activity in OZR but not LZR. It is concluded that inhibition of jejunal Na+,K+-ATPase activity through D1 dopamine receptors is dependent on salt intake in OZR, whereas in LZR, the enzyme failed to respond to the activation of D1 dopamine receptors irrespective of their salt intake.

Animals↗

Clinical and laboratory features of systemic lupus erythematosus (SLE) in Pakistani patients.

OBJECTIVES: To study the clinico-pathological features of systemic lupus erythematosus (SLE) in Pakistani patients at the time of presentation in the four teaching hospitals of Rawalpindi-Islamabad area. SETTINGS: Department of Immunology, Armed Forces Institute of Pathology (AFIP), Rawalpindi, Military Hospital (MH), Rawalpindi, Armed Forces Institute of Urology (AFIU), Rawalpindi, Combined Military Hospital (CMH), Rawalpindi, Department of Rheumatology, Pakistan Institute of Medical Sciences (PIMS), Islamabad. SUBJECTS: Patients suffering from SLE, diagnosed on the basis of the ARA criteria. MAIN OUTCOME MEASURES: Clinico-pathological features at the time of presentation. RESULTS: Twelve male patients in age range 5-30 years (mean 21.6 years) and 38 female patients in age range 8-37 years (mean 22.2 years) were included in the study, showing a female to male ratio of 3:1. Fever was the most common presenting feature (100%), followed by arthralgias/arthritis (98%), malar rash (64%) and oral ulcers (58%). Laboratory results showed antinuclear antibody to be positive in all patients followed by anti double stranded DNA antibodies (anti DNA antibodies: 64%), anti extractable nuclear antigen antibodies (anti ENA antibodies: 64%) and evidence of complement consumption in 64% of the patients. Erythrocyte Sedimentation Rate (ESR) was found to be increased with a mean of 64 mm first hour fall in males and a mean of 87 mm first hour fall in the female patients. The C reactive protein was detected to be normal or marginally increased inspite of the increased ESR with mean of 7 mg/l for male patients and 5 mg/1 for the females. CONCLUSION: The subject patient population presented almost universally with fever and arthralgias or arthritis in combination with malar rash or oral ulcers and in some patients a combination of all of the above was observed. A combination of positive anti nuclear antibody test, evidence for consumption of the complement in form of low C4 and C3, increased ESR and low C reactive protein were found to be a sensitive and cost effective set of laboratory findings for the diagnosis of patients suffering from SLE. The above mentioned set of clinical and laboratory features would help in the correct and early diagnosis of patients suffering from SLE, a relatively rare disease, in the busy medical out patient departments in our set up.

Adult↗

Studies on dopaminergic and GABAergic markers in striatum reveals a decrease in the dopamine transporter in schizophrenia.

Changes in the interaction between dopaminergic and GABAergic systems in the striatum have been suggested to be important in the pathology of schizophrenia. If that hypothesis is correct, these changes could produce inter-related changes in the dopaminergic and GABAergic systems in the striatum from schizophrenic subjects. To test this proposition we measured important markers on dopaminergic and GABAergic neurons in striatum obtained post-mortem from schizophrenic and non-schizophrenic subjects. There was a significant decrease in the density of the dopamine transporter (mean+/-SEM: 230+/-31 vs. 334+/-22fmol/mg ETE; P=0.01), but not nitric oxide synthase, dopamine D(2)-like, D(1)-like, D(3) or GABA(A) receptors in subjects with schizophrenia. There were no inter-related changes in the dopaminergic or GABAergic markers. In the schizophrenic subjects, the density of dopamine D(1)-like receptors decreased with age and was positively correlated with the density of dopamine D(2)-like receptors. This study does not readily add weight to the hypothesis that changes in the interaction between dopamine and GABA in the striatum are important in the pathology of schizophrenia. However, our findings could indicate that changes in the dopamine transporter within the striatum, either because of decreased transporter numbers per se or as a result of innervating neuronal loss, may be involved in the pathology of the illness.

Adult↗

Salt intake and intestinal dopaminergic activity in adult and old Fischer 344 rats.

We have earlier shown that the renal dopaminergic system failed to respond to high salt (HS) intake in old (24-month-old) Fisher 344 rats (Hypertension 1999;34:666-672). In the present study, intestinal Na+,K+-ATPase activity and intestinal dopaminergic tonus were evaluated in adult and old Fischer 344 rats during normal salt (NS) and HS intake. Basal intestinal Na+,K+-ATPase activity (nmol Pi/mg protein/min) in adult rats (142+/-6) was higher than in old Fischer 344 rats (105+/-7). HS intake reduced intestinal Na+,K+-ATPase activity by 20% (P<0.05) in adult, but not in old rats. Dopamine (1 microM) failed to inhibit intestinal Na+,K+-ATPase activity in both adult and old Fischer 344 rats (NS and HS diets). In adult animals, co-incubation of pertussis toxin with dopamine (1 microM) produced a significant inhibitory effect in the intestinal Na+,K+-ATPase activity. L-DOPA and dopamine tissue levels in the intestinal mucosa of adult rats were higher (45+/-9 and 38+/-4 pmol/g) than those in old rats (27+/-9 and 14+/-1 pmol/g). HS diet did not change L-DOPA and DA levels in both adult and old rats. DA/L-DOPA tissue ratios, an indirect measure of dopamine synthesis, were higher in old (1.1+/-0.2) than in adult rats (0.6+/-0.1). Aromatic L-amino acid decarboxylase (AADC) activity in the intestinal mucosa of old rats was higher than in adult rats. HS diet increased the AADC activity in adult rats, but not in old rats. It is concluded that intestinal dopaminergic tonus in old Fisher 344 rats is higher than in adult rats and is accompanied by lower basal intestinal Na+,K+-ATPase activity. In old rats, HS diet failed to alter the intestinal dopaminergic tonus or Na+,K+-ATPase activity, whereas in adult rats increases in AADC activity were accompanied by decreases in Na+,K+-ATPase activity. The association between salt intake, increased dopamine formation and inhibition of Na+,K+-ATPase at the intestinal level was not as straightforward as that described in renal tissues.

Aging↗

Extended treatment with typical and atypical antipsychotic drugs differential effects on the densities of dopamine D2-like and GABAA receptors in rat striatum.

In situ radioligand binding and quantitative autoradiography have been used to measure the density of striatal D1-like, D2-like, and GABAA receptors in rats treated with haloperidol at 0.01 or 0.1 mg/kg/ day or chlorpromazine, olanzapine or clozapine at 0.1 or 1.0 mg/kg/day for 1, 3 or 7 months. [3H]SCH23390 binding to D1-like receptors was not changed by any drug treatments. There were significant increases in [3H]nemonapride binding to D2-like receptors at different time points due to treatment with haloperidol, chlorpromazine and olanzapine. By contrast, treatment with clozapine and olanzapine caused a time-dependent decrease in [3H]muscimol binding to the GABAA receptor. These data suggest that treatment with atypical antipsychotic drugs, but not typical antipsychotic drugs, affect striatal GABAergic neurons. In addition, it would appear that clozapine might be unique in that it does not increase dopamine-D2 like receptor density at doses which would be predicted to have antipsychotic effects in humans. The extent to which such changes are involved in the therapeutic effects of drugs such as olanzapine and clozapine remains to be determined.

Animals↗

Relaxation of rat aorta by adenosine in diabetes with and without hypertension: role of endothelium.

Effects of diabetes on the responses of aortic rings of normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive (SHR) rat to adenosine analogues were examined. Streptozotocin-induced diabetes caused an increase in blood glucose and plasma levels of cholesterol and triglycerides in normotensive (diabetic-WKY) as well as hypertensive (diabetic-SHR) rats. In diabetic-SHR group, the body weight was significantly low (50%) as compared to SHR (non-diabetic). Diabetic-SHR group showed the largest heart weight-to-body weight ratio indicating cardiac enlargement. The relaxation responses to adenosine analogues were obtained in endothelium-intact and -denuded aortic rings precontracted with phenylephrine. The IC(50) values of adenosine analogues were lower in endothelium-intact aortic rings of WKY as compared to diabetic-WKY and -SHR. Aortic rings from diabetic-SHR showed the greatest attenuation in adenosine analogue-mediated relaxation. Removal of endothelium from the aortic rings inhibited the relaxant response of adenosine analogues and abolished the differences among the groups. Nitric oxide (NO) synthase inhibitor L-monomethylarginine (L-NMMA) caused a significant rightward shift in the concentration-response curves in WKY and diabetic-WKY groups, only a small shift in SHR and no change in diabetic-SHR group indicating that it is primarily the inhibition of NO release which is responsible for attenuation of adenosine receptor responses in SHR and diabetic-WKY and there was absence of NO release in diabetic-SHR. Forskolin and sodium nitroprusside equally relaxed the aortic rings in all the groups. This suggested that there was no abnormality in the relaxant property of vascular smooth muscle due to hypertension and/or diabetes. Therefore, it is concluded that streptozotocin-induced diabetes in SHR aggravates the severity of vascular endothelial dysfunction which led to impairment in adenosine receptor-mediated vascular responses.

Adenosine↗

Activation of dopamine D(1)-like receptor causes phosphorylation of alpha(1)-subunit of Na(+),K(+)-ATPase in rat renal proximal tubules.

Dopamine causes inhibition of Na(+),K(+)-ATPase activity via activation of dopamine D(1)-like receptors. It is the phosphorylation of Serine(18) of the alpha(1)-subunit of Na(+),K(+)-ATPase which results in the inhibition of the enzyme activity; however, such a phosphorylation by dopamine D(1)-like receptor agonist has not been demonstrated in the proximal tubules. We show here by immunoprecipitation and detection with phosphoserine antibody that SKF 38393, a dopamine D(1)-like receptor agonist, causes phosphorylation of the alpha(1)-subunit of Na(+),K(+)-ATPase. The effect of (+/-)-1-phenyl-2,3,4,5-tetrahydro-(1H)-3-benzazepine-7,8-diol hydrochloride, SKF 38393, is blocked by R(+)-7-choro-8-hydroxy-3-methyl-1-phenyl-2,3,4,5-tetrahydro-1H-benzazepine hydrochloride, SCH 23390, a dopamine D(1)-like receptor antagonist, and staurosporin, a protein kinase C inhibitor. The phosphorylation is also increased by phorbol 12-13 dibutyrate ester. However, Rp-cAMP triethylamine, an inhibitor of protein kinase A, does not affect the SKF 38393-mediated phosphorylation of Na(+),K(+)-ATPase. Therefore, these results provide the evidence that dopamine D(1)-like receptor activation causes phosphorylation of the alpha(1)-subunit of Na(+),K(+)-ATPase in renal proximal tubules via protein kinase C pathway.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗

Role of endothelium in adenosine receptor-mediated vasorelaxation in hypertensive rats.

The present study was designed to investigate the role of endothelium derived relaxing factor nitric oxide (NO) in adenosine A2 receptor mediated vasorelaxation in normotensive (WKY) and hypertensive (SHR) rat aortic ring preparations. Adenosine analogues, 2-chloroadenosine (CAD) and 5-ethylcarboxamidoadenosine (NECA) produced concentration-dependent (10(-9)-10(-4) M) relaxation in phenylephrine (1 x 10(-6) M) precontracted vascular rings, which was significantly shifted to the right in SHR compared to WKY rats. Endothelium removal attenuated CAD and NECA relaxation responses in both SHR and WKY and abolished the difference in relaxation between SHR and WKY vascular tissues. The relaxation response to CAD was antagonised by adenosine A2 receptor antagonist, 8-sulfophenyltheophylline (8-SPT, 50 x 10(-6) M). The antagonism by 8-SPT was lower in SHR as compared to WKY tissues. L-monomethylarginine (L-LMMA) (30 x 10(-6) M) significantly shifted the CAD relaxation to the right, which was reversed by the addition of L-arginine (100 x 10(-6) M) in both SHR and WKY rats. However, the rightward shift by L-NMMA was smaller in SHR compared to WKY vascular tissues. Vasorelaxation response to acetylcholine (1 x 10(-6) M) was significantly inhibited (50%) in SHR rings compared to WKY. The relaxation produced by sodium nitroprusside (10(-9)-10(-5) M) in endothelium-intact and -denuded aortic rings showed no difference between SHR and WKY. Isoproterenol produced concentration-dependent (10-9-10-5 M) relaxation, which was shifted to the right in SHR compared to WKY rings with an intact endothelium, while the removal of endothelium abolished the difference in the response between SHR and WKY. The results suggest: (i) adenosine A2 receptors mediate vasorelaxation in part through endothelium possibly by releasing nitric oxide (NO); (ii) the impairment of endothelium may be one of the factors for the attenuation of adenosine receptor and receptor-mediated responses in SHR.

Adenosine↗

Dopamine fails to inhibit Na,H-exchanger in proximal tubules of obese Zucker rats.

Dopamine via the activation of D1-like receptors inhibits Na,K-ATPase and Na,H-exchanger and subsequently increases sodium excretion. We have previously reported that dopamine failed to inhibit Na,K-ATPase in the proximal tubules (PTs) of obese Zucker rats. The present study was designed to determine the effect of dopamine on Na,H-exchanger in PTs of lean and obese Zucker rats, and examine D1-like receptor-coupled signal transduction pathway mediating the inhibition of Na,H-exchanger. We found that dopamine inhibited Na,H-exchanger in the PTs of lean rats but this response was absent in obese rats. In brush border membranes, [3H]SCH 23390 binding revealed a approximately 45% reduction in D1-like receptor binding sites in obese compared to lean rats. Dopamine stimulated cAMP accumulation in PTs of lean but not in obese rats. Forskolin-mediated stimulation of cAMP was similar in lean and obese rats. Dopamine as well as forskolin and dibutyryl cAMP-mediated stimulation of protein kinase A (PKA) was reduced in PTs of obese compared to lean rats. The data suggest that reduction in D1-like receptor binding sites, defective coupling with signaling pathway and inability of PKA activation may be responsible for the failure of dopamine to inhibit Na,H-exchanger in PTs of obese rats. This phenomenon may contribute to an increase in sodium reabsorption and development of hypertension in obese Zucker rats.

Animals↗

Defective renal dopamine D1-like receptor signal transduction in obese hypertensive rats.

It is reported that dopamine promotes renal sodium excretion via activation of D1-like dopamine receptors located on the proximal tubules. In spontaneously hypertensive rats the natriuretic and diuretic response to exogenously administered and endogenously produced dopamine is reduced, which results from a diminished dopamine-induced inhibition of the enzyme, Na+,K+-ATPase. The present study was designed to examine dopamine-receptor mediated inhibition of Na+,K+-ATPase and its associated signal transduction pathway in the proximal tubules of Zucker obese and lean control rats. The obese animals were hypertensive, hyperinsulinaemic and hyperglycaemic compared with the lean rats. While dopamine caused inhibition of Na+,K+-ATPase activity in lean rats, this effect was significantly attenuated in the obese animals. There was significant reduction in D1-like receptor numbers in the basolateral membranes of obese rats compared with lean rats with no change in the affinity to the ligand [3H]SCH 23390 between the two groups of rats. Dopamine failed to stimulate G proteins as measured by [35S]GTPgammaS binding in the obese rats. Also, dopamine was unable to cause phospholipase-C activation in obese rats, but it did activate phospholipase-C in lean rats. These results show that reduction in D1-like receptor numbers and a defect in receptor-G protein coupling may account for the inability of dopamine to activate the D1-like receptor-coupled signal transduction pathway and cause inhibition of Na+,K+-ATPase in the obese hypertensive rats.

Animals↗

Diminished natriuretic response to dopamine in old rats is due to an impaired D1-like receptor-signaling pathway.

BACKGROUND: Dopamine (DA) causes natriuresis and diuresis, which results from activation of D1-like receptor (D1R) located on proximal tubules. Earlier, we reported that DA failed to inhibit Na,K-ATPase in proximal tubules of old Fischer 344 rats. The present study was designed to investigate the functional consequence of this phenomenon. METHODS: Measurements of the functional (natriuretic and diuretic) response to intravenously infused DA and SKF 38393 (D1R agonist) in adult (6 month) and old (24 month) Fischer 344 rats were taken. Biochemical measurements were carried out to determine the potential defects in D1R and its signaling pathway in proximal tubules of old rats. RESULTS: We found that intravenous infusion of DA and SKF 38393 caused natriuresis and diuresis in adult rats, but this response was blunted in old rats. In the isolated proximal tubules, DA and SKF 38393 inhibited Na,H-exchanger (NHE) in adult rats; however, this inhibition was attenuated in old rats. Radioligand binding revealed approximately 46% reduction in D1R binding sites in brush border membranes (BBMs) in old compared with adult rats. SKF 38393 stimulated [35S]GTPgammaS binding in BBM in adult rats, but not in old rats, suggesting an impaired D1R-G protein coupling. DA and SKF 38393 stimulated adenylyl cyclase (AC) activity in adult but not in the old rats. Forskolin and NaF stimulated AC activity in a comparable manner in adult and old rats, indicating no defect in AC and G proteins. DA and SKF 38393 failed to stimulate protein kinase A (PKA) activity in proximal tubules of old rats. Dibutyryl-cAMP-mediated PKA activation was also absent in old rats. CONCLUSIONS: A decrease in D1R binding sites, a coupling defect with G proteins, and a defect in PKA activation lead to diminished DA-mediated inhibition of NHE in old rats, which may contribute to the blunted natriuretic response to DA in these animals.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗

Dopamine inhibits na,h-exchanger via D1-like receptor-mediated stimulation of protein kinase a in renal proximal tubules.

Dopamine causes natriuresis and diuresis via activation of D1-like receptors located in the renal proximal tubules. It is reported that this response to dopamine results from the inhibition of Na,H-exchanger and Na,K-ATPase. Earlier studies have suggested a role of protein kinase A (PKA) in the inhibition of Na,H-exchanger, however, the effect of dopamine or the dopamine receptor subtype responsible for the stimulation of PKA has not been reported. Present study was designed to examine the effect of dopamine and D1-like receptor agonist, SKF 38393, on the stimulation of PKA activity in rat renal proximal tubules. Dopamine and SKF 38393 (1 nM - 1 microM) caused stimulation of PKA activity, an effect which was antagonized by a D1-like receptor antagonist, SCH 23390 (10 microM). Stimulation of PKA activity was also seen with forskolin and di-butyryl cAMP. We also observed that dopamine and SKF 38393 inhibited Na,H-exchanger activity in the proximal tubules. This response was blocked by SCH 23390 and Rp-cAMPS triethylamine, a selective inhibitor of PKA. Similarly, forskolin and di-butyryl cAMP inhibited Na,H-exchanger activity. The data provide direct evidence showing that dopamine, through the activation of D1-like receptors stimulates PKA activity which in turn inhibits Na,H-exchanger in the proximal tubules.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗

Respiratory symptoms and wheat flour exposure: a study of flour millers.

The objective of this study was to determine the prevalence of respiratory symptoms and their relationship to sensitization to wheat flour allergens and fungal amylase, in a group of workers from the UK flour milling industry. A cross-sectional study was used to evaluate symptoms, using a structured interview technique, and sensitization, using skin prick test findings, from 679 employees in flour milling and packing operations at 18 flour mills. A total of 147 workers (147/679, 22%) described upper respiratory tract symptoms of some kind. In the majority (139/147, 95%) these symptoms were of an occasional or transitory nature and were related to short-term exposures to high levels of dust. Three individuals (3/679, 0.4%) were identified whose symptoms were thought to be the result of allergy to wheat flour. The prevalence of positive skin prick tests to wheat flour allergens and to fungal amylase was 1.2% (8/678) and 0.9% (6/678), respectively. Measurements of total inhalable dust exposure for personnel exposed to flour dust were taken at 10 of the sites (116 samples). For production personnel the levels were typically between 1 and 10 mg/m3 (8-h time weighted average), with a median of 6.2 mg/m3. Hygiene operatives had appreciably higher exposure than production personnel, with a median of 18.7 mg/m3. Overall, 43% (50/116) of all samples exceeded 10 mg/m3 (8-h time weighted average). The findings suggest that the risk of sensitization to wheat flour allergens from current dust exposures in flour mills is very low. Wheat allergy was responsible in only a small proportion of the total who had respiratory symptoms. The principal causation of symptoms experienced by the workforce was considered to be a non-specific irritant effect related to short-term exposures to high levels of total inhalable dust.

Amylases↗

PediaSure in the treatment of severe malnutrition in Pakistani children.

OBJECTIVES: We used "PediaSure" a high-density supplemental high caloric feed, for the purpose of nutrition therapy of malnourished children during the initial 2 weeks of rehabilitation. METHODOLOGY: Thirty-one severely malnourished children between the ages of 1-5 years of age completed the study. After management of acute medical complications, they were started on "Pediasure" as their source of calories, for 2 weeks. Their weight gain clinical tolerance, stool output were monitored, as were hematological and biochemical parameters. RESULTS: The study revealed a significant increase in caloric intake (p < 0.01) at the end of 2 weeks. There was also a significant improvement in weight gain of these children, averaging to 7.5 gm/kg/day. The Z score weight for age improved as well, (p = < 0.01) over the 2 week period. The biochemical parameters registered an increase in their serum potassium levels, but no untoward chemical imbalance was noted. Tolerance for PediSure was very high, only one child was excluded from the study due to limited intake. None of the children developed diarrhea. CONCLUSION: We conclude that "PediaSure" can be used effectively in the initial stage of nutrition rehabilitation of severely malnourished children.

Child, Preschool↗