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Biomedical subjects

L Ali

Publications and source records attributed to L Ali.

33 records · Page 2Linked to original sources

Hypoglycemic effects of three plants from eastern Himalayan belt.

Rhizome of Costus speciosus, tuber of Nephrolepsis tuberosa, and bulb of Stephania hernandifolia, used by the local people and traditional healers in the Eastern Himalayan belt, were studied for their effects on serum glucose levels in nondiabetic and diabetic rat models at different prandial states. The results showed that in nondiabetic rat C speciosus and N tuberosa had no significant effect in the fasting or postprandial state when freeze-dried juices were fed simultaneously with glucose. However, when fed 30 min before the glucose load both C speciosus (p < 0.05) and N tuberosa (p < 0.003) showed hypoglycemic effect. To the contrary, S hernandifolia increased the serum glucose levels of nondiabetic rats in all the series of experiments (p < 0.05 or p < 0.01). In NIDDM model rats N tuberosa opposed the rise in serum glucose level when it was fed 30 min before the glucose load (p < 0.02), whereas S hernandifolia had a tendency to raise the serum glucose level. In IDDM model rats, none of these three freeze-dried juice showed any effect in the fasting state. However, C speciosus showed significant hypoglycemic effect (p < 0.002) when the juice was fed with simultaneous glucose load. In marked contrast to the findings with nondiabetic and NIDDM model rats S hernandifolia showed significant hypoglycemic effect (p < 0.05-0.006) in both the stages (fed simultaneously with, and 30 min before the glucose load) of prandial states of the IDDM model rats. The results indicated that these three plants have interesting possibilities as a source of oral hypoglycemic agents.

Animals↗

Studies on hypoglycemic effects of fruit pulp, seed, and whole plant of Momordica charantia on normal and diabetic model rats.

Extracts of Momordica charantia fruit pulp, seed, and whole plant were tested for their hypoglycemic effects on normal and diabetic rat models. The results show that during the oral glucose tolerance test the peak blood glucose values in rats are obtained much earlier (15-45 min) than in human subjects (around 60 min). Pulp juice of M. charantia lowered fasting blood glucose levels in normal rats (p < 0.05 at 120 min); the effect was more pronounced with the saponin-free methanol extract of the pulp juice (p < 0.05 at 60 min and p < 0.01 at 120 min). The pulp juice also had a significant hypoglycemic effect in the glucose-fed normal rats when the extract was fed 45 minutes before the oral glucose load [percentage increments over basal value (M +/- SE): 85 +/- 10 in the control group vs. 54 +/- 7 in the pulp juice group, p < 0.01]. In the IDDM model rats the pulp juice had no significant effect on blood glucose levels either in fasting or postprandial states. In the NIDDM model rats the saponin-free methanol extract of juice produced a significant hypoglycemic effect both in fasting (p < 0.05 at 120 min) and in postprandial states (sum of percentage increments over basal value: 140 +/- 26 in the control vs. 71 +/- 7 in the pulp juice group, p < 0.05). Methanol extracts of seed and of whole plant, and saponin-free methanol extract of whole plant produced no hypoglycemic effects in normal or IDDM model rats either in fasting or in postprandial states.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Glucose stimulation of ouabain-resistant efflux of Na+ from rat pancreatic islets.

1. Integrating flame photometry was employed for measuring the mobilization of sodium from rat pancreatic islets after substitution of extracellular Na+ by N-methylglucamine. 2. Glucose accelerated the initial loss of sodium both in the absence and presence of ouabain (1 mM). In the latter case the effect was maximal at 5 mM of the sugar. 3. Amiloride (0.1 mM), an inhibitor of Na(+)-H+ exchange, prevented the effect of glucose on the ouabain-resistant Na+ efflux, increasing the rate of outward transport in the absence of the sugar. 4. Extracellular K+ and arginine (10 mM) mimicked the action of glucose in promoting a ouabain-resistant mobilization of sodium. 5. Whereas the hypoglycaemic sulphonylurea tolbutamide (100 microM) did not modify the outward transport of Na+, the ouabain-resistant component of this process was partially suppressed after bumetanide (100 microM) inhibition of the chloride-dependent co-transport of Na+ and K+. 6. It is suggested that the glucose-induced lowering of the steady-state content of islet sodium involves an increased outward transport mediated at least in part by mechanisms other than stimulation of the Na(+)-K+ pump.

Animals↗

Free and bound sodium in pancreatic beta-cells exposed to glucose and tolbutamide.

The effects of glucose and tolbutamide on the sodium handling of the pancreatic beta-cells were evaluated by measuring the total sodium content in intact islets from ob/ob-mice by integrating flame photometry and the free ion in individual beta-cells by dual wavelength fluorometry. Whereas increasing the glucose concentration from 3 to 20 mM resulted in a lowering of sodium, the addition of 100 microM tolbutamide caused a rise. The above-mentioned effects were most marked (about 50%) for the physiologically significant free sodium. The data indicate a more important role for Na+ in the regulation of insulin release than so far acknowledged. Increase of Na+ may contribute to the secretory response to hypoglycemic sulfonylureas by providing an additional rise of cytoplasmic Ca2+.

Animals↗

Effects of depolarizing agents on the sodium content of rat pancreatic islets.

Rat pancreatic islets were used for studying the effects of depolarization on their sodium content. The islet sodium was markedly affected by small variations of extracellular K+. As with increased K+, the presence of low concentrations of glucose (5 mM) and arginine (2 mM) decreased the sodium content. The latter substances did not lower the sodium concentration below the value obtained by depolarization with excessive K+, nor was it possible to obtain a further decrease when 10 mM arginine was combined with 5 mM glucose. The sodium content was also reduced in the presence of 10 mM L-leucine, 10 mM 2-ketoisocaproate and 0.1 mM Ba2+. Tolbutamide differed from the other depolarizing agents in that it increased the sodium concentration, an effect manifested also in the presence of excessive K+. The observation that depolarizing agents other than sulfonylureas do not increase but actually reduce sodium implies that islet cells are exceptional among electrically excitable cells. The observed reduction of sodium may reflect activation of a voltage-sensitive carrier mechanism for outward transport of Na+.

Animals↗

The effects of glibenclamide and its non-sulfonylurea analogue HB 699 on the sodium content of rat pancreatic islets.

Sodium contents were determined in rat pancreatic islets using integrating flame photometry. Whereas the sodium content decreased in the presence of glucose, it increased when 0.1-100 mumol/l glibenclamide was added to a medium containing 3 mmol/l glucose. The complexity of the glibenclamide action became evident with its reversal after removal of extracellular Ca2+ and the observation that the sulfonylurea counteracted the increase of sodium obtained after removal of K+. The effects of glibenclamide were mimicked by 1 mmol/l of its non-sulfonylurea analogue HB 699 with the exception that the latter compound being without suppressive action on the sodium content in medium deprived of Ca2+. Also exposure to 1 mmol/l sulfadiazine resulted in a Ca2+-dependent increase of sodium. The results suggest a role for sodium in amplifying the secretory response to the increased entry of Ca2+ obtained with the depolarisation of the beta-cells with glibenclamide or HB 699.

Animals↗

Sulphonamide modulation of sodium content in rat pancreatic islets.

Sodium was measured in rat pancreatic islet exposed to tolbutamide, glipizide, diazoxide or sulfisomidine. When added to a medium with physiologically balanced cations these sulphonamides induced a significant rise of the islet content of sodium. The insulin-releasing compounds, tolbutamide and glipizide, had effects opposite to those of the hyperglycemic diazoxide in counteracting the increase of sodium obtained with removal of K+. The tolbutamide-induced increase in sodium was reversed to a decrease when Ca2+ was omitted from the incubation medium. The increase of sodium, which was also seen with non-hypoglycemic sulphonamides, is itself not sufficient for initiating insulin release. However, it may well represent an important mechanism contributing to the secretory response initiated by Ca2+ entry into the sulfonylurea-depolarized beta-cell.

Animals↗

Opposing effects of glucose and tolbutamide on the sodium content of rat pancreatic islets.

Integrating flame photometry was employed for measuring sodium in rat pancreatic islets incubated in media buffered with HEPES or bicarbonate. The sodium content decreased by nearly 40% when the islets were exposed to 5 mmol/l glucose, no further reduction being seen with additional rise of the concentration to 20 mmol/l. Whereas the depressing effect of glucose was mimicked by 100 mumol/l quinine, increased sodium contents were noted after inhibition of the Na/K pump (removal of extracellular K+ or addition of 1 mmol/l ouabain) or exposure of the islets to 1 mmol/l tolbutamide. Although promoting sodium accumulation in the islet cells, tolbutamide counteracted the increase in sodium obtained on withdrawal of K+ from the incubation medium. It is suggested that tolbutamide in addition to its major effect in promoting the entry of Ca2+ also facilitates insulin release by suppressing the outward transport of this ion.

Animals↗

Possible treatment of some genetic deficiency diseases--a hypothesis.

A conceptual hypothesis for the possibility of treatment of genetic deficiency diseases utilizing genetic engineering techniques is presented. It is proposed that the gene responsible for the synthesis of a protein which is missing in the patient may be inserted into the patient's stem cells using already established techniques of gene splicing and delivery. The so modified stem cells, if put back into the patient's system (e.g. bone marrow), by virtue of their ability of self multiplication are likely to start synthesizing and continue to produce missing protein. Since stem cells are also capable of differentiating into various blood cells, the nucleated blood cells are also likely to begin production of the protein whose gene was inserted into the stem cells. In this way a blood protein synthesized by any organ (e.g. liver) in normal persons may be synthesized by stem cells or their differentiated forms in the patient resulting in correction of the deficiency. Certain genetically deficient animals may be used to prove this hypothesis.

Genetic Engineering↗

Aerodynamic measures of coarticulation in /VNC/ sound sequences.

Simultaneous measurements were made of voice, oral air flow, and nasal air flow for two speakers producing seven repetitions of 12 differing contexts containing Vowel + Nasal + Oral Consonant sequences in a search for the temporal pattern of nasal coarticulation. Analysis indicated a rather stereotyped degree of overlap of nasal air flow during the oral consonant, about 36% of the duration of the oral consonant. Carryover of nasal air flow into the oral consonant appears to reflect mechano-inertial limitations of a sluggish velum.

Adult↗

Intrusive stops in nasal-fricative clusters: an aerodynamic and acoustic investigation.

An aerodynamic investigation of the occurrence of intrusive stop consonants occurring in nasal-fricative consonant clusters in English revealed that intrusive stops were cued perceptually by silent gaps often followed by burst releases preceding the fricative consonant. In articulatory-aerodynamic terms, intrusive stops appear to result from a prolonged oral occlusion of the nasal stop which is released with a vigorous burst release just prior to complete formation of the following fricative slit constriction.

Acoustics↗

Pancreatitis in fibrocalculous pancreatic diabetes mellitus is not associated with common mutations in the trypsinogen gene.

BACKGROUND: A distinct type of pancreatitis associated with diabetes, termed fibrocalculous pancreatic diabetes (FCPD), has been reported in tropical developing countries including Bangladesh. The molecular basis for autosomal dominant hereditary pancreatitis (HP) has recently been attributed to mutations in exons 2 and 3 of the trypsinogen gene. We have investigated the hypothesis that mutations in the aforementioned exons of this gene might also predispose to FCPD. METHODS: Seventy Bangladeshi and 50 South Indian unrelated FCPD patients and seven South Indian families with FCPD probands were studied. Pancreatic calcification was confirmed by abdominal X-ray, ultrasound and/or ERCP. Established mutations of exons 2 and 3 of the trypsinogen gene were studied in these subjects by PCR-RFLP analysis and DNA sequencing. RESULTS: The mutations found in hereditary pancreatitis were not observed in this collection of FCPD subjects, and complete DNA sequencing of exons 2 and 3 of the fourth cationic trypsinogen gene also excluded any new mutations. CONCLUSIONS: These results indicate that chronic pancreatitis of FCPD is unlikely to be caused by common mutations in the trypsinogen gene.

Adult↗

An epidemological study of smoking at Abbottabad.

BACKGROUND: Smoking is a type of environmental pollution and is injurious to health. We conducted an epidemiological study of different forms of smoking like cigarette, Hookah (Hubble-Bubble) and cigar in Abbottabad. METHODS: 600 randomly selected subjects residing in different localities of Abbottabad were included. A specifically designed questionnaire was filled. RESULTS: Out of the study population 200 (33%) were found to be smoking. CONCLUSIONS: A significant proportion of Abbottabad population smokes. This city is supposed to be a relatively less polluted hill station where a lot of people come for vacations.

Humans↗