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Biomedical subjects

S Hassan

Publications and source records attributed to S Hassan.

At least 73 records · Page 4Linked to original sources
PubMed1990

Utilization of dietary sodium selenite, barley, oats and meat meal selenium by the chick.

The biological availability of selenium (Se) in barley, oats and meat meal as compared to that in sodium selenite was determined by whole blood glutathione peroxidase (GSH-Px) activity and Se concentration depletion-repletion bioassays. One day old White Leghorn chicks, initially of low-Se status, were further depleted for Se by feeding a low-Se casein basal diet (0.03 mg Se/kg diet) adequate in vitamin E for the first two weeks of life. Repletion treatments of Se at graded levels supplemented by the natural sources or sodium selenite were then provided for 4 weeks. A multiple regression equation was calculated to relate the final whole blood GSH-Px activity and Se concentration to the dietary intake of Se. The percent biological availability of Se present in the natural sources was evaluated by slope ratio analyses in comparison to the standard, sodium selenite (100%). The activity of whole blood GSH-Px established a relative bioavailability for barley, oats and meat meal Se of 85, 41 and 25%, respectively (as mu kat/l), and 81, 51 and 17%, respectively (as mu kat/g Hb). The estimated bioavailability of Se in the different natural sources, as measured by blood Se concentration was: barley, 104%; oats, 99% and meat meal, 69% in comparison to that of sodium selenite. Thus, selenite Se was superior to the natural Se sources for the induction of GSH-Px activity. Barley Se appeared to be of higher biological value to chicks than did oats and meat meal Se. Even though meal Se was retained in appreciable amounts in chick blood, it showed the poorest utilization for the synthesis of blood GSH-Px.

Animal Feed↗
PubMed1990

Histopathological and biochemical changes associated with selenium and vitamin E deficiency in chicks.

One day old unsexed White Leghorn chicks obtained either from commercial hens fed adequate levels of selenium (Se) and vitamin E (VE) (Comm. chicks), or from hens depleted in both nutrients (Depl. chicks), were fed a low Se-VE semi-synthetic basal diet. The dietary Se content was kept constantly low, while graded levels of VE as dl-alpha-tocopheryl acetate (dl-alpha Ta), (0, 5, 10 or 15 mg VE/kg diet) were fed for six weeks. An efficient carry-over of Se and VE from hens to their progeny was observed by a significant increase in their muscle Se, liver Se-glutathione peroxidase (Se-GSH-Px), and VE content at hatching. In the Depl. chicks, signs of Se-VE deficiency, i.e. exudative diathesis (ED) were observed at hatching, indicating that the deficiency lesions had developed during the embryonic period, whereas these signs were not observed in Comm. chicks on the depletion diets until they were 2 weeks old. The VE supplemental level of 15 mg/kg was not adequate to provide a complete protection against ED. Exudative diathesis was associated with low levels of muscle Se, liver Se-GSH-Px and VE and was also accompanied by a simultaneous increase in the liver non-Se-GSH-Px. Autopsy findings and histopathological lesions were observed only in subcutaneous tissue and skeletal muscle. The subcutaneous tissue was edematous with hyaline vascular lesions and hemorrhages. The thigh muscles were more susceptible to deficiency lesions than were the breast muscles, and showed in acute stages degenerative processes of the muscle fibers including calcium deposits, vascular lesions and hemorrhages. In subacute and chronic cases, reparative changes and muscle damage may develop independently of the hyaline vasculosis. To prevent ED, adequate Se and VE in chick diet is essential after hatching, irrespective of their tissue reserves of both nutrients at 1 day of age.

Animals↗
PubMed1990

Response of whole blood, erythrocyte and plasma vitamin E content to dietary vitamin E intake in the chick.

Whole blood, red blood cells (RBC), and plasma vitamin E (VE) levels in chicks fed dietary VE (dl-alpha-tocopheryl acetate, dl-alpha Ta) supplementation in steps of 0.0, 5.0, 10.0, 15.0, 20.0 and 30.0 mg/Kg were determined to examine their usefulness as an index of VE status. The increase in VE level was significant and linear in whole blood (r = 0.90), RBC (r = 0.89) and plasma (r = 0.93) in response to dietary VE intake. There was a close correlation between VE in plasma vs whole blood (r = 0.90), plasma vs RBC (r = 0.91) and whole blood vs RBC (r = 0.95). The plasma VE content was 1.2-1.8 times greater than that of whole blood, and 6.6-12.5 times greater than that of RBC. The plasma total lipids content was not affected by the dietary VE intake, whereas the level of VE in the plasma total lipids was significantly increased with increasing supplementation. Alpha tocopherol was the major isomer (ca 92%) of VE in whole blood, RBC and plasma at hatching. The small proportions of beta-tocopherol (ca 2%), gamma-tocopherol (ca 5%) and alpha-tocotrienol (ca 1%) observed at 1 day of age had decreased or totally disappeared by 7 days of age after feeding the VE-free basal diet. The data showed that in the chick, the whole blood and RBC levels of VE were as sensitive and reliable indexes of dietary VE status as was that of the plasma.

Animals↗
PubMed1989

Evidence that glutamate mediates axon-to-Schwann cell signaling in the squid.

High-frequency stimulation (100 Hz) of isolated giant axons of the small squid Alloteuthis subulata and the large squid Loligo forbesi caused the periaxonal Schwann cell resting potential (Em = -40 mV) to hyperpolarize up to 11 mV in direct proportion to train duration and action potential amplitude. In both species, the Schwann cell also hyperpolarized up to 17 mV with the application of L-glutamate (10(-9) to 10(-6) M), in a dose-dependent manner. By contrast, in the presence of 10(-8) M d-tubocurarine (d-TC) to block the cholinergic component of the Schwann cell response, Schwann cells depolarized 8-9 mV during electrical stimulation of the axon or application of L-glutamate. In the presence of 10(-5) M 2-amino-4-phosphonobutyrate (2-APB), the hyperpolarization to glutamate and to axon stimulation was blocked, whereas the cholinergic (carbachol-induced) hyperpolarization was unaffected. In experiments with Alloteuthis, L-aspartate (10(-7) M) also caused a Schwann cell hyperpolarization, but this was not blocked by 2-APB. In tests with glutamate receptor agonists and antagonists, quisqualate (10(-5) M) produced a hyperpolarization blocked by 10(-4) M L-glutamic acid diethylester (GDEE), which also blocked the response to axonal stimulation. Kainic acid (10(-4) M) also caused a hyperpolarization, but n-methyl-D-aspartate (NMDA; 10(-4) M), ibotenate (10(-5) M), alpha-amino-3-hydroxy-5-methyl-isoxazole proprionate (AMPA; (10(-4) M), and isethionate (10(-5) M) had no effect.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1988

Studies of axon-glial cell interactions and periaxonal K+ homeostasis--II. The effect of axonal stimulation, cholinergic agents and transport inhibitors on the resistance in series with the axon membrane.

The small electrical resistance in series with the axon membrane is generally modeled as the intercellular pathway for current flow through the periaxonal glial (Schwann cell) sheath. The series resistance of the medial giant axon of the crayfish, Procambarus clarkii, was found to vary with conditions known to affect the electrical properties of the periaxonal glia. Series resistance was estimated from computer analysed voltage waveforms generated by axial wire-constant current and space clamp techniques. The average series resistance for all axons was 6.2 +/- 0.5 omega cm2 (n = 128). Values ranged between 1 and 30 omega cm2. The series resistance of axons with low resting membrane resistance (less than 1500 omega cm2) increased an average of 30% when stimulated for 45 s to 7 min (50 Hz) whereas the series resistance of high membrane resistance (greater than 1500 omega cm2) axons decreased an average of 10%. Carbachol (10(-7) M) caused the series resistance of low membrane resistance axons to decrease during stimulation but had no effect on high membrane resistance axons. d-Tubocurare (10(-8) M) caused the series resistance of high membrane resistance axons to increase during stimulation but had no effect on low membrane resistance axons. Bumetanide, a Na-K-Cl cotransport inhibitor and low [K+]o, prevented the stimulation-induced increase in series resistance of low membrane resistance axons but had no effect on the high membrane resistance axons. The results suggest that the series resistance of axons varies in response to the activity of the glial K+ uptake mechanisms stimulated by the appearance of K+ in the periaxonal space during action potential generation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Studies of axon-glial cell interactions and periaxonal K+ homeostasis--III. The effect of anisosmotic media and potassium on the relationship between the resistance in series with the axon membrane and glial cell volume.

The effect of anisosmotic physiological solutions and [K+]o on the resistance in series with the axon membrane were studied in medial giant axons of the crayfish, Procambarus clarkii, to determine if changes in series resistance are correlated with changes in glial cell volume and volume regulatory responses. Series resistance was estimated from computer analysed voltage waveforms generated by constant current and space clamp techniques using piggy-back axial wire current passing and glass pipette recording electrodes. Axons subjected to anisosmotic physiological solution in the range of 23 to 175% of isosmolar solution demonstrated that the series resistance of axons changes in a manner similar to that expected for a volume change in isolated cells. In hyperosmotic solution the series resistance changes biphasically, initially decreasing followed by a recovery of the series resistance, similar to the regulatory volume increase described for glial cells in culture. The increase in series resistance following the initial decrease is inhibited by bumetanide (0.1 mM). Ouabain (1 mM), an inhibitor of the volume decreasing Na-K pump, causes the series resistance to increase significantly above that seen for the no-drug control. Bumetanide, an inhibitor of the volume increasing Na-K-Cl cotransporter, inhibits the volume regulatory response to anisosmotic media. Treating the axon with three times normal external [K+] causes the series resistance to decrease approximately 15% while five times normal [K+] leads to a 15% increase in series resistance. Both ouabain and d-tubocurare (10(-p8) M) prevent the three-fold [K+]-induced decrease in series resistance while carbachol (10(-7) M) and bumetanide have little effect. On the other hand, ouabain enhances the five-fold [K+]-induced increase in series resistance while carbachol and bumetanide cause the five-fold [K+] response to be in a decreasing direction. d-Tubocurare has little effect on the five-fold [K+]-induced increase in series resistance. The study demonstrates that under the conditions of these experiments changes in series resistance are a reflection of changes in cell volume modulated by ouabain- and bumetanide-sensitive K+ uptake mechanisms. The effects of carbachol and d-tubocurare on the series resistance suggest that their effects are modulated through their actions on the glial cell membrane potential and the electrochemical gradient for K+, which in turn controls the amount of K+ that appears in the periaxonal space.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1988

Periaxonal K+ regulation in the small squid Alloteuthis. Studies on isolated and in situ axons.

A novel giant axon preparation from the squid Alloteuthis is described. Properties of in situ and isolated axons are similar. Periaxonal K+ accumulation is a function of the physiological state of the animal and of the axon and its sheathing layers. Carefully dissected isolated axons, and axons in situ in a healthy mantle, show much less K+ accumulation than previously reported in squid. It is suggested that the Schwann cells are involved in the observed K+ regulation.

Action Potentials↗
PubMed1988

Urinary C-peptide in the neonate correlates both to maternal glucose tolerance and to fetal size at birth.

In 18 women with gestational diabetes the variables of an oral glucose tolerance test (fasting and 2-hour blood glucose values and area under the blood glucose curve) performed in the last trimester of pregnancy correlated significantly with the urinary C-peptide excretion during the first 12 hours of the life (r = 0.47, 0.71, and 0.60, respectively). In a combined group with 28 type II pregnant diabetic women there was also a significant correlation between the urinary C-peptide excretion of the infants and their skinfold. Assay of the urinary C-peptide excretion of the neonate, reflecting its insulin production, seems to be a sensitive parameter to study the influence of the maternal carbohydrate metabolism in the offspring.

Birth Weight↗
PubMed1985

Effect of a hydantoin prostaglandin analogue, BW245C, during oral dosing in man.

Following an open pilot study, the effects of repeated oral doses of BW245C, a hydantoin prostaglandin analogue, were studied in man. Six healthy volunteers received 150 micrograms BW245C or placebo 6-hourly for 5 days according to a double blind randomised balanced design with 7 days interval between treatments. Measurements of headache, facial flushing, heart rate, blood pressure, systolic time intervals, ECG, platelet aggregation responses to ADP and of subjective effects were made before and 1 and 3 h after the first dose of BW245C/placebo on days 1, 3 and 5 of dosing. BW245C produced significantly (p less than 0.05) higher headache scores than placebo on days 3 and 5; facial flushing, nasal stuffiness and abdominal discomfort were more frequent on BW245C than placebo. Heart rate, derived from the ECG, was significantly (p less than 0.05) higher and pre-ejection period significantly (p less than 0.05) shorter on BW245C at 1 h after dosing on each day. Left ventricular ejection time index, QS2 index, PR interval, QRS duration and T wave height were unchanged. Heart rate, counted at the radial pulse, and systolic and diastolic blood pressure, all measured lying and standing, were similar for BW245C and placebo. Platelet aggregation responses were not significantly different between the two treatments. The results indicate that repeated oral doses of BW245C, sufficient to cause moderately uncomfortable subjective effects, do not inhibit platelet aggregation.

Adenosine Diphosphate↗
PubMed1984

Biopotency of vitamin E in barley.

Investigations were carried out to establish the total biopotency of the natural vitamin E isomers in barley compared with that of DL-alpha-tocopheryl acetate. The chick was used as an experimental animal. Prevention of nutritional encephalomalacia (NE) and chick liver-storage and plasma-storage assays of vitamin E were the methods used in the study. The individual tocopherols and tocotrienols, both in the tissue samples and in the grain and barley oil, were analysed using high-pressure liquid chromatography (HPLC) with fluorescence detection. The diagnosis of NE was based on careful clinical and histopathological observations. It can be concluded from the results that full protection against NE in the chicks was obtained with a supplementation level of 7.5 mg DL-alpha-tocopheryl acetate/kg diet (i.e. a total vitamin E content of 11.20 mg/kg diet) or with a supplement of 8.7 g barley oil/kg diet (i.e. a total vitamin E content of 22.99 mg from barley oil/kg diet). This gave a biopotency factor of 0.49 for barley for prevention of NE of the chicks, as compared to that of DL-alpha-tocopheryl acetate. Using regression analysis a statistically linear relationship could be observed between the total dietary vitamin E level and the response, as measured by the total vitamin E content in the liver and plasma, both in the groups supplemented with DL-alpha-tocopheryl acetate and in the groups supplemented with corresponding amounts of vitamin E in barley oil. The liver and plasma responses to the total vitamin E in the barley-oil diet compared with those of the DL-alpha-tocopheryl acetate reference diet gave identical values for the regression coefficients, i.e. in both liver-storage and plasma-storage assays the value for slopes of dose-response lines was 0.37. This means that the biopotency of the total vitamin E in barley was 37% of that of dietary DL-alpha-tocopheryl acetate. Thus, barley is not as rich a source of vitamin E as could be supposed on the basis of the chemical determination of its total vitamin E content. It was possible to verify this experimentally established biopotency of 0.37 for the total vitamin E in barley by converting the chemically determined amounts of the vitamin E isomers in barley into DL-alpha-tocopheryl acetate equivalents by multiplying them with internationally accepted potency factors for the individual natural isomers (DL-alpha-tocopheryl acetate 1.00, D-alpha-tocopherol 1.49, D-beta-tocopherol 0.60, D-gamma-tocopherol 0.15, D-alpha-tocotrienol 0.37).(ABSTRACT TRUNCATED AT 400 WORDS)

Animal Feed↗