Dynamics of exciton formation and relaxation in GaAs quantum wells.
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Biomedical subjects
Publications and source records attributed to J Shah.
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The structural and thermotropic properties of the hydrated mixed-chain phosphatidylcholines (PCs), C(8):C(18)-PC and C(10):C(18)-PC, have been studied by X-ray diffraction and differential scanning calorimetry. For fully hydrated C(8):C(18)-PC, the reversible chain melting transition is observed at 9.9 degrees C (delta H = 7.3 kcal/mol). X-ray diffraction at 0 degrees C (below the chain melting transition) shows a small bilayer repeat distance, d = 51.0 A, and a sharp, symmetric wide-angle reflection at 4.1 A, characteristic of a mixed interdigitated bilayer gel phase [see McIntosh, T. J., Simon, S. A., Ellington, J. C., Jr., & Porter, N. A. (1984) Biochemistry 23, 4038-4044; Hui, S. W., Mason, J. T., & Huang, C. (1984) Biochemistry 23, 5570-5577]. At 30 degrees C (above the chain melting transition), a diffuse band is observed at 4.5 A characteristic of an L alpha phase but with an increased bilayer periodicity, d = 61 A. Both the calculated lipid bilayer thickness (d1) and that determined directly from electron density profiles (dp-p) show unusual increases as a consequence of chain melting. In contrast, fully hydrated C(10):C(18)-PC shows an asymmetric endothermic transition at 11.8 degrees C. Below the chain melting transition, two lamellar phases are present, corresponding to coexisting interdigitated (d = 52.3 A) and noninterdigitated (d = 62.5 A) bilayer gel phases. The relative amounts of these phases depend upon the low-temperature incubation and/or hydration conditions, suggesting conversions, albeit kinetically complex, between metastable, and stable phases. The different behavior of C(8):C(18)-PC and C(10):C(18)-PC, as well as their positional isomers, is rationalized in terms of the molecular conformation of PC.
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We undertook a retrospective review of 247 previously untreated consecutive patients from 1965 to 1986 with primary squamous cell carcinoma of the supraglottic or glottic larynx to ascertain the prevalence of neck node metastases by neck level. The 247 patients underwent a total of 262 radical neck dissections. Patients were grouped by clinical neck status at the time of neck dissection: elective dissection in the NO neck; immediate therapeutic dissection in the N+ neck; and subsequent therapeutic dissection in the NO neck that over time converted clinically to N+. Detailed analysis revealed a predominance of neck node metastases in levels II, III, and IV for all clinical neck groups. Level V was rarely involved, but always in conjunction with neck node metastases in levels II, III, or IV (ie, N2 disease). Level I was rarely involved; involvement occurred with neck node metastases in levels II, III, or IV 75% of the time. Level I involvement correlated with T3 or T4 primary tumors exhibiting histologic extralaryngeal spread. These data support the trend toward selective limited neck dissection in both NO and N1 patients.
Ticlopidine is a potent inhibitor of platelet aggregation. Absorption of ticlopidine after oral dosing is rapid and complete. Ticlopidine is extensively metabolized with a relative minor component of unchanged ticlopidine in plasma. The randomized crossover study described here was undertaken to examine the effect of food and antacid on the oral bioavailability of a single dose of ticlopidine (250 mg) in normal volunteers. After postprandial treatment the rate and extent of absorption of ticlopidine was earlier and greater relative to fasting treatment [tmax = 1.71 +/- 0.33 hr (fed) vs 1.92 +/- 0.56 hr (fasting) and AUC0-infinity = 2.164 +/- 0.813 micrograms X hr/mL (fed) vs 1.808 +/- 1.052 micrograms X hr/mL (fasting)]. The oral bioavailability of ticlopidine was increased by 20% when taken after a meal. In contrast, absorption of ticlopidine administered after antacid treatment was approximately 20% lower than under fasting conditions. Administration of ticlopidine with food is recommended to maximize gastrointestinal tolerance.
A reduction in the density of small arterioles (rarefaction) has been reported in several vascular beds of the spontaneously hypertensive rat (SHR). There have been conflicting reports on the existence of rarefaction in the pial vasculature of SHR. In this study, we determined whether there was rarefaction of pial arterioles in several models of hypertension. We studied SHR; two-kidney, one-clip Goldblatt hypertensive rats; deoxycorticosterone-salt hypertensive rats; and Dahl salt-sensitive rats fed high salt diet. The two groups of normotensive controls were Wistar--Kyoto rats and Dahl salt-sensitive rats fed low salt diet. The duration of hypertension was about 2 months. Density of first-, second-, third-, and fourth-order arterioles was determined by counting the number of vessels from enlarge photographs. We also measured the lengths of segments of the arterioles. We did not observe any evidence of rarefaction of arterioles in the pial vasculature in any of the hypertensive groups of rats. We conclude that (i) rarefaction of arterioles does not occur in the pial microvasculature after approximately 2 months of hypertension and (ii) rarefaction of pial arterioles does not account for abnormalities in the cerebral circulation of hypertensive rats such as protection of the blood-brain barrier or changes in autoregulation of cerebral blood flow.
The intraperitoneal route is frequently used for the administration of insulin in diabetic continuous ambulatory peritoneal dialysis patients. However, there is conflicting evidence as to whether the dosage of intraperitoneal insulin should be increased or decreased during peritonitis in these patients. Glucose and insulin absorption and glycaemic control were evaluated in 2-hour exchanges using 15 ml of 2.5% dextrose dialysis solution in diabetic rats with (group 1) and without (group 2) peritonitis. Fasting blood glucose values at the beginning of the study exchanges were mean +/- SD 17.9 +/- 3.3 mmol/l in group 1 and 18.2 +/- 3.5 mmol/l in group 2. Even though group 1 had a higher percentage absorption of dialysate glucose (65 +/- 19 vs. 47 +/- 7%; p less than 0.05) and higher percentage absorption of dialysate insulin (49 +/- 12 vs. 44 +/- 14%; p less than 0.1), the hypoglycaemic response to the standard intraperitoneal dose of insulin was similar in each group. Plasma C peptide levels remained very low in both groups, thus excluding significant endogenous release of insulin. These data indicate that peritonitis per se does not change intraperitoneal insulin requirements during standardized peritoneal dialysis exchanges in diabetic rats. Insulin requirements may also be unaltered during peritonitis in diabetic continuous ambulatory peritoneal dialysis patients, provided that dialysate glucose load and oral carbohydrate intake are kept constant.
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Animal models demonstrate a cancer-protective effect of vitamin A. However, human epidemiologic studies correlate the intake of the precursor, beta-carotene, rather than active vitamin A, to a reduced risk for certain cancers. This suggests that beta-carotene may have cancer-protective properties independent of its vitamin A activity. In the present rat study, effects of beta-carotene or active vitamin A on carcinogen metabolizing enzyme activity were evaluated. The activity of intestinal aryl hydrocarbon hydroxylase (AHH, EC 1.14.14.1) was higher in rats fed a purified diet supplemented with beta-carotene than in rats fed the control diet containing adequate vitamin A as retinyl palmitate (165 +/- 30 vs. 90 +/- 18 pmol/min x mg), P less than (0.05). Supplementing the control diet with retinyl acetate had no effect. This AHH-enhancing effect of beta-carotene on the activity of the intestinal mucosal enzyme was not seen on the hepatic enzyme, which is consistent with the nearly complete conversion of beta-carotene to vitamin A prior to reaching the liver. These results demonstrate an effect of beta-carotene on carcinogen metabolism which is independent of its vitamin A activity. This may help explain human epidemiologic data, and may lead to further work which would allow for prudent dietary recommendations toward a reduction in cancer risk.
Ethanol-induced neurotransmitter release in unstimulated synaptosomes was found to be independent of extrasynaptosomal Ca2+ concentration, indicating a redistribution of intracellular Ca2+. The effects of alcohol on microsomal Ca2+ uptake and release were studied. In vitro addition of 100 mM ethanol had no effect on ATP-dependent Ca2+ accumulation in the microsomes. However, the same amount of ethanol released 25% of total accumulated Ca2+ from the microsomes. Ethanol induced Ca2+ release in a concentration-dependent manner over the range 30 mM-500 mM. The amount of Ca2+ release increased with higher alcohols. The effect of alcohol was temperature-dependent and inhibited at 0 degrees C. These results indicate that the known stimulatory effects of ethanol on resting release of neurotransmitters may be due to the microsomal release of Ca2+.
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The ionic mechanism of inositol trisphosphate (InsP3)-induced Ca2+ release was investigated in microsomes (microsomal fractions) isolated from rat brain. InsP3 stimulated Ca2+ release from microsomes incubated in media containing 100 mM-KCl. The InsP3-induced Ca2+ release was insensitive to a variety of Ca2+-channel blockers; however, the K+-channel blockers tetraethylammonium chloride (TEA; 1 mM) and 9-tetraethylammonium chloride (9-TEA; 1 mM) blocked InsP3-induced Ca2+ release. Moreover, addition of InsP3 increased 86Rb+ influx into the microsomes. The influx of 86Rb+ also was sensitive to TEA and 9-TEA. The above results suggest that InsP3-induced Ca2+ release requires an opposite flow of K+ ions, and modulation of K+ channels by TEA and 9-TEA may underlie the inhibition of InsP3-induced Ca2+ release from brain microsomes by these agents.
We evaluated 191 consecutive adults with pulmonary tuberculosis in order to develop methods to determine which patients should be initially hospitalized. Using stepwise discriminant analysis, we found the six factors that were most strongly associated with an unfavorable short-term outcome (respiratory failure or death): lymphopenia, advanced age, concomitant smear-positive extrapulmonary tuberculosis, alcoholism, a high percentage of neutrophils on the differential white blood cell count, and lack of radiographic evidence of cavitation. We derived a scoring system incorporating these variables and separated patients into high- and low-risk groups. The system was prospectively validated by applying it to a separate group of 179 patients. Lymphocyte-transformation tests in 32 patients revealed an association between clinical markers of poor prognosis and minimal lymphocyte proliferation to a heat-killed strain of Mycobacterium tuberculosis.
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The effects of different ionic media on Ca2+ uptake and release in isolated brain microsomes were investigated. KCl (100 mM) provided the best medium for Ca2+ uptake in the presence of ATP. The effect of myo-inositol 1,4,5-trisphosphate (IP3) on Ca2+ release was examined and was maximum at 0.2 microM. IP3-induced Ca2+ release was dependent on extramicrosomal free Ca2+ concentration with maximal release at 5.0 microM free Ca2+. Replacement of KCl by sucrose or NaCl did not show any response to IP3. Electron microscopy showed that the microsomal fraction consisted of characteristic endoplasmic reticulum-derived vesicular profiles and were free of mitochondria or plasma membrane contamination. Our results support the concept that the endoplasmic reticulum is the target for IP-3 induced mobilization of Ca2+ in the cell.