Rotational band structures in 127Cs: Shape changes induced by h11/2 neutron alignment.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to Y Liang.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Urine and serum ferritin levels were measured by a double-antibody radio-immunoassay in 96 normal adults and 57 patients with urologic malignancies. In the 96 adults, the urine ferritin levels ranged from 0 to 28 ng/ml. Elevated urine ferritin levels were observed in all 7 patients with renal pelvic carcinoma, 4 of 13 patients with renal carcinoma, 1 of 13 patients with well-differentiated (Grade I) bladder carcinoma, 8 of 19 patients with median-differentiated (Grade II) bladder carcinoma, and all 5 patients with poorly-differentiated (Grades III, IV) bladder carcinoma. These results indicated that urine ferritin assay was helpful in discriminating well-differentiated bladder carcinoma from the poorly-differentiated (P less than 0.01) in addition to differentiating renal pelvic carcinoma from renal carcinoma (P less than 0.05).
Human immunodeficiency virus (HIV) is now considered as the causative agent of acquired immunodeficiency syndrome (AIDS). A high risk of AIDS has been reported among patients with hemophilia who received lyophilized commercial factor VIII and IX concentrates of American origin. At a prevalent survey from September to December 1985, HIV antibodies were found in all four patients with hemophilia treated with the batch number W87307, 955 I.U. of American commercial factor VIII concentrate supplied by Armour Pharmaceutical Company, USA. One of the sero-positive patients developed AIDS-related complex (ARC) and died of cerebral hemorrhage. The other three sero-positive patients had abnormalities in cell-mediated immunity. Of them two developed left lumbosacral radiculopathy and hemorrhagic herpes zoster and one remained well so far.
This paper reports an outbreak of diphtheria and the result of appropriate preventive and therapeutic measures in Anshan area from Dec. 1984 to Dec. 1987. This epidemic of diphtheria occurred mainly in a camp of reform though labour organization and in a spring sanatorium among a population of young adult people with higher level of antibodies. It was proved that the special infection origin was a strain of nontoxic diphtheria bacilli. After a combined management including of injection of a refined diphtheria toxoid and an environment disinfection, the incidence of the disease dropped markedly.
Explore the source record for details and available documents.
Acesulfame K is an artificial sweetener which has been used in the food industry for some years. As yet no metabolic effects have been reported. It was reported that the sweetener can induce a cephalic phase of insulin secretion. To analyse the mechanism of this phenomenon, we studied the effect of Acesulfame K on insulin secretion in vivo. Male Wistar rats, weighing 250-300 g were fasted overnight and anaesthetized with phenobarbital. A silicon catheter was inserted into the right cervical vein for injection of test substances and for obtaining blood samples. In some experiments, another catheter was inserted into the left cervical vein for continuous infusion. Blood samples were drawn at 0, 5, 10, 15, 30 and 60 min after injection, and at -10, 0, 10, 20, 30, 40, 60, 80, 100 and 120 min after the infusion started. Injection of Acesulfame K (150 mg/kg body weight) increased the plasma insulin concentration at 5 min from 27.3 +/- 3.0 microU/ml to 58.6 +/- 4.2 microU/ml without any significant change in the blood glucose. Infusion of Acesulfame K (20 mg/kg body weight/min) for one hour maintained the insulin concentration at a high level (about 85-100 microU/ml) during this period, and at the same time blood glucose was gradually reduced from 103.0 +/- 7.3 to 72.0 +/- 7.2 mg/dl. When using different amounts of Acesulfame K, the insulin secretion was stimulated in a dose-dependent fashion. The effect of Acesulfame K on insulin secretion was similar to that observed by injecting or infusing the same doses of glucose (150 mg/kg) body weight for injection and 20 mg/kg body weight/min for infusion), except that no hyperglycemia was observed with Acesulfame K.(ABSTRACT TRUNCATED AT 250 WORDS)
The effect of the artificial sweetener Acesulfame K on insulin release in vitro was investigated. Pancreatic islets were obtained from Male Wistar rats. Acesulfame K produced a significant increase in insulin release from incubated islets. This effect was dose- and glucose-dependent. When islets were incubated with different amounts of Acesulfame K (2.5, 7.5 and 15 mM) and 15 mM glucose in the media for one hour, insulin concentrations were 140.2 +/- 21.1, 246.7 +/- 32.4 and 313.9 +/- 37.7 microU/ml, respectively. When 15 mM Acesulfame K was added to a media containing 0, 2.5, 5, 10 and 15 mM glucose, insulin release from incubated islets after 60 min were 25.6 +/- 6.4, 65.4 +/- 12.1, 109.0 +/- 10.0, 229.6 +/- 28.0 and 313.9 +/- 37.7 microU/ml. Incubating islets in the media containing arginine or acetylcholine increased insulin release significantly. However, when Acesulfame K was added to the media containing either arginine or acetylcholine, no further potentiating effect could be detected. The effect of Acesulfame K on insulin secretion was decreased by noradrenaline. However, the addition of naloxone, atropine and propranolol had no significant effect. Somatostatin inhibited insulin release from isolated pancreatic islets, but did not antagonize the action of Acesulfame K. When 2.5 mM Acesulfame K was added to a medium containing somatostatin, the inhibitory effect of somatostatin was totally neutralized. In a perifusion system, Acesulfame K stimulated both phases of insulin secretion. In conclusion, Acesulfame K acts directly on the pancreatic islets and potentiates glucose-induced insulin release.
Explore the source record for details and available documents.
L-Leucine and its hydrochloride salt have been deposited on the clay minerals kaolin and bentonite, and the amino acid/clay preparations have been irradiated in a 3000 Ci60Co gamma-ray source for radiation dosages that achieved 2-89% radiolysis of the leucine. The undecomposed leucine was thereupon recovered and both percent radiolysis and percent radioracemization were determined. Similar studies were made using solid L-leucine and its hydrochloride, and L-leucine in 0.1 M aqueous solution. It has been found that radiolysis and radio-racemization in these and the previously studied leucine systems follow pseudo-first-order rate laws, and the corresponding specific rate constants are evaluated and compared. Leucine and its hydrochloride salt proved to be the most stable to both radiolysis and radioracemization, followed by leucine and its HCl salt on kaolin, followed by leucine and its HCl salt on bentonite, with leucine (and its HCl and Na salts) in aqueous solution being least stable to both radiolysis and (except for the HCl salt) radioracemization. Implications of these observations as regards the Vester-Ulbricht mechanism for the origin of optical activity are discussed.
Explore the source record for details and available documents.
A brief review is presented of the Vester-Ulbricht beta-decay Bremsstrahlen hypothesis for the origin of optical activity, and of subsequent experiments designed to test it. Certain of our experiments along these lines, begun in 1974 and involving the irradiation of racemic and optically active amino acids in a 61.7 KCi 90Sr-90Y Bremsstrahlen source, have now been completed and are described. After 10.89 years of irradiation with a total Bremsstrahlen dose of 2.5 X 10(9) rads, crystalline DL-leucine, norleucine, and norvaline suffered 47.2, 33.6, and 27.4% radiolysis, respectively, but showed no evidence whatsoever of asymmetric degradation. D- and L-Leucine underwent about 48% radiolysis and showed 2.4-2.9% radioracemization. Other samples in solution were too severely degraded to analyze. Probable intrinsic reasons for the failure of the Vester-Ulbricht mechanism to afford asymmetric radiolysis in the present and related experiments involving beta-decay Bremsstrahlen are enumerated.
Explore the source record for details and available documents.
Explore the source record for details and available documents.