Electron addition spectrum in the supersymmetric t-J model with inverse-square interaction.

The electron addition spectrum A+(k,omega) is obtained analytically for the one-dimensional (1D) supersymmetric t-J model with 1/r2 interaction. The result is obtained first for a small-sized system and its validity is checked against the numerical calculation. Then the general expression is found which is valid for arbitrary size of the system. The thermodynamic limit of A+(k,omega) has a simple analytic form with contributions from one spinon, one holon, and one antiholon-all of which obey fractional statistics. The upper edge of A+(k,omega) in the (k,omega) plane includes a delta-function peak which reduces to that of the single-electron band in the low-density limit.

Exact dynamical structure factor of the degenerate haldane-shastry model

The dynamical structure factor S(q,omega) of the K-component ( K = 2, 3, 4) spin chain with a 1/r(2) interaction is derived exactly at zero temperature for the arbitrary size of the system. The result is interpreted in terms of a free quasiparticle picture which is a generalization of the spinon picture in the SU(2) case. The excited states consist of K quasiparticles each of which is characterized by a set of K-1 quantum numbers. Divergent singularities of S(q,omega) at the spectral edges are derived analytically. The analytic result is checked numerically for finite systems.

Novel benzoxazole 2,4-thiazolidinediones as potent hypoglycemic agents. Synthesis and structure-activity relationships.

A new series of benzoxazole 2,4-thiazolidinediones was synthesized and evaluated for hypoglycemic activity in genetically obese and diabetic yellow KK mice. 2-Arylmethyl- and 2-(heteroarylmethyl)benzoxazole derivatives showed far more potent activity than known 2,4-thiazolidinedione derivatives such as ciglitazone, troglitazone and pioglitazone. A facile synthesis of benzoxazole 2,4-thiazolidinediones was also established using aminophenol 2,4-thiazolidinedione (11) as a key intermediate. Details of synthesis and structure-activity relationships for this series are described.

[512 x 2048 matrix whole body scintigraphy with laser imaging system].

Although we could acquire a detailed 512 x 2048 matrix whole body scintigraphy, the 512 x 2048 matrix whole body scintigraphy was divided to the upper and lower half of the body, because a many of CRT system displayed only 1024 x 1024 matrix with non interlace mode. We made 12 dots of normal vertical image distance to 0 dot with laser imaging system (Li-10 Konica medical inc.), and we printed these divided whole body images in the four partition of the film. The lead bar phantom (interval from 6 mm to 3 mm) filled with 99mTcO4- was studied by both 512 x 2048 matrix whole body scanning mode and 256 x 1024 whole body scanning mode in the basic study. And the distance between the lead bar phantom and the gamma camera was changed from 10 mm to 100 mm. We studied 41 patients with metastatic bone tumor (14 breast cancer, 7 lung cancer, 7 prostate cancer, 5 others, 6 unknown origin) clinically. However the 512 x 2048 matrix whole body scan was better quality of images than 256 x 1024 matrix whole body scan at 100 mm distance in the basic study. The abnormal uptake of metastatic sites was shown equally in both 512 x 2048 and 256 x 1024 matrix whole body scintigraphy. The 512 x 2048 matrix whole body scan was better quality of images than 256 x 1024 matrix whole body scan in 26 out of 41 patients, equal in 10 out of 41 patients and worse in 3 out of 41 patients. The matrix size of 512 x 2048 matrix whole body scintigraphy (0.98 mm2) was smaller than that of 256 x 1024 matrix whole body scintigraphy (1.95 mm2).(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of aminopeptidase inhibitors actinonin and amastatin on chemotactic and phagocytic responses of human neutrophils.

Actinonin and amastatin are low-molecular-weight inhibitors of aminopeptidases associated with cell surfaces. The purpose of this study was to determine their effects on human neutrophil functions such as chemotaxis and phagocytosis. Both actinonin and amastatin enhanced chemotaxis to the chemotactic peptide N-formyl-methionyl-leucyl-phenylalanine. On the other hand, the effects of both agents on neutrophil phagocytosis were varied. Bacterial attachment to neutrophils was slightly affected by these agents. However, actinonin enhanced the internalization of bacteria by neutrophils. Neutrophil leucine aminopeptidase activity was also determined and was found to be weakly inhibited by these agents.

Effects of methyl (+) (3S)-1,2,3,4-tetrahydro-3-hydroxymethyl-beta-carboline-2- carbodithioate(THC), a new hepatoprotective agent, on protein synthesis and chronic liver injury induced by carbon tetrachroride in rats.

The effects of oral administration of methyl (+) (3S)-1,2,3,4-tetrahydro-3-hydroxymethyl-beta-carboline-2-carbodithioa te (THC) on protein synthesis in the liver and chronic liver injury induced by carbon tetrachloride (CCl4) in rats were studied. THC increased liver weight and the contents of protein and ribonucleic acid, but not deoxyribonucleic acid, in the liver. THC also accelerated the 14C-leucine incorporation into hepatic microsomal and cytosol proteins in rats when the animals were treated with THC 24 h before sacrifice. In addition, when the animals were treated with THC during the latter half of a 5 weeks CCl4-treatment period, THC had a marked therapeutic effect on CCl4-induced chronic liver injury in rats by an improvement of the decreased body weight gain, suppression of the elevated serum enzyme activities (glutamic pyruvic transaminase, glutamic oxaloacetic transaminase and alkaline phosphatase) and increases in the decreased serum total protein and glucose contents. In the liver, THC also improved the decreased protein content, the increased triglyceride content and histopathological changes. These results suggested that THC stimulates protein synthesis in the liver and has a therapeutic effect on chronic liver injury induced by CCl4.

Effects of methyl (+)(3S)-1,2,3,4-tetrahydro-3-hydroxy-methyl-beta-carboline-2- carbodithioate (THC), a new hepatoprotective agent, on acute liver injuries induced by various hepatotoxic substances in mice and rats.

The effects of oral administration of methyl (+)(3S)-1,2,3,4-tetrahydro-3-hydroxymethyl-beta-carboline-2-carbodith ioate (THC) on acute liver injuries induced by carbon tetrachloride (CCl4), bromobenzene (B.B.), D-galactosamine (GALN) and alpha-naphthylisothiocyanate (ANIT) in rats and allyl alcohol (A.A.) in mice were studied. THC suppressed the elevation of plasma transaminase activities and hepatic lipid contents induced by CCl4 in rats when the animals were treated with THC for 4 consecutive days simultaneously with CCl4 administration. THC also suppressed the elevation of hepatic lipid contents induced by the 4 d-treatment of rats with CCl4 when administered for 4 consecutive days from the next day after treatment with CCl4. This effect of THC was histopathologically confirmed. In addition, pretreatment with THC protected rats against liver injuries induced by B.B., GALN, and ANIT, but not against A.A. in mice. This protection was evident from the suppression of elevated activities of plasma transaminase and/or elevated contents of hepatic lipid induced by these hepatotoxic substances. Furthermore, THC inhibited the formation of lipid peroxide in rat liver microsomes with an IC50 of 3.2 microM. These results suggested that THC protected rats against liver injuries induced by CCl4, B.B., GALN and ANIT and had a protective effect on the microsomal membrane against lipid peroxide in vitro.