Search PubMed⌕ Search

Biomedical subjects

K Nakata

Publications and source records attributed to K Nakata.

At least 487 records · Page 27Linked to original sources

The injury and repair of human articular cartilage: a morphological study of 192 cases of coxarthrosis.

The examination of articular cartilage from 192 osteoarthritic hip joints has shown a combination of cell and matrix injury on the one hand and cell and matrix regeneration on the other. The reparative cartilage tissue has three sources, bone, synovium and cartilage, which are both intrinsic and extrinsic. The observation of reparative cartilage in every case examined, and of significant amounts in more than 50% of the cases, indicates that the cartilage has considerable potential for repair. In particular, intrinsic repair which is of cartilage origin, in our opinion, has a very significant role in the articular cartilage.

Bone Regeneration↗

Prediction of splice junctions in mRNA sequences.

A general method based on the statistical technique of discriminant analysis is developed to distinguish boundaries of coding and non-coding regions in nucleic acid sequences. In particular, the method is applied to the prediction of splicing sites in messenger RNA precursors. Information used for discrimination includes consensus sequence patterns around splice junctions, free energy of snRNA and mRNA base pairing, and statistical differences between coding and non-coding regions such as periodic appearance of specific bases in coding regions reflecting the non-random usage of degenerate codons. Given the reading frame of an exon (but not the exon/intron boundaries), the method will predict the following exon, namely, the intron to be excised out. When applied to human sequences in the GenBank database, the method correctly identified 80% of true splice junctions.

Base Sequence↗

[Pharmacological studies of N-(2-mercapto-2-methylpropanoyl)-L-cysteine (SA96). V. Effects of SA96 in combination with indomethacin or prednisolone on adjuvant arthritis in rats].

SA96 in combination with indomethacin or prednisolone was investigated for their effects on the adjuvant arthritis in Lewis rats. SA96 given orally at a dose of 10 mg/kg inhibited the inflammation of adjuvant treated foot and untreated foot and the increase of serum Cu concentration which followed the development of adjuvant arthritis, but 2 mg/kg had no effect. Indomethacin given orally at a dose of 0.1 mg/kg or prednisolone given orally at a dose of 0.4 mg/kg also inhibited the adjuvant arthritis. Prednisolone suppressed the decrease of A/G ratio. Indomethacin and prednisolone, however, had no effects on the increase of serum Cu concentration. SA96 at a dose of 10 mg/kg in combination with indomethacin was more effective than the treatment of each drug alone on inflammation of adjuvant treated and untreated foot, serum Cu concentration, erythrocyte sedimentation rate and A/G ratio. The combination of SA96 at a dose of 2 mg/kg or 10 mg/kg with prednisolone had similar synergistic effects towards the adjuvant arthritis in rats.

Animals↗

[Pharmacological studies on N-(2-mercapto-2-methylpropanoyl)-L-cysteine(SA96). IV. Effects of SA96 and its main metabolite, SA679, on denaturation of human gamma-globulin and adjuvant arthritis in rats].

SA96 and its main metabolite, SA679, were investigated for their effects on denaturation of human gamma-globulin and bovine serum albumin (BSA) and on adjuvant arthritis in Lewis rats. The heat denaturation of human gamma-globulin and BSA enhanced by Cu2+ was inhibited by SA96, SA679 and D-penicillamine, and the inhibitory effect of SA96 was the most potent. In adjuvant arthritis rats, SA96 given orally at a dose of 10 mg/kg from the same day as the adjuvant injection inhibited significantly the swelling of adjuvant treated foot and untreated foot, increase of the relative organ weights of the adrenals, liver and kidney, and increase of serum Cu concentration; but at a dose of 100 mg/kg, it did not show any effects on these parameters. On the other hand, SA96 given from three days before the adjuvant injection showed the inhibitory effects at a dose of 100 mg/kg as well as 10 mg/kg. These results suggest that the effect of SA96 on adjuvant arthritis in rats depends on its administration schedule. SA679 also inhibited the adjuvant arthritis at a dose of 100 mg/kg, but its effect was less potent than that of SA96.

Animals↗

Responses of plasma cyclic AMP, serum immunoreactive insulin, C-peptide immunoreactivity and blood sugar levels to glucagon in patients with liver diseases.

Levels of plasma cyclic AMP, serum immunoreactive insulin (IRI), serum c-peptide immunoreactivity (CPR) and blood sugar (BS) were determined 0, 15, 30, 45 and 60 min after a glucagon injection (0.01 mg per kg body weight) in normal controls, patients with acute hepatitis and liver cirrhosis. Plasma cyclic AMP responses to glucagon in liver disease patients varied widely in peak value, and only in patients with fulminant hepatitis and decompensated liver cirrhosis with poor prognosis was the response suppressed. The peak response of BS was found significantly later in liver cirrhosis patients than in normal controls. IRI and CPR responses to glucagon were lower in acute hepatitis patients than in normal controls and liver cirrhosis patients. IRI levels and their sum were also lower in acute hepatitis patients, although CPR levels were not significantly different. Thus, the ratio of the sum of CPR from 0 to 60 min to that of IRI was significantly higher in acute hepatitis, indicating impaired pancreatic secretion of insulin to glucagon stimulation as well as increased uptake of insulin by the liver in acute hepatitis.

Adult↗

Pharmacological studies of N-(2-mercapto-2-methylpropanoyl)-L-cysteine (SA96) (3). Effects of SA96 on experimental allergic reactions.

The effects of an antirheumatic agent, N-(2-mercapto-2-methylpropanoyl)-L-cysteine (SA96), were investigated on allergic reactions in rats and guinea pigs. The effects of SA96 were compared with those of D-penicillamine (D-Pc). SA96 given twice orally at the doses of 10 to 50 mg/kg significantly caused inhibitions of 28%, 29% and 44% against passive cutaneous anaphylaxis (PCA), reversed cutaneous anaphylaxis (RCA) and reversed passive Arthus (RPA) reactions, which are classified as Type I, Type II and Type III allergic reactions, respectively. D-Pc also showed inhibitions of 30%, 23% and 18% on Type I, Type II and Type III reactions, respectively, and inhibitions on Type II and Type III reactions were not significant. On the other hand, SA96 (10 to 50 mg/kg twice) had no influence on the Type IV allergic reaction, delayed hypersensitivity, while D-Pc (20 mg/kg twice) showed an enhancement of 27% on the Type IV reaction. In the in vitro study, SA96 inhibited the hemolytic complement activity at 10(-4) to 10(-2) M and the macrophage migration at 1 X 10(-4) to 5 X 10(-3) M in a dose-dependent manner. These in vitro activities of SA96 were more potent than those of D-Pc. These results showed that SA96 had some different immunopharmacological properties on experimental allergic reactions as compared with those of D-Pc.

Anaphylaxis↗