[Effectiveness and limitations of anticoagulant therapy].
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Biomedical subjects
Publications and source records attributed to Y Nakamoto.
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It was clinically evaluated by double blind method whether co-enzyme Q10 has protective effects on hair loss caused by anthracycline antibiotics. Six cases of acute leukemia, 2 blastic crisis of CML and 11 malignant lymphoma were entered to this study. DCMP regimen for acute leukemia for VEPA for lymphoma were performed. Coenzyme Q10 (or placebo) of 120 mg/day was orally administered. The grade of hair loss was classified into five groups. Five cases were only given to DM and 3 cases receiving DM and CoQ10. ADM was 6 cases and 5 were combined with CoQ10. No significant diffehence in effect of CoQ10 administration rence was recognized between two groups statistically. Elevations of GOT and GPT were less frequent in the group receiving CoQ10.
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Effects of heparin, urokinase, and ancrod were concurrently compared on intraglomerular coagulation using a model of progressive Masugi nephritis. Evaluations were performed with light and immunofluorescent microscopy. Treatment significantly reduced crescent formation, more markedly with ancrod. In contrast, endocapillary proliferation was enhanced in the groups treated with urokinase and, especially, ancrod. Ancrod appeared to be most effective in decreasing the glomerular deposition of fibrinogen-related materials as judged from the immunofluorescence, and a relatively high dose was required for urokinase to be comparable with ancrod. However, in some glomeruli from two of 13 animals given ancrod, mesangiolytic lesion developed. Thus, although promising, ancrod has many problems to be solved before using it to control endocapillary proliferation and mesangiolysis.
Cyclic AMP (cAMP) inhibited septum formation in Escherichia coli PA3092 and induced cell filamentation at elevated temperatures. This phenomenon was first observed in E. coli PA3092 and is due to a temperature-sensitive mutation. We tentatively named this mutation fic (filamentation induced by cAMP). The fic gene was located near rpsL (formerly strA) on the E. coli K-12 map. the inhibitory effect of cAMP on cell division and filamentation in a fic mutant was not observed in a crp mutant. When cAMP was removed from the culture medium, filaments were divided into rods as the intracellular cAMP level decreased. These results suggest that the cAMP-cAMP receptor protein complex causes filamentation in the fic mutant, E. coli PA3092.
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Glomerular lesions associated with hepatic disease were evaluated. Among 752 consecutive patients with hepatitis and cirrhosis, nephritic urinary changes appeared in 1.0% of chronic hepatitis and 9.2% of cirrhotics, but none in patients with acute or subacute hepatitis. Kidney tissue was obtained from 141 cases, of which 59 underwent immunofluorescent studies. Except for a few with possibly coincidental glomerulonephritis, the main glomerular pathology was mesangial depositive or proliferative lesions with frequent circumferential mesangial interposition. The highest incidence (up to 69.2%) occurred in liver cirrhosis. The glomerular immunohistology was not necessarily homogeneous. In acute or subacute hepatitis, IgG or IgM, if present, was dominant. The more chronic the course the liver disease followed, the more frequently significant IgA deposition emerged, occurring in 60.5% of cirrhotics. The IgA positive cases often disclosed paramesangial dense deposits, which is one of the characteristics of primary IgA nephritis. Hepatic IgA nephritis exhibited a lower nephritogenicity and a proneness to show mesangial interposition when compared with primary or purpuric IgA nephritis. The possible origin of glomerular IgA associated with liver disease is discussed.
A possible role of HBsAg in hepatic glomerulonephritis was evaluated in kidney specimens from 104 patients with various diseases. Huang's method using formalin-fixed and paraffin-embedded sections was applied to the kidney from 65 cases. Only 4 (3.8%) with liver cirrhosis had glomerular HBsAg deposition; 3 on frozen and one on paraffin sections. In one case of crescentic glomerulonephritis, HBsAg appeared to have had a pathogenetic role with glomerular immunofluorescence dominant for IgM, less intense IgG and negative IgA. The glomerular HBsAg in the remaining 3 patients with hepatic IgA glomerulonephritis was likely to be concomitant or superimposed. One of them had a nephrotic syndrome for which corticosteroid treatment was given, resulting in a near-complete remission and disappearance of HBsAg in the glomeruli, but the glomerular immunohistology was unaffected by the treatment. The present findings suggest that HBsAg has only a minor role.
Cell division of Escherichia coli K-12 strain PA3092 was inhibited by the addition of adenosine 3',5'-phosphate (cAMP), and the cellular morphology was changed from rods into filaments. Nucleoids in the filaments were regularly distributed and septum formation was perfectly inhibited. This inhibition of cell division by cAMP was reversed by the addition of guanosine 3',5'-monophosphate. To examine whether the inhibitory effect of cAMP on cell division in E. coli PA3092 was specific, its effect in several parental strains was investigated. Induction of cell filamentation by cAMP was observed in E. coli PA309 and P678, but not in E. coli W505, W1, Y10, or the wild-type strain. This result suggests that filamentation by cAMP in E. coli PA3092, PA309, and P678 was due to the mutagenesis by which E. coli P678 was derived from E. coli W595.
The transport of cephalothin (CET) to the exudate was investigated in croton oil-induced inflammatory rats following the intramuscular administration of CET-aqueous solution, CEt-O/W emulsion, or CET-W/O emulsion. The lymphatic transport of CET was the highest following the administration of W/O emulsion. The exudate level of CET was in a decreasing order of W/O emulsion, O/W emulsion, and aqueous solution. In the rat whose blood vessels at femoral rectus, the site of administration, were ligated, the plasma level was decreased by the administration of aqueous solution, but not by W/O emulsion. The exudate level of CET was significantly higher in case of W/O emulsion. Possible mechanisms involved are discussed.
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The effect of gel preparation on the rate of absorption of a rectally administered insulin which was suspended in a polyacrylic acid aqueous gel base (0.1%, pH 6.5) was investigated in the alloxan diabetic rats and rabbits. The preparation was administered into the in situ rectal loop in rats or infused directly into the rectum in rabbits, and the change in the blood glucose level and plasma insulin value was taken as a measure to evaluate the rate of rectal absorption of insulin. The blood glucose lowering effect in both rats and rabbits was dose-dependent, namely, a slight effect was observed at 1 IU/kg followed by a significant effect with 3 and 5 IU/kg, and a sharp hypoglycemic effect was recorded with 10 IU/kg which lasted for 5 hr. The plasma insulin level exhibited a rapid increase at 30 minutes after the dosing of the insulin by the polyacrylic acid aqueous gel base. However, the plasma level quickly diminished in 1 hr. Contrary to our expectation, an addition of a non-ionic surfactant such as Tween 80 under pH 4--8 did not show further enhancement of the absorption. In an attempt to simulate a clinical condition in which insulin was given after a meal, the insulin gel was administered into the rectal loop in diabetic rats following the i.v. injection of glucose. A satisfactory result was obtained in which 5 IU/kg dose was able to suppress a rise in the blood glucose after the glucose loading.
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