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Biomedical subjects

M Tsuji

Publications and source records attributed to M Tsuji.

At least 415 records · Page 23Linked to original sources
PubMed1987

Estimation and characterization of glycosylated carbonic anhydrase I in erythrocytes from patients with diabetes mellitus.

Glycosylated form of carbonic anhydrase isozyme I was found in human erythrocytes. The percent of glycosylated enzyme of the total erythrocyte carbonic anhydrase I of patients with diabetes mellitus was significantly higher than that from normal controls. Characterization of the glycosylated carbonic anhydrase I was studied using an enzyme purified from diabetic patients. The glycosylated enzyme showed a slightly acidic isoelectric point in comparison with that of a nonglycosylated enzyme. The specific activity of the glycosylated enzyme was approximately 40% of that of the normal enzyme, and the immunological activity decreased to 52% of that of the normal enzyme. Estimation of carbohydrates which may form a ketoamine linkage with the enzyme was studied using [3H]-labelled glycosylated enzyme synthesized by incubation of the enzyme with [3H]-D-glucose in vitro, and it was found that one mol of glucose binds to one mol of enzyme. Exposure of red cells to a higher concentration of glucose in diabetics brought about glycosylation of carbonic anhydrase, which is associated with its low activity enzymatically and immunologically.

Adult↗
PubMed1987

[Evaluation of plasma 6-keto-prostaglandin F1 alpha and thromboxane B2 in diabetic neuropathy].

The relationship between diabetic neuropathy on the one hand and microangiopathy and arteriosclerosis on the other was studied by determining plasma 6-keto-prostaglandin F1 alpha (PGF1 alpha) and plasma thromboxane B2 (TXB2) in diabetics with neuropathy. The subjects were 13 patients with insulin independent diabetes mellitus with polyneuropathy (DN+ group), 9 cases which had no neuropathy (DN- group) and 6 control cases. The patients with severe retinopathy, nephropathy and hypertension were excluded. Plasma 6-keto-PGF1 alpha and plasma TXB2 concentration were determined by radioimmunoassay. The motor neuron conduction velocity (M.C.V.) was measured through the tibial nerve in all diabetics. Plasma 6-keto-PGF1 alpha was 116.3 +/- 4.2 pg/ml (mean +/- SE) in the DN+ group and 139.9 +/- 3.0 in the DN- group, each group showing a significant fall over the control with 150.8 +/- 4.5. Plasma 6-keto-PGF1 alpha in the DN+ group showed a significant decrease in comparison with that in the DN- group. As to plasma TXB2, there was no significant difference among the three groups. The M.C.V. fell off significantly in the DN+ group with 52.9 +/- 3.2 m/sec. Furthermore, a significant positive correlation was observed between M.C.V. and plasma 6-keto-PGF1 alpha. The following is the summary of these results. A decrease in plasma 6-keto-PGF1 alpha was observed in diabetics with polyneuropathy. A decrease in the production of prostacyclin (PGI2) due to impairment of vascular endothelium in the nerve tissue was surmised. The decrease in plasma 6-keto-PGF1 alpha presumably stimulates the activity of platelet agglutination and causes an ischemic change in the nerve tissue.(ABSTRACT TRUNCATED AT 250 WORDS)

6-Ketoprostaglandin F1 alpha↗
PubMed1987

Shared idiotopes between anti-class II monoclonal antibodies and major histocompatibility complex recognition site of T cells.

We have raised a number of monoclonal antibodies (mAb) against idiotopes (Id) on monoclonal anti-murine class II (anti-Ak or Ek) antibodies. Two anti-Id mAb among 31 were found to cross-react with some T cells but not with macrophages and B cells of H-2k animals. They were able to block syngeneic mixed lymphocyte reaction (SMLR) and antigen-induced major histocompatibility complex (MHC)-restricted T cell proliferation of H-2k but not of other haplotypes. These results indicated that antibodies were recognizing Id associated with the MHC restriction site of T cells. The injection of these anti-Id mAb into H-2k mice resulted in the stimulation of self-class II-reactive T cell clones as determined by SMLR. They were also able to stimulate in non-H-2k strains to prime H-2k alloreactive T cell clones. Some animals developed anti-class II (anti-Iak) antibodies by the injection of anti-Id. These results indicated that certain anti-Id (anti-anti-class II) antibodies cross-reacted with T cell receptors which carried class II restriction specificity and were involved in allorecognition. These antibodies were found to have an ability to alter the T cell repertoire in vivo by stimulating such MHC-restricted clones.

Animals↗
PubMed1987

Studies on aromatase inhibition with 4-androstene-3,6,17-trione: its 3 beta-reduction and time-dependent irreversible binding to aromatase with human placental microsomes.

The metabolism of 4-androstene-3,6,17-trione (AT), previously described as a suicide substrate for aromatase, and its irreversible binding to aromatase were studied by using human placental microsomes. AT was rapidly converted into 3 beta-reduced metabolite (3-OHAT) with an enzyme other than aromatase in the microsomes in the presence of NADPH under either aerobic or anaerobic conditions. The conversion was efficiently prevented by a steroid 5 alpha-reductase inhibitor. 3-OHAT was characterized as a competitive (Ki = 6.5 microM) and irreversible inhibitor of aromatase. Both 14C-labeled AT and 3-OHAT were demonstrated to be irreversibly bound to aromatase probably through a sulfur atom of the enzyme in time-dependent manners in the presence of NADPH, being accompanied with time-dependent losses of the enzyme activity. It was shown that the process of an apparent time-dependent loss of aromatase activity caused by AT even under conditions allowing its 3 beta-reduction should principally depend on the action of the parent inhibitor AT itself and not on that of the metabolite 3-OHAT.

Androstenes↗
PubMed1987

Hypophysectomy does not alter the effects of somatostatin or growth hormone on canine splanchnic biogenic amine release.

We have demonstrated previously that growth hormone (GH) and somatostatin (somatotropin release inhibitory factor, SRIF) exert comparable effects on the release of splanchnic biogenic amines. The purpose of the present investigation was to study further the response of the two hormones and see whether the similarity persists in dogs completely deprived of endogenous GH. Experiments were conducted in seven hypophysectomized dogs fitted with an indwelling portal catheter. Two to 4 weeks after surgery the responsiveness of their catecholaminergic neurons was tested by an injection of human beta-endorphin (20 micrograms/kg); it caused a rise in portal catecholamine levels equivalent to that seen in intact dogs. Then the effect of a spike concentration of SRIF or GH on hepatic portal and peripheral levels of free serotonin and catecholamines was studied, all by radioenzymatic methods. The intravenous injection of ovine GH (100 micrograms/kg) or equimolar amounts of SRIF (7.5 micrograms/kg) produced in the hepatic portal circulation a transient but statistically significant rise of serotonin and a concomitant reduction in the concentration of dopamine, norepinephrine, and epinephrine. No changes were found in the peripheral circulation. The response patterns to SRIF or GH were virtually identical, which is in keeping with our other data, suggesting that the effect of GH on splanchnic biogenic amine secretion is SRIF-dependent and mediated by SRIF-containing neurons.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Exact mechanisms contributing to instability and refractoriness to therapy in patients with unstable angina: coronary arteriographic evaluation.

Ninety one patients with unstable angina were evaluated by clinical and angiographic study. Of 91 patients, 42 (46%) responded poorly to the intensive medical treatment. Emergency coronary arteriography was then performed on these patients. The important pathoanatomical mechanisms contributing to instability of angina pectoris and/or refractoriness to the intensive medical treatment were observed in 19 of 42 patients (45%). These include: 1) More severe disease with left main lesion; 2) Refractory coronary spasm; 3) Coronary dissection; 4) Rapid progression of atherosclerosis; 5) Ulcerating plaque and 6) Coronary thrombus. Our results presented here suggest that an appropriate knowledge regarding pathophysiology might improve the approach to treatment.

Adult↗
PubMed1987

Focal fatty change of the liver adjacent to the falciform ligament: CT and sonographic findings in five surgically confirmed cases.

Five cases of surgically confirmed focal fatty infiltration of the liver were detected by CT and sonography. In all five cases, the abnormality was located at the anterolateral edge of the medial segment of the liver. It was seen as a small area of low attenuation adjacent to the falciform ligament on CT and as an echogenic area next to the ligamentum teres on sonography. Dynamic CT performed during infusion of contrast medium via the superior mesenteric artery (arterial portography) showed portal blood flow within the lesion and was useful for excluding the presence of a hepatic tumor. Focal fatty infiltration of the liver adjacent to the falciform ligament constitutes a diagnostic pitfall on CT and sonography.

Fatty Liver↗
PubMed1987

Clinical usefulness of intrathecal injection of methylcobalamin in patients with diabetic neuropathy.

Seven men and four women with symptomatic diabetic neuropathy were treated with methylcobalamin (2,500 micrograms in 10 ml of saline) injected intrathecally. Treatment was begun when patients had good metabolic control, as determined by measurements of plasma glucose and hemoglobin, and was repeated several times with a one-month interval between injections. Three patients were re-treated one year after the last intrathecal injection. Symptoms in the legs, such as paresthesia, burning pains, and heaviness, dramatically improved. The effect appeared within a few hours to one week and lasted from several months to four years. The mean peroneal motor-nerve conduction velocity did not change significantly. The mean (+/- SD) concentration of methylcobalamin in spinal fluid was 114 +/- 32 pg/ml before intrathecal injection (n = 5) and 4,752 +/- 2,504 pg/ml one month after intrathecal methylcobalamin treatment (n = 11). Methylcobalamin caused no side effects with respect to subjective symptoms or characteristics of spinal fluid. These findings suggest that a high concentration of methylcobalamin in spinal fluid is highly effective and safe for treating the symptoms of diabetic neuropathy.

Adult↗