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Biomedical subjects

H Takami

Publications and source records attributed to H Takami.

At least 163 records · Page 9Linked to original sources
PubMed1996

Open reduction of chronic lunate and perilunate dislocations.

Four patients with chronic lunate and perilunate dislocations were treated by open reduction and internal fixation. The interval between injury and operation was 7, 8, 14 and 18 weeks, respectively. Both palmar and dorsal surgical approaches were needed to reduce the old dislocation in all cases. A case of dorsal trans-scaphoid perilunate dislocation showed concurrent partial disruption of the scapholunate ligament. Transient vascular compromise of either the lunate or the proximal scaphoid fragment was noted in three patients. Despite the delay in treatment, all patients had satisfactory outcomes.

Adult↗
PubMed1996

[Tumor markers: neoplasmas in digestive organs].

Because they show high levels in hepatocellular carcinoma, alpha-fetoprotein and des-gamma-carboxyprothrombin are clinically useful tumor markers for differentiating hepatocellular carcinoma from other hepatic diseases. The two are useful complementary markers of hepatocellular carcinoma because they do not correlate with each other. A typical marker of pancreatic cancer is carbohydrate antigen (CA) 19-9. Over a period of more than 10 years, many markers resembling CA19-9 have been identified, but none are markedly superior to CA19-9, and the sensitivity of these markers in pancreatic cancer is only 65%-80%. Tumor markers are not useful for the early diagnosis of either hepatocellular carcinoma or pancreatic cancer. They are, however, considered to be useful for monitoring after treatment.

Biomarkers, Tumor↗
PubMed1996

Diltiazem preserves direct vasodilator response but fails to suppress intimal proliferation in rat allograft coronary artery disease.

BACKGROUND: We investigated the effect of diltiazem on transplant coronary artery disease in rat cardiac allografts both with standard histologic techniques and by measuring coronary vascular resistance and vasodilator response of the coronary arteries. METHODS: Hearts from Lewis rats were transplanted into Fischer 344 rats in an abdominal position without immunosuppression as a chronic rejection model. The rats were randomly divided into two groups: (1) no drug intervention (control; n = 36) and (2) diltiazem in drinking water (n = 33). Syngeneic transplants, Lewis donor to Lewis recipient, were used for isograft comparison (n = 17). Rat allografts were observed for length of survival, and at 4 months the surviving allografts were transferred to Langendorff perfusion, where coronary vascular resistance and its response to acetylcholine and nitroglycerin were examined. Allografts were also examined histologically and assigned transplant coronary artery disease and cellular rejection grades. RESULTS: Graft survival at 4 months was 43%, 38%, and 100% in control, diltiazem, and isograft groups, respectively. In the control group baseline coronary vascular resistance was much higher than in isografts (243 +/- 52 versus 35.3 +/- 6.2 cm H2O center dot gm center dot min/ml, p < 0.05) and the response to acetylcholine and nitroglycerin was significantly lower than that in the isografts (acetylcholine 6.2% +/- 4.8% versus 16.4% +/- 3.3%, p < 0.05; nitroglycerin 5.6% +/- 4.7% versus 12.6% +/- 5.7%, p < 0.05). In the diltiazem group baseline coronary vascular resistance (191 +/- 72 cm H2O center dot gm center dot min/ml) and the response to acetylcholine (7.3% +/- 2.9%) were similar to those in the control group (p = not significant); however, the response to nitroglycerin was better than that in the control group and in fact similar to that in the isograft group (13.6% +/- 7.0%; p < 0.05 versus control group, p = not significant versus isograft group). Histologic examination showed no coronary artery disease in isografts but equivalent marked transplant coronary artery disease and inflammation in both the control (transplant coronary artery disease grade 2.9 +/- 0.6, cellular rejection grade 3.6 +/- 0.7) and diltiazem (transplant coronary artery disease grade 3.0 +/- 0.8, cellular rejection grade 4.3 +/- 0.9) groups. CONCLUSION: In this transplant coronary artery disease model, diltiazem did not suppress the development of coronary intimal proliferation, but it did help preserve the vasodilative properties of the allograft coronary arteries in response to nitroglycerin, a direct vasodilator.

Animals↗
PubMed1995

(E)-4-(2-[[3-(indol-5-yl)-1-oxo-2-butenyl]amino]phenoxy)butyric acid derivatives: a new class of steroid 5 alpha-reductase inhibitors in the rat prostate. 1.

A series of (E)-4-(2-[[3-(indol-5-yl)-1-oxo-2-butenyl]amino]phenoxy)butyric acid derivatives was prepared, and the derivatives were demonstrated to be potent inhibitors of steroid 5 alpha-reductase in the rat prostate. The structure-activity relationships were as follows. An alpha-branched alkyl or benzyl substituent of proper size at position 1 of the indole is crucial for optimal enzyme inhibitory activity. N-Methylation of the amide NH resulted in complete loss of activity. Thus, coplanarity of the benzene ring and amide moiety is essential for such activity. Among the compounds prepared, (E)-4-(2-[[3-[1-[bis(4-fluorophenyl)methyl]indol-5-yl]-1-oxo-2- butenyl]-amino]phenoxy)butyric acid (57, KF18678) was one of the most potent compounds (rat prostate 5 alpha-reductase IC50 = 3.3 nM).

5-alpha Reductase Inhibitors↗
PubMed1995

Germline mutations of the RET proto-oncogene in eight Japanese patients with multiple endocrine neoplasia type 2A (MEN2A).

Multiple endocrine neoplasia type 2A (MEN2A) is a dominantly inherited cancer syndrome characterized by medullary thyroid carcinoma, pheochromocytoma, and parathyroid hyperplasia. The gene responsible for MEN2A was localized by linkage analysis to chromosome 10q11.2 in 1987, and recently mutations in RET, a proto-oncogene in the candidate region, were discovered in patients with MEN. The majority of mutations found so far in MEN2A patients have been located in nucleotide sequences encoding cysteine residues in the extracellular domain of RET. To characterize MEN2A germline alterations in the Japanese population, we screened DNA from eight unrelated patients for mutations in exons 10 and 11 of the RET proto-oncogene and found mutations in all eight patients, at codons 618, 620, or 634; each of these sites encodes a cysteine residue in the extracellular domain of RET. The mutations were confirmed in other affected individuals in the respective families by digestion of polymerase chain reaction (PCR) products containing the mutated codons with restriction enzymes (Rs alpha I, CfoI, or AluI) for which cleavage sites had been generated by the specific genetic alteration. These PCR-restriction enzyme systems will be useful for genetic diagnosis in members of families carrying these mutations.

Base Sequence↗
PubMed1995

Pregnancy outcome among long-term survivors with acute leukemia.

By means of a mail questionnaire, we evaluated the influence of treatment for acute leukemia on offspring of long-term survivors and determined whether the outcome of pregnancy in patients (or spouses) induced relapse of acute leukemia. In 322 replies from the 445 institutions where a questionnaire was sent, there were 1136 adult long-term survivors. We analyzed the 43 adults who had become pregnant or become a father after postremission therapy. The mean age at the leukemia onset was 26.4 and 21.6 years for males and females. Forty-six normal children (26 boys and 20 girls) were born of long-term survivors including 7 pairs of siblings and a pair of twin sisters. There were no malformed babies. There were five abortions. The average duration until delivery was 79 months after diagnosis, and 49 months after the final postremission therapy. Four of 38 parents of live offspring died (3 relapse, 1 other disease), and the other 34 parents of live offspring were in complete remission at the point of this survey. The adverse effect of treatment on the offspring of long-term survivors could not be clarified in this survey. Additional lifetime follow-up of long-term survivors with acute leukemia and their offspring may be necessary.

Acute Disease↗
PubMed1995

Traumatic rupture of the extensor tendons at the musculotendinous junction.

Ten cases of closed extensor tendon rupture at the musculotendinous junction are reported. In five patients the rupture occurred at work, and in five during athletic activities. In each instance, indirect tendon injury resulted from a strong stretching force applied to a contracting muscle. In one case, rupture of the extensor pollicis longus tendon occurred proximal to the extensor retinaculum. In eight cases of complete tendon rupture direct repair was impossible. Of these eight patients, five were treated by side-to-side juncture and three by tendon transfer. Two patients with incomplete rupture were treated by splinting. All patients improved after treatment.

Adult↗
PubMed1995

The mechanism of cold-induced platelet aggregation in the presence of heparin.

Low temperature induces platelet aggregation, but this phenomenon is slight and poorly reproduced. However, heparin potentiated the reaction in a dose dependent manner. The degree of aggregation increased as the temperature at which the platelet-rich plasma was chilled was lowered, and as the time of chilling lengthened. Acetylsalicylic acid, a cyclooxygenase inhibitor, and staurosporin, an inhibitor of protein kinase C, partially inhibited cold-induced platelet aggregation (CIPA), suggesting that at least part of the reaction mechanism involves production of thromboxane A2 and activation of protein kinase C. Prostaglandin E1 (PGE1), which inhibits platelet responses through elevating platelet cyclic AMP, completely blocked CIPA, suggesting that PGE1 dependent pathway in platelets plays an important role for CIPA. The inhibition of CIPA by these inhibitors suggests that CIPA is aggregation with platelet activation but not platelet agglutination. Extracellular Ca2+ is essential for CIPA because ethylene glycol-bis (beta-aminoethylether) N, N, N', N'-tetraacetic acid (EGTA), extracellular Ca2+ chelating agent, completely inhibited CIPA. Monoclonal antibodies against glycoprotein (GP) IIb/IIIa (10E5, P2) and Ang-Gly-Asp-Ser-peptide (RGDS-peptide) which inhibit fibrinogen binding to GPIIb/IIIa completely blocked CIPA but monoclonal antibodies against GPIb (6D1, SZ2) partially. In addition, CIPA occurred only when fibrinogen was added to washed platelets suspension. These results indicate that CIPA is dependent on binding of fibrinogen to GPIIb/IIIa and GPIb is partly related with the reaction.

Amino Acid Sequence↗
PubMed1995

[Parathyroid crisis].

Parathyroid crisis is an unusual form of primary hyperparathyroidism characterized by life-threatening hypercalcemia. We encountered nine patients with primary hyperparathyroidism, who showed various clinical symptoms including psychoneurotic symptoms, as a result of marked hypercalcemia. The average age of the patients was 49 (29 to 77), with an even distribution between men and women. Marked hypercalcemia (16.1 +/- 2.0 mg/dl) was accompanied by high levels of parathyroid hormone. Physiological saline solution, furosemide and calcitonin were administered to the nine patients for ten to thirty-fore days, respectively, in order to correct hypercalcemia and dehydration, and then parathyroidectomy was performed. Postoperative courses were uneventful, and the psychoneurotic symptoms improved markedly. No renal or cardiac dysfunction was observed. Since surgery (parathyroidectomy) is effective for the present condition, it seems important to quickly relieve dehydration and to operate early rather than to offer prolonged treatment by medication.

Adult↗
PubMed1995

[Quantitative bleeding time].

Bleeding time, which reflects the interaction of the platelets with the damaged vessel wall and the subsequent formation of the primary hemostatic plug, has been widely used in the diagnosis of bleeding disorders, especially platelet abnormalities. We have developed a computerized method to measure the bleeding pattern and the amount of blood loss from the bleeding time incision (quantitative bleeding time). In 87 normal subjects (51 males and 36 females), the bleeding time was 389 +/- 137 sec and the amount of blood loss was 15.7 +/- 7.2 microliters (mean +/- S.D.). The bleeding pattern was classified into four types (I-IV). Type II showed the prolongation of the bleeding time, continuous constant bleeding, and considerably large amount of blood loss from the incision. This type which includes severe von Willebrand disease and serious thrombocytopenia is related to the severe bleeding tendency. Type III exhibited the prolongation of the bleeding time keeping a trace of blood loss from the incision. In type III patients, the bleeding tendency was generally mild despite the prolonged bleeding time as in patients with moderate thrombocytopenia or aspirin ingestion. Measurement of bleeding pattern and blood loss will provide a useful information to evaluate the defect of primary hemostasis.

Adolescent↗
PubMed1995

[Familial occurrence of thyroid tumors].

In 1986, familial medullary thyroid carcinoma (FMTC) was recognized clinically as a distinct entity, clearly distinguished from multiple endocrine neoplasia (MEN), being characterized by the development of MTC in the absence of any additional neoplasms. Ret proto-oncogene was first identified in 1985 using transformation assay. The gene was mapped to the chromosome 10, similar to MEN and FMTC, and was expressed at high levels in MTC. In 1993, ret mutations were identified in patients with MEN2A and FMTC, and many other mutations has been clarified up to today. What is the normal function of RET and how ret mutations lead to tumor formation in MEN and FMTC are focus of intensive studies at present.

Chromosomes, Human, Pair 10↗
PubMed1995

[Response-oriented salvage chemotherapy with mitoxantrone, etoposide and enocitabine for previously treated acute myeloid leukemia. Tohoku Leukemia Study Group].

Twenty-two patients with previously treated acute myeloid leukemia (AML) received salvage chemotherapy with mitoxantrone, 5 mg/m2/d on days 1 to 3, etoposide, 70 mg/m2/d on days 1 to 5, and enocitabine, 170 mg/m2/d on days 1 to 7 (BHAC-ME). Additional mitoxantrone, etoposide (both for up to 2 days) and enocitabine (for up to 7 days) were given if the bone marrow obtained on day 8 was not severely hypoplastic. Mitoxantrone and etoposide had been previously administered in 14 and 15 patients, respectively. Seven patients had primary resistance; 14 patients had first relapse (4 early and 10 late): and 2 patients had second relapse. Overall, seven patients (31%) achieved a complete remission; 7/14 with first relapse, and 0/8 with primary resistance or second relapse. Four patients, 3 with primary resistance and 1 with first relapse, died of infectious complication in aplasia. First relapse patients who had been previously treated both with mitoxantrone and etoposide, had a lower CR rate than the other first relapse patients [2/8 (25%) vs 5/6 (86%)], although patient characteristics such as duration of first CR, initial karyotype, and performance status, were similar between the two groups. We conclude that response-oriented BHAC-ME regimen is still active in first relapse AML patients unless they have received both mitoxantrone and etoposide previously.

Acute Disease↗