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Biomedical subjects

K Tsuji

Publications and source records attributed to K Tsuji.

At least 325 records · Page 18Linked to original sources
PubMed1995

Residual beta-cell function and HLA-A24 in IDDM. Markers of glycemic control and subsequent development of diabetic retinopathy.

To identify risk factors for diabetic retinopathy in insulin-dependent diabetes mellitus (IDDM), we studied the relationships among residual beta-cell function, human leukocyte antigen (HLA), long-term glycemic control, and development of diabetic retinopathy in 128 IDDM patients. Residual beta-cell function was assessed by serum C-peptide immunoreactivity (CPR) response to a 100-g oral glucose load (delta CPR). The patients were stratified into three groups: those with delta CPR of < 0.033 nmol/l (group 1, n = 50), those with delta CPR of 0.033-0.1 nmol/l (group 2, n = 38), and those with delta CPR of > 0.1 nmol/l (group 3, n = 40). The cumulative incidence rate of background retinopathy was higher in the order of groups 1, 2, and 3 (P = 0.032). Group 1 progressed to preproliferative retinopathy at an earlier stage than did groups 2 and 3 combined (P = 0.028). Further progression to proliferative retinopathy tended to be earlier in group 1 than in groups 2 and 3 combined (P = 0.083). The mean HbA1c value rose from 9.01 +/- 1.06% (mean +/- SD) in group 3 to 9.75 +/- 0.79% in group 2 to 10.48 +/- 1.12% in group 1 (P < 0.0001). In group 1, 89.6% of the patients had HLA-A24, whereas 50 and 43.6% of the patients had this antigen in groups 2 and 3 respectively (P < 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1995

Chimeric TLS/FUS-CHOP gene expression and the heterogeneity of its junction in human myxoid and round cell liposarcoma.

Myxoid liposarcomas have a unique and specific t(12;16)q13;p11) chromosomal translocation. The breakpoint has recently been identified and shown to involve the TLS/FUS gene on chromosome 16 and the CHOP gene on chromosome 12. This translocation causes fusion of these genes resulting in the expression of a novel chimeric TLS/FUS-CHOP message. Using the polymerase chain reaction with primer sets derived from sequences of TLS/FUS and CHOP cDNAs, we could amplify three types of the fusion transcripts from seven of seven samples of myxoid and round cell liposarcomas. In six of the seven positive samples, two kinds of chimeric messenger RNAs were found that have been reported previously. However, the last sample had a novel chimeric message that had an extra sequence of 33 bp derived from the TLS/FUS gene. Thus, it was shown that these fusion transcripts had a varying extent of the sequence of TLS/FUS gene incorporated at the site of the fusion. However, the TLS/FUS-CHOP fusion transcripts were not detected in two pleomorphic liposarcomas or in three myxoid variants of malignant fibrous histiocytomas. Our findings indicate that in liposarcomas TLS/FUS-CHOP fusion transcripts have variations at the junction of chimeric messages, which was the case for Ewing's sarcoma. Detection of the chimeric message by reverse transcription polymerase chain reaction was also suggested to be a useful approach for the diagnosis of myxoid and round cell liposarcomas that have (12;16) translocation, and for distinguishing them from pleomorphic liposarcoma and myxoid variant of malignant fibrous histiocytomas.

Adult↗
PubMed1995

[Acute promyelocytic leukemia following ulcerative colitis].

We report a case of acute promyelocytic leukemia (APL) following ulcerative colitis (UC). A 23-year-old man was diagnosed as UC in January 1991 and had been treated with salazosulfapyridine and prednisolone with good effect. In September 1993, he developed bleeding tendency and a diagnosis of APL with disseminated intravascular coagulation was made based on the results of bone marrow aspiration and coagulation profile. Complete remission was achieved with All-trans retinoic acid together with combined chemotherapy. He died of sepsis during consolidation chemotherapy in December 1993. Autopsy revealed no recurrence of UC.

Adult↗
PubMed1995

[A new modality of locoregional chemotherapy based on biochemical double modulation of 5-fluorouracil with both leucovorin and cisplatin against liver metastases of colorectal cancer].

A new modality of locoregional chemotherapy based on biochemical double modulation of 5-fluorouracil (FU) with both leucovorin (LV) and cisplatin (CDDP) against liver metastases of colorectal cancer was devised. The schedule for the locoregional therapy was as follows; bolus infusion of LV (6 mg/body) followed by 30-minute infusion of CDDP (10 mg/body) and 30-minute infusion of 5-FU (250 mg/body). Four colorectal cancer patients with numerous metastases to both lobes of liver were given intraarterial administration of above anticancer drugs every 1-2 weeks after resection of primary lesions. On the one hand, 3 colorectal cancer patients, who developed a few metastases to both lobes of liver, were treated preventively by the same schedule every 2-3 weeks after the resection of metastatic tumors. As for the clinical (radiographic) response, complete response and partial response were observed in 1 and 2 of 4 patients, respectively. The response rate was 75%. No new lesions appeared for over 1 year by the preventive treatment in 2 of 3 patients, whereas new lesions appeared in one patient at 3 months after discontinuation of treatment because of mild toxicity. The toxicity, however, was within acceptable limits. These results indicated that biochemical double modulation of 5-FU with both LV and CDDP is a very promising locoregional chemotherapy against liver metastases of colorectal cancer.

Aged↗
PubMed1995

[Fontan-type procedure for an adult case of double-outlet right ventricle (S, D, L)].

The double-outlet right ventricle with L-malposition (DORV (S, D, L)) is one of the rare congenital heart diseases. Intracardiac rerouting with a internal conduit has been indicated in principle to it as the radical operation. DORV (S, D, L) is often combined with the pulmonic stenosis (PS), and Rastelli's operation is indicated to the case in which release of PS is difficult. We report a case of DORV (S, D, L) combined with PS and the hypoplastic right ventricle which is treated by the Fontan-type procedure. The patient was a 35-year-old female who had undergone Glenn's operation at 10 years of age under the diagnosis of transposition of the great arteries. Recently she complained of aggravation of the cyanosis and dyspnea on exertion. After thorough examinations, the disease was diagnosed as DORV (S, D, L) with doubly committed VSD which was combined with severe PS, hypoplastic right ventricle (29% of normal) and left-sided juxtaposition of atrial appendages. The development of her distal pulmonary arteries was estimated well enough (PA-index 448 mm2/m2). We judged that intracardiac rerouting with an internal conduit could not be applied due to her severe pulmonic stenosis, and that Rastelli's operation as the biventricular repair was also impossible because of her hypoplastic right ventricle. Thus we adopted the Fontan-type procedure with a new septation in the right atrium, namely oblique partition, and attained a good result. To our knowledge, this case is the fourth case report in Japan of DORV (S, D, L) treated with the Fontan-type procedure.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Exon redefinition by a point mutation within exon 5 of the glucose-6-phosphatase gene is the major cause of glycogen storage disease type 1a in Japan.

Glycogen storage disease (GSD) type 1a (von Gierke disease) is an autosomal recessive disorder caused by a deficiency in microsomal glucose-6-phosphatase (G6Pase). We have identified a novel mutation in the G6Pase gene of a individual with GSD type 1a. The cDNA from the patient's liver revealed a 91-nt deletion in exon 5. The genomic DNA from the patient's white blood cells revealed no deletion or mutation at the splicing junction of intron 4 and exon 5. The 3' splicing occurred 91 bp from the 5' site of exon 5 (at position 732 in the coding region), causing a substitution of a single nucleotide (G to T) at position 727 in the coding region. Further confirmation of the missplicing was obtained by transient expression of allelic minigene constructs into animal cells. Another eight unrelated families of nine Japanese patients were all found to have this mutation. This mutation is a new type of splicing mutation in the G6Pase gene, and 91% of patients and carriers suffering from GSD1a in Japan are detectable with this splicing mutation.

Adult↗
PubMed1995

[Usefulness of the DNA-HLA class II typing in corneal transplantation].

DNA-HLA (human leukocyte antigen) typing was performed for ocular tissues in order to determine the usefulness of the method in corneal transplantation. Each type of ocular tissue was dissected from eye bank eyes (n = 3). DNA was extracted, and HLA-DRB1, DQB1, and DPB1 genes were amplified using PCR (polymerase chain reaction) method. DNA can be extracted and amplified from each ocular tissue except for the crystalline lens, but DNA from iris and choroid can be amplified only after diluting the samples 10 to 100 times. HLA class II antigens were successfully determined in these ocular tissues by the RFLP (restriction fragment length polymorphism) method. The method was applied to the corneal tissues of donor and recipient used for the corneal transplantation (n = 7). HLA class II antigens can be determined in both the donor and recipient corneal samples, and the results of recipients' HLA typing were the same as those determined using the blood samples. These results indicate that the DNA-HLA typing can be used for ocular tissues. Since DNA-HLA typing is more accurate than the conventional serological typing, the method is promising for the study of HLA class II typing in corneal transplantation.

Aged↗
PubMed1995

[A surgical repair of partial anomalous pulmonary venous drainage to the high superior vena cava].

A 7-year-old boy with partial anomalous pulmonary venous drainage to the high superior vena cava (SVC) underwent surgical repair by Williams procedure. Right upper pulmonary vein was drained to the left atrium via the SVC and the surgically enlarged sinus venosus type ASD. SVC was ligated and divided. SVC was then anastomosed to RA appendage pedicle directly. Autologous pericardium was patched anteriorly to create a new SVC pathway. The postoperative course was uneventful without arrhythmia and cardiac catheterization 1 month postoperation revealed no stenosis of the SVC and right upper pulmonary venous return.

Anastomosis, Surgical↗
PubMed1995

[Myelofibrosis complicated by T-cell lymphoma followed by leukemic transformation].

A 37-year-old man was admitted because of pancytopenia with leukoerythroblastosis and anisocytosis in January 1986. Bone marrow aspiration resulted in a dry tap and biopsy showed marked myelofibrosis. Three months after admission, generalized lymph node swelling and multiple skin tumors were recognized. A biopsied lymph node revealed lymphoblastic lymphoma. The surface markers of lymphoma cells showed an immature T-cell phenotype, whereas T-cell receptor beta and gamma chain genes showed germ line configuration. The patient was treated with combination chemotherapy in June 1986. A month later, he developed leukemic transformation with features of acute myelocytic leukemia and he died of pneumonia. Autopsy disclosed extramedullary hematopoiesis in the liver and spleen. Primary myelofibrosis complicated by T-cell lymphoma is extremely rare.

Adult↗
PubMed1994

Sodium dodecyl sulfate polyacrylamide gel- and replaceable polymer-filled capillary electrophoresis for molecular mass determination of proteins of pharmaceutical interest.

Performance of commercially available replaceable SDS polymer-filled capillary electrophoresis (rPGCE) systems were evaluated for the determination of the molecular mass of proteins of pharmaceutical interest. The mass values obtained by these systems were compared with those obtained by SDS-PAGE and high-performance size exclusion chromatographic (HPSEC). The molecular masses of proteins determined by rPGCE were not significantly different and agreed closely with those obtained by SDS-PAGE and with the theoretical values of the proteins. HPSEC gave the least reliable data. Performance of the SDS crosslinked polyacrylamide gel-filled capillary electrophoresis system was superior to that of the commercially available rPGCE systems. Nevertheless, the rPGCE systems present significant advantages over the conventional SDS-PAGE and HPSEC methods for rapid analysis and improved precision for the determination of the molecular masses of proteins of pharmaceutical interest.

Electrophoresis, Polyacrylamide Gel↗
PubMed1994

Rapid decrease in ATP content without recovery phase during glutamate-induced cell death in cultured spinal neurons.

Glutamate neurotoxicity in the cultured neurons from rat spinal cord was evaluated on the basis of endogenous ATP content in the cells. A short exposure of the neurons to glutamate induced an immediate and rapid decrease in ATP content. Then, after removal of glutamate, no recovery of ATP content was observed for 24 h, eventually resulting in neuronal death. These findings suggest that the glutamate-induced neuronal death in vitro is apparently similar to but essentially different from so-called 'delayed' neuronal death in vivo after a brief ischemia in hippocampal CA1 neurons in which a transient recovery of ATP level occurs after its dramatic reduction.

Adenosine Triphosphate↗
PubMed1994

HLA-DR4 antigen and lymph node metastases in poorly differentiated adenocarcinoma of the stomach.

BACKGROUND: The authors investigated whether HLA antigens could act as a predictor of the risk of lymph node metastasis in patients with gastric cancer. METHODS: The microcytotoxicity assay was used to examine 51 HLA antigens of the A, B, C, DR, and DQ loci in 573 patients who underwent resection of gastric cancer. The incidence of HLA antigens in patients with or without lymph node metastasis was analyzed using the chi-square method. RESULTS: The incidence of patients with HLA-DR4 antigen with or without lymph node metastasis was 45.9% and 34.8%, respectively (P = 0.0098, corrected P = 0.49). The relative risk of lymph node metastasis in patients with HLA-DR4 was 1.6. In poorly differentiated adenocarcinoma, the incidence of HLA-DR4 antigen in patients with lymph node metastasis was significantly higher (47.5%) than in patients without lymph node metastasis (18.5%), if corrected P values were tested (P = 0.0007, corrected P = 0.0387). The relative risk of lymph node metastasis in patients with poorly differentiated adenocarcinoma with DR4 was 4.0. CONCLUSIONS: The data suggest an association between the presence of HLA-DR4 and an increased risk of lymph node metastasis, especially in poorly differentiated adenocarcinoma.

Adenocarcinoma↗
PubMed1994

Adenosine enhances intracellular Ca2+ mobilization in conjunction with metabotropic glutamate receptor activation by t-ACPD in cultured hippocampal astrocytes.

2Cl-Adenosine, a non-metabolized adenosine agonist, enhanced the increase in intracellular Ca2+ concentration ([Ca2+]i) in cultured hippocampal astrocytes induced by (+-)-1-aminocyclopentane-trans-1,3-dicarboxylic acid (t-ACPD), a metabotropic glutamate agonist. In the absence of 2Cl-adenosine, the half effective concentration (EC50) of t-ACPD was about 80 microM. On the other hand, in the presence of 1 microM 2Cl-adenosine, the EC50 of t-ACPD shifted to about 5 microM, although the maximum [Ca2+]i did not change. The synergistic effect of 2Cl-adenosine with t-ACPD on [Ca2+]i elevation was not inhibited by the elimination of extracellular Ca2+, but was inhibited by A1-specific adenosine antagonists. These results indicate that adenosine can act via the A1 receptor as an endogenous co-activator of the metabolic processes induced by metabotropic glutamate receptor activation.

Adenosine↗
PubMed1994

The study of tumor necrosis factor beta gene polymorphism in lung cancer patients.

BACKGROUND: In recent years numerous reports have discussed the relationship between the human leukocyte antigen and lung cancer. However, the genetic background of lung cancer has not yet been precisely clarified. METHODS: To investigate the genetic background of lung cancer, the human leukocyte antigens in 159 normal healthy control subjects and 102 lung cancer patients were studied, and restriction fragment length polymorphism analysis of the tumor necrosis factor (TNF) beta gene in 165 normal healthy control subjects and 135 lung cancer patients was performed. RESULTS: Lung cancer patients showed a high frequency of human leukocyte antigen B61; however, no statistical difference was found. In the lung cancer patients, the TNF beta 10.5/10.5-kb allele was found at a low frequency, 38.5%, compared to 53.3% in normal controls (chi 2 = 7.51, P = 0.011, corrected P = 0.033, relative risk = 0.77). In the relationship between the histologic types and the TNF beta gene, the TNF beta 10.5/10.5-kb allele showed low frequencies: 38.5% in adenocarcinoma, 38.2% in squamous cell carcinoma, and 27.8% in small cell carcinoma, although no statistical difference was shown. In relation to the postoperative survival period, the TNF beta 10.5/10.5-kb allele was associated with prolonged survival. CONCLUSIONS: The TNF beta 10.5/10.5-kb allele may be associated with resistance to lung cancer and with a better prognosis.

Adenocarcinoma↗
PubMed1994

Craniosynostosis and hemizygosity for D7S135 caused by a de novo and apparently balanced t(6;7) translocation.

Craniosynostosis (CRS) is frequently seen in the del(7p) syndrome, and the gene for this cranial anomaly (CRS1) has been assigned to 7p21. We present a 3-year-old boy with CRS involving the sagittal and coronal sutures, who had a de novo and apparently balanced translocation, t(6;7)(q16.2;p15.3). Southern blot analysis of several loci on 7p14-->pter showed that the patient was heterozygous for HOX1I and IL6, possibly homozygous for D7S149, but hemizygous for D7S135 with a loss of the paternal allele. These findings suggest the localization of a candidate gene for CRS1 to be on 7p15.3 in the close proximity to the D7S135 locus.

Blotting, Southern↗
PubMed1994

Recovery from ultraviolet-induced growth arrest of primary rat hepatocytes by p53 antisense oligonucleotide treatment.

Recent evidence suggests that wild-type p53 prevents cell-cycle progression after DNA damage, which may provide a sufficient period for the cells to repair the genetic lesions that may otherwise lead to cell death or cellular transformation. We tested whether this hypothesis is generally applicable to parenchymal cells of internal organs. When primary neonatal rat hepatocytes were exposed to a nonlethal dose of ultraviolet light, actinomycin D, or mitomycin C, most cells expressed abundant p53 with an abnormally extended half life in their nuclei, and their growth was arrested despite treatment with growth factors (epidermal growth factor and insulin). When DNA-damaged cells were treated with p53-antisense oligonucleotides, p53 expression was significantly suppressed, and an appreciable fraction of the cells entered S phase. However, when damaged cells were administered p53-sense or retinoblastoma susceptibility gene-antisense oligonucleotides, there was no recovery from growth arrest. The data strongly suggest that p53 is a component of at least one signal transduction pathway leading to growth arrest in DNA-damaged cells.

Animals↗