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Biomedical subjects

T Yamazaki

Publications and source records attributed to T Yamazaki.

At least 415 records · Page 23Linked to original sources
PubMed1996

Heliquinomycin, a new inhibitor of DNA helicase, produced by Streptomyces sp. MJ929-SF2 I. Taxonomy, production, isolation, physico-chemical properties and biological activities.

Heliquinomycin was isolated as a part of a program designed to find inhibitors of DNA helicase from microbial sources. It was purified from the culture broth of Streptomyces sp. MJ929-SF2 by solvent extraction and serial chromatographies of centrifugal partition chromatography, Sephadex LH-20 and Capcell Pak C18 (HPLC). The isolated red powder was analyzed to have the molecular formula of C33H30O17. It inhibited partially purified DNA helicase from HeLa cell in a non-competitive manner with the inhibition constant (Ki) of 6.8 mM. Heliquinomycin exhibited biological activity against microorganisms including MRSA, and cultured cell lines.

Animals↗
PubMed1996

[Comparative study of mRNA expression of E-cadherin and collagenase IV in early and advanced cancers].

During the process of invasion, tumor cells must detach from the primary neoplasm and degrade host stroma. E-cadherin is responsible for the cell-cell adhesion and collagenase IV is the one of the matrix metalloproteinases. We determined whether the levels of mRNA for E-cadherin and collagenase IV were differently expressed within 12 cases of early and 13 cases of advanced gastric cancers using a rapid calorimetric in situ hybridization assay for mRNA. In 6 of 12 early cancers, we found a decreased expression of E-cadherin mRNA in the invasion edge compared to the main tumor. In advanced gastric cancers, 3 out of 13 cancers also exhibited this finding. Higher expression of the collagenase IV at the invasion edge of the tumor compared to the main tumor was observed in half of the early and advanced gastric cancer cases. Inverse expression levels of E-cadherin and collagenase IV mRNA were observed in 6 of 12 early cancers. However, only one of 13 advanced cancer cases expressed the same finding.

Adenocarcinoma↗
PubMed1996

[Mobile right atrial thrombus: a case report of surgical removal].

A 71-year-old man was admitted due to brain infarction. An abnormal floating mass was found in the right atrium by echocardiography. The mass was assumed to be a thrombus. The patient was failed to be in danger of pulmonary embolism, so it was decided to remove surgically. The thrombus was removed under cardiopulmonary bypass including the atrial wall where it was attached, because it was difficult to rule out the possibility of cardiac tumor macroscopically. The tumor showed pathological findings of thrombus. Postoperative course was uneventful.

Aged↗
PubMed1996

[Diagnosis of superficial-type early carcinoma of the gallbladder by endoscopic ultrasonography--comparison with ultrasonography].

The detectability of superficial-type carcinoma of the gallbladder by ultrasonography (US) and endoscopic ultrasonography (EUS) were investigated. Eight patients with such carcinoma of the gallbladder were reviewed. They had undergone both US and EUS previous to surgery. The tumor was detected in 3 patients by US, 2 patients with IIa + IIb-type carcinoma and 1 patient with IIa-type carcinoma. Those lesions were visualized as localized thickening of the gallbladder wall or as broad-based tumor. In 2 patients, lesions were not initially detected by US, but were shown by US after the examination by EUS. The tumor was detected by EUS also in 1 case of IIb + IIa-type carcinoma besides those 3 patients mentioned above. All four of these lesions were visualized as broad-based tumor by EUS. It was difficult to detect pure IIb-type or small IIa-type carcinoma even by EUS. In patients with concomitant acute cholecystitis or gallbladder stone, it was difficult to evaluate the abnormal findings of the gallbladder wall.

Aged↗
PubMed1996

A novel nonsense mutation associated with an exon skipping in a patient with hereditary protein S deficiency type I.

The genetic defect in a patient with hereditary type I protein S (PS) deficiency was investigated. All the exons and intron-exon junctions of the patient's PS gene were amplified by PCR and subjected to heteroduplex screening. Only the PCR product of exon 4 revealed heteroduplex bands. A novel nonsense mutation, Ser62 (TCA) to Stop (TGA) was found in exon 4. RT-PCR detected the aberrant mRNA in the patient's platelets, which was markedly reduced in amount and lacked the region of exon 4, suggesting that the nonsense mutation affected the mutated mRNA metabolism and induced exon skipping. The skipping of exon 4 causes an in-frame deletion of 29 amino acids which just construct the thrombin-sensitive region of the PS molecule. The loss of such an important domain as well as the quantitative decrease in the mutated mRNA appear to be responsible for the type I PS deficiency in this patient.

Exons↗
PubMed1996

[Detection of rifampicin-resistant strains of Mycobacterium tuberculosis by a non-radioactive PCR-SSCP method].

PCR-SSCP method to detect genetic mutations in rpoB gene as a marker of rifampicin-resistance was developed by Telenti et al., and we have modified it applying non-radioactive PhastSystem for more practical use in the detection of rifampicin-resistance of Mycobacterium tuberculosis. PCR products amplified with the primers specific to rpoB gene using extracted DNA from 89 strains of M. tuberculosis were sequenced and the amino acid sequences were morphism was determined by the PhastSystem. The bands were stained by silver staining. Among 89 strains of M. tuberculosis, 43 were confirmed as rifampicin-resistant (RFPr) and 46 were rifampicin-sensitive (RFPs) by the culture on the drug-containing media. All of the 43 RFPr strains had one or more mutations in the DNA sequence of rpoB gene, while none of the RFPs strains had such mutations. However, by PCR-SSCP, only 20 out of 43 RFPr strains showed clear differences in the band pattern of electrophoresis from that of RFPs strains. Other 23 RFPr strains had only slight differences in the band pattern of the PCR-SSCP from that of RFPs strains. But it was noticed that the main bands of RFPr strains were distinguishable from the main bands of RFPs strains even their patterns were similar. Thus, it is possible to apply a non-radioactive PCR-SSCP for the detection of rifampicin resistance of M. tuberculosis with further improvement of the condition of gel electrophoresis or staining techniques.

Amino Acid Sequence↗
PubMed1996

Effects of heat shock and teprenone on ethanol-induced damage to cultured rabbit gastric mucosal cells.

We examined whether or not heat shock and teprenone (a gastric mucosal protective drug), through the induction of heat shock proteins (HSPs), protect cultured rabbit gastric mucosal cells from ethanol-induced damage. Cell viability was assessed by mitochondrial function and membrane permeability assays. Exposure of mucosal cells to 5% ethanol for 1h caused an about 50% reduction in viability. When the cells had been heated at 43 degrees C for 1 h, the cell damage caused by ethanol was significantly prevented. However, pretreatment with teprenone at 1-100 microM failed to prevent the ethanol-induced damage. Western blot analysis with an anti-HSP-72 antibody showed that HSP-72 was apparently induced by heat treatment, but not by teprenone. Both the cytoprotection and induction of HSP-72 on heat treatment were potently inhibited by cycloheximide and actinomycin D. These results demonstrate that, in rabbit gastric mucosal cells, the induction of HSPs is strongly associated with cytoprotection against ethanol-induced damage, but that teprenone has no effect on the cytoprotection or HSP induction.

Animals↗
PubMed1996

[A clinico-pathological study of early gallbladder carcinoma].

We performed a clinico-pathological study on cases with early gallbladder carcinoma to elucidate its morphological characteristics. Thirty cases (33 lesions) were included, invasion was confined to the mucosa in 24 of these cases and involvement of both the mucosa and muscularis propria was seen in 6 cases. The results are as follows: 1) In all cases with I p-type cancer, the depth of invasion was limited to the mucosa. 2) In I s cases in which the tumor had a broad base, 10mm in size or less, the depth of invasion was up to the muscularis propria. 3) In cases with II a-type carcinoma in which the base was less than 15mm in size, no involvement of the subserosa was observed. In conclusion, it is suggested that with lesions diagnosed by imaging modalities as I p-type cancers, broad-based tumors with a base of 10mm or less, or II a-like lesions with a base less than 15mm, there is a high probability that the depth of invasion is limited to the mucosa or up to the muscularis propria.

Adult↗
PubMed1996

[Two cases of pneumonia caused by Sho-saiko-to].

We describe two cases of pneumonia caused by Sho-saiko-to. Patient 1 was a 61-year-old man with type-C liver cirrhosis. About 50 days after starting to take Sho-saiko-to, he complained of fever and diarrhea, and progressive dyspnea developed. Analysis of arterial blood obtained in the emergency room showed severe hypoxemia:, PaO2 26 Torr. A chest radiograph and a CT scan showed bilateral diffuse fine granular and ground-glass opacities predominantly in the upper lung fields. Despite repeated pulse therapy with methylprednisolone and aggressive medical treatment including mechanical ventilation, the patient remained in respiratory distress, which was later complicated by gastrointestinal bleeding. He died on the 45th hospital day. The bronchoalveolar lavage contained abnormally high fluid percents of lymphocytes and neutrophils. Postmortem examination of the lungs revealed alveolar septal thickening, marked hyperplasia of type 2 pneumocytes, and no hyaline membrane formation. Patient 2 was a 68-year-old man. Eighty days after he began taking Sho-saiko-to, he presented with a 4-day history of shortness of breath accompanied by fewer and progressive coughing. On arrival of the hospital, arterial blood gas analysis showed mild hypoxemia (PaO2, 61 Torr) and a chest radiograph revealed bilateral irregular infiltrates in the lower lung fields. Analysis of bronchoalveolar lavage fluid showed an abnormally high percent of lymphocytes (especially CD8 + lymphocytes), and examination of a biopsy specimen revealed exudates of fibrin and neutrophils in the alveolar spaces and patechy intraluminal organization. The response to prednisolone was good and he was discharged on the 40th hospital day in stable condition. Drug lymphocyte stimulation tests of peripheral blood to Sho-saiko-to were positive in both patients. Patients 2 was though to have a typical case of Sho-saiko-to-induced pneumonia, patient 1 was thought to have fulminating variant of this disease.

Aged↗
PubMed1996

A point mutation in glycoprotein IX coding sequence (Cys73 (TGT) to Tyr(TAT)) causes impaired surface expression of GPIb/IX/V complex in two families with Bernard-Soulier syndrome.

Bernard-Soulier syndrome (BSS) is a rare inherited bleeding disorder which is caused by abnormal expression or function of the glycoprotein (GP) Ib/IX/V complex, a platelet major receptor for von Willebrand factor. We studied four BSS patients in two unrelated families in which the same and novel mutation was found. Flow cytometric analysis showed that GPIX was completely absent but residual amounts of GPIb alpha and GPV were detectable in these patients. We analyzed all coding regions of GPIb alpha, GPIb beta, GPV and GPIX which were amplified from the patients' genomic DNA by the polymerase chain reaction (PCR). In all four cases, we identified a point mutation in the GPIX coding region that changes the codon for cysteine 73 (TGT) to a codon for tyrosine (TAT). Furthermore, we confirmed by a transient expression study that the mutation caused the loss of adequate surface expression of GPIX. Since cysteine might be important for the secondary structure, this mutation of GPIX gene would lead to a dramatic conformational change of GPIX protein, resulting in the reduced surface expression. We concluded that this novel point mutation of the GPIX gene was responsible for BSS in these families.

Adult↗
PubMed1996

Clinical analysis of malignant lymphomas of tonsils.

Data of 38 patients with primary tonsil lymphoma, treated during the past 14 years was analysed. All cases were non-Hodgkin lymphomas. There were 11 patients with Stage 1, 14 with Stage II, 8 with Stage III, and 4 with Stage IV tonsillar lymphomas. The applied chemotherapies were CHOP or MACOP-B regimen. The overall 5-year survival rate was 64.4%. Further analysis of the intermediate grade group showed that 5-year survival rates were 72.7%) for patients younger than 60 years old, in contrast to 35.0% for patients aged 60 or older (p 0.0049). Five-year survival rates were 100%) for Stage I, 32.4% for Stage II, 55.6% for Stage III, and 100%) for Stage IV patients (p = 0.0878). In patients with Stage II tonsillar lymphomas, 5-year survival rates were below 100% for CHOP regimen, 100% for MACOP-B regimen, 66.7% for radiation alone, and 0% for radiation followed by chemotherapy (p = 0.1966). In patients with Stage III tonsillar lymphomas, 5-year survival rates were below 100% for MACOP-B regimen, and 0% for initial radiation followed by chemotherapy (p = 0.2568). The factors influencing survival were age, stage, and treatment modality. For Stage I patients without bulky mass, radiation therapy is sufficient. For Stage II patients or Stage I patients with a bulky mass, CHOP regimen (followed by radiation) is the choice of treatment. For Stage III or IV patients,, MACOP-B regimen is promising.

Combined Modality Therapy↗