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Biomedical subjects

M Terada

Publications and source records attributed to M Terada.

At least 235 records · Page 13Linked to original sources
PubMed1996

Tolrestat improves nerve regeneration after crush injury in streptozocin-induced diabetic rats.

To delineate the ability of diabetic nerves to regenerate and to determine the effect of aldose reductase (AR) inhibitors (ARIs) on nerve regeneration in diabetic neuropathy, we evaluated nerve regeneration electrophysiologically and morphologically after sciatic nerve crush injury in three groups of male Sprague-Dawley rats: untreated diabetic (streptozocin [STZ]-induced, n = 16), tolrestat-treated diabetic (n = 16), and age-matched controls (n = 16). Compound muscle action potentials (CMAPs) appeared 4 weeks after crush injury in the control group and 5 weeks after injury in both diabetic groups. Motor nerve conduction velocity (MNCV) in the crushed nerves was decreased in both diabetic groups compared with the control group throughout the experiment. However, this decrease was significantly prevented at 24 weeks with tolrestat treatment. Morphologically, the density of myelinated nerve fibers (MNFs) and the number of MNFs per fascicle were significantly decreased in untreated diabetic rats, but tolrestat significantly prevented the former decrease at 5 weeks and the latter at 24 weeks. The mean diameter of large MNFs (>4 microm) was smaller in the untreated diabetic group than in the control group, but this decrease also was significantly prevented with tolrestat treatment. These results suggest that nerve regeneration is impaired in diabetic neuropathy and that tolrestat can prevent this impairment.

Animals↗
PubMed1996

Determination of ester-type local anesthetic drugs (procaine, tetracaine, and T-caine) in human serum by wide-bore capillary gas chromatography with nitrogen-phosphorus detection.

A sensitive method for simultaneous determination of ester-type local anesthetic drugs (procaine, tetracaine, and T-caine) has been developed using wide-bore capillary gas chromatography with nitrogen-phosphorus detection (GC-NPD). The extraction procedure, the experimental conditions for heptafluorobutyryl (HFB) derivative formation, and the percentage of the ester-type local anesthetic drugs from the human serum are described. The HFB derivatives of ester-type local anesthetic drugs showed sensitivity of approximately 2-3 fold higher than that without derivatization. The detection limits of HFB derivatives of the ester-type local anesthetic drugs were approximately 60-70 pg on column. Recoveries from the human serum were 85-94%. This method could be used to determine concentrations as low as 24-28 ng/mliters of the ester-type local anesthetic drugs.

4-Aminobenzoic Acid↗
PubMed1996

Quantification of the CD55 and CD59, membrane inhibitors of complement on HIV-1 particles as a function of complement-mediated virolysis.

Previous studies have demonstrated that the murine monoclonal antibody (MoAb) NM-01 activates the human complement classical pathway resulting in lysis of human immunodeficiency virus (HIV). The present study was performed to determine the availability of the V3-loop of gp120 relative to the complement regulatory proteins, CD55 (DAF) and CD59 (HRF20) molecules on HIV. The results demonstrate that CD55 and CD59 exist on HIV virions, along with gp120 molecules. These findings suggest that activation of human complement on free viral particles is induced by MoAb NM-01 and that this occurs regardless of the presence of CD55 and CD59 molecules. The destruction of viral particles was demonstrated by a decrease in infectivity. The involvement of human complement in this process was confirmed with an immunoelectron microscopy technique by the presence of a human C9 to prove membrane attack complex (MAC). The results indicate that NM-01 can induce complement activation because of the ratios of CD55 and CD59 to gp120 molecules on HIV virions. The availability of the gp120 V3 domain on the virion is sufficient for binding of NM-01 and thereby the formation of MAC that results in virolysis.

Antibodies, Monoclonal↗
PubMed1996

[A statistical investigation of the influence of allergic factors on intractable asthma by multiple logistic regression].

The relationships of the development of intractability in bronchial asthma with 17 factors, namely 1) sex, 2) age, 3) age of onset, 4) period from onset, 5) severity of asthma, 6) type of asthma, 7) family history of asthma within the third degree of consanguinity, 8) history of smoking, 9) past history of atopic dermatitis, 10) past history of allergic rhinitis, 11) past history of chronic sinusitis, 12) past history of nasal polyp, 13) necessity of oral beta-adrenergic agonists, 14) necessity of inhaled beta-adrenergic agonists, 15) necessity of oral xanthine agents, 16) necessity of inhaled anticholinergic agents and 17) necessity of inhaled corticosteroids, were analyzed by multiple logistic regression in 160 asthmatic patients. Evaluation of each factor according to the relative risk indicated that asthmatic patients tended to become intractable with the following categories (relative risk--reference category): more than 40 years old (5.2 in the fifth and sixth decades, 4.4 in the seventh and eighth decades--the third and fourth decades); the fifth decade or later onset (7.3--the first decade); non-atopic type (2.1--atopic type); positive family history of asthma (2.8--negative one); an ex- and current smoker (3.1--no smoker); negative past histories of atopic dermatitis and allergic rhinitis (4.1 in the former, 2.4 in the latter--positive one respectively); positive past histories of chronic sinusitis and nasal polyp (5.1 in the former, 6.6 in the latter--negative one respectively). Especially, relative risk in asthmatic patients with simultaneous positive past histories of chronic sinusitis and nasal polyp was about 16 times as high as in ones without both histories. This finding suggested these histories strongly participated in the development of intractability in bronchial asthma.

Adult↗
PubMed1996

[Continuous systemic venous oxygen saturation monitoring immediately after Fontan procedure].

Changes in cardiac output (CO), systemic venous oxygen saturation (SvO2), systemic oxygen consumption, and urinary output immediately after Fontan procedure were measured in 10 patients at the intensive unit (ICU) to assess the effects of aorusal from anesthesia, hypothermic management, and respiratory condition. The measurements were taken at the following phases; phase A in deep sedation under hypothermia (33-35 degrees C rectal temperature) and controlled ventilation; phase B in mild sedation under normothermia and controlled ventilation; phase C when awake under normothermia and assisted ventilation; phase D when awake under assisted ventilation; phase D when awake under normothermia immediately after extubation; and phase E 24 hours after extubation. Oxygen delivery (O2 Del.) and fractional oxygen fractions were calculated in each phase. Two patients whose SvO2 values were below 55% during the postoperative course needed reoperation for atrioventricular valve regurgitation in one case for PV stenosis in the other case. CO increased significantly (p < 0.05) after extubation (phase D), compared with that of controlled ventilation (phase B). Under hypothermia (phase A), urinary output was relatively higher with lower CO. There was a significant correlation between SvO2 and CO (R = 0.61) in phase A, however there was no correlation in phase E. Fractional oxygen extraction in phase A was significantly lower than in phase B. In conclusion, the continuous SvO2 measurements reflected real-time changes in cardiac output in the immediate post-Fontan patients. Induced hypothermia was beneficial in increasing urinary output presumably through the correction of maldistribution of cardiac output in post-Fontant patients. Arousal from anesthesia and spontaneous ventilation seemed advantageous for increasing cardiac output, hence, early extubation should be encouraged in the management of post-Fontan patients.

Blood Gas Monitoring, Transcutaneous↗
PubMed1996

[Spiral volumetric CT venography of the lower extremities: preliminary report].

Twelve cases, including varicose veins (7), deep venous thrombosis (3), A-V malformation (1) and skin ulcer (1), were examined by three-dimensional CT venography (3D CTV), and comparison was made with conventional ascending venography. In the "double phase method," the first phase scan (40 seconds) of the femoral region was performed in order to rule out deep venous thrombosis, and the second phase scan (30 seconds) of the lower leg was performed to visualize varicose veins. Veins of the thigh and popliteal space were relatively well visualized. It is thought that 3D-CTV is particularly useful for spatially evaluating deep venous thrombosis and varicose veins.

Arteriovenous Malformations↗
PubMed1996

[Atherosclerosis obliterance; thrombolytic therapy].

Thrombolytic therapy used to be considered ineffective for chronic arteriosclerotic obiterance. However, direct infusion of a thrombotic agent into the thrombus through a vascular catheter was shown to be more effective than expected. We have performed high-dose intra-thrombotic urokinase injection for arteriosclerotic obiterance of iliac and femoropopliteal arterial region since 1985. In this procedure, urokinase is infused at 10,000 unit/ minute through a catheter inserted into the thrombus. In the 65 lesions treated by this method, the initial success rate was 85%, and the cumulative 1-year patency rate was 72%. The mean total dose of urokinase was 620,000 units. Here we discussed thrombolytic therapy for chronic arteriosclerosis obliterance based on our experience.

Arteriosclerosis Obliterans↗
PubMed1996

Rapid and clear detection of ABO genotypes by simultaneous PCR-RFLP method.

We reported a new approach of ABO genotyping by a polymerase chain reaction and restriction fragment length polymorphism method. Instead of amplifying the loci containing the positions of nucleotides 258 and 700 of cDNA of the A transferase separately, we successfully amplified these 2 loci together in one reaction mixture using 2 sets of primers. The amplified DNA products were digested at the same time with restriction enzymes Kpn I and Alu I. The digested DNA products were then separated by electrophoresis on polyacrylamide gel. In addition, we evaluated the influence of various amplification parameters (concentration of template DNA, primers, Taq DNA polymerase, MgCl2, and number of cycles). In particular, high Mg2+ concentration (3.5 mM) made effective amplification of this locus without producing any unspecific band. By using that optimized condition for PCR, together with a simultaneous approach, our study proved to be time saving, more economic, and convenient in interpreting the results.

ABO Blood-Group System↗
PubMed1996

[Mutation frequency of the p16/CDKN2 gene and amplification of the cyclin E gene in human primary gastric carcinomas].

There are many observations of genetic alterations of genes when a cell enters into S phase from G1. Here we report that four (16%) of 25 primary esophageal carcinomas were found to be mutated in the p16/CDKN2 gene, and that no mutations were observed in 19 surgical specimens of gastric adenocarcinomas. No amplification of the Cyclin D1 gene in gastric carcinoma has been known, while amplification of the Cyclin E gene was observed in six (14%) of 42 surgical specimens of gastric carcinomas.

Animals↗
PubMed1996

[Genetic events during development of esophageal squamous cell carcinoma].

Various molecular genetic abnormalities have been reported in esophageal carcinoma. These include amplification of the chromosome 11q13 region containing cyclin D1, EXP1 and EMS1 genes, and the oncogenes, the epidermal growth factor receptor gene, EGFR/c-ERBB1, and c-myc. Loss of heterozygosity (LOH) at several chromosome loci and point mutation of the p53 and p16/CDKN2 tumor suppressor genes have also been described. Mutations of p53 gene and LOH at 3p and 9q loci were investigated in esophageal epithelial dysplasia. In contrast, amplification of cyclin D1, EGFR, c-myc and other genes was accumulated in advanced tumors with invasion. Cyclin D1 amplification is found more in metastatic lesions than in primary tumors.

Carcinoma, Squamous Cell↗
PubMed1996

[Recovery from descending necrotizing mediastinitis and multiple organic failure after seven months of mechanical ventilation].

A 61-year-old man with a history of hypertension and diabetes mellitus had a tooth extracted. Nine days later, he was admitted to the hospital with complaints of high fever, dyspnea, and anterior chest pain. Physical examination revealed a drowsy man with a fever of 38.2 degrees C, blood pressure of 66/44 mmHg, and marked redness and swelling from the neck to anterior part of the chest. Laboratory examination indicated severe infection and multiple organ failure, consisting of cardiac, respiratory, renal, and hepatic failure, with disseminated intravascular coagulation. Chest X-ray and CT-scan films showed abscesses extending from the neck to the mediastinum, and bilateral pleural effusion. Immediately, he was treated with catecholamines, furosemide, mechanical ventilation with a high concentration of oxygen, continuous drainage, repeated skin incisions, and broad-spectrum antibiotics. In addition, steroid pulse therapy was administered for persistent respiratory failure. On the 28th hospital day, a fistula developed between the trachea and the mediastinum, and an intratracheal tube had to be inserted through the fistula. On the 212 th hospital day, after intravenous hyperalimentation, continuous intravenous insulin infusion, and administration of broad-spectrum antibiotics, catecholamines, and furosemide, the patient was weaned from mechanical ventilation. A restrictive ventilatory defect due to ankylosis and atrophy of underused muscles was noted after weaning, but the PaO2 was high with a low dose of oxygen (1 to 2 l/min), and 21 months later, the blood gases were normal while the patient was breathing room air. As of January, 1996, he was undergoing rehabilitation to promote his recovery from ankylosis, muscle atrophy, and speech dysfunction.

Catecholamines↗
PubMed1996

Cyclin D1 amplification as a new predictive classification for squamous cell carcinoma of the esophagus, adding gene information.

The cyclin D1, referred to as PRAD-1, has been mapped to the 11q13 region, and its expression has been detected in squamous cell lines and several primary esophageal carcinomas. We assessed cyclin D1 amplification in 122 squamous cell carcinomas of the esophagus. Samples for DNA extraction were obtained from formalin-fixed paraffin-embedded specimens, and 10 microgram of each DNA sample were subjected to slot blot analysis. The presence of more than three gene copies was considered evidence of gene amplification. Amplification of cyclin D1 was detected in 28 (23%) of 122 cases of squamous cell carcinoma of the esophagus. There were no significant differences between the clinicopathological background factors in groups positive and negative for cyclin D1 amplification, but the survival rate of patients exhibiting amplification was significantly lower (P < 0.001). The groups were stratified according to the pN (pathological N category) factor and pT (pathological T category) factor in the TNM classification, and the cumulative survival rates in the amplification groups were always significantly lower. Amplification of cyclin D1 was correlated with distant organ metastasis after curative operations, but there was no significant difference in lymph node recurrence rates of patients with or without amplification. Cyclin D1 amplification had the second highest partial regression coefficient in the multivariate analysis, after the pN factor. Amplification of cyclin D1 was independent of the TNM classification as a prognostic factor, and was a useful marker for predicting outcome and distant organ metastasis in patients with squamous cell carcinoma of the esophagus. It appears that appropriate treatment can be selected by evaluating both TNM factors and cyclin D1 amplification.

Adult↗
PubMed1996

Immunohistochemical detection of K-sam protein in stomach cancer.

The K-sam gene, originally isolated as an amplified gene from the stomach cancer cell line KATO-III, is characterized by its preferential amplification in the undifferentiated type (diffuse type) of stomach cancer and encodes one of the receptors for heparin-binding growth factors or fibroblast growth factors. The K-sam gene has been isolated by different methods and has been designated BEK, TK14, and Cek2. The receptor for keratinocyte growth factor was also found to be encoded by the same gene. To examine the expression of the K-sam protein in stomach cancer, polyclonal antibody pK1-2 was raised against the extracellular domain of the gene product. This antibody detected K-sam proteins by Western blot and flow cytometry analyses in stomach cancer cell lines KATO-III and HSC39, in which the K-sam gene is amplified and overexpressed. By immunohistochemical analysis, 20 of 38 cases of the undifferentiated type of advanced stomach cancer were K-sam positive, whereas none of 11 cases of the differentiated or intestinal type revealed K-sam staining. The K-sam product was observed predominantly in diffusely infiltrative lesions. In one autopsy case, the K-sam protein was detected only focally in the primary tumor, whereas markedly increased staining for the K-sam product was detected diffusely in the metastasized tumor in the lymph node and liver. These results suggest that K-sam overexpression is associated with the malignant phenotype of the undifferentiated type of stomach cancer, such as infiltrative growth and metastasis.

Amino Acid Sequence↗
PubMed1995

Tumorigenicity and gene amplification potentials of cyclin D1-overexpressing NIH3T3 cells.

Cyclin D1 is a key regulator of the G1-S transition in cell cycle, and its gene is amplified and overexpressed in many cancers. To address the gene amplification potential of the cells in which the cyclin D1 gene expression is deregulated, we have established NIH3T3 clones with various levels of cyclin D1 transgene message. Those transfectants showed anchorage independent growth and tumorigenicity without in vitro morphological transformation. The degree of the transformed phenotype apparently correlated with the cyclin D1 expression level. Upon selection by N-(phosphonoacetyl)-L-aspartate (PALA), the cyclin D1-transfected NIH3T3 cells showed a higher ability to develop PALA-resistant colonies by amplifying the CAD gene, as compared to the parental NIH3T3 cells.

3T3 Cells↗