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Biomedical subjects

Y Satoh

Publications and source records attributed to Y Satoh.

At least 145 records · Page 8Linked to original sources
PubMed1999

Nocardia asteroides pneumonia, subcutaneous abscess and meningitis in a patient with advanced malignant lymphoma: successful treatment based on in vitro antimicrobial susceptibility.

Nocardia asteroides pneumonia, subcutaneous abscess and meningitis without brain abscesses developed in a patient with advanced non-Hodgkin's lymphoma, who had received corticosteroid therapy and cancer chemotherapy for a long time. At the time of nocardial pneumonia, profound lymphocytopenia and hypogammaglobulinemia was seen. The severely immunosuppressed condition most likely accounted for the uncommon infection, nocardiosis. The organism isolated from the sputum, subcutaneous abscess and cerebrospinal fluid was strongly resistant to cotrimoxazole, which is the recommended standard treatment, but it was susceptible to imipenem (IPM) and erythromycin (EM) in an in vitro antimicrobial susceptibility study. The patient's nocardiosis responded well to chemotherapy including IPM and EM.

Abscess↗
PubMed1999

[Extravasation of contrast media in acute subdural hematoma during three-dimensional CT angiography: a case report].

We report a case of acute subdural hematoma in which extravasation of contrast medium was demonstrated using three-dimensional computed tomographic angiography (3D-CTA). An 83-year-old man was found lying down on the floor but he was conscious. Thirty minutes later, he lost consciousness and was transferred to our hospital in a comatose state with right hemiparesis. Plain CT scan showed a left temporoparietal acute subdural hematoma with subarachnoid hemorrhage. CT scan also demonstrated an iso-density area beneath a high-density around the left Sylvian fissure. We performed an emergent 3D-CTA to rule out ruptured aneurysm as the cause of hemorrhage. However, 3D-CTA revealed no cerebral aneurysm, but extravasation of contrast medium from the cortical artery of the left temporal cortex was noted. The patient immediately underwent total evacuation of subdural hematoma by small temporoparietal craniectomy under local anesthesia. We found 3D-CTA to be a useful, less-invasive method for diagnosing the hemorrhagic cause and localizing the bleeding point. It is expected that with more routine use of 3D-CTA in patients with acute subdural hematoma, extravasation of the contrast medium will be seen more frequently. Subdural hematoma with extravasation of contrast medium required emergent surgery, and 3D-CTA findings facilitated the selection of the surgical method according to the bleeding point.

Acute Disease↗
PubMed1999

[Phase I study of a combination chemotherapy of nedaplatin and cisplatin].

A new platinum complex, nedaplatin, has been reported to be effective for both ovarian and cervical cancers. We designated a phase I dose-escalation study of a combination chemotherapy of nedaplatin and cisplatin to investigate the dose-limiting toxicity (DLT) and the maximum tolerated dose (MTD). Six patients, including two with advanced cervical cancer, three with ovarian clear cell adenocarcinoma and one with endometrial clear cell adenocarcinoma, were enrolled in this study. The doses of the two agents were escalated alternatively, i.e., a tandem method, from 40 to 80 mg/m2 by 20 mg/m2. Nedaplatin and cisplatin were administrated by intravenous drip infusion and repeated after an interval of at least 4 weeks, as a rule. The major toxicity observed was hematotoxicity. One of the 6 patients dropped out of this study because of severe hematotoxicity after 80 mg/m2 of nedaplatin and 60 mg/m2 of cisplatin were administered. With a dose of 80 mg/m2 nedaplatin and 80 mg/m2 cisplatin, severe neutropenia was found in all 6 patients, and thrombocytopenia and anemia were found in 1 patient, respectively. A slight hearing loss was detected by audiometry in 5 patients, but no one was inconvenienced in daily life. Mild nausea and vomiting were also observed in all 6 patients. In conclusion, the DLT of this combination therapy was hematotoxicity and the MTD was 80 mg/m2 for nedaplatin and 60 mg/m2 for cisplatin, respectively. Thus, 60 mg/m2 of nedaplatin and 60 mg/m2 of cisplatin may be recommended for combined administration.

Adenocarcinoma, Clear Cell↗
PubMed1999

Abnormal FHIT transcripts found in both lung cancer and normal lung tissue.

Occurrence of abnormal transcripts of the FHIT (fragile histidine triad) gene has been reported in various types of cancer. On the other hand, aberrant transcripts are sometimes found in non-neoplastic tissues, so the relationship between the presence of abnormal transcripts of the FHIT gene and cancer pathogenesis is controversial. We investigated alterations in the FHIT locus, detected by nested reverse transcription-polymerase chain reaction and/or allelic status, in 88 primary lung cancers and normal lung tissues, and 22 normal lung tissues with metastatic lung cancer as a control. The frequencies of abnormal transcripts were 59% in lung cancer, 35% in paired normal lung, and 64% in normal control lung; the difference in frequencies between lung cancer and paired normal lung was significant, while that between lung cancer and normal control lung was not. Sequence analysis revealed that there were no cancer-specific abnormal transcripts entirely missing two or more exons, nor were the abnormal transcripts of lung cancer identical with those of paired normal lung in the same individual. Furthermore, we found no correlation between loss of heterozygosity in the FHIT locus and occurrence of abnormal FHIT transcripts. These results suggest that the presence of abnormal FHIT transcripts, in terms of their frequency and variety, is not cancer-specific in lung carcinogenesis, and the abnormality may be mainly due to abnormal splicing and processing of the transcripts. To estimate the precise function of the FHIT gene, further study of the FHIT protein in lung carcinogenesis is needed.

Acid Anhydride Hydrolases↗
PubMed1998

Two novel oleanolic acid saponins having a sialyl Lewis X mimetic structure from Achyranthes fauriei root.

Two novel triterpene glycosides, achyranthosides E and F, were isolated as methyl esters from the root of Achyranthes fauriei, an antiinflammatory medicinal plant. Their structures were characterized as oleanolic acid glucuronides having unique substituents composed of C6H9O5 and C9H15O7, respectively, at the C-3 position of glucuronic acid. These compounds are active components which can inhibit the excess recruiting of neutrophiles to injured tissues 1,000 times more potently than sialyl Lewis X.

Magnetic Resonance Spectroscopy↗
PubMed1998

Productive infection of Epstein-Barr virus (EBV) in EBV-genome-positive epithelial cell lines (GT38 and GT39) derived from gastric tissues.

We characterized the expression of Epstein-Barr virus (EBV) on two epithelial cell lines, GT38 and GT39, derived from human gastric tissues. The EBV nuclear antigen (EBNA) was detected in all cells of both cell lines. The EBV immediate-early BZLF 1 protein (ZEBRA), the early antigen diffuse component (EA-D), and one of the EBV envelope proteins (gp350/220) were expressed spontaneously in small proportions in the cells. EBNA 1, EBNA2, latent membrane protein 1, ZEBRA, and EA-D molecules were then observed by Western blotting in the cells. The lytic cycle was enhanced with treatment with 12-O-tetradecanoylphorbol-13-acetate (TPA) or n-butyrate. The virus particles were observed in the TPA treated GT38 cells by electron microscopy. Infectious EBV was detected with the transformation of cord blood lymphocytes and also with the induction of early antigen to Raji cells by the supernatants of both cells lines. A major single and minor multiple fused terminal fragments and a ladder of smaller fragments of the EBV genome were detected with a Xhol probe in both cell lines. These epithelial cells lines and viruses will be useful in studying their association with EBV in gastric epithelial cells.

Animals↗
PubMed1998

Decreased expression of the metastasis suppressor gene KAI1 in gastric cancer.

KAI1 was immunohistochemically detected in the lower part of fundic glands and intestinal metaplasia in non-cancerous gastric tissues, while only 11.0% (8/73) of cancerous tissues were shown to be positive. The relationship between various clinicopathological characteristics of patients with gastric cancer and KAI1 expression in their tumors was then analyzed to reveal that the incidence of positivity was 16.6% (8/48) of patients with stage Ia-IIIa and 0% (0/25) of patients with stage IIIb-IVb (P < 0.05) and that the incidence of peritoneal or hepatic metastasis tended to be lower in KAI1-positive tumors than in negative ones. These results suggest that decreased KAI1 expression may be related to the progression of gastric cancer.

Adenocarcinoma↗
PubMed1998

Relationship between dihedral angles of N1 and C9 substituents in 1,4-benzodiazepines and dual cholecystokinin-A and -B antagonistic activities.

Introduction of a methyl moiety to the C9 position of a 1,4-benzodiazepine ring system afforded dual CCK-A and -B antagonistic activity. Novel derivatives having ethyl, isopropyl and chloro substituents at C9 were prepared in order to obtain more potent antagonistic activities. AM1(MOPAC93) calculations of the dihedral angles between the N1 and C9 substituents indicated that dihedral angles for dual antagonistic activities were between 50 degrees and 60 degrees. A methyl moiety was selected as the most suitable C9 substituent in this series for potent dual CCK-A and -B receptor antagonistic properties.

Animals↗
PubMed1998

Lambert-Eaton syndrome antibodies inhibit acetylcholine release and P/Q-type Ca2+ channels in electric ray nerve endings.

1. The types of voltage-dependent calcium channels (VDCCs) present in the cholinergic terminals isolated from the electric organ of the ray, Narke japonica, were characterized on the basis of their pharmacological sensitivity to specific antagonists. Inhibition of these channel types by autoantibodies from patients with the Lambert-Eaton syndrome (LES) was then studied to determine the specificity of the pathogenic IgG. 2. In normal untreated synaptosomal preparations, maximal doses of N- and P and/or Q-type Ca2+ channel antagonists, omega-conotoxin GVIA and omega-agatoxin IVA, inhibited depolarization-evoked ACh release by 47 % and 43 %, respectively. Calciseptine, an L-type VDCC antagonist, caused a 20 % reduction in the release. This indicates that the exocytotic release process is predominantly mediated by N- and P/Q-type VDCCs. 3. LES IgG or sera caused an inhibition of ACh release by 39-45 % in comparison with the control antibody-treated preparations. The ionomycin-induced ACh release, however, was not altered by the antibodies. Additionally, the same LES antibodies inhibited whole-cell calcium currents (ICa) in bovine adrenal chromaffin cells. Thus, the pathogenic antibodies exert their action on VDCCs present in the synaptosomes. 4. The efficacy of three Ca2+ channel antagonists in blocking ACh release was determined in preparations pretreated with LES IgG. omega-Agatoxin IVA produced only an additional 3-5 % reduction in release beyond that obtained with LES antibodies. Despite the pretreatment with LES IgG, omega-conotoxin GVIA and calciseptine inhibited the release to nearly their control levels. 5. These results indicate that LES antibodies mainly downregulate P/Q-type Ca2+ channels which contribute to presynaptic transmitter release from the cholinergic nerve terminals of electric organ. 6. The present findings are consistent with the hypothesis that P/Q-type VDCCs at the neuromuscular junction are the target of LES antibodies and that their inhibition by the antibodies produces the characteristic neuromuscular defect in this disease.

Acetylcholine↗
PubMed1998

Simultaneous assessment of the hemodynamic, cardiomechanical, and electrophysiological effects of terfenadine on the in vivo canine model.

Prolongation of the QT interval, sometimes leading to torsades de pointes, has been clinically reported during terfenadine treatment. However, information regarding the cardiovascular profile of terfenadine is still limited, particularly in in vivo animal models. In the current study, we examined the cardiovascular effects of terfenadine using halothane-anesthetized, closed-chest in vivo canine models (n = 6) to better simulate the clinical situation. Intravenous infusion of 0.3 mg/kg of terfenadine over 10 min, which would attain the antihistaminic plasma concentration, reduced the heart rate and left ventricular contractility and prolonged the repolarization period as well as the ventricular effective refractory period. An additional infusion of a ten times higher dose of terfenadine over 10 min caused hypotension and increased left ventricular preload and atrioventricular conduction time, in addition to potentiating the changes observed by the lower dose. A reverse use-dependent prolongation of the repolarization period was observed after the higher dose infusion. Moreover, early afterdepolarization-like potential was detected in four out of six experiments. Since each suppressive effect can become deleterious during terfenadine overdose, caution must be taken for those patients with potential cardiac dysfunction and with the risk of elevated plasma drug concentrations.

Analysis of Variance↗
PubMed1998

The long-term survival rates of patients after repair of abdominal aortic aneurysms.

This study was undertaken to examine the long-term survival rates of patients following abdominal aortic aneurysm (AAA) repair in comparison with an age-matched normal population, and to determine by multivariate analysis the factors influencing long-term survival. Of 125 patients who underwent AAA repair prior to July 1986, 13 died during hospitalization. Of these 13 patients, 6 who suffered aneurysmal rupture all died within 30 days. The survival rate of patients with ruptured aortic aneurysms was significantly lower than that of those with nonruptured aneurysms. Of the 112 patients surviving hospitalization, 85 died within 0.48 to 24 years after their operation. The long-term survival rate of patients who had suffered a preoperative cardiovascular event was significantly lower than that of those who had not suffered a preoperative cardiovascular event. The actual survival rate was significantly lower than the expected survival rate. According to a multivariate analysis, the significant predictors of late survival were age, aneurysmal rupture, and chronic renal failure in all the patients, and age, chronic renal failure, and pre- and postoperative cardiovascular events in patients who did not die in hospital. These findings indicate the importance of improving immediate perioperative management of ruptured AAA and that cardiovascular events should be prevented, or treated during long-term follow-up.

Adult↗
PubMed1998

[Postoperative infections related to pacing wires, pulmonary arterial catheters, and drainage tubes temporarily inserted during open-heart surgery].

Bacterial examinations of temporary pacing wires (P-wires), pulmonary arterial (P-A) catheters, and drainage tubes temporarily inserted during open-heart surgery were performed in 213 patients. Bacteria were detected in 19 (2.8%) of 672 specimens gathered from the subject patients, with coagulase-negative Staphylococcus (CNS) being most frequently observed. P-wires accounted for 17 out of 19 of the culture-positive specimens, and 7 of the P-wires remained in place for more than two weeks. The frequency of infection with the P-wires was significantly higher than with the P-A catheters or drainage tubes. The period of time that the P-wire was left in place significantly longer than for P-A catheter or drainage tube. There was, however, no statistically significant difference between the culture-positive and negative groups in respect to age, detention periods, operation times, CPB times, or length of ICU stay. As a result of these findings, we have concluded that P-wires should be removed as soon as possible following surgery, and in any case, a meticulous care should be taken to prevent transcutaneous infection.

Adolescent↗
PubMed1998

The effects of coenzyme Q10 treatment on maternally inherited diabetes mellitus and deafness, and mitochondrial DNA 3243 (A to G) mutation.

The characteristic clinical features of diabetes mellitus with mitochondrial DNA (mtDNA) 3243(A-G) mutation are progressive insulin secretory defect, neurosensory deafness and maternal inheritance, referred to as maternally inherited diabetes mellitus and deafness (MIDD). A treatment for MIDD to improve insulin secretory defects and reduce deafness has not been established. The effects of coenzyme Q10 (CoQ10) treatment on insulin secretory response, hearing capacity and clinical symptoms of MIDD were investigated. 28 MIDD patients (CoQ10-DM), 7 mutant subjects with impaired glucose tolerance (IGT), and 15 mutant subjects with normal glucose tolerance (NGT) were treated daily with oral administration of 150 mg of CoQ10 for 3 years. Insulin secretory response, blood lactate after exercise, hearing capacity and other laboratory examinations were investigated every year. In the same way we evaluated 16 MIDD patients (control-DM), 5 mutant IGT and 5 mutant NGT subjects in yearly examinations. The insulin secretory response assessed by glucagon-induced C-peptide secretion and 24 h urinary C-peptide excretion after 3 years in the CoQ10-DM group was significantly higher than that in the control-DM group. CoQ10 therapy prevented progressive hearing loss and improved blood lactate after exercise in the MIDD patients. CoQ10 treatment did not affect the diabetic complications or other clinical symptoms of MIDD patients. CoQ10 treatment did not affect the insulin secretory capacity of the mutant IGT and NGT subjects. There were no side effects during therapy. This is the first report demonstrating the therapeutic usefulness of CoQ10 on MIDD.

Adult↗
PubMed1998

Portal vein reconstruction with conventional polytetrafluoroethylene grafts: an experimental study in dogs.

The purpose of this study was to examine the short- and long-term performance of conventional polytetrafluoroethylene (PTFE) grafts for portal vein reconstruction. The grafts were placed as a portal vein replacement in 11 mongrel dogs. At 1 month and 6 months, the grafts were then retrieved and examined for patency, while also undergoing a pathological analysis. During the observation period (at 55 days), one dog died of an unknown cause with a patent graft. The patency rates of the other 10 grafts were 83% (5/6) at 1 month and 100% (4/4) at 6 months. However, the neointima formation was incomplete even 6 months after implantation. In conclusion, although conventional PTFE grafts may be used as a synthetic alternative to autogenous vein grafts, every effort should be made to use autogenous vein grafts before considering conventional PTFE grafts.

Animals↗
PubMed1998

Expression analysis of two mutant human ornithine transcarbamylases in COS-7 cells.

Ornithine transcarbamylase (OTC) is located in the mitochondrial matrix of the liver and small intestine and catalyzes the second step of the urea cycle. OTC deficiency (OTCD) is an X-linked inborn error of metabolism and causes hyperammonemia. We reported in 1992 the A152V and G195R mutations in patients with OTCD. These mutant OTC cDNAs were prepared by site-directed mutagenesis using the polymerase chain reaction (PCR). The wild-type and mutant cDNAs were transiently expressed in COS-7 cells. The wild-type cDNA gave an OTC activity of 1180 +/- 47 nmol/min per mg protein. The OTC activities of the A152V and the G195R mutants were 3.7% and 2.5% of that of wild-type, respectively. Immunoblot analysis showed that the quantities of OTC proteins in the A152V and G195R mutants were 29% and 12% of that of wild-type, respectively. In pulse-labeling and pulse-chase experiments, the precursor form of OTC was synthesized and processed to the mature form. The A152V mutant OTC was processed to the mature form as rapidly as the wild-type precursor. However, the processed, mature form of the mutant OTC was rapidly degraded, presumably in the mitochondrial matrix. These results indicate that OTCD with the A152V mutation is due both to rapid degradation of the processed, mature form, and to a lower specific activity of the remaining protein.

Animals↗
PubMed1998

Analysis of bilirubin uridine 5'-diphosphate (UDP)-glucuronosyltransferase gene mutations in seven patients with Crigler-Najjar syndrome type II.

Crigler-Najjar syndrome (CN) type II is caused by a reduction in hepatic bilirubin uridine 5'-diphosphate (UDP)-glucuronosyltransferase activity. Recently, there has been progress in mutation analysis of patients with CN type II. Here, we analyzed both the coding and the promoter regions of the gene in seven Japanese patients with CN type II from five unrelated families. The mutations found in this study were classified into three types. The first type was composed of double homozygous missense mutations (Gly71Arg and Tyr486Asp) in exons 1 and 5. These mutations, which were detected in five patients from three unrelated families, were the commonest. The second type, which was detected in one patient, consisted of a single homozygous missense mutation (Arg209Trp) in exon 1. The third type, which was detected in one patient and was a new type of mutation combination, was composed of a homozygous insertion mutation of the TATAA element and a heterozygous missense mutation (Pro229Gln) in exon 1. Although the first and the second type of mutations are recessive, the third type appears to be dominant with incomplete penetrance, since the allele frequency of the insertion mutation of the TATAA element is very high (40%).

Adult↗
PubMed1998

Acetylcholine-induced calcium signaling along the rat colonic crypt axis.

BACKGROUND & AIMS: Acetylcholine-induced calcium signaling dynamics have been described in cell monolayers derived from colonic mucosa, but not in intact colonic crypts. The aim of this study was to characterize the spatiotemporal characteristics of calcium signaling induced by acetylcholine in isolated intact rat colonic crypts and to identify the muscarinic receptor subtype coupled to this signaling pathway. METHODS: Isolated crypts from the distal colon of male Wistar rats were loaded with the calcium-sensitive dye Fura-2 and imaged with a charge-coupled device video camera. RESULTS: Acetylcholine mobilized intracellular calcium with an EC50 of 3.9 micromol/L. The response was initiated at the base of the crypt and progressed toward the surface. The velocity of propagation was dose dependent. Addition of muscarinic antagonists inhibited the response (pKb values calculated for pirenzepine and 4-DAMP, 6.08 and 8.65, respectively). Microperfusion of acetylcholine initiated a calcium signal throughout the lower half of the crypt. Microinjection of inositol 1,4,5-triphosphate induced a propagation of a calcium signal along the crypt axis. Heptanol inhibited the velocity of acetylcholine-induced wave propagation by 33%. CONCLUSIONS: M3 muscarinic receptors are coupled to the mobilization of calcium from intracellular stores of intact, isolated rat colonic crypts. Intercellular communication potentiates the propagation of the acetylcholine-induced calcium signal along the crypt axis.

Acetylcholine↗