Biomedical subjects

T Kitagawa

Publications and source records attributed to T Kitagawa.

At least 199 records · Page 11Linked to original sources

PubMed1996

[Surgical experience of two different types of unroofed coronary sinus].

We experienced two cases with uncommon unroofed coronary sinus. The first patient, a 55-year-old man, had a partially unroofed mid-portion of the coronary sinus. His symptoms and physical state were similar to that of atrial septal defect (ASD). Echocardiogram and angiogram revealed that the coronary sinus (CS) communicated with the left atrium (LA). We confirmed that CS had an enlarged orifice and lacked a part of its roof through the right atriotomy and the atrioseptotomy. We directly closed the defect between the LA and the CS. His postoperative course was satisfactory. The second patient, a 46-year-old man, showed mild cyanosis. He had a completely unroofed CS with left superior vena cava (LSVC), absent inferior vena cava (IVC) and hemiazygos continuity. The LSVC directly drained to the LA, and the CS was absent. A part of the posterior wall of the LA was like a groove which laid from the orifice of the LSVC to the coronary sinus ASD. The roof of this groove was covered with fibrous tissue, which was shaped like a network structure. We thought that this network was a residue of the septum between the CS and the LA. Thus we resected this structure, and reconstructed the roof by equine pericardial patch to drain the venous blood from the LSVC to the right atrium. Anomaly in the patient may be the transitional type between the completely unroofed CS and the partially unroofed CS.

Coronary Vessel Anomalies↗

PubMed1996

[A case of advanced hepatoma cured by repeated percutaneous isolated liver perfusion using hepatic venous isolation and charcoal hemoperfusion].

We have reported the treatment results of percutaneous isolated liver perfusion using hepatic venous isolation and charcoal hemoperfusion (HVI.CHP) for unresectable liver cancers. This is a case of multiple advanced hepatoma cured completely by repeated per cutaneous isolated liver perfusion. The patient was a 58-year-old woman who was referred to our hospital for a hepatic tumor detected by abdominal computed tomograpy (CT). On admission, she showed HBs antigen positive, mild anemia and liver dysfunction, and elevation of tumor markers. Abdominal CT demonstrated nodular tumors in segment 4. In addition, hepatic angiography additionally revealed multiple bilobar metastases. We treated this case with high-dose intraarterial adriamycin (150 mg/body) using HVI.CHP. There after, the patient received intermittent intraarterial low-dose epirubicin infusions (30 mg/body, 5 times) via an implantable catheter system. Furthermore, she was given a second high-dose of adriamycin (130 mg/body) under HVI.CHP 7 months after the first treatment. Despite repeated high-dose treatments, she had no severe side effects. The levels of tumor markers, including AFP and PIVKA-II, decreased to normal range, and all tumor nodules have disappeared in abdominal CT studies at present, 20 months after the initial treatment. In conclusion, our experience suggests that advanced hepatoma with multiple bilobar lesions, as in this case, would be cured by repeated percutaneous isolated liver perfusion using HVI.CHP.

Antineoplastic Combined Chemotherapy Protocols↗

PubMed1996

[Effect of amiloride on the early and late stage of postischemic recovery in isolated perfused rat hearts--possible involvement of Na+/H+ and Na+/Ca2+ exchange].

To investigate whether Na+/H+ exchange or Na+/Ca2+ exchange involves in the ischemic-reperfusion injury, we examined the effect of amiloride, a potent inhibitor of Na+/H+ exchange, on the ischemic reperfused rat heart. When, the hearts were loaded with 0.1 mM amiloride preischemically, the recovery of left ventricular developed pressure was significantly improved than that of the control group, whereas the recovery of heart rate was not influenced by amiloride pretreatment at 30 min of reperfusion. Measurement of intracellular cations revealed that intracellular Na+ accumulation in the early stage (within 5 min) of reperfusion was inhibited by amiloride pretreatment. On the other hand, in the late stage (from 5 min to 30 min) of reperfusion, Ca2+ overload was inhibited by amiloride. These results suggest that Na+/H+ exchange mainly participates in the early stage of reperfusion injury and Na+/Ca2+ exchange system, secondary to the Na+/H+ exchange, participates in the late stage of the reperfusion injury. Moreover, pretreatment with amiloride also decreased creatine phosphokinase activity in the coronary effluent and completely abolished the incidence of ventricular arrhythmia during reperfusion. It is assumed that the improvement of postischemic cardiac dysfunction induced by amiloride pretreatment may be attributable to its inhibition on the resultant Ca2+ accumulation during ischemia.

Amiloride↗

PubMed1996

[Lymphedema].

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Adolescent↗

PubMed1996

Mechanism of ATP-induced Ca2+ efflux from freshly isolated adult rat cardiomyocytes: possible involvement of Na+/Ca2+ exchange.

Physiological stimulation causes a rise in intracellular Ca2+ concentration in cardiomyocytes. However, it has not yet been elucidated what mechanisms are involved in the reduction of cytosolic free Ca2+ levels, including those which underlie Ca2+ efflux from the cells. In the present study, we examined the effect of extracellular adenosine 5'-triphosphate (ATP) on Ca2+, efflux from freshly isolated adult rat cardiomyocytes. The isolated cardiomyocytes were preloaded with 45CaCl2 for one hour. Then, the fractional release of 45Ca2+ from the cells was measured consecutively. ATP stimulated the efflux of 45Ca2+ from isolated adult rat cardiomyocytes in a concentration-dependent manner (0.01-1 mM). The 45Ca2+ efflux from the cells was also stimulated by adenosine-5'-O-(3-thiotriphosphate) (ATP-gamma S), alpha, beta-methylene-ATP and adenosine 5'-diphosphate (ADP), but not by adenosine 5'-monophosphate (AMP) or adenosine. The effect of ATP was inhibited by a specific purinergic P2-receptor antagonist, but not by a P1-receptor antagonist. From these results, it is conceivable that the effect of ATP on Ca2+ efflux from cardiomyocytes is mediated through P2-purinoceptors. The ATP-stimulated 45Ca2+ efflux was not affected by removal of extracellular Ca2+, but was dependent on the presence of extracellular Na+. Moreover, ATP caused a 22Na+ influx into the cells. These results suggest that ATP stimulates extracellular Na(+)-dependent 45Ca2+ efflux from freshly isolated adult rat cardiomyocytes, probably through its stimulatory effect on plasma membrane P2-purinoceptors which may couple to Na+/Ca2+ exchange.

Adenosine Triphosphate↗

PubMed1996

Effect of cromakalim on ischemic and reperfused immature heart: experiments with isolated neonatal New Zealand white rabbit hearts.

To elucidate whether K+ channels are involved in the ischemia-reperfusion injury in immature heart, we examined the effect of cromakalim, a potent opener of ATP-sensitive K+ channel (KATP channel), on the ischemic and reperfused neonatal New Zealand white rabbit heart. The experiments were divided into control group and cromakalim pretreated group. When, the heart was loaded with 10 microM cromakalim preischemically, the recovery of heart rate and left ventricular developed pressure were significantly improved than those of the control group. Pretreatment with cromakalim also decreased lactate excretion in the coronary effluent. Measurements of cation contents with atomic absorption method revealed that intracellular K+ content was lower in cromakalim pretreated group at preischemia, end of ischemia and 20 min after ischemia. Intracellular accumulation of Na+ and Ca2+ at reperfusion period was inhibited by cromakalim pretreatment. From these results, it is assumed that cromakalim might act on KATP channels of plasma membrane and reduces the K+ content of the cardiomyocytes which in turn inhibits Na+ and Ca2+ accumulation during the reperfusion period. Prevention of Na+ and Ca2+ accumulation after ischemia might be a reason for cardioprotective effect of cromakalim on neonatal New Zealand white rabbit heart.

Animals↗

PubMed1995

Spectroscopic and electrochemical studies on active-site transitions of the type 1 copper protein pseudoazurin from Achromobacter cycloclastes.

The single type 1 copper protein pseudoazurin from Achromobacter cycloclastes gives reversible electrochemical behavior at a (4-pyridyl)disulfide-modified gold electrode. Measurements carried out at 25.0 degrees C indicate a midpoint reduction potential of E 1/2 = 260 mV versus normal hydrogen electrode at pH 7.0 and a peak-to-peak separation of delta Ep = 59 mV. The diffusion coefficient and heterogeneous electron transfer rate constant are estimated to be 2.23 x 10(-6) cm2 s-1 and 3.7 x 10(-2) cm s-1, respectively. Also, controlled potential electrolysis indicates a 1-electron transfer process and a formal reduction potential of 259 mV versus normal hydrogen electrode for the Cu(II)/Cu(I) couple. The heterogeneous electron transfer rate constant determined at the (4-pyridyl)disulfide-modified gold electrode at pH 4.6 is 6.7 x 10(-3) cm s-1, consistent with a slower process at the positively charged electrode surface. At pH 11.3, UV-visible, EPR, and resonance Raman spectra indicate a conversion of the distorted tetrahedral copper geometry to a trigonal structure. The trigonal form has elongated axial bonding and an axial EPR spectrum. At pH 11.3, the reduction potential is further decreased, and Cu-S bands in resonance Raman spectra at 330-460 cm-1 are shifted to higher energy (approximately 10 cm-1), consistent with a stronger Cu-S bond.

Alcaligenes↗

PubMed1995

Frequent development of pancreatic carcinomas in the Rana nigromaculata group.

In 1979, 2 species of pond frogs (Rana nigromaculata and Rana plancyi plancyi) were imported from China, and hybrids were made between these and Japanese, Korean, and Taiwanese pond frogs (R. nigromaculata, Rana plancyi fukienensis and Rana brevipoda) that had been kept for a number of years in the Laboratory for Amphibian Biology of Hiroshima University. From 1982, development of tumors, especially in the peritoneal cavity, was noticed frequently in the hybrids and also later, although rarely, in the Japanese pond frogs. Such tumors had never previously been observed among pond frogs in the laboratory. Histological and immunohistochemical studies identified the i.p. tumors to be pancreatic carcinomas with occasional production of insulin and/or somatostatin. Ultrastructural investigation revealed both endocrine and exocrine secretion granules together with C-type retrovirus particles in the carcinoma cells. Other tumors included a retroperitoneal rhabdomyosarcoma, liver adenomas, and an unclassifiable mesenchymal tumor of the foot pad.

Animals↗

PubMed1995

Identification of an enhancer responsible for tumor marker gene expression by means of transgenic rats.

The glutathione transferase P (GST-P) gene is known for its specific expression during chemical hepatocarcinogenesis of the rat and is used as a tumor marker for hepatocellular carcinoma. We have shown recently that the upstream 2.9-kb region of the GST-P gene is sufficient for conferring tumor-specific expression of the gene in vivo (S. Morimura et al., Proc. Natl. Acad. Sci. USA, 90: 2065-2068, 1993). To further identify crucial sequence elements regulating the unique expression of this gene, we have established six independent lines of transgenic rats bearing distinct areas of the GST-P gene that are connected to the chloramphenicol acetyltransferase coding region and analyzed changes of the chloramphenicol acetyltransferase activity during the course of chemical hepatocarcinogenesis. We demonstrate here that the enhancer, glutathione transferase P enhancer I, that is located 2.5 kb upstream of the GST-P gene is required and sufficient for its tumor-specific expression of the gene among other controlling elements. This approach to transgene expression could be used to define other enhancers, the activity of which is dependent on cellular changes such as carcinogenesis, development, and differentiation.

Animals↗

PubMed1995

Evidence that portal vein decompression improves survival of canine quarter orthotopic liver transplantation.

The minimum graft volume still remains unclear in reduced-size liver transplantation (RLT). This study reports the improved survival of canine RLT using a quarter graft with the aid of a portahepatic vein shunt (PHVS). In beagles, the donor liver was reduced to the right lateral and caudate lobes (quarter graft) with or without provision of PHVS, and transplanted orthotopically in the recipient. The PHVS was established by an end-to-end anastomosis of the portal vein branch and the hepatic vein in the resected left lateral lobe. Liver chemistries including arterial blood ketone body ratio (AKBR) were serially measured during and after surgery. All seven animals with PHVS survived more than 3 days (mean +/- SD; 5.3 +/- 1.7 days), whereas all six without PHVS died within 3 days (1.8 +/- 0.8 days, P < 0.01). Portal vein pressures immediately after recirculation in animals with and without PHVS were 8.5 +/- 1.2 mmHg and 16.9 +/- 3.1 mmHg, respectively (P < 0.01). Regardless of the presence or absence of PHVS, AKBR dropped to a level lower than 0.7 during the anhepatic period and returned promptly to above 1.0 as early as 30 min after recirculation. Thereafter, the AKBR values in animals with PHVS remained higher than 1.0, whereas those in animals without PHVS showed a progressive decrease, showing a statistically significant difference between the two groups after 12 hr (P < 0.05). Graft function, as assessed by AKBR, was well correlated with survival and other liver chemistries. These results indicate that, in an extreme RLT, portal hypertension is a risk factor predisposing to graft failure, most likely by increasing microvascular injury after recirculation.

Animals↗

PubMed1995

Ultraviolet resonance Raman studies of quaternary structure of hemoglobin using a tryptophan beta 37 mutant.

Environmental changes of tyrosine and tryptophan residues of hemoglobin (Hb) upon its T to R transition of quaternary structure were investigated with ultraviolet resonance Raman (UVRR) spectroscopy excited at 235 nm. DeoxyHb A (T-form) showed a UVRR spectrum distinctly different from those of the ligated Hbs (R-form) including oxyHb, COHb, and metHb A, whereas the ligated Hbs exhibited similar UVRR spectra irrespective of the ligand species and the oxidation state of the heme. To characterize the spectral change of Trp-beta 37 at the alpha 1 beta 2 interface due to the quaternary structure transition, the UVRR spectra of Hb A were compared with the corresponding spectra of Hb Hirose (Trp-beta 37-->Ser). A difference spectrum between deoxyHb A and deoxyHb Hirose showed only Trp resonance Raman (RR) bands, which were reasonably ascribed to Trp-beta 37 in deoxyHb A. RR bands at 873 cm-1 (W17) and at 1360 and 1343 cm-1 (W7, Fermi doublet) indicated that the indole ring of Trp-beta 37 in deoxyHb A formed a strong hydrogen bond at the N1H site in hydrophobic environments. Tyr residues in deoxyHb Hirose seemed to be in the same environments as those of deoxyHb A. In contrast, the difference spectrum between Hb A and Hb Hirose in the ligated state displayed peaks for RR bands of both Trp and Tyr. The difference spectra were unaltered by the addition of 5 mM inositol hexaphosphate. This means that the differences were not caused by the tetramer to dimer dissociation but by a conformation change within a tetramer. Comparison of the Hb A-Hb Hirose difference spectra in the oxy and deoxy states revealed that the oxygenation-induced changes of Trp RR bands arose mostly from Trp-beta 37 with the small portion of remaining changes coming from Trp-beta 15, demonstrating that Trp-beta 37 plays a pivotal role in the quaternary structural change in Hb A.

Amino Acid Sequence↗

PubMed1995

Bilateral asymmetry in bone weight at various skeletal sites of the rat.

BACKGROUND: Morphological and functional asymmetry in the limbs has generally been regarded as a human characteristic that is of genetic or of both genetic and environmental origin. The aim of this study was to determine the presence of lateral dominance in bone weight of the forelimb of the rat. METHODS: Wistar rats (77) were used, 45 controls and 32 experimental animals, implanted with a steel weight subcutaneously under the right forelimb. Bones examined for bilateral asymmetry in bone weight were the mandibula, the bones of fore- and hindlimbs, calcaneus, and talus of the tarsus. The weight of each dry bone was measured to the nearest milligram. RESULTS: Significant bilateral asymmetry in the forelimb was evident in male and female rats, with the left side having more bone mass than the right. Bilateral differences were more pronounced in the females than the male rats. Greater asymmetry was evident in the experimental group compared to the control rats. CONCLUSIONS: These findings demonstrate that asymmetry is present not only in humans, but also in lower animals such as rats. Greater asymmetry in the experimental rat group is indicative of the influence of environmental factors or physical stress on asymmetry. We conclude that genetics might control the development of asymmetry, but physical stress may alter the functional expression of the asymmetry.

Animals↗

PubMed1995

Frequent loss of heterozygosity on chromosome 4 in diethylnitrosamine-induced C3H/MSM mouse hepatocellular carcinomas in culture.

Genetic changes, in particular the loss of heterozygosity (LOH) and the presence of c-Ha-ras codon 61 point mutations, were investigated in diethylnitrosamine-induced hepatocellular carcinomas (HCCs) in C3H/MSM F1 mice. (MSM are wild mice.) LOH analysis of 48 primary tumors with microsatellite probes covering at least one proximal and one distal site of each autosome revealed no obvious positive results for LOH. Analysis of 23 cell lines established from seven of these HCCs, however, showed LOH on chromosome 4 in all (seven of seven), even in early passages (G2-G3). With regard to other chromosomes, LOH was observed only rarely on chromosomes 16 and 19. These allelotype features were maintained in later passages (G11-G14), with only a few additional occurrences of LOH appearing on chromosomes 1, 6, and 8. Extensive analyses with multiple microsatellite probes from chromosome 4 and with 52 cell lines established from 24 HCCs of 18 mice revealed LOH in 22 of the tumors (92%), with the shortest region about 10 cM distal to the alpha-interferon gene. No c-Ha-ras oncogene activation in codon 61 was observed. These data indicate that loss of tumor suppressor genes on chromosome 4 may play an important role in mouse hepatocarcinogenesis in progression in vivo or in immortalization in vitro or both.

Alleles↗

PubMed1995

Markedly increased renal disease mortality and incidence of renal replacement therapy among IDDM patients in Japan in contrast to Allegheny County, Pennsylvania, USA. Diabetes Epidemiology Research International (DERI) U.S.-Japan Mortality Study Group.

The aim of this study was to evaluate factors related to the markedly increased risk of dying from diabetic renal disease in Japanese insulin-dependent diabetic patients compared to those in the USA. The study was based on two population-based cohorts consisting of 1374 cases from Japan and 995 cases from Allegheny County, Pennsylvania, USA, who were diagnosed between 1 January 1965 and 31 December 1979. The living status and dialysis experience were determined as of 1 January 1990. The duration-adjusted renal-failure-related mortality rates in the Japanese cohort and the USA cohort were 277.2 and 130.9 per 100,000 person-years, and the duration-adjusted incidence rates of dialysis were 564.9 and 295.6 per 100,000 person-year, respectively. After adjustment for sex, age at onset, calendar year of onset, and duration of diabetes, individuals with insulin-dependent diabetes in the Japanese cohort were still 2.4-fold more likely to receive dialysis compared to those in the USA cohort. Ten of the 36 renal-failure-related deaths in the Japanese cohort had never been treated by dialysis, while all renal-failure-related deaths in the USA cohort had been treated by dialysis. Survival after initiation of dialysis in the Japanese cohort was virtually the same as the USA cohort. These data suggest that a greater frequency of diabetic end-stage renal disease and reduced access to acceptance at dialysis underlie much of the excess of diabetic renal deaths in Japan.

Adolescent↗

PubMed1995

Hepatocarcinogenesis in rodents and humans.

In hepatocarcinogenesis in rodents, induction of foci and nodules comprising clonally proliferated initiated cells is considered to be essential for the future development of carcinomas. Nodules in human cirrhotic liver, though known to be associated with a high hepatocellular carcinoma risk, have generally been regarded as regenerative in nature, and not the result of clonal or neoplastic cell proliferation, on a morphological basis. However, when we analyzed 83 cirrhotic nodules from 11 HBV carrier patients, utilizing hepatitis B virus (HBV) integration as a marker for clonal proliferation, we found the existence of clonal populations of more than 10(5) hepatocytes in 26 (31.3%) of them. Although such clonal cell populations are morphologically not discernible from neighboring hepatocytes, they may have particular histogenetic significance in human hepatocarcinogenesis and clearly deserve further investigation. Allelotype analysis of mouse hepatocellular carcinomas (HCC), induced by a single dose of diethyl nitrosaminine in C3H/MSM F1 hybrids, revealed no remarkable alterations in the original tumors when microsatellite probes were used, but loss of heterozygosity of chromosome 4 at extremely high frequency (95%) in cultured cell lines derived from these HCC. The shortest common region was about 10 cM distal to the interferon alpha gene, in which the p16 gene is located. The results indicated that loss of gene function, most probably including that of the p16 gene, may be essential for immortalization of cultured hepatocytes but that it may not play any role in initiation or early events in mouse hepatocarcinogenesis in vivo. The mouse HCC used for analysis in this study may be comparable with human HCC at an early stage, for which only very limited genetic alterations have so far been identified.

Alleles↗

PubMed1995

Tissue-specific activation of tumor marker glutathione transferase P transgenes in transgenic rats.

By means of transgenic rats, we have recently shown that the GPEI enhancer of the glutathione transferase P (GST-P) gene, which has two one-base-missmatched AP-1 sites locating palindromically with three-base spacing in between, is sufficient for conferring tumor-specific activation of the gene in vivo. It is noted that there is another consensus AP-1 site near the promoter of this gene. By using seven independent transgenic rats, bearing distinct areas of the GST-P gene that are connected to the chloramphenicol acetyltransferase (CAT) coding sequence, we analyzed CAT expression in various tissues (brain, lung, liver, kidney, spleen) in these transgenic rats. We found that the ECAT gene, which has sufficient of the upstream regulatory region (approx. 2.9 kb) of the gene containing GPEI, is trans-activated in the kidney and lung of transgenic rats in a similar manner to endogenous GST-P. When either the GPEI core sequence or the AP-1 site near the promoter is deleted, CAT expression decreases to almost background level. Substitution of the GPEI core or the AP-1 site near the promoter to this silent construct (5CATGPEIcore) reconstituted CAT expression in the transgenic rats. In these rats, CAT was expressed in the brain and lung rather than in the kidney, showing a somewhat different pattern from the endogenous GST-P. In the brain tissue of the 5CATGPEIcore transgenic rat, CAT was demonstrated in the glia cells, which is consistent with endogenous GST-P expression. These results suggest that a relatively long upstream region (approx. 2.9 kb) is required for tissue-specific expression of the GST-P gene and that GST-P expression in the brain may be regulated differently from its expression in other organs.

Animals↗

PubMed1995

Technique for constructing the pulmonary trunk for tetralogy of Fallot with pulmonary atresia.

In expectation of the growth of a new pulmonary arterial trunk in total correction of tetralogy of Fallot with pulmonary atresia, we used pedicled autologous pericardium combined with left atrial appendage as the posterior wall of a new pulmonary arterial trunk. In cases of long discontinuity between the right ventricular infundibulum and left pulmonary artery, our technique could be recommended for early repair of tetralogy of Fallot with pulmonary atresia.

Child, Preschool↗

PubMed1995

Distal residue-CO interaction in carbonmonoxy myoglobins: a molecular dynamics study of three distal mutants.

Six 90-ps molecular dynamics trajectories, two for each of three distal mutants of sperm whale carbonmonoxy myoglobin, are reported; solvent waters within 16 A of the active site have been included. In both His64GIn trajectories, the distal side chain remains part of the heme pocket, forming a "closed" conformation similar to that of the wild type 64N delta H tautomer. Despite a connectivity more closely resembling the N epsilon H histidine tautomer, close interactions with the carbonyl ligand similar to those observed for the wild type 64N epsilon H tautomer are prevented in this mutant by repulsive interactions between the carbonyl O and the 64O epsilon. The aliphatic distal side chain of the His64Leu mutant shows little interaction with the carbonyl ligand in either His64Leu trajectory. Solvent water molecules move into and out of the active site in the His64Gly mutant trajectories; during all the other carbonmonoxy myoglobin trajectories, including the wild type distal tautomers considered in an earlier work, solvent molecules rarely encroach closer than 6 A of the active site. These results are consistent with a recent structural interpretation of the wild type infrared spectrum, and the current reinterpretation that the distal-ligand interaction in carbonmonoxy myoglobin is largely electrostatic, not steric, in nature.

Allosteric Site↗