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Biomedical subjects

K Goto

Publications and source records attributed to K Goto.

At least 397 records · Page 22Linked to original sources
PubMed1996

Establishment of two human renal cell carcinoma cell lines with different chemosensitivity.

Two cell lines, SKR1 and NKK1, were established from renal cell carcinomas (RCC) with different histopathologic characteristics: SKR1 from grade 3, solid type, pleomorphic cell type carcinoma in a 66-year-old male and NKK1 from grade 2, alveolar type, clear cell carcinoma in a 49-year-old female. Electron microscopic study showed the presence of microvilli on cell surface and desmosome-like structures between cells in both lines. Doubling time and plating efficiency of SKR1 were 28 h and 37%, respectively, whereas those of NKK1 were 45 h and 22%, respectively. The chromosome number of both cell lines was 100% aneuploid with a mode of 74 chromosomes for SKR1 and 84 for NKK1. Both SKR1 and NKK1 induced tumors at the site of subcutaneous injection of nude mice. The morphologic characteristics of the tumor were similar to those of each original tumor. NKK1 was about 20 times more resistant to doxorubicin and vinblastine as compared to SKR1. Expression of P-glycoprotein was considered to be one of the factors responsible for such multidrug resistant phenotype of NKK1 cells. These two lines with different chemosensitivity may be a useful model for developing new therapeutic strategies for RCC.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1996

Acute emphysematous cholecystitis associated with pneumobilia: a case report.

This report describes a rare case of acute emphysematous cholecystitis with pneumobilia in the common bile duct. The patient was a 66-year-old woman with a part history of diabetes mellitus, and operations for gastric and breast carcinoma. The chief complaint was pain in the right hypochondrium with severe right hypochondrial tenderness and distention of the gallbladder detected on examination. Laboratory tests showed leukocytosis, marked elevation of CRP, jaundice, liver dysfunction, and hyperglycemia. Gas was detected in the gallbladder on plain abdominal X-rays and CT scans of the abdomen, and a small amount of gas was also observed in the common bile duct. On the day of admission, percutaneous transhepatic gallbladder drainage (PTGBD) was carried out under ultrasound guidance, and Clostridium perfingens and E. coli were detected in the bile. Imaging after PTGBD showed no cystic duct obstruction. On the 12th day after PTGBD, cholecystectomy and choledochotomy with primary closure were performed. The postoperative course was good and the patient was discharged on the 15th day after surgery.

Acute Disease↗
PubMed1996

Hepatic embolization through extrahepatic collateral pathways after hepatic arterial embolization for the hepatocellular carcinoma.

Extrahepatic collateral pathways developing after repeated transcatheter arterial embolization (TAE) for hepatocellular carcinoma (HCC) make therapeutic arterial embolization for recurrent lesions extremely difficult. TAE was performed through the collateral pathways using a sophisticated micro-catheter with good trackability and pushability and a coaxial system. Twenty-three TAEs were undertaken through the collateral pathways in 13 patients with recurrent HCC who had extrahepatic collateral pathways after the previous hepatic arterial TAE. There were 69 extrahepatic collateral pathways, with partially obstructed hepatic arteries. On the average, three feeding arteries were seen in the liver. The main extrahepatic collateral pathways were the inferior phrenic artery and epicholedocal artery, 18 vessels and 29 vessels, respectively, accounting for about 80% of the total collateral pathways. TAEs were successful in all cases and the number of embolized vessels was 2.1 on average. The average time of the first collateral TAE after the initial conventional hepatic arterial TAE was 2.3 years. Excellent prognosis was observed with a one-year survival rate of 77% and 3-year survival rate of 38% after the collateral TAE. We consider that collateral TAE for recurrent HCC with obstruction of the hepatic artery is the procedure of choice, is technically feasible, and provides better prognosis for the patients.

Adult↗
PubMed1995

Localization of mRNA for phosphatidylinositol 3-kinase in brain of developing and mature rats.

In the adult brain, the gene expression for phosphatidylinositol 3-kinase was weak in almost all neurons with relatively high levels in the olfactory bulb, hippocampus, and cerebellum. On the embryonic days high levels of the gene expression were found throughout the entire neuraxis, then decreased gradually to adult levels during postnatal development. The present finding suggests that phosphatidylinositol 3-kinase may contribute not only to neurogenesis but also to some important physiological roles in differentiating and mature neurons.

Amino Acid Sequence↗
PubMed1995

Initiating and responsible enzyme of arginine vasopressin degradation in human placenta and pregnancy serum.

The hydrolysis of arginine vasopressin (AVP) by human placental subcellular fractions and pregnancy sera was studied in the presence of selective inhibitors and the antibody against pregnancy serum oxytocinase (P-LAP) (EC 3.4.11.3) by measuring liberated amino acids by high-performance liquid chromatography (HPLC). AVP degradation by placental subcellular fractions and pregnancy sera was inhibited by bestatin. The IC50 values of bestatin on AVP degradation by placental subcellular fractions and pregnancy sera were similar to that of this inhibitor on the P-LAP measured by L-Leu-p-nitroamnilide as a substrate (LAP activity), which we reported previously. Our immunotitration study clearly showed that the initiating and responsible protease in AVP degradation in human placenta and pregnancy serum is P-LAP. Since N-benzylcarbonyl-valyl-prolinal (Z-Val-prolinal), a selective inhibitor of post-proline endopeptidase, and phosphoramidon, a putative endopeptidase-24.11 inhibitor, could not significantly influence the degradation of AVP by placental microsomal fractions. Neither enzyme seems to be actively involved in AVP degradation.

Amino Acid Sequence↗
PubMed1995

Ultraviolet B irradiation increases endothelin-1 and endothelin receptor expression in cultured human keratinocytes.

The effect of ultraviolet B (UVB) irradiation on endothelin-1 (ET-1) and ET receptor expression was examined using cultured normal human keratinocytes. Keratinocytes secreted ET-1 in the medium at a level of 2.1 pg/day/10(5) cells. UVB irradiation up to 10 mJ/cm2 increased ET-1 secretion 3-fold, and potentiated expression of mRNA for ET-1. Both ETA and ETB receptor mRNAs were detected in keratinocytes, and their expression was up-regulated by 5 mJ/cm2 UVB irradiation.

Base Sequence↗
PubMed1995

Role of nitric oxide and neuropeptides in neurogenic vasodilatation of the guinea pig mesenteric artery.

Although dense networks of adrenergic nerves are present and noradrenaline causes vasoconstriction, electrical field stimulation failed to elicit any constriction of the isolated ring preparation of the guinea pig mesenteric artery. In the presence of an active tone, a vasodilator response was elicited by electrical field stimulation in endothelium-removed tissues. Nonadrenergic, noncholinergic nerves mediate the electrical field stimulation-induced vasodilator response, since guanethidine and atropine did not affect while tetrodotoxin abolished it. Multiple mediators seem to participate in this vasodilatation. NADPH-diaphorase-positive nerves, calcitonin gene-related peptide (CGRP)- and vasoactive intestinal peptide (VIP)-immunoreactive nerves were present in the mesenteric artery. Nitro-L-arginine but not nitro-D-arginine suppressed the electrical field stimulation-induced vasodilator response with rapid onset and L-arginine restored it. VIP and CGRP relaxed the tissue in a dose-dependent manner. Pretreatment of the animals with capsaicin partly reduced the electrical field stimulation-induced vasodilator response. CGRP-(8-37), a CGRP antagonist, slightly attenuated the vasodilator response induced by both electrical field stimulation and CGRP. Glibenclamide, an inhibitor of ATP-sensitive K+ channels, decreased the nitro-L-arginine- and capsaicin-insensitive component of the electrical field stimulation-induced vasodilator response. Zinc protoporphyrin IX, an inhibitor of CO formation, did not affect the electrical field stimulation-induced response. In the presence of nitro-L-arginine without an active tone, electrical field stimulation induced a vasoconstrictor response that was sensitive to bunazosin and guanethidine. The results show that the electrical field stimulation-induced vasodilator response of the mesenteric artery of guinea pigs is mediated by nitric oxide (NO), CGRP and some yet unidentified substance(s). Elimination of the vasodilator response unmasked the adrenergic vasoconstrictor response to electrical field stimulation.

Animals↗
PubMed1995

Characteristic induction of hepatic metallothionein in mice by tumor transplantation.

Based on the previous finding that hepatic metallothionein (MT) level was tumor-growth dependently elevated in tumor-transplanted mice, the mode of induction of hepatic MT in tumor-bearing mice was comparatively studied with inflammation-induced and stress-subjected mice. The prefeeding with zinc (Zn)-deficient diet for 1 wk suppressed both the growth of tumor and the increase of hepatic MT and Zn in tumor-bearing mice. The postfeeding with Zn-deficient diet also suppressed hepatic MT induction in the course of tumor growth. On the other hand, in the other two experimental model mice, the prefeeding with Zn-deficient diet did not suppress the increase of hepatic MT and Zn. Further, the dexamethasone treatment stimulated hepatic MT induction in tumor-bearing mice, but rather reduced that in inflammation-induced mice. These results suggest that hepatic MT was induced uniquely in tumor-bearing mice and that Zn may play a key role for the induction of hepatic MT by tumor transplantation.

Animals↗
PubMed1995

Molecular identification of guanine-nucleotide-binding regulatory proteins which couple to endothelin receptors.

The coupling of two endothelin receptor subtypes (ET(A) and ETB) to several types of guanine-nucleotide-binding regulatory protein (G protein) was examined. Two subtypes of receptor cDNAs were transfected alone or together with four different G protein alpha subunit cDNAs in COS-7 cells. In ET(A) receptor-transfected cells, endothelin-1 (ET-1) activated phosphatidylinositol-specific phospholipase C as measured by the production of phosphatidylinositol 1,4,5-trisphosphate [Ins(1,4,5)P3]. ETB-receptor-transfected cells also produced Ins(1,4,5)P3 on stimulation by ET-1. The ET-1-induced production of Ins(1,4,5)P3 was markedly higher in G alpha q-cotransfected or G alpha 11-cotransfected cells than in cells transfected with each receptor alone. ET-1 also stimulated production of cAMP in ET(A) or ETB receptor-transfected cells. The production of cAMP was synergistically amplified by G alpha s co-transfection with each receptor. In contrast, when G alpha i2 was co-transfected with the ET(A) or ETB receptor, ET-1 displayed an inhibitory action on forskolin-stimulated cAMP accumulation. Pertussis-toxin treatment of the G alpha i2-transfected cells resulted in abolition of the endothelin-induced inhibition of cAMP accumulation. These observations indicate that both ET(A) and ETB receptors are able to couple to Gq, G11, Gs and Gi2, and suggest that endothelin receptors stimulate multiple effectors via several types of G protein simultaneously. The overall effects induced by endothelin may differ in cell types depending on the level of expression of each G-protein subtype in the cell.

Animals↗
PubMed1995

Hydrophobic accessible surface areas are proportional to binding energies of serine protease-protein inhibitor complexes.

For analysis of enzyme-protein inhibitor interactions, we calculated the buried hydrophobic and hydrophilic accessible surface areas (ASAs) of enzymes and primary contact regions. In the five enzyme-protein inhibitor complexes so far analyzed, we found that the hydrophobic ASAs buried between the enzyme and the primary contact region are proportional to their experimental binding energies. This finding indicates that the hydrophobic interaction drives the binding of enzymes with protein inhibitors.

Animals↗
PubMed1995

Increase in choroidal blood flow in rabbits with endothelin-1 induced transient complete obstruction of retinal vessels.

BACKGROUND: In a previous paper, we reported that retinal blood flow (RBF) ceased immediately after injection of 1 nmol endothelin-1 (ET-1) and no recovery of RBF was detected for at least 50 min. In this study, we confirmed the same duration of RBF cessation and measured choroidal blood flow (CBF) for 180 min. METHODS: We measured CBF in a rabbit model of transient complete obstruction of retinal vessels induced by intravitreal injection of a high dose of ET-1, using the hydrogen clearance method. We also investigated the effects of intravitreal injection of ET-1 on intraocular pressure (IOP), blood pressure, pulse rate and blood gases. RESULTS: CBF was significantly greater in the ET-1-injected eyes than in the control eyes 40-130 min after injection of ET-1 (P < 0.05). The maximal CBF ratio in the ET-1-injected eyes was 128 +/- 7.4% at 40 min. CBF decreased to the pre-injection level at 140 min after the injection of ET-1. There was no significant change in blood pressure, pulse rate and blood gases throughout this experiment, and there was no significant difference in IOP between ET-1-injected eyes and control eyes. CONCLUSION: It seems likely that the increase in CBF resulted from some local mechanisms of control that compensated for the decrease in RBF induced by intravitreal injection of ET-1. This model may be useful for investigation of the regulatory system of intraocular circulation, including endothelin receptors.

Animals↗
PubMed1995

Prevalence of HTLV-I-associated uveitis in the Kanto Plain, Japan.

BACKGROUND: Seroprevalence of antibody to human T-lymphotropic virus type I (HTLV-I) is high in the island of Kyushu, Japan. Reports on the etiological analysis of HTLV-I in patients with uveitis primarily document cases in this island. We studied the seroprevalence of HTLV-I at the Department of Ophthalmology in Yokohama City University Hospital and in Odawara Municipal Hospital, which are in the Kanto Plain on the island of Honshu, Japan. METHODS: The subjects were 741 patients who visited the two hospitals. The presence of serum antibodies against HTLV-I was assessed using the method of particle agglutination. RESULTS: Of 454 patients with nonuveitic ocular diseases, 9 (1.98%) were seropositive. Of 143 patients with definite diagnosis of uveitis, 1 (0.70%) was seropositive. Of 144 patients with non-specific uveitis (etiology undefined), 8 (5.56%) were seropositive. Thus, the prevalence of serum antibodies to HTLV-I was higher in patients with non-specific uveitis than in patients with specific uveitis or nonuveitic ocular diseases. Common ocular symptoms of 8 HTLV-I-infected patients with non-specific uveitis were compatible with the clinical features of uveitis described as HTLV-I-associated uveitis (HAU). CONCLUSION: It is important to suspect HAU in patients with uveitis of unknown etiology, even outside known areas of prevalence.

Adult↗
PubMed1995

Human hand impedance characteristics during maintained posture.

The present paper examines human hand impedance characteristics, including inertia and viscosity as well as stiffness, in multi-joint arm movements. While a subject maintains a given hand location, small external disturbances are applied to his hand by a manipulandum. The corresponding force-displacement vectors are measured and sampled over time in order to estimate the hand impedance by means of a second-order linear model. The experimental results in different subjects and hand locations are summarized as follows: (1) the estimated inertia matrices of the human hand well agrees with computed values using a two-joint arm model, (2) spatial variations of the stiffness ellipses are consistent with the experimental results of Mussa-Ivaldi et al. (1985), (3) hand stiffness and viscosity increase with the grip force of the subject, and (4) viscosity and stiffness ellipses tend to have similar orientation. The accuracy of the impedance estimation method is validated with a mechanical spring-mass system with known parameters.

Adult↗
PubMed1995

L-arginine and endogenous nitric oxide protect the gastric mucosa from endothelin-1-induced gastric ulcers in rats.

We have reported that endothelin-1 induces gastric ulcer characterized by a potent long-lasting vasoconstriction of the regional microvasculature. Nitric oxide synthesized from L-arginine has been shown to regulated gastric mucosal blood flow, and inhibition of its synthesis has been shown to delay the healing of gastric ulcers. We examined the effect of exogenous L-arginine and the inhibition of nitric oxide synthesis on the development of endothelin-1-induced gastric ulcers. In rats anesthetized with urethane, a continuous intravenous infusion of L- or D-arginine (10 mg.kg-1.min-1) was followed, 15 min later, by a submucosal injection of endothelin-1 (200 pmol/kg) in the anterior wall of the gastric body. In another group, rats were intravenously pretreated with N omega-nitro-L-arginine-methyl ester (1-10 mg/kg), a nitric oxide synthesis inhibitor, and then injected with endothelin-1 (40 pmol/kg). Twenty-four h later, L-arginine, but not D-arginine, had significantly reduced the extent and the severity of the endothelin-1-induced ulcer (mucosal wall damage, 18.11 +/- 4.79% and 88.14 +/- 7.06%, respectively; mean +/- SD, P < 0.001), and the nitric oxide synthesis inhibitor (10 mg/kg) had increased the endothelin-1-induced mucosal damage (ulcer length, 3.8 +/- 1.2 mm and 1.1 +/- 0.2 mm, respectively, P < 0.01). Continuous gastric mucosal blood flow measurements showed that L-arginine antagonized the endothelin-1-induced vasoconstriction. L-arginine protected the gastric mucosa from the ulcerogenic action of endothelin-1 and antagonized its vasoconstrictive action. The inhibition of endogenous nitric oxide potentiated the ulcerogenic effect of endothelin-1 on rat gastric mucosa.

Analysis of Variance↗
PubMed1995

Bosentan antagonizes the effects of endothelin-1 on rat gastric blood flow and mucosal integrity.

Bosentan, a new type of orally effective, mixed (ETA+ETB) endothelin receptor antagonist has been recently introduced and tested in a variety of experimental models. We studied the effect of bosentan on the changes in gastric mucosal hemodynamics and mucosal integrity, induced by the exogenous application of endothelin-1, in rats. Bosentan (10 mg/kg iv) pretreated rats were injected with endothelin-1 (500-1000-2000 pmol/kg, iv) and gastric mucosal hemodynamics were monitored. After combined oral (30 mg/kg) and systemic pretreatment with bosentan we studied the effects of submucosal injection of endothelin-1 (50 pmol) on blood flow and gastric mucosa. Bosentan antagonized the vasodilator, vasoconstrictor and ulcerogenic effects of endothelin-1 in the rat gastric mucosa. These results show that bosentan can be a useful probe in the study of endogenous endothelin in the gastrointestinal tract.

Administration, Oral↗
PubMed1995

DNA rearrangements in Japanese facioscapulohumeral muscular dystrophy patients: clinical correlations.

Facioscapulohumeral muscular dystrophy (FSHD) is an autosomal dominant muscular disorder in which the disease locus has been mapped to chromosome 4q35-qter. In most patients, the DNA rearrangements associated with FSHD have been found in the EcoRI fragment detected by the p13E-11 probe, and deletions of the 3.2 kb repeat units within the fragment are thought to cause the disease. To examine FSHD-associated DNA rearrangements in the Japanese population, we performed Southern blot analysis of the genomic DNA, using the p13E-11 and pFR-1 probes, in 158 Japanese individuals, including 38 FSHD patients from 19 families. We found that all but one (a possible affected recombinant) of the Japanese FSHD patients (97.4%) had specific smaller (< 28 kb) EcoRI fragments which cosegregated with the disease; this included four patients who had severe inflammatory changes in the muscle and eight patients with de novo DNA rearrangements. We found no FSHD patient who had a fragment larger than 28 kb. By contrast, only two of 35 Japanese controls (5.7%) had EcoRI fragments smaller than 28 kb. Our patients showed anticipation, i.e. decreased size of the EcoRI fragment in parallel with earlier onset of the disease (r = 0.531, P = 0.003, with younger age at onset in children (17.8 +/- 7.0) than their affected parents (31.5 +/- 14.8) (P = 0.019). However, since each family had a specific small EcoRI fragment associated with the disease, the differing clinical severity within a family cannot be explained by the size of the fragment alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗