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Biomedical subjects

K Yasuda

Publications and source records attributed to K Yasuda.

At least 433 records · Page 24Linked to original sources
PubMed1998

[Effects of ulinastatin on PMNL and vascular endothelial injury in patients undergoing open heart surgery with CPB].

Activated leukocytes are thought to contribute to respiratory dysfunction, alterations in microvascular permeability, disseminated intravascular coagulation, and thrombosis, all of which can complicate cardiopulmonary bypass (CPB). We have measured the levels of circulating proinflammatory cytokines (IL-6, 8), polymorphonuclear leukocytes elastase (PMNL-E), and vascular endthelial factors (ET-1, TM, sICAM-1) in patients undergoing open heart surgery with CPB. Patients were divided into a control group and a ulinastatin group. We have examined the effects of ulinastatin on these humoral mediators and postoperative pulmonary function. Every factor except IL-8 increased after CBP in control group. IL-6 and PMNL-E declined sharply to normal level in a few hours, but it took several days after surgery for ET-1, TM, and sICAM-1 to return to preoperative levels. Ulinastatin significantly suppressed the elevation of PMNL-E after CPB, indirectly suppressing the increase of other factors. There was no significant relationship between levels of humoral mediators and postoperative pulmonary function between the two groups. Our results suggest that ulinastatin alleviates the damage of vascular endothelium due to CPB (first attack), and this may be beneficial to reduce excessive inflammatory reaction against secondary insults.

Aged↗
PubMed1998

Heterogeneity in E2 region of GBV-C/hepatitis G virus and hepatitis C virus.

GB virus C/hepatitis G virus (GBV-C/HGV) is related distantly to hepatitis C virus (HCV). HCV has a hypervariable region (HVR), and exists as quasispecies in vivo. Although GBV-C/HGV also has replaceable amino acids in the presumed antigenic region, the existence and fluctuation of population of heterogeneous virus have not been evaluated. In this study, the heterogeneity of GBV-C/HGV and HCV was investigated by the single-strand conformation polymorphism (SSCP) analysis in six concomitantly infected patients. Two patients were observed for 4 years without any treatment, and four were treated with interferon-alpha (IFN). By SSCP analysis, amplicons of GBV-C/HGV RNA were separated into 1-5 bands on gels for each patient. The amplicons had different nucleotide but the same amino acid sequences in the presumed antigenic region. The amplicons of HCV RNA, separated into 1-4 bands, had different nucleotide and amino acid sequences in the HVR. In the two patients without treatment, the predominant strain of GBV-C/HGV was unchanged for the 4 years. In the four patients administered IFN, some strains of GBV-C/HGV disappeared after IFN therapy, whereas other strains persisted. The mean genetic distance among GBV-C/HGV strains represented by SSCP analysis was significantly lower than that of HCV (P < 0.05). The data indicate that: 1) GBV-C/HGV can be devoid of antigenic drift unlike HCV; 2) GBV-C/HGV has no HVR as seen in HCV in the presumed antigenic region; and 3) the sensitivity to IFN differs among GBV-C/HGV strains in the same hosts, as with HCV.

Adult↗
PubMed1998

Surgical experiences with peripheral arterial aneurysms due to vasculo-Behçet's disease.

BACKGROUND: Vascular involvement of Behçet's disease is currently considered as an important sign of the clinical evolution of patients with Behçet's disease. In addition, Behçet's disease is important in that it causes peripheral arterial aneurysms. METHODS: In this report, 4 patients with vasculo-Behçet's peripheral arterial aneurysms are presented. These aneurysms were distributed in the carotid artery (n=1), popliteal artery (n=1) and femoral arteries (n=3). Operative procedures included patch closure of a perforated wall for the carotid aneurysm, arterial reconstruction with the autogenous saphenous vein for the femoral and popliteal aneurysms. RESULTS: All four patients tolerated the operation well, however, two of four patients required re-operation due to anastomotic insufficiency later. CONCLUSIONS: Aneurysms associated with Behçet's disease have a sudden onset in many cases and often result in rupture. Appropriate operative procedures, including an adequate choice of anastomotic sites and reinforcement of the suture, may reduce the incidence of complications in patients with arterial aneurysms due to Behçet's disease.

Adolescent↗
PubMed1998

[Long-term results of operation for acute type A aortic dissection].

We report results of surgical treatment in 30 patients with acute type A aortic dissection. The average age of the 25 patients without the Marfan syndrome was 59.2 (range 51-76), and male/female ratio was 11/14. The average age of the five patients with the Marfan syndrome was 36.8 (range 27-48), and male/female ratio was 2/3. As an adjunct, we used deep hypothermic circulatory arrest during ascending aortic replacement, while selective cerebral perfusion was employed during aortic arch replacement. Operative procedures for the non-Marfan patients included 14 ascending aortic replacement and 11 ascending and aortic arch replacement, while the Marfan patients underwent extensive aortic replacement that included three aortic arch replacement combined with the Bentall operation, one extensive replacement from the ascending aorta to the descending thoracic aorta and one ascending and aortic arch replacement. One patient died early after the operation and the early mortality rate was 3.3%. No patient developed new brain complication related to the operation. During the follow-up period, three patients died and two patients required a total of three subsequent distal operations. Cumulative survival rate was 89% at one year, 85% at three years, 85% at five years. Cumulative cardiovascular event-free rate was 89% at one year, 85% at three years, 77% at five years. Early and long-term results of surgical treatment for acute type A aortic dissection was satisfactory. This seems to result from the use of deep hypothermic circulatory arrest and selective cerebral perfusion as an adjunct and application of aortic arch replacement when the aortic arch is dilated or intimal tear is located in the aortic arch or more distally.

Aged↗
PubMed1998

[Responsibility of the lateral geniculate nucleus in photosensitive epilepsy: dipole tracing method].

We studied the location of the electric generator of photoparoxysmal discharges using a scalp-skull-brain dipole tracing (DT) method. By this method, the location of epileptic discharges on each scalp EEG was calculated as an equivalent current dipole (ECD) in 8 cases of epilepsy who had photoparoxysmal discharges. We divided these cases into groups A and B (4 cases each), comprising of patients with and without visually-induced seizures, respectively. The ECDs of the 3 cases in group A corresponded to the small area adjacent to the lateral geniculate nucleus on MRI superimposed. On the other hand, the ECDs of all cases in group B located at the corpus callosum. This study suggests the pathways of epileptic discharges from the epileptic focus are different between two groups. It is supposed that neural activity of the lateral geniculate nucleus might be responsible for the generator mechanism of photoparoxysmal discharges which evokes photosensitive epilepsy.

Adolescent↗
PubMed1998

Pancreaticoduodenal artery aneurysm with celiac trunk occlusion. Report of a case.

A case of superior mesenteric artery branch aneurysm is described. A 43-year-old female patient was hospitalized after the incidental discovery of a low echogenic mass next to the superior mesenteric artery trunk. A selective superior mesenteric arteriography confirmed aneurysms of the inferior pancreaticoduodenal artery and an aortogram demonstrated occlusion of the celiac trunk. Bypass between the abdominal aorta and the common hepatic artery and resection of aneurysms were performed. The possible etiology and operative procedure are discussed.

Adult↗
PubMed1998

Successful repair of cardio-Behçet's disease with aortic and mitral regurgitation.

A case of Behçet's disease with cardiac involvement of aortic and mitral regurgitation is presented. The patient underwent aortic and mitral valve replacement, along with plication of the ascending aorta. Histological examination revealed chronic inflammation with degenerative changes, consistent with Behçet's disease. Anti-inflammatory therapy using prednisolone was maintained throughout the postoperative period. This is the first case of cardio-Behçet's disease surgically treated for both aortic and mitral valves with a successful long-term survival.

Aortic Valve Insufficiency↗
PubMed1997

The nature of detrusor bladder neck dyssynergia in non-neurogenic bladder dysfunction.

There have been two major opinions on the pathology or nature of the bladder neck contracture. One is an organic fibrosis, and the other is an accentuated sympathetic nervous function, or detrusor bladder neck dyssynergia. The existence of active detrusor bladder neck dyssynergia in neurogenic bladder was reported in a urodynamical manner using microtip transducer catheters. However, it has not been confirmed whether or not detrusor bladder neck dyssynergia is responsible for bladder neck contracture in patient without neurogenic bladder. The present study was designed to determine by means of video urodynamic study whether or not bladder neck contracture would be of the same nature as detrusor bladder neck dyssynergia in non-neurogenic bladder subjects. The study included 32 male subjects of 16-84 years old (average 52.3): 17 bladder neck contracture subjects including 7 subjects associated with minimum complications (4 with trapped benign prostatic hyperplasia and 3 with incomplete neurological lesion) and 15 non-bladder neck contracture subjects (10 healthy volunteers, 2 chronic prostatitis, 3 prostatodynia). A 5-microtip transducer catheter was used to measure the pressure in the bladder and at the bladder neck, the external urethral sphincter and the bulbous urethra during voiding. Proper localization of the transducers was done with an image intensifier. Bladder outlet obstruction localized at the bladder neck (diameters smaller than 0.75 cm) on voiding cystourethrogram was defined as bladder neck contracture. Detrusor bladder neck dyssynergia was defined where pressures were higher at the level of bladder neck than in the bladder during detrusor contraction. An alpha-blocker, terazosin hydrochloride (0.5 mg, b.i.d., two weeks), was orally administered to subjects judged to have detrusor bladder neck dyssynergia by the above methods for the purpose of confirming whether detrusor bladder neck dyssynergia was really due to accentuated sympathetic nervous function. Detrusor bladder neck dyssynergia was found in seven cases with bladder neck contracture: 6 cases with bladder neck contracture with minimum complications and only 1 case with bladder neck contracture without complications (p < 0.01). Detrusor bladder neck dyssynergia was found at the beginning and ending of micturition, but not at maximum flow. In six cases with detrusor bladder neck dyssynergia, the condition disappeared after terazosin. In conclusion, detrusor bladder neck dyssynergia was not thought to be a major factor of voiding dysfunction in bladder neck contracture in non-neurogenic bladder. In the presence of sympathetic hyperactivity or in cases with increased number of alphareceptors, detrusor bladder neck dyssynergia occurs, being predominantly noted in trapped benign prostatic hyperplasia and neurological disorder patients.

Adolescent↗
PubMed1997

Gastric inhibitory polypeptide activates MAP kinase through the wortmannin-sensitive and -insensitive pathways.

The signal transduction pathways of a cloned human gastric inhibitory polypeptide (GIP) receptor have been investigated in CHO cells stably expressing this receptor. Exposure of GIP receptor expressing cells to GIP significantly increased MAP kinase activity. Time course analysis showed that a rapid and marked increase in MAP kinase activation was detected and that this activation reached maximal levels 10 min after the addition of GIP. Dose-response analysis showed that GIP activated MAP kinase activity in a dose-dependent manner with an ED50 value of 5.9 x 10(-10) M of GIP. Wortmannin, a potent inhibitor of phosphatidylinositol 3-kinase (PI3-kinase), partially inhibited GIP-induced MAP kinase activation, suggesting that GIP activates MAP kinase through two different, wortmannin-sensitive and -insensitive pathways. It has been demonstrated that in CHO cells cAMP attenuates MAP kinase activity by inhibiting Raf-1. Since GIP elevates intracellular cAMP, we examined the effects of cAMP on MAP kinase activation. Interestingly, forskolin, which increased intracellular cAMP levels, significantly inhibited MAP kinase activation by GIP, but did not affect MAP kinase activation by GIP in the presence of wortmannin, suggesting that the wortmannin-sensitive pathway activates an MAP kinase cascade at or above the level of Raf-1 and that the wortmannin-insensitive pathway activates an MAP kinase cascade below the level of Raf-1. These findings demonstrate that the GIP receptor is linked to the MAP kinase cascade via at least two different pathways.

Androstadienes↗
PubMed1997

A bacterial cloning vector using a mutated Aequorea green fluorescent protein as an indicator.

The bacterial cloning vector, pGreenscript A, derived from the mutated Aequorea green fluorescent protein (GFP-S65A) gene, when expressed in E. coli produced colonies that showed yellow color under daylight and strong green fluorescence under long-wave ultraviolet light. The vector was used to select for inserted foreign genes based on the loss of the yellow color/green fluorescence of E. coli cells caused by the insertional inactivation of GFP production.

Amino Acid Sequence↗
PubMed1997

Development of non-insulin-dependent diabetes mellitus in the double knockout mice with disruption of insulin receptor substrate-1 and beta cell glucokinase genes. Genetic reconstitution of diabetes as a polygenic disease.

Non-insulin-dependent diabetes mellitus (NIDDM) is considered a polygenic disorder in which insulin resistance and insulin secretory defect are the major etiologic factors. Homozygous mice with insulin receptor substrate-1 (IRS-1) gene knockout showed normal glucose tolerance associated with insulin resistance and compensatory hyperinsulinemia. Heterozygous mice with beta cell glucokinase (GK) gene knockout showed impaired glucose tolerance due to decreased insulin secretion to glucose. To elucidate the interplay between insulin resistance and insulin secretory defect for the development of NIDDM, we generated double knockout mice with disruption of IRS-1 and beta cell GK genes by crossing the mice with each of the single gene knockout. The double knockout mice developed overt diabetes. Blood glucose levels 120 min after intraperitoneal glucose load (1.5 mg/g body wt) were 108 +/- 24 (wild type), 95 +/- 26 (IRS-1 knockout), 159 +/- 68 (GK knockout), and 210 +/- 38 (double knockout) mg/dl (mean +/- SD) (double versus wild type, IRS-1, or GK; P < 0.01). The double knockout mice showed fasting hyperinsulinemia and selective hyperplasia of the beta cells as the IRS-1 knockout mice (fasting insulin levels: 0.38 +/- 0.30 [double knockout], 0.35 +/- 0.27 [IRS-1 knockout] versus 0.25 +/- 0.12 [wild type] ng/ml) (proportion of areas of insulin-positive cells to the pancreas: 1.18 +/- 0.68%; P < 0.01 [double knockout], 1.20 +/- 0.93%; P < 0.05 [IRS-1 knockout] versus 0.54 +/- 0.26% [wild type]), but impaired insulin secretion to glucose (the ratio of increment of insulin to that of glucose during the first 30 min after load: 31 [double knockout] versus 163 [wild type] or 183 [IRS-1 knockout] ng insulin/mg glucose x 10(3)). In conclusion, the genetic abnormalities, each of which is nondiabetogenic by itself, cause overt diabetes if they coexist. This report provides the first genetic reconstitution of NIDDM as a polygenic disorder in mice.

Animals↗