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Biomedical subjects

K Kaneko

Publications and source records attributed to K Kaneko.

At least 325 records · Page 18Linked to original sources
PubMed1997

Anatomy of the round ligament in female infants and children with an inguinal hernia.

BACKGROUND: The ligament which runs along an inguinal hernia sac in females is believed to be the round ligament of the uterus. According to most standard textbooks, the round ligament of the uterus terminates at the labium majorum. This study examined the termination of the ligament. METHODS: The anatomy of the ligament was examined in 248 female children (aged 1 month to 11 years) with an inguinal hernia. The anterior wall of the hernia sac, consisting of the inner and outer membranes, was opened and the inner membrane of the sac was pulled up with forceps; the hernia sac was then separated from the surrounding tissue. The termination of the ligament was observed. RESULTS: The ligament did not end at the labium majorum but terminated in the hernia sac. The ligament was attached to the mid portion of the fallopian tube near the ovary. CONCLUSION: These findings suggest that the ligament which runs along the hernia sac is the suspensory ligament of the ovary.

Child↗
PubMed1997

[A case of right ventricular myxoma].

A 43-year-old male presented with a history of occasional syncopal episodes and general fatigue for 4 months. On admission, a grade 4/6 systolic murmur was noted, and the electrocardiogram demonstrated frequent premature supraventricular beats. An echocardiogram revealed the presence of a multi-lobular mass in the right ventricle which prolapsed into the pulmonary artery during systole. Ultrafast computed tomography demonstrated a pedunculated mass arising from the right ventricular free well. At operation, the soft mass was excised through the tricuspid valve under cardiac arrest. Histopathologically, the tumor was diagnosed as a myxoma. Myxoma of the right ventricle occurs very rare. We review the literature relevant to cardiac myxoma.

Adult↗
PubMed1997

Protein plugs cause symptoms in patients with choledochal cysts.

OBJECTIVES: Symptoms in patients with choledochal cysts are believed to be caused by pancreaticobiliary maljunction. However, this anomaly alone cannot explain the occurrence of symptoms. The aim of this study was to elucidate the etiology of the symptomatology in patients with choledochal cysts. METHODS: Clinical data and preoperative and operative cholangiopancreatography were reviewed in 55 consecutive patients with choledochal cysts seen between 1980 and 1996. RESULTS: The bile duct was significantly larger in the symptomatic phase than in the asymptomatic phase. External biliary drainage resulted in rapid resolution of symptoms in 11 patients. A radiolucent filling defect in the pancreaticobiliary duct was found in 22 patients (40.0%). The defects were in the common channel in 15 patients and near the common channel in 7 patients. Filling defects disappeared spontaneously or after irrigation in 19 patients. In three patients, the material in the common channel removed during surgery was fragile and consisted of more than 98% protein. CONCLUSION: The filling defects were protein plugs. The simultaneous occurrence of symptoms and signs may be explained by disturbances in bile and pancreatic secretory flow caused by a protein plug in the common channel.

Adolescent↗
PubMed1997

[Size estimation method for patch used in reconstruction of LV cavity].

The reconstruction of LV cavity is accomplished by suturing a patch to the viable myocardium to exclude the infarcted area from the high LV pressures. However, there is no clear guideline to estimate the size of patch used for LV reconstruction. We have designed a new method to determine the correct patch size, and applied it in 5 cases. The suture line of the patch is at the junction of contractile (functional) and infarcted portions of LV. The patch size is determined by the length of AB, termed "a", as the base, where "point A" represents the junction on the LV anterior wall side, and "point B" the junction of the LV posterior wall side, from RAO 30 degrees projection of the left ventriculogram obtained by cardiac catheterization. In LV aneurysm, we designed the patch in the range of a/2 < l < or = pi a/2, where patch length on RAO 30 degrees is considered "l". An effort was made to reconstruct to normalize LV volume and contour by designing the patch size to be a/2 < l < a, particularly when the contractile portion was enlarged by aneurysm. On the other hand, in post AMI VSD, LV contractile portion is not enlarged in early stage. Therefore, the patch was designed in the range of a < l < or = pi a/2 to maintain LV volume. Postoperative LV volume can be calculated prior to surgery, by using the lengths of the designed patch. Postoperative analysis indicated that the actual LV volume and contour were almost identical to our estimation. This method is very useful in planning the patch size for LV reconstruction.

Aged↗
PubMed1997

Expression of interleukin-6 in the ventricles and coronary arteries of patients with myocardial infarction.

While an overproduction of interleukin-6 (IL-6) has been observed in patients with acute myocardial infarction (AMI), its clinical significance and localization in the ischemic myocardium have not been elucidated. We examined immunohistochemically the expression of IL-6 in 12 autopsied patients with AMI who had died within seven days of the infarction. Twenty sections of ischemic myocardium and nine of the coronary arteries involved were stained with anti-IL-6 and anti-atrial natriuretic peptide (ANP). The diameter of the myocardium was analyzed. The greatest expression of IL-6 in the infarcted myocardium occurred in patients who had died three to four days after the onset (2.7 +/- 0.4), as judged by a scheme for grading IL-6 expression. Patients who died within one to two days (1.0 +/- 0.3) or five to eight days (0.6 +/- 0.4) less frequently showed an overproduction of IL-6. The IL-6-positive myocardium co-expressed ANP and was significantly (p < 0.05) hypertrophied, when compared with the IL-6-negative myocardium. The diameter of IL-6-positive myocardial myocytes was significantly (p < 0.02) increased in patients who died within one to two days (1.6 +/- 0.2), three to four days (1.8 +/- 0.3), or five to eight days (2.0 +/- 0.2) after the AMI. The involved coronary arteries expressed IL-6 in the intimal and smooth muscle cells, as did atherosclerotic coronary arteries not involved in AMI. An overproduction of IL-6 was confirmed in the injured myocardium with hypertrophy in patients who died of AMI within seven days after onset. The hypertrophied injured myocardium co-expressed IL-6 and ANP. The expression of IL-6 in the myocardium in AMI appears to be associated with the mechanism of cardiac hypertrophy.

Adult↗
PubMed1997

Comparative effects of gallopamil and verapamil on the mechanical and electrophysiological parameters of isolated guinea-pig myocardium.

The effects of gallopamil, D600, a methoxy derivative of verapamil, on the mechanical and electrophysiological parameters of isolated guinea-pig myocardial preparations were compared with those of verapamil. Both gallopamil and verapamil produced concentration-dependent negative chronotropic and negative inotropic effects in isolated right atrial and right ventricular papillary muscles, respectively. The negative chronotropic and negative inotropic potencies of gallopamil were 7.2 and 4.3 times higher than those of verapamil, respectively. Gallopamil decreased the action potential duration of isolated papillary muscles without substantially affecting other action potential parameters, while verapamil decreased not only the action potential duration but also the maximum rate of rise and amplitude. In voltage-clamped single ventricular myocytes, gallopamil as well as verapamil decreased the L-type Ca2+ current amplitude. The potency orders for the shortening of the action potential duration and inhibitory effects of the L-type Ca2+ current amplitudes were verapamil > gallopamil. These results indicate that gallopamil has higher negative chronotropic and inotropic potency than verapamil as a result of factors other than L-type Ca2+ current inhibition.

Animals↗
PubMed1996

Cloning of a novel signal-transducing adaptor molecule containing an SH3 domain and ITAM.

We molecularly cloned a cDNA coding for a novel phosphotyrosine molecule with a 70 kDa molecular mass, named STAM (signal transducing adaptor molecule), which is tyrosine-phosphorylated rapidly after stimulation with various cytokines such as IL-2, IL-3, IL-4, IL-7, GM-CSF, EGF and PDGF. STAM contains an SH3 (Src-homology 3) domain and the ITAM (immunoreceptor tyrosine-based activation motif), suggesting that STAM acts as an adaptor molecule involved in signal transducing pathways from the cytokine receptors.

Adaptor Proteins, Signal Transducing↗
PubMed1996

A new model for pancreaticobiliary maljunction without bile duct dilatation: demonstration of cell proliferation in the gallbladder epithelium.

Patients with pancreaticobiliary maljunction without bile duct dilatation (PBMWBDD) develop gallbladder carcinoma frequently. No models of PBMWBDD exist, and no previous studies have clearly demonstrated changes in the gallbladder relating to carcinogenesis. We, therefore, examined the cell kinetics of the gallbladder epithelium in a new experimental model of PBMWBDD. A cat model was produced by performing choledocho-pancreatic side-to-side ductal anastomosis in nine animals. Five cats, in which the choledocho-pancreatic ducts were exposed only, served as controls. After 6 months, the gallbladders of these cats were removed and stained with anti-proliferating cell nuclear antigen (PCNA) antibody (PC10, Dako). The labeling index (LI) was determined from the percentage of positive nuclei in three microscopic fields. The diameter of the common bile duct was not different between the models and the controls. In the models, the number of PCNA positive cells was significantly increased. The mean (+/- standard deviation) PCNA LI was 28.1 +/- 12.2% in the models and 4.3 +/- 1.6% in the controls (P < 0.01). These studies clearly indicate that this model is suitable for studying PBMWBDD and that PBMWBDD has a prominent proliferating effect on the gallbladder epithelium which may play an important role in gallbladder carcinogenesis.

Amylases↗
PubMed1996

Bradykinin enhances GLUT4 translocation through the increase of insulin receptor tyrosine kinase in primary adipocytes: evidence that bradykinin stimulates the insulin signalling pathway.

It has been suggested that bradykinin stimulates glucose uptake in experiments in vivo and in cultured cells. However, its mechanism has not yet been fully elucidated. In this study, the effects of bradykinin on the insulin signalling pathway were evaluated in isolated dog adipocytes. The bradykinin receptor binding study revealed that dog adipocytes possessed significant numbers of bradykinin receptors (Kd = 83 pmol/l, binding sites = 1.7 x 10(4) site/ cell). Reverse transcription-polymerase chain reaction amplification showed the mRNA specific for bradykinin B2 receptor in the adipocytes. Bradykinin alone did not increase 2-deoxyglucose uptake in adipocytes; however, in the presence of insulin (10(-7) mol/l) it significantly increased 2-deoxyglucose uptake in a dose-dependent manner. Bradykinin also enhanced insulin stimulated GLUT4 translocation from the intracellular fraction to the cell membrane, and insulin induced phosphorylation of the insulin receptor beta subunit and insulin receptor substrate-1 (IRS-1) without affecting the binding affinities or numbers of cell surface insulin receptors in dog adipocytes. The time-course of insulin stimulated phosphorylation of the insulin receptor beta subunit revealed that phosphorylation reached significantly higher levels at 10 min, and stayed at the higher levels until 120 min in the presence of bradykinin, suggesting that bradykinin delayed the dephosphorylation of the insulin receptor. It is concluded that bradykinin could potentiate insulin induced glucose uptake through GLUT4 translocation. This effect could be explained by the potency of bradykinin to upregulate the insulin receptor tyrosine kinase activity which stimulates phosphorylation of IRS-1, followed by GLUT4 translocation.

Adipocytes↗
PubMed1996

CETP is a determinant of serum LDL-cholesterol but not HDL-cholesterol in healthy Japanese.

Cholesteryl ester transfer protein (CETP) is one of the factors that regulate plasma levels of HDL-cholesterol. To identify the factors that may regulate CETP activity, and to determine to what extent CETP is correlated with physiologic concentrations of lipoprotein, we performed an epidemiologic study in 586 healthy volunteers (317 males and 269 females mean age 52.2 +/- 10.9 years). CETP activity in these subjects was 192.96 +/- 48.73 (mean +/- S.D.) nmol/ml/h and distributed to a wide range (60-450 nmol/ml/h). Using multiple regression analysis, we found significant positive correlations between CETP activity and LDL-cholesterol (P < 0.03), apolipoprotein (apo) E (P < 0.005) and LCAT activity (P < 0.001). CETP activities showed significant negative correlation with apo A-I (P < 0.03). However, CETP activity showed no significant correlation either with HDL cholesterol or with apo B. One-way layout analysis of variance showed that alcohol drinking and cigarette smoking significantly reduced CETP activity, but there was no significant association between CETP activity and body mass index. Although CETP activities were significantly higher in females than in males (P < 0.001), multiple regression analysis showed no correlation between CETP activity and age in either the males or the females. Our results suggest that CETP activity regulates the concentration of apo A-I and LDL-cholesterol, and that such activity may be influenced by gender, alcohol consumption and cigarette smoking.

Adult↗
PubMed1996

The effects of single and repeated phencyclidine administration on [125I] iomazenil binding in the rat brain.

We measured [125I] iomazenil binding, labeling the central-type benzodiazepine receptor in 37 discrete rat brain areas following single (7.5 mg/kg, i.p.) and repeated (7.5 mg/kg/day x 14 days, i.p.) treatment with phencyclidine (PCP), a non-competitive antagonist of the N-methyl-D-aspartate(NMDA)-type glutamate receptor, using in vitro quantitative autoradiographic receptor binding assay. Both single and repeated PCP treatment produced heterogeneous changes in the rat brain in a similar manner, the magnitude of change in [125I] iomazenil binding being generally greater in the repeated treatment group than in the single treatment group. A significant increase in [125I] iomazenil binding was observed in the superficial layer (layer I-IV) of the parietal cortex in both of the PCP treatment groups and the CA1 of the hippocampus of the repeated PCP-treated group. There was a significant decrease in [125I] iomazenil binding in the piriform cortex of the repeated PCP-treated group. These results suggest that the blockade of NMDA receptor-mediated glutamatergic neurotransmission by PCP produces the compensational alterations in the central-type benzodiazepine receptor antagonist binding, and that the observed diversity may be due to dissimilar modes of organizations between glutamatergic and the GABA(gamma-aminobutyric acid)-benzodiazepine receptor complex.

Animals↗