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Biomedical subjects

Y Yazaki

Publications and source records attributed to Y Yazaki.

At least 811 records · Page 45Linked to original sources
PubMed1983

Reconstitution of heavy chain and light chain 1 in cardiac subfragment-1 from hyperthyroid and euthyroid rabbit hearts.

It is now established that cardiac myosin from hyperthyroid rabbit hearts (TXM) exhibits high Ca2+ ATPase activity. The high Ca2+ ATPase activity of TXM was completely retained in cardiac myosin subfragment-1 (S-1) (1.33 +/- 0.04 mumol Pi/mg per min; euthyroid, 0.51 +/- 0.04). Cardiac S-1 from hyperthyroid and euthyroid rabbits (TXS-1 and NS-1) had the same pattern in SDS-polyacrylamide gel electrophoresis. The possible influence of heavy and light chains of TXM on increasing the ATPase activity was examined by reconstitution in the S-1 preparation. Crosswise reconstitution was performed using cardiac S-1 heavy chain (90,000 daltons) and light chain 1 (LC1) (27,000 daltons) from hyperthyroid and euthyroid hearts. Reconstitution was verified by using radiolabeled LC1. More than 95% of S-1 was recovered with full ATPase activity. When TXS-1 was reconstituted with LC1 from euthyroid hearts, the reconstituted molecule retained high ATPase activity. On the other hand, NS-1 reconstituted with LC1 from hyperthyroid hearts failed to increase the ATPase activity. The ATPase activity of S-1 was determined by the source of the heavy chain. These results suggest that the high Ca2+ ATPase activity of cardiac myosin and S-1 from hyperthyroid animals arises from the molecular alteration of the heavy chain induced by thyroxine administration.

Animals↗
PubMed1983

Serial changes in cytosolic, mitochondrial, and lysosomal enzymes and cardiac myosin light chain II in plasma following coronary ligation in conscious closed-chest dogs.

We studied serial changes in various myocardial enzymes and cardiac myosin light chain II (LCII) in plasma following coronary ligation in 14 conscious closed-chest dogs. Cytoplasmic enzymes [creatine phosphokinase (CPK) and supernatant glutamic oxaloacetic transaminase (sGOT)] reached maximum at 12-24 hr and returned to normal at 72-96 hr. The mitochondrial isozyme of GOT (mGOT) began to rise at 6-9 hr, peaked at 12-30 hr (4.8-42.2 IU/liter), and stayed higher at 96 hr than before infarction. Glutamate dehydrogenase (GLDH), another mitochondrial enzyme, began to elevate at 6-16 hr and reached maximum at 24-60 hr (6.2-20.5 U/liter); GLDH also showed higher levels at 96 hr than before infarction. N-Acetyl-beta-glucosaminidase (NAG), a lysosomal enzyme, showed a biphasic pattern in every case. The first peak appeared at 3-12 hr, and the second one at 36-72 hr. Myosin LCII began to rise at 3-9 hr, peaked at 30-120 hr (34-136 ng/ml), and remained elevated for 7 to 10 days. Determination of these myocardial enzymes or LCII in plasma is useful for the diagnosis of acute myocardial infarction.

Acetylglucosaminidase↗
PubMed1983

Myocardial infarct size from serum cardiac myosin light chain. Clinical and experimental studies.

The relationship between myocardial infarct size and serum cardiac light chain (LC) levels was studied in experimental and clinical myocardial infarction. In dogs with left anterior descending coronary artery occlusion, regression analysis showed good correlation between infarct size and LC II release, but CPK-MB release failed to correlate with infarct size because of a decreasing value of cumulative CPK with larger sized infarctions. In patients with acute myocardial infarction, Peak LC I levels correlated well with CPK release, since the phenomenon of the decreased CPK release in larger sized infarction was not so distinctive in human cases. Thus, LC determination may better quantitate the extent of myocardial damage as well as provide a specific and sensitive method for diagnosis of acute myocardial infarction.

Animals↗
PubMed1983

Evaluation of methods for estimating infarct size by myosin LC2: comparison with cardiac enzymes.

The relationship between histologically determined infarct size and release or peak levels of circulating cardiac enzymes and myosin light chain 2 (LC2) was studied. Myocardial infarction was produced by ligating the left anterior descending coronary artery in 18 conscious closed-chest dogs. Creatine phosphokinase (CPK), cytosolic and mitochondrial isozymes of aspartate transaminase (sAST and mAST) in the plasma, and LC2 in the serum were measured serially until 10 days after infarction, when infarct size was determined histologically [range 4.0-38.8% of the left ventricular weight (%LV)]. Infarct size correlated most closely with LC2 release (r = 0.82, P less than 0.001) and less closely with peak sAST (r = 0.59, P less than 0.01), peak mAST (r = 0.49, P less than 0.05), peak CPK (r = 0.22), and CPK release (r = 0.14). The correlation between infarct size and CPK release was improved by limiting the analysis to the dogs with infarct size of less than 20% LV (n = 11, r = 0.53, P less than 0.1). Because, among cardiac enzymes and LC2, CPK activity decayed most rapidly in the lymph fluid when incubated in vitro, degeneration of CPK in the lymph stream may contribute to the nonlinear relationship between infarct size and CPK release.

Animals↗
PubMed1983

[10 cases of congenital cystic dilatation of the common bile duct].

Ten cases of congenital cystic dilatation of the common bile duct (including insufficiency form) were examined for mode of pancreatico-biliary anastomosis and cholangiographic findings. The results were as follows. Male to female ratio was 1:9 in this series. Regarding the mode of pancreatico-biliary anastomosis, type I (pancreatic duct flowing into common bile duct) tended to occur frequently in patients 30 years old or more, while type II (common bile duct flowing into pancreatic duct) in patients under 30 years old. With respect to clinical symptoms, no cases had triad (jaundice, abdominal pain and palpation of mass), but abdominal pain occurred in all the cases. Jaundice and palpation of mass were seen in 30% and 10% of the cases, respectively. Regarding the age at the onset and the duration of the disease, type I occurred in elderly cases with a longer duration of disease, while type II occurred in young cases with a shorter duration of disease. The degree of distention increased in proportion to the severity of the peripheral stenosis of the biliary duct. Complication with biliary tract carcinoma was seen in 2 type I cases. Among the type I cases, those with mild distention were considered to be insufficient form.

Adult↗
PubMed1983

[Clinical significance of HBeAg and anti-HBe in HBsAg positive liver diseases].

Variation of incidence of HBe antigen (HBeAg) and HBe antibody (anti-HBe) was examined by use of RIA in 72 patients with HBsAg positive liver diseases. 1) Percentage of positive HBeAg was highest (71.5%) in chronic active hepatitis with lobular distortion, followed by chronic active hapatitis without lobular distortion (70.0%) and acute hepatitis in asymptomatic HBsAg carriers (66.7%). In contrast, it was low in chronic inactive hepatitis (35.7%) and liver cirrhosis (38.5%). None of liver cancers showed HBeAg positive reaction. 2) Percentage of positive HBe antibody (anti-HBe) was highest in liver cancer (100%), followed by liver cirrhosis (61.5%) and chronic inactive hepatitis (50.0%). In acute hepatitis from asymptomatic HBsAg carriers no anti-HBe was found. In chronic active hepatitis the percentage of positive anti-HBe was low, 21.4 and 30.0% with and without lobular distortion, respectively. 3) In 45 patients with persistently positive HBsAg liver diseases, fluctuations of HBeAg and anti-HBe were followed over a period of one year in relation to serum GPT values, an indicator of clinical conditions. Serum GPT tended to fluctuate or to remain high in patients with persistently positive HBeAg or with sporadically positive HBeAg or anti-HBe, whereas it tended to become low or normal with persistently positive anti-HBe or with seroconversion from HBeAg to anti-HBe. However, there were some exceptions to this tendency. From these results we concluded that it is clinically of significant value to determine HBeAg and anti-HBe levels for the effective assessment of the activity and time course of HBsAg positive liver diseases.

Adolescent↗
PubMed1983

[The effect of paromomycin sulfate on Diphyllobothrium latum].

Nine vital tapeworms were expelled from 7 patients with diphyllobothriasis latum by the modified Damaso De Rivas' method. Seven worms of them placed in 1% and 5% paromomycin solution (37 degrees C, pH 6.8--6.9) and 2 were in physiological saline at 37 degrees C as controls. In both 1% and 5% solution, the movement of worms stopped completely within 15 minutes. When they were taken out from the solution and washed thoroughly with physiological saline solution, they did not move any longer and died soon. As for the controls, they were moving with animation in physiological saline at 37 degrees C even after 60 minutes. Pathohistologically (H.E. stain), the scolex was seriously affected down to the immature proglottid; degeneration and desquamation of the villi and cuticle with somatic cells exposed and edematous swelling of the whole body. Somatic cells had degenerative necrosis, plasmatomy and disorder in the disposition of the circular muscle and longitudinal muscle were marked. Scanning electronmicroscopy revealed that the worms treated with paromomycin had the scolex remarkably impaired and destroyed the villous epithelial layer and cuticle of the immature proglottid adjacent to the scolex desquamated exposing somatic cells regardless of the duration of exposure to and the concentration of paromomycin, while in the controls, the scolex was normal and the worm surface was closely covered with normal villi. Aminoglycoside antibiotics are known to have neurotoxic effect in general. It seems to be related to this neurotoxicity that paromomycin solution stopped the movement of worms. The changes occurring in the tapeworms were irreversible and the worms died soon. It is suggested that when patients with diphyllobothriasis latum are administered with paromomycin, the alterations of the worms induced by paromomycin are accelerated by potent human digestive juice.

Animals↗
PubMed1982

An extensive primary myocardial fibrosis in progressive systemic sclerosis--a case report with autopsy findings.

An extensive myocardial fibrosis due to progressive systemic sclerosis (PSS) was described in a 36-year-old normotensive woman without pulmonary hypertension. An electrocardiogram showed low voltage and a pseudo-infarctional pattern in leads V1 through V3. Right ventricular dilatation and generalized left ventricular hypokinesis were present, but her pulmonary artery pressure was normal. Serum creatine kinase (CK) was elevated to 2305 U/L and CK-MB isoenzyme was as high as 7.1%. Simultaneously performed isoenzyme analysis of CK from the homogenate of the skeletal muscle of the patient showed a similar pattern, thus confirming that serum CK originated mainly from the skeletal muscle lesions. Autopsy findings demonstrated diffuse myocardial fibrosis and relatively unremarkable changes in the lungs and the kidneys. Our case serves as a warning that primary myocardial fibrosis could be, in some cases, so extensive that it might lead to a rapidly aggravated myocardial dysfunction and eventual death.

Adult↗
PubMed1982

Effects of dietary sodium on brain angiotensin II receptors in spontaneously hypertensive rats.

The effects of dietary sodium on the characteristics of angiotensin II (A II) receptor sites in the hypothalamus-thalamus-septum-midbrain (HTSM) region were examined in spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). Twenty-four SHR and 24 WKY were divided into two groups respectively, which were maintained on high sodium diets or low sodium diets for 4 weeks, respectively. The binding capacity and affinity of the A II receptors were measured by radioreceptor assay. In WKY, the binding capacity of the A II receptors in the high sodium group was significantly lower than that in the low sodium group. On the other hand, the binding capacity of A II receptors in the high sodium group was significantly lower than that in the low sodium group. On the other hand, the binding capacity of A II receptors was not significantly different between high and low sodium groups in SHR. The secretion of arginine vasopressin (AVP) increased significantly in SHR with high sodium intake. The present results suggest that in WKY the decrease of the binding capacity of the A II receptors in the HTSM region in response to a high sodium intake serves to attenuate an osmotical stimulus to AVP secretion. However, in SHR such a regulatory mechanism as adjusting the binding capacity of the A II receptors is lacking, and this seems to be responsible, at least in part, for the enhanced secretion of AVP on the sodium loading.

Angiotensin II↗
PubMed1981

Heterogeneity of 27,000 dalton-light chain of cardiac ventricular myosin.

Electrophoretic analysis on sodium pyrophosphate gels of myosin light chain 1 (LC-1; 27,000 daltons) from rabbit ventricular heart muscle revealed the presence of two distinct components named LC-1a (10%) and LC-1b (90%). After thyroxine administration, a shift toward LC-1a (45%) was observed. Canine cardiac ventricular light chain 1 (27,000 daltons) had equal amounts of LC-1a' (50%) and LC-1b' (50%), which corresponded to LC-1a and LC-1b of rabbit heart, respectively. However, heterogeneity of light chain 2 (20,000 daltons) was not observed. It is concluded that cardiac ventricular myosin has two heterogeneous 27,000 dalton-light chains and that the proportion of these proteins varies according to the thyroid status and animal species.

Animals↗
PubMed1981

The importance of vasopressin in the mechanism maintaining hypertension in the rat.

The further role of vasopressin in the pathogenesis of hypertension was studied in two different types of hypertensive rats in which the intravenous injection of a vasopressin antiserum reduced arterial blood pressure substantially. The increased secretion of vasopressin was demonstrated in deoxycorticosterone acetate (DOCA)-salt hypertensive and spontaneously hypertensive rats with high salt intake. Angiotensin II binding of the brain receptor which has been postulated to modify osmotically stimulated vasopressin release from neurohypophysis was not affected by sodium balance in these types of hypertensive rats, whereas the decrease in the brain receptor binding of angiotensin II was observed in the control rats. The lack of the adjusting control system in the brain angiotensin II receptors for sodium balance may be, at least in a part, responsible for the enhancement of vasopressin secretion in the hypertensive rats compared to that in the control rats with high salt intake. Since pressor responsiveness to vasopressin was increased in the rats with DOCA-salt hypertension, vasopressin may function as a direct pressor agent in the maintenance of high blood pressure in this type of hypertension.

Angiotensin II↗
PubMed1981

Assessment of myocardial infarct size by serial changes in serum cardiac myosin light chain II in dogs.

The relationship between myocardial infarct size and serum levels of cardiac myosin light chain II (LC II; 20000 daltons) was studied in 24 dogs with left anterior descending coronary artery occlusion. LC II in the serum was measured by the radioimmunoassay which we have recently developed. In our assay, 0.1--5.0 ng of LC II were effectively measurable. Serum LC II levels rose rapidly and stayed elevated long after coronary occlusion. Infarct size was determined by gross inspection. In 24 dogs, infarct size ranged from 0.3 to 41.7 per cent of left ventricular weight. LC II release was calculated by the formula of Shell and associates. Regression analysis showed good correlation between infarct size and LC II release (r = 0.78). Infarct size also correlated with maximal LC II level (r = 0.77), and LC II level 24 hours after coronary occlusion (r = 0.69). Detection of circulating LC II is a useful method since it can be applied to the diagnosis of acute myocardial infarction at the early as well as late stage and infarct size can be assessed by analysis of serum LC II levels.

Animals↗