Assignment of the human genes for desmocollin 3 (DSC3) and desmocollin 4 (DSC4) to chromosome 18q12.
Explore the source record for details and available documents.
Animals↗
Biomedical subjects
K Kawamura
Publications and source records attributed to K Kawamura.
Anatomy of the sinus node, AV node, and His bundle of the heart of the sperm whale (Physeter macrocephalus), with a note on the absence of an os cordis.
BACKGROUND: Atrioventricular (AV) conduction time in large whales is only slightly greater than in smaller mammals even though their hearts are enormously larger. Little is known of the detailed histology or cytology of the conduction system of large whales. Such knowledge could be useful in defining the nature of cardiac rhythm and conduction of the whale as well as smaller mammals including humans. METHODS: We studied hearts from seven sperm whales. After fixation in formaldehyde and later dissection, specimens were prepared for histological examination. RESULTS: Cell size, histological organization, and innervation of the sperm whale's sinus node, AV node, and His bundle are similar to most mammalian hearts, except the sinus node is substantially larger. There is no central fibrous body between the atrial and ventricular septa, and the whale has no os cordis. Only the upper quarter of the interventricular septum is fully formed; below that there is only a thin layer of fatty connective tissue between the two ventricles. CONCLUSIONS: Given our morphological findings, we believe that the whale's comparatively short AV conduction time may be best explained by the sinus node and AV node functioning as coupled relaxation oscillators. Absence of an os cordis or central fibrous body or strong attachment between the two ventricles may pose both electrophysiological and hemodynamic hazards when the whale is no longer in its normally buoyant aquatic environment.
Animals↗
Natural antibodies against the immunoglobulin F(ab')2 fragment cause elimination of antigens recognized by the F(ab')2 from the circulation.
A humanized monoclonal IgG1 antibody, designated hC4G1, recognizes the fibrinogen receptor glycoprotein (GP)IIb/IIIa on platelets and inhibits platelet aggregation. When the F(ab')2 fragment of hC4G1 (F(ab')2 hC4G1) was administered to cynomolgus monkeys, all the monkeys showed inhibition of platelet aggregation ex vivo. Unexpectedly, a significant decrease in platelet count was observed in 5 of 18 monkeys. Antibodies against F(ab')2 hC4G1 were detected in the plasma of these monkeys by ELISA. Antibody activity in the plasma of these monkeys was significantly correlated with the intensity of platelet decrease (r = 0.84). The natural monkey antibodies to F(ab')2 hC4G1 were directed against the C-terminal region of F(ab')2 fragment common to all human and humanized IgG antibodies. Natural homo-reactive antibodies were also detected in human plasma from 15 of 40 healthy volunteers. Specificity was closely similar to that of the monkey antibodies. Affinity-purified human homoreactive antibodies enhanced phagocytosis of platelets treated with the F(ab')2 hC4G1. Monkey plasma with high homo-reactive antibody activity was confirmed to decrease platelet count when administered together with F(ab')2 hC4G1 to a monkey with low antibody activity. These results suggest that F(ab')2 of humanized and human antibodies causes elimination of the corresponding antigens from the circulation by homo-reactive antibodies.
Animals↗
Bone marrow metastasis of neuroblastoma analyzed by MRI and its influence on prognosis.
Bone marrow metastases (BM mets) of neuroblastoma were analyzed by magnetic resonance imaging (MRI). BM mets were demonstrated in 45 femurs of 23 patients with neuroblastoma by MRI. They were classified into two patterns, nodular (N) type and diffuse (D) type, on MRI, with an incidence of 16% (7/45) and 84% (38/45), respectively. No bone metastases (B mets) were accompanied by N type BM mets, whereas all of them were accompanied by D type BM mets. The rate of disappearance of N type BM mets after chemotherapy was 100% (7/7) and was significantly higher than that (26%, 10/38) of D type BM mets. The rate of disappearance (58%, 11/19) of BM mets in bones without associated B mets was also significantly higher than that (23%, 6/26) of BM mets in bones with associated B mets. BM mets present in bones with B mets tended to persist after chemotherapy. The survival rate of patients with residual BM mets after chemotherapy was significantly lower than that of patients without residual BM mets. This suggests that powerful systematic chemotherapy and additional targeted therapy to lesions remaining after chemotherapy are needed to improve the cure rate of patients with advanced neuroblastoma.
Bone Marrow↗
Cellular and molecular characterization of transdifferentiation in the process of morphallaxis of budding tunicates.
In the budding tunicate, Polyandrocarpa misakiensis, a bud consists of two epithelial sheets, of which the inner, atrial epithelium shows developmental multipotency. It contains pigment granules in the cytoplasm and expresses a few differentiation markers on the cell surface. During bud development, these features are lost and new differentiation markers appear in organ rudiments that arise from the atrial epithelium. This transdifferentiation of the multipotent epithelium requires at least one cycle of cell division. It may be triggered by endogenous retinoids, probably retinoic acid (RA). RA acts on mesenchymal cells, which then secrete proteases that would serve as an actual transdifferentiation factor of the atrial epithelium.
Animals↗
Induction from posterior hypothalamus is essential for the development of the pituitary proopiomelacortin (POMC) cells of the toad (Bufo japonicus).
The role of the posterior hypothalamus in the development of the epithelial hypophysis was studied in Bufo embryos. In animals from which the central part of the neural plate (NP) had been surgically removed at the open neurula stage, the infundibulum did not develop, and the epithelial hypophysis was formed away from the normal site without morphological connection with the brain. Immunoreactive MSH cells and ACTH cells, i.e., the pituitary POMC cells, were not detected in any of the surgically treated animals, while other types of secretory cells (PRL, GH, TSH and GTH cells) were invariably present. In view of the fact that POMC cells originate in the anterior neural ridge, and not in the neural plate, the embryonic brain seems to exert an inductive influence upon the primordial pituitary POMC cells. Since these cells differentiate in a tail graft, isolated from the brain at a later stage (tail-bud stage), the inductive stimuli must be conveyed from/via the posterior hypothalamus to the pituitary anlage between the open neurula and the tail-bud stages.
Adrenocorticotropic Hormone↗
Growth, development and nutritional status in Japanese children under 2 years on continuous ambulatory peritoneal dialysis.
We examined the growth, development and nutritional status over a period of 10 years of 15 young children (< 2 years old) on continuous ambulatory peritoneal dialysis (CAPD). There were 6 males and 9 females with a mean age of 12.5 months, mean weight of 6.3 kg, mean height of 66.2 cm at the start of CAPD and a mean duration of therapy of 2.6 years. Height, weight, head circumference, development quotient (DQ), blood chemistry and dietary intake were assessed over a period of 10 years. The patients' mean height standard deviation score (SDS) did not change significantly (from -2.51 to -2.74) during CAPD therapy. The mean growth velocity index (GVI) during CAPD was 76.5% and correlated positively with energy intake but not with protein intake. The mean DQ was low (67.0%) at the start of CAPD and 69.3% at the end of CAPD. DQ did not correlate with energy intake, GVI, head circumference SDS or with the weight/height ratio; however, 2 patients with low DQ (< 60%) had a low energy intakes. Although most patients had a low DQ, the IQ at 5-6 years of age was normal in all patients except 1 without cerebral disease. Our study showed minimal growth (delta SDS) and mental developmental (IQ) delays during CAPD therapy, but an adequate nutritional intake must be assured to obtain the above results.
Blood Proteins↗
Human heart-type cytoplasmic fatty acid-binding protein as an indicator of acute myocardial infarction.
Human heart-type cytoplasmic fatty acid-binding protein (HH-FABPc) has been proposed as an early biochemical indicator of acute myocardial infarction (AMI). However, skeletal muscles also contain HH-FABPc identical to that found in the heart. Before HH-FABPc can be clinically employed as an indicator of AMI, its content in various tissues other than the heart must be known. Accordingly, we measured the HH-FABPc content of various human muscles and organs, using a sandwich enzyme-linked immunosorbent assay (ELISA) for HH-FABPc. HH-FABPc was abundant in the ventricles (0.46 mg/g wet weight and 1.5% of the cytoplasmic protein in the left ventricle), while the atria contained slightly less HH-FABPc (0.25 mg/g wet weight and 0.7% of the cytoplasmic protein in the left atrium). Of the skeletal muscles tested, the diaphragm contained about one-quarter of the HH-FABPc content of the heart, but other skeletal muscles contained very low levels of this protein. Other than the muscles, the kidneys contained less than one-tenth of the HH-FABPc in the heart, and negligible amounts were found in the liver and small intestine. The distribution of HH-FABPc in the heart and skeletal muscles was comparable to that of cardiac-specific creatine kinase (CK-MB) activity, and was inverse to the distribution of myoglobin. The plasma myoglobin/HH-FABPc ratio, determined in patients with AMI and those without AMI, closely reflected that in the heart and skeletal muscles. These findings indicate that HH-FABPc may be useful as a specific indicator of AMI, and the plasma myoglobin/HH-FABPc ratio could provide valuable information for the diagnosis of AMI.
Adult↗
Congenital hypomyelination neuropathy: decreased expression of the P2 protein in peripheral nerve with normal DNA sequence of the coding region.
Congenital hypomyelination neuropathy (Lyon type) is characterized by a non-progressive clinical course and a histopathological formation of atypical onion-bulb. We have studied the immunohistochemical expression of the major peripheral myelin proteins including P0 protein, myelin basic protein (MBP) and P2 protein in three such patients. No significant difference was observed between the patients and the controls, as to the P0 and MBP staining. In contrast, P2 protein antiserum scarcely stained the patients' nerve fibers except for a few scattered adequately myelinated fibers. Assuming the pathogenetic contribution of the extremely decreased P2 protein to the disease, we investigated P2 protein gene by sequencing all coding regions but failed to detect any change in the nucleotide sequence. Further investigation including the analysis of promoter region of P2 protein gene is needed to elucidate the mechanism of congenital hypomyelination neuropathy.
Base Sequence↗
Analysis of enterovirus genotypes using single-strand conformation polymorphisms of polymerase chain reaction products.
Enterovirus genotypes were identified rapidly by reverse (RT-PCR) followed by single-strand conformation polymorphism (SSCP) analysis. The primer pair was chosen from the highly conserved sequence at the 5' non-coding region of enterovirus genomes. RT-PCR amplified a 154 bp sequence in all samples from 14 serotypes of enteroviruses, including group A and B Coxsackie viruses, echoviruses and polioviruses. SSCP analysis of these products revealed different electrophoretic profiles. Thus, SSCP analysis will be useful for differentiating the genotypes of enteroviruses, and may be applicable for rapid diagnosis of enteroviral infection.
Base Sequence↗
Effect of sulfo-N-succinimidyl palmitate on the rat heart: myocardial long-chain fatty acid uptake and cardiac hypertrophy.
Abnormal long-chain fatty acid metabolism has been suggested as having a role in the genesis of certain cardiac diseases, and depressed myocardial long-chain fatty acid uptake has been clinically demonstrated in some patients with hypertrophic cardiomyopathy. However, the site where long-chain fatty acid metabolism is affected in cardiomyopathy remains unclear. Although cardiac hypertrophy is reported to be induced in rats by a fat-free diet, little is known of the consequences of depressed myocardial long-chain fatty acid uptake. Sulfo-N-succinimidyl derivatives of long-chain fatty acids have been shown to irreversibly inhibit long-chain fatty acid transport. To investigate the possible linkage of abnormal long-chain fatty acid uptake with cardiac hypertrophy, myocardial long-chain fatty acid uptake was blocked in rats using a sulfo-N-succinimidyl derivative of palmitate (SSP). SSP was intraperitoneally administered to rats for 12 weeks, and its effects on physiological parameters, and cardiac morphology were studied, SSP treatment (20 mg/kg) caused a 12% increase in heart weight (663.7 +/- 33.6 mg in controls v 741.2 +/- 26.5 mg after SSP treatment) and an 11% increase in the heart weight to body weight ratio (2.46 +/- 0.10 in controls v 2.72 +/- 0.17 after SSP) without any significant change of body weight. No significant differences were observed in blood pressure, heart rate, and serum hormones (insulin and triiodothyronine) between the control and SSP-treated groups.(ABSTRACT TRUNCATED AT 250 WORDS)
Analysis of Variance↗
Isolation of myocardial membrane long-chain fatty acid-binding protein: homology with a rat membrane protein implicated in the binding or transport of long-chain fatty acids.
Abnormal myocardial long-chain fatty acid uptake is suspected of being involved in certain types of heart disease, but the mechanism by which the heart takes up long-chain fatty acids remains unclear. The sulfo-N-succinimidyl derivatives of long-chain fatty acids have been reported to undergo covalent binding to a membrane protein and to irreversibly inhibit the transport of long-chain fatty acids by rat adipocytes (Harmon et al., 1991). It has been suggested that the membrane protein bound by these derivatives is a candidate transporter for long-chain fatty acids in adipocytes. However, myocardial membrane long-chain fatty acid-binding proteins have not yet been fully investigated. Rat hearts were isolated and perfused with a sulfo-N-succinimidyl derivative of tritium-labeled palmitate ([3H]SSP). Then the [3H]SSP-binding protein was characterized by sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) autoradiography and histological autoradiography. Myocardial palmitic acid uptake was examined after pretreatment of isolated perfused rat hearts with SSP. The SSP-binding protein was isolated from bovine hearts by successive chromatography, and the amino acid sequences of lysylendopeptidase-digested peptide fragments were determined. SDS-PAGE autoradiography revealed that [3H]SSP bound to an 85-90 kDa protein derived from the myocardial microsomal fraction, and histological autoradiography demonstrated that [3H]SSP radioactivity was localized to the myocardial cell membrane. Pre-incubation with SSP inhibited palmitic acid uptake by isolated perfused rat hearts. A [3H]SSP-binding protein was also found in canine and bovine hearts, and was isolated from the bovine cardiac membrane fraction. Amino acid sequencing revealed that four peptide fragments showed strong sequence homology with rat adipocyte membrane protein, which is implicated in the binding or transport of long-chain fatty acids (Abumrad et al., 1993). We conclude that the SSP-binding protein is localized to the myocardial cell membrane and might be involved in the uptake or transport of long-chain fatty acids.
Amino Acid Sequence↗
A case of steatocystoma multiplex with prominent cysts on the scalp treated successfully using a simple surgical technique.
The case described is a 35-year-old male with multiple cysts on the upper half of his body. This patient was diagnosed as having steatocystoma multiplex, based on clinical and histological findings. The lesions consisted of widespread and unusually prominent cysts, which were removed by a simple surgical technique using a dermatological trepan and artery forceps. We provide here a detailed description of the surgical procedures employed.
Adult↗
CT screening for unrecognized coronary sequel of Kawasaki disease.
Explore the source record for details and available documents.
Adolescent↗
Establishment of cell lines from multipotent epithelial sheet in the budding tunicate, Polyandrocarpa misakiensis.
We report here the in vitro culture of the atrial epithelium, which is the major formative tissue of the budding tunicate, Polyandrocarpa misakiensis. Preliminary studies suggested that both pH and osmotic pressure of the basic seawater medium should be lowered significantly (pH 6.8, 800-830 mOsm). In the growth medium consisting of modified millipore-filtered seawater, Dulbecco's modified Eagle medium and 3% fetal bovine serum, cells spread out from the epithelial explant and proliferated with a doubling time of about 13 hours. They could be cloned and cultured successively. They contained the Polyandrocarpa lectin gene, showing that they were indeed of tunicate origin. At a low cell density (< 3 x 10(2) cells/mm2), clonal cells took a spherical form and contained several granules in the cytoplasma. At a high cell density (> 3 x 10(4) cells/mm2), on the other hand, they gave rise to smaller cells without any specialized features and, finally, to dark flattened cells. Consistent with this observation, confluent cells lost the atrial epithelium-specific antigen, which reappeared on the cell surface when they were re-plated at a low density. In conclusion, we have established for the first time tunicate cell lines. They appeared to differentiate and dedifferentiate repeatedly in our culture system.
Animals↗
Effects of nicorandil on left ventricular systolic and diastolic function in patients with hypertrophic cardiomyopathy.
Various evidence suggest that myocardial ischemia is a major factor in the progression of hypertrophic cardiomyopathy (HCM). In this study, we investigated the effects of nicorandil on left ventricular (LV) systolic and diastolic function in 12 symptomatic patients with HCM using echocardiography and radionuclide angiography. Nicorandil (6 mg), when administered intravenously, produced no significant changes in any parameter, including LV filling dynamics. However, accelerated LV peak early filling velocity (0.51 +/- 0.13 to 0.59 +/- 0.14 m/sec, p < 0.01), and reduced peak velocity in atrial contraction (0.54 +/- 0.17 to 0.50 +/- 0.15 m/sec, p < 0.05) were observed by Doppler echocardiography after 4 weeks of oral administration of 10 mg nicorandil 3 times daily. This oral administration did not affect heart rate, blood pressure, LV outflow gradient, or LV systolic function. The same favorable results were observed in a wall motion analysis with radionuclide angiography: peak filling rate (PFR) in global LV (3.21 +/- 0.76 to 3.52 +/- 0.87 end-diastolic volume (EDV)/sec, p < 0.02), and apical (4.73 +/- 1.18 to 5.42 +/- 1.55 EDV/sec, p < 0.01) and lateral (4.78 +/- 1.60 to 5.52 +/- 1.51 EDV/sec, p < 0.05) segments was increased, and the time to peak filling rate (TPF) in septal (245 +/- 31 to 203 +/- 40 msec, p < 0.01) and lateral (222 +/- 54 to 193 +/- 34 msec, p < 0.05) segments was reduced. These findings indicate that nicorandil has beneficial effects on LV diastolic function in HCM. These favorable effects may be due to the improvement of subendocardial ischemia.
Adult↗
Comparable effects of angiotensin II and converting enzyme blockade on hemodynamics and cardiac hypertrophy in spontaneously hypertensive rats.
Angiotensin-converting enzyme inhibitors may regress left ventricular hypertrophy (LVH) without decreasing blood pressure (BP). The aim of the present study was to compare the effects of low and high doses of lisinopril and the angiotensin II receptor antagonist TCV116 (TCV) on LVH and hemodynamics in spontaneously hypertensive rats (SHR). Lisinopril (0.5 and 3 mg/kg per day) and TCV (0.3 mg/kg per day) were given to 8-week-old male SHR daily for 2 weeks. Untreated SHR and Wistar-Kyoto rats (WKY) served as controls. Untreated SHR had a greater left ventricular (LV) weight than WKY (p < 0.01). Lisinopril (3 mg/kg per day) decreased both LV weight and BP. Lisinopril (0.5 mg/kg per day) significantly decreased LV weight, but not BP. In contrast, although TCV significantly decreased BP, LVH was not suppressed. Renal blood flow (RBF) in untreated SHR was less than that in WKY (p < 0.05), but was increased with either lisinopril (3 mg/kg per day)-treated rats (p< 0.05). These findings suggest that factors other than afterload reduction play a role in the regression of LVH with lisinopril, whereas a longer duration of treatment and/or a higher dose may be necessary with TCV. Despite the decrease in BP, TCV normalized RBF in SHR, perhaps due to the blockade of renal angiotensin II.
Angiotensin II↗
V-onc mutation associated with host cell growth in retroviral tumors.
In sarcomagenesis in rats infected neonatally with feline sarcoma virus (ST-FeSV), v-fes product (P85) was previously shown by us to be a predictive and preventive determinant. In order to explore the part played by P85 in tumor suppression, DNA was extracted from precancerous granulomas and from slow or rapid growing sarcomas induced by neonatal injection of the virus. The v-fes signal from extracted DNA was analyzed by PCR-SSCP. The prototype v-fes gene signal was detected in most lesions and found to be generally amplified in rapid growing sarcomas and in some granulomas. Several v-fes homologs showing varying mobilities in gel were seen in most sarcomas and some granulomas with or without the prototype v-fes signal. In slow growing sarcomas and granulomas induced in hosts that were immunized with ST-FeSV induced syngeneic sarcoma and proved to carry IgG antibody to P85, the prototype v-fes gene was found to be down-regulated and v-fes homologs were found to be reduced in number or eliminated. These results suggest that the development of v-fes mutations is associated with the growth potential of cells carrying the v-fes gene, and that host immunity to v-onc product influences the development of virogene rearrangements and results in slow and suppressed growth of tumors caused by neonatal infection with retrovirus.
Animals↗