IgA nephropathy demonstrating clinico-serologic features of acute post-streptococcal glomerulonephritis.
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Adult↗
Biomedical subjects
S Kawashima
Publications and source records attributed to S Kawashima.
Spatial resolution of fodrin proteolysis in postischemic brain.
One of the major obstacles in investigating in vivo proteolytic phenomena has been the inaccessibility to spatial information as to where in the tissue the reaction proceeds because the orthodox method employing electrophoretic analysis requires homogenization of samples and thus results in loss of such spatial information. To overcome this technical drawback, we have developed methodology to produce antibodies that specifically distinguish a proteolyzed form of a given protein from its intact form. Here we describe our immunohistochemical observation of calpain-catalyzed fodrin proteolysis in postischemic gerbil hippocampus, using an antibody exclusively specific to the proteolyzed 150-kDa form of fodrin alpha subunit. Our data establish a novel discovery that transient (10 min) global forebrain ischemia followed by reperfusion induces at least two distinct phases of fodrin proteolysis in hippocampus: an early phase in molecular layer and in stratum oriens of CA3 and CA1 sectors within 15 min and a late drastic and persistent phase in the entire CA1 after 4-24 h. The former may be one of the early events initiating the complex cascade leading to the delayed neuronal death, while the latter should be considered as a more direct cause for the actual degeneration in CA1.
Animals↗
Purification and characterization of a Z-Leu-Leu-Leu-MCA degrading protease expected to regulate neurite formation: a novel catalytic activity in proteasome.
A tripeptide aldehyde protease inhibitor, benzyloxycarbonyl(Z)-Leu-Leu-leucinal (ZLLLa1), initiates neurite outgrowth in PC12 cells at an optimal concentration of 30nM. This result suggests the existence of a protease which regulates neurite formation in PC12 cells. We report here an attempt to identify this target protease in bovine brain using Z-Leu-Leu-Leu-4-methylcoumaryl-7-amide (ZLLL-MCA), in which the aldehyde moiety of ZLLLa1 was changed to 4-methylcoumaryl-7-amide to serve as a substrate for the protease. As a result, we have purified a proteasome with a molecular weight of about 660 kDa as a ZLLL-MCA degrading protease. The activity of the proteasome was inhibited efficiently by ZLLLa1, and was different from known catalytic activities of proteasome in some aspects, suggesting it to be a novel one. Thus, the proteasome may be involved in the regulation of neurite formation in PC12 cells.
Amino Acid Sequence↗
Activation of nitric oxide synthase from cultured aortic endothelial cells by phospholipids.
Nitric oxide is a recently discovered biomolecule with a broad range of actions and synthesized by nitric oxide synthases. We investigated effects of lipids on particulate nitric oxide synthase purified from cultured bovine aortic endothelial cells by monitoring the conversion of L-[3H]arginine to L-[3H]citrulline. Phosphatidylcholine, lysophosphatidylcholine, and phosphatidylethanolamine dose-dependently enhanced the enzyme activity up to 3 fold in the presence of Ca2+, calmodulin, NADPH, FAD, and (6R)-5,6,7,8-tetrahydrobiopterin. These phospholipids increased the Vmax of nitric oxide synthase without altering the Km for L-arginine and the affinities for Ca2+ and calmodulin. These findings suggest that phospholipids play an important role in modulating endothelial nitric oxide synthase activity.
Amino Acid Oxidoreductases↗
Calpain activity alters in rat myocardial subfractions after ischemia or reperfusion.
To examine whether calpain is activated during ischemic or reperfusion injury, we measured calpain activity of the subfractions of rat myocardia after global ischemia for 60 min or the ischemia followed by 30 min reperfusion by the Langendorff procedure. The myocardial homogenate was fractionated into 600 x g, 10,000 x g and 100,000 x g pellet fractions as well as 10,000 x g supernatant fraction. The supernatant fraction was further subjected to DEAE cellulose and phenyl-Sepharose chromatographies to separate mu- and m-calpains. The m-calpain activity of the DEAE fractions after global ischemia for 60 min was higher but that after ischemia-reperfusion was lower than that of the control. On the other hand, the ischemia-reperfusion but not ischemia by itself raised the calpain activity of the phenyl-Sepharose fraction (mu-calpain) and the 10,000 x g pellet measured at 100 microM and 5 mM Ca2+. Treatment with verapamil but not with ryanodine during ischemia attenuated the increase in m-calpain activity. A dot-blotting analysis of calpain antigenicity showed a decrease in soluble but no change in the particulate fractions after ischemia-reperfusion. An immunoblotting technique did not detect proteolysis of the calpain 80-kDa subunit. These observations suggest that calpain is activated by Ca2+ influx during ischemia and reperfusion without gross changes in its amount. Some unknown processes other than translocation or autolysis are thought to be involved in the alterations.
Animals↗
A variety of calpain/calpastatin systems in mammalian erythrocytes.
Calpain and its endogenous inhibitor, calpastatin, were isolated from erythrocytes of various mammals and their properties were compared. It has been widely believed that mammalian erythrocytes contain only mu-calpain. However, rat and human erythrocytes were found to contain two species of calpain, identified as mu-calpain and m-calpain from their elution positions on DEAE-cellulose column chromatography and their Ca(2+)-requirements. Thus, it is apparent that rat and human erythrocytes contain not only mu-calpain, but m-calpain as well. On the other hand, rabbit erythrocytes contain only mu-calpain. Western blot analysis showed that human and rabbit erythrocytes contain predominantly 70-kDa calpastatin (erythrocyte-type), but unnegligible amounts of 110-kDa calpastatin (tissue-type) are also present. Rat erythrocytes were shown to contain a calpastatin with a molecular mass of approx. 100 kDa almost exclusively; this molecular mass was in perfect coincidence with the mass of the calpastatin in rat lung. These results strongly suggest that rat erythrocytes contain a tissue-type calpastatin. No essential change in the calpain/calpastatin system during maturation of rabbit reticulocytes into mature erythrocytes was observed.
Animals↗
A novel domain sequence of connectin localized at the I band of skeletal muscle sarcomeres: homology to neurofilament subunits.
A cDNA of 4.0 kb was cloned from a chicken embryo skeletal muscle cDNA library, using an antibody to muscle elastic protein connectin (titin), the molecular mass of which is estimated to be 3,000 kDa. Immunoelectron microscopy revealed that the antiserum raised against the product of the cDNA expressed in E. coli bound to the epitopes of the connectin filament near the N2 line of chicken breast muscle sarcomeres. The predicted amino acid sequence contains eight immunoglobulin C2 motifs and regions highly homologous with the high and medium molecular weight subunits of neurofilament. In addition, there are regions homologous with desmoplakin, calsequestrin, and calpastatin.
Amino Acid Sequence↗
Immunohistochemical localization of calpains and calpastatin in the rabbit eye.
The localization of the two Ca-activated extralysosomal proteases m-calpain and mu-calpain in the eye of the adult rabbit was examined by immunohistochemistry, using poly- and monoclonal antibodies against the corresponding rabbit antigens. Immunoreactivity against the two forms of calpains was observed in the epithelial cells on the external and internal surface of the cornea as well as in the epithelial cells covering the iris and ciliary body. The sclera and choroid layers showed a relatively weak immunoreactivity. Using anti m-calpain antibodies, the pigment epithelium in the retina was heavily labelled as well as the outer and inner plexiform layers. The other and inner borders of the Müller cells were clearly labelled. The outer segments of the receptor cells showed a strong immunoreactivity for both mu-calpain and m-calpain. Labelling was also observed in the retinal ganglion cells and in the nerve fiber layer. The immunohistochemical localization of calpastatin, an endogenous inhibitor of both m- and mu-calpain was also examined. A high level of calpastatin immunoreactivity was observed in the outer segments of the receptor cells. The results may be compatible with a role for calpains, especially m-calpain, in the secretory/phagocytic process and as modulators of the cytoskeleton in cell processes.
Animals↗
Thyroid nodules in female uremic patients on maintenance hemodialysis.
We investigated the incidence of thyroid nodules in female uremic patients on maintenance hemodialysis using a high-frequency sonographic scanner. In 47 (21.0%) of the 224 female normal controls and 33 (55.0%) of the 60 female patients, thyroid nodules were detected. The difference in these incidences between controls and patients was significant. There were no differences in age, duration of hemodialysis, the level of blood urea nitrogen, parathyroid hormone or thyroid stimulating hormone between the patients with thyroid nodules and those without nodules. Although there is a correlation between uremia and the development of thyroid nodules, the details of the underlying mechanism of their association remain unclear.
Adult↗
Photoperiodic regulation of follicle-stimulating hormone binding to gonads and of plasma gonadotropin concentrations in Indian weaver birds.
Previous studies showed that changes of gonadal weight and of follicle-stimulating hormone (FSH) receptor number in response to fluctuations in natural environmental conditions are smaller in female than in male Indian weaver bird (Ploceus phillippinus). Therefore, we studied whether the response to artificial photoperiodic changes differs between the sexes. Birds were transferred to short-day (SD) photoperiods during the breeding phase (June). Other birds were subjected to long-day (LD) photoperiods during the nonbreeding phase (December). Exposure to SD for 10 weeks induced a marked testicular weight decrease. Similarly, FSH binding per unit testicular weight as well as per two testes decreased after SD exposure. The influence of photoperiodic manipulations on the ovarian weight was much smaller than that on the testicular weight. SD exposure did not alter FSH binding either per unit ovarian weight or per ovary. Plasma gonadotropin concentration significantly decreased in both sexes subjected to SD environment. On the other hand, exposure to LD significantly increased testicular weight. LD exposure slightly increased ovarian weight, but the increase was statistically not significant. FSH binding per unit testicular weight markedly increased 10 weeks after transfer to LD. The total FSH binding per two testes showed a parallel change with the testicular weight. However, there was no significant increase in FSH binding per unit ovarian weight during 10 weeks of LD exposure. Although LD exposure for 10 weeks significantly increased the total FSH binding per ovary, the rate of increase was much smaller than that in the testes. The plasma gonadotropin level in both sexes was increased by LD exposure. Scatchard plot analyses of FSH binding indicated that FSH binding changes were due to changes in binding site number. These results suggest that photoperiod regulates FSH receptor numbers particularly in the testis. Such an effect is manifested by marked changes in the testicular weight under different photoperiodic conditions in the subtropical bird.
Animals↗
Culture of rat brain preoptic area neurons: effects of sex steroids.
The aim of the present study was to investigate the direct effects of testosterone (T), estradiol-17 alpha (E2) and 5 alpha-dihydrotestosterone (5 alpha-DHT) on the survival of neurons and the morphology of neuronal processes (the total process length, the number of processes and the number of process branchings) of the cells derived from neonatal rat preoptic area (POA) to analyze the bases of morphological sexual dimorphism of the POA. The POA cells were exposed to sex steroids during 2-14 days of culture in serum-free medium. Neuronal survival was significantly greater in cultures treated with 1.0 nM T than controls. Although T at any concentration tested (0.1, 1.0 or 10.0 nM) failed to affect the mean value of the process length, a significant difference was observed in the frequency distribution of total process length between 1.0 nM T-treated cultures and control cultures. By 1.0 nM T, the number of process branchings was also significantly increased. In contrast, the number of neurons and the total process length of neurons were not affected by 5 alpha-DHT. However, the number of process branchings was significantly increased by 0.1 nM 5 alpha-DHT. E2 had no significant effect on any of these parameters. These results suggest that T directly enhances the survival of neurons and increases the dendritic and/or axonic field of the POA, which serves, at least partly, for the development of morphological sexual dimorphism in the rat.
Androgens↗
The gene for Machado-Joseph disease maps to human chromosome 14q.
Machado-Joseph disease (MJD) is an autosomal dominant, multisystem neurodegenerative disorder involving predominantly cerebellar, pyramidal, extrapyramidal, motor neuron and oculomotor systems. Although it was first reported in families of Portuguese-Azorean descent, MJD has also been described in non-Azorean families from various countries, being one of the most common hereditary spinocerebellar degenerations. With the use of highly polymorphic microsatellite DNA polymorphisms, we have assigned the gene for MJD to the long arm of chromosome 14 (14q24.3-q32) by genetic linkage to microsatellite loci D14S55 and D14S48 (multipoint lod score Zmax = 9.719).
Chromosome Mapping↗
Paradoxical forearm vasodilatation and haemodynamic improvement during cardiopulmonary baroreceptor unloading in patients with congestive heart failure.
1. To examine the contribution of paradoxical reflex forearm vasodilatation during unloading of cardiopulmonary baroreceptors to systemic haemodynamics, the responses of central and peripheral haemodynamics during lower-body negative pressure were measured in 24 patients with chronic congestive heart failure (New York Heart Association functional class II-IV) and were compared with those of 10 normal subjects. 2. Lower-body negative pressure of less than -20 mmHg caused a significant forearm vasoconstriction in normal subjects but not in patients with congestive heart failure. In the individual cases, however, eight patients (subgroup A) had a significant forearm vasoconstriction, whereas 10 patients (subgroup B) had a paradoxical forearm vasodilatation. The remaining six patients had a blunted forearm vascular response. Baseline pulmonary capillary wedge pressure (26 +/- 3 versus 20 +/- 1 mmHg, means +/- SEM) and left ventricular wall stress in end-diastole (57 +/- 6 versus 37 +/- 4 g/cm2) were significantly (P < 0.05) higher in subgroup B than in subgroup A. 3. During lower-body negative pressure of -20 mmHg, the plasma level of noradrenaline, systemic vascular resistance and cardiac index did not change significantly in subgroup A. In subgroup B, however, during this orthostatic stimulus systemic vascular resistance fell significantly from a baseline value of 2023 +/- 109 to 1740 +/- 110 dyn s-1 cm-5 (P < 0.01) and cardiac index increased significantly from a baseline value of 2.0 +/- 0.1 to 2.5 +/- 0.2 1 min-1 m-2 (P < 0.01) despite there being no significant change in the plasma level of noradrenaline. 4. After treatment, a second bout of lower-body negative pressure was applied to seven patients in subgroup B. The forearm vascular response to the second bout of lower-body negative pressure was normalized. 5. These data suggest that the patients with more severe heart failure show a paradoxical forearm vasodilatation during mild lower-body negative pressure and that this altered cardiopulmonary baroreflex control of the circulation serves to improve the depressed cardiac performance.
Adult↗
Suppression of spontaneous development of uterine adenomyosis by a Chinese herbal medicine, keishi-bukuryo-gan, in mice.
Keishi-bukuryo-gan (KBG) is a traditional Chinese herbal remedy and has been used for the treatment of gynecological disorders, such as hypermenorrhea, dysmenorrhea, and infertility. The effects of KBG on the development of uterine adenomyosis, which is characterized by an abnormal growth of glands and stroma into and beyond the smooth muscle layers of the uterus, were examined in an experimental animal model using the SHN strain of mice. Mice fed handmade chow containing relatively high doses of KBG (0.5% and 1%) showed a significantly lower incidence of adenomyosis and lower activity of thymidylate synthetase (TS) in the uteri than mice fed control handmade chow containing no KBG. The long-term exposure to KBG between 25 and 120 days of age hardly affected the estrous cycle, food intake and body weight. However, mice provided with chow containing a low dose of KBG (0.1%) showed no difference in the incidence of adenomyosis as compared with the controls. The inhibitory effects of the high doses of KBG were nullified by pituitary isografting, which has been proved to enhance the development of adenomyosis. The present mouse data support the view in humans that the oral administration of KBG is a useful tool for the treatment of uterine adenomyosis.
Animals↗
11q trisomy detected by fluorescence in situ hybridization.
A patient with psychomotor developmental delay, multiple minor anomalies, congenital heart disease and left inguinal hernia is reported. His karyotype was 45,X/46,X,+mar (3:37 cells), and the marker chromosome was identified as t(Y;11)(q12;q14?) using fluorescence in situ hybridization and fluorescent chromosome painting. He was diagnosed as mosaic for de novo 11q trisomy.
Abnormalities, Multiple↗
Suppression of spontaneous development of uterine adenomyosis and mammary hyperplastic alveolar nodules by Chinese herbal medicines in mice.
The effects of traditional Chinese herbal remedies, Shakuyaku-kanzo-to (SKT) and Hachimijiou-gan (HJG), on the spontaneous development of uterine adenomyosis and mammary hyperplastic alveolar nodules (HAN) were examined in an experimental animal model using SHN strain of mice. Female mice were provided with the chow containing 1% of SKT or HJG during 25-150 days of age. At 150 days of age, SKT treatment showed significantly lower incidence of adenomyosis, and HJG treatment resulted in a significantly lower incidence of HAN when compared to a control chow containing no medicines. Long-term exposure to these herbal medicines affected little serum prolactin (PRL) level, estrous cycle, food intake and body growth. Thus, the present mouse data suggest that the oral administration of these herbal medicines is a useful tool for the treatment of uterine adenomyosis or mammary disorder such as cystic mastitis.
Adenomyoma↗
High density lipoprotein reverses inhibitory effect of oxidized low density lipoprotein on endothelium-dependent arterial relaxation.
We have recently reported that oxidized low density lipoprotein (ox-LDL) inhibits endothelium-dependent arterial relaxation through its increased lysophosphatidylcholine (LPC). In this study we examined whether high density lipoprotein (HDL) has any effect on the inhibition of endothelium-dependent relaxation by ox-LDL in isolated strips of rabbit thoracic aorta. Both low density lipoprotein (LDL) and HDL were isolated from normal human plasma, and LDL was oxidized by exposure to copper. Preincubation of arterial strips with ox-LDL (0.1-0.5 mg protein/ml) inhibited endothelium-dependent relaxation to acetylcholine (ACh) in a concentration-dependent manner. HDL (1 mg protein/ml) by itself had no effect on the relaxation to ACh. In the presence of HDL, the inhibition by ox-LDL was markedly reduced. Although synthetic L-alpha-palmitoyl LPC (5 micrograms/ml) completely abolished a relaxation to ACh, the preincubation of arterial strips with HDL completely prevented the LPC-induced inhibition. Moreover, a relaxation to ACh was almost completely recovered when the strips were washed with buffer containing HDL even after LPC-induced inhibition had occurred. HDL markedly reduced the incorporation of [1-14C]palmitate-labeled LPC ([14C]LPC) into cultured bovine aortic endothelial cells and promoted the release of cell-incorporated [14C]LPC into the medium, resulting in a reduction of the remaining [14C]LPC in the cells. Agarose electrophoresis after incubation of a mixture of ox-LDL labeled with [14C]LPC and unlabeled HDL demonstrated a transfer of [14C]LPC from ox-LDL to HDL. These results indicate that HDL reverses the ox-LDL-induced impairment of endothelium-dependent relaxation by removing LPC from ox-LDL and preventing LPC from acting on the endothelium.(ABSTRACT TRUNCATED AT 250 WORDS)
Acetylcholine↗
[Regulatory mechanisms of endothelial nitric oxide synthase activity and its modification by lipids and cytokines].
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Adenosine Triphosphate↗