Biomedical subjects
Publications and source records attributed to K Obara.
A 25-year-old Japanese woman had both ulcerative colitis and Takayasu's disease and was positive for HLA-A24, BW52, and DR2. She was found to have thickening of the wall of the carotid artery on contrast-enhanced computerized tomography of the neck and chest. Prednisolone, beraprost, and sulfapyridine achieved rapid remission of both diseases.
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An autopsy was performed on a 42-year-old Japanese female who had been suffering from both ulcerative colitis (UC) and Takayasu's disease. Her UC started at age 27 with bloody stool, and Takayasu's disease was diagnosed at age 30 on the basis of absence of pulse in her left arm. After more than ten years she died of multiple cerebral infarction. An autopsy study revealed the scarring stage of UC in the entire colon and aortitis in the aortic arch and its major branches and pulmonary arteries. Her HLA type was positive for HLA-A2, 24, Bw52 and 61. Clinical features of a total of 13 Japanese cases that had both UC and Takayasu's disease have been reviewed in the Japanese and Western literature.
To elucidate the role of macrophages in diabetic glomerulosclerosis (DGS), an immunohistologic study was performed using monoclonal antibodies to common leukocyte antigen (DAKO-LC), T cells (T3), B cells (CD22), and macrophages (MAC 387, Leu-M5, and EBM-11). Kidney biopsy specimens were obtained from 28 patients with non-insulin-dependent diabetes mellitus. Cells were identified by a three-layer immunoperoxidase technique applied to cold ethanol-fixed, paraffin-embedded sections and quantitated as the number of cells per glomerular cross-sections and number of cells per square millimeter of glomerulus. The severity of the diffuse lesions in each glomerulus was graded semiquantitatively. The average grades for all the glomeruli were calculated and registered as an index of DGS for a biopsy specimen. There was no relationship between the index of DGS and the number of T or B cells. However, the number of macrophages and common leukocyte-positive cells increased significantly in the moderate stage of glomerulosclerosis compared with the mild or advanced stage. The results suggest that macrophages may transiently infiltrate during the moderate stage of diffuse DGS, contributing to irreversible structural damage.
Following acute, localized lesions of the central nervous system, arising from any cause, there are immediate depressions of neuronal synaptic functions in other areas of the central nervous system remote from the lesion. These remote effects result from deafferentation, a phenomenon known as "diaschisis". After an interval of time, which will vary directly with the severity of the lesion, functional recovery occurs due to synaptic reactivation of neurones. This is favourably influenced by rehabilitation. Diaschisis most commonly manifests itself by such neurological signs as impaired consciousness or cognitive impairments including dementia, dyspraxias, dystaxias, dysphasias, incoordination and sensory neglect. The nature of diaschisis has been demonstrated by widespread depressions of local cerebral blood flow and metabolism extending far beyond the anatomical lesion. Recovery of function is associated with recovery of local perfusion and metabolism.
The effects of okadaic acid (OA) and calyculin A (CL-A), potent inhibitors of protein phosphatases type 1 (PP1) and type 2A (PP2A), on inward current carried by Ba2+ through voltage-dependent Ca2+ channel in guinea pig teniae coli smooth muscle cells were investigated using whole-cell patch-clamp technique. High concentrations of OA (5 x 10(-8)-5 x 10(-6) M) and CL-A (10(-9)-10(-7) M) dose dependently increased the inward current. The concentration producing apparent half-maximum enhancing effect values for OA and CL-A were 1.12 x 10(-7) and 1.78 x 10(-9) M, respectively. CL-A appeared to be approximately 100-fold more potent in increasing the inward current than OA. Lower concentrations of OA (10(-10)-2 x 10(-8) M) and CL-A (10(-11)-10(-9) M) decreased the inward current. The maximum inhibitory effects of OA and CL-A were observed at 10(-8) M OA and 5 x 10(-10) M CL-A, respectively. CL-A is approximately 100 times more effective inhibitor of PP1 than OA, and lower concentrations of OA and CL-A used in the present study inhibit PP2A activity, but they have no or little effect on PP1 activity (Ishihara, H., B. L. Martin, D. L. Brautigan, H. Karaki, H. Ozaki, Y. Kato, N. Fusetani, S. Watabe, K. Hashimoto, D. Uemura and D. J. Hartshorne. Biochem. Biophys. Res. Commun. 159: 871-877, 1989). In the absence of ATP in pipette solution, OA and CL-A did not affect the inward current.(ABSTRACT TRUNCATED AT 250 WORDS)
By using a radioimmunoassay specific for endothelin-1 (ET-1), we measured urinary excretion of ET-1-like immunoreactivity (LI) in 63 spot urine samples of 48 patients with primary vesicoureteral reflux (VUR). And also, urinary excretion of N-acetyl-beta-D-glucosaminidase (NAG), beta 2-microglobulin (beta-2-MG), microalbumin (Alb) and creatinine (Cr) were measured. There was no significant correlation in any of the pairs ET-1 and NAG, ET-1 and beta 2-MG, and ET-1 and Alb. Comparing the grade of reflux according to the International Classification with urinary ET-1, urinary ET-1/Cr levels in patients with grade 2, 3 and 4 VUR were higher than normal, and the ratio of more than normal urinary ET-1/Cr increased in proportion to the grade of reflux, but it conversely decreased in grade 5. In conclusion, urinary ET-1 may be an indicator of renal tubular injury in patients with primary VUR, and its meaning may be different from conventional urinary parameters.
The voltage-dependent Ca2+ channels (VDC) in smooth muscle cell membranes are the major pathway by which Ca2+ enters the cell during contraction. It has been reported that VDC can be modulated by reversible channel protein phosphorylation and dephosphorylation reactions. In intestinal smooth muscle cell, muscarinic agents have been reported to increase the break-down of phosphatidylinositol 4,5-bisphosphate, which indicates that inositol-1,4,5-trisphosphate and diacylglycerol (DG) can be generated. DG activates protein kinase C. Carbachol (CCh), phorbol 12,13-dibutyrate and phosphatase inhibitors, okadaic acid and calyculin A increased the inward currents passing through the L-type VDCs. These effects were inhibited by protein kinase inhibitors, H-7 and staurosporine. The CCh effect was also inhibited by GDP beta S. Therefore, it seems possible that DG, a product of phosphatidylinositol break-down might mediate muscarinic effects on L-type VDC, the last via stimulation of protein kinase C, and that L-type VDC activity might be modulated by protein kinase C-mediated phosphorylation and protein phosphatase type-1-mediated dephosphorylation of the channel or related protein(s) in guinea pig taenia coli smooth muscle cells.
An experimental reconstruction of the urinary bladder using specially designed bovine cross linked atelocollagen sponge was performed after partial cystectomy in 12 male rabbits. Bladder reconstruction with hybrid type biomaterials using both atelocollage sponge and cultured autologous cells were performed in 5 rabbits (the 1st group). The autologous cells were collected from the mucosa and muscular layer of the urinary bladder and were seeded on the atelocollagen sponge before reconstruction. Reconstruction using atelocollagen sponge without autologous cells were performed in the other 7 rabbits (the 2nd group). In 9 of these 12 rabbits, atelocollagen sponge was successfully implanted in the native urinary bladder. Histopathological findings revealed that seeded autologous cells and growth of surrounding host cells could be seen similarly in the atelocollagen sponge but these could not be differentiated by these could not be differentiated by routine histopathological techniques. In conclusion, these results showed a possibility of construction of artificial urinary tract using both atelocollagen sponge and autologous cells.
The mechanism of increased nocturnal urine production in adult patients complaining of nocturia has seldom been reported. The objective of this clinical study is to investigate the circadian rhythm of both urine production and plasma arginine-vasopressin (AVP) level, and the efficacy of intranasal instillation of 1-deamino-8-D-arginine-vasopressin (DDAVP) in adult patients complaining of nocturia. Eight patients (seven men, one woman) who ranged in age from 44 to 77 years (mean 64.1 years) were examined. Three of them suffered from Shy-Drager syndrome, and no patient had shown any improvement of symptoms in spite of administration of anti-cholinergic agents and restriction of water intake. Nocturnal urine volume was more than bladder capacity in all patients, and no patient showed normal elevation of nocturnal plasma AVP level. Intranasal administration of DDAVP of 5 or 10 micrograms revealed marked decrease in nocturia, and nocturnal urine volume (p < 0.01). There were mild side effects (headache, nasal obstruction, and hyponatremia) not requiring any treatment. In conclusion, DDAVP is a safe and effective treatment for adult patients complaining of nocturia due to hyperproduction of nocturnal urine and inappropriate nocturnal secretion of AVP.
This report describes a patient with food-dependent exercise-induced anaphylaxis (FEA). A 25-year-old female has had three episodes of syncopal attack associated with urticaria in the past two years: the attacks have been developed by exercise after taking meals made of wheat flour. She has an allergic predisposition to metals. No abnormal findings were observed in the routine work up for syncope including, ECG, 24-hour Holter ECG, UCG, tilt table test, and EEG examinations. A provocative test for FEA was performed. It included food (sandwich) intake followed by exercise. The serum histamine concentration was elevated to a three times higher than the control value after the provocation. Accordingly, she was diagnosed as FEA and advised not to take wheat flour prior to physical exercise. No syncopal episode has been observed during the 16 months since the diagnosis.
Two adult patients with type I glycogen storage disease (I-GSD) had chronic renal disease with heavy proteinuria. Renal biopsies showed focal glomerular sclerosis, interstitial fibrosis, tubular atrophy or vacuolation, and prominent arteriosclerosis. Marked glomerular hypertrophy was demonstrated histometrically. Oil red O staining in one patient revealed numerous lipid deposits in the glomerular mesangium, tubular epithelial cells and interstitium. Electron microscopy in the other patient revealed diffuse thickening of the glomerular basement membrane (GBM) and lipid droplets within the mesangium. The glomerular hypertrophy, thickening of the GBM, and subsequent sclerosis were similar to those in insulin-dependent diabetes mellitus. These findings may explain the similarities between the natural histories of renal involvement in the two disorders. Particularly, glomerular hypertrophy may be a key step leading to glomerular sclerosis, which is the predominant finding I-GSD. Hyperlipidemia, which is commonly seen in I-GSD, may also accelerate the glomerular sclerosing process.
An expression cDNA library was constructed with poly(A)-rich RNA extracted from the collar of the giant African snail, Achatina fulica Férussac. A 1.9-kbp cDNA clone encoding a precursor of antibacterial glycoprotein of the snail, achacin, was isolated from the cDNA expression library. The cDNA sequence contains an open reading frame with 1593-nucleotide residues. The deduced amino acid sequence of this achacin precursor starts with a 29-residue leader peptide followed by a 502-residue mature peptide (56 kDa) with four possible N-glycosylation sites, Asn-Xaa-Ser or Asn-Xaa-Thr. The Northern-blot analysis proved that the achacin precursor was specifically expressed in the tissue of snail collar and processed to mature achacin. cDNA inserts encoding achacin precursor were subcloned into expression plasmids. Three kinds of expressed polypeptides were cross-reacted with rabbit antiserum raised against achacin. The largest polypeptide (M(r) 63,000) should be the achacin precursor.
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Explore the source record for details and available documents.
1. The responses of guinea-pig urinary bladder smooth muscle to intramuscular nerve stimulation were investigated by isometric tension recording. 2. The nerve mediated contractions, evoked by field stimulation with a stimulus of 0.5 msec duration, a frequency of 15 Hz and a voltage of 50 V, were inhibited by atropine (10(-6) M) and alpha, beta-MeATP (10(-4) M) to about 80% and 20%, respectively, of control. 3. Simultaneous application of atropine (10(-6) M) and alpha, beta-MeATP (10(-4) M) abolished the contraction evoked by selective nerve stimulation. 4. Terodiline (10(-4) M), one of Ca2+ antagonists, inhibited the contraction evoked by both nerve selective stimulation and exogenously applied ATP. 5. Based on these results we suggested that in guinea-pig urinary bladder, ATP was a predominant excitatory transmitter and the nerve-mediated contraction and exogenous ATP were mainly dependent upon Ca2+ influx.
Expression of a fusion protein composed of dihydrofolate reductase and a derivative of growth hormone-releasing factor resulted in the formation of inclusion bodies in Escherichia coli at 37 degrees C. Among various chemicals, such as detergents, protein denaturants, and acetic acid, tested for the ability to dissolve the inclusion bodies, acetic acid, Brij-35, deoxycholic acid sodium salts, guanidine-HCl, and urea showed a strong solubilizing effect without damaging the DHFR activity. Acetic acid was useful in terms of preparing GRF derivatives, since it could be easily removed by lyophilization, and this made it easy to perform the succeeding BrCN treatment for cutting out the GRF derivative from the fusion protein. The GRF derivative was purified by reversed phase HPLC from the BrCN digest of the acetic acid extract, and its growth hormone-releasing activity was demonstrated. However, for obtaining a highly purified fusion protein itself, solubilization of inclusion bodies by urea was preferred because urea was the only agent which did not cause serious precipitation of the regenerated fusion protein after 10-fold dilution of the extracted inclusion bodies with buffer. The fusion protein was highly purified by means of a methotrexate affinity chromatography.