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Biomedical subjects

Y Yoshikawa

Publications and source records attributed to Y Yoshikawa.

At least 289 records · Page 16Linked to original sources

Molecular analysis of structural protein genes of the Yamagata-1 strain of defective subacute sclerosing panencephalitis virus. III. Nucleotide sequence of the hemagglutinin gene.

The full-length cDNA corresponding to the mRNA for the hemagglutinin (H) protein of the Yamagata-1 strain of the subacute sclerosing panencephalitis (SSPE) virus was cloned and the nucleotide sequence was determined. The mRNA corresponding to the H protein was composed of 1952 nucleotides and contained a single large open reading frame, which encoded 620 amino acids with a predicted molecular weight of 69,723. This cDNA clone expressed the H protein in Cos 7 cells, and the transfected cells showed hemadsorption. The nucleotide and amino-acid sequence homology with the Edmonston strain of MV were 98.0% and 96.6%, respectively. The deduced amino acid sequence had a single hydrophobic domain near the N-terminus that was long enough to serve as an anchor in the membrane. Five potential glycosylation sites were found on the H protein at identical positions as in the H protein of MV. Cysteine and proline were located at almost identical positions as those of the H protein of MV. In addition, monoclonal antibody study revealed that three epitopes, including the domains that were involved in the biological activities of the H protein of MV, were conserved on the Yamagata-1 strain. These results suggested that the H protein of the Yamagata-1 strain of defective SSPE virus is structurally and functionally similar to that of the Edmonston strain of MV.

Amino Acid Sequence↗

Molecular analysis of structural protein genes of the Yamagata-1 strain of defective subacute sclerosing panencephalitis virus. IV. Nucleotide sequence of the fusion gene.

The full-length cDNA corresponding to the mRNA of the fusion (F) protein of the Yamagata-1 strain of subacute sclerosing panencephalitis (SSPE) virus was cloned, and its complete nucleotide sequence was determined. The F gene was composed of 2369 nucleotides and contained a single large coding region, which is located between two noncoding regions. The 5'-terminal noncoding region consisted of 584 nucleotides comprising 44.9% cytosine, and had several inverted repetitious sequences. The 3'-terminal noncoding region had a relatively low homology of 91.7% with the MV. The coding region was expanded for nucleotides 585-2189, which encoded 534 amino acids with a molecular weight of 57,963. The homology of the amino acid sequence of the F protein between the MV and SSPE virus was 96.27%, and the positions of cysteine and proline were almost identical in the two viruses. The functional domains of SSPE-virus F protein closely resembled those of MV F protein, including the cleavage site, a signal sequence, the fusion-related stretch, the transmembrane region, and four potential glycosylation sites. Four antigenic epitopes on the MV F protein were also conserved on the SSPE-virus F protein. However, deletion of one nucleotide (position 2155) of the SSPE virus was found when compared with the MV, and shifted the coding frame, causing the substitutions of 27 C-terminal amino acids of the MV F protein with 11 different residues. The variations of the C-terminal region of the F protein were observed with two other SSPE viruses, suggesting that this may be a common property of SSPE virus that differs from MV.

Amino Acid Sequence↗

Renal amyloidosis characterized by abnormally thick fibrils.

A renal biopsy of a 57-year-old man with nephrotic syndrome revealed marked glomerular deposition of Congo red-positive, bire-fringent material characteristic for amyloid. Ultrastructurally, however, this material is composed of nonbranching, haphazardly arranged fibrils of approximately three times the thickness of typical amyloid fibrils. To our knowledge, there has been no report of such a finding, and this unique case enlarges the morphologic spectrum of renal fibrillosis.

Amyloidosis↗

Edematous changes in the central nervous system of zitter rats with genetic spongiform encephalopathy.

The pathogenesis of progressive spongy degeneration in zitter rats with genetic spongiform encephalopathy was examined histopathologically and biochemically in the context of edematous change in the central nervous system (CNS). Histopathological studies revealed that vacuolation in the CNS of zitter rats progressed with aging and the severity of spongy degeneration was markedly divergent in different areas in the CNS. Edematous change was confirmed by a consistently higher water content in the brain of zitter rats than in that of normal SD/J rats at all ages. Furthermore, a close relationship between spongy degeneration and edematous change in the CNS was demonstrated by regional measurement of specific gravity (SPGR) of brain tissues and quantification of the spongy degeneration by computer-image analysis. The brain regions with lighter SPGR were more severely affected by spongy degeneration. These results suggest that edematous change is related to the pathogenesis of spongy degeneration in the CNS of the zitter rat.

Animals↗

Diversity of matrix protein in subacute sclerosing panencephalitis and measles virus-infected cells.

Expression of the viral matrix (M) proteins in Vero cells infected with 18 strains of subacute sclerosing panencephalitis (SSPE) virus and measles virus was examined by immunocytochemistry and Western blot analysis using an anti-M monospecific serum and two sera against the M protein specific synthetic peptides. By immunocytochemistry using the anti-M monospecific serum, M protein was detected in all of the virus-infected cells regardless of cell-free virus production. M proteins of the seven non-productive strains were found to vary significantly in their epitope, in their reactivity to different assay systems, and in their molecular weight, whereas M proteins of the other 11 productive strains were detected consistently. These results suggest diversification of M protein of the non-productive strains.

Amino Acid Sequence↗

Temporary breakdown of immunological tolerance to dsDNA and nucleohistone antigens in rabbits infected with rinderpest virus.

The rabbit-passaged L strain of rinderpest virus (RV) causes the transient induction of anti-nuclear antibodies (ANA) in rabbits. It has been shown by an indirect immunofluorescence test that the target antigens of these ANA are DNA and/or DNA-histone complexes (nucleohistone). Here detailed examinations of the target antigens were carried out by ELISA, and it was revealed that rabbit sera contained three types of antibodies: antibodies reacting equally with both dsDNA and ssDNA; those reacting with ssDNA alone; and those reacting with nucleohistone. Epitopes recognized by the third type consisted of complexes of dsDNA and H2A + H2B or of dsDNA and H2B. All types of antibodies were antigen specific. Since the diversity of ANA among experimental rabbits was large, it was suggested that genetic background is important in the induction of anti-dsDNA antibodies in this system. Moreover, early induction of antibodies to nucleohistone and the rapid disappearance of ANA suggest that B cell proliferation/maturation for continuous production of ANA requires factors other than RV infection. This system may help elucidate the mechanisms of ANA induction and the development of autoimmune diseases.

Animals↗

Immune complex-induced disseminated intravascular coagulation (DIC). An experimental study.

Disseminated intravascular coagulation (DIC) was induced in rabbits by administration of antibody and antigen. The rabbits were sensitized passively by i.v. injection of antiferritin antiserum and challenged simultaneously by an i.p. inoculation of ferritin. After the challenge, circulating white blood cells, platelets and plasma fibrinogen levels showed an early fall, reaching minimum values at 3, 10 and 6 h, respectively. Fibrin thrombi appeared first at 2 h, reached a maximum at 5-7 h, and had mostly disappeared by 24 h. Formation of fibrin thrombi was frequent in the lung, liver, kidney and spleen. Early morphological changes included neutrophilic infiltration and accumulation of platelets in capillaries. Ferritin-antiferritin complexes were noted among fibrin thrombi or phagocytized by reticuloendothelial cells and neutrophils. The capacity of Kupffer cells to remove circulating immune complexes was saturated transiently; at this time fibrin thrombosis in various organs was most widespread and severe. It seems likely that formation of antigen-antibody complexes in the microcirculation initiates activation of platelets and neutrophils with subsequent release of mediators responsible for triggering DIC. Activation of complement was another possible factor inducing the reaction. In addition, blockade of the reticuloendothelial system promotes the progression of DIC. It is considered that the methods described constitute a useful model for further elucidation of immune complex-induced DIC.

Animals↗

[Relation between dentofacial skeletal patterns and the deflection of the roots of mandibular canine and premolars].

We conducted an investigation of the relation between dentofacial skeletal patterns and the deflection of the roots of mandibular canines and premolars. Data on root deflection, rated as mesial, distal, or undeflected, were obtained from orthopantomographs taken of 130 patients who were judged to meet certain criteria on their initial orthodontic examinations. The significance of the relation between these data and the dentofacial patterns, determined by radiographic cephalometric analysis, was then examined statistically. This determined that in cases of severe mandibular prognathism (ANB less than -2 degrees), the roots of 1st and 2nd premolars exhibited significantly more mesial deflection. This result suggests that the mesial deflection of these roots is caused by the differential growth rates of basal and alveolar bone in cases of severe mandibular prognathism.

Alveolar Process↗

[Effects of alpha-1-blocking agent in the treatment of detrusor sphincter dyssynergia].

Effects of adrenergic alpha-1-blocking agent, prazosin, in the treatment of detrusor external-sphincter dyssynergia (DSD) were evaluated in both experimental and clinical aspects. Experimentally, in the urethral pressure profile in dogs, the maximum urethral closing pressure was depressed after intravenous injection of 1 mg prazosin. When experimental DSD was obtained in dogs by stimulating electrically the unilateral 2nd sacral root, intra-venous injection of 1 mg prazosin inhibited contraction of the external urethral sphincter. Clinically, 74 patients with DSD based on neurogenic bladder from cerebral vascular attack (CVA) (13 cases) and spinal cord injury (61 cases) were retrospectively surveyed in terms of therapeutical effects of prazosin for DSD. Spinal cord injury was subdivided to 4 groups for clinical evaluation; cervical cord injury (C) with complete paralysis, thoracic cord injury (Th) with complete paralysis, lumbar cord injury (L) with complete paralysis and spinal cord injury with incomplete paralysis. Patients with CVA and spinal cord injury with incomplete paralysis showed good response rates in subjective improvement, 69% and 60% respectively. However, those with spinal cord injury with complete paralysis showed a poor response (28% for C, 23% for Th and 14% for L). The amount of residual urine significantly decreased after treatment, in all the groups except that of lumbar cord injury with complete paralysis. In all the groups, however, even after the drug treatment the amount of residual urine ranged from 80 to 170 ml and the rates of needing clean intermittent catheterization unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

[A case report of rheumatoid arthritis which showed acute renal failure, nephrotic syndrome and drug-related lupus-like syndrome caused by D-penicillamine].

The patient was a 74 years-old male who had suffered arthralgia since April 1986. Gold therapy was performed from June 1986 based on a diagnosis of rheumatoid arthritis (RA). This treatment was ineffective and administration of D-penicillamine (D-Pc) was started from March 1987, which alleviated the arthralgia. However, proteinuria appeared, and the nephrotic syndrome (NS) and acute renal failure (ARF) gradually developed. Four items, not including the renal symptoms, fulfilled the diagnostic criteria for systemic lupus erythematosus (SLE). Thereafter, D-Pc was withdrawn, and the symptoms were improved by hemodialysis and steroid therapy. This case was considered to be NS and ARF caused by treatment of RA with rather small doses of D-Pc (18.3 g in total), but the involvement of other factors could not be ruled out. Since the four items conforming to the SLE diagnostic criteria were alleviated by steroid therapy, the case was considered to be drug-related lupus-like syndrome. In recent years, D-Pc has frequently been used in the treatment of RA and its effects have been confirmed. However, side effects often appear, and considerable caution is required in the presence of drug-related SLE as well as proteinuria. When drug-related SLE is suspected, withdrawal of the drug concerned and steroid therapy appear to be useful.

Acute Kidney Injury↗

[Evaluation of plasma tissue plasminogen activator (I-PA) levels in patients with liver diseases].

Previous studies have demonstrated that plasma tissue plasminogen activator (t-PA) level was elevated in patients with liver disease. In this study, t-PA antigen levels were investigated in patients with acute hepatitis (AH; N = 12), chronic hepatitis (CH; N = 8), compensated liver cirrhosis (CLC; N = 40), decompensated liver cirrhosis (DLC; N = 23) and hepatocellular carcinoma (HCC; N = 35). The increased t-PA levels (higher than 14 ng/ml) were found in 33% (4/12) of AH on the early hospital days, 25% (2/8) of CH, 45% (18/40) of CLC and 91% (21/23) of DLC, and 60% (21/35) of Hcc cases. In patient with LC, the correlations between t-PA levels and serum total bilirubin (T.Bill) and hepatic synthetic functions were investigated. The results were that the t-PA levels correlated positively with T. Bil and negatively with liver synthetic functions such as albumin, protein C and choline-esterase, indicating that t-PA increased almost in proportion to the deterioration of hepatic function. Serial determination of t-PA in patients with HCC treated by transcatheter arterial embolization (TAE) revealed that TAE failed to normalize the t-PA levels. In one case of HCC complicated with disseminated intravascular coagulation (DIC), t-PA showed a marked increase at acute phase of DIC and subsequent decrease after the successful treatment for DIC by gabexate mesilate (FOY) infusion. These results suggest that increased t-PA in liver disease is due mainly to deterioration of hepatic function, and that secondary fibrinolytic state, such as DIC, is also a contributing factor.

Adult↗

Splenic amyloidosis: correlations between chemical types of amyloid protein and morphological features.

Sixty-one autopsy cases of splenic amyloidosis were reviewed to assess the relationship between the morphological patterns and chemical types of amyloid protein. On the basis of immunohistochemical reactions of amyloid protein, the cases were classified into 34 cases of AA and 27 of AL amyloidosis. Amyloid deposition in the spleen was divided into three major sites: the red pulp, the white pulp, and blood vessels. Red pulp involvement by amyloid was noted in 52% of the AL cases but in none of the AA cases. White pulp amyloid deposition was found in 70% of the AL and 35% of the AA cases. This difference was statistically significant (P less than 0.001). On the other hand, vascular deposition of amyloid was invariably noted in all cases with AA or AL amyloidosis, affecting the AA cases rather severely. These results strongly suggest that the widely held concept of deposition of amyloid as predominantly vascular in AL amyloidosis and parenchymal in AA amyloidosis requires revision. Our findings indicate that parenchymal, especially the red pulp, involvement is a consistent feature of AL amyloidosis, whereas vascular involvement is a finding common to both types of systemic amyloidosis.

Adult↗

[A case of emphysematous cystitis].

Emphysematous cystitis is a rare but interesting disease. A case is reported of cystitis emphysema with acute pyelonephritis and uncontrolled diabetes. The patient was a 54-year-old woman complaining of gross hematuria and fever. A submucosa emphysema in bladder was found by cystoscopy . Radiography showed the gas around the bladder. The patient was administered antibiotics, then symptoms was improved. We reviewed 12 cases of emphysematous cystitis reported in Japan and summarized the pathophysiologic features of this entity.

Acute Disease↗

Encephalitis induced by a canine distemper virus in squirrel monkeys.

Intracerebral inoculation with canine distemper virus (CDV) caused acute neurological signs of viral encephalitis in squirrel monkeys. Electroencephalogram revealed an abnormal sharp wave and seizure discharges resembling those of epilepsy. There was parenchymal inflammation, perivascular cuffs, neuronal degeneration, and glial reactions. Virus antigen was detected immunohistologically in the neurons and ependymal cells. Thus, CDV infection in squirrel monkeys provides an animal model for viral encephalitis and epilepsy.

Acute Disease↗

[A case of adult Still's disease with pulmonary hypertension].

The patient was a 29-year-old woman. She was well until autumn 1983, when she presented with polyarthralgia, fever above 39 degrees C, hepatosplenomegaly, swelling of lymphnode and salmon pink rash. Laboratory tests revealed marked leucocytosis with shift to the left, elevated ESR, strong positivity of CRP and abnormal liver function tests. However, anti-nuclear antibody and RA factor were negative. She was diagnosed as adult onset Still's disease (AOSD) by characteristic clinical course and laboratory data. During her disease course these abnormal findings could be well controlled neither by nonsteroidal anti-inflammatory drugs, immunosuppressive agents nor corticosteroids. Two and half years after the first admission, she began to complain of dry cough, dyspnea on efforts. Auscultation revealed an increased pulmonic sound and systolic murmur of cardiac apex. Chest X-Rays showed enlarged main pulmonary arteries. The lung fields were normal. Pulmonary function tests gave no evidence of a significant obstructive or restrictive defect but showed the low DLco and hypoxemia. Ventilation-perfusion lung scanning failed to reveal pulmonary embolism. Finally, right heart catheterization confirmed the pulmonary precapillary hypertension. Her pulmonary hypertension has progressed rapidly, strongly suggesting poor prognosis. Her pulmonary hypertension associated with no apparent parenchymal involvement was thought to be caused by a pulmonary vascular change probably related to AOSD. This case is a first case of AOSD with pulmonary hypertension.

Adult↗

Membranous glomerulonephritis in diabetic patients: a study of 15 cases and review of the literature.

Glomerular diseases other than diabetic glomerulosclerosis (DGS) occurring in diabetic patients may pose a diagnostic challenge to both clinicians and pathologists. We studied 15 cases of membranous glomerulonephritis (MG) in patients with diabetes mellitus focusing on the morphologic changes of the kidney. Light microscopic observation revealed nodular and/or diffuse DGS in 12 cases and no DGS in three. Periodic acid-silver methenamine stain showed spikes or chain-like structures in the glomerular capillary wall in 13 cases, indicating the presence of MG. Ultrastructurally, MG was classified into Stage I (N = 2), II (N = 8), III (N = 4), or IV (N = 1). Six out of nine cases with Stages I and II MG showed a thickened lamina densa of the glomerular basement membrane (GBM), suggesting diabetic influence on the GBM. Moreover, MG in some of the cases suggested atypical ultrastructural features including (a) the presence of large immune type deposits separated by tall spikes (N = 4), (b) high electron density of deposits in spite of their intramembranous location (N = 4), and (c) the presence of immune type deposits of mesangial (N = 3) and subendothelial (N = 2) locations. It is postulated that these atypical features are caused by altered turnover of the GBM, impaired glomerular clearance of immune complexes, changes of the glomerular capillary wall as the result of hemodynamic alterations, and/or nonenzymatic glycosylation in diabetic milieu.

Adolescent↗

Development of heat-stable recombinant rinderpest vaccine.

Recombinant vaccinia virus (RVV) containing the full-length cDNA of rinderpest virus (RV)-haemagglutinin (H) gene was constructed. The H gene was inserted into the attenuated vaccine strain of vaccinia virus (VV), Le 16 m0, with two different promoters, namely cowpox virus A-type inclusion body (ATI) promoter or VV 7.5 kilodalton (P7.5) promoter. These RVVs produced the same sized fully glycosylated RV-H protein in RK 13 cells as that of the authentic RV-H. Their heat stability in the lyophylized state was similar to that of the parental VV. All rabbits immunized with these RVVs produced virus neutralizing (VN) antibody to RV as well as anti RV-H antibody. Four weeks after immunization, these animals were challenged with RV intravenously. None of the RVV-immunized rabbits developed any clinical signs of RV infection except one which was immunized with RVV containing the ATI promoter and developed low VN titer. These results indicate the possibility of developing a heat-stable recombinant vaccine for the eradication of rinderpest in tropical countries without cold storage systems.

Animals↗