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Biomedical subjects

H Tsukagoshi

Publications and source records attributed to H Tsukagoshi.

At least 163 records · Page 9Linked to original sources

Choreoathetoid movements associated with a spleno-renal shunt.

A 73-year-old woman without liver cirrhosis developed choreoathetoid movements of the limbs due to portal-systemic encephalopathy. A prominent spleno-renal shunt was demonstrated by non-invasive methods (abdominal computed tomography and sonography) as well as arterial portography. The choreoathetoid movements were improved by a protein-restricted diet and administration of lactulose. A portal systemic shunt should be considered when investigating choreoathetosis, even in patients without liver cirrhosis.

Aged↗

HTLV-I-associated meningitis.

A 69-year-old woman with human T-cell lymphotropic virus type I (HTLV-I) positive chronic myelopathy became comatose with acute meningitis. Most of the cells in the cerebrospinal fluid were similar to those found in adult T-cell leukaemia/lymphoma, which suggests that there is a close relationship between HTLV-I and this form of meningitis.

Aged↗

Systemic amyloid deposition in old age and dementia of Alzheimer type: the relationship of brain amyloid to other amyloid.

We investigated amyloid deposition in the brain and other organs in 105 consecutive autopsy cases, aged 59 to 101 years. They consisted of two groups; 15 patients with dementia of Alzheimer type (DAT) and 90 patients without DAT. Amyloid deposition was found in 93% of all cases. The incidence of amyloid deposition increased with age. The number of organs affected with amyloid deposition in each case also increased with age. The incidence of amyloid deposition in each organ was as follows; 88% in pituitary gland, 66% in brain [amyloid of senile plaque (SP) (61%) and/or cerebral amyloid angiopathy (CAA) (56%)], 33% in pancreas, 3% in heart, and less in others. In immunohistochemical studies using the antisera to the various kinds of amyloid or related proteins, amyloid beta protein was demonstrated in brain amyloids including SP and CAA, but not in others. Cardiac amyloid was positive for prealbumin. Pituitary amyloid and CAA were positive for amyloid P-component. The incidence of brain amyloids in DAT were significantly higher than that in non-DAT. There was no significant difference in the incidence of pituitary and pancreatic amyloid between DAT and non-DAT. In the non-DAT patients, there were significant positive correlations in amyloid deposition between the brain and pituitary gland and between the brain and pancreas. Acceleration of amyloid deposition would be a process confined to the brain in the patients with DAT. The pathogenesis of the accelerated deposition of brain amyloids is discussed from the point of view of amyloidosis.

Aged↗

Immunolocalization of cathepsins B, H and L in skeletal muscle of X-linked muscular dystrophy (mdx) mouse.

The amounts of non-collagen proteins (muscle structural proteins) and the activity of creatine kinase were significantly decreased in muscles of 28-day-old mdx mice. The activities of lysosomal thiol proteases such as cathepsins B and L were increased in muscles of mdx mice at as early as 10 days of age. Endogenous thiol proteinase inhibitor and various lysosomal hydrolases also showed increased activities. The localization of cathepsins B, H and L, and endogenous thiol proteinase inhibitor was investigated using the respective specific antibodies. While only invading macrophages were stained strongly with anticathepsin B and H, and anti-thiol proteinase inhibitor antibodies, cathepsin L was localized in muscle cells as well as in invading macrophages. Cathepsin L in muscle cells itself may initially degrade muscle structural proteins, before lysosomal thiol proteases, mainly derived from macrophages, degrade them in skeletal muscles of mdx mice.

Age Factors↗

Localized amyloidosis of the uterine cervix.

Localized amyloidosis of the uterine cervix was found in a 56-year-old woman. The firm enlarged cervix showed massive tumorous amyloid deposition. In the amyloid deposits there were foci of ossification and calcification. An infiltrate of multinucleated giant cells, histiocytes, lymphocytes, and plasma cells was seen adjacent to the amyloid deposits. Immunohistochemically, the amyloid reacted with antisera against A-lambda, amyloid protein of immunoglobulin lambda light chain origin. This indicated that the amyloid protein was of immunoglobulin origin in this rare case of localized amyloidosis of the uterine cervix.

Amyloidosis↗

Skeletal muscle amyloid deposition in AL- (primary or myeloma-associated), AA- (secondary), and prealbumin-type amyloidosis.

Amyloid deposition in the quadriceps femoris muscle was investigated in 12 cases of systemic amyloidosis including 6 of AL-(primary or myeloma-associated) type, 2 of AA- (secondary) type, and 4 of prealbumin- (familial or sporadic) types. Clinically, muscle weakness was found in 7 patients. Among the 7 patients, one of the AL-type suffered from systemic myopathy showing progressive muscular stiffness, pseudohypertrophy, and weakness. The other 6 presented with polyneuropathy. Pathologically, no amyloid was found to be deposited in the AA-type. In all of the AL- and prealbumin-types, amyloid deposition was found in the blood vessels and peri- and endomysium. The degrees of amyloid deposition were marked in one case of the AL-type, which was considered to be suffering from amyloid myopathy, moderate in one of the AL-type, and slight in the rest of the AL-type and all of the prealbumin-type. Our observations and descriptions in the literature indicate that the presence and degrees of amyloid deposition in the skeletal muscles would be related to the types of amyloid proteins in amyloidosis. It seems likely that the affinity of amyloid to the skeletal muscles is variable in AL-type, probably depending on the molecular heterogeneity of AL protein, is low in prealbumin-type, and is almost absent in AA-type.

Adult↗

Myoclonic activity associated with cefmetazole, with a review of neurotoxicity of cephalosporins.

We reported a case of a 66-year-old female with uremia who developed myoclonic activity after administration of cefmetazole (4g/2 days). Curiously, the level of the antibiotics (236 micrograms/ml) in the cerebrospinal fluid (CSF) was higher than that in the blood (103 micrograms/ml). Myoclonic activity faded away after cessation of the antibiotics. This is the first case reported developing neurotoxicity associated with intravenous administration of cefmetazole. In addition, the curious pharmacokinetic dynamics of cephalosporin in uremia is discussed.

Aged↗

[A case of chronic polyneuropathy associated with chronic type B hepatitis].

A case of chronic polyneuropathy associated with chronic type B hepatitis was described. A 31 year-old male was admitted to our hospital with a 2-year history of progressive weakness and sensory disturbances of all limbs. There was past history of acute type B post-transfusion hepatitis after subtotal gastrectomy. On examination there was generalized muscle weakness, particularly in movements of the hands and feet with areflexia. He had a steppage gait. Sensory examination revealed moderately decreased pinprick, light touch, vibration and position sense in the distal portion of all extremities. On admission, hepatitis associated antigen and antibody were negative and positive, respectively. The level of circulating immune complexes was high with the titer of 6.6 micrograms/ml by Clq assay and 16X by Raji cell assay. Liver biopsy revealed fibrosis and periportal inflammatory infiltrate compatible with the diagnosis of chronic viral hepatitis. Sural nerve biopsy showed marked loss of large myelinated fibers and epineural vasculitis with the thickened blood vessel wall and mononuclear cell infiltrates. There have been increasing evidences that extrahepatic manifestations are caused by vasculitis due to HBs antigen-antibody immune complex deposits. On the basis of findings in the literature it seems possible that chronic polyneuropathy may be related to the vasculitis due to HBs antigen-antibody complex deposits after hepatitis B virus infection.

Adult↗