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Biomedical subjects

H Shiraki

Publications and source records attributed to H Shiraki.

At least 91 records · Page 5Linked to original sources

Double encephalitis with herpes simplex virus and cytomegalovirus in an adult.

A 51-year-old housewife developed symptoms of a cold followed by high fever, delirium, coma, rigidity of extremity muscles, positive Babinski sign and generalized convulsions, while complement-fixing antibody titre to herpes simplex virus in the sera raised over 128 X and declined to 8 X in the course. She finally expired of bronchopneumonia following status epilepticus after 94 days of illness. Severe necrosis with extensive hemorrhage in the white matter was predominant in the temporal, insular and orbitofrontal cortex, thalamus and globus pallidus. Focal rarefaction of the cerebral cortex with a very few eosinophilic intranuclear inclusions in the oligodendroglia and nerve cells, nerve cell destruction in the substantia nigra with glial nodules and perivascular inflammatory cell cuffs were observed. Abundant cytomegalic inclusion cells, originating from hypertrophic astrocytes, were present in the necrotic areas of cerebrum as well as in the rarefied tissue in the subependymal layers of the brainstem and cerebellum. Electron-microscopic study of the cytomegalic cells demonstrated the presence of numerous virions in both nucleus and cytoplasm. Fortuitour infection of the brain by cytomegalovirus with necrotizing encephalitis by herpes simplex virus is unique. The cause of double viral infections and severe lesions by less virulent strains is discussed.

Astrocytes↗

The neuropathology of subacute myelo-optico-neuropathy, "SMON", in the humans: --with special reference to the quinoform intoxication.

The detailed neuropathology of the 16 autopsy cases of the acute to chronic "SMON" of different ages together with those reported before and at the "SMON" Research Commission has been described and reviewed. This was compared with the alreadyknown neurological disorders, particularly systemic and/or pseudosystemic degeneration of the long tracts of the spinal cord with polyneuropathy together with the "SMON"-like diseases caused by certain neurotoxic and/or neurotropic agents. It has been concluded that "SMON" can be belonged to a subgroup of some endemic diseases within the main group of combined degenerations associated with complex nutritional deficiency or toxic interference of tissue metabolism. Since an excess and mal-administration of quinoform in quantity, time and space were identified in a great majority of the autopsy cases, quinoform could comprize the most important etiology for the "SMON" onset. This view also was supported by the almost complete reconstruction of the neuropathology of the human "SMON" in the experimental animals intoxicated with quinoform which disclosed a precise neurotropism from the autoradiograms of the same animals. As compared with the similar lesions in SLE,hepatocerebral diseases, etc., the pathogenesis and clinicopathological relationship of "SMON" was speculated. The accerelating and/or modifying factors for the SMON" onset aside from quinoform were discussed.

Adolescent↗