Neuronal and oligodendroglial infection by the WW strain of Theiler's virus.

Newborn ICR mice were infected by intracerebral inoculation of 10(5.3) LD50 of the WW strain of Theiler's virus and examined serially by virologic and ultrastructural methods. Maximal titers of 10(6) LD50 developed in the brain by day 8 when 90 per cent of the animals were dead or moribund. The virus first appeared and was most prominent in the thalamus, basal ganglia, and midbrain. It spread from these areas throughout the cortex, brainstem, and spinal cord but spared the cerebellar cortex. Both neurons and oligodendroglia were infected. Infected cells first showed dispersion of polyribosomes, accumulation of vesicles, and widening of perinuclear cisternae. Normal cytoplasmic organelles and the nucleus were displaced by an accumulation of viral crystals, membranous profiles, and fibrillar material. Within degenerating cells the nuclear chromatin became clumped and marginated and the cytoplasm was filled either with vesicles or masses of paracrystalline viral arrays. These changes were accompanied by a vigorous inflammatory response of lymphocytes, plasma cells, macrophages, neutrophils, and eosinophils. Lysis of oligodendroglia during acute infection with the WW strain of Theiler's virus may provide a stimulus for the late autoimmune demyelination that has been described in animals that survive the acute encephalitis.     

Use of carbon labeling to demonstrate the role of blood monocytes as precursors of the ‘ameboid cells’ present in the corpus callosum of postnatal rats

Cells with features suggestive of ameboid motion and phagocytic properties are observed in the rat corpus callosum during the first few days of life. These cells, herafter referred to as ‘ameboid cells’, have been investigated in several ways. An electron microscopic study of the corpus callosum in 5- to 7-day-old rats indicated that most ‘ameboid cells’ were typical macrophages, but some displayed features of monocytes, while others appeared to be transitional between the two types. These observations raised the possibility that blood monocytes were the precursors of ‘ameboid cells’. This possibility was tested by injecting a suspension of carbon particles into the circulation of rats of various ages to label and trace monocytes. Within 15 minutes after injection, carbon particles were seen between cells in blood smears as well as in the lumen of capillaries, but not between cells and axons in corpus callosum. By a half hour, a few of the circulating monocytes, and with time, up to half of them, contained carbon particles. Five days after injection, carbon particles were observed in cells of the corpus callosum identified as ‘ameboid cells’ of the monocytic and macrophagic type. Such carbon-containing cells were seen in many of the animals injected at the age of 0–1 day, in few of those injected at 3–5 days, and in none of the older animals. Since free carbon had not been observed in corpus callosum spaces, it was concluded that ‘ameboid cells’ did not pick up carbon locally. The alternative was that blood monocytes, after ingesting carbon particles in the circulation, migrated to the corpus callosum and settled as ‘ameboid cells’. In the hope of obtaining a direct confirmation of this conclusion, blood cells obtained from carbon-injected Lewis rats were centrifuged in a Percoll gradient to obtain a fraction which contained 70–80% monocytes, less than 2% granulocytes, and 20–30% lymphocytes. Carbon was present in up to half on the monocytes and 1% of the granulocytes, but not in the lymphocytes; and it was calculated that over 99% of the carbon-labeled cells were monocytes. The cell fraction was then introduced into the blood circulation of 2- to 3-day-old syngeneic Lewis rats, and the animals were sacrificed 5 days later. Occasional carbon-labeled cells appeared not only in liver, spleen and connective tissue, but also in the corpus callosum, where they were identified as ‘ameboid cells’ of the monocytic and macrophagic type. Even though such cells were infrequent, their presence conclusively demonstrated that at least some ‘ameboid cells’ of the corpus callosum were derived from circulating blood monocytes.     

Fine structural studies of radiation-resistant human squamous cell carcinomas1

Abstract Squamous cell carcinomas of the oral cavity are relatively common lesions, and often can be controlled by radiation therapy. Recently, a series of these tumors has been encountered which did not respond positively to irradiation, necessitating subsequent extensive surgery. This report describes some fine structural changes which were observed in squamous cell carcinomas following exposure to x-irradiation. In addition to the common, keratin-forming differentiated cell, others which were observed were secretory-like, undifferentiated and phagocytic cells. Undifferentiated tumor cells occasionally became incorporated, at least temporarily, as a component of the blood vessel wall, perhaps reflecting metastatic potentiality. It is proposed that irradiation may either increase potential avenues of tumor cell differentiation or inactivate inhibitors thereof.     

Corpus luteum formation in the fetus

A well-developed corpus luteum was found at autopsy in a premature infant who died 26 hours post partum. Intrauterine pituitary-gonadal development and regulation are briefly reviewed and a possible mechanism of intrauterine fetal ovulation is presented.     

Helicobacter pylori and severe nausea and vomiting during pregnancy

Helicobacter pylori is a bacterial infection of the stomach, which may aggravate nausea and vomiting in pregnancy. Studies have found conflicting evidence of the role of H. pylori in severe nausea and vomiting in pregnancy and hyperemesis gravidarum. Several women suffering from weight loss and experiencing continued nausea and vomiting were tested for H. pylori antibody during their pregnancy. This article reviews the outcomes of women with both positive and negative H. pylori tests, the treatment of H. pylori, and its controversial role in managing severe nausea and vomiting in pregnancy.