Congenital laryngeal anomalies associated with tracheal agenesis

Forty-eight cases of tracheal agenesis have been reported to date. Previous authors have studied gross postmortem laryngeal specimens. Of 37 cases wherein laryngeal findings were mentioned, only 14 were reported to be abnormal. This report details two more cases of tracheal agenesis and includes a detailed histopathologic study of the laryngeal anomalies by serial horizontal section. Although one of these specimens appeared normal at autopsy, both were found to have several abnormalities when studied microscopically in horizontal section. Both have an elliptical cricoid cartilage, an abnormality originally discovered by one of us (G.F.T.) using the same technique.     

Inhibition of cellular immune reactions by zymosan

Mice treated intraperitoneally with zymosan showed a strong inhibition of the DTHR (delayed-type hypersensitivity reaction) against sheep erythrocytes (SE), ovalbumin (OA), and alloantigen. Furthermore, the rejection time of skin transplants was nearly doubled while antibody formation against SE was significantly enhanced. When a DTHR against OA and an antibody formation against SE were induced at the same time in the same animals, than the suppressive and stimulating effects cancelled each other. These results are discussed with regard to the sensitivity of lymphocyte subpopulations, which may be different if exposed to phagocytosis-induced oxygen radicals.     

Studies of human myelin proteins during old age

The electrophoretic protein patterns of myelin isolated from frontal and callosal white matter were studied in adult man up to the age of 90 years. The proportions of the four major myelin proteins remained virtually unchanged as did the total protein content of white matter and of purified myelin. The total mass of purified myelin that could be recovered from white matter gradually decreased with age, suggesting an age-related loss of myelin sheath and probably neurons as well, without detectable alterations of the regular protein composition of myelin. In most cases basic protein of myelin was preceded by one or two minor protein components on electrophoresis. One of them is tentatively identified as "prebasic" protein similar to the one previously observed in other species, because of its close electrophoretic apposition to the main basic protein. The second component was found less frequently and was thought to arise from specific types of proteolysis of myelin proteins. Prolonged time intervals between death and autopsy had little, if any, effect on the proportions of basic protein and proteolipid protein. Similar results were obtained when bovine brain was incubated under conditions designed to simulate post-mortem autolysis. It was there fore concluded that meaningful data on proteins of human central myelin may be obtained even though an autopsy was not performed within a few hours of death.     

Cloning of murine IL-22 receptor alpha 2 and comparison with its human counterpart

We have identified the mouse and rat homologs of human interleukin-22 receptor alpha 2 (IL-22R alpha 2) and compared the localization, structure, and expression of the encoding murine and human genes. The mouse IL-22R alpha 2-encoding gene is located on chromosome 10A3 between, like in human, the genes for interferon-gamma R1 and IL-20R1. It spans a region of approximately 10 kb therefore being three times shorter than the human gene. Although the overall gene structure in both species is similar, the mouse gene lacks a counterpart to the third coding exon of the human gene known to be alternatively spliced. Like in human, mouse and rat IL-22R alpha 2 exist only as soluble receptors as deduced from the lack of transmembrane and intracellular domains encoding sequences. Quantitative expression analyses showed, analogically to the human system, a limited tissue distribution of mouse IL-22R alpha 2 mRNA. Differential modulation of IL-22R alpha 2 mRNA expression was observed upon systemic inflammation in mice in spleen, thymus, and lymph node.     

Damage of purkinje cell axons following chronic phenytoin administration: An animal model of distal axonopathy

Summary An animal model of central distal axonopathy following chronic administration of phenytoin is described. Male C57/BL6J mice received diphenylhydantoin (DPH) in the daily diet (liquid diet Stardit, supplemented with vitamins) over a period of 8 weeks. Control and experimental animals were pair-fed.Twelve mice of both groups were perfused via the left ventricle with glutaraldehyde. Representative samples of the cerebral cortex (area 3), cerebellum (vermis and deep cerebellar nuclei), thalamus, hypothalamus, and liver were embedded in araldite. Semithin sections and electron microscopy of the cerebellar vermis revealed marked dystrophic changes in the Purkinje cell axons. The presynaptic segments of Purkinje cell axons in the deep cerebellar nuclei showed massive enlargement and swelling due to accumulation of spherical particles and tubular structures in the axoplasm. These structures represent a proliferation of the smooth endoplasmic reticulum.Identical changes were found in hepatocytes of treated animals. Because phenytoin induces hepatic microsomal enzymes, we suggest that phenytoin-related Purkinje cell damage may be produced by an induction of Purkinje cell microsomes with proliferation of the smooth endoplasmic reticulum which causes a swelling and enlargement of presynaptic segments of Purkinje cell axons in deep cerebellar nuclei. Chronic phenytoin administration to mice is a new model of phenytoin-induced encephalopathy and of distal axonopathy of cerebellar neurons.Supported by the Deutsche ForschungsgemeinschaftPresented in Part at the Joint Meeting of the German and Scandinavian Neuropathologists, Turku, Finland, June 3–4, 1983     

CT stereotactic biopsy in the differential diagnosis of deeply situated intracerebral hematomas

The diagnosis of intracerebral haematomas, especially of those which are relatively small, occupy little space and are deeply situated, presents considerable problems. The problem is even greater when the expected acute case history and the acute beginning of the symptoms do not occur and unusual localisations are found. The consequences of this are false diagnoses and the treatment of these patients within the framework of blanket diagnosis "intracerebral tumours" or "space occupying processes" without any confirmation of the histological diagnosis. - Using a sample of 26 patients where the histological diagnosis of non-recent intracerebral hemorrhages had been confirmed (out of a series of 818 CT-stereotactically biopsied patients punctured by us from the beginning of 1983 until the end of 1984), the problem of establishing a diagnosis is exposed. - A histological diagnoses should in any case be confirmed before any thorough and deep-reaching therapy is begun, since false diagnoses and misinterpretations can cause serious consequences for the patient.