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Biomedical subjects

J J Townsend

Publications and source records attributed to J J Townsend.

At least 55 records · Page 3Linked to original sources
PubMed1985

Macrophage response to herpes simplex encephalitis in immune competent and T cell-deficient mice.

Corneal inoculation of Nude (athymic) mice and Balb/c mice with herpes simplex virus Type I produces a brainstem encephalitis with demyelination of the trigeminal root entry zone. The extent of CNS demyelination is less in the immune-deficient athymic mice 7 days after infection compared to the immune-competent Balb/c mice. Both groups demonstrate a macrophage response and beginning myelin disruption approximately 3 days after corneal infection when herpes viral particles are first observed within central nervous system cells. Five to seven days after infection when differences in the extent of demyelination between the immune-competent and immune-deficient animals become evident, the Balb/c mice demonstrate T cells and increasing numbers of macrophages at the trigeminal root entry zones. These findings suggest an interaction between macrophages and T cells which leads to an extension of the demyelination in the immune competent Balb/c mice and that lack of T cells is important in limiting demyelination in Nude (athymic) mice.

Animals↗
PubMed1983

Schwann cell remyelination in experimental herpes simplex encephalitis at the trigeminal root entry zone.

Inoculation of mice on the cornea with herpes simplex virus, type I, results in demyelination of central nervous system (CNS) axons at the trigeminal root entry zone. This study examined the process of remyelination in this area. Between eight and 15 days after corneal infection, increasing numbers of Schwann cells appeared on the CNS side of the trigeminal root entry zone, where they encircled the demyelinated CNS axons. Remyelination of CNS axons by Schwann cells began between 12 and 15 days and increased during the following weeks. Remodeling of remyelinated internodes continued during the nine weeks of observation. No infectious virus could be cultured 15 days after infection, although latent virus was recovered from the dorsal root ganglia at this time. The disruption of astrocytes on the CNS side of the trigeminal root entry zone during the early stages of infection and the proximity of Schwann cells to the CNS trigeminal root entry zone appear to be important factors affecting CNS remyelination.

Animals↗
PubMed1982

Brain pyruvate carboxylase and the pathophysiology of biotin-dependent diseases.

Given the cerebellar symptomatology of biotin-dependent diseases and other lactic acidoses, we hypothesized that cerebellar pyruvate carboxylase activity might be differentially low or especially sensitive to cofactor deprivation. Accordingly, pyruvate carboxylase activity was measured in selected areas of normal and biotin-deficient rat brain. Control cerebellar hemisphere and vermis specific activities were identical, and slightly higher than cerebral and brainstem activities. In biotin-deficient rats, hepatic pyruvate carboxylase activity was 3% of control, whereas pyruvate carboxylase activities of all brain sections were 53 to 71% of control. Brain histology was normal. Cerebellar pyruvate carboxylase activity is therefore not distinctly low or labile and is in fact preferentially maintained despite severe cofactor deprivation.

Animals↗
PubMed1982

Lymphocytic adenohypophysitis of pregnancy simulating a pituitary adenoma: a distinct pathological entity. Report of two cases.

Diffuse lymphocytic infiltration of the adenohypophysis occurring in temporal relation to pregnancy was found in two patients, each of whom had an intrasellar mass with suprasellar extension that caused compression of the optic chiasm. The pathology and etiology of this lesion is discussed. This entity should be considered when evaluating patients with a pituitary mass lesion that presents in temporal association to pregnancy, particularly if there is evidence of hypopituitarism rather than a hypersecreting, endocrine-active adenoma.

Adenoma↗
PubMed1982

Immunochemical features of a case of progressive rubella panencephalitis.

Progressive rubella panencephalitis (PRP), a slowly progressive and fatal central nervous system (CNS) disorder due to rubella virus, is characterized by high cerebrospinal fluid (CSF) levels of immunoglobulins, oligoclonal bands and high CSF:serum rubella antibody titre ratios. Sera, CSF and neutral extracts of brain, spleen, lymph node and kidney obtained at autopsy from a case were analysed for immunoglobulin isotype and content by enzyme linked immunosorbent assays. Comparable titres of rubella specific IgA and IgG were found in sera and CSF, but accounted for a disproportionate amount of the isotype specific immunoglobulins of CSF (0.19%, 14.0%) as compared to serum (0.02%, 0.69%). The percentage of isotype specific immunoglobulins were not increased in extracts of most visceral tissues compared to serum, however, rubella specific IgA and IgG were disproportionately increased in extracts from most regions of brain sampled (1-60-fold and 8-27-fold respectively). No rubella specific IgM could be conclusively demonstrated in any specimen. Immunoprecipitation studies showed that the IgG reacted with the major glycoproteins (gp62, gp47-56 complex) and non-glycosylated polypeptide (p38) of radiolabelled rubella virions and infected cell lysates. These studies support the conclusion that a major portion of the rubella specific antibody is produced within the CNS of patients with PRP.

Antibodies, Viral↗
PubMed1981

The demyelinating effect of corneal HSV infections in normal and nude (athymic) mice.

Nude (athymic) mice and their immune competent Balb/c litter mates were infected with herpes simplex virus (HSV) type I on the scarified cornea. Seven to eight days after infection the trigeminal root entry zone was examined by light and electron microscopy. The immune competent Balb/c litter mates demonstrated marked central nervous system (CNS) demyelination when compared to the T cell-deficient animals who showed mild edematous change and minimal CNS demyelination ultrastructurally 7 days after infection. Viral titers were similar in both groups at this time. These studies further substantiate a role for the cell-mediated immune system in the CNS demyelination 1 week after corneal infection with HSV.

Animals↗
PubMed1981

The relationship of astrocytes and macrophages to CNS demyelination after experimental herpes simplex virus infection.

Corneal inoculation of mice with herpes simplex virus type I (HSV) produces central nervous system (CNS) demyelination 7 to 8 days after infection. The demyelination originates at the junction between PNS and CNS in the trigeminal root entry zone. The pathogenesis for this selective demyelination is unknown. Immunosuppression with cyclophosphamide reduces the extent of demyelination, but does not eliminate the lesion entirely. This report concerns the electron microscopic evaluation of the events preceding demyelination. The astrocytes forming the CNS junction are heavily infected 62 hours after corneal inoculation before myelin breakdown. These cells then undergo lysis, releasing viral and cellular debris. Perivascular monocytes appear in the CNS at this time, and proceed to phagocytize the dying cells. These monocytes may be important in transferring antigenic information to the cell-mediated immune system, which responds by producing extensive CNS demyelination by 6 to 7 days postinfection.

Animals↗
PubMed1981

Isolated hypertrophic interstitial neuropathy of the trigeminal nerve associated with trigeminal neuralgia. Case report of an entity not previously described.

Hypertrophic interstitial neuropathy (HIN) of the trigeminal nerve was observed in a patient with trigeminal neuralgia who had no other neurological abnormalities. Pathological documentation confirmed focal HIN. No similar histologically documented case of isolated trigeminal nerve involvement by HIN has been reported previously.

Adult↗
PubMed1980

An autoradiographic study of human gliomas: growth kinetics of anaplastic astrocytoma and glioblastoma multiforme.

When 3H-thymidine was administered either intravenously or intra-arterially to 9 patients with gliomas (5 glioblastoma multiforme, 3 anaplastic astrocytoma, and one mixed glioma) shortly before operation, and tissue obtained from the biopsy and, subsequently, at autopsy was examined by autoradiography, it was found that 2 of the glioblastomas diluted out the labelling in the two- to four-month interval between labelling and autopsy, whereas 3 other glioblastomas and the 2 anaplastic astrocytomas retained labelled neoplastic cells in parts of the tumours at autopsy after intervals of from three weeks to five months following labelling. Most patients whose tumours demonstrated foci of labelled cells at autopsy survived longer (1.5 to 7 years). Certain neoplastic cells in anaplastic astrocytomas and some glioblastomas appear either to limit cell division or to differentiate even in an environment favourable to cell proliferation.

Adolescent↗
PubMed1980

Continuous cataplexy in a patient with a midbrain tumor: the limp man syndrome.

A patient with glioblastoma of the rostral brainstem and hypothalamus exhibited bilateral internuclear ophthalmoplegia and vertical nystagmus; he suffered episodes of cataplexy, narcolepsy, and sleep paralysis. A peculiar fluctuation of posture and tone ("limp man syndrome") proved to be a manifestation of continuous cataplexy, as documented by H-reflex recordings. This is the first report of a remarkable movement disorder caused by continuous, fluctuating, partial cataplexy, and is the second report of an association between cataplexy and a tumor of the rostral brainstem.

Adult↗
PubMed1980

Giant aneurysm and cerebral ischemia.

A case is reported of a patient harboring a giant aneurysm of the left middle cerebral artery who presented with a reversible ischemic neurological deficit. The etiology of the cerebral ischemia is discussed, with reference to the literature. In addition, results obtained from evaluation of the luminal surface of the aneurysmal dome with the scanning electron microscope are described.

Adult↗
PubMed1979

An infant with Cushing's disease due to an adrenocorticotropin-producing pituitary adenoma.

An 8-month old male with Cushing's disease is presented; his clinical presentation and appearance were typical of infants with glucocorticoid excess. Concentrations of cortisol, 17-hydroxyprogesterone, and adrenal androgens were strikingly elevated. High doses of dexamethasone did not suppress the excretion of urinary free cortisol or 17-hydroxycorticoids, and administration of ACTH elicited no further rise in plasma cortisol. Responses of LH, FSH, and PRL to iv LRF and TRF were appropriate for age, but neither TSH nor ACTH rose significantly. Plasma ACTH values were elevated to 700 pg/ml. An intracranial mass lesion superior and anterior to the sella turcica was demonstrated by computerized axial tomography and angiography. An inoperable pituitary adenoma was a massive surrounding fibroblastic reaction was found at craniotomy. The pathological diagnosis of an ACTH-producing pituitary adenoma was confirmed by immunohistochemistry and by the in vitro secretion of ACTH by cells cultured from the tumor.

17-Hydroxycorticosteroids↗
PubMed1979

Recurrent transient ischemic attacks secondary to an embolizing saccular middle cerebral artery aneurysm. Case report.

Over a 1-year period, a 60-year-old woman had nine episodes of transient weakness, clumsiness, and hypesthesia of the right upper extremity. Angiography revealed normal extracranial vessels and a left middle cerebral artery aneurysm. The aneurysmal sac, removed at operation, had an organized thrombus, which was believed to be the cause of the transient ischemic attacks. Postoperatively, the patient has remained free of neurological symptoms.

Female↗
PubMed1979

Prolactin-secreting pituitary adenomas in multiple endocrine adenomatosis, type I.

In three unrelated families, four patients with multiple endocrine adenomatosis, type I, had confirmed or highly probable prolactin-secreting pituitary adenomas. In one patient, selective transsphenoidal tumor resection resulted in normal prolactin levels and resumption of menses. Heretofore, the majority of pituitary tumors in such patients had been thought to be nonsecreting chromophobe adenomas, but recent studies have shown that, in sporadic cases, as many as three fourths of "nonsecreting" pituitary tumors in fact secrete prolactin. Thus, based on our experience and reports of others, we believe that prolactin-secreting tumors may be common in patients with pituitary tumors as part of the syndrome of multiple endocrine adenomatosis, type I, and we recommend that serum prolactin be measured when evaluating these patients and their families.

Adult↗