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Biomedical subjects

J J Dinn

Publications and source records attributed to J J Dinn.

18 recordsLinked to original sources
PubMed1991

Neuropathologic findings in AIDS and human immunodeficiency virus infection--report on 30 patients.

Central nervous system findings in 30 fatal cases of human immune deficiency viral (HIV) infection are described. Twenty seven patients had acquired immune deficiency syndrome (AIDS) and three patients had serological evidence of HIV infection only (HIV seropositive). Twenty nine patients had neuropathologic abnormalities at autopsy and frequently had more than one neuropathologic process. Neurologic disease was the dominant clinical feature in nineteen patients. The spectrum of neuropathologic disease is similar to that described in other series encompassing direct HIV infection of brain; indirect CNS involvement by opportunistic pathogens differing slightly from other series in their relative frequency; lymphoma and neurovascular disease. This, the first report which serves to document the level of neurologic disease in Irish patients with AIDS and HIV infection should help to provide meaningful information for use in the planning of neurologic and rehabilitation services for these patients.

Acquired Immunodeficiency Syndrome↗
PubMed1990

The emerging AIDS epidemic in Ireland--clinicopathological findings in 23 early cases.

A longitudinal study with follow up to the end of 1989 was carried out on 23 patients with AIDS who had attended St. James's Hospital, Dublin, by the end of 1987. Until then only 33 cases of AIDS had been reported in Ireland. The patients, all of whom had antibodies to human immunodeficiency virus (HIV), were predominantly male, young (mean age 31.3 years) and belonged about equally to three major risk groups: homosexuals, intravenous drug abusers (IVDA) and haemophiliacs. AIDS was diagnosed because of oesophageal candidiasis (8 cases), Kaposi's sarcoma (4), mycobacterial infection (4), pneumocystis carinii pneumonia (3), toxoplasmosis (2) or encephalopathy (2). Malignant lymphoma and a variety of infections occurred in the course of illness, and neurological involvement developed in 11 patients (48%). Mortality following diagnosis of AIDS was 39% at one year and 64% after two years. Autopsy in 10 of the 16 deaths contributed much to defining the extent and nature of the disease. The demographic pattern, risk group status, survival and range of complications were broadly similar to the pattern of AIDS as seen elsewhere in developed countries. However, compared to the profile of disease reported from the United States, oesophageal candidiasis (52%) and Mycobacterium tuberculosis (22%) were more prominent, pneumocystis carinii pneumonia (39%), Kaposi's sarcoma (22%) and Mycobacterium avium intracellulare (13%) were less frequent and cryptococcal infection was not identified. These regional variations in the frequency of the various complications and particularly the prominence of tuberculosis, probably reflect the interaction of the immunocompromised patient with the local environment and may have important diagnostic and therapeutic implications.

Acquired Immunodeficiency Syndrome↗
PubMed1986

Aggressive oncocytic neuroendocrine tumour ('oncocytic paraganglioma') of the cauda equina.

An oncocytic neuroendocrine tumour ('oncocytic paraganglioma') of the cauda equina is reported. The tumour was predominantly intradural, with extension into and destruction of surrounding vertebral bone. The tumour had an organoid pattern, and the tumour cells had abundant non-argyrophilic eosinophilic cytoplasm. Immunocytochemical stains for neurone-specific enolase, S-100 protein, keratin and carcinoembryonic antigen were positive, but stains for glial fibrillary acidic protein were negative. On ultrastructural examination, there were numerous mitochondria and scattered 200 nm dense-core membrane-bound granules, that rarely clustered in small aggregates. Intermediate filaments were focally arranged in long compact bundles. The histogenesis of tumours reported as cauda equina paragangliomas is discussed.

Actin Cytoskeleton↗
PubMed1985

Natural history of acromegalic peripheral neuropathy.

Eleven sural nerve biopsies from nine acromegalic patients, with and without peripheral neuropathy, were examined utilizing routine sections, single teased fibres and electron microscopy. The initial basic pathological lesion in both groups consisted of demyelination combined with hypertrophic formations affecting the Schwann cell system of the small diameter fibres. Second biopsies from two patients with neuropathy demonstrate the natural history of the lesion. The progression to eventual end-stage neuropathy is documented and is due to the marked onion bulb formation. Recovery is unlikely. Our findings indicate that the development of peripheral neuropathy in acromegaly is a serious complication. Deterioration, both clinically and pathologically, can be expected if the growth hormone remains persistently elevated.

Acromegaly↗
PubMed1981

Pathogenesis of subacute combined degeneration: a result of methyl group deficiency.

Four pairs of monkeys were maintained in an atmosphere of nitrous oxide under conditions which had previously been shown to produce subacute combined degeneration (SCD) of the spinal cord. The diet of one of each pair was supplemented with methionine. In every case the monkey with the unsupplemented diet became ataxic at around 10 weeks and the disorder progressed over a period of 2-3 weeks until the animal was moribund. During this period there was no detectable clinical change in the monkeys receiving methionine supplementation. Microscopical examination of the spinal cord and peripheral nerves of the unsupplemented monkeys showed the classical changes of SCD. The histological changes correlated with the clinical observations. Sections form the methionine-supplemented monkeys showed no change or only slight changes. These results suggest that, in these animals, inability to resynthesise methionine from homocysteine leads to SCD. It seems probable that the primary lesion producing SCD in human beings with pernicious anaemia is also inability to maintain methionine biosynthesis.

Animals↗
PubMed1979

Distribution of herpes simplex virus in acute necrotising encephalitis.

A 49-yr-old female developed a rapidly progressive neurological illness. The gross, light microscopic and electron-microscopic examination of the brain revealed all of the characteristic features of acute necrotising encephalitis with predominant involvement of the left limbic system. The distribution of herpes simplex virus suggests that the olfactory apparatus is the route of infection.

Acute Disease↗
PubMed1978

Lipoid proteinosis; a clinical, pathological and genetic study.

The clinical, pathological, and genetic findings in two closely related families in which a number of cases of lipoid proteinosis occurred are described. The necropsy findings, particularly the neuropathological aspects, in a patient who died from a coincidental pancreatic carcinoma are detailed. The genetic aspects are reviewed.

Aged↗
PubMed1971

Neurosarcoidosis.

Explore the source record for details and available documents.

Adrenal Cortex Hormones↗
PubMed1970

Schwann cell dysfunction in uraemia.

Examination of individual sural nerve fibres revealed segmental demyelination, in 10 out of 12 subjects with uraemia. Peripheral neuropathy was present in only two cases. The complex biochemical changes occurring with dialysis unmask the underlying demyelination in subjects with a latent neuropathy. This would explain the precipitation of a neuropathy in those subjects submitted for repeated dialysis. The possible correlation between creatinine retention, dialysis, and metabolic dysfunction in the Schwann cell system is discussed.

Adult↗