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Biomedical subjects

A J Larner

Publications and source records attributed to A J Larner.

At least 145 records · Page 8Linked to original sources
PubMed1989

Recurrent Listeria monocytogenes meningitis in a heart transplant recipient.

A case of recurrent Listeria monocytogenes meningitis is reported, the two episodes arising 4 months and 8 months after the patient had received a heart transplant. Both episodes immediately followed increased doses of corticosteroids for allograft rejection. The source of infection was not identified. Previous reports and possible explanations of recurrent L. monocytogenes infection are reviewed.

Heart Transplantation↗
PubMed1988

The aetiology of appendicitis.

Although inflammatory disease of the vermiform appendix has been recognized as such for more than 100 years, its aetiology remains a subject of controversy. Since early this century consumption of a low fibre diet has been implicated. More recently this theory has been challenged and the role of infection emphasized.

Acute Disease↗
PubMed1987

The molecular pathology of haemophilia.

The great success of recombinant DNA technology in unravelling the pathology of the thalassaemias at a molecular level has encouraged the application of these methods to other single gene disorders of man in the hope of gaining a deeper insight into the biochemical defects underlying them. An example of this approach is provided by the sex-linked recessive disorders of blood clotting: haemophilia and Christmas disease. These clinically indistinguishable, life-long disorders result from the deficiency or abnormality of the clotting proteins factor VIII and factor IX, respectively, which both participate in the activation of factor X in the intrinsic pathway of blood coagulation. This paper looks at the information concerning the molecular biology and pathology of the haemophilias which has recently been forthcoming. The genes for factor VIII and factor IX have both been successfully cloned within the past five years, with that of factor VIII, achieved in 1984, being a particular tour de force. It encompasses 0.1 per cent of the human X chromosome and is the largest gene yet characterised. Gene cloning is the starting point from which gene probes can be designed to elucidate the molecular pathology of the haemophilias. The implications of these discoveries for the practice of clinical medicine are reviewed, with special emphasis on prenatal diagnosis and carrier detection by means of restriction fragment length polymorphisms, and replacement therapy with recombinant factor VIII.

Genetic Engineering↗
PubMedDate not supplied

The cerebellum in Alzheimer's disease.

The cerebellum is a relatively neglected area of the Alzheimer's disease (AD) brain, probably because it was formerly thought to be spared by the disease. However, a number of pathological changes have now been revealed in the AD cerebellum, principally by immunocytochemical studies, including widespread deposits of diffuse amyloid, ubiquitin-immunoreactive dystrophic neurites, and increased microglia, but tau-immunoreactive neurofibrillary tangles have not been seen. Although the observed changes may be merely epiphenomenal to the pathological processes occurring in the AD neocortex and hippocampus, the morphological and immunocytochemical differences between AD cerebral cortex and cerebellar cortex may nonetheless give insights into the molecular factors involved in the development of the neuropathological lesions of AD brain.

Alzheimer Disease↗
PubMedDate not supplied

The cortical neuritic dystrophy of Alzheimer's disease: nature, significance, and possible pathogenesis.

It has been increasingly appreciated in the last decade that the neocortex of the Alzheimer's disease brain is characterized by a widespread neuritic dystrophy, spatially distinct from that observed surrounding neuritic amyloid plaques. The nature and significance of this cortical neuritic dystrophy and its possible pathogenesis are the topics of this review. It may represent a regenerative sprouting response of neurons to partial deafferentation following cell loss; alternatively it may reflect a primary aberrant growth phenomenon leading to cell loss. Such changes could result from derangement of neurite growth-promoting and growth-inhibitory factors in the Alzheimer's disease brain.

Alzheimer Disease↗