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Biomedical subjects

A Boulton

Publications and source records attributed to A Boulton.

27 records · Page 2Linked to original sources
PubMed1991

A comparison of fluoxetine and amitriptyline in the treatment of major depression.

Fluoxetine, a new serotonin uptake blocking antidepressant, was compared with amitriptyline in a double-blind study. Patients were diagnosed as having major depression, according to DSM-III criteria, when interviewed with the Diagnostic Interview Schedule. There was significant improvement in patient and observer ratings of depression in both groups, with no difference between groups. Recent memory improved significantly in the fluoxetine group but not in the amitriptyline group. Numbers of patients reporting side-effects were similar but the profiles of side-effects were different, with more patients on amitriptyline reporting anticholinergic and intolerable side-effects.

Adolescent↗
PubMed1985

Lymphoid cells of BB/W diabetic rats are cytotoxic to islet beta cells in vitro.

Assays were developed to detect cell-mediated immune destruction of pancreatic islet beta cells by lymphoid cells isolated from diabetic BioBreeding/Worcester (BB/W) rats. Splenic lymphoid cells from diabetic (D), diabetes-prone (DP), and diabetes-resistant (DR) BB/W rats were incubated for 2 days with monolayer cultures of major histocompatibility complex (MHC)-compatible Wistar-Furth (WF) rat islet cells or a rat islet cell line (RIN), and islet beta cell survival was determined by measuring insulin content in the cultures. D splenic lymphoid cells significantly decreased insulin content in WF rat islet (-32%) and RIN cultures (-77%). DP cells also significantly reduced the insulin content in WF rat islet (-20%) and RIN cultures (-63%), whereas DR cells had no significant effect. Islet-directed cytotoxicity was detected also by the release of 51Cr from RIN cells incubated for 8 h with BB/W spleen cells. Cytotoxicity was linearly related to the number of effector spleen cells. At a target: effector of 1:20, lysis (mean +/- SEM) of RIN target cells by spleen cells from D rats (21.6 +/- 2.0%) and DP rats (16.5 +/- 4.1%) was significantly greater than the effect of DR spleen cells (5.4 +/- 1.0%). D and DP splenic lymphoid cells activated in vitro for 2 days with concanavalin A exhibited a doubling of cytotoxicity to RIN islet cells. These results provide direct evidence for lymphoid cell-mediated immune damage to islet beta cells in diabetic BB rats.

Animals↗
PubMed1981

The influence of topology and glycosylation on the fate of heterologous secretory proteins made in Xenopus oocytes.

Secretory proteins made in Xenopus laevis oocytes under the direction of heterologous messenger RNA are modified, topologically segregated and exported. Thus the oocyte may serve as a useful surrogate secretory system and we have studied some of the factors governing access to the export pathway. Unglycosylated chicken ovalbumin, synthesized and trapped in the cytosol, is not secreted but glycosylated ovalbumin, found sequestered within vesicles, is exported from oocytes. However, ovalbumin, which is transferred across the endoplasmic reticulum in the presence of tunicamycin and which is indistinguishable by immunoprecipitation, by two-dimensional gel electrophoresis and by concanavalin-A--Sepharose binding from the cytosolic form, is still secreted. Guinea-pig milk proteins and human interferon are also exported from tunicamycin-treated frog cells. These observations demonstrate that access to the endoplasmic reticulum but not glycosylation is a mandatory intermediate step in secretion, and emphasize the advantages of the oocyte as a surrogate system for the study of the later events in the gene expression pathway.

Animals↗
PubMedDate not supplied

What causes neuropathic pain?

Although the etiology of diabetic neuropathic pain remains enigmatic, two types of neuropathic pain are now recognized: nerve trunk pain following a discrete often vascular lesion as seen in ocular mononeuropathy and hyperalgesic pain as seen in diffuse involvement of peripheral sensory fibers. Our understanding of the causes of hyperalgesic pain has been furthered by studying structural changes in sural nerve biopsies from subjects with symptomatic neuropathy or by assessing biochemical changes that lead to positive symptoms. Recent evidence suggests that both small and large fibers are involved in painful neuropathy, and axonal atrophy may contribute to pain generation. The observation that acute painful neuropathy may follow either periods of unstable glycemic control or sudden improvement of control ("insulin neuritis") suggests that blood glucose flux may precipitate pain. Sudden changes in glycemia may contribute to the generation of impulses in nociceptive fibers or even induce relative hypoxia and axonal atrophy. Pain might arise from ectopic impulses in dorsal root ganglion cells or may even be of spinal or central origin. Thus, a combination of structural and functional changes in peripheral nerve is most likely to lead to the generation of neuropathic pain.

Analgesics↗