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J Hinde

Publications and source records attributed to J Hinde.

5 recordsLinked to original sources
PubMed2001

A score test for testing a zero-inflated Poisson regression model against zero-inflated negative binomial alternatives.

Count data often show a higher incidence of zero counts than would be expected if the data were Poisson distributed. Zero-inflated Poisson regression models are a useful class of models for such data, but parameter estimates may be seriously biased if the nonzero counts are overdispersed in relation to the Poisson distribution. We therefore provide a score test for testing zero-inflated Poisson regression models against zero-inflated negative binomial alternatives.

Animals↗
PubMed2000

Genetic bounty.

Explore the source record for details and available documents.

Australia↗
PubMed1986

Morphometric analysis of small intestinal mucosa. III. The quantitation of crypt epithelial volumes and lymphoid cell infiltrates, with reference to celiac sprue mucosae.

With the aid of computerised image-analysis, morphometric techniques were used to measure the volumes of crypt epithelium, with reference to a constant test area (10(4) microns2) of muscularis mucosae, in untreated and treated celiac sprue mucosae in comparison with four other groups of control jejunal specimens. Crypt epithelial lymphocyte populations were also analyzed in terms of absolute numbers (N), mean nuclear (DN) and cytoplasmic (DCYT) diameters, and mean nuclear (VN) and cell (VCELL) volumes. Untreated celiac sprue crypts, despite a 3-5 fold increase in volume over control mucosae, contained a markedly expanded population of lymphocytes which was localised predominantly to the upper crypt regions and comprised approximately 6% large lymphocytes (DN greater than 6 microns: DCYT greater than 9 micron). These changes were entirely reversed by dietary treatment and hence were considered to be gluten-driven. The infiltrate might reflect the expression of gluten receptors on maturing upper crypt enterocytes: but why these lymphocytes do not cause any apparent injury to crypt epithelium (unlike surface epithelium) or influence its well-known compensatory response, remains unclear.

Adult↗
PubMed1985

Inflammatory component of celiac sprue mucosa. I. Mast cells, basophils, and eosinophils.

To study mast cell, basophil, and eosinophil populations within celiac sprue mucosae in comparison with various disease-control specimens, toluidine blue-stained 1-micron plastic sections were analyzed morphometrically by light microscopy. Within lamina propria of celiac sprue mucosae each population of cells was markedly expanded and fell to control levels during gluten restriction. Changes within surface and crypt epithelium, however, were not significantly different from those in the severer, "flat" disease-control lesions, and were not affected by gluten restriction. Basophils were not identified within surface or crypt epithelium of any specimen analyzed. The influx of eosinophils and basophils into lamina propria occurred by emigration via pericryptal venules. Mature mast cells were not seen within the microvasculature, neither were these cells undergoing mitosis: thus their origin was from unidentified precursors. The gluten-dependent alterations in each of these cell populations in celiac sprue mucosae are consistent with secondary effector mechanisms, probably resulting from cell-mediated reactions that occur primarily within the lamina propria, rather than the epithelium.

Basophils↗