Search PubMed⌕ Search

Biomedical subjects

M Morin

Publications and source records attributed to M Morin.

188 records · Page 11Linked to original sources
PubMedDate not supplied

Sudden death in turkeys with perirenal hemorrhage: pathological observations and possible pathogenesis of the disease.

A pathological study was conducted on 32 turkeys that died of sudden death with perirenal hemorrhage syndrome. Turkeys were selected from routine necropsy cases in a diagnostic laboratory. A higher incidence was observed in heavy tom turkeys. In addition to the characteristic gross lesions of perirenal hemorrhage, splenomegaly, and pulmonary congestion, turkeys in most cases had a hypertrophic cardiopathy. Microscopic lesions included moderate-to-marked acute passive congestion of all tissues examined (32/32), severe perirenal hemorrhage (32/32), and splenic lymphoid depletion (25/32). Changes in the thyroid follicular epithelium of most birds suggested an increased glandular activity. No lesions suggestive of arterial hypertension were observed. Adenoviral infection was detected in only four of 32 birds. Bacteriological cultures revealed no significant pathogen. Results suggest that sudden death in turkeys with perirenal hemorrhage is caused by an acute congestive heart failure consecutive to a hypertrophic cardiopathy. The perirenal hemorrhage would be a consequence of a severe passive congestion in kidneys.

Animals↗
PubMedDate not supplied

Picogram concentrations of endotoxin stimulate synthesis of IL-1 beta and TNF alpha by human peripheral blood mononuclear cells exposed to recombinant human C5a.

Endotoxemia, complement activation, and the generation of C5a occur in the course of sepsis, trauma, and the adult respiratory distress syndrome, clinical situations in which TNF and IL-1 are thought to play an important role. In the present studies, we examined the effect of picogram concentrations of endotoxin (LPS) on the synthesis of IL-1 beta and TNF alpha by human PBMC exposed to recombinant human C5a (rhuC5a). rhuC5a induced the synthesis of IL-1 beta by PBMC made in response to otherwise substimulatory levels of LPS. In the presence of rhuC5a, LPS concentrations from 10 pg to 1000 pg/ml substantially amplified IL-1 beta synthesis by PBMC compared to LPS alone. Since rhuC5a can induce transcription of IL-1 beta with minimal translation to cytokine protein, these studies support the concept that fM concentrations of LPS can combine with rhuC5a to provide the "second signal" for optimal translation of IL-1 beta mRNA.

Complement C5a↗
PubMedDate not supplied

[Evaluation studies of experimental carcinogenesis].

In many cases, epidemiological studies demonstrate carcinogenic risk of occupational exposures and industrial processes, but do not allow to assess carcinogenic potential of the various substances involved in exposures (speciation). Expert judgment combining human and animal data is needed for classifying and labelling of the pure substances. For decision aiding purpose, a method was established for reviewing critically experimental carcinogenesis: 1. Standardized toxicological profiles are established according to pure substances, species, strains and administration routes. 2. Methodological evaluation is made using a scheme based on 3 critical parameters: study duration which should extend to the life expectancy of the species under study; sample size, the statistical significance of negative experiments being ascertained depending on size of samples; survival rates of groups, since sufficient numbers of animals should be at risk during most of their life span. 3. Classification of the results for risk assessment, taking into account the relevance of the administration routes.

Animals↗
PubMedDate not supplied

A generalized inclusion body disease in the budgerigar (Melopsittacus undulatus) caused by a papovavirus-like agent.

High mortality rates have been reported in budgerigars between one and 15 days of age in 19 aviaries in the Province of Quebec. The most consistent signs of disease were abdominal distention, lack of down feathers on the back and abdomen, lack of filoplumes on the head and neck, and retarded growth of the tail and contour feathers in birds that either survived or died later. Internal gross lesions were hydropericardium, enlarged heart and liver with multiple pinpoint white spots or large, yellow foci, pale or congested kidneys, congested lungs, and ascites. Histologic examination revealed large, slightly basophilic inclusion bodies in the enlarged nuclei of many different cells. These inclusion bodies were composed of viral particles. Multiple foci of coagulation necrosis were scattered in the myocardium and liver parenchyma, and granulovacuolar degeneration was common in renal tubular epithelial cells. Ballooning degeneration was multifocal in the epidermis and very extensive in the epithelial cells of developing feather follicles, and this led to their partial or complete destruction. Viral particles 50 to 55 nm in diameter were observed in negatively stained preparations from different organs of affected birds. These particles had the size and morphology of a papovavirus. In experimentally infected 25-day-old budgerigars, histologic examinations revealed the presence of intranuclear inclusions in hepatocytes, epithelial cells of the kidney tubules, and reticular cells of the spleen, despite the absence of clinical signs. We feel that this disease is caused by a papovavirus-like agent that can replicate in many tissues of the body, causing widespread lesions responsible for the high mortality rate of very young budgerigars and for the absence and/or incomplete development of feathers.

Animals↗