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Biomedical subjects

W G Siller

Publications and source records attributed to W G Siller.

At least 19 recordsLinked to original sources
PubMed1985

Deep pectoral myopathy: a penalty of successful selection for muscle growth.

Deep pectoral myopathy (DPM) is a disease that affects commercial poultry selected for large breast muscle development. The muscle affected by the disease is the supracoracoid muscle and usually one side of the breast musculature atrophies. The necrotic muscle has a characteristic pale green color. Heavy breeds of turkeys and broilers can be induced to show DPM by electrical stimulation of the breast muscle itself or by vigorous wing flapping; older birds are more susceptible. The cause of DPM is a fascial compartment too small to accommodate the enclosed supracoracoid muscle during vigorous exercise when the muscle increases its weight (and overall size) by about 20%. The inelastic compartment essentially strangulates the swollen, activated muscle. A possible means of correcting DPM is to train or exercise the flight muscles during the rapid growth phase of chicks or poults. Feed, for example, could be positioned above floor level so that birds would have to flutter up to reach it. There is also evidence to suggest a genetic component to the disease. Hence, an indicator such as high plasma creatine kinase levels may be used as a selection criterion.

Age Factors↗
PubMed1984

X chromosome-linked muscular dystrophy (mdx) in the mouse.

An X chromosome-linked mouse mutant (gene symbol, mdx) has been found that has elevated plasma levels of muscle creatine kinase and pyruvate kinase and exhibits histological lesions characteristic of muscular dystrophy. The mutants show mild clinical symptoms and are viable and fertile. Linkage analysis with four X chromosome loci indicates that mdx maps in the Hq Bpa region of the mouse X chromosome. This gives a gene order of mdx-Tfm-Pgk-1-Ags, the same as for the equivalent genes on the human X chromosome.

Animals↗
PubMed1983

Experimentally induced fatty liver and kidney syndrome in the young turkey.

Turkeys were fed up to four weeks of age on diets of low biotin content and then fasted for 18 hours. Three birds developed clinical signs of fatty liver and kidney syndrome (FLKS) and on autopsy had pale and swollen livers and kidneys. Morphological studies showed fatty accumulations in liver, kidney, heart and proventriculus but no signs of inflammatory or degenerative changes. The infiltrated lipid had an abnormal fatty acid composition, with an increased proportion of monounsaturated fatty acids. Affected birds suffered from severe hypoglycaemia and hepatic glycogen was depleted. These findings demonstrate that FLKS can be induced experimentally in turkeys.

Animals↗
PubMed1980

Incorporation of 3H-oleic acid by the proximal convoluted tubule cells of the chick (Gallus domesticus). Electron microscopic autoradiographic study.

Lipid metabolism in the cells of the renal proximal convoluted tubules (PCT) was investigated in healthy fowls and in fowls with the Fatty Liver and Kidney Syndrome (FLKS). The tissue was fixed at 10-25 min intervals after intravenous injection of 3H-oleic acid. The distribution of autoradiographic grains was analysed by the "circle method". In normal cells most of the silver grains were associated with the cytoplasmic organelles. Lipid droplets and Golgi elements had the highest specific activity relative to the nuclear activity, which was little above background level. Lysosome-like bodies and mitochondria had lower values. In the cells of the FLKS-affected birds a large porportion of the grains was located over the lipid droplets, which are abundant in this condition. The specific activity of the cytoplasmic organelles was barely 2-fold higher than the nuclear activity. The results suggest that there is a diminished incorporation of esterified fatty acids by the organelles of these cells and that the excess is transferred to the lipid droplets. The identity of low electron density particles observed in the PCT cell of severely affected birds is discussed.

Animals↗
PubMed1980

Pathology of deep pectoral myopathy of broilers.

Deep pectoral myopathy occurred in 39 of 204 apparently healthy and 46 of 146 ill, adult broiler breeders from Poultry Research Centre flocks. Both sexes and two commercial strains were similarly affected. The myopathy was not associated with any disease except pododermatitis. The supracoracoid was the only muscle affected. It was bilaterally involved in 33 chickens. The lesions were grouped macroscopically into three categories: acute oedema progressing to a green necrosis, centrally located cicatrix, and replacement of the caudal region by fibroadipose tissue. Microscopcially the green lesion consisted of necrotic, anucleate muscle fibres devoid of inflammatory cells and surrounded by a fibrous capsule that had a reactive inner border and externally abutted on normal and regenerating muscle or fibro-adipose tissue. Considered with the ultrastructural findings of early loss of glycogen and disintegration of sarcoplasmic reticulum, mitochondria, nuclei and Z lines, these findings indicate that the condition is an ischaemic necrosis. There was no evidence that its primary cause was occlusive vascular lesions. The muscle was able to regenerate unless extensive secondary neurological lesions were present.

Animals↗
PubMed1978

Deep pectoral myopathy: an experimental simulation in the fowl.

Surgical occlusion of the subclavian artery of domestic fowls has been found to induce a condition closely resembling, in location and histopathology, the deep pectoral myopathy of turkeys. The operative procedure is described and the significance of the collateral blood supply in the pathogenesis of the lesion is briefly discussed.

Animals↗
PubMed1977

Changes in plasma lipid and glucose levels during the onset of fatty liver and kidney syndrome in chics.

Plasma glucose, free fatty acid and triglyceride levels were measured during the onset of fatty liver and kidney syndrome in chicks. Intial studies indicated that behavioural and clinical changes characteristically associated with the syndrome were observed only during the 24 h preceding death. A more detailed examination of the blood changes was made on fasted birds. Typically, affected birds could be distinguished from healthy fasted birds by a hypoglycaemia which developed within 2.5 h of the removal of food, and a slightly higher and more sustained elevation of free fatty acid levels. Triglyceride values were not generally different from those found in normal birds. Although moderate to large amounts of lipid were occasionally observed in the kidneys of healthy fasted birds, only in affected birds was significant lipid infiltration of the kidneys associated with a similar level of lipid infiltration of the liver. In extreme cases death from fatty liver and kidney syndrome could occur within 4 h of the removal of food.

Animals↗
PubMed1976

Biotin deficiency and fatty liver and kidney syndrome in chicks given purified diets containing different fat and protein levels.

1. The occurence of biotin deficiency and fatty liver and kidney syndrome (FLKS) in chicks was studied using a 2x2x2x2 factorial-design experiment in which the variables were dietary biotin, fat and protein, and starvation. 2. The severity of biotin deficiency, using growth retardation and severity of dermal lesions as criteria, was least when the low-biotin diet also contained low levels of fat and protein. Addition of fat or protein increased the severity of the deficiency. Tissue fatty acid composition was affected by biotin deficiency only in those birds given the low-protein, low-fat diet. The main change was an increase in the ratio, 16:1 fatty acids :18:0 fatty acids. Plasma glucose and free fatty acid levels in non-fasted birds were unaffected by the dietary variables. 3. Mortality from FLKS with the diet containing low biotin, fat and protein levels was 52% at 28d, but was reduced or eliminated when the dietary level of any of these ingredients was increased. 4. Starvation considerably increased the incidnece of FLKS in the period immediately after fasting, and also affected plasma glucose and free fatty acid concentrations. Liver fatty acid composition, indicated an increase in the proportion of 18:0 at the expense of 16:1 and concentrations increased in proportion, at the expense of 18:0. 5. The relationship between biotin deficiency and FLKS, and a possible mechanism for the induction of FLKS by starvation are discussed.

Adipose Tissue↗
PubMed1976

An ultrastructural study of the liver, kidney and myocardium in the fatty liver and kidney syndrome in the fowl.

In birds with the fatty liver and kidney syndrome large lipid droplets measuring up to 4 mum in diameter were observed in increased numbers in liver, kidney and heart muscle, particularly in the livers and the proximal convoluted tubules (PCT) of the kidneys. In the hepatocytes and the PCT a much smaller type of lipid particle (LP) was also observed, both intracellularly within the cisternae of the Golgi-ER system and outside the plasma membranes in the space between neighbouring parenchymal cells, within the space of Disse and among the basal processes of the PCT. The origin of these LP is discussed.

Animals↗
PubMed1975

The adrenal cortico-medullary ratio in the fowl.

1. A new integrating method of assessing the proportions of cortical and medullary tissue in the avian adrenal gland is described and statistically evaluated. 2. It is shown that a single "central" section of the adrenal gland will suffice to obtain accurate results. 3. Each section was projected on to a grid of about 2500 intersection points and the ratio of points falling on cortical or medullary tissue was determined. 4. Applications of this method to normal fowls showed that there were significant breed, sex and, particularly, age differences in the cortico-medullary ratio of the fowl's adrenal glands.

Adrenal Cortex↗
PubMed1975

The histopathology of fatty liver and kidney syndrome in chicks.

Studies of the general histopathology of the fatty liver and kidney syndrome in chickens have shown abnormal accumulations of the lipid in a variety of organs but no degenerative or inflammatory reactions. Lipid was found in some skeletal muscles, alimentary tract, autonomic ganglia, central nervous system and pineal gland as well as in the liver, kidney and heart. Small amounts of lipid were sometimes seen in the exocrine pancreas, adrenal medulla and epithelium of the thyroid follicles. Lipid deposits in the liver were primarily associated with the hepatic structural unit. The glycogen content of the hepatic cell was reduced. The lipid-metabolising gastrocnemius muscle contained abnormal amounts of lipid but this did not apply to the carbohydrate-metabolising pectoralis major muscle. The thymus did not contain excessive lipid but was significantly smaller in affected than in control birds of similar ages. There was loss of tinctorial distinction between the cortex and medulla of the adrenal gland associated with decreased basophilia of the latter region. Many of these morphological changes can be correlated with previously reported biochemical findings and they are discussed in relation to the hyperlipaemia and hypoglycaemia which characterise the disease.

Adrenal Glands↗