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Biomedical subjects

D H Read

Publications and source records attributed to D H Read.

At least 37 records · Page 2Linked to original sources
PubMed1992

An association between complete and incomplete stress fractures of the humerus in racehorses.

Twenty-one horses had a complete unilateral humeral fracture during race training or racing at a California racetrack during the period 24 February 1990 to 10 July 1991. Fractures occurred approximately equally in left and right limbs, and in males and females. Most fractures occurred during training, and in 2- and 3-year-old horses. Only 5 of 16 Thoroughbred horses with known racing records had previously raced more than once, and their mean time between races was less than the time between their last race and fracture (P = 0.07). Ten of 13 humeri studied further had gross evidence of periosteal callus bridging one portion of the fracture line, indicative of a pre-existing stress fracture.

Animals↗
PubMed1986

Hyperglycemia and reproductive defects in non-diabetic gravidas: a mouse model test of a new theory.

The frequent association of various reproductive anomalies with maternal diabetes is explained by a theory that predicts such defects will occur even in transient moderate hyperglycemia in non-diabetic gravidae. A first test of this hypothesis produced strongly supportive results in a mouse model. Thirteen C57BL/6J dams on a grain (control) diet produced (in the 4th week after first mating) 64 pups, 62 surviving to maturity. In the same time interval on a high sucrose diet, fourteen isogenic dams produced only 5 pups, none surviving 5 days (p much less than .001). Additional ongoing studies of the underlying glucose-ascorbate antagonism and of early vs. perinatal hyperglycemia are described briefly.

Animals↗
PubMed1986

Experimentally induced thiamine deficiency in beagle dogs: pathologic changes of the central nervous system.

Brain and spinal cord were examined in twenty-two 2- to 5-month-old Beagle dogs fed a purified thiamine-deficient ration for 84 +/- 42 (range, 32 to 134) days. Eleven dogs were used as principals, 6 were pair-fed controls, and 5 were controls fed ad libitum. Thiamine at 300 micrograms/kg of body weight was administered IM to control groups once a week. Lesions occurred in 2 topographic patterns in the brain of 8 of the principals. In pattern I, only the caudal colliculi were involved. In pattern II, the suprasplenial gyri of the cerebral cortex and the claustra, caudal colliculi, cerebellar nodulus, and medial vestibular nuclei were commonly involved. In both patterns I and II, gray matter was primarily involved, and in bilateral structures, the 2 sides were affected. Lesions were not limited to a given cerebral lamina or layer of the cerebellum, whereas sulcal areas were relatively spared, and the cingulate gyri were completely spared. Microscopic appearance of the lesions varied greatly among locations and individual principals. Collectively, regressive and reparative changes indicated that there was a progressive process which began with spongiosis and ended with tissue necrosis. These included hydropic vacuolation of the neuropil and myelin sheaths followed by demyelination, neuronal cell body necrosis, hypertrophy and hyperplasia of endothelial cells, necrosis of glia, neutrophil infiltration, disintegration of neuropil, and, finally, accumulation of lipid-containing phagocytes. Axonal degeneration was variable. Neuronal necrosis in the brain stem was characterized by acute swelling and lysis and by shrinkage of the cell body in cerebral and cerebellar cortex and basal ganglia.

Animals↗
PubMed1985

Glycemic modulation of tumor tolerance in a mouse model of breast cancer.

Marked sensitivity of tumor tolerance to blood glucose level is demonstrated in a mouse model of human breast cancer. A theory is cited that explains the high association of hyperglycemia with malignancy, especially breast cancer, via glycemic modulation of cellular immunity. Three groups of BALB/C mice were injected with an aggressive mammary tumor and placed on three dietary regimens designed to produce three different glycemic levels. Mortalities 70 days after injection were 16 of 24 hyperglycemic mice, 8 of 24 normoglycemic, and 1 of 20 hypoglycemic (chi-square p less than .005). Taken together with other experiments and human data discussed briefly, this result suggests that glycemic modulation of tumor tolerance should be evaluated in human trials.

Animals↗
PubMed1983

Osmolal excretion after open heart surgery.

Water and osmolal balance was investigated during the peri-operative period in twenty unselected adult patients presenting for open heart surgery. On the day before surgery the mean urine output was 1.13 litres/sq m/24 hours and osmolal output 430 mOs/sq m/24 hours. Using a haemodilution cardiopulmonary bypass technique, patients received 2.62 litres/sq m and 792 mOs/sq m in the operating room. The pattern of excretion of this water and solute load was identified. Patients were still in positive balance on the day following surgery despite a considerable diuresis, with solute retention exceeding water retention.

Adult↗
PubMed1983

Pre-oxygenation--how long?

Pre-oxygenation was studied in 12 fit volunteers and 20 patients using an oxygen flow of 8 litres/minute delivered from a standard anaesthetic machine via a Magill or Bain breathing attachment. End-tidal nitrogen concentrations of 4% or less were achieved within 3 minutes; the fastest times were achieved using the Magill breathing system when the reservoir bag was filled with oxygen prior to application to the face. Gas-tight fits of face masks on patients were found to be essential.

Anesthesia, Inhalation↗
PubMed1982

Adrenal and hepatic calcium stearate crystal deposits in dogs fed a thiamine-deficient diet.

The nature and histologic environment of birefringent crystals found incidentally at necropsy in the liver and adrenal glands of dogs fed a thiamine-deficient diet were studied. The crystals were identified as calcium stearate by ultrastructural and x-ray microdiffraction techniques. Crystals were observed intracellularly within cytoplasmic vacuoles and extracellularly within sinusoids. Generally, crystals were also observed in pair-fed controls that were given a purified diet (equal in weight to that consumed by the thiamine-deficient animals) plus supplemental thiamine. Crystal deposits were found in trace amounts in a few of the ad libitum-fed controls. Although thiamine deficiency may be involved in promoting crystal deposition in the adrenal cortex, calcium stearate crystal formation within the adrenal glands and the liver appears unrelated to dietary thiamine deficiency per se, but is probably related to deficiency of an unidentified nutrient in the purified thiamine-deficient diet.

Adrenal Glands↗
PubMed1981

Experimentally induced thiamine deficiency in beagle dogs: clinical observations.

Twenty-three 2- to 5-month-old Beagle dogs were fed a purified thiamine-deficient ration (2 to 3 micrograms of thiamine/100 g of ration) at a rate of 40 to 70 g/kg of body weight/day depending on age. Eleven dogs were used as principles, 6 as pair-fed controls, and 6 as ad libitum-fed controls. Controls were treated once a week with an IM dose of 300 micrograms of thiamine hydrochloride/kg of body weight. Three stages of clinical disease occurred in the principals: (i) an initial short (18.0 +/- 7.9 days) stage of induction, during which the dogs usually grew suboptimally, but were otherwise healthy, (ii) an intermediate stage of preliminary clinical signs of deficiency, characterized by a variable period (58.5 +/- 37.0 days) of progressive inappetance, failure to grow, loss of body weight, and coprophagia, and (iii) a terminal stage, which, in most dogs, was abrupt in onset and short (7.6 +/- 6.0 days) and consisted of either a neurologic syndrome or sudden unexpected death syndrome. Eight of the principals developed the neurologic syndrome characterized by anorexia, emesis, CNS depression, paraparesis, sensory ataxia, torticollis, circling, exophthalmos, tonic-clonic convulsions, profound muscular weakness, recumbency, and then died. Common reflex abnormalities included exaggerated patella reflex, proprioceptive and supporting reflex deficits, induced torticollis and ventroflexion of head, and absent eye menace (blink) reflex. Three other principals developed the sudden unexpected death syndrome. Common signs of deficiency were inappetance and paresis. Two were found dead and 1, with severe ECG abnormalities (including elevation of ST segment and tall or deeply inverted T waves), was killed.

Animals↗
PubMed1977

Polioencephalomalacia of dogs with thiamine deficiency.

A naturally occurring neurological disease occurred in six dogs fed cooked meat. Clinical signs were anorexia, progressive spastic paraparesis, recumbency, convulsions and death. The disease was characterized by bilaterally symmetrical spongy change and necrosis of brainstem nuclei with a lesion distribution pattern similar to that in thiamine deficient foxes and cats. An associated thiamine deficiency was evidenced by decreased thiamine levels in the blood of one dog and in the food of another, and rapid remission of clinical signs in a dog given thiamine hydrochloride. Thermal destruction of thiamine through cooking of the foods probably caused the dietary deficiency.

Animals↗
PubMed1976

Neuronal-visceral GM1 gangliosidosis in a dog with beta-galactosidase deficiency.

A 9-month-old dog with a history of progressive motor dysfunction was shown to have a deficiency in brain beta-galactosidase activity. The canine disease, like that of children with GM1 gangliosidosis, is characterized by accumulation of GM1 ganglioside in the brain, liver, and spleen, and membranous cytoplasmic bodies in neurons. The dog's pedigree suggests an autosomal recessive pattern of inheritance.

Animals↗
PubMedDate not supplied

Bovine post-parturient haemoglobinuria: two distinct entities in New Zealand.

Haematological and biochemical features of sixteen cases of post-parturient haemoglobinuria (PPH) from 15 farms in the Waikato and Bay of Plenty regions are described. Characteristically there was a marked regenerative anaemia as well as spherocytosis and haemoglobinaemia. Heinz body formation occurred in 140% of erythrocytes depending on the case. Nine of 11 cases examined had subnormal serum inorganic phosphorus concentrations. On two of eight farms there was widespread anaemia in clinically healthy herd mates and in one of these the anaemia was associated with large numbers of Heinz bodies. Hypophosphataemia was widespread in four of ten herds and individual cows were hypophosphataemic in all ten. Six of eight herds had a low selenium status as determined by glutathione peroxidase activity in whole blood. Hypocupraemia and hypomagnesaemia were not consistent findings. It is concluded that there are two distinct entities of PPH in the region. On one farm the disease was typical of that seen in Northland, New Zealand. The clinical case was a young cow and there was widespread subclinical Heinz body anaemia in herd mates. All but one of the cows sampled in that herd had normal serum inorganic phosphorus levels. On most other farms PPH closely resembled that described from North America. Affected cases were miltiparous, high producing and had low serum inorganic phosphorus levels. The possible pathogenesis of these two entities is discussed.

Journal Article↗
PubMedDate not supplied

Pathologic and bacteriologic findings in 27-week-old commercial laying hens experimentally infected with Salmonella enteritidis, phage type 4.

Two strains of 27-wk-old commercial laying chickens (strain A, brown-egg-laying type and strain B, white-egg-laying type) were inoculated either orally (PO) or intravenously (IV) with a field isolate of Salmonella enteritidis phage type 4. Chickens were sequentially necropsied at regular intervals throughout the 17-wk observation period. Gross and microscopic lesions were most evident between 1 and 14 days postinoculation (DPI). Gross lesions consisted of enlarged livers with white foci, enlarged and mottled white spleens, fibrinous exudate in the peritoneum, and atretic, misshapen ovarian follicles. Microscopic lesions included multifocal coagulative necrosis of hepatocytes and inflammation, fibrinous exudation in vascular sinuses of the spleen, and fibrinosuppurative inflammation of the peritoneum and ovarian follicles. The proportion of reproductive organ infections (ovary and oviduct) in the IV group, 83% (20/24, P = 0.007; 50% and 33% for strains A and strain B birds, respectively), was higher than that of the PO group, 46% (11/24; 29% and 17% for strains A and B, respectively), for the first 16 days of observation postinoculation. The proportion of fecal shedding for the IV group of birds was significantly (P = 0.009) lower, 29% (7/24; 33% and 25% respectively for strain A and strain B birds, respectively), than the PO group, 67% (16/24; 75% and 58% for strain A and strain B birds, respectively). Three (2.6%) of 234 egg pools were culture-positive for group D Salmonella from strain A chickens (1 of 119 pools from the IV group and 2 of 115 pools from the PO group of birds). Chickens infected with the field strain of S. enteritidis phage type 4 harbored the organism in tissues only for a brief time, most clearing within 8 DPI and nearly all within 16 DPI. Overall the percentage of culture-positive birds did not differ significantly (P > 0.05) between birds with and without lesions, but isolation of S. enteritidis tended to be more frequent when lesions were evident. This experiment also demonstrated that brown-egg-laying-type chickens were more susceptible than white-egg-laying-type chickens to S. enteritidis phage type 4 isolated from California based on gross and microscopic lesions and bacteriologic findings.

Administration, Oral↗