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At least 613 records · Page 34Linked to original sources
PubMed1996

The toxicity of repeated exposures to rolipram, a type IV phosphodiesterase inhibitor, in rats.

Rolipram is a selective inhibitor of Type IV phosphodiesterase isozymes (PDE IV) which is often used as a baseline comparator for compounds in this class. To document the toxicological effects of rolipram, it was administered to female rats at 0, 10, 30 or 100 mg/kg/day orally for up to 2 weeks. One treatment-related death in the 100 mg/kg/day dose group was observed on day 3, and all rats at this dose level were considered moribund and euthanatized on day 5. Several clinical signs were observed in treated rats, including increased salivation, slight distention of the abdomen, emaciated appearance, and ataxia. After 14 days of treatment, the rats were necropsied and tissues examined microscopically. A number of compound-related histopathological changes were observed in rats receiving 30 or 100 mg/kg/day. Myocardial degeneration and necrosis, endocardial fibrosis, epicarditis, and arteritis/periarteritis of intramural and extramural coronary arteries were observed in the heart. A necrotizing vasculitis and inflammation were observed in the mesentery and interstitial areas of the liver, affecting medium-sized portal arteries and veins. Focal necrosis was also observed in the glandular mucosa of the stomach at these 2 dose levels. Other treatment-related effects included squamous hyperplasia and hyperkeratosis with or without ulceration in the nonglandular stomach of at least one animal from all treatment groups. Enlarged salivary glands were noted at necropsy in animals treated with 100 mg/kg/day, and this finding correlated microscopically with dilatation and degeneration of ducts and acini in the sublingual gland with secondary inflammation and edema. The results of this study demonstrate that rolipram, a selective inhibitor of the type IV class of PDE, can cause effects on the heart and vasculature of rats which heretofore have been ascribed only to selective inhibitors of the PDE III class of isozymes. Therefore, these organs should be closely examined in studies with other PDE IV inhibitors. In addition, the gastrointestinal tract and salivary glands were sites for rolipram-induced toxicity and may be targets of other PDE IV inhibitors.

Animals↗
PubMed1978

Total body potassium fat free weight and maximal aerobic power in children with anorexia nervosa.

Body composition and aerobic work performance have been studied in 5 boys and 10 girls suffering from anorexia nervosa. The average ages of the two groups of children were 15.4 (boys) and 15.2 (girls) years respectively. Measurements of body composition included height, weight (W), body potassium (40K), skinfold thickness (SFT) at triceps and subscapularis, blood volume (BV) and femoral condylar and radioulnar breadths. From these measurements estimates of fat free weight (FFW), skeletal weight (S) and lean body mass (LBM) were made. Work performance was assessed by measurement of the maximal aerobic power (VO2 max). The patients had lost on average 26% of their former body weight. The boys had on average greater than 7% of their body weight as fat compared with greater than 9% in the girls. However, the loss of weight was not solely due to loss of body fat, but could also be ascribed to a decrease in soft fatfree tissue. LBM or FFW could be estimated as well from SFT as from 40k. vo2 max averaged 1.43 1/min (35.1 ml/kg/min) in the anorexic boys and 1.24 l/min (33.2 ml/kg/min) in the girls and was associated with FFW and LBM. However, VO2 max was lower in relation to LBM than in healthy children of the same age. Thus it was suggested that the emaciation in anorexia is directly attributable to loss of both fat and muscle and accounts in part for the reduction of aerobic power observed. However, an important factor may be the debilitating effect of starvation on the patient, particularly in its advanced and later stages, which reduces his/her level of habitual physical activity.

Adolescent↗
PubMed1985

Severe anorexia nervosa treated with total parenteral nutrition. Clinical course and influence on clinical chemical analyses.

Severe anorexia nervosa in which psychiatric treatment has failed is a life-threatening condition since the degree of emaciation can be profound. Nine young women with a weight loss of 25-50% of their habitual weights were given total parenteral nutrition (TPN) over 3-8 weeks through a tunneled central venous silicone catheter. They initially received a mean of 55 kcal/kg body weight/24 hours increasing to 65-70 kcal/kg body weight during the first week. The initial bradycardia and hypotension were normalized and body weight increased with a mean of 2.5 kg/week. All patients showed a general somato-psychic improvement after two weeks of TPN. The electrolyte disturbances seen at the beginning were normalized during the first weeks of treatment and the previously reported life-threatening electrolyte disturbances and dehydration in connection with TPN treatment were not seen. The only adverse effect registered was a rise in liver enzymes in two patients who were given greater than 80 kcal/kg and day. With a reduction of the caloric supply these changes normalized, and TPN could be continued. After 3-8 weeks the oral intake had normalized and TPN was discontinued. This study confirms that TPN can be used successfully and with minimal risk in severe anorexia nervosa until the patients have normalized their oral intake.

Adolescent↗
PubMed2003

A genetic mouse model carrying the nonfunctional xeroderma pigmentosum group G gene.

A genetic mouse model with a disrupted XPG allele was generated by insertion of neo cassette sequences into exon 3 of the XPG gene by using embryonic stem (ES) cell techniques. The xpg-deficient mice showed distinct developmental characteristics. Their body was marked smaller than that in wild-type littermates since the postnatal day 6, and this postnatal growth failure became more severe with developmental proceeding. Their life span was very short, all of the mutants died by postnatal day 23 after showing great weakness and emaciation. In addition, the mutant homozygous mice also showed some progressive neurological signs, like the lower level of activity and a progressive ataxia. Further examination indicated there was developmental retardation of the brain in the mutant mice. Their brain weight, and thickness of cerebral cortex and cerebellar cortex were significant different from the controls. These characteristics, like small size brain, brain developmental retardation and progressive neurological dysfunctions in the homozygotes were similar to the typical clinical phenotype of the XPG patients and Cockayne syndrome, we believe that the xpgdeficient mice will be an animal model for studying the function of the XP-G protein in nucleotide-excision repair and mechanisms related to the clinic symptoms of XP-G and Cockayne syndrome in humans.

Animals↗
PubMed2004

Clinical Hepatozoon canis infection in a dog in Turkey.

A five-year-old female dog was presented with a four-week history of inappetence, weight loss, and skin and gait abnormalities. Physical examination revealed weakness, depression, incoordination of the posterior limbs, emaciation, skin and hair coat alterations, peripheral lymphadenopathy, pale mucous membranes and fever. Laboratory analysis of samples revealed abnormalities which included anaemia, neutrophilic leucocytosis, thrombocytopenia, low serum glucose and albumin concentrations, and increased serum alkaline phosphatase activity. The diagnosis was confirmed microscopically, by demonstrating the presence of Hepatozoon canis gametocytes within neutrophils in Giemsa-stained peripheral blood smears. Treatment consisting of toltrazuril and a trimethoprim-sulfamethoxazole combination was effective in relieving the clinical signs and clearing the blood of H. canis gametocytes. To the authors' knowledge, this is the first detailed clinical description of H. canis infection in a dog in Turkey.

Animals↗
PubMed1992

Amyloidosis, hemochromatosis, and atherosclerosis in a roseate flamingo (Phoenicopterus ruber).

An aged male roseate flamingo, in a private collection in the British Virgin Islands, was found acutely "down." After four days of supportive therapy, the flamingo succumbed. At necropsy gross lesions included emaciation; collapsed and thickened, yellow abdominal air sac; dark red liver, partially covered by friable yellow material; and a raised, intimal plaque in the aorta near the iliac trifurcation. Histologic examination revealed severe, diffuse, pyogranulomatous air sacculitis with associated locally extensive pleuroperitonitis/perihepatitis. Pansystemic, predominantly periarteriolar distribution of amyloid deposition was evident, as was massive intrahepatocellular accumulation of iron pigment (hemachromatosis/hemosiderosis). A locally extensive, nonobstructive, fibroatheromatous plaque was present in the distal aorta. Amyloidosis, hemochromatosis/hemosiderosis, and atherosclerosis have been recognized in Phoenicopteriformes and other marine or aquatic birds. Their pathogenesis and pathogenicity remain a matter of debate.

Amyloidosis↗
PubMed2002

Clinicoepidemiological and biochemical profile of malnutrition-modulated diabetes mellitus.

Malnitrition-modulated diabetes mellitus ((MMDM) was previously known as protein-deficient diabetes mellitus (PDDM). Its clinical picture is similar to that of type 1 diabetes, but it develops over a background of chronic malnutrition from childhood. In spite of severe hyperglycemia, ketonuria never occurs. MMDM patients are extremely lean and require high doses of insulin-over 2.0 U/kg/day for good glycemic control. Even when optimally controlled, these patients maintain their leanness. Infections of the skin and soft tissues and pulmonary tuberculosis are often seen, whereas micro- and macrovascular complications are rare, even after long-term follow-up. Ultrasonographic evaluation of the abdomen clearly differentiates MMDM from fibrocalculous pancreatic diabetes. Absence of ketonuria and ketosis despite very severe hyperglycemia in emaciated young subjects is the most significant marker of MMDM.

Adolescent↗
PubMed2002

Elk restoration in Ontario, Canada: infectious disease management strategy, 1998-2001.

Ontario has embarked upon a program to restore elk (Cervus elaphus) that were once native to that province. A comprehensive disease-management strategy has ensured that elk are free of infectious diseases such as brucellosis and tuberculosis prior to shipment to Ontario. Postmortem analysis occurs on elk mortalities in Ontario to ensure that elk are not infected with diseases such as chronic wasting disease and tuberculosis. Between 1998 and 2001, a total of 443 elk were transported from Elk Island National Park, Alberta, and released in four different areas of Ontario. Cumulative mortality for elk in all areas was 26% from 1998 to January 2001. The primary causes of mortality were post-release stress-induced emaciation (21%), wolf predation (20%), transport/handling injuries (10%), bacterial infections (10%), and drowning (7%). Female calves had the highest mortality rates (37%) compared to the other sex and age cohorts (23-24%). Preliminary findings suggest an inverse correlation between the length of time elk are held in enclosures prior to release and the distance they disperse from the release site. The 2001 estimated population of elk in Ontario is about 400 individuals.

Age Factors↗
PubMed1975

Ibaraki disease and its relationship to bluetongue.

Ibaraki disease, an epizootic disease of cattle in Japan resembling bluetongue, is characterized by fever and lesions affecting the mucous membranes, the skin, the musculature and vascular system. Degeneration of striated muscular tissue is observed in the oesophagus, larynx, pharynx, tongue and the skeletal muscles. Oedema and haemorrhage are marked in the mouth, lips, abomasum, around the coronets, etc., and are occasionally followed by degeneration of the epithelium leading to erosions or ulcerations. Severe lesions affecting the oesophageal and laryngopharyngeal musculature cause difficulty in swallowing which in turn produces dehydration and emaciation, and occasionally the aspiration pneumonia, which constitute the major causes of death of affected animals. These clinical and pathological findings indicate the similarity of the disease to bluetongue in sheep and cattle. Ibaraki disease was first recognised in Japan in 1959 and 1960. Seasonally its occurrence is limited to late summer and autumn, and geographically to the central and western parts of Japan, roughly south of 37 degrees north latitude. It is absent from the higher altitudes. The seasonal and geographical incidence suggests the possibility of an arthropod vector; but direct evidence for such a vector is still lacking. Serological data suggest the presence of Ibaraki virus on Bali Island in Indonesia and in Taiwan. The disease can be transmitted serially in calves by the intravenous inoculation of blood obtained at the height of a febrile reaction. Ibaraki virus can be isolated in bovine cell cultures from both natural and experimentally produced cases of the disease. The virus multiplies and induces cytopathic effects in primary cultures of bovine, sheep and hamster lung origin, and L cells; but it does not grow in primary cultures of horse and swine kidney nor in HeLa cell cultures. The virus is readily passaged serially in 4 to 5-day-old eggs by yolk-sac inoculation and incubation at 33.5 degrees C. It multiplies in the brains of mice of any age after incracerebral inoculation but younger mice give a better viral growth and develop encephalitis. No evidence has been obtained that rabbits and guinea pigs are susceptible to Ibaraki virus...

Animals↗
PubMed1978

Diarrhoea in piglets inoculated with rotavirus.

A rotavirus isolated from a field outbreak of diarrhoea in artificially reared piglets was purified, filtered and administered orally to gnotobiotic and conventional piglets. Four successive passages of the virus in gnotobiotic piglets produced severe diarrhoea within 20 to 24 hours of administration. The diarrhoea lasted several days causing dehydration, emaciation, loss of body weight and some deaths. Virus was demonstrated in the faeces of the infected piglets by electron microscopy. Conventionally reared piglets developed little or no diarrhoea when given virus, whereas artificially reared piglets developed moderate to severe diarrhoea which lasted from 3 to 8 days with some deaths. No clinical disease was obvious in surviving piglets following challenge with the virus 10 or 17 days after initial infections.

Animal Nutritional Physiological Phenomena↗
PubMed1980

A transmissible chicken tumour associated with reticuloendotheliosis virus infection.

Histiocytic lymphosarcomas of the intestine, liver, spleen and sciatic nerve were found at necropsy in a 36-week-old laying hen that was culled from a flock of 1800 birds because of emaciation. Type C particles were observed in ultrathin sections of liver and spleen. The serum of the hen contained reticuloendotheliosis virus (REV) antigen, and antibody against REV, but lacked antibodies reactive with Marek's disease virus or subgroups A and B of Rous sarcoma virus. The tumour was transmitted to chickens using a suspension of the initial tumours. These experimental tumours were then transmitted to further chickens, using cultured spleen cells, viable spleen cells that had been stored frozen, and disrupted spleen cells. The tumours, which developed after incubation periods as short as 2 weeks, were histologically similar to those in the original hen. A few chickens also developed feather abnormalities. The chickens with experimentally transmitted tumours developed antibody against REV and REV antigen was demonstrated in cultured cells from these chickens. The chickens failed to develop antibody against Rous sarcoma virus and only 1 of 29 developed antibody against Marek's disease virus.

Animals↗
PubMed1981

Caseous lymphadenitis in goats.

Two dairy goat stud herds were surveyed for Corynebacterium ovis infection by clinical examination and serum tests using both the haemolysis inhibition and double immunodiffusion techniques for detection of C. ovis antitoxin. In one herd, of 53 goats 11 had abscesses from which C. ovis was recorded; 33 and 29 goats were positive to the haemolysis inhibition and double immunodiffusion tests respectively. Serums from 10 and 9 of 23 kids gave reactions positive to the respective tests with 19 of 23 kids having been born to does with demonstrable antibody. In a second herd of 57 goats 16 had superficial abscesses containing C. ovis; serums from 34 and 45 goats gave positive reactions to the haemolysis inhibition and double immunodiffusion tests respectively. The prevalence of caseous lymphadenitis in these stud herds was a cause of economic loss to the owners through euthanasia of severely affected goats, reduced milk production and emaciation, the cost of labour and drugs for treatment, jeopardisation of income from boarding or mating with outside stock and the appearance of goats at stud shows, and sale of valuable breeding stock to local and export markets.

Animals↗
PubMed1982

Dieldrin poisoning and botulism in Australian pelicans (Pelecanus conspicillatus).

Autopsies and laboratory examinations of material from 24 Australian pelicans found sick or dead in southern coastal Queensland in 1977 to 1979 revealed dieldrin poisoning in 8 from the Brisbane region and botulism in 8 from Brisbane, Bundaberg and Gladstone. In those diagnosed as dieldrin poisoning, brain and liver samples contained 12.1 to 27.4 and 34.0 to 48.1 mg/kg dieldrin respectively. All of these birds were emaciated, 2 had convulsed and 1 had muscle tremors. Low and probably insignificant residues of DDE were detected in many birds. Type C botulism was confirmed in 4 of the 6 birds tested with specific antiserums. A large number of parasites including mites, lice, nematodes, cestodes, trematodes, coccidia and Sarcocystis sp were found but were thought to have had only a limited effect on the health of these birds.

Animal Population Groups↗
PubMed1982

White liver disease of sheep.

Outbreaks of ovine white liver disease (WLD) on 7 farms in eastern Victoria were investigated. Most occurred in late spring and mainly affected lambs 3 to 6 months old, with a morbidity of 20 to 100% and mortality of 8 to 15%. Clinically affected lambs showed illthrift, emaciation and bilateral, serous, ocular discharge. Clinical pathology showed mild anaemia, elevated serum liver enzymes (GGT, OCT, AST) and low levels of serum vitamin B12. Grossly, the livers were pale, fatty and friable; microscopically there was parenchymal fatty change, bile duct proliferation and ceroid pigmentation. Liver cobalt values were consistently low (mean 0.4 +/- 0.4 mumol/kg D.W.). Levels of cobalt in pasture from 2 properties were very low (0.34 mumol/kg D.W.) The diagnosis of white liver disease was made on the basis of clinical features, specific liver pathology and low cobalt status. Treatment trials established that cobalt injections or oral bullet administration resulted in clinical improvement, significant weight gains, and improved serum vitamin B12 levels. WLD did not recur in previously affected sheep using these treatments. However, when blocks containing cobalt were available continuously, WLD recurred 2 years after the initial outbreak.

Animals↗
PubMed1986

An outbreak of sarcocystosis in dairy cattle.

Sixteen of 32 Friesian calves, 8 to 10 weeks old, died over 4 weeks. The calves were housed in pens previously used by dogs. Clinical signs included anorexia, pale mucous membranes, rapid weight loss, coughing and palpably enlarged superficial lymph nodes. At necropsy, calves were emaciated and had generalised enlargement of lymph nodes, pale mottling of skeletal muscles, excess peritoneal, thoracic and pericardial fluid and subpleural and subepicardial haemorrhages. Histologically there was a lymphadenitis, myositis, myocarditis, glomerulonephritis, interstitial pneumonitis and encephalitis. Schizonts of a sporozoan parasite, presumably Sarcocystis cruzi were found in the endothelial cells of blood vessels in many organs.

Animals↗
PubMed1987

Suppurative splenitis and peritonitis in a horse after gastric ulceration caused by larvae of Gasterophilus intestinalis.

A 12-year-old Thoroughbred mare, with a history of anorexia, dramatic weight loss, fluctuating pyrexia and intermittent diarrhoea after an episode of colic, was presented for examination with depression, emaciation and ataxia. Thoracic and abdominal paracenteses yielded copious quantities of inflammatory exudate. Palpation per rectum revealed an enlarged spleen. The primary alterations in haematology included a severe leucocytosis with a left shift, and a hyperproteinaemia characterised by hypoalbuminaemia and hypergammaglobulinaemia. Post-mortem examination revealed a low grade pleurisy and peritonitis with fluid accumulation in both cavities. A suppurative gastritis with full thickness perforations of the stomach wall associated with Gasterophilus intestinalis larvae had extended to the juxtaposed organ initiating an extensive suppurative splenitis. Streptococcus zooepidemicus was cultured.

Animals↗
PubMed1990

Enteritis in sheep and goats due to Yersinia enterocolitica infection.

Yersinia enterocolitica biotype 5, serotype 02,3 was isolated from the intestine of 38 sheep and 8 goats submitted to the laboratory for disease diagnosis. Infected animals were usually young, had diarrhoea and were in poor condition or emaciated. A number were moribund or dead when submitted. Characteristic microabscesses were demonstrated in the intestine of 5 of 38 sheep and 3 of 8 goats and no alternative cause of morbidity or mortality was established in these animals. Of the 33 sheep and 5 goats infected with Y. enterocolitica in which microabscesses were not demonstrated, a number of other diagnoses were made, including internal parasitism (18), selenium deficiency or white muscle disease (6) and cobalt deficiency (2), so that morbidity and mortality were possibly unrelated to Y. enterocolitica infection. Five of 6 sheep exposed experimentally by mouth to Y. enterocolitica biotype 5, serotype 02,3 developed an intestinal infection. Although infected sheep showed no clinical evidence of disease and haematological and biochemical indices remained normal, multiple intestinal microabscesses typical of yersiniosis were demonstrated in 3 of 5 infected sheep. It is concluded that Y. enterocolitica biotype 5, serotype 02,3 is an enteropathogen of sheep and goats. Since sheep and goats may be the specific hosts of this bacterium, its virulence for these species is apparently low. Morbidity and mortality may, therefore, be unusual manifestations of infection.

Animals↗
PubMed1990

The pathology of Johne's disease in sheep.

The clinical, gross and histopathological findings in 50 sheep affected with Johne's disease are described. Clinically 90% were emaciated and 20% showed severe diarrhoea. On necropsy there was thickening of the walls of the intestines, particularly of the ileum, caecum and less frequently the jejunum, but in 36% of sheep the changes were only mild. Histologically there was a granulomatous enteritis, typhlitis and colitis, with the most severe changes in the terminal ileum. High numbers of acid-fast organisms were present in the terminal ileum in over 70% of sheep. Mycobacterium paratuberculosis was cultured from only 8% of the sheep examined.

Animals↗