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Biomedical subjects

D F Kelly

Publications and source records attributed to D F Kelly.

At least 73 records · Page 4Linked to original sources
PubMed1995

Multisystemic inflammatory disease in a borzoi dog.

A six-week-old female borzoi puppy from a brother-sister mating developed a generalised illness characterised by anorexia, temporary intention tremor, episodic pyrexia, tachypnoea, conjunctivitis, otitis and neck pain. Haematological abnormalities included an inflammatory leukogram and regenerative anaemia. Blood cultures remained sterile; clinical chemistry values were unremarkable. The puppy had recurrent seizures and was euthanased when 18 weeks old. Post mortem examination revealed a multisystemic inflammatory disease involving thyroids, lymph nodes, spleen, pancreas, bladder and lung, but no lesions to account for the neurological signs. The cause of this generalised disease was not recognised. The histological features are unusual and resemble those described in other dogs of this breed.

Animals↗
PubMed1995

Delayed hyponatremia after transsphenoidal surgery for pituitary adenoma. Report of nine cases.

Hyponatremia, usually attributed to the syndrome of inappropriate secretion of antidiuretic hormone, typically occurs in a delayed fashion following transsphenoidal removal of a pituitary adenoma. In a series of 99 consecutive patients who underwent transsphenoidal surgery for pituitary adenoma, nine patients developed delayed hyponatremia, seven of whom were symptomatic. Of these seven patients, four had been discharged from the hospital and required readmission on postoperative Day 7 to 9. In the nine patients who developed hyponatremia, on the average, serum sodium levels began to fall on Day 4 and reached a nadir on Day 7 (mean serum sodium nadir 123 mmol/L). The development of delayed hyponatremia was associated with the presence of a macroadenoma in eight of the nine patients. Seven of the nine patients had serum sodium levels less than 130 mmol/L and required treatment. One patient was treated with fluid restriction alone and six were treated with both fluid restriction and intravenous urea therapy. Twenty-four and 48 hours after urea administration, serum sodium levels rose by an average of 6 and 10 mmol/L, respectively, and at discharge, levels averaged 136 mmol/L. Intravenous administration of urea provides a rapid yet safe means of correcting symptomatic hyponatremia when fluid restriction alone is inadequate. In this article, the authors discuss the pathogenesis of delayed hyponatremia.

Adenoma↗
PubMed1995

Steroids in head injury.

Failure of high-dose corticosteroid therapy to ameliorate intracranial hypertension or improve long-term neurologic outcome in patients with traumatic brain injury has been shown in several prospective, randomized clinical trials. Additionally, the risk of complications, including elevations in serum glucose levels and gastrointestinal hemorrhage, although relatively low, make routine use of glucocorticoids further unwarranted in head-injured patients.

Brain Edema↗
PubMed1994

Neurosurgical postoperative care.

The goals of postoperative neurosurgical intensive care are early detection of neurologic deterioration and maintenance or reestablishment of systemic and neurologic homeostatsis. Encompassed within these goals is an effort to prevent postoperative complications or to minimize their impact once they have occurred. This article focuses on postoperative care following intracranial surgery. Criteria for admission to the intensive care unit are discussed.

Brain Diseases↗
PubMed1993

Neonatal mortality in a pair of identical twin calves: clinical and post mortem observations.

Parturition was induced, on day 278 of pregnancy, of identical twin male Blonde d'Aquitaine calves; the parturition was assisted by gentle traction. The calves died approximately four minutes and eight hours after birth. Detailed post mortem examinations revealed soft tissue haemorrhage, fractured ribs and intrapulmonary amniotic material. The calf which lived for four minutes had persistent fetal atelectasis and a solitary cartilage embolus in a meningeal vein. Atrioventricular valvular telangiectases were incidental findings in both calves. The observations suggest first that parturient trauma may contribute to neonatal mortality, secondly that the need for intensive neonatal care may be greater than is usually considered appropriate, thirdly that a post mortem examination may reveal unexpected lesions whose effects may contribute to the calves' failure to thrive, and finally that a critical assessment of neonatal pathology is restricted by the lack of data on the perinatal physiological status of the bovine dam and fetus.

Animals↗
PubMed1993

The effect of fluorine substitution on the hepatotoxicity and metabolism of paracetamol in the mouse.

The widely used analgesic paracetamol (P) produces fulminant hepatocellular necrosis in humans when taken in overdose. The toxicity is mediated by drug oxidation and depletion of hepatic glutathione. We have, therefore, explored the effects of fluorine substitution on the hepatotoxicity of P in female CD1 mice. 3-Fluoro-4-hydroxyacetanilide (1FPO), 3,5-difluoro-4-hydroxyacetanilide (2FPO), 2,6-difluoro-4-hydroxyacetanilide (2FPN) and 2,3,5,6-tetrafluoro-4-hydroxyacetanilide (4FP) were synthesized, characterized and investigated for their potential to cause hepatotoxicity in the mouse. Introduction of fluorine into P increases the oxidation potential of the drug. The oxidation potentials of paracetamol and its fluorinated analogues were measured by cyclic voltametry and found to increase in the order P < 1FPO < 2FPO < 2FPN < 4FP. Serum transaminase (ALT) and hepatic glutathione were measured 24 and 6 hr, respectively, after administration of a single dose (2.65 mmol/kg) of each compound to female CD1 mice. There was significant elevation of ALT in mice given P, 1FPO and 2FPO, but not in those which received either 2FPN or 4FP. Hepatic glutathione was reduced significantly by administration of P and IFP, but not after administration of 2FPO, 2FPN or 4FP. Accordingly, glucuronide and sulphate conjugates, but not thioether metabolites, were detected in urine after administration of 14C-labelled 2FPO, 2FPN and 4FP. These data indicate that introduction of fluorine into the 2 and 6 positions increases the oxidation potential of paracetamol which in turn reduces the propensity of the molecule to undergo oxidative bioactivation, and thereby reduces the in vivo toxicity of the molecule.

Acetaminophen↗
PubMed1993

Idiopathic hepatic fibrosis in 15 dogs.

Idiopathic hepatic fibrosis was diagnosed by liver biopsy in 15 young dogs, of which nine were German shepherds. Clinical signs included ascites, anorexia, weight loss and hepatic encephalopathy. Erythrocyte microcytosis was a consistent clinical feature, and clinical chemistry generally revealed hypoproteinaemia and high serum activities of alkaline phosphatase and, to a smaller extent, alanine aminotransferase. Fasting blood ammonia and serum bile acid concentrations were increased in most dogs examined, and all the dogs tested had prolonged retention of sulfobromophthalein at 30 minutes. Multiple acquired portosystemic shunts were revealed by laparotomy and/or portography. Non-inflammatory fibrosis was present to different degrees in all the dogs' livers, and on the basis of its predominant location these were classified as having central perivenous fibrosis, diffuse pericellular fibrosis or periportal fibrosis. The response to symptomatic treatment and anti-fibrotic therapy with glucocorticosteroids or colchicine was variable. Seven dogs died or were euthanased shortly after diagnosis, but one dog survived two-and-a-half years, and three dogs were still alive more than four years after the initial diagnosis.

Alanine Transaminase↗
PubMed1993

Diagnosis of grass sickness by ileal biopsy.

Ileal biopsies were obtained from 18 horses with grass sickness, 15 horses with other alimentary disease and three horses without gastrointestinal disease. Samples of small intestine were also obtained from nine cases of obstruction due to small intestinal strangulation. Histological examination revealed that severe enteric neuropathy in the absence of other significant morphological changes was confined to the horses with grass sickness.

Animals↗
PubMed1993

Enteric neuropathy in horses with grass sickness.

The degeneration of enteric neurones has been recorded in grass sickness, but the distribution of the lesions in the gut and their possible relationship with the severity of the clinical signs has not been established. Samples obtained from 11 anatomically defined sites along the gastrointestinal tract of eight control horses without gastrointestinal disease, five horses with acute grass sickness and three horses with chronic grass sickness were examined histologically. The organisation of the enteric ganglia was similar to that in other large mammalian species. Minor exceptions included the presence of fundic mucosal nerve cell bodies and blood vessels within submucosal ganglia. All the horses with grass sickness had severe enteric neuropathy, widespread in the acute cases but localised to the distal small intestine in the chronic cases. These neuronal lesions are consistent with, and may explain the intractable gastrointestinal propulsive deficit that characterises grass sickness.

Acute Disease↗
PubMed1993

Cerebral healing after craniotomy to evacuate a Coenurus cerebralis cyst.

An 11-month-old ewe developed neurological signs caused by a space-occupying lesion in the left cerebral hemisphere. Successful surgical evacuation of a Coenurus cerebralis cyst was carried out, the neurological signs regressed and the ewe produced twins in the following breeding season. Sixteen months after the surgical treatment the ewe was found dead and necropsy revealed a vegetative endocarditis. In the brain, at the site of cyst evacuation, there was a collapsed subcortical cavity lined by siderotic fibrovascular tissue and surrounded by a modest glial reaction. These observations confirm that the clinical signs of cerebral coenuriasis are related to the space-occupying effect of the parasitic cyst and indicate that partial replacement by gliomesodermal tissue plays a part in healing of the collapsed cyst.

Animals↗
PubMed1992

Spongiform encephalopathy in a captive puma (Felis concolor).

A captive adult puma developed ataxia, a hypermetric gait and whole body tremor. The signs progressed over a period of six weeks. Histopathological examination following euthanasia demonstrated spongiform encephalopathy, gliosis and mild non-suppurative meningoencephalitis. Immunostaining with a polyclonal antiserum revealed prion protein (PrP) associated with these changes in sections of cervical spinal cord and medulla. This is the first confirmed case of a scrapie-like spongiform encephalopathy described in a non-domestic cat in the United Kingdom.

Animals↗
PubMed1992

Anaplastic sarcoma in the caudal thigh of a horse.

A 16-year-old showjumping gelding was examined because of a non-painful, slowly progressive caudal thigh swelling, which was associated with 2/10th lameness at the trot. Radiography, real time beta-mode ultrasonography and gamma-scintigraphy of the caudal thigh for the presence of chip fractures, sequestrum formation and, or, abscessation were inconclusive. Radiographic examination of the chest revealed multifocal, nodular cannon ball-like opacities throughout the entire lung fields from which a diagnosis of a primary soft tissue tumour with metastasis to the thorax was made. An anaplastic sarcoma was diagnosed port mortem in the candal thigh. At no time did the horse show signs of respiratory embarrassment.

Animals↗
PubMed1992

Boxer colitis.

Explore the source record for details and available documents.

Animals↗
PubMed1992

Induction and enhancement of feline infectious peritonitis by canine coronavirus.

Preexisting antibody to feline infectious peritonitis virus (FIPV) causes acceleration and enhancement of disease on subsequent infection of cats with FIPV. Other workers have shown that canine coronavirus (CCV) can infect cats subclinically, but have found no evidence of enhancement of, or protection against, subsequent FIPV infection. With various isolates of CCV, we determined that 1 strain of CCV can induce transient mild diarrhea in cats and, furthermore, that previous infection with CCV causes acceleration and enhancement of subsequent infection with FIPV. In addition, sequential inoculation of cats with another strain of CCV caused lesions indistinguishable from those of FIP, without exposure at any time to FIPV.

Animals↗