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Biomedical subjects

J Hardy

Publications and source records attributed to J Hardy.

At least 289 records · Page 16Linked to original sources
PubMed1993

Pituitary microadenomas: early enhancement with dynamic CT--implications of arterial blood supply and potential importance.

In a search for early contrast medium enhancement, which can indicate the presence of direct arterial supply, a retrospective review of dynamic computed tomographic (CT) scans was performed in 260 patients with a pituitary microadenoma smaller than 10 mm in diameter. Fifty patients underwent examination with dynamic CT for nonendocrinologic disease as a control group to establish the normal pattern of pituitary gland enhancement. One hundred seventy microadenomas (65.4%) displayed the usual dynamic CT pattern (ie, they did not show early enhancement before that of the portal system of the pituitary gland: those pituitary microadenomas appeared less enhanced than the normal pituitary gland during the entire examination). On the other hand, in 90 microadenomas (34.6%), early partial or complete enhancement was seen within the microadenoma before the normal portal enhancement of the gland. Therefore, analysis with dynamic CT yields two groups of pituitary microadenomas separable on the basis of blood supply: those with portal blood supply only and those with partial or predominantly direct arterial blood supply; in theory, the second group avoids hypothalamic control.

Adenoma↗
PubMed1993

Heterogeneity in Alzheimer's disease.

The genetic data implicating mutations framing the beta-amyloid segment of the amyloid precursor protein as causes of Alzheimer's disease are reviewed and integrated with information on the normal processing of the amyloid precursor protein. The data indicating that there is a second and quantitatively major locus for early-onset Alzheimer's disease on the long arm of chromosome 14 are reviewed. The prediction that this second genetic locus will produce a protein intimately involved in the metabolism of the amyloid precursor protein is reiterated, together with the prediction that all causes of Alzheimer's disease will directly involve this process.

Alzheimer Disease↗
PubMed1992

Use of telemetry functions in the assessment of implanted antitachycardia device efficacy.

Twenty patients (aged 50 +/- 21 years and mean left ventricular ejection fraction 37 +/- 17%) with recurrent ventricular arrhythmias were treated with an investigational, implantable combined antitachycardia-pacing cardioverter defibrillator. The device's telemetry capabilities include both stored (1-second snapshots) and real-time display of endocardial and device-circuit signals. The device can store these before, during and after up to 50 tachycardia and antitachycardia pacing episodes. All stored events are indexed to a 24-hour internal clock. During 10.1 +/- 5.1 months of follow-up, the device was used in 11 of 20 patients. In the entire group, antitachycardia pacing was activated on 44 +/- 14 occasions per patient (total 874) and shock delivery occurred on 8 +/- 14 occasions per patient (total 156). Reconstruction by stored telemetry of all device-therapy episodes was possible. Twenty-six percent of all shocks delivered were not appropriate and were due to atrial arrhythmias in 2 patients and dysfunction of the sensing lead in 3. The absence of a relation between symptoms and appropriate shock delivery was documented in 1 patient. Antitachycardia pace acceleration occurred in 5.3% of cases; 7% of attempts at pacing were unsuccessful and needed shock therapy. It is concluded that the enhanced telemetry available in newer antitachycardia devices enables more accurate assessment of device use and enhances diagnosis of inappropriate therapy delivery.

Electric Countershock↗
PubMed1992

Complications of nasogastric intubation in horses: nine cases (1987-1989).

Pharyngeal or esophageal trauma was diagnosed in 9 horses after nasogastric intubation. Evidence of trauma (edema or ulceration) was detected in the pharynx of 3 horses and in the esophagus of 6 horses. Complications associated with nasogastric intubation were first observed in 5 horses while they were intubated and in 4 horses after extubation. Clinical signs of pharyngeal or esophageal trauma were similar, and included salivation, bruxism, coughing, and nasal discharge. Treatment, including extubation, enteral feeding through a small nasogastric tube, or esophagostomy distal to the affected site, was attempted in 6 horses. Three of 6 treated horses survived, but 4 of 5 horses with perforated esophagus were euthanatized.

Animals↗
PubMed1992

Pathological changes in the brain of a patient with familial Alzheimer's disease having a missense mutation at codon 717 in the amyloid precursor protein gene.

The brain of a 61-year-old patient with familial Alzheimer's disease, showing a missense (valine----glycine) mutation at codon 717 of the amyloid precursor gene, has been examined at postmortem. Sections of brain showed pathological features entirely typical of Alzheimer's disease with no unusual characteristics. It seems therefore that this particular mutation is indeed pathogenic and that the altered amyloid precursor protein resulting from expression of this mutation is processed in a way that triggers or promotes the pathological cascade of Alzheimer's disease.

Adult↗
PubMed1992

A phase II study of sulofenur, a novel sulfonylurea, in recurrent epithelial ovarian cancer.

A total of 16 patients with recurrent epithelial ovarian cancer were treated with sulofenur (LY 186641), a novel oral sulfonylurea. All subjects had received previous chemotherapy. Anaemia occurred in all 16 patients, 14 of whom required a blood transfusion, and 2/16 patients received methylene blue for breathlessness due to methaemaglobinaemia. Treatment was discontinued in 2/16 cases due to rising liver enzyme values, which reverted to normal on cessation of the drug. There was no nausea or alopecia. Only two minor responses were seen. Plasma drug levels were insufficient to result in antitumour activity as extrapolated from animal data. Further studies that attempt to increase the bioavailability and improve the therapeutic index are warranted.

Adolescent↗
PubMed1992

An 'anatomical cascade hypothesis' for Alzheimer's disease.

The molecular mechanisms of the cytopathology of Alzheimer's disease are very rapidly being elucidated. However, the factors that restrict the effects of this disease to specific neuroanatomical systems are less well understood. In this brief article a possible hypothesis is outlined to explain this apparent specific localization.

Alzheimer Disease↗
PubMed1992

A locus for familial early-onset Alzheimer's disease on the long arm of chromosome 14, proximal to the alpha 1-antichymotrypsin gene.

Although mutations in the beta-amyloid precursor protein gene (APP) on chromosome 21 cause some cases of early-onset Alzheimer's disease (AD), most cases evidently do not have mutations in APP. We analysed ten early-onset families for linkage to APP and markers elsewhere in the genome. One family (F172) was consistent with linkage to chromosome 21 and was subsequently found to have an APP Val to Ile mutation. Of the others, all but one were consistent with linkage to markers in the middle long arm of chromosome 14. However, no family showed independent evidence of linkage with two point analysis and only one showed independent evidence of linkage on multipoint analysis. Therefore, we cannot rule out heterogeneity at these loci although tests for heterogeneity were not significant.

Adult↗
PubMed1992

Inherited prion disease with 144 base pair gene insertion. 2. Clinical and pathological features.

A large family with autosomal dominant segregation of presenile dementia, and other neurological and behavioural features is described. At various times, family members have carried diagnoses of Alzheimer's disease, Huntington's disease, Parkinson's disease, myoclonic epilepsy, atypical dementia, Pick's disease, Creutzfeldt-Jakob disease and Gerstmann-Sträussler syndrome. Molecular genetic studies have enabled classification of this disease at the molecular level as one of the group of inherited prion diseases. Here we describe the phenotype of inherited prion disease (PrP 144 bp insertion).

Adult↗
PubMed1992

Screening for mutations in the open reading frame and promoter of the beta-amyloid precursor protein gene in familial Alzheimer's disease: identification of a further family with APP717 Val-->Ile.

Following the identification of mutations in the beta-amyloid precursor protein (APP) gene in familial, early onset Alzheimer's disease (AD), we have developed a screening protocol using single strand conformation analysis (SSCA) to screen exon 17 for the known mutations within APP. In addition, we used this protocol to screen the other seventeen exons of APP and a three hundred and thirty base pair regulatory region of the promoter for new mutations in 9 families with early onset AD. Exons 16 and 17, which encode the deposited beta-amyloid peptide, were screened in a further 10 families. Our screening procedure identifies all the reported mutations within APP. While we have identified a further family with APP717 Val-->Ile, we did not find any previously undescribed mutations. Screening of other exons of APP in 2 families in which we have previously reported mutations at APP717, failed to reveal other sequence abnormalities supporting the hypothesis that the mutations at APP717 cause the disease in these families. These data suggest that mutations in APP are a rare cause of familial early onset AD (3/21 families tested) and that within APP most, possibly all, mutations which cause AD are in exon 17.

Adult↗