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Biomedical subjects

M Gardner

Publications and source records attributed to M Gardner.

122 records · Page 7Linked to original sources
PubMed1974

Congenital and genetic skin disorders with tumor formation.

There are a great number of genetic and congenital disorders with skin manifestations ("genodermatoses") with tumor formation. Some of these tumors are benign (hamartomas, in part) and others are malignant. There is a large group of heredodegenerative disorders with such complications as lymphosarcoma and leukemia. There are congenital tumors with malignancy developing. Lastly, there are the chromosomal abnormalities with skin manifestations and tumors, usually malignant. This will be an ever increasing field and the use of fibroblast and virus cultures will become more important in ascertaining the cause of malignancy.

Adolescent↗
PubMed1972

In vitro antimicrobial susceptibility of anaerobic bacteria isolated from clinical specimens.

The minimal inhibitory concentrations of 601 clinical isolates of anaerobic bacteria to 10 different antimicrobial agents were determined by an agar-dilution technique. Nearly all strains were resistant to kanamycin and gentamicin, although moderate activity to both drugs was noted with Fusobacterium sp., anaerobic cocci, some strains of Bacteroides melaninogenicus, and nonsporeforming gram-positive bacilli. Chloramphenicol at 12.5 mug/ml inhibited all but three of the strains tested. Tetracycline at 6.25 mug/ml had high activity against all groups tested, with the exception that only 39% of strains of Bacteroides fragilis were inhibited at this concentration. Excluding certain species of Bacteroides, the majority of anaerobes were inhibited by penicillin at 3.1 mug/ml or less and by cephalothin at 12.5 mug/ml or less. Lincomycin at 6.2 mug/ml or less was active against nearly all strains. Erythromycin at a concentration of 3.1 mug/ml was active against B. fragilis; however, erythromycin was less active against the other groups. Most of the minimal inhibitory concentrations of lincomycin exceeded those of clindamycin by fourfold. Rifampin inhibited virtually all strains at 3.1 mug/ml.

Anaerobiosis↗
PubMedDate not supplied

Simian AIDS--evidence for a retroviral etiology.

This paper reviews the major features of a simian model of acquired immunodeficiency ('SAIDS'), SAIDS occurs endemically in colonies of macaque monkeys in the United States and resembles AIDS in humans in overall clinical manifestations, pathology, and immune deficiency. An infectious type D retrovirus, related to but distinct from the Mason-Pfizer monkey virus, has been identified as the primary cause of SAIDS. The relevance of these findings for human AIDS is discussed.

Acquired Immunodeficiency Syndrome↗
PubMedDate not supplied

Antimalarial activity of rifampicin in vitro and in rodent models.

The antimalarial activity of rifampicin, a specific inhibitor of bacterial ribonucleic acid (RNA) polymerase, was confirmed with Plasmodium falciparum in vitro and with P. chabaudi in vivo. The viability of ring forms of P. falciparum, measured by [3H]hypoxanthine and [14C]isoleucine uptake, was significantly reduced within 5 h of exposure to 2.5 microM rifampicin, the 50% inhibitory concentration. Streptolydigin and tagetitoxin, other specific inhibitors of bacterial RNA polymerase, were much less effective as antimalarials. A rifampicin-tolerant sub-line of P. falciparum was selected in vitro. When released from drug pressure, the tolerant line showed appreciably greater rates of incorporation of precursors and growth than the parent line, but over a period of months these characteristics gradually reverted. Rifampicin was effective against a chloroquine-resistant line of P. falciparum and the rifampicin-tolerant line had increased chloroquine sensitivity. Treatment of patent parasitaemias of P. chabaudi in mice with more than 100 mg/kg rifampicin twice daily significantly reduced the parasitaemia within 24 h and parasites were barely detectable on blood films by the fourth day. Recrudescence occurred on release of drug pressure.

Aminoglycosides↗
PubMedDate not supplied

Reduction in dissociation due to aging and cognitive deficit.

Our objective was to investigate whether dissociative experiences occur less frequently in older psychiatric patients than in younger adult patients, and to examine the role of cognitive deficits in the frequency of dissociative events. Fifty-two outpatients 60 years and older were administered the Dissociative Experiences Scale (DES) and the Mini-Mental State Exam (MMSE). Their scores were compared with those of 50 outpatients 35 to 55 years old. Each group included patients sampled from the Mental Health Center (MHC) and University Medical Center clinics. Older patients showed significantly lower DES and MMSE median scores than younger patients. Cognitive deficit reflected by reduced MMSE scores also was associated with reduced DES scores for younger and older patients. Older patients with little or no cognitive deficit continued to show reduced DES scores. Decreases in dissociativity continue well beyond the fourth decade and do not rely on age-related cognitive deficit. Factors related to the aging process seem to mediate reductions in dissociativity independent of reductions mediated by cognitive deficit. The use of the DES for screening without adjusting for age and cognitive status is questioned.

Adult↗
PubMedDate not supplied

Nursing diagnosis as content organizer.

The junior year faculty in a baccalaureate nursing program reorganized nursing content around nursing diagnosis. This revision served to highlight nursing process better, made the sequence of classes more logical, reduced repetition and made the relationship of individual classes to each other clearer. Students and faculty concluded that skills in analysis, synthesis, and problem solving were greatly enhanced by this format.

Curriculum↗
PubMedDate not supplied

Localization of a gene responsible for arrhythmogenic right ventricular dysplasia to chromosome 3p23.

BACKGROUND: Arrhythmogenic right ventricular dysplasia (ARVD), a familial cardiomyopathy occurring with a prevalence of 1 in 5000, is characterized by replacement of myocytes with fatty and fibrous tissue. Clinical manifestations include structural and functional abnormalities of the right ventricle and arrhythmias, leading to a sudden death rate of 2.5% per year. Four loci have been mapped, but no gene has been identified as yet. METHODS AND RESULTS: We identified a large family of >200 members with ARVD segregating as an autosomal dominant trait affecting 10 living individuals. The diagnosis of ARVD was based on international diagnostic criteria including history, physical examination, ECG, echocardiogram, right ventricular angiogram, endomyocardial biopsy, and 24-hour ambulatory ECG. Blood was collected for DNA from 149 family members. Analysis of 257 polymorphic microsatellite markers by genetic linkage excluded previously known loci for ARVD and identified a novel locus at 3p23. Analysis of an additional 20 markers further defined the region. A peak logarithm of the odds score of 6.91 was obtained with marker D3S3613 at theta=0% recombination. Haplotype analysis identified a shared region between markers D3S3610 and D3S3659 of 9. 3 cM. CONCLUSIONS: A novel locus for ARVD has been mapped to 3p23 and the region narrowed to 9.3 cM. Identification of the gene will allow genetic screening and a specific diagnosis for a disease with protean nonspecific findings. It should also provide insight fundamental to understanding cardiac chamber-specific gene expression and/or the mechanism of myocyte apoptosis observed in this disease.

Adult↗
PubMedDate not supplied

Diagnosis and management of heart failure. Canadian Cardiovascular Society.

Many of the recommendations presented in this consensus report are summarized in Figure 2. All patients with known or suspected heart failure should undergo a detailed history and physical examination. Other causes for the symptoms and/or clinical signs indicative of heart failure should be excluded. Routine biochemical tests, as well as a standard chest x-ray and ECG, should be performed on all patients with heart failure. Precipitating or aggravating causes of heart failure should be eliminated. Patients with potentially surgically correctable lesions, such as constrictive pericarditis, valvular disease or left ventricular aneurysm, should be referred for cardiological evaluation and the appropriate surgery. Patients with ischemic induced heart failure should be assessed for possible revascularization by either angioplasty or bypass surgery. Pending clinical findings and the degree of systolic or diastolic dysfunction present, determined by noninvasive tests, the panel made recommendations concerning the choice of various therapeutic agents. These clinical guidelines have been developed for practising physicians who manage patients with heart failure. The process by which consensus recommendations were developed by the Canadian Cardiovascular Society was based on the principle that guidelines have the best chance of succeeding if they are developed by those who will be using them. Strategies that ensure physicians are aware of the current guidelines, and that their implementation leads to measurable improvement in the diagnosis and management of patients with heart failure must be developed. Consensus reports represent an ongoing process which is subject to revision when further conclusive evidence is obtained by ongoing and future clinical trials.

Cardiac Output, Low↗