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Biomedical subjects

C H Scoggin

Publications and source records attributed to C H Scoggin.

At least 37 records · Page 2Linked to original sources
PubMed1984

Aerosolized terbutaline sulfate in the treatment of bronchospasm.

Terbutaline sulfate, a relatively selective beta2 agonist, is indicated for the treatment of bronchospasm associated with chronic obstructive pulmonary disease. Studies have shown that when administered via an aerosol, terbutaline has a rapid onset, a prolonged duration of action, and a low incidence of systemic side effects. Because the drug is delivered directly to the bronchi, one can administer low doses of aerosolized terbutaline and achieve a bronchodilatory effect comparable to that achieved with higher doses of the oral form.

Adult↗
PubMed1983

Two-dimensional electrophoresis of peptides from human-CHO cell hybrids containing human chromosome 21.

Peptide expression influenced by human chromosome 21 was examined by comparing two-dimensional electrophoretograms of a human-hamster hybrid cell containing human chromosome 21 with its parent hamster cell and a revertant of the hybrid which had segregated the chromosome 21 genes for SOD-1, GARS, and a cytotoxic cell-surface antigen. Certain peptides were found in the hybrid but not in the hamster cell. Some, but not all, of these peptides segregated with markers for chromosome 21. Hamster peptides were also found which apparently were suppressed in the hybrid. Finally, one peptide was identified which was unique to the revertant cell. These findings may be of potential relevance to Down's syndrome.

Animals↗
PubMed1983

Factitious illness. Dramatic deceit versus reality.

Patients with factitious illness present a particular challenge. Because they may be clever in their deception, they may be difficult to recognize as the fabricators of their apparent medical problem(s). Findings vary from relatively simple problems such as fever to more complex and often dramatic complaints of bleeding and pain. Differential diagnosis should include other, often more easily managed disorders such as somatoform disorders, malingering, antisocial personality, and schizophrenia. Because no definitive treatment exists, patients often consult many physicians, often in diverse geographical locations.

Diagnosis, Differential↗
PubMed1982

Down's syndrome as a model disease.

Aneuploid chromosomal disorders may offer insight into the pathogenesis of certain common diseases. The birth defects and mental retardation that characterize Down's syndrome are well recognized. In addition, the altered chromosomal content that occurs in the syndrome apparently affects the prevalence of a variety of disorders, such as malignancy, endocrine dysfunction, infection, atherosclerosis, and premature aging. Because the single distinguishing factor in Down's syndrome is the presence of an excess of a part of chromosome 21, the genetic information contained in this chromosomal segment seems to be responsible for the disease manifestations. Techniques of somatic cell genetics and molecular biology allow mapping of human genes and study of their expression. With such methods it should be possible to understand Down's syndrome and other aneuploid disorders and to apply these considerations to other areas of medicine.

Adolescent↗
PubMed1981

Cardiopulmonary resuscitation by medical and surgical house-officers.

In teaching hospitals the responsibility for cardiopulmonary resuscitation usually rests with the house-staff, yet most house-officers receive no formal training in life support. The life-support skills of 45 medical and surgical house-officers in a university teaching hospital were tested by means of simulated cardiac arrests. House-officers were graded on the basis of a performance checklist derived from the standards of the American Heart Association. No house-officer received a pass score in basic life support (BLS). Only 29% could properly compress and ventilate the mannequin. In advanced cardiac life support (ACLS) only one-third could intubate in 35 s or less; only 31%, 40%, and 33% could manage ventricular fibrillation, asystole, and complete heart block, respectively. Some house-officers were unable to operate the defibrillator or assemble resuscitation equipment. Many house-officers displayed helplessness and anxiety during the simulations; fourteen (40%) were prompted to register for additional advanced life-support courses. The performance of medical and surgical house-officers was equal. House-officers who had received prior life-support training performed better in BLS (p less than 0.001) but not in ACLS. It was concluded that (a) most medical and surgical house-officers are not reasonably proficient in BLS and ACLS, and (b) cardiac arrest simulation is a motivating exercise which permits analysis of each house-officer's life-support skills. House-officers should have more training and practice in life support, or they should not have primary responsibility for cardiopulmonary resuscitations.

Clinical Competence↗
PubMed1981

Hydrogen peroxide causes the fatal injury to human fibroblasts exposed to oxygen radicals.

Oxygen radicals are suspected as being a cause of the cellular damage that occurs at sites of inflammation. The phagocytic cells that accumulate in areas of inflammation produce superoxide, hydrogen peroxide, hydroxyl radical, and probably singlet oxygen in the extracellular fluid. The mechanism by which these oxygen molecules kill cells is unknown. To determine which of the oxygen species is responsible for the cellular killing, we exposed human fibroblasts in culture to oxygen radicals generated by the enzymatic action of xanthine oxidase upon acetaldehyde. Using the amount of chromium-51 released from labeled fibroblasts as an index of cellular death, we found that cells were protected only by interventions that reduce hydrogen peroxide concentration. Agents that inactivate superoxide, hydroxyl radical, and singlet oxygen were ineffective in limiting oxygen radical-induced cellular death.

Cell Survival↗
PubMed1981

Two-dimensional electrophoresis of human-CHO cell hybrids containing human chromosome 11.

Two-dimensional electrophoresis-electrofocusing with polyacrylamide gels is described in which the pattern of peptide spots obtained from hybrid cells of CHO containing the single human chromosome 11 are compared with those from the hybrid which has undergone reversion so as to lose this chromosome. At least eight distinct spots unique to the cell containing chromosome 11 have been located on the electrophoretogram. Experiments are described demonstrating applicability of the method to hybrids containing specific deletion mutants of chromosome 11, an approach which makes possible regional mapping of the loci responsible for specific peptides. The methodology appears applicable to study of gene expression under the influence of hormones and other agents and to the comparison of normal and disease situations.

Animals↗
PubMed1981

The cellular basis of aging.

Normal cells have only a finite life span before they die. The process known as aging may occur as a result of continued damage to the cell or as a result of expression of predetermined information within the genetic structure of the cell. Both processes lead to progressive cellular dysfunction which is evidenced by the organs of the body as aging. By understanding how individual cells age we will gain insight into how the body as a whole ages. The impact of such knowledge on science and society is a matter of both conjecture and concern.

Aging↗
PubMed1979

Accentuated hypoxemia at high altitude in subjects susceptible to high-altitude pulmonary edema.

To investigate the hypotheses that activated coagulation, catecholamine release, or arginine vasopressin release are involved in the pathogenesis of high-altitude pulmonary edema (HAPE), we measured these variables in seven subjects susceptible to HAPE and in nine control subjects at an altitude of 1,600 m, and after 6 and 12 h at a simulated altitude of 4,150 m. Each subject was studied twice, once after 3 days of placebo medication and once after 3 days of premedication with aspirin and dipyridamole. At high altitude, HAPE-susceptible subjects showed significantly exaggerated hypoxemia and a slightly higher end-tidal carbon dioxide partial pressure that did not account fully for the hypoxemia. Fibrinolytic activity was significantly accelerated in both groups at high altitude, whereas other coagulation measurements, catecholamines and arginine vasopressin levels, and pulmonary function tests were not significantly changed. Similar findings were obtained after both placebo and platelet-inhibitor premedication. The results indicate that none of the three hypothesized mechanisms, i.e., activated coagulation, excessive catecholamine release, or antidiuresis, would account for HAPE susceptibility. Instead, HAPE-susceptible subjects exhibited exaggerated hypoxemia associated with relative hypoventilation and a widened alveolar-arterial gas pressure difference.

Adolescent↗
PubMed1979

Moderate alcohol dose and chronic obstructive pulmonary disease: not a cause of hypoventilation.

Six patients with chronic obstructive pulmonary disease (COPD) (forced expiratory volume in one second, 1.01 +/- 0.08 L [mean +/- SEM] ) were given either 1 mL of 100% alcohol per kilogram of body weight in an aqueous solution or a similar volume of water in a crossover design on consecutive days. All subjects became intoxicated and the peak alcohol concentration was 137 +/- 11 mg/dL, 40 minutes after ingestion. No significant difference was found in either PaO2 or PaCO2 between the alcohol and control period. A significant decrease in arterial pH occurred following alcohol (P less than .05), and represented a mild metabolic acidosis. Alcohol ingestion resulted in an increase in oxygen consumption (P less than .05) and carbon dioxide production (P less than .05) but no change in respiratory rate. It appears that small to moderate amounts of alcohol will not cause marked changes in oxygen tension or alveolar hypoventilation in patients with severe COPD who do not have marked hypercapnia. Nevertheless, other effects of alcohol on the cardiopulmonary system and the concomitant use of sedatives have to be considered before condoning the use of alcohol.

Aged↗
PubMed1978

Familial aspects of decreased hypoxic drive in endurance athletes.

One difference between endurance athletes and nonathletes is decreased ventilatory responsiveness to hypoxia and hypercapnia. It has never been clear whether these decreased responses are a consequence of conditioning or precede participation in endurance athletics. Recent studies demonstrating clusters of decreased ventilatory responses to hypoxia in families of patients with unexplained respiratory failure suggest that decreased responses in endurance athletes might be familial. To investigate this possibility, ventilatory response to hypoxia and hypercapnia were measured in 16 nonathletic, healthy parents and siblings of five successful long-distance runners. Response were compared to 34 nonathletic controls. As measured by the shape parameter A, hypoxic response was decreased to a similar extent in runners 74 +/- 6.4 (mean +/- SE) (P less than 0.05) and their relatives 69 +/- 15.2 (P less than 0.01) compared to control 128 +/- 11.3. Hypercapnic responses were slightly, but not significantly, decreased in runners and their families. We conclude familial influences made a major contribution to the decreased hypoxic ventilatory response seen in long-distance runners.

Adolescent↗
PubMed1978

Hereditary aspects of decreased hypoxic response.

Decreased ventilatory responses to hypoxia and hypercapnia have been demonstrated in a variety of disorders; however, the etiology of these decreased drives remains virtually unknown. Recent observations have suggested a familial influence on hypoxic and hypercapnic ventilatory response, but it is unclear whether this influence is the result of hereditary or environmental influences. Therefore we measured the ventilatory response to isocapnic hypoxia (HVR) and hyperoxic hypercapnia in 12 pairs of identical and 12 pairs of nonidentical twins. Significant correlation (P less than 0.01) was found for HVR within identical twin pairs but not within nonidentical twin pairs. Identical twins resembled each other more closely with respect to HVR than was the case for nonidentical twins (P less than 0.0125). This was independent of body size, blood PCO2, or pH. No such correlation could be found for ventilatory response to hyperoxic hypercapnia. It is concluded that hereditary influences affect HVR and it is speculated that such influences may play a role in clinical conditions characterized by decreased hypoxic ventilatory responses.

Adolescent↗