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Biomedical subjects

D Penney

Publications and source records attributed to D Penney.

12 recordsLinked to original sources
PubMed1991

A percutaneous liver biopsy technique in ducks (Anas platyrhynchos) experimentally infected with duck hepatitis B virus.

Aylesbury ducks (Anas platyrhynchos) chronically infected with the duck hepatitis B virus provide a useful model for studying hepadna-virus infection, replication and the effects of antiviral therapy. In these studies, it is necessary to have an effective method for obtaining repeat liver specimens for histological and molecular analyses. We have therefore developed a percutaneous liver biopsy technique which has a low rate of complications, can be performed at repeated intervals, and provides sufficient quantities of liver tissue for histological and nucleic acid hybridization analysis.

Animals↗
PubMed1989

Serum markers for prediction of pulmonary radiation syndromes. Part I: Surfactant apoprotein.

Detection of a biochemical marker indicating radiation lung injury prior to the onset of clinical pathologic events could prove valuable in patient management. An increased level of alveolar surfactant is one of the earliest detectable changes following lung irradiation, starting within hours of irradiation and persisting a maximum of 2-6 weeks. However, because broncho-alveolar lavage is impracticable and endothelial cell damage due to radiation results in changes in permeability of vessel wall with leakage of alveolar proteins into serum, identification of serum markers was sought. A series of experiments in rabbits are described that clearly demonstrate serum surfactant apoprotein is an accurate marker and predictor for later lethal radiation pneumonitis. At 3-7 days after graded single doses to lung, surfactant was found in the serum paralleling the dose response for lethality. Control studies with a physiologic agent such as terbutaline release alveolar surfactant, but no serum surfactant was detected. Monitoring serum surfactant could direct preventive intervention prior to clinicopathologic manifestation of pulmonary radiation syndromes.

Animals↗
PubMed1989

Hypothermia protects brain function in acute carbon monoxide poisoning.

The role of body temperature in the morbidity and mortality resulting from acute severe carbon monoxide (CO) poisoning (2400 ppm CO, 90 min) was investigated using an unanesthetized animal model. Modified Levine prepared female rats (left common carotid artery and jugular cannulated) displayed a lower rate of recovery period (4 hr) re-warming, and an increased mortality rate and behaviorally-assessed neurologic index (NI) compared to normal rats. This indicated their greater susceptibility to CO hypoxia, although the degree of CO-induced hypothermia was the same in both groups. The whole-body cooling of Levine rats to a similar extent prior to CO exposure increased somewhat the post-CO re-warming rate, and marginally decreased NI and mortality during CO exposure (in-CO). In contrast, maintenance of constant body temperature by external heating during CO exposure resulted in a negative post-CO re-warming rate and sharply increased NI and in-CO mortality. Normal euthermic rats were much less severely affected by CO. The results suggest that hypothermia, whether CO-induced or produced by prior cooling, provides measurable protection of brain function during acute severe CO poisoning, and that maintenance of body temperature increases in-CO mortality and interferes with ability to thermoregulate and increases NI in survivors.

Animals↗
PubMed1988

A comparison of the adherence of fimbriated and nonfimbriated Haemophilus influenzae type b to human adenoids in organ culture.

Adherence of fimbriated and nonfimbriated variants of a single strain of Haemophilus influenzae type b to organ cultures of human adenoidal tissue was measured by three assays, two of which were quantitative. In one assay, the adherence of radioactively labeled bacteria was measured; the numbers of CFU of bacteria per gram of adenoidal tissue were 16.0 +/- 6.7 for fimbriated bacteria and 10.2 +/- 4.0 for nonfimbriated bacteria (P less than 0.05). In the second assay, adherent CFU were determined directly; the results were 23.4 +/- 17.2 CFU/g of tissue for fimbriated bacteria and 5.1 +/- 2.2 CFU/g for the nonfimbriated variant (P less than 0.02). By combining data from the two assays it appears that fimbriated and nonfimbriated bacteria do not compete for the same site on the tissue, and that the adherent bacteria do not change their state of fimbriation under the assay conditions used. In contrast, the third assay, scanning electron microscopy, showed very poor adherence of nonfimbriated bacteria. Fimbriated bacteria, on the other hand, adhered in clusters to nonciliated epithelial cells. Overall, the data indicate that fimbriae enhance adherence of H. influenzae type b to a type of tissue that is a normal site of human colonization and that nonfimbriated bacteria adhere by a distinctly different mechanism.

Adenoids↗
PubMed1976

Effect of acute carbon monoxide poisoning on serum lactate dehydrogenase and creatine phosphokinase.

Young adult rats were exposed to 1,500 ppm CO in air for 2 hr. Blood carboxyhemoglobin (COHb) concentration immediately postexposure was 55.68 +/- 0.90%. Serum lactate dehydrogenase (LDH) activity peaked at 117% above control 2 hr postexposure, while serum creatine phosphokinase (CPK) activity was maximal at 132% above control immediately following termination of exposure. Serum LDH activity declined to control within 8 hr, while serum CPK undershot controls at 8 hr and returned to the control value by 24 hr.

Animals↗
PubMed1976

Effects of early severe malnutrition on heart and skeletal muscle lactate dehydrogenase.

Following weaning, rats from litter sizes of 15 to 20 were subjected to severe food restriction for 10 weeks, and compared to rats from litter size 5 fed ad libitum. Percent M (muscle type) lactate dehydrogenase, M and H (heart type) subunit activity and lactate dehydrogenase activity (per g wet weight) determined both electrophoretically and spectrophotometrically were all significantly lower in separated left and right ventricles of the malnourished rats. There were no differences in skeletal muscle lactate dehydrogenase activity. Following 5 weeks of ad libitum feeding, the previously malnourished rats showed large increases in body weight. Now only the right ventricle showed slight decreases in H subunit and lactate dehydrogenase activity; other measurements in the right ventricle and all in the left ventricle had returned to control levels. Skeletal muscle lactate dehydrogenase activity was not different from controls.

Age Factors↗
PubMed1975

Hematological alterations and response to acute hypobaric stress.

Exposure of rats to simulated altitude (15,000 ft) for 1 day and 3 and 9 wk produced progressive polycythemia, elevated 2,3-diphosphoglycerate levels and raised P50 values; the latter two parameters decreased toward control values after 9 wk. Carbon monoxide (38-43% HbCO) exposure produced polycythemia after 3- and 9-wk exposure, no change in 2,3-DPG and a fall in P50 value. Ten days' treatment with sodium cyanate produced a large decrease in 2,3-DPG and P50. Survival during 90 min of acute hypobaria (0.3 atm) under Nembutal anesthesia was highest with NaOCN (75%), intermediate with 3- and 9-wk exposure to altitude and CO (56-58%) lower in 1-day altitude exposure (44%) and lowest in controls (5%). Heart and ventilation rate was monitored during this hypobaric test and response patterns established for each exposure/treatment. In states of extreme oxygen deprivation the results suggest, in order of importance, the survival value of 1) increased oxygen-hemoglobin affinity, and 2) polycythemia.

Altitude↗
PubMed1975

Cardiac anoxia tolerance of carbon monoxide-poisoned, hypoxia-exposed and normal rats.

Under nitrogen anoxia heart rate (HR) persists at a high level for 1 min longer in rats exposed chronically to carbon monoxide and hypoxia than in unexposed control rats. Although declining sharply, HR of exposed animals continues higher than HR of controls during min 1-4 of anoxia. However, during min 5 and 6 of anoxia HR of CO-poisoned rats becomes similar to that of controls, while HR of hypoxia-exposed rats remains above control HR for 3 min longer. The data are discussed in light of cardiovascular changes induced by CO and hypobaric hypoxia.

Animals↗