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Biomedical subjects

C Peterson

Publications and source records attributed to C Peterson.

At least 307 records · Page 17Linked to original sources
PubMed1984

Helplessness and hospitalization: more remarks.

Our recent research (Raps, Peterson, Jonas, & Seligman, 1982), in which we concluded that hospitalization may cause learned helplessness among patients, was criticized because (a) perceived control was not directly assessed and (b) factors other than helplessness might explain the observed data. On a general level, we agree with these criticisms because our investigation was not fine grained. However, we suggest that field research in the helplessness tradition should be evaluated in part on the basis of convergence between field and laboratory findings and that the criticisms of our study ignore this convergence.

Helplessness, Learned↗
PubMed1984

Attributional style and the generality of learned helplessness.

According to the logic of the attribution reformulation of learned helplessness, the interaction of two factors influences whether helplessness experienced in one situation will transfer to a new situation. The model predicts that people who exhibit a style of attributing negative outcomes to global factors will show helplessness deficits in new situations that are either similar or dissimilar to the original situation in which they were helpless. In contrast, people who exhibit a style of attributing negative outcomes to only specific factors will show helplessness deficits in situations that are similar, but not dissimilar, to the original situation in which they were helpless. To test these predictions, we conducted two studies in which undergraduates with either a global or specific attributional style for negative outcomes were given one of three pretreatments in the typical helplessness triadic design: controllable bursts of noise, uncontrollable bursts of noise, or no noise. In Experiment 1, students were tested for helplessness deficits in a test situation similar to the pretreatment setting, whereas in Experiment 2, they were tested in a test situation dissimilar to the pretreatment setting. The findings were consistent with predictions of the reformulated helplessness theory.

Adult↗
PubMed1984

Growth and lignification in seedlings exposed to eight days of microgravity.

Four-day-old pine seedlings and mung bean and oat seeds were prepared for flight on the third Space Transport System Mission (STS-3). The seedlings and seeds were planted in six mini-growth chambers (two chambers per species) which were placed in a plant growth unit (PGU). Another set of seedlings and seeds was prepared and placed in another PGU as the 1 g control. The flight PGU was positioned in the orbiter mid-deck locker area about 11 h prior to launch. The pine seedlings and germinating mung bean and oat seeds were exposed to 194 h of microgravity. The PGU was received at a temporary laboratory about 75 min post-landing. Plants were observed, photographed and the atmospheric gases analyzed at the landing site. The plants were then brought to our Houston laboratory where they were measured and analyzed for lignin and protein content and for phenylalanine ammonia-lyase (PAL) and peroxidase activities. Flight seedlings were shorter than the controls in all three species. Twenty-five to 40 per cent of the mung bean and oat roots were growing upward, and the mung beans showed signs of disorientation. Flight mung beans showed a significant reduction in lignin content in comparison to the controls, and PAL and peroxidase activities were reduced in flight pine seedlings. The results generally support the postulate that lignin synthesis is reduced in near-weightlessness and show other interesting findings.

Avena↗
PubMed1984

Synaptosomal calcium metabolism during hypoxia and 3,4-diaminopyridine treatment.

A decline in the calcium-dependent release of neurotransmitters appears to underlie the decreased neuronal function that accompanies reduced oxygen tensions (hypoxia). To determine if alterations in calcium uptake are primary to these changes, synaptosomal calcium uptake was measured in the presence of 100%, 2.5%, or 0% oxygen. Calcium uptake declined 60.2 +/- 0.1 and 82.4 +/- 2.5% with 2.5% and 0% when compared with 100% oxygen, respectively. 3,4-Diaminopyridine stimulated calcium uptake by synaptosomes when they were incubated in low-potassium media. It also diminished the hypoxic-induced decline in calcium uptake to 30.6 +/- 3.1 and 33.5 +/- 3.1% with 2.5% and 0% oxygen, respectively. External binding to the synaptosomal plasma membrane declined to 29.2 +/- 0.3 or 11.8 +/- 0.9% when the oxygen tension was reduced to 2.5% or 0% oxygen. 3,4-Diaminopyridine increased this superficial binding from 111.7 +/- 0.3 to 86.5 +/- 0.9 or 23.4 +/- 0.9% with 100%, 2.5%, or 0% oxygen when compared with 100% oxygen without 3,4-diaminopyridine, respectively. Thus, the decline in neuronal processing that accompanies acute hypoxia may be due to altered calcium homeostasis, which diminishes neurotransmitter release.

4-Aminopyridine↗
PubMed1984

Apparent correlation between structure and carcinogenicity of phenylenediamines and related compounds.

The carcinogenicity of 23 phenylenediamines and related compounds was reviewed. An extensive analysis of the methods used indicated that the bioassays were conducted well. The data suggest that the carcinogenicity of 4-substituted 1,3-phenylenediamines is reduced substantially or eliminated completely by oxidation of one or both amine groups or by N-substitution. Oxidation of a methyl substituent on nitroaniline to a carboxyl group eliminated all carcinogenic activity. It required dichlorination to make ring-substtuted 1,4-phenylenediamine carcinogenic whereas only one chlorine atom was needed to make 1,2- and 1,3-phenylenediamine carcinogenic. While the available data suggest that as a class, 4-substituted 1,3-phenylenediamines are carcinogenic more often than ring-substituted 1,4-phenylenediamines, the type of added substituent and its position on the benzene ring also are important in exerting carcinogenic activity.

Animals↗
PubMed1984

Significance of the low-density lipoprotein (LDL) receptor pathway for the in vitro accumulation of AD-32 incorporated into LDL in normal and leukemic white blood cells.

The accumulation of the lipophilic cancer chemotherapeutic agent AD-32 as free drug and incorporated into low-density lipoprotein (LDL) (AD-32-LDL) has been studied in wbcs from normal subjects and from patients with acute myelogenous leukemia exhibiting high-affinity uptake and degradation of 125I-LDL. The rate of degradation of 125I-LDL in the leukemic cells was four to 25 times higher than that in normal wbcs. The accumulation of LDL-incorporated AD-32 was greater than that of the free drug and could be reduced by the addition of native LDL in excess. AD-32-LDL was as effective as native LDL in inhibiting the degradation of 125I-LDL. Preincubation of wbcs in a lipoprotein-deficient medium enhanced both the degradation of 125I-LDL and the cellular drug accumulation on incubation with AD-32-LDL. Heparin inhibited both the high-affinity degradation of 125I-LDL and the cellular accumulation of LDL-incorporated drug. However, comparison of the high-affinity degradation rate of 125I-LDL and the accumulation of LDL-incorporated AD-32 showed that the cellular drug accumulation markedly exceeded that which could be explained by high-affinity uptake and degradation of AD-32-LDL. Furthermore, saturation of the cellular uptake of LDL-incorporated drug occurred at higher LDL concentrations than saturation of 125I-LDL degradation. The results indicate that cellular uptake of AD-32-LDL is partly mediated by the LDL receptor pathway and partly by a nonspecific mechanism.

Aged↗
PubMed1984

Elevated low density lipoprotein receptor activity in leukemic cells with monocytic differentiation.

The receptor-mediated degradation of 125I-low density lipoprotein (LDL) was compared in normal white blood cells and leukemic cells. The cells were isolated from the peripheral blood and bone marrow of healthy subjects and patients with newly diagnosed leukemia. The cells from most of the 40 consecutive patients with acute myelogenous leukemia showed markedly higher degradation rates as compared to mononuclear cells and granulocytes from peripheral blood and nucleated cells from the bone marrow of healthy individuals. Leukemic cells from patients with monocytic (FAB-M5) or myelomonocytic leukemia (FAB-M4) exhibited the highest degradation rates. The rate of receptor-mediated degradation of 125I-LDL was also high in leukemic cells from all three patients with chronic myelogenous leukemia in blast crisis, as well as in two of three patients with acute undifferentiated leukemia. In contrast, leukemic cells isolated from two patients with acute lymphoblastic leukemia showed low rates. In most cases, there was little difference in LDL receptor activity between leukemic cells isolated from peripheral blood and those from bone marrow. Hypocholesterolemia was a frequent finding in the leukemic patients. There was an inverse correlation between the plasma cholesterol level and the rate of receptor-mediated degradation of 125I-LDL by the leukemic cells. Studies are now in progress to investigate the possibilities of using LDL as a carrier of cytotoxic drugs in the treatment of leukemia.

Acute Disease↗
PubMed1983

Aging and 3,4-diaminopyridine alter synaptosomal calcium uptake.

The molecular basis of the cognitive changes that accompany aging is unknown. Since several lines of evidence suggest that senescence may alter calcium homeostasis, 45calcium uptake was determined in brain synaptosomes from aged rats. In low potassium (5 mM KCl) media, aging altered calcium influx: 104.2% (3 months), 100.0% (6 months), 76.7% (15 months), or 58.6% (27 months). In 31 mM KCl media, uptake declined with age from 106.6% (3 months) to 100.0% (6 months), 67.8% (15 months), or 45.8% (27 months). 3,4-Diaminopyridine elevated the potassium-stimulated calcium influx 2.3% (3 months), 10.2% (6 months), 31.8% (15 months), or 78.8% (27 months) when they are compared to non-drug-treated synaptosomes of the same age. The calcium that binds superficially to the plasma membrane changed as the age increased from 3 months (105.4%) to 6 months (100.0%), 15 months (116.1%), or 27 months (141.4%). 3,4-Diaminopyridine reduced this binding at 15 or 27 months to 109.3 or 121.4%, when compared to the 6 month old rats respectively. The decline in synaptosomal calcium uptake may alter neuronal metabolism which leads to the reduction in mental function that accompanies aging.

4-Aminopyridine↗
PubMed1983

Acetylcholine and oxidative metabolism in septum and hippocampus in vitro.

Regulation of acetylcholine metabolism varied in brain slices from hippocampus and septum which have different proportions of cholinergic nerve cell bodies and nerve endings. Anoxia (0% oxygen) inhibited acetylcholine synthesis (-77%) and its calcium-dependent release (-87%) from hippocampal slices but had no effect on synthesis or release by septal slices. [1,5-14C]Citrate incorporation into acetylcholine was higher in septum than in hippocampus, which suggested that citrate metabolism differs regionally. (-)Hydroxycitrate, a specific inhibitor of ATP citrate (pro3S)-lyase (EC 4.1.3.8), reduced [U-14C]glucose incorporation into acetylcholine more in septal than in hippocampal slices. 14CO2 production from glucose or citrate was similar in control and experimental conditions in the two regions. These findings indicate that acetylcholine metabolism varies regionally, which may partially explain the selective vulnerability of certain brain areas to anoxia and other metabolic insults.

Acetylcholine↗
PubMed1983

Problem-solving deficits and depressive symptoms among children.

Depressive symptoms among 40 fourth- and fifth-grade students as measured by the Children's Depression Inventory, correlated highly with impaired problem solving at block designs (r = .64) and anagrams (r = .67). Similar impairments have been found among depressed adults, suggesting that depression among children may be continuous with depression among adults.

Child↗
PubMed1983

Adrenergic neurons: are they present on microvessels in cheek pouches of hamsters?

Catecholaminergic innervation was investigated in the cheek pouch, mesentery, and cremaster muscle of the hamster. These tissues were removed from normal hamsters after anesthetization with sodium pentobarbital. They were prepared immediately for visualization of catecholamines by using a glyoxylic acid fluorescent technique. Visualization was accomplished via a Zeiss fluorescent microscope with a 470-nm barrier and a 420-nm excitation filter. No fluorescence was observed in or around the microvessels of the cheek pouch; however, intense fluorescence was demonstrated around and along microvessels in the mesentery and cremaster muscle. Thus, within the limitations of this technique, this study demonstrates that local catecholamines, either as a component of adrenergic neurons or a part of the local tissue milieu, are nondetectable in the microvessels within the cheek pouch as compared to mesenteric and muscle tissue of the hamster.

Adrenergic Fibers↗
PubMed1983

Amelioration of age-related neurochemical and behavioral deficits by 3,4-diaminopyridine.

Alterations of the cholinergic system may be responsible for age-related changes in behavior. The in vitro calcium dependent release of acetylcholine and tight rope test performance decline in parallel during senescence. 3,4-Diaminopyridine, which enhances calcium influx by nerve terminals, diminishes these age-related alterations. In aged mice (30 month old), 3,4-diaminopyridine increases the calcium dependent release of acetylcholine (260%) and improves tight rope test performance (428%). These results support the hypothesis that alterations in calcium homeostasis underlie some of the cholinergic and behavioral deficits that accompany senescence.

4-Aminopyridine↗
PubMed1983

Cholinergic drugs and 4-aminopyridine alter hypoxic-induced behavioral deficits.

To test the hypothesis that decreased acetylcholine (ACh) metabolism during hypoxia is behaviorally important, the effects of cholinergic drugs and 4-aminopyridine, an enhancer of ACh release, were examined in hypoxic mice. Chemical hypoxia (150 mg/kg NaNO2) reduced tight rope test scores from 13.2 +/- 0.2 to 2.8 +/- 0.3. 4-Aminopyridine partially reversed the scores of hypoxic mice (7.3 +/- 0.7). Physostigmine improved performance by hypoxic mice (7.9 +/- 0.4) when it was given before NaNO2 and this effect was blocked by pretreatment with atropine (3.5 +/- 0.4) or mecamylamine (2.4 +/- 0.6). Neostigmine (0.002-0.2 mg/kg) was ineffective. Performance also improved if atropine (7.0 +/- 0.5) or mecamylamine (7.2 +/- 0.5) was given before NaNO2. Nicotine (5.5 +/- 0.7) or the muscarinic agonist arecoline (5.4 +/- 0.5) improved performance when given during the hypoxic episode, and when the drugs were combined, the score was even higher (8.2 +/- 1.0). Neither epinephrine (0.002-2.0 mg/kg) nor norepinephrine (0.00002-2.0 mg/kg) improved performance by hypoxic mice. These results suggest that hypoxia produces a behaviorally important impairment of the cholinergic system perhaps through a primary alteration of acetylcholine release.

4-Aminopyridine↗
PubMed1983

Danger: T.R. at work.

State credential processes may require applicant groups to specify the dangers to the public and clients of unregulated practice. A model for the equitable display of therapeutic recreation concerns is proposed as well as a classification of negative worker behaviors. The self-study process described has implications for education, personnel justifications and the development of standards and ethics.

Credentialing↗