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Biomedical subjects

J M Davis

Publications and source records attributed to J M Davis.

At least 379 records · Page 21Linked to original sources
PubMed1989

Are disturbances in lipid-protein interactions by phospholipase-A2 a predisposing factor in affective illness?

Current theories of affective disorders do not account for many of the biological markers replicated in patient studies. We link many biological findings in a reasonable physiological relationship, compatible with mechanisms of action of pharmacological and electroshock therapies for depression. We propose that excessive phospholipase-A2 (PLA2) activity disrupts membrane fluidity, composition, and therefore, the activity, of membrane-dependent proteins. Similar disruptions in these proteins are documented in depressed patients and can be accounted for by excessive PLA2 activity. This paradigm accounts for disturbances in the activity of Na-K-ATPase, beta2- and alpha2-adrenergic receptors, MAO, norepinephrine and serotonin uptake, and imipramine binding. Disturbances in other membrane-dependent proteins, tyrosine and tryptophan hydroxylase, can explain the biogenic amine hypothesis. Inhibition of glucocorticoid receptor and TRH receptor binding to their respective ligands by PLA2 may explain patient nonsuppression in the Dexamethasone Suppression Test and poor response in the TRH stimulation test. Physiological regulators of PLA2 activity; calcium, cortisol, estrogen, progesterone, and PGE2 are documented abnormalities in some patients with affective disorders and consistent with excessive PLA2 activity. Thus, postpartum depression and premenstrual tension syndrome may be described in the paradigm. The mechanisms of action of tricyclic antidepressants, lithium, electroconvulsive shock, and some novel antimanic agents can be described in terms of alterations of PLA2 activity. Interestingly, ethanol perturbs membrane fluidity and membrane-bound enzymes in a manner similar to excessive PLA2 activity. A hereditary factor predisposing patients to affective disorders may be a gene defect at either PLA2 or in its regulation.

Brain↗
PubMed1989

Human inhumanity.

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History, 18th Century↗
PubMed1989

Leukotriene B4 generation in patients with established pulmonary failure.

We investigated the cause of the reduced leukotriene B4 (LTB4) production seen in neutrophils from patients with established adult respiratory distress syndrome compared with control neutrophils. Lymphocytes/monocytes from controls were found to synergistically enhance the amount of LTB4 produced when incubated with neutrophils. This synergistic effect was not seen in cells from patients with adult respiratory distress syndrome. Fatty-acid analysis of neutrophils from patients with adult respiratory distress syndrome and controls showed remarkable similarity in all quantities of fatty acids measured except for arachidonic acid, where there was a 22% reduction in patients' cells compared with controls. Assay of the rate of generation of LTB4 and its degradation product, 20-hydroxy LTB4, revealed that reduced LTB4 generation in patients' neutrophils was not due to increased degradation of LTB4 by hydroxylase enzymes. When the amount of LTB4 being generated per milliliter of whole blood was analyzed in the patients with adult respiratory distress syndrome and compared with controls, it was determined that the potential to generate LTB4 in patients in the intensive care unit was three to five times greater than in controls.

Fatty Acids↗
PubMed1989

Changes in pulmonary mechanics following caffeine administration in infants with bronchopulmonary dysplasia.

The effects of caffeine upon pulmonary mechanics were measured in 16 infants with bronchopulmonary dysplasia (BPD). Pulmonary function tests were performed immediately prior to and 1 hour following a dose of 10 mg/kg of caffeine. A 37% increase in minute ventilation (mean +/- SEM; 436.6 +/- 26.3 to 580.8 +/- 30.7 ml/min/kg) was seen with caffeine administration (P less than 0.001), primarily from a 42% increase in tidal volume (6.2 +/- 0.4 to 8.5 +/- 0.4 ml/kg) (P less than 0.001). Total lung resistance decreased by 20% (134.6 + 24.2 to 105.3 +/- 20.1 cmH2O/L/sec) (P = 0.01), and total pulmonary compliance improved by 47% (0.642 +/- 0.104 to 0.908 +/- 0.190 ml/cmH2O/kg) (P less than 0.01). In five matched control infants with BPD, no effects of placebo upon pulmonary mechanics were detected. Since caffeine has a wide therapeutic index with few side effects, it may be an effective adjunct in the treatment of infants with BPD.

Airway Resistance↗
PubMed1989

Increased 3H-clonidine binding in the platelets of patients with depressive and schizophrenic disorders.

To examine whether alpha 2-adrenergic receptor function is altered in affective and schizophrenic disorders, we determined 3H-clonidine binding in platelets obtained from 33 normal control subjects and from 24 patients with depressive, 22 patients with schizophrenic, 18 with bipolar, and 8 patients with schizoaffective disorders during a drug-free period. The maximum number of binding sites (Bmax) and apparent dissociation constant (Kd) for high affinity 3H-clonidine binding was computed by Scatchard analysis. Comparison of the diagnostic groups indicated that the Bmax in depressed, schizophrenic, and schizoaffective patients was significantly higher than in normal controls, but there were no significant Bmax differences between bipolar patients and controls. Comparison of the Kd among the diagnostic groups indicated no significant differences among the groups or between patient diagnostic groups and normal controls. Baseline Bmax in schizophrenic patients was significantly correlated with the decrease in Brief Psychiatric Rating Scale (BPRS) scores after treatment, suggesting a relationship between baseline Bmax and clinical response. Treatment with lithium caused a significant decrease in the baseline Bmax, whereas treatment with desipramine or trifluoperazine did not cause significant changes in the baseline Bmax. Our results thus indicate an increase in the number of alpha 2-adrenergic receptors in depressed and schizophrenic patients as compared to normal controls.

Bipolar Disorder↗
PubMed1989

Plasma and CSF HVA before and after pharmacological treatment.

Plasma and cerebrospinal fluid (CSF) levels of the major dopamine metabolite homovanillic acid (HVA) were measured in psychiatric patients after an average washout period of 19 days, and again after 4 weeks of pharmacological treatment. Absolute values of plasma HVA did not correlate with absolute values of CSF HVA either at baseline or after treatment. However, changes in plasma HVA were highly correlated with changes in CSF HVA. Further, while baseline levels of plasma and CSF HVA were not significantly correlated with baseline clinical measures, clinical improvement was associated with decreases in both plasma and CSF HVA. This reached statistical significance for the plasma HVA level/clinical response relationship.

Adult↗
PubMed1989

Weight control and calorie expenditure: thermogenic effects of pre-prandial and post-prandial exercise.

The thermogenic effects of pre- and postprandial exercise was examined in seven lean active females. Energy expenditure was measured for 3 h via open circuit indirect calorimetry after four separate treatments: Exercise Only (25 min treadmill run at 60% VO2 max), Meal Only (910 kcal mixed meal), Exercise-Meal and Meal-Exercise. The thermogenic response to the Exercise-Meal treatment was similar to the Meal Only treatment. However, the Meal-Exercise treatment resulted in a greater energy expenditure than the Meal Only and Exercise-Meal treatments. The Exercise Only treatment showed the lowest thermogenic response. These data suggest that exercise following a meal would be more beneficial than exercise before a meal in increasing and maintaining an elevated energy expenditure.

Adult↗
PubMed1989

Prenatal and postnatal effects of low-level lead exposure: integrated summary of a report to the U.S. Congress on childhood lead poisoning.

This article provides an integrated summary of a report to Congress from the Federal government (ATSDR) on childhood lead poisoning in the United States, with particular reference to low-level lead exposure and its effects on the fetus and the preschool child. As mandated by Section 118(f)(1)(C) of the 1986 Superfund Amendments and Reauthorization Act (SARA), ATSDR has examined the full spectrum of human in utero and postnatal lead toxicity, with emphasis on low-level neurotoxicity and adverse impacts on growth indices in risk populations. Especially important has been assessment of the relative persistence of these effects in later life as discernible from a number of longitudinal studies now under way around the world. Included in the Congressional report were discussions of dose-effect and dose-response relationships using blood lead levels as the indicator of lead dose.

Child, Preschool↗
PubMed1989

Medicine is changing.

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Attitude of Health Personnel↗
PubMed1989

Inflammation generating potential of long and short fibre amosite asbestos samples.

Previous studies have shown that long thin asbestos fibres are more pathogenic in in vivo and more active in in vitro assays than short fibre samples. In the present study a long fibre amosite asbestos sample and a short fibre sample prepared from it were tested for ability to cause inflammation in the peritoneal cavity of the mouse; a UICC sample intermediate in fibre size and an inert compact dust, TiO2, were also tested. The ability of the dust samples to cause inflammation, as judged by macrophage and neutrophil recruitment, was ranked in the order long fibre greater than UICC greater than short fibre greater than TiO2. Ability of amosite samples to cause inflammation was therefore related to the proportion of long fibres. The enhanced ability of long fibres to cause inflammation and cause macrophage activation is probably a key factor in the ability of long fibres to cause pulmonary fibrosis and may also be important in fibre carcinogenesis.

Animals↗
PubMed1989

Lung injury in the neonatal piglet caused by hyperoxia and mechanical ventilation.

Neonatal lung injury from hyperoxia and mechanical hyperventilation was studied in newborn piglets hyperventilated (arterial PCO2 15-20 Torr) for 24-48 h with 100% O2 and compared with unventilated controls. Pulmonary function testing was performed, and biochemical indicators of lung injury were analyzed from tracheobronchial aspirates at 0, 24, and 48 h. Lung sections were obtained for light and electron microscopy, and bronchoalveolar lavage fluid was analyzed for surfactant composition and activity. At 24 h significant changes in tracheobronchial aspirate albumin concentrations (up 78%) and percent of polymorphonuclear cells (up 16%) were demonstrated. At 48 h a 35% decrease in dynamic lung compliance (P less than 0.05) and a 36% increase in pulmonary resistance (P less than 0.05) were noted. Further biochemical abnormalities occurred with total cell counts increased by 271% (P less than 0.02), albumin 163% (P less than 0.05), total protein 217% (P less than 0.01), and elastase 108% (P less than 0.02). Pathological analyses revealed mild lung injury at 24 h and marked inflammation, abnormal inflation patterns, flattening of Clara cells, fibrinous exudate and edema, early collagen formation, and cell necrosis observed at 48 h. Bronchoalveolar lavage surfactant had normal biophysical activity. Results demonstrate that exposure of neonatal piglets to O2 and mechanical hyperventilation for 48 h cause severe progressive lung injury.

Animals↗
PubMed1989

Endogenous opioids may protect the perinatal brain in hypoxia.

Endogenous opioids are released in great amounts in perinatal asphyxia. The role of this release has been unclear. In a study of cerebral blood flow and oxygen metabolism in 5 hypoxic newborn lambs, naloxone blocking of opioid receptors resulted in a proportional increase in telencephalic cerebral blood flow and oxygen metabolism. It is suggested that endogenous opioid release protects the neonatal brain in hypoxia by diminishing the cerebral metabolic rate of oxygen.

Animals↗
PubMed1989

Beta-blockers in portal hypertension. An overview.

This paper describes a meta-analysis of data from the 5 primary and 15 secondary prevention studies in patients with portal hypertension, in which beta-blockers were compared with inactive control. These studies involved 1525 patients. Overall, the number of patients who suffered bleeding events was 38% lower in the groups treated with beta-blockers (p less than 0.001). The percentage reductions in bleeding-related deaths and in total mortality were 35% and 18%, respectively (p = 0.007 and p = 0.024). More detailed analysis supports the conclusion that propranolol, the beta-blocker predominantly used in these studies, is effective in both the primary and secondary prevention of bleeding events and mortality due to portal hypertension.

Adrenergic beta-Antagonists↗
PubMed1989

Treatment of hypertension with a fixed ratio combination of long-acting propranolol and bendrofluazide, and influence of age of the subject.

The efficacy of sustained-release propranolol 160 mg (Inderal LA), bendrofluazide 5 mg and the combination preparation Inderex (bendrofluazide 5 mg and Inderal LA) in the treatment of hypertension was investigated. Twenty-one patients over a wide age range were studied, as it was of particular interest to find whether differing responses across a range of age groups might exist 24 hours post-dosing. Blood pressure control was greater with Inderex than with either Inderal LA or bendrofluazide. No significant difference between different age groups on the three treatments was demonstrated. There was some evidence, not statistically significant, suggesting potassium values to be lower on bendrofluazide and on Inderex. Serum glutamate oxaloacetate transaminase (SGOT) values were raised on bendrofluazide. Inderex is more effective in lowering blood pressure than either bendrofluazide or Inderal LA alone, and as a single capsule given once daily encourages compliance in comparison with combination treatments.

Adult↗