Soda consumption and hospital admissions among Californian adults with asthma

Introduction: Asthma prevalence has been increasing consistently since 1995 in California. Recent studies have found that consuming soda and sugar-containing drinks may pose a risk for asthma. Research that examines the relationship between soda intake and asthma among adult asthmatics is limited. Objective: This study investigated the relationship between sugar-sweetened soda consumption and asthma hospitalization among adult asthmatics in California. Methods: This cross-sectional study was based on the 2011–2012 California Health Interview Survey (CHIS) data and included 3,784 adults who were diagnosed with asthma by a doctor and who currently reported either that they still had asthma, or that they had suffered from an asthma attack in the last 12 months. The analysis was survey weighted. The exposure variable was soda intake measured as the number of times soda was consumed in the last week. The health outcome measure was overnight hospital admission due to asthma. Logistic regression was used to examine the association between soda consumption and overnight hospital admission after adjusting for age, education, sex, race/ethnicity, weight status, smoking status, and self-rated health. Results: Adults with asthma who drank soda three or more times per week reported higher odds of overnight hospitalization (adjusted odds ratio = 2.77, 95% CI: 1.51–5.10, p = 0.001). Conclusions: Our findings suggest that efforts designed to limit soda consumption would benefit asthma suffers by reducing hospital admissions. This, however, needs further research to confirm a direct causal association.     

Prostaglandin E2 type 1 receptors contribute to neuronal apoptosis after transient forebrain ischemia

Cyclooxygenase-2-derived prostaglandin E₂ (PGE₂) contributes to excitotoxic and ischemic neuronal cell death by engaging neuronal PGE₂ type 1 receptors (EP1R). Our previous studies have shown that EP1R signaling resulted in disturbances of intracellular Ca²⁺ homeostasis and suppression of the pro-survival protein kinase AKT. The aim of this study was to investigate whether these pathophysiological mechanism have a role in the neuronal cell death after transient forebrain ischemia. Mice were subjected to ischemia/reperfusion by bilateral common carotid artery occlusion. Hippocampal cornu ammonis area 1 (CA1) neuronal cell death was determined 5 days after reperfusion. Animals treated with the EP1R antagonist SC51089 or EP1R-deficient mice (EP1^−/−) showed significantly less neuronal injury as compared to vehicle-treated wild-type controls. Benefits of EP1R blockage were still evident 14 days after injury. Better neuronal survival was correlated with reduced neuronal caspase-3 activity and decreased nuclear translocation of the apoptosis-inducing factor . Neuroprotection could be reverted by intracerebroventricular administration of the phosphoinositide 3-kinase inhibitor {"type":"entrez-nucleotide","attrs":{"text":"LY294002","term_id":"1257998346","term_text":"LY294002"}}LY294002 and was not further increased by the calcineurin inhibitor FK506. These data implicate EP1R in postischemic neuronal apoptosis possibly by facilitating AKT inhibition.     

Reduced insulin-induced phosphatidylinositol-3-kinase activation in peripheral blood mononuclear leucocytes from patients with Alzheimer's disease

The epidemiological finding of an increased risk of dementia in patients with diabetes mellitus has raised the hypothesis that a dysfunction of the insulin receptors plays a role in the pathogenesis of Alzheimer's disease (AD). A possible link is suggested by the evidence that the insulin-stimulated phosphatidylinositol-3-kinase (PI-3-K)/phospho-Akt pathway negatively controls the glycogen synthase kinase-3beta. The activation of this enzyme mediates the hyperphosphorylation of the tau protein, a relevant step in the formation of the neurofibrillary tangles associated with AD. We hypothesized that the neurodegeneration associated with AD is related to an impairment of the intracellular signalling stimulated by insulin receptors. To test this hypothesis we assessed the PI-3-K/phospho-Akt pathway following in-vitro challenge with insulin in peripheral blood mononuclear cells from subjects with AD (n = 20) and controls (n = 20). We found that the stimulation of PI-3-K is blunted in patients with AD with respect to control. The reduction did not correlate with the extent of cognitive decline or with scores at neuropsychological tests exploring attention, memory, language or visuospatial abilities. The study supports the hypothesis that an impaired control of glycogen synthase kinase-3beta activity by insulin receptor-mediated signalling plays a role in the pathogenesis of AD, facilitating tau protein phosphorylation and neurofibrillary tangle formation.     

Explosive-aggressive behavior related to bilateral subthalamic stimulation

We describe a patient with Parkinson's Disease who underwent bilateral subthalamic nucleus deep brain stimulation and later presented with episodes of aggressive behavior disorder with disturbed impulse control and an inability to control anger likely related to the deep brain stimulation "switch-on stimulation". We hypothesize that increasing voltage intensity could influence neighboring passing fibers coming from basal limbic system that are involved in the regulation of affect and emotional behavior. We suggest investigating these neuropsychological disturbances considering their influence on quality of life after surgery.     

Diltiazem and reinfarction in patients with non-Q-wave myocardial infarction. Results of a double-blind, randomized, multicenter trial

We performed a multicenter, double-blind, randomized study to evaluate the effect of diltiazem on reinfarction after a non-Q-wave myocardial infarction. Nine centers enrolled 576 patients: 287 received diltiazem (90 mg every six hours) and 289 received placebo. Treatment was initiated 24 to 72 hours after the onset of infarction and continued for up to 14 days. The primary end point, reinfarction, was defined as an abnormal reelevation of MB creatine kinase in plasma within 14 days. Reinfarction occurred in 27 patients in the placebo group (9.3 percent) and in 15 in the diltiazem group (5.2 percent)--a 51.2 percent reduction in cumulative life-table incidence (P = 0.0297; 90 percent confidence interval, 7 to 67 percent). Diltiazem reduced the frequency of refractory postinfarction angina (a secondary end point) by 49.7 percent (P = 0.0345; 90 percent confidence interval, 6 to 73 percent). Mortality was similar in the two groups (3.1 and 3.8 percent, respectively, in the placebo and diltiazem groups), but adverse drug reactions (most of which were mild) were more common in the diltiazem group. Nevertheless, the drug was well tolerated, despite concurrent treatment with beta-blockers in 61 percent of the patients. We conclude that diltiazem was effective in preventing early reinfarction and severe angina after non-Q-wave infarction and that it was also safe and generally well tolerated.     

A cognitive-existential analysis of counselor responses to HIV-positive substance misusers in an outpatient methadone program and a residential therapeutic community.

Counselors of HIV-afflicted substance abusers not only must apply counseling strategies directed toward curbing drug use, but also are called upon to assess suicide risk, attend to the promotion of social support, treat adverse affective reactions, and respond to spiritual and existential concerns. The present study attempted to explore systematically the self-reported feelings, thoughts, and behaviors of counselors as they confront such demands. All counselors reported experiencing increased stress as a result of working with HIV-afflicted clients, and cognitive distortions were sometimes noted in counselor responses. However, more generally, thoughts seemed clearly formulated, and planned behaviors appeared directed toward rendering the best treatment possible.     

The effects of short-term venous congestion on forearm venous volume and reactive hyperemia blood flow in human subjects

Congestive heart failure is associated with a reduction in limb venous volume at an effective venous pressure of 30 mm Hg (VV[30]). Further, an attenuated arteriolar dilation in response to a metabolic stimulus has been demonstrated. It was the purpose of this study to determine to what extent the chronic elevation in venous pressure seen in heart failure might explain these abnormalities of the limb circulation. Ten normal human volunteers were subjected to venous congestion of one arm for three hours at 70 mm Hg. A mercury-in-rubber strain gauge plethysmograph was used to measure forearm VV [30] and forearm blood flow at rest after release of five minutes of arterial occlusion (the reactive hyperemia response). Congestion reduced VV [30] 22%, resting forearm blood flow 49% and peak reactive hyperemia blood flow 25%. Thus, chronic venous congestion per se may significantly reduce limb venous volume as well as resting and reactive hyperemia blood flow.