The California Department of Health Services evaluated carpal tunnel syndrome (CTS), a median nerve entrapment condition associated with forceful and repetitive wrist motion, among grocery store workers at a large California supermarket where a CTS cluster had been reported. Forceful and repetitive wrist motion was measured, in three exposure levels, through a job classification scheme based upon type of work tasks and average time per week spent performing these tasks. A medical questionnaire and measurements of median sensory nerve conduction were used to measure CTS. CTS prevalence was 23% based upon a sample of 56 participants drawn from a workforce of 69 employees. A relative risk of 8.3 (95% confidence interval 2.6-26.4) for a history of CTS-like symptoms between the high and low exposure level groups held up after adjustment for the potential confounders of age, sex, alcohol consumption, and high-risk medical history. It was concluded that the basic principles of good ergonomic design should be used to prevent or diminish the risk of musculoskeletal injury in the workplace.
Alcoholism causes serious neurologic disease that may be due, in part, to the ability of ethanol to interact with neural cell membranes and change neuronal function. Adenosine receptors are membrane-bound proteins that appear to mediate some of the effects of ethanol in the brain. Human lymphocytes also have adenosine receptors, and their activation causes increases in cAMP levels. To test the hypothesis that basal and adenosine receptor-stimulated cAMP levels in lymphocytes might be abnormal in alcoholism, we studied lymphocytes from 10 alcoholic subjects, 10 age-and sexmatched normal individuals, and 10 patients with nonalcoholic liver disease. Basal and adenosine receptor-stimulated cAMP levels were reduced 75% in lymphocytes from alcoholic subjects. Also, there was a 76% reduction in ethanol stimulation of cAMP accumulation in lymphocytes from alcoholics. Similar results were demonstrable in isolated T cells. Unlike other laboratory tests examined, these measurements appeared to distinguish alcoholics from normal subjects and from patients with nonalcoholic liver disease. Reduced basal and adenosine receptor-stimulated levels of cAMP in lymphocytes from alcoholics may reflect a change in cell membranes due either to chronic alcohol abuse or to a genetic predisposition unique to alcoholic subjects.Despite the widespread incidence of alcoholism, the molecular events accounting for intoxication, tolerance, and physical dependence after alcohol abuse are poorly understood. Ethanol is believed to intercalate into cell membranes, producing acute and adaptive changes in membrane fluidity (1, 2) or membrane constituents (3,4). Adenosine receptors are membrane-bound proteins that appear to mediate some of the effects of ethanol in the central nervous system (5). We recently reported (6) that ethanol acutely increases adenosine receptor-stimulated cAMP levels in a clonal neural cell line (neuroblastoma-glioma hybrid and that with time these cells adapt to the presence of ethanol, showing a reduction in adenosine receptor-stimulated cAMP levels. After chronic exposure to ethanol, the NG108-15 cells require ethanol to achieve normal levels of adenosine receptorstimulated cAMP, which may indicate a form of cellular "dependence." This process is completely reversible upon ethanol withdrawal.These observations suggest that intact single cells adapt to the presence of ethanol. Moreover, depressed adenosine receptor-stimulated cAMP levels in cells might be a biochemical change of pathophysiologic significance in chronic alcoholism. Since human lymphocytes have the same A2 adenosine receptors as the neuroblastoma cells (7), we could test directly whether alcoholics have altered cAMP levels. We undertook a controlled study of basal and adenosine receptor-stimulated cAMP levels in lymphocytes of chronic alcoholics, normal subjects, and patients with nonalcoholic liver disease. Mixed lymphocytes and T cells from chronic alcoholics showed a striking reduction in basal and adenosine receptor-stimulated cAMP levels. Moreov...
Although the toxic effects of lead have been known for centuries, lead intoxication is still widespread in the United States. Without baseline tests of neuropsychological, neurobehavioral and neurophysiological testing it may be difficult to detect subtle changes in neurological function after lead exposure. This may be further confounded by partial chelation treatment and exposure to neurotoxic mixtures or inability to quantitate alcohol consumption. We undertook a cross-sectional study to address these problems in 24 exposed and 29 control subjects in a plant that manufactured electrical components using fritted leaded glass to coat capacitors and transistors. Potentially exposed workers had blood lead levels ranging between 3 micrograms/dL to 135 micrograms/dL. Industrial hygiene monitoring revealed the plant's air lead levels ranged from 61 micrograms/m3 to 1,700 micrograms/m3 in excess of OSHA permissible exposure limits of 40 micrograms/m3/10 hr day. Using a specially designed battery of neurophysiological, neurobehavioral and neuropsychological screening tests, we demonstrated a significant difference from controls in measures of psychomotor speed, motor strength and verbal memory. Although limited by the cross-sectional design, these findings support the hypothesis that the battery of neurophysiological, neuropsychological and neurobehavioral tests can detect a significant inter-group differences between lead-exposed and control subjects.
Dengue virus (DENV) causes a spectrum of diseases ranging from asymptomatic, mild febrile to a life-threatening illness: dengue hemorrhagic fever. The main clinical symptom of dengue is fever, similar to that of malaria. The prevalence of dengue virus infection, alone or in association with other endemic infectious diseases in children in Cameroon is unknown. The aim of this study was to determine the prevalence of dengue, malaria and HIV in children presenting with fever and associated risk factors. Dengue overall prevalence was 20.2%, Malaria cases were 52.7% and HIV cases represented 12.6%. The prevalence of dengue-HIV co-infection was 6.0% and that of Malaria-dengue co-infection was 19.5%. Triple infection prevalence was 4.3%. Dengue virus infection is present in children and HIV-Dengue or Dengue- Malaria co-infections are common. Dengue peak prevalence was between August and October. Sex and age were not associated with dengue and dengue co-infections. However, malaria as well as HIV were significantly associated with dengue (P = 0.001 and 0.028 respectively). The diagnosis of dengue and Malaria should be carried out routinely for better management of fever.
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