Mass chemotherapy for intestinal Taenia solium infection: effect on prevalence in humans and pigs

Mass treatment of the human population with niclosamide was carried out in 2 villages in rural Guatemala where Taenia solium was endemic, to determine how this would affect the epidemiology of the parasite. Intestinal taeniasis was diagnosed by microscopy and coproantigen testing, and porcine cysticercosis by a specific Western blot. Before mass treatment, the prevalence of human taeniasis was 3.5%; 10 months after treatment it was 1%, a significant decrease (P < 10(-4)). All tapeworms that could be identified to the species level were T. solium. Similarly, the seroprevalence of antibodies to cysticercosis in pigs declined from 55% before treatment to 7% 10 months after treatment, once again a significant decrease (P < 10(-6)). These effects were seen in both villages. The possible use of mass chemotherapy as a tool in the control of T. solium is discussed.     

Measurement of serum levels of exogenously administered FSH and LH during ovulation induction therapy

The available surgical and non-surgical therapy options for treatment of gallstone disease are presented. Conventional cholecystectomy is regarded as standard therapy of symptomatic cholecystolithiasis. Other modes of therapy may be indicated under certain circumstances, depending on the results of imaging procedures. In this context conventional X-ray examination, oral and intravenous cholecystography, sonography, computed tomography, endoscopic retrograde cholangiography/cholecystography, and magnetic resonance imaging are discussed and their influence on therapeutic decisions is explained.     

Global self-ratings of health and mortality: hazard in the North Carolina Piedmont

We analyzed the first 5 years of surveillance data from the Established Population for the Epidemiologic Studies of the Elderly (EPESE) in the Piedmont of North Carolina (n = 4162) to estimate the effect of a global self-rating of health on survival. Covariates used in Cox proportional hazard models included sociodemographic factors, chronic medical conditions, activities of daily living, use of health services, health risk behaviors, cognitive function, affective mood, and negative life events. Adjusted risk of mortality associated with poor (compared to excellent) self-ratings of health was significantly elevated among urban men only. Confounders of the association between survival and overall health assessment varied widely by subgroup. Pooled estimates from heterogeneous populations may mask significant subgroup differences both in the pattern of variables that mediate crude risk and also in the magnitude of residual risk of global self-ratings of health.     

A PET study of the neural systems of stuttering

The cause of stuttering is unknown. Failure to develop left-hemispheric dominance for speech is a long-standing theory although others implicated the motor system more broadly, often postulating hyperactivity of the right (language nondominant) cerebral hemisphere. As knowledge of motor circuitry has advanced, theories of stuttering have become more anatomically specific, postulating hyperactivity of premotor cortex, either directly or through connectivity with the thalamus and basal ganglia. Alternative theories target the auditory and speech production systems. By contrasting stuttering with fluent speech using positron emission tomography combined with chorus reading to induce fluency, we found support for each of these hypotheses. Stuttering induced widespread overactivations of the motor system in both cerebrum and cerebellum, with right cerebral dominance. Stuttered reading lacked left-lateralized activations of the auditory system, which are thought to support the self-monitoring of speech, and selectively deactivated a frontal-temporal system implicated in speech production. Induced fluency decreased or eliminated the overactivity in most motor areas, and largely reversed the auditory-system underactivations and the deactivation of the speech production system. Thus stuttering is a disorder affecting the multiple neural systems used for speaking.     

An alternative method for the quantitation of neuronal damage after experimental middle cerebral artery occlusion in rats: analysis of behavioral deficit

We tested the hypothesis that increasing durations of focal ischemia that have been shown to result in enlargement of cortical infarct will be associated with progression of behavioral dysfunction that can be measured by a battery of tests sufficiently sensitive and reproducible to detect a positive effect of pharmacotherapy. Untreated or N-methyl-D-aspartate receptor antagonist (CNS-1102)-treated spontaneously hypertensive rats underwent 45, 60, 90, or 120 min of tandem middle cerebral and common carotid artery occlusion followed by reperfusion. We then evaluated the extent of damage and its recovery for up to 21 days using nine behavioral tests aimed at analyzing strength, coordination, and bilateral asymmetry. Also using a graded bioassay that employs a curve-fitting computer program (ALLFIT) to correlate duration of ischemia with degree of behavioral dysfunction, we calculated the average of maximal behavioral dysfunction and duration of ischemia required to produce half-maximal behavioral dysfunction and compared these values in untreated controls with analogous values obtained from animals treated with CNS-1102. Three behavioral tests, forearm flex, tape (somatosensory neutralization), and foot-fault placing, were each separately and combined able to distinguish between the degrees of damage produced by increasing durations of ischemia. The behavioral abnormalities assessed using the tape test were reversible within a week, whereas those using forearm flex or foot-fault tests persisted for at least 21 days. CNS-1102 significantly reduced behavioral dysfunction measured by all three tests. This analysis of behavioral dysfunction represents a useful experimental model to grade efficacy of therapies aimed at protecting the brain from damage produced by acute stroke and might also be used to assess recovery from preexisting ischemic damage.     

Whole-body kinetics and dosimetry of L-3--123I-iodo-alpha-methyltyrosine

BACKGROUND: Desflurane anesthesia can produce cerebral metabolic depression and increase cerebral blood flow. We evaluated the effect of desflurane on brain tissue oxygen pressure (PO2), carbon dioxide pressure (PCO2) and pH during neurosurgery. METHODS: Following a craniotomy, the dura was opened and a Paratrend 7 sensor, which measures PO2, PCO2, pH and temperature, was inserted into brain tissue. In 6 control patients in group 1, anesthesia was maintained constant with 3% end-tidal desflurane over 60 min, including a 30-min stabilization period. In group 2, 9 patients were ventilated with 3% desflurane under baseline conditions. After a 30-min stabilization period, baseline tissue gases and pH were measured and end-tidal desflurane was increased to 6% and then 9% for 15-min intervals. Mean arterial pressure (MAP) was maintained with intravenous phenylephrine. RESULTS: Under baseline conditions, cardiovascular and brain tissue measures were similar between the 2 groups. Increasing end-tidal desflurane from 3% to 9% produced burst-suppression EEG in all patients and significantly increased tissue PO2 and pH and decreased PCO2. No parameters changed significantly in the control group during steady-state anesthesia. CONCLUSION: These results show that 9% desflurane can improve brain tissue metabolic status before temporary brain artery occlusion if cerebral perfusion pressure is maintained. This may be particularly important in patients with symptoms of ischemia before surgery.