Levodopa is the most efficacious and widely used symptomatic drug for Parkinson's disease (PD). There is currently, however, a great deal of interest focused on the possibility that levodopa-induced increases in dopamine (DA) turnover may increase oxidative damage derived from the breakdown of DA. Increased oxidative damage following levodopa may contribute to the progressive degeneration of remaining host nigral neurons as well as interfere with development and function of embryonic nigral neurons in neural grafting trials. There is abundant evidence that levodopa is toxic to embryonic nigral DA neurons in both cell culture and neural grafting models. These findings have prompted a number of studies on mechanisms of levodopa toxicity to identify effective means of ameliorating potential oxidative stress related to levodopa in PD. In the current study we have utilized cultures of embryonic nigral DA neurons to address the fundamental question of whether levodopa-induced toxicity is related to DA production or whether dopa itself contributes to cell death. We compared the degree of nigral DA cell death following chronic administration of: 1) levodopa (e.g.: l-dopa); 2) its less active stereoisomer d-dopa; and 3) DA. We examined the rank order of toxicity of these compounds in two species of rats, Fisher 344 (F344) and Sprague-Dawley (SD). Results indicate a toxicity profile of: DA > l-dopa >> d-dopa. In addition, although there was no difference in response of F344 and SD cultures to l-dopa, the SD cultures were significantly more susceptible to the neurotoxic effects of DA. Taken collectively, these results suggest that levodopa-induced toxicity is related primarily to DA production rather than oxidation of dopa to toxic metabolites, and that some strain related differences do exist.

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A lthough the development of pulmonary arterial hypertension (PAH) in mixed connective tissue disease (MCTD) is now recognised as the most important life threatening factor, an effective treatment for PAH has not been established. The response to steroid treatment of PAH related to MCTD varies. Furthermore, Raynaud's phenomenon is the most common symptom of MCTD and one symptom of the 1996 revised criteria for MCTD in Japan.

Pulmonary embolism has become a cause of great concern to health care professionals. Despite strides in research and availability of sensitive diagnostic tests, the mortality and morbidity related to this entity continues to cause tremendous economic burden. Patients present with an array of symptoms ranging from mild dyspnea to hemodynamic instability and even death. Prompt recognition of symptoms along with early risk stratification can be lifesaving. Management focuses on achieving hemodynamic stability and reducing clot burden. Approved treatment modalities include anticoagulation, systemic or catheter directed thrombolytic therapy and surgical embolectomy. In this article we will review catheter-directed thrombolytic therapy, specifically the EKOS® or the EkoSonic endovascular system. EKOS® uses ultrasoundfacilitated catheter-directed thrombolysis. The rationale behind this therapy is using shorter infusion times and lower dosage of the thrombolytic therapy, thereby reducing the complications associated with their use.

OBJECTIVES: This study evaluated the efficacy of radiographic screening for tuberculosis in correctional facilities. METHODS: Inmates at an admission facility in New York, NY, were screened for tuberculosis by registry cross-match, symptom interviews, tuberculin testing, and chest radiography. RESULTS: Thirty-two cases of tuberculosis were detected among 4172 inmate admissions (767 cases per 100,000). Twenty-five inmates (78%) were previously diagnosed but incompletely treated; all were identified by registry cross-match. Seven inmates (22%) were newly diagnosed, of whom four (57%) were asymptomatic, had negative skin tests, and were detected only by their abnormal radiographs. CONCLUSIONS: Screening strategies that limit radiographic testing to inmates with either positive skin tests or symptoms may result in missed opportunities for diagnosing active tuberculosis.