Chest
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Randomized Controlled Trial
Factors affecting quality of anticoagulation control amongst atrial fibrillation patients on warfarin:The SAMe-TT2R2 (Sex female, Age less than 60, Medical history, Treatment strategy [rhythm control], Tobacco use [doubled], Race [doubled] score.
When oral anticoagulation with adjusted-dose vitamin K antagonist (VKA) is used, the quality of anticoagulation control (as reflected by the time in therapeutic range [TTR] of the international normalized ratio [INR]) is an important determinant of thromboembolism and bleeding. Our objective was to derive a validated scheme using patient-related clinical parameters to assess the likelihood of poor INR control among patients with atrial fibrillation (AF) on VKA therapy. ⋯ Common clinical and demographic factors can influence the quality of oral anticoagulation. We incorporated these factors into a simple score (SAMe-TT₂R₂) that can predict poor INR control and aid decision-making by identifying those patients with AF who would do well on VKA (SAMe-TT₂R₂ score = 0-1), or conversely, those who require additional interventions to achieve acceptable anticoagulation control (SAMe-TT₂R₂ score ≥ 2).
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Inflammatory diseases of the lung are a major cause of morbidity and mortality. Allergic lung inflammation often stems from the overproduction of type 2 cytokines. The resulting type 2 inflammation is frequently caused by an inappropriate immune response to relatively harmless allergens and often associates with asthma. ⋯ Indeed, ILC2s appear to be critical for the induction of adaptive immunity and, thus, play a central role for immune regulation. As one of the first responders in the entire Th2 cascade, ILC2 might serve as the early tile in a Th2 domino effect. As such, ILC2s present an attractive target for future drug development.
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ICU admissions are ever increasing across the United States. Following critical illness, physical functioning (PF) may be impaired for up to 5 years. We performed a systematic review of randomized controlled trials evaluating the efficacy of interventions targeting PF among ICU survivors. The objective of this study was to identify effective interventions that improve long-term PF in ICU survivors. ⋯ The only effective intervention to improve long-term PF in critically ill patients is exercise/PT; its benefit may be greater if started earlier. Further research in this area comparing different interventions and timing is needed.
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Comparative Study
Lobe-Specific Mediastinal Nodal Dissection is Sufficient During Lobectomy by VATS or Thoracotomy for Early Stage Lung Cancer.
Lobectomy with complete mediastinal lymphadenectomy is considered standard for patients with early-stage non-small cell lung cancer (NSCLC). However, the benefits of complete lymphadenectomy are unproven. There is evidence suggesting a predictable pattern of mediastinal nodal drainage. This study analyzed the frequency and pattern of mediastinal nodal disease and its impact on outcome in patients with early-stage NSCLC. ⋯ Mediastinal N2 metastases follow predictable lobe-specific patterns in patients with negative preoperative CT scans and PET scans. Lobe-specific N2 nodal evaluation results in a recurrence rate similar to that of complete mediastinal evaluation. Lobe-specific mediastinal nodal evaluation appears acceptable in patients with early-stage NSCLC.
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Comparative Study
Sleep-disordered-breathing in Ehlers-Danlos Syndrome (a genetic model of obstructive sleep apnea).
The objective of this study was to investigate the presence of sleep-disordered breathing (SDB) in patients with Ehlers-Danlos syndrome. Ehlers-Danlos syndrome is a genetic disorder characterized by cartilaginous defects, including nasal-maxillary cartilages. ⋯ In patients with Ehlers-Danlos syndrome, abnormal breathing during sleep is commonly unrecognized and is responsible for daytime fatigue and poor sleep. These patients are at particular risk for SDB because of genetically related cartilage defects that lead to the development of facial structures known to cause SDB. Ehlers-Danlos syndrome may be a genetic model for OSA because of abnormalities in oral-facial growth. Early recognition of SDB may allow treatment with orthodontics and myofacial reeducation.