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 Anticoagulant plasma concentrations and patient characteristics might affect the benefit-risk balance of therapy. The study objective was to assess the impact of model-predicted rivaroxaban exposure and patient characteristics on outcomes in patients receiving rivaroxaban for venous thromboembolism (VTE) prophylaxis (VTE-P) after hip/knee replacement surgery. Post hoc exposure-response analyses were conducted using data from the phase 3 RECORD1-4 studies, in which 12,729 patients were randomized to rivaroxaban 10 mg once daily or enoxaparin for ≤ 39 days. Multivariate regression approaches were used to correlate model-predicted individual rivaroxaban exposures and patient characteristics with outcomes. In the absence of measured rivaroxaban exposure, exposure estimates were predicted based on individual increases in prothrombin time (PT) and by making use of the known correlation between rivaroxaban plasma concentration and dynamics of PT. No significant associations between rivaroxaban exposure and total VTE or major bleeding were identified. A significant association between exposure and a composite of major or non-major clinically relevant (NMCR) bleeding from day 4 after surgery was observed. The relationship was shallow, with an approximate predicted absolute increase in a composite of major or NMCR bleeding from 1.08 [95% confidence interval (CI) 0.76-1.54] to 2.18% (95% CI 1.51-3.17) at the 5th and 95th percentiles of trough plasma concentration, respectively. In conclusion, based on the underlying data and analysis, no reliable target window for exposure with improved benefit-risk could be identified within the investigated exposure range. Hence, monitoring rivaroxaban levels is unlikely to be beneficial in VTE-P.We report a rare case of fatal intoxication in a 40-year-old man caused by injection of a fluid containing organic mercury, allegedly in an attack with a syringe fixed to the tip of an umbrella. The man suffered from severe neurological symptoms and progressive multiorgan failure and died 10 months later in refractory status epilepticus. Autopsy revealed severe brain atrophy and non-specific kidney damage. Neuropathological examination showed neuronal loss especially in the occipital lobe, distinct granule cell necrosis in the cerebellum and Wallerian degeneration in the brainstem. Postmortem toxicological analysis revealed extremely increased levels of mercury in liver and kidney tissue as well as methylmercury levels in peripheral blood.Urinothorax is a cause of pleural effusion that is often missed due to its perceived rarity.  https://www.selleckchem.com/products/ABT-263.html  Here, we present a case of urinothorax secondary to percutaneous nephrolithotomy resulting in lung collapse and death. This case highlights urinothorax as a cause of death, its biochemical profile, and diagnostic features on autopsy. A 39-year-old female presented to the ED with low back pain and dysuria. Abdominal and pelvic CT showed a large staghorn calculus in the right kidney which was then treated with percutaneous nephrolithotomy. On post-operative day (POD) 1, the patient was febrile, had decreased breath sounds, and complained of pain with deep inspiration. Chest x-ray revealed increased right pleural fluid. On POD 3, the patient continued to have difficulty breathing and was eventually found apneic. Resuscitation was unsuccessful. Autopsy revealed a collapsed right lung associated with a 1200 mL pleural effusion, which was cloudy, yellow, and smelled like urine. The cause of death was listed as complications of percutaneous nephrolitotomy, with urinothorax and collapse of lung. While rare, urinothoraces must be considered as a cause of pleural effusion due to risk of respiratory failure and death. Diagnosis relies on pleural fluid analysis and history, especially with regard to genitourinary obstruction and surgeries.Multiple organ dysfunction syndrome (MODS), also referred to as external challenge-induced multiple organ injury, is characterized by dysfunction of two or more organs during infection or following shock or trauma. The pathogenesis of MODS is multifactorial and involves systemic inflammation and cell stress responses including cell death; sepsis is defined as an infection with MODS. Gut microbiota contributes significantly to organ dysfunction and to the pathobiology of sepsis. However, the relationship between the development of sepsis and the composition of gut microbiota is equivocal and is only now starting to be elucidated. Recent studies by our group and others reveal that enteric microbial composition and function are disrupted during sepsis, and that microbial products can either promote or alleviate the progression of sepsis. Here, we summarize the current research on the functional link between gut microbiota and sepsis, and argue the point that gut microbiota is a potential therapeutic target in the management of sepsis.The gut microbiota consists of a dynamic multispecies community living within a particular niche in a mutual synergy with the host organism. Recent findings have revealed roles for the gut microbiota in the modulation of host immunity and the development and progression of immune-mediated diseases. Besides, growing evidence supports the concept that some metabolites mainly originated from gut microbiota are linked to the immune regulation implicated in systemic inflammatory and autoimmune disorders. In this chapter, we describe the recent advances in our understanding of how host-microbiota interactions shape the immune system, how they affect the pathogenesis of immune-associated diseases and the impact of these mechanisms in the efficacy of disease therapy.The gut microbiome contains trillions of commensal microorganisms that maintain a symbiotic relationship with the host, and its profound effects on gastrointestinal diseases have been widely described.  https://www.selleckchem.com/products/ABT-263.html  Recently, gut microbiota have emerged as important factors in endocrine system diseases. Disruption of the gut microbiota affects neuroendocrine homeostasis and promotes peripheral endocrine system diseases, including obesity, diabetes, and hyperuricemia. This chapter provides a comprehensive overview of the biological mechanisms of gut microbiota that participate in endocrine system pathologies and discusses potential novel therapies for these diseases.