Related StoriesACC's public reporting system provides information regarding hospitals' performanceStudy: Post hospital syndrome is usually significant risk factor for sufferers undergoing elective surgeryCHOP's Buerger Middle for Advanced Pediatric Treatment celebrates grand starting MyRounding allows our leaders to fully capture real-time patient responses in an organized manner so that we are able to proactively meet individual and family needs and continually improve and sustain the best patient experience, said Guler. With the MyRounding platform, health care facilities can gather data and offer instant reviews to nurses and administrators on patient feedback and experience.Suhr, M.D.: Efficacy and Protection of RNAi Therapy for Transthyretin Amyloidosis Transthyretin amyloidosis is a life-threatening disorder caused by the deposition of hepatocyte-derived transthyretin amyloid in various tissues and organs.1,2 Circulating transthyretin is derived from the liver3 and can form amyloid deposits in peripheral nerves and in the gastrointestinal system, heart, and kidneys. Transthyretin can be synthesized by the retina and choroid plexus,4,5 which can result in leptomeningeal and vitreal deposits. More than 100 genetic variants of the gene encoding transthyretin are associated with autosomal dominant forms of the disease, known as familial amyloidotic polyneuropathy6-8 and familial amyloidotic cardiomyopathy.9-11 The most typical mutation associated with familial amyloidotic polyneuropathy is V30M; in addition to polyneuropathy, cardiac involvement can be manifested early as conduction disturbances in individuals with the V30M mutation and as cardiomyopathy in a few individuals with the V30M mutation who’ve advanced disease and in sufferers with familial amyloidotic polyneuropathy with various other mutations.12,13 The predominant mutation connected with familial amyloidotic cardiomyopathy is V122I; individuals with this mutation are susceptible to isolated cardiac involvement and will not have polyneuropathy.9 Most individuals are heterozygous for the TTR mutations, and the amyloid deposits consist of mutant and nonmutant transthyretin.14,15 Liver transplantation is conducted in sufferers with familial amyloidotic polyneuropathy but has substantial restrictions, including transplant availability and substantial mortality and morbidity.16-20 Also, transplantation eliminates the production of mutant however, not nonmutant transthyretin, so further deposition of non-mutant transthyretin occurs after transplantation, resulting in cardiomyopathy and worsening of neuropathy.