Paul Y. Kwo, M.D., Parvez S. Mantry, M.D., Eoin Coakley, M.D., Helen S. Te, M.D., Hugo E. Vargas, M.D., Robert Brown, Jr., M.D., M.P.H., Fredric Gordon, et.al.
Hepatitis C virus (HCV) presents a global health care challenge, with approximately 170 million people chronically infected.1 In 2012, approximately 24,000 liver transplantations were performed worldwide, with the largest proportion performed because of HCV-induced liver disease.2,3 In the United States, more than 40% of registrants on the liver-transplant waiting list are infected with HCV.3,4 After liver transplantation, recurrence of HCV infection is universal among recipients with viremia before transplantation.5,6 Fibrosis progression may be accelerated and HCV viral loads may be markedly increased in patients receiving post-transplantation immunosuppressive therapy as compared with patients not undergoing transplantation.
Amesh A. Adalja, M.D., Eric Toner, M.D., and Thomas V. Inglesby, M.D.
In this article, we review the clinical management of deliberate infection with several pathogens of greatest bioweapons concern. On the basis of historical incidents coupled with information on ease of dissemination, contagiousness, mortality rates, public health impact, ability to engender panic, and the need for special preparedness,1-3 the Centers for Disease Control and Prevention (CDC) stratifies pathogens and toxins into three risk categories — A, B, and C — with category A meriting the highest level of concern and preparedness.4,5
Jason A. Regules, M.D., John H. Beigel, M.D., Kristopher M. Paolino, M.D., Jocelyn Voell, R.N., M.S., Amy R. Castellano, L.P.N., Paula Muñoz, B.S., James E. Moon, M.D., et.al.
The current Ebola virus disease (EVD) outbreak has resulted in more than 24,000 cases and 10,000 reported deaths as of March 25, 2015.1 Although the primary strategy to stop the transmission of human Ebola virus remains the identification and isolation of contacts and the use of appropriate personal protective equipment, the development and deployment of a safe and efficacious vaccine would provide an important public health tool that could be used to interrupt transmission within outbreaks and prevent subsequent occurrences.
Claire E. Wainwright, M.B., B.S., M.D., J. Stuart Elborn, M.D., Bonnie W. Ramsey, M.D., Gautham Marigowda, M.D., Xiaohong Huang, Ph.D., Marco Cipolli, M.D., Carla Colombo, M.D., Jane C. Davies, M.D., Kris De Boeck, M.D., Patrick A. Flume, M.D., Michael W. Konstan, M.D., Susanna A. McColley, M.D., Karen McCoy, M.D., Edward F. McKone, M.D., Anne Munck, M.D., Felix Ratjen, M.D., Steven M. Rowe, M.D., M.S.P.H., David Waltz, M.D., and Michael P. Boyle, M.D., for the TRAFFIC and TRANSPORT Study Groups*
Cystic fibrosis is a genetic disease that is associated with high rates of premature death.1-4 It is a multisystem disease that is characterized by pancreatic insufficiency and chronic airway infections associated with loss of lung function, repeated pulmonary exacerbations, and, ultimately, respiratory failure.5
Cystic fibrosis is caused by gene mutations that result in deficient or dysfunctional cystic fibrosis transmembrane conductance regulator (CFTR) protein, an anion channel that is normally present in the epithelial membrane
Melina Claussnitzer, Ph.D., Simon N. Dankel, Ph.D., Kyoung-Han Kim, Ph.D., Gerald Quon, Ph.D., Wouter Meuleman, Ph.D., Christine Haugen, M.Sc., Viktoria Glunk, M.Sc., Isabel S. Sousa, M.Sc., Jacqueline L. Beaudry, Ph.D., Vijitha Puviindran, B.Sc., Nezar A. Abdennur, M.Sc., Jannel Liu, B.Sc., Per-Arne Svensson, Ph.D., Yi-Hsiang Hsu, Ph.D., Daniel J. Drucker, M.D., Gunnar Mellgren, M.D., Ph.D., Chi-Chung Hui, Ph.D., Hans Hauner, M.D., and Manolis Kellis, Ph.D.
Obesity affects more than 500 million people worldwide and contributes to type 2 diabetes, cardiovascular disorders, and cancer.1 Obesity is the result of a positive energy balance, whereby energy intake exceeds expenditure, resulting in the storage of energy, primarily as lipids in white adipocytes. Energy balance is modulated by food consumption and physical activity, as well as by the dissipation of energy as heat through constitutive thermogenesis in mitochondria-rich brown adipocytes in brown fat and through inducible thermogenesis in beige adipocytes in white fat.