Climate change refers to long-term shifts in weather conditions and patterns of extreme weather events. It may lead to changes in health threat to human beings, multiplying existing health problems. This review examines the scientific evidences on the impact of climate change on human infectious diseases. It identifies research progress and gaps on how human society may respond to, adapt to, and prepare for the related changes. Based on a survey of related publications between 1990 and 2015, the terms used for literature selection reflect three aspects--the components of infectious diseases, climate variables, and selected infectious diseases. Humans' vulnerability to the potential health impacts by climate change is evident in literature. As an active agent, human beings may control the related health effects that may be effectively controlled through adopting proactive measures, including better understanding of the climate change patterns and of the compound disease-specific health effects, and effective allocation of technologies and resources to promote healthy lifestyles and public awareness. The following adaptation measures are recommended: 1) to go beyond empirical observations of the association between climate change and infectious diseases and develop more scientific explanations, 2) to improve the prediction of spatial-temporal process of climate change and the associated shifts in infectious diseases at various spatial and temporal scales, and 3) to establish locally effective early warning systems for the health effects of predicated climate change.

dence of active viral replication at the time of transplantation Prophylactic hepatitis B immunoglobulin (HBIg) re-(hepatitis B e antigen [HBeAg]-positive or HBV DNA-posiduces the risk of reinfection in hepatitis B surface antitive by hybridization assay) seem to have the greatest risk gen (HBsAg)-positive liver transplant recipients. In the of recurrent infection. 3,4 Prophylactic hepatitis B immunomedical center of this study, high-dose HBIg immunoglobulin (HBIg) has been shown to reduce the incidence of prophylaxis is administered at a fixed dose of 10,000 IU recurrent HBV infection and improve survival in HBsAg-posmonthly, and in this study, the long-term efficacy of this itive transplant recipients. 5 Previously reported studies have treatment regimen was examined. Of 52 HBsAg-positive used target antibody to HBsAg (anti-HBs) titers to determine liver transplant recipients, 24 were administered HBIg the frequency of HBIg administration. 6-9 Using trough antiimmunoprophylaxis, and 28 were administered no speHBs levels of 100-300 mIU/mL, recurrent HBV infection has cific therapy; the 2-year recurrence rates (defined by the reappearance of HBsAg) were 19% and 76%, respectively. developed in 10%-50% of patients, and rates of reinfection Fifty-four percent of the HBIg-treated patients were pos-may be as high as 80% in patients with indices of active viral itive for HBeAg or hepatitis B virus (HBV) DNA (by hy-replication pretransplantation. 3,[6][7][8][9] The optimal schedule of bridization assay) pretransplantation. In patients ad-HBIg administration is yet to be defined, and the long-term ministered monthly HBIg, intrapatient and interpatient consequences of HBIg administration are unknown. variability in trough antibody to HBsAg (anti-HBs) titerThe HBIg protocol used at our institution provides intravewas significant, highlighting the potential difficulties of nous HBIg daily during the first week posttransplantation using anti-HBs titer to guide therapy. Trough anti-HBs and then on a fixed schedule of 10,000 IU monthly until titers were less in patients who became HBsAg positive recurrence of infection is documented. This regimen offers than in patients who remained HBsAg-negative (490 vs. the advantage of ease of administration and monitoring. This 1290 mIU/mL) (P Å .0001), reflecting either the cause or study focuses on the long-term efficacy and safety of this effect of HBV reinfection. Of 9 patients who remained treatment protocol and seeks to define appropriate treatment HBsAg-negative and who were administered monthly end points.

The spatial spread of the highly pathogenic avian influenza virus H5N1 and its long-term persistence in Asia have resulted in avian influenza panzootics and enormous economic losses in the poultry sector. However, an understanding of the regional long-distance transmission and seasonal patterns of the virus is still lacking. In this study, we present a phylogeographic approach to reconstruct the viral migration network. We show that within each wild fowl migratory flyway, the timing of H5N1 outbreaks and viral migrations are closely associated, but little viral transmission was observed between the flyways. The bird migration network is shown to better reflect the observed viral gene sequence data than other networks and contributes to seasonal H5N1 epidemics in local regions and its large-scale transmission along flyways. These findings have potentially far-reaching consequences, improving our understanding of how bird migration drives the periodic reemergence of H5N1 in Asia.

Recent papers report transition metal-free couplings of haloarenes to arenes to form biaryls, triggered by alkali metal tert-butoxides in the presence of various additives. These reactions proceed through radical intermediates, but understanding the origin of the radicals has been problematic. Electron transfer from a complex formed from potassium tert-butoxide with additives, such as phenanthroline, has been suggested to initiate the radical process. However, our computational results encouraged us to search for alternatives. We report that heterocycle-derived organic electron donors achieve the coupling reactions and these donors can form in situ in the above cases. We show that an electron transfer route can operate either with phenanthrolines as additives or using pyridine as solvent, and we propose new heterocyclic structures for the respective electron donors involved in these cases. In the absence of additives, the coupling reactions are still successful, although more sluggish, and in those cases benzynes are proposed to play crucial roles in the initiation process. Results An explosion of interest has arisen in dehalogenative couplings between haloarenes and arenes to form biphenyls under transition metal-free conditions 1-28 since the original report of coupling of iodobenzene with pyridine and pyrazine by Itami in 2008. 1 The excitement is easily understood, since these reactions avoid the use of costly complexes of palladium, which are the normal catalysts. A common feature of the recent reactions is the use of sodium or potassium tert-butoxide as base. The absence of any signicant contamination with transition metals like palladium, 1,2 together with the properties of the new coupling reactions, has led to a general consensus that the reactions proceed by aryl radical intermediates. 1,6 The corollary coupling between haloarenes and styrenes, also triggered by alkali metal butoxides, 3,7,12 likely follows the same route. The general case for a radical mechanism was well summarised in an essay by Studer and Curran 9 and an attractive proposal from that source is shown in Fig. 1A. Here, the aryl radical 2 adds to benzene to form the arylcyclohexadienyl radical 3. Deprotonation by butoxide affords the radical anion 4,

Coupling of haloarenes to arenes has been facilitated by a diverse range of organic additives in the presence of KO(t)Bu or NaO(t)Bu since the first report in 2008. Very recently, we showed that the reactivity of some of these additives (e.g., compounds 6 and 7) could be explained by the formation of organic electron donors in situ, but the role of other additives was not addressed. The simplest of these, alcohols, including 1,2-diols, 1,2-diamines, and amino acids are the most intriguing, and we now report experiments that support their roles as precursors of organic electron donors, underlining the importance of this mode of initiation in these coupling reactions.