Melting, Solidification, and Crystallization of a Thermoplastic Polyurethane as a Function of Hard Segment Content

Thermoplastic polyurethanes (TPU) with varying hard segment contents (HSC) are monitored during melting and solidifying (20 K/min , Tmax = 220 ° C) by small-angle and wide-angle X-ray scattering (WAXS and SAXS). Hard segments: MDI/BD. Soft segments: PTHF1000. The neat materials are injection-molded, having small amorphous hard domains (chord length d⎯⎯h ∼ 35% show sharp Bragg peaks and larger hard domains ( d⎯⎯h > 7 nm ). When heated, small domains melt, but crystallization in the remaining large domains is not detected. Upon cooling, large agglomerates segregate first, which crystallize immediately. Segregation starts for HSC = 42% at 160 °C and for HSC = 75% at 210 °C. When HSC ≤ 30%, the morphologies before and after are similar, but afterward, many hard blocks are dissolved in the soft phase at the expense of the hard domain fraction. In heating and cooling the melts, multiple homogenization and segregation processes are observed, which are explained by the agglomeration of hard blocks of different lengths in the colloidal fluid

HIV interactions with monocytes and dendritic cells: viral latency and reservoirs

HIV is a devastating human pathogen that causes serious immunological diseases in humans around the world. The virus is able to remain latent in an infected host for many years, allowing for the long-term survival of the virus and inevitably prolonging the infection process. The location and mechanisms of HIV latency are under investigation and remain important topics in the study of viral pathogenesis. Given that HIV is a blood-borne pathogen, a number of cell types have been proposed to be the sites of latency, including resting memory CD4+ T cells, peripheral blood monocytes, dendritic cells and macrophages in the lymph nodes, and haematopoietic stem cells in the bone marrow. This review updates the latest advances in the study of HIV interactions with monocytes and dendritic cells, and highlights the potential role of these cells as viral reservoirs and the effects of the HIV-host-cell interactions on viral pathogenesis

Epidemiology of carbapenem-resistant Enterobacteriaceae: a 5-year experience at a tertiary care hospital

Darunee Chotiprasitsakul,1 Sirawat Srichatrapimuk,2 Suppachok Kirdlarp,1 Alexander D Pyden,3 Pitak Santanirand4 1Division of Infectious Diseases, Department of Medicine, Faculty of Medicine Ramathibodi Hospital, Mahidol University, Bangkok, Thailand; 2Chakri Naruebodindra Medical Institute, Faculty of Medicine Ramathibodi Hospital, Mahidol University, Samutprakan, Thailand; 3Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA; 4Clinical Microbiology Laboratory, Department of Pathology, Faculty of Medicine Ramathibodi Hospital, Mahidol University, Bangkok, Thailand Purpose: The incidence of carbapenem-resistant Enterobacteriaceae (CRE) has been increasing worldwide. Ertapenem resistance is mediated by non-carbapenemase mechanisms, and has less of an effect on susceptibility to imipenem and meropenem. This study aimed to study the epidemiology of CRE, and to compare risk factors and related mortality between non-susceptibility to ertapenem alone Enterobacteriaceae (NSEE), with non-susceptibility to other carbapenems (imipenem, meropenem, or doripenem) Enterobacteriaceae (NSOCE) at a tertiary care hospital in Thailand. Methods: All CRE isolated were identified between December 2011 and December 2016. Quarterly incidence rate was estimated. Hospital-wide carbapenem consumption was calculated as defined daily doses (DDD). Relationships between hospital-wide carbapenem consumption and incidence of CRE were tested. Factors associated with NSEE and NSOCE, and risk factors associated with 14- and 30-day mortality in patients with CRE infection were determined. Results: The quarterly CRE incidence increased significantly from 3.37 per 100,000 patient-days in the last quarter of 2011 to 32.49 per 100,000 patient-days in the last quarter of 2016. (P for trend <0.001). Quarterly hospital-wide carbapenem consumption increased 1.58 DDD per 1,000 patient-days (P for trend=0.004). The Poisson regression showed the expected increase of CRE incidence was 1.02 per 100,000 patient-days for a 1 DDD per 1,000 patient-days increase in carbapenem consumption (P<0.001). There were 40 patients with NSEE and 134 patients with NSOCE in the 5-year study period. The NSEE group had significantly lower carbapenem exposure compared with the NSOCE group (adjusted odds ratio: 0.25; P=0.001). No difference in 14-day and 30-day all-cause mortality between the two groups was observed. Conclusion: The incidence of CRE has risen significantly at our institution. Previous carbapenem use was associated with NSOCE. This hospital-wide carbapenem use was significantly associated with the increasing incidence of CRE. Keywords: CRE, risk factors, incidence, carbapenems, antimicrobial stewardshi