Fabrication of a ternary biocomposite film based on polyvinyl alcohol, cellulose nanocrystals, and silver nanoparticles for food packaging.

Silver nanoparticles (AgNPs) were loaded on deprotonated cellulose nanocrystals (CNCd) and incorporated into polyvinyl alcohol (PVA) to develop novel active food packaging films. The AgNPs were fabricated using the liquid phase chemical reduction method using the sodium borohydride reductant of AgNO3. The analysis using X-ray diffraction (XRD), Fourier transform infrared spectroscopy (FT-IR), Thermogravimetric analysis (TGA), Differential scanning calorimetry (DSC), and Ultraviolet-visible spectroscopy (UV-Vis) showed that the CNCd surface had a homogeneous distribution of AgNPs with a diameter of about 100 nm. Additionally, CNCd/Ag was successfully incorporated into the PVA film. The developed PVA/CNCd/Ag film showed significantly improved mechanical properties, thermal stability, and UV barrier properties compared to a neat PVA film. The PVA/CNCd/Ag composite film could significantly preserve bananas for 14 days, preventing deterioration and allowing extended storage periods. This composite film generally shows promise in food packaging and prolongs food's shelf life.

Mucosal adjuvant activity of cholera toxin requires Th17 cells and protects against inhalation anthrax.

Cholera toxin (CT) elicits a mucosal immune response in mice when used as a vaccine adjuvant. The mechanisms by which CT exerts its adjuvant effects are incompletely understood. We show that protection against inhalation anthrax by an irradiated spore vaccine depends on CT-mediated induction of IL-17-producing CD4 Th17 cells. Furthermore, IL-17 is involved in the induction of serum and mucosal antibody responses by CT. Th17 cells induced by CT have a unique cytokine profile compared with those induced by IL-6 and TGF-beta, and their induction by CT requires cAMP-dependent secretion of IL-1beta and beta-calcitonin gene-related peptide by dendritic cells. These findings demonstrate that Th17 cells mediate mucosal adjuvant effects of CT and identify previously unexplored pathways involved in Th17 induction that could be targeted for development of unique mucosal adjuvants.

Prognostication in Anoxic Brain Injury.

Cardiac arrest is a common cause of coma with frequent poor outcomes. Palliative medicine teams are often called upon to discuss the scope of treatment and future care in cases of anoxic brain injury. Understanding prognostic tools in this setting would help medical teams communicate more effectively with patients' families and caregivers and may promote improved quality of life overall. This article reviews multiple tools that are useful in determining outcomes in the setting of postarrest anoxic brain injury.

Long-term outcome of biologic graft: a case report.

INTRODUCTION: Biologic grafts have been shown to support tissue regeneration in various animal models. Very few reports in the literature exist to show tissue remodeling in patients after placement of a biologic graft. CASE PRESENTATION: We report the case of a 69-year-old Caucasian man with a history of small bowel carcinoid resection and concurrent recurrent ventral hernia repair with component separation and underlay biologic graft placement who underwent re-operation for metastatic carcinoid tumor to his liver. Complete incorporation of the biologic graft was observed. Tissue analysis of the incised midline fascia revealed tissue remodeling at the site of the previous abdominal wall defect. CONCLUSION: Placement of a biologic graft in ventral hernia repair supports tissue regeneration similar to that previously reported in animal models.

Interleukin 1 receptor signaling regulates DUBA expression and facilitates Toll-like receptor 9-driven antiinflammatory cytokine production.

The interleukin 1 receptor (IL-1R) and the Toll-like receptors (TLRs) are highly homologous innate immune receptors that provide the first line of defense against infection. We show that IL-1R type I (IL-1RI) is essential for TLR9-dependent activation of tumor necrosis factor receptor-associated factor 3 (TRAF3) and for production of the antiinflammatory cytokines IL-10 and type I interferon (IFN). Noncanonical K63-linked ubiquitination of TRAF3, which is essential for type I IFN and IL-10 production, was impaired in Il1r1(-/-) CD11c(+) dendritic cells. In contrast, degradative ubiquitination of TRAF3 was not affected in the absence of IL-1R1 signaling. Deubiquitinating enzyme A (DUBA), which selectively cleaves K63-linked ubiquitin chains from TRAF3, was up-regulated in the absence of IL-1R1 signaling. DUBA short interference RNA augmented the TLR9-dependent type I IFN response. Mice deficient in IL-1RI signaling showed reduced expression of IL-10 and type I IFN and increased susceptibility to dextran sulphate sodium-induced colitis and failed to mount a protective type I IFN response after TLR9 ligand (CpG) administration. Our data identifies a new molecular pathway by which IL-1 signaling attenuates TLR9-mediated proinflammatory responses.

Conventional dendritic cells regulate the outcome of colonic inflammation independently of T cells.

We explored the physiological role of conventional dendritic cells (cDCs) in acute colitis induced by a single cycle of dextran sodium sulfate administration. Depending on their mode of activation and independently of T cells, cDCs can enhance or attenuate the severity of dextran sodium sulfate-induced colitis. The latter beneficial effect was achieved, in part, by IFN-1 induced by Toll-like receptor 9-activated cDCs. IFN-1 inhibits colonic inflammation by regulating neutrophil and monocyte trafficking to the inflamed colon and restraining the inflammatory products of tissue macrophages. These data highlight a novel role of cDCs in the regulation of other innate immune cells and position them as major players in acute colonic inflammation.