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The purpose of this investigation was to develop titanium nitride (TiN)/titanium (Ti) coating on orthodontic nickel–titanium (NiTi) wires and to study the stress corrosion of specimens in vitro , simulating the intra-oral environment in as realistic a manner as possible. TiN/Ti coatings were formed on orthodontic NiTi wires by physical vapor deposition (PVD). The characteristics of untreated and TiN/Ti-coated NiTi wires were evaluated by measurement of corrosion potential ( E corr ), corrosion current densities ( I corr ), breakdown potential ( E b ), and surface morphology in artificial saliva with different pH and three-point bending conditions. From the potentiodynamic polarization and SEM results, the untreated NiTi wires showed localized corrosion compared with the uniform corrosion observed in the TiN/Ti-coated specimen under both unstressed and stressed conditions. The bending stress influenced the corrosion current density and breakdown potential of untreated specimens at both pH 2 and pH 5.3. Although the bending stress influenced the corrosion current of the TiN/Ti-coated specimens, stable and passive corrosion behavior of the stressed specimen was observed even at 2.0 V (Ag/AgCl). It should be noted that the surface properties of the NiTi alloy could determine clinical performance. For orthodontic application, the mechanical damage destroys the protective oxide film of NiTi; however, the self-repairing capacity of the passive film of NiTi alloys is inferior to Ti in chloride-containing solutions. In this study, the TiN coating was found able to provide protection against mechanical damage, while the Ti interlayer improved the corrosion properties in an aggressive environment.

Cellular inflammatory response plays an important role in ischemic brain injury and anti-inflammatory treatments in stroke are beneficial. Dietary supplementation with docosahexaenoic acid (DHA) shows anti-inflammatory and neuroprotective effects against ischemic stroke. However, its effectiveness and its precise modes of neuroprotective action remain incompletely understood. This study provides evidence of an alternative target for DHA and sheds light on the mechanism of its physiological benefits. We report a global inhibitory effect of 3 consecutive days of DHA preadministration on circulating and intracerebral cellular inflammatory responses in a rat model of permanent cerebral ischemia. DHA exhibited a neuroprotective effect against ischemic deficits by reduction of behavioral disturbance, brain infarction, edema and blood-brain barrier disruption. The results of enzymatic assay, Western blot, real-time reverse transcriptase polymerase chain reaction and flow cytometric analysis revealed that DHA reduced central macrophages/microglia activation, leukocyte infiltration and pro-inflammatory cytokine expression and peripheral leukocyte activation after cerebral ischemia. In parallel with these immunosuppressive phenomena, DHA attenuated post-stroke oxidative stress, c-Jun N-terminal kinase (JNK) phosphorylation, c-Jun phosphorylation and activating protein-1 (AP-1) activation but further elevated ischemia-induced NF-E2-related factor-2 (Nrf2) and heme oxygenase-1 (HO-1) expression. DHA treatment also had an immunosuppressive effect in lipopolysaccharide/interferon-γ-stimulated glial cultures by attenuating JNK phosphorylation, c-Jun phosphorylation and AP-1 activation and augmenting Nrf2 and HO-1 expression. In summary, we have shown that DHA exhibited neuroprotective and anti-inflammatory effects against ischemic brain injury and these effects were accompanied by decreased oxidative stress and JNK/AP-1 signaling as well as enhanced Nrf2/HO-1 expression.

Background & Aims Active bleeding is a poor prognostic indicator in patients with acute esophageal variceal bleeding. This study aimed at determining indicators of 6-week re-bleeding and mortality in patients with "active" esophageal variceal bleeding, particularly emphasizing the presenting symptoms and timing of endoscopy to define the treatment strategy. Methods From July 2005 to December 2009, cirrhotic patients with endoscopy-proven active esophageal variceal bleeding were evaluated. Cox proportional hazards regression analysis was used to determine the indicators of 6-week re-bleeding and mortality. Outcome comparisons were performed by Kaplan–Meier method and log rank test. Results In 101 patients, the overall 6-week and 3-month re-bleeding rates were 25.7% (n=26) and 29.7% (n=30), respectively. The overall 6-week and 3-month mortality was 31.7% (n=32) and 38.6% (n=39), respectively. Door-to-endoscopy time (hr), MELD score, and portal vein thrombosis were indicators of 6-week re-bleeding, while hematemesis upon arrival, MELD score, and hepatocellular carcinoma were indicators of 6-week mortality. Overall mortality was poorer in hematemesis than in non-hematemesis patients (39.7% vs. 10.7%, p =0.007). In hematemesis patients, 6-week re-bleeding rate (18.9% vs. 38.9%, p =0.028) and mortality (27% vs. 52.8%, p =0.031) were lower in those with early (⩽12h) than delayed (>12h) endoscopy. In non-hematemesis patients, early and delayed endoscopy had no difference on 6-week re-bleeding rate (17.6% vs. 18.2%, p =0.944) and mortality (11.8% vs. 9.1%, p =0.861). Conclusions It is likely that early endoscopy (⩽12h) is associated with a better outcome in hematemesis patients, but a randomized trial with larger case numbers is required before making a firm conclusion.

Numerous studies have demonstrated that the disease pathogenesis of Japanese encephalitis involves cytokine-mediated bystander damage. The mechanisms involved in the regulation of Japanese encephalitis virus (JEV)-induced cytokine expression are not well defined but rely mainly on the tight regulation of transcription factor NF-κB. The Src-family tyrosine kinases participate in diversity of cellular signaling and have been demonstrated in JEV-infected cells. A direct link leading from Src activation to NF-κB activation in JEV-induced cytokine expression is incompletely understood. Here, we report that Src-related Ras/Raf/extracellular signal-regulated kinase (ERK) cascades participate in NF-κB activation and consequent tumor necrosis factor-alpha (TNF-α) and interleukin-1 beta (IL-1β) expression in JEV-infected microglia. Central microglia were capable of producing TNF-α and IL-1β after JEV infection. However, JEV infection had a negligible effect on triggering TNF-α and IL-1β production by neurons and astrocytes. The expression of TNF-α and IL-1β caused by JEV was accompanied by increased Src phosphorylation, Ras membrane association, Raf serine-338 as well as tyrosine-340 phosphorylation, ERK phosphorylation, NF-κB DNA binding activity, and decreased Raf serine-259 phosphorylation. Pharmacological studies revealed that the integrity of lipid raft and the activation of Src, Ras, Raf, ERK, and NF-κB all contributed to JEV-induced TNF-α and IL-1β expression. Pharmacological and biochemical studies further suggested that Src, upon activation, might transmit signals to the Raf/ERK cascades via Ras-dependent and -independent mechanisms that in turn might lead to NF-κB activation. Overall, our results show that the lipid raft might play a role in mediating JEV-initiated Src/Ras/Raf/ERK/NF-κB signaling and TNF-α/IL-1β expression in microglia.

A near-field ultrasound stimulation system was designed for use in in vitro and in vivo trials. The intensity of ultrasound was studied to optimize the osseointegration of the dental titanium implant into the adjacent bone. MG63 osteoblast-like cells were seeded on commercial purity titanium (CP-Ti) plate, and then sonicated for 3 min/day at a frequency of 1 MHz and intensities of 0.05, 0.15 and 0.30 W/cm(2), using either pulsed or continuous ultrasound. Cells were analyzed to determine viability (inhibition of (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) reduction) and alkaline phosphatase (ALP). Tissue culture was performed in vitro by placing a CP-Ti plate in a cultured rat neonatal calvarial defect in response to ultrasound stimulation. In the in vivo trial, screw-shaped CP-Ti implants were inserted into the metaphysis of rabbit tibia, and then stimulated by ultrasound for 10 min daily for 30 d. All samples were processed for histomorphometric evaluation and analyzed by image system. Color Doppler ultrasonography was inspected to evaluate the supply of blood flow. Pulsed ultrasound groups had higher MTT and ALP than control. Tissue culture indicated that pulsed ultrasound groups promoted cell migration and new bone regeneration more effectively than in the control. In animal study, blood flow and mature type I collagen fibers were more prevalent around titanium implants, and bone formation was accelerated in pulsed ultrasound groups. In conclusion, low-intensity pulsed ultrasound at 0.05-0.3 W/cm(2) may accelerate cell proliferation and promote the maturation of collagen fibers and support osteointegration.

This study attempted to accelerate the peripheral nerve regeneration, using the high outflow rate of asymmetric poly(dl-lactic acid-co-glycolic acid) (PLGA) nerve conduits. Asymmetric PLGA nerve conduits of monomer ratio 85/15 were prepared by immersion-precipitation method to serve as possible materials. In this study, mandrels were immersed into a 20% (wt/wt) of PLGA/1,4-dioxane solution and precipitated in a non-solvent bath followed by freeze-drying. Different concentrations of isopropyl alcohol (95%, 40% and 20%) were used as precipitation baths where non-asymmetric (95%) and asymmetric (40% and 20%) conduits could easily form. The asymmetric nerve conduits that consisted of macrovoids on the outer layer, and interconnected micropores in the inner sublayer, possessed characters of larger outflow rate than inflow rate. The asymmetric conduits were implanted to 10mm right sciatic nerve defects in rats. Autografts, silicone and non-asymmetric PLGA conduits were performed as the control and the contrast groups. Implanted graft specimens of all groups were harvested for histological analysis at 4 and 6 weeks following surgery. The asymmetric PLGA conduits maintained a stable supporting structure and inhibited exogenous cells invasion during entire regeneration process. Asymmetric PLGA conduits were found to have statistically greater number of regenerated axons at the midconduit and distal nerve site of implanted grafts, as compared to the silicone and non-asymmetric groups at 4 and 6 weeks. Of interest was that the results of 4 weeks in asymmetric groups were better than the non-asymmetric groups at 6 weeks in number of axons. According to the results of permeability, the asymmetric structure in the conduit wall seemed to enhance the removal of the blockage of the waste drain from the inner inflamed wound in the early stage, which may have improved the efficacy of the peripheral nerve regeneration. The asymmetric structure could be adequately employed in the future as optimal nerve conduits in peripheral nerve regeneration.

This study attempted to improve the efficacy of peripheral nerve regeneration, using the stimulus of low-intensity ultrasound (US) on poly(DL-lactic acid-co-glycolic acid) (PLGA) nerve guidance conduits seeded with Schwann cells. The possible differences between the ultrasonic effects of biodegradable and nonbiodegradable materials used as conduits were also investigated, by comparison with a group of silicone conduits. The PLGA conduits were seeded with or without Schwann cells (6 x 10(3) cells). All conduits were implanted 10 mm into right sciatic nerve defects in rats and underwent 12 ultrasonic treatment sessions over 2 weeks. Ultrasound was applied at a frequency of 1 MHz and an intensity of 0.2 W/cm2 spatial average temporal peak (SATP) for 5 min/day. Histologic analysis was used to evaluate the recovery of the nerve after 6 weeks. Ultrasonically stimulated animals, especially those whose PLGA conduits, seeded with Schwann cells, exhibited considerably more myelinated axons with a larger mean area at the midconduit of the implanted grafts than those in any other group. Ultrasonic stimulation of a silicone conduit induced the generation of mass fibrous tissues that covered the nerve conduits and retarded axon regeneration. These results showed that ultrasonic stimulation may directly stimulate the seeded Schwann cells within the PLGA conduits to regenerate nerves. Nevertheless, the applying of US may not allow incorporation with the silicone rubber as a material from which to form nerve guidance conduits.

The aim of this study is to prepare networks of Bloom number 300 gelatin and genipin as degradable biomaterials. The cross-linking ability of genipin on gelatin was studied and discs were made from the genipin-fixed gelatin. The swelling ratio, the degree of cross-linking, and the rate of degradation of the discs were measured using ninhydrin assay and differential scanning calorimetry (DSC) experiments. The results indicated that genipin is a good cross-linker for the gelatin. Additionally, varying the concentration of genipin can control the rate of degradation and the degree of cross-linking of the genipin-fixed gelatin. Finally, the concentration of genipin should exceed 0.5% of the overall weight of the gelatin-based material if a complete cross-linking reaction between gelatin and genipin molecules is required.