Nanostructured-lipid carriers-Chitosan hydrogel beads carrier system for loading of resveratrol: A new method of topical application.

The aim of this study was to develop nanostructured-lipid carriers (NLC) encapsulated by Chitosan hydrogel beads for the efficient topical carrier. Dynamic light scattering (DLS), X-ray diffraction (XRD), Differential scanning calorimetry (DSC), and attenuated total reflectance-Fourier transform infrared spectroscopy (ATR-FTIR) were conducted to study the influence of the encapsulation on the characteristic of resveratrol-loaded NLC, and the results showed that there was no impact on resveratrol-loaded NLC. Chitosan hydrogel beads could significantly improve the physical stability of resveratrol-loaded NLC. In vitro release study revealed that resveratrol-loaded NLC-Chitosan hydrogel beads had a more significant sustained-release effect on resveratrol. In vitro transdermal studies suggested that the skin permeation of resveratrol was promoted by the effect of Chitosan hydrogel beads and increased resveratrol distribution in the skin. In vitro cytotoxicity showed that resveratrol-loaded NLC-Chitosan hydrogel beads did not exert a hazardous effect on L929 cells. Hence, NLC-Chitosan hydrogel beads might be a promising method for topical applications of resveratrol.

Residues and chiral signatures of organochlorine pesticides in sediments from Xiangshan Bay, East China Sea.

Residual levels and enantiomeric signatures of hexachlorocyclohexanes (HCHs) and dichlorodiphenyltrichloroethanes (DDTs) in surface sediments from Xiangshan Bay, East China Sea were investigated. The concentrations of ∑HCHs (sums of α-, ß-, γ-, and δ-HCH) and ∑DDTs (sums of p, p'-DDT, p, p'-DDD,p, p'-DDE, o, p'-DDT, and o, p'-DDD) ranged from 0.14 to 0.67 ng g⁻¹ and 0.61 to 22.38 ng g⁻¹, respectively. A slight potential health risk to the organism was then indicated for the residual levels of DDTs according to the ERL/ERM guidelines. Moreover, the predominant ß-HCH implied that the technical HCH contamination was mainly due to the historical usage. But the high ratio of DDT/∑DDTs depicted a cocktail input pattern of fresh and weathered DDTs. The enantiomeric fractions (EFs) of α-HCH, o, p'-DDT, and o, p'-DDD were also determined. The degradation of α-HCH was enantioselective in all sediments samples, resulting in an enrichment of (-)-enantiomers. However, the racemic residues of o, p'-DDT and o, p'-DDD were observed in all sediments samples.

Refeeding Hypophosphatemia in Patients Receiving Parenteral Nutrition: Prevalence, Risk Factors, and Predicting Its Occurrence.

BACKGROUND: Patients receiving parenteral nutrition (PN) support may develop refeeding hypophosphatemia (RH), and its prevalence is highly variable in the literature. Identifying at-risk patients is crucial to minimize clinical complications. The National Institute for Health and Clinical Excellence (NICE) guidelines are used widely to assess the risk of RH, but they lack validation. We aim to (1) identify the prevalence of RH by multiple diagnostic criteria; (2) assess the predictive ability of the NICE guidelines for RH; and (3) identify important risk factors for RH and evaluate their predictive abilities for RH in a new model. METHODS: This is a single-center retrospective study on adult patients with PN ≥48 hours. Prevalence of RH was determined by 4 established diagnostic criteria. Prognostic accuracy of the NICE guidelines were assessed by the area under the receiver operating characteristic (ROC) curve. Multivariable logistic regressions were performed to develop a new risk-assessment model. RESULTS: Of 149 enrolled patients, 23%-48% (35 to 72 of 149 patients) developed RH (depending on the diagnostic criteria used). The NICE guidelines demonstrated poor discrimination across all diagnostic criteria (ROC, 0.43-0.53). Critical illness, the use of diuretics, and hypomagnesemia prior to PN were independently associated with RH. These risk factors formed the new model for predicting RH and had good discrimination (ROC 0.74; 95% confidence interval, 0.66-0.82). CONCLUSION: Prevalence of RH varied according to established diagnostic criteria. The current NICE guidelines poorly predict the occurrence of RH, and modification is likely beneficial. A new risk-assessment model was developed; nevertheless, further validation is required.

Infection with Hematodinium sp. in mud crabs Scylla serrata cultured in low salinity water in southern China.

Dinoflagellates in the genus Hematodinium are important parasites of wild marine crustaceans, but are rarely reported in waters with salinities < 11 or from cultured crustaceans. Since 2005, the mud crab Scylla serrata, which is cultured along the coast of southeastern China, has suffered from an acute epizootic locally known as 'milky disease'. The disease mainly occurrs from September to November. The clinical signs are largely similar to those of crabs suffering from bitter crab disease (BCD) or pink crab disease (PCD), which are caused by parasites of the genus Hematodinium. To determine whether Hematodinium sp. is a pathogen of milky disease, histopathological examinations of mud crab haemolymph, hepatopancreas, heart and gill were conducted. In addition, previously reported Hematodinium molecular probes were applied to infected material. The results indicate that Hematodinium sp. is at least one of the main pathogens of milky disease. The salinity in S. serrata culture ponds was < 9. To our knowledge, this is the first report showing the Hematodinium infection in a cultured crustacean in low salinity water.

GLYX-13, a NMDA Receptor Glycine-Site Functional Partial Agonist, Attenuates Cerebral Ischemia Injury In Vivo and Vitro by Differential Modulations of NMDA Receptors Subunit Components at Different Post-Ischemia Stage in Mice.

Excessive activation of NMDA receptors (NMDARs) is implicated in pathological synaptic plasticity also known as post-ischemic long-term potentiation (i-LTP) which was produced by glutamate mediated excitotoxicity after stroke. In the past decades, many NMDARs inhibitors failed in clinical investigations due to severe psychotomimetic side effects. GLYX-13 is a NMDAR modulator with glycine site partial agonist properties and has potential protective effects on ischemic neuronal death. However, the underlying molecular mechanism of GLYX-13 attenuating the ischemic neuronal damage remains elusive. Our study was conducted to examine the molecular, cellular and behavioral actions of GLYX-13 in stroke, and further characterize the mechanism underlying the neuroprotective actions via modulation of the NMDAR subunit composition. In present study we found that in vitro oxygen-glucose deprivation (OGD) stroke model, GLYX-13 blocked i-LTP and restored the ratio of NR2A/NR2B subunit composition. The glycine site of NMDARs full coagonist D-serine completely blocked the effects of GLYX-13 on i-LTP. Besides, in vivo middle cerebral artery occlusion (MCAO) model, GLYX-13 decreased the cerebral infarct volume and reduced injury of hippocampus. Western analysis showed that GLYX-13 down-regulated the expression of phosphorylated NR2B (Tyr1472) and up-regulated phosphorylated NR2A (Tyr1325). Furthermore, GLYX-13 treatment along with NR2B specific antagonist (Ro256981) failed to exhibit any additional neuro-protective effects, whereas the application of NR2A antagonist (NVP-AAM007) abolished the neuroprotective effects of GLYX-13, which suggested that the protective action of GLYX-13 should be by its regulation of NMDAR subunit components. Our study provides important insights on the potential protective mechanism of GLYX-13 in ischemia and proposes the glycine site of NMDARs as a novel target for developing therapeutic strategies to store synaptic function in stroke.

miRNA-155 upregulation and complement factor H deficits in Down's syndrome.

Down's syndrome, a congenital disorder associated with cognitive impairment and early-onset Alzheimer's disease, is a progressive genetic pathology resulting from full or partial triplication of chromosome 21. Down's syndrome brain is typified by activated microglia, increases in inflammatory signaling, and an aberrant immune system. In these studies, a screening of micro-RNA (miRNA) from Down's syndrome brain and peripheral tissues indicated an upregulation of a chromosome 21-encoded miRNA-155 and a decrease in the abundance of the miRNA-155 mRNA target complement factor H (CFH), an important repressor of the innate immune response. Stressed primary human neuronal-glial cells indicated both miRNA-155 increase and CFH downregulation, an effect that was reversed using anti-miRNA-155. These findings suggest that immunopathological deficits associated with Down's syndrome can, in part, be explained by a generalized miRNA-155-mediated downregulation of CFH that may contribute to both brain and systemic immune pathology.