Effectiveness and safety of Wuling capsule for post stroke depression: A systematic review

SummaryObjectiveTo review the effectiveness and safety of Wuling capsule for post stroke depression (PSD) systematically.MethodsWe searched electronic databases for randomized controlled trials (RCTs) that compared either Wuling capsule with placebo, no treatment or Wuling capsule plus conventional treatment with conventional treatment alone in adults with post stroke depression. Relevant resources were also retrieved. Two reviewers screened the citations, assessed the risk of bias and extracted data independently.ResultsA total of 16 studies involving 1378 patients were identified for this review. There were 3 trials comparing Wuling capsule with no treatment control and 13 trials comparing Wuling capsule plus conventional treatment (Deanxit, Fluoxetine, Sertraline, Paroxetine or Citalopram) with conventional treatment alone. Meta-analyses indicated Wuling capsule used alone or integrated with conventional treatment was effective for PSD in terms of HAMD (Hamilton depression scale) scores, response rate and with less adverse effects, of which, HAMD scores decreased significantly in favor of Wuling capsule from onset time to 1 week (SMD=1.27, 95%CI: 0.71–1.83, P<0.00001), 2 weeks (SMD=1.45, 95%CI: 0.57–2.33, P=0.001), 4 weeks (SMD=2.84, 95%CI: 2.15–3.52, P<0.00001), 6 weeks (SMD=2.70, 95%CI: 2.15–3.24, P<0.00001), and 8 weeks (SMD=4.53, 95%CI: 3.55–5.50, P<0.00001) and overall effect (SMD=2.40, 95%CI: 1.75–3.05, P<0.00001) (SMD=standardized mean difference).ConclusionWuling capsule appeared to present certain antidepressant effect compared to no treatment control. With a combination of several Western medicines, Wuling capsule could be helpful in strengthening efficacy and reducing the incidence of adverse events as an alternative choice in the treatment of PSD. However, due to the limited number of included trials and relatively moderate methodological quality in the majority of studies, further large scale and rigorously designed trials are warranted to confirm the effectiveness and safety of Wuling capsule for post stroke depression

Effects of Vanadium doping on BaFe2As2

We report an investigation of the structural, magnetic and electronic properties of Ba(Fe(1-x)V(x))2As2 using x-ray, transport, magnetic susceptibility and neutron scattering measurements. The vanadium substitutions in Fe sites are possible up to 40\%. Hall effect measurements indicate strong hole-doping effect through V doping, while no superconductivity is observed in all samples down to 2K. The antiferromagnetic and structural transition temperature of BaFe2As2 is gradually suppressed to finite temperature then vanishes at x=0.245 with the emergence of spin glass behavior, suggesting an avoided quantum critical point (QCP). Our results demonstrate that the avoided QCP and spin glass state which were previously reported in the superconducting phase of Co/Ni-doped BaFe2As2 can also be realized in non-superconducting Ba(Fe(1-x)V(x))2As2.Comment: 5 pages, 6 figure

Human Gingiva-Derived Mesenchymal Stem Cells Elicit Polarization of M2 Macrophages and Enhance Cutaneous Wound Healing

Increasing evidence has supported the important role of mesenchymal stem cells (MSCs) in wound healing, however, the underlying mechanism remains unclear. Recently, we have isolated a unique population of MSCs from human gingiva (GMSCs) with similar stem cell-like properties, immunosuppressive, and anti-inflammatory functions as human bone marrow-derived MSCs (BMSCs). We describe here the interplay between GMSCs and macrophages and the potential relevance in skin wound healing. When cocultured with GMSCs, macrophages acquired an anti-inflammatory M2 phenotype characterized by an increased expression of mannose receptor (MR; CD206) and secretory cytokines interleukin (IL)-10 and IL-6, a suppressed production of tumor necrosis factor (TNF)-α, and decreased ability to induce Th-17 cell expansion. In vivo, we demonstrated that systemically infused GMSCs could home to the wound site in a tight spatial interaction with host macrophages, promoted them toward M2 polarization, and significantly enhanced wound repair. Mechanistically, GMSC treatment mitigated local inflammation mediated by a suppressed infiltration of inflammatory cells and production of IL-6 and TNF-α, and an increased expression of IL-10. The GMSC-induced suppression of TNF-α secretion by macrophages appears to correlate with impaired activation of NFκB p50. These findings provide first evidence that GMSCs are capable to elicit M2 polarization of macrophages, which might contribute to a marked acceleration of wound healing. © AlphaMed Press

Metabolically Specific In Situ Fluorescent Visualization of Bacterial Infection on Wound Tissues

The ability to effectively detect bacterial infection in human tissues is important for the timely treatment of the infection. However, traditional techniques fail to visualize bacterial species adhered to host cells in situ in a target-specific manner. Dihydropteroate synthase (DHPS) exclusively exists in bacterial species and metabolically converts p-aminobenzoic acid (PABA) to folic acid (FA). By targeting this bacterium-specific metabolism, we have developed a fluorescent imaging probe, PABA-DCM, based on the conjugation of PABA with a long-wavelength fluorophore, dicyanomethylene 4H-pyran (DCM). We confirmed that the probe can be used in the synthetic pathway of a broad spectrum of Gram-positive and negative bacteria, resulting in a significantly extended retention time in bacterial over mammalian cells. We validated that DHPS catalytically introduces a dihydropteridine group to the amino end of the PABA motif of PABA-DCM, and the resulting adduct leads to an increase in the FA levels of bacteria. We also constructed a hydrogel dressing containing PABA-DCM and graphene oxide (GO), termed PABA-DCM@GO, that achieves target-specific fluorescence visualization of bacterial infection on the wounded tissues of mice. Our research paves the way for the development of fluorescent imaging agents that target species-conserved metabolic pathways of microorganisms for the in situ monitoring of infections in human tissues. </p

Fresh raspberry phytochemical extract inhibits hepatic lesion in a Wistar rat model

Background: Red raspberry possesses potent antioxidant capacity and antiproliferative activity against cancer in vitro. Methods: The objective of this study was to determine the protective effects of raspberry 80% acetone extract in a rat hepatic lesions model induced by diethylnitrosamine (DEN). Rats were treated with the red raspberry extract (0.75, 1.5 or 3.0 g/kg of body weight) by gavage starting 2 h after DEN administration and continuing for 20 weeks. Results: A dose-dependent inhibition by red raspberry extract of DEN-induced hepatic nodule formation which stands for hepatic lesions was observed. Corresponding hepatic nodule incidence rates were 45.0, 40.0, 25.0 and 5.0% in positive control, low, middle and high groups, respectively (P < 0.01 or 0.05). Gross findings, histopathological and ultrastructural evaluations of hepatic lesion were performed on 9, 8, 5 and 1 hepatic nodule in positive control, low, middle and high doses of groups, respectively, identified in rats from the respective groups of 20. A decreasing trend of proportions of hepatocellular carcinoma masses accompanied the increasing doses of red raspberry extract. Conclusions: These findings demonstrate that the potent capacity of red raspberry diet could not only suppress DEN-induced hepatic lesions in rats, but also reduce the definite diagnostic features of neoplasm

Expression of fatty acid related gene promotes astaxanthin heterologous production in Chlamydomonas reinhardtii

Natural astaxanthin is a high-value ketone carotenoid mainly derived from Haematococcus pluvialis, which is an excellent antioxidant for human consumption. To study the role of lipids in accumulation of astaxanthin, the H. pluvialis-derived astaxanthin synthesis pathway genes (β-carotene ketolase gene, BKT and β-carotene hydroxylase gene, BCH) and fatty acid elongation gene (mitochondrial trans-2-enoyl-coa reductase gene, MECR) were heterologously co-expressed in C. reinhardtii. Zeaxanthin, the precursor of astaxanthin synthesis, was significantly increased after BKT and BCH were expressed. In contrast, the α-carotene that competes with astaxanthin synthesis for lycopene decreased significantly. This redistribution of carbon flow was conducive to the synthesis of astaxanthin. In addition, the transformant only expressed astaxanthin metabolism related genes (BKT, BCH) would lead to an increase in total lipid, a decrease in monounsaturated fatty acids and an increase in polyunsaturated fatty acids. On this basis, the expression of MECR gene further increased the total lipid, and the relative content of different fatty acids also changed. The astaxanthin content of algal strains transformed with BKT and BCH genes was nearly 50% higher than that of the wild type. On this basis, the astaxanthin content of transformants expressing MECR gene related to long-chain fatty acid synthesis was increased by 227.5%. In this study, an astaxanthin production model similar to H. pluvialis by combining carotenoid metabolism and fatty acid metabolism was constructed in C. reinhardtii. The results suggest that the increase in astaxanthin is indeed linked to the regulation of fatty acid metabolism, and this link may involve the type of fatty acids and the dynamics of astaxanthin ester in cells. The strategy of promoting the synthesis of fatty acids has potential to achieve efficient production of astaxanthin in C. reinhardtii

Genome-Wide and Differential Proteomic Analysis of Hepatitis B Virus and Aflatoxin B1 Related Hepatocellular Carcinoma in Guangxi, China

Both hepatitis B virus (HBV) and aflatoxin B1 (AFB1) exposure can cause liver damage as well as increase the probability of hepatocellular carcinoma (HCC). To investigate the underlying genetic changes that may influence development of HCC associated with HBV infection and AFB1 exposure, HCC patients were subdivided into 4 groups depending upon HBV and AFB1 exposure status: (HBV(+)/AFB1(+), HBV(+)/AFB1(-), HBV(-)/AFB1(+), HBV(-)/AFB1(-)). Genetic abnormalities and protein expression profiles were analyzed by array-based comparative genomic hybridization and isobaric tagging for quantitation. A total of 573 chromosomal aberrations (CNAs) including 184 increased and 389 decreased were detected in our study population. Twenty-five recurrently altered regions (RARs; chromosomal alterations observed in ≥10 patients) in chromosomes were identified. Loss of 4q13.3-q35.2, 13q12.1-q21.2 and gain of 7q11.2-q35 were observed with a higher frequency in the HBV(+)/AFB1(+), HBV(+)/AFB1(-) and HBV(-)/AFB1(+) groups compared to the HBV(-)/AFB(-) group. Loss of 8p12-p23.2 was associated with high TNM stage tumors (P = 0.038) and was an unfavorable prognostic factor for tumor-free survival (P=0.045). A total of 133 differentially expressed proteins were identified in iTRAQ proteomics analysis, 69 (51.8%) of which mapped within identified RARs. The most common biological processes affected by HBV and AFB1 status in HCC tumorigenesis were detoxification and drug metabolism pathways, antigen processing and anti-apoptosis pathways. Expression of AKR1B10 was increased significantly in the HBV(+)/AFB1(+) and HBV(-)/AFB1(+) groups. A significant correlation between the expression of AKR1B10 mRNA and protein levels as well as AKR1B10 copy number was observed, which suggest that AKR1B10 may play a role in AFB1-related hepatocarcinogenesis. In summary, a number of genetic and gene expression alterations were found to be associated with HBV and AFB1- related HCC. The possible synergistic effects of HBV and AFB1 in hepatocarcinogenesis warrant further investigations