Parkinson’s disease (PD) is a multifactorial neurodegenerative disease manifesting mitochondrial damages and neuroinflammation. Qi is defined as a natural power that can regulate the energy flow in Oriental medicine, whereas mitochondria generate energy power in Western medicine. We investigated whether Qi-enhancing component in Oriental herb medicines could activate mitochondrial activities. Quercetin was found as a major bioactive compound in most Qi-activating Oriental herb medicines through online search for active compounds in several Oriental Medicine databases. We then investigated if quercetin could reverse 1-methyl-4-phenylpyridinium (MPP+)-induced mitochondrial dysfunction and lipopolysaccharide (LPS)-induced neuroinflammation. Mitochondrial activities were monitored based on complex 1 NADH dehydrogenase activities, ATP contents, mitochondrial membrane potential, cellular/mitochondrial reactive oxygen species, and oxygen consumption rate in SH-SY5Y cells. Quercetin at concentration up to 20 µg/ml was not cytotoxic to SH-SY5Y cells. Pre-treatment with quercetin significantly protected mitochondrial damages in 1 mM MPP+- or 100 ng/ml LPS-treated cells. Quercetin increased expression levels of tyrosine hydroxylase and mitochondria controlling proteins. When in vivo effects of quercetin were assessed by immunohistochemical staining of tissue sections from LPS-injected mice brains, quercetin reduced the activation of microglia and astrocytes in the hippocampus and substantia nigra of LPS-injected mice. Our data suggest that Qi-activating quercetin might be therapeutically effective for neuroinflammation-mediated neurodegeneration by alleviating mitochondrial damages.Bimetallic nanomaterials, which exhibit a combination of the properties associated with two different metals, have enabled innovative applications in nanoscience and nanotechnology. Here, we introduce the fabrication of dendritic Au/Ag bimetallic nanostructures for surface-enhanced Raman scattering (SERS) and catalytic applications. The dendritic Au/Ag bimetallic nanostructures were prepared by combining the electrochemical deposition and replacement reaction. The formation of Au nanoparticle shell on the surface of Ag dendrites greatly improves the stability of dendritic nanostructures, followed by a significant SERS enhancement. In addition, these dendritic Au/Ag bimetallic nanostructures are extremely efficient in degrading 4-nitrophenol (4-NP) compared with the initial dendritic Ag nanostructures. These experimental results indicate the great potential of the dendritic Au/Ag bimetallic nanostructures for the development of excellent SERS substrate and highly efficient catalysts.Shiga toxin-producing Escherichia coli (STEC) pathotype secretes two types of AB5 cytotoxins (Stx1 and Stx2), responsible for complications such as hemorrhagic colitis (HC) and hemolytic uremic syndrome (HUS) in infected patients, which could lead to sequels and death. Currently, there is no effective treatment against the cytotoxic effect of these toxins. However, in order to approve any therapy molecule, an animal experiment is required in order to evaluate the efficacy and safety of therapeutic approaches. The use of alternative small host models is growing among human infectious disease studies, particularly the vertebrate zebrafish model, since relevant results have been described for pathogen-host interaction. In this sense, the present work aimed to analyze the toxic effect of Shiga toxins in zebrafish embryo model in order to standardize this method in the future to be used as a fast, simple, and efficient methodology for the screening of therapeutic molecules. Herein, we demonstrated that the embryos were sensitive in a dose-dependent manner to both Stx toxins, with LD50 of 22 μg/mL for Stx1 and 33 μg/mL for Stx2, and the use of anti-Stx polyclonal antibody abolished the toxic effect. Therefore, this methodology can be a rapid alternative method for selecting promising compounds against Stx toxins, such as recombinant antibodies.Assisted reproduction technologies have substantially advanced since the birth of the first in vitro fertilization baby, and innovations within in vitro fertilization laboratories have been of paramount importance for the overall assisted reproduction technology success rates. However, one of the milestones in the history of in vitro fertilization is irrefutably the introduction of conventional ovarian stimulation. The objective of the present review is to provide an update on conventional ovarian stimulation, by giving an overview of treatment milestones, together with the latest innovations currently being investigated. The realization of an assisted reproduction technology treatment depends on many steps that can be medically manipulated and must be harmoniously combined, starting from the follicular phase and ending with luteal phase support. New technologies in the pharmaceutical sector are fundamental to optimize efficiency and tailor treatment approaches to individual needs. The present review aims to offer physicians a useful summary of the more recent publications and to facilitate the translation of research findings into daily clinical practice.Practices of Provider-Initiated HIV Testing and Counseling (PITC) remains suboptimal in Côte d’Ivoire. The aim of this survey was to identify the practices and obstacles to PITC among healthcare professionals in Côte d’Ivoire. A nationally representative cross-sectional survey was conducted in 2018 by telephone among three separate samples of midwives, nurses and physicians practicing in Côte d’Ivoire. The number of HIV tests proposed during consultation in the month preceding the survey was collected for each professional. Factors associated with the number of proposed tests were identified through ordinal logistic regression models. A total of 298 midwives, 308 nurses and 289 physicians were interviewed. Midwives proposed the test more frequently, followed by nurses and physicians. Among midwives, a higher number of proposed tests was associated with the perception that HIV testing does not require specific consent compared to other diseases (aOR 4.00 [95% CI 1.37-14.29]). Among nurses, having received HIV training and the presence of community HIV counselors were associated with a higher number of proposed tests (aOR 2.01 [1.31-3.09] and aOR 1.75 [1.14-2.70], respectively). For physicians, the presence of a voluntary testing center was associated with a higher number of proposed tests (aOR 1.69 [1.01-2.86]). PITC practices and barriers differed across professions. Beyond improving environmental opportunities such as dedicated staff or services, strengthening the motivations and capabilities of healthcare professionals to propose testing could improve PITC coverage.Activation of hepatic stellate cells (HSCs) is a prominent driver of liver fibrosis. This study was designed to investigate the effect of exosomes derived from natural killer (NK) cells on HSC activation and liver fibrosis. The exosomes were isolated from NK-92MI cells (NK-Exo) and identified by transmission electron microscopy, nanoparticle tracking analysis, and western blot. Then NK-Exo was administered into TGF-β1-treated LX-2 cells (human HSC line) and mice with CCl4-induced liver fibrosis. LX-2 cell proliferation was determined by CCK-8 assay. The levels of α-SMA and CoL1A1 were measured by qRT-PCR and western blot to evaluate HSC activation. Serum levels of AST and ALT were measured. Hematoxylin-eosin, Masson staining, and Sirius Red staining were performed to assess the pathological changes and collagen deposition. Cell supernatant derived from NK-92MI cells inhibited TGF-β1-induced HSC proliferation and activation in LX-2 cells, and this effect was counteracted by the exosome inhibitor GW4869. Further assays confirmed that NK-Exo treatment significantly inhibited TGF-β1-induced HSC proliferation and activation. Moreover, NK-Exo administration alleviated CCl4-induced liver fibrosis in mice. NK-Exo inhibited TGF-β1-induced HSC activation and CCl4-induced liver fibrosis.A new series of tetrahydroacridine derivatives with the fluorobenzoyl moiety was synthesized and evaluated for cytotoxic activity against lung cancer cell lines A549 and colorectal cancer HT29. The cytotoxic activity of the compounds was compared on the somatic cell line-EAhy926. Compounds showed high cytotoxic activity on A549 cells (IC50 183.26-68.07 μM) and HT29 cells (IC50 68.41-19.70 μM), higher than controls-etoposide (IC50 451.47 μM) toward A549 and 5-fluorouracil (IC50 1626.85 μM) against HT29. Derivative 4 was the most cytotoxic to A549, whereas for the cell lines HT29 compound 6. Selected compounds showed similar cytotoxicity to the EAhy926 cell line (IC50 about 50 μM). In the hyaluronidase inhibition assay, all compounds exhibited anti-inflammatory activity, including 4 exhibiting the best inhibitory activity-IC50 of 52.27 μM when the IC50 heparin was 56.41 μM. Mathematical modeling was performed to determine LD50 after intraperitoneal, oral, intravenous and subcutaneous administration and to predict potential mutagenicity and carcinogenicity of the compounds analyzed. Obtained results showed that tested derivatives are slightly toxic compounds, and LD50 values (mg/kg) ranged from 680 to 1200 (oral rat model), the analyzed compounds have low mutagenic potential, and differences between derivatives are insignificant and very low probability of carcinogenicity. To confirm mathematical calculations, an in vivo test was carried out on a laboratory mouse model for two selected compounds. It allowed to qualify compounds 6 to category 4 of the GHS scale, and 4 to category 3 of the GHS scale.Previous studies have shown that some specific long non-coding RNAs are dysregulated in vascular walls and abnormally expressed in vascular disease. LncRNA HLA complex group 18 (HCG18) is a member of the HLA complex group, which has been rarely investigated in human diseases. In this study, we aimed to investigate the role of HCG in vascular smooth muscle cells. HCG18 was over-expressed by adenovirus transfection and knocked down in vascular smooth muscle cells by shRNA. Cell proliferation was detected by CCK-8 assays. Flow cytometry was employed to test the impacts of HCG18 on vascular smooth muscle apoptotic cells. The expression of associated genes in protein and mRNA levels was detected by western blotting, immunofluorescence and qRT-PCR. The interactions between HCG18 and fused in sarcoma (FUS) were confirmed by RNA EMSA and RIP assays. The expression of serum HCG18 was decreased in hypertensive patients and PDGF-BB-treated vascular smooth muscle cells. HCG18 inhibited proliferation and induced apoptotic cells in vascular smooth muscle cells. In addition, we also found that HCG18 can inhibit vascular smooth muscle cell phenotypic switching from a contractile to a secretory phenotype. Finally, our results showed that HCG18 enhanced apoptotic cells by directly binding with FUS. Our findings reveal that HCG18 is involved in the regulation of proliferation, apoptosis and the expression levels of markers of the contractile and synthetic phenotype.We have computed the low energy minima for the two endomorphin peptides, N-acetyl-Tyr-Pro-Trp-Phe-NHCH3 (endomorphin 1) and Tyr-Pro-Phe-Phe-NHCH3 (endomorphin 2) in aqueous solution. These peptides block pain without inducing the harmful side effects of the opiates that bind to the same mu opiate receptor but have short half lives. From over 1000 starting conformations for each peptide, we find less than 200 low energy structures whose conformational energies were ≤ 5 kcal/mole of the energy of the global minimum. The most probable conformations calculated using the Boltzmann distribution for both peptides were similar to one another. Using the letter representation for backbone conformational states, these most probable structures were D A E E for endomorphin 1 and E A E E for endomorphin 2. Both of these structures form reverse turns at Pro 2-Trp (Phe) 3 resulting in the juxtaposition of the aromatic rings of Tyr 1 and Phe 4. The Trp residue of endomorphin 1 points to the back of the reverse turn. These features may be useful in the design of non-peptide analogues that will have longer half-lives than the peptides.