Discrimination and classification of tobacco wastes by identification and quantification of polyphenols with LC–MS/MS

The chemical composition of polyphenols in tobacco waste was identified by HPLC-PDA–ESI/MS/MS and the contents of chlorogenic acids and rutin in 10 varieties of tobacco wastes were determined by HPLC–UV. The relationships between the contents of active polyphenols and the varieties of tobacco wastes were interpreted by hierarchical cluster analysis (HCA) and principal component analysis (PCA). The results showed that 15 polyphenols were identified in a methanolic extract of dried tobacco waste. The tobacco wastes were characterized by high levels of chlorogenic acids (3-CQA, 5-CQA, and 4-CQA) and rutin; their ranges in the 10 tobacco varieties were 0.116–0.196, 0.686–1.781, 0.094–0.192, and 0.413–0.998 %, respectively. According to multivariate statistics models, two active compound variables can be considered important for the discrimination of the varieties of tobacco wastes: chlorogenic acids and rutin. Consequently, samples of 10 tobacco varieties were characterized into three groups by HCA based on the PCA pattern. In conclusion, tobacco waste could be used as a new pharmaceutical material for the production of natural chlorogenic acids and rutin in the ethnopharmacological industry

The interaction between different types of activated RAW 264.7 cells and macrophage inflammatory protein-1 alpha

<p>Abstract</p> <p>Background</p> <p>Two major ways of macrophage (MΦ) activation can occur in radiation-induced pulmonary injury (RPI): classical and alternative MΦ activation, which play important roles in the pathogenesis of RPI. MΦ can produce chemokine MΦ inflammatory protein-1α (MIP-1α), while MIP-1α can recruit MΦ. The difference in the chemotactic ability of MIP-1α toward distinct activated MΦ is unclear. We speculated that there has been important interaction of MIP-1α with different activated MΦ, which might contribute to the pathogenesis of RPI.</p> <p>Methods</p> <p>Classically and alternatively activated MΦ were produced by stimulating murine MΦ cell line RAW 264.7 cells with three different stimuli (LPS, IL-4 and IL-13); Then we used recombinant MIP-1α to attract two types of activated MΦ. In addition, we measured the ability of two types of activated MΦ to produce MIP-1α at the protein or mRNA level.</p> <p>Results</p> <p>Chemotactic ability of recombinant MIP-1α toward IL-13-treated MΦ was the strongest, was moderate for IL-4-treated MΦ, and was weakest for LPS-stimulated MΦ (p < 0.01). The ability of LPS-stimulated MΦ to secrete MIP-1α was significantly stronger than that of IL-4-treated or IL-13-treated MΦ (p < 0.01). The ability of LPS-stimulated MΦ to express MIP-1α mRNA also was stronger than that of IL-4- or IL-13-stimulated MΦ (p < 0.01).</p> <p>Conclusions</p> <p>The chemotactic ability of MIP-1α toward alternatively activated MΦ (M2) was significantly greater than that for classically activated MΦ (M1). Meanwhile, both at the mRNA and protein level, the capacity of M1 to produce MIP-1α is better than that of M2. Thus, chemokine MIP-1α may play an important role in modulating the transition from radiation pneumonitis to pulmonary fibrosis <it>in vivo</it>, through the different chemotactic affinity for M1 and M2.</p

Protection Effect of Zhen-Wu-Tang on Adriamycin-Induced Nephrotic Syndrome via Inhibiting Oxidative Lesions and Inflammation Damage

Zhen-wu-tang (ZWT), a well-known formula in China, is widely used to treat chronic kidney diseases. However, very little information on ZWT’s mechanism of action is currently available. In this study, we investigated the possible protective role and underlying mechanism of ZWT on nephrotic syndrome (NS) induced by Adriamycin (intravenous injection, 6.0 mg/kg) in rats using biochemical and histopathological approaches. ZWT decreased urine protein excretion and the serum levels of total cholesterol, triglycerides, blood urea nitrogen, and creatinine significantly in diseased rats. A decrease in plasma levels of total protein and albumin was also recorded in nephropathic rats. Pathological results show an improved pathological state and recovering glomerular structure in ZWT treatment groups. ZWT decreased renal IL-8 level but increased renal IL-4 level. In addition, rats subjected to ZWT exhibited less IgG deposition in glomerulus compared with model group. RT-PCR results showed that ZWT decreased the mRNA expression of NF-κB p65 and increased the mRNA expression of IκB. Furthermore, ZWT reduced the level of MDA and increased SOD activity. These results demonstrated that ZWT ameliorated Adriamycin-induced NS in rats possibly by inhibiting Adriamycin-induced inflammation damage, enhancing body’s antioxidant capacity, thereby protecting glomerulus from injury

Variants in MME are associated with autosomal-recessive distal hereditary motor neuropathy

© 2019 The Authors. Annals of Clinical and Translational Neurology published by Wiley Periodicals, Inc on behalf of American Neurological Association. Objective: To identify a new genetic cause in patients segregating distal hereditary motor neuropathy (dHMN) with an autosomal recessive pattern. Methods: Whole-exome sequencing was conducted in two siblings and was combined with segregation analysis. Additionally, 83 unrelated dHMN patients with unknown genetic cause were screened. RNA analysis was performed using blood lymphocytes and HEK293 cells transfected with mutant plasmids. Immunohistochemistry and Western blot analysis was applied to the nerve tissue. The enzymatic activities of mutant proteins were measured in the cultured cells to verify the pathogenicity of variants. Results: The clinical features of the patients showed late-onset phenotype of distal motor neuropathy without sensory involvement. We identified that compound heterozygous variants of c.1342C\u27T and c.2071_2072delGCinsTT in the membrane metalloendopeptidase (MME) gene co-segregated with the phenotype in a dHMN family. In an additional group of 83 patients with dHMN, compound heterozygous variants of c.1416+2T\u27C and c.2027C\u27T in MME were identified in one patient. The splice site variant c.1416+2T\u27C results in skipping of exon 13. The stop variant c.1342C\u27T induces mRNA degradation via nonsense-mediated mRNA decay. Transcript levels of MME in the lymphocytes showed no significant differences between the patients and controls. We also identified that MME variants were associated with mild decrease in protein expression in the sural nerve and significant impairments of enzymatic activity. Interpretation: Variants in the MME gene were associated with not only a Charcot-Marie-Tooth neuropathy phenotype but also with an autosomal-recessive dHMN phenotype. Loss of function may play a role in the pathogenesis of dHMN

Psoriasis-associated variant Act1 D10N with impaired regulation by Hsp90

Act1 is an essential adaptor molecule in IL-17-mediated signaling and is recruited to the IL-17 receptor upon IL-17 stimulation. Here, we report that Act1 is a client protein of the molecular chaperone, Hsp90. The Act1 variant (D10N) linked to psoriasis susceptibility is defective in its interaction with Hsp90, resulting in a global loss of Act1 function. Act1-/- mice modeled the mechanistic link between Act1 loss of function and psoriasis susceptibility. Although Act1 is necessary for IL-17-mediated inflammation, Act1-/- mice exhibited a hyper TH17 response and developed spontaneous IL-22-dependent skin inflammation. In the absence of IL-17-signaling, IL-22 is the main contributor to skin inflammation, providing a molecular mechanism for the association of Act1 (D10N) with psoriasis susceptibility

Production of doubly-charged Δ\Delta baryon in e+e−e^{+}e^{-} annihilation at energies from 2.3094 to 2.6464 GeV

The processes $e^{+}e^{-} \to \Delta^{++}\bar{\Delta}^{--}$ and $e^{+}e^{-}\to \Delta^{++} \bar{p} \pi^{-} + c.c.$ are studied for the first time with $179~{\rm pb}^{-1}$ of $e^{+}e^{-}$ annihilation data collected with the BESIII detector at center-of-mass energies from $2.3094$ GeV to $2.6464$ GeV. No significant signal for the $e^{+}e^{-}\to \Delta^{++}\bar{\Delta}^{--}$ process is observed and the upper limit of the Born cross section is estimated at each energy point. For the process $e^{+}e^{-} \to \Delta^{++} \bar{p} \pi^{-} + c.c.$, a significant signal is observed at center-of-mass energies near 2.6454 GeV and the corresponding Born cross section is reported.Comment: 10 pages, 4 figure

Search for an axion-like particle in J/ψJ/\psi radiative decays

We search for an axion-like particle (ALP) $a$ through the process $\psi(3686)\rightarrow\pi^+\pi^-J/\psi$, $J/\psi\rightarrow\gamma a$, $a\rightarrow\gamma\gamma$ in a data sample with $(2708.1\pm14.5)\times10^6$ $\psi(3686)$ events collected by the BESIII detector. No significant ALP signal is observed over the expected background, and the upper limits on the branching fraction of the decay $J/\psi\rightarrow\gamma a$ and the ALP-photon coupling constant $g_{a\gamma\gamma}$ are set at the 95\% confidence level in the mass range of 0.165\leq m_a\leq2.84\,\mbox{GeV}/c^2. The limits on $\mathcal{B}(J/\psi\rightarrow\gamma a)$ range from $8.3\times10^{-8}$ to $1.8\times10^{-6}$ over the search region, and the constraints on the ALP-photon coupling are the most stringent to date for 0.165\leq m_a\leq1.468\,\mbox{GeV}/c^2.Comment: 10 pages, 5 figure

Search for a scalar partner of the X(3872)X(3872) via ψ(3770)\psi(3770) decays into γηη′\gamma\eta\eta' and γπ+π−J/ψ\gamma\pi^{+}\pi^{-}J/\psi

Using a data sample corresponding to an integrated luminosity of 2.93 fb$^{-1}$ collected at a center-of-mass energy of 3.773~GeV with the BESIII detector at the BEPCII collider, we search for a scalar partner of the $X(3872)$, denoted as $X(3700)$, via $\psi(3770)\to \gamma\eta\eta'$ and $\gamma\pi^{+}\pi^{-}J/\psi$ processes. No significant signals are observed and the upper limits of the product branching fractions ${\cal B}(\psi(3770)\to\gamma X(3700))\cdot {\cal B}(X(3700)\to \eta\eta')$ and ${\cal B}(\psi(3770)\to\gamma X(3700))\cdot {\cal B}(X(3700)\to\pi^{+}\pi^{-}J/\psi)$ are determined at the 90\% confidence level, for the narrow $X(3700)$ with a mass ranging from 3710 to 3740 MeV/$c^2$, which are from 0.8 to 1.8 $(\times 10^{-5})$ and 0.9 to 3.4 $(\times 10^{-5})$, respectively

Measurement of branching fractions of Λc+\Lambda_{c}^{+} decays to Σ+K+K−\Sigma^{+} K^{+} K^{-}, Σ+ϕ\Sigma^{+}\phi and Σ+K+π−(π0)\Sigma^{+} K^{+} \pi^{-}(\pi^{0})

Based on 4.5 fb$^{-1}$ data taken at seven center-of-mass energies ranging from 4.600 to 4.699 GeV with the BESIII detector at the BEPCII collider, we measure the branching fractions of $\Lambda_{c}^{+}\rightarrow\Sigma^{+}+hadrons$ relative to $\Lambda_{c}^{+}\rightarrow \Sigma^+ \pi^+ \pi^-$. Combining with the world average branching fraction of $\Lambda_{c}^{+}\rightarrow \Sigma^+ \pi^+ \pi^-$, their branching fractions are measured to be $(0.377\pm0.042\pm0.018\pm0.021)\%$ for $\Lambda_{c}^{+}\rightarrow\Sigma^{+} K^{+} K^{-}$, $(0.200\pm0.023\pm0.010\pm0.011)\%$ for $\Lambda_{c}^{+}\rightarrow\Sigma^{+} K^{+} \pi^{-}$, $(0.414\pm0.080\pm0.029\pm0.023)\%$ for $\Lambda_{c}^{+}\rightarrow\Sigma^{+}\phi$ and $(0.197\pm0.036\pm0.008\pm0.011)\%$ for $\Lambda_{c}^{+}\rightarrow\Sigma^{+}K^{+} K^{-}$(non-$\phi$). In all the above results, the first uncertainties are statistical, the second are systematic and the third are from external input of the branching fraction of $\Lambda_{c}^{+}\rightarrow \Sigma^+ \pi^+ \pi^-$. Since no signal for $\Lambda_{c}^{+}\rightarrow\Sigma^{+} K^{+} \pi^{-}\pi^{0}$ is observed, the upper limit of its branching fraction is determined to be 0.11\% at the 90$\%$ confidence level