Confronting pentaquark photoproduction with new LHCb observations

The newly measurement of production fractions of $P_c$ states by LHCb collaboration have put restriction on their branching ratios of $J/\psi p$ decay, thus constraining their photoproduction in $\gamma p\to J/\psi p$ reaction. We show the tension between LHCb results and the current experiments in search of $P_c$ photoproduction. We also find that the present information of branching ratios of $P_c\to J/\psi p$ has already confronted sharply with the models which study the nature of $P_c$

Data driven isospin analysis of timelike octet baryons electromagnetic form factors and charmonium decay into baryon-anti-baryon

Inspired by the recent precise data, we perform model-independently an isospin decomposition of the timelike octet baryons electromagnetic form factors. As noted in our previous work, the relative magnitude of isoscalar and isovector component is determined with the input of data on various isospin channels. Herein we further assert that {their relative phase can be constraint by the phase difference of oscillatory modulation of effective form factors} between isospin channels. The framework is extended to analyze the data of differential cross sections and applied to the form factors of nucleon and hyperons with detail and isospin non-conservation of charmonium decay into baryon-anti-baryon as well. We address that isospin analysis is meaningful when the isospin broken scale is compared to or smaller than the uncertainties of data.Comment: 11 pages, 7 figure

J/ψ→ppˉϕJ/\psi \rightarrow p\bar{p}\phi decay in the isobar resonance model

Based on the effective Lagrangian approach, the $J/\psi \to p \bar{p} \phi$ decay is studied in an isobar resonance model with the assumption that the $\phi$-meson is produced from intermediate nucleon resonances. The contributions from the $N^*_{1/2^-}(1535)$, $N^*_{3/2^+}(1900)$, $N^*_{1/2^-}(2090)$ and $N^*_{1/2^+}(2100)$ states are considered. In terms of the coupling constants $g^{2}_{\phi N N^{*}}$ and $g^{2}_{\phi N N^{*}}$ extracted from the data of the partial decay widths of the $N^*$s to the $N\pi$ channel, the reaction cross section of the $\pi^{-}p\rightarrow n\phi$ process and the partial decay widths of the $J/\psi\rightarrow p\bar{p}\eta$ and $J/\psi\rightarrow p\bar{n}\pi^{-}$ processes, respectively, the invariant mass spectrum and the Dalitz plot for $J/\psi \to p \bar{p} \phi$ are predicted. It is shown that there are two types of results. In the type I case, a large peak structure around 2.09GeV implies that a considerable mount of $N\phi$ or $qqqs\bar s$ component may exist in the narrow-width $N^*_{1/2^-}(2090)$ state, but for the wide-width $N^*_{1/2^+}(2100)$ state, it has little $qqqs\bar s$ component. In the type II case, a small peak around 2.11GeV may only indicate the existence of a certain mount of $p\phi$ or $qqqs\bar s$ component in the narrow-width $N^*_{1/2^+}(2100)$ state, but no information for the wide-width $N^*_{1/2^-}(2090)$ state. Further BESIII data with high statistics would help us to distinguish the strange structures of these $N^*$s

Rotective effect of Fengliao-Changweikang extracts, a traditional Chinese herbal medicine formula,on mucosa in rat with chronic gastritis

Background: Fengliao-Changwei-Kang(FCK), the Chinese patent drug, is a famous traditional Chinese herbal medicine formula. It has a significant effect on the clinic treatment of gastrointestinal diseases  including gastritis, enteritis and diarrhea for many years. However, there is few research on the  protective effects of FCK on the gastric mucosa of chronic gastritis (CG) model rat. Objective: The present study aimed to explore the effects of FCK extract on mucosa in rats with Chronic Gastritis.Materials and Methods: 50 SD mice were randomly divided into 5 groups with 10 in each group（five per sex). The groups are respectively control group, model group, low, middle and high FCK extracts (FCK I, II and III) group. The CG rat model was induced by synthetic methods. FCK I, II and III group were  administrated with FCK extracts at 2.16g• kg, 4.32g• kg, 8.94g• kg once per day for 21 consecutive  days, and the control group and model group were administrated the same volume of distilled water at 10mL/kg once per day. 16 hours after the last administration, the rats were anesthetized and their blood and stomach were drawn from vena cava and abdominal cavity. The serum levels of EGF was measured by enzyme linked immunosorbent assay(ELISA) method, the expression of growth factor receptor (EGFR) in gastric mucosa was detected by immunohistochemical method, and the mRNA expressions of NF-κB p65 was detected in-situ hybridization.Results: The inflammation grades and the expressions of NF-κB p65 mRNA in gastric mucosa of the model group were markedly higher than those of the control group (P<0.05). The inflammation grades of gastric mucosa and the expressions of NF-κB p65 mRNA in gastric mucosa the FCK extract group are significantly lower than those of the model group, and the FCK extract group at 8.64g/kg could greatly increase the serum levels of EGF and the expressions of EGFR in gastric mucosa. High EGF level was found in FCK extract group at 4.32g/kg, but low in FCK extract groups at 2.16g/kg. There were no marked differences among the rats from control group, model group and FCK extract group on ratio of Ll/L2 (P>0.05).Conclusions: FCK extract could alleviate mucosal inflammation by down regulating the expressions of NF-κB p65 mRNA and promote tissue repair by up regulating EGFR expression in gastric mucosa cell.Keywords: chronic gastritis; fengliao-changwei-kang extract; epidermal growth factor receptor; nuclear factor kappa B

Brain derived neurotrophic factor (BDNF) contributes to the pain hypersensitivity following surgical incision in the rats

<p>Abstract</p> <p>Background</p> <p>The pathogenic role of brain derived neurotrophic factor (BDNF) in the incisional pain is poorly understood. The present study explores the role of the BDNF in the incision-induced pain hypersensitivity.</p> <p>Methods</p> <p>A longitudinal incision was made in one plantar hind paw of isoflurane-anesthetized rats. Dorsal root ganglias (DRG) and spinal cords were removed at various postoperative times (1–72 h). Expression pattern of BDNF was determined by immunohistochemistry and double-labeling immunofluorescence. Lidocaine-induced blockade of sciatic nerve function was used to determine the importance of afferent nerve activity on BDNF expression in the DRG and spinal cord after incision. BDNF antibody was administered intrathecally (IT) or intraperitoneal (IP) to modulate the spinal BDNF or peripheral BDNF after incision.</p> <p>Results</p> <p>After hind-paw incision, the BDNF was upregulated in the ipsilateral lumbar DRG and spinal cord whereas thoracic BDNF remained unchanged in response to incision. The upregulated BDNF was mainly expressed in the large-sized neurons in DRG and the neurons and the primary nerve terminals in the spinal cord. Sciatic nerve blockade prevented the increase of BDNF in the DRG and spinal cord. IT injection of BDNF antibody greatly inhibited the mechanical allodynia induced by incision whereas IP administration had only marginal effect.</p> <p>Conclusion</p> <p>The present study showed that incision induced the segmental upregulation of BDNF in the DRG and spinal cord through somatic afferent nerve transmission, and the upregulated BDNF contributed to the pain hypersensitivity induced by surgical incision.</p

Expression of telomerase inhibits hydroxyl radical-induced apoptosis in normal telomerase negative human lung fibroblasts

AbstractIn tumor cells telomerase activity is associated with resistance to apoptosis and the introduction of the human telomerase reverse transcriptase (hTERT) subunit into normal human cells is associated with life span extension of the cells. To determine the role of telomerase in regulating apoptosis, telomerase negative human embryo lung fibroblasts were transfected with the hTERT gene. Unlike the control fibroblasts, the telomerase-expressing cells had elongated telomeres and were resistant to apoptosis induced by hydroxyl radicals. The results indicate that expression of telomerase and, thus, the maintenance of telomere length in normal human somatic cells caused resistance to not only cellular senescence but also apoptosis. Moreover, we found that hydroxyl radical-induced apoptosis in telomerase-expressing and control fibroblasts was caspase-3 independent. These findings have revealed a new type of interrelation between telomerase and caspase-3, which may indicate that in this case the expressed telomerase may inhibit apoptosis at a site not related to the caspase-3 cascade