The bound state problem of S-wave heavy quark meson-aitimeson systems

We investigated systematically whether the S-wave ($\bar{Q}q$) meson and the ($Q\bar{q}$) meson may form S-wave bound states in a chiral SU(3) quark model by solving the resonating group method equation. Here $Q=c$ or $b$ and $q=u$, $d$ or $s$. Our preliminary calculation disfavors the existence of $I=\frac12$ ($\bar{Q}l$)-($Q\bar{s}$) molecules ($l=u,d$) while favors the existence of isoscalar $B\bar{B}$, $B^*\bar{B}^*$ (J=2) and $B\bar{B}^*$ (C=+) molecules. The existence of isovector (charm-anticharm) and (charm-bottom) molecules is also disfavored. Therefore the resonance-like structure $Z^+(4051)$ is unlikely to be an S-wave $D^*\bar{D}^*$ molecule.Comment: 8 pages, 7 tables, accepted by Phys. Rev.

QqQˉqˉ′Qq\bar Q\bar q' States in Chiral SU(3) Quark Model

In this work, we study the masses of $Qq\bar Q\bar q'$ states with J^{PC}=0^{++}, 1^{++}, 1^{+-} and 2^{++} in the chiral SU(3) quark model, where Q is the heavy quark (c or b) and q (q') is the light quark (u, d or s). According to our numerical results, it is improbable to make the interpretation of $[cn\bar c\bar n]_{1^{++}}$ and $[cn\bar c\bar n]_{2^{++}}$ (n=u, d) states as X(3872) and Y(3940), respectively. However, it is interesting to find the tetraquarks in the $bq\bar b\bar q'$ system

Chronic stress and intestinal permeability: Lubiprostone regulates glucocorticoid receptor‐mediated changes in colon epithelial tight junction proteins, barrier function, and visceral pain in the rodent and human

BackgroundChronic psychological stress is associated with increased intestinal epithelial permeability and visceral hyperalgesia. Lubiprostone, an agonist for chloride channel‐2, promotes secretion and accelerates restoration of injury‐induced epithelial barrier dysfunction. The mechanisms underlying how lubiprostone regulates colon epithelial barrier function and visceral hyperalgesia in chronic stress remain unknown.MethodsMale rats were subjected to water avoidance stress for 10 consecutive days. Lubiprostone was administered daily during the stress phase. Visceromotor response to colorectal distension was measured. Human colon crypts and cell lines were treated with cortisol and lubiprostone. The transepithelial electrical resistance and FITC‐dextran permeability were assayed. Chromatin immunoprecipitation was conducted to assess glucocorticoid receptor binding at tight junction gene promoters.Key ResultsLubiprostone significantly decreased chronic stress‐induced visceral hyperalgesia in the rat (P < 0.05; n = 6). WA stress decreased occludin and claudin‐1 and increased claudin‐2 in rat colon crypts, which was prevented by lubiprostone. Cortisol treatment induced similar alterations of tight junction protein expression in Caco‐2/BBE cells (P < 0.05) and significantly changed paracellular permeability in monolayers (P < 0.01). These changes were blocked by lubiprostone. Glucocorticoid receptor and its binding at occludin promoter region were decreased in cortisol‐treated cells and human colon crypts, which was largely reversed by lubiprostone. In rat colonic cells, glucocorticoid receptor and its co‐chaperone proteins were down‐regulated after corticosterone treatment and lubiprostone reversed these changes.Conclusions & InferencesLubiprostone preferentially prevents chronic stress‐induced alterations of intestinal epithelial tight junctions, barrier function, and visceral hyperalgesia that was associated with modulation of glucocorticoid receptor expression and function.Lubiprostone preferentially prevents chronic stress‐induced alterations of intestinal epithelial tight junctions, barrier function, and visceral hyperalgesia that was associated with modulation of glucocorticoid receptor expression and function.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/147799/1/nmo13477.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/147799/2/nmo13477_am.pd