A cobordism realizing crossing change on sl2\mathfrak{sl}_2 tangle homology and a categorified Vassiliev skein relation

In this paper, we discuss degree 0 crossing change on Khovanov homology in terms of cobordisms. Namely, using Bar-Natan's formalism of Khovanov homology, we introduce a sum of cobordisms that yields a morphism on complexes of two diagrams of crossing change, which we call the "genus-one morphism." It is proved that the morphism is invariant under the moves of double points in tangle diagrams. As a consequence, in the spirit of Vassiliev theory, taking iterated mapping cones, we obtain an invariant for singular tangles that extending sl(2) tangle homology; examples include Lee homology, Bar-Natan homology, and Naot's universal Khovanov homology as well as Khovanov homology with arbitrary coefficients. We also verify that the invariant satisfies categorified analogues of Vassiliev skein relation and the FI relation.Comment: 35 pages, 5 figures. Changed title, Refinement of some part

The effect of the gastrointestinal hormones on colonic mucosal blood flow

The effect of intravenous administration of various gastrointestinal hormones or peptides on the colonic mucosal blood flow was investigated by a reflex spectrum apparatus (TS-200, Sumitomo Denko Co). Various gastrointestinal hormones (pentagastrin, secretin, substance P, vasoactive intestinal polypeptide) were administered via the femoral vein at different doses. The hormones were administered over 30 minutes using a chronofuser at a rate of 0.1 ml/min. Serial measurements of cecal mucosal blood flow were performed. Saline was administered to the control group. 1) Pentagastrin was administered at doses of 1μg/kg/hr, 50μg/kg/hr, 100μg/kg/hr, and 200μg/kg/hr. Cecal mucosal blood flow decreased when the dose of pentagastrin was increased. The intravascular supply of oxygen also decreased in a dose dependent manner. Each dose of the gastrointestinal hormone caused a reduction in blood pressure. 2) Secretin was administered at doses of 5μg/kg/hr, 50μg/ kg/hr, and 100μg/kg/hr. Each tested dose of this gastrointestinal hormone acted to maintain cecal mucosal blood flow. The blood pressure remained unchanged throughout the experiment. 3) Substance P was administered at doses of 1μg/kg/hr and 5μg/kg/hr. Cecal mucosal blood flow and the intravascular oxygen supply increased after administration of this gastrointestinal hormone. The blood pressure decreased transiently at the start of administration, but later gradually returned to the baseline values. 4) Vasoactive intestinal polypeptide (VIP) was administered at doses of 1μg/kg/hr, 5μg/kg/hr, and 10μg/kg/hr. VIP caused the cecal mucosal blood flow to increase in a dosedependent manner. The intravascular oxygen, supply also increased signific antly after administration of this gastrointestinal hormone. The blood pressure initially de creased after administration of each test dose of VIP, after which it gradually started to increase. 5) To identify the factors responsible for the increase in cecal mucosal blood flow at the start of VIP administration at a dose of 5μg/kg/h of VIP, the blood concentrations of VIP, cyclic AMP, phospholipase, prostaglandin E_2, prostaglandin: E, and 6 keto-prostaglandin:F_1α were examined at regular intervals. However, no significant changes with regard to these substances were noted

Regulation of Colonic Mucosal Blood Flow by Exogenous Ecosanoids in the Rat

We measured colonic mucosal blood flow using a reflectance spectrophotometry in Wistar rats during and after continuous injection of prostaglandins (PGs: PGE1, PGE2 and PGI2), as vasodilators, and thromboxane A2 (TXA2) as a vasoconstrictor. Administration of PGs increased colonic mucosal blood volume and oxyhemoglobin saturation of the colonic mucosal tissue, representing a parameter of mucosal oxygenation. The dose used did not change arterial blood pressure. These results suggest that PGs regulate colonic mucosal hemodynamics and oxygenation, and may thus act as cytoprotective substances. On the other hand, TXA2 injection diminished colonic mucosal blood flow compared with the same dose of PGI2 injection and acted against PGI2. Our results suggest that TXA2 and PGI2 regulate colonic mucosal hemodynamics

Requirement of Gαq/Gα11 Signaling in the Preservation of Mouse Intestinal Epithelial Homeostasis

Background & AimsProliferation, differentiation, and morphogenesis of the intestinal epithelium are tightly regulated by a number of molecular pathways. Coordinated action of intestine is achieved by gastrointestinal hormones, most of which exert these actions through G-protein–coupled receptors. We herein investigated the role of Gαq/11-mediated signaling in intestinal homeostasis.MethodsIntestinal tissues from control (Gnaqflox/floxGna11+/+), Int-Gq knock-out (KO) (VilCre+/-Gnaqflox/floxGna11+/+), G11 KO (Gnaqflox/floxGna11-/-), and Int-Gq/G11 double knock-out (DKO) (VilCre+/-Gnaqflox/floxGna11-/-) mice were examined by microscopy, transmission electron microscopy, and immunohistochemistry. The effect of Gαq/11-mediated signaling was studied in the cell lineage, proliferation, and apoptosis. Dextran sodium sulfate (DSS) colitis was induced to study the role of Gαq/11 in colon.ResultsPaneth cells were enlarged, increased in number, and mislocalized in Int-Gq/G11 DKO small intestine. Paneth cells also reacted with PAS and Muc2 antibody, indicating an intermediate character of Paneth and goblet cells. The nuclear β-catenin, T-cell factor 1, and Sox9 expression were reduced severely in the crypt base of Int-Gq/G11 DKO intestine. Proliferation was activated in the crypt base and apoptosis was enhanced along the crypt. Int-Gq/G11 DKO mice were susceptible to DSS colitis. Proliferation was inhibited in the crypt of unaffected and regenerative areas. Cystic crypts, periodic acid–Schiff–positive cells, and Muc2-positive cells were unusually observed in the ulcerative region.ConclusionsThe Gαq/11-mediated pathway plays a pivotal role in the preservation of intestinal homeostasis, especially in Paneth cell maturation and positioning. Wnt/β-catenin signaling was reduced significantly in the crypt base in Gαq/G11-deficient mice, resulting in the defective maturation of Paneth cells, induction of differentiation toward goblet cells, and susceptibility to DSS colitis