Homotopy analysis solutions for the asymmetric laminar flow in a porous channel with expanding or contracting walls

In this paper, the asymmetric laminar flow in a porous channel with expanding or contracting walls is investigated. The governing equations are reduced to ordinary ones by using suitable similar transformations. Homotopy analysis method （HAM） is employed to obtain the expres- sions for velocity fields. Graphs are sketched for values of parameters and associated dynamic characteristics, especially the expansion ratio, are analyzed in detail.

Effect of the ginsenoside Rb1 on the spontaneous contraction of intestinal smooth muscle in mice

AIM: To investigate the effect and the possible mechanism of ginsenoside Rb1 on small intestinal smooth muscle motility in mice. METHODS: Intestinal smooth muscle strips were isolated from male ICR mice (5 wk old), and the effect of ginsenoside Rb1 on spontaneous contraction was recorded with an electrophysiolograph. The effect of ginsenoside Rb1 on ion channel currents, including the voltage-gated K + channel current (IK V ), calcium-activated potassium channel currents (IK Ca ), spontaneous transient outward currents and ATP-sensitive potassium channel current (IK ATP ), was recorded on freshly isolated single cells using the whole-cell patch clamp technique. RESULTS: Ginsenoside Rb1 dose-dependently inhibited the spontaneous contraction of intestinal smooth muscle by 21.15% ± 3.31%, 42.03% ± 8.23% and 67.23% ± 5.63% at concentrations of 25 μmol/L, 50 μmol/L and 100 μmol/L, respectively (n=5,P<0.05). The inhibitory effect of ginsenoside Rb1 on spontaneous contraction was significantly but incompletely blocked by 10 mmol/L tetraethylammonium or 0.5 mmol/L 4-aminopyridine, respectively (n=5, P<0.05). However, the inhibitory effect of ginsenoside Rb1 on spontaneous contraction was not affected by 10 μmol/L glibenclamide or 0.4 μmol/L tetrodotoxin. At the cell level, ginsenoside Rb1 increased outward potassium currents, and IK V was enhanced from 1137.71 ± 171.62 pA to 1449.73 ± 162.39 pA by 50 μmol/L Rb1 at +60 mV (n=6, P<0.05). Ginsenoside Rb1 increased IK Ca and enhanced the amplitudes of spontaneous transient outward currents from 582.77 ± 179.09 mV to 788.12 ± 278.34 mV (n=5, P<0.05). However, ginsenoside Rb1 (50 μmol/L) had no significant effect on IK ATP (n=3, P<0.05). CONCLUSION: These results suggest that ginsenoside Rb1 has an inhibitory effect on the spontaneous contraction of mouse intestinal smooth muscle mediated by the activation of IK V and IK Ca , but the K ATP channel was not involved in this effect.

THRESHOLD CONDITION FOR CHOCKING IN OPEN CHANNELS AND EXCAVATION OF TAILRACE

On the basis of energy and continuity equations a general threshold condition for chocking in open channels is obtained and a representation in terms of the Froude number at the upstream section and other parameters is given to predict whether the chocking phenomenon occurs or not at the downstream section. From the general threshold condition for chocking the limit contraction ratios of the channel width are introduced for both with and without the energy losses and a criterion for excavation of the tailrace to avoid chocking is derived. An example shows that using these criterion and the representation proposed for calculating flow depth it is very easy to determine the scheme of the excavation of the open channels.

The role of TRPP2 in agonist-induced gallbladder smooth muscle contraction

TRPP2 channel protein belongs to the superfamily of transient receptor potential(TRP) channels and is widely expressed in various tissues, including smooth muscle in digestive gut. Accumulating evidence has demonstrated that TRPP2 can mediate Ca^(2+) release from Ca^(2+) stores. However, the functional role of TRPP2 in gallbladder smooth muscle contraction still remains unclear. In this study, we used Ca^(2+) imaging and tension measurements to test agonist-induced intracellular Ca^(2+) concentration increase and smooth muscle contraction of guinea pig gallbladder, respectively. When TRPP2 protein was knocked down in gallbladder muscle strips from guinea pig, carbachol(CCh)-evoked Ca^(2+) release and extracellular Ca^(2+) influx were reduced significantly, and gallbladder contractions induced by endothelin 1 and cholecystokinin were suppressed markedly as well. CCh-induced gallbladder contraction was markedly suppressed by pretreatment with U73122, which inhibits phospholipase C to terminate inositol 1,4,5-trisphosphate receptor(IP3) production, and 2-aminoethoxydiphenyl borate(2APB), which inhibits IP3 recepor(IP3R) to abolish IP3R-mediated Ca^(2+) release. To confirm the role of Ca^(2+) release in CCh-induced gallbladder contraction, we used thapsigargin(TG)-to deplete Ca^(2+) stores via inhibiting sarco/endoplasmic reticulum Ca^(2+)-ATPase and eliminate the role of store-operated Ca^(2+) entry on the CCh-induced gallbladder contraction. Preincubation with 2 μmol L^(-1) TG significantly decreased the CCh-induced gallbladder contraction. In addition, pretreatments with U73122, 2APB or TG abolished the difference of the CCh-induced gallbladder contraction between TRPP2 knockdown and control groups. We conclude that TRPP2 mediates Ca^(2+) release from intracellular Ca^(2+) stores, and has an essential role in agonist-induced gallbladder muscle contraction.