PGE2 inhibits basolateral 50 pS potassium channels in the thick ascending limb of the rat kidney.

To study the inhibition of the inwardly rectifying basolateral 50 pS potassium channels by PGE(2) we performed patch-clamp studies on the basolateral membrane of the rat kidney thick ascending limb. PGE(2)'s effect was mimicked by the selective EP1- and EP3-receptor agonist, sulprostone, but was prevented by inhibiting protein kinase-C with calphostin-C. The mitogen-activated protein kinase inhibitor PD98059 (ERK) or SB203580 (p38) increased basal channel activity; however, while neither alone prevented the inhibitory effect of PGE(2), but using both of them together completely abolished PGE(2)'s effect on channel activity.

Arachidonic acid inhibits basolateral K channels in the cortical collecting duct via cytochrome P-450 epoxygenase-dependent metabolic pathways.

We used the patch-clamp technique to study the effect of arachidonic acid (AA) on basolateral 18-pS K channels in the principal cell of the cortical collecting duct (CCD) of the rat kidney. Application of AA inhibited the 18-pS K channels in a dose-dependent manner and 10 microM AA caused a maximal inhibition. The effect of AA on the 18-pS K channel was specific because application of 11,14,17-eicosatrienoic acid had no effect on channel activity.

Thirty-nine-month xylitol chewing-gum programme in initially 8-year-old school children: a feasibility study focusing on mutans streptococci and lactobacilli.

Aim: To investigate the use of xylitol-containing chewing-gums in public elementary schools as a means to affect the growth of salivary and plaque mutans streptococci and salivary lactobacilli.

Design: Over a period of 24 months, 750 8- to 9-year-old children chewed xylitol (X group; n = 255) or xylitol-sorbitol (XS group; n = 264) gum on school days (454 days over 2 years), or chewed no gum at all (C group; n = 231). Consumption of xylitol in the X and the XS groups was 6.

Sodium-dependent regulation of renal amiloride-sensitive currents by apical P2 receptors.

The epithelial sodium channel (ENaC) plays a major role in the regulation of sodium balance and BP by controlling Na(+) reabsorption along the renal distal tubule and collecting duct (CD). ENaC activity is affected by extracellular nucleotides acting on P2 receptors (P2R); however, there remain uncertainties over the P2R subtype(s) involved, the molecular mechanism(s) responsible, and their physiologic role. This study investigated the relationship between apical P2R and ENaC activity by assessing the effects of P2R agonists on amiloride-sensitive current in the rat CD.

Expression of tetraspan protein CD63 activates protein-tyrosine kinase (PTK) and enhances the PTK-induced inhibition of ROMK channels.

In the present study, we tested the role of CD63 in regulating ROMK1 channels by protein-tyrosine kinase (PTK). Immunocytochemical staining shows that CD63 and receptor-linked tyrosine phosphatase alpha (RPTPalpha) are expressed in the cortical collecting duct and outer medulla collecting duct. Immunoprecipitation of tissue lysates from renal cortex and outer medulla or 293T cells transfected with CD63 reveals that CD63 was associated with RPTPalpha both in situ and in transfected cells.

K restriction inhibits protein phosphatase 2B (PP2B) and suppression of PP2B decreases ROMK channel activity in the CCD.

We used Western blot analysis to examine the effect of dietary K intake on the expression of serine/threonine protein phosphatase in the kidney. K restriction significantly decreased the expression of catalytic subunit of protein phosphatase (PP)2B but increased the expression of PP2B regulatory subunit in both rat and mouse kidney. However, K depletion did not affect the expression of PP1 and PP2A.

A fully automated robotic system for microinjection of zebrafish embryos.

As an important embodiment of biomanipulation, injection of foreign materials (e.g., DNA, RNAi, sperm, protein, and drug compounds) into individual cells has significant implications in genetics, transgenics, assisted reproduction, and drug discovery.

Carbon monoxide stimulates the Ca2(+)-activated big conductance k channels in cultured human endothelial cells.

We used the whole-cell patch-clamp technique to study K channels in the human umbilical vein endothelial cells and identified a 201 pS K channel, which was blocked by tetraethylammonium and iberiotoxin but not by TRAM34 and apamin. This suggests that the Ca(2+)-activated big-conductance K channel (BK) is expressed in endothelial cells. Application of carbon monoxide (CO) or tricarbonylchloro(glycinato)ruthenium(II), a water soluble CO donor, stimulated the BK channels.

PGE2 inhibits apical K channels in the CCD through activation of the MAPK pathway.

We used the patch-clamp technique and Western blot analysis to explore the effect of PGE(2) on ROMK-like small-conductance K (SK) channels and Ca(2+)-activated big-conductance K channels (BK) in the cortical collecting duct (CCD). Application of 10 microM PGE(2) inhibited SK and BK channels in the CCD. Moreover, either inhibition of PKC or blocking mitogen-activated protein kinase (MAPK), P38 and ERK, abolished the effect of PGE(2) on SK channels in the CCD.

Role of gp91phox -containing NADPH oxidase in mediating the effect of K restriction on ROMK channels and renal K excretion.

Previous study has demonstrated that superoxide and the related products are involved in mediating the effect of low K intake on renal K secretion and ROMK channel activity in the cortical collecting duct (CCD). This study investigated the role of gp91(phox)-containing NADPH oxidase (NOXII) in mediating the effect of low K intake on renal K excretion and ROMK channel activity in gp91(-/-) mice. K depletion increased superoxide levels, phosphorylation of c-Jun, expression of c-Src, and tyrosine phosphorylation of ROMK in renal cortex and outer medulla in wild-type (WT) mice.

Inhibitor of growth 4 (ING4) is up-regulated by a low K intake and suppresses renal outer medullary K channels (ROMK) by MAPK stimulation.

Dietary K intake plays an important role in the regulation of renal K secretion: a high K intake stimulates whereas low K intake suppresses renal K secretion. Our previous studies demonstrated that the Src family protein-tyrosine kinase and mitogen-activated protein kinase (MAPK) are involved in mediating the effect of low K intake on renal K channels and K secretion. However, the molecular mechanism by which low K intake stimulates MAPK is not completely understood.

Adenosine stimulates the basolateral 50 pS K channels in the thick ascending limb of the rat kidney.

We used the patch-clamp technique to examine the effect of adenosine on the basolateral K channels in the thick ascending limb (TAL) of the rat kidney. A 50-pS inwardly rectifying K channel was detected in the basolateral membrane, and the channel activity was decreased by hyperpolarization. Application of adenosine (10 microM) increased the activity of basolateral 50 pS K channels, defined by NP(o), from 0.

Angiotensin II inhibits the ROMK-like small conductance K channel in renal cortical collecting duct during dietary potassium restriction.

Base-line urinary potassium secretion in the distal nephron is mediated by small conductance rat outer medullary K (ROMK)-like channels. We used the patch clamp technique applied to split-open cortical collecting ducts (CCDs) isolated from rats fed a normal potassium (NK) or low potassium (LK) diet to test the hypothesis that AngII directly inhibits ROMK channel activity. We found that AngII inhibited ROMK channel activity in LK but not NK rats in a dose-dependent manner.

Effect of hydrogen peroxide on ROMK channels in the cortical collecting duct.

We used the patch-clamp technique to study the effect of H(2)O(2) on the apical ROMK-like small-conductance K (SK) channel in the cortical collecting duct (CCD). The addition of H(2)O(2) decreased the activity of the SK channels and the inhibitory effect of H(2)O(2) was larger in the CCD from rats on a K-deficient diet than that from rats on a normal-K or a high-K diet. However, application of H(2)O(2) did not inhibit the SK channels in inside-out patches.

Inhibition of MAPK stimulates the Ca2+ -dependent big-conductance K channels in cortical collecting duct.

The kidney plays a key role in maintaining potassium (K) homeostasis. K excretion is determined by the balance between K secretion and absorption in distal tubule segments such as the connecting tubule and cortical collecting duct. K secretion takes place by K entering principal cells (PC) from blood side through Na+, K+ -ATPase and being secreted into the lumen via both ROMK-like small-conductance K (SK) channels and Ca2+ -activated big-conductance K (BK) channels.

[The effect of shanzha xiaozhi capsule on the blood lipid and the function of endothelial cells in patients with dislipide mia].

Objective: To explore the Mechanism of Shanzha xiaozhi Capsule improving the functions of endonthelial cells in patients with dislipide mia.

Methods: To measurate the blood lipid and the levels of plasma Endothelin (ET) and nitrodi oxide (NO) in 30 patients with dislipide mia before and after taking the Shanzha xiaozhi Capsule, and there were 10 normal persons in control group, which were measured the blood lipid and the levels of ET and NO only one time.

Results: After treatment with Shanzha xiaozhi Capsule, the levels of triglyceride (TG), total cholesterol (TC), low density lipoprotein cholestero (LDL-C), ET were markedly reduced (P < 0.

Mitogen-activated protein kinases inhibit the ROMK (Kir 1.1)-like small conductance K channels in the cortical collecting duct.

It was demonstrated previously that low dietary potassium (K) intake stimulates Src family protein tyrosine kinase (PTK) expression via a superoxide-dependent signaling. This study explored the role of mitogen-activated protein kinase (MAPK) in mediating the effect of superoxide anions on PTK expression and ROMK (Kir 1.1) channel activity.

Low Na intake suppresses expression of CYP2C23 and arachidonic acid-induced inhibition of ENaC.

We previously demonstrated that arachidonic acid (AA) inhibits epithelial Na channels (ENaC) through the cytochrome P-450 (CYP) epoxygenase-dependent pathway (34). In the present study, we tested the hypothesis that low Na intake suppresses the expression of CYP2C23, which is mainly responsible for converting AA to epoxyeicosatrienoic acid (EET) in the kidney (11) and attenuates the AA-induced inhibition of ENaC. Immunostaining showed that CYP2C23 is expressed in the Tamm-Horsfall protein (THP)-positive and aquaporin 2 (AQP2)-positive tubules.

Clinical and pathological study of lichen-planus-like keratosis in China.

Lichen-planus-like keratosis is usually diagnosed pathologically; rarely, a definitive diagnosis can be made grossly in the clinic. Only a few cases of lichen-planus-like keratosis have been reported in China. The purpose of this study was to investigate the clinical and pathological features of lichen-planus-like keratosis in China.

Salt-sensitive hypertension is associated with dysfunctional Cyp4a10 gene and kidney epithelial sodium channel.

Functional and biochemical data have suggested a role for the cytochrome P450 arachidonate monooxygenases in the pathophysiology of hypertension, a leading cause of cardiovascular, cerebral, and renal morbidity and mortality. We show here that disruption of the murine cytochrome P450, family 4, subfamily a, polypeptide 10 (Cyp4a10) gene causes a type of hypertension that is, like most human hypertension, dietary salt sensitive. Cyp4a10-/- mice fed low-salt diets were normotensive but became hypertensive when fed normal or high-salt diets.

Ischemia impairs the association between connexin 43 and M3 subtype of acetylcholine muscarinic receptor (M3-mAChR) in ventricular myocytes.

We used Western blot analysis to examine the expression of connexin 43 and M2/M3 acetylcholine muscarinic receptors (mAChR) and their interaction in ventricular myocytes from control and the ischemic heart. We confirmed that the connexin 43 and M2/ M3-mAChR were expressed in ventricular myocytes. Moreover, we showed that M3-mAChR was expressed in non-glycosylated (72 kDa) and glycosylated forms (115 kDa).

Cosmetic dermatitis in Chinese eczema patients patch tested with a modified European standard series of allergens.

The prevalence of cosmetic allergic contact dermatitis (CACD) in Chinese eczema patients (CEP) has not been reported. The purpose of our study was to analyse CACD in CEP and examine the frequency of patch test (PT) reactions to common cosmetic-related allergens (CRA). 378 consecutive CEP patch tested with a modified European standard series of allergens during a 2-year period in our clinic were analysed.

Regulation of ROMK (Kir1.1) channels: new mechanisms and aspects.

This brief review attempts to provide an overview regarding recent developments in the regulation of ROMK channels. Studies performed in ROMK null mice suggest that ROMK cannot only form hometetramers such as the small-conductance (30-pS) K channels but also construct heterotetramers such as the 70-pS K channel in the thick ascending limb (TAL). The expression of ROMK channels in the plasma membrane is regulated by protein tyrosine kinase (PTK), serum and glucorticoid-induced kinase (SGK), and with-no-lysine-kinase 4.

Coupling of sequencing batch reactor and mesh filtration: operational parameters and wastewater treatment performance.

Wastewater treatment performance of the combined process of sequencing batch reactor (SBR) and mesh filtration bio-reactor was investigated with a synthetic wastewater. In this system, the filtration was performed only by the water level difference between the reactor and the effluent port, with the help of a sludge layer which accumulated on the mesh filter. A half volume of the mixed liquor was filtrated for ca.

Adenosine inhibits ENaC via cytochrome P-450 epoxygenase-dependent metabolites of arachidonic acid.

We used the patch-clamp technique to examine the effect of adenosine on epithelial sodium channel (ENaC) activity in rat cortical collecting duct (CCD). Application of adenosine inhibits ENaC activity, and the effect of adenosine was mimicked by cyclohexyladenosine (CHA), an A(1) adenosine-receptor agonist that reduced channel activity from 1.32 to 0.