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Biomedical subjects

J S Woo

Publications and source records attributed to J S Woo.

At least 19 recordsLinked to original sources
PubMed2006

Controlled delivery of a hydrophilic drug from a biodegradable microsphere system by supercritical anti-solvent precipitation technique.

The purpose of this study was to prepare microspheres loaded with hydrophilic drug, bupivacaine HCl using poly(D,L-lactic-co-glycolic acid) (PLGA) and poly(L-lactic acid) (PLLA). Microspheres were prepared with varying the PLGA/PLLA ratio with two different levels of bupivacaine HCl (5 and 10%) using a supercritical anti-solvent (SAS) technique. Microspheres ranging from 4-10 microm in geometric mean diameter could be prepared, with high loading efficiency. Powder X-ray diffraction (PXRD) revealed that bupivacaine HCl retained its crystalline state within the polymer and was present as a dispersion within the polymer phase after SAS processing. The release of bupivacaine HCl from biodegradable polymer microspheres was rapid up to 4 h, thereafter bupivacaine HCl was continuously and slowly released for at least 7 days according to the PLGA/PLLA ratio and the molecular weight of PLLA.

Absorbable Implants↗
PubMed2001

Simplified retrograde systemic perfusion for removal of air from the aorta in an infant.

Total circulatory arrest with full venous drainage can result in air entering the arterial system through several possible sites such as the aortic cannulation site or collateral vessels. Air present in the arterial system during total circulatory arrest imposes a special problem. We describe a simple technique of short-term retrograde systemic perfusion to remove air from the arterial system before restarting systemic arterial perfusion after total circulatory arrest.

Aortic Diseases↗
PubMed2001

Effect of pentoxifylline on ischemic acute renal failure in rabbits.

Previous studies have demonstrated that levels of tumor necrosis factor-alpha (TNF-alpha) or its mRNA expression are increased in acute renal failure of various types including ischemia/reperfusion injury. This study was undertaken to determine whether pentoxifylline (PTX), an inhibitor of TNF-alpha production, provides a protective effect against ischemic acute renal failure in rabbits. Renal ischemia was induced by clamping bilateral renal arteries for 60 min. Animals were pretreated with PTX (30 mg/kg, i.v.) 10 min before release of clamp. At 24 h of reperfusion of blood after ischemia, changes in renal function, renal blood flow, and the expression of TNF-alpha mRNA were evaluated. Ischemia/reperfusion caused a marked reduction in GFR, which was accompanied by an increase of serum creatinine levels. Such changes were significantly attenuated by PTX pretreatment. PTX ameliorated the impairment of renal tubular function, but it had no effect on the reduction of renal blood flow induced by ischemia/reperfusion. The protective effect of PTX on functional changes was supported by morphological studies. The impairment of glucose and phosphate reabsorption in postischemic kidneys was associated with a depression in the expression of Na+-glucose and Na+-Pi transporters. The expression of TNF-alpha mRNA was increased after reperfusion, which was inhibited by PTX pretreatment. The PTX pretreatment in vitro prevented the release of lactate dehydrogenase induced by an oxidant t-butylhydroperoxide in rabbit renal cortical slices, but it did not produce any effect on the oxidant-induced lipid peroxidation, suggesting that PTX protection is not resulted from its antioxidant action. These results suggest that PTX may exert a protective effect against ischemic acute renal failure by inhibiting the production of TNF-alpha in rabbits.

Acute Kidney Injury↗
PubMed2001

Nonselective left internal mammary artery angiography during right transradial coronary angiography: a simple, rapid, and safe technique.

Internal mammary artery angiography is increasingly required, but the technique for left internal mammary artery (LIMA) angiography during right transradial coronary angiography is not well established. The authors investigated the feasibility and safety of a new, simple, and rapid nonselective technique. Following right transradial coronary angiography, LIMA angiography was performed using a 5 French (Fr) Judkins JL-3.5 catheter in 110 patients. The catheter, placed in the ascending aorta with its natural curve, was withdrawn slowly while being rotated clockwise to engage its tip in the proximal left subclavian artery. Contrast material was injected while sphygmomanometer cuff inflation was applied to the left upper arm. In the last 50 patients, the angiography was performed twice randomly with and without the cuff inflation. In 108 patients (98%), the catheter was successfully engaged in the subclavian artery in a mean of 11 +/- 8 seconds (range, 3-136) from the time when it was withdrawn from the ascending aorta, and nonselective LIMA angiography was successfully performed. The image quality of the angiograms was satisfactory in 103 (95%) of the 108 patients. In the last 50 patients, the image quality of the angiograms was determined satisfactory in 48 (96%) and 45 (90%) patients, with and without the cuff inflation, respectively. The difference was statistically not significant. There were no complications, including arterial dissection and thromboembolism. In conclusion, nonselective LIMA angiography can be readily and safely performed during right transradial coronary angiography using a 5 Fr Judkins JL-3.5 catheter.

Aged↗
PubMed2000

Role of lipid peroxidation and poly(ADP-ribose) polymerase activation in oxidant-induced membrane transport dysfunction in opossum kidney cells.

This study was undertaken to examine the role of lipid peroxidation and poly(ADP-ribose) polymerase (PARP) activation in H(2)O(2)-induced inhibition of Na(+)-dependent phosphate (Na(+)-Pi) uptake in opossum kidney (OK) cells. H(2)O(2) inhibited Na(+)-Pi uptake in a dose-dependent manner. H(2)O(2)-induced inhibition of Na(+)-Pi uptake was prevented by dithiothreitol and glutathione. A potent antioxidant, DPPD, had no effect on H(2)O(2) inhibition of Na(+)-Pi uptake, despite completely inhibiting lipid peroxidation induced by H(2)O(2). However, in primary cultured rabbit proximal tubular cells, the effect of H(2)O(2) on Na(+)-Pi uptake was significantly prevented by DPPD, suggesting a species difference in the role of lipid peroxidation in the inhibition of Na(+)-Pi uptake occurring with H(2)O(2). t-Butylhydroperoxide (tBHP) caused the inhibition of Na(+)-Pi uptake that was prevented by DPPD in OK cells and rabbit proximal tubular cells. The PARP inhibitor 3-aminobenzamide completely protected the inhibition of Na(+)-Pi uptake induced by H(2)O(2) but not by tBHP. H(2)O(2)-induced ATP depletion was prevented by 3-aminobenzamide but not by DPPD. tBHP-induced ATP depletion was prevented by DPPD, whereas it was not altered by 3-aminobenzamide. Effects of H(2)O(2) and tBHP on Na(+)-Pi uptake and ATP depletion were prevented by an iron chelator, deferoxamine, suggesting that the oxidants inhibit Na(+)-Pi uptake through an iron-dependent mechanism. The extent of DNA damage by tBHP was similar to that by H(2)O(2). These results indicate that the effect of H(2)O(2) on membrane transport function in OK cells is associated with PARP activation but not lipid peroxidation, whereas the effect of tBHP is associated with lipid peroxidation.

Animals↗
PubMed2000

Mechanism of reduced GFR in rabbits with ischemic acute renal failure.

A reduction in glomerular filtration rate (GFR) is a primary characteristic of ischemic acute renal failure. The present study was undertaken to examine the roles of angiotensin II, tubuloglomerular-feedback (TGF) mechanism, and tubular obstruction for the GFR reduction in the post-ischemic kidney. Renal ischemia was induced by occlusion of the bilateral renal arteries for 60 min, and renal function was examined at 2 and 24 h after the onset of reflow. After the end of 2-h reflow, the GFR was not significantly changed, but the urine flow increased significantly. On the other hand, at the end of 24-h reflow, the GFR and urine flow decreased markedly along with increased filtration fraction. The renal blood flow significantly decreased at 24 h, but not 2 h, after reflow, which was accompanied by increased total renal vascular resistance. Furosemide infusion (1 mg/min/kg) after 24 h of reflow prevented the reduction in GFR and filtration fraction without no changes in renal blood flow and total renal vascular resistance. Pretreatment of enalapril and losartan did not prevent the reduction in GFR, indicating that angiotensin II was not involved. In morphological examinations, tubular obstruction was seen in the proximal and distal tubules of kidneys both at 2 and 24 h after the onset of reflow. In two rabbits subjected to 48 h of reflow, the tubular obstruction was not observed, despite GFR remained depressed. These results suggest that the late reduction in GFR in postischemic kidneys is not mediated by angiotensin II, but is mediated, at least in part, by the TGF mechanism. The tubular obstruction may be not prerequisite for the GFR reduction in rabbits.

Acute Kidney Injury↗
PubMed2000

Effect of arachidonic acid metabolic inhibitors on hypoxia/reoxygenation-induced renal cell injury.

The present study was undertaken to examine the role of arachidonic acid (AA) metabolites in hypoxia/reoxygenation (H/R)-induced renal cell injury in rabbit renal cortical slices using AA metabolic inhibitors. Inhibitors of cyclooxygenase (indomethacin and diclofenac sodium) and lipoxygenase pathways (nordihydroguaiaretic acid, caffeic acid, and eicosapentaenoic acid) reduced H/R-induced LDH release in a dose-dependent manner, whereas an inhibitor of cytochrome P-450 monooxygenase pathway ethoxyresorufin was not effective. AA increased LDH release in control slices, and the effect was not altered by indomethacin and nordihydroguaiaretic acid. The protective effect of indomethacin was not affected by addition of PGE2, a main product of cyclooxygenase pathway in the kidney. H2O2-induced LDH release was prevented by inhibitors of lipoxygenase but not by inhibitors of cyclooxygenase and cytochrome P-450 monooxygenase H/R-induced LDH release was not altered by iron chelators, phenanthroline and deferoxamine, and a potent antioxidant, N,N'-diphenyl-p-phenylenediamine, suggesting that the H/R-induced cell injury is not attributed to a generation of reactive oxygen species. Morphological studies showed that H/R-induced structural changes including cell necrosis were significantly prevented by indomethacin. These results suggest that inhibitors of cyclooxygenase and lipoxygenase pathways exert a direct protective effect against the H/R-induced cell injury in renal tubules. Whether these effects are mediated by alterations of AA metabolic pathways is not certain.

Animals↗
PubMed2000

Protective role of superoxide dismutase in rat eustachian tubal mucosa against acute otitis media induced by upper respiratory tract infection.

Superoxide dismutase has been known to play a role as an anti-oxidative system against oxidative injury during acute inflammation. To investigate the role of superoxide dismutase in eustachian tubal mucosa during acute otitis media (AOM), an animal model was made. Sprague-Dawley rats were inoculated with Streptococcus pneumoniae through the nasal cavity following development of virus-induced upper respiratory infection. The animals were divided into three groups according to their tympanic cavity conditions following bacterial inoculation; inoculated animals with no resultant AOM (no-AOM), animals with resultant AOM (AOM) and animals with resolving otitis media (recovery). The changes of superoxide dismutase in each tubal mucosa were compared with that of the normal control using immunohistochemistry and immunoblotting methods. On Western blot, there were little changes of optical density and surface area in no-AOM (213.5 +/- 22.4, 13.2 +/- 0.8 mm2) and recovery group (219.3 +/- 18.7, 14.8 +/- 0.7 mm2) compared to the normal control (223.5 +/- 26.2, 16.7 +/- 0.4 mm2). However, a marked decrease was found in the AOM model (167.6 +/- 19.3, 6.5 +/- 0.9 mm2). These findings suggest that superoxide dismutase may play a role in protecting tubal mucosa from free radical injury during AOM.

Acute Disease↗
PubMed1999

Topical oleo-hydrogel preparation of ketoprofen with enhanced skin permeability.

In an attempt to improve the skin penetration of ketoprofen, various transdermal formulations were prepared, and their in vitro skin permeability and in vivo percutaneous absorption were evaluated. In vitro permeation studies were performed using a modified Franz cell diffusion system in which permeation parameters such as cumulative amount at 8 hr Q8hr, steady-state flux Jss, or lag time tL were determined. In the in vivo percutaneous absorption study using the hairless mouse, maximum concentration Cmax and area under the curve at 24 hr AUC24h were measured. The optimal transdermal formulation (oleo-hydrogel formulation) of ketoprofen showed a Q8hr value of 227.20 micrograms/cm2, a Jss value of 29.61 micrograms/cm2/hr, and a tL value of 0.46 hr. The Q8hr and Jss values were about 10-fold (p < .01) higher than those (Q8hr = 19.61 micrograms/cm2; Jss = 2.66 micrograms/cm2/hr) from the K-gel and about 3.5-fold (p < .01) than those (Q8hr = 60.00 micrograms/cm2; Jss = 7.99 micrograms/cm2/hr) of the K-plaster. In the in vivo percutaneous absorption, the Cmax (6.82 micrograms/ml) and AUC24h (55.74 micrograms.hr/ml) values of the optimal formulation were significantly (p < .01) higher than those of K-gel and K-plaster. The relative bioavailability of the oleo-hydrogel following transdermal administration in reference to oral administration was about 37%, and the Cmax value (4.73 micrograms/cm2) in the hypodermis following topical administration was much higher than those from the conventional products (Cmax of K-gel and K-plaster were 0.92 +/- 0.19 microgram/cm2 and 1.27 +/- 0.37 microgram/cm2, respectively). These data demonstrate that the oleo-hydrogel formulation of ketoprofen was more beneficial than conventional products (K-gel and K-plaster) in enhancing transdermal permeation and skin absorption of ketoprofen. Furthermore, there was a good correlation between in vitro permeation parameters and in vivo percutaneous absorption parameters.

Administration, Cutaneous↗
PubMed1998

Difference in H2O2 toxicity between intact renal tubules and cultured proximal tubular cells.

The present study was undertaken to examine the response to H2O2 and t-butylhydroperoxide (t-BHP) in various in vitro model systems of renal proximal tubules: rabbit renal cortical slices, freshly isolated rabbit proximal tubules, rabbit primary cultured proximal tubular cells, and opossum kidney (OK) cells. t-BHP increased lactate dehydrogenase release and lipid peroxidation in a concentration-dependent manner over the concentration range of 0.2 to 3 mM in cortical slices, whereas H2O2 caused a similar concentration-dependent increase in both parameters at 5-100 mM. The sensitivity of isolated tubules to both peroxides was similar to that of cortical slices. In primary cultured cells and OK cells, however, the cytotoxicity of H2O2 was identical to that of t-BHP. The cytotoxicity of t-BHP was not different among all the systems examined. The specific activity of catalase in cortical slices was similar to that of isolated tubules, but it was much higher than that of primary cultured cells or opossum kidney cells. Glutathione (GSH) peroxidase activity was not different among all the systems examined. The expression of catalase mRNA in cortical slices and isolated tubules was higher than that in primary cultured cells, whereas those of superoxide dismutase, glutathione peroxidase, or beta-actin were not different among the systems. These results indicate that intact proximal tubules are more resistant to H2O2 than are cultured proximal tubular cells, and the resistance is due to a higher specific activity of catalase resulting from the increased expression of its mRNA.

Animals↗
PubMed1998

The effect of galE gene inactivation on lipopolysaccharide profile of Helicobacter pylori.

The galE gene product, UDP-galactose 4-epimerase, mediates the incorporation of galactose in extracellular polysaccharide materials such as the O-side chain of lipopolysaccharide (LPS). The O-side chain in H. pylori LPS has been shown to cross-react with Lewis x and/or y blood group antigens, suggesting its potential involvement in H. pylori-linked autoimmune disease. To study its role in H. pylori LPS biosynthesis, the galE gene was cloned, sequenced, and a galE-knockout H. pylori strain was constructed. The H. pylori galE gene encoded a protein of 344 amino acids with a molecular weight of 39K. The LPS profile from the galE-knockout H. pylori strain showed a lower molecular weight than that of the parental strain, indicating the involvement of the galE gene in LPS biosynthesis of H. pylori.

Amino Acid Sequence↗
PubMed1998

REP-PCR fragments as biomarkers for differentiating gastroduodenal disease-specific Helicobacter pylori strains.

We previously identified four potential putative gastroduodenal disease fragments by using the interspersed repetitive extragenic palindromic DNA sequence based PCR (REP-PCR) technique. We investigated these fragments with regard to their disease specificity. The putative disease-specific REP-PCR fragments were cloned, mapped by restriction enzymes, cross-hybridized, and confirmed by Southern hybridization. The four fragments were also used as probes against REP-PCR amplicons from H. pylori isolates obtained from gastritis (N = 20), duodenal ulcer (N = 30), and gastric cancer patients (N = 30). Three of these fragments (1.4- and 0.76-kb for gastritis; 1.35 kb for duodenal ulcer) were amplified without any discrimination between any disease-specific H. pylori isolates. However, amplification following hybridization with the fourth 0.81-kb fragment was observed only from gastritis (60%) and duodenal ulcer (52%) but with none (0%) of gastric cancer patients. Nucleotide sequence analysis of the 0.81-kb fragment revealed that it was an open reading frame of the hypothetical protein HP0373 matched to the position of 380,966 to 383,068 nucleotides of the H. pylori complete genome sequence. Hence, the REP-PCR sequence was not a extragenic palindromic DNA sequence. The hypothetical protein was also present in all the tested isolates. The REP-PCR fingerprinting technique is useful to differentiate disease-specific H. pylori strains based on the interspersed repetitive extragenic palindromic DNA sequences; however, it may not be useful to identify disease-specific virulence determinant(s) without being confirmed by DNA sequence analysis and functional studies.

Amino Acid Sequence↗
PubMed1998

Adenylyl cyclase is involved in desensitization and recovery of ATP-stimulated Cl- secretion in MDCK cells.

We investigated the process of and recovery from desensitization of the P2 receptor-mediated stimulation of Cl- secretion in Madin-Darby canine kidney (MDCK) cell monolayers by assaying the response of short-circuit current (Isc). When the cells were exposed to repeated 3-min challenges of ATP or UTP interspersed with 5-min washes, the response of Isc desensitized rapidly followed by spontaneous recovery. The pattern of inhibition by various channel blockers or enzyme inhibitors revealed that both the initial and recovered responses of Isc have the same ionic and signaling mechanisms. The desensitization and recovery processes were confined to the membrane exposed to the repeated challenges. When added during the desensitized phase, 8-bromoadenosine 3',5'-cyclic monophosphate enhanced the ATP-stimulated Isc response, whereas it did not during the initial or recovered phases. ATP-induced increases of intracellular adenosine 3',5'-cyclic monophosphate showed similar desensitization and recovery in parallel with the changes in the responses of Isc. The desensitization process was attenuated by pretreatment with cholera toxin or pertussis toxin. Taken together, our results suggest that the adenylyl cyclase system plays a role in the desensitization and recovery mechanism of the ATP-stimulated Cl- secretion in MDCK cells.

Adenosine Triphosphate↗
PubMed1997

Agrin inhibits neurite outgrowth but promotes attachment of embryonic motor and sensory neurons.

Agrin is a secreted glycoprotein with the ability to cluster cell surface molecules, including the nicotinic acetylcholine receptor (AchR) on muscle cells. Alternate splicing of agrin mRNA results in a family of agrin proteins which differ in their clustering potency. Neuronal-specific isoforms with the highest clustering activity play a role in clustering postsynaptic proteins at the neuromuscular junction. However, the function of agrin isoforms expressed in many nonneuronal tissues, and only weakly active in clustering assays, remains obscure. Monolayer cultures of Chinese hamster ovary (CHO) cells expressing a neuronal (agrin-19) or a nonneuronal (agrin-0) form of agrin were used to assay the effect of agrin on neurite outgrowth and cell attachment. These results were compared to outgrowth on control CHO cells expressing only drug resistance and on regions of CHO-agrin monolayers not expressing detectable levels of agrin. Neurite extension on confluent monolayers of agrin-0- or -19-expressing CHO cells was reduced substantially below that of controls. In one experiment neurite lengths were compared at 2 and 3 days after plating and suggested that neurite outgrowth may be stopped and not simply retarded. Attachment of sensory or motoneurons was nearly twofold higher to agrin monolayers than to control cells, showing that the inhibition is not a result of a nonpermissive environment. An agrin construct missing the C-terminal half, removing the major site of variability and clustering activity, was also tested. This construct did not reduce outgrowth, suggesting that the C-terminal half of the protein may be important in stopping growth as well as inducing clustering. These results expand the role of agrin in synaptogenesis as it may provide a stop signal at the myofiber surface and may anchor the presynaptic fibers to the eventual motor endplate .

Agrin↗
PubMed1997

Failure to isolate Helicobacter pylori from stray cats indicates that H. pylori in cats may be an anthroponosis--an animal infection with a human pathogen.

The recent isolation of Helicobacter pylori from cats obtained from a commercial supplier has potentially important public health implications. The present study investigated whether H. pylori infection was common in stray cats. Twenty-five cats were examined for the presence of H. pylori by histological examination, culture and two polymerase chain reaction (PCR) assays. Histologically, the gastric biopsy specimens from all cats showed large spiral organisms typical of H. felis and not H. pylori. Samples from 23 cats yielded bacterial growth and two had no growth. Colonies grossly similar to H. pylori were tested for catalase, oxidase, urease and Gram's stain reactions. None was H. pylori. All samples tested as positive by the Helicobacter 16S rRNA genus-specific PCR assay and only six cats and a mouse stomach infected with H. heilmannii gave positive results with the adhesin subunit A (hpaA)-specific PCR assay, which is consistent with either H. pylori or H. heilmannii. The helicobacters identified in these samples by PCR were not cultivable and hence were probably H. heilmannii. H. pylori infection is uncommon in stray cats and owning pet cats should not be a threat to public health in relation to H. pylori infection.

Adhesins, Bacterial↗
PubMed1997

cGMP stimulates sodium and chloride currents in rat tracheal airway epithelia.

To test the hypothesis that guanosine 3',5'-cyclic monophosphate (cGMP) regulates ion transport in airway epithelial cells, we measured short-circuit current (I(sc)) and (22)Na+ fluxes in primary cultured rat tracheal epithelial cells. In Cl- -containing Ringer solution, I(sc) was increased by approximately 17 microA/cm2 after application of 1 mM 8-bromoguanosine 3',5'-cyclic monophosphate (8-BrcGMP), whereas, in Cl- -free solutions, the Na+ -mediated component was approximately 5 microA/cm2, suggesting a cGMP stimulation of Cl-secretory current and a smaller Na+ absorptive current. Inward and net mucosal-to-serosal (22)Na+ flux was doubled in the presence of 2 mM 8-BrcGMP. To determine whether nucleotide-gated channels play a role in this transepithelial Na+ absorption, blockers of nucleotide-gated cation channels were used to inhibit I(sc). The cGMP-stimulated Na+-mediated I(sc) was blocked by as little as 500 nM dichlorobenzamil or 50 microM L-cis-diltiazem, which are known blockers for cyclic nucleotide-gated cation channels. These agents also blocked the basal (non-cGMP-stimulated) current when measured in the presence of 10 microM amiloride, which blocks current through 5-pS amiloride-sensitive Na+ channels. To document whether the distribution of nucleotide-gated nonselective cation channels was consistent with a role in airway epithelial transport, in situ hybridization was performed. In situ hybridization of mRNA encoding for nucleotide-gated cation channels was found in epithelial cell layers of rat trachea, bronchi, bronchioles, and alveolar cells but not in smooth muscle layers or tracheal cartilage. Reverse transcriptase-polymerase chain reaction, restriction enzyme analysis, and sequencing of the cDNA transcribed from mRNA of whole lung and tracheal epithelial cells indicate that a channel highly homologous to the retinal nucleotide-gated nonselective cation channel (CNG1) is present. Thus these data, along with evidence supporting the existence of signal transduction pathways elevating intracellular levels of cGMP, indicate that cGMP regulates transepithelial ion transport in lung epithelial tissues.

Amiloride↗
PubMed1997

Role of purinergic receptors in chloride secretion in Caco-2 cells.

Purinergic receptors play an important role in regulating Cl- secretion in epithelial cells. To explore further the role of these receptors in the intestine, we utilized the human intestinal epithelial cell line, Caco-2, grown on permeable membrane supports and assayed for Cl- secretion by measuring the short-circuit current (Isc). Stimulation of Isc by extracellular nucleotides could be detected by day 4 and increased by day 10 postseeding. The magnitude of stimulation of Isc at 10 microM in cells at day 10 was UTP > ATP > UDP > > 2-methylthioadenosine 5'-triphosphate (2-MeS-ATP) = ADP on the apical side and UTP = 2-MeS-ATP = ATP > ADP > > UDP on the basolateral side. Cross-desensitization studies suggested that two different receptors are expressed in the apical membrane, a P2U purinoceptor and a uridine nucleotide receptor. Two different receptors are also expressed in the basolateral membrane, a P2U receptor and another that reacts with both 2-MeS-ATP and ADP. This latter receptor has an unusual pharmacological profile, with a reactivity for 2-MeS-ATP > ADP but not for ATP. Responses to purinergic receptor agonists were inhibited by pretreatment with 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid-acetoxymethyl ester, thapsigargin, or quinine. Thus we suggest that an increase in intracellular Ca2+ and subsequent opening of Ca(2+)-activated K+ channel play a role in increasing driving force for Cl- to exit across the apical membrane. The role of the cystic fibrosis transmembrane conductance regulator as a Cl- exit pathway on the apical membrane was also established.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗