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TWIK-related acid-sensitive K + channel(TASK)is an important member of the two-pore-domain potassium channels family. It is widely expressed in the central nervous system and peripheral tissues and is extremely sensitive to hypoxia and pH changes in extracellular fluid. TASK participates in regulating the expression of respiratory center and the respiratory movement and also plays certain role in sleep regulation. This article reviews the recent advances in the roles of TASK in the regulation of respiration and sleep.

This study was aimed to investigate the effects of the intermediate-conductance Ca(2+)-activated K(+) (IKCa1) channels on the proliferation, migration, invasion ability and monoclonal immunoglobulin (IgE) secretion of multiple myeloma (MM) cells. Trypan blue exclusion was used to evaluate the impact of clotrimazole (CLO, an inhibitor of the KCa1) on the survival ability of MM cell line U266; transwell chamber and matrigel experiments were used to evaluate the impact of CLO on the ability of the migration and invasion of U266 cells; the influence of CLO on IgE secretion in U266 cells was detected by ELISA. The results showed that small dose of CLO ( ≤ 1.0 µmol/L) could not inhibit the viability of U266 cells. The Transwell and Matrigel invading tests displayed that the cell number moving into lower chamber of transwell decreased after U266 cells treated with small dose of CLO ( ≤ 1.0 µmol/L). After treating the cells with 1.00 µmol/L CLO for 24 h and 48 h, the concentration of IgE in cell supernatant was (4.98 ± 0.39) and (4.38 ± 0.32) ng/ml, while those in control group were (15.41 ± 1.88) and (19.73 ± 2.01) ng/ml, respectively, suggesting significant difference between them(P < 0.05). It is concluded that CLO can decrease the ability of migration and monoclonal immunoglobulin secretion of multiple myeloma cells by blocking the IKCa1, thus this study provides a new think for the targeted therapy of MM.

Objective: To investigate the changes of open probability (Po) of large conductance Ca(2+)-activated K(+) channel (BK channel) in diabetic coronary smooth muscle cells and elucidate the underlying cellular electrophysiology mechanisms of coronary dysfunction., Methods: Rat coronary smooth muscle cells were isolated from control group and diabetic group. BK single channel currents were recorded by patch clamp technique in inside-out configuration. Open probabilities were calculated and compared between two groups. After exposure to DHS-1, a specific BK channel activator, Po at 0.2 and 1 µmol/L free Ca(2+) were compared between control and diabetic groups., Results: In the presence of 0.2 µmol/L free Ca(2+), the Po at baseline was significantly lower in diabetic rats than in control rats (0.0032 ± 0.0012 vs. 0.095 ± 0.036, P < 0.05). Cytoplasmic application of DSH-1 significantly increased the Po to 0.335 ± 0.096 (P < 0.05 vs. baseline) in control rats, whereas DSH-1 had no effect in diabetic rats (Po = 0.022 ± 0.018, P > 0.05 vs. baseline). In the presence of 1 µmol/L free Ca(2+), the Po at baseline was also significantly lower in diabetic rats than in control rats (0.210 ± 0.055 vs. 0.458 ± 0.077, P < 0.05). Cytoplasmic application of DHS-1 further robustly enhanced Po to 0.823 ± 0.019 (P < 0.05 vs. baseline) in control rats and to 0.446 ± 0.098 in diabetic rats (P < 0.05 vs. baseline of diabetic rats; P < 0.05 vs. control rats with DHS-1)., Conclusion: The decrease of Po of BK single channel in coronary smooth muscle cells may be a potential cause for coronary dysfunction in diabetic rats.

Objective: To investigate the expression and functional role of the small conductance Ca(2+)-activated K(+) channels in human atrial myocytes., Methods: We collected the right atrial appendage tissues from 8 patients with congenital heart defect with sinus rhythm undergoing open-heart surgery. Immunohistochemistry was performed to identify the expression of 3 isoforms of SK channel (SK1, SK2 and SK3). Using the classical two-step enzymatic isolation method, perforated patch clamp and conventional voltage-clamp techniques were performed to record the action potentials (APs) and the whole-cell Ca(2+)-activated K(+) current (I(K, Ca)) in the single atrial myocyte. We compared the changes in action potential duration (APD) before and after the application of a specific SK channels blocker apamin (100 nmol/L)., Results: Human atrial myocytes showed positivity for all the SK1, SK2 and SK3 isoform channels. Patch-clamp recording confirmed the presence of I(K,Ca), and apamin significantly prolonged APD at 90% repolarization (APD(90)), but produced no obvious effect on APD(50)., Conclusion: The three isoforms of SK channels are all expressed in human atrial myocytes. SK channels play a prominent role in the late phase of repolarization in human atrial myocytes, which is distinct from their functional roles in neurons where they mediate the process of afterhyperpolarization following APs.

Objective: To investigate the changes of large conductance Ca(2+)-activated K(+) channel (BK channel) on coronary smooth muscle cells from diabetic rats., Methods: Streptozotocin-induced rat diabetic animal model was used. Coronary smooth muscle cells were isolated by enzyme digestion. BK currents in control and diabetic groups were recorded by patch clamp technique in whole cell configuration, and BK channel protein expression was detected by Western blot. Calcium concentration was measured by fluorescence assay., Results: Compared with control group, BK current densities in diabetic group were significantly decreased when test potentials > 100 mV (P < 0.05). BK current densities were (275 ± 40) pA/pF in control group (n = 8) and (70 ± 10) pA/pF in diabetic group (n = 6) at 150 mV test potentials. α-subunit protein expression was similar between the groups (P > 0.05), however, β1-subunit protein expression was significantly reduced in diabetic group than in control group (P < 0.05). Calcium concentrations were significantly increased in diabetic group control group (151 ± 18) nmol/L (n = 6) than in control group (92 ± 7) nmol/L (n = 5, P < 0.05)., Conclusion: Observed β1-subunit downregulation, BK current density decrease and cytosolic calcium concentration increase in smooth muscle cells of diabetic coronary arteries may be associated with coronary dysfunction in diabetic rats.

Aim: To study the protection mechanisms of K(ATP) channels on hippocampal CA1 neurons during chronic severe hypoxia., Methods: p53 expression, DNA fraction, and cell apoptosis were examined in cultured hippocampal neurons in control group, hypoxia group, hypoxia group treated with K(ATP) channels antagonist and hypoxia group treated with K(ATP) channels agonist., Results: In the group of a 12 h long exposure to oxygen concentration of 0%, diazoxide (100 micromol/L), the K(ATP) channels agonist, reduced p53 expression and the hypoxia-induced apoptosis. In contrast, tolbutamide (100 micromol/L), the K(ATP) channels antagonist, significantly rose p53 expression and the hypoxia-induced apoptosis, which could be reversed by p53 inhibitor TSA., Conclusion: K(ATP) channels protect hippocampal neurons against chronic severe hypoxia by suppressing p53 expression.

The objective of this paper was to investigate the effect of mitochondrial ATP-sensitive K(+) (MitoK(ATP)) channels on the expression of hypoxia inducible factor-1alpha (HIF-1alpha) and cell proliferation in pulmonary arterial smooth muscle cells (PASMCs) of rats. Cultured PASMCs were divided into six groups as follows: (1) normoxia group: cultured under normoxia for 24 h; (2) normoxia + diazoxide group: cultured under normoxia with diazoxide, an opener of MitoK(ATP) channel, for 24 h; (3) normoxia + 5-HD group: cultured under normoxia with 5-hydroxydecanoate (5-HD), an antagonist of MitoK(ATP) channel, for 24 h; (4) hypoxia group: cultured under hypoxia (37 degrees C, 5% O(2), 5% CO(2), 90% N(2)) for 24 h; (5) hypoxia + diazoxide group: cultured under hypoxia (37 degrees C, 5% O(2), 5% CO(2), 90% N(2)) with diazoxide for 24 h; (6) hypoxia + 5-HD group: cultured under hypoxia (37 degrees C, 5% O(2), 5% CO(2), 90% N(2)) with 5-HD for 24 h. The relative changes in mitochondrial potential were tested with Rhodamine 123 (R-123) fluorescence technique. Immunohistochemical method was used to trace the expression of HIF-1alpha. The proliferation of PASMCs was examined by MTT colorimetric assay. The results were as follows: The intensity of R-123 fluorescence in normoxia + diazoxide group was significantly increased as compared with that in normoxia group (P<0.05), and the intensity of R-123 fluorescence in hypoxia + diazoxide group was also significantly increased as compared with that in hypoxia group (P<0.05). 24-hour hypoxia or 24-hour hypoxia + diazoxide markedly increased the intensity of R-123 fluorescence in PASMCs as compared with normoxia (P<0.05), and the change was more prominant in hypoxia + diazoxide group than that in hypoxia group (P<0.05). There was no significant difference in the intensity of R-123 fluorescence between normoxia group and normoxia + 5-HD group (P>0.05). However, 5-HD weakened the effect of 24-hour hypoxia on the intensity of R-123 fluorescence. The intensity of R-123 fluorescence in hypoxia + 5-HD group was significantly decreased as compared with that in hypoxia group (P<0.05). After exposure to hypoxia or hypoxia + diazoxide for 24 h, the expression of HIF-1alpha and the proliferation of PASMCs were significantly increased as compared with that in normoxia or normoxia + diazoxide group (P<0.05), and the change was more significant in hypoxia + diazoxide group than that in hypoxia group (P<0.05). There was no significant difference in the expression of HIF-1alpha and the proliferation of PASMCs between normoxia group and normoxia + 5-HD group (P>0.05). However, the expression of HIF-1alpha and the proliferation of PASMCs in hypoxia + 5-HD group were significantly decreased as compared with that in hypoxia group (P<0.05). All these results suggest that the opening of MitoK(ATP) channels followed by a depolarization of mitochondrial membrane might contribute to the increase of the expression of HIF-1alpha and the proliferation of PASMCs. This might be a mechanism of the development of hypoxic pulmonary hypertension.

The basic electrophysiological characteristics of large conductance K(+)-channels in the basolateral cell membrane of outer hair cells (OHC) from the guinea pig cochlea were studied with patch-clamp technique. Acutely isolated OHC preparations were obtained by enzymatic digestion and excised patches were made in cell-attached configuration to record single-channel currents led by patch-clamp micropipette and fed to patch-clamp amplifier. Data were sampled and analyzed on-line with a computer. The result showed that the typical properties of single channels of large conductance K(+)-channels were: 1. The channel was activated by depolarization of membrane and it showed a marked voltage-dependence. The channel had a unitary conductance of about 133 pS and the channel current reversed at about -30mV under asymmetrical K+ concentration gradient. 2. Tetraethylammonium (TEA, > 10 mmol/L), a potassium channel blocker, dose-dependently abolished the outward current. 3. The open probability (Po) and mean open time of this channel was markedly increased with elevation of cytoplasmic Ca2+ concentration. These results suggest that a population of voltage-dependent and Ca(2+)-activated K+ channel exists in the basolateral membrane of OHC of the guinea pig; it is characterized by a very high unitary conductance and high sensitivity to Ca2+ and is blocked by K+ channel blocker. This work provided valuable basic materials for further study on the regulation and drug influence of the type of single channels.

Objective To explore the molecular mechanism of prolonged atrial repolarization in rats with reperfusion atrial arrhythmia. Methods Sixteen Langendorff isolated heart perfusion models made by male SD rats were randomly divided into control group （group C, n = 8） and hypothermic ischemia-reperfusion group （group IR, n = 8）. According to the occurrence of atrial arrhythmia after reperfusion, group IR was further subdivided into reperfusion non-atrial arrhythmia subgroup （group N-RAA） and reperfusion atrial arrhythmia subgroup （group RAA ）.Group C was perfused with 37 ℃ K-H solution for 120 min. In group IR, the isolated heart was perfused with 37 ℃ K-H solution for 30 min and stopped, and the isolated heart was perfused with 4 ℃ Thomas solution（ 20 mL/kg） for 60 mins. When the heart stopped for 30 mins, the isolated heart was perfused with a half dose of 4 ℃ Thomas solution （10 ℃）. During cardioplegia, the isolated heart was protected by low temperature Thomas solution （4 ℃）, and then reperfused for 30 mins with 37 ℃ K-H solution. The monophasic action potential （MAP） of the right atrium was recorded at balanced perfusion for 30 mins （T0）, balanced perfusion for 105 mins in group C/reperfusion for 15 mins in group IR（T1） and balanced perfusion for 120 mins in group C/reperfusion for 30 min in group IR（T2）; The duration of 50% and 90% repolarization of monophasic action potential （MAPD50 and MAPD90） was measured. After electrophysiological monitoring, the expression of Kir2.1 and CaMKⅡ in right atrium was detected by Western blot. Results Compared with T0, MAPD50 and MAPD90 at T1 and T2 were significantly prolonged in group R-AA （P < 0.05）, and MAPD90 at T1 and T2 in group R-NAA and group R-AA were significantly longer than those in group C （P < 0.05）.Compared with group R-NAA, MAPD50 and MAPD90 in group R-AA were significantly prolonged at T1 and T2 （P < 0.05）. The results of Western blot showed that the expression of Kir2.1 in group R-NAA and group R-AA was significantly lower than that in group C （P < 0.05）, and that in group R-AA was significantly lower than that in group R-NAA （P < 0.05）. The expression of CaMKⅡ in group R-NAA and group R-AA was significantly higher than that in group C （P < 0.05）, and the expression of CaMKⅡ in group R-AA was significantly higher than that in group R-NAA. Conclusion The prolonged duration of atrial repolarization in rats with hypothermic ischemia-reperfusion atrial arrhythmia may be related to the down-regulation of Kir2.1 expression and the upregulation of CaMKⅡ expression. [ABSTRACT FROM AUTHOR]

Copyright of Journal of International Reproductive Health/Family Planning is the property of Editorial Board of the Journal of International Reproductive Health/Family Planning and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

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Copyright of Chinese Journal of Tissue Engineering Research / Zhongguo Zuzhi Gongcheng Yanjiu is the property of Chinese Journal of Tissue Engineering Research and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Chinese Journal of Tissue Engineering Research / Zhongguo Zuzhi Gongcheng Yanjiu is the property of Chinese Journal of Tissue Engineering Research and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objectives: To observe the effect of ginger-salt-partitioned moxibustion on ATP-sensitive potassium (K ATP ) channel of bladder in detrusor overactivity (DO) rats., Methods: Female SD rats were randomly divided into sham operation, model, moxibustion and antagonist groups ( n =9 in each group). Thorax (T) 10 spinal cord transection was performed by surgery. Ginger-salt partitioned moxibustion was applied to "Shenque" (CV8) for 3 cones, once daily for 14 consecutive days. Rats of the antagonist group were intraperitoneally injected with K ATP channel specific antagonist glibenclamide (10 μg·kg -1 ·d -1 ) once daily for 14 consecutive days. Urodynamic tests were performed after treatment. The distribution and expression of K ATP channel tetrameric subunit (SUR2B) in the bladder of rats was observed by immunofluorescence. The protein and mRNA expression levels of SUR2B in bladder tissue were detected by Western blot and qPCR respectively., Results: Compared with the sham operation group, rats of the model group showed intensive and large phasic contractions of the detrusor during bladder filling, the frequency and amplitude of phasic contractions of the detrusor 5 min before leakage were significantly increased ( P <0.001)；the voiding threshold pressure was significantly decreased ( P <0.001)；the bladder perfusion volume was increased ( P <0.001)；the SUR2B protein and mRNA expression in bladder tissue were significantly reduced ( P <0.001). Compared with the model group and the antagonist group, the above-mentioned indicators in the moxibustion group were all reversed ( P <0.01, P <0.001, P <0.05)., Conclusions: Ginger-salt partitioned moxibustion can reduce the frequency and amplitude of detrusor phase contraction during bladder filling and prolong the time of first phase contraction in DO rats, which may be associated with up-regulating the expression level of K ATP channel protein and mRNA, promoting the outflow of potassium ions, and inhibiting the inflow of calcium ions, thus improve the stability of detrusor during storage.

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Copyright of Chinese Journal of Tissue Engineering Research / Zhongguo Zuzhi Gongcheng Yanjiu is the property of Chinese Journal of Tissue Engineering Research and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Shandong Medical Journal is the property of Shandong Medical Health Newspapers and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective To observe the protective function and mechanism of melatonin (MT) against white matter lesions in corpus callosum induced by chronic cerebral hypoperfusion (CCH) in cerebral small vessel disease (cSVD) rats. Methods Forty -four adult male Sprague - Dawley rats were divided into sham group, bilateral common carotid artery occlusion (BCCAO) group, MT1 group [BCCAO + melatonin 5 mg/(kg⋅d)] and MT2 group [BCCAO + melatonin 10 mg/(kg⋅d)]. Four weeks after operation, social activity (sniffing time and crossing number) was assessed to reflect apathetic behavior. Myelin basic protein (MBP) in corpus callosum was detected by immunofluorescence. Transmission electron microscope was used to compare the G-ratio. Western blotting test was used to detect phosphorylation level of mammalian target of rapamycin (mTOR). Results BCCAO group rats showed fewer sniffing time (t = 58.000, P = 0.000) and crossing number (t = 20.000, P = 0.000), lower level of MBP expression (t = 20.400, P = 0.000), higher level of G-ratio (t = - 9.800, P = 0.000), and lower pmTOR/mTOR ratio (t = 20.336, P = 0.000) than those of sham group; after treatment of melatonin [5 or 10 mg/(kg⋅d)], MT1 group and MT2 group showed more sniffing time (t = - 12.600, P = 0.001; t = - 26.000, P = 0.000) and crossing number (t = - 8.400, P = 0.000; t = - 10.200, P = 0.000), higher pmTOR/mTOR ratio (t = - 6.022, P = 0.014; t = - 8.800, P = 0.001) than those of BCCAO group but still lower than those of sham group (t = 45.400, P = 0.000; t = 32.000, P = 0.000; t = 11.600, P = 0.000; t = 9.800, P = 0.000; t = 14.314, P = 0.000; t = 11.536, P = 0.000); while showed higher level of MBP expression (t = - 16.800, P = 0.001; t = - 20.600, P = 0.000), and lower level of G-ratio (t = 8.600, P = 0.041; t = 9.200, P = 0.030) than those of BCCAO group but similar with sham group (P > 0.05, for all); MT2 group showed longer sniffing time than MT1 group (t = - 13.400, P = 0.000). Conclusions Melatonin could ameliorate apathetic behavioral and white matter lesions in corpu callosums in rats with cSVD, which might be related to the up-regulate of phosphorylation level of mTOR. [ABSTRACT FROM AUTHOR]

Copyright of Shandong Medical Journal is the property of Shandong Medical Health Newspapers and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Shandong Medical Journal is the property of Shandong Medical Health Newspapers and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

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Copyright of Journal of Clinical Hepatology / Linchuang Gandanbing Zazhi is the property of Journal of Clinical Hepatology and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Chinese Journal of Tissue Engineering Research / Zhongguo Zuzhi Gongcheng Yanjiu is the property of Chinese Journal of Tissue Engineering Research and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Shandong Medical Journal is the property of Shandong Medical Health Newspapers and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Shandong Medical Journal is the property of Shandong Medical Health Newspapers and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Shandong Medical Journal is the property of Shandong Medical Health Newspapers and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)