Bing shuo Chen - Academia.edu (original) (raw)
Papers by Bing shuo Chen
The Kaohsiung journal of medical sciences, 2015
The inwardly rectifying K(+) current [IK(IR)] allows large inward K(+) currents at potentials neg... more The inwardly rectifying K(+) current [IK(IR)] allows large inward K(+) currents at potentials negative to K(+) equilibrium potential (EK) and it becomes small outward K(+) currents at those positive to EK. How changes of such currents enriched in glial cells can influence the functions of glial cell, neurons, or both is not clearly defined, although mutations of Kir4.1 channels have been demonstrated to cause serious neurological disorders. In this study, we identified the presence of IK(IR) in human glioma cells (U373 and U87 cells). The amplitude of IK(IR) in U373 cells was subject to inhibition by amitriptyline, arecoline, or BaCl2. The activity of inwardly rectifying K(+) channels was also clearly detected, and single-channel conductance of these channels was calculated to be around 23 pS. Moreover, based on a simulation model derived from neuron-glial interaction mediated by ion flux, we further found out that incorporation of glial IK(IR) conductance into the model can signifi...
![Research paper thumbnail of Potent Activation of Large-Conductance Ca2+-Activated K+ Channels by the Diphenylurea 1,3-Bis-[2-hydroxy-5-(trifluoromethyl)phenyl]urea (NS1643) in Pituitary Tumor (GH3) Cells](https://attachments.academia-assets.com/100032987/thumbnails/1.jpg)
](Molecular Pharmacology, 2008
1,3-Bis-[2-hydroxy-5-(trifluoromethyl)phenyl]urea (NS1643) is reported to be an activator of huma... more 1,3-Bis-[2-hydroxy-5-(trifluoromethyl)phenyl]urea (NS1643) is reported to be an activator of human ether-à-go-go-related gene current. However, it remains unknown whether it has any effects on other types of ion channels. The effects of NS1643 on ion currents and membrane potential were investigated in this study. NS1643 stimulated Ca 2ϩ-activated K ϩ current [I K(Ca) ] in a concentration-dependent manner with an EC 50 value of 1.8 M in pituitary tumor (GH 3) cells. In inside-out recordings, this compound applied to the intracellular side of the detached channels stimulated large-conductance Ca 2ϩ-activated K ϩ (BK Ca) channels with no change in single-channel conductance. It shifted the activation curve of BK Ca channels to less depolarized voltages without altering the gating charge of the channels. NS1643-stimulated channel activity depended on intracellular Ca 2ϩ , and mean closed time during exposure to NS1643 was reduced. NS1643 (3 M) had little or no effect on peak amplitude of ether-à-go-go-related gene-mediated K ϩ current evoked by membrane hyperpolarization, although it increased the amplitude of late-sustained components of K ϩ inward current, which was suppressed by paxilline but not by azimilide. NS1643 (3 M) had no effect on L-type Ca 2ϩ current. This compound reduced repetitive firing of action potentials, and further application of paxilline attenuated its decrease in firing rate. In addition, NS1643 enhanced BK Ca-channel activity in human embryonic kidney 293T cells expressing ␣-hSlo. In summary, we clearly show that NS1643 interacts directly with the BK Ca channel to increase the amplitude of I K(Ca) in pituitary tumor (GH 3) cells. The ␣-subunit of the channel may be a target for the action of this small compound.
Journal of Anesthesia, 2012
Purpose There is still a lack of evidence to support the use of specific anesthetic agents during... more Purpose There is still a lack of evidence to support the use of specific anesthetic agents during major operations that could affect the development of postoperative acute lung injury (ALI). This study determined the protective effect of inhaled isoflurane in a rat model of endotoxininduced ALI. Methods Rats were exposed to volatile isoflurane (1.5 % in oxygen) or pure oxygen via a facemask for 2 h. After a 3-h recovery period, rats were reanesthetized and ALI was induced by intratracheal instillation of lipopolysaccharide (LPS, 1 mg/kg in 0.5 ml saline). In some animals, a specific inducible nitric oxide synthase (iNOS) inhibitor, 1400W, (10 mg/kg, i.p.) was administered before exposure to isoflurane. Animals were sacrificed 12 h later for analysis. Pulmonary artery vasomotor function and alveolocapillary permeability were assessed. Expression of iNOS and CD11b, and activity of myeloperoxidase in the lung were analyzed. Results The maximal relaxation response to acetylcholine was significantly potentiated in rats pretreated with isoflurane. Lung wet-to-dry ratio was reduced in the lung of isoflurane-treated animals. Expression of iNOS and CD11b were attenuated in the lung tissue obtained from rats receiving isoflurane. Furthermore, enzymatic activity of myeloperoxidase was also reduced in the lung preexposed to isoflurane. However, these pulmonary protective effects of isoflurane were significantly abolished by pretreatment with 1400W. Conclusion Pretreatment with volatile isoflurane attenuated inflammatory process in the lung tissue of rats with LPS-induced ALI, and this preconditioning pulmonary protective effect was mainly mediated by activation of endogenous iNOS in the lung.
British Journal of Anaesthesia, 2009
Background. Dexmedetomidine (DEX), a selective agonist of a 2-adrenergic receptors, is recognized... more Background. Dexmedetomidine (DEX), a selective agonist of a 2-adrenergic receptors, is recognized to facilitate analgesia and anaesthesia in humans. Despite the potential for wide use, its effects on ion currents and membrane potential in neurones remain largely unclear. Methods. We investigated the effects of DEX on ion channels in NG108-15 neuronal cells differentiated with dibutyryl cyclic AMP and in cultured cerebellar neurones. Results. DEX suppressed the amplitude of delayed rectifier K + current [I K(DR) ] in a concentration-dependent manner with an IC 50 value of 4.6 mM in NG108-15 cells. No change in the steady-state inactivation of I K(DR) was evident in the presence of DEX. A minimal binding scheme was also used to evaluate DEX-induced block of I K(DR). Inhibition of I K(DR) by DEX was still observed in cells preincubated with yohimbine (10 mM) or efaroxan (10 mM). DEX depressed the peak amplitude of Na + current (I Na), whereas it had minimal effect on L-type Ca 2+ current. Under current-clamp configuration, DEX increased the duration of action potentials (APs). I K(DR) and I Na in response to AP waveforms were more sensitive to block by DEX than those elicited during rectangular pulses. In isolated cerebellar granule cells, DEX also effectively suppressed I K(DR). Conclusions. The effects of DEX are not limited to its interactions with a 2-adrenergic receptors. Inhibitory effects on I K(DR) and I Na constitute one of the underlying mechanisms through which DEX and its structurally related compounds might affect neuronal activity in vivo.
Anesthesia & Analgesia, 2001
Journal of Clinical Gastroenterology, 2009
Background: Despite the increasing popularity of propofol for sedation in colonoscopy, the optima... more Background: Despite the increasing popularity of propofol for sedation in colonoscopy, the optimal regimen is still controversial. Both propofol alone and propofol in combination with meperidine are frequently used during colonoscopy, but the impact of adding meperidine has not been evaluated. This study aimed to investigate if adding meperidine to propofol offers any advantage in terms of patient tolerance, recovery time, and postcolonoscopy discomforts. Method: Consecutive patients admitted to the physical checkup department of our hospital were randomized to receive either meperidine plus propofol (combination group, n = 100) or propofol alone (propofol group, n = 100) for sedated colonoscopy. The patients' tolerance and postcolonoscopy discomforts (pain, bloating, dizziness, and nausea/vomiting) were assessed with a 0-10 visual analog scale. The recovery times were assessed with 5-minute and 10-minute Aldrete scores. Results: The dose of propofol was less in the combination group than the propofol group (129.80 ± 37.93 mg vs. 147.90 ± 47.85, mean ± SD, P = 0.003). The endoscopists, anesthetists, and nurses all rated patients' tolerance in favor of the combination group than the propofol group (
Proceedings of the National Academy of Sciences, 2012
HIV-1 envelope glycoprotein is the primary target for HIV-1–specific antibodies. The native HIV-1... more HIV-1 envelope glycoprotein is the primary target for HIV-1–specific antibodies. The native HIV-1 envelope spike on the virion surface is a trimer, but trimeric gp140 and monomeric gp120 currently are believed to induce comparable immune responses. Indeed, most studies on the immunogenicity of HIV-1 envelope oligomers have revealed only marginal improvement over monomers. We report here that suitably prepared envelope trimers have nearly all the antigenic properties expected for native viral spikes. These stable, rigorously homogenous trimers have antigenic properties markedly different from those of monomeric gp120s derived from the same sequences, and they induce potent neutralizing antibody responses for a cross-clade set of tier 1 and tier 2 viruses with titers substantially higher than those elicited by the corresponding gp120 monomers. These results, which demonstrate that there are relevant immunologic differences between monomers and high-quality envelope trimers, have impor...
Journal of Theoretical Biology, 2009
The rapidly inactivating (I(Naf)) and noninactivating Na(+) currents (I(Na)(()(NI)())) were chara... more The rapidly inactivating (I(Naf)) and noninactivating Na(+) currents (I(Na)(()(NI)())) were characterized in NG108-15 neuronal cells differentiated with dibutyryl cyclic AMP in this study. Standard activation and inactivation protocols were used to evaluate the steady-state and kinetic properties of the I(Naf) present in these cells. The voltage protocols with a slowly depolarizing ramp were implemented to examine the properties of I(Na)(()(NI)()). Based on experimental data and computer simulations, a window component of the rapidly inactivating sodium current (I(Naf)(()(W)())) was also generated in response to the slowly depolarizing ramp. The I(Naf)(()(W)()) was subtracted from I(Na)(()(NI)()) to yield the persistent Na(+) current (I(Na)(()(P)())). Our results demonstrate the presence of I(Na)(()(P)()) in these cells. In addition to modifying the steady-state inactivation of I(Naf), ranolazine or riluzloe could be effective in blocking I(Naf)(()(W)()) and I(Na)(()(P)()). The ability of ranolazine and riluzole to suppress I(Na)(()(P)()) was greater than their ability to inhibit I(Naf)(()(W)()). In current-clamp recordings, current-induced voltage oscillations were applied to elicit action potentials (APs) through a gradual transition between spontaneous depolarization and upstroke. Ranolazine or riluzole at a concentration of 3 microM then effectively suppressed the AP firing generated by oscillatory changes in membrane current. The data suggest that a small rise in I(Na)(()(NI)()) facilitates neuronal hyper-excitability due the decreased threshold of AP initiation. The underlying mechanism of the inhibitory actions of ranolazine or riluzole on membrane potential in neurons or neuroendocrine cells in vivo may thus be associated with their blocking of I(Na)(()(NI)()).
The Kaohsiung journal of medical sciences, 2015
The inwardly rectifying K(+) current [IK(IR)] allows large inward K(+) currents at potentials neg... more The inwardly rectifying K(+) current [IK(IR)] allows large inward K(+) currents at potentials negative to K(+) equilibrium potential (EK) and it becomes small outward K(+) currents at those positive to EK. How changes of such currents enriched in glial cells can influence the functions of glial cell, neurons, or both is not clearly defined, although mutations of Kir4.1 channels have been demonstrated to cause serious neurological disorders. In this study, we identified the presence of IK(IR) in human glioma cells (U373 and U87 cells). The amplitude of IK(IR) in U373 cells was subject to inhibition by amitriptyline, arecoline, or BaCl2. The activity of inwardly rectifying K(+) channels was also clearly detected, and single-channel conductance of these channels was calculated to be around 23 pS. Moreover, based on a simulation model derived from neuron-glial interaction mediated by ion flux, we further found out that incorporation of glial IK(IR) conductance into the model can signifi...
Molecular Pharmacology, 2008
1,3-Bis-[2-hydroxy-5-(trifluoromethyl)phenyl]urea (NS1643) is reported to be an activator of huma... more 1,3-Bis-[2-hydroxy-5-(trifluoromethyl)phenyl]urea (NS1643) is reported to be an activator of human ether-à-go-go-related gene current. However, it remains unknown whether it has any effects on other types of ion channels. The effects of NS1643 on ion currents and membrane potential were investigated in this study. NS1643 stimulated Ca 2ϩ-activated K ϩ current [I K(Ca) ] in a concentration-dependent manner with an EC 50 value of 1.8 M in pituitary tumor (GH 3) cells. In inside-out recordings, this compound applied to the intracellular side of the detached channels stimulated large-conductance Ca 2ϩ-activated K ϩ (BK Ca) channels with no change in single-channel conductance. It shifted the activation curve of BK Ca channels to less depolarized voltages without altering the gating charge of the channels. NS1643-stimulated channel activity depended on intracellular Ca 2ϩ , and mean closed time during exposure to NS1643 was reduced. NS1643 (3 M) had little or no effect on peak amplitude of ether-à-go-go-related gene-mediated K ϩ current evoked by membrane hyperpolarization, although it increased the amplitude of late-sustained components of K ϩ inward current, which was suppressed by paxilline but not by azimilide. NS1643 (3 M) had no effect on L-type Ca 2ϩ current. This compound reduced repetitive firing of action potentials, and further application of paxilline attenuated its decrease in firing rate. In addition, NS1643 enhanced BK Ca-channel activity in human embryonic kidney 293T cells expressing ␣-hSlo. In summary, we clearly show that NS1643 interacts directly with the BK Ca channel to increase the amplitude of I K(Ca) in pituitary tumor (GH 3) cells. The ␣-subunit of the channel may be a target for the action of this small compound.
Journal of Anesthesia, 2012
Purpose There is still a lack of evidence to support the use of specific anesthetic agents during... more Purpose There is still a lack of evidence to support the use of specific anesthetic agents during major operations that could affect the development of postoperative acute lung injury (ALI). This study determined the protective effect of inhaled isoflurane in a rat model of endotoxininduced ALI. Methods Rats were exposed to volatile isoflurane (1.5 % in oxygen) or pure oxygen via a facemask for 2 h. After a 3-h recovery period, rats were reanesthetized and ALI was induced by intratracheal instillation of lipopolysaccharide (LPS, 1 mg/kg in 0.5 ml saline). In some animals, a specific inducible nitric oxide synthase (iNOS) inhibitor, 1400W, (10 mg/kg, i.p.) was administered before exposure to isoflurane. Animals were sacrificed 12 h later for analysis. Pulmonary artery vasomotor function and alveolocapillary permeability were assessed. Expression of iNOS and CD11b, and activity of myeloperoxidase in the lung were analyzed. Results The maximal relaxation response to acetylcholine was significantly potentiated in rats pretreated with isoflurane. Lung wet-to-dry ratio was reduced in the lung of isoflurane-treated animals. Expression of iNOS and CD11b were attenuated in the lung tissue obtained from rats receiving isoflurane. Furthermore, enzymatic activity of myeloperoxidase was also reduced in the lung preexposed to isoflurane. However, these pulmonary protective effects of isoflurane were significantly abolished by pretreatment with 1400W. Conclusion Pretreatment with volatile isoflurane attenuated inflammatory process in the lung tissue of rats with LPS-induced ALI, and this preconditioning pulmonary protective effect was mainly mediated by activation of endogenous iNOS in the lung.
British Journal of Anaesthesia, 2009
Background. Dexmedetomidine (DEX), a selective agonist of a 2-adrenergic receptors, is recognized... more Background. Dexmedetomidine (DEX), a selective agonist of a 2-adrenergic receptors, is recognized to facilitate analgesia and anaesthesia in humans. Despite the potential for wide use, its effects on ion currents and membrane potential in neurones remain largely unclear. Methods. We investigated the effects of DEX on ion channels in NG108-15 neuronal cells differentiated with dibutyryl cyclic AMP and in cultured cerebellar neurones. Results. DEX suppressed the amplitude of delayed rectifier K + current [I K(DR) ] in a concentration-dependent manner with an IC 50 value of 4.6 mM in NG108-15 cells. No change in the steady-state inactivation of I K(DR) was evident in the presence of DEX. A minimal binding scheme was also used to evaluate DEX-induced block of I K(DR). Inhibition of I K(DR) by DEX was still observed in cells preincubated with yohimbine (10 mM) or efaroxan (10 mM). DEX depressed the peak amplitude of Na + current (I Na), whereas it had minimal effect on L-type Ca 2+ current. Under current-clamp configuration, DEX increased the duration of action potentials (APs). I K(DR) and I Na in response to AP waveforms were more sensitive to block by DEX than those elicited during rectangular pulses. In isolated cerebellar granule cells, DEX also effectively suppressed I K(DR). Conclusions. The effects of DEX are not limited to its interactions with a 2-adrenergic receptors. Inhibitory effects on I K(DR) and I Na constitute one of the underlying mechanisms through which DEX and its structurally related compounds might affect neuronal activity in vivo.
Anesthesia & Analgesia, 2001
Journal of Clinical Gastroenterology, 2009
Background: Despite the increasing popularity of propofol for sedation in colonoscopy, the optima... more Background: Despite the increasing popularity of propofol for sedation in colonoscopy, the optimal regimen is still controversial. Both propofol alone and propofol in combination with meperidine are frequently used during colonoscopy, but the impact of adding meperidine has not been evaluated. This study aimed to investigate if adding meperidine to propofol offers any advantage in terms of patient tolerance, recovery time, and postcolonoscopy discomforts. Method: Consecutive patients admitted to the physical checkup department of our hospital were randomized to receive either meperidine plus propofol (combination group, n = 100) or propofol alone (propofol group, n = 100) for sedated colonoscopy. The patients' tolerance and postcolonoscopy discomforts (pain, bloating, dizziness, and nausea/vomiting) were assessed with a 0-10 visual analog scale. The recovery times were assessed with 5-minute and 10-minute Aldrete scores. Results: The dose of propofol was less in the combination group than the propofol group (129.80 ± 37.93 mg vs. 147.90 ± 47.85, mean ± SD, P = 0.003). The endoscopists, anesthetists, and nurses all rated patients' tolerance in favor of the combination group than the propofol group (
Proceedings of the National Academy of Sciences, 2012
HIV-1 envelope glycoprotein is the primary target for HIV-1–specific antibodies. The native HIV-1... more HIV-1 envelope glycoprotein is the primary target for HIV-1–specific antibodies. The native HIV-1 envelope spike on the virion surface is a trimer, but trimeric gp140 and monomeric gp120 currently are believed to induce comparable immune responses. Indeed, most studies on the immunogenicity of HIV-1 envelope oligomers have revealed only marginal improvement over monomers. We report here that suitably prepared envelope trimers have nearly all the antigenic properties expected for native viral spikes. These stable, rigorously homogenous trimers have antigenic properties markedly different from those of monomeric gp120s derived from the same sequences, and they induce potent neutralizing antibody responses for a cross-clade set of tier 1 and tier 2 viruses with titers substantially higher than those elicited by the corresponding gp120 monomers. These results, which demonstrate that there are relevant immunologic differences between monomers and high-quality envelope trimers, have impor...
Journal of Theoretical Biology, 2009
The rapidly inactivating (I(Naf)) and noninactivating Na(+) currents (I(Na)(()(NI)())) were chara... more The rapidly inactivating (I(Naf)) and noninactivating Na(+) currents (I(Na)(()(NI)())) were characterized in NG108-15 neuronal cells differentiated with dibutyryl cyclic AMP in this study. Standard activation and inactivation protocols were used to evaluate the steady-state and kinetic properties of the I(Naf) present in these cells. The voltage protocols with a slowly depolarizing ramp were implemented to examine the properties of I(Na)(()(NI)()). Based on experimental data and computer simulations, a window component of the rapidly inactivating sodium current (I(Naf)(()(W)())) was also generated in response to the slowly depolarizing ramp. The I(Naf)(()(W)()) was subtracted from I(Na)(()(NI)()) to yield the persistent Na(+) current (I(Na)(()(P)())). Our results demonstrate the presence of I(Na)(()(P)()) in these cells. In addition to modifying the steady-state inactivation of I(Naf), ranolazine or riluzloe could be effective in blocking I(Naf)(()(W)()) and I(Na)(()(P)()). The ability of ranolazine and riluzole to suppress I(Na)(()(P)()) was greater than their ability to inhibit I(Naf)(()(W)()). In current-clamp recordings, current-induced voltage oscillations were applied to elicit action potentials (APs) through a gradual transition between spontaneous depolarization and upstroke. Ranolazine or riluzole at a concentration of 3 microM then effectively suppressed the AP firing generated by oscillatory changes in membrane current. The data suggest that a small rise in I(Na)(()(NI)()) facilitates neuronal hyper-excitability due the decreased threshold of AP initiation. The underlying mechanism of the inhibitory actions of ranolazine or riluzole on membrane potential in neurons or neuroendocrine cells in vivo may thus be associated with their blocking of I(Na)(()(NI)()).