The effects of protein kinase C （PKC） on the tension and the activity of voltage-dependent delayed rectifier potassium channel （K,,） were examined in normal and passively sensitized human airway smooth muscle （H...The effects of protein kinase C （PKC） on the tension and the activity of voltage-dependent delayed rectifier potassium channel （K,,） were examined in normal and passively sensitized human airway smooth muscle （HASM）, by measuring tones and whole-cell patch clamp techniques, and the Kv activities and membrane potential （Em） were also detected. The results showed that phorbol 12-myristate 13-acetate （PMA）, a PKC activator, caused a concentration-dependent constriction in normal HASM rings. The constriction of the passively sensitized muscle in asthma serum group was significantly higher than that of the normal group （P〈0.05）, and the constrictions of both groups were completely abolished by PKC inhibitor Ro31-8220 and calcium channel inhibitor nifedipine. Kv activities of HASM cells were significantly inhibited by PMA, and the Em became more positive, as compared with the DMSO （a PMA menstruum）-treated group （P〈0.01）. This effect could be blocked by Ro31-8220 （P〈0.01 ）. It was concluded that activation of PKC could increase the tones of HASM, which might be related to the reduced Kv activity. In passively sensitized HASM rings, this effect was more notable.展开更多
Background Potassium (K +) channels are important in regulating cell membrane potential and excitability. Although bronchial myocytes from asthmatic rats show a significant reduction in voltage-dependent delayed rec...Background Potassium (K +) channels are important in regulating cell membrane potential and excitability. Although bronchial myocytes from asthmatic rats show a significant reduction in voltage-dependent delayed rectifier potassium channel (Kv) current density and higher excitability, the activity and expression of Kv in human bronchial smooth muscle cells (HBSMCs) have never been studied. The ob jective of this study was to investigate the effect of passive sensitization by asthmatic serum on the activity of Kv and the expression of Kv isoform Kv1.5 in HBSMCs.Methods HBSMCs were randomly divided into two groups: control group (containing 10% serum from nonatopic individuals) and sensitized group (containing 10% asthmatic serum), then cultured for 24 hours. Whole-cell patch clamp, immunofluorescence staining, reverse transcription-polymerase chain reaction and Western blot techniques were used to study the effect of passive sensitization on the activity of Kv and the expression of Kv1.5 in HBSMCs.Results The membrane potential in passively sensitized HBSMCs was significantly depolarized to -(26.7±5.2) mV compared with -(41.3±6.4) mV in the cont rol group (P<0.01). Passive sensitization caused a significant inhibition of Kv currents in HBSMCs, resulting in a downward shift in the current-voltage (Ⅰ-Ⅴ) relationship curve. At +50mV, the peak Kv current density of passively sensitized HBSMCs was significantly decreased from (54.6±8.7) picoamperes per picofarad ( pA/pF) to (32.1±7.1) pA/pF (P<0.01). The expression level of Kv1.5 mRNA in passively sensitized HBSMCs was significantly lower than that in the control group (0.76±0.07 vs 1.04±0.13, P<0.05). The expression of Kv1.5 protein of passively sensitized HBSMCs was also significantly reduced compared to that from the control group (984±168 vs 2200±380, P<0.05).Conclusions The activity and expression of Kv were all decreased in HBSMCs passively sensitized by asthmatic serum compared with nonsensitized cells. These changes might be involved in the mechanisms of formation and development of asthma.展开更多
Objective To investigate changes in the delayed rectifier K + channel (Kv) function and the regulation of Kv by the protein kinase C (PKC) pathway in bronchial myocytes from asthmatic rats. Methods The Kv currents an...Objective To investigate changes in the delayed rectifier K + channel (Kv) function and the regulation of Kv by the protein kinase C (PKC) pathway in bronchial myocytes from asthmatic rats. Methods The Kv currents and membrane potentials in bronchial myocytes from asthmatic rats and from controls were observed, using whole cell voltage- and current-patch clamp techniques.Results Bronchial myocytes from asthmatic rats showed a significant reduction in Kv-current density (51.6±9.4 pA/pF, n=14, P<0.01) in comparison with those from control rats (72.4±12.3 pA/pF, n=14) at +50 mV. The current-voltage relationship curve exhibited a significant downward shift. Bronchial myocytes from asthmatic rats had no significantly different capacitances (P>0.05), but had more positive membrane potential ( P<0.01) compared with those from controls. 1 μmol/L phorbol 12-myristate 13-acetate, a PKC activator, caused an obvious reduction in Kv-current density (P<0.01) and a significant downward shift in the current-voltage relationship curve, an effect which was partly abolished by 1 μmol/L Ro31-8220 (a PKC inhibitor); 1 μmol/L phorbol 12-myristate 13-acetate caused more positive membrane potential (Em), from -36.8±5.7 mV to -30.4±7.3 mV, in rat bronchial myocytes (P<0.05). This effect was partly abolished by 1 μmol/L Ro31-8220. Conclusions Bronchial myocytes from asthmatic rats have inhibited Kv function, more positive membrane potential, and higher excitability, all of which can also be induced by PKC activation. These characteristics may contribute to the development of airway hyperreactivity in asthma.展开更多
In multi-cell cooperative multi-input multi-output （MIMO） systems, base station （BS） can exchange and utilize channel state information （CSI） of adjacent cell users to manage co-channel interference. Users quant...In multi-cell cooperative multi-input multi-output （MIMO） systems, base station （BS） can exchange and utilize channel state information （CSI） of adjacent cell users to manage co-channel interference. Users quantize the CSIs of desired channel and interference channels using finite-rate feedback links, then BS can generate cooperative block diagonalization （BD） precoding matrices using the obtained quantized CSI at transmitter to supress co-channel interference. In this paper, a novel adaptive bit allocation scheme is proposed to minimize the rate loss due to imperfect CSI. We derive the closed-form expression of rate loss caused by both channel delay and limited feedback. Based on the derived rate loss expression, the proposed scheme can adaptively allocate more bits to quantize the better channels with smaller delays and fewer bits to worse channels with larger delays. Simulation results show that the proposed scheme yields higher performance than other allocation schemes.展开更多
5G networks apply adaptive modulation and coding according to the channel condition reported by the user in order to keep the mobile communication quality.However,the delay incurred by the feedback may make the channe...5G networks apply adaptive modulation and coding according to the channel condition reported by the user in order to keep the mobile communication quality.However,the delay incurred by the feedback may make the channel quality indicator(CQI)obsolete.This paper addresses this issue by proposing two approaches,one based on machine learning and another on evolutionary computing,which considers the user context and signal-to-interference-plus-noise ratio(SINR)besides the delay length to estimate the updated SINR to be mapped into a CQI value.Our proposals are designed to run at the user equipment(UE)side,neither requiring any change in the signalling between the base station(gNB)and UE nor overloading the gNB.They are evaluated in terms of mean squared error by adopting 5G network simulation data and the results show their high accuracy and feasibility to be employed in 5G/6G systems.展开更多
Background：Stellate ganglion （SG） plays an important role in cardiovascular diseases.The electrical activity of SG neurons is involved in the regulation of the autonomic nervous system.The aim of this research was ...Background：Stellate ganglion （SG） plays an important role in cardiovascular diseases.The electrical activity of SG neurons is involved in the regulation of the autonomic nervous system.The aim of this research was to evaluate the effects offluvastatin on the electrophysiological characteristics of SG neurons in a rabbit model of myocardial ischemia （MI）.Methods：The MI model was induced by abdominal subcutaneous injections of isoproterenol in rabbits.Using whole-cell patch clamp technique,we studied the characteristic changes of ion channels and action potentials （APs） in isolated SG neurons in control group （n =20）,MI group （n =20） and fluvastatin pretreated group （fluvastatin group,n =20）,respectively.The protein expression of sodium channel in SG was determined by immunohistochemical analysis.Results：MI and the intervention of fluvastatin did not have significantly influence on the characteristics of delayed rectifier potassium channel currents.The maximal peak current density of sodium channel currents in SG neurons along with the characteristics of activation curves,inactivation curves,and recovery curves after inactivation were changed in the MI group.The peak current densities of control group,MI group,and fluvastatin group （n =10 in each group） were-71.77 ± 23.22 pA/pF,-126.75 ± 18.90 pA/pF,and-86.42 ± 28.30 pA/pF,respectively （F=4.862,P =0.008）.Fluvastatin can decrease the current amplitude which has been increased by MI.Moreover,fluvastatin induced the inactivation curves and post-inactive recovery curves moving to the position of the control group.But the expression of sodium channel-associated protein （Nav 1.7） had no significantly statistical difference among the three groups.The percentages of Nav 1.7 protein in control group,MI group,and fluvastatin group （n =5 in each group） were 21.49 ± 7.33%,28.53 ± 8.26%,and 21.64 ± 2.78%,respectively （F =1.495,P =0.275）.Moreover,MI reduced the electrical activity of AP and increased amplitude of AP,fluvastatin pretreatment could recover amplitude and electrical activity of AP.The probability of neurons induced continuous APs were 44.44%,14.29%,and 28.57% in control group,MI group,and fluvastatin group,respectively.Conclusions：Fluvastatin pretreatment can recover electrophysiology characteristics of ion channel and AP in SG neurons in a rabbit model of MI.It could be considered as potential method for treating coronary heart diseases.展开更多
基金This project was supported by a grant from the National Natural Sciences Foundation of China (No. 30270583)
文摘The effects of protein kinase C （PKC） on the tension and the activity of voltage-dependent delayed rectifier potassium channel （K,,） were examined in normal and passively sensitized human airway smooth muscle （HASM）, by measuring tones and whole-cell patch clamp techniques, and the Kv activities and membrane potential （Em） were also detected. The results showed that phorbol 12-myristate 13-acetate （PMA）, a PKC activator, caused a concentration-dependent constriction in normal HASM rings. The constriction of the passively sensitized muscle in asthma serum group was significantly higher than that of the normal group （P〈0.05）, and the constrictions of both groups were completely abolished by PKC inhibitor Ro31-8220 and calcium channel inhibitor nifedipine. Kv activities of HASM cells were significantly inhibited by PMA, and the Em became more positive, as compared with the DMSO （a PMA menstruum）-treated group （P〈0.01）. This effect could be blocked by Ro31-8220 （P〈0.01 ）. It was concluded that activation of PKC could increase the tones of HASM, which might be related to the reduced Kv activity. In passively sensitized HASM rings, this effect was more notable.
基金ThisstudywassupportedbytheNationalNaturalScienceFoundationofChina (No 3 0 2 70 5 83 )
文摘Background Potassium (K +) channels are important in regulating cell membrane potential and excitability. Although bronchial myocytes from asthmatic rats show a significant reduction in voltage-dependent delayed rectifier potassium channel (Kv) current density and higher excitability, the activity and expression of Kv in human bronchial smooth muscle cells (HBSMCs) have never been studied. The ob jective of this study was to investigate the effect of passive sensitization by asthmatic serum on the activity of Kv and the expression of Kv isoform Kv1.5 in HBSMCs.Methods HBSMCs were randomly divided into two groups: control group (containing 10% serum from nonatopic individuals) and sensitized group (containing 10% asthmatic serum), then cultured for 24 hours. Whole-cell patch clamp, immunofluorescence staining, reverse transcription-polymerase chain reaction and Western blot techniques were used to study the effect of passive sensitization on the activity of Kv and the expression of Kv1.5 in HBSMCs.Results The membrane potential in passively sensitized HBSMCs was significantly depolarized to -(26.7±5.2) mV compared with -(41.3±6.4) mV in the cont rol group (P<0.01). Passive sensitization caused a significant inhibition of Kv currents in HBSMCs, resulting in a downward shift in the current-voltage (Ⅰ-Ⅴ) relationship curve. At +50mV, the peak Kv current density of passively sensitized HBSMCs was significantly decreased from (54.6±8.7) picoamperes per picofarad ( pA/pF) to (32.1±7.1) pA/pF (P<0.01). The expression level of Kv1.5 mRNA in passively sensitized HBSMCs was significantly lower than that in the control group (0.76±0.07 vs 1.04±0.13, P<0.05). The expression of Kv1.5 protein of passively sensitized HBSMCs was also significantly reduced compared to that from the control group (984±168 vs 2200±380, P<0.05).Conclusions The activity and expression of Kv were all decreased in HBSMCs passively sensitized by asthmatic serum compared with nonsensitized cells. These changes might be involved in the mechanisms of formation and development of asthma.
基金ThisstudywassupportedbytheNationalNaturalScienceFoundationofChina (No 3 0 2 70 5 83 ) .
文摘Objective To investigate changes in the delayed rectifier K + channel (Kv) function and the regulation of Kv by the protein kinase C (PKC) pathway in bronchial myocytes from asthmatic rats. Methods The Kv currents and membrane potentials in bronchial myocytes from asthmatic rats and from controls were observed, using whole cell voltage- and current-patch clamp techniques.Results Bronchial myocytes from asthmatic rats showed a significant reduction in Kv-current density (51.6±9.4 pA/pF, n=14, P<0.01) in comparison with those from control rats (72.4±12.3 pA/pF, n=14) at +50 mV. The current-voltage relationship curve exhibited a significant downward shift. Bronchial myocytes from asthmatic rats had no significantly different capacitances (P>0.05), but had more positive membrane potential ( P<0.01) compared with those from controls. 1 μmol/L phorbol 12-myristate 13-acetate, a PKC activator, caused an obvious reduction in Kv-current density (P<0.01) and a significant downward shift in the current-voltage relationship curve, an effect which was partly abolished by 1 μmol/L Ro31-8220 (a PKC inhibitor); 1 μmol/L phorbol 12-myristate 13-acetate caused more positive membrane potential (Em), from -36.8±5.7 mV to -30.4±7.3 mV, in rat bronchial myocytes (P<0.05). This effect was partly abolished by 1 μmol/L Ro31-8220. Conclusions Bronchial myocytes from asthmatic rats have inhibited Kv function, more positive membrane potential, and higher excitability, all of which can also be induced by PKC activation. These characteristics may contribute to the development of airway hyperreactivity in asthma.
基金supported by the Important National Science & Technology Specific Projects(2010ZX03005-001-0)the Hi-Tech Research and Development of China(2006AA01Z272)the New Century Excellent Talents in University(NCET):(NCET-11-0593)
文摘In multi-cell cooperative multi-input multi-output （MIMO） systems, base station （BS） can exchange and utilize channel state information （CSI） of adjacent cell users to manage co-channel interference. Users quantize the CSIs of desired channel and interference channels using finite-rate feedback links, then BS can generate cooperative block diagonalization （BD） precoding matrices using the obtained quantized CSI at transmitter to supress co-channel interference. In this paper, a novel adaptive bit allocation scheme is proposed to minimize the rate loss due to imperfect CSI. We derive the closed-form expression of rate loss caused by both channel delay and limited feedback. Based on the derived rate loss expression, the proposed scheme can adaptively allocate more bits to quantize the better channels with smaller delays and fewer bits to worse channels with larger delays. Simulation results show that the proposed scheme yields higher performance than other allocation schemes.
基金supported by the Motorola Mobility,the National Council for Scientific and Technological Development(No.433142/2018-9)Research Productivity Fellowship(No.312831/2020-0)the Pernambuco Research Foundation(FACEPE)。
文摘5G networks apply adaptive modulation and coding according to the channel condition reported by the user in order to keep the mobile communication quality.However,the delay incurred by the feedback may make the channel quality indicator(CQI)obsolete.This paper addresses this issue by proposing two approaches,one based on machine learning and another on evolutionary computing,which considers the user context and signal-to-interference-plus-noise ratio(SINR)besides the delay length to estimate the updated SINR to be mapped into a CQI value.Our proposals are designed to run at the user equipment(UE)side,neither requiring any change in the signalling between the base station(gNB)and UE nor overloading the gNB.They are evaluated in terms of mean squared error by adopting 5G network simulation data and the results show their high accuracy and feasibility to be employed in 5G/6G systems.
文摘Background：Stellate ganglion （SG） plays an important role in cardiovascular diseases.The electrical activity of SG neurons is involved in the regulation of the autonomic nervous system.The aim of this research was to evaluate the effects offluvastatin on the electrophysiological characteristics of SG neurons in a rabbit model of myocardial ischemia （MI）.Methods：The MI model was induced by abdominal subcutaneous injections of isoproterenol in rabbits.Using whole-cell patch clamp technique,we studied the characteristic changes of ion channels and action potentials （APs） in isolated SG neurons in control group （n =20）,MI group （n =20） and fluvastatin pretreated group （fluvastatin group,n =20）,respectively.The protein expression of sodium channel in SG was determined by immunohistochemical analysis.Results：MI and the intervention of fluvastatin did not have significantly influence on the characteristics of delayed rectifier potassium channel currents.The maximal peak current density of sodium channel currents in SG neurons along with the characteristics of activation curves,inactivation curves,and recovery curves after inactivation were changed in the MI group.The peak current densities of control group,MI group,and fluvastatin group （n =10 in each group） were-71.77 ± 23.22 pA/pF,-126.75 ± 18.90 pA/pF,and-86.42 ± 28.30 pA/pF,respectively （F=4.862,P =0.008）.Fluvastatin can decrease the current amplitude which has been increased by MI.Moreover,fluvastatin induced the inactivation curves and post-inactive recovery curves moving to the position of the control group.But the expression of sodium channel-associated protein （Nav 1.7） had no significantly statistical difference among the three groups.The percentages of Nav 1.7 protein in control group,MI group,and fluvastatin group （n =5 in each group） were 21.49 ± 7.33%,28.53 ± 8.26%,and 21.64 ± 2.78%,respectively （F =1.495,P =0.275）.Moreover,MI reduced the electrical activity of AP and increased amplitude of AP,fluvastatin pretreatment could recover amplitude and electrical activity of AP.The probability of neurons induced continuous APs were 44.44%,14.29%,and 28.57% in control group,MI group,and fluvastatin group,respectively.Conclusions：Fluvastatin pretreatment can recover electrophysiology characteristics of ion channel and AP in SG neurons in a rabbit model of MI.It could be considered as potential method for treating coronary heart diseases.
