该文建立了当归四逆汤物质基准的高效液相色谱(HPLC)特征图谱及多指标含量测定方法,阐明了当归四逆汤物质基准的关键质量属性,完善了其质量控制体系。使用的色谱柱为Pomenex Luna C 18(250 mm×4.6 mm,5μm),流动相为乙腈-0.05%磷...该文建立了当归四逆汤物质基准的高效液相色谱(HPLC)特征图谱及多指标含量测定方法,阐明了当归四逆汤物质基准的关键质量属性,完善了其质量控制体系。使用的色谱柱为Pomenex Luna C 18(250 mm×4.6 mm,5μm),流动相为乙腈-0.05%磷酸水溶液,体积流量为1.0 mL·min-1,梯度洗脱,进样量为10μL,柱温30℃,检测波长为230 nm和290 nm。15批物质基准特征图谱的相似度均大于0.89;两个检测波长下共确定45个共有峰,并指认7个共有成分,分别为芍药苷、阿魏酸、甘草苷、甘草酸铵、细辛脂素、桂皮醛和藁本内酯;15批物质基准的平均出膏率为15.00%;芍药苷、甘草酸铵、细辛脂素、桂皮醛和藁本内酯的含量分别为8.226~13.46、1.929~6.535、0.02002~0.03430、0.07661~0.5433和0.07594~0.1406 mg·g^(-1)。该研究为经典名方当归四逆汤物质基准的质量控制和复方制剂的开发提供了科学依据。展开更多
TMEM16F is involved in many physiological processes such as blood coagulation,cell membrane fusion and bone mineralization.Activation of TMEM16F has been studied in various central nervous system diseases.High TMEM16F...TMEM16F is involved in many physiological processes such as blood coagulation,cell membrane fusion and bone mineralization.Activation of TMEM16F has been studied in various central nervous system diseases.High TMEM16F level has been also found to participate in microglial phagocytosis and transformation.Microglia-mediated neuroinflammation is a key factor in promoting the progression of Alzheimer’s disease.However,few studies have examined the effects of TMEM16F on neuroinflammation in Alzheimer’s disease.In this study,we established TMEM16F-knockdown AD model in vitro and in vivo to investigate the underlying regulatory mechanism about TMEM16F-mediated neuroinflammation in AD.We performed a Morris water maze test to evaluate the spatial memory ability of animals and detected markers for the microglia M1/M2 phenotype and NLRP3 inflammasome.Our results showed that TMEM16F was elevated in 9-month-old APP/PS1 mice.After TMEM16F knockdown in mice,spatial memory ability was improved,microglia polarization to the M2 phenotype was promoted,NLRP3 inflammasome activation was inhibited,cell apoptosis and Aβplaque deposition in brain tissue were reduced,and brain injury was alleviated.We used amyloid-beta(Aβ_(25-35))to stimulate human microglia to construct microglia models of Alzheimer’s disease.The levels of TMEM16F,inducible nitric oxide synthase(iNOS),proinflammatory cytokines and NLRP3 inflammasome-associated biomarkers were higher in Aβ_(25-35) treated group compared with that in the control group.TMEM16F knockdown enhanced the expression of the M2 phenotype biomarkers Arg1 and Socs3,reduced the release of proinflammatory factors interleukin-1,interleukin-6 and tumor necrosis factor-α,and inhibited NLRP3 inflammasome activation through reducing downstream proinflammatory factors interleukin-1βand interleukin-18.This inhibitory effect of TMEM16F knockdown on M1 microglia was partially reversed by the NLRP3 agonist Nigericin.Our findings suggest that TMEM16F participates in neuroinflammation in Alzheimer’s 展开更多
Background：Bipolar electro-coagulation has a reported efficacy in treating epilepsy involving functional cortex by pure electro-coagulation or combination with resection.However,the mechanisms of bipolar electro-coag...Background：Bipolar electro-coagulation has a reported efficacy in treating epilepsy involving functional cortex by pure electro-coagulation or combination with resection.However,the mechanisms of bipolar electro-coagulation are not completely known.We studied the acute cortical blood flow and histological changes after bipolar electro-coagulation in 24 patients with intractable temporal lobe epilepsy.Methods：Twenty-four patients were consecutively enrolled,and divided into three groups according to the date of admission.The regional cortical blood flow （rCBF）,electrocorticography,the depth of cortex damage,and acute histological changes （H and E staining,neuronal staining and neurofilament （NF） staining） were analyzed before and after the operation.The t-test analysis was used to compare the rCBF before and after the operation.Results：The rCBF after coagulation was significantly reduced （P 〈 0.05）.The spikes were significantly reduced after electro-coagulation.For the temporal cortex,the depth of cortical damage with output power of 2-9 W after electro-coagulation was 0.34 ± 0.03,0.48 ± 0.06,0.69 ± 0.06,0.84 ± 0.09,0.98 ± 0.08,1.10 ± 0.1 l,1.11 ± 0.09,and 1.22 ± 0.11 mm,respectively.Coagulation with output power of 4-5 W completely damaged the neurons and NF protein in the molecular layer,external granular layer,and external pyramidal layer.Conclusions：The electro-coagulation not only destroyed the neurons and NF protein,but also reduced the rCBF.We concluded that the injuries caused by electro-coagulation would prevent horizontal synchronization and spread of epileptic discharges,and partially destroy the epileptic focus.展开更多
Quantum communication has been rapidly developed due to its unconditional security and successfully implemented through optical fibers and free-space air in experiments. To build a complete quantum communication netwo...Quantum communication has been rapidly developed due to its unconditional security and successfully implemented through optical fibers and free-space air in experiments. To build a complete quantum communication network involving satellites in space and submersibles in ocean, the underwater quantum channel has been investigated in both theory and experiment. However, the question of whether the polarization encoded qubit can survive through a long-distance and high-loss underwater channel, which is considered as the restricted area for satellite-borne radio waves, still remains. Here, we experimentally demonstrate the transmission of blue-green photonic polarization states through 55-m-long water. We prepare six universal quantum states at the single photon level and observe their faithful transmission in a large marine test platform. We obtain complete information of the channel by quantum process tomography. The distance demonstrated in this work reaches a region allowing potential real applications, representing a step further towards air-to-sea quantum communication.展开更多
Purpose： we once reported blast-induced traumatic brain injury （bTBI） in confined space. Here, bTBI was studied again on goats in the open air using 3.0 kg trinitrotoluene. Methods： The goats were placed at 2, 4, ...Purpose： we once reported blast-induced traumatic brain injury （bTBI） in confined space. Here, bTBI was studied again on goats in the open air using 3.0 kg trinitrotoluene. Methods： The goats were placed at 2, 4, 6 and 8 m far from explosion center. Trinitrotoluene （TNT） was used as the source of the blast wave and the pressure at each distance was recorded. The systemic physiology, electroencephalogram, serum level of S-100beta, and neuron specific enolase （NSE） were determined pre and post the exposure. Neuroanatomy and neuropathology were observed 4 h after the exposure. Results： Simple blast waveforms were recorded with parameters of 702.8 kPa-0.442 ms, 148.4 kPa- 2.503 ms, 73.9 kPa-3.233 ms, and 41.9 kPa-5.898 ms at 2, 4, 6 and 8 m respectively. Encephalic blast overpressure was on the first time recorded in the literature by us at 104.2 kPa-0.60 ms at 2 m, where mortality and burn rate were 44% and 44%. Gross examination showed that bTBI was mainly manifested as congestive expansion of blood vessels and subarachnoid hemorrhage, which had a total incidence of 25% and 19% in 36 goats. Microscopical observation found that the main pathohistological changes were enlarged perivascular space （21/36, 58%）, small hemorrhages （9/36, 25%）, vascular dilatation and congestion （8/36, 22%）, and less subarachnoid hemorrhage （2[36, 6%）. After explosion, serum levels of S- 10013 and NSE were elevated, and EEG changed into slow frequency with declined amplitude. The results indicated that severity and incidence of bTBI is related to the intensity of blast overpressure. Conclusion： Blast wave can pass through the skull to directly injure brain tissue.展开更多
文摘该文建立了当归四逆汤物质基准的高效液相色谱(HPLC)特征图谱及多指标含量测定方法,阐明了当归四逆汤物质基准的关键质量属性,完善了其质量控制体系。使用的色谱柱为Pomenex Luna C 18(250 mm×4.6 mm,5μm),流动相为乙腈-0.05%磷酸水溶液,体积流量为1.0 mL·min-1,梯度洗脱,进样量为10μL,柱温30℃,检测波长为230 nm和290 nm。15批物质基准特征图谱的相似度均大于0.89;两个检测波长下共确定45个共有峰,并指认7个共有成分,分别为芍药苷、阿魏酸、甘草苷、甘草酸铵、细辛脂素、桂皮醛和藁本内酯;15批物质基准的平均出膏率为15.00%;芍药苷、甘草酸铵、细辛脂素、桂皮醛和藁本内酯的含量分别为8.226~13.46、1.929~6.535、0.02002~0.03430、0.07661~0.5433和0.07594~0.1406 mg·g^(-1)。该研究为经典名方当归四逆汤物质基准的质量控制和复方制剂的开发提供了科学依据。
基金supported by the National Natural Science Foundation of China,No.82072941(to QHX)Liaoning Province Key R&D Program Guidance Project,No.2020JH2/10300044Science and Technology Plan Project of Shenyang,No.20-205-4-050(both to XHS)。
文摘TMEM16F is involved in many physiological processes such as blood coagulation,cell membrane fusion and bone mineralization.Activation of TMEM16F has been studied in various central nervous system diseases.High TMEM16F level has been also found to participate in microglial phagocytosis and transformation.Microglia-mediated neuroinflammation is a key factor in promoting the progression of Alzheimer’s disease.However,few studies have examined the effects of TMEM16F on neuroinflammation in Alzheimer’s disease.In this study,we established TMEM16F-knockdown AD model in vitro and in vivo to investigate the underlying regulatory mechanism about TMEM16F-mediated neuroinflammation in AD.We performed a Morris water maze test to evaluate the spatial memory ability of animals and detected markers for the microglia M1/M2 phenotype and NLRP3 inflammasome.Our results showed that TMEM16F was elevated in 9-month-old APP/PS1 mice.After TMEM16F knockdown in mice,spatial memory ability was improved,microglia polarization to the M2 phenotype was promoted,NLRP3 inflammasome activation was inhibited,cell apoptosis and Aβplaque deposition in brain tissue were reduced,and brain injury was alleviated.We used amyloid-beta(Aβ_(25-35))to stimulate human microglia to construct microglia models of Alzheimer’s disease.The levels of TMEM16F,inducible nitric oxide synthase(iNOS),proinflammatory cytokines and NLRP3 inflammasome-associated biomarkers were higher in Aβ_(25-35) treated group compared with that in the control group.TMEM16F knockdown enhanced the expression of the M2 phenotype biomarkers Arg1 and Socs3,reduced the release of proinflammatory factors interleukin-1,interleukin-6 and tumor necrosis factor-α,and inhibited NLRP3 inflammasome activation through reducing downstream proinflammatory factors interleukin-1βand interleukin-18.This inhibitory effect of TMEM16F knockdown on M1 microglia was partially reversed by the NLRP3 agonist Nigericin.Our findings suggest that TMEM16F participates in neuroinflammation in Alzheimer’s
文摘Background：Bipolar electro-coagulation has a reported efficacy in treating epilepsy involving functional cortex by pure electro-coagulation or combination with resection.However,the mechanisms of bipolar electro-coagulation are not completely known.We studied the acute cortical blood flow and histological changes after bipolar electro-coagulation in 24 patients with intractable temporal lobe epilepsy.Methods：Twenty-four patients were consecutively enrolled,and divided into three groups according to the date of admission.The regional cortical blood flow （rCBF）,electrocorticography,the depth of cortex damage,and acute histological changes （H and E staining,neuronal staining and neurofilament （NF） staining） were analyzed before and after the operation.The t-test analysis was used to compare the rCBF before and after the operation.Results：The rCBF after coagulation was significantly reduced （P 〈 0.05）.The spikes were significantly reduced after electro-coagulation.For the temporal cortex,the depth of cortical damage with output power of 2-9 W after electro-coagulation was 0.34 ± 0.03,0.48 ± 0.06,0.69 ± 0.06,0.84 ± 0.09,0.98 ± 0.08,1.10 ± 0.1 l,1.11 ± 0.09,and 1.22 ± 0.11 mm,respectively.Coagulation with output power of 4-5 W completely damaged the neurons and NF protein in the molecular layer,external granular layer,and external pyramidal layer.Conclusions：The electro-coagulation not only destroyed the neurons and NF protein,but also reduced the rCBF.We concluded that the injuries caused by electro-coagulation would prevent horizontal synchronization and spread of epileptic discharges,and partially destroy the epileptic focus.
基金National Basic Research Program of China(973 Program)(2017YFA0303700)National Natural Science Foundation of China(NSFC)(61734005,11761141014,11690033)+1 种基金Science and Technology Commission of Shanghai Municipality(STCSM)(15QA1402200,16JC1400405,17JC1400403)Shanghai Municipal Education Commission(SMEC)(16SG09,2017-01-07-00-02-E00049)
文摘Quantum communication has been rapidly developed due to its unconditional security and successfully implemented through optical fibers and free-space air in experiments. To build a complete quantum communication network involving satellites in space and submersibles in ocean, the underwater quantum channel has been investigated in both theory and experiment. However, the question of whether the polarization encoded qubit can survive through a long-distance and high-loss underwater channel, which is considered as the restricted area for satellite-borne radio waves, still remains. Here, we experimentally demonstrate the transmission of blue-green photonic polarization states through 55-m-long water. We prepare six universal quantum states at the single photon level and observe their faithful transmission in a large marine test platform. We obtain complete information of the channel by quantum process tomography. The distance demonstrated in this work reaches a region allowing potential real applications, representing a step further towards air-to-sea quantum communication.
基金special funds for major state basic research project,China，grants from the National Natural Science Foundation of China，grant from the funds of the State Key Laboratory of Trauma,Burn and Combined Injury
文摘Purpose： we once reported blast-induced traumatic brain injury （bTBI） in confined space. Here, bTBI was studied again on goats in the open air using 3.0 kg trinitrotoluene. Methods： The goats were placed at 2, 4, 6 and 8 m far from explosion center. Trinitrotoluene （TNT） was used as the source of the blast wave and the pressure at each distance was recorded. The systemic physiology, electroencephalogram, serum level of S-100beta, and neuron specific enolase （NSE） were determined pre and post the exposure. Neuroanatomy and neuropathology were observed 4 h after the exposure. Results： Simple blast waveforms were recorded with parameters of 702.8 kPa-0.442 ms, 148.4 kPa- 2.503 ms, 73.9 kPa-3.233 ms, and 41.9 kPa-5.898 ms at 2, 4, 6 and 8 m respectively. Encephalic blast overpressure was on the first time recorded in the literature by us at 104.2 kPa-0.60 ms at 2 m, where mortality and burn rate were 44% and 44%. Gross examination showed that bTBI was mainly manifested as congestive expansion of blood vessels and subarachnoid hemorrhage, which had a total incidence of 25% and 19% in 36 goats. Microscopical observation found that the main pathohistological changes were enlarged perivascular space （21/36, 58%）, small hemorrhages （9/36, 25%）, vascular dilatation and congestion （8/36, 22%）, and less subarachnoid hemorrhage （2[36, 6%）. After explosion, serum levels of S- 10013 and NSE were elevated, and EEG changed into slow frequency with declined amplitude. The results indicated that severity and incidence of bTBI is related to the intensity of blast overpressure. Conclusion： Blast wave can pass through the skull to directly injure brain tissue.
