BACKGROUND： The effect of pituitary adenylate cyclase activating polypeptide （PACAP） during traumatic brain injury （TBI） and whether it can modulate secondary injury has not been reported previously. The present ...BACKGROUND： The effect of pituitary adenylate cyclase activating polypeptide （PACAP） during traumatic brain injury （TBI） and whether it can modulate secondary injury has not been reported previously. The present study evaluated the potential protective effects of ventricular infusion of PACAP in a rat model of TBI.METHODS： Male Sprague Dawley rats were randomly divided into 3 treatment groups （n=6, each）： sham-operated, vehicle （normal saline）＋TBI, and PACAP＋TBI. Normal saline or PACAP （1 μg/5 μL） was administered intracerebroventricularly 20 minutes before TBI. Right parietal cortical contusion was produced via a weight-dropping method. Brains were extracted 24 hours after trauma. Histological changes in brains were examined by HE staining. The numbers of CD4＋ and CD8＋ T cells in blood and the spleen were detected via flow cytometry.RESULTS： In injured brain regions, edema, hemorrhage, inflammatory cell infiltration, and swollen and degenerated neurons were observed under a light microscope, and the neurons were disorderly arrayed in the hippocampi. Compared to the sham group, average CD4＋ CD8＋ lymphocyte counts in blood and the spleen were significantly decreased in rats that received TBl＋vehicle, and CD4- CD8＋ were increased. In rats administered PACAP prior to TBI, damage was attenuated as evidenced by significantly increased CD4＋, and decreased CD8＋, T lymphocytes in blood and the spleen.CONCLUSION： Pretreatment with PACAP may protect against TBI by influencing periphery T cellular immune function.展开更多
AIM:To investigate precore/basal core promoter(PC/BCP) mutants throughout hepatitis B virus(HBV) infection and to determine their relationship to hepatitis B early antigen(HBeA g) titers.METHODS:We enrolled 191 patien...AIM:To investigate precore/basal core promoter(PC/BCP) mutants throughout hepatitis B virus(HBV) infection and to determine their relationship to hepatitis B early antigen(HBeA g) titers.METHODS:We enrolled 191 patients in various stages of HBV infection at the Huashan Hospital and the Taizhou Municipal Hospital from 2010 to 2012.None of the patients received antiviral therapy.HBV DNA from serum,was quantified by real-time PCR.The HBV genotype was determined by direct sequencing of the S gene.We used the Simpleprobe ultrasensitivequantitative method to detect PC/BCP mutants in each patient.We compared the strain number,percentage,and the changes in PC/BCP mutants in different phases,and analyzed the relationship between PC/BCP mutants and HBe Ag by multiple linear regression and logistic regression.RESULTS:Patients with HBV infection(n = 191) were assigned to groups by phase:Immune tolerance(IT) = 55,Immune clearance(IC) = 67,Low-replicative(LR) = 49,and HBeA g-negative hepatitis(ENH) = 20.Of the patients(male,112; female,79) enrolled,122 were HBe Ag-positive and 69 were HBe Ag-negative.The median age was 33 years(range:18-78 years).PC and BCP mutation detection rates were 84.82%(162/191) and 96.86%(185/191),respectively.In five HBe Ag-negative cases,we detected double mutation G1896A/G1899 A.The logarithm value of PC mutant quantities(log10 PC) significantly differed in IT,IC,and LR phases,as well as in the ENH phase(F = 49.350,P < 0.001).The logarithm value of BCP mutant quantities(log10 BCP) also differed during the four phases(F = 25.530,P < 0.001).Log10 PC and log10 BCP values were high in the IT and IC phases,decreased in the LR phase,and increased in the ENH phase,although the absolute value at this point remained lower than that in the IT and IC phases.PC mutant quantity per total viral load(PC%) and BCP mutant quantity per total viral load(BCP%) differed between phases(F = 20.040,P < 0.001; F = 10.830,P < 0.001),with PC% and BCP% gradually increasing in successive phases.HBeA g titers negatively correlated with PC%(Spearman's rho =-0.354,P < 0.001) and BCP%(Spearman's rho =-0.395,P < 0.001).The negative correlation between PC% and HBeA g status was significant(B =-5.281,P = 0.001),but there was no such correlation between BCP% and HBeA g status(B =-0.523,P = 0.552).CONCLUSION:PC/BCP mutants become predominant in a dynamic and continuous process.Log10 PC,log10 BCP,PC% and BCP% might be combined to evaluate disease progression.PC% determines HBeA g status.展开更多
AIM： To investigate the effects of electrical stimulation of hypothalamic paraventricular nuclei （PVN） on gastric mucosal cellular apoptosis and proliferation induced by gastric ischemia/reperfusion （I/R） injury....AIM： To investigate the effects of electrical stimulation of hypothalamic paraventricular nuclei （PVN） on gastric mucosal cellular apoptosis and proliferation induced by gastric ischemia/reperfusion （I/R） injury. METHODS： For different experimental purposes, stimulating electrode plantation or electrolytic destruction of the PVN was applied, then the animals＇ GI/R injury model was established by clamping the celiac artery for 30 min and allowing reperfusing the artery for 30 rain, 1 h, 3 h or 6 h respectively. Then histological, immunohistochemistry methods were used to assess the gastric mucosal damage index, the gastric mucosal cellular apoptosis and proliferation at different times. RESULTS： The electrical stimulation of PVN significantly attenuated the GI/R injury at 30 min, i h and 3 h after reperfusion. The electrical stimulation of PVN decreased gastric mucosal apoptosis and increased gastric mucosal proliferation. The electrolytic destruction of the PVN could eliminate the protective effects of electrical stimulation of PVN on GI/R injury. These results indicated that the PVN participated in the regulation of GI/R injury as a specific area in the brain, exerting protective effects against the GI/R injury, and the protection was associated with the inhibition of cellular apoptosis and the promotion of gastric mucosal proliferation. CONCLUSION： Stimulating PVN significantly inhibits the gastric mucosal cellular apoptosis and promots gastric mucosal cellular proliferation. This may explain the protective mechanisms of electrical stimulation of PVN against GI/R injury.展开更多
By dispersing La1-xSrxMnO3 (LSMO) granule into PbZrxTi1-xO3 (PZT) matrix, the 0-3 type LSMO/PZT composite film is synthesized through chemical solution method. The asymmetry of the top and bottom electrodes introduces...By dispersing La1-xSrxMnO3 (LSMO) granule into PbZrxTi1-xO3 (PZT) matrix, the 0-3 type LSMO/PZT composite film is synthesized through chemical solution method. The asymmetry of the top and bottom electrodes introduces novel electrostatic screening on LSMO/PZT interface. As electric polarization is switched between upward and downward orientations, the evolution of exchange bias, diode transport, and magnetoresistance is observed. The result implies the electrostatic switch of magnetic core-shell in the present film. In detail, as the spontaneous polarization is upward or downward in the PZT matrix, the ferromagnetic/antiferromagnetic or ferromagnetic/ferromagnetic core-shell structure is formed in LSMO granule, respectively. This work would develop a novel device for spintronics and metamaterial.展开更多
We review the description and modeling of transport phenomena among the electron systems coupled via scalar or vector photons.It consists of three parts.The first part is about scalar photons,i.e.,Coulomb interactions...We review the description and modeling of transport phenomena among the electron systems coupled via scalar or vector photons.It consists of three parts.The first part is about scalar photons,i.e.,Coulomb interactions.The second part is with transverse photons described by vector potentials.The third part is onϕ=0 or temporal gauge,which is a full theory of the electrodynamics.We use the nonequilibrium Green’s function(NEGF)formalism as a basic tool to study steady-state transport.Although with local equilibrium it is equivalent to the fluctuational electrodynamics(FE),the advantage of NEGF is that it can go beyond FE due to its generality.We have given a few examples in the review,such as transfer of heat between graphene sheets driven by potential bias,emission of light by a double quantum dot,and emission of energy,momentum,and angular momentum from a graphene nanoribbon.All of these calculations are based on a generalization of the Meir–Wingreen formula commonly used in electronic transport in mesoscopic systems,with materials properties represented by photon self-energy,coupled with the Keldysh equation and the solution to the Dyson equation.展开更多
文摘BACKGROUND： The effect of pituitary adenylate cyclase activating polypeptide （PACAP） during traumatic brain injury （TBI） and whether it can modulate secondary injury has not been reported previously. The present study evaluated the potential protective effects of ventricular infusion of PACAP in a rat model of TBI.METHODS： Male Sprague Dawley rats were randomly divided into 3 treatment groups （n=6, each）： sham-operated, vehicle （normal saline）＋TBI, and PACAP＋TBI. Normal saline or PACAP （1 μg/5 μL） was administered intracerebroventricularly 20 minutes before TBI. Right parietal cortical contusion was produced via a weight-dropping method. Brains were extracted 24 hours after trauma. Histological changes in brains were examined by HE staining. The numbers of CD4＋ and CD8＋ T cells in blood and the spleen were detected via flow cytometry.RESULTS： In injured brain regions, edema, hemorrhage, inflammatory cell infiltration, and swollen and degenerated neurons were observed under a light microscope, and the neurons were disorderly arrayed in the hippocampi. Compared to the sham group, average CD4＋ CD8＋ lymphocyte counts in blood and the spleen were significantly decreased in rats that received TBl＋vehicle, and CD4- CD8＋ were increased. In rats administered PACAP prior to TBI, damage was attenuated as evidenced by significantly increased CD4＋, and decreased CD8＋, T lymphocytes in blood and the spleen.CONCLUSION： Pretreatment with PACAP may protect against TBI by influencing periphery T cellular immune function.
基金Supported by National Science and Technology Major Project of China,No.2012ZX10002007-001-002 and No.2013ZX10002001(to Zhang JM)the National Natural Science Foundation of China,No.81271833 and No.81471933(to Zhang JM)+1 种基金the Science and Technology Plan Project of Taizhou,Zhejiang province,No.1402ky19(to Tu WH and Hou W)the Scientific Research Project of Taizhou University,Zhejiang province,No:2014PY054(to Tu WH and Hou W)
文摘AIM:To investigate precore/basal core promoter(PC/BCP) mutants throughout hepatitis B virus(HBV) infection and to determine their relationship to hepatitis B early antigen(HBeA g) titers.METHODS:We enrolled 191 patients in various stages of HBV infection at the Huashan Hospital and the Taizhou Municipal Hospital from 2010 to 2012.None of the patients received antiviral therapy.HBV DNA from serum,was quantified by real-time PCR.The HBV genotype was determined by direct sequencing of the S gene.We used the Simpleprobe ultrasensitivequantitative method to detect PC/BCP mutants in each patient.We compared the strain number,percentage,and the changes in PC/BCP mutants in different phases,and analyzed the relationship between PC/BCP mutants and HBe Ag by multiple linear regression and logistic regression.RESULTS:Patients with HBV infection(n = 191) were assigned to groups by phase:Immune tolerance(IT) = 55,Immune clearance(IC) = 67,Low-replicative(LR) = 49,and HBeA g-negative hepatitis(ENH) = 20.Of the patients(male,112; female,79) enrolled,122 were HBe Ag-positive and 69 were HBe Ag-negative.The median age was 33 years(range:18-78 years).PC and BCP mutation detection rates were 84.82%(162/191) and 96.86%(185/191),respectively.In five HBe Ag-negative cases,we detected double mutation G1896A/G1899 A.The logarithm value of PC mutant quantities(log10 PC) significantly differed in IT,IC,and LR phases,as well as in the ENH phase(F = 49.350,P < 0.001).The logarithm value of BCP mutant quantities(log10 BCP) also differed during the four phases(F = 25.530,P < 0.001).Log10 PC and log10 BCP values were high in the IT and IC phases,decreased in the LR phase,and increased in the ENH phase,although the absolute value at this point remained lower than that in the IT and IC phases.PC mutant quantity per total viral load(PC%) and BCP mutant quantity per total viral load(BCP%) differed between phases(F = 20.040,P < 0.001; F = 10.830,P < 0.001),with PC% and BCP% gradually increasing in successive phases.HBeA g titers negatively correlated with PC%(Spearman's rho =-0.354,P < 0.001) and BCP%(Spearman's rho =-0.395,P < 0.001).The negative correlation between PC% and HBeA g status was significant(B =-5.281,P = 0.001),but there was no such correlation between BCP% and HBeA g status(B =-0.523,P = 0.552).CONCLUSION:PC/BCP mutants become predominant in a dynamic and continuous process.Log10 PC,log10 BCP,PC% and BCP% might be combined to evaluate disease progression.PC% determines HBeA g status.
基金grants from the National Natural Science Foundation of China, No. 30370533, 30570671the Educational Department Science Research Foundation of Jiangsu Province, No. 99KJB310005,05KJB310134
文摘AIM： To investigate the effects of electrical stimulation of hypothalamic paraventricular nuclei （PVN） on gastric mucosal cellular apoptosis and proliferation induced by gastric ischemia/reperfusion （I/R） injury. METHODS： For different experimental purposes, stimulating electrode plantation or electrolytic destruction of the PVN was applied, then the animals＇ GI/R injury model was established by clamping the celiac artery for 30 min and allowing reperfusing the artery for 30 rain, 1 h, 3 h or 6 h respectively. Then histological, immunohistochemistry methods were used to assess the gastric mucosal damage index, the gastric mucosal cellular apoptosis and proliferation at different times. RESULTS： The electrical stimulation of PVN significantly attenuated the GI/R injury at 30 min, i h and 3 h after reperfusion. The electrical stimulation of PVN decreased gastric mucosal apoptosis and increased gastric mucosal proliferation. The electrolytic destruction of the PVN could eliminate the protective effects of electrical stimulation of PVN on GI/R injury. These results indicated that the PVN participated in the regulation of GI/R injury as a specific area in the brain, exerting protective effects against the GI/R injury, and the protection was associated with the inhibition of cellular apoptosis and the promotion of gastric mucosal proliferation. CONCLUSION： Stimulating PVN significantly inhibits the gastric mucosal cellular apoptosis and promots gastric mucosal cellular proliferation. This may explain the protective mechanisms of electrical stimulation of PVN against GI/R injury.
基金Project supported by the Science Foundation of North University of China(Grant No.2017026)the Applied Basic Research Foundation of Shanxi Province,China(Grant No.201801D221143)+1 种基金the Scientific and Technological Innovation Programs of Higher Education Institutions in Shanxi,China(Grant No.2019L0535)the National Natural Science Foundation of China(Grant No.11847012).
文摘By dispersing La1-xSrxMnO3 (LSMO) granule into PbZrxTi1-xO3 (PZT) matrix, the 0-3 type LSMO/PZT composite film is synthesized through chemical solution method. The asymmetry of the top and bottom electrodes introduces novel electrostatic screening on LSMO/PZT interface. As electric polarization is switched between upward and downward orientations, the evolution of exchange bias, diode transport, and magnetoresistance is observed. The result implies the electrostatic switch of magnetic core-shell in the present film. In detail, as the spontaneous polarization is upward or downward in the PZT matrix, the ferromagnetic/antiferromagnetic or ferromagnetic/ferromagnetic core-shell structure is formed in LSMO granule, respectively. This work would develop a novel device for spintronics and metamaterial.
基金supported by NSFC under grant No.12204346,MOE tier 2 grant R-144-000-411-112MOE Academic Research Tier 1 Fund A-8000990-00-00.
文摘We review the description and modeling of transport phenomena among the electron systems coupled via scalar or vector photons.It consists of three parts.The first part is about scalar photons,i.e.,Coulomb interactions.The second part is with transverse photons described by vector potentials.The third part is onϕ=0 or temporal gauge,which is a full theory of the electrodynamics.We use the nonequilibrium Green’s function(NEGF)formalism as a basic tool to study steady-state transport.Although with local equilibrium it is equivalent to the fluctuational electrodynamics(FE),the advantage of NEGF is that it can go beyond FE due to its generality.We have given a few examples in the review,such as transfer of heat between graphene sheets driven by potential bias,emission of light by a double quantum dot,and emission of energy,momentum,and angular momentum from a graphene nanoribbon.All of these calculations are based on a generalization of the Meir–Wingreen formula commonly used in electronic transport in mesoscopic systems,with materials properties represented by photon self-energy,coupled with the Keldysh equation and the solution to the Dyson equation.
