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Metastasis and resistance are main causes to affect the outcome of the current anticancer therapies. Heat shock protein 90 (Hsp90) as an ATP-dependent molecular chaperone takes important role in the tumor metastasis and resistance. Targeting Hsp90 and downregulating its expression show promising in inhibiting tumor metastasis and resistance. In this study, a redox-responsive dual-drug nanocarrier was constructed for the effective delivery of a commonly used chemotherapeutic drug PTX, and a COA-modified 4-arm PEG polymer (4PSC) was synthesized. COA, an active component in oleanolic acid that exerts strong antitumor activity by downregulating Hsp90 expression, was used as a structural and functional element to endow 4PSC with redox responsiveness and Hsp90 inhibitory activity. Our results showed that 4PSC/PTX nanomicelles efficiently delivered PTX and COA to tumor locations without inducing systemic toxicity. By blocking the Hsp90 signaling pathway, 4PSC significantly enhanced the antitumor effect of PTX, inhibiting tumor proliferation and invasiveness as well as chemotherapy-induced resistance in vitro. Remarkable results were further confirmed in vivo with two preclinical tumor models. These findings demonstrate that the COA-modified 4PSC drug delivery nanosystem provides a potential platform for enhancing the efficacy of chemotherapies.
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Reducing the inflammatory response is a major goal in the therapy of rheumatoid arthritis (RA). Herein, we integrated palladium nanoparticles (Pd NPs) with selenium nanoparticles (Se NPs) and obtained a multiple nanosystem (Pd@Se-HA NPs) that could simultaneously scavenge hydroxyl radicals (⋅OH) and provide a photothermal effect. The Pd@Se-HA NPs were constructed by a simple self-assembly method in which Se NPs were electrostatically bonded to Pd NPs; hyaluronic acid (HA) was linked to the NPs by ester bonding to provide macrophage targeting ability. The experiments show that the combined therapy of eliminating ⋅OH with Se NPs and utilizing PTT with Pd NPs could effectively reduce the inflammatory response in macrophages more effectively than either individual NP treatment. In addition, the outer layer of HA could specifically target the CD44 receptor to enhance the accumulation of Pd@Se NPs at the lesion, further enhancing the therapeutic effect. After treatment for 15 days, the Pd@Se-HA NPs nearly eliminated the inflammatory response in the joints of mice in an induced RA model, and prevented joint damage and degradation.
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MiR-142-3p has been reported to act as a tumor suppressor in breast cancer. However, the regulatory effect of miR-142-3p on drug resistance of breast cancer cells and its underlying mechanism remain unknown. Here, we found that miR-142-3p was significantly downregulated in the doxorubicin (DOX)-resistant MCF-7 cell line (MCF-7/DOX). MiR-142-3p overexpression increased DOX sensitivity and enhanced DOX-induced apoptosis in breast cancer cells. High-mobility group box 1 (HMGB1) is a direct functional target of miR-142-3p in breast cancer cells and miR-142-3p negatively regulated HMGB1 expression. Moreover, overexpression of HMGB1 dramatically reversed the promotion of apoptosis and inhibition of autophagy mediated by miR-142-3p up-regulation. In conclusion, miR-142-3p overexpression may inhibit autophagy and promote the drug sensitivity of breast cancer cells to DOX by targeting HMGB1. The miR-142-3p/HMGB1 axis might be a novel target to regulate the drug resistance of breast cancer patients.
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Aim To measure the methylation rate of bone marrow mesenchymal stem cells (BMMSCs) using ultra-performance liquid chromatography-tandem mass spectrometry, and determine the methylation rate in the process of senescence.Methods The DNA extracted from BMMSCs would be digested into individual deoxynucleosides using enzymatic hydrolysis.To quantify the global genomic DNA methylation rate,we developed a method using ultra-performance liquid chromatography-tandem mass spectrometry with multiple reaction monitoring to simultaneously measure the levels of 5-methyl deoxycytidine and deoxyguanosine in digested genomic DNA.Results The DNA methylation rate could be analyzed within two minutes after hydrolyzing 1μg DNA for an hour.The detection limit of DNA methylation rate was 5.00×10-4.The coefficient of variance of the intra-day and inter-day precision was within 7.12×10-2 and 0.119, respectively.With the subculture of BMMSCs, the methylation rate gradually decreased.The methylation rate of stem cells was the lowest in 4~6 generation, and gradually increased with the subculture.Conclusions Using this method, the preliminary data on DNA methylation of BMMSCs in the process of senescence are obtained.The method is simple and convenient for sample preprocessing, and the method is fast and accurate with good sensitivity and repeatability.
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Aim To investigate whether human umbili-cal cord mesenchymal stem cells(hUC-MSCs)exposed to inflammatory conditions could release large amounts of exosomes to induce regulatory T cells(Treg).Meth-ods hUC-MSCs were isolated by enzyme digestion method.(In vitro)interferonγ(IFN-γ)was added in-to hUC-MSCs to mimic inflammatory microenviron-ments,then exosomes were extracted from the superna-tant of normal conditional medium or IFN-γpretreated hUC-MSCs.Both sources of exosomes,Nor-hUC-exo and IFN-γ-stimulated hUC-exo, were identified by Nanoparticle Trafficking Analysis (NTA )and Western blot for the exosome-enriched protein CD63 .Next,hu-man peripheral blood mononuclear cells (PBMCs ) stimulated with PHA were respectively co-cultured with hUC-MSCs,IFN-γ-pretreated-hUC-MSCs,hUC-MSCs exosomes or IFN-γ-stimulated-hUC-MSCs exosomes for 5 days to assess the exosomes-T cells communication. The proliferation rate of PBMCs and frequency of CD4 +/CD25 +/Foxp3 + Treg were measured by flow cytometry.Results The isolated cells from human um-bilical cord tissue,which were positive for CD73, CD44,CD29,CD90 and HLA-ABC,but were nega-tive for CD31 and CD34,were mesenchymal stem cells indeed.After IFN-γtreatment,hUC-MSCs secreted nu-merous exosomes(P<0.05 ).Morerover,there was a significantly higher level of CD63 ,but no difference in diameter between Nor-hUC-exo and IFN-γ-stimulated hUC-exo.IFN-γ-stimulated hUC-exo had a superior a-bility compared with Nor-hUC-exo to suppress the pro-liferation of PHA stimulated PBMCs due to their upreg-ulation of the percentage of Treg (1 1.53 ±0.88% vs 6.60 ±0.56%,P <0.01 ).Conclusion hUC-MSCs could promote the expression of Treg to modulate im-munosuppression through exosomes,especially for IFN-γ-licenced exosomes,which might carry much immu-notherapeutic potential.
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Aim To investigate the effect of Sonic Hedgehog on normal hearts and hypoxic-ischemic myo-cardial cells. Methods A method for left anterior de-scending artery ( LAD ) ligation was employed to con-struct the myocardial infarction model, and ultrasonic cardiogram was used for identification. Western blot and immunofluorescence staining were used to detect expressions of Shh, Ptch-1, Smo and Gli-1 in H9C2 cells and H2 O2-induced H9C2 cells, and that in 12 ca-ses of myocardial infarction tissues and 9 cases of nor-mal myocardium, respectively. Agonist and antagonist of Shh pathway were adminstered in the hypoxic-ische-mic myocardial H2 O2-induced H9C2 cell model, and once again expressions and strength of Shh, Ptch-1, Smo, Gli-1 were detected. Results Shh and Gli-1 were not expressed in normal hearts, but expressed in hearts with myocardial infarction;Ptch-1 and Smo were expressed in both normal hearts and hearts with myo-cardial infarction. Under the action of agonist, expres-sions of Shh and Gli-1 increased in the hypoxic-ische-mic H9C2 cell model. Similarly, Shh and Gli-1 were not expressed in normal H9C2 cells, but in H2 O2-in-duced H9C2 cells, and Ptch-1 and Smo were expressed in both normal H9C2 and in H2 O2-induced H9C2 cells. Conclusion Shh signaling pathway can be acti-vated in the condition of ischemia and oxidative stress, and then it promotes the repairing of myocardial cell damage.
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AIM:Increasing evidence indicates that inflammation contributes to the initiation and perpetuation of atrial fibrillation ( AF) .Al-though tumor necrosis factor ( TNF)-αlevels are increased in patients with AF , the role of TNF-αin the pathogenesis of AF remains unclear.Recent research has revealed that T-type Ca2+currents ( ICa,T ) play an important role in the pathogenesis of AF .METH-ODS:In this study , we used the whole-cell voltage-clamp technique and biochemical assays to explore the role of TNF-αin the regula-tion of ICa,T in atrial myocytes.RESULTS:We found that compared with sinus rhythm (SR) controls, T-type calcium channel (TCC) subunit mRNA levels were decreased , while TNF-αexpression levels were increased , in human atrial tissue from patients with AF .In murine atrial myocyte HL-1 cells, after cultured for 24 h, 12.5, 25 and 50 μg/L TNF-αsignificantly reduced the protein expression levels of the TCC α1G subunit in a concentration-dependent manner .The peak current was reduced by the application of 12.5 or 25μg/L TNF-αin a concentration-dependent manner [from ( -15.08 ±1.11) pA/pF in controls to ( -11.89 ±0.83) pA/pF and (-8.54 ±1.55) pA/pF in 12.5 and 25 μg/L TNF-αgroups, respectively].TNF-αapplication also inhibited voltage-dependent inactivation of ICa,T shifted the inactivation curve to the left .CONCLUSION:These results suggest that TNF-αis involved in the path-ogenesis of AF, probably via decreasing ICa,T function in atrium-derived myocytes through impaired channel function and down -regula-tion of channel protein expression .This pathway thus represents a potential pathogenic mechanism in AF .
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OBJECTIVE:To explore the genome-wide methylation differences between coronary heart disease (CHD) patients and healthy volunteers,and to investigate the relationsip of DNA methylation with CHD from epigenetics. METHODS:In case-control study,subjects were divided into CHD group(50 cases)and health control group(50 cases). DNA of 2 groups were sequenced with methylated DNA immunoprecipitation sequencing technology. The genome-wide methylation differences were analyzed and compared between 2 groups. RESULTS:The number of methylation peak in CHD group was higher than health group,with statistical signfi-cance(P<0.05). The methylation peak mainly distributed in 5'UTR,Intron functional elements. The number of reads in AQP1,SHB and other gene promoters in CHD group were lower than health group,and its methylation level decreased. The number of reads in GRK5 and serveal gene promoters on chrX in CHD group were higher than helath group,and its methylation level increased,with sta-tistical significance(P<0.01). CONCLUSIONS:The genome-wide methylation level of CHD patients are higher than those of healthy volunteers. The occurence of CHD is possibly associated with the change of methylation level of related gene promoters.
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Aim To explore the anti-apoptotic function of cardiac progenitor cells(CPCs)-derived exosome in vitro.Method CPCs were isolated from mouse heart using Magnetic Cell Sorting(MACS)system.Flow Cy-tometry(FC)determine the purity of stem cell surface antigen-1 positive(Sca-1 +)CPCs.Exosome was puri-fied from conditional medium,and confirmed by West-ern blot using CD63 as a marker,Nanoparticle Traffic-king Analysis(NTA)was used to detect the diameters and concentration of exosome.Then the cells were di-vided into control groups and CPC-exosome pre-protec-tion groups.H2 O2 was added into H9c2 cells to induce oxidative stress.Western blot was adopted to determine the expression of cleaved caspase-3.Results ① Im-munofluorescence showed that CPCs isolated by MACS were positively expressing Sca-1 protein;FC analysis showed that typical purity of Sca-1 +CPCs from the first preparations was more than 95%.② WB demonstrated that CD63 of exosome isolated from CCMwas positively expressed,and NTA results showed that the diameters of exosome were (82.33 ±3.06)nm(n =3).Micro-scope detected PKH-26 labeled exosome appeared in the cytoplasma of H9c2 cells.③ Western blot showed the CPC-exosome pre-protection groups significantly down-regulated the levels of cleaved caspase-3 com-pared to the control groups(P <0.05).Conclusion CPC can secrete exosome which carries many important cargos,which can effectively gather in H9c2 cells. CPC-exosome can protect H9c2 cells from the oxidative stress induced by H2 O2 .Our results highlight a new perspective strategy for cardiac disease.
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AIM:To investigate whether the association of connexin 43 ( Cx43 ) and L-type calcium channel involved in the pathogenesis of atrial fibrillation ( AF) .METHODS:The biochemical assays and whole-cell patch-clamp technique were used to study the expression of Cx43 in human atrial tissue.The co-localization of Cx43 and L-type calcium channel, and the regulation of L-type calcium current in atrial myocytes were investigated.RESULTS:The expression of Cx43 at mRNA and protein levels was decreased in human atrial tissues of AF patients.In cultured atrium-derived myocytes ( HL-1 cells) , knockdown of Cx43 significantly inhibited the mRNA expression of L-type calcium channelα1c subunit, as well as L-type calcium current.Co-localization of Cx43 with L-type calcium channel α1c subunit in mouse atrial myocytes was observed.CONCLUSION:The decrease in Cx43 is involved in the pathogenesis of AF, probably through reducing the L-type calcium current in atrial myoctyes by co-localization with L-type calcium channel, thus representing the potential pathogenesis in atrial fibrillation.
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It was previously revealed that noncoding RNAs, especially microRNAs, control cardiac genes and regulate heart function.Recently, growing evidence from high-throughput genomic platforms has confirmed that long non-coding RNAs ( lncRNAs) serve as new and enigmatic regulators in cardiac development and homeostasis.Nevertheless, lit-tle is known about their characteristics compared to microRNAs.Here, we review the latest progress on lncRNAs in cardiac biology and diseases, summarizing detailed knowledge of their functions and novel cardiac-related gene regulatory mecha-nisms in epigenetic processes.Finally, we highlight that lncRNAs could be promising therapeutic targets and diagnostic bi-omarkers in cardiac pathophysiology.
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[ ABSTRACT] AIM:To investigate the role of encapsulated protein transfected into human bone marrow mesen-chymal stem cells ( hBMSCs) by polyethyleneimine ( PEI) , and to optimize the best mole ratio of PEI-proteins.METH-ODS:6 groups of DNase I-PEI complexes were constructed and the best mole ratio was explored by laser scattering analy-sis.The appearance of complexes was presented under transmission electron microscope.Meanwhile, 4 groups of construc-ted GFP-PEI complexes were utilized to transfect into the hBMSCs, which were isolated and expand in vitro.The fluores-cence intensity of transfected cells was observed under confocal microscope.In addition, the cytotoxicity of the complexes on the cell proliferation was detected by MTT assay.The activity of the intracellular proteins was testified by aβ-galactosi-dase staining experiment.RESULTS:When the mole ratio of PEI and protein was adjusted to 4∶1, the complex transfec-tion efficiency was the best, and β-galactosidase color test turned blue.CONCLUSION:PEI has the character of encap-sulating various proteins to nano-complexes.The proteins transfected into bone marrow mesenchymal stem cells are con-firmed to have functional activity.As a protein carrier, PEI is of high efficiency and low toxicity, thus providing a new way for stem cell reprogramming.
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The provenances of Rongshui miniature pigs ( RMPs) were purchased from Rongshui, Guangxi, in 2012.130 RMPs were transported to Sanshui, Guangdong,China, which were breed according to the laboratory animal standards.83 RMPs were selected randomly from the first filial generations ( F1 ).The basic data were collected including breed characteristics, reproductive performance, grow curve, hematology, biochemical markers of serum and urine, organ coefficient, Chromosome analysis.According to the national and local standards, the quality control standards of RMP were set up including microbiological, parasitic, environment and facilities, fodder, pathology, genetic.The results showed that RMPs adapt to the climate of Guangdong.The natural mating and conceive rate was 88.3% with the pregnancy of 112 days.The average number of firstborn and still-born was 6.1 and 7.9 respectively.RMP was small body size with the adult body weight of 17.21 ±5.20 kg and 16.35 ±5.23 kg in female and male respectively.RMP was very tame.The mitochondrial genome analysis suggested RMP belonged a typical miniature pig breed in China, which is ancient than Lanyu pig.RMP could be breed as a new kind of laboratory animal.
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Objective Assembly whole mitochondrial genome sequence of Rongshui miniature pig ( RMP ) breed and analysis the structure of mitochondrion based on the next-generation sequecing method.Comparison of phylogenetic relationship and genetic diversity among different pig breeds.Methods We collected peripheral venous blood sample from RMP and constructed two paired-end sequencing libraries.A whole-genome shotgun sequencing strategy and Illumina Genome Analyser sequencing technology were used in our study.Results The mitochondrial genome of RMP consists of 13 protein coding genes, 2 ribosomal RNA genes, 22 transfer RNA genes and the length of pig is 16888 bp.The GC content of this pig mitochondrial genome is about 44 %.Based on phlogenetic analysis, population genetic analysis, our findings confirmed that the ancestral cluster in East Asia mainly occurred among Diannan 7#pig, Hainan wild boar, Lanyu and RMP.Conclusion RMP, a typical miniature pig breed in China, is an earlier ancestor than Lanyu pig breed.
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BACKGROUND:Inducing pluripotent stem cels has been considered as a promising treatment for ischemic heart disease. However, an ideal inducing method has not been found yet. OBJECTIVE:To investigate the role of sodium-calcium exchanger (NCX1) promoter in the differentiation of mouse induced pluriptent stem cels (miPS) into cardiomyocytes. METHODS: The pLVX-IRES-ZsGreen1 vectors which contain NCX1 promoter constructed by recombinant DNA technology were co-transfected to 293FT cels with ViraPowerTM Lentiviral Packaging Mix. The recombinant lentiviruses infected with miPS were selected and purified by puromycin. miPS were recovered and passaged to form embryoid bodies. The embryoid bodies were induced by differentiation medium containing various concentrations of the virus titer. The number of beating embryoid bodies were calculated. The expression profiles of the myocardial intra-markers were tested to determine the differentiation efficiency of iPSC by RT-PCR and immunofluorescence analysis. RESULTS AND CONCLUSION:pLVX-IRES-ZsGreen1 vectors which contain NCX1 promoter were constructed and confirmed by PCR. Virus could be packaged, purified and concentrated successfuly. The recombinant lentivirus to transduce miPS was sorted by flow cytometry. In contrast to NCX1-/GFP- cels, NCX1+/GFP+ cels were differentiated and developed prominent beating areas with sustained contractile activity for additional 4 days, and demonstrated positive expression of gap communication marker CX43 and cardiac troponin. The expressions of GATA4, MEF2c and Nkx2.5 in the NCX1+ cels were 4.2, 7.5, and 2.5 times those in NCX1- cels. Results showed the NCX1 promoter can promote the cardiac differentiation of miPS .
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BACKGROUND:Porous poly(3-hydroxybutyrate-co-4-hydroxybutyrate)/calcium metaphosphate composite membranes prepared previously is too thick and uneven in holes. OBJECTIVE:To prepare the thin even porous poly(3-hydroxybutyrate-co-4-hydroxybutyrate)/calcium metaphosphate composite membrane, and to evaluate the cytocompatibility and differentiation capacity. METHODS:Porous and nonporous, thin and even poly(3-hydroxybutyrate-co-4-hydroxybutyrate)/calcium metaphosphate composite membranes were prepared by phase separation method. Its thickness and weight loss rate were determined. Human bone marrow mesenchymal stem cel s were cocultured with porous and nonporous poly(3-hydroxybutyrate-co-4-hydroxybutyrate)/calcium metaphosphate composite membranes for 7 days. Ultrastructure of composite membranes was observed under the scanning electron microscopy. Surface markers of the bone marrow mesenchymal stem cel s on the composite membranes were analyzed using flow cytometry. RESULTS AND CONCLUSION:The thickness of the porous and nonporous composite membranes was (0.041 ± 0.005) mm and (0.058±0.004) mm. Weight loss rates of porous and nonporous composite membranes were respectively 19.93%and 7.64%at 24 hours. Calcium metaphosphate particles were evenly distributed in porous and nonporous composite membrane. Cel s spread entirely, showing spindle shape. Calcium metaphosphate particles were evenly distributed in porous composite membrane. Pore in porous composite membranes was also uniformly distributed, and pore size was about 2-8μm. Cel s spread entirely, showing polygonal shape with multiple tentacles. The tentacles of some cel s entered into the scaffold. CD105, CD90, CD44, CD29 and CD73 expression was detected in porous and nonporous composite membranes. There was no significant difference in cel-positive rate. Poly(3-hydroxybutyrate-co-4-hydroxybutyrate)/calcium metaphosphate composite membranes prepared in this study has good biocompatibility and could not promote cel differentiation.
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BACKGROUND:Calcium metaphosphate has excel ent biocompatibility, degradability, and cel affinity. Human bone marrow mesenchymal stem cel s can grow and proliferate in the pores of the porous calcium metaphosphate, but less is known about calcium metaphosphate nanoparticles. OBJECTIVE:To prepare calcium metaphosphate nanoparticles, and to analyze the effect of calcium metaphosphate nanoparticles at different concentrations on apoptosis of human bone marrow mesenchymal stem cel s by flow cytometry. METHODS:The calcium metaphosphate nanoparticles were prepared by wet bal mil ing. Scanning electron microscopy and transmission electron microscopy were used to observe the morphology of the calcium metaphosphate nanoparticles, and the crystal structure of nanoparticles was analyzed by X-ray diffraction. Calcium metaphosphate nanoparticles were mixed in the CYAGON Oricel TM basal medium, and the concentrations of calcium metaphosphate nanoparticles in the medium were 10, 1, 0.1 mg/L. Human bone marrow mesenchymal stem cel s were cultured for 7 days in the above-mentioned media, and apoptosis of human bone marrow mesenchymal stem cel s was analyzed by flow cytometry. RESULTS AND CONCLUSION:Calcium metaphosphate nanoparticles were successful y prepared by wet bal mil ing, irregular in shape, and the mean diameter was 10-30 nm. X-ray diffraction results showed the crystal structure of nonaparticles was mainlyβ-Ca(PO3)2. The cel ratio of G0/G1 phase and G2/M phase in 10 mg/L group was obviously higher than that in 1, 0.1 mg/L groups (P<0.01). The cel apoptosis rates during the early, middle, late stages in 10 mg/L group were obviously higher than those in 1, 0.1 mg/L groups (P<0.01), and the total cel apoptosis was also significantly increased in 10 mg/L group (P<0.01). These findings indicate that human bone marrow mesenchymal stem cel s proliferation can be inhibited by calcium metaphosphate nanoparticles, and apoptosis rate is increased significantly when the concentration of calcium metaphosphate nanoparticles increases from 1 mg/L to 10 mg/L.
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The effects of ketamine on transient outward potassium current (I(to)) of isolated human atrial myocytes were investigated to understand the mechanism of part of its effects by whole-cell patch-clamp. Atrial myocytes were enzymatically isolated from specimens of human atrial appendage obtained from patients under going cardiac valve displacing. Ito is recorded in voltage-clamp modes using the patch-clamp technique at room temperature. Currents signals were recorded by an Axopatch 200B amplifier with the Digidata 1322A-pClamp 9.0 data acquisition system. Ketamine decreased I(to) of human atrial myocytes in a dose-dependent manner. The current-voltage curve was significantly lowered, 30, 100, 300, and 1000 micromol x L(-1) ketamine decreased respectively I(to) current density about (13.62 +/- 0.04)%, (38.92 +/- 0.05)%, (72.24 +/- 0.10)% and (83.84 +/- 0.05)% at the potential of 50 mV, with an IC50 of 121 micromol x L(-1). The I(to) activation curve, inactivation curve and the recovery curve were not altered by ketamine. So, ketamine concentration-dependently decreased I(to) of human atrial myocytes.
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Objective To analyze a rare genotype with β-thalassemia intermadia.Methods Phenotypic analysis was performed using routine hematological tests to measure red blood cell parameters and high performance liquid chromatography (HPLC)was used to measure hemoglobin fractions.The β-globin gene mutations were conducted using reverse-dot-blot and DNA sequencing of the breakpoint region were characterized with gap-PCR.Results The proband had a trait of thalassemia intermedia with reduced hemoglobin (86 g/L).The proband's father had a trait of microcytic hypochromic with reduced mean corpuscular volume(MCV),mean corpuscular hemoglobin (MCH) (63.7 fl and 20.4 pg,respectively) and an elevated level of HbA2.He had the phenotype of heterozygosity for β-thalassemia.The preband's mother,grandmother and sister had a trait of heterezygote for hereditary persistence of fetal hemoglobin (HPFH) with elevated level of HbF,which were 28.3%,21.1% and 33.7%,respectively.After molecular characterization of the family members,the proband was identified as a patient with β-thalassemia intermedia caused by co-existence of β-thalassemia(β41-42) and HPFH-6.The father was heterozygoas for β-thaiassemia (β41-42/βN) and the mother,grandmother and sister were all heterozygons for HPFH-6.Condusions A rare β-thalassemia intermedia case resulting from compound heterezygote of β41-42 with HPFH-6 is found.This study may provide clinical experiences for antenatal diagnosis.
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Aim To investigate changes of MAP2 expression level in rat hippocampal pyramidal cells induced by chronic stress, and to explore effects of tianeptine on them. Methods 25 rats were divided randomly into three groups:Control group,Stress group and Stree-tianeptine group. The forced-swimming was performed to rats in stress group and stress-tianeptine. Using the immunohistochemistry and the computerized image technique, expression levels of phosphorated MAP2 and the number the Positive cells were assayed quantitatively in each group. Results Compared with control group (149.34?1.81), the phosphorated MAP2 average gray degree in pyramidal cells of stress group (144.99?4.40) was significantly lower, that of the stress-tianeptine group (148.84?2.73) was significantly higher than that of stress group; The number of phosphorated MAP2 positive cells in stress group (40.36?1.35) was significantly less compared withthat of control group (42.73?1.56); that of stress-tianeptine group (42.14?1.62) was significantly more than that of stress group. Conclusion It is suggested that tianeptine could inhibit the enhancement of phosphorated MAP2 expression in hippocampal pyramidal cells induced by chronic stress.