Spinal cord injury is considered one of the most difficult injuries to repair and has one of the worst prognoses for injuries to the nervous system.Following surgery,the poor regenerative capacity of nerve cells and t...Spinal cord injury is considered one of the most difficult injuries to repair and has one of the worst prognoses for injuries to the nervous system.Following surgery,the poor regenerative capacity of nerve cells and the generation of new scars can make it very difficult for the impaired nervous system to restore its neural functionality.Traditional treatments can only alleviate secondary injuries but cannot fundamentally repair the spinal cord.Consequently,there is a critical need to develop new treatments to promote functional repair after spinal cord injury.Over recent years,there have been seve ral developments in the use of stem cell therapy for the treatment of spinal cord injury.Alongside significant developments in the field of tissue engineering,three-dimensional bioprinting technology has become a hot research topic due to its ability to accurately print complex structures.This led to the loading of three-dimensional bioprinting scaffolds which provided precise cell localization.These three-dimensional bioprinting scaffolds co uld repair damaged neural circuits and had the potential to repair the damaged spinal cord.In this review,we discuss the mechanisms underlying simple stem cell therapy,the application of different types of stem cells for the treatment of spinal cord injury,and the different manufa cturing methods for three-dimensional bioprinting scaffolds.In particular,we focus on the development of three-dimensional bioprinting scaffolds for the treatment of spinal cord injury.展开更多
CD36 is a highly glycosylated integral membrane protein that belongs to the scavenger receptor class B family and regulates the pathological progress of metabolic diseases.CD36 was recently found to be widely expresse...CD36 is a highly glycosylated integral membrane protein that belongs to the scavenger receptor class B family and regulates the pathological progress of metabolic diseases.CD36 was recently found to be widely expressed in various cell types in the nervous system,including endothelial cells,pericytes,astrocytes,and microglia.CD36 mediates a number of regulatory processes,such as endothelial dysfunction,oxidative stress,mitochondrial dysfunction,and inflammatory responses,which are involved in many central nervous system diseases,such as stroke,Alzheimer’s disease,Parkinson’s disease,and spinal cord injury.CD36 antagonists can suppress CD36 expression or prevent CD36 binding to its ligand,thereby achieving inhibition of CD36-mediated pathways or functions.Here,we reviewed the mechanisms of action of CD36 antagonists,such as Salvianolic acid B,tanshinone IIA,curcumin,sulfosuccinimidyl oleate,antioxidants,and small-molecule compounds.Moreover,we predicted the structures of binding sites between CD36 and antagonists.These sites can provide targets for more efficient and safer CD36 antagonists for the treatment of central nervous system diseases.展开更多
Colorectal cancer(CRC)stands among the top prevalent cancers worldwide and holds a prominent position as a major contributor to cancer-related mortality globally.Absent in melanoma 2(AIM2),a constituent of the interfe...Colorectal cancer(CRC)stands among the top prevalent cancers worldwide and holds a prominent position as a major contributor to cancer-related mortality globally.Absent in melanoma 2(AIM2),a constituent of the interferoninducible hematopoietic interferon-inducible nuclear antigens with 200 amino acid repeats protein family,contributes to both cancer progression and inflammasome activation.Despite this understanding,the precise biological functions and molecular mechanisms governed by AIM2 in CRC remain elusive.Consequently,this study endeavors to assess AIM2’s expression levels,explore its potential antitumor effects,elucidate associated cancer-related processes,and decipher the underlying signaling pathways in CRC.Our findings showed a reduced AIM2 expression in most CRC cell lines.Elevation of AIM2 levels suppressed CRC cell proliferation and migration,altered cell cycle by inhibiting G1/S transition,and induced cell apoptosis.Further research uncovered the participation of P38 mitogen-activated protein kinase(P38MAPK)in AIM2-mediated modulation of CRC cell apoptosis and proliferation.Altogether,our achievements distinctly underscored AIM2’s antitumor role in CRC.AIM2 overexpression inhibited proliferation and migration and induced apoptosis of CRC cells via activating P38MAPK signaling pathway,indicating AIM2 as a prospective and novel therapeutic target for CRC.展开更多
Hypoxic injuries during fetal distress have been shown to cause reduced expression of micro RNA-27a（mi R-27a）,which regulates sensitivity of cortical neurons to apoptosis.We hypothesized that miR-27 a overexpression...Hypoxic injuries during fetal distress have been shown to cause reduced expression of micro RNA-27a（mi R-27a）,which regulates sensitivity of cortical neurons to apoptosis.We hypothesized that miR-27 a overexpression attenuates hypoxia- and ischemia-induced neuronal apoptosis by regulating FOXO1,an important transcription factor for regulating the oxidative stress response.miR-27 a mimic was transfected into hippocampal neurons to overexpress miR-27 a.Results showed increased hippocampal neuronal viability and decreased caspase-3 expression.The luciferase reporter gene system demonstrated that mi R-27 a directly binded to FOXO1 3′UTR in hippocampal neurons and inhibited FOXO1 expression,suggesting that FOXO1 was the target gene for mi R-27 a.These findings confirm that mi R-27 a protects hippocampal neurons against oxygen-glucose deprivation-induced injuries.The mechanism might be mediated by modulation of FOXO1 and apoptosis-related gene caspase-3 expression.展开更多
Backgroud： Wingless-type MMTV integration site family member 5a （Wnt5a） is involved in carcinogenesis.However, little data are available in Wnt5a signaling with hepatocellular carcinoma （HCC）. In thepresent study...Backgroud： Wingless-type MMTV integration site family member 5a （Wnt5a） is involved in carcinogenesis.However, little data are available in Wnt5a signaling with hepatocellular carcinoma （HCC）. In thepresent study, we investigated the expression of hepatic Wnt5a in HCC and the role of Wnt5a in HCCprogression and outcome.展开更多
AIM: To interfere with the activation of nuclear factor-κB(NF-κB) with metformin and explore its effect in reversing multidrug resistance(MDR) of hepatocellular carcinoma(HCC) cells.METHODS: Expression of P-glycopro...AIM: To interfere with the activation of nuclear factor-κB(NF-κB) with metformin and explore its effect in reversing multidrug resistance(MDR) of hepatocellular carcinoma(HCC) cells.METHODS: Expression of P-glycoprotein(P-gp) and NF-κB in human HepG 2 or HepG 2/adriamycin(ADM) cells treated with pC MV-NF-κB-small interference RNA(siR NA) with or without metformin, was analyzed by Western blot or fluorescence quantitative PCR. Cell viability was tested by CCK-8 assay. Cell cycle and apoptosis were measured by flow cytometry and Annexin-V-PE/7-AnnexinV apoptosis detection double staining assay, respectively. RESULTS: P-gp overexpression in HepG 2 and HepG 2/ADM cells was closely related to mdr1 mR NA(3.310 ± 0.154) and NF-κB mR NA(2.580 ± 0.040) expression. NF-κB gene transcription was inhibited by specific siR NA with significant down-regulation of P-gp and enhanced HCC cell chemosensitivity to doxorubicin. After pretreatment with metformin, Hep G2/ADM cells were sensitized to doxorubicin and P-gp was decreased through the NF-κB signaling pathway. The synergistic effect of metformin and NF-κB siR NA were found in HepG 2/ADM cells with regard to proliferation inhibition, cell cycle arrest and inducing cell apoptosis. CONCLUSION: Metformin via silencing NF-κB signaling could effectively reverse MDR of HCC cells by downregulating MDR1/P-gp expression.展开更多
Background:Hepatic Golgi protein-73(GP73)expression is related to hepatocellular carcinoma(HCC)progression.The aim of this study was to investigate the dynamic expression of GP73 mRNA and protein during hepatocytes ma...Background:Hepatic Golgi protein-73(GP73)expression is related to hepatocellular carcinoma(HCC)progression.The aim of this study was to investigate the dynamic expression of GP73 mRNA and protein during hepatocytes malignant transformation.Methods:Human GP73 expressions in 88 HCC tissues and their self-control surrounding tissues were examined by immunohistochemistry,and survival time of HCC patients was evaluated by the Kaplan-Meier method.HCC model of Sprague-Dawley rats was made by diet containing 2-fluorenylacetamide.The rats were divided into the control,hepatocyte degeneration,precanceration,and HCC groups to observe GP73 protein and mRNA alterations during hepatocytes malignant transformation.Results:The GP73 expression was significantly higher in the cancerous tissues than that in the surrounding tissues,with shorter survival time,and the positive rates of GP73 protein in human HCC tissues were 53.3%at stage I,84.0%at stage II,84.6%at stage III,and 60.0%at stage IV,respectively.The positive rates of hepatic GP73 protein and mRNA in the rat models were none in the control group,66.7%and 44.4%in the hepatocytes degeneration group,88.9%and 77.8%in the hepatocytes precanceration group,and 100%in the HCC group,respectively.There was a positive correlation(r=0.91,P<0.01)between hepatic GP73 and serum GP73 during rat hepatocytes malignant transformation.Conclusions:Abnormal GP73 expression may be a sensitive and valuable biomarker in hepatocarcinogensis.展开更多
Glial cells play an important role in signal transduction,energy metabolism,extracellular ion homeostasis and neuroprotection of the central nervous system.However,few studies have explained the potential effects of e...Glial cells play an important role in signal transduction,energy metabolism,extracellular ion homeostasis and neuroprotection of the central nervous system.However,few studies have explained the potential effects of exosomes from glial cells on central nervous system health and disease.In this study,the genes expressed in exosomes from astrocytes and microglia were identified by deep RNA sequencing.Kyoto Encyclopedia of Genes and Genomes analysis indicated that several pathways in these exosomes are responsible for promoting neurodegenerative diseases,including Alzheimer's disease,Parkinson's disease and Huntington's disease.Gene ontology analysis showed that extracellular exosome,mitochondrion and growth factor activity were enriched in exosomes from the unique astrocyte group,while extracellular exosome and mitochondrion were enriched in exosomes from the unique microglia group.Next,combined with the screening of hub genes,the protein-protein interaction network analysis showed that exosomes from astrocytes influence neurodegenerative diseases through metabolic balance and ubiquitin-dependent protein balance,whereas exosomes from microglia influence neurodegenerative diseases through immune inflammation and oxidative stress.Although there were differences in RNA expression between exosomes from astrocytes and microglia,the groups were related by the hub genes,ubiquitin B and heat shock protein family A(Hsp70) member 8.Ubiquitin B appeared to be involved in pleiotropic regulatory functions,including immune regulation,inflammation inhibition,protein catabolism,intracellular protein transport,exosomes and oxidative stress.The results revealed the clinical significance of exosomes from glia in neurodegenerative diseases.This study was approved by the Animal Ethics Committee of Nantong University,China(approval No.S20180102-152) on January 2,2018.展开更多
BACKGROUND: Cardiac arrest(CA) is a common and serious event in emergency medicine. Despite recent improvements in resuscitation techniques, the survival rate of patients with CA is unchanged. The present study was un...BACKGROUND: Cardiac arrest(CA) is a common and serious event in emergency medicine. Despite recent improvements in resuscitation techniques, the survival rate of patients with CA is unchanged. The present study was undertaken to observe the effect of mild hypothermia(MH) on the reactive oxygen species(ROS) and the effect of neurological function and related mechanisms.METHODS: Sixty-five healthy male Sprague Dawley(SD) adult rats were randomly(random number) divided into 2 groups: blank control group(n=5) and CPR group(n=60). CA was induced by asphyxia. The surviving rats were randomly(random number) divided into two groups: normothermia CPR group(NT) and hypothermia CPR group(HT). Normothermia of 37 °C was maintained in the NT group after return of spontaneous circulation(ROSC), hypothermal intervention of 32 °C was carried out in the HT group for 4 hours immediately after ROSC. Both the NT and HT groups were then randomly divided into 2 subgroups 12 hours and 24 hours after ROSC(NT-12, NT-24, HT-12, HT-24 subgroups). During observation, the neurological defi cit scores(NDSs) was recorded, then the bilateral hippocampi were obtained from rats' head, and monoplast suspension of fresh hippocampus tissue was made immediately to determine the level of intracellular ROS by flow cytometry. Transmission electron microscope was used to observe the ultramicro changes of cellular nucleus and mitochondria. Reverse transcription-polymerase chain reaction(RT-PCR) was used to determine the expression of caspase-3 m RNA, and western-blotting(WB) was used to determine the level of LC3 in frozen hippocampus tissue. Measured data were analyzed with paired sample t test and One-Way ANOVA.RESULTS: Of 60 rats with CA, 44(73%) were successfully resuscitated and 33(55%) survived until the end of the experiment. The NDSs of rats in the NT and HT groups were more signifi cantly reduced than those in the BC group(F=8.107, P<0.05), whereas the NDSs of rats in the HT-12 and HT-24 subgroups were significantly increased in comparison with those NDSs of rats in the NT-12 and NT-24 subgroups, respectively(t=9.692, P<0.001; t=14.374, P<0.001). The ROS in hippocampus nerve cells in the NT and HT groups signifi cantly increased compared to the BC group(F=16.824, P<0.05), whereas the ROS in the HT-12 and HT-24 subgroups significantly reduced compared with that ROS in the NT-12 and NT-24 subgroups, respectively(t=9.836, P<0.001; t=7.499, P<0.001). The expression of caspase-3 m RNA in hippocampus nerve cells in the NT and HT groups were signifi cantly increased compared to the BC group(F=24.527, P<0.05), whereas the expression of caspase-3 m RNA in rats of the HT-12 and HT-24 subgroups was signifi cantly reduced compared to the NT-12 and NT-24 subgroups, respectively(t=6.935, P<0.001; t=4.317, P<0.001). The expression of LC3B-II/I in hippocampus nerve cells of rats in the NT and HT groups signifi cantlyincreased compared to the BC group(F=6.584, P<0.05), whereas the expression of LC3B-II/I in rats of the HT-12 and HT-24 subgroups significantly reduced compared to the NT-12 and NT-24 subgroups, respectively(t=10.836, P<0.001; t=2.653, P=0.02). Ultrastructure damage of nucleus and mitochondria in the NT group was more evident than in the BC group, and eumorphism of nucleus and mitochondria were maintained in rats of the HT group compared with the NT group.CONCLUSION: Mild hypothermia lessened the injury of nerve cells and improved the neurological function of rats that survived from cardiac arrest by reducing the ROS production of nerve cells and inhibiting the expression of caspase-3 m RNA and LC3, leading to cellular apoptosis and massive autophagy in rats that survived from cardiac arrest after CPR.展开更多
BACKGROUND： It has been demonstrated that curcumin can increase the activities of various anti-oxidase in blood and tissue, effectively eliminate various free radicals, reduce the production of peroxisome, and allevi...BACKGROUND： It has been demonstrated that curcumin can increase the activities of various anti-oxidase in blood and tissue, effectively eliminate various free radicals, reduce the production of peroxisome, and alleviate oxidative stress reaction. Whether it has the same effect on microglia？ OBJECTIVE： To observe the effects of curcumin on the expressions of inducible nitric oxide synthase （iNOS）, nuclear factor- κ B （NF- κ B）, and superoxide dismutase （SOD） in microglial cell line BV stimulated by lipopolysaccharide （LPS）. DESIGN： An observational comparative study. SETTING： Research Room of Biochemistry, Medical College of Nantong University. MATERIALS： Mice microglia cell line BV, iNOS and NF- κ B reporter gene plasmids were presented by Dr. Bhat.NR. from the Medical University of South Carolina （USA）. Curcumin was produced by the Xi＇an Branch of China Chengdu Scholar Bio-Tech. Co.,Ltd.; LPS （E.Coli O26：B6）, anti-mice iNOS monoclonal antibody, horseradish peroxidase labeled goat-anti-mice IgG were the products of Sigma Company （USA）. METHODS： The experiments were carried out in the Research Room of Biochemistry, Medical College of Nantong University from May 2006 to April 2007. （1） Detection of iNOS： The cells were seeded onto 24-well plate at the density of 1 × 10^5, After the cells had adhered to the cover glasses, the cells were grouped as negative control group （the primary antibody was replaced by phosphate buffered solution PBS）; normal control group （the cells were normally cultured）; LPS-treated group （the cells were treated with LPS for 24 hours）; curcumin＋LPS group （the cells were treated with curcumin for 1 hour and LPS for 24 hours）. The expressions of iNOS protein were detected with immunocytochemical staining. （2） Determination of iNOS and NF- κ B gene activities： According to the introduction of the kit for transfection, iNOS or NF- κ B report gene plasmids were transiently transfected with Lipofectaminer^TM2000 liposomes into the cells in the 24-well plate for 24 hours. The cells were divided into normal control group （the cells were normally cultured after transfected with report gene plasmids）; blank plasmid group （the cells were normally cultured after transfected with blank plasmids）; LPS-treated group （the cells were treated with LPS for 4 hours after transfected with report gene plasmids）; curcumin＋LPS group （the cells were treated with curcumin for 1 hour and LPS for 24 hours after transfected with report gene plasmids）. The content of luciferase in the cell lysis buffer was determined after cell lysis. （3） Determination of SOD activity： The cells were seeded into culture bottle at the density of 1 × 10^6, and the divided into four groups, including normal control group （the cells were normally cultured）; LPS-treated group （the cells were treated with LPS for 24 hours）; curcumin＋LPS group （the cells were treated with curcumin for 1 hour and LPS for 24 hours）; vitamin C＋LPS group （the cells were treated with vitamin C for 1 hour and LPS for 24 hours）. The SOD activity was determined with xanthine oxidase and quantitative colorimetric assay. MAIN OUTCOME MEASURES： The expressions of iNOS protein, iNOS and NF- κ B, and the activity of SOD were observed. RESULTS： （1） Expression of iNOS protein in microglia： The expression of iNOS protein in the LPS-treated group was obviously higher than that in the negative control group （P 〈 0.01）; Those in the curcumin＋LPS group were significantly decreased as compared with that in the LPS-treated group （P 〈 0.01 ） （2） Expressions of iNOS and NF- κ B genes： The expressions of iNOS and NF- κ B genes in the LPS-treated group were significantly higher than those in the normal control group （P 〈 0.01）; Those in the curcumin＋LPS group were significantly lower than those in the LPS-treated group （P 〈 0.01）. （3） SOD activity： The activity of SOD in the LPS-treated group was significantly lower than those in the normal control group （P 〈 0.01）. It in the curcumin＋LPS group and vitamin C ＋LPS group was significantly higher than that in the LPS-treated group （P 〈 0.01）. CONCLUSION： Curcumin could inhibit the expression of iNOS in the activated microglia, and it also has the abilities in eliminating free radicals and antagonizing lipid peroxidation.展开更多
Objective:The aim of this study was to analyze the expression features of hypoxia inducible factor-1α (HIF-1α) in hepatocellular carcinoma (HCC) and effects of HIF-1α silencing on HepG2 cells.Methods:HIF-1α expres...Objective:The aim of this study was to analyze the expression features of hypoxia inducible factor-1α (HIF-1α) in hepatocellular carcinoma (HCC) and effects of HIF-1α silencing on HepG2 cells.Methods:HIF-1α expression was analyzed in the self-control HCC specimens by immunohistochemistry.After HepG2 cells with miRNA transfection,the expression of HIF-1α was determined at mRNA or protein level by real-time polymerase chain reaction (PCR) or Western blotting.Vascular endothelial growth factor (VEGF) and angiopoietin-2 (ANG-2) were determined by ELISA.Alterations of cell cycles and apoptosis of HepG2 cells were measured using a flow cytometer.Results:Positive HIF-1α was brown and granule-like in the cytoplasm or nucleus.Significant difference was found between HCC (80%) and its surrounding tissues (100%,χ2=22.35,P < 0.001) and HIF-1α expression related to tumor size.At 72 h after miRNA transfection,the expression of HIF-1α in HepG2 cells was down-regulated by 87% at mRNA or 65% at protein level,with VEGF and ANG-2 decreased to 54% and 36%,respectively.After RNA interference combined with anti-cancer drug,the apoptotic rate of HepG2 cells was increasing from 22.46% ± 0.61% to 36.99% ± 0.88%,with up-regulation of G1 phase (65.68% ± 0.91%) and down-regulation of S phase (19.47 ± 1.34 %).Conclusion:Abnormal expression of HIF-1α is associated with development of HCC,and HIF-1α gene silencing can effectively inhibit HepG2 cell proliferation.展开更多
Objective:To investigate the level and influencing factors of benefit discovery in patients with breast cancer after operation.Methods:Convenient sampling method was used to evaluate the change of benefit discovery le...Objective:To investigate the level and influencing factors of benefit discovery in patients with breast cancer after operation.Methods:Convenient sampling method was used to evaluate the change of benefit discovery level of 60 patients with breast cancer after operation in a cancer ward of a hospital by using Chinese version of benefit discovery rating scale and general information questionnaire.Results:The level of benefit discovery of breast cancer patients at different stages was statistically different(P<0.05).Age and education level entered the multiple linear stepwise regression equation of influencing factors of benefit discovery level of breast cancer patients(P<0.05).Conclusion:Targeted nursing measures should be taken to improve the quality of life of patients with breast cancer.展开更多
AIM To investigate the dynamic alteration of mitochondrial carnitine palmitoyl transferase Ⅱ(CPT-Ⅱ) expression during malignant transformation of rat hepatocytes.METHODS Sprague-Dawley male rats were fed with normal...AIM To investigate the dynamic alteration of mitochondrial carnitine palmitoyl transferase Ⅱ(CPT-Ⅱ) expression during malignant transformation of rat hepatocytes.METHODS Sprague-Dawley male rats were fed with normal, high fat(HF), and HF containing 2-fluorenylacetamide(2-FAA) diet, respectively. According to the Hematoxylin and Eosin staining of livers, rats were divided into control, fatty liver, degeneration, pre-cancerous, and cancerous groups. Liver lipids were dyed with Oil Red O, CPT-Ⅱ alterations were analyzed by immunohistochemistry, and compared with CPT-Ⅱ specific concentration(μg/mg protein). Levels of total cholesterol(Tch), triglyceride(TG), and aminotransferases [alanine aminotransferase(ALT), aspartate aminotransferase(AST)] were determined by the routine methods.RESULTS After intake of HF and/or HF+2-FAA diets, the rat livers showed mass lipid accumulation. The lipid level in the control group was significantly lower than that in other groups. The changes of serum TG and Tch levels were abnormally increasing, 2-3 times more than those in the controls(P < 0.05). During the rat liver morphological changes from normal to cancer development process with hepatocyte injury, serum AST and ALT levels were significantly higher(4-8 times, P < 0.05) than those in the control group. The specific concentration of CPT-Ⅱ in liver tissues progressively decreased during hepatocyte malignant transformation, with the lowest CPT-Ⅱ levels in the cancer group than in any of the other groups(P < 0.05).CONCLUSION Low CPT-Ⅱ expression might lead to abnormal hepatic lipid accumulation, which should promote the malignant transformation of hepatocytes.展开更多
AIM: To investigate member 3a of Wingless-type MMTV integration site family (Wnt3a) expression in cancerous and surrounding tissues and the relationship between clinicopathologic features of hepatocellular carcinoma (...AIM: To investigate member 3a of Wingless-type MMTV integration site family (Wnt3a) expression in cancerous and surrounding tissues and the relationship between clinicopathologic features of hepatocellular carcinoma (HCC) and Wnt3a expression.METHODS: Wnt3a expression and cellular distribution and clinicopathologic characteristics in cancerous tissue and matched surrounding tissues were analyzed in 80 HCC patients from January 2006 to August 2008 by tissue microarrays and immunohistochemistry. The overall and disease-free survival rates were estimated using the Kaplan-Meier method and compared with the log-rank test. The prognostic analysis was carried out with univariate and multivariate Cox regressions models.RESULTS: The incidence of oncogenic Wnt3a expression in the cancerous group was up to 96.25% (77 of 80), which was significantly higher (χ<sup>2</sup> = 48.818, P < 0.001) than that in the surrounding group (46.25%, 37 of 80). Brown Wnt3a staining gradually increased with clinical staging that showed very strong staining in advanced HCC. The clinicopathologic features of high Wnt3a expression in HCC were related to poorly-differentiated grade (χ<sup>2</sup> = 20.211, P < 0.001), liver cirrhosis (χ<sup>2</sup> = 8.467, P < 0.004), hepatitis B virus (HBV) infection (χ<sup>2</sup> = 12.957, P < 0.001), higher tumor-node-metastasis stage (χ<sup>2</sup> = 22.960, P < 0.001), and 5-year survival rate (χ<sup>2</sup> = 15.469, P < 0.001).CONCLUSION: Oncogenic Wnt3a expression associated with HBV infection and cirrhotic liver might be an independent prognostic factor for HCC.展开更多
Septic encephalopathy is a frequent complication of sepsis,but there are few studies examining the role of micro RNAs（mi Rs） in its pathogenesis.In this study,a mi R-219 mimic was transfected into rat hippocampal ne...Septic encephalopathy is a frequent complication of sepsis,but there are few studies examining the role of micro RNAs（mi Rs） in its pathogenesis.In this study,a mi R-219 mimic was transfected into rat hippocampal neurons to model mi R-219 overexpression.A protective effect of mi R-219 was observed for glutamate-induced neurotoxicity of rat hippocampal neurons,and an underlying mechanism involving calmodulin-dependent protein kinase II γ（Ca MKIIγ） was demonstrated.mi R-219 and Ca MKIIγ m RNA expression induced by glutamate in hippocampal neurons was determined by quantitative real-time reverse transcription-polymerase chain reaction（q RT-PCR）.After neurons were transfected with mi R-219 mimic,effects on cell viability and apoptosis were measured by 3-（4,5-dimethylthiazolyl-2）-2,5-diphenyltetrazolium bromide（MTT） assay and flow cytometry.In addition,a luciferase reporter gene system was used to confirm Ca MKIIγ as a target gene of mi R-219.Western blot assay and rescue experiments were also utilized to detect Ca MKIIγ expression and further verify that mi R-219 in hippocampal neurons exerted its effect through regulation of Ca MKIIγ.MTT assay and q RT-PCR results revealed obvious decreases in cell viability and mi R-219 expression after glutamate stimulation,while Ca MKIIγ m RNA expression was increased.MTT,flow cytometry,and caspase-3 activity assays showed that mi R-219 overexpression could elevate glutamate-induced cell viability,and reduce cell apoptosis and caspase-3 activity.Moreover,luciferase Ca MKIIγ-reporter activity was remarkably decreased by co-transfection with mi R-219 mimic,and the results of a rescue experiment showed that Ca MKIIγ overexpression could reverse the biological effects of mi R-219.Collectively,these findings verify that mi R-219 expression was decreased in glutamate-induced neurons,Ca MKIIγ was a target gene of mi R-219,and mi R-219 alleviated glutamate-induced neuronal excitotoxicity by negatively controlling Ca MKIIγ expression.展开更多
Acute kidney injury(AKI)affects approximately 13.3 million individuals and contributes to about 1.7 million deaths globally per year.As estimated 85% of those affected live in the developing world[1].Although there ar...Acute kidney injury(AKI)affects approximately 13.3 million individuals and contributes to about 1.7 million deaths globally per year.As estimated 85% of those affected live in the developing world[1].Although there are various measures to prevent or treat AKI,including renal protective drugs and continuous renal replacement therapy,most of them have limited success or are still in their infancy[2,3].展开更多
To the Editor:Recently,we reviewed almost all the articles reporting surfeit locus containing the six sequenceunrelated housekeeping genes Surfeit 1 to Surfeit 6 since 1988 and one of the family members,surfeit 4(SURF...To the Editor:Recently,we reviewed almost all the articles reporting surfeit locus containing the six sequenceunrelated housekeeping genes Surfeit 1 to Surfeit 6 since 1988 and one of the family members,surfeit 4(SURF 4)gene interested us.In this article,we will summarize the characteristics and protein localization of SURF4 gene,as well as its possible physiological functions and pathogenesis in various diseases and cancers,expecting to explore its clinical application values.展开更多
Spinal cord injury(SCI)often leads to permanent disability,which is mainly caused by the loss of functional recovery.In this review,we aimed to investigate why the healing process is interrupted.One of the reasons for...Spinal cord injury(SCI)often leads to permanent disability,which is mainly caused by the loss of functional recovery.In this review,we aimed to investigate why the healing process is interrupted.One of the reasons for this interruption is the formation of a glial scar around the severely damaged tissue,which is usually covered by reactive glia,macrophages and fibroblasts.Aiming to clarify this issue,we summarize the latest research findings pertaining to scar formation,tissue repair,and the divergent roles of blood-derived monocytes/macrophages,ependymal cells,fibroblasts,microglia,oligodendrocyte progenitor cells(OPCs),neuron-glial antigen 2(NG2)and astrocytes during the process of scar formation,and further analyse the contribution of these cells to scar formation.In addition,we recapitulate the development of therapeutic treatments targeting glial scar components.Altogether,we aim to present a comprehensive decoding of the glial scar and explore potential therapeutic strategies for improving functional recovery after SCI.展开更多
基金supported by the National Natural Science Foundation of China,No.82171380(to CD)Jiangsu Students’Platform for Innovation and Entrepreneurship Training Program,No.202110304098Y(to DJ)。
文摘Spinal cord injury is considered one of the most difficult injuries to repair and has one of the worst prognoses for injuries to the nervous system.Following surgery,the poor regenerative capacity of nerve cells and the generation of new scars can make it very difficult for the impaired nervous system to restore its neural functionality.Traditional treatments can only alleviate secondary injuries but cannot fundamentally repair the spinal cord.Consequently,there is a critical need to develop new treatments to promote functional repair after spinal cord injury.Over recent years,there have been seve ral developments in the use of stem cell therapy for the treatment of spinal cord injury.Alongside significant developments in the field of tissue engineering,three-dimensional bioprinting technology has become a hot research topic due to its ability to accurately print complex structures.This led to the loading of three-dimensional bioprinting scaffolds which provided precise cell localization.These three-dimensional bioprinting scaffolds co uld repair damaged neural circuits and had the potential to repair the damaged spinal cord.In this review,we discuss the mechanisms underlying simple stem cell therapy,the application of different types of stem cells for the treatment of spinal cord injury,and the different manufa cturing methods for three-dimensional bioprinting scaffolds.In particular,we focus on the development of three-dimensional bioprinting scaffolds for the treatment of spinal cord injury.
基金supported by the National Major Project of Research and Development,No.2022YFA1105500(to SZ)the National Natural Science Foundation of China,No.81870975(to SZ)Innovation Program for Graduate Students in Jiangsu Province of China,No.KYCX223335(to MZ)。
文摘CD36 is a highly glycosylated integral membrane protein that belongs to the scavenger receptor class B family and regulates the pathological progress of metabolic diseases.CD36 was recently found to be widely expressed in various cell types in the nervous system,including endothelial cells,pericytes,astrocytes,and microglia.CD36 mediates a number of regulatory processes,such as endothelial dysfunction,oxidative stress,mitochondrial dysfunction,and inflammatory responses,which are involved in many central nervous system diseases,such as stroke,Alzheimer’s disease,Parkinson’s disease,and spinal cord injury.CD36 antagonists can suppress CD36 expression or prevent CD36 binding to its ligand,thereby achieving inhibition of CD36-mediated pathways or functions.Here,we reviewed the mechanisms of action of CD36 antagonists,such as Salvianolic acid B,tanshinone IIA,curcumin,sulfosuccinimidyl oleate,antioxidants,and small-molecule compounds.Moreover,we predicted the structures of binding sites between CD36 and antagonists.These sites can provide targets for more efficient and safer CD36 antagonists for the treatment of central nervous system diseases.
基金supported by the Gusu Medical Key Talent Project of Suzhou City of China(GSWS2020005)the New Pharmaceutics and Medical Apparatuses Project of Suzhou City of China(SLJ2021007)+3 种基金the Suzhou City Key Clinical Disease Diagnosis and Treatment Technology Special Project,China(LCZX202129)Wujiang Science and Educational Health Revitalization Fund Project,Suzhou,China(WWK202015)the Scientific Research Project of Suzhou Ninth People’s Hospital,Suzhou,China(YK202008)and Suzhou“Science and Education”Youth Science and Technology Project,Suzhou,China(KJXW2020075).
文摘Colorectal cancer(CRC)stands among the top prevalent cancers worldwide and holds a prominent position as a major contributor to cancer-related mortality globally.Absent in melanoma 2(AIM2),a constituent of the interferoninducible hematopoietic interferon-inducible nuclear antigens with 200 amino acid repeats protein family,contributes to both cancer progression and inflammasome activation.Despite this understanding,the precise biological functions and molecular mechanisms governed by AIM2 in CRC remain elusive.Consequently,this study endeavors to assess AIM2’s expression levels,explore its potential antitumor effects,elucidate associated cancer-related processes,and decipher the underlying signaling pathways in CRC.Our findings showed a reduced AIM2 expression in most CRC cell lines.Elevation of AIM2 levels suppressed CRC cell proliferation and migration,altered cell cycle by inhibiting G1/S transition,and induced cell apoptosis.Further research uncovered the participation of P38 mitogen-activated protein kinase(P38MAPK)in AIM2-mediated modulation of CRC cell apoptosis and proliferation.Altogether,our achievements distinctly underscored AIM2’s antitumor role in CRC.AIM2 overexpression inhibited proliferation and migration and induced apoptosis of CRC cells via activating P38MAPK signaling pathway,indicating AIM2 as a prospective and novel therapeutic target for CRC.
基金supported by the National Natural Science Foundation of China,No.81101159the Natural Science Foundation of Jiangsu Province of China,No.BK20151268
文摘Hypoxic injuries during fetal distress have been shown to cause reduced expression of micro RNA-27a（mi R-27a）,which regulates sensitivity of cortical neurons to apoptosis.We hypothesized that miR-27 a overexpression attenuates hypoxia- and ischemia-induced neuronal apoptosis by regulating FOXO1,an important transcription factor for regulating the oxidative stress response.miR-27 a mimic was transfected into hippocampal neurons to overexpress miR-27 a.Results showed increased hippocampal neuronal viability and decreased caspase-3 expression.The luciferase reporter gene system demonstrated that mi R-27 a directly binded to FOXO1 3′UTR in hippocampal neurons and inhibited FOXO1 expression,suggesting that FOXO1 was the target gene for mi R-27 a.These findings confirm that mi R-27 a protects hippocampal neurons against oxygen-glucose deprivation-induced injuries.The mechanism might be mediated by modulation of FOXO1 and apoptosis-related gene caspase-3 expression.
基金supported by grants from the National Natural Science Foundation of China(81673241,81401988 and 81702419)Jiangsu Medical Science(BE2016698)+2 种基金Jiangsu Government Scholarship for Overseas Studies(JS-2014-209 and JS-2014-208)Projects of Nantong Health and Family Planning Commission Fund(WQ2016083)Jiangsu Graduate Innovation of China(KYCX17_1934)
文摘Backgroud： Wingless-type MMTV integration site family member 5a （Wnt5a） is involved in carcinogenesis.However, little data are available in Wnt5a signaling with hepatocellular carcinoma （HCC）. In thepresent study, we investigated the expression of hepatic Wnt5a in HCC and the role of Wnt5a in HCCprogression and outcome.
基金Supported by Projects of Jiangsu Elitist Peak in Six Fields,Nos.2013-WSN-078,2013-WSW-011,and 2014-YY-028the QingL an Program of Jiangsu Higher Education,the Youth Science Foundation of Nantong Health Department,No.WQ2014005the International Science and Technology Cooperation Program,No.2013DFA32150
文摘AIM: To interfere with the activation of nuclear factor-κB(NF-κB) with metformin and explore its effect in reversing multidrug resistance(MDR) of hepatocellular carcinoma(HCC) cells.METHODS: Expression of P-glycoprotein(P-gp) and NF-κB in human HepG 2 or HepG 2/adriamycin(ADM) cells treated with pC MV-NF-κB-small interference RNA(siR NA) with or without metformin, was analyzed by Western blot or fluorescence quantitative PCR. Cell viability was tested by CCK-8 assay. Cell cycle and apoptosis were measured by flow cytometry and Annexin-V-PE/7-AnnexinV apoptosis detection double staining assay, respectively. RESULTS: P-gp overexpression in HepG 2 and HepG 2/ADM cells was closely related to mdr1 mR NA(3.310 ± 0.154) and NF-κB mR NA(2.580 ± 0.040) expression. NF-κB gene transcription was inhibited by specific siR NA with significant down-regulation of P-gp and enhanced HCC cell chemosensitivity to doxorubicin. After pretreatment with metformin, Hep G2/ADM cells were sensitized to doxorubicin and P-gp was decreased through the NF-κB signaling pathway. The synergistic effect of metformin and NF-κB siR NA were found in HepG 2/ADM cells with regard to proliferation inhibition, cell cycle arrest and inducing cell apoptosis. CONCLUSION: Metformin via silencing NF-κB signaling could effectively reverse MDR of HCC cells by downregulating MDR1/P-gp expression.
基金This study was supported by grants from the Ministry of S&T National Key Research and Development Program of China(2018YFC0116902)the National Natural Science Foundation of China(81673241,81702419,31872738,81873915)and Project of Jiangsu Medical Science(BE2016698).
文摘Background:Hepatic Golgi protein-73(GP73)expression is related to hepatocellular carcinoma(HCC)progression.The aim of this study was to investigate the dynamic expression of GP73 mRNA and protein during hepatocytes malignant transformation.Methods:Human GP73 expressions in 88 HCC tissues and their self-control surrounding tissues were examined by immunohistochemistry,and survival time of HCC patients was evaluated by the Kaplan-Meier method.HCC model of Sprague-Dawley rats was made by diet containing 2-fluorenylacetamide.The rats were divided into the control,hepatocyte degeneration,precanceration,and HCC groups to observe GP73 protein and mRNA alterations during hepatocytes malignant transformation.Results:The GP73 expression was significantly higher in the cancerous tissues than that in the surrounding tissues,with shorter survival time,and the positive rates of GP73 protein in human HCC tissues were 53.3%at stage I,84.0%at stage II,84.6%at stage III,and 60.0%at stage IV,respectively.The positive rates of hepatic GP73 protein and mRNA in the rat models were none in the control group,66.7%and 44.4%in the hepatocytes degeneration group,88.9%and 77.8%in the hepatocytes precanceration group,and 100%in the HCC group,respectively.There was a positive correlation(r=0.91,P<0.01)between hepatic GP73 and serum GP73 during rat hepatocytes malignant transformation.Conclusions:Abnormal GP73 expression may be a sensitive and valuable biomarker in hepatocarcinogensis.
基金supported by the National Natural Science Foundation of China,No.81870975 (to SLZ)Innovation and Entrepreneurship Training Program for College Students in Jiangsu Province of China,No.202010304034Z (to FYZ)。
文摘Glial cells play an important role in signal transduction,energy metabolism,extracellular ion homeostasis and neuroprotection of the central nervous system.However,few studies have explained the potential effects of exosomes from glial cells on central nervous system health and disease.In this study,the genes expressed in exosomes from astrocytes and microglia were identified by deep RNA sequencing.Kyoto Encyclopedia of Genes and Genomes analysis indicated that several pathways in these exosomes are responsible for promoting neurodegenerative diseases,including Alzheimer's disease,Parkinson's disease and Huntington's disease.Gene ontology analysis showed that extracellular exosome,mitochondrion and growth factor activity were enriched in exosomes from the unique astrocyte group,while extracellular exosome and mitochondrion were enriched in exosomes from the unique microglia group.Next,combined with the screening of hub genes,the protein-protein interaction network analysis showed that exosomes from astrocytes influence neurodegenerative diseases through metabolic balance and ubiquitin-dependent protein balance,whereas exosomes from microglia influence neurodegenerative diseases through immune inflammation and oxidative stress.Although there were differences in RNA expression between exosomes from astrocytes and microglia,the groups were related by the hub genes,ubiquitin B and heat shock protein family A(Hsp70) member 8.Ubiquitin B appeared to be involved in pleiotropic regulatory functions,including immune regulation,inflammation inhibition,protein catabolism,intracellular protein transport,exosomes and oxidative stress.The results revealed the clinical significance of exosomes from glia in neurodegenerative diseases.This study was approved by the Animal Ethics Committee of Nantong University,China(approval No.S20180102-152) on January 2,2018.
基金supported by a grant from a science andtechnology project"Health of Science and Education"of Suzhouin 2013(KJXW2013026)
文摘BACKGROUND: Cardiac arrest(CA) is a common and serious event in emergency medicine. Despite recent improvements in resuscitation techniques, the survival rate of patients with CA is unchanged. The present study was undertaken to observe the effect of mild hypothermia(MH) on the reactive oxygen species(ROS) and the effect of neurological function and related mechanisms.METHODS: Sixty-five healthy male Sprague Dawley(SD) adult rats were randomly(random number) divided into 2 groups: blank control group(n=5) and CPR group(n=60). CA was induced by asphyxia. The surviving rats were randomly(random number) divided into two groups: normothermia CPR group(NT) and hypothermia CPR group(HT). Normothermia of 37 °C was maintained in the NT group after return of spontaneous circulation(ROSC), hypothermal intervention of 32 °C was carried out in the HT group for 4 hours immediately after ROSC. Both the NT and HT groups were then randomly divided into 2 subgroups 12 hours and 24 hours after ROSC(NT-12, NT-24, HT-12, HT-24 subgroups). During observation, the neurological defi cit scores(NDSs) was recorded, then the bilateral hippocampi were obtained from rats' head, and monoplast suspension of fresh hippocampus tissue was made immediately to determine the level of intracellular ROS by flow cytometry. Transmission electron microscope was used to observe the ultramicro changes of cellular nucleus and mitochondria. Reverse transcription-polymerase chain reaction(RT-PCR) was used to determine the expression of caspase-3 m RNA, and western-blotting(WB) was used to determine the level of LC3 in frozen hippocampus tissue. Measured data were analyzed with paired sample t test and One-Way ANOVA.RESULTS: Of 60 rats with CA, 44(73%) were successfully resuscitated and 33(55%) survived until the end of the experiment. The NDSs of rats in the NT and HT groups were more signifi cantly reduced than those in the BC group(F=8.107, P<0.05), whereas the NDSs of rats in the HT-12 and HT-24 subgroups were significantly increased in comparison with those NDSs of rats in the NT-12 and NT-24 subgroups, respectively(t=9.692, P<0.001; t=14.374, P<0.001). The ROS in hippocampus nerve cells in the NT and HT groups signifi cantly increased compared to the BC group(F=16.824, P<0.05), whereas the ROS in the HT-12 and HT-24 subgroups significantly reduced compared with that ROS in the NT-12 and NT-24 subgroups, respectively(t=9.836, P<0.001; t=7.499, P<0.001). The expression of caspase-3 m RNA in hippocampus nerve cells in the NT and HT groups were signifi cantly increased compared to the BC group(F=24.527, P<0.05), whereas the expression of caspase-3 m RNA in rats of the HT-12 and HT-24 subgroups was signifi cantly reduced compared to the NT-12 and NT-24 subgroups, respectively(t=6.935, P<0.001; t=4.317, P<0.001). The expression of LC3B-II/I in hippocampus nerve cells of rats in the NT and HT groups signifi cantlyincreased compared to the BC group(F=6.584, P<0.05), whereas the expression of LC3B-II/I in rats of the HT-12 and HT-24 subgroups significantly reduced compared to the NT-12 and NT-24 subgroups, respectively(t=10.836, P<0.001; t=2.653, P=0.02). Ultrastructure damage of nucleus and mitochondria in the NT group was more evident than in the BC group, and eumorphism of nucleus and mitochondria were maintained in rats of the HT group compared with the NT group.CONCLUSION: Mild hypothermia lessened the injury of nerve cells and improved the neurological function of rats that survived from cardiac arrest by reducing the ROS production of nerve cells and inhibiting the expression of caspase-3 m RNA and LC3, leading to cellular apoptosis and massive autophagy in rats that survived from cardiac arrest after CPR.
基金the Natural Science Foundation of Jiangsu Province, No.BK2004047the scientific and Technological Foundation of Nantong University, No.05z075
文摘BACKGROUND： It has been demonstrated that curcumin can increase the activities of various anti-oxidase in blood and tissue, effectively eliminate various free radicals, reduce the production of peroxisome, and alleviate oxidative stress reaction. Whether it has the same effect on microglia？ OBJECTIVE： To observe the effects of curcumin on the expressions of inducible nitric oxide synthase （iNOS）, nuclear factor- κ B （NF- κ B）, and superoxide dismutase （SOD） in microglial cell line BV stimulated by lipopolysaccharide （LPS）. DESIGN： An observational comparative study. SETTING： Research Room of Biochemistry, Medical College of Nantong University. MATERIALS： Mice microglia cell line BV, iNOS and NF- κ B reporter gene plasmids were presented by Dr. Bhat.NR. from the Medical University of South Carolina （USA）. Curcumin was produced by the Xi＇an Branch of China Chengdu Scholar Bio-Tech. Co.,Ltd.; LPS （E.Coli O26：B6）, anti-mice iNOS monoclonal antibody, horseradish peroxidase labeled goat-anti-mice IgG were the products of Sigma Company （USA）. METHODS： The experiments were carried out in the Research Room of Biochemistry, Medical College of Nantong University from May 2006 to April 2007. （1） Detection of iNOS： The cells were seeded onto 24-well plate at the density of 1 × 10^5, After the cells had adhered to the cover glasses, the cells were grouped as negative control group （the primary antibody was replaced by phosphate buffered solution PBS）; normal control group （the cells were normally cultured）; LPS-treated group （the cells were treated with LPS for 24 hours）; curcumin＋LPS group （the cells were treated with curcumin for 1 hour and LPS for 24 hours）. The expressions of iNOS protein were detected with immunocytochemical staining. （2） Determination of iNOS and NF- κ B gene activities： According to the introduction of the kit for transfection, iNOS or NF- κ B report gene plasmids were transiently transfected with Lipofectaminer^TM2000 liposomes into the cells in the 24-well plate for 24 hours. The cells were divided into normal control group （the cells were normally cultured after transfected with report gene plasmids）; blank plasmid group （the cells were normally cultured after transfected with blank plasmids）; LPS-treated group （the cells were treated with LPS for 4 hours after transfected with report gene plasmids）; curcumin＋LPS group （the cells were treated with curcumin for 1 hour and LPS for 24 hours after transfected with report gene plasmids）. The content of luciferase in the cell lysis buffer was determined after cell lysis. （3） Determination of SOD activity： The cells were seeded into culture bottle at the density of 1 × 10^6, and the divided into four groups, including normal control group （the cells were normally cultured）; LPS-treated group （the cells were treated with LPS for 24 hours）; curcumin＋LPS group （the cells were treated with curcumin for 1 hour and LPS for 24 hours）; vitamin C＋LPS group （the cells were treated with vitamin C for 1 hour and LPS for 24 hours）. The SOD activity was determined with xanthine oxidase and quantitative colorimetric assay. MAIN OUTCOME MEASURES： The expressions of iNOS protein, iNOS and NF- κ B, and the activity of SOD were observed. RESULTS： （1） Expression of iNOS protein in microglia： The expression of iNOS protein in the LPS-treated group was obviously higher than that in the negative control group （P 〈 0.01）; Those in the curcumin＋LPS group were significantly decreased as compared with that in the LPS-treated group （P 〈 0.01 ） （2） Expressions of iNOS and NF- κ B genes： The expressions of iNOS and NF- κ B genes in the LPS-treated group were significantly higher than those in the normal control group （P 〈 0.01）; Those in the curcumin＋LPS group were significantly lower than those in the LPS-treated group （P 〈 0.01）. （3） SOD activity： The activity of SOD in the LPS-treated group was significantly lower than those in the normal control group （P 〈 0.01）. It in the curcumin＋LPS group and vitamin C ＋LPS group was significantly higher than that in the LPS-treated group （P 〈 0.01）. CONCLUSION： Curcumin could inhibit the expression of iNOS in the activated microglia, and it also has the abilities in eliminating free radicals and antagonizing lipid peroxidation.
基金Supported by grants from Jiang su Health Key Project(No.K201102)Nantong City Social Development Project (No. S2009027)
文摘Objective:The aim of this study was to analyze the expression features of hypoxia inducible factor-1α (HIF-1α) in hepatocellular carcinoma (HCC) and effects of HIF-1α silencing on HepG2 cells.Methods:HIF-1α expression was analyzed in the self-control HCC specimens by immunohistochemistry.After HepG2 cells with miRNA transfection,the expression of HIF-1α was determined at mRNA or protein level by real-time polymerase chain reaction (PCR) or Western blotting.Vascular endothelial growth factor (VEGF) and angiopoietin-2 (ANG-2) were determined by ELISA.Alterations of cell cycles and apoptosis of HepG2 cells were measured using a flow cytometer.Results:Positive HIF-1α was brown and granule-like in the cytoplasm or nucleus.Significant difference was found between HCC (80%) and its surrounding tissues (100%,χ2=22.35,P < 0.001) and HIF-1α expression related to tumor size.At 72 h after miRNA transfection,the expression of HIF-1α in HepG2 cells was down-regulated by 87% at mRNA or 65% at protein level,with VEGF and ANG-2 decreased to 54% and 36%,respectively.After RNA interference combined with anti-cancer drug,the apoptotic rate of HepG2 cells was increasing from 22.46% ± 0.61% to 36.99% ± 0.88%,with up-regulation of G1 phase (65.68% ± 0.91%) and down-regulation of S phase (19.47 ± 1.34 %).Conclusion:Abnormal expression of HIF-1α is associated with development of HCC,and HIF-1α gene silencing can effectively inhibit HepG2 cell proliferation.
文摘Objective:To investigate the level and influencing factors of benefit discovery in patients with breast cancer after operation.Methods:Convenient sampling method was used to evaluate the change of benefit discovery level of 60 patients with breast cancer after operation in a cancer ward of a hospital by using Chinese version of benefit discovery rating scale and general information questionnaire.Results:The level of benefit discovery of breast cancer patients at different stages was statistically different(P<0.05).Age and education level entered the multiple linear stepwise regression equation of influencing factors of benefit discovery level of breast cancer patients(P<0.05).Conclusion:Targeted nursing measures should be taken to improve the quality of life of patients with breast cancer.
基金Supported by the National Natural Science Foundation,No.81673241,No.81200634,No.81370982the program of Jiangsu Key Research Plan,No.BE2016698the International Science and Technology Cooperation Program of China,No.2013DFA32150
文摘AIM To investigate the dynamic alteration of mitochondrial carnitine palmitoyl transferase Ⅱ(CPT-Ⅱ) expression during malignant transformation of rat hepatocytes.METHODS Sprague-Dawley male rats were fed with normal, high fat(HF), and HF containing 2-fluorenylacetamide(2-FAA) diet, respectively. According to the Hematoxylin and Eosin staining of livers, rats were divided into control, fatty liver, degeneration, pre-cancerous, and cancerous groups. Liver lipids were dyed with Oil Red O, CPT-Ⅱ alterations were analyzed by immunohistochemistry, and compared with CPT-Ⅱ specific concentration(μg/mg protein). Levels of total cholesterol(Tch), triglyceride(TG), and aminotransferases [alanine aminotransferase(ALT), aspartate aminotransferase(AST)] were determined by the routine methods.RESULTS After intake of HF and/or HF+2-FAA diets, the rat livers showed mass lipid accumulation. The lipid level in the control group was significantly lower than that in other groups. The changes of serum TG and Tch levels were abnormally increasing, 2-3 times more than those in the controls(P < 0.05). During the rat liver morphological changes from normal to cancer development process with hepatocyte injury, serum AST and ALT levels were significantly higher(4-8 times, P < 0.05) than those in the control group. The specific concentration of CPT-Ⅱ in liver tissues progressively decreased during hepatocyte malignant transformation, with the lowest CPT-Ⅱ levels in the cancer group than in any of the other groups(P < 0.05).CONCLUSION Low CPT-Ⅱ expression might lead to abnormal hepatic lipid accumulation, which should promote the malignant transformation of hepatocytes.
基金Supported by the International S&T Cooperation Program,No.2013DFA32150 of China
文摘AIM: To investigate member 3a of Wingless-type MMTV integration site family (Wnt3a) expression in cancerous and surrounding tissues and the relationship between clinicopathologic features of hepatocellular carcinoma (HCC) and Wnt3a expression.METHODS: Wnt3a expression and cellular distribution and clinicopathologic characteristics in cancerous tissue and matched surrounding tissues were analyzed in 80 HCC patients from January 2006 to August 2008 by tissue microarrays and immunohistochemistry. The overall and disease-free survival rates were estimated using the Kaplan-Meier method and compared with the log-rank test. The prognostic analysis was carried out with univariate and multivariate Cox regressions models.RESULTS: The incidence of oncogenic Wnt3a expression in the cancerous group was up to 96.25% (77 of 80), which was significantly higher (χ<sup>2</sup> = 48.818, P < 0.001) than that in the surrounding group (46.25%, 37 of 80). Brown Wnt3a staining gradually increased with clinical staging that showed very strong staining in advanced HCC. The clinicopathologic features of high Wnt3a expression in HCC were related to poorly-differentiated grade (χ<sup>2</sup> = 20.211, P < 0.001), liver cirrhosis (χ<sup>2</sup> = 8.467, P < 0.004), hepatitis B virus (HBV) infection (χ<sup>2</sup> = 12.957, P < 0.001), higher tumor-node-metastasis stage (χ<sup>2</sup> = 22.960, P < 0.001), and 5-year survival rate (χ<sup>2</sup> = 15.469, P < 0.001).CONCLUSION: Oncogenic Wnt3a expression associated with HBV infection and cirrhotic liver might be an independent prognostic factor for HCC.
基金supported by the National Natural Science Foundation of China,No.81101159the Natural Science Foundation of Jiangsu Province of China,No.BK20151268
文摘Septic encephalopathy is a frequent complication of sepsis,but there are few studies examining the role of micro RNAs（mi Rs） in its pathogenesis.In this study,a mi R-219 mimic was transfected into rat hippocampal neurons to model mi R-219 overexpression.A protective effect of mi R-219 was observed for glutamate-induced neurotoxicity of rat hippocampal neurons,and an underlying mechanism involving calmodulin-dependent protein kinase II γ（Ca MKIIγ） was demonstrated.mi R-219 and Ca MKIIγ m RNA expression induced by glutamate in hippocampal neurons was determined by quantitative real-time reverse transcription-polymerase chain reaction（q RT-PCR）.After neurons were transfected with mi R-219 mimic,effects on cell viability and apoptosis were measured by 3-（4,5-dimethylthiazolyl-2）-2,5-diphenyltetrazolium bromide（MTT） assay and flow cytometry.In addition,a luciferase reporter gene system was used to confirm Ca MKIIγ as a target gene of mi R-219.Western blot assay and rescue experiments were also utilized to detect Ca MKIIγ expression and further verify that mi R-219 in hippocampal neurons exerted its effect through regulation of Ca MKIIγ.MTT assay and q RT-PCR results revealed obvious decreases in cell viability and mi R-219 expression after glutamate stimulation,while Ca MKIIγ m RNA expression was increased.MTT,flow cytometry,and caspase-3 activity assays showed that mi R-219 overexpression could elevate glutamate-induced cell viability,and reduce cell apoptosis and caspase-3 activity.Moreover,luciferase Ca MKIIγ-reporter activity was remarkably decreased by co-transfection with mi R-219 mimic,and the results of a rescue experiment showed that Ca MKIIγ overexpression could reverse the biological effects of mi R-219.Collectively,these findings verify that mi R-219 expression was decreased in glutamate-induced neurons,Ca MKIIγ was a target gene of mi R-219,and mi R-219 alleviated glutamate-induced neuronal excitotoxicity by negatively controlling Ca MKIIγ expression.
文摘Acute kidney injury(AKI)affects approximately 13.3 million individuals and contributes to about 1.7 million deaths globally per year.As estimated 85% of those affected live in the developing world[1].Although there are various measures to prevent or treat AKI,including renal protective drugs and continuous renal replacement therapy,most of them have limited success or are still in their infancy[2,3].
基金supported by the Scientific Research Fund of Jiangsu Provincial Department of Health(No.H2017075)Taizhou People’s Hospital Innovation Team Fund(No.CXTDB201904).
文摘To the Editor:Recently,we reviewed almost all the articles reporting surfeit locus containing the six sequenceunrelated housekeeping genes Surfeit 1 to Surfeit 6 since 1988 and one of the family members,surfeit 4(SURF 4)gene interested us.In this article,we will summarize the characteristics and protein localization of SURF4 gene,as well as its possible physiological functions and pathogenesis in various diseases and cancers,expecting to explore its clinical application values.
基金supported by the National Key Basic Research Program of China,No.2017YFA0104701The National Natural Science Foundation of China,No.81801281,81870975,81671230The Natural Science Foundation of Jiangsu Province(BK20202013).
文摘Spinal cord injury(SCI)often leads to permanent disability,which is mainly caused by the loss of functional recovery.In this review,we aimed to investigate why the healing process is interrupted.One of the reasons for this interruption is the formation of a glial scar around the severely damaged tissue,which is usually covered by reactive glia,macrophages and fibroblasts.Aiming to clarify this issue,we summarize the latest research findings pertaining to scar formation,tissue repair,and the divergent roles of blood-derived monocytes/macrophages,ependymal cells,fibroblasts,microglia,oligodendrocyte progenitor cells(OPCs),neuron-glial antigen 2(NG2)and astrocytes during the process of scar formation,and further analyse the contribution of these cells to scar formation.In addition,we recapitulate the development of therapeutic treatments targeting glial scar components.Altogether,we aim to present a comprehensive decoding of the glial scar and explore potential therapeutic strategies for improving functional recovery after SCI.
