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Objective To explore the molecular mechanism of SHMT2 regulating the invasion and migration of breast cancer cells. Methods Bioinformatics analysis was used to verify the role of SHMT2 in breast cancer tissues. Transwell assay was used to detect the changes of invasion and migration abilities of breast cancer cells. Co-immunoprecipitation, knockdown plasmid transfection and Western blot were used to determine the regulatory relationship between different proteins. Results Bioinformatics analysis showed that the expression level of SHMT2 in invasive breast cancer tissues was significantly higher than that in adjacent normal tissues (P < 0.001). The 5-year disease-specific survival and overall survival in the SHMT2 high expression group were significantly lower than those in the SHMT2 low expression group (both P < 0.001). Transwell assay showed that SHMT2 knockdown significantly reduced the invasion ability (t=5.375, P=0.0058) and migration ability (t=6.274, P=0.0033) of MCF7 cells. Western blot showed that SHMT2 could combine to HAX1, and knockdown of SHMT2 reduced the protein level of HAX1. Transwell assay showed that the inhibitory effect of SHMT2 knockdown on the migration of MCF7 cells could be reversed by overexpression of HAX1 (t=6.274, P=0.0033; t=8.041, P=0.0013), while SHMT2 inhibitor (SHIN1, 10 nmol/L) significantly inhibited the migration of MCF7 cells induced by SHMT2 overexpression (t=10.16, P=0.0005; t=8.741, P=0.0009). Conclusion SHMT2 was closely related to the poor prognosis of breast cancer, and was a key factor in the invasion and migration of breast cancer cells. The mechanism was that SHMT2 increased the invasion and migration ability of breast cancer cells by binding to and up-regulating HAX1. It was verified that SHMT2 inhibitor could significantly reduce the migration ability of breast cancer cells. This study explored the therapeutic potential of SHMT2 inhibitor in metastatic breast cancer, and found potential intervention targets for its clinical treatment.
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Ovarian cancer is the most lethal malignancy of the female genital tract. Genetic predisposition, usage of hormone, relative disease and reproduction, and lifestyle factors are possible risk factors for ovarian cancer. Women can be stratified into high risk and general populations according to the ovarian cancer risk. Screening and prevention were reviewed for the two populations. Population-based trials in the general population have not demonstrated that screening improves early detection or survival. Strengthening the awareness of tumor prevention and conducting effective screening and prevention in the high-risk population are cost-effective methods to reduce the incidence and mortality of ovarian cancer.
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Objective@#To examine the effects of Berberine(BBR)on inflammatory pathways related to endoplasmic reticulum stress(ERS)in the penumbra area following focal cerebral ischemia-reperfusion injury in type 2 diabetic rats.@*Methods@#A total of 72 healthy male Sprague-Dawley rats were fed a high-fat, high-sugar diet and injected with streptozotocin to establish a type 2 diabetes mellitus model.The diabetic rats were randomly divided by digital lottery method into a Sham operation group(Sham group), a diabetic rat + BBR treatment group(BBR group), a diabetic middle cerebral artery occlusion(MCAO)model group(MCAO group), and a diabetic rats MCAO + BBR treatment group(MCAO + BBR group). Six rats were included in each group.The two treatment groups received prespecified doses of BBR through gastric perfusion at 48 h, 24 h before surgery, and 6h after surgery.The MCAO model was prepared by a suture occlusion method.The neurological deficit scores were performed, and the expression of tumor necrosis factor-α(TNF-α)and interleukin-1β(IL-1β)was detected by enzyme-linked immunosorbent assay(ELISA). The mRNA expression of ERS marker protein GRP78 was detected by quantitative real time polymerase chain reaction(RT-qPCR), and the expression of ERS-related inflammatory pathway proteins[78 Glucoseregulated protein(GRP78)、Pancreatic endoplasmic reticulum Rinase(PERK)、nuclear factor-κB(NF-κB)]was detected by Western blot.@*Results@#the cerebral ischemic penumbra area, after 2 h of ischemia and 24 h of reperfusion, the neurological deficit score in the MCAO group was higher than that in the MACO+ BBR group [(2.83±0.41)vs.(1.67±0.52), P<0.05], and the expression levels of pro-inflammatory cytokines(TNF-α and IL-1β)and ERS-related inflammatory pathway proteins(GRP78, PERK and NF-κB p65)were also significantly increased(all P<0.05). However, BBR treatment was able to alleviate the neurological dysfunction caused by cerebral ischemia-reperfusion in type 2 diabetic rats(P<0.05). Similarly, BBR treatment also reduced the expression levels of pro-inflammatory factors(TNF-α and IL-1β)and ERS-related inflammatory pathway proteins(GRP78, PERK and NF-κB p65)in the cerebral ischemic penumbra area(all P<0.05).@*Conclusions@#Through inhibiting ERS-related inflammatory pathways, BBR plays a neuroprotective role to alleviate cerebral ischemia-reperfusion injury in type 2 diabetic rats.
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Objective To examine the effects of Berberine(BBR)on inflammatory pathways related to endoplasmic reticulum stress(ERS) in the penumbra area following focal cerebral ischemia-reperfusion injury in type 2 diabetic rats.Methods A total of 72 healthy male Sprague-Dawley rats were fed a high-fat,high-sugar diet and injected with streptozotocin to establish a type 2 diabetes mellitus model.The diabetic rats were randomly divided by digital lottery method into a Sham operation group(Sham group),a diabetic rat + BBR treatment group(BBR group),a diabetic middle cerebral artery occlusion(MCAO)model group (MCAO group),and a diabetic rats MCAO + BBR treatment group (MCAO + BBR group).Six rats were included in each group.The two treatment groups received prespecified doses of BBR through gastric perfusion at 48 h,24 h before surgery,and 6h after surgery.The MCAO model was prepared by a suture occlusion method.The neurological deficit scores were performed,and the expression of tumor necrosis factor-α(TNF-a)and interleukin-1β(IL-1β) was detected by enzyme-linked immunosorbent assay(ELISA).The mRNA expression of ERS marker protein GRP78 was detected by quantitative real time polymerase chain reaction(RT-qPCR),and the expression of ERS-related inflammatory pathway proteins 678 Glucoseregulated protein(GRP78)、Pancreatic endoplasmic reticul um Rinase (PERK)、nuclear factor-κB (NF-κB)] was detected by Western blot.Results the cerebral ischemic penumbra area,after 2 h of ischemia and 24 h of reperfusion,the neurological deficit score in the MCAO group was higher than that in the MACO+BBR group [(2.83 ± 0.41) vs.(1.67± 0.52),P ＜0.05],and the expression levels of pro-inflammatory cytokines(TNF-α and IL-1β)and ERS-related inflammatory pathway proteins(GRP78,PERK and NF-κB p65)were also significantly increased(all P＜0.05).However,BBR treatment was able to alleviate the neurological dysfunction caused by cerebral ischemia-reperfusion in type 2 diabetic rats (P＜0.05).Similarly,BBR treatment also reduced the expression levels of pro-inflammatory factors(TNF-α and IL-1β)and ERS-related inflammatory pathway proteins(GRP78,PERK and NF-κB p65)in the cerebral ischemic penumbra area(all P＜0.05).Conclusions Through inhibiting ERS-related inflammatory pathways,BBR plays a neuroprotective role to alleviate cerebral ischemia-reperfusion injury in type 2 diabetic rats.
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OBJECTIVE@#To assess the effect of miR-137 on the proliferation and apoptosis of human umbilical vein endothelial cells (HUVECs) induced by high glucose and its mechanism.@*METHODS@#HUVECs cells were divided into low-glucose group (5.5 mmol/L glucose-treated cells), high-glucose group (33.36 mmol/L glucose-treated cells), anti-NC group (cells treated with 33.36 mmol/L glucose after anti-NC transfection) and anti-miR-137 group (cells treated with 33.36 mmol/L glucose after anti-miR-137 transfection). After 48 hours, qRT-PCR was used to determine the expression of miR-137. CCK-8 assay and flow cytometry were used to detect cell proliferation and apoptosis rate, respectively. The targeting relationship between miR-137 and AKT2 was validated by dual fluorescence reporter gene detection system and AKT2 protein expression after overexpression or inhibition of miR-137.@*RESULTS@#High glucose could significantly up-regulate the expression of miR-137 in HUVECs cells, and the expression of miR-137 in HUVECs cells transfected with miR-137 inhibitor was significantly decreased (P<0.05). High glucose can significantly inhibit HUVECs cell proliferation and induce apoptosis, while inhibition of miR-137 expression can weaken the effect of high glucose on HUVECs cell proliferation inhibition and apoptosis promotion (P<0.05). Inhibiting AKT2 expression could weaken the inhibitory effect of miR-137 inhibitor on HUVECs cell proliferation and apoptosis (P<0.05).@*CONCLUSION@#Inhibiting the expression of miR-137 gene can attenuate the proliferation inhibition and apoptosis promotion of HUVECs induced by high glucose, and the mechanism is related to activating the expression of AKT2.
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Humans , Apoptosis , Cell Proliferation , Cells, Cultured , Glucose , Human Umbilical Vein Endothelial Cells , Cell Biology , MicroRNAs , Genetics , Proto-Oncogene Proteins c-akt , GeneticsABSTRACT
OBJECTIVE@#To investigate the effects of genipin on promoting brown adipose tissue activation and white adipose tissue browning.@*METHODS@#The male C57BL/6J mice were divided into three groups: normal control group, genipin group and cold-stimulus group.Genipin group were treated consecutively with genipin at a dose of 15 mg/kg once a day for 9 days, normal control group were treated with the saline.The mice with cold-stimulus were exposed to 4℃ environment for 5 days.Daily food amount and body weight were measured.Morphological changes were observed in the subscapular region, inguinal region and epididymis around the adipose tissue.The expression of uncoupling protein 1 (UCP1) was determined by real-time PCR and Western blot respectively.@*RESULTS@#The wet weight of white fat in genipin-treated mice was decreased by 16% , and 28% in that of cold-stimulus mice, compared with the normal control group (P＜0.05).After treatments of genipin and cold-stimulus, the color of white adipose tissues was darker, and the size of lipid droplets in adipocytes was smaller, whereas the number was increased.Compared with the normal control group, UCP1 expression was increased obviously in fat tissues, including the subcutaneous and visceral white adipose tissues, and brown adipose tissue after treated with genipin and cold-stimulus (P＜0.05).@*CONCLUSION@#Genipin promoted activation of brown adipose tissue and browning of white adipose tissue by upregulating UCP1 expression, which could contribute to the loss of body weight against obesity.
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Animals , Male , Mice , Adipose Tissue, Brown , Adipose Tissue, White , Cholagogues and Choleretics , Pharmacology , Iridoids , Pharmacology , Mice, Inbred C57BL , Obesity , Drug Therapy , Uncoupling Protein 1 , Up-RegulationABSTRACT
Objective@#To assess the effect of miR-137 on the proliferation and apoptosis of human umbilical vein endothelial cells (HUVECs) induced by high glucose and its mechanism.@*Methods@#HUVECs cells were divided into low-glucose group (5.5 mmol/L glucose-treated cells), high-glucose group (33.36 mmol/L glucose-treated cells), anti-NC group (cells treated with 33.36 mmol/L glucose after anti-NC transfection) and anti-miR-137 group (cells treated with 33.36 mmol/L glucose after anti-miR-137 transfection). After 48 hours, qRT-PCR was used to determine the expression of miR-137. CCK-8 assay and flow cytometry were used to detect cell proliferation and apoptosis rate, respectively. The targeting relationship between miR-137 and AKT2 was validated by dual fluorescence reporter gene detection system and AKT2 protein expression after overexpression or inhibition of miR-137.@*Results@#High glucose could significantly up-regulate the expression of miR-137 in HUVECs cells, and the expression of miR-137 in HUVECs cells transfected with miR-137 inhibitor was significantly decreased (P<0.05). High glucose can significantly inhibit HUVECs cell proliferation and induce apoptosis, while inhibition of miR-137 expression can weaken the effect of high glucose on HUVECs cell proliferation inhibition and apoptosis promotion (P<0.05). Inhibiting AKT2 expression could weaken the inhibitory effect of miR-137 inhibitor on HUVECs cell proliferation and apoptosis (P<0.05).@*Conclusion@#Inhibiting the expression of miR-137 gene can attenuate the proliferation inhibition and apoptosis promotion of HUVECs induced by high glucose, and the mechanism is related to activating the expression of AKT2.
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Objective To investigate the effect of Berberine on insulin resistance and its mechanism in Otsuka Long-Evans Tokushima Fatty(OLETF) rats with metabolic syndrome(MS).Methods LETO(Long-evans Tokushima Otsuka)rats(the control group receiving standard normal diet,n=10)and diabetic OLETF rats(the MS group receiving high-fat diet for 24 weeks,n=30).Rats in the MS group were randomly divided into 3 subgroups(n=10,each subgroup).Each subgroup was gavaged with normal saline,high-dose Berberine(100 mg · kg-1 · d-1)and low-dose Berberine (50 mg · kg-1 · d-1) respectively,and the high-fat diet remained unchanged.After 6 weeks of berberine treatment,body weight,blood glucose and lipid metabolism parameters were determined.The oral glucose tolerance test(OGTT) and insulin tolerance test(ITT) were used to detect insulin resistance.Expression levels of the protein and mRNA of 78 kDa glucose-regulated protein (GRP7 8),Caspase-12 and CCAAT/enhancer-binding protein(C/EBP) homologous protein(CHOP) in skeletal muscles were detected by Western blot and RT-PCR.Results After Berberine treatment,the body weight,fasting plasma glucose,fasting insulin[(28.9 ± 2.0) mU/L,(31.5± 2.4) mU/L vs.(36.9 ± 4.7) mU/L],total cholesterol,triglycerides,and low-density lipoprotein cholesterol were decreased,while the high-density lipoprotein cholesterol(HDL-C) levels were increased in MS rats with high-dose berberine and low-dose berberine as compared with the control group (P ＜ 0.05) respectively.Berberine treatment could reduce the protein and mRNA expression levels of GRP78,Capase-12 and CHOP in the skeletal muscle of MS rats(P＜0.05).Conclusions Berberine may alleviate insulin resistance in rats with metabolic syndrome by reducing endoplasmic reticulum stress in skeletal muscle.
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Eighty percent of bacterial infections are related to the formation of bacterial biofilm. Compared with planktonic bacteria, bacterial biofilm is 10-1 000 times more resistant to antibiotics, which is the main cause of current bacterial drug resistance. A comprehensive understanding of the characteristics and resistance mechanisms of bacteria biofilm will help us treat the stubborn infections caused by the bacterial biofilm better and solve the problem of bacterial drug resistance. In this review, the composition and quorum sensing of bacterial biofilm, two major patterns of biofilm formation and drug resistance mechanisms were presented. Furthermore, representative compounds with anti-biofilm activity and compounds synergistic with antibiotics in anti-biofilm actions were introduced. Nano drug delivery strategies used for anti-biofilm in recent years as well as a novel drug delivery system-molecularly imprinted polymer was also introduced.
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To compare the therapeutic effects of different treatment methods on the nude mice bearing colon cancer HT29 cells. BalB/C nude mice colon cancer stem cell models were established and randomly divided into the following four groups, with 8 nude mice in each group: blank control group, DC-CIK group, Huaier group, and Huaier combined with DC-CIK group (combined treatment group). The mice in DC-CIK group and combined treatment group received 1×10⁶ DC-CIK cells treatment by tail vein injectionafter the tumor stem cells were inoculated for 4 days,2 times a week for three weeks. The mice in Huaier group and combined treatment group received intragastric administration at the dose of 20 g/60 kg body weight, 0.2 mL/time, once a day for a total of three weeks. The mice in control group received equal volume of normal saline. Tumor size and body weight of nude mice were measured every 2 days during treatment for three weeks in each group. After the treatment, the nude mice were sacrificed to measure the tumor weight and the tumor inhibition rate was calculated. The RT-PCR method was used to detect the expression levels of the key genes in the signal pathway. After the end of the treatment, the quality of the tumor in the Huaier group, DC-CIK group and combined treatment group was significantly lower than that in the control group; the quality in combined treatment group was significantly lower than that in Huaier group and DC-CIK group.Among them, the tumor inhibition rate reached 46.77% in the combined treatment group. In respect of changes in expression levels of key genes in the signaling pathway, the mRNA expression levels of key genes PI3KR1 and Akt in PI3K/Akt pathway, key genes Wnt1 and CTTNB1 in Wnt/-catenin pathway, and key genes Notch1, Notch2, Notch3 in Notch pathway in the combined treatment group were lower than those in DC-CIK group and Huaier group. The Huaier combined with DC-CIK group showed best therapeutic effect among different treatment methods for HT29 stemcell colon tumors in nude mice, providing a new idea for clinical treatment of colon cancer.
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Animals , Humans , Mice , Cell Line, Tumor , Colonic Neoplasms , Drug Therapy , Complex Mixtures , Pharmacology , Mice, Inbred BALB C , Mice, Nude , Neoplastic Stem Cells , Signal TransductionABSTRACT
Objective To explore the mediating effect of coping styles on the relationship between social support and self-management among young patients with newly-diagnosed type 2 diabetes(T2DM).Methods A total of 169 young patients with newly-diagnosed T2DM at China-Japan Friendship Hospital were investigated with the Medical Coping Mmodes Questionnaire,Social Support Rating Scale and the Summary of Diabetes Self-Care Activities.Results Among young patients with newly-diagnosed T2DM,there was a positive correlation between social support and confronce coping style(r =0.250,P＜0.01).The confronce coping style was positively correlated with self-management(r=0.367,P＜0.01).Confronce coping style could explain 15.3%variance of self-management(P＜0.01).Confronce coping style had a mediating effect on the relationship between social support and self-management.Conclusions Confronce coping style has a predictive role on self-management among young patients with newly-diagnosed T2DM,and confronce coping style has a mediating effect between social support and self-management.
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Objective To observe the anti-relapse and anti-graft versus host disease (GVHD) effects and side effects of ruxolitinib on patients who have relapsed leukemia after allo-hematopoietic stem cell transplantation (HSCT).Methods The clinical data of four patients sufferring from relapsed leukemia were collected and analyzed retrospectively.Three cases had a positive gene and 1 case had a extramedullary recurrence.All of them had serious GVHD involving multiparts,as the result of attenuating immunosuppressant aggressively.One case had central nervous system leukemia before allo-HSCT.Those patients were treated with ruxolitinib,according to the degree of GVHD,the treatment strategy and curative effect of GVHD,and the residual condition of original leukemia.Then,the degree of GVHD,the residual condition of original leukemia and the side effects of ruxolitinib were revaluated once a month after taking ruxolitinib.Results One case achieved completer remission (CR) and there partial remission (PR) in consideration of GVHD.Up to date,2 cases had no relapse in any level and 2 cases replased according to any of the results related to bone marrow aspiration.Conclusion Ruxolitinib is effective in patients with GVHD after allo-HSCT and doesn't influence GVL effect or increase the risk of relapse at the same time.Ruxolitinib doesn't have obvious side effects when treating GVHD.
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Competing endogenous RNA (ceRNA) is a class of RNA which includes mRNA,pseudogenes,long non-coding RNA (lncRNA),circular RNA (circRNA).ceRNA weakens its inhibitory effect on mRNA translation through competitive binding with shared microRNA (miRNA).Many studies have confirmed that the disorder of ceRNA is closely related to the occur-ence of breast cancer,gastric cancer,lymphoma and other tumors.With the improvement of researches,ceRNA may be used as a tumor marker of clinical diagnosis and therapeutic target.
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Objective To investigate the health status and nutrition-related diseases of residents in Pudong New Area,Shanghai and provide information for shaping the relevant national policies and guiding the people''s health dietary.Methods By means of a stratified multi-stage cluster random household sampling survey were performed questionnaire,physical examination and laboratory assay for 737 residents above the age of 15.Results The mean±standard deviation of the men''s height was (168.79±6.81) cm,and the women''s mean height (157.47±6.53) cm.And the rates of malnourishment,overweight,obesity and central obesity were 4.37%,48.91%,14.48% and 49.25%,and the prevalence rate of hypertension was 45.18%.Among residents above 18 years old,the abnormal rate of total cholesterol and triglycerides were 28.69% and 23.50%.Conclusion Nutrition-related chronic diseases will be an important public health problem in Pudong New Area.
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<p><b>OBJECTIVE</b>To investigate the effect of oridonin on the human acute lymphocytic leukemia cell line Jurkat and its mechanism.</p><p><b>METHODS</b>Jurkat cells were cultured in vitro and treated with various concentrations (0, 1.25, 2.5, 5, and 10 μmol/L) of oridonin for different lengths of time (24, 48, and 72 hours). The proliferation of Jurkat cells was analyzed by MTT assay. The changes in nuclear morphology were evaluated by fluorescence microscopy at 12 hours after treatment with various concentrations of oridonin. The expression levels of Brg1, P53, and C-myc were determined by semi-quantitative Western blot in Jurkat cells treated with various concentrations of oridonin for 24 hours or 5 μmol/L oridonin for various lengths of time (0, 2, 6, 12, and 24 hours). The expression levels of P53 and C-myc and proliferation of Jurkat cells were evaluated after Brg1 expression was knocked down by Brg1-specific siRNA.</p><p><b>RESULTS</b>Compared with the control group, the proliferation of oridonin-treated Jurkat cells was significantly inhibited in a concentration- and time-dependent manner (P<0.05). According to the florescence microscopic analysis, oridonin treatment led to nuclear pyknosis in Jurkat cells. Compared with the control group, Jurkat cells treated with 5 μmol/L oridonin had reduced expression of Brg1 and C-myc but elevated expression of P53. Brg1 knock-down led to a significant reduction in proliferation of Jurkat cells (P<0.05), up-regulated expression of P53, and down-regulated expression of C-myc.</p><p><b>CONCLUSIONS</b>Oridonin can inhibit the proliferation of Jurkat cells, probably via the Brg1 signaling pathway.</p>
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Humans , Antineoplastic Agents, Phytogenic , Pharmacology , Cell Proliferation , DNA Helicases , Physiology , Diterpenes, Kaurane , Pharmacology , Dose-Response Relationship, Drug , Down-Regulation , Jurkat Cells , Nuclear Proteins , Physiology , Precursor Cell Lymphoblastic Leukemia-Lymphoma , Drug Therapy , Proto-Oncogene Proteins c-myc , Signal Transduction , Physiology , Transcription Factors , Physiology , Tumor Suppressor Protein p53ABSTRACT
<p><b>OBJECTIVE</b>To compare and analyze the differentially expressed plasma proteome between patients with stable angina pectoris (SAP) and healthy donors to identify the biomarkers for early diagnosis of SAP.</p><p><b>METHODS</b>Plasma samples from 60 patients with SAP and 60 healthy controls were collected. Twenty samples (100 mL each) randomly selected from each group were pooled and after removing high-abundance proteins from the pooled plasma, two-dimensional gel electrophoresis (2DE) was performed to isolate the total proteins. The protein spots with more than 2 fold changes were selected after 2D analysis using software, and the differentially expressed proteins were identified by MALDI TOF/TOF mass spectrometer. ELISA was performed to detect hemoglobin subunit delta (HBD) levels in 40 randomly selected samples from each group for verification of the results of 2DE.</p><p><b>RESULTS</b>A total of 7 differentially expressed proteins were found in plasma samples from patients with SAP, including 3 up regulated proteins (serum albumin, hemoglobin subunit alpha and hemoglobin subunit delta,) and 4 down?regulated ones (apolipoprotein L1, apolipoprotein C3, apolipoprotein E and complement C4B). ELISA results showed that HBD level was increased in SAP plasma, which was consistent with the results of 2DE.</p><p><b>CONCLUSION</b>Patients with SAP have different plasma protein profiles from those of healthy controls, and HBD may serve as a potential specific biomarker for early diagnosis of SAP.</p>
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Objective: To detect the expression of CD133, E-cadherin and WWOX in colorectal cancer, analyze the correlations and pathological significance of the biomarkers
Methods: Two hundred and ten patients with colorectal cancer treated surgically between January 2007 and December 2015 were analyzed retrospectively. All patients had pathologic specimens and integrated clinical data. Pathologic specimens were retrieved for immunohistochemical examination of the expressions of CD133, WWOX and E-cadherin. The clinical data of these patients including gender, age, tumor location, tumor size, tumor differentiation, invasion depth, hepatic metastases, lymphatic metastasis, UICC stage and recurrence of tumor were retrieved to investigate their demographics and clinical characteristics
Results: In 210 specimens of colorectal cancer, the positive expression rate of CD133, E-cadherin and WWOX was 61.9%, 40.5% and 41.9%, respectively. The expression of CD133, E-cadherin and WWOX was significantly correlated with lymphatic metastasis, hepatic metastases and UICC stage [p<0.05]. The expression of CD133 was negatively correlated with WWOX and E-cadherin [p<0.05], and the expression of WWOX was positively correlated with E-cadherin in specimens [p<0.05]
Conclusion: A detection of CD133, E-cadherin and WWOX can facilitate physicians in predicting the progression and prognosis of colorectal cancer
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Bone marrow microenvironment is a complex network consisting of hematopoietic stem/pro-genitor cells (HSPCs),non-hematopoietic cells,extracellular matrix and various cytokines.Its components interact to support normal hematopoiesis.Emerging evidence indicates that the dysfunction of mesenchymal stem cells,myeloid-derived suppressor cells,cytokines and the epigenetic alterations of HSPCs in the bone marrow microenvironment could influence normal hematopoiesis.Abnormal hematopoiesis contributes to the occurrence of hematological malignancies,such as myelodysplastic syndromes (MDS).Animal models have confirmed that bone marrow microenvironment plays an important role in the original generation and maintenance of malignant diseases of hematopoietic system.
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Objective To ascertain the gross α/β levels in drinking water in Inner Mongolia and to estimate the annual effective dose to the local residents from radionuclides in drinking water.Methods A total of 768 water samples were collected from 101 counties distributed over 12 cities of Inner Mongolia.Low background α/β measuring instrument was used to measure the radioactivity level;On this basis,use EPA Federal Guidance Report 11 universal method to estimate the annual effective dose to the local residents via intake of radionuclides from drinking water.Results The gross α radioactivity range was 0.016-1.003 Bq/L for tap water,O.016-0.975 Bq/L for factory water,0.017-1.544 Bq/L for river water,0.120-0.672 Bq/L for lake water,0.016-0.492 Bq/L for reservoir water,0.016-1.139 Bq/L for well water,0.032-3.156 Bq/L for spring water,respectively.The gross β radioactivity range was 0.030-0.828 Bq/L for tap water,0.031-0.571 Bq/L for factory water,0.066-0.873 Bq/L for river water,0.169-2.268 Bq/L for lake water,0.046-0.519 Bq/L for reservoir water,0.071-0.526 Bq/L for well water,0.087-1.063 Bq/L for spring water,respectively.Conclusions In Inner Mongolia,the gross α/β mean value in tap water is less than the World Health Organization-recommended value and the average annual effective dose from tap water is also less than the WHO-recommended value O.1 mSv/a.The gross α/β radioactivity from the other water samples is also within the range of the nationwide average.
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<p><b>BACKGROUND</b>Brain acid soluble protein 1 (BASP1) is identified as a novel potential tumor suppressor in several cancers. However, its role in thyroid cancer has not been investigated yet. In the present study, the antitumor activities of BASP1 against the growth and migration of thyroid cancer cells were evaluated.</p><p><b>METHODS</b>BASP1 expression in thyroid cancer tissues and normal tissues were examined by immunohistochemical staining and the association between its expression and prognosis was analyzed. pcDNA-BASP1 carrying full length of BASP1 cDNA was constructed to restore the expression of BASP1 in thyroid cancer cell lines (BHT-101 and KMH-2). The cell proliferation in vitro and in vivo was evaluated by WST-1 assay and xenograft tumor models, respectively. Cell cycle distribution after transfection was analyzed using flow cytometry. Cell apoptosis after transfection was examined by annexin V/propidium iodide assay. The migration was examined using transwell assay.</p><p><b>RESULTS</b>BASP1 expression was abundant in normal tissues while it is significantly decreased in cancer tissues (P = 0.000). pcDNA-BASP1 restored the expression of BASP1 and significantly inhibited the growth of BHT-101 and KMH-2 cells as well as xenograft tumors in nude mice (P = 0.000). pcDNA-BASP1 induced G1 arrest and apoptosis in BHT-101 and KMH-2 cells. In addition, pcDNA-BASP1 significantly inhibited the cell migration.</p><p><b>CONCLUSIONS</b>Downregulation of BASP1 expression may play a role in the tumorigenesis of thyroid cancer. Restoration of BASP1 expression exerted extensive antitumor activities against growth and migration of thyroid cancer cells, which suggested that BASP1 gene might act as a potential therapeutic agent for the treatment of thyroid cancer.</p>