Animals ; Antibodies ; chemistry ; genetics ; Genetic Engineering ; Humans ; Immunoglobulins ; genetics ; Immunohistochemistry ; Protein Engineering

Air Pollutants, Occupational ; analysis ; Chromatography, Gas ; methods ; Indenes ; analysis ; Workplace

Background and purpose: Pancreatic cancer is often diagnosed at advanced stage, therefore, chemotherapy remains the cornstone of treatment for advanced pancreatic cancer. However, no standard regimen has been established as second-line therapy for advanced pancreatic cancer. The purpose of the study was to evaluate the efifcacy and safety of albumin-bound paclitaxel plus S-1 for the treatment of advanced pancreatic cancer patients in second-line setting after the failure of gemcitabine treatment. Methods:Clinical outcomes of 19 patients with advanced pancreatic cancer were analyzed. These patients received albumin-bound paclitaxel plus S-1 as second-line therapy after the failure of gemcitabine treatment. Albumin-bound paclitaxel was administered at a dose of 125 mg/m2 over 30 minutes on day 1 and 8 of a 21-day cycle. From d1-14, all patients received oral S-1 40 mg/m2, twice daily. Results:All patients were available for evaluation. Of the 19 patients, 1 case got complete response (CR), 4 cases had partial response (PR) and 9 cases had stable disease (SD). The objective response rate (ORR) was 26.3%, the disease control rate (DCR) was 73.7%and the median progression free survival (PFS) was 5.2 months. The main toxicities include hematological toxicity, myodynia, gastrointestinal reactions, sensory neuropathy, fatigue and alopecia. Conclusion:The combination of albumin-bound paclitaxel and S-1 is effective and tolerated in the treatment of advanced pancreatic cancer patients who resistant to gemcitabine.

Objective To investigate the suppression to 2-glycoprotein-1-specific B cell response by human recombinant 2-glycoprotein-1 domain Ⅰ dimer(rh?2-GP1-DⅠ2) in rh?2-GP1 immunized mice.Methods The effects of treatment using rh?2-GP1-DⅠ2 on titer and ratio of anti-?2-GP1 were analyzed by solid phase ELISA.The number of splenic ?2-GP1-specific antibody-forming cells(AFC) was counted by ELISPOT.Results The levels of anti-?2-GP1 from rh?2-GP1 immunized mice treated with rh?2-GP1-DⅠ2 were significantly decreased compared with those in negative controls(P

Objective:To observe the change of CD4+CD25+regulatory T cells and Th17 cells in mice with experimental anti-phospholipid antibody syndrome ( EAPS ) .Methods: EAPS model was established by immunizing BALB/c mice with recombinant humanβ2 glycoprotein 1 (rhβ2GP1).The levels of serum anti-β2 glycoprotein 1 (anti-β2GP1),anti-cardiolipin antibody (aCA),IL-17,IL-2,IL-6 and TGF-βwere tested by ELISA.The rate of abortion,activated partial thromboplastin time (APTT) and platelet count were also detected.Flow cytometry was applied to detect the percentages of the CD4+CD25+regulatory T cells and Th17 cells in peripheral blood mononuclear cells.Results:Compared with the control group,the levels of anti-β2 GP1,aCA,IL-17,IL-2 and IL-6 were significantly increased,the rate of abortion was increased,APTT time was prolonged and the levels of TGF-βand platelet count were de-creased in model mice (P<0.05).No significant difference was detected of percentage of Treg cells in PBMC at the eighth weeks in model group (P>0.05),but percentage of Treg cells was lower than that in control group after 12 weeks (P<0.05);the percentage of Th17 cells in model group was higher than that in control group (P<0.05).In addition,the ratio of Treg/Th17 cells was lower in model mice than that in control group.Conclusion: The imbalance of CD4+CD25 Treg/Th17 cells may participate in the pathogenesis of EAPS.

Adenofibroma ; metabolism ; pathology ; Antigens, CD34 ; metabolism ; Child, Preschool ; Diagnosis, Differential ; Female ; Humans ; Kidney Neoplasms ; metabolism ; pathology ; surgery ; Neoplasms, Germ Cell and Embryonal ; metabolism ; pathology ; surgery ; Nephroma, Mesoblastic ; metabolism ; pathology ; Sarcoma, Clear Cell ; metabolism ; pathology ; Stromal Cells ; metabolism ; pathology ; Vimentin ; metabolism

12E7 Antigen ; Adolescent ; Adult ; Antigens, CD ; metabolism ; Biomarkers, Tumor ; metabolism ; Brain Neoplasms ; secondary ; Cell Adhesion Molecules ; metabolism ; Child ; Child, Preschool ; Diagnosis, Differential ; Extremities ; Female ; Follow-Up Studies ; Humans ; Immunohistochemistry ; In Situ Hybridization, Fluorescence ; Infant ; Ki-67 Antigen ; metabolism ; Male ; Neuroectodermal Tumors, Primitive ; metabolism ; pathology ; Oncogene Proteins, Fusion ; metabolism ; Repressor Proteins ; metabolism ; Sarcoma, Ewing ; metabolism ; pathology ; Sarcoma, Synovial ; diagnosis ; metabolism ; pathology ; surgery ; Soft Tissue Neoplasms ; diagnosis ; metabolism ; pathology ; surgery ; Vimentin ; metabolism ; Young Adult

OBJECTIVETo explore the effect of negative emotions on serum levels of adrenocorticotropic hormone (ACTH) and neuropeptide Y (NYP) in hepatitis B liver cirrhosis (HBLC) patients.

METHODSTotally 617 HBLC patients were assigned to the negative emotion group (415 cases) and the non-negative emotion group (202 cases) judged by negative emotions. Case numbers of various grading Child-Pugh were recorded in the two groups. Their liver functions were compared between the two groups. Serum levels of ACTH and NPY were detected using double antibody sandwich enzyme-linked immunosorbent assay (ELISA) in the two groups.

RESULTSThere was no statistical difference in Child-Pugh grading between the two groups (χ2 = 0.65, P = 0.72). Compared with the non-negative emotional group, serum ACTH levels decreased significantly in the negative emotion group with statistical difference (P < 0.05). There was no statistical difference in serum ACTH levels between the two groups (P > 0.05).

CONCLUSIONThe negative emotion of HBLC patients was not related to the serum ACTH level, but to relatively lower-concentration serum NPY levels.

Adrenocorticotropic Hormone ; blood ; Emotions ; Hepatitis B ; blood ; psychology ; Humans ; Liver Cirrhosis ; blood ; psychology ; Neuropeptide Y ; Serum

Objective To detect the impact of reactive oxygen species ( ROS) on mitochondrial morphology and distri-bution during mitosis.Methods A viral vector in which the fluorescence gene was specifically under the control of mito-chondrial promoter was constructed and confirmed through DNA sequencing and Western blotting.After transfecting HeLa s3 cell with packaged virus, the HeLa s3-COX4tp-EGFP cell line stably expressing the mitochondrial fluorescence signal was obtained.With immunofluorescent staining, the impact of ROS on the morphology and distribution of mitochondria dur-ing mitosis was inspected.Result The cell line constantly expressing mitochondrial fluorescence signals was successfully constructed.Meanwhile,it was found that H2 O2 treatment could significantly change the morphology and distribution of mi-tochondria during mitosis by confocal microscopy.Conclusion Our study demonstrates that ROS can affect the morphology and distribution of mitochondria during mitosis.This research help study the relationship between the mitochondrial function and the regulation of mitosis in the future.

Aim To investigate the effects of irbesartan on Wnt/β-catenin signaling pathway in tubular epithelial-mesenchymal transition(EMT)in HKCs induced by high-glucose.Methods Human kidney proximal tubular epithelial cell line(HKCs)cultured in vitro was divided into four groups:normal-glucose group,mannitol control group,high-glucose group and high-glucose plus irbesartan group.Immunocytochemistry staining was used to observe the expression of β-catenin;the protein expression of Wnt4,β-catenin,E-cadherin and α-SMA was assessed by Western blot;Wnt4 and β-catenin mRNA were detected by reverse transcription-polymerase chain reaction(RT-PCR).Results Compared with normal-glucose and mannitol control group,both the protein and the mRNA of Wnt4 were up-regulated in HKCs stimulated by high-glucose.α-SMA expression significantly increased but E-cadherin decreased in HG group.The cytoplastic and nuclear fraction of β-catenin enhanced with highglucose stimulation.But no difference of the total protein and mRNA of β-catenin was observed between highglucose-treatment and control groups.Highglucose induced Wnt4 and β-catenin expression in a time-dependent manner,both peaking at 24 h.Irbesartan reduced the promotional effect of HG on Wnt4 and α-SMA expression,and nuclear translocation of β-catenin.HG-mediated inhibition of E-cadherin was also restored by irbesartan.Conclusion These data supported a functional role for Wnt/β-catenin signaling pathway during epithelial-mesenchymal transition of HKCs induced by high glucose and suggested that irbesartan might reverse tubular EMT by regulating activity of Wnt/β-catenin pathway.