Fistula ; complications ; surgery ; Humans ; Male ; Maxilla ; pathology ; Middle Aged ; Osteomyelitis ; complications ; surgery

Adenocarcinoma ; genetics ; pathology ; virology ; Carcinoma in Situ ; genetics ; pathology ; virology ; Cervical Intraepithelial Neoplasia ; genetics ; pathology ; virology ; Cervix Uteri ; pathology ; virology ; Cytological Techniques ; DNA, Viral ; analysis ; Female ; Follow-Up Studies ; Humans ; Neoplasm Grading ; Papillomaviridae ; genetics ; isolation & purification ; Papillomavirus Infections ; diagnosis ; Uterine Cervical Neoplasms ; genetics ; pathology ; virology

Adult ; Bone Plates ; Female ; Humans ; Male ; Middle Aged ; Pubic Symphysis Diastasis ; surgery

To investigate the function of ALK3 gene, the gene regulation and the signaling pathway related to ventricular septum defect during heart development. The model mice with ALK3 gene knock-out via alpha-MHC-Cre/lox P system were bred. The mRNA expression level of control group was compared with that of experiment group and ALK3 downstream genes were screened using PCR-select cDNA subtraction microarray. The mRNA of control group was extracted from E11.5 normal mouse hearts, and that of experiment group, from E11.5 hearts of mice with alpha-MHC Cre(+/-) ALK3(F/+) genotype. It was found that the mice with ALK3 gene knock-out produced heart defects involving the interventricular septum. The platelet-activating factors acetylhydrolase and the transcription factor Pax-8 and so on, were down-regulated. However, the Protein Tyrosine Kinase (PTK) of Focal Adhesion Kinase (FAK) subfamily and beta subtype protein 14-3-3 were up-regulated in the alpha-MHC Cre(+/-) ALK3(F/-) mice. These data provide support that ALK3 gene played an important role during heart development. The platelet-activating factors acetylhydrolase and Pax-8 genes could be important ALK3 downstream genes in the BMP signaling pathway during interventricular septum development. PTK and beta subtype protein 14-3-3 might be regulatory factors in this pathway.
1-Alkyl-2-acetylglycerophosphocholine Esterase ; genetics ; metabolism ; 14-3-3 Proteins ; genetics ; metabolism ; Animals ; Bone Morphogenetic Protein Receptors, Type I ; genetics ; metabolism ; Genotype ; Heart Septal Defects, Ventricular ; genetics ; Mice ; Mice, Knockout ; Oligonucleotide Array Sequence Analysis ; PAX8 Transcription Factor ; Paired Box Transcription Factors ; genetics ; metabolism ; Protein-Tyrosine Kinases ; genetics ; metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Signal Transduction ; genetics ; physiology

OBJECTIVETo investigate the effects of Compound Salvia injection (CSI) on the number and activity of endothelial progenitor cells (EPCs).

METHODMononuclear fraction of human umbilical cord blood was obtained by density gradient centrifugation and plated on fibronectin coated culture dishes. Cells were divided in to five groups: group control, group VEGF, group CSI 50, group CSI 10 and group CSI 2 (supplemented with none cytokine, VEGF 10 ng x mL(-1), CSI 50, 10, 2 microg x mL(-1), respectively). After six days in culture, cell clusters were viewed with an inverted microscope, fluorescence-activated cell sorting (FACS) analysis of PE-CD34 and FITC-VE-Cadherin was performed to detect number of EPCs, adhesion assay was performed by replating cells on fibronectin coated dishes, and then counting adherent cells.

RESULTNumbers of EPCs of group VEGF, group CSI 10 and group CSI 2 were significantly increased as compared with those of group control ( P < 0.01, P < 0.05, P < 0.01, respectively), and numbers of EPCs of group CSI 2 were more than those of group CSI 10 and group V (P < 0.01). Compared with group control, number of EPCs of group CSI 50 was significantly decreased (P < 0.01). Compared with group control, numbers of clusters and adhesive EPCs of group CSI 10 and group CSI 2 were significantly increased, while those of group CSI 50 were significantly decreased.

CONCLUSIONLow concentration CSI can significantly promote EPCs augmentation and enhance its functional activity, while high concentration CSI significantly restrains it.

Blood Cell Count ; Cell Adhesion ; drug effects ; Dose-Response Relationship, Drug ; Drug Combinations ; Drugs, Chinese Herbal ; administration & dosage ; isolation & purification ; pharmacology ; Endothelium, Vascular ; cytology ; Fetal Blood ; cytology ; Humans ; Injections ; Plants, Medicinal ; chemistry ; Salvia miltiorrhiza ; chemistry ; Stem Cells ; cytology ; drug effects

Acute Disease ; Adolescent ; Adult ; Aged ; China ; epidemiology ; Female ; Humans ; Male ; Middle Aged ; Pesticides ; poisoning ; Poisoning ; epidemiology

OBJECTIVETo explore the effect of treatment with immunocyte therapy on benzene-induced haemopoietic dysfunction.

METHODSMono-nuclear cells (MNC) were separated from 40 - 50 ml peripheral blood in patients and mixed with interleukin-2 and granulocyte macrophage colony stimulating factor (GM-CSF) for six day cultivation. The new formed immunocytes were collected and transfused into the patients. Bone marrow aspiration and biopsy were taken before and after therapy for all patients with severe benzene poisoning. Blood samples were stained by flow cytometry for detecting CD(4) and CD(8) positive cells.

RESULTSOf 20 patients with chronic benzene poisoning, 9 were severe benzene poisoning. All examination including blood count, bone marrow biopsy and T cell subpopulation restored to normal after immunocyte therapy. Laboratory tests (liver and kidney function, and myocardial enzymes) were observed periodically and showed normal during therapy. Follow-up study (the longest time was more than 15 months) showed that bone marrow haemopietic function of all treated patients were in normal range.

CONCLUSIONBone marrow haemopoietic dysfunction caused by benzene poisoning may be closely related to disorder of immune function. Immunocyte therapy may significantly improve bone marrow haemopoietic dysfunction induced by benzene poisoning.

Adult ; Anemia, Aplastic ; chemically induced ; immunology ; therapy ; Benzene ; poisoning ; Bone Marrow ; immunology ; pathology ; Female ; Flow Cytometry ; Follow-Up Studies ; Humans ; Male ; Occupational Diseases ; chemically induced ; immunology ; therapy ; Peripheral Blood Stem Cell Transplantation ; methods ; Treatment Outcome

OBJECTIVEConventional deletion of ALK3, also termed as bone morphogenetic protein (BMP) receptor IA, in mice might result in early embryonic lethality. To investigate the function of ALK3 in cardiac development, the cardiac-specific deletion of ALK3 in mice was made by Dr. Schneider, using Cre recombinase driven by the alpha-MHC promoter that Dr. Fukushipe worked out. Such specific deletion of ALK3 caused death in mid-gestation with defects in the trabeculae, interventricular septum, and endocardial cushion. Since ALK3 is not a cardiac-specific gene, it is extremely important to identify ALK3 downstream genes.

METHODSAlpha-MHC Cre+/-, ALK3 F/- and alpha-MHC Cre+/-, ALK3 F/+ embryos were obtained after 20 alpha-MHC Cre+/-, ALK3 +/- mice and 20 ALK3 F/F mice were mating. The ALK3 downstream genes were screened using microarray made in Germany that could identify 25000 genes in mouse. Two populations of mRNA, one derived from the embryonic heart (11.5 days) of alpha-MHC Cre+/-, ALK3 F/- mice, and the other derived from the alpha-MHC Cre+/-, ALK3 F/+ mice, were compared. Cardiac-specific ALK3 downstream genes were identified using real time quantitative RT-PCR and in situ hybridization.

RESULTSThe expression of 12 genes, such as Pax-8 and Hox-3.5 were down-regulated in alpha-MHC Cre+/-, ALK3 F/- mouse heart. The expression of 16 genes including Ras-related protein Rab-5b and EPS-8 protein was up-regulated in the group of alpha-MHC Cre+/-, ALK3 F/-. It was found that the Box protein Pax-8 gene was down-regulated by 7.1 fold (P < 0.001) in the alpha-MHC Cre+/-, ALK3 F/- mice by real time quantitative RT-PCR. It was also revealed that the Box protein Pax-8 gene was expressed stronger in alpha-MHC Cre+/-, ALK3 F/+ than alpha-MHC Cre+/-, ALK3 F/- E11.5 days mouse heart by means of in situ hybridization.

CONCLUSIONThe Box protein Pax-8 gene is an important and cardiac-specific ALK3 downstream gene in the BMP signaling pathway during inter-ventricular septum development.

Animals ; Bone Morphogenetic Protein Receptors ; DNA-Binding Proteins ; genetics ; Down-Regulation ; Female ; Heart ; embryology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Myocardium ; metabolism ; pathology ; Nuclear Proteins ; Oligonucleotide Array Sequence Analysis ; PAX8 Transcription Factor ; Paired Box Transcription Factors ; Receptors, Growth Factor ; genetics ; physiology ; Reverse Transcriptase Polymerase Chain Reaction ; Trans-Activators ; genetics

OBJECTIVETo evaluate the efficacy and prognostic factors of transarterial interventional therapy (TAIT) in patient with liver metastasis from malignancy of the alimentary tract.

METHODS266 patients with unresectable liver metastases from malignancy of the alimentary tract received totally 754 sessions of transarterial interventional therapy. Cox regression was used in the proportional hazard analysis.

RESULTSThe overall response rate of TAIT was 45.4%, The median survival time (MS) was 14.3 months in this series. The 0.5-, 1-, 2-, 3-, 5-year cumulative survival rate (CSR) was 83.1%, 56.8%, 17.7%, 9.3% and 1.5% , respectively. No severe adverse reaction was observed except nausea, vomiting and mild fever as well as pain in the hepatic area. It was found that portal vein tumor thrombosis (PVTT), the blood supply of tumor, metastasis from esophageal carcinoma, the number of metastasis, multi-lobe involvement, resection nature of primary tumor were independent factors affecting survival.

CONCLUSIONTransarterial interventional therapy is effective for treatment of liver metastasis from malignancy of the alimentary tract. Portal vein tumor thrombosis, metastasis from esophageal carcinoma, multiple metastatic lesions, multi-lobe involvement are poor prognostic factors, while complete resection of the primary tumor and rich blood supply of metastatic lesion are good independent prognostic factors.

Adult ; Aged ; Aged, 80 and over ; Antineoplastic Combined Chemotherapy Protocols ; therapeutic use ; Chemoembolization, Therapeutic ; Cisplatin ; administration & dosage ; Colorectal Neoplasms ; pathology ; surgery ; Doxorubicin ; administration & dosage ; Esophageal Neoplasms ; pathology ; surgery ; Female ; Fluorouracil ; administration & dosage ; Follow-Up Studies ; Gastrointestinal Stromal Tumors ; pathology ; surgery ; Humans ; Infusions, Intra-Arterial ; Iodized Oil ; Liver Neoplasms ; secondary ; therapy ; Male ; Middle Aged ; Neoplastic Cells, Circulating ; Portal Vein ; pathology ; Remission Induction ; Retrospective Studies ; Stomach Neoplasms ; pathology ; surgery ; Survival Rate

Objective To observe the effects of ryanodine on rapamycin treated endothelial outgrowth cells (EOCs). Methods The mononuclear cells were harvested from umbilical cord blood by Ficoll density gradient centrifugation, then induced into EOCs tnd expanded in vitro. The endothelial characteristics of EOCs were identified by immunostaining and fluorescent staining. The EOCs were pretreated with or without ryanodine ( 10 μmol/L) for 1 h, and then treated with or without rapamycin ( 10nmoL/L) for 24 h. Proliforation was evaluated by CCK8 and migration was measured by Transwell. The protein expression of EOCs was evaluated by immunobloting technique with total eNOS antibody and phosphoeNOS(Thr495) antibody. Results Compared with control group, the proliferation and migration capacities of EOCs were significantly reduced while the phosphorylation of eNOS ( Thr495 ) protein was significantly upregulated in rapamycin group( P ＜ 0. 05 ), expression of total eNOS was not affected by rapamycin ( P ＞0. 05). Compared with rapamycin group, the proliferation and migration capacities of EOCs were significantly increased and the phosphorylation of eNOS(Thr495) protein was significantly downregnlated in ryanodine + rapamycin group( P ＜0. 05). The proliferation and migration capacities, the phosphorylation of eNOS (Thr495) protein and the expression of total eNOS were not affected by ryanodine alone ( P ＞ 0. 05 ).ConclusionsRapamycin reduced proliferation and migration capacities while upregulated the phosphorylation of eNOS (Thr495) protein of EOCs and these effects could bepartly reversed by cotreatment with ryanodine.