The definition of esophagogastric junction (EGJ) adenocarcinoma and progress in multidisciplinary treatment for the tumor were revised in this review. Siewert classification is especially useful for the surgical approach of EGJ adenocarcinoma. Siewert I should be treated as esophageal cancer, and Ivor-Lewis esophagogastrectomy (right thoracotomy and laparotomy) is recommended as an extended two-field lymphadenectomy. For Siewert II or III tumors, left thoracophreno-laparotomy is preferred, especially in case of positive thoracic lymph nodes or positive resection margin. If there is any contraindication against thoracotomy, or a high operating risk, a transhiatal esophagectomy with lower mediastinal lymphadenectomy is an alternative. Preoperative chemoradiotherapy or perioperative chemotherapy improves overall survival and the rate of complete resection for patients with large tumor or lymph node metastasis. Neoadjuvant chemoradiotherapy is associated with high but acceptable postoperative complications. Adjuvant chemoradiotherapy remains a rational standard therapy for curatively resected EGJ cancer with T3 or greater lesion or positive nodes.
Adenocarcinoma ; surgery ; therapy ; Combined Modality Therapy ; Esophageal Neoplasms ; surgery ; therapy ; Esophagogastric Junction ; Humans ; Stomach Neoplasms ; surgery ; therapy

Apoptosis ; physiology ; Cell Cycle ; physiology ; Humans ; Neoplasms ; etiology ; metabolism ; Tankyrases ; genetics ; physiology ; Telomerase ; metabolism ; physiology ; Telomere ; genetics ; metabolism ; Telomere-Binding Proteins ; genetics ; physiology ; Telomeric Repeat Binding Protein 1 ; genetics ; physiology ; Telomeric Repeat Binding Protein 2 ; genetics ; physiology

AIM: To establish the quality standard for Huangqi Fufang Granules(Radix Astragali, Fructus Schisandrae Chinensis, Radix Cyathulae, etc.). METHODS: Fructus Schisandrae Chinensis, Radix Cyathulae were identified by TLC, and the content of astragaloside Ⅳ was determined by TLC scanning. RESULTS: Fructus Schisandrae Chinensis, Radix Cyathulae could be identified by TLC. Astragaloside Ⅳ showed a good linear relationship at a range of 1.0?g～6.0?g, r =0.9992. The average recovery was 99.19%, and RSD was 0.63%. CONCLUSION: The methods are simple, accurate and specific, and can be used for the quality control of Huangqi Fufang Granules.

Objective To investigate theeffect of ischemic postconditioning (IPO) on ischemia/reperfusion injury via mitochondrial pathway.Methods Male Sprague-Dawley rats were divided into three groups by means of random number table.Rats in IRI group and IPO group received liver transplantation.The portal vein in IRI group was opened immediately after liver implantation to restore the blood supply.The graft rats in IPO group received IPO before the portal vein was completely opened: 60-s ischemia and 60-s reperfusion of the portal vein,repeated 6 times).The rats in the sham-operation group were only subject to dissociation of the liver ligament.Six h after portal vein reperfusion,liver function was tested.The expression of Bcl-2 mRNA and Bax mRNA was detected by using real time-PCR.The protein expression of Cyt-c was detected by using Western blotting.The apoptosis and necrosis of liver tissue and the mitochondrial transmembrane potential were detected by using flow cytomertry.The changes of mitochondrial structure were observed under an electron microscope.Results The liver functions in IRI group and IPO group were significantly worse (P＜0.05),the levels of Bax mRNA were significantly higher (P＜0.05),the levels of Bcl-2 mRNA were significantly lower (P＜0.05),the levels of Cyt-c protein were significantly higher (P＜0.05),the levels of apoptosis and necrosis were significantly higher (P＜0.05),and mitochondrial transmembrane potential (MTP) of liver cells was significantly lower (P＜0.05) than in sham operation group.The changes of all the parameters in IRI group were more significant than in IPO group (P ＜ 0.05).The morphological changes of the liver mitochondria were also significantly aggravated in IRI group as compared with IPO group.Conclusion IPO reduced IRI by inhibiting the mitochondrial signaling pathway in rats undergoing liver transplantation.

Aim To investigate the molecular mechanisms of differentiation in human leukemia HL-60 cells induced by diallyl disulfide(DADS)using suppression subtractive hybridization(SSH).Methods In our privious study,the subtractive cDNA library was constructed successfully and efficiently. 30 clones were randomly analyed with restriction enzyme.The inserts of cDNAs were analyzed by restrictive enzyme EcoR I.Positive clones were sequenced and the homology of resulting cDNA sequences were analyzed through bioinformatics software Blastn.Results 18 clones contained 100～600 bp cDNA inserts.10 differantiation genes were obtained and involved in cell cycle,signal transduction,metabolism and RNA binding.And 3 of 10 genes,p21,STAT1 and CAMTA1 were up-regulated and detected by RT-PCR,the results matched with SSH.Conclusion sThere are tight correlation between the differentiation induced by DADS and three-upregulated gene:p21,STAT1 and CAMTA1.

It has been shown, however, that in terms of immune function, a transitional stage of dendritic cell maturation exists between immature myeloid dendritic cells (imDCs) and mature dendritic cells (DCs), which were named semimature dendritic cells (smDCs). Therefore, the theory that DCs can be classified as imDCs and mDCs has been challenged because of finding smDCs. SmDCs and imDCs are regarded as tolerogenic dendritc cells while what concrete mechanism taken by smDCs and imDCs in transplantation immunity has yet to know. The authors analyzed the important roles and the advanced molecular mechanism of smDCs and imDCs in transplantation immunity in order to update and widen understand underlying tolerogenic dendritic cells.

Animals ; Hypothermia ; blood ; Hypoxia ; blood ; Malondialdehyde ; blood ; Myocardial Ischemia ; blood ; Rabbits ; Superoxide Dismutase ; blood

Antineoplastic Agents ; administration & dosage ; Drug Delivery Systems ; Genetic Therapy ; methods ; Hematologic Neoplasms ; drug therapy ; therapy ; Humans

Objective To observe the effects of ulinastatin on the expressions of tumor necrosis factor-α (TNF-α) in the lung tissues of rats with acute lung injmy induced by phosgene, and to explore the mechanism of ulinastafin in treating acute lung injury. Method Sixty-four clean grade healthy male SD rots were randomly divided(random number) into eight groups with eight in each group. Group A1 in which rats were exposed to air. Group A2 in which rots wereexposed to air and treated with saline. Group A3 in which rats were exposed to air and treated with dexamethasone. Group A4 in which mrs were exposed to air and treated with ulinastatin. Group B1 in which rots were exposed to phosgene without treatment. Group B2 in which rats were exposed to phosgene and treated with saline. Group B3 in which rats were exposed to phosgene and treated with dexamethasone. Group B4 in which rats were exposed to phosgene and treated with ulinastatin. The expressions of TNF-α in the lung tissues were measured by using immunohistocheistry. Lung tissues were observed grossly and under 200-fold light microscope to identify the positive expressions in kytoplasm. Results In group B1 and group B2, the wet weight, dry weight and wet/dry weight ratio og right lower lobe of lung were higher thai those in group A1 and group A4( P <0.01 ), and those in group B4 and group B3 were significantly lower than those in group B1(P<0.01 ), but still higher than those in group A1 and A4(P<0.01). The gross observation suggested that the surfaces of lung tissues in group A1and group A2 were slick and rose pink without congestion, dropsy or infarction; the surfaces of lung tissue in groups B1 and B2 appeared with congestion, dropsy and many petechia. The surfaces of lung tissue in groups B3 and B4 were similar to those in groups B1 and B2. Under the light microscope, the structure, of lungs in groups A1 and A2 were clear without congestion, effusion or inflammatory cell infiltration. In groups B1 and B2, the engorgement of lung capillary vessels, congestion and tiny thrombosis were found and there abundant edematous fluid and inflammatory cell infiltration in lung stroma and alveolus with focal pulmonary atelectasis in some lung tissue section. The tissues in groups B3 and B4 showed congestion, dropsy, tiny thrombosis and inflammatory cell infiltration, but these changes were slighter than those in groups B1 and B2. The expressions of TNF-α in groups B1, B2, B3, and B4 were significantly higher thanthose in groups A1 and A2( P < 0.01 ), but the expressions of TNF-α IN group B4 was lower than that in groups B1 and B2(P<0.01). Conclusions Ulinastatin could lessen the lung injury by reducing the expressions of pro-inflammatory cytokines such as TNF-α.

Aim To investigate JAKs/STATs signal transduction change in HL-60 cells differentiation induced by diallyl disulfide(DADS)and molecular mechanism regulating the differentiation.Methods After incubation of HL-60 cells with DADS or AG490(50 ?mol?L -1),the cell differentiation indexes were observed by cytomorphology, NBT reduction ability assay,cell myeloid differentiation antigen CD11b by flow cytometry. Kinase activity of JAKs/STATs was tested by western-blotting and expressions of nucleus transcription genes stats,c-myc,c-fos,c-jun were detected by immumocyte chemistry method.Results Cell differentiation index changes indicated that HL-60 cells were induced differentiation toward granulocytic lineage by DADS, Western blot test demonstrated that constitive phosphorylation of Jak1,stat3 kinase was suppressed. Stat3,c-myc gene expression decreased and c-fos, c-jun gene expression increased in HL-60 cells treated with DADS through immunocyte chemistry.Conclusion Inhibition of phosphative Jak1, Stat3 was involved in HL-60 cells differentiation induced by DADS, its molecular mechanism might be related to modulation of gene expression associated proliferation and differentiation,and inhibition of DNA systhesis, induction differentiation.