Axillary reverse mapping (ARM) is anatomic theoretical foundation based on breast and upper limb lymph axillary lymph injected into different lymphatic populations, ARM can display upper limb lymphatic channels through different tracers during the periods of axillary lymph node dissection and sentinel lymph node dissection, to reduce the rate of postoperative upper extremity edem.Although ARM has a positive effect, it exists a controversy in safety and the relationship between its node and sentinel lymph node.

Breast conserving surgery has become the first choice for the treatment of early breast cancer.However,the safety margin is still one of the important issues for surgeons in the implementation of breast conserving surgery.Because variety of clinical factors have some effects on the safety margin,at present,no consensus on safe margin of breast conserving surgery is reached,and the controversy still goes on.

Objective: To elucidate the relationship between Notch3 expression and chemosensitivity of human colon carcinoma cell line SW620 to topotecan. Methods: Notch3 siRNA was transfected into SW620 cells, and the expression of Notch3 in SW620 cells was examined by Western blotting. After transfected with Notch3 siRNA for different time peri-ods, SW620 cells were further treated with topotecan, and the proliferation of SW620 cells was detected by MTT assay; the apoptosis of SW620 cells was detected by Hoechst 33342 staining and flow cytometry. Caspase-3 activation in SW620 cells was examined by caspase-3 activation kit. Results: Notch3 siRNA transfection remarkably inhibited Notch3 protein expression in SW620 cells. The IC_(50) of topotecan in Notch3 siRNA-transfected group was significantly decreased compared with that in the Ctrl siRNA group (P <0.05). Silence of Notch3 expression in SW620 cells by Notch3 siRNA remarkably promoted apoptosis (P < 0.05) and caspase-3 activation (P < 0.05) of SW620 cells induced by topotecan. Conclusion: Notch3 down-regulation by siRNA in SW620 cells can enhance the chemosensitivity cells to topotecan.

Portal vein tumor thrombus is a common complication of primary liver cancer,in the event,and often indicates that his condition has office in the late irreversible,the prognosis is extremely poor.This article describes the treatment of portal vein tumor thrombus of existing methods,to promote muhidisciplinary treatment,improve survival in patients with advanced liver cancer.

At present, more and more studies show that epithelial-mesenchymal transition (EMT) is closely associated with cancer stem cell formation and tumor cell invasion, migration and metastasis.EMT not only enhances the capacity of cancer cell invasion and metastasis, but also makes the cell obtain self regeneration and other stem cell characteristics and promotes the production of cancer stem cells.As a result, the investigation of the relationship between EMT and common stem cells can be served as a new approach for searching for effective ways to control tumor invasion and metastasis.It also can provide new targets for the treatment of tumor.

Objective:To construct pEGFP-C1-Smad4 expression vector and to observe the influence of Smad4 over-expression on the proliferation of human gastric cancer SGC7901 cells and its relationship with nuclear factor kappa B (NF-?B). Methods:Recombinant expression vector pEGFP-C1-Smad4 was constructed and was used to transfect human gastric cancer SGC7901 cells. EGFP expression in transfected cells was detected by fluoroscopy. Smad4 and NF-?B expression in transfectant was examined by Western blotting. Effect of Smad4 over-expression on activation of NF-?B and proliferation of transfected SGC7901 cells were examined by electrophoretic mobility shift assay (EMSA) and MTT assay,respectively. Results:Expression of EGFP in transfected SGC7901 cells was observed under fluorescence microscope. Smad4 was over-expressed in transfected SGC7901 cells,accompanied by down-regulation of NF-?B p65 expression in the tranfectants. EMSA and MTT demonstrated that Smad4 over-expression significantly inhibited the activation of NF-?B and the proliferation of SGC7901 cells (P

Objective To explore the regulatory function of over-expression of NOTCH-1 in TNF?-induced apoptosis of gastric carcinoma carcinoma BGC-823 cells.Methods BGC-823 cells were infected with retrovirus recombined with intracellular domain of NOTCH-1.The cell clones,into which objective genes had been transfected,were obtained after screening with G-418.Before and after incubation with TNF?,MTT assay,flow cytometry,Western blot and EMSA were used to detect cell growth,apoptosis,expressions of NOTCH-1,NF-?B and caspase-3 activity.Results There was stronger expression of NOTCH-1 and its target gene HES-1 in the cells transfected with NOTCH-1 gene than that of control.After TNF? treatment,the rates of killing and apoptosis in NOTCH-1-transfected cells were all lower than those in control cells.Moreover,we showed over-expression of NOTCH-1 suppressed caspase-3 activation induced by TNF?.However,TNF?-induced activation of NF-?B was not affected by over-expression of NOTCH-1.Conclusion Over-expression of NOTCH-1 significantly protects BGC-823 cells from apoptosis and growth suppression induced by TNF?.This effect is mediated,at least in part,through inhibition of caspase-3 activation independent of NF-?B.

Primary liver cancer is a high incidence and common malignant tumor in China. Portal vein tumor thrombus is one of the biologic marks of advanced liver cancer and difficult to be cured, and the prognosis is extremely poor. This paper systematically describes the formation mechanism, diagnosis,classification and prognosis of portal vein tumor thrombus. It would provide a theoretical basis for this clinical problem in order to reasonably understand and actively treat it.

Type-2 innate lymphoid cells ( ILC2 ) is a new member of the innate lymphoid cell family which has been recently discovered. These cell arise from lymphoid progenitors in the bone marrow and,under the control of the transcriptional regulators and Gata3,producing IL-5,IL-9 and IL-13 is a sign of the matura-tion. These cells are critical components of the innate immune response to parasitic worm infections and have al-so been implicated in the pathogenesis of asthma. This paper summarizes the role of ILC2 in the pathogenesis of asthma and its therapy research progress.

BACKGROUND:Studies have found that bone marrow mesenchymal stem cel s, under certain conditions, can be induced to differentiate into neurons and glial cel s, which to some extent solves the problem of the source of seed cel s. Induction methods currently used are different, and their efficiencies are not the same.
OBJECTIVE:To observe the effects of different antioxidants on differentiation of rat bone marrow mesenchymal stem cel s into neuron-like cel s in vitro.
METHODS:Bone marrow mesenchymal stem cel s from Wistar rats were divided into four groups:non-intervention group,β-mercaptoethanol group, retinoic acid group,β-mercaptoethanol+retinoic acid group. Changes in cel morphology and positive rate of neuron-specific enolase and microtubule-associated protein 2 were observed and detected at 5 hours, 12 hours, 1 day, 3 days, 5 days, 7 days, and 10 days after induction.
RESULTS AND CONCLUSION:Except non-intervention group, bone marrow mesenchymal stem cel s in the other three groups were gradual y becoming spindle-shaped, and gave birth to many smal protrusions that were interconnected into a network, showing neuron-like cel morphology. Immunocytochemical staining showed that the efficiency of theβ-mercaptoethanol+retinoic acid group was the highest at 10 days after induction, and the positive rates of neuron-specific enolase and microtubule-associated protein 2 were 71.63%and 79.72%, respectively. The results show thatβ-mercaptoethanol can be combined with retinoic acid to accelerate the differentiation of bone marrow mesenchymal stem cel s into neuron-like cel s.