In recent years, the incidence of adenocarcinoma of esophagogastric junction (AEG) keeps increasing. Siewert type II and type III AEG invades at 2-4 cm in the lower esophagus, and it has a higher rate of lower mediastinal lymph node metastasis. Lower mediastinal lymph node clearing through the abdomino-transhiatal (TH) approach is preferred, which can be accomplished by entering the lower mediastinum through the hiatus and mobilize the esophagus upward and the surrounding lymph and connective tissue for approximately 6.5 cm. Using the infracardiac bursa (IBC) as an anatomical landmark improves the safety and operability of the thorough dissection of the lower mediastinum. Total resection of the mesenterium at the esophagogastric junction can entirely dissect the lower mediastinal lymph nodes, which conforms to the safety principles in oncology.

OBJECTIVETo investigate the changes of CD4T lymphocytes in peripheral blood of patients with follicular lymphoma and its clinical significance.

METHODSBlood samples were collected for detection of whole blood cells, including absolute monocyte count (AMC), absolute lymphocyte count (ALC), hemoglobin (Hb), platelet count (Plt). Age, sex, pathological grade, number of involved lymph nodes, bone marrow involvement (BMI), Ann Arbor stage, B symptoms, serum lactate dehydrogenase (LDH) and serum β-2 microglobulin (β2-MG) were recorded, the prognostic stratification was performed by using FLIPI and FLIPI-2. The T lymphocyte subsets were analyzed by flow cytometry, including the absolute number of CD4T lymphocytes (ACD4C) and the absolute number of CD8T lymphocytes (ACD8C).

RESULTSPatients were with higher Ann Arbor stage, Hb<120 g/L, LDH greater than the upper limit of normal, the number of lymph nodes were involved> 4, the bone marrow was involvement, β2-MG levels were high FLIPI score and FLIPI-2 score, AMC level was higher (P<0.05). There were no significant differences in ACD4C levels among different groups. Patients with AMC≥0.89×10/L showed a shorter progression-free survival (PFS) and a shorter overall survival time (OS) (P=0.010,0.002) as compared with patients with AMC<0.89×10/L. The patients with ACD4C>0.16×10/L had longer progression-free survival and overall survival time, as compared with patients with ACD4C ≤0.16×10/L (P=0.016,0.012). Low ACD4C and high AMC related with shorter PFS and OS (P=0.013, 0.020). Univariate Cox regression analysis showed that age (P=0.026), bone marrow involvement (P=0.017), elevated LDH (P=0.001), β2-MG (P=0.014), FLIPI and FLIP2 score (P= 0.004 and 0.000) related with a shorter PFS. Multivariable Cox regression analysis showed that Hb (P=0.015), elevated LDH (P=0.003), β2-MG (P=0.045), bone marrow involvement (P=0.016) and FLIPI-2 score(P=0.003) related with short OS. ACD4C ≤0.16×10/L was a factor influencing prognosis of FL patients (PFS and OS) (P<0.05).

CONCLUSIONSLow ACD4C levels relatees with poor prognosis of patients with FL, and the ACD4C levels may be an important predictor for FL disease and prognosis.

Acute myeloid leukemia (AML) is a malignant clonal hematologic disease from hematopoietic stem and progenitor cells. The isocitrate dehychogenase 2 (IDH2) gene mutation has been recently found, which may be associated with the course of AML. The incidence of IDH2 gene mutation in the patients with acute myeloid leukemia is high, especially in the AML patients with normal karyotype. Different subtypes of IDH2 mutation, or companing other molecular biology, will make different influence on clinical features and progress of patients with AML. IDH2 mutation is stable, which can be used as the test sign of AML and minimal residual disease (MRD), and for guiding the clinical treatment and predicting the progress. In this article, the research progress of IDH2 mutation in acute myeloid leukemia is reviewed.
Humans ; Isocitrate Dehydrogenase ; genetics ; Leukemia, Myeloid, Acute ; genetics ; Mutation ; Neoplasm, Residual ; Prognosis

The electrophysiological activity of the gastrointestinal tract and the mechanical anti-reflux structure of the gastroesophageal junction are the basis of the anti-reflux function of the stomach. Proximal gastrectomy destroys the mechanical structure and normal electrophysiological channels of the anti-reflux. Therefore, the residual gastric function is disordered. Moreover, gastroesophageal reflux is one of the most serious complications. The emergence of various types of anti-reflux surgery through the mechanism of reconstructing mechanical anti-reflux barrier and establishing buffer zone, and the preservation of, the pacing area and vagus nerve of the stomach, the continuity of the jejunal bowel, the original gastroenteric electrophysiological activity of the gastrointestinal tract, and the physiological function of the pyloric sphincter, are all important measures for gastric conservative operations. There are many types of reconstructive approaches after proximal gastrectomy. The design based on the anti-reflux mechanism and the functional reconstruction of mechanical barrier, and the protection of gastrointestinal electrophysiological activities are important considerations for the selected of reconstructive approaches after proximal gastrectomy. In clinical practice, we should consider the principle of individualization and the safety of radical resection of tumor to select a rational reconstructive approaches after proximal gastrectomy.
Humans ; Stomach Neoplasms/surgery* ; Gastrectomy ; Gastroesophageal Reflux ; Esophagogastric Junction/surgery* ; Pylorus/pathology*

In 2008, WHO made the JAK2V617F gene mutation as one of the specific molecular diagnostic markers of BCR/ABL-negative myeloproliferative neoplasms (MPN). In 2013 two research teams demonstrated that whole genome sequencing technology (WGS) was used to detect calreticulin gene mutation in essential thrombocythaemia (ET) and primary myelofibrosis (PMF) patients with JAK2V617F⁻ and MPL⁻ mutations. In this review, the relationship of CALR gene mutation with MPN is briefly summarized.
Bone Marrow Neoplasms ; genetics ; Calreticulin ; genetics ; Humans ; Janus Kinase 2 ; genetics ; Mutation ; Myeloproliferative Disorders ; genetics ; Receptors, Thrombopoietin ; genetics

During the past few years, a novel family of CD4⁺T cell lineage was detected and named as Th17 cells because of its unique ability expressing IL-17, which also can produce IL-17A, IL-17F, IL-21, IL-22 and IL-26. Some cytokines, such as TGF-β, IL-6, L-23 may promote the differentiation of Th17 subset, whereas some cytokines, such as IL-21, IL-2, IFN-γ, may have inhibitory effects. Th17 cells serving as immune effectors play an important role in autoimmune diseases caused by chronic inflammation injury. More and more studies confirmed that Th17 cells have closely correlations with the development of aplastic anemia, and may be a new target in the diagnosis, therapy, prognosis and prophylaxis of aplastic anemia.
Anemia, Aplastic ; immunology ; Autoimmune Diseases ; Cell Differentiation ; Cytokines ; Humans ; Inflammation ; Th17 Cells ; cytology ; immunology

This study was aimed to investigate the inducing-apoptosis effect of brucine on human monocytic leukemia cell line THP-1 cells and its possible mechanism. The inhibition effect of brucine on growth of THP-1 cells was measured by CCK-8 method. Morphological changes of THP-1 cells treated with brucine was detected by acridine orange/ethidium bromide (AO/EB)double staining. Annexin-V/PI double labeling method was used to assay the apoptosis rate of THP-1 cells. The effect of brucine on THP-1 cell cycle distribution was detected by PI single staining. RT-PCR was used to detect the expression of BCL-2 and BAX. The results showed that the brucine could inhibit the THP-1 cell growth in concentration and time-dependent manners at the range of 50 to 400 µg/ml. The cells stained with AO/EB revealed that the brucine induced the nuclear chromatin condensation. After the THP-1 cells were treated with brucine of 400µg/ml for 48 hours, most nucleic were stained as orange-red, and condensed, displaying the late apoptotic cell morphology. Annexin-V/PI detection showed that brucine could induce apoptosis of THP-1 cells in a concentration-dependent manner. Compared with the control group, more cells in brucine-treated group were arrested at G0/G1 phase in a concentration-dependent manner. RT-PCR detection revealed that the expression of BCL-2 was down-regulated strikingly and BAX was up-regulated. It is concluded that brucine can efficiently inhibit cell growth and block THP-1 cells in G0/G1 phase. The mechanism of THP-1 cell apoptosis induced by brucine may be related to the inhibition of BCL-2 and activation of BAX.
Apoptosis ; drug effects ; Cell Cycle ; drug effects ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Humans ; Proto-Oncogene Proteins c-bcl-2 ; metabolism ; Strychnine ; analogs & derivatives ; pharmacology ; bcl-2-Associated X Protein ; metabolism

PRAS40 (proline-rich Akt substrate 40 kD) associates with mammalian target of rapamycin complex 1(mTORC1), serine 183 site (Ser183) of PRAS40 can be phosphorylated by mTORC1. To prepare the phosphorylated PRAS40 (Ser183) antibody, We chosen 10-amino acid including Ser183 as antigen peptide through antigenicity and hydrophobicity analysis, hinged on keyhole limpet hemocyanin (KLH), and used the KLH-peptide to immunize rabbits. After antibody serum titer detection by enzyme linked immunosorbent assay (ELISA), the antibody was purified with rProtein A sepharose fast flow and dephosphorylated antigen membrane. The antibody titrate reached 1:10 000 after purification and its special property was enhanced with absorption treatment of dephosphorylated antigen membrane. In addition, we used rabbit anti-PRAS40 antibody and the phosphorylated PRAS40 (Ser183) antibody to detect PRAS40 expression in several cell lines, including the normal cells HL7702, HEK293, tumor cells HepG2, A549 and S180. There were no quite difference among these cells; otherwise, we observed the decreased phosphorylation level of Ser183 after amino acid withdrawal treatment. Therefore, the polyclonal phosphorylated PRAS40 (Ser183) antibody was specific to PRAS40 (Ser183) site and could be used for the function study of PRAS40.
Adaptor Proteins, Signal Transducing ; Animals ; Antibodies ; analysis ; Cell Line, Tumor ; Humans ; Male ; Mechanistic Target of Rapamycin Complex 1 ; Multiprotein Complexes ; Phosphoproteins ; chemistry ; immunology ; Proteins ; genetics ; metabolism ; Proto-Oncogene Proteins c-akt ; metabolism ; Rabbits ; Serine ; metabolism ; TOR Serine-Threonine Kinases

ObjectiveTo investigate the effects of dopamine D1 receptor (D1R) tool drugs and combined acupuncture and medicine on striatal expressions of D1R and dopamine transporters (DAT) in middle cerebral artery occlusion (MCAO)-reperfusion rats.MethodForty-seven male SD rats were randomly grouped, used to make a model and given corresponding interventions. The materials were taken and fixed six hrs later. Striatal D1R and DAT expressions were detectedby an immunohistochemical method in different groups.ResultThe neurological deficit score was significantly higher in the model group than in the blank group. Electroacupuncture treatment decreased the score significantly (P<0.05). D1R expression was significantly down-regulated in the antagonist, electroacupuncture and electroacupuncture plus antagonist groups compared with the model group (P<0.05). There was no statistically significant difference in D1R expression between the model group and the antagonist or electroacupuncture plus antagonist group (P>0.05). DAT expression was significantly down-regulated in the other groups compared with the model group (P<0.05). There was no statistically significant difference in D1R expression between all groups except the model group (P>0.05).ConclusionCerebral ischemia-reperfusion can result in high D1R and DAT expressions in rat striatum on the ischemic side. Electroacupuncture, D1R antagonists and a combination of the two can significantly down-regulate D1R expression and have a protective effect on the brain. The effects of electroacupuncture and D1R antagonists can not be added to each other. D1R signaling pathway may be one of ways by which electroacupuncture produces a protective effecton the brain.

BACKGROUNDTissue-engineered bioartificial muscle-based gene therapy represents a promising approach for the treatment of heart diseases. Experimental and clinical studies suggest that systemic administration of insulin-like growth factor-1 (IGF-1) protein or overexpression of IGF-1 in the heart exerts a favorable effect on cardiovascular function. This study aimed to investigate a chronic stage after myocardial infarction (MI) and the potential therapeutic effects of delivering a human IGF-1 gene by tissue-engineered bioartificial muscles (BAMs) following coronary artery ligation in Sprague-Dawley rats.

METHODSLigation of the left coronary artery or sham operation was performed. Primary skeletal myoblasts were retrovirally transduced to synthesize and secrete recombinant human insulin-like growth factor-1 (rhIGF-1), and green fluorescent protein (GFP), and tissue-engineered into implantable BAMs. The rats that underwent ligation were randomly assigned to 2 groups: MI-IGF group (n = 6) and MI-GFP group (n = 6). The MI-IGF group received rhIGF-secreting BAM (IGF-BAMs) transplantation, and the MI-GFP group received GFP-secreting BAM (GFP-BAMs) transplantation. Another group of rats served as the sham operation group, which was also randomly assigned to 2 subgroups: S-IGF group (n = 6) and S-GFP group (n = 6). The S-IGF group underwent IGF-1-BAM transplantation, and S-GFP group underwent GFP-BAM transplantation. IGF-1-BAMs and GFP-BAMs were implanted subcutaneously into syngeneic rats after two weeks of operation was performed. Four weeks after the treatment, hemodynamics was performed. IGF-1 was measured by radioimmunoassay, and then the rats were sacrificed and ventricular samples were subjected to immunohistochemistry. Reverse transcriptase-polymerase chain reaction (RT-PCR) was used to examine the mRNA expression of bax and Bcl-2. TNF-α and caspase 3 expression in myocardium was examined by Western blotting.

RESULTSPrimary rat myoblasts were retrovirally transduced to secrete rhIGF-1 and tissue-engineered into implantable BAMs containing parallel arrays of postmitotic myofibers. In vitro, they secreted consistent levels of hIGF (0.4 - 1.2 µg×BAM(-1)×d(-1)). When implanted into syngeneic rat, IGF-BAMs secreted and delivered rhIGF. Four weeks after therapy, the hemodynamics was improved significantly in MI rats treated with IGF-BAMs compared with those treated with GFP-BAMs. The levels of serum IGF-1 were increased significantly in both MI and sham rats treated with IGF-BAM. The mRNA expression of bax was lower and Bcl-2 expression was higher in MI-IGF group than MI-GFP group (P < 0.05). Western blotting assay showed TNF-α and caspase 3 expression was lower in MI-IGF group than MI-GFP group after therapy.

CONCLUSIONSrhIGF-1 significantly improves left ventricular function and suppresses cardiomyocyte apoptosis in rats with chronic heart failure. Genetically modified tissue-engineered BAMs provide a method delivering recombinant protein for the treatment of heart failure.

Animals ; Apoptosis ; Caspase 3 ; analysis ; Desmin ; analysis ; Genetic Therapy ; Heart Failure ; pathology ; physiopathology ; therapy ; Insulin-Like Growth Factor I ; genetics ; secretion ; Myoblasts, Skeletal ; metabolism ; Myocytes, Cardiac ; pathology ; Rats ; Rats, Sprague-Dawley ; Recombinant Proteins ; secretion ; Retroviridae ; genetics ; Tissue Engineering ; Tumor Necrosis Factor-alpha ; analysis ; Ventricular Function, Left