Tumor dormancy is a phase of occurrence and progress of cancer.In recent years,with the further study of circulating tumor cells,disseminated tumor cells and cancer stem cells,it is found that they are closely related to the tumor dormancy.Moreover,tumor microenvironment is another important factor in tumor dormancy.

The paper introduces the system structure of the knowledge discovery system of digital library of medical university,including knowledge service interaction layer,knowledge discovery processing layer,data mining & transmission layer and basic data resource layer,and discusses the knowledge service mode of the digital library of medical university supported by knowledge discovery,namely,the knowledge service mode based on embedded system,document database and collaborative mode.

Acetylation regulated by histone deacetylases (HDAC) has a broad influence on plenty of physiological processes and regulation of malignant tumor.HDAC inhibitors can promote tumor cell apoptosis and have little effect on normal cells,so they have been developed a new kind of anti-tumor agent,and part of them have entered clinical trials.Vorinostat and romidepsin have been approved by FDA for treating cutaneous T cell lymphoma patients with progressive,persistent and recurrent disease.Studies of the molecular mechanisms of the HDAC inhibitors will contribute to the further clinical application.

AIM: To investigate the molecular mechanisms of apoptosis and to elucidate the apoptosis signaling pathway triggered by etoposide in Jurkat human leukemia cells. METHODS: Apoptosis was detected using annexin V - FITC and propidium iodide (PI) staining, respectively, and annexin V - FITC positive cells and hypodiploid cells were analyzed by flow cytometry. Mitochondrial membrane potential (△Ψm) was detected using 3,3' - dihexyloxycarbocyanine iodide [ DiOC6 (3)] staining and △Ψm low cells were analyzed by flow cytometry. Preparation of cytosolic extracts and isolation of mitochondria were completed by centrifugation. Western blotting analysis was used to evaluate the level of cytochrome c, caspase - 3, and poly ( ADP - ribose) polymerase (PARP) expression. RESULTS: Etoposide induced apoptosis showing phosphatidylserine externalization and DNA fragmentation in a time - dependent manner and the apoptosis could be inhibited by a broad caspase inhibitor benzyloxycarbonyl - Val - Ala - Asp - fluoromethylketone ( zVAD. fmk). Collapse of △Ψm induced by etoposide preceded DNA fragmentation and phosphatidylserine externalization. In contrast, it was not blocked by zVAD. fmk. Etoposide caused cytochrome c release from mitochondria into cytosol, subsequent activation of caspase-3 (32 kD) presented with an intermediate (20 kD) and its active product (17kD), and cleavage of full- length PARP (116 kD) into the so- called apoptotic 85 kD fragment. CONCLUSION:Etoposide - induced Jurkat cell apoptosis is initiated through mitochondria signaling pathway with cytochrome c release into cytoplasm and caspase is the ultimate executioner of cell apoptosis.

Objective:We clarify the relationship between dysfunction of gastric motility and the plasma motilin,in order to study the pathogenesis,diagnosis and therapy of the hepatocirrhosis with dyspepsia.Methods:The liquid gastric emptying (GE),electrogastrograpgy(EGG) and plasma motilin were examined in 51 patients with hepatocirrhosis.Results:The dysfunction of gastric motility is associated with the liver function,gastric rhythm and upper gastrointestinal symptom.The plasma motilin concentration increased significantly in patients with hepatocirrhosis as compared with that of controls (P<0.01).The sorbefacient prokinetic drug (prepulsid) can improve the function of gastric power,but the lever of motilin no change.Conclusion:The patients with hepatocirrhosis have the dysfunction of gastric motility,and gastric emptying delayed,and there is a relation between GE and the liver function.We evaluate that this disorder is associated with the low sensitivity about stomach to the plasma molitin in this case.We can judge the degree of the liver damage,gastric emptying delayed.gastric rhythm by testing the gastric motilin.Drug can deal it.

Objective To assess ventilation administration during fiberoptic bronchoscopy (FB) in neonates. Methods Twenty-three neonates divided into two group (A group 12 neonates, B group 11 neonates) received FB. All were given pressure support ventilation (PSV)by a Y-like facility which connected to fiberoptic bronchoscope suction hole. In A group,after the tip of fiberoptic bronchoscope arrived at the carina, PSV was administrated. In B group, PSV was administrated in the entire process during FB, SpO2 and electrocardio were monitoring. Artery blood samples for blood gas analysis were obtained at four stages of just before FB,with the tip of the bronchoscope at the supralarynx,just before withdrawing bronchoscope out off trachea and within 20-30 minutes after FB. The arterial blood oxygen tension (PaO2), arterial blood carbon dioxide tension (PaCO2) and SpO2 just before FB served as baseline. The same indexes of other three stages were compared with the baseline. Results All 23 neonates were studied completely. When the tip of fiberoptic bronchoscope advanced from nostril to the supralarynx, SpO2, PaO2 and PaCO2 in two groups were similar to the baseline. In A group, when the tip below the glottis, cyanosis occurred, and SpO2 decreased significantly ( P＜0. 01 ) in 11 cases (92%) by 25% ; When tip at the carina, after PSV, cyanosis disappeared, and SpO2 returned to the baseline level, PaO2 keep on the baseline just before withdrawing the bronchoscope out of the trachea. SpO2 ,PaO2 in all B group neonates keep on the baseline during FB. After the tip below the glottis,PaCO2 in all neonates of the two groups increased significantly ( P＜0. 01 ), but returned to baseline within 20-30 minutes after FB. Conclusion FB can cause significant hypoxemia and hypercapnia in neonates. PSV through fiberoptic bronchoscope can be considered a safe and beneficial ventilation technique for maintaining oxygenation during FB.

Objective To observe the effects of Huoxue Xifeng Decoction (HXD) on endothelin-1 (ET-1) and nitric oxide (NO) levels in the blood and brain tissue of focal cerebral infarction (FCI) rats. Methods Forty male Wistar rats were randomized into 5 groups:sham-operation, FCI model and HXD-high, HXD-middle, HXD-low dose groups, with 8 rats in each group. The model of FCI rats was established by photo-chemistry method, and intragastric administration were continue 7 days before operation. HXD-high, HXD-middle, HXD-low dose groups were given HXD 20, 10, 5 g/(kg?d) respectively, and other groups were given the same volume distilled water. Blood and brain tissue samples were gotten 24 h after operation, and radio-immunity method was used to measure ET-1 level, spectrophotometric method was used to measure NO level. Results Compared with FCI model group, HXD decreased ET-1 level in plasma and brain tissue after infarction, and decreased NO level in the brain tissue, increased NO level in serum (P

The effects of Trichostatin A (TSA) on histone deacetylase 8 (HDAC8) expression, proliferation and cell cycle arrest in T-lymphoblastic leukemia cell line Molt-4 cells in vitro were investigated. The effect of TSA on the growth of Molt-4 cells was studied by MTT assay. Flow cytometry was used to examine the cell cycle. The expression of HDAC8 was detected by using immunocytochemistry and Western blot. The results showed that proliferation of Molt-4 cells was inhibited in TSA-treated group in a time- and dose-dependent manner. The IC50 of TSA exposures for 24 h and 36 h were 254.3236 and 199.257 microg/L respectively. The cell cycle analysis revealed that Molt-4 was mostly in G0/G1 phase, and after treatment with TSA from 50 to 400 microg/L for 24 h, the percents of G0/G1 cells were decreased and cells were arrested in G2/M phase. Treatment of TSA for 24 h could significantly inhibit the expression of HDAC8 protein in Molt-4 cells (P<0.01). It was concluded that TSA could decrease the expression of HDAC8 in Molt-4 cells, which contributed to the inhibition of proliferation and induction of cell cycle arrest in Molt-4 cells.

Objective To observe the clinical effect of phloroglucinol combined with diazepam in prolonging the latency of primipara and the influence on the safety of mother and infant after medication .Methods A total of 180 cases with a naturally occurring post-partum latency≥8 h and no progress of patients in Weifang Tranditional Chinese Hospital from June 2015 to June 2016 in this study were divided into control group and observation group with 90 cases in each group.The observation group were treated with phloroglucinol combined with diazepam,the control group were treated with diazepam.Two groups appeared uterine inertia when the discretion of intravenous infusion of 0.5% oxytocin injection.Two groups were observed to 16h, still no progression of labor related to obstetric intervention.Observed of cervix big open situation,cervical opened time, cervical edema rate, cervical laceration rate, the rate of vaginal delivery, two hours postpartum hemorrhage, Apgar scores of newborns and the adverse reaction of medicine. Results The duration from drug administration to full dilation of cervix in obseve group was significantly shorter than the control group(P<0.05),the rate of cervical edema in the observation group was significantly lower than the control group(P<0.05), but no statistically difference in the cervical laceration.The the rate of vaginal delivery in observation group decreased significantly when compared with the control group ( P<0.05 ) , two hours postpartum hemorrhage and the Apgar scores of newborns had no significant differcences.Conclusion Puerpera latency prolonged application of phloroglucinol combined with diazepam can significantly speed up the cervix to open the time , and reduce cervical edema and improve vaginal delivery rate,and cervical laceration,two hours postpartum hemorrhage and neonatal complications had no effect.

The CD19-targeted chimeric antigen receptor (CAR) T-cell treatment has achieved clinical success in treating B-cell lineage hematopoietic malignancies. This accomplishment involved the precise and efficient elimination of tumor cells by tumor-associated an-tigen-redirected immune cells. As a result, the reinitiation of several CAR T-cell (CART) based clinical trials in solid tumors was promot-ed. However, developing a feasible and efficient CAR T based therapeutic modality for solid tumors is urgently needed given the differ-ential properties between liquid and solid tumors. In this review, we discuss the advances in the management of cytotherapeutic mo-dality for solid tumors. The aspects considered include toxicity management, target selection, and primer or conditioning treatment.