Objective The aim is to observe the role and mechanism of estradiol ( E2 ) on the proliferation of rat hippocampal neural stem cells ( NSCs ) .Methods Twenty hippocampi from embryonic 17-day ( E17 ) SD rats were dissociated and plated into culture flasks with NSCs specific medium containing different concentrations of estradiol .The proliferation and the vitality of NSCs were detected by immunofluorescence against BrdU and MTT assay .The expression of estrogen receptors ( ERαand ERβ) was measured by immunofluorescence staining combined with Nestin double labeling . Results BrdU and MTT assay results showed that the cell number increased when the concentration of estradiol increased from 10 -10 to 10 -8 mol/L.The number of cell proliferation and the viability of cells were best at the concentration of 10 -8 mol/L compared to the other groups .However, when the estradiol concentration was increased from 10-8 to 10 -6 mol/L, the cell proliferative capacity declined gradually .Double immunofluorescence labeling showed that the two types of estrogen receptors ( ERαand ERβ) were expressed in the cultured hippocampal NSCs .Conclusion Estradiol promotes the proliferation of hippocampal NSCs in a certain concentration range , and ERαand ERβmay be involved in the estradiol-induced proliferation .

Objective To determine the expression of disabled homolog 2 interacting protein (DAB2IP) gene in the basal cell carcinoma (BCC) of the skin,and to investigate its clinical significance.Methods Clinical data were retrospectively analyzed in 105 outpatients and inpatients who received skin mass resection in Department of Dermatology,Guangdong Second Provincial General Hospital and Guangzhou Institute of Dermatology between January 2012 and November 2017.Totally,79 patients with pathologically diagnosed BCC of the skin served as patient group,and 26 patients with pathologically diagnosed skin tag but without other clinical manifestations served as control group.Immunohistochemical staining was performed to determine the expression of DAB2IP in the two groups,and correlations of the DAB2IP expression with the clinical phenotype and pathological features of BCC of the skin were analyzed.Statistical analysis was carried out with SPSS21.0 software by using chi-square test for the comparison of enumeration data.Results The protein expression of DAB2IP was observed in 11 (42.3％) of 26 patients in the control group,as well as in 74 (93.7％) of 79 patients in the patient group,and there was a significant difference in the positive rate of DAB2IP protein between the two groups (x2 =33.50,P ＜ 0.05).The expression of DAB2IP was uncorrelated with gender or age of patients with BCC of the skin,or with the tumor size (all P ＞ 0.05).The positive rate of DAB2IP protein significantly differed between the patients with superficial BCC (5/7) and those with invasive BCC (95.8％,69/72;x2 =6.47,P ＜ 0.05).Of the 79 patients with BCC of the skin,Ki-67 protein was detected in 31 (39.2％),and the cancer cells expressing Ki-67 protein also expressed DAB2IP protein.Conclusion The expression of DAB2IP increases in BCC of the skin,which may be associated with the occurrence and infiltration of BCC of the skin.

Objective To study the proliferation of CRTH2 (CD4+ CD294+ Th2)cells promoted by pneumococcal vaccine through antigen presentation of dendritic cells (DCs),so as to provide a new approach for amplification and sorting of Th2 cells.Methods CDs induced from peripheral blood mononuclear cells were cocultured with T lym-phocytes after loading pneumococcal vaccine antigen,mixed lymphocyte reaction (MLR)was detected by cell count-ing kit-8(CCK8),DCs and CRTH2 cells were analyzed by flow cytometry.Results Pneumococcal vaccine could promote the maturation of DCs,together with TNF-a,it was adjuvant for maturation of DCs.Pneumococcal vaccine antigen-loaded DCs could increase the rate of subsets of CRTH2 cells on day 5([0.93±0.10]%)compared with day 1([0.70±0.02]%),and absolute number also increased (both P <0.05).Conclusion Amplification of CRTH2 cells can be greatly promoted by pneumococcal vaccine antigen-loaded DCs,which might be one of the effective way to induce amplification of Th2 cells.

OBJECTIVETo study on visible display of Meridian on the dummy human body.

METHODSTube model-building method and computer technique were used, and data came from Voxel-Man dummy human body development platform.

RESULTSThe visual effect of re-building Meridian is very good and it can display the different layers of anatomic structures on the Meridian lines.

CONCLUSIONThe visible display of Meridian on the dummy human body is preliminary realized, which provides data carriers for establishing the platform of Meridian study.

Human Body ; Humans ; Meridians

OBJECTIVETo study the effect of human alpha-mannosidase Man2c1 transgene on tumor growth and metastasis in mice.

METHODSHepatoma cell H22 or squamous epithelial carcinoma cell S180 was subcutaneously inoculated into the right armpit of mice (wild type mice and 28#, 35#, and 54# transgenic mice). Tumor size was measured every week. Mice were sacrificed on day 9 or 10 and then the tumors were exercised and weighted. Tumors and lungs were fixed in formaldehyde and sectioned. The sections were stained with hematoxylin/eosin and examined under microscope. The red blood cells in spleen were destroyed by Tris-NH4Cl. Natural killer (NK) cell activity was detected with Yac-1 cell as target.

RESULTSH22 and S180 tumors grew faster in all the three transgenic mice (28#, 35#, and 54#) than in wild type mice. The average size and weight of tumors between the transgenic mice and wild type mice were significantly different (P<0.05). Most tumors in the transgenic mice invaded the surrounding tissues. In contrast, nearly all the tumors in wild type mice were capsulized. Three of 10 28# transgenic mice, 5 of 10 35# transgenic mice, 3 of 10 54# transgenic mice, and 1 of 10 wild type mice showed lung metastasis of H22 tumor. Two of 6 28# transgenic mice, 3 of 6 35# transgenic mice, 1 of 6 54# transgenic mice, and 0 of 6 wild type mice showed lung metastasis of S180 tumor. No difference of NK activity in spleen cells was observed between the transgenic mice and wild type mice.

CONCLUSIONShMan2c1 transgene promotes growth, invasion, and metastasis of transplanted H22 and S180 tumors in mice. hMan2cl transgene does not affect NK activity in splenocytes.

Animals ; Cell Line, Tumor ; Humans ; Killer Cells, Natural ; immunology ; Lung Neoplasms ; secondary ; Mannosidases ; genetics ; Mice ; Mice, Transgenic ; Neoplasm Invasiveness ; Neoplasm Transplantation ; Neoplasms, Experimental ; immunology ; metabolism ; pathology ; Spleen ; immunology ; Transgenes

OBJECTIVESTo study the effects of tumor suppressor in lung cancer-1 (TSLC1) on human hepatocyte carcinoma cell line HepG2.

METHODSA full length of TSLC1 cDNA was amplified from RNA of normal human liver cells by RT-PCR, and it was cloned into a pCI-neo expression vector and transfected into human hepatocellular carcinoma cell line HepG2. The HepG2 cells transfected with this plasmid (experimental group) and those treated with pCI-neo vector (control group) and without any treatment (blank group) were compared. Cell morphology was studied microscopically and cell growth was analyzed with MTT assay. FACSort flow cytometry analysis was performed to assess the cell cycle distribution and apoptosis.

RESULTSA stable cell line expressing TSLC1 protein was successfully established. Morphologically, cells of the experimental group were tightly aggregated when compared with those of the control and blank groups. The growth of TSLC1-transfected cells was significantly suppressed in vitro compared with those of the control and blank groups. The amount of G0-G1 cells was 63.66%+/-3.83% (P less than 0.01) in the experimental group, while those of the control and blank groups were 47.45%+/-0.91% and 54.47%+/-0.96% respectively. The amount of S phase cells in the experimental group, 22.90%+/-6.04%, was significantly lower (P less than 0.05) than that of the control group (36.58%+/-0.61%) and the blank group (33.61%+/-2.99%), which suggested a G0-G1 cell cycle arresting. The number of cells in early and late phase apoptosis (17.09%+/-0.20% and 16.11%+/-0.40% respectively) were significantly higher than those of the control and blank groups (P less than 0.01).

CONCLUSIONSTSLC1 strongly inhibits the growth of HepG2 cells in vitro and induces apoptosis of the cells, suggesting that TSLC1 may have a tumor suppressor function in HCC.

Apoptosis ; genetics ; Cell Adhesion Molecule-1 ; Cell Adhesion Molecules ; Cell Proliferation ; Hep G2 Cells ; Humans ; Immunoglobulins ; genetics ; Membrane Proteins ; genetics ; Transfection ; Tumor Suppressor Proteins ; genetics

OBJECTIVETo investigate the prognostic factors of small cell lung cancer (SCLC) and establish a reliable model of clinical prognostic index.

METHODSKaplan-Meier and Cox regression were used to analyze the relationship between survival time and prognostic factors in 60 cases of SCLC. The prognostic factors included clinical and laboratory parameters, serum cytokeratin fragment 19 (CYFRA21-1), carcinoembryonic antigen (CEA), neuron-specific enolase (NSE), CA125, interleukin-2 (IL-2) and soluble interleukin-2 receptors (sIL-2R).

RESULTSKaplan-Meier analysis showed that poor prognosis was in patients with KPS < 80 or extensive disease and unrelated to other clinical parameters such as age, sex and smoking index, and in patients with serum NSE > 30 micro g/L, CEA > 5.0 micro g/L, CA125 > 37 KU/L and sIL-2R > 500 KU/L. Serum IL-2 and CYFRA21-1 were also elevated, but had no significant prognostic value. Multivariate analysis indicated that serum NSE, stage and treatment of disease were independent prognostic factors. The three prognostic factors enabled establishment of a prognostic index (PI) based on a simple algorithm: PI = NSE (0 if < or = 30 micro g/L, 1 if > 30 microg/L) + stage (0 = LD, 1 = ED) + CEA (0 if < or = 5.0 microg/L, 1 if > 5.0 microg/L).

CONCLUSIONThe stage of disease, systemic treatment and the level of serum NSE are independent prognostic factors. Without considering the influence of treatment-related factors on survival, the levels of serum CEA, NSE and stage of disease before treatment are significant independent prognostic factors. PI calculated on the basis of CEA, NSE and stage is recommended to predict the survival of SCLC.

Adult ; Aged ; Biomarkers, Tumor ; blood ; Brain Neoplasms ; secondary ; Carcinoma, Small Cell ; mortality ; secondary ; therapy ; Female ; Follow-Up Studies ; Humans ; Liver Neoplasms ; secondary ; Lung Neoplasms ; mortality ; pathology ; therapy ; Male ; Middle Aged ; Multivariate Analysis ; Neoplasm Staging ; Prognosis ; Proportional Hazards Models ; Survival Rate

Cell Line ; Humans ; Liver ; metabolism ; Membrane Potential, Mitochondrial ; Mitochondria, Liver ; metabolism ; Proliferating Cell Nuclear Antigen ; biosynthesis ; Proteins ; pharmacology

This study was undertaken to observe the effect of acute stress on seizure occurrence in chronic period of epileptic model rats. Lithium-pilocarpine (LiCl-PILO)-induced epileptic rat model was constructed. At the spontaneous recurrent seizure period, acute stress stimulations such as cat's urine and foot electrical shock were applied to observe the behavioral changes and seizure occurrence. The results showed that after the cat's urine stimulation, the self-directed behaviors of the epileptic model rats decreased significantly, while the risk assessment behaviors increased significantly. The seizure occurrence, however, was not observed during the 45 min after the stimulation. Applying electrical foot shocks also did not evoke seizures in epileptic model rats. On the contrast, intra-peritoneal injection of low dose of pentylenetetrazole (PTZ, 30 mg/kg) evoked seizure more efficiently, and the duration of seizure activity was extensively prolonged in epileptic model rats than that of control rats. Taken together, these results indicate that although applying stress stimulations such as cat's urine and electrical foot shock cause several behavioral changes, they are not severe enough to evoke seizure in epileptic model rats.
Animals ; Behavior, Animal ; Disease Models, Animal ; Epilepsy ; chemically induced ; physiopathology ; Lithium Chloride ; adverse effects ; Pentylenetetrazole ; adverse effects ; Pilocarpine ; adverse effects ; Rats ; Seizures ; physiopathology ; Stress, Physiological

OBJECTIVETo determine the diagnostic value of B72.3, BerEP4 and calretinin in differentiating metastatic carcinoma cells from reactive mesothelial cells (RMC) in serous effusions by using immunocytochemical method (ICC), and to investigate the feasibility of ThinPrep (TP) preparation for ICC.

METHODSOne hundred fifty eight serous effusion specimens were examined by ICC on cell block (CB) sections (CB-ICC) using antibodies against of B72.3, BerEP4 and calretinin. Fourty-nine of the samples, ICC on ThinPrep slides (TP-ICC) and CB-ICC were performed concurrently.

RESULTSThe sensitivities of B72.3 and Ber-EP4 for detecting carcimoma cells were 76.9% and 69.2% respectively, and when combined the sensitivity was increased to 89.7%. The sensitivity and specificity of Calretinin for detecting mesothelial cells were 90.9% and 87.2% respectively. The sensitivity of B72.3 in differentiating cancer cells from reactive mesothelial cells by CB-ICC and TP-ICC was 78.9% and 68.4%. It was 78.9% and 68.4% of BerEP4 respectively. No statistical significance was observed between CB-ICC and TP-ICC in differentiating metastatic carcinoma cells from reactive mesothelial cells.

CONCLUSIONThe combination of antibodies of B72.3, Ber-EP4 and calretinin is quite helpful as an auxiliary in differentiating metastatic carcinoma cells from reactive mesothelial cells. ThinPrep preparation slides may effectively replace the cell block sections for ICC in differential diagnosis of serous effusions.

Antibodies, Monoclonal ; Antibodies, Neoplasm ; Ascitic Fluid ; metabolism ; pathology ; Calbindin 2 ; Cytodiagnosis ; Diagnosis, Differential ; Humans ; Pericardial Effusion ; diagnosis ; pathology ; Pleural Effusion, Malignant ; diagnosis ; pathology ; S100 Calcium Binding Protein G