Objective:To investigate the changes of CD4+T cells,CD8+T cells and myeloid derived suppressor cells( MDSC) in immune organs of lung cancer mice.Methods: Lung cancer mouse models were made by subcutaneously injection of Lewis lung cancer cell line( LLC).The CD4+T cell,CD8+T cell and MDSC were detected by flow cytometry.Results:Compared to that of normal control mice,the ratio and numbers of CD4+and CD8+T cell were significantly decreased in the spleen and lymph nodes of lung cancer mice.The number of CD4+T cells had no significant change while CD8+T cells decreased in the bone marrow of lung cancer mice.However,the ratio and number of MDSC were significantly increased in the bone marrow,spleen and lymph nodes of lung cancer mice compared to that of normal control mice.Conclusion: The development of lung cancer leads to decreased T cells and increased MDSC;which may induce immune tolerance to tumor cells.

Objective To explore changes of the myeloid derived suppressor cell (MDSC), regulatory T cell (Treg), traditional T cell, and their mechanisms in lung tumor mice. Methods Twenty C57BL/6 mice were randomly divided into the experimental and the normal control groups. The experimental group was injected with Lewis lung cancer cells (LLC, 100μL 1 × 106) subcutaneously to prepare the lung tumor model mice, the normal control group was given the same amount of saline (NC). Spleen cells were obtained from LLC and NC groups. Flow cytometry was used to detect the ratio and number changes of MDSC, Treg, CD4+and CD8+T cells in the lung tumor of mice. CD4+and CD8+T cell apoptosis were detected by Annexin-Ⅴstaining, and their proliferation were detected by 5-bromine deoxidization uracil nucleoside (BrdU) incorporation. Results Compared with normal control mice, the ratio and number of MDSC in spleen increased significantly in LLC group (P<0.01), in addition, the ratio of CD4+Foxp3+Treg in CD4+T cells and their number in spleen increased significantly in LLC group. However, the ratio and number of CD4+and CD8+T cells in spleen decreased significantly in LLC group (P<0.05). The proliferation of CD4+and CD8+T cells decreased significantly in LLC group compared with that of NC group (P<0.05), while the apoptosis of CD8+T cells increased significantly (P<0.05). Conclusion MDSC and Treg cells increase in lung tumor model mice, which inhibit proliferation of CD4+and CD8+T cells and promote apoptosis of CD8+T cells.

Objective To explore the effects of PSE on hemodynamics and Liver function in LCPH. Methods 30 patients with LCPH are treated by PSE. The hemodynamics changes of patients with LCPH are evaluated with color Doppler diasonograph. The changes of main clinical features which is related to LCPH , serum ALT and albumn were investigated . Results The hemodynamics indexs of LCPH are all changed significantly (P0. 05) between four and two weeks after PSE. But the main symptoms, signs of LCPH and liver function are improved after PSE . Conclutions PSE plays an important role in hemdynamics and liver function of LCPH. After PSE, Portal hypertension decreases effectively and liver function is improved.

AIM: To investingate the potential role of apoptosis in the development of acute lung injury(ALI) following limbs ischemia-reperfusion(LIR) in rats and the effects of raurine. METHODS: The model of LIB injury in rats was made. By using TUNEL, electrophoresis, reverse-transcription polymerase chain reaction(RT-PCR) and immunohistochemistry techniques, pulmonary apoptosis, Fas/FasL expressions and Ca~(2+), reactive oxygen species (ROS),the ratio of DNA double chain in tissue were detected in different groups.RESULTS: The rapid appearance of apoptosis in alveolar epithelial cells and pulmonary vascular endothelial cells were observed after LIR in rats. The ratio of DNA double chain decreased and tissue Ca~(2+) increased. The expression of Fas/FasL mRNA and protein was up-regulated in lung tissue of rats after LIR, which was related to the elevation of alveolar epithelial cells and pulmonary vascular endothelial cell apoptosis. Taurine decreased alveolar epithelial cell and pulmonary vascular endothelial cell apoptosis not by down-regulating expression of Fas/FasL system. CONCLUSIONS: These results suggest that the excessive apoptosis and Fas/FasL system expression may play a role in the pathogensis of ALI following LIB in rats, and taurine decreases alveolar epithelial cell and pulmonary vascular endothelial cell apoptosis.

Objective To assess the value of selective renal arterial embolization in treating mononephrous renal angiomyolipoma. Methods 1 6 patients with mononephrous renal angiomyolipoma were retrospectively analyzed.To observe and analyze the changes in renal function,lesions reduction and its complications.Results Symptoms have been improved significantly after treatment,no se-rious complications were observed during operation and postoperation.The creatinine level in postoperation was lower than the pre-operative level,followed-up after 1year.Conclusion Selective renal artery embolization is a safe and effective method for the treat-ment of mononephrous renal angiomyolipoma.

AIM To evaluate the possible role of endogenous nitric oxide (NO) in the development of lung injury after hind limbs ischemia reperfusion (LIR), and the effect of taurine on endogenous NO on the model of lung injury following LIR. METHODS Wistar rats were divided into three groups: control group, ischemia reperfusion group (IR) and taurine+IR (Tau+IR). The changes of PaO 2 ,PaCO 2,lung index (LI) and lung permeability index (LPI) were observed. The content of malondialdehyde (MDA), NO and endothelin (ET) in both plasma and the lung as well as the content of nitric oxide synthase (NOS) and taurine in the lung were detected. The immunohistochemical method was used to detect level in the expression of NOS protein. RESULTS Taurine improved the pulmonary respiratory following LIR significantly, lightened lung edema, decreased the content of ET in both plasma and lung tissue, increased the content of NO in both plasma and lung tissue and promoted the level in the expression of NOS protein. CONCLUSION Using taurine may lighten lung injury following LIR and this protective effect may due to increasing the content of endogeneous NO and decreasing the level of ET.

Objective:To investigate the effect of miR-150 gene deletion on the breeding and hematologic parameters of mice. Methods:The nest litter size,wean rate and weight changes of miR-150 knock out (miR-150ko) and C57BL/6J mice were com-pared. The hematology indexes were analyzed by automated blood cell counter, the serum biochemical parameters were analyzed by automatic biochemical analyzer. Results:The nest litter size and wean rate of miR-150ko mice were significantly decreased compared with that of C57BL/6J mice. The number of total white blood cells,intermediate cells,neutrophils,and the percentage of neutrophils and intermediate cells were significantly increased in miR-150ko mice compared with that of C57BL/6J mice. However,the number and per-centage of platelets and lymphocytes decreased significantly in miR-150ko mice. In addition,the levels of serum glucose and TC were in-creased significantly in miR-150ko mice compared with that of C57BL/6J mice. Conclusion: miR-150 gene deletion impairs the breeding and has complex impact on hematologic parameters of mice.

Objective To study the clinical efficiency and possible side effects of lower tidal volume combined with sustained inflation(SI) on acute respiratory distress syndrome (ARDS) for post operative carcinoma surgery patients.Methods Fifty one hypoxemia post operative carcinoma surgery patients from Jan.2007 to Dec.2009 in Cancer Hospital and Institute,Chinese Academy of Medical Sciences and Peking Union Medical College were included.Their cirrculation was stable.Mechanical ventilation could not be removed due to ARDS.Noninvasive continuous artery blood pressure ( NBP),pulse oximetric saturation ( SPO2 ),arterial blood gas ( ABG ) analysis,static compliance of respiratory system (Cst) were monitored and recorded.Patients were ventilated on volume control mode.Tidal volumes (VT) was set to 6 ml/kg.SI were conducted by continuous positive airway pressure of 35 cm H2O,sustaining for 40 seconds.Positive end-expiratory pressure (PEEP),FiO2,respiratory rate (F),Pplateau inspiratory pressures (Pplat),the peak inspiratory pressures (Ppeak),VT,Cst and ABG before SI applying and at 10 min,24 h,48 h after SI applying were measured.Results The level of PaO2 and FiO2 were significantly lowered,VT and Crs increased significantly,Ppeak,Pplat,and F were improved significantly at 10 min,24 h and 48 h after SI in all cases.No complication occurred.All patients were discharged without adverse event.Conclusions Hypoxemia of ARDS following carcinoma surgery could be improved by lower tidal volume combined with SI.

Objective To explore the effect of p21Waf1/Cip1 methylation changes on the process of cellular senescence .Methods Bisulfite sequencing was used to analyze the methylation changes of p21Waf1/Cip1 in the process of cellular senescence;p21Waf1/Cip1 ex‐pression was detected by RT‐PCR and Western‐blot ;Middle‐aged 2BS cells was treated by 5‐aza‐CdR and cellular senescence was detected by MTT and SA‐β‐Gal staining .Results Bisulfite sequencing analysis of p21Waf1/Cip1 promoter showed that CpGs were methylated by 1 .25% in the young 2BS cells ,by 27 .27% in the middle‐aged 2BS cells ,while only by 0 .64% in the senescent cells . The expression of p21Waf1/Cip1 was low in the young(28 PD) 2BS cells ,it increased first(35 PD) but decreased later in the middle‐aged(42 PD) cells .In the senescent 2BS cells ,p21Waf1/Cip1 expression was further increased .5‐aza‐CdR treatment resulted in de‐creased growth rate but increasedβ‐Gal staining of middle‐aged 2BS cells .Conclusion The process of cellular senescence is regula‐ted by the status of p21Waf1/Cip1 methylation ,and p21Waf1/Cip1 demethylation accelerates cellular senescence .

BACKGROUND: Limb ischemia reperfusion (LIR) as a stressor leads to gastric mucosal injury, and then results in the occurrence of stress ulcer.OBJECTIVE: To observe the effects of LIR on gastric mucosal injury, investigate part of the mechanism, and the role of several transient limb ischemia in the occurrence of gastric mucosal injury.DESIGN: A randomized grouping design and controlled animal experiment.SETTING: Department of Pathophysiology of North China Coal Medical College.MATERIALS: The experiment was carried out in the pathophysiological laboratory of North China Coal Medical College from January to June 2002. Fifty-four healthy adult male Wistar rats were randomly divided into three groups with 18 rats in each group. Ischemia reperfusion (I/R) group: The rats were duplicated into models according to the Rosenthal method that under superficial anesthesia with ether, the roots of both hindlimbs were ligated by wrapping with rubber strap, blood flow was blocked for 4 hours and then recovered to perfusion for 4 hours, and finally killed by bleeding from abdominal aorta. Ischemic preconditioning group: Before model establishment, blood flow of both hindlimbs was blocked for 5 minutes, and then recovered to perfusion for 5 minutes, which was repeated for four times, and the following operations were the same as those in the I/R group. Control group: The operations were the same as those in the I/R group,but both hindlimbs were ligated at relaxation without blocking the blood flow.METHODS: Sections of gastric mucosa were prepared, and then observed under light microscope and electron microscope, and the index of gastric mucosal injury was determined according to the Guth standard. The colorimetric assay was performed with 721 spectrophotometer at 650 nm, and the amount of gastric combining mucus was calculated.Meanwhile, the blood flow of gastric mucosa, contents of phospholipid and hexosamine in gastric mucus, content of nitric oxide in plasma and gastric tissue and activity of nitric oxide synthase (NOS) in gastric mucosa were determined.MAIN OUTCOME MEASURES: Index of gastric mucosal injury, amount of gastric combining mucus, blood flow of gastric mucosa, contents of phospholipid and hexosamine in gastric mucus, contents of nitric oxide in plasma and gastric tissue and NOS activity in gastric mucosa.RESULTS: All the 54 rats were involved in the analysis of results. ① In the I/R group, gastric mucosal injury was serious, edema, hyperemia, erosion and disintegration of gland of mucosal glands were observed, infiltration of inflammatory cells (formation of ulcer) was observed in basal and inferior mucosa. In the ischemic preconditioning group, the gastric mucosa was complete, and the damaged severity was milder than that in the I/R group; Under electron microscope, the organell structures of gastric parietal and chief cells were incomplete and destroyed. The cell injuries in the ischemic preconditioning group were milder than those in the I/R group (index of injury: 18.00±10.71, 34.00±15.01, P＜ 0.01). ② The blood flow and combining mucosal amount of gastric mucosa, contents of phospholipid and hexosamine in gastric mucus in the ischemic preconditioning group and I/R group were all obviously lower than those in the control group [(2.12±0.56), (10.84±2.56), (25.52±2.97) mL/(kg·h); (2.01±0.91), (2.79±0.73), (3.99±0.87) mg;(7.68±1.95), (9.74±1.04), (11.98±1.98) mg/g; (3.83±1.18), (5.42±0.47), (5.76±1.21) mg/g, P ＜ 0.05, 0.01], those the above indexes were all higher in the ischemic preconditioning group than in the I/R group. ③ The contents of nitric oxide in plasma and gastric tissue and NOS activity in gastric mucosa in the ischemic preconditioning group and I/R group were significantly lower than those in the control group [(250.0±5.6), (270.0±11.3), (210.0±7.4) μmol/L; (9.34±0.67), (11.34±1.00), (7.50±0.67) μ kat/g, P ＜ 0.01], those were also signficantly higher in the ischemic preconditioning group than in the I/R group.CONCLUSION: As a stressor, LIR can lead to gastric mucosal injury, and cause stress ulcer.Ischemic preconditioning can alleviate the gastric mucosal injury following LIR