Objective To observe the protective effect of N-NAC on radiation-induced lung injury. Methods 86 cases of thoracic neoplasm patients were chosen and randomly divided into two groups,group RT +N(n =43)and group RT(n =43).Two groups were observed by CT after radiotherapy.Acute and chronical toxicities were graded by RTOG.TGF-β1,IL-1,IL-4,TNF were observed before and after the radiotherapy.Results After 3 monthsof radiotherapy,RTOG≥2 was 23.4%(RT +N),while RTOG≥2 was 53.1%(RT).there was significant differencebetween the two groups(P <0.01).At 6,9 and 12 months,fibrosis was present in 28.4%,25.4%,22.4% receivingRT vs 58.4%,54.4%,52.4% receiving RT +N,there was significant difference between the two groups(P <0.05).TGF-β1,IL-1,IL-4,TNF were observed which showed that The RT +N were lower than RT.Conclusion N-NAC can reduce incidence rate of lung injury in radiotherapy,and can reduce the content and the release of TGF-β1,IL-1,IL-4,TNF.

Objective To study the characteristics of dynamic susceptibility-contrast(DSC)MR perfusion curves,color images and perfusion values in pre-operative brain metastasis.Methods Twenty- eight brain metastases underwent DSC MR perfusion imaging by using a first-pass T_2~* echo-planar sequence. The patients' data were transferred to on-line workstation.Time-signal intensity curves,color perfusion maps and rCBV,rMTT values in both tumor parenchyma and peri-tumor edema were analyzed,and independent t- test was used and P0.05).Conclusion Different originated brain metastases have nearly same characteristics in DSC MR perfusion imaging.

OBJECTIVETo study the relationship between imbalanced synthesis of human chorionic gonadotropin (hCG) alpha and beta subunits and the pathology of pregnancy-induced hypertension (PIH).

METHODSTotal hCG, free alphahCG and betahCG were measured in serum samples collected from 60 cases of PIH and 30 normal gravid women by radioimmunoassay. The ratio of total hCG/betahCG, betahCG/FalphahCG, (FalphahCG+betahCG)/betahCG were calculated. Immunohistochemical staining was performed in 13 placenta from each group.

RESULTSIn PIH group the levels of FalphahCG, total hCG and betahCG were significantly higher than those of normal group (FalphahCG: 528 +/-421 IU/L compared with 222 +/-129 IU/L; betahCG: 39396 +/-6412 IU/L compared with 24265 +/-5575 IU/L; total hCG: 66597 +/-9294 IU/L compared with 36078 +/-4767 IU/L, all P<0.001). The betahCG/FalphahCG ratio in PIH was lower than that of normal group (91.23 +/-53.38 Compared with 119.4 +/-80.1, P<0.05); (FalphahCG+betahCG)/betahCG ratio and total hCG/betahCG ratio in two groups were (1.022 +/-0.026 compared with 1.015 +/-0.011; 1.802 +/-0.339 compared with 1.807 +/-0.258, respectively P>0.05). The immunohistochemical intensity of betahCG and FalphahCG in syncytiotrophoblast was significantly increased in 13 PIH compared with the control.

CONCLUSIONThese data suggested that the imbalanced synthesis of hCG alpha and beta subunits may cause hypertension.

Adult ; Chorionic Gonadotropin ; biosynthesis ; Chorionic Gonadotropin, beta Subunit, Human ; biosynthesis ; Female ; Glycoprotein Hormones, alpha Subunit ; biosynthesis ; Humans ; Hypertension, Pregnancy-Induced ; etiology ; metabolism ; Pregnancy

OBJECTIVE: To evaluate the free alpha subunit of human chorionic gonadotropin (FalphahCG) as a marker for pregnancy-induced hypertension (PIH). METHODS: The study group consisted of 74 pregnant women with hypertension. PIH admitted at 21-43 weeks of gestation. The control group was 37 non-PIH women. Serum FalphahCG was measured by radioimmunoassay with monoclonal technology. Using Youden's index of the receiver operator characteristic curve(ROC), a threshold value was determined. RESULTS: FalphahCG levels in PIH women were significantly higher than in the control group women [(556+/-428)IU/L compared with (232+/-131)IU/L,P<0.001].Using 260 IU/L of FalphahCG as the threshold value yields a sensitivity of 81.1% and specificity of 75.7% with a Youden's index of 0.57 for predicting PIH. CONCLUSION: Serum FalphahCG may serve as a useful marker to predict PIH.

Objective To study the role of SIRT 1 in apoptosis of PC 12 neuronal cells induced by lipopolysaccharide (LPS). Methods PC12 cells were cultured with different concentrations of LS (50 μg/mL,500 μg/mL,750 μg/mL,1000 μg/mL and 1250 μg/mL),and some other PC12 cells were routinely cultured as controls. MTT assay was employed to identify the cell survival 24 h after the inducement,and accordingly,the suitable LPS concentration for subsequent experiments was determined based on MTT results. And then, cell apoptosis in the experimental groups under the suitable LPS concentration at different times (1/2,2,18,24,and 48 h) and control group was noted by flow cytometry and Hoechst 33258 staining; Western blotting was used to detect the SIRT1 level in PC12 cells. Results Hoechst 33258 staining indicated that a few apoptotic bodies were noted 1/2 h after inducement,expressing as karyopyknosis and karyorrhexis; apoptotic bodies began to increase 18 h after inducement,reaching their peak level 24 h after inducement; and a decreased trend was observed 48 h after inducement. Flow cytometry indicated that significantly higher apoptosis rate at each time point was noted as compared with that in the control group (P＜0.05); and Hoechst 33258 staining showed the same result. Western blotting revealed that the SIRT1 expression was (1.84±0.04) in the control group,decreasing to (1.17±0.09) 1/2 h after the inducement,and reaching the lowest level (0.62±0.03) 24 h after the inducement; and then, the expression was increased to (0.77±0.02) 48 h after the inducement;significant difference on the expression at each time point was noted as compared with that in the control group (P＜0.05). Conclusion LPS can induce PC12 cell apoptosis and SIRT1 protein expression is inhibited,indicating that SIRT1 may take part in the apoptosis and play a protective role to PC12 cells.

OBJECTIVETo study the effects of neuron specific enolase (NSE) gene silencing on the cell proliferation and apoptosis of lung cancer cells in vitro.

METHODSNSE protein expression was detected in human small cell lung cancer cell line NCI-H446 and non-small cell lung cancer cell line A549 by immunocytochemistry, and a small interference RNA (siRNA) was transfected into the cells to inhibit NSE gene expression. The changes in the cell cycle, apoptosis, Ki67 protein and caspase-3 activity in the transfected cells were observed by flow cytometry, Western blotting and colorimetric assay, respectively.

RESULTSBoth A549 and NCI-H446 cells expressed NSE protein. Transfection of siRNA for NSE gene significantly inhibited the expression of NSE gene in the cells, resulting in an inhibition rate exceeding 90%. NSE gene silencing caused significantly decreased cell percentage in S phase and the expression of Ki67 protein, and increased the cell apoptotic rate and caspase-3 activity.

CONCLUSIONNSE gene expression promotes the cell proliferation and inhibits the cell apoptosis in lung cancer cells with neuroendocrine differentiation, which might be a causative factor contributing to increased malignancy of the cells.

Adenocarcinoma ; enzymology ; genetics ; pathology ; Apoptosis ; genetics ; Caspase 3 ; metabolism ; Cell Line, Tumor ; Cell Proliferation ; Humans ; Ki-67 Antigen ; metabolism ; Lung Neoplasms ; enzymology ; genetics ; pathology ; Phosphopyruvate Hydratase ; genetics ; RNA Interference ; Small Cell Lung Carcinoma ; enzymology ; genetics ; pathology

Aged ; Anti-Inflammatory Agents ; therapeutic use ; Cyclophosphamide ; therapeutic use ; Female ; Humans ; Immunosuppressive Agents ; therapeutic use ; Methylprednisolone ; therapeutic use ; POEMS Syndrome ; complications ; diagnosis ; drug therapy ; pathology ; Plasma Cells ; pathology ; gamma-Globulins ; therapeutic use

Objective To explore the clinical and imaging features of Hallervorden-Spatz syndrome (HSS) and its deep brain stimulation (DBS) treatment.Methods A 12-year-old boy with HSS,admitted to our hospital from June 2010,was chosen in our study; the clinical and imaging features and the DBS therapy outcome were retrospectively analyzed.Results The patient (12 years old) was at an early onset,predominantly presented with dystonia,cognitive impairment,dysarthria and pyramidal signs; the symptoms were rapidly progressive.Brain MRI revealed a typical "eye-of-tiger" sign.Significant improvement of motor function after DBS of the internal globus pallidus (Gpi) and no significant improvement of cognitive dysfunction and dysarthria were noted; and the benefit of surgery was maintained during the 1 year follow-up.Conclusion The characteristic imaging manifestations and clinical features are very important for HSS diagnosis; DBS of the internal globus pallidus (Gpi) can improve the motor function; and DBS is one of the limited optional therapies for HSS.

Female ; GTP-Binding Protein gamma Subunits ; genetics ; Humans ; Male ; Mutation ; Pedigree ; Silver-Russell Syndrome ; diagnosis ; genetics

OBJECTIVETo determine the expression of TREM-1 (triggering receptor expressed on myeloid cells-1) in macrophages after coxsackievirus B3 (CVB3) infection and the cardiomyocytes viability after culturing with supernatant of macrophages in the absence and presence of TREM-1 inhibitor LP-17 to explore if TREM-1 is involved in the pathogenesis of CVB3 infection induced inflammation and cardiomyocytes injury.

METHODSTREM-1 mRNA and TREM-1 and DAP-12 protein expression in macrophages were detected by Real-time PCR at 0, 1, 4, 8 and 12 h and by Western blot at 0, 16, 24 and 48 h post CVB3 infection. TNF-α secretion of macrophages was measure by ELISA, vitality and the apoptosis degree of cardiomyocytes was assessed by CCK8 and Annexin V-FITC after the cardiomyocytes were cultured with the supernatant of macrophages in normal control group, CVB3 infection group and LP-17 pretreated CVB3 infection group.

RESULTSTREM-1 mRNA expression was significantly upregulated at 4, 8, and 12 h (peaked at 8 h) and TREM-1 protein expression was significantly upregulated at 16 and 24 h and returned to baseline level at 48 h after CVB3 infection. The protein expression of DAP-12, a direct downstream signaling molecule of TREM-1, also significantly increased at 24 and 48 h post CVB3 infection (P < 0.01). Level of macrophages secreted TNF-α post CVB3 infection was significantly reduced in LP-17 pretreated cells (P < 0.01), LP-17 pretreatment also significantly improved viability and significantly reduced apoptosis of cardiomyocytes cultured with supernatant of CVB3 infected macrophages (P < 0.01).

CONCLUSIONTREM-1 might be an important mediator post CVB3 infection and a major player on inducing excess macrophages-related inflammation and resulting in an indirect injury to cardiomyocytes.

Animals ; Coxsackievirus Infections ; metabolism ; Culture Media, Conditioned ; Macrophages ; metabolism ; Male ; Myocarditis ; metabolism ; virology ; Myocytes, Cardiac ; cytology ; virology ; Rats ; Rats, Sprague-Dawley ; Receptors, Immunologic ; metabolism