Objective To establish the orthotopic bladder cancer model of multidrug resistance as the human' s, and detect its resistance condition. Methods Two groups of nude rats 4-6 weeks of age were inculated with 1×107 cell of T24 or T24-ADM, following with observation and putting down their meat, drink,mental condition, urine and abdominal mass growth. Animals were sacrificed after 4 weeks later, then their bladder were weighted and measured, histopathologic assessment was performed,mdr1 was detected by PCR,and cells from the bladder tumors were detected of multidrug resistence by MTT. Results Group of nude rats inculated with T24-ADM generated tumors about 80 % (8/10), the one inculated with T24 was 90 % (9/10)and about 2-3 days early. The blank group had no rats emerge tumors in bladder mucosa at all. Bladder weight and volume: (0.8±0.3) g, (1.0±0.5) g, (875±158) mm3, (903±192) mm3, difference between the two groups had no significant (t = 1.332 and t = 1.215, P＞0.05). Histopathologic detection: The two groups of bladder cancer tissue biopsies can be seen more chaotic arrangement of cell structure, cell body shape is irregular, to the depth of myometrial invasion in different without breaking the film. Between the two groups there were no significantly differences. PCR detection of mdr1 expression differences between the two groups was significant (t = 3.612, P ＜0.01). Cytological detection of drug-resistant cell volume is slightly larger, and no significant difference in morphology. MTT detection: cells from the inculated T24-ADM mice bladder tumor were more resistance to ADM than the ones from the inculated T24 mice bladder tumor (F = 412.107, P＜0.01), and for several other drugs were also resistant. Conclusion Cell transplantation was successfully used to establish bladder cancer model in situ of T24-ADM, and with multi-drug resistance characteristics. The model laid the foundation for further multi-drug resistance research of bladder cancer.

Objective To investigate the correlation between mutiple-voxel magnetic resonance spectroscopy (1H-MRS) parameter choline/creatine (Cho/Cr) and distribution of glioma stem cells (GSCs). Methods Sixteen patients with high-grade glioma approved by pathology, admitted to our hospital form August 2012 and March 2015, were enrolled in our study. They were performed 1H-MRS before surgery, and apparently different regions of Cho/Cr were identified. With the help of intraoperative neuronavigation, different Cho/Cr tissue samples were gained accurately (Cho/Cr hypermetabolism group and Cho/Cr hypometabolism group). The different distribution of glioma stem cells in glioma tissues of the two groups was detected via neurosphere culture; immunohistochemistry and Western blotting were employed to detect the CD133 and nestin expressions. Results Neurospheres were successfully cultured from different glioma tissues, and the sphere formation rate from Cho/Cr hypermetabolism group was significantly higher as compared with that from Cho/Cr hypometabolism group (13.94±3.55 vs. 8.04± 1.47, P<0.05). The immunohistochemistry results indicated that the expressions of CD133 and nestin in the Cho/Cr hypermetabolism group were significantly higher as compared with those in the Cho/Cr hypometabolism group ([22.96±2.28]% vs. [18.04±1.36]%, [25.47±2.43]% vs. [19.74±1.66]%, P<0.05). Western blotting showed that the relative protein expressions of CD133 and nestin in the Cho/Cr hypermetabolism group were significantly higher as compared with those in the Cho/Cr hypometabolism group (0.50±0.17 vs. 0.30±0.08, 0.45±0.13 vs. 0.27±0.07, P<0.05); and the protein expressions of CD133 and nestin were positively correlated with Cho/Cr (r=0.972, P=0.000; r=0.762, P=0.000). Conclusion 1H-MRS parameter Cho/Cr reveals the distribution differences of cancer stem cells in high-grade gliomas, which can assist in finding and resecting the glioma stem cells-rich region.

ObjectiveTo investigate the molecular mechanism of the anti-inflammatory effect of Erchentang in the lung tissue of the rat model of chronic obstructive pulmonary disease （COPD） via the heparin-binding factor （Midkine）/transmembrane receptor protein （Notch2）/Hey1 signaling pathway. MethodSixty SD rats were randomized into normal group， model group， modified Erchentang （5， 10， 20 g·kg^-1·d^-1） groups， and Notch1 pathway inhibitor （γ-secretase inhibitor， DAPT， 0.02 g·kg^-1） group， with 10 rats in each group. The rat model of COPD was established by cigarette smoke combined with lipopolysaccharide （LPS）. After the modeling， the rats were administrated with corresponding drugs by gavage， and those in the normal and model groups were administrated with normal saline by gavage for 21 days. The levels of Midkine， cytokine-induced neutrophil chemoattractant-1 （CINC-1）， macrophage-derived chemokine （MDC）， chemokine ligand 5 （CXCL5）， neutrophil elastase （NE）， and nuclear factor-kappa B （NF-κB） p65 in bronchoalveolar lavage fluid （BALF） were determined by enzyme-linked immunosorbent assay （ELISA）. Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR） and immunohistochemistry were respectively employed to determine the mRNA and protein levels of Midkine， Notch2， and Hey1 in the lung tissue. ResultCompared with the normal group， the modeling increased the levels of Midkine， CINC-1， MDC， CXCL5， NE， and NF-κB p65 in BALF （P<0.01） and up-regulated the mRNA and protein levels of Midkine， Notch2， and Hey1 in the lung tissue （P<0.01）. Compared with the model group， medium- and high-dose modified Erchentang and DAPT lowered the levels of Midkine， CINC-1， MDC， CXCL5， and NF-κB p65 in BALF （P<0.01） and down-regulated the mRNA levels of Midkine， Notch2， and Hey1 （P<0.01）. ConclusionModified Erchentang may inhibit the inflammation in COPD rats by down-regulating the expression of Midkine， Notch2， and Hey1 and reducing the content of Midkine， CINC-1， MDC， and CXCL5.

ObjectiveTo observe the effect of modified Erchentang on the expression of key molecules in the Jagged1/Notch1/Hes1 signaling pathway in lung tissues of rats with chronic obstructive pulmonary disease （COPD） and explore its anti-inflammatory effect and molecular mechanism on COPD through the Jagged1/Notch1/Hes1 signaling pathway. MethodSixty SD rats were randomly divided into normal group， model group， low-， medium-， and high-dose modified Erchentang groups （5， 10， 20 g·kg^-1）， and γ-secretase inhibitor DAPT group （0.02 g·kg^-1）， with 10 rats in each group. The COPD model was induced in rats by cigarette smoking combined with intratracheal instillation of lipopolysaccharide （LPS）. Rats were treated with corresponding drugs by gavage， while those in the normal group and the model group were treated with the same amount of normal saline by gavage. The serum levels of Notch1， soluble intercellular adhesion molecule-1 （sICAM-1）， activated leukocyte cell adhesion molecule （ALCAM）， and soluble vascular adhesion molecule-1 （sVCAM-1） were detected by enzyme-linked immunosorbent assay （ELISA）. The mRNA expression of Jagged1， Notch1， and Hes1 was detected by Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR）. The protein expression of Jagged1， Notch1， Notch1 intracellular domain （NICD1）， and Hes1 in lung tissues of rats was detected by immunohistochemistry （IHC）. ResultCompared with the normal group， the model group showed increased serum content of Notch1， sICAM-1， ALCAM， and sVCAM-1 （P<0.01）， increased mRNA expression of Jagged1， Notch1， and Hes1 in lung tissues （P<0.01）， and increased protein expression of Jagged1， Notch1， NICD1， and Hes1 （P<0.01）. Compared with the model group， the medium- and high-dose modified Erchentang groups and the DAPT group showed decreased serum content of Notch1， sICAM-1， ALCAM， and sVCAM-1 （P<0.05， P<0.05）， down-regulated mRNA expression of Jagged1， Notch1， and Hes1 （P<0.05， P<0.01）， and reduced protein expression of Jagged1， Notch1， NICD1， and Hes1（P<0.05， P<0.01）. ConclusionModified Erchentang may inhibit the inflammatory response in the lung of COPD rats， and its mechanism may be related to the resistance of inflammatory injury in the lung by decreasing the mRNA expression of Jagged1， Notch1， and Hes1 and inhibiting the release of Notch1， sICAM-1， ALCAM， and sVCAM-1.