Objective To investigate the effects of Gualou Guizhi Granules on excitatory toxic damage of PC12 induced by glutamate; To primarily explore the involved protective mechanism of Gualou Guizhi Granules. Methods Excitatory toxic damage of PC12 induced by glutamate was used to establish models. Cells were divided into normal group, glutamate group, and Gualou Guizhi Granules low- (200 μg/mL), medium- (400 μg/mL) and high-dose (800 μg/mL) groups. MTT and LDH assay methods were used to detect PC12 activity; Caspase-3 activity detection method and Annexine V/PI double staining method were used to detect cell apoptosis; Western blot and RT-PCR were used to detect Bcl-2, Bax protein and mRNA expression. Results Compared with glutamate group, MTT showed that all Gualou Guizhi Granules groups could improve PC12 activity, and LDH showed that cell activity in all Gualou Guizhi Granules groups decreased; Annexine V/PI double staining method showed that all Gualou Guizhi Granules groups could decrease the PC12 apoptosis; Caspase-3 activity detection method showed that all Gualou Guizhi Granules groups could decrease the activity of Caspase-3; Western blot and RT-PCR showed that all Gualou Guizhi Granules groups could reduce Bax expression and increase Bcl-2 expression. Conclusion Gualou Guizhi Granules have certain protective effects on excitatory toxic damage of PC12 induced by glutamate, which may be related to its anti-apoptotic activity.

Resorption and osteolysis of periimplant bones resulting from the wear debris of artificial joint will cause long-term loosening. A new type of rolling knee artificial joint without UHMWPE based on the mechanics of rolling friction is designed for alleviating this problem. Because of low friction force, the resistance of extension and flexion is reduced strikingly and the stress on the interface between prosthesis and bone is reduced evidently. In addition, the bio-toxicity caused by the wear debris of UHMWPE will not occur absolutely. In consequence, the rolling artificial joint can prevent the trend of long-term loosening of the prosthesis efficiently.
Animals ; Arthroplasty, Replacement, Knee ; Ceramics ; chemistry ; Computer-Aided Design ; Dogs ; Humans ; Knee Prosthesis ; Materials Testing ; Polyethylenes ; Prosthesis Design ; Vitallium ; chemistry

Four types of 3D mathematical mode of the muscle groups applied to the human mandible have been developed. One is based on electromyography (EMG) and the others are based on linear programming with different objective function. Each model contains 26 muscle forces and two joint forces, allowing simulation of static bite forces and concomitant joint reaction forces for various bite point locations and mandibular positions. In this paper, the method of image processing to measure the position and direction of muscle forces according to 3D CAD model was built with CT data. Matlab optimization toolbox is applied to solve the three modes based on linear programming. Results show that the model with an objective function requiring a minimum sum of the tensions in the muscles is reasonable and agrees very well with the normal physiology activity.
Bite Force ; Computer Simulation ; Electromyography ; Humans ; Mandible ; physiology ; Programming, Linear

Objective To analyze the clinical factors for pathologic complete response ( pCR) after preoperative neoadjuvant chemoradiotherapy ( neo?CRT) for locally advanced rectal cancer. Methods From 2005 to 2012, 297 patients with locally advanced rectal cancer and complete clinical data were enrolled as subjects. Those patients were diagnosed with biopsy and treated with neo?CRT ( radiotherapy by 3?dimonsional conformal radiotherapy or volumetric?modulated arc therapy) followed by radical surgery. The logistic regression model was used for the multivariate analyses of the correlation of pCR with age, gender, distance between tumor and the anal verge, serum level of carcinoembryonic antigen ( CEA ) before treatment, hemoglobin level before treatment, cT staging, and cN staging. Results In all patients, 78 ( 26?7%) patients had pCR after treatment. The numbers of patients with pCR were 42( 34?4%) in patients with stage T1?T3 disease and 37(21?1%) in patients with stage T4 disease. In the patients with serum CEA levels no higher than 5?33 ng/ml, 55(36?4%) had pCR after treatment, while in the patients with serum CEA levels higher than 5?33 ng/ml, only 24( 16?4%) had pCR. The univariate analysis revealed that age, gender, distance between tumor and the anal verge, anemia before treatment, or cN staging were not related to pCR. The multivariate analysis showed that stage cT1?T3 and a serum CEA level no higher than 5?33 ng/ml before treatment were influencing factors for pCR after neo?CRT for locally advanced rectal cancer ( P=0?031,P=0?000) . Conclusions The clinical staging and the serum CEA level before treatment are influencing factors for pCR after neo?CRT for locally advanced rectal cancer. The serum CEA level before treatment can be considered as a predictor of pCR after neo?CRT for locally advanced rectal cancer.

ObjectiveTo investigate the mechanism by which Shenbai Jiedu prescription （SBJDF） inhibits the proliferation of colorectal cancer （CRC） HCT116 cells. MethodAfter 48 h treatment of HCT116 cells with SBJDF （0， 0.25， 0.5， 1， 2， 4 g·L^-1）， the viability of HCT116 cells were determined by methyl thiazolyl tetrazolium （MTT） colorimetry. Following the classification of cells into blank control group and SBJDF （1， 2， 4 g·L^-1） groups， the effect of SBJDF on HCT116 cell morphology was observed under an inverted microscope. The effects of SBJDF on the proliferation of HCT116 cells and mitochondrial membrane potential （Δψm） were detected by colony formation assay and JC-1 probe， respectively. The flow cytometry was then performed for determining cell cycle distribution and apoptosis. The effects of SBJDF on cell cycle-， apoptosis-， and nuclear factor kappa-B （NF-κB） signaling pathway-related proteins were determined by Western blot. ResultSBJDF effectively inhibited the vitality of HCT116 cells and changed their morphology in a concentration-dependent manner. Compared with the blank control group， SBJDF at 1， 2， 4 g·L^-1 significantly reduced cell colony formation （P<0.05， P<0.01），and SBJDF at 2 and 4 g·L^-1 arrested the HCT116 cell cycle at G₀/G₁ phase （P<0.05， P<0.01）. Compared with the blank control group， SBJDF at 1， 2， 4 g·L^-1 remarkably down-regulated the protein expression of CyclinD₁ （P<0.05， P<0.01）. SBJDF at 2 and 4 g·L^-1 lowered the CyclinA₂ and cyclin-dependent kinase 4 （CDK4） （P<0.05， P<0.01）. SBJDF at 4 g·L^-1 reduced the cyclin-dependent kinase 1 （CDK1） （P<0.01）. Compared with the blank control group， SBJDF at 2 and 4 g·L^-1 induced HCT116 cell apoptosis， down-regulated the protein expression of anti-apoptosis-related proteins Bcl-2 and Bcl-xl as well as the NF-κB signaling pathway-related proteins IκB kinase α （IKKα），inhibitor α of NF-κB （IκBα），and phospho-NF-κB p65 （p-p65） （P<0.05， P<0.01）， and diminished the mitochondrial membrane potential of HCT116 cells. ConclusionSBJDF inhibits the proliferation of HCT116 cells， which may be related to its inhibition of the activation of NF-κB signaling pathway and the induction of cell cycle arrest and apoptosis.

ObjectiveTo study the mechanism of Shenbai Jiedu prescription inhibiting the proliferation of HCT116 colorectal cancer （CRC） cells by regulating the phosphatase and tensin homolog deleted on chromosome ten （PTEN）/phosphatidylinositol 3-kinase （PI3K）/ protein kinase B （Akt） signaling pathway. MethodShenbai Jiedu prescription was extracted by water extraction and alcohol precipitation to prepare freeze-dried powder. HCT116 cells were cultured in vitro， and treated with different concentrations of Shenbai Jiedu prescription （2， 4， 8， 16 g·L^-1）. The inhibitory effect of Shenbai Jiedu prescription on the proliferation of HCT116 cells was tested by methyl thiazolyl tetrazolium （MTT）. Real-time quantitative PCR was used to detect the mRNA expression levels of PTEN， PI3K， Akt， glycogen synthase kinase-3β （GSK-3β）， c-Myc， survivin and Cyclin D₁. Western blot was employed to measure the protein expression levels of PTEN， phosphorylated PTEN （p-PTEN）， PI3K， Akt， phosphorylated Akt （p-Akt）， GSK-3β， phosphorylated GSK-3β （p-GSK-3β）， c-Myc， survivin and Cyclin D₁， β-catenin nuclear import was explored by immunofluorescence assay. ResultCompared with the control group， Shenbai Jiedu prescription inhibited the proliferation of HCT116 cells in a dose-dependent manner （P<0.01）. Compared with the control group， the mRNA expression levels of PTEN and GSK-3β were up-regulated whereas those of PI3K， Akt， c-Myc， survivin and CyclinD₁ were down-regulated after treatment with Shenbai Jiedu prescription （P<0.01）. The protein expression levels of PTEN， p-PTEN and GSK-3β were up-regulated whereas those of PI3K， Akt， p-Akt， GSK-3β， p-GSK-3β， c-Myc， survivin and CyclinD₁ were down-regulated （P<0.05， P<0.01）. Immunofluorescence assay showed that Shenbai Jiedu prescription suppressed β-catenin nuclear import in HCT116 cells. ConclusionShenbai Jiedu prescription inhibited the proliferation of HCT116 cells via the mechanism of regulating the PTEN/PI3K/Akt signaling pathway.

ObjectiveTo explore the biological foundation of colorectal adenoma in damp-heat accumulation syndrome and the possible anti-tumor mechanism of Shenbai Jiedu prescription. MethodEight patients with colorectal adenoma in damp-heat accumulation syndrome， 11 patients with non-damp-heat accumulation syndrome， and 10 patients with colorectal cancer recruited by Jiangsu Provincial Hospital of Traditional Chinese Medicine from February 2019 to December 2020 meeting the inclusion criteria were clinically obtained， and the tissue of the three groups of patients was subjected to transcriptome sequencing to screen for the differentially expressed genes between the syndrome and the diseases. The intersection of the differentially expressed genes between the syndrome and the disease was taken for further screening of the differentially expressed genes sequentially increasing or sequentially decreasing in patients with non-damp-heat accumulation syndrome， damp-heat accumulation syndrome， and colorectal cancer， and functional enrichment analysis and signaling pathway enrichment analysis were carried out. Real-time polymerase chain reaction （Real-time PCR） was used to detect the effect of Shenbai Jiedu prescription on the expression of the above key differential genes. ResultBy comparing the damp-heat accumulation syndrome and non-damp-heat accumulation syndrome， a total of 384 differentially expressed genes were screened， of which 203 were up-regulated genes， and 181 were down-regulated genes. By comparing the colorectal adenoma of colorectal cancer and damp-heat accumulation syndrome， a total of 2 965 differentially expressed genes were screened， of which 2 460 were up-regulated genes， and 505 were down-regulated genes. The intersection of differentially expressed genes of the two groups was taken， and a total of 58 differentially expressed genes with the same changes were screened. The gene ontology functions were mainly enriched in UDP-galactose： β-N-acetylglucosamine beta-1，3-galactosyltransferase activity， N-acetyllactosaminide beta-1，3-N-acetylglucosaminyltransferase activity， and poly-N-acetyllactosamine biosynthetic process. Kyoto Encyclopedia of Genes and Genomes （KEGG） signaling pathways were mainly enriched in glycosphingolipid biosynthesis-globo and isoglobo series， glycosphingolipid biosynthesis-lacto and neolacto series， and IL-17 signaling pathway. Shenbai Jiedu prescription significantly inhibited the expression of key genes involved in the enrichment， such as FOSB and B3GALT5， in a dose-dependent manner （P<0.05）. ConclusionGlycolipid metabolism may be the biological foundation of colorectal adenoma in damp-heat accumulation syndrome， and Shenbai Jiedu prescription may inhibit colorectal adenoma carcinogenesis by down-regulating the expression of FOSB and B3GALT5.