ObjectiveTo investigate the protective effect of tanshinoneⅡA on the expression of S100A1 protein after acute myocardial ischemia injury in rats.Methods Sixty Wistar rats were randomly divided into sham operation group, acute myocardial ischemia model group and tanshinoneⅡA pretreatment group by random number table. The acute myocardial ischemia model was established by thoracotomy and penetration of a thread and occlusion around the root part of the left anterior descending coronary artery, while the sham operation group was established only by thoracotomy and penetration of a thread around the root part of that artery but without occlusion; 3 days before the operation, in the tanshinoneⅡA pretreatment group, intraperitoneal injection of tanshinoneⅡA solution(at a dose of 1.5 mg/kg) was applied, while in the sham and acute myocardial ischemia groups, intraperitoneal injection of an equal volume of saline was given. Myocardial cell apoptosis was detected by the terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling(TUNEL), the levels of serum superoxide dismutase (SOD), malondialdehyde(MDA), creatine kinase(CK), lactate dehydrogenase(LDH) and S100A1 protein were examined and the level of expression of S100A1 protein in myocardial tissue was assayed by immunohistochemical staining and Western Blot.Results Compared with the sham operation group, the myocardial cell apoptosis rate, the contents of MDA, CK, LDH, S100A1 and the level of S100A1 expression in myocardial ischemia group and tanshinoneⅡA pretreated group were significantly increased, while SOD activity was decreased obviously; compared with the myocardial ischemia model group, the myocardial cell apoptosis rate, the contents of MDA, CK, LDH, S100A1 and the level of S100A1 protein expression were significantly reduced〔apoptosis rate:(32.1±4.2)% vs.(72.4±5.4)%, MDA(μmol/L): 9.1±2.2 vs. 17.3±5.2, CK(U/L): 83.3±12.2 vs. 107.5±12.4, LDH (μmol·s-1·L-1): 84.0±16.4 vs. 114.4±16.0, S100A1(μg/L): 37.6±6.0 vs. 78.4±8.6,P<0.05 orP<0.01〕, while the activity of SOD was increased markedly in tanshinoneⅡA pretreated group(kU/L:72.8±10.2 vs. 49.6±8.8,P<0.01). TUNEL staining showed that in the myocardial ischemia model group and tanshinoneⅡA pretreated group, the myocardial cells represented positive staining(brown-yellow in color), irregular in shape with nuclear pyknosis, cell detachment from the surrounding tissue and other characteristics. And in sham operation group,the staining of majority of cells was negative. The results of immunohistochemistry showed that S100A1 protein staining was relatively deep in the myocardial ischemia model group and tanshinoneⅡA pretreated group, and in the latter group, the color of S100A1 protein positive staining was not as deep as that in the former group. Western Blot showed that the S100A1 protein expression in myocardial ischemia model group was 2.8 folds of that of the sham operation group, while the S100A1 protein expression in tanshinoneⅡA pretreated group was significantly decreased compared with that of myocardial ischemia model group(bothP<0.05),which was 1.5 folds of that of the sham operation group.ConclusionTanshinoneⅡA may play a role in inhibiting the expression of S100A1 protein to protect against acute myocardial ischemia injury, suggesting that this agent have a potential effect for treatment of myocardial ischemia.

Objective To investigate the effects of Mus81 gene silencing on the chemosensitivity of human colon cancer HCT116 cells to oxaliplatin and explore the underlying mechanisms. Methods lentiviral-mediated RNAi was employed to inhibit Mus81 gene in human colon cancer HCT116 cells. MTT assay was employed to evaluate oxaliplatin chemosensitivity of HCT116. Cell apoptosis rate was detected by Annexin V-APC staining and the expression levels of p53, while Bax and Bcl-2 in HCT116 cells were detected by Real-time PCR and Western blot. Results Oxaliplatin IC50 of Mus81 depleted HCT116 cells was significantly decreased. After oxaliplatin treatment, the cell apoptosis rate of Mus81 silenced HCT116 cells was increased by 77.6% (P < 0.05), and the expression of p53 and Bax in these cells was obviously increased but the expression of Bcl-2 was significantly decreased (P < 0.01). Introducing Mus81 gene in Mus81 depleted HCT116 cells could reduce apoptosis rate. Conclusion Mus81 gene silencing can significantly improve oxliplatin chemosensitivity of HCT116 cells possibly by promoting cell apoptosis through regulating the expression of p53, Bax and Bcl-2.

Objective To explore the clinical diagnostic value of polyclonal all immunoglobulin.Methods The specimens of pa-tients were simultaneously tested and identified by quantitative immunoglobulins,Immunofixation electrophoresis of serum and u-rine,urine protein electrophoresis,and other ways.Results From 1 patients with rheumatoid arthritis were detected the serum IgG, M,A,KAP and LAM,and urine KAP and LAM,at the same time show the increment of the polyclonal polyclonal all immune glob-ulin hematic disease.Conclusion Polyclonal all immune globulin hematic disease often appear in the complications of chronic in-flammation,which should be paid attention during its in clinical doctors.

Objective: Reveal the global expression profile of serum exosomal proteins of Crouzon syndrome patients. Methods: We isolated microvesicles from serum of Crouzon children with a C342Y mutation in FGFR2 by ultracentrifugation, which were further characterized by electron microscopy and immunoblotting. The protein profiling in normal subjects and Crouzon patients was systematically compared by iTRAQ proteomic analysis. Results: The result demonstrated that microvesicles were between 30—100 nm in diameter, round shape with cup-like concavity and expressed exosomal marker tumor susceptibility gene (TSG) 101 and flotillin (Flot) 1. We identified a total number of 62 proteins, among which 22 proteins overlap with ExoCarta database and were different between the Crouzon patient and the normal subject. The Ingenuity Pathway Analysis showed that the functions of these proteins are mostly involved in Developmental Disorder, Hereditary Disorder, Skeletal and Muscular Disorders, which are all related to the clinical manifestations of Crouzon syndrome. In addition, the proteins were focused on the network of "Organismal Injury and Abnormalities, Hematological System Development and Function, Cell-To-Cell Signaling and Interaction" . The central protein FN1 was presented as the key protein in the network. Conclusions Our data demonstrated that serum exosomes harbor informative proteins and FN1 was selected as a potential candidate for its role in promoting osteoblast adhesion, proliferation and mineralization.

OBJECTIVETo investigate expression of Her-2/neu (c-erbB-2) and its significance in ovarian epithelial tumors.

METHODS106 specimens and clinical history of ovarian epithelial tumors were collected including 54 cases of malignant, 33 cases of borderline and 19 benign cases. There were 19 cases of stages I and II and 35 cases of stages III and IV in ovarian carcinoma and all borderline malignant cases were stage I according to FIGO's standard. Immunohistochemical staining for Her-2/neu was performed by LSAB method.

RESULTSThe positives rates of Her-2/neu of benign, borderline and malignant tumors were 47.4% (9/19), 84.8% (28/33,), and 85.2% (46/54), respectively. Both borderline and malignant cases were found to have higher expression of Her-2/neu than those of benign cases (P < 0.02 and P < 0.01) respectively. Overexpression of Her-2/neu showed in 14/54 (25.9%) of malignant cases, 3/33 (9.1%) of borderline, and none of benign cases. Overexpression of Her-2/neu in malignant tumors cases with metastasis was higher than those without metastasis (P < 0.001).

CONCLUSIONOverexpression of Her-2/neu is associated with biological aggressiveness of ovarian cancer.

Craniosynostosis (CS) is a congenital skeletal disease caused by premature fusion of one or more cranial sutures. According to whether accompanied by injuries in other organ systems besides craniofacial deformity, CS can be divided into syndromic craniosynostosis (SCS) and non-syndromes craniosynostosis (NSC), accounting for 85% and 15% respectively. Especially, SCS can lead to more serious clinical symptoms. The occurrence of CS is influenced by both environmental and genetic factors, including monogenic mutation, chromosome abnormality and gene polymorphism. Common related genes include FGFR1, FGFR2, FGFR3, TWIST1, MSX1, ERF, TCF12. Most of published genetic studies on CS are concentrated in the European population, showing different genetic pathogenesis between SCS and NSC. Studies on molecular genetics of CS is important in the clinical diagnosis, treatment and genetic counseling. We reviewed the research status and progress of the pathogenesis of CS through the development of CS, as well as the genetic studies of SCS and NSC.

Objective:To explore the common pathogenic gene mutation in non-syndromic craniosynostosis in Chinese population.Methods:Patients with non-syndromic craniosynostosis were recruited in Huashan Hospital Affiliated to Fudan University from March 2018 to December 2020. A clinical questionnaire was designed to collect the general information of the patients. The gene panel was designed by entering the keywords craniosynostosis and gene panel in PubMed, extracting all relevant literature from January 1995 to May 2017. The gene library was sequenced on the Illumina HiSeq X platform, and bioinformatic analysis and pathogenic analysis were performed.Results:A total of 237 literatures were reviewed in the PubMed and Ovid databases, and the total sample was 3375 patients, of which 1822 cases (54%) were detected with corresponding mutations, involving 21 pathogenic genes. Based on the mutation detection rate of not less than 0.4%, 12 genes were selected in the gene panel: FGFR2, TWIST1, FGFR3, EFNB1, FGFR1, SKI, POR, RAB23, TCF12, MSX2, SMAD3 and ERF. A total of 109 patients with non-syndromic craniosynostosis were recruited in this study, including 62 males and 47 females; the average age was 2.1 years old. All participants denied family history. The average age at childbearing of father was 28.3 years old and of mother was 26.7 years old. 14 different pathogenic/ probable pathogenic mutation loci were found in the gene sequences of 19 patients. The mutation rate was 17.4%. The 14 mutation varients were distributed in 5 genes (FGFR2, TWIST1 , TCF12, EFNB1 , and FGFR3) . The 14 mutations can be classified into 5 missense mutations, 3 nonsense mutations, 1 splice mutation, 1 frameshift mutation and 4 in-frame deletion mutations, 11 of which have not been reported. These 11 novel mutations were mainly concentrated in two genes, TWIST1 and TCF12. The mutation types included: 3 loss-of-function, 4 frameshift deletions, 3 missense mutations, and 1 frameshift insertion, of which 7 were de novo mutation.Conclusions:TWIST1 and TCF12 are common pathogenic genes in Chinese patients with non-syndromic craniosynostosis.

Objective:To explore the feasibility and safety of the prophylactic optic canal decompression in frontol-orbital fibrous dysplasia surgery by three-dimensional simulation design and computer assisted navigation.Methods:A retrospected study was conducted in Huashan Hospital affiliated to Fudan University.Patients with stable fronto-orbital fibrous dysplasia were recruited from January 2016 to June 2020. Preoperatively, three-dimensional simulation design was used to design the scope of resection. Then a subtotal resection of fibrous dysplasia lesion was performed by computer assisted navigation and reshaping of the orbit rim was achieved by preserving the fronto-orbital bandeau. Meanwhile, the intracanal and intraorbital parts of optic nerve canal decompression was performed. Follow-up of the pre-op and post-op difference of the frontal bulge point, the lateral forehead point and orbitofrontal point of the affected side, the degree of proptosis, visual acuity and fundus were analyzed by paired t test. Results:A total of 7 patients were recruited, including 2 males and 5 females, with an average age of 22.5 years. The average follow-up time was 11.4 months, and the difference in exophthalmos between the two sides improved from an average of (6.7±1.6) mm before operation to an average of(2.9±1.1) mm at 6 months after operation, which was statistically significant ( P<0.001). The difference between the pre-op and post-op of the frontal bulge point on the affected side also improved from (18.1±3.4) mm before surgery to (3.1±3.5)mm( P=0.001) immediately after surgery and (4.0±3.6) mm( P=0.001)at 6 months after surgery. The difference of lateral forehead point improved from(21.4±4.1) mm before surgery to (1.8±1.9) mm( P<0.001) immediately after surgery and (2.5±2.1) mm( P<0.001) at 6 months after surgery, and the difference of orbitofrontal point improved from(12.2±2.5) mm before surgery to (2.3±3.0) m( P=0.004) immediately after surgery and (2.7±2.9) mm( P=0.006) at 6 months after surgery. The average uncorrected visual acuity of the affected side before operation was 4.5, and it was 4.6 6 months after operation, with no statistical difference( P>0.05). Conclusions:Using 3D simulation to design the scope of resection and computer assisted navigation to decompress the optic canal in patients with stable fronto-orbital fibrous dysplasia, which can safely and effectively protect the optic nerve and accurately improve the frontal-orbital shape.

Objective:To explore the feasibility and safety of the prophylactic optic canal decompression in frontol-orbital fibrous dysplasia surgery by three-dimensional simulation design and computer assisted navigation.Methods:A retrospected study was conducted in Huashan Hospital affiliated to Fudan University.Patients with stable fronto-orbital fibrous dysplasia were recruited from January 2016 to June 2020. Preoperatively, three-dimensional simulation design was used to design the scope of resection. Then a subtotal resection of fibrous dysplasia lesion was performed by computer assisted navigation and reshaping of the orbit rim was achieved by preserving the fronto-orbital bandeau. Meanwhile, the intracanal and intraorbital parts of optic nerve canal decompression was performed. Follow-up of the pre-op and post-op difference of the frontal bulge point, the lateral forehead point and orbitofrontal point of the affected side, the degree of proptosis, visual acuity and fundus were analyzed by paired t test. Results:A total of 7 patients were recruited, including 2 males and 5 females, with an average age of 22.5 years. The average follow-up time was 11.4 months, and the difference in exophthalmos between the two sides improved from an average of (6.7±1.6) mm before operation to an average of(2.9±1.1) mm at 6 months after operation, which was statistically significant ( P<0.001). The difference between the pre-op and post-op of the frontal bulge point on the affected side also improved from (18.1±3.4) mm before surgery to (3.1±3.5)mm( P=0.001) immediately after surgery and (4.0±3.6) mm( P=0.001)at 6 months after surgery. The difference of lateral forehead point improved from(21.4±4.1) mm before surgery to (1.8±1.9) mm( P<0.001) immediately after surgery and (2.5±2.1) mm( P<0.001) at 6 months after surgery, and the difference of orbitofrontal point improved from(12.2±2.5) mm before surgery to (2.3±3.0) m( P=0.004) immediately after surgery and (2.7±2.9) mm( P=0.006) at 6 months after surgery. The average uncorrected visual acuity of the affected side before operation was 4.5, and it was 4.6 6 months after operation, with no statistical difference( P>0.05). Conclusions:Using 3D simulation to design the scope of resection and computer assisted navigation to decompress the optic canal in patients with stable fronto-orbital fibrous dysplasia, which can safely and effectively protect the optic nerve and accurately improve the frontal-orbital shape.

Objective:To explore the common pathogenic gene mutation in non-syndromic craniosynostosis in Chinese population.Methods:Patients with non-syndromic craniosynostosis were recruited in Huashan Hospital Affiliated to Fudan University from March 2018 to December 2020. A clinical questionnaire was designed to collect the general information of the patients. The gene panel was designed by entering the keywords craniosynostosis and gene panel in PubMed, extracting all relevant literature from January 1995 to May 2017. The gene library was sequenced on the Illumina HiSeq X platform, and bioinformatic analysis and pathogenic analysis were performed.Results:A total of 237 literatures were reviewed in the PubMed and Ovid databases, and the total sample was 3 375 patients, of which 1 822 cases (54%) were detected with corresponding mutations, involving 21 pathogenic genes. Based on the mutation detection rate of not less than 0.4%, 12 genes were selected in the gene panel: FGFR2, TWIST1, FGFR3, EFNB1, FGFR1, SKI, POR, RAB23, TCF12, MSX2, SMAD3 and ERF. A total of 109 patients with non-syndromic craniosynostosis were recruited in this study, including 62 males and 47 females; the average age was 2.1 years old. All participants denied family history. The average age at childbearing of father was 28.3 years old and of mother was 26.7 years old. Fourteen different pathogenic/probable pathogenic mutation loci were found in the gene sequences of 19 patients. The mutation rate was 17.4%(19/109). The 14 mutation varients were distributed in 5 genes (FGFR2, TWIST1, TCF12, EFNB1, and FGFR3). The 14 mutations can be classified into 5 missense mutations, 3 nonsense mutations, 1 splice mutation, 1 frameshift mutation and 4 in-frame deletion mutations, 11 of which have not been reported. These 11 novel mutations were mainly concentrated in two genes, TWIST1 and TCF12. The mutation types included: 3 loss-of-function, 4 frameshift deletions, 3 missense mutations, and 1 frameshift insertion, of which 7 were de novo mutation.Conclusions:TWIST1 and TCF12 are common pathogenic genes in Chinese patients with non-syndromic craniosynostosis.