Objective To explore the effect of minimally invasive and mini-incision surgery (MIS) in total hip arthroplasty (THA) on late osteonecrosis of femoral head (ONFH). Methods From March 2003, Eighteen patients (22 hips) with ONFH underwent MIS in THA. Their ages ranged from 24to 57 years, including 13 males and 5 females. The mean body mass index ranged from 17.1 to 30.1(24.6 on average). The Harris hip score was 46 points before operation. Modified posterior-lateral approach was adopted, and the MIS THA was performed by cementless prosthesis. As a comparison, 18 patients (22 hips) were performed by conventional THA at the same period. The data, including bleeding volume during operation, incision length, operative time, and postoperative function recovery, were compared. Results Follow-ups were done for 6 to 20 months (11 months on average). Dislocation occurred in one patient that underwent conventional THA 2 days after operation. No complication occurred in MIS THA group. The incision lengths ranged from 8.7 to 10.5 cm (9.3 cm on average) in MIS THA group, being statistically different (Plt;0.01). There was no significant difference in Harris scoring of the function between the two groups both before the operation and after the operation (Pgt;0.05). The operative time was almost the same, but the bleeding volume in MIS THA group was less (Plt;0.05). The function recovery was faster in MIS THA group.Conclusion The MIS THA is an alternative to the treatment of late ONFH. The advantages of MIS THA are fewer trauma, less bleeding volume, and faster recovery. The MIS THA should be performed by surgeons with rich experiences in THA and hospitals with necessary instruments.
Objective To summarize the role of matrix metalloproteinases (MMPs) in occurrence and development of gastric cancer. Methods Domestic and international publications online involving MMPs of gastric cancer in recent years were collected and reviewed. Results The occurrence and development of gastric cancer was a multi-step and multi-factorial complicated progress, whose etiology and pathogenesis were still unclarified. MMPs were a class of proteolytic enzymes, which played an important role in the proliferation, metastasis, angiogenesis of gastric cancer and apoptosis of tumor cells and their surrounding normal cells by regulating the microenvironment of the growth of tumor. Conclusion MMPs promote the evolution of gastric cancer in variable ways, the mechanisms of which should be comprehended to provide a theoretical basis for the future treatment of gastric cancer.
Stage T1 lung cancer refers to the tumor with maximum diameter≤3 cm, surrounded by the pleural membrane of the lung or viscera, and does not exceed the lobar bronchus under the bronchoscope. The prognosis is generally good, but some of them are more invasive, and more aggressive treatments are needed to achieve the best prognosis. This article reviews which T1 lung cancers are susceptible to metastasis and their risk factors. It is hoped that such patients will receive the attention of relevant scholars, and when they are encountered clinically, a more aggressive approach will be taken to extend their life expectancy．
Objective To systematically review the prognostic value of perineural invasion (PNI) for patients with early-stage cervical cancer. Methods We searched PubMed, EMbase, The Cochrane Library (Issue 10, 2016), CNKI, WanFang Data, CBM and VIP databases to collect case-control studies about prognostic value of PNI in cervical cancer from inception to October, 2016. Two reviewers independently screened literature, extracted data and assessed the risk of bias of included studies. Then meta-analysis was performed by using RevMan 5.3 software. Results Seven case-control studies from eight articles involving 1 218 patients were included. The results of meta-analysis showed that: (1) On Cox's model multivariate analysis, PNI was not identified as an independent risk factor for disease free survival (DFS) (HR=0.73, 95%CI 0.33 to 1.58,P=0.42) or overall survival (OS) (HR=0.89, 95%CI 0.41 to 1.94,P=0.77) with no significant difference; (2) On Kaplan-Meier-curves, DFS (HR=1.86, 95%CI 1.20 to 2.88,P=0.006) and OS (HR=2.43, 95%CI 1.63 to 3.62,P<0.000 1) were both significantly decreased in patients with PNI positive group. Conclusion PNI represents a decreasing disease-free survival and overall survival in patients with early-stage cervical cancer, and is one of the poor prognosis factors which be informed management decisions regarding adjuvant therapy. However, there is no evidence that PNI is an independent factor affecting the prognosis. In view of the limitation of the studies, a large sample prospective controlled trial is warranted to verify the above conclusion.
Objective To investigate the role of chemokine receptor CXCR7 in the development and progression of pancreatic carcinoma. Methods The short hairpin RNA (shRNA) targeting CXCR7 was designed and delivered into AsPC-1 pancreatic carcinoma cells to knock down CXCR7 expression. The cell proliferation, cell cycle, and apoptosis after CXCR7 knockdown was determined by MTT and flow cytometry, respectively. The invasive ability of pancreatic carcinoma cells was evaluated by using the Transwell system. Results Compared with the blank control group (BC group), transfection of AsPC-1 cells with CXCR7-shRNA resulted in a significantly decreased expression of CXCR7 at both mRNA and protein levels (P<0.05), and the ability of proliferation and invasion significantly decreased (P<0.05). Knockdown of CXCR7 also significantly increase apoptosis (P<0.05), induce cell cycle arrest at G0/G1 phase (P<0.05). Conclusions Taken together, the present study showes that the knockdown of CXCR7 expression may play an important role in pancreatic carcinoma development, invasion, and metastasis, CXCR7 may be a potential therapeutic target for the treatment of pancreatic carcinoma.
Objective To detect the tissue factor (TF) mRNA expression in hepatocellular carcinoma and to elucidate its significance. Methods TF mRNA was detected by reverse transcription-polymerase chain reaction （RT-PCR） in 27 cases of human hepatocellular carcinoma tissue specimen with their adjacent tissues and in 27 non-tumorous process tissues. Then the relationship between mRNA expression and pathological data were analyzed. Results The expression and the relative expression intensity of TF in hepatocellular carcinoma tissues were 62.96%（17/27） and 0.567±0.268 respectively, which were significantly higher than those in their adjacent tissues 〔33.33%(9/27), 0.469±0.184〕 and in 27 non-tumorous process tissue 〔29.63%(8/27), 0.353±0.121〕, Plt;0.05. The relative expression intensity of TF were associated with tumor size, intrahepatic and extrahepatic metastasis and portal vein invasion, but unrelated to gender, AFP level, differentiation, HBsAg, cirrhosis, number of tumor lesions, and lymph node metastasis (Pgt;0.05). Conclusion Expression of TF mRNA were significantly higher in hepatocellular carcinoma and in the invasive and metastatic tissue, which indicated that TF may play an important role in carcinogenesis, invasion and metastasis of hepatocellular carcinoma.
Objective To investigate the blood clotting dysfunction of invasive pulmonary aspergillosis(IPA)and the therapeutic effect of low molecular hepafin in a mouse model．Methods The neutropenic IPA mouse model was constructed by being given cyclophosphamide to depress immunologic function，and then intranasally challenged with Aspergillus fumigatus conidia．(1)Blood clotting function were assessed by bleeding time，clotting time，platelet count and antithrombase-III(AT-III)activity．Seventy-two mice were randomly assigned into 4 groups．Group A received only normal saline．group B received normal saline to substitute the cycloph0sphamide，and the rest equal to group D．Group C received normal saline to substitute the AspergiUus fumigatus conidia suspension，and the rest equal to group D．Group D(model group)received cyclophosphamide(intraperitoneally，150 mg／kg，d4，d1)and Aspergillus fumigatus conidia suspension(intranasally，40 μL／mouse，1．5×10∧5／mL，d0)．Six mice were randomly sacrificed in each group for analysis of blood clotting function per 24 h after inoculation for 3 times．(2)Therapeutic effect of low molecular heparin was determined by survival time of IPA mice．One hundred and eighteen mice were randomly assigned into 4 groups after challenged with 6×10 conidia／mouse and received one of the following regimens daily from dl to d7 after challenge，vehicle(group E，n=29)，low molecular heparin(group F，n=30，subcutaneous injection，1000 IU／kg，qd×7 d)，amphotericin B(group G，n=29，intraperitoneal，1 m kg，qd×7 d)，low molecular heparin plus amphotericin B(group H，n=30)．Mice survivals were recorded once daily to d21 after innoculation．Results (1)AT-III activity of group D decreased significantly 24 h after innoculation．Bleeding time and clotting time decreased significantly and AT—III activity decreased sequentially 48 h after innoculation．The platelet decreased significantly 72 h after innoculation，and bleeding time shoaened further．Clotting time was longer than that 0f 48 h．but still shorter than norm al and AT-III activity decreased sequentially．There were significant differences when comparing group D with group A，B and C(all Plt;0.01)．And there was no significant difference between group A，B and C(all Pgt;0．05)．(2)Survival analysis indicated that the therapeutic effect of low molecular hepafin plus amphotericin B was better than that of amphotericin B or low molecular heparin alone．No therapeutic effect was found in group F(group E vs group F，Pgt;0．05，both group E and group F compared with group H，P lt;0．01．Group H vs group G，P lt;0．05．Both group E and group F compared with group G，P lt;0．05)．Conclusions The results suggest that there is blood clotting dysfunction in IPA mice and AT—III activity may be an early index to monitor the disfunction．Compared with the therapeutic effect of amphoterinein B alone，low molecular hepafin plus amphoterincin B can prolong survival of neutropenic IPA mice
ObjectiveTo investigate the influence of heat shock protein A2 (HSPA2) on the biological behavior of pancreatic adenocarcinoma cells and its mechanism. MethodsThe expressions of HSPA2 were determined in the human pancreatic adenocarcinoma cell lines (PANC-1, BxPC-3, and AsPC-1) using the Western blot. Subsequently, the cells with the lowest and highest HSPA2 expressions among these three lines were selected for conducting overexpression and knockdown experiments targeting HSPA2, respectively. The cellular proliferation, cell clonogenesis, migration, and invasion capabilities were assessed using MTT, clonogenic assay, and Transwell assay, respectively. Additionally, the impact of HSPA2 on the expression of key markers of epithelial-mesenchymal transition (EMT) was examined using the Western blot. The potential target molecules of HSPA2 were identified through immunoprecipitation assay and mass spectrometry. The rescue experiments further explored the regulatory relation between the HSPA2 and its target molecules. The influence of HSPA2 on pancreatic adenocarcinoma growth was investigated through establishment of xenograft tumor model in nude mice. ResultsThe HSPA2 exhibited the lowest expression in the PANC-1 cells and the highest expression in the AsPC-1 cells among the three cell lines. Subsequent functional studies demonstrated that the overexpression of HSPA2 in the PANC-1 cells markedly promoted proliferation, cell clonogenesis, migration, and invasion, while the knockdown of HSPA2 expression in the AsPC-1 cells markedly inhibited these processes. The Western blot analysis further showed that the HSPA2 overexpression downregulated E-cadherin expression and upregulated N-cadherin and Vimentin expressiones, whereas the HSPA2 knockdown produced opposite effects. The rescue experiments indicated that the HSPA2 promoted the EMT in pancreatic adenocarcinoma cells by upregulating Yes associated protein (YAP). The subcutaneous xenograft tumor experiments in the nude mice showed that the HSPA2 knockdown inhibited tumor growth. ConclusionThe results of this study suggest that HSPA2 promotes EMT via upregulating YAP, which facilitates proliferation, migration, and invasion of pancreatic adenocarcinoma cells.
ObjectiveTo investigate the influence of hypoxia on pro-metastasis induced by epithelial-mesenchymal transition (EMT) of human lung adenocarcinoma. MethodsThe human lung cancer cell line H460 was cultured in hypoxic condition and the morphologic changes of the cells were observed under the microscope. The EMT-related markers including E-cadherin and vimentin were detected by Western blot. Transwell migration assay and transwell invasion assay were employed to detect the migratory and invasive activity of cancer cells. ResultsHypoxic induced morphological changes were consistent with the mesenchymal phenotype, such as an elongated fibroblastic morphology, and conversion from a tightly packed epithelial cobblestone pattern to a loosely packed scattered phenotype. Compared with the control group, hypoxic attenuated the quantity of E-cadhenrin, but increased vimentin, which resulted in promotion of migration and invasion of H460. ConclusionHypoxia induces EMT in H460 and enhances the invasive and migratory abilities of lung cancer cells.