Objective To investigate the clinical value of computer-assisted navigation system (CANS) in pedicle screw placement. Methods From August 2002 to June 2006, we carried out 66 cases of pedicle screw placement under the guidance of CANS; 66 cases of traditional pedicle screw placement were set as a control. Results The mean operation time of CANS group was significantly shorter [(142.3?5.3) min vs (173.4?7.1) min; t=-28.301, P=0.000] and the blood loss was significantly fewer [(798.3?10.9)ml vs (912.2?14.3) ml; t=-51.463, P=0.000] than those in the control. X-ray and CT scan respectively showed that the placement of pedicle screw in CANS group was significantly more accurate than that in the control. (?2=29.424, P=0.000; ?2=36.829, P=0.000). Conclusion Pedicle screw placement under the guidance of CANS is more accurate, safe, and micro-invasive than traditional operation.

Pdx-1, an important transcription factor highlighting in the early pancreatic development, islet functions and pancreatic disorders, needs to be more investigated in zebrafish, and siRNA is still seldom applied in zebrafish embryo-related research. Our aim was to explore the role of pdx-1 in pancreatic development of zebrafish embryos by using siRNA approach. Microinjection, reverse transcriptase-PCR (RT-PCR), in situ hybridization and immunofluorescent staining were used in this research, and the morphology of the islet in normal zebrafish embryos, and in those treated with the siRNA specific to pdx-1 (siPDX-1) or siGFP was observed and compared. The expression of pdx-1 was detected in the stages of 1-cell, 2-cell, 4-cell, 8-cell, 16-cell, 16-hour by RT-PCT. The in situ hybridization and immunofluorescent staining results showed that siPDX-1 disturbed the formation of the islet in zebrafish embryos. Pdx-1 played multiple roles in maintaining the phenotype of the islet during embryogenesis in zebrafish.
Embryo, Nonmammalian ; Homeodomain Proteins/genetics ; Homeodomain Proteins/*metabolism ; Islets of Langerhans/cytology ; Islets of Langerhans/*embryology ; Islets of Langerhans/metabolism ; RNA Interference ; RNA, Small Interfering/*genetics ; Trans-Activators/genetics ; Trans-Activators/*metabolism ; Zebrafish

One confirmed diagnosiscase of severe human infection by avian influenza H7N9 admitted to intensive care unit (ICU) of the Second Affiliated Hospital of Guizhou Medical University on January 12th, 2017 was reported. The patient was treated with the sepsis bundle, and recovered finally, including a series of comprehensive treatments, such as respiratory support, circulation support, antiviral, anti-inflammation, immunization enhancement, critical nursing, fluid management, nutritional support and treatment of complications. The critical patient was admitted on January 27th, and the treatment was successful. It has important significance to rescue the severe human infection from avian influenza H7N9 by the sepsis bundle.

Pdx-1, an important transcription factor highlighting in the early pancreatic development,islet functions and pancreatic disorders, needs to be more investigated in zebrafish, and siRNA is still seldom applied in zebrafish embryo-related research.Our aim was to explore the role of pdx-1 in pan-creatic development of zebrafish embryos by using siRNA approach. Microinjection, reverse tran-scriptase-PCR (RT-PCR), in situ hybridization and immunofluorescent staining were used in this re-search, and the morphology of the islet in normal zebrafish embryos, and in those treated with the siRNA specific to pdx-1 (siPDX-1) or siGFP was observed and compared. The expression of pdx-1 was detected in the stages of 1-cell, 2-cell, 4-cell, 8-cell, 16-cell, 16-hour by RT-PCT. The in situ hy-bridization and immunofluorescent staining results showed that siPDX-I disturbed the formation of the islet in zebrafish embryos. Pdx-1 played multiple roles in maintaining the phenotype of the islet during embryogenesis in zebrafish.

Objective To discuss whether mild hyperuricemia can lead to kidney damage and the protection of decreased uric acid,through observing that hyperuricemia did damage to glomerulus endothelial function and cell proliferation of vascular smooth muscle in rats. Methods Fifty-four male SD rats were divided into four groups,the control group,model group (Oxonate),allopurinol group and Oxonate+allopurinol group.Rats were administered on a low sodium diet and their systolic blood pressure (SBP) were measured each 10 days.ELISA was used to detect rat plasma markers of endothelial function damage [nitric oxide (NO),type-1 plasminogen activator inhibitor (PAI-1),endothelin 1 (ET-1)] and cell proliferation of vascular smooth muscle[plateletderived growth factor (PDGF),cycloxygenase 2 (COX2),monocyte chemotactic protein-1 (MCP-1)],and the markers of inflammatory reaction[interleukin-18 (IL-18),tumor necrosis factor α(TNF-α)].PDGF and nitric oxide synthase (NOS) levels of rats were detected by immunohistochemical method.Renal tissue pathology of rats was observed. Results Compared to the control group,the plasmic concentration of COX2,ET-1,IL-18,PAI-1,PDGF,TNF-o,MCP-1 increased,and NO decreased significantly in rats of model group (all P＜0.05),expression of NOS significantly reduced and PDGF increased (all P＜0.05).Under light microscope,vascular wall thickening,intimal proliferation and lumen slight stricture without uric acid crystals in renal tissue were found in model group,which were obviously improved by using allopurinol. Conclusion Mild hyperuricemia can do damage to endothelial function of glomerulus and lead to vascular cell proliferation,which can be improved through decreasing uric acid.

BACKGROUNDTo study the apoptosis-inducing effect of Tanshinone and its molecular mechanism on human lung cancer cells.

METHODSHuman lung cancer cell line (SPC-A-1) was treated in vitro with 0.5 mg/L Tanshinone IIA for five days, and the cells treated with all trans retinoic acid (RA) or DDP as controls. Changes in cell morphology, apoptotic index and apoptosis related gene expression were detected by electron microscope, FCM and DNA-end-labeling.

RESULTSMany apoptotic cells were observed by light and electron microscopes. FCM examination showed that apoptotic index in Tanshinone group was much higher than that of DDP and control groups, but no difference was found statistically compared with RA group. The expression of p53, Fas and Bax genes in Tanshinone group was up-regulated markedly, but Bcl-2 was obviously down-regulated.

CONCLUSIONSTanshinone IIA can induce apoptosis in human lung cancer cell line (SPC-A-1) . Up-regulating expression of p53, Bax, Fas and down-regulating Bcl-2 expression might be its molecular mechanisms.

BACKGROUNDTo study the growth-inhibiting effect and its molecular mechanism of Tanshinone on human lung carcinoma cell line.

METHODSHuman lung adenocarcinoma cell line (SPC-A-1) was treated in vitro with 0.5μg/ml Tanshinone IIA for five days, and the cells treated with all trans retinoic acid (RA) and DDP as control. Changes in cell morphology, proliferation dynamics, cell cycle distribution and tumor-related gene expression were detected.

RESULTSThe cell growth and rate of clone formation of SPC-A-1 cells were markedly inhibited in Tanshinone group than RA group. Flow cytometry demonstrated that S phase cells decreased and G₀/G₁ phase cells increased in Tanshinone group. Expression of p53, p21 was up-regulated obviously but CDKN₂ was down-regulated markedly by Tanshinone IIA.

CONCLUSIONSTanshinone IIA can inhibit cell growth and clone formation in human lung cancer cell line (SPC-A-1) and its possible molecular mechanism may be inhibiting DNA synthesis by up-regulating p53, p21 and down-regulating CDKN₂.

BACKGROUNDTo observe the growth-inhibiting effect of anticancer ketonon on A549 cell line and PLA-801D cell line and to explore its mechanism based on the antineoplastic effects of Tanshinon.

METHODSA549 and PLA-801D cell lines were treated with anticancer ketonon by techniques of cell culture in vitro . The growth curves and dose-effect curves were drawn up. The ability of clone formation was determined. It was observed and analysed by light microscopy and flow cytometry.

RESULTSThe growth of A549 and PLA 801D cell lines was evidently inhibited. Ability of clone formation was inhibited. The apoptosis index of cells was increased after treated with anticancer ketonon and the cell cycle was blocked at G0/G1 phase.

CONCLUSIONSAnticancer ketonon can significantly inhibit the growth of human lung cancer cells probably through inducing the apoptosis of cancer cells.

BACKGROUNDIt has been proved that Tanshinone has obvious anticancer effect, but its mechanisms of anticancer are still unknown. Anticancer Ketonon is complex antitumor drug which Tanshinone is combined with other anticancer elements. This study aims to explore the antineoplastic effects of Anticancer Ketonon on Lewis lung cancer and the mechanisms in mice.

METHODSThe mice were divided into three groups: Ketonon group, 5-fluorouracil (5-Fu) group and control group. The former two groups were treated with responsive drugs after subcutaneous inoculation of Lewis lung cancer. The last group was only treated with normal saline after inoculation. Apoptosis index and cell cycle were measured by flow cytometry.

RESULTSTwo experiments were carried out in male and female mice respectively. The tumor inhibitory rates of Anticancer Ketonon were 38.9% and 32.2% respectively, those of 5-FU were 59.6% and 53.9%. Compared with those of control groups, the tumor weights in Ketonon group and 5-Fu group were statistically decreased (P < 0.05). Metastasis rates of the lung in the three groups were not statistically different (P > 0.05). The apoptosis index of Ketonon group was significantly higher than that of control group (P < 0.05), but the cell cycle was not statistically changed compared with that of control group (P > 0.05).

CONCLUSIONSAnticancer Ketonon has antineoplastic effect on Lewis lung cancer in mice and the mechanism may be associated with inducing apoptosis of tumor cells.

Objective: To explore the relationship between mobile phone dependence (MPD) and academic burden among junior middle school students in Guizhou Province, under the "double reduction" policy by using a multi level model, so as to provide a basis for preventing the occurrence of MPD. Methods: From December 2021 to January 2022, 7 868 students from grade 1 to grade 3 in 3 cities (prefecture) of Guizhou Province were selected by multi stage stratification random sampling method, and on site investigation was conducted by self compiled questionnaire and Self rating Questionnaire for Adolescent Problematic Mobile Phone Use(SQAPMPU). Using MLwiN 2.30 to fit a multi level model of the relationship between MPD and academic burden among junior middle school students. Results: The MPD detection rate of junior middle school students in Guizhou Province was 20.9%. The multi level model revealed that MPD of junior middle school students was clustered at the level of school and class ( χ 2= 1 565.32 , P <0.01), and high perceived academic pressure had a positive predictive effect on MPD among junior middle school students ( β =1.96). Homework duration ≥90 min/d at weekends had a negative predictive effect on MPD ( β =-0.55), while participation in off campus training on learning days had a positive predictive effect ( β =1.66)( P <0.05). Conclusion The MPD occurrence level is higher among junior middle school students in Guizhou Province. Perceived academic pressure, time spent on homework during weekends, off campus training and other academic burdens have an impact on MPD among junior middle school students, which should be a cause of concern for schools, families and social departments.