Can internet use change sport participation behavior among residents? Evidence from the 2017 Chinese General Social Survey.

Purpose: The popularization of the internet has promoted the implementation of China's national fitness strategy and created conditions for Chinese residents to participate in sports. The internet is an essential medium for disseminating sports knowledge, and the use of the internet can change sport participation behaviors. Therefore, the internet can be used to popularize sports knowledge and promote the participation of all people in sports and thus improve the health of the entire population. This study attempts to empirically analyse how the use of the internet changes sport participation behavior. Method: Utilizing data from the 2017 China General Social Survey, a probit model, ivprobit model, and bias-corrected non-parametric percentile bootstrap test were used to analyse the impact of internet use on sport participation behavior. Results: The empirical results show that internet use significantly increased the probability of participation in sports by Chinese residents. Heterogeneity test results showed that internet use was more effective in promoting sport participation in middle-aged groups, groups of older persons, unmarried groups, and groups with a high school education or above. The mediating effect test results showed that internet use influenced residents' participation in sports by promoting social interaction, leisure and entertainment, and learning and recharging. Conclusions: The internet has changed participation in sports; specifically, the use of the internet promotes sport participation. Additionally, internet use has a more obvious impact on improving the sport participation behavior of middle-aged, older, unmarried, and middle- and higher-educated individuals. Internet social interaction, internet entertainment and internet learning are effective channels to encourage Chinese residents to participate in sports and improve their health.

[Toxoplasma gondii Infection in HIV-infected Individuals in Henan Province].

Genomic DNA was extracted from 1 038 peripheral blood samples from HIV-infected individuals in Henan Province. One-step single-tube nested PCR was performed to amplify the 529 bp repeating sequences of Toxoplasma gondii. Of the 1 038 samples （762 from males and 276 from females）, 66 showed positive PCR results, with a positive rate of 6.4%. The PCR positive rate in males and females was 6.3% （48/762） and 6.5% （18/276） respectively. The PCR positive rate in the married HIV individuals was 4.9%（25/508）, and that in unmarried, divorced and widowed HIV individuals was 7.7% （41/530）（χ2 = 3.451, P> 0.05）. The PCR positive rate in HIV individuals with a high-school educational level or above was 6.9%（34/489）, and that in those below the high-school level was 5.8% （32/549）（χ2 = 0.545, P> 0.05）. The highest infection rate was in the age group of 20-40 years（7.6%, 31/410）. In addition, the Toxoplasma infection rate in those with and without a history of venereal diseases, and those with an unknown history was 8.0%（9/113）, 6.5%（50/773） and 4.6%（7/152） respectively （χ2 = 0.355, P> 0.05）.

Emodin inhibits angiogenesis in pancreatic cancer by regulating the transforming growth factor-ß/drosophila mothers against decapentaplegic pathway and angiogenesis-associated microRNAs.

Emodin is a traditional Chinese medicine, which has been demonstrated to inhibit the growth of pancreatic cancer cells. However, the underlying molecular mechanisms remain to be elucidated. The present study investigated whether emodin suppresses angiogenesis in pancreatic cancer. A nude mouse pancreatic cancer xenograft model was established using SW1990 human pancreatic cancer cells by surgical orthotopic implantation. Different doses of emodin were injected into the abdominal cavities of the tumor­bearing mouse models and controls three times each week for 2 weeks. The tumors were measured and weighed, the expression of cluster of differentiation 34 was detected using immunochemistry, and microvessel densities were calculated. Reverse transcription­quantitative polymerase chain reaction (RT­qPCR) and western blotting were performed to determine the mRNA and protein expression levels of transforming growth factor (TGF)­ß and drosophila mothers against decapentaplegic (Smad) homologs. The angiogenesis­associated microRNAs (miR), miR­20, miR­155 and miR­210 were assessed by RT­qPCR. A negative dose­dependent association was revealed between treatment with emodin and the volume and weight of tumors and microvessel density. Emodin was associated with lower mRNA and protein expression levels of TGF­ß1 and its downstream target, angiopoietin­like 4, and higher mRNA and protein expression levels of TGF­ß receptor (TßR)I, TßRII and Smad4. Notably, treatment with emodin was associated with lower expression levels of miR­155 and miR­210 and higher expression levels of miR­20b. The present study suggested that treatment with emodin may repress angiogenesis in pancreatic cancer by altering the activities of the TGF-ß/Smad pathway and angiogenesis-associated miR-20b, miR-155, and miR-210.

Blue rubber bleb nevus syndrome: a case report and literature review.

Blue rubber bleb nevus syndrome (BRBNS) is a rare disease characterized by multiple venous malformations and hemangiomas in the skin and visceral organs. The lesions often involve the cutaneous and gastrointestinal systems. Other organs can also be involved, such as the central nervous system, liver, and muscles. The most common symptoms are gastrointestinal bleeding and secondary iron deficiency anemia. The syndrome may also present with severe complications such as rupture, intestinal torsion, and intussusception, and can even cause death. Cutaneous malformations are usually asymptomatic and do not require treatment. The treatment of gastrointestinal lesions is determined by the extent of intestinal involvement and severity of the disease. Most patients respond to supportive therapy, such as iron supplementation and blood transfusion. For more significant hemorrhages or severe complications, surgical resection, endoscopic sclerosis, and laser photocoagulation have been proposed. Here we present a case of BRBNS in a 45-year-old woman involving 16 sites including the scalp, eyelid, orbit, lip, tongue, face, back, upper and lower limbs, buttocks, root of neck, clavicle area, superior mediastinum, glottis, esophagus, colon, and anus, with secondary severe anemia. In addition, we summarize the epidemiology, clinical manifestations, diagnosis, differential diagnosis and therapies of this disease by analyzing all previously reported cases to enhance the awareness of this syndrome.

Effect of beta-3 adrenoceptor stimulation on the levels of ApoA-I, PPARα, and PPARγ in apolipoprotein E-deficient mice.

The beta-3 adrenoceptor (ß3-AR) protects against the progression of atherosclerosis. However, the specific mechanism of this antiatherosclerotic effect is still not clear. Thus, the aim of this study was to understand the antiatherosclerotic effects of ß3-AR. Thirty-six male homozygous apolipoprotein E-deficient mice and wild-type C57BL/6J mice were randomized into 6 treatment groups: wild-type, atherosclerotic model, atorvastatin, low-dose ß3-AR agonist, high-dose ß3-AR agonist, and ß3-AR antagonist groups. The serum lipids, aortic-free cholesterol (FC), and cholesteryl ester (CE) concentrations were measured at the end of the treatments. The mRNA expression levels of liver apolipoprotein A-I (apoA-I), peroxisome proliferator-activated receptor-α (PPARα), and peroxisome proliferator-activated receptor-γ (PPARγ) were detected by quantitative real-time PCR. Protein expression levels of apoA1, PPARα, and PPARγ in the liver were determined by western blot analysis. Treatment with ß3-AR significantly increased the plasma levels of high-density lipoprotein cholesterol and apoA-I, whereas the levels of total cholesterol, triglycerides, and low-density lipoprotein cholesterol decreased. The ß3-AR agonist treatment markedly decreased both the FC and the CE concentrations in the aorta compared with the atherosclerotic model mice. The ß3-AR agonist increased the mRNA and protein expression levels of apoA-I, PPARα, and PPARγ in the liver. This study demonstrates that long-term ß3-AR activation can regulate lipid metabolic disorders and reduces the aortic FC and the CE concentrations. These effects may be related to apoA-I, PPARα, and PPARγ.

Ginsenoside Rg3 inhibition of vasculogenic mimicry in pancreatic cancer through downregulation of VE­cadherin/EphA2/MMP9/MMP2 expression.

Ginsenoside Rg3 (Rg3), a trace tetracyclic triterpenoid saponin, is extracted from ginseng and shown to have anticancer activity against several types of cancers. This study explored the effect of Rg3 on pancreatic cancer vasculogenic mimicry. Altered vasculogenic mimicry formation was assessed using immunohistochemistry and PAS staining and associated with the expression of vascular endothelial-cadherin (VE-cadherin), epithelial cell kinase (EphA2), matrix metalloproteinase (MMP)-2 and MMP-9. The effect of Rg3 on the regulation of pancreatic cancer vasculogenic mimicry was evaluated in vitro and in vivo. The data showed vasculogenic mimicry in pancreatic cancer tissues. In addition, the expression of VE-cadherin, EphA2, MMP-2 and MMP-9 proteins associated with formation of pancreatic cancer vasculogenic mimicry. Rg3 treatment reduced the levels of vasculogenic mimicry in nude mouse xenografts in vitro and in vivo, while the expression of VE-cadherin, EphA2, MMP-2 and MMP-9 mRNA and proteins was downregulated by Rg3 treatment in vitro and in tumor xenografts. In conclusion, ginsenoside Rg3 effectively inhibited the formation of pancreatic cancer vasculogenic mimicry by downregulating the expression of VE-cadherin, EphA2, MMP9 and MMP2. Further studies are required to evaluate ginsenoside Rg3 as an agent to control pancreatic cancer.

Simultaneous determination of 12 illicit drugs in whole blood and urine by solid phase extraction and UPLC-MS/MS.

A rapid and sensitive method based on solid phase extraction and ultra performance liquid chromatography-electrospray ionization tandem mass spectrometry (UPLC-ESI-MS/MS) for the simultaneous determination of amphetamine, methamphetamine, 3,4-methylenedioxyamphetamine, 3,4-methylene-dioxymethamphetamine, N-methyl-1-(3,4-methyl-enedioxyphenyl)-2-butanamine, 3,4-methylenedioxyethylamphetamine, p-methoxymethamphetamine, ephedrine, N-methylephedrine, cathinone, methcathinone, and ketamine in whole blood and urine was developed and validated. Following solid phase extraction, the analytes were separated on ACQUITY UPLC BEH Phenyl column (100mm×2.1mm, 1.7µm) under gradient elution using a mobile phase containing of acetonitrile and 0.3% formic acid in water at a flow rate of 0.4mLmin(-1) and analyzed by a triplequadrupole mass spectrometer in the multiple reaction monitoring (MRM) mode. The proposed method was linear for each analyte with correlation coefficients over 0.99. Recovery validation studies showed accuracy bias below 4.4%. Acceptable precision was also obtained with a relative standard deviation below 8.9%. The sensitivity of the assay was found to be adequate for the quantitation of the illicit drugs in whole blood and urine sample and was higher than reported methods. The present method was proved to be reliable and robust for drug screening in forensic toxicological analysis.

The distinct mechanisms of the antitumor activity of emodin in different types of cancer (Review).

Emodin, a tyrosine kinase inhibitor, is a natural anthraquinone derivative found in the roots and rhizomes of numerous plants. The inhibitory effect of emodin on mammalian cell cycle modulation in specific oncogene-overexpressing cells has formed the basis for using this compound as an anticancer drug. Previous reviews have summarized the antitumor properties of emodin. However, the specific molecular mechanisms of emodin-mediated tumor inhibition have not been completely elucidated over the last 5 years. Recently, there has been great progress in the preclinical study of the anticancer mechanisms of emodin. Our recent study revealed that emodin has therapeutic effects on pancreatic cancer through various antitumor mechanisms. Notably, the therapeutic efficacy of emodin in combination with chemotherapy was found to be higher than the comparable single chemotherapeutic regime, and the combination therapy also exhibited fewer side-effects. Despite these encouraging results, further investigation is warranted as emodin has been shown to modulate one or more key regulators of cancer growth. This review provides an overview of the distinct mechanisms of anticancer action of emodin in different body systems identified over the past 5 years. These new breakthrough findings may have important implications for targeted cancer therapy and for the future clinical use of emodin.

[Determination of aconitine, hypaconitine and mesaconitine in Shenfu injection].

To establish a method for the content determination of indexes for measuring aconitic compounds contained in Shenfu injection, in order to provide basis for the evaluation of the curative effect of monkshood in Shenfu injection. The sample were purified and enriched with HF-LPME. ACQUITY UPLC BEH C18 column (2.1 mm x 50 mm, 1.7 microm) was adopted and eluted with a gradient program, with acetonitrile-10 mmol x L(-1) NH4HCO3 (pH 10) as the mobile phases. The flow rate was 0.45 mL x min(-1). The content was determined with ESI and MRM. The results showed that aconitine, hypaconitine and mesaconitine showed a good linear relationship, with r > 0.999, within the range of 0.1-100 ng x L(-1). The recoveries were detected to be 100.1%, 97.4%, 97.5%, with RSD being 1.2%, 1.1%, 1.5%, respectively. This method was used to prove the safety of Shenfu injection, and provide scientific basis for correct evaluation of curative effect of monkshood, as well as a reliable, simple and practical means for quality control of monkshood-containing Chinese materia medica preparations.

Effects of ß3-adrenoceptor on scavenger receptor class B type 1 and its signal transduction pathway in apolipoprotein E knockout mice.

It is clear that activated ß3-adrenoceptor can improve disorders of lipid metabolism, however there are few reports concerning the anti-atherosclerotic effects of ß3-adrenoceptor in the artery of apolipoprotein E knockout (Apoe(-/-)) mice. In the present study, we aimed at investigating the effects of ß3-adrenoceptor on lipids, atherosclerosis plaques, scavenger receptor class B type 1 and its signal transduction in Apoe(-/-) mice. Ten C57BL/6J mice were used as a control, and fifty age-matched Apoe(-/-) mice were randomly divided into five groups: atherosclerotic model (saline), positive control (atorvastatin), low-dose ß3-adrenoceptor agonist, high-dose ß3-adrenoceptor agonist and ß3-adrenoceptor antagonist groups. After 26 weeks on the high-fat diet, the mice received the above treatments for 12 weeks. Thoracic aortas, serum lipids, SR-B1, P-MeK1/2, P-ErK1/2 and protein kinase Cα(PKCα) activity were detected. We found that the levels of serum total cholesterol, triglyceride, very low-density lipoprotein/low-density lipoprotein cholesterol and the area of atherosclerotic plaques were significantly decreased in ß3-adrenoceptor agonist-treated mice (P<0.01), while the levels of high-density lipoprotein cholesterol, thoracic aortic lumen area, activity of liver PKCα, the protein expression of SR-B1, P-MeK1/2 and P-ErK1/2 were significantly increased (P<0.01), compared with the atherosclerotic model mice. Effects of the high-dose agonist were superior to those of the low-dose (P<0.01). These findings suggest that activation of ß3-adrenoceptor reduce the plaque area in the thoracic aorta and play an important anti-atherosclerotic role by regulating lipid metabolism disorders and the SR-B1 signal transduction pathway.

ß3-Adrenoceptor activation attenuates atherosclerotic plaque formation in ApoE(-/-) mice through lowering blood lipids and glucose.

AIM: To examine the effects of ß3-adrenoceptor (ß3-AR) activation on atherosclerotic plaque development in ApoE(-/-) mice. METHODS: Thirty six week-old male ApoE(-/-) mice on a high-fat diet were treated with atorvastatin (10 mg·kg(-1)·d(-1), po), BRL37344 (ß3-AR agonist, 1.65 or 3.30 µg/kg, ip, twice a week) or SR52390A (ß3-AR antagonist, 50 µg/kg, ip, twice a week) for 12 weeks. Wild-type C57BL/6J mice receiving a normal diet were taken as healthy controls. At the end of the treatments, serum levels of triglycerides (TG), total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), non-high density lipoprotein cholesterol (nHDL-C), glucose and insulin were measured. The thoracic aortas were dissected out, the area of atherosclerotic plaques and extent of fibrosis in the plaques were examined using HE and Masson's trichome staining, respectively. RESULTS: Compared to wild-type mice, ApoE(-/-) mice fed on a high-fat diet exhibited prominent hyperlipidemia and insulin resistance, associated with large area of atherosclerotic plaques and great extent of fibrosis in aortas. Atorvastatin significantly decreased the serum levels of TC and nHDL-C, and reduced the plaque area and collagen content in aortas. BRL37344 significantly decreased the serum levels of TG, TC, nHDL-C, glucose and insulin, and increased HDL-C and the insulin sensitivity, and dose-dependently reduced the plaque area and collagen content in aortas. SR52390A treatment did not affect any parameters studied. CONCLUSION: The ß3-AR agonist impedes the progression of atherosclerosis in ApoE(-/-) mice, through improvement of the lipid and glucose profiles.

Involvement of the phosphoinositide 3-kinase/Akt pathway in apoptosis induced by capsaicin in the human pancreatic cancer cell line PANC-1.

Capsaicin, one of the major pungent ingredients found in red peppers, has been recently demonstrated to induce apoptosis in various malignant cell lines through an unclear mechanism. In this study, the effect of capsaicin on proliferation and apoptosis in the human pancreatic cancer cell line PANC-1 and its possible mechanism(s) of action were investigated. The results of a Cell Counting Kit-8 (CCK-8) assay revealed that capsaicin significantly decreased the viability of PANC-1 cells in a dose-dependent manner. Capsaicin induced G0/G1 phase cell cycle arrest and apoptosis in PANC-1 cells as demonstrated by a flow cytometric assessment. Caspase-3 expression at both the protein and mRNA level was promoted following capsaicin treatment. Furthermore, we revealed that phospho-PI3 Kinase p85 (Tyr458) and phospho-Akt (Ser473) in PANC-1 cells were downregulated in response to capsaicin. Moreover, capsaicin gavage significantly inhibited the growth of pancreatic cancer PANC-1 cell xenografts in athymic nude mice. An increased number of TUNEL-positive cells and cleaved caspase-3 were observed in capsaicin-treated mice. In vivo, capsaicin downregulated the expression of phospho-PI3 Kinase p85 (Tyr458) and phospho-Akt (Ser473). In conclusion, we have demonstrated that capsaicin is an inhibitor of growth of PANC-1 cells, and downregulation of the phosphoinositide 3-kinase/Akt pathway may be involved in capsaicin-induced apoptosis in vitro and in vivo.

Emodin induces Panc-1 cell apoptosis via declining the mitochondrial membrane potential.

In this study, we investigated the apoptotic effect of emodin on human pancreatic cancer cell line Panc-1 in vitro and in vivo as well as the possible mechanisms involved. In vitro, human pancreatic cancer cell line Panc-1 was exposed to varying concentrations of emodin (0, 10, 20, 40 or 80 µmol/l). Then the mitochondrial membrane potential (MMP) was analyzed by JC-1 staining, cell apoptosis was analyzed by flow cytometry (FCM) and cell proliferation was analyzed by MTT. In vivo, nude mice orthotopically implanted were randomly divided into five groups to receive treatments by different doses of emodin: control group (normal saline 0.2 ml), E10 group (emodin 10 mg/kg), E20 group (emodin 20 mg/kg), E40 group (emodin 40 mg/kg) and E80 group (emodin 80 mg/kg). Each mouse was treated 5 times by intraperitoneal injection of emodin every 3 days. During the treatment, the feeding stuff was recorded. One week after the last treatment, we recorded the body weight and the maximum diameter of tumor in each group before the mice were sacrificed. Then the cell apoptosis of the tumor was tested by TUNEL assay. The results in vitro showed that the MMP of the cells declined and the apoptosis rate increased with the emodin concentration increasing and the cell proliferation of each group was inhibited in a dose- and time-dependent manner by emodin. The feeding stuff curve did not decline significantly in E40 group and the apoptosis rate of the tumor cells in this group was higher than the lower-dose groups. Taken together, our results demonstrate that emodin may induce the pancreatic cancer cell apoptosis via declining the MMP and a moderate dose of emodin improved the living state of the model mice.

Antitumor activity of emodin against pancreatic cancer depends on its dual role: promotion of apoptosis and suppression of angiogenesis.

BACKGROUND: Emodin has been showed to induce apoptosis of pancreatic cancer cells and inhibit tumor growth in our previous studies. This study was designed to investigate whether emodin could inhibit the angiogenesis of pancreatic cancer tissues and its mechanism. METHODOLOGY/PRINCIPAL FINDING: In accordance with our previous study, emodin inhibited pancreatic cancer cell growth, induced apoptosis, and enhanced the anti-tumor effect of gemcitabine on pancreatic caner cells in vitro and in vivo by inhibiting the activity of NF-κB. Here, for the first time, we demonstrated that emodin inhibited tumor angiogenesis in vitro and in implanted pancreatic cancer tissues, decreased the expression of angiogenesis-associated factors (NF-κB and its regulated factors VEGF, MMP-2, MMP-9, and eNOS), and reduced eNOS phosphorylation, as evidenced by both immunohistochemistry and western blot analysis of implanted tumors. In addition, we found that emodin had no effect on VEGFR expression in vivo. CONCLUSIONS/SIGNIFICANCE: Our results suggested that emodin has potential anti-tumor effect on pancreatic cancer via its dual role in the promotion of apoptosis and suppression of angiogenesis, probably through regulating the expression of NF-κB and NF-κB-regulated angiogenesis-associated factors.

[Posterior interbody fusion versus improved transforaminal lumbar interbody fusion in segmental spinal fixation for aged spondylolisthesis with lumbar spinal canal stenosis].

OBJECTIVE: To assess the clinical and radiographic outcomes of posterior lumbar fixation and posterior interbody fusion or improved transforaminal lumbar interbody fusion for Meyerding grade II/III spondylolisthesis so as to address the suitability of a dynamic stabilization. METHODS: A total of 28 consecutive patients underwent posterior lumbar fixation and posterior interbody fusion or improved transforaminal lumbar interbody fusion for Meyerding grade II/III spondylolisthesis. Among them, 13 patients underwent posterior interface fusion (PLIF) and pedicle screw fixation. And improved transforaminal lumbar interbody fusion (ITLIF) and placement of the same system were performed in 15 patients. Their clinical, economic, functional, and radiographic data were recorded both pre- and postoperatively. RESULTS: The average changes of economic and functional scores on the Prolo scale were 1.36 and 1.48 respectively. In patients with posterior interbody fusion; the average preoperative vertebral slippage was 46.9% (range: 25 - 75%) versus 14.6% (range: 15 - 25%) postoperatively. In patients with ITLIF, the average changes in economic and functional scores were 1.75 and 1.63 respectively. And the average preoperative vertebral slippage was 45.2% (range: 28 - 78%) compared with 26.3% (range: 14 - 28%) postoperatively. When two fusion techniques were compared, an overall superior reliability and resistance of systems was associated with the ITLIF procedure. But their clinical outcomes did not differ greatly (P > 0.05). CONCLUSIONS: The application of a segmental pedicle screw fixation is both feasible and efficacious.

Oridonin enhances antitumor activity of gemcitabine in pancreatic cancer through MAPK-p38 signaling pathway.

Gemcitabine is currently the best treatment available for pancreatic cancer (PaCa); however, patients with the disease develop resistance to the drug over time. Agents that can either enhance the effects of gemcitabine or overcome chemoresistance to the drug are required for the treatment of PaCa. Oridonin is one such agent which is safe and multitargeted, and has been linked with the suppression of survival, proliferation, invasion and angiogenesis of cancer. In this study, we investigated whether oridonin could sensitize PaCa to gemcitabine in vitro and in vivo. In vitro, oridonin inhibited the proliferation of the PaCa cell line, BxPC-3, potentiated the apoptosis induced by gemcitabine, induced G1 cell cycle arrest and activated p38 and p53; these results were significant when oridonin was combined with gemcitabine. In vivo, we found that oridonin significantly suppressed tumor growth and this effect was further enhanced by gemcitabine (P<0.05). Tumors from nude mice injected with BxPC-3 PaCa cells and treated with a combination of oridonin and gemcitabine showed a significant upregulation in p38 and p53 activation (P<0.05 vs. control, P<0.05 vs. gemcitabine or oridonin alone). Taken together, our results demonstrate that oridonin can potentiate the effects of gemcitabine in PaCa through the mitogen-activated protein kinase (MAPK)-p38 signaling pathway, which is dependent on p53 activation.

Emodin potentiates the antitumor effects of gemcitabine in PANC-1 pancreatic cancer xenograft model in vivo via inhibition of inhibitors of apoptosis.

Pancreatic cancer is a highly aggressive malignant disease. Gemcitabine is currently the standard first-line chemotherapeutic agent for pancreatic cancer. As members of apoptosis inhibitors, Survivin and XIAP play an important role in chemotherapy resistance in pancreatic cancer. Emodin has therapeutic potential against cancers. This study was designed to investigate whether combination therapy with gemcitabine and emodin enhanced antitumor efficacy in pancreatic cancer. The application of the combination therapy triggered significantly higher frequency of pancreatic cancer cell apoptosis. Our research demonstrated that the combination of emodin and gemcitabine resulted in significantly reduced tumor volumes compared to gemcitabine or emodin treatment alone. Immunohistochemistry and western immunoblot analyses showed that Survivin and XIAP expression were downregulated in emodin and the combination groups compared to the other two groups. Reverse transcriptase polymerase chain reaction analyses showed that Survivin and XIAP mRNA expression in emodin and the combination groups were downregulated significantly compared to the other two groups. Furthermore, the expression of the nuclear transcription factor κB (NF-κB) protein and NF-κB mRNA were downregulated in the emodin and the combination groups. DNA-binding activity of NF-κB was inhibited in emodin and combination groups compared to the other groups. This study suggests that emodin potentiates the antitumor effects of gemcitabine in PANC-1 cell xenografts via promotion of apoptosis and IAP suppression.

Enhanced antitumor efficacy of gemcitabine by evodiamine on pancreatic cancer via regulating PI3K/Akt pathway.

Evodiamine has therapeutic potential against cancers. This study was designed to investigate whether combination therapy with gemcitabine and evodiamine enhanced antitumor efficacy in pancreatic cancer. In vitro application of the combination therapy triggered significantly higher frequency of pancreatic cancer cells apoptosis, inhibited the activities of PI3K, Akt, PKA, mTOR and PTEN, and decreased the activation of NF-κB and expression of NF-κB-regulated products. In vivo application of the combination therapy induced significant enhancement of tumor cell apoptosis, reductions in tumor volume, and inhibited activation of mTOR and PTEN. In conclusion, evodiamine can augment the therapeutic effect of gemcitabine in pancreatic cancer through direct or indirect negative regulation of the PI3K/Akt pathway.

[Surgical treatment of postoperative deep wound infection after posterior lumbar interlumbar fusion of the lumbar stenosis].

OBJECTIVE: To study surgical treatment for the deep wound infections after the operation of posterior lumbar interlumbar fusion (PLIF) in lumbar spinal stenosis. METHODS: From December 2005 to December 2010,10 patients with the deep wound infection of the PLIF were analyzed retrospectively, including 4 males and 6 females, with a mean age of 52.8 years (ranged from 34 to 70 years). All the patients were treated with debridement and the drainage. The sensitive antibiotics were used. The VAS score, erythrocyte sedimentation rate (ESR), C reactive protein (CRP), and JOA lumbar score were used to compare the clinical results pre-and post-operation. RESULTS: All the patients were followed up, and the mean duration was 24 months (ranged from 19 to 28 months). One patient developed to an intervertebral space infection and the cage was removed. One patient suffered a radical central nerve system infection and died after the debridement. Other 8 patients got a good clinical result. The VAS score decreased from preoperative 8.0 +/- 0.4 to postoperative 2.8 +/- 0.3; JOA score improved from preoperative 10.30 +/- 3.02 to postoperative 24.10 +/- 2.85; ESR decreased from preoperative (85.0 +/- 17.0) mm/h to postoperative (14.0 +/- 6.0) mm/h; both CRP and WBC decreased from preoperative (73.5 +/- 14.3) mg/L, (11.1 +/- 1.8) x 10(9)/L to postoperative (5.1 +/- 1.1) mg/L, (7.4 +/- 0.5) x 10(9)/L respectively. CONCLUSION: Treatment of patients with deep wound infections after PLIF with debridement, drainage, and sensitive antibiotics could get a good long-term clinical result, which is important to treat the patients with high-risk factors. Early diagnosis and operation is the key to deal with the patients with deep wound infections after PLIF.

[Comparison between bipedicular approach and uni-extrapedicular approach in application of vertebroplasty].

OBJECTIVE: To analyze the advantages and disadvantages of bipedicular approach and uni-extrapedicular approach of vertebroplasty in treating osteoporotic vertebral compression fractures (OVCFs). METHODS: From January 2008 to December 2010,53 patients with OVCFs were retrospectively analyzed. There were 24 males, 30 females with an average age of 66.9 years (ranged,59 to 88 years). Among them, 26 cases were treated with bipedicular approach, 28 cases were treated with uni-extrapedicular approach. The data of bone cement injection, radiology exposure times, operation time, bone cement leakage and vessels nerve complications were observed. Cobb angle, vertebral compression ration were observed by imaging data, and evaluate recovery of deformity. RESULTS: The data of bone cement injection, radiology exposure times, operation time, VAS score were (6.6 +/- 0.8) ml and (6.8 +/- 1.5) ml, (21.7 +/- 4.0) times and (17.9 +/- 3.6) times, (40.5 +/- 5.5) min and (31.6 +/- 9.1) min, (2.8 +/- 0.6) scores and (3.1 +/- 0.5) scores respectively. Cobb angle,vertebral compression ration were (7.6 +/- 2.0) degrees and (6.9 +/- 2.6) degrees, (18.1 +/- 5.8)% and (16.5 +/- 6.1)%. There were no vascular nerve complications occurred. For bone cement leakage, 3 cases (11%) in bipedicular approach and 3 cases (11%)in uni-extrapedicular approach. There was no significant differences between two groups in VAS score, recovery of vetebral body, Cobb angle, bone cement injection and bone cement leakage, but had significant differences in radiology exposure times and operation time (P<0.05). CONCLUSION: Both of two approaches can treat OVCFs well, especially extropedicle approach which could reduce operation time and radiation shoot frequency.