Preparation of Ni@Pd Core-Shell Nanoparticles Supported on KIT-6 by Ultrasound-Assisted Galvanic Replacement for Dodecahydro-N-ethylcarbazole Dehydrogenation.

Using Ni as a template and reductant, Ni core-Pd shell nanoparticles (Ni@Pd NPs) supported on KIT-6 (Ni@Pd/K6) were prepared by a galvanic replacement reaction under ultrasonic radiation. The characterization results show that the Ni@Pd core-shell NPs with an average diameter of 1.9 ± 0.3 nm are uniformly dispersed on KIT-6. The d-band center position of Pd in Ni@Pd core-shell NPs can be affected by both ligand and strain effects. The relationship between the d-band center of Pd and the selectivity of intermediates is a nearly straight curve. The dehydrogenation efficiency of dodecahydro-N-ethylcarbazole on Ni@Pd(6:1)/K6 is 100% only for 3 h at 180 °C and 95.5% for 6 h at 160 °C, which is better than the reported catalysts. The outstanding catalytic dehydrogenation performance of Ni@Pd(6:1)/K6 can be attributed to the synergistic effect of the ligand and strain effect, the high dispersion of core-shell NPs, and the weak H2 binding ability of the catalyst.

Sema7A protects against high-fat diet-induced obesity and hepatic steatosis by regulating adipo/lipogenesis.

OBJECTIVE: Obesity and related diseases are becoming a growing risk for public health around the world due to the westernized lifestyle. Sema7A, an axonal guidance molecule, has been known to play a role in neurite growth, bone formation, and immune regulation. Whether Sema7A participates in obesity and metabolic diseases is unknown. As several SNPs in SEMA7A and its receptors were found to correlate with BMI and metabolic parameters in the human population, we investigated the potential role of Sema7A in obesity and hepatic steatosis. METHODS: GWAS and GEPIA database was used to analyze SNPs in SEMA7A and the correlation of Sema7A expression with lipid metabolism related genes. Sema7A-/- mice and recombinant Sema7A (rSema7A) were used to study the role of Sema7A in HFD-induced obesity and hepatic steatosis. Adipose tissue-derived mesenchymal stem cells (ADSCs) were used to examine the role of Sema7A in adipogenesis, lipogenesis and downstream signaling. RESULTS: Deletion of Sema7A aggravated HFD-induced obesity. Sema7A deletion enhanced adipogenesis in both subcutaneous and visceral ADSCs, while the addition of rSema7A inhibited adipogenesis of ADSCs and lipogenesis of differentiated mature adipocytes. Sema7A inhibits adipo/lipogenesis potentially through its receptor integrin ß1 and downstream FAK signaling. Importantly, administration of rSema7A had protective effects against diet-induced obesity in mice. In addition, deletion of Sema7A led to increased hepatic steatosis and insulin resistance in mice. CONCLUSIONS: Our findings reveal a novel inhibitory role of Sema7A in obesity and hepatic steatosis, providing a potential new therapeutic target for obesity and metabolic diseases.

The role of triclosan-coated suture in preventing surgical infection: A meta-analysis.

OBJECTIVES: In this meta-analysis, we aimed to compare the differences in surgical site infection (SSI) between triclosan-coated and uncoated sutures after hip and knee arthroplasty. MATERIALS AND METHODS: We searched PubMed, Embase, and Cochrane databases for randomized-controlled studies (RCTs) comparing triclosan-coated sutures with uncoated sutures for the prevention of SSIs after hip and knee arthroplasty. Literature screening and data curation were performed according to inclusion and exclusion criteria and the risk of bias was assessed for included research using Cochrane Handbook criteria. RESULTS: Three RCTs with a total of 2,689 cases were finally included, including 1,296 cases in the triclosan-coated suture group and 1,393 cases in the control group. The overall incidence of SSI was lower in the group with triclosan antimicrobial sutures (1.9%) than in the uncoated suture group (2.5%), but the difference was statistically significant (odds ratio=0.76, 95% confidence interval: [0.45-1.27], p=0.30). The differences in the results of the incidence of superficial SSI and deep SSI were not statistically significant (p>0.05). CONCLUSION: The application of triclosan antimicrobial sutures did not reduce the incidence of SSI after hip and knee arthroplasty compared to the controls, and it needs further high-quality RCT studies to be improved.

Superhydrophobic Mechano-Bactericidal Surface with Photodynamic Antibacterial Capability.

Bacterial invasion and proliferation on various surfaces pose a serious threat to public health worldwide. Conventional antibacterial strategies that mainly rely on bactericides exhibit high bacteria-killing efficiency but might trigger the well-known risk of antibiotic resistance. Here, we report a superhydrophobic mechano-bactericidal surface with photodynamically enhanced antibacterial capability. First, bioinspired nanopillars with polycarbonate as the bulk material were replicated from anodized alumina oxide templates via a simple hot-pressing molding method. Subsequently, a facile bovine serum albumin phase-transition method was used to introduce chlorin e6 onto the nanopillar-patterned surface, which was then perfluorinated to render the surface superhydrophobic. Benefiting from its strong liquid super-repellency and photodynamically enhanced mechano-bactericidal properties, the superhydrophobic nanopillar-patterned surface exhibits 100% antibacterial efficiency after 30 min visible light irradiation (650 nm, 20 mW cm-2). More strikingly, the surface exhibited impressive long-lasting antimicrobial performance, maintaining a very high bactericidal efficiency (≥99%) even after 10 cycles of bacterial contamination tests. Also, the superhydrophobic nanopillar-patterned surface displays good hemocompatibility with a much lower than the 5% hemolysis rate. Overall, this work offers a new method for significantly enhancing the antibacterial efficiency of structural antimicrobial surfaces without involving any bactericidal agents, and this functional surface shows great potential in the field of advanced medical materials and hospital surfaces.

Bio-Inspired Self-Adaptive Nanocomposite Array: From Non-antibiotic Antibacterial Actions to Cell Proliferation.

Pathogenic bacterial infection and poor native tissue integration are two major issues encountered by biomaterial implants and devices, which are extremely hard to overcome within a single surface, especially for those without involvement of antibiotics. Herein, a self-adaptive surface that can transform from non-antibiotic antibacterial actions to promotion of cell proliferation is developed by in situ assembly of bacteriostatic 3,3'-diaminodipropylamine (DADP)-doped zeolitic imidazolate framework-8 (ZIF-8) on bio-inspired nanopillars. Initially, the nanocomposite surface shows impressive antibacterial effects, even under severe bacterial infection, due to the combination of mechano-bactericidal activity from a nanopillar structure and bacteriostatic activity contributed by pH-responsive release of DADP. After the complete degradation of the ZIF-8 layer, the refurbished nanopillars not only can still physically rupture bacterial membrane but also facilitate mammalian cell proliferation, due to the obvious difference in cell size. More strikingly, the nanocomposite surface totally avoids the usage of antibiotics, eradicating the potential risk of antimicrobial resistance, and the surface exhibited excellent histocompatibility and lower inflammatory response properties as revealed by in vivo tests. This type of self-adaptive surface may provide a promising alternative for addressing the intractable implant-associated requirements, where antibiotic-free antibacterial activity and native tissue integration are both highly needed.

Single-cell transcriptional profiling of human carotid plaques reveals a subpopulation of endothelial cells associated with stroke incidences.

The differences in plaque histology between symptomatic and asymptomatic patients have been widely accepted. Whether there is a heterogeneity of cells between symptomatic and asymptomatic plaques remains largely unclear. To reveal the potential heterogeneity within different plaques, which may contribute to different stroke incidences, we obtained the scRNA-seq data from symptomatic and asymptomatic patients and identified eight cell types present in plaques. Further analysis of endothelial cells (ECs) revealed three distinct EC subpopulations appeared to be endowed with specific biological functions such as antigen processing and presentation, cell adhesion, and smooth muscle cell proliferation. Of note, the differentially expressed genes of the EC 2 subpopulation showed that the genes involved in cell adhesion were up-regulated in asymptomatic plaques compared to symptomatic plaques. Integrating the data of intraplaque haemorrhage and plaque stability, the 5th top-enriched biological process was cell adhesion in the stable or non-haemorrhaged plaques compared to unstable plaques or haemorrhaged plaques. Among these cell adhesion-related genes, the intersection gene AOC3 may play a vital role in plaque haemorrhage and plaque stability. Targeting cell adhesion and the specialized genes may provide potential new therapeutic directions to prevent asymptomatic patients from stroke.

Bioinspired nanopillar surface for switchable mechano-bactericidal and releasing actions.

Constructing safe and effective antibacterial surfaces has continuously received great attention, especially in healthcare-related fields. Bioinspired mechano-bactericidal nanostructure surfaces could serve as a promising strategy to reduce surface bacterial contamination while avoiding the development of antibiotic resistance. Although effective, these nanostructure surfaces are prone to be contaminated by the accumulation of dead bacteria, inevitably compromising their long-term antibacterial activity. Herein, a bioinspired nanopillar surface with both mechano-bactericidal and releasing actions is developed, via grafting zwitterionic polymer (poly(sulfobetaine methacrylate) (PSBMA)) on ZnO nanopillars. Under dry conditions, this nanopillar surface displays remarkable mechano-bactericidal activity, because the collapsed zwitterionic polymer layer makes no essential influence on nanopillar structure. Once being incubated with aqueous solution, the surface could readily detach the killed bacteria and debris, owing to the swelling of the zwitterionic layer. Consequentially, the surface antibacterial performances can be rapidly and controllably switched between mechano-bactericidal action and bacteria-releasing activity, guaranteeing a long-lasting antibacterial performance. Notably, these collaborative antibacterial behaviors are solely based on physical actions, avoiding the risk of triggering bacteria resistance. The resultant nanopillar surface also enjoys the advantages of substrate-independency and good biocompatibility, offering potential antibacterial applications for biomedical devices and hospital surfaces.

Biocompatible mechano-bactericidal nanopatterned surfaces with salt-responsive bacterial release.

Bio-inspired nanostructures have demonstrated highly efficient mechano-bactericidal performances with no risk of bacterial resistance; however, they are prone to become contaminated with the killed bacterial debris. Herein, a biocompatible mechano-bactericidal nanopatterned surface with salt-responsive bacterial releasing behavior is developed by grafting salt-responsive polyzwitterionic (polyDVBAPS) brushes on a bio-inspired nanopattern surface. Benefiting from the salt-triggered configuration change of the grafted polymer brushes, this dual-functional surface shows high mechano-bactericidal efficiency in water (low ionic strength condition), while the dead bacterial residuals can be easily lifted by the extended polymer chains and removed from the surface in 1 M NaCl solution (high ionic strength conditions). Notably, this functionalized nanopatterned surface shows selective biocidal activity between bacterial cells sand eukaryotic cells. The biocompatibility with red blood cells (RBCs) and mammalian cells was tested in vitro. The histocompatibility and prevention of perioperative contamination activity were verified by in vivo evaluation in a rat subcutaneous implant model. This nanopatterned surface with bacterial killing and releasing activities may open new avenues for designing bio-inspired mechano-bactericidal platforms with long-term efficacy, thus presenting a facile alternative in combating perioperative-related bacterial infection. STATEMENT OF SIGNIFICANCE: Bioinspired nanostructured surfaces with noticeable mechano-bactericidal activity showed great potential in moderating drug-resistance. However, the nanopatterned surfaces are prone to be contaminated by the killed bacterial debris and compromised the bactericidal performance. In this study, we provide a dual-functional antibacterial conception with both mechano-bactericidal and bacterial releasing performances not requiring external chemical bactericidal agents. Additionally, this functionalized antibacterial surface also shows selective biocidal activity between bacteria and eukaryotic cells, and the excellent biocompatibility was tested in vitro and in vivo. The new concept for the functionalized mechano-bactericidal surface here illustrated presents a facile antibiotic-free alternative in combating perioperative related bacterial infection in practical application.

Piezoelectric Based Touch Sensing for Interactive Displays-A Short Review.

Interactive display is an important part of electronic devices. It is widely used in smartphones, laptops, and industrial equipment. To achieve 3-dimensional detection, the piezoelectric touch panel gains great popularity for its advantages of high sensitivity, low cost, and simple structure. In order to help readers understand the basic principles and the current technical status, this article introduces the work principles of the piezoelectric touch panel, widely-used piezoelectric materials and their characteristics, as well as the applications of the piezoelectric touch panel. The challenges and future trends are also discussed.

Single-cell RNA-seq reveals cellular heterogeneity of mouse carotid artery under disturbed flow.

Disturbed blood flow (d-flow) has been known to induce changes of the cells in the arterial wall, increasing the risk of atherosclerosis. However, the heterogeneity of the vascular cell populations under d-flow remains less understood. To generate d-flow in vivo, partial carotid artery ligation (PCL) was performed. Seven days after ligation, single-cell RNA sequencing of nine left carotid arteries (LCA) from the PCL group (10,262 cells) or control group (14,580 cells) was applied and a single-cell atlas of gene expression was constructed. The integrated analysis identified 15 distinct carotid cell clusters, including 10 d-flow-relevant subpopulations. Among endothelial cells, at least four subpopulations were identified, including Klk8hi ECs, Lrp1hi ECs, Dkk2hi ECs, and Cd36hi ECs. Analysis of GSVA and single-cell trajectories indicated that the previously undescribed Dkk2hi ECs subpopulation was mechanosensitive and potentially transformed from Klk8hi ECs under d-flow. D-flow-induced Spp1hi VSMCs subpopulation that appeared to be endowed with osteoblast differentiation, suggesting a role in arterial stiffness. Among the infiltrating cell subpopulations, Trem2hi Mφ, Birc5hi Mφ, DCs, CD4+ T cells, CXCR6+ T cells, NK cells, and granulocytes were identified under d-flow. Of note, the novel Birc5hi Mφ was identified as a potential contributor to the accumulation of macrophages in atherosclerosis. Finally, Dkk2hi ECs, and Cd36hi ECs were also found in the proatherosclerotic area of the aorta where the d-flow occurs. In conclusion, we presented a comprehensive single-cell atlas of all cells in the carotid artery under d-flow, identified previously unrecognized cell subpopulations and their gene expression signatures, and suggested their specialized functions.

Sema4D correlates with tumour immune infiltration and is a prognostic biomarker in bladder cancer, renal clear cell carcinoma, melanoma and thymoma.

Sema4D, a member of the immune semaphorin family, plays crucial roles in the immune regulation, bone resorption and nervous system. It is also involved in angiogenesis and tumour progression. However, systemic studies on the correlation between Sema4D expression and the immune infiltration or clinical outcomes in tumours are still limited. Here, we analysed the landscape of Sema4D expression and its prognostic value in the cancer genome atlas pan-cancer as well as the correlation between Sema4D and immune cell infiltration by Tumour Immune Estimation Resource and Gene Expression Profiling interactive analysis online tools. Results showed that a higher Sema4D expression was significantly correlated with a favourable overall survival in diverse solid tumours including bladder cancer (Hazards Ratio (HR)=0.68, p = .0095), kidney renal clear cell carcinoma (HR = 0.61, p = .0016), melanoma (HR = 0.58, p = 6.6e-05) and thymoma (HR = 0.1, p = .011). Interestingly, Sema4D expression has positive correlation with various tumour infiltrating immune cells and immune cell biomarkers in these tumours. These results suggest that Sema4D could be a prospective biomarker for calculating hazard ratio of tumour patients and their tumour immune infiltration levels.

Differentially expressed genes related to oxidoreductase activity and glutathione metabolism underlying the adaptation of Phragmites australis from the salt marsh in the Yellow River Delta, China.

The common reed (Phragmites australis) is a dominant species in the coastal wetlands of the Chinese Yellow River Delta, where it tolerates a wide range of salinity. Recent environmental changes have led to the increase of soil salinity in this region, which has degraded much of the local vegetation. Clones of common reeds from the tidal marsh may have adapted to local high salinity habitat through selection on genes and metabolic pathways conferring salt tolerance. This study aims to reveal molecular mechanisms underlying salt tolerance in the tidal reed by comparing them to the salt-sensitive freshwater reed under salt stress. We employed comparative transcriptomics to reveal the differentially expressed genes (DEGs) between these two types of common reeds under different salinity conditions. The results showed that only three co-expressed genes were up-regulated and one co-expressed gene was down-regulated between the two reed types. On the other hand, 1,371 DEGs were exclusively up-regulated and 285 DEGs were exclusively down-regulated in the tidal reed compared to the control, while 115 DEGs were exclusively up-regulated and 118 DEGs were exclusively down-regulated in the freshwater reed compared to the control. From the pattern of enrichment of transcripts involved in salinity response, the tidal reed was more active and efficient in scavenging reactive oxygen species (ROS) than the freshwater reed, with the tidal reed showing significantly higher gene expression in oxidoreductase activity. Furthermore, when the reeds were exposed to salt stress, transcripts encoding glutathione metabolism were up-regulated in the tidal reed but not in the freshwater reed. DEGs related to encoding glutathione reductase (GR), glucose-6-phosphate 1-dehydrogenase (G6PDH), 6-phosphogluconate dehydrogenase (6PD), glutathione S-transferase (GST) and L-ascorbate peroxidase (LAP) were revealed as especially highly differentially regulated and therefore represented candidate genes that could be cloned into plants to improve salt tolerance. Overall, more genes were up-regulated in the tidal reed than in the freshwater reed from the Yellow River Delta when under salt stress. The tidal reed efficiently resisted salt stress by up-regulating genes encoding for oxidoreductase activity and glutathione metabolism. We suggest that this type of common reed could be extremely useful in the ecological restoration of degraded, high salinity coastal wetlands in priority.

Molecular docking-assisted screening reveals tannic acid as a natural protein disulphide isomerase inhibitor with antiplatelet and antithrombotic activities.

Protein disulphide isomerase (PDI) promotes platelet activation and constitutes a novel antithrombotic target. In this study, we reported that a PDI-binding plant polyphenol, tannic acid (TA), inhibits PDI activity, platelet activation and thrombus formation. Molecular docking using plant polyphenols from dietary sources with cardiovascular benefits revealed TA as the most potent binding molecule with PDI active centre. Surface plasmon resonance demonstrated that TA bound PDI with high affinity. Using Di-eosin-glutathione disulphide fluorescence assay and PDI assay kit, we showed that TA inhibited PDI activity. In isolated platelets, TA inhibited platelet aggregation stimulated by either GPVI or ITAM pathway agonists. Flow cytometry showed that TA inhibited thrombin- or CRP-stimulated platelet activation, as reflected by reduced granule secretion and integrin activation. TA also reduced platelet spreading on immobilized fibrinogen and platelet adhesion under flow conditions. In a laser-induced vascular injury mouse model, intraperitoneal injection of TA significantly decreased the size of cremaster arteriole thrombi. No prolongation of mouse jugular vein and tail-bleeding time was observed after TA administration. Therefore, we identified TA from natural polyphenols as a novel inhibitor of PDI function. TA inhibits platelet activation and thrombus formation, suggesting it as a potential antithrombotic agent.

[Source Analysis and Health Risk Assessment of PAHs in PM2.5 During Winter in Liaocheng City].

To investigate the mass concentrations, sources, and health effects of polycyclic aromatic hydrocarbons (PAHs) in ambient particulate matter (PM) in Liaocheng City during winter, 14 types of PAHs in PM2.5 were determined from January to February of 2017. The sources of the PAHs were analyzed by using diagnostics ratios and the principal component analysis (PCA)-multiple linear regression (MLR) model,and the health risk of PAHs was assessed by BaP equivalent concentrations (BaPeq) and incremental lifetime cancer risk (ILCR). The results showed that the mass concentrations of PAHs in PM2.5 during winter were (64.89±48.23) ng·m-3, Fla, Pyr, and Chry were predominant species, accounting for 15.5%, 12.8%, and 12.7% of the total concentrations of PAHs, respectively. Moreover, the ring distribution of the PAHs was dominated by four-ring PAHs. The pollution during the pre-Spring Festival and firework Ⅱwere the most severe during the sampling period. The results of the PCA-MLR model suggested that PAHs originated mostly from coal burning, biomass burning, and vehicle emissions. The toxicity exposure index (TEQ) in Liaocheng City during winter was (6.37±4.92) ng·m-3. The results of the risk model revealed that the ILCR of adults was higher than that of children, and both groups of ILCR for winter were in the range of the risk threshold. This suggests that a potential risk in terms of inhalation PAH exposure for residents in Liaocheng City.

Activation of p47phox as a Mechanism of Bupivacaine-Induced Burst Production of Reactive Oxygen Species and Neural Toxicity.

Bupivacaine has been shown to induce neurotoxicity through inducing excessive reactive oxygen species (ROS), but the underlying mechanism remains unclear. NOX2 is one of the most important sources of ROS in the nervous system, and its activation requires the membrane translocation of subunit p47phox. However, the role of p47phox in bupivacaine-induced neurotoxicity has not been explored. In our in vitro study, cultured human SH-SY5Y neuroblastoma cells were treated with 1.5 mM bupivacaine to induce neurotoxicity. Membrane translocation of p47phox was assessed by measuring the cytosol/membrane ratio of p47phox. The effects of the NOX inhibitor VAS2870 and p47phox-siRNA on bupivacaine-induced neurotoxicity were investigated. Furthermore, the effect of VAS2870 on bupivacaine-induced neurotoxicity was assessed in vivo in rats. All these changes were reversed by pretreatment with VAS2870 or transfection with p47phox-siRNA in SH-SY5Y cells. Similarly, pretreatment with VAS2870 attenuated bupivacaine-induced neuronal toxicity in rats. It is concluded that enhancing p47phox membrane translocation is a major mechanism whereby bupivacaine induced neurotoxicity and that pretreatment with VAS2870 or local p47phox gene knockdown attenuated bupivacaine-induced neuronal cell injury.

Diphenyleneiodonium Mitigates Bupivacaine-Induced Sciatic Nerve Damage in a Diabetic Neuropathy Rat Model by Attenuating Oxidative Stress.

BACKGROUND: Increased oxidative stress has been linked to local anesthetic-induced nerve injury in a diabetic neuropathy (DN) rat model. The current study explores the effects of diphenyleneiodonium (DPI) chloride, an NADPH oxidase (NOX) inhibitor, on bupivacaine-induced sciatic nerve injury in DN rats. METHODS: A rat DN model was established through high-fat diet feeding and streptozotocin injection. The model was confirmed via testing (i) blood glucose, (ii) hindpaw allodynia responses to von Frey (VF) monofilaments, (iii) paw withdrawal thermal latency (PWTL), and (iv) nerve conduction velocity (NCV). Bupivacaine (Bup, 0.2 mL, 5 mg/mL) was used to block the right sciatic nerve. DPI (1 mg/kg) was injected subcutaneously 24 hours and 30 minutes before the sciatic block. At 24 hours after the block, NCV, various reactive oxygen species, and Caspase-3 were evaluated to determine the extent of sciatic nerve injury. RESULTS: The DN rat model was successfully established. Compared with the DN control group, the postblock values of VF responses (DN-Con, 16.5 ± 1.3 g; DN + Bup, 19.1 ± 1.5 g, P < .001) and PWTL significantly increased (DN-Con, 13.3 ± 1.1 seconds; DN + Bup, 14.6 ± 1.1 seconds, P = .028); the NCV of sciatic nerve was significantly reduced (DN-Con, 38.8 ± 2.4 m/s, DN + Bup, 30.5 ± 2.0 m/s, P = .003), and sciatic nerve injury (as indicated by axonal area) was more severe in the bupivacaine-treated DN group (DN-Con, 11.6 ± 0.3 µm, DN + Bup, 7.5 ± 0.3 µm, P < .001). In addition, DPI treatment significantly improved nerve function (VF responses, 17.3 ± 1.3 g; PWTL, 13.4 ± 1.1 seconds; NCV, 35.6 ± 3.1 m/s) and mitigated loss of axonal area (9.6 ± 0.3 µm). Compared to the DN + Bup group (without DPI), the levels of lipid peroxides and hydroperoxides, as well as the protein expression of NOX2, NOX4, and Caspase-3, were significantly reduced in the DN + Bup + DPI group (P < .05). CONCLUSIONS: Subcutaneous injection of DPI appears to protect against the functional and neurohistological damage of bupivacaine-blocked sciatic nerves in a high-fat diet/streptozotocin-induced DN model.

MiR-223-3p targeting SEPT6 promotes the biological behavior of prostate cancer.

MicroRNAs (miRNAs) present frequently altered expression in urologic cancers including prostate, bladder, and kidney cancer. The altered expression of miR-223 has been reported in cancers and other diseases in recent researches. MiR-223 is up-regulated in systemic lupus erythematosus and rheumatoid arthritis. In neoplastic diseases, miR-223 is proved to be up-expressed in plasma or serum and cancer tissues compared with normal tissues in pancreatic cancer, gastric cancer, et al. However, whether altered expression of miR-223 is associated with prostate cancer (PCa) and what it is potential functions in PCa remained unveiled. In this study, we firstly found miR-223-3p were up-regulated in prostate cancer tissues and then we study functional role of miR-223-3p in PCa using DU145, PC3 and LNCaP cell lines. Our data suggested that miR-223-3p might target gene SEPT6 and promoted the biological behavior of prostate cancer. Notably, we found increasing SEPT6 expression might reverse the biological activity induced by miR-223-3p, which might be a potential therapeutic target for PCa.

Diagnosis and surgical treatment of nutcracker syndrome: a single-center experience.

OBJECTIVES: To report our experience in the diagnosis and surgical treatment of the nutcracker syndrome, which is uncommon, with few larger series published. METHODS: We retrospectively analyzed 23 patients with the nutcracker syndrome who presented to our institution from July 1998 to July 2007. A diagnosis of the nutcracker syndrome was suspected from the clinical examination, ultrasound, computed tomography, and magnetic resonance imaging findings. The diagnosis was confirmed by determination of the renocaval gradient using phlebography of the left renal vein (LRV). Because of recurrent gross hematuria and persistent orthostatic proteinuria, 7 patients (4 females and 3 males) underwent LRV transposition. Other patients with mild and tolerable symptoms were treated conservatively. The follow-up range was 14-122 months (mean 42.6). RESULTS: All 23 patients met the criteria for establishing the diagnosis of the nutcracker syndrome. Ultrasonography, computed tomography, and magnetic resonance imaging revealed entrapment of the LRV between the superior mesenteric artery and aorta. The renocaval pressure gradient was > or = 4 mm Hg (normal < 1 mm Hg) in all patients. The hematuria and proteinuria disappeared in the 7 patients who underwent LRV transposition, and only 1 patient continued to have pelvic pain. No complications occurred during surgery. The postoperative complications included paralytic ileus in 2 and retroperitoneal hematoma in 1 patient. No improvement or only partial improvement was observed in most patients receiving conservative treatment. CONCLUSIONS: The diagnosis of the nutcracker syndrome is determined from the clinical examination and radiographic findings. In patients who require surgical treatment, LRV transposition is an efficient surgical approach with an acceptable risk of complications. However, in some cases, pelvic pain may persist despite removal of the obstruction of the renal venous backflow.

Hypothetic association between greater sympathetic activity and prostate cancer.

Among men, prostate cancer is the most common cancer diagnosed, and the second leading cause of death from cancer in the industrialized countries. In spite of substantial progress in research, diagnosis and treatment, the causes of prostate cancer remain largely unknown. In this paper, we propose the hypothesis that prostate cancer represents another entity in the constellation of disease incited by the greater sympathetic activity that develops with age. However, the specific mechanisms of changes of increased prostatic cell proliferation and carcinogenesis caused by the autonomic nervous system have not yet been clarified. In regard to this matter, future studies should outline a more complete mechanism.