Establishment of a prognostic model to predict chemotherapy response and identification of RAC3 as a chemotherapeutic target in bladder cancer.

Cisplatin-based chemotherapy is considered the primary treatment option for patients with advanced bladder cancer (BCa). However, the objective response rate to chemotherapy is often unsatisfactory, leading to a poor 5-year survival rate. Furthermore, current strategies for evaluating chemotherapy response and prognosis are limited and inefficient. In this study, we aimed to address these challenges by establishing a chemotherapy response type gene (CRTG) signature consisting of 9 genes and verified the prognostic value of this signature using TCGA and GEO BCa cohorts. The risk scores based on the CRTG signature were found to be associated with advanced clinicopathological status and demonstrated favorable predictive power for chemotherapy response in the TCGA cohort. Meanwhile, tumors with high risk scores exhibited a tendency toward a "cold tumor" phenotype. These tumors showed a low abundance of T cells, CD8+ T cells and cytotoxic lymphocytes, along with a high abundance of cancer-associated fibroblasts. Moreover, they displayed higher mRNA levels of these immune checkpoints: CD200, CD276, CD44, NRP1, PDCD1LG2 (PD-L2), and TNFSF9. Furthermore, we developed a nomogram that integrated the CRTG signature with clinicopathologic risk factors. This nomogram proved to be a more effective tool for predicting the prognosis of BCa patients. Additionally, we identified Rac family small GTPase 3 (RAC3) as a biomarker in our model. RAC3 was found to be overexpressed in chemoresistant BCa tissues and enhance the chemotherapeutic resistance of BCa cells in vitro and in vivo by regulating the PAK1-ERK1/2 pathway. In conclusion, our study presents a novel CRTG model for predicting chemotherapy response and prognosis in BCa. We also highlight the potential of combining chemotherapy with immunotherapy as a promising strategy for chemoresistant BCa and that RAC3 might be a latent target for therapeutic intervention.

HIO3-HIO2-Driven Three-Component Nucleation: Screening Model and Cluster Formation Mechanism.

Iodine oxoacids (HIO3 and HIO2)-driven nucleation has been suggested to efficiently contribute to new particle formation (NPF) in marine atmospheres. Abundant atmospheric nucleation precursors may further enhance HIO3-HIO2-driven nucleation through various multicomponent nucleation mechanisms. However, the specific enhancing potential (EP) of different precursors remains largely unknown. Herein, the EP-based screening model of precursors and enhancing mechanism of the precursor with the highest EP on HIO3-HIO2 nucleation were investigated. The formation free energies (ΔG), as critical parameters for evaluating EP, were calculated for the dimers of 63 selected precursors with HIO2. Based on the ΔG values, (1) a quantitative structure-activity relationship model was developed for evaluating ΔG of other precursors and (2) atmospheric concentrations of 63 (precursor)1(HIO2)1 dimer clusters were assessed to identify the precursors with the highest EP for HIO3-HIO2-driven nucleation by combining with earlier results for the nucleation with HIO3 as the partner. Methanesulfonic acid (MSA) was found to be one of the precursors with the highest EP. Finally, we found that MSA can effectively enhance HIO3-HIO2 nucleation at atmospheric conditions by studying larger MSA-HIO3-HIO2 clusters. These results augment our current understanding of HIO3-HIO2 and MSA-driven nucleation and may suggest a larger impact of HIO2 in atmospheric aerosol nucleation.

A clinically practical model for the preoperative prediction of lymph node metastasis in bladder cancer: a multicohort study.

BACKGROUND: The aim of this study was to construct a clinically practical model to precisely predict lymph node (LN) metastasis in bladder cancer patients. METHODS: Four independent cohorts were included. The least absolute shrinkage and selection operator regression with multivariate logistic regression were applied. The diagnostic efficacy of LN score and CT/MRI was compared by accuracy, sensitivity, specificity, and area under curve (AUC). RESULTS: A total of 606 patients were included to develop a basic prediction model. After multistep gene selection, the LN metastasis prediction model was constructed with 5 genes. The model can accurately predict LN metastasis with an AUC of 0.781. For clinically practical use, we transformed the model into a Fast LN Scoring System using the SYSMH cohort (n = 105). High LN score patients exhibited a 72.2% LN metastasis rate, while low LN score patients showed a 3.4% LN metastasis rate. The LN score achieved a superior accuracy than CT/MRI (0.882 vs. 0.727). Application of LN score can correct the diagnosis of 88% (22/25) patients who were misdiagnosed by CT/MRI. DISCUSSION: The clinically practical LN score can precisely, rapidly, and conveniently predict LN status, which will assist preoperative diagnosis for LN metastasis and guide precise therapy.

TSPAN18 facilitates bone metastasis of prostate cancer by protecting STIM1 from TRIM32-mediated ubiquitination.

BACKGROUND: Bone metastasis is a principal cause of mortality in patients with prostate cancer (PCa). Increasing evidence indicates that high expression of stromal interaction molecule 1 (STIM1)-mediated store-operated calcium entry (SOCE) significantly activates the calcium (Ca2+) signaling pathway and is involved in multiple steps of bone metastasis in PCa. However, the regulatory mechanism and target therapy of STIM1 is poorly defined. METHODS: Liquid chromatography-mass spectrometry analysis was performed to identify tetraspanin 18 (TSPAN18) as a binding protein of STIM1. Co-IP assay was carried out to explore the mechanism by which TSPAN18 inhibits STIM1 degradation. The biological function of TSPAN18 in bone metastasis of PCa was further investigated in vitro and in vivo models. RESULT: We identified that STIM1 directly interacted with TSPAN18, and TSPAN18 competitively inhibited E3 ligase tripartite motif containing 32 (TRIM32)-mediated STIM1 ubiquitination and degradation, leading to increasing STIM1 protein stability. Furthermore, TSPAN18 significantly stimulated Ca2+ influx in an STIM1-dependent manner, and then markedly accelerated PCa cells migration and invasion in vitro and bone metastasis in vivo. Clinically, overexpression of TSPAN18 was positively associated with STIM1 protein expression, bone metastasis and poor prognosis in PCa. CONCLUSION: Taken together, this work discovers a novel STIM1 regulative mechanism that TSPAN18 protects STIM1 from TRIM32-mediated ubiquitination, and enhances bone metastasis of PCa by activating the STIM1-Ca2+ signaling axis, suggesting that TSPAN18 may be an attractive therapeutic target for blocking bone metastasis in PCa.

Whole-body tumor segmentation from PET/CT images using a two-stage cascaded neural network with camouflaged object detection mechanisms.

BACKGROUND: Whole-body Metabolic Tumor Volume (MTVwb) is an independent prognostic factor for overall survival in lung cancer patients. Automatic segmentation methods have been proposed for MTV calculation. Nevertheless, most of existing methods for patients with lung cancer only segment tumors in the thoracic region. PURPOSE: In this paper, we present a Two-Stage cascaded neural network integrated with Camouflaged Object Detection mEchanisms (TS-Code-Net) for automatic segmenting tumors from whole-body PET/CT images. METHODS: Firstly, tumors are detected from the Maximum Intensity Projection (MIP) images of PET/CT scans, and tumors' approximate localizations along z-axis are identified. Secondly, the segmentations are performed on PET/CT slices that contain tumors identified by the first step. Camouflaged object detection mechanisms are utilized to distinguish the tumors from their surrounding regions that have similar Standard Uptake Values (SUV) and texture appearance. Finally, the TS-Code-Net is trained by minimizing the total loss that incorporates the segmentation accuracy loss and the class imbalance loss. RESULTS: The performance of the TS-Code-Net is tested on a whole-body PET/CT image data-set including 480 Non-Small Cell Lung Cancer (NSCLC) patients with five-fold cross-validation using image segmentation metrics. Our method achieves 0.70, 0.76, and 0.70, for Dice, Sensitivity and Precision, respectively, which demonstrates the superiority of the TS-Code-Net over several existing methods related to metastatic lung cancer segmentation from whole-body PET/CT images. CONCLUSIONS: The proposed TS-Code-Net is effective for whole-body tumor segmentation of PET/CT images. Codes for TS-Code-Net are available at: https://github.com/zyj19/TS-Code-Net.

Analysis of the typing of adenovirus and its clinical characteristics in children with acute respiratory tract infection.

BACKGROUND: The purpose of this study was to investigate the typing of adenovirus (AdV) infection in children hospitalized with acute respiratory tract infection (ARTI) and its clinical characteristics. METHODS: Samples from 7832 hospitalized children with ARTIs from January 2021 to June 2022 were tested by multiplex PCR for AdV. AdV hex neighborhood genes were amplified and sequenced for typing by nested PCR. RESULTS: Three hundred twenty-eight cases were positive for AdV with rate of 4.48% (328/7832). No statistical difference in the rate of AdV detection was observed in different ages (P > 0.05). Among the 328 cases, 305 cases underwent amplification and sequence determination of AdV five-neighborhood, six-neighborhood and fibronectin genes. Only 237 cases were sequenced successfully for all 3 genetic fragments. The typing results of 231 cases with 3 genes were consistent, with 49.78% (115/231) of type 3, 41.56% (96/231) of type 7 and 8.66% (20/231) of other types identified. The main clinical symptoms in 231 children hospitalized with ARTI who were AdV positive were cough, sputum not easily coughable, Wheezing or shortness of breath and fever. Clinical diagnoses of 231 cases included: acute bronchitis 3.03% (7/231), capillary bronchitis 16.45% (38/231), pneumonia (mild/severe) 76.62% (177/231) (68.40% (158/231) in mild and 8.23% (19/231) in severe cases), bronchial asthma combined with pulmonary infection 3.46% (8/231). Higher percentage of shortness of breath, multilobar infiltration, and pleural effusion were found in type 7. Calcitoninogen in type 7 were significantly higher than those of type 3 and other types, and the white blood cell count was lower than those of type 3 and other types, and the difference was statistically significant (P < 0.05). CONCLUSION: AdV type 3 and 7 were frequently found in hospitalized children with acute lower respiratory tract involvement. AdV type 7 seems to be associated with more severe outcome.

UBE2S as a novel ubiquitinated regulator of p16 and ß-catenin to promote bone metastasis of prostate cancer.

Bone metastasis is the main site of metastasis and causes the most deaths in patients with prostate cancer (PCa). The mechanism of bone metastasis is complex and not fully clarified. By RNA sequencing and analysing key pathways in bone metastases of PCa, we found that one of the most important characteristics during PCa bone metastasis was G1/S transition acceleration caused by low protein levels of p16INK4a (p16). Interestingly, we demonstrated that UBE2S bound and degraded p16 through K11- rather than K48- or K63-linked ubiquitination, which accelerated PCa tumour cell G1/S transition in vivo and in vitro. Moreover, UBE2S also stabilized ß-catenin through K11-linked ubiquitination, leading to enhanced migration and invasion of tumour cells in PCa bone metastasis. Based on our cohorts and public databases, UBE2S was overexpressed in bone metastases and positively correlated with a high Gleason score, advanced nodal metastasis status and poor prognosis in PCa. Finally, targeting UBE2S with cephalomannine inhibited proliferation and invasion in vitro, and bone metastasis of PCa in vivo. This study innovatively discovered that UBE2S plays an oncogenic role in bone metastasis of PCa by degrading p16 and stabilizing ß-catenin via K11-linked ubiquitination, suggesting that it may serve as a multipotent target for metastatic PCa treatment.

5­Aza­dC suppresses melanoma progression by inhibiting GAS5 hypermethylation.

The in­depth study of melanoma pathogenesis has revealed that epigenetic modifications, particularly DNA methylation, is a universal inherent feature of the development and progression of melanoma. In the present study, the analysis of the tumor suppressor gene growth arrest­specific transcript 5 (GAS5) demonstrated that its expression was downregulated in melanoma, and its expression level had a certain negative association with its methylation modification level. The promoter of GAS5 presented with detectable CpG islands, and methylation­specific polymerase chain reaction analysis demonstrated that GAS5 was actually modified by methylation in melanoma tissues and cells; however, no methylation modification of GAS5 was detected in normal tissues. Following the treatment of melanoma cells with 5­Aza­2'­deoxycytidine (5­Aza­dC), GAS5 methylation was significantly reversed. The analysis of melanoma cell proliferation revealed that 5­Aza­dC inhibited A375 and SK­MEL­110 cell proliferation in a time­dependent manner. Further analysis of apoptosis demonstrated that 5­Aza­dC significantly increased the apoptosis level of the two cell lines. Moreover, migration analysis of melanoma cells revealed that 5­Aza­dC significantly reduced cell migration. Furthermore, 5­Aza­dC significantly decreased the invasive ability of the two cell lines. However, when the expression of GAS5 was silenced, the effects of 5­Aza­dC on cell proliferation, apoptosis, invasion and migration were not significant. Furthermore, the subcutaneous injection of A375 cells in nude mice successfully resulted in xenograft tumor formation. However, following an intraperitoneal injection of 5­Aza­dC, the volume and weight of xenograft tumors and Ki­67 expression were significantly reduced, and caspase­3 activity and GAS5 expression were enhanced; following the silencing of GAS5, the antitumor effect of 5­Aza­dC was significantly blocked. On the whole, the present study demonstrates that 5­Aza­dC inhibits the growth of melanoma, and its function may be related to the methylation modification of GAS5.

Characteristics and Risk Assessments of Mercury Pollution Levels at Domestic Garbage Collection Points Distributed within the Main Urban Areas of Changchun City.

The mercury that is released from the centralized treatment of municipal solid waste is an important source of atmospheric mercury. We chose the main urban area of Changchun as a representative area. Environmental factors such as total mercury content, temperature, wind speed, and other factors were measured in samples from the trash cans of two types of collection points (trash cans and garbage stations), the topsoil under the selected trash cans, and the ambient air above the selected trash cans. The potential ecological risks of mercury pollution were evaluated. The results showed that the mercury content levels of all sample types in the refuse transfer station were higher than the garbage cans and there were no significant differences observed between soil surface mercury and garbage cans. The mercury content levels in the atmosphere and the surface soil at the garbage collection points were found to increase along the cascade relationship of the garbage collection. However, there were no correlations observed between the atmospheric mercury content levels and the surface soil mercury content levels with the attachments and the sum of the former two. There were no correlations observed between surface soil and the attachments, or among the attachments, surface soil, and the atmospheric mercury content levels. The mercury content levels in the attachments, surface soil, and atmosphere of the garbage collection points in the study area were negatively correlated with the loop lines. Meanwhile, the potential ecological risk indexes of the garbage cans and garbage stations were found to be high. The chronic non-carcinogenic risks of mercury to children and adults were determined to be very low. The risks of mercury to children were higher when compared with adults. The highest non-carcinogenic risks of mercury pollution were determined to be within the central area of Changchun.

Gaseous Elemental Mercury Exchange Fluxes over Air-Soil Interfaces in the Degraded Grasslands of Northeastern China.

Mercury (Hg) is a global pollutant that may potentially have serious impacts on human health and ecologies. The gaseous elemental mercury (GEM) exchanges between terrestrial surfaces and the atmosphere play important roles in the global Hg cycle. This study investigated GEM exchange fluxes over two land cover types (including Artemisia anethifolia coverage and removal and bare soil) using a dynamic flux chamber attached to the LumexR RA915+ Hg analyzer during the growing season from May to September of 2018, in which the interactive effects of plant coverage and meteorological conditions were highlighted. The daily mean ambient levels of GEM and the total mercury concentrations of the soil (TSM) were determined to be 12.4 ± 3.6 to 16.4 ± 5.6 ng·m-3 and 32.8 to 36.2 ng·g-1, respectively, for all the measurements from May to September. The GEM exchange fluxes (ng·m-2·h-1) during the five-month period for the three treatments included the net emissions from the soil to the atmosphere (mean 5.4 to 7.1; range of -27.0 to 47.3), which varied diurnally, with releases occurring during the daytime hours and depositions occurring during the nighttime hours. Significant differences were observed in the fluxes between the vegetation coverage and removal during the growing months (p < 0.05). In addition, it was determined that the Hg fluxes were positively correlated with the solar radiation and air/soil temperature levels and negatively correlated with the air relative humidity and soil moisture under all the conditions (p < 0.05). Overall, the results obtained in this study demonstrated that the grassland soil served as both a source and a sink for atmospheric Hg, depending on the season and meteorological factors. Furthermore, the plants played an important inhibiting role in the Hg exchanges between the soil and the atmosphere.

Targeting WD repeat domain 5 enhances chemosensitivity and inhibits proliferation and programmed death-ligand 1 expression in bladder cancer.

BACKGROUND: Chemotherapy and/or immunotherapy are first-line treatments for advanced muscle-invasive bladder cancer (BCa), but the unsatisfactory objective response rate to these treatments yields poor 5-year patient survival. Discovery of therapeutic targets essential for BCa maintenance is critical to improve therapy response in clinic. This study evaluated the role of targeting WD repeat domain 5 (WDR5) with the small molecule compound OICR-9429 and whether it could be used to treat bladder cancer. METHODS: We analysed the expression and clinical prognosis of WDR5 in a TCGA cohort. The pharmacological role of OICR-9429 was further investigated in vitro and in vivo. RNA sequencing, western blot, and chromatin immunoprecipitation (ChIP) were utilized to explored the mechanism underlying OICR-9429-induced WDR5 inhibition. RESULTS: First, we found that WDR5 expression was upregulated in BCa and was associated with histologic grade, metastasis status, histologic subtype, and molecular subtype. High WDR5 expression level was also correlated with shorter overall survival (OS) in BCa. The WDR5 inhibitor OICR-9429 reduced cell viability by decreasing H3K4me3 levels but not WDR5 levels in T24, UM-UC-3, and TCCSUP BCa cells. OICR-9429 suppressed the proliferation of BCa cells by blocking the G1/S phase transition. Next, OICR-9429 enhanced apoptosis and chemosensitivity to cisplatin in BCa cells. In addition, OICR-9429 independently inhibited the motility and metastatic behaviour of BCa cells. In vivo experiments further revealed that OICR-9429 suppressed tumour growth, enhanced chemosensitivity, and reduced the toxicity of cisplatin in BCa. Notably, WDR5 was positively correlated with programmed death-ligand 1 (PD-L1) expression, and OICR-9429 suppressed immune evasion by blocking PD-L1 induced by IFN-γ. Mechanistically, some cell cycle-, antiapoptosis-, DNA repair-, metastasis-, and immune evasion-related genes, including BIRC5, XRCC2, CCNB1, CCNE2, PLK1, AURKA, FOXM1, and PD-L1 were identified to be directly regulated by OICR-9429 in a H3K4me3-dependent manner. CONCLUSIONS: Our novel finding is that the WDR5 inhibitor, OICR-9429, suppressed proliferation, metastasis and PD-L1-based immune evasion while enhancing apoptosis and chemosensitivity to cisplatin in BCa by blocking the WDR5-MLL complex mediating H3K4me3 in target genes. Hence, our findings offer insight into a multipotential anticancer compound, OICR-9429, which enhances the antitumour effect of cisplatin or immunotherapy in BCa.

WD repeat domain 5 promotes chemoresistance and Programmed Death-Ligand 1 expression in prostate cancer.

Purpose: Advanced prostate cancer (PCa) has limited treatment regimens and shows low response to chemotherapy and immunotherapy, leading to poor prognosis. Histone modification is a vital mechanism of gene expression and a promising therapy target. In this study, we characterized WD repeat domain 5 (WDR5), a regulator of histone modification, and explored its potential therapeutic value in PCa. Experimental Design: We characterized specific regulators of histone modification, based on TCGA data. The expression and clinical features of WDR5 were analyzed in two dependent cohorts. The functional role of WDR5 was further investigated with siRNA and OICR-9429, a small molecular antagonist of WDR5, in vitro and in vivo. The mechanism of WDR5 was explored by RNA-sequencing and chromatin immunoprecipitation (ChIP). Results: WDR5 was overexpressed in PCa and associated with advanced clinicopathological features, and predicted poor prognosis. Both inhibition of WDR5 by siRNA and OICR-9429 could reduce proliferation, and increase apoptosis and chemosensitivity to cisplatin in vitro and in vivo. Interestingly, targeting WDR5 by siRNA and OICR-9429 could block IFN-γ-induced PD-L1 expression in PCa cells. Mechanistically, we clarified that some cell cycle, anti-apoptosis, DNA repair and immune related genes, including AURKA, CCNB1, E2F1, PLK1, BIRC5, XRCC2 and PD-L1, were directly regulated by WDR5 and OICR-9429 in H3K4me3 and c-Myc dependent manner. Conclusions: These data revealed that targeting WDR5 suppressed proliferation, enhanced apoptosis, chemosensitivity to cisplatin and immunotherapy in PCa. Therefore, our findings provide insight into OICR-9429 is a multi-potency and promising therapy drug, which improves the antitumor effect of cisplatin or immunotherapy in PCa.

High developmental pluripotency­associated 4 expression promotes cell proliferation and glycolysis, and predicts poor prognosis in non­small­cell lung cancer.

The developmental pluripotency­associated 4 (Dppa4) gene serves critical roles in cell self­renewal, as well as in cancer development and progression. However, the regulatory role of Dppa4 in non­small­cell lung cancer (NSCLC) and its underlying mechanisms remain elusive. The aim of the present study was to investigate the biological function of Dppa4 in NSCLC and its underlying mechanism of action. Dppa4 expression was measured in NSCLC tissue samples and cell lines, and its effect on cell proliferation and the expression of glycolytic enzymes was determined. In addition, the underlying mechanisms of Dppa4­induced alterations in glycolysis were analyzed. Univariate and multivariate analyses were also performed to analyze the prognostic significance of clinicopathological characteristics. Dppa4 was found to be highly expressed in NSCLC tissues and cell lines. Furthermore, it was observed that Dppa4 was correlated with the degree of tumor differentiation and TNM stage. Univariate and multivariate analyses identified Dppa4 expression and clinical stage as prognostic factors for NSCLC patients. Kaplan­Meier analysis further revealed that patients with lower Dppa4 expression exhibited a better prognosis. In NSCLC cells, Dppa4 knockdown inhibited cell proliferation, while Dppa4 overexpression enhanced cell proliferation, which was likely mediated by glycolysis promotion. Dppa4 knockdown had no evident effect on the majority of enzymes examined; however, glucose transporter type 4 (GLUT­4) and pyruvate kinase isozyme M2 were significantly upregulated, and hexokinase II (HK­II) and lactate dehydrogenase B (LDHB) were downregulated following Dppa4 knockdown. By contrast, Dppa4 overexpression resulted in downregulation of GLUT­4, and upregulation of HK­II, enolase and LDHB, whereas it had no effect on other enzymes. Since the most evident effect was observed on LDHB, further functional experiments demonstrated that this enzyme reversed the promoting effects of Dppa4 in NSCLC. In conclusion, Dppa4 promotes NSCLC progression, partly through glycolysis by LDHB. Thus, the Dppa4­LDHB axis critically contributes to glycolysis in NSCLC cells, thereby promoting NSCLC development and progression.

Wuqinxi Qigong as an Alternative Exercise for Improving Risk Factors Associated with Metabolic Syndrome: A Meta-Analysis of Randomized Controlled Trials.

Background: The improvement of living standards has led to increases in the prevalence of hypokinetic diseases. In particular, multifactorial complex diseases, such as metabolic syndrome, are becoming more prevalent. Currently, developing effective methods to combat or prevent metabolic syndrome is of critical public health importance. Thus, we conducted a systematic review to evaluate the existing literature regarding the effects of Wuqinxi exercise on reducing risk factors related to metabolic syndrome. Methods: Both English- and Chinese-language databases were searched for randomized controlled trials investigating the effects of Wuqinxi on these outcomes. Meanwhile, we extracted usable data for computing pooled effect size estimates, along with the random-effects model. Results: The synthesized results showed positive effects of Wuqinxi exercise on systolic blood pressure (SBP, SMD = 0.62, 95% CI 0.38 to 0.85, p < 0.001, I2 = 24.06%), diastolic blood pressure (DBP, SMD = 0.62, 95% CI 0.22 to 1.00, p < 0.001, I2 = 61.28%), total plasma cholesterol (TC, SMD = 0.88, 95% CI 0.41 to 1.36, p < 0.001, I2 = 78.71%), triglyceride (TG, SMD = 0.87, 95% CI 0.49 to 1.24, p < 0.001, I2 = 67.22%), low-density lipoprotein cholesterol (LDL-C, SMD = 1.24, 95% CI 0.76 to 1.72, p < 0.001, I2 = 78.27%), and high-density lipoprotein cholesterol (HDL, SMD = 0.95, 95% CI 0.43 to 1.46, p < 0.001, I2 = 82.27%). In addition, regression results showed that longer-duration Wuqinxi intervention significantly improved DBP (ß = 0.00016, Q = 5.72, df = 1, p = 0.02), TC (ß = -0.00010, Q = 9.03, df = 1, p = 0.01), TG (ß = 0.00012, Q = 6.23, df = 1, p = 0.01), and LDL (ß = 0.00011, Q = 5.52, df = 1, p = 0.02). Conclusions: Wuqinxi may be an effective intervention to alleviate the cardiovascular disease risk factors of metabolic syndrome.

Applied anatomy of the lower cervical pedicle screw insertion / 中华创伤杂志(英文版)

<p><b>OBJECTIVE</b>To ascertain an accurate approach to inserting the pedicle screw into C3-C7 segments of the cervical vertebra.</p><p><b>METHODS</b>Anatomic morphology of lateral mass and pedicle, and their anatomic relationship with the adjacent tissue were observed on C3-C7 segments of 25 adult embalmed cadavers (50 sides).</p><p><b>RESULTS</b>1) The inferior edge of the base of the posterior tubercle of the transverse process and the inferior edge of the pedicle were connected with each other on 25 adult embalmed cadavers (50 sides). The transverse section which passed through the median point between the superior edge and the inferior edge of the base of the posterior tubercle of the transverse process, and the transverse section which passed through the central axis between the superior edge and the inferior edge of the pedicle, were in the same horizontal plane. The superior and inferior position of placing the pedicle screw was determined by this transverse section, which passed through the median point between the superior and the inferior edge of the base of the posterior tubercle of the transverse process. 2) There was a directed internal-downwards "triangular sulcule" between the base of the posterior tubercle of the transverse process and the anterolateral edge of the inferior articular process. The anterior wall of the triangular sulcule was the base of the posterior tubercle of the transverse process, the posterior wall was the anterolateral edge of the inferior articular process, and the bottom of the sulcule was connected with the interior edge of the pedicle. The vertical length between the top of triangle and the planes of inferior edge of the pedicle was (2.78+/-1.71) mm. The inferior edge of the cervical pedicle could be detected using a blunt probe along the "triangular sulcule" between the base of the posterior tubercle of the transverse process and the anterolateral edge of the inferior articular process in surgical operation. 3) The lateral fovea of the articular process was observed on all lateral masses (50 sides). The internal and external position of the entrance point could depend on anatomic landmarks: the lateral edge of the lateral fovea of the articular process. The horizontal length between the lateral fovea of the articular process and the entrance point was (3.14+/-1.45) mm. 4) The diameter of pedicle screw, about (2.78+/-1.71) mm, was the transverse diameter of the cancellous bone of the greatest narrow part of the cervical pedicle.</p><p><b>CONCLUSIONS</b>The median point between the superior edge and the inferior edge of the base of the posterior tubercle of the transverse process, the lateral fovea of the articular process, and the triangular sulcule between the base of the posterior tubercle of the transverse process and the anterolateral edge of inferior articular process, are easy to be exposed and identified in surgical operation. The pedicle screw can be precisely inserted through this method.</p>