Amorphous conversion in pyrolytic symmetric trinuclear nickel clusters trigger trifunctional electrocatalysts.

The pursuit of multifunctional electrocatalysts holds significant importance due to their comprehension of material chemistry. Amorphous materials are particularly appealing, yet they pose challenges in terms of rational design due to their structural disorder and thermal instability. Herein, we propose a strategy that entails the tandem (low-temperature/250-350 °C) pyrolysis of molecular clusters, enabling preservation of the local short-range structures of the precursor Schiff base nickel (Ni3[2(C21H24N3Ni1.5O6)]). The temperature-dependent residuals demonstrate exceptional activity and stability for at least three distinct electrocatalytic processes, including the oxygen evolution reaction (η10 = 197 mV), urea oxidation reaction (η10 = 1.339 V), and methanol oxidation reaction (1358 mA cm-2 at 0.56 V). Three distinct nickel atom motifs are discovered for three efficient electrocatalytic reactions (Ni1 and Ni1' are preferred for UOR/MOR, while Ni2 is preferred for OER). Our discoveries pave the way for the potential development of multifunctional electrocatalysts through disordered engineering in molecular clusters under tandem pyrolysis.

Non-POEMS osteosclerotic multiple myeloma: Clinical characteristics and differential diagnosis.

Osteosclerosis in multiple myeloma (MM) is typically associated with rare POEMS syndrome, characterized by polyneuropathy (P), organomegaly (O), endocrinopathy (E), M-protein (M), and skin changes (S). However, osteosclerosis in multiple myeloma (MM) without POEMS syndrome, defined as non-POEMS Osteosclerotic MM, is exceedingly rare. We report a 70-year-old man with rib pain, remarkably high bone mineral density and diffuse osteosclerosis. The diagnosis of non-POEMS osteosclerotic MM was confirmed by biopsy and aspiration of bone marrow through surgery. A literature review spanning from 1990 identified 12 cases of similar non-POEMS osteosclerotic MM, including 5 males and 7 females with a mean age of 59.7 ± 10.6 years. The non-POEMS osteosclerotic MM can be divided into two subtypes, the osteosclerotic lesion subtype and the diffuse osteosclerosis subtype. Absence of polyneuropathy and organomegaly are the main factors that differentiate non-POEMS osteosclerotic MM from POEMS. A hyperactive osteoblastic process might be the etiology of diffuse osteosclerosis. Further research is needed to understand its etiology and pathophysiology.

KDF1 Promoted Proliferation, Migration and Invasion of Lung Adenocarcinoma Cells through Activating STAT3 and AKT Pathway.

KDF1 has been reported to be correlated with carcinogenesis. However, its role and mechanism are far from clear. To explore the possible role and underlying mechanism of KDF1 in lung adenocarcinoma (LUAD), we investigated KDF1 expression in LUAD tissues and the influence of KDF1 in the phenotype of LUAD cells (A549 and PC-9) as well as the underlying mechanism. Compared to non-tumor lung epithelial cells, KDF1 was upregulated in the cancer cells of the majority of LUAD patients, and its expression was correlated with tumor size. Patients with enhanced KDF1 in cancer cells (compared with paired adjacent non-neoplastic lung epithelial cells) had shorter overall survival than patients with no increased KDF1 in cancer cells. Knockdown of KDF1 inhibited the migration, proliferation and invasion of LUAD cells in vitro. And overexpression of KDF1 increased the growth of the subcutaneous tumors in mice. In terms of molecular mechanisms, overexpression of KDF1 induced the expression of AKT, p-AKT and p-STAT3. In KDF1-overexpressing A549 cells, inhibition of the STAT3 pathway decreased the level of AKT and p-AKT, whereas inhibition of the AKT pathway had no effect on the activation of STAT3. Inhibition of STAT3 or AKT pathways reversed the promoting effects of KDF1 overexpression on the LUAD cell phenotype and STAT3 inhibition appeared to have a better effect. Finally, in the cancer cells of LUAD tumor samples, the KDF1 level was observed to correlate positively with the level of p-STAT3. All these findings suggest that KDF1, which activates STAT3 and the downstream AKT pathway in LUAD, acts as a tumor-promoting factor and may represent a therapeutic target.

Healthcare quality and safety assessment based on annual scorekeeping.

Objective: To explore the practice of medical quality and safety evaluation system based on annual score under the background of establishing modern hospital management system and strengthening national public hospital performance evaluation. Methods: Statistical analysis was used to study the improvement of medical quality and safety in hospitals after the implementation of score evaluation, and the existing problems were analyzed according to the actual situation and related requirements. Results: The hospital's medical quality and safety evaluation system ran smoothly, the evaluation indexes could be implemented, and the evaluation results were used properly. The improvement of hospital medical quality and operation efficiency has achieved good results. Conclusion: The evaluation system of medical quality and safety for physicians and medical technicians based on annual score can achieve the whole process, all-round, personalized and information-based evaluation, and promote the high-quality development of hospitals. It is necessary to further improve the range of evaluation and carry out the evaluation of the evaluation system by relevant personnel.

An inflammation-related signature could predict the prognosis of patients with kidney renal clear cell carcinoma.

Background: Kidney renal clear cell carcinoma (KIRC) is an inflammation-related carcinoma, and inflammation has been recognized as an important factor in inducing carcinogenesis. To further explore the role of inflammation in KIRC, we developed an inflammation-related signature and verified its correlation with the tumor micro-environment. Methods: After the differential inflammation-related prognostic genes were screened by Lasso regression, the inflammation-related signature (IRS) was constructed based on the risk score of multivariate Cox regression. Then, the prognostic value of the IRS was evaluated by Kaplan-Meier analysis, receiver operating characteristic (ROC) curve analysis and multivariate Cox regression. Gene set variation analysis (GSVA) was applied to screen out enriched signaling pathways. Infiltrated immune cells, tumor mutational burden (TMB) and immune checkpoints were explored by CIBERSORTx and maftool. Results: Four genes (TIMP1, PLAUR, CCL22, and IL15RA) were used to construct the IRS in patients with KIRC. Kaplan-Meier analysis and multivariate Cox regression identified that the IRS could independently predict the prognosis of patients with KIRC in the training and validation groups. The diagnostic value of the nomogram increased from 0.811 to 0.845 after adding the IRS to the multiparameter ROC analysis. The GSVA results indicated that IRS was closely related to primary immunodeficiency and antigen processing and presentation. The immune checkpoint LAG3 was highly expressed in patients with high-risk score (p < 0.05), while CD274 (PD-L1) and HAVCR2 were highly expressed in patients with low-risk score (p < 0.001). There was a significant positive correlation between the high-risk score group and CD8+ T, activated CD4+ memory T, gamma and delta regulatory T and M0 macrophage cells, while the low-risk score group was negatively associated with B memory, plasma, resting CD4+ memory T, activated NK, M1 macrophages and resting mast cells. Conclusion: We found that the IRS might serve as a biomarker to predict the survival of KIRC. Moreover, patients with high or low-risk score might be sensitive to immune drugs at different immune checkpoints.

Identification of autophagy-related genes as potential biomarkers for type 1 diabetes mellitus.

Background: Type 1 diabetes mellitus (T1DM) is a metabolic disease in which the autoimmune destruction of pancreatic islet ß-cells occurs. This study sought to investigate the role of autophagy-related genes and immune cells in the development of T1DM. Methods: We acquired the raw gene expression profiles of 302 T1DM and 422 normal control peripheral blood samples from the Gene Expression Omnibus (GEO) database. The differentially expressed genes (DEGs) were identified using the Limma package, and Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were performed. The Search Tool for the Retrieval of Interacting Genes/Proteins (https://string-db.org/) and Cytoscape autophagy genes were intersected with the DEGs for the immune cell analysis and the correlation analysis. Results: A total of 568 DEGs were identified in the T1DM and normal samples, of which 301 were upregulated and 267 were downregulated. The results of the functional and pathway enrichment analyses showed that the DEGs were closely associated with autophagy and immunity. Member RAS oncogene family (RAB11A), protein tyrosine phosphatase non-receptor type 11, lamin A/C, heat shock protein70, heat shock protein family A member 4, cluster of differentiation 8A, caspase 3 (CASP3), exportin 1, proto-oncogene, non-receptor tyrosine kinase, SMAD family member 4, and sirtuin 1 (SIRT1) were located at the center of the protein-protein interaction network as the core genes. The peripheral blood T cells were more elevated in the T1DM subjects than the normal subjects. RAB11A, CASP3, and SIRT1 are autophagy-associated genes. RAB11A and CASP3 were positively correlated with most immune cells, while SIRT1 was negatively correlated with most immune cells. Conclusions: Autophagy-related genes (i.e., RAB11A, CASP3, and SIRT1) and immune cells (i.e., T and B cells) may play important regulatory roles in the development of T1DM. Our findings provide novel insights into and potential targets for T1DM prediction and treatment.

IL-1B can serve as a healing process and is a critical regulator of diabetic foot ulcer.

Background: Diabetic foot ulcer (DFU) is the main cause of disability in diabetic patients. However, the molecular changes underlying the occurrence and progression of DFU remain unclear. We conducted this study to examine gene alterations in different DFU patients. Methods: GSE143735 and GSE134431 transcriptome data sets were acquired from the Gene Expression Omnibus database, and differential expression analyses of the genes in these data sets were performed. A functional enrichment analysis of the differentially expressed genes (DEGs) was performed using clusterProfiler package in R. To examine the correlations between DEGs and significant immune-related genes, we identified the intersecting ulcer-related DEGs, healing-related DEGs, and immune-related DEGs. Finally, we further investigate the relationship between the selected genes with immune cell regulation via a single-sample gene set enrichment analysis, and the infiltration of 28 immune cells in common diabetes samples, unhealed DFU samples, and healed samples DFU were compared. Results: We found 238 upregulated genes and 207 downregulated genes in the diabetic foot (DF) patients with ulcers compared to the DF patients without ulcers, and 74 upregulated genes and 28 downregulated genes in the healed samples compared to the unhealed samples. To examine the main biological functions, we conducted a functional enrichment analysis. The results showed that the biological functions of functional enrichment analysis included neutrophil degranulation, leukocyte chemotaxis, myeloid leukocyte migration, phagosome, cytokine-cytokine receptor interaction, and the chemokine signaling pathway. Interleukin (IL)-1B was more highly expressed in patients with ulcers and healed DFU patients than those without ulcers and unhealed DFU patients. Finally, the immune cell abundance difference results showed that activated cluster of differentiation (CD)8 T cells, central memory CD8 T cells, T follicular helper cells, myeloid-derived suppressor cells, natural killer T cells and monocytes were more highly infiltrated in normal diabetes patients and healed DFU patients than unhealed DFU patients. However, no difference was found between DF patients with and without ulcers. Conclusions: IL-1B is an inflammation gene that can be used to assess and regulate DFU progression.

CPEB3 overexpression caused by miR-106b-5p inhibition inhibits esophageal carcinoma in-vitro progression and metastasis.

This study investigates the role of CPEB3 in esophageal cancer (EC) progression. The prognosis of EC patients was shown by survival analysis. CPEB3-targeting microRNAs were predicted by bioinformatics tools and further validated by dual-luciferase assay and RNA immunoprecipitation. CPEB3 expression in EC cell lines and EC tissues was analyzed by quantitative reverse transcription PCR. The viabilities of KYSE150 and EC9706 cells were measured by MTT and Cell Counting Kit-8 assays. The migration, invasion and tube formation of KYSE150 and EC9706 cells were examined by wound healing, Transwell and tube formation assay, respectively. E-cadherin, N-cadherin, fibronectin, vimentin and vascular endothelial growth factor (VEGF), epidermal growth factor receptor (EGFR) [and phosphorylation (p)] and STAT3 levels (and phosphorylation) in KYSE150 and EC9706 cells were determined by western blot analysis or quantitative reverse transcription PCR. In addition, a xenograft tumor model was established through subcutaneously implanting KYSE150 and EC9706 cells transfected with Lv-CPEB3 or Lv-control viruses. CPEB3 expression was downregulated in EC cells and tissues, and its overexpression inhibited viability, migration, invasion and the expressions of N-cadherin, fibronectin, vimentin and VEGF, EGFR, p-EGFR and p-STAT3 levels in KYSE150 cells, but promoted E-cadherin expression. Small interfering RNA (siRNA)-CPEB3 inversely affected these phenotypes and gene expressions in EC9706 cells. miR-106b-5p targeted CPEB3 and negatively regulated CPEB3 expression. miR-106b-5p mimics reversed the effect of CPEB3 overexpression on KYSE150 cells, and miR-106b-5p inhibitor reversed the effect of siRNA-CPEB3 on EC9706 cells. In mice, tumor volumes, weights and Ki-67 expression were lower in mice treated with Lv-CPEB3 than that with Lv-control. CPEB3 overexpressed by miR-106b-5p inhibition suppressed EC progression involved in EGFR and STAT3 signaling.

The Significance of INHBE Expression in the Cancer Cells of Clear-Cell Renal Cell Carcinoma.

BACKGROUND: Activins and inhibins are structurally related dimeric glycoprotein hormones belonging to the transforming growth factor-ß superfamily but whether they are also involved in malignancy is far from clear. No study has reported the expression of INHBE in kidney cancer. The purpose of this study was to examine the expressions of INHBE in the tumor tissue of patients with clear-cell renal cell carcinoma (ccRCC) and to explore the pathologic significance. METHODS: The INHBE mRNA expression in the tumor tissue of ccRCC patients was analyzed by using RNA sequencing data from the TCGA database. To examine the expression of inhibin ßE protein, 241 ccRCC patients were recruited and immunohistochemistry was performed on the tumor tissue of these patients along with 39 normal renal samples. The association between the inhibin ßE expression level and patient's clinicopathological indices was evaluated. RESULTS: In the normal renal tissue, inhibin ßE was found to be expressed mainly by renal tubular epithelial cells. In the tumor tissue, inhibin ßE was expressed mainly in cancer cells. The expressions of INHBE mRNA and protein in the tumor tissue of ccRCC patients increased significantly compared with those in normal renal samples. There was a significant correlation between the level of inhibin ßE in the tumor tissue and tumor grade. Patients with a lower inhibin ßE expression in the tumor tissue were found to have a longer overall survival and disease-specific survival. CONCLUSIONS: INHBE might be involved in the pathogenesis of ccRCC and function as a tumor promoter.

KDF1, a Novel Tumor Suppressor in Clear Cell Renal Cell Carcinoma.

KDF1 has been identified as a key regulator of epidermal proliferation and differentiation, but it is unknown whether KDF1 is involved in the pathogenesis of malignancy. No study has reported the expression and function of KDF1 in renal cancer. To explore the pathologic significance of KDF1 in clear cell renal cell carcinoma (ccRCC), the expression level of KDF1 protein in the tumor tissue of ccRCC patients was examined by immunohistochemistry and Western blot while the expression level of KDF1 mRNA was analyzed by using the data from TCGA database. In vitro cell experiments and allogeneic tumor transplantation tests were performed to determine the effects of altered KDF1 expression on the phenotype of ccRCC cells. Both the KDF1 mRNA and protein were found to be decreasingly expressed in the tumor tissue of ccRCC patients when compared with the adjacent non-tumor control tissue. The expression level of KDF1 in the tumor tissue was found to correlate negatively with the tumor grade. Patients with higher KDF1 in the tumor tissue were found to have longer overall survival and disease-specific survival time. KDF1 was shown to be an independent factor influencing the disease-specific survival of the ccRCC patients. Overexpression of KDF1 was found to inhibit the proliferation, migration and invasion of ccRCC cells, which could be reversed by decreasing the expression of KDF1 again. ccRCC cells with KDF1 overexpression were found to produce smaller transgrafted tumors. These results support the idea that KDF1 is involved in ccRCC and may function as a tumor suppressor.

High SEC61G expression predicts poor prognosis in patients with Head and Neck Squamous Cell Carcinomas.

Background: Overexpression of the membrane protein SEC61 translocon gamma subunit (SEC61G) has been observed in a variety of cancers; however, its role in head and neck squamous cell carcinomas (HNSCC) is unknown. This study aimed to elucidate the relationship between SEC61G and HNSCC based on data from The Cancer Genome Atlas (TCGA) database. Methods: Data for HNSCC patients were collected from TCGA and the expression level of SEC61G was compared between paired HNSCC and normal tissues using the Wilcoxon rank-sum test. The relationship between clinicopathologic features and SEC61G expression was also analyzed using the Wilcoxon rank-sum test and logistic regression. Receiver operating characteristic (ROC) curves were generated to evaluate the value of SEC61G as a binary classifier using the area under the curve (AUC value). The association of clinicopathologic characteristics with prognosis in HNSCC patients was assessed using Cox regression and the Kaplan-Meier methods. A nomogram, based on Cox multivariate analysis, was used to predict the impact of SEC61G on prognosis. Functional enrichment analysis was performed to determine the hallmark pathways associated with differentially expressed genes in HNSCC patients exhibiting high and low SEC61G expression. Results: The expression of SEC61G was significantly elevated in HNSCC tissues compared to normal tissues (P < 0.001). The high expression of SEC61G was significantly correlated with the T stage, M stage, clinical stage, TP53 mutation status, PIK3CA mutation status, primary therapy outcome, and cervical lymph node dissection (all P < 0.05). Meanwhile, ROC curves suggested the significant diagnostic ability of SEC61G for HNSCC (AUC = 0.923). Kaplan-Meier survival analysis showed that patients with HNSCC characterized by high SEC61G expression had a poorer prognosis than patients with low SEC61G expression (hazard ratio = 1.95, 95% confidence interval 1.48-2.56, P < 0.001). Univariate and multivariate analyses revealed that SEC61G was independently associated with overall survival (P = 0.027). Functional annotations indicated that SEC61G is involved in pathways related to translation and regulation of SLITs/ROBOs expression, SRP-dependent co-translational protein targeting to the membrane, nonsense-mediated decay, oxidative phosphorylation, and Parkinson's disease. Conclusion: SEC61G plays a vital role in HNSCC progression and prognosis; it may, therefore, serve as an effective biomarker for the prediction of patient survival.

Aptamer-Regulated Gold Nanosol Plasmonic SERS/RRS Dimode Assay of Trace Organic Pollutants Based on TpPa-Loaded PdNC Catalytic Amplification.

As with excellent catalytic performance, palladium nanoclusters (PdNCs) have a wide range of applications. However, the traditional PdNCs are easy to agglomerate in the analysis system and lose their catalytic activity. A covalent organic framework (COF) has a definite structure, good stability, and easy surface functionalization. So, it is of great significance to develop stable PdNCs with high catalytic activity and then combine with advanced analysis techniques to analyze ultratrace small-molecule pollutants in the environment. In this research, a stable PdNC dispersed on a COF (PdTpPa) catalyst is prepared and we find it with strong catalysis for the NaH2PO2-HAuCl4 catalytic reaction. Furthermore, this nanocatalytic indicator reaction can be tracked by surface-enhanced Raman spectroscopy (SERS) and resonance Rayleigh scattering (RRS) dual-mode. Combined with a highly specific aptamer-modifying technique, a highly sensitive and selective SERS/RRS dimode assay platform for trace organic pollutants has been developed. The detection limits of oxytetracycline (OTC), glyphosate (GLY), tetracycline (TEC), and bisphenol A (BPA) are 0.64, 0.03, 6.2 × 10-3, and 0.53 × 10-3 ng/mL, respectively. This work also provides ideas for the application of COF materials and Pd nanocatalysts in the molecular spectral detection of trace pollutants.

Metallothionein 1M suppresses tumorigenesis in hepatocellular carcinoma.

Members of the metallothionein (MT) family are involved in metal detoxifcation and in the protection of cells against certain electrophilic carcinogens. In present study, it was found that MT1M was downregulated in more than 77.1% (91/118) of hepatocellular carcinoma (HCC) tissues compared with adjacent non-tumor tissues. Furthermore, overexpression of MT1M inhibited cell viability, colony formation, cell migration and invasion in HCC cell lines and tumor cell growth in xenograft nude mice, and activated cell apoptosis in HCC cell lines. In addition, immunohistochemistry analysis showed MT1M was negative or weak staining in tumor tissues but moderate or strong staining in adjacent non-tumor tissues. The sensitivity and specificity of MT1M for HCC diagnosis were 76.27% and 89.83%, respectively. In conclusion, MT1M was identified as a potential tumor marker for HCC and may serve as a useful therapeutic agent for HCC gene therapy.

The efficacy of thalidomide on preventing and treating radiation-induced oral mucosi-tis in nasopharyngeal carcinoma / 中国肿瘤临床

Objective:To evaluate the efficacy and safety of thalidomide on preventing and treating radiation-induced oral mucositis (RIOM) in nasopharyngeal carcinoma (NPC). Methods:A total of 60 patients with NPC were randomly divided into treatment group and control group. The treatment group took thalidomide and gargled with mixture of saline+gentamycin+dexamethasone when ra-diotherapy started, and the control group gargled only with mixture of saline+gentamycin+dexamethasone. The time of occurrence and degree of RIOM in both groups were registered at the same time. Results:The incidence of RIOM in treatment group was lower than that in control group (P<0.05). For the incidence of 3 or 4 grade RIOM, the treatment group was also lower than the control group. No statistical difference in terms of objective response rate was found between the two groups (P>0.05). There was no statisti-cally significant difference between the treatment group and the control group in the oral average dose, V30, V35, V40, V45, V50, and V54 (P>0.05). There was no statistically significant difference between the treatment group and the control group in the use of nutri-tion agents, hormones and antibiotics (P>0.05). There was no statistical difference between the groups in the drowsiness, peripheral nerve toxicity, hematologic toxicity and gastrointestinal reaction (P>0.05). Conclusion:Thalidomide can reduce the incidence and se-verity of RIOM for radiotherapy of patients with NPC, which deserves clinic application.

Expression and prognostic role of MEKK3 and pERK in patients with renal clear cell carcinoma.

Mitogen-activated protein kinase/extracellular signal-regulated kinase kinase kinase 3 (MEKK3) is an important serine/threonine protein kinase and a member of the MAPK family. MEKK3 can effectively activate the MEK/ERK signaling pathway and promote an autocrine growth loop critical for tumor genesis, cell proliferation, terminal differentiation, apoptosis and survival. To explore the relationship between MEKK3 and cell apoptosis, clinicopathology and prognosis, we characterize the expression of MEKK3, pERK and FoxP3 in the renal clear cell carcinoma (RCCC). Protein expression was detected by tissue microarray and immunochemistry in 46 cases of RCCC and 28 control cases. Expression levels of CD3+ ,CD3+CD4+,CD3+CD8+,CD4+CD25+, CD4+CD25+ FoxP3+ were assessed by flow cytometry and analyzed for their association with pathological factors, correlation and prognosis in RCCC. Expression of MEKK3, pERK and FoxP3 was significantly up-regulated in RCCC as compared to control levels (p<0.01), associated with pathological grade (p<0.05)and clinical stage (p<0.05). CD4+CD25+ Foxp3+ Treg cells were also significantly increased in RCCC patients (p<0.05). Cox multivariate regression analysis showed that MEKK3, pERK expression and patholigical stage were independent prognostic factors in patients with RCCC (p<0.05). MEKK3 can be used as an important marker of early diagnosis and prognostic evaluation in RCCC. It may be associated with imbalance of anti-tumor immunity and overexpression of pERK. Expression of MEKK3 and pERK are significantly increased in RCCC, with protein expression and clinical stage acting as independent prognostic factors.

MEKK3 and survivin expression in cervical cancer: association with clinicopathological factors and prognosis.

Mitogen-activated protein kinase/extracellular signal-regulated kinase kinase kinase 3 (MEKK3) is an important protein kinase and a member of the MAPK family, which regulates cellular responses to environmental stress and serves as key integration points along the signal transduction cascade that not only link diverse extracellular stimuli to subsequent signaling molecules but also amplify the initiating signals to ultimately activate effector molecules and induce cell proliferation, differentiation and survival. To explore the relationship between MEKK3 and cell apoptosis, clinicopathology and prognosis, we characterize the expression of MEKK3 and survivin in cervical cancer. MEKK3 and survivin expression was measured by RT-PCR and Western blotting of fresh surgical resections from 30 cases of cervical cancer and 25 cases of chronic cervicitis. Protein expression was detected by tissue microarray and immunochemistry (En Vision) in 107 cases of cervical cancer, 86 cases of cervical intraepithelial neoplasia (CIN), and 35 cases of chronic cervicitis. Expression patterns were analyzed for their association with clinicopathological factors and prognosis in cervical cancer. Expression of MEKK3 and survivin mRNA was significantly higher in cervical cancer than in the controls (p<0.05). MEKK3 and survivin expression differed significantly between cervical carcinoma, CIN, and cervicitis (p<0.05) and correlated with clinical stage, infiltration depth, and lymph node metastasis (p<0.05). MEKK3 expression was positively correlated with survivin (p<0.05). Kaplan-Meier survival analysis showed that MEKK3 and survivin expression, lymph node metastasis, depth of invasion, and FIGO stage reduce cumulative survival. Cox multivariate regression analysis showed that MEKK3, survivin, and clinical staging are independent prognostic factors in cervical cancer (p<0.05). Expression of MEKK3 and survivin are significantly increased in cervical cancer, their overexpression participating in the occurrence and development of cervical cancer, with protein expression and clinical staging acting as independent prognostic factors for patients with cervical cancer.

Expression and function analysis of mitotic checkpoint genes identifies TTK as a potential therapeutic target for human hepatocellular carcinoma.

The mitotic spindle checkpoint (SAC) genes have been considered targets of anticancer therapies. Here, we sought to identify the attractive mitotic spindle checkpoint genes appropriate for human hepatocellular carcinoma (HCC) therapies. Through expression profile analysis of 137 selected mitotic spindle checkpoint genes in the publicly available microarray datasets, we showed that 13 genes were dramatically up-regulated in HCC tissues compared to normal livers and adjacent non-tumor tissues. A role of the 13 genes in proliferation was evaluated by knocking them down via small interfering RNA (siRNA) in HCC cells. As a result, several mitotic spindle checkpoint genes were required for maintaining the proliferation of HCC cells, demonstrated by cell viability assay and soft agar colony formation assay. Then we established sorafenib-resistant sublines of HCC cell lines Huh7 and HepG2. Intriguingly, increased TTK expression was significantly associated with acquired sorafenib-resistance in Huh7, HepG2 cells. More importantly, TTK was observably up-regulated in 46 (86.8%) of 53 HCC specimens. A series of in vitro and in vivo functional experiment assays showed that TTK overexpression promoted cell proliferation, anchor-dependent colony formation and resistance to sorafenib of HCC cells; TTK knockdown restrained cell growth, soft agar colony formation and resistance to sorafenib of HCC cells. Collectively, TTK plays an important role in proliferation and sorafenib resistance and could act as a potential therapeutic target for human hepatocellular carcinoma.

Prevalence survey on pterygium among people aged 40 and above in Hengli Town of Dongguan / 国际眼科杂志(Guoji Yanke Zazhi)

AlM:To investigate the prevalence of pterygium of the household population aged 40 and above in Hengli Town of Dongguan. METHODS: Using the method of cluster random sampling, select 3 628 people aged 40 and above in four villages and one community for visual examination, intraocular pressure check, slit lamp examination and questionnaire. RESULTS: The actual number of subjects was 3 393 people, and examination rate was 93. 52%. We detected 843 patients with pterygium. The prevalence of pterygium was 24. 85%. CONCLUSlON:There is high prevalence of pterygium in Dongguan area. The prevalence of pterygium is related with age and working environment, but has no relation with gender.

Sarcomatoid thymic carcinoma arising in metaplastic thymoma: a case report.

Metaplastic thymoma is an extremely rare tumor. To date, only 17 cases of metaplastic thymoma have been reported. To the best of the authors' knowledge, this is the second reported case of a sarcomatoid carcinoma arising in metaplastic thymoma; the carcinoma in this case is larger than that in the previous case. A 63-year-old woman with cough and asthenia for 2 weeks was admitted to the hospital. Computed tomography (CT) revealed a giant mass on the right side of the front mediastinum medium. The mediastinal tumor was excised, and additional pathological examinations, immunohistochemical tests, and electron-microscopic tests were performed. The tumor was diagnosed as a sarcomatoid carcinoma arising in metaplastic thymoma. Here, the authors discuss the clinical pathology of the sarcomatoid carcinoma arising in metaplastic thymoma and describe the biological behaviors with respect to the pathological features.