Association between advanced lung cancer inflammation index and all-cause and cardiovascular mortality among stroke patients: NHANES, 1999-2018.

Background: Stroke was a major global public health challenge, and its prognosis was remarkably associated with inflammation levels and nutritional status. The advanced lung cancer inflammation index (ALI) was a comprehensive indicator that combined inflammation and nutritional status. Currently, the relationship between ALI and the prognosis of stroke patients was not yet known. The purpose of the current study was to estimate their relationship. Methods: Cohort data from the National Health and Nutrition Examination Survey (NHANES) 1999-2018 were collected. The association between ALI and all-cause and cardiovascular disease (CVD) mortality in stroke patients was estimated using a multivariable adjusted Cox model. Their non-linear relationship was analyzed by restricted cubic spline analysis. Sensitivity analysis was constructed through stratified analysis and interaction analysis. Results: 1,440 stroke patients were included in this study. An elevated ALI was significantly related to a reduced risk of all-cause mortality in stroke patients but not related to CVD mortality. A reverse J-shaped non-linear association between ALI and all-cause mortality in stroke patients, with an inflection point at 83.76 (the lowest of the mortality risk). On the left side of the inflection point, for each 10 U increase in ALI, there was a 16% reduction in the risk of all-cause mortality. However, on the right side, the risk increased by 6%. There was no remarkable interaction between stratified variables and ALI. Conclusion: This was the first study on the relationship between ALI and all-cause and CVD mortality in stroke patients. Elevated ALI was closely associated with a reduced risk of all-cause mortality. A reverse J-shaped non-linear relationship existed between the two, with an inflection point at 83.76. These findings implied that controlling the ALI of stroke patients within an appropriate range was crucial for their prognosis (such as weight management, albumin supplementation, anti-inflammatory treatment). The dynamic variation in ALI was also advantageous for clinicians in establishing personalized ALI criteria to maximize the long-term survival of stroke patients.

NEDD1 overexpression increases cell proliferation, tumor immune escape, and drug resistance in LUAD.

Background: Neural Precursor Cell Expressed Developmentally Down-Regulated Protein 1 (NEDD1) serves as a crucial factor in promoting cellular mitosis by directly facilitating wheel assembly and daughter centriole biogenesis at the lateral site of parent centrioles, ultimately driving centrosome replication. The amplification of centrosomes and the abnormal expression of centrosome-associated proteins contribute to the invasion and metastasis of non-small cell lung cancer cells. However, the specific mechanism by which NEDD1 contributes to the progression of lung adenocarcinoma (LUAD) remains unexplored. Therefore, the objective of this study is to uncover the role played by NEDD1 in LUAD. Methods: To verify the expression of NEDD1 in pan-carcinoma. The feasibility of NEDD1 as a prognostic marker for LUAD in TCGA and GEO databases was verified. Subsequently, Cox proportional hazard regression analysis was used to screen the prognostic factors of LUAD, so as to analyze the correlation between prognostic factors and NEDD1 expression. For another, NEDD1-related genes were screened for pathway enrichment analysis to verify their possible functions. In addition, the expression of NEDD1 in LUAD was verified by qPCR and IHC, then siRNA was used to construct NEDD1-knocked lung cancer cells for subsequent cytobehavioral experiments. Finally, the distribution of NEDD1 in single-cell samples was revealed, and then the correlation between its overexpression and LUAD immune escape and drug resistance was analyzed. Results: LUAD exhibits upregulation of NEDD1, which in turn promotes the proliferation, migration, invasion, and epithelial-mesenchymal transition of lung cancer cells, thereby contributing to a poor prognosis. Furthermore, the overexpression of NEDD1 is closely associated with immune escape and drug resistance in LUAD. Conclusion: NEDD1 serves as a reliable prognostic marker for LUAD, and its upregulation is associated with increased immune escape and drug resistance. Given these findings, NEDD1 holds potential as a novel therapeutic target for the treatment of LUAD.

Astragaloside IV promotes exosome secretion of endothelial progenitor cells to regulate PI3KR2/SPRED1 signaling and inhibit pyroptosis of diabetic endothelial cells.

BACKGROUND AIMS: Treating chronic non-healing diabetic wounds and achieving complete skin regeneration has always been a critical clinical challenge. METHODS: In order to address this issue, researchers conducted a study aiming to investigate the role of miR-126-3p in regulating the downstream gene PIK3R2 and promoting diabetic wound repair in endothelial progenitor cell (EPC)-derived extracellular vesicles. The study involved culturing EPCs with astragaloside IV, transfecting them with miR-126-3p inhibitor or mock plasmid, interfering with high glucose-induced damage in human umbilical vein endothelial cells (HUVECs) and treating diabetic skin wounds in rats. RESULTS: The healing of rat skin wounds was observed through histological staining. The results revealed that treatment with miR-126-3p-overexpressing EPC-derived extracellular vesicles accelerated the healing of rat skin wounds and resulted in better tissue repair with slower scar formation. In addition, the transfer of EPC-derived extracellular vesicles with high expression of miR-126-3p to high glucose-damaged HUVECs increased their proliferation and invasion, reduced necrotic and apoptotic cell numbers and improved tube formation. In this process, the expression of angiogenic factors vascular endothelial growth factor (VEGF)A, VEGFB, VEGFC, basic fibroblast growth factor and Ang-1 significantly increased, whereas the expression of caspase-1, NRLP3, interleukin-1ß, inteleukin-18, PIK3R2 and SPRED1 was suppressed. Furthermore, miR-126-3p was able to target and inhibit the expression of the PIK3R2 gene, thereby restoring the proliferation and migration ability of high glucose-damaged HUVEC. CONCLUSIONS: In summary, these research findings demonstrate the important role of miR-126-3p in regulating downstream genes and promoting diabetic wound repair, providing a new approach for treating chronic non-healing diabetic wounds.

lncRNA CERS6-AS1 upregulates the expression of ANLN by sponging miR-424-5p to promote the progression and drug resistance of lung adenocarcinoma.

Long non-coding RNAs (lncRNAs) play a crucial role in tumor generation and progression. However, the exact functional significance and underlying molecular mechanism by which lncRNA CERS6-AS1 operates in the context of lung adenocarcinoma (LUAD) remain unknown. We aimed to evaluate the potential role of the CERS6-AS1/miR-424-5p/ANLN axis in the progression of LUAD through bioinformatics and cytobehavioral experiments, and to provide a new insight into the combined treatment of LUAD. Based on the TCGA database, the expression of CERS6-AS1 in pan-cancer was evaluated, and its prognostic performance in LUAD was evaluated by ROC curve, survival curve and COX analysis. In addition, quantification of CERS6-AS1 expression levels in LUAD patients and lung cancer cells using quantitative real-time polymerase chain reaction (RT-qPCR), and further validate the functional significance of CERS6-AS1 in promoting the proliferation, migration, and invasion abilities of lung cancer cells. The competitive endogenous RNA (ceRNA) network was constructed, and miR-424-5p inhibitors were applied to CERS6-AS1 knockdown cells. The potential downstream genes associated with the regulatory axis of CERS6-AS1/miR-424-5p were analyzed by PPI network and gene enrichment analysis (KEGG). Finally, we evaluated the prognostic value of high expression of ANLN in LUAD and its effects on immune cell infiltration, tumor mutation burden, chemotherapy response, and immunotherapy. CERS6-AS1 expression was significantly elevated in both LUAD patients and lung cancer cells. In the CERS6-AS1 knockdown assay, the proliferation, invasion, migration and epithelial-mesenchymal transformation (EMT) of cancer cells were significantly inhibited. Notably, there was a prominent upregulation of miR-424-5p expression in cells where CERS6-AS1 was knocked down. Co-transfection of siRNA and miR-424-5p inhibitors into lung cancer cells restored the restriction on lung cancer cells. Anillin (ANLN) has been identified as a potential target gene for miR-424-5p and as a prognostic and immune biomarker associated with immune cell infiltration and tumor mutational burden in LUAD. Additionally, ANLN impacts the efficacy of chemotherapy and immunotherapy in LUAD patients. This study reveals a novel regulatory mechanism in which CERS6-AS1 may contribute to the progression of LUAD by influencing the expression of ANLN as a competitive sponge for miR-424-5p.

3 L split-dose polyethylene glycol is superior to 2 L polyethylene glycol in colonoscopic bowel preparation in relatively high-BMI (≥ 24 kg/m2) individuals: a multicenter randomized controlled trial.

BACKGROUND: Whether body mass index (BMI) is a risk factor for poor bowel preparation is controversial, and the optimal bowel preparation regimen for people with a high BMI is unclear. METHODS: We prospectively included 710 individuals with high BMIs (≥ 24 kg/m2) who were scheduled to undergo colonoscopy from January to November 2021 at 7 hospitals. Participants were randomly allocated into 3 L split-dose polyethylene glycol (PEG) group (n=353) and 2 L PEG group (n=357). The primary outcome was the rate of adequate bowel preparation, and the secondary outcomes included Boston Bowel Preparation Scale (BBPS) score, polyp detection rate, cecal intubation rate, and adverse reactions during bowel preparation. Furthermore, we did exploratory subgroup analyses for adequate bowel preparation. RESULTS: After enrollment, 15 individuals didn't undergo colonoscopy, finally 345 participants took 3 L split-dose PEG regimen, and 350 participants took 2 L PEG regimen for colonoscopic bowel preparation. 3 L split-dose PEG regimen was superior to 2 L PEG regimen in the rate of adequate bowel preparation (81.2% vs. 74.9%, P = 0.045), BBPS score (6.71±1.15 vs. 6.37±1.31, P < 0.001), and the rate of polyp detection (62.0% vs. 52.9%, P = 0.015). The cecal intubation rate was similar in both groups (99.7%). Regarding adverse reactions, individuals were more likely to feel nausea in the 3 L PEG group (30.9% vs. 19.3%; P = 0.001); however, the degree was mild. In the subgroup analysis for adequate bowel preparation, 3 L split-dose PEG regimen performed better than 2 L PEG regimen in the overweight (BMI 25-29.9 kg/m2 ) (P = 0.006) and individuals with constipation (P = 0.044), while no significant differences were observed in relatively normal (BMI 24-24.9 kg/m2) (P = 0.593) and obese individuals (BMI ≥ 30 kg/m2) (P = 0.715). CONCLUSIONS: 3 L split-dose PEG regimen is superior to 2 L PEG regimen for colonoscopic Bowel Preparation in relatively high-BMI individuals, especially overweight individuals (BMI 25-29.9 kg/m2 ). TRIAL REGISTRATION: This trial was registered in the Chinese Clinical Trials Registry (ChiCTR2000039068). The date of first registration, 15/10/2020, http://www.chictr.org.cn.

A Risk Model for Prognosis and Treatment Response Prediction in Colon Adenocarcinoma Based on Genes Associated with the Characteristics of the Epithelial-Mesenchymal Transition.

The epithelial-mesenchymal transition (EMT) is an important process during metastasis in various tumors, including colorectal cancer (CRC). Thus, the study of its characteristics and related genes is of great significance for CRC treatment. In this study, 26 EMT-related gene sets were used to score each sample from The Cancer Genome Atlas program (TCGA) colon adenocarcinoma (COAD) database. Based on the 26 EMT enrichment scores for each sample, we performed unsupervised cluster analysis and classified the TCGA-COAD samples into three EMT clusters. Then, weighted gene co-expression network analysis (WGCNA) was used to investigate the gene modules that were significantly associated with these three EMT clusters. Two gene modules that were strongly positively correlated with the EMT cluster 2 (worst prognosis) were subjected to Cox regression and least absolute shrinkage and selection operator (LASSO) regression analysis. Then, a prognosis-related risk model composed of three hub genes GPRC5B, LSAMP, and PDGFRA was established. The TCGA rectal adenocarcinoma (READ) dataset and a CRC dataset from the Gene Expression Omnibus (GEO) were used as the validation sets. A novel nomogram that incorporated the risk model and clinicopathological features was developed to predict the clinical outcomes of the COAD patients. The risk model served as an independent prognostic factor. It showed good predictive power for overall survival (OS), immunotherapy efficacy, and drug sensitivity in the COAD patients. Our study provides a comprehensive evaluation of the clinical relevance of this three-gene risk model for COAD patients and a deeper understanding of the role of EMT-related genes in COAD.

Digital radio-over-fiber system based on differential pulse code modulation and space division multiplexing.

In this paper, we present and experimentally demonstrate a digital-radio-over-fiber (D-RoF) architecture based on differential pulse code modulation (DPCM) and space division multiplexing (SDM). At low quantization resolution, DPCM can effectively reduce quantization noise and obtain significant signal-to-quantization noise ratio (SQNR) gain. We experimentally study the 7-core and 8-core multicore fiber transmission of 64-ary quadrature amplitude modulation (64QAM) orthogonal frequency division multiplexing (OFDM) signals with a bandwidth of 100 MHz in a fiber-wireless hybrid transmission link. Compared to PCM-based D-RoF, the error vector magnitude (EVM) performance in the DPCM-based D-RoF is effectively improved when the quantization bits (QBs) are 3-5 bits. In particular, when the QB is 3 bits, the EVM of the DPCM-based D-RoF is 6.5% and 7% lower than that of the PCM-based system in 7-core- and 8-core-multicore fiber-wireless hybrid transmission links, respectively.

Requiring Reconsideration of Differences of Aeromonas Infections Between Extra-Intestinal and Intestinal in Hospitalized Patients.

Purpose: The purpose of this study is to examine the variations between extra-intestinal and intestinal infections of Aeromonas in terms of strain types, risk factors, drug susceptibility results, and the distribution of drug resistance and virulence genes. Patients and Methods: A total of 188 Aeromonas strains were identified to the species level using housekeeping genes (rpoD, gyrB, and gyrA). The risk factors for Aeromonas extra-intestinal and intestinal infection, as well as mortality, were retrospectively examined in this study. The broth microdilution method was used to investigate the antimicrobial susceptibility profiles. Touchdown polymerase chain reaction (PCR) assays and DNA sequencing were employed to confirm virulence and the presence of drug resistance genes. Results: The housekeeping genes identified 188 strains into 7 species. Extra-intestinal isolates generally contained A. caviae and A. hydrophila, while intestinal were A. veronii (p=0.0001). Extra-intestinal infections (158/188) were the main type and accounted for 24/27 of all fatalities. Malignant tumors, hepatobiliary diseases, anemia, and hypoproteinemia were linked to infections. Poor results were associated with septic shock. Using the broth microdilution method, over 80% isolates were susceptible to most antimicrobials, except for ceftazidime (79.8%) and ceftriaxone (69.7%). Except for imipenem, intestinal strains were more susceptible to other medications than extra-intestinal. Using touch-down polymerase chain reaction testing and DNA sequencing, 6 strains, 31 strains, and a strain only had bla TEM, bla CphA, and bla VIM, respectively. Two Aeromonas hydrophila each possessed bla CphA+ bla CTXM-M-9, and bla CphA + bla CTX-M-1 + bla CTX-M-15-like + bla TEM; two Aeromonas caviae each possessed bla NDM + bla CTX-M-1 +bla CTX-M-15-like + bla TEM, and bla NDM + bla TEM. Thirty-four of the 42 strains mentioned above were isolated from extra-intestinal. Act, aexT, and ascF-G, were in intestinal more frequently, but alt, hlyA, ela, and lip were in extra-intestinal more frequently. Conclusion: Aeromonas inside and outside intestinal differed in their clinical characteristics, drug susceptibility, drug resistance and virulence genes.

LncRNA PCAT6 promotes proliferation, migration, invasion, and epithelial-mesenchymal transition of lung adenocarcinoma cell by targeting miR-545-3p.

BACKGROUND: Lung cancer is a high incidence cancer on a worldwide basis and has become a major public health problem. Lung adenocarcinoma (LUAD) makes up approximately half of all lung cancers and is a threat to human health. Long non-coding RNAs (lncRNAs) is an important regulator of the development and progression of lung adenocarcinoma. In this manuscript we examined the role and potential mechanism of lncRNA PCAT6 in the development of LUAD. METHODS AND RESULTS: Differences in lncRNA PCAT6 levels between LUAD samples and normal samples were first explored in the GEPIA database. We found that lncRNA PCAT6 expression was elevated, which was also validated in lung adenocarcinoma tissues and cell lines. Using western blotting, CCK-8, EdU, wound healing and transwell assays, we found that knockdown of lncRNA PCAT6 inhibited EMT, proliferation, migration, and invasion of LUAD cells. We noted a predicted a binding site for lncRNA PCAT6 and miR-545-3p through conducting bioinformatic analyses, and their binding was subsequently verified by a dual-luciferase reporter assay. Rescue experiments confirmed that miR-545-3p inhibitor partially abolished the inhibition function of lncRNA PCAT6 knockdown on LUAD cells. In addition, we predicted the downstream target genes of miR-545-3p and verified them by RT-qPCR. We found that EGFR was reduced in the silence of lncRNA PCAT6 and upregulated after miR-545-3p inhibition. CONCLUSION: This study demonstrates that lncRNA PCAT6 promotes a more aggressive LUAD phenotype by sponging miR-545-3p. This finding may provide new ideas for the treatment of lung cancer.

Accurate Identification and Virulence Detection of Aeromonas: a Single-Center Retrospective Study on the Clinical Features and Outcomes Associated with Aeromonas Bacteremia in Southwestern China.

In this study, Aeromonas spp. were re-identified, and the clinical aspects associated with Aeromonas bacteremia, as well as drug resistance and virulence genes, were elucidated. A total of 188 isolates were classified into 7 Aeromonas spp. using housekeeping gene sequencing, which was the standard to assess the accuracy of the VITEK MALDI-TOF system and the VITEK2 Compact system. The VITEK MS system and housekeeping gene sequencing had a 39.89% clear coincidence rate, whereas the VITEK2 Compact system and the standard had a 2.13% coincidence rate. Aeromonas bacteremia was associated with septic shock, hematologic malignancy, and post-hepatitic cirrhosis. Hematological malignancy, hypoproteinemia, systemic steroid use, central venous catheterization, and virulence genes act and ast were linked to poor outcomes. Aeromonas bacteremia had a 37.5% mortality rate; however, differences in mortality rates among Aeromonas spp. were observed. According to the broth microdilution method, over 90% of isolates were sensitive to most antimicrobials, except ceftriaxone (83.33%) and imipenem (83.33%). Polymerase chain reaction and DNA sequencing verified the presence of drug resistance genes; blaCphA was detected in 3 isolates, while blaNDM-1 was found in one isolate. In summary, common methods for identifying Aeromonas spp. are ineffective. Immunocompromised patients have a higher risk of infection and mortality. Furthermore, carbapenem resistance is a serious problem.

Long non-coding RNA FAM83A antisense RNA 1 (lncRNA FAM83A-AS1) targets microRNA-141-3p to regulate lung adenocarcinoma cell proliferation, migration, invasion, and epithelial-mesenchymal transition progression.

The current paper investigates how long non-coding RNA (lncRNA) FAM83A antisense RNA 1 (lncRNA FAM83A-AS1) affected the epithelial-mesenchymal transformation (EMT), growth, invasion and migration of lung adenocarcinoma (LUAD) via targeting miRNA-141-3p. The GEPIA and ENCORI databases were used to analyze differences in lncRNA FAM83A-AS1 levels within LUAD samples. FAM83A-AS1 and miR-141-3p levels were assessed using qRT-PCR among 30 LUAD samples and surrounding normal tissues. In addition, we analyzed how FAM83A-AS1 affected proliferation, invasion, migration, and EMT processes of LUAD cells by targeting miR-141-3p through EdU, CCK-8 assay, scratch assay, transwell migration and invasion assay, immunofluorescence (IF) staining and WB assay. MicroRNAs targeting FAM83A-AS1 were screened using AnnoLnc2 and identified by RT-qPCR. Dual-luciferase assays were utilized to evaluate the connection between FAM83A-AS1 and miR-141-3p. FAM83A-AS1 expression was remarkably raised in lung cancer cells and tissue samples; however, miR-141-3p level markedly reduced relative to healthy samples. FAM83A-AS1 silencing suppressed EMT, growth, invasion and migration of LUAD cells. MiR-141-3p was the possible FAM83A-AS1 binding target negatively associated with FAM83A-AS1. The miR-141-3p inhibitor partly abolished the FAM83A-AS1 knockdown-induced inhibition on EMT, cell growth, invasion and migration in LUAD cells. In addition, miR-141-3p down-regulation abolished the inhibition of E-box-bound zinc finger protein 1 and 2 protein production following FAM83A-AS1 knockdown. According to our results, FAM83A-AS1/miR-141-3p axis plays an important role in LUAD occurrence and development. FAM83A-AS1 sponged miR-141-3p to down-regulate the level of the latter within LUAD and thereby encouraging LUAD development and suggesting a possible novel therapeutic approach for LUAD.

[Clinical Value of White Light Image, Endoscopic Ultrasonography and Magnifying Endoscopy with Narrow Band Imaging in Evaluation of Indications for Endoscopic Treatment of Early Gastric Cancer].

OBJECTIVE: To explore the application value of white light image (WLI), endoscopic ultrasonography (EUS) and magnifying endoscopy with narrow band imaging (ME-NBI) in the endoscopic treatment of early gastric cancer (EGC), and to provide basis for decision-making in clinical diagnosis and treatment. METHODS: The clinicopathological data of EGC patients who underwent endoscopic submucosal dissection (ESD) at West China Hospital, Sichuan University between December 2013 and October 2020 were included. The accuracy, sensitivity, specificity, positive predictive value and negative predictive value of EGC invasive depth were compared between WLI and EUS. The role of ME-NBI in predicting the differentiation types of EGC was analyzed. RESULTS: A total of 280 patients (291 lesions) were enrolled in the study. Among them, 199 patients (207 lesions) received EUS and 160 patients (168 lesions) received ME-NBI. The overall accuracy of WLI in diagnosing the invasive depth of EGC was 87.0%, significantly higher than that of EUS (46.4%, P<0.001). When WLI was combined with EUS, the diagnostic accuracy (87.4%) was not significantly improved. The overall accuracy of determining the differentiation degree of EGC with ME-NBI was 92.3% (155/168), and the accuracy of determining undifferentiated EGC with ME-NBI was significantly lower than that of differentiated EGC (41.2% vs. 98.0%, P<0.001). CONCLUSION: In the evaluation of indications for endoscopic treatment of EGC, WLI showed better performance in predicting the invasive depth of EGC, while EUS demonstrated limited value. ME-NBI showed better accuracy for predicting the differentiation degree of most EGC, especially for differentiated EGC.

The Development of Rickets in Children and Nursing Contributions to Treatment.

Rickets is one of the most prevalent non-communicable diseases in children in the developing world. It is often found in cultures in which children follow strict vegetarian diets and are not exposed to vitamin D-enhanced foods. While a rare occurrence, X-linked hypophosphatemic rickets may be the most frequent type of the disease seen outside the Third World today. However, there is not much credible information on the extent of the development of rickets. Therefore, pediatric nurses must be able to recognize children at risk and provide best practice care for the prevention and treatment of rickets. When caring for children in hospitals, communities or classrooms, nurses play a vital role in identifying children at risk for hypovitaminosis D and advising families to, if possible, follow safe diets and take supplements in order to avoid health complications associated with low levels of vitamin D. This study examines the prevalence and variables contributing to rickets, including hypovitaminosis vitamin D, the consequent orthopedic problems and the role of nurses in preventing and managing the pathogenesis of rickets and ultimately avoiding extreme deficits that result in bone deformities and the need for corrective surgery.

Deoxycytidine Kinase (DCK) Mutations in Human Acute Myeloid Leukemia Resistant to Cytarabine.

Resistance to cytarabine is an important cause of therapy failure in persons with acute myeloid leukemia (AML). Deoxycytidine kinase, encoded by DCK, catalyzes phosphorylation of cytarabine to cytarabine monophosphate, a necessary step for eventual incorporation of cytarabine triphosphate into DNA and for clinical efficacy. Whether DCK mutations make AML cells resistant to cytarabine is controversial. We studied DCK mutations and messenger RNA (mRNA) concentrations in leukemia cells from 10 subjects with AML who received cytarabine-based therapy and relapsed and in 2 artificially induced cytarabine-resistant AML cell lines. DCK mutations were detected in 4 subjects with AML relapsing after achieving a complete remission and receiving high-dose cytarabine postremission therapy. Most mutations were in exons 4-6 and were not present before therapy. DCK was also mutated in cytarabine-resistant but not parental AML cell lines. DCK mRNA concentrations were significantly decreased in cytarabine-resistant K562 and SHI-1 cells compared with cytarabine-sensitive parental cells. Mutation frequency of DCK and mRNA concentration did not correlate with the extent of cytarabine resistance indicating other factors operate. Overexpression of wild-type DCK restored cytarabine sensitivity to previously resistant leukemia cell lines. Our data contribute to the understanding of cytarabine resistance in persons with AML.

Long non-coding RNA SNHG1 regulates rheumatoid synovial invasion and proliferation by interaction with PTBP1.

Fibroblast-like synoviocytes (FLSs) in rheumatoid arthritis (RA) present proliferative and aggressive cell phenotype. RA-FLSs are the essential effector cells that lead to symptoms like synovial inflammation and joint destruction. Currently, the cause of RA-FLSs involving in the pathological process of RA remains unknown. Accumulate researches have demonstrated that lncRNAs may play a critical role in regulating the biological behaviors of RA-FLSs, but the mechanism is still unclear. Here, we found that lncRNA small nucleolar RNA host gene 1 (SNHG1) is up-regulated in RA-FLSs compared with FLSs from trauma arthritis and osteoarthritis patients. The results suggest that SNHG1 in RA-FLSs helps to sustain the cellular functions of proliferation, migration and invasion. Furthermore, the regulation mechanism depends on the interaction between SNHG1 and polypyridine tract-binding protein 1 (PTBP1). This interaction influences PTBP1 expression that participates in the regulation of RA-FLSs biological behaviors. Our results suggest that up-regulated SNHG1 of RA-FLSs may contribute to synovial aggression and disease progression in RA and be favourable for RA treatment target RA-FLSs.

The influence of exhaust gas compositions in MnO2 dry DeSO x filter for diesel emission control.

Sulfur dioxide purification has adverse effects on the environment and the human body. In this study, the dry desulfurization process from exhaust gas exhaust by dry DeSO x filter is investigated for constructing a sulfur-based capture-and-reuse system. The activated MnO2 having a high-specific surface area (HSSA MnO2) is utilized as an absorbent to indicate high SO2 capture performance in the low-temperature region. To improve the capture performance, (SO2 concentration, space velocity, and gas composite) is analysed on SO2 capture performance of dry DeSO x filter. Results showed that SO2 capture performance in high SO2 concentration was constant regardless of space velocity. However, in low SO2 concentration, the SO2 capture performance decreased with increasing space velocity. Moreover, the presence of H2O in the flow gas exhibited a beneficial effect on SO2 capture performance.

Validation of the diagnostic efficiency of folate receptor-positive circulating tumor cells in lung cancers: a prospective observational study.

BACKGROUND: This study sought to validate the clinical value of folate receptor-positive circulating tumor cell (FR+CTC) for the diagnosis of lung cancers. METHODS: Seventy-five lung cancer patients and 71 non-malignant participants (including 48 benign lung disease patients and 23 healthy subjects) were enrolled in this study. Three milliliters of the whole blood sample was collected from all the participants (before surgery for cancer patients). FR+CTC analysis was performed using "CytoploRare Detection Kit". The expression level of serum biomarkers, including carcinoembryonic antigen (CEA), cytokeratin fragment 19 (CYFRA21-1), and neuron-specific enolase (NSE), were also tested in cancer and benign lung disease patients. RESULTS: The median FR+CTC level in lung cancers (10.5 CTC units/3 mL blood) was significantly higher than that of the non-malignant group (5.9 CTC units/3 mL blood, P<0.0001). No significant difference in FR+CTC level was observed between patients with different age, gender, and pathological subtype (P>0.05), except for clinical stage (stages I-III versus stage IV: P=0.0169). With 7.9 CTC units/3 mL blood as the cut-off threshold, FR+CTC showed superior sensitivity (78.7%) and specificity (81.7%) in the diagnosis of lung cancers. The detection rate of FR+CTC was significantly higher compared to CEA (24.0%), CYFRA21-1 (48.0%), and NSE (16.0%). The diagnostic efficiency of FR+CTC was similar in stage I lung cancers (n=25, sensitivity =68.0% and specificity =90.1%). CONCLUSIONS: Our results support that FR+CTC is an independent and efficacious biomarker in the diagnosis of lung cancers. FR+CTC detection can be used to assist in early-stage thoracic cancer diagnosis.

Chinese and Europeans with acute myeloid leukemia have discordant mutation topographies.

Although the topography of mutations in persons of predominately European-descent with acute myeloid leukemia (AML) is well-described this is less so in Asians. We studied AML-related mutations in 289 consecutive Chinese (mostly Han) with newly-diagnosed de novo AML. Full-length coding sequence of NPM1 and CEBPA, IDH1 and IDH2 hotspot mutations and WT1 mutations in exons 7 and 9 were analyzed by PCR as were correlations with clinical and laboratory variables. CEBPA mutations were detected in 20% of subjects (95% confidence interval [CI] 15, 25%), NPM1 mutations in 20% (15, 25%), IDH1 mutations in 4% (1, 6%), IDH2 mutations in 11% (7, 15%) and WT1 mutations in 6% (3, 9%). A comparison of these data with mutation frequencies in persons of predominately European-descent with AML indicates a higher frequency of CEBPA mutations, a similar frequency of IDH2 mutations and lower frequencies of NPM1, IDH1 and WT1 mutations. Our data indicate different topographies of AML-associated mutations in Chinese compared with persons of predominately European descent suggesting genetic background, life-style, environment and perhaps other variables may influence these differences.

A preliminary study on the relationship between circulating tumor cells count and clinical features in patients with non-small cell lung cancer.

BACKGROUND: To evaluate the clinical value of circulating tumor cells (CTC) count in peripheral venous blood of patients with non-small cell lung carcinoma (NSCLC). METHODS: A total of 50 NSCLC patients who were diagnosed in Wuxi No. 2 People's Hospital from January 2013 to December 2013 were selected as the NSCLC group, 35 patients with lung benign tumor as the benign group, and 28 healthy subjects as the normal control group. Venous blood samples (3 mL) were collected in all subjects for counting the CTC, and a result of ≥8.7 was judged to be positive. The relationships between the positive rate of CTC and the age, sex, pathological type, and clinical stage of NSCLC were analyzed. RESULTS: CTC count was significantly higher in NSCLC group than in benign group and normal control group. In NSCLC patients, CTC count was not significantly correlated with sex, age, or the pathological type (P>0.05) but was closely related to clinical stage (P<0.01). Among NSCLC patients, CTC count significantly increased along with tumor progression. CONCLUSIONS: CTC count shows certain correlation with the clinical features of NSCLC and thus can, to certain extent, reflect the status of the disease.