Atmospheric PM2.5 exposure and risk of ischemic heart disease: A systematic review and meta-analysis of observational studies.

Fine particulate matter <2.5 µm in diameter (PM2.5) has been validated to associate with cardiovascular diseases (CVD) incidence and mortality. So far, no study has quantitatively evaluated the relationship between the atmospheric PM2.5 exposure and ischemic heart disease (IHD). We conducted a meta-analysis to illustrate the relationship between PM2.5 and IHD. Published articles were systematically searched (until June 2022) from PubMed, EMBASE, Cochrane Library. A random-effect model was performed to summarize the total relative risks (RRs) and 95% confidence intervals (CIs). Meta-analysis was performed using Stata 12.0 software. A total of 28 studies among 23 cohorts (23.38 million individuals and 256256 IHD cases) were included. With PM2.5 increasing 10 µg/m3, the total RRs of IHD incidence and mortality were 1.07 (95% CI: 0.99-1.17), 1.21 (95% CI: 1.15-1.28), respectively. In sub-analyses, our study revealed that the combined RRs of exposure to PM2.5 on IHD mortality in Asian and European population [1.11 (95% CI: 0.93-1.33); 1.06 (95% CI: 1.02-1.11)] were much lower compared with American and Canadian people [1.27 (95% CI: 1.17-1.37); 1.30 (95% CI: 1.24-1.35)]. Furthermore, study duration, size and some adjustments were related with the total RR. Our findings indicated that exposure of an increase in the concentration of atmospheric PM2.5 may increase the risk of IHD incidence and mortality. Further evidence is needed to confirmed the association.

Short-term exposure to ambient air pollution and atrial fibrillation hospitalization: A time-series study in Yancheng, China.

Atrial fibrillation (AF) is an important cardiovascular disease that causes a great burden of disease. However, there is limited evidence of a link between air pollution exposure and AF. This study aimed to explore the short-term association between air pollution and AF. We obtained daily hospitalization of AF in two major hospitals of Yancheng, China from May, 2015 to May, 2020. Generalized additive models with quasi-Poisson regression were used to assess the associations between six criteria air pollutants and AF hospitalization. We explored the lag patterns, and visualized the concentration-response relationships. The robustness of the association was tested by two-pollutant model, and we explored potential effect modification by age, sex and season. A total of 15,171 inpatients from two hospitals were collected in this study with an average daily count of eight patients. We observed consistent and significant associations between six air pollutants and AF on lag 0-4 days. A 10 ug/m3 increase in PM2.5 was associated with 2.81% (95%CI: 1.44%, 4.20%) changes in AF, and the effect estimate was 1.67% (95%CI: 0.77%, 2.59%) for PM10, 4.90% (95%CI: 1.69%, 8.22%) for NO2, 6.81% (95%CI: 0.46%, 13.57%) for SO2, 1.82% (95%CI: 0.60%, 3.06%) for O3; a 0.1 mg/m3 increase in CO was associated with 2.55% (95%CI: 0.91%, 4.21%) increments in AF. Associations of PM2.5 and PM10 were robust after adjusting for SO2, NO2, CO, and O3, but not vice versa. Female patients and those aged less 70 years had larger risk of AF associated with air pollution exposure. The concentration-response curves of the six pollutants were almost linear and increasing with no obvious thresholds. This time-series study in Yancheng demonstrated increased risk of AF and a delayed effect over lag 0-4 days. Our findings suggested need of prevention and protection against these environmental risk factors for AF in health departments.

Short-term exposure to coarse particulate matter and outpatient visits for cardiopulmonary disease in a Chinese city.

Limited studies have been conducted to evaluate the short-term relationships between exposure to coarse particulate matter (PM2.5-10) and outpatient visits in China. We designed this time-series analysis in a Chinese city Yancheng, to explore the relationship of PM2.5-10 with outpatient visits for cardiopulmonary diseases. The study period was from 2013 to 2015. A typical generalized additive model was used. We explored the lag patterns by building a series of lag of exposure. We also built two-pollutant models to ascertain the independence of PM2.5-10. Stratified analyses were applied to compare the season-specific associations. Finally, we pooled the concentration-response (C-R) curves for PM2.5-10 and outpatient visits. We recorded a daily average of 85 and 43 outpatient visits for cardiovascular and respiratory causes, respectively. PM2.5-10 exposures of lag 05 day yielded the best estimates for both outcomes. Per 10-µg/m3 increase in PM2.5-10, there was a 1.69% (95% confidence interval [CI]: 0.68%-2.72%) increase in outpatient visits for respiratory causes, and a 0.85% (95% CI: 0.13%-1.57%) increase for cardiovascular causes. The association kept robust after adjusting for PM2.5 and O3, and there were larger associations in warm seasons. The C-R curves had a larger slope for respiratory diseases in relatively lower concentrations (<30 µg/m3), and PM2.5-10 was positively associated with cardiovascular diseases in higher concentrations (>30 µg/m3). This study indicated significant associations of PM2.5-10 with cardiopulmonary outpatient visit. Such results may be used for health risk assessment and policy making for particulate air pollution control.

Sinoporphyrin Sodium-Mediated Sonodynamic Therapy Inhibits RIP3 Expression and Induces Apoptosis in the H446 Small Cell Lung Cancer Cell Line.

BACKGROUND/AIMS: Sonodynamic therapy (SDT) is expected to be a new method to solve the clinical problems caused by advanced metastasis in patients with lung cancer. The use of ultrasound has the advantage of being noninvasive, with deep-penetration properties. This study explored the anti-tumor effect of SDT with a new sonosensitizer, sinoporphyrin sodium (DVDMS), on the human small cell lung cancer H446 cell line in vitro and in vivo. METHODS: Absorption of DVDMS was detected by a fluorescence spectrophotometer, and DVDMS toxicity was determined using a Cell Counting Kit-8. Mitochondrial membrane potential (MMP) was assessed using the JC-1 fluorescent probe. Cell apoptosis was measured by flow cytometry, and apoptosis-related proteins were detected by western blotting. The expression of cytokines was measured using an enzyme-linked immunosorbent assay and quantitative real-time PCR. To verify the in vitro results, we detected tumor volumes and weight changes in a xenograft nude mouse model after DVDMS-SDT. Hematoxylin and eosin staining was used to observe changes to the tumor, heart, liver, spleen, lung, and kidney of the mice, and immunohistochemistry was used to examine changes in the expression of tumor CD34 and receptor-interacting protein kinase-3 (RIP3), while terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling was used to observe apoptosis in tumor tissues. RESULTS: DVDMS-SDT-treated H446 cells increased the rate of cellular apoptosis and the levels of reactive oxygen species (ROS), cleaved caspase-3, cleaved caspase-8, cleaved caspase-9, and caspase-10, and decreased the levels of MMP, RIP3, B-cell lymphoma 2, vascular endothelial growth factor, and tumor necrosis factor-α. The sonotoxic effect was mediated by ROS and was reduced by a ROS scavenger (N-acetyl-L-cysteine). In the in vivo mouse xenograft model, DVDMS-SDT showed efficient anti-cancer effects with no visible side effects. CONCLUSION: DVDMS-SDT induced apoptosis in H446 cells, in part by targeting mitochondria through the mitochondria-mediated apoptosis signaling pathway, and the extrinsic apoptosis pathway was also shown to be involved. Both apoptosis and changes in RIP3 expression were closely related to the generation of ROS. DVDMS-SDT will be advantageous for the management of small cell lung cancer due to its noninvasive characteristics.

Nonmuscle myosin heavy chain IIA mediates Epstein-Barr virus infection of nasopharyngeal epithelial cells.

EBV causes B lymphomas and undifferentiated nasopharyngeal carcinoma (NPC). Although the mechanisms by which EBV infects B lymphocytes have been extensively studied, investigation of the mechanisms by which EBV infects nasopharyngeal epithelial cells (NPECs) has only recently been enabled by the successful growth of B lymphoma Mo-MLV insertion region 1 homolog (BMI1)-immortalized NPECs in vitro and the discovery that neuropilin 1 expression positively affects EBV glycoprotein B (gB)-mediated infection and tyrosine kinase activations in enhancing EBV infection of BMI1-immortalized NPECs. We have now found that even though EBV infected NPECs grown as a monolayer at extremely low efficiency (<3%), close to 30% of NPECs grown as sphere-like cells (SLCs) were infected by EBV. We also identified nonmuscle myosin heavy chain IIA (NMHC-IIA) as another NPEC protein important for efficient EBV infection. EBV gH/gL specifically interacted with NMHC-IIA both in vitro and in vivo. NMHC-IIA densely aggregated on the surface of NPEC SLCs and colocalized with EBV. EBV infection of NPEC SLCs was significantly reduced by NMHC-IIA siRNA knock-down. NMHC-IIA antisera also efficiently blocked EBV infection. These data indicate that NMHC-IIA is an important factor for EBV NPEC infection.

Interleukin-22 promotes lung cancer cell proliferation and migration via the IL-22R1/STAT3 and IL-22R1/AKT signaling pathways.

Lung cancer continues to be an enormous burden on current health care systems throughout the world, with more than a million deaths every year. Previous studies have shown that interleukin-22 (IL-22) promotes survival and resistance to chemotherapy in human lung cancer cells. However, the association of IL-22 expression with recurrence of lung cancer is still unclear. In this study, we found that expression of IL-22 was upregulated in tumor tissues and serum from patients with recurrent non-small cell lung cancer (NSCLC) as compared to primary NSCLC samples. Treatment with IL-22 promoted cell proliferation and enhanced migration and invasion in A549 and H125 cell lines. Furthermore, we revealed that phosphorylation of STAT3 and AKT was highly induced by treatment with IL-22 via IL-22R1. IL-22R1 was also consistently overexpressed in recurrent NSCLC tissues. Finally, we found that siRNA-mediated depletion of IL-22R1 completely abrogated the effects of IL-22 treatment on cell proliferation and migration activity in NSCLC cell lines. Our findings indicate that IL-22 and IL-22R1 may be novel therapeutic targets for treatment of advanced NSCLC.

Interleukin-17 levels correlate with poor prognosis and vascular endothelial growth factor concentration in the serum of patients with non-small cell lung cancer.

OBJECTIVE: The aim of this study was to explore the clinical role of serum interleukin-17 in patients with non-small-cell lung cancer (NSCLC). MATERIALS AND METHOD: IL-17 expression and microvessel density (MVD) were measured via immunohistochemistry in 58 NSCLC tissues. Serum IL-17 and VEGF levels in NSCLC patients (n = 43) and healthy controls (n = 37) were analyzed via enzyme-linked immunosorbent assay. RESULTS: Serum IL-17 was elevated and the levels positively correlated with VEGF concentration in NSCLC patients. Multivariate analyses revealed that serum IL-17 levels were an independent prognostic factor in NSCLC. CONCLUSION: IL-17 may play a role in NSCLC progression by promoting angiogenesis.

Advances in malignant peritoneal mesothelioma.

BACKGROUND: Malignant mesothelioma is a rare, insidious, and aggressive tumor arising from the mesothelial surface of pleural and peritoneal cavities, the pericardium, or the tunica vaginalis, with an increasing incidence worldwide, high misdiagnosis rate, and overall negative prognosis. A total of 20% of all cases is peritoneum in origin. METHODS: The present study is a review of literatures focusing on the advances in epidemiology, clinical presentations, radiological features, diagnosis, misdiagnosis, management, and prognostic factors of malignant peritoneal mesothelioma (MPM) occurred in the past decades. RESULTS: Asbestos, SV40, and radiation exposures have been demonstrated to be correlated with the pathogenesis of MPM. The main presentations are abdominal distension and pain. Computed tomography (CT), magnetic resonance imaging (MRI), and positron-emission tomography (PET) play an important role in the preoperative imaging and staging. Definitive diagnosis is made on the basis of immunohistochemistry. Prognostic factors have been identified and verified. Negative indicators include advanced age, male gender, poor performance status, non-epithelial histology, and absence of surgery. The management of MPM has evolved from single chemotherapy to multimodality treatment of cytoreductive surgery (CRS) and hyperthermic intraperitoneal chemotherapy (HIPEC), chemotherapy, radiotherapy, and immunotherapy. Promising results have been achieved after a combined treatment of CRS and HIPEC, with an elevated median survival time of 29.5-92 months and a 5-year survival rate of 39-63%. CONCLUSIONS: CRS and HIPEC represent the standard treatment strategy for selected patients with MPM, and patients with unresectable tumors can benefit from the combined treatment of chemotherapy, radiotherapy, and immunotherapy.

Newly identified biomarkers for detecting circulating tumor cells in lung adenocarcinoma.

Circulating tumor cells (CTCs) have been implicated in cancer prognosis and follow up. Detection of CTCs was considered significant in cancer evaluation. However, due to the heterogeneity and rareness of CTCs, detecting them with a single maker is usually challenged with low specificity and sensitivity. Previous studies concerning CTCs detection in lung cancer mainly focused on non-small cell lung carcinoma. Currently, there is no report yet describing the CTC detection with multiple markers in lung adenocarcinoma. In this study, by employing quantitative real-time PCR, we identified four candidate genes (mRNA) that were significantly elevated in peripheral blood mononuclear cells and biopsy tissue samples from patients with lung adenocarcinoma: cytokeratin 7 (CK7), Ca(2+)-activated chloride channel-2 (CLCA2), hyaluronan-mediated motility receptor (HMMR), and human telomerase catalytic subunit (hTERT). Then, the four markers were used for CTC detection; namely, positive detection was defined if at least one of the four markers was elevated. The positive CTC detection rate was 74.0% in patients with lung adenocarcinoma while 2.2% for healthy controls, 6.3% for benign lung disease, and 48.0% for non-adenocarcinoma non-small cell lung carcinoma. Furthermore, in a three-year follow-up study, patients with an increase in the detection markers of CTCs (CK7, CLCA2, HMMR or hTERT) on day 90 after first detection had shorter survival time compared to those with a decrease. These results demonstrate that the combination of the four markers with specificity and sensitivity is of great value in lung adenocarcinoma prognosis and follow up.

Phase separation in innate immune response and inflammation-related diseases.

Inflammation induced by nonspecific pathogenic or endogenous danger signals is an essential mechanism of innate immune response. The innate immune responses are rapidly triggered by conserved germline-encoded receptors that recognize broad patterns indicative of danger, with subsequent signal amplification by modular effectors, which have been the subject of intense investigation for many years. Until recently, however, the critical role of intrinsic disorder-driven phase separation in facilitating innate immune responses went largely unappreciated. In this review, we discuss emerging evidences that many innate immune receptors, effectors, and/or interactors function as "all-or-nothing" switch-like hubs to stimulate acute and chronic inflammation. By concentrating or relegating modular signaling components to phase-separated compartments, cells construct flexible and spatiotemporal distributions of key signaling events to ensure rapid and effective immune responses to a myriad of potentially harmful stimuli.

Epstein-Barr virus-encoded LMP2A induces an epithelial-mesenchymal transition and increases the number of side population stem-like cancer cells in nasopharyngeal carcinoma.

It has been recently reported that a side population of cells in nasopharyngeal carcinoma (NPC) displayed characteristics of stem-like cancer cells. However, the molecular mechanisms underlying the modulation of such stem-like cell populations in NPC remain unclear. Epstein-Barr virus was the first identified human tumor virus to be associated with various malignancies, most notably NPC. LMP2A, the Epstein-Barr virus encoded latent protein, has been reported to play roles in oncogenic processes. We report by immunostaining in our current study that LMP2A is overexpressed in 57.6% of the nasopharyngeal carcinoma tumors sampled and is mainly localized at the tumor invasive front. We found also in NPC cells that the exogenous expression of LMP2A greatly increases their invasive/migratory ability, induces epithelial-mesenchymal transition (EMT)-like cellular marker alterations, and stimulates stem cell side populations and the expression of stem cell markers. In addition, LMP2A enhances the transforming ability of cancer cells in both colony formation and soft agar assays, as well as the self-renewal ability of stem-like cancer cells in a spherical culture assay. Additionally, LMP2A increases the number of cancer initiating cells in a xenograft tumor formation assay. More importantly, the endogenous expression of LMP2A positively correlates with the expression of ABCG2 in NPC samples. Finally, we demonstrate that Akt inhibitor (V) greatly decreases the size of the stem cell side populations in LMP2A-expressing cells. Taken together, our data indicate that LMP2A induces EMT and stem-like cell self-renewal in NPC, suggesting a novel mechanism by which Epstein-Barr virus induces the initiation, metastasis and recurrence of NPC.

Luffa echinata Roxb. induces human colon cancer cell (HT-29) death by triggering the mitochondrial apoptosis pathway.

The antiproliferative properties and cell death mechanism induced by the extract of the fruits of Luffa echinata Roxb. (LER) were investigated. The methanolic extract of LER inhibited the proliferation of human colon cancer cells (HT-29) in both dose-dependent and time-dependent manners and caused a significant increase in the population of apoptotic cells. In addition, obvious shrinkage and destruction of the monolayer were observed in LER-treated cells, but not in untreated cells. Analysis of the cell cycle after treatment of HT-29 cells with various concentrations indicated that LER extracts inhibited the cellular proliferation of HT-29 cells via G2/M phase arrest of the cell cycle. The Reactive oxygen species (ROS) level determination revealed that LER extracts induced apoptotic cell death via ROS generation. In addition, LER treatment led to a rapid drop in mitochondrial membrane potential (MMP) as a decrease in fluorescence. The transcripts of several apoptosis-related genes were investigated by RT-PCR analysis. The caspase-3 transcripts of HT-29 cells significantly accumulated and the level of Bcl-XL mRNA was decreased after treatment with LER extract. Furthermore, the ratio of mitochondria-dependent apoptosis genes (Bax and Bcl-2) was sharply increased from 1.6 to 54.1. These experiments suggest that LER has anticancer properties via inducing the apoptosis in colon cancer cells, which provided the impetus for further studies on the therapeutic potential of LER against human colon carcinoma.

Prediction of Axillary Lymph Node Metastasis in Invasive Breast Cancer by Sound Touch Elastography.

The aims of this study were to investigate the value of sound touch elastography (STE) in predicting axillary lymph node metastasis (ALNM) in patients with invasive breast cancer (IBC) and to explore whether lysyl oxidase (LOX) is correlated with increasing stiffness and promotion of metastasis in IBC. A total of 142 lesions in 142 patients were assessed by STE. The STE values of IBCs in the two groups were compared and the best cutoff values for diagnosing ALNM determined. Immunohistochemistry was used to detect LOX expression. Collagen fiber and elastic fiber content was determined by Masson and Weigert elastic fiber staining. Correlation analyses were performed to identify the associations of the data. The optimal cutoff values of Emax (maximum stiffness value of the tumor) and Smax (maximum stiffness value of the shell) for predicting ALNM of IBC were 94.58 and 148.78 kPa. Immunohistochemistry and Masson and Weigert elastic fiber staining were performed on 67 samples. LOX expression and collagen volume fraction were significantly higher in the ALNM+ group than in the ALNM- group (p = 0.04 and 0.03), except for elastic fiber content (p = 0.628). Moreover, Emax, Smax and LOX expression were positively correlated with collagen volume fraction (r = 0.624, 0.512, and 0.533, respectively). Emax and Smax were found to be predictors for ALNM of IBC. STE could serve as a non-invasive method for assessing lymph node status before surgery. Overexpression of LOX and increased collagen fiber contributed to the increased stiffness in the lesions and metastases of IBC.

Association between fine particulate matter and heart failure hospitalizations: a time-series analysis in Yancheng, China.

BACKGROUND: Heart failure (HF) is a global public health problem of increasing importance. The association between acute exposure to air pollution and HF has been well established in developed countries, but little evidence is available in developing countries where air pollution levels are much higher. OBJECTIVES: To explore the associations between PM2.5 and HF hospitalizations in Yancheng, China. METHODS: In this time-series study, daily HF hospitalizations admitted in three major hospitals in Yancheng from May 1, 2015 to Apr 30, 2020 were collected. We used a generalized additive model with quasi-Poisson regression to investigate the association between PM2.5 and HF hospitalizations. The robustness of the associations was tested using two-pollutant models, and we examined the potential effect modification by age, gender, and season via stratification analyses. Lastly, we pooled the concentration-response curves. RESULTS: A total of 10,466 HF hospitalizations were recorded, with a daily average of 6 cases. We observed the most robust estimates on lag 0 day, and the associated increment in HF was 1.28% (95% CI 0.45%, 2.11%) for a 10-µg/m3 increase of PM2.5. The association remained after adjustment of O3, but not for NO2, CO, and SO2. The PM2.5-HF associations were positive in females, patients aged ≥ 65 years, and in cold season. The C-R relationship curve was generally increasing below 30 µg/m3. CONCLUSION: This study provided evidence on the association of PM2.5 with acute exacerbation of chronic heart failure, which may benefit future prevention strategy and policymaking.

Plasmonic Heating-Promoted Photothermal Synthesis of α-Cyanoacrylonitriles Over Au/h-BN Catalysts.

Plasmonic nanoparticle-involved materials play an essential role in the field of photothermal conversion. Herein, we report the application of photothermal heterogeneous catalysts consisting of gold nanoparticles decorated on defect-rich h-BN sheets (Au/h-BN) for the photocatalytic synthesis of α-cyanoacrylonitriles under mild conditions. It has been demonstrated the-NH2 groups present in the defect-rich h-BN act as the catalytically active sites, while plasmonic heating from the gold nanoparticles can drive the reaction by providing local heat. Au/h-BN catalyst can work for a broad substrate scope in the synthesis of α-cyanoacrylonitriles, and a plausible -NH2 group-involved reaction mechanism has been proposed. This work may open up new avenues in photothermal catalysis by combining plasmonic materials and catalytic sites in one system.

Low-work-function LaB6 for realizing photodynamic-enhanced photothermal therapy.

There is great potential for photodynamic therapy (PDT)-enhanced photothermal therapy (PTT) to be used for tumor therapy, especially for the single material-mediated process that could greatly simplify the experimental arrangements. This study presents a new cancer phototherapeutic agent consisting of low-work-function lanthanum hexaboride particles, which are excellent light absorbers in the near-infrared (NIR) region. The photothermal effect and reactive oxygen species production were realized by LaB6 under NIR light irradiation. Theoretical calculations based on density functional theory confirmed that the strong NIR light absorption by LaB6 was attributed to the local plasmonic resonance effect and the excellent photodynamic effect derived from the low work function. In vivo treatment of HepG2 tumor-bearing mice revealed that LaB6-mediated phototherapy resulted in excellent tumor inhibitory effects, and no adverse effects on mice were observed. These results indicate that LaB6 is a promising phototherapeutic agent for cancer synergetic phototherapy.

Prognostic significance and therapeutic implications of centromere protein F expression in human nasopharyngeal carcinoma.

BACKGROUND: Our recent cDNA microarray data showed that centromere protein F (CENP-F) is significantly upregulated in primary cultured nasopharyngeal carcinoma (NPC) tumor cells compared with normal nasopharyngeal epithelial cells. The goal of this study was to further investigate the levels of CENP-F expression in NPC cell lines and tissues to clarify the clinical significance of CENP-F expression in NPC as well as the potential therapeutic implications of CENP-F expression. METHODS: Real-time RT-PCR and western blotting were used to examine CENP-F expression levels in normal primary nasopharyngeal epithelial cells (NPEC), immortalized nasopharyngeal epithelial cells and NPC cell lines. Levels of CENP-F mRNA were determined by real-time RT-PCR in 23 freshly frozen nasopharyngeal biopsy tissues, and CENP-F protein levels were detected by immunohistochemistry in paraffin sections of 202 archival NPC tissues. Statistical analyses were applied to test for prognostic associations. The cytotoxicities of CENP-F potential target chemicals, zoledronic acid (ZOL) and FTI-277 alone, or in combination with cisplatin, in NPC cells were determined by the MTT assay. RESULTS: The levels of CENP-F mRNA and protein were higher in NPC cell lines than in normal and immortalized NPECs. CENP-F mRNA level was upregulated in nasopharyngeal carcinoma biopsy tissues compared with noncancerous tissues. By immunohistochemical analysis, CENP-F was highly expressed in 98 (48.5%) of 202 NPC tissues. Statistical analysis showed that high expression of CENP-F was positively correlated with T classification (P < 0.001), clinical stage (P < 0.001), skull-base invasion (P < 0.001) and distant metastasis (P = 0.012) inversely correlated with the overall survival time in NPC patients. Multivariate analysis showed that CENP-F expression was an independent prognostic indicator for the survival of the patient. Moreover, we found that ZOL or FTI-277 could significantly enhance the chemotherapeutic sensitivity of NPC cell lines (HONE1 and 6-10B) with high CENP-F expression to cisplatin, although ZOL or FTI-277 alone only exhibited a minor inhibitory effect to NPC cells. CONCLUSION: Our data suggest that CENP-F protein is a valuable marker of NPC progression, and CENP-F expression is associated with poor overall survival of patients. In addition, our data indicate a potential benefit of combining ZOL or FTI-277 with cisplatin in NPC suggesting that CENP-F expression may have therapeutic implications.

Author Correction: Interleukin-17 promotes angiogenesis by stimulating VEGF production of cancer cells via the STAT3/GIV signaling pathway in non-small-cell lung cancer.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

Association between ambient temperature and daily emergency hospitalizations for acute coronary syndrome in Yancheng, China.

Acute coronary syndrome (ACS) is a major public health concern worldwide. Few studies have directly evaluated the associations between ambient temperature and ACS incidence. To explore the association between ambient temperature and ACS emergency hospitalizations in the area of subtropical monsoon climate, data on ACS emergency hospitalizations were collected from two highest-ranking hospitals in the central urban area of Yancheng, China, from January 1, 2013, to December 31, 2018. We applied the time-series method to investigate the potentially lagged and non-linear effects of ambient temperature on ACS using the generalized linear model combined with the distributed lag non-linear model after adjusting for time trend, day of the week, holiday, and relative humidity. We identified a total of 5303 cases of ACS emergency hospitalizations during the study period. The exposure-response curves between ambient temperature and ACS hospitalizations were inverse "J-shaped." The effects of extreme low temperature on ACS hospitalizations occurred on the present day and lasted for 3 days, followed by the harvesting effect. The effects of extreme high temperature occurred on the present day and lasted for 5 days. The cumulative relative risks of ACS were 2.14 [95% confident interval (CI): 1.32 to 3.47] for extremely low temperature and 1.66 (95% CI: 1.33 to 2.06) for extremely high temperature over the lag of 0-5 days, compared with the reference temperature (25.0 °C). Both low and high temperatures were significantly associated with higher risks of emergency hospital admissions for ACS in Yancheng, China.

Diurnal temperature range is a risk factor for coronary heart disease death.

BACKGROUND: Although the relation between day-to-day temperature change and coronary heart disease (CHD) mortality is well established, it is unknown whether temperature variation within 1 day, ie, diurnal temperature range (DTR), is an independent risk factor for acute CHD death. METHODS: We used time-series and case-crossover approaches to assess the relation between DTR and daily CHD mortality between 2001 and 2004 in Shanghai, China. Specifically, we used exposures averaged over periods varying from 1 to 5 days to assess the effects of DTR on CHD mortality. We estimated the percent increase in the number of daily deaths related to CHD that were associated with DTR, after adjustment for daily meteorologic conditions (temperature and relative humidity) and levels of outdoor air pollutants. RESULTS: Both time-series and case-crossover analyses showed that DTR was significantly associated with the number of daily deaths related to CHD. A 1 degrees C increase in 2-day lagged DTR corresponded to a 2.46% (95% CI, 1.76% to 3.16%) increase in CHD mortality on time-series analysis, a 3.21% (95% CI, 2.23% to 4.19%) increase on unidirectional case-crossover analysis, and a 2.13% (95% CI, 1.04% to 3.22%) increase on bidirectional case-crossover analysis. CONCLUSIONS: Our findings suggest that DTR is an independent risk factor for acute CHD death.