Profiles of Cough and Associated Risk Factors in Nonhospitalized Individuals With SARS-CoV-2 Omicron Variant Infection: Cross-Sectional Online Survey in China.

BACKGROUND: Cough is a common symptom during and after COVID-19 infection; however, few studies have described the cough profiles of COVID-19. OBJECTIVE: The aim of this study was to investigate the prevalence, severity, and associated risk factors of severe and persistent cough in individuals with COVID-19 during the latest wave of the Omicron variant in China. METHODS: In this nationwide cross-sectional study, we collected information of the characteristics of cough from individuals with infection of the SARS-CoV-2 Omicron variant using an online questionnaire sent between December 31, 2022, and January 11, 2023. RESULTS: There were 11,718 (n=7978, 68.1% female) nonhospitalized responders, with a median age of 37 (IQR 30-47) years who responded at a median of 16 (IQR 12-20) days from infection onset to the time of the survey. Cough was the most common symptom, occurring in 91.7% of participants, followed by fever, fatigue, and nasal congestion (68.8%-87.4%). The median cough visual analog scale (VAS) score was 70 (IQR 50-80) mm. Being female (odds ratio [OR] 1.31, 95% CI 1.20-1.43), having a COVID-19 vaccination history (OR 1.71, 95% CI 1.37-2.12), current smoking (OR 0.48, 95% CI 0.41-0.58), chronic cough (OR 2.04, 95% CI 1.69-2.45), coronary heart disease (OR 1.71, 95% CI 1.17-2.52), asthma (OR 1.22, 95% CI 1.02-1.46), and gastroesophageal reflux disease (GERD) (OR 1.21, 95% CI 1.01-1.45) were independent factors for severe cough (VAS>70, 37.4%). Among all respondents, 35.0% indicated having a productive cough, which was associated with risk factors of being female (OR 1.44, 95% CI 1.31-1.57), having asthma (OR 1.84, 95% CI 1.52-2.22), chronic cough (OR 1.44, 95% CI 1.19-1.74), and GERD (OR 1.22, 95% CI 1.01-1.47). Persistent cough (>3 weeks) occurred in 13.0% of individuals, which was associated with the risk factors of having diabetes (OR 2.24, 95% CI 1.30-3.85), asthma (OR 1.70, 95% CI 1.11-2.62), and chronic cough (OR 1.97, 95% CI 1.32-2.94). CONCLUSIONS: Cough is the most common symptom in nonhospitalized individuals with Omicron SARS-CoV-2 variant infection. Being female, having asthma, chronic cough, GERD, coronary heart disease, diabetes, and a COVID-19 vaccination history emerged as independent factors associated with severe cough, productive cough, and persistent cough.

Smoking index and COPD duration as potential risk factors for development of osteoporosis in patients with non-small cell lung cancer - A retrospective case control study evaluated by CT Hounsfield unit.

Objective: To investigate the effect of smoking index (calculated as number of cigarettes per day × smoking years) and chronic obstructive pulmonary disease (COPD) duration on osteoporosis (OP)evaluated by opportunistic chest CT in patients with non-small cell lung cancer (NSCLC). Methods: A total of 101 patients diagnosed with NSCLC were included in our cohort study. Among them, 50 patients with a history of smoking and COPD were assigned to the experimental group, while 51 patients without a history of smoking and COPD were assigned to the control group. Hounsfield unit (HU) value was measured by conventional chest CT to investigate the bone mineral density; and the mean values of axial HU value in the upper, middle and lower parts of T4, T7, T10 and L1 vertebral bodies were measured as the study variables. Results: There were no significant differences in gender, age, body mass index, type of lung cancer, clinical stage of lung cancer and comorbidities between the two groups (P = 0.938，P = 0.158，P = 0.722,P = 0.596,P = 0.813,P = 0.655). The overall mean HU values of T4, T7, T10, L1 in the experimental group were 116.60 ± 30.67, 110.56 ± 30.03, 109.18 (96.85-122.95), 94.63 (85.20-104.12) and 106.86 ± 22.26, respectively, which were significantly lower than those in the control group (189.55 ± 34.57, 174.54 ± 35.30, 172.73 (156.33-199.50), 158.20 (141.60-179.40) and 177.50 ± 33.49) (P ＜0.05). And in the experimental group, smoking index and COPD duration were significantly and negatively correlated with HU values (r = -0.627, -0.542, P ＜0.05, respectively). Conclusion: Patients with NSCLC who have a history of smoking and COPD exhibit a notably lower HU value compared to the control groups. Additionally, it has been observed that the smoking index and duration of COPD may be influential factors affecting bone mineral density in NSCLC patients.

Ultrasonic Elastography-guided Pleural Biopsy for the Diagnosis of Pleural Effusion: A Multicenter Prospective Study of Diagnostic Test Performance.

Rationale: The diagnostic yield of traditional ultrasound-guided pleural biopsy remains unsatisfactory, particularly when the pleural thickness is ⩽5 mm and/or no pleural nodules are detected. Pleural ultrasound elastography (UE) has a better diagnostic yield than traditional ultrasound for malignant pleural effusion (MPE). However, studies on UE-guided pleural biopsies are lacking. Objectives: To evaluate the feasibility and safety of UE-guided pleural biopsy. Methods: In this multicenter prospective single-arm trial, patients with pleural effusion whose pleural thickness was ⩽5 mm with no pleural nodules were enrolled between July 2019 and August 2021. The diagnostic yield of UE-guided pleural biopsy for pleural effusion and its sensitivity for detecting MPE were evaluated. Results: Ninety-eight patients (mean age, 62.4 ± 13.2 yr; 65 men) were prospectively enrolled. The diagnostic yield of UE-guided pleural biopsy for making any diagnosis was 92.9% (91/98), and its sensitivity for MPE was 88.7% (55/62). In addition, its sensitivity for pleural tuberculosis was 69.6% (16/23). The rate of postoperative chest pain was acceptable, and there was no pneumothorax. Conclusions: UE-guided pleural biopsy is a novel technique for diagnosing MPE with good diagnostic yield and sensitivity. Clinical trial registered with https://www.chictr.org.cn (ChiCTR2000033572).

Atorvastatin ameliorated PM2.5-induced atherosclerosis in rats.

PM2.5 provokes atherosclerotic events. Atorvastatin presents anti-inflammatory and antioxidant activities, and may ameliorate PM2.5-induced atherosclerosis development. The purpose of this study was to investigate the cardiotoxic effect of fine particulate matter (PM2.5) on atherosclerosis (AS) in rats, and the intervention effects of atorvastatin (ATO) on PM2.5-induced AS development. AS model was established using 32 male Wistar rats through intraperitoneal injection of vitamin D3 combined with a high-fat diet (10% fat and 4% cholesterol). The rats were randomly divided into 4 groups: control group, PM2.5-exposed group, ATO group, and ATO treated PM2.5-exposed group. PM2.5 increased levels of TC, TG, LDL, MDA, IL-6, and TNF-α, as well as decreased SOD levels. Besides, PM2.5 also enhanced AI. After the treatment of ATO, most levels of various contents in serum, including TC, TG, LDL, MDA, IL-6, TNF-α, hS-CRP, and ox-LDL, significantly decreased compared to the PM2.5-exposed group. Moreover, after the treatment of ATO, AI was significantly reduced compared to the PM2.5-exposed group. In addition, PM2.5 exacerbated the nuclear translocation and ATO resulted in an obvious decrease in PM2.5-induced nuclear translocation. The present study suggests that PM2.5 could induce oxidative damage and systemic inflammatory response in atherosclerosis model rats, while ATO could ameliorate PM2.5-induced atherosclerosis development, possibly by lowering lipid, inhibiting inflammation, and suppressing oxidation.

A Systematic Review and Meta-Analysis Comparing the Safety and Efficacy of Spinal Anesthesia and Spinal Anesthesia Combined with Obturator Nerve Block in Transurethral Resection of Bladder Tumors.

Background: Transurethral resection of bladder tumors (TURBT) is the main surgical treatment for bladder cancer, but during TURBT, it is easy to stimulate the obturator nerve passing close to the lateral side of the bladder wall and induce involuntary contraction of the adductor muscle group of the thigh innervated by it, which will affect the surgical process and lead to adverse reactions. Obturator nerve block (ONB) helps to prevent the obturator nerve reflex. This study systematically evaluated and meta-analyzed the reports on the co-application of ONB and spinal anesthesia (SA) in TURBT in recent years to provide evidence for clinical diagnosis and treatment. Methods: The clinical randomized controlled literature studies of ONB combined with SA in TURBT published in PubMed, EMBASE, the Cochrane Library, CNKI (China National Knowledge Infrastructure), and Wanfang databases from January 2000 to December 2021 were searched. After screening the qualified literature studies, the literature quality was assessed by the Jadad scale. The incidence of obturator nerve reflex, the incidence of bladder perforation, length of hospital stay, and tumor recurrence rate were used as outcome indicators. The meta-analysis was performed with the R language toolkit. Results: A total of 444 articles were initially retrieved, and after the screening, a total of 8 articles were included in the selection, and a total of 635 patients with ureterovesical tumor resection were included. The meta-analysis showed that the use of SA + ONB anesthesia during TURBT was associated with a smaller incidence of bladder perforation (RR = 0.24, 95% CI (0.11, 0.53), Z = -3.48, P=0.0005), a smaller incidence of obturator nerve reflex (RR = 0.22, 95% CI (0.13, 0.36), Z = -6.11, P=0.0001), a significantly shorter length of hospital stay (MD = -1.81, 95% CI (-2.65, -0.97), Z = -4.24, P=0.0001), and a significantly lower tumor recurrence rate (RR = 0.46, 95% CI (0.29, 0.73), Z = -3.30, P=0.001) compared with SA alone. Conclusion: The application of SA combined with ONB in TURBT can effectively reduce the incidence of obturator nerve reflex, reduce the incidence of bladder perforation, shorten the hospital stay and reduce the tumor recurrence rate.

Identification of hub genes in bladder cancer based on weighted gene co-expression network analysis from TCGA database.

BACKGROUND: Muscular invasive bladder cancer (MIBC) is a common malignant tumor in the world. Because of their heterogeneity in prognosis and response to treatment, biomarkers that can predict survival or help make treatment decisions in patients with MIBC are essential for individualized treatment. AIM: We aimed to integrate bioinformatics research methods to identify a set of effective biomarkers capable of predicting, diagnosing, and treating MIBC. To provide a new theoretical basis for the diagnosis and treatment of bladder cancer. METHODS AND RESULTS: Gene expression profiles and clinical data of MIBC were obtained by downloading from the Cancer Genome Atlas database. A dataset of 129 MIBC cases and controls was included. 2084 up-regulated genes and 2961 down-regulated genes were identified by differentially expressed gene (DEG) analysis. Then, gene ontology analysis was performed to explore the biological functions of DEGs, respectively. The up-regulated DEGs are mainly enriched in epidermal cell differentiation, mitotic nuclear division, and so forth. They are also involved in the cell cycle, p53 signaling pathway, PPAR signaling pathway, and so forth. The weighted gene co-expression network analysis yielded five modules related to pathological stages and grading, of which blue and turquoise were the most relevant modules for MIBC. Next, Using Kaplan-Meier survival analysis to identify further hub genes, the screening criteria at p ≤ .05, we found CNKSR1, HIP1R, CFL2, TPM1, CSRP1, SYNM, POPDC2, PJA2, and RBBP8NL genes associated with the progression and prognosis of MIBC patients. Finally, immunohistochemistry experiments further confirmed that CNKSR1 plays a vital role in the tumorigenic context of MIBC. CONCLUSION: The research suggests that CNKSR1, POPDC2, and PJA2 may be novel biomarkers as therapeutic targets for MIBC, especially we used immunohistochemical further to validate CNKSR1 as a therapeutic target for MIBC which may help to improve the prognosis for MIBC.

Identification of SLITRK6 as a Novel Biomarker in hepatocellular carcinoma by comprehensive bioinformatic analysis.

Hepatocellular carcinoma (HCC) is the most common primary malignancy of the adult liver and morbidity are increasing in recent years, however, there is still no effective strategy to prevent and diagnose HCC. Therefore, it is urgent to research the effective biomarker to predict clinical outcomes of HCC tumorigenesis. In the current study, differentially expressed genes in HCC and normal tissues were investigated using the Gene Expression Omnibus (GEO) dataset GSE144269 and The Cancer Genome Atlas (TCGA). Gene differential expression analysis and weighted correlation network analysis (WGCNA) methods were used to identify nine and 16 key gene modules from the GEO dataset and TCGA dataset, respectively, in which the green module in the GEO dataset and magenta module in TCGA were significantly correlated with HCC occurrence. Third, the enrichment score of gene function annotation results showed that these two key modules focus on the positive regulation of inflammatory response and cell differentiation, etc. Besides, PPI network analysis, mutation analysis, and survival analysis found that SLITRK6 had high connectivity, and its mutation significantly impacted overall survival. In addition, SLITRK6 was found to be low expressed in tumor cells. To summarize, SLITRK6 mutation was found to significantly affect the occurrence and prognosis of HCC. SLITRK6 was confirmed as a new potential gene target for HCC, which may provide a new theoretical basis for personalized diagnosis and chemotherapy of HCC in the future.

IFN regulatory Factor-1 induced macrophage pyroptosis by modulating m6A modification of circ_0029589 in patients with acute coronary syndrome.

BACKGROUND: Pyroptosis is identified as a novel form of inflammatory programmed cell death and has been recently found to be closely related to atherosclerosis (AS). We found that IFN regulatory factor-1(IRF-1) effectively promotes macrophage pyroptosis in patients with acute coronary syndrome (ACS). Subsequent studies have demonstrated that circRNAs are implicated in AS. However, the underlying mechanisms of circRNAs in macrophage pyroptosis remain elusive. METHODS: We detected the RNA expression of hsa_circ_0002984, hsa_circ_0010283 and hsa_circ_0029589 in human PBMC-derived macrophages from patients with coronary artery disease (CAD). The lentiviral recombinant vector for hsa_circ_0029589 overexpression (pLC5-GFP-circ_0029589) and small interference RNAs targeting hsa_circ_0029589 and METTL3 were constructed. Then, macrophages were transfected with pLC5-GFP-circ_0029589, si-circ_0029589 or si-METTL3 after IRF-1 was overexpressed and to explore the potential mechanism of hsa_circ_0029589 involved in IRF-1 induced macrophage pyroptosis. RESULTS: The relative RNA expression level of hsa_circ_0029589 in macrophages was decreased, whereas the N6-methyladenosine (m6A) level of hsa_circ_0029589 and the expression of m6A methyltransferase METTL3 were validated to be significantly elevated in macrophages in patients with ACS. Furthermore, overexpression of IRF-1 suppressed the expression of hsa_circ_0029589, but induced its m6A level along with the expression of METTL3 in macrophages. Additionally, either overexpression of hsa_circ_0029589 or inhibition of METTL3 significantly increased the expression of hsa_circ_0029589 and attenuated macrophage pyroptosis. CONCLUSION: Our observations suggest a novel mechanism by which IRF-1 facilitates macrophage pyroptosis and inflammation in ACS and AS by inhibiting circ_0029589 through promoting its m6A modification.

IFN Regulatory Factor 1 Mediates Macrophage Pyroptosis Induced by Oxidized Low-Density Lipoprotein in Patients with Acute Coronary Syndrome.

BACKGROUND: Atherosclerosis (AS) is recognized as a chronic inflammatory disease. It is caused by the interaction between inflammatory cells such as macrophages, dendritic cells, and lipoproteins. Evidence has revealed that macrophage pyroptosis in lesion contributes to the formation of the necrotic core and thinning of the fibrous cap, which plays crucial roles in the onset of acute coronary syndrome (ACS). IFN regulatory factor 1 (IRF-1) is a pleiotropic transcription factor involved in various immune processes and cell death. We propose that IRF-1 may be implicated in macrophage pyroptosis in the pathogenesis of AS and ACS. METHODS: Patients with stable angina, unstable angina, acute myocardial infarction, and clinical presentation of chest pain were enrolled. The expression of IRF-1 in human PBMC-derived macrophages was analyzed. Then, overexpression and inhibition of IRF-1 was performed in macrophages from patients with ACS to explore the possible role and mechanism of IRF-1 involvement in macrophage pyroptosis. RESULTS: The expression of IRF-1 in macrophages was upregulated in ACS patients. The overexpression or inhibition of IRF-1 effectively modulated caspase-1 activation, as well as macrophage lysis, expression of gasdermin D-N (GSDMD-N), production of IL-1ß and IL-18, and activation of NLRP3-ASC inflammasome, which were all inhibited by caspase-1 inhibitor. Further experiments revealed that pyroptosis and the downstream inflammatory response in AS induced by IRF-1 is a process that is dependent on reactive oxygen species (ROS) generation. CONCLUSION: Our observations suggest that IRF-1 potently activates ox-LDL-induced macrophage pyroptosis and may play an important role in AS and ACS.

Sodium butyrate alleviates lipopolysaccharide-induced endometritis in mice through inhibiting inflammatory response.

Endometritis is commonly occurred in dairy cows after calving and results in a great deal of property damage. Although numerous studies have been performed to find the therapeutic agents for endometritis, the incidence of this disease remains high. Short-chain fatty acids (SCFAs), the major metabolic products of anaerobic bacteria fermentation in the gut, have been reported to exhibit anti-inflammatory properties. Therefore, the purpose of this study was to investigate the protective effects and mechanisms of sodium butyrate (SB) on lipopolysaccharide (LPS)-induced endometritis in mice. The mice were administered by intraperitoneal injection of SB at 1 h before LPS injection. 24 h later, the uterus tissues were collected. Hematoxylin and eosin (H & E) stained sections of uterus were used to determine the degree of the damage. Uterine myeloperoxidase (MPO) activity was used to analyze neutrophil granulocytes concentration. The levels of pro-inflammatory cytokines tumor necrosis factor-α (TNF-α) and interleukin-1ß (IL-1ß) were measured by ELISA. The activation of the NF-κB signaling pathway proteins were detected by Western blot analysis. The results showed that SB significantly attenuated the pathological injury of the uterus tissues. SB also suppressed LPS-induced MPO activity and the production of inflammatory cytokines TNF-α and IL-1ß. Furthermore, Western blot analysis showed that SB inhibited the activation of NF-κB signaling pathway. In addition, SB could inhibit histone deacetylases. In summary, SB protects against LPS-induced endometritis through HDAC inhibition.

Protective effects of polydatin on LPS-induced endometritis in mice.

Endometritis, a common inflammation of the uterus, often causes severe damage to human and animal reproductive health. Polydatin is a polyphenol extracted from the rhizome of Polygonum cuspidatum that has anti-inflammatory and anti-oxidative effects. The purpose of this study was to investigate the underlying protective effects and mechanisms of polydatin against lipopolysaccharide (LPS)-induced endometritis in mice. The mouse model of endometritis was established by injection of LPS through the vagina. The uterine tissues of each group were gathered to analyze histopathological changes, inflammatory cytokine production, and the degree of activation of the NF-κB and Nrf2 signaling pathways. The myeloperoxidase (MPO) activity assay indicated that polydatin treatment significantly alleviated inflammatory cell infiltration in LPS-induced endometritis mice. Furthermore, polydatin treatment remarkably impeded the expression of TNF-α, IL-1ß, and IL-6 by ELISA assay. Hematoxylin-eosin staining (H&E) showed that polydatin significantly decreased impairment of the uterus. In addition, polydatin was also found to suppress LPS-induced NF-κB activation in a dose-dependent manner. The expression of Nrf2 and HO-1 was enhanced by polydatin treatment. All the results suggest that polydatin helpfully alleviates LPS-induced endometritis by suppressing the NF-ĸB signaling pathway and activating the Nrf2 signaling pathway.

MiR-182 promotes cell proliferation, migration and invasion by targeting FoxF2 in endometrial carcinoma cells.

miR-182 has been reported to be up-regulated in many tumors, including endometrial carcinoma (EC). However, effects of miR-182 on the development of EC and possible molecular mechanisms have not been fully reported. The purpose of this study was to investigate the function of miR-182 and its potential mechanism in EC cell line RL95-2. At first, the expression of miR-182 in RL95-2 cells was inhibited using miR-182 inhibitor and detected by qRT-PCR. The expression of its target FoxF2 was also changed using lentiviral-mediated over-expression vector or interfering RNA vector. Cell migration and invasion, cell cycle progress and colony formation of RL95-2 cells were examined and statistically analyzed after the inhibition of miR-182 and/or altered expression of FoxF2. The inhibition of miR-182 significantly increased the expression of FoxF2, decreased the numbers of migrated and invaded cells, as well as the number of colonized cells, induced cell cycle arrest to the G1 phase, and suppressed epithelial-mesenchymal transition. Lentiviral-mediated over-expression of FoxF2 showed similar functions to miR-182 inhibition, whereas lentiviral-mediated down-regulation of FoxF2 displayed the opposite effects. The effects of miR-182 inhibitor on cell proliferation, migration, and invasion were reversed when the expression of both miR-182 and FoxF2 were suppressed. Our findings indicate miR-182 acts as an oncogenic miRNA and promotes cell proliferation, migration, and invasion by targeting FoxF2 in EC.

Statin Attenuated Myocardial Inflammation Induced by PM2.5 in Rats.

BACKGROUND: Here, the study aims to explore the effect of PM2.5 exposure on atherosclerosis in rats. MATERIALS AND METHODS: 32 Wistar rats were selected in our study. An atherosclerosis model was established. All rats were evenly divided into four groups, including normal control group (NC), model control group (MC), model PM2.5 group (PM2.5) and model Atorvastatin group (Atorvastatin). The rats in NC and model control group were treated with saline 1 ml/kg body weight by tail intravenous injection, while the rats in PM2.5 group were exposed to PM2.5 suspension. The rats in atorvastatin group were given atorvastatin by gavage with 10 mg·kg-1·per day for 12 weeks until PM2.5 injection. After 24 h, all rats in each group were sacrificed. Pathological analysis, immunohistochemistry (IHC) and electrophoretic mobility shift assays (EMSA) were carried out. RESULTS: PM2.5 exposure significantly reduced the levels of triglyceride (TG), high density lipoprotein (HDL) and superoxide dismutase (SOD), but promoted the levels of total cholesterol (TC), low density lipoprotein (LDL), atherosclerosis index (AI), malondialdehyde (MDA), tumor necrosis factor-α (TNF-α) and high-sensitivity C-reactive protein (hs-CRP) in the rats of PM2.5 group than MC group (p < 0.05). PM2.5 group showed activated nuclear factor-kappa B (NF-κB), seriously damaged myocardial coronary branches and the highest nuclear translocation rate. Atorvastatin significantly improved the levels of TG, HDL, SOD, interleukin-6 (IL-6), and reduced the levels of TC, LDL, AI, MDA, TNF-α, hs-CRP, oxidized low-density lipoprotein (ox-LDL) and blood pressure, even the nuclear translocation rate. CONCLUSIONS: PM2.5 exposure contributes to atherosclerosis in rats, which correlate with the levels of cholesterol, oxidative stress and inflammatory response. Atorvastatin could attenuate myocardial inflammation caused by PM2.5 exposure in rats.

Regulation of epithelial-mesenchymal transition by tumor-associated macrophages in cancer.

It should be urgently better understood of the mechanism that contributes cancer aggressiveness. Epithelial-mesenchymal transition (EMT) plays a fundamental role in tumor progression and metastasis formation by invasion, resistance to cell death and senescence, resistance to chemotherapy and immunotherapy, immune surveillance, immunosuppression and inflammation, confers stem cell properties. Tumor-associated macrophages (TAMs) are key orchestrators and a set of macrophages in tumor microenvironment. They are major players in the connection between inflammation and cancer. TAMs could promote proliferation, invasion and metastasis of tumor cells, stimulate tumor angiogenesis, and inhibit anti-tumor immune response mediated by T cell followed by promoting tumor progression. Recently, studies showed that TAMs played critical role in the regulation of EMT in cancer, although the underlying mechanism of TAMs-mediated acquisition of EMT has been largely unclear. This review will discuss recent advances in our understanding of the role of TAMs in the regulation of EMT during tumorigenesis and summarize the recent ongoing experimental and pre-clinical TAMs targeted studies.

Association between TNF-α gene 308G>A polymorphism and lung cancer risk: a meta-analysis.

Many studies have investigated the association between tumor necrosis factor alpha (TNF-α) gene 308G/A polymorphism and lung cancer risk, but the results were inconsistent. We thus comprehensively searched the PubMed, EMBASE, and BIOSIS Previews databases and extracted data from all eligible articles to estimate the association between TNF-α gene 308G/A polymorphism and lung cancer risk. The pooled odds ratio (OR) with 95 % confidence intervals (CIs) were calculated. Twelve case-control studies in 11 articles involving 2,436 cases and 2,573 controls were included in the meta-analysis to assess the association between TNF-α gene 308G>A polymorphism and susceptibility to lung cancer. Overall, TNF-α gene 308G>A polymorphism was significantly associated with an increased risk of lung cancer for A vs. G (OR = 1.13, 95 % CI 1.00 ~ 1.27, P = 0.04). Subgroup analysis by ethnicity showed that there was a significant association between TNF-α gene 308G>A polymorphism and increased risk of lung cancer in Asians, but not in Caucasians. In subgroup analysis by tumor type, there were significant associations between TNF-α gene 308G>A polymorphism and increased risk of lung cancer in small cell lung cancer (SCLC) for AA+AG vs. GG, in non-small cell lung cancer (NSCLC) for A vs. G, AA vs. GG, and AA+AG vs. GG. No association between the genotypes and different stages of lung cancer was detected. The meta-analysis suggests that TNF-α gene 308G>A polymorphism is associated with an increased risk of lung cancer, particularly among Asians, both for SCLC and NSCLC, considering tumor type.

Papillary serous carcinoma of the cervix mixed with squamous cells: A report of the first case.

OBJECTIVE: Primary papillary serous carcinoma (PPSC) of the cervix is rarely recognized, with the aggressive and unpredictable course. Here we report a case of primary adenosquamous papillary serous carcinoma of the cervix in a woman who underwent comprehensive treatment. CASE: A 53-year-old woman presented with irregular vaginal bleeding in hospital. The patient with a diagnosis of PPSC by an intracolposcopic biopsy received radical hysterectomy with bilateral salpingo-oophorectomy, right pelvic lymphadenectomy, left pelvic lymph node dissection, and postoperative concurrent chemoradiotherapy. Postoperative immunohistochemistry showed that CK5/6, CK7, P16, CEA, CA12-5 and P53 were positive. During 17 months after operation, the patient demonstrated distant metastases of lymph nodes and finally died of brain metastasis. CONCLUSIONS: Papillary serous adenocarcinoma of the cervix mixed with squamous cell carcinoma has not been reported since now, and here, this is the first documented case. Despite surgery and concurrent chemoradiotherapy, which were reported as effective therapeutic strategies for papillary serous adenocarcinoma of the cervix, the patient showed a poorer prognosis. Taken together, papillary serous adenosquamous carcinoma of the cervix could be more malignant than pure papillary serous adenocarcinoma.