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Recent studies suggest that rare variants exhibit stronger effect sizes and might play a crucial role in the etiology of lung cancers (LC). Whole exome plus targeted sequencing of germline DNA was performed on 1045 LC cases and 885 controls in the discovery set. To unveil the inherited causal variants, we focused on rare and predicted deleterious variants and small indels enriched in cases or controls. Promising candidates were further validated in a series of 26,803 LCs and 555,107 controls. During discovery, we identified 25 rare deleterious variants associated with LC susceptibility, including 13 reported in ClinVar. Of the five validated candidates, we discovered two pathogenic variants in known LC susceptibility loci, ATM p.V2716A (Odds Ratio [OR] 19.55, 95%CI 5.04–75.6) and MPZL2 p.I24M frameshift deletion (OR 3.88, 95%CI 1.71–8.8); and three in novel LC susceptibility genes, POMC c.*28delT at 3′ UTR (OR 4.33, 95%CI 2.03–9.24), STAU2 p.N364M frameshift deletion (OR 4.48, 95%CI 1.73–11.55), and MLNR p.Q334V frameshift deletion (OR 2.69, 95%CI 1.33–5.43). The potential cancer-promoting role of selected candidate genes and variants was further supported by endogenous DNA damage assays. Our analyses led to the identification of new rare deleterious variants with LC susceptibility. However, in-depth mechanistic studies are still needed to evaluate the pathogenic effects of these specific alleles. [ABSTRACT FROM AUTHOR]

The etiology of lung cancer (LC) is a multifactorial and reflects the interaction between environment and genetic factors. Single nucleotide polymorphism (SNPs) in the promoter region of some cytokines may affect the overall expression of the cytokine, and, hence, involve in the development of cancer. This study aimed to evaluate the association of two SNPs in the promoter region of TNF-á gene and serum of TNF-á level of in the development of LC. A total of 50 patients with LC and other age-matched 40 apparently healthy individuals were enrolled in this casecontrol study. From each participant, 5 mL of peripheral blood were collected. DNA was isolated from leukocytes and TNF-á gene was amplified with two specific sets of primers. Genotyping was achieved by restriction fragment length polymorphism (RFLP). Serum level of TNF-á was measured using enzyme linked immune-sorbent assay (ELISA). The frequency of GG, GA and AA genotypes of the SNPTNF-á-308G/A among patients was 38%, 44% and 18%, respectively compared with 60%, 37.5% and 2.5% respectively among controls. Logistic regression test revealed a significant difference in the frequency of variant genotype (AA) between the two groups (OR=11.37, 95%CI = 1.32-97.78, P=0.027). The variant allele (A allele) of this polymorphism almost 2-time more frequent in patients than controls with a significant difference (OR=2.47,95%CI=1.27-4.82, P=0.012). No significant differences in the frequencies of genotypes and allele of TNF-á-863C/A between patients and controls. serum level of TNF-á in patients was 15 pg/mL (range 0-84 pg/mL) which is higher than that of controls (median 7 pg/mL, range 0-86 pg/mL) with a significant difference (P=0.022). These data suggest the importance of TNF-á-308G/A gene polymorphism as a risk factor for LC. Serum levels of TNFá increased in patients with active LC. [ABSTRACT FROM AUTHOR]

Canada is proposing a ban on asbestos, and the US Environmental Protection Agency has listed it among the first 10 materials it is investigating under the new Toxic Substances Control Act revisions. However, this effort is currently running up against enormous industry and political opposition. Here, we detail the activities in the early 1970s of the Friction Materials Standards Institute, an industry trade association, to stifle earlier attempts to regulate asbestos use in brake linings, one of the oldest and most obvious sources of asbestos exposure to mechanics, among others. [ABSTRACT FROM AUTHOR]

Cancer stem cells (CSCs) play a central role in the development of cancer. The canonical Wnt/β-catenin pathway is critical for maintaining stemness of CSCs. Phytochemicals from dietary compounds possess anti-CSCs properties and have been characterized as promising therapeutic agents for the prevention and treatment of many cancers. To date, the involvement and function of miR-19, a key oncogenic miRNA, in regulating Wnt/β-catenin pathway and lung CSCs has not been defined. Meanwhile, the effect of sulforaphane (SFN) on lung CSCs also remains to be elucidated. Here, we reported that lung CSCs up-regulated miR-19a and miR-19b expression. Overexpression of miR-19a/19b enhanced the ability of tumorsphere formation, up-regulated the expression of lung CSCs markers, increased Wnt/β-catenin pathway activation and β-catenin/TCF transcriptional activity in lung CSCs. In contrary, down-regulation of miR-19 suppressed lung CSCs activity and Wnt/β-catenin activation. We further revealed that miR-19 activated Wnt/β-catenin pathway by directly targeting GSK3β, the key negative modulator of this pathway. Moreover, we showed that SFN exhibited inhibitory effect on lung CSCs through suppressing miR-19 and Wnt/β-catenin pathway. Taken together, these data illustrate the role of miR-19 in regulating lung CSCs traits and miR-19/GSK3β/β-catenin axis in SFN intervention of lung CSCs. Findings from this study could provide important new insights into the molecular mechanisms of lung CSCs regulation as well as its target intervention. [ABSTRACT FROM AUTHOR]

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The etiology of peripheral squamous cell lung cancer (PSCCa) remains unknown. Here, we show that this condition spontaneously develops in mice in which the genes for two oxysterol receptors, Liver X Receptor (LXR) α (Nr1h3) and β (Nr1h2), are inactivated. By 1 y of age, most of these mice have to be euthanized because of severe dyspnea. Starting at 3 mo, the lungs of LXRα,βDko mice, but not of LXRα or LXRβ single knockout mice, progressively accumulate foam cells, so that by 1 y, the lungs are covered by a "golden coat." There is infiltration of inflammatory cells and progressive accumulation of lipid in the alveolar wall, type 2 pneumocytes, and macrophages. By 14 mo, there are three histological lesions: one resembling adenomatous hyperplasia, one squamous metaplasia, and one squamous cell carcinoma characterized by expression of transformation-related protein (p63), sex determining region Y-box 2 (Sox2), cytokeratin 14 (CK14), and cytokeratin 13 (CK13) and absence of thyroid transcription factor 1 (TTF1), and prosurfactant protein C (pro-SPC). RNA sequencing analysis at 12 mo confirmed a massive increase in markers of M1 macrophages and lymphocytes. The data suggest a previously unidentified etiology of PSCCa: cholesterol dysregulation and M1 macrophage-predominant lung inflammation combined with damage to, and aberrant repair of, lung tissue, particularly the peripheral parenchyma. The results raise the possibility that components of the LXR signaling may be useful targets in the treatment of PSCCa. [ABSTRACT FROM AUTHOR]

Radon causes lung cancer when it is trapped inside the lungs. Therefore it is very important to analyze the radon concentration in water and soil samples. In the present investigation, water and soil samples collected from 20 different locations of Jodhpur and Nagaur districts of Northern Rajasthan, India have been studied by using RAD7. The measured radon concentration in water samples varies from 0.5 to 15 Bq l −1 . The observed values lie within the safe limit as set by UNSCEAR, 2008. The total annual effective dose due to radon in water corresponding to all studied locations has been found to be well within the safe limit of 0.1 mSv y −1 as recommended by World Health Organization ( WHO, 2004 ) and European Council ( EU, 1998 ). The measurements carried out on radon concentration in soil samples reveal a variation from 1750 to 9850 Bq m −3 . These results explore that the water of Jodhpur and Nagaur districts is suitable for drinking purpose without posing any health hazard but soil hazards depend upon its permeability and radon concentration. [ABSTRACT FROM AUTHOR]

Early detection through low-dose computed tomographic screening for lung cancer and implementation of smoking cessation can reduce mortality related to lung cancer. While studies delineating the relationship between smoking cessation strategies and lung cancer screening programs remain sparse, we aim to review available data on their importance both individually and synergistically. Strategies and obstacles for implementation are also discussed. [ABSTRACT FROM AUTHOR]

Lung cancer encompasses a heterogeneous group of malignancies. Here we discuss how the remarkable diversity of major lung cancer subtypes is manifested in their transforming cell of origin, oncogenic dependencies, phenotypic plasticity, metastatic competence and response to therapy. More specifically, we review the increasing evidence that links this biological heterogeneity to the deregulation of cell lineage-specific pathways and the transcription factors that ultimately control them. As determinants of pulmonary epithelial differentiation, these poorly characterized transcriptional networks may underlie the etiology and biological progression of distinct lung cancers, while providing insight into innovative therapeutic strategies. [ABSTRACT FROM AUTHOR]

The classification of outdoor air pollution as carcinogenic for humans strengthens the increasing concern about particulate matter (PM). We previously demonstrated that PM exposure produces an antiapoptotic effect resulting from polycyclic aromatic hydrocarbons (PAH) and water-soluble components. In this study, we investigated transition metallic compounds, particularly iron, in order to decipher their underlying molecular mechanisms that prevent apoptosis. Human bronchial epithelial cells were exposed for 4 h to different PM samples with established antiapoptotic effect (e.g. PM-AW) or not (e.g. PM-VS) or to their metallic components (Fe, Mn, Zn and Al) before apoptosis induction by the calcium ionophore A23187 or Staurosporine. PM-AW, Fe, Mn and Al significantly reduced induced apoptosis. The antiapoptotic effect of Fe was enhanced by benzo(a)pyrene, a typical PAH compound, but was totally reversed by the iron chelator, deferiprone. Furthermore, particles and iron triggered cellular ROS generation and prevented the depletion in glutathione levels observed during A23187-induced apoptosis. In contrast to benzo(a)pyrene, PM-AW and Fe rapidly activated NRF2, subsequently upregulated several target genes ( HO1 , NQO1 and GPX1 ) and modulated some genes which control cell death ( BCL2 , BAX and p53 ). The key role of the NRF2 pathway in the antiapoptotic effect mediated by Fe and PM was demonstrated using siRNA technology. Our results suggest that the iron component participates in the antiapoptotic effect of PM by activating a NRF2-dependent antioxidant process. As resisting to cell death is one of the hallmarks of cancer cells, these findings provide additional clues for understanding the development of lung cancer after atmospheric pollution exposure. [ABSTRACT FROM AUTHOR]

Smoking is the second reason for developing lung cancer. Our goal was to determine how the amount of Po in the tobacco is distributed among the cigarette parts and what percentage reaches the respiratory system, calculating the effective dose. Po from tobacco, filter and ash samples were measured from seven Romanian cigarette brands by alpha spectrometry. The obtained average results were 13.97 ± 1.75 mBq/cigarette in the tobacco; 1.61 ± 0.25 mBq/cigarette in the filter and 3.33 ± 0.29 mBq/cigarette in the ash. The dose originating from active smoking was estimated to have an average of 8.36 ± 0.91 μSv/year, while the passive smoking dose reaching the respiratory system was 5.92 ± 0.49 μSv. [ABSTRACT FROM AUTHOR]

Genetic variations in NFKB1 have been associated with cancer risk. This investigation intended to evaluate the possible association between common variants in NFKB1 and lung cancer risk and gene–gene and gene–environment interactions. A study containing 384 Chinese lung cancer cases and 387 cancer-free controls was conducted. 5 htSNPs (rs3774934, rs13117745, rs230541, rs1801, rs3774965) in NFKB1 and interaction with common variants in NFKB1 and PPP1R13L and CD3EAP and smoking-duration were assessed. No association with lung cancer risk was detected for individual htSNP in four genetic models, but the haplotype consisting of the wild-type alleles of rs3774934 G , rs13117745 C , rs230541 A , and rs1801 G was associated with lowered lung cancer risk after adjustment for smoking duration [OR (95% CI) = 0.71 (0.51–0.98), P = 0.036]. There was no interaction between NFKB1 polymorphisms and PPP1R13L and CD3EAP and smoking status in relation to lung cancer risk. Two significant models: smoking duration as main effect ( P < 0.0010) and smoking duration– PPP1R13L rs1970764 combination ( P = 0.0040–0.0050) were tested. The results suggest that NFKB1 common variants and smoking duration and smoking duration– PPP1R13L rs1970764 interaction could be concerned with the lung cancer development in a Chinese population. The present findings add to the evidence implicating inflammation in lung cancer etiology. [ABSTRACT FROM AUTHOR]

Dyspnea is a symptom that severely affects the quality of life of terminally ill patients. Its frequency differs considerably between studies. We aimed to characterize the frequency of dyspnea in a palliative care hospital ( PCH) and to identify factors predisposing to dyspnea, particularly during the very last days of life, as a function of the underlying disease. Episodes of dyspnea were identified by the computerized extraction of prospectively collected data from the reports of care assistants or from medical observations recorded in the medical files for all stays at our PCH during the last 6 years. There were 6455 hospital stays, 88% ending in the death of the patient; 13,282 episodes of dyspnea were recorded during 2608 hospital stays (40%). Dyspnea was more frequently observed in cases of cancer than in other conditions ( RR = 1.30; 95% CI: 1.14-1.48). Pulmonary metastasis increased the risk of dyspnea from 37% to 51% ( RR = 1.37; 95% CI: 1.29-1.46). Dyspnea frequency varied with the primary cancer site, from 24% (brain cancer) to 60% (esophageal cancer). The data for cancer patients staying for more than 6 days who subsequently died indicated that 8% of patients experienced dyspnea exclusively during the last 4 days of the life, independently of the site of the primary cancer. Dyspnea during the last few days of life requires systematic assessment. Exclusively terminal dyspnea should be distinguished from more precocious dyspnea, as the pathophysiological mechanisms and treatments of these two forms are probably different. [ABSTRACT FROM AUTHOR]

Objective The examination of lung cancer by histology type is important for monitoring population trends that have implications for etiology and prevention, screening and clinical diagnosis, prognosis and treatment. We provide a comprehensive description of recent histologic lung cancer incidence rates and trends in the USA using combined population-based registry data for the entire nation. Materials and methods Histologic lung cancer incidence data was analyzed from CDC's National Program of Cancer Registries (NPCR) and the National Cancer Institute's Surveillance, Epidemiology and End Results (SEER) Program. Standardized rates and trends were calculated for men and women by age, race/ethnicity, and U.S. Census region. Rate ratios were examined for differences in rates between men and women, and annual percent change was calculated to quantify changes in incidence rates over time. Results Trend analysis demonstrate that overall rates have decreased, but incidence has remained stable for women aged 50 or older. Adenocarcinoma and squamous cell carcinoma were the two most common histologic subtypes. Adenocarcinoma rates continued to increase in men and women, and squamous cell rates increased in women only. All histologic subtype rates for white women exceeded rates for black women. Histologic rates for black men exceeded those for white men, except for small cell carcinoma. The incidence rate for Hispanics was nearly half the rate for blacks and whites. Conclusion The continuing rise in incidence of lung adenocarcinoma, the rise of squamous cell cancer in women, and differences by age, race, ethnicity and region points to the need to better understand factors acting in addition to, or in synergy with, cigarette smoking that may be contributing to observed differences in lung cancer histology. [ABSTRACT FROM AUTHOR]

BACKGROUND Lung cancer incidence rates overall are declining in the United States. This study investigated the trends by histologic type and demographic characteristics. METHODS Surveillance, Epidemiology, and End Results (SEER) program rates of microscopically confirmed lung cancer overall and squamous cell, small cell, adenocarcinoma, large cell, other, and unspecified carcinomas among US whites and blacks diagnosed from 1977 to 2010 and white non-Hispanics, Asian/Pacific Islanders, and white Hispanics diagnosed from 1992 to 2010 were analyzed by sex and age. RESULTS Squamous and small cell carcinoma rates declined since the 1990s, although less rapidly among females than males. Adenocarcinoma rates decreased among males and only through 2005, after which they then rose during 2006 to 2010 among every racial/ethnic/sex group; rates for unspecified type declined. Male/female rate ratios declined among whites and blacks more than among other groups. Recent rates among young females were higher than among males for adenocarcinoma among all racial/ethnic groups and for other specified carcinomas among whites. CONCLUSIONS US lung cancer trends vary by sex, histologic type, racial/ethnic group, and age, reflecting historical cigarette smoking rates, duration, cessation, cigarette composition, and exposure to other carcinogens. Substantial excesses among males have diminished and higher rates of adenocarcinoma among young females have emerged as rates among males declined more rapidly. The recognition of EGFR mutation and ALK rearrangements that occur primarily in adenocarcinomas are the primary basis for the molecular revolution that has transformed lung cancer diagnosis and treatment over the past decade, and these changes have affected recent type-specific trends. Cancer 2014;120:2883-2892. © 2014 American Cancer Society. [ABSTRACT FROM AUTHOR]

Non-small-cell lung cancers (NSCLCs), the most common lung cancers, are known to have diverse pathological features. During the past decade, in-depth analyses of lung cancer genomes and signalling pathways have further defined NSCLCs as a group of distinct diseases with genetic and cellular heterogeneity. Consequently, an impressive list of potential therapeutic targets was unveiled, drastically altering the clinical evaluation and treatment of patients. Many targeted therapies have been developed with compelling clinical proofs of concept; however, treatment responses are typically short-lived. Further studies of the tumour microenvironment have uncovered new possible avenues to control this deadly disease, including immunotherapy. [ABSTRACT FROM AUTHOR]

Lung cancer is the leading cause of cancer-related deaths for both men and women. Early diagnosis of lung cancer has a 5-year survival rate of 48.8%, however, nearly 35% of stage I patients relapses after surgical resection, thus portending a poor prognosis. Therefore, detecting lung cancer in early stage and further identifying the high-risk patients would allow the opportunity to provide adjuvant therapy and possibly increase survival. There is considerable evidence that the immune system produces an autoantibody response to neoplastic cells. The detection of such autoantibodies has been shown to have diagnostic and prognostic value. Here we took advantage of the high-throughput Luminex technique to multiplex a total of 14 tumor-associated autoantigens to detect the autoantibody from the patients sera. The 14 antigens were expressed by in vitro transcription/translation system with HaloTag at N-terminus. The fusion proteins were then covalently immobilized onto the Luminex microspheres conjugated by the halo-link ligand, thus eliminating the protein purification procedure. Sera samples from cancer patients and healthy controls were interacted with the microsphere-antigen complex to measure the autoantibodies. We have developed a quick multiplex detection system for measuring autoantibody signature from patient sera with minimal cross-reaction. A panel of seven autoantibody biomarkers has generated an AUC>80% in distinguishing the lung cancers from healthy controls. This study is the first report by combining Luminex platform and HaloTag technology to detect humoral immune response in cancer patients. Due to the flexibility of the Luminex technology, this approach can be applied to others conditions such as infectious, neurological, and metabolic diseases. One can envision that this multiplex Luminex system as well as the panel of seven biomarkers could be used to screen the high-risk population with subsequent CT test based on the blood test result. [ABSTRACT FROM AUTHOR]

Lung cancer is the most common malignancy and the leading cause of cancer deaths worldwide. While smoking is by far the leading cause of lung cancer, other environmental and genetic factors influence the development and progression of the cancer. Since unique mutations patterns have been observed in individual cancer samples, identification and characterization of the distinctive lung cancer molecular profile is essential for developing more effective, tailored therapies. Until recently, personalized DNA sequencing to identify genetic mutations in cancer was impractical and expensive. The recent technological advancements in next-generation DNA sequencing, such as the semiconductor-based Ion Torrent sequencing platform, has made DNA sequencing cost and time effective with more reliable results. Using the Ion Torrent Ampliseq Cancer Panel, we sequenced 737 loci from 45 cancer-related genes to identify genetic mutations in 76 human lung cancer samples. The sequencing analysis revealed missense mutations in KRAS, EGFR, and TP53 genes in the breast cancer samples of various histologic types. Thus, this study demonstrates the necessity of sequencing individual human cancers in order to develop personalized drugs or combination therapies to effectively target individual, breast cancer-specific mutations. [ABSTRACT FROM AUTHOR]

INTRODUCTION: In cardiac tamponade, there is a filling restriction of the heart due to increased pressure of the pericardial cavity secondary to pericardial effusion. Pressure can reach values greater than that of the right heart cavities, compromising their filling, and, secondarily, affecting the preload of the left ventricle. CASE REPORT: A 52-year old male, with type 2 diabetes mellitus, consulted to the emergency department of Victor Rios Ruiz Hospital of Los Angeles, Chile for epigastric colic pain, nausea, vomiting, abdominal distention, choluria, oliguria, anorexia, constipation, asthenia, adynamia and malaise. He is admitted to the surgery ward on the suspicion of acute cholecystitis. Abdominal ultrasound showed perihepatic and perisplenic free fluid and increased caliber of the inferior vena cava, associated with bilateral pleural effusion. Hypotension, paradoxical pulse and jugular engorgement developed, so he is transferred to the ICU where echocardiography confirmed cardiac tamponade. Pericardiocentesis was performed, which showed malignant cells on microscopy. A computerized tomography (CT scan) showed a solid mass in the left inferior lung lobe, a nodule in the middle lobe and multiple mediastinal and hiliar bilateral lymphoadenopaties. DISCUSSION: Malignant pericardial effusion commonly presents as cardiac tamponade, being the lung cancer its main etiology. The prognosis of pericardial effusion in lung cancer is rather ominous, with an overall survival of less than 3 months. [ABSTRACT FROM AUTHOR]

Genome-wide association studies (GWAS) have identified a number of genetic variants associated with lung cancer risk. However, these loci explain only a small fraction of lung cancer hereditability and other variants with weak effect may be lost in the GWAS approach due to the stringent significance level after multiple comparison correction. In this study, in order to identify important pathways involving the lung carcinogenesis, we performed a two-stage pathway analysis in GWAS of lung cancer in Han Chinese using gene set enrichment analysis (GSEA) method. Predefined pathways by BioCarta and KEGG databases were systematically evaluated on Nanjing study (Discovery stage: 1,473 cases and 1,962 controls) and the suggestive pathways were further to be validated in Beijing study (Replication stage: 858 cases and 1,115 controls). We found that four pathways (achPathway, metPathway, At1rPathway and rac1Pathway) were consistently significant in both studies and the P values for combined dataset were 0.012, 0.010, 0.022 and 0.005 respectively. These results were stable after sensitivity analysis based on gene definition and gene overlaps between pathways. These findings may provide new insights into the etiology of lung cancer. [ABSTRACT FROM AUTHOR]

Lung cancer, which is mainly affected by environmental factors, is a lethal malignancy. It is also important to investigate the effect of genetic factors on lung cancer aetiology. In this study, we aimed to investigate the distribution of CYP1A1*2C, GSTT1 and GSTM1 polymorphisms in Turkish lung cancer patients to determine whether any promoting effect of polymorphisms could cause development of lung cancer. For this purpose, genomic DNA samples obtained from peripheral blood of 128 patients with lung cancer and 122 healthy subjects were analyzed. Genotyping of polymorphic enzymes were carried out by polymerase chain reaction–restriction fragment length polymorphism methods. Although there were no significant differences between groups in terms of CYP1A1 polymorphism, the carriers of CYP1A1Ile/Val genotype (odds ratio [OR] = 1.224, 95% confidence interval [CI]: 0.585–2.564) or CYP1A1Val/Val genotype (OR = 3.058, 95% CI: 0.312–30.303) had an increased risk of lung cancer development. There was no statistical difference between groups in terms of both GSTT1 null genotype (OR = 1.114, 95% CI: 0.590–2.105) and GSTM1 null genotype (OR = 0.776, 95% CI: 0.466–1.290). This is the first case–control study investigating CYP1A1Ile/Val, GSTT1 and GSTM1 polymorphisms in Turkish lung cancer patients. Although we suggest that other genes in addition to the proposed genes could play a role in lung cancer development, the results of our study will contribute to the possible associations between CYP1A1Ile/Val, GSTT1 and GSTM1 gene polymorphism on the risk of lung cancer. [ABSTRACT FROM AUTHOR]

Epidemiological studies have shown that respirable exposure to emitted cement particulate matter is associated with adverse health risk for human. The underlying mechanisms, however, are poorly understood. To examine the effect of cement, nine blinded cement-related particulates (<10 μm) were assessed with regard to their induction of the proinflammatory cytokines IL-6 and IL-8 in human primary epithelial cells (pEC) from oropharyngeal mucosa as well as from nonsmall-cell lung carcinoma (non-SCLC) cells A549. It was demonstrated that the cement specimens did not act cytotoxic as assessed by the lactate dehydrogenase (LDH) assay. The basal and IL-1β-induced IL-8 expression was suppressed, in contrast to an unchanged IL-6. At the transcript level the basal and induced IL-6 and IL-8 gene expression was not influenced by cement dust. To discover the mechanism by which cement influenced the IL-8 expression the following experiments were performed. Submerse exposure experiments have shown that the release of IL-8 was suppressed by cement dust. Furthermore, the incubation of IL-8 with cement-related specimens under cell-free condition led to a loss of immunoreactive IL-8. An immunological masking of IL-8 by free soluble components of respiratory epithelial cells was excluded. Thus, the decrease of IL-8 protein content after cement exposure seems to be a result of the adsorption of IL-8 protein to cement particles and the inhibition of IL-8 release. In conclusion, due to absent cytotoxic and inflammatory effects of cement-related specimens in both human pEC and A549 cell models it remains open how cement exposure may lead to the respiratory adverse effects in humans. © 2010 Wiley Periodicals, Inc. Environ Toxicol, 2012. [ABSTRACT FROM AUTHOR]

Abstract: Superiorvena cava (SVC) obstruction is typically dramatic, but the diagnosis is usually easy. However, elucidation of the etiology is more difficult. In this case report we present a case of 46-year-old smoker who presented with SVC syndrome, evaluation and investigations revealed a dissecting aortic aneurysm as an etiology. This highlights the fact that a dissecting aortic aneurysm can masquerade as a mediastinal mass bearing a resemblance with bronchogenic carcinoma in a chronic smoker. An index of suspicion and imaging modalities like a computed tomography scan is diagnostic. [Copyright &y& Elsevier]

The article reports on the cases of oral cancer in India and mentions that 86 percent of total oral cancer patients are from India. Topics discussed includes oral cancer due to consumption of chewing tobacco, ailments caused due to tobacco use such as heart and lung diseases and increasing cases of cervical and breast cancers among women in India.

The article focuses on higher exposure to nicotine, cotinine, tobacco-related carcinogens and volatile organic compounds associated with water pipe smoking. Topics discussed include the 73-fold increase in nicotine among others found among participants of a study on the risks associated with water pipe smoking, the potential for nicotine dependance among water pipe smokers and Centers for Disease Control and Prevention data on the use of hookahs among young adults.