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Background: Although many studies suggested the benefit of smoking cessation among pregnant women in reducing the risk of preterm birth (PTB), the timing of the effect of the cessation remains inconclusive. Objectives: To examine the association of trimester‐specific smoking cessation behaviours with PTB risk. Methods: We included 199,453 live births in Western New York between 2004 and 2018. Based on self‐reported cigarette smoking during preconception and in each trimester, we created six mutually exclusive groups: non‐smokers, quitters in each trimester, those who smoked throughout pregnancy, and inconsistent smokers. Risk ratios (RRs) and 95% confidence intervals (CIs) were estimated using Poisson regression to examine the association between smoking cessation and PTB. Effect modification by illegal drug use, maternal age, race and ethnicity and pre‐pregnancy body mass index (BMI) was investigated multiplicatively by ratio of relative risk and additively by relative excess risk due to interaction (RERI). Results: Overall, 6.7% of women had a PTB; 14.1% smoked throughout pregnancy and 3.4%, 1.8% and 0.8% reported quitting smoking during the first, second and third trimesters, respectively. Compared to non‐smokers, third‐trimester cessation (RR 1.20, 95% CI 1.01, 1.43) and smoking throughout pregnancy (RR 1.27, 95% CI 1.21, 1.33) were associated with a higher PTB risk, while quitting smoking during the first or second trimester, or inconsistent smoking was not associated with PTB. A positive additive interaction was identified for maternal age and late smoking cessation or smoking throughout pregnancy on PTB risk (RERI 0.17, 95% CI 0.00, 0.36), and a negative interaction was observed for pre‐pregnancy BMI ≥30 kg/m2 (ratio of relative risk 0.70, 95% CI 0.63, 0.78; RERI −0.42, 95% CI −0.56, −0.30). Conclusion: Compared to non‐smokers, smoking throughout pregnancy and third‐trimester smoking cessation are associated with an increased risk of PTB, while quitting before the third trimester may not increase PTB risk. [ABSTRACT FROM AUTHOR]

Palmitoylation, a critical lipid modification of proteins, is involved in various physiological processes such as altering protein localization, transport, and stability, which perform essential roles in protein function. Palmitoyltransferases are specific enzymes involved in the palmitoylation modification of substrates. S‐palmitoylation, as the only reversible palmitoylation modification, is able to be deacylated by deacyltransferases. As an important mode of programmed cell death, apoptosis functions in the maintenance of organismal homeostasis as well as being associated with inflammatory and immune diseases. Recently, studies have found that palmitoylation and apoptosis have been demonstrated to be related in many human diseases. In this review, we will focus on the role of palmitoylation modifications in apoptosis. [ABSTRACT FROM AUTHOR]

Research findings remain inconsistent whether caffeine consumption is associated with invasive breast cancer. We aimed to examine the association between caffeine intake from coffee and tea and incident invasive breast cancer among postmenopausal women. We included 79 871 participants in the Women's Health Initiative Observational Study in the current analysis. Incident invasive breast cancers were identified through September 30, 2015. Caffeine intake (mg/day) from caffeinated and decaffeinated coffee and tea was estimated based on self‐reported frequency (cups/day) and average caffeine amount in each beverage. Cox proportional hazards regression models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs). Subgroup analyses were conducted to explore whether associations of caffeine intake from coffee and tea with invasive breast cancer were different by age, race and ethnicity, smoking status, body mass index, history of hormone therapy use, alcohol intake and subtypes of breast cancer. During a median follow‐up of 16.0 years, 4719 incident invasive breast cancers were identified. No significant association was found between caffeine intake from coffee and tea and invasive breast cancer incidence after adjusting for demographic, lifestyle and reproductive factors: HRs (95% CIs) for increasing quartiles of caffeine intake compared to the lowest were 1.03 (0.94, 1.12), 1.04 (0.95, 1.13) and 1.03 (0.94, 1.13), respectively (P‐for‐trend =.54). No significant associations of coffee and tea intake (cups/day) with overall breast cancer risk were found. Our findings are consistent with others showing no clear association of caffeine consumption with invasive breast cancer among postmenopausal women. What's new? Caffeine intake is variously linked to mechanisms behind prevention and promotion of breast cancer. Hence, it remains unclear whether caffeine has a role in breast carcinogenesis. Here, associations between caffeine intake from coffee and tea and incident invasive breast cancer were investigated among postmenopausal women. Analyses reveal no association between breast cancer risk and caffeine intake from coffee or tea. This null association held regardless of demographic, lifestyle and reproductive factors. While additional studies could shed light on relationships between caffeine and breast carcinogenesis, these findings support the idea that caffeine has little impact on postmenopausal invasive breast cancer risk. [ABSTRACT FROM AUTHOR]

Helicobacter pylori (Hp) is crucial in gastric carcinogenesis, but infection alone is not a sufficient cause, and the interaction between Hp infection and other risk factors has not been adequately studied. We conducted a pooled analysis of seven case‐control studies from the Stomach cancer Pooling (StoP) Project, comprising 1377 cases and 2470 controls, to explore the interaction among Hp infection and tobacco smoking, alcohol drinking, socioeconomic status (SES) and dietary salt intake on the risk of gastric cancer. We estimated summary odds ratios (ORs) and the corresponding 95% confidence intervals (CIs) by multivariate unconditional logistic regression. The analysis showed no consistent interaction between Hp infection and cigarette smoking, while interaction was more than multiplicative for alcohol drinking (OR = 1.38, 95% CI: 1.07‐1.77, P‐interaction 0.02) and high intake of salt (OR = 2.62, 95% CI: 1.88‐3.65, P‐interaction = 0.04). The interaction with SES followed the multiplicative model (P = 0.49), resulting in a weakening among infected individuals of the protective effect of high SES among observed Hp‐negative individuals. The interactions found were more pronounced in subjects with history of peptic ulcer. The interactions with Hp infection were stronger for cigarette smoking and dietary salt in the case of noncardia cancer, and for alcohol and SES in the case of cardia cancer. No differences were found when stratifying for histologic type. This large‐scale study aimed to quantify the interaction between Hp infection and other modifiable risk factors of gastric cancer revealed that the benefit of combined Hp eradication and lifestyle modification on gastric cancer prevention may be larger than commonly appreciated. What's new? Why do some Helicobacter pylori infections lead to gastric cancer, but not others? In this study, the authors investigated the interaction between H. pylori and other gastric cancer risk factors, including tobacco smoking, alcohol drinking, socioeconomic status (SES) and dietary salt. They combined seven case‐control studies and performed pooled analysis to quantify the interaction between risk factors. They found that the associations with alcohol and salt were more than multiplicative. Smoking and SES, on the other hand, combined with H. pylori infection in a multiplicative fashion. Thus, lifestyle modifications could boost the benefit of eradicating H. pylori. [ABSTRACT FROM AUTHOR]

Graphs can be used to represent the direct and indirect relationships between variables, and elucidate complex relationships and interdependencies. Detecting structure within a graph is a challenging problem. This problem is studied over a range of fields and is sometimes termed community detection, module detection, or graph partitioning. A popular class of algorithms for module detection relies on optimizing a function of modularity to identify the structure. In practice, graphs are often learned from the data, and thus prone to uncertainty. In these settings, the uncertainty of the network structure can become exaggerated by giving unreliable estimates of the module structure. In this work, we begin to address this challenge through the use of a nonparametric bootstrap approach to assessing the stability of module detection in a graph. Estimates of stability are presented at the level of the individual node, the inferred modules, and as an overall measure of performance for module detection in a given graph. Furthermore, bootstrap stability estimates are derived for complexity parameter selection that ultimately defines a graph from data in a way that optimizes stability. This approach is utilized in connection with correlation graphs but is generalizable to other graphs that are defined through the use of dissimilarity measures. We demonstrate our approach using a broad range of simulations and on a metabolomics dataset from the Beijing Olympics Air Pollution study. These approaches are implemented using bootcluster package that is available in the R programming language. [ABSTRACT FROM AUTHOR]

Gastrointestinal cancer patterns are distinct among populations. Our study aims to compare the incidence and risk of gastrointestinal cancers between Chinese American and non‐Hispanic whites in Los Angeles, CA, USA, to those of people indigenous to Shanghai to elucidate the changing patterns of gastrointestinal cancers. Cancer incidence data from 1988 to 2012 were extracted from the Cancer Incidence in Five Continents plus database. The age standardized incidence and estimated annual percentage change were calculated to estimate the temporal trends of gastrointestinal cancers. Traditional Poisson regression models and three‐factor constrained Poisson regression models were applied to compare the gastrointestinal cancer risk across populations. The incidences of oesophageal, stomach, liver and gall bladder cancers were higher among indigenous Chinese residents of Shanghai than among the other two populations in Los Angeles. While the incidences of colorectal and pancreatic cancer were higher among non‐Hispanic whites, Chinese American immigrants were considered to be at an intermediate level for most gastrointestinal cancers. The gender‐specific gastrointestinal cancer disparities across populations, especially between Shanghai Chinese and non‐Hispanic US whites, were significant regardless of age, period or cohort scale. However, the regional differences in gastrointestinal cancer rates decreased over time. Most gastrointestinal cancer patterns in Chinese American immigrants were more aligned to those of their new country of residence than to those of their original country. The disparities in gastrointestinal cancers across populations indicate that environmental factors might play a key role in cancer genesis. Shift in environmental exposures may result in significant changes in gastrointestinal cancer incidence. What's new? China has among the highest incidences of gastrointestinal (GI) cancers in the world. But how much of this is due to genetics, and how much to environmental factors? In this epidemiological study, the authors found that, while Chinese‐American immigrants had somewhat higher rates of GI cancers than whites in the same city, they had significantly lower rates than Chinese residents of urban Shanghai. These results indicate that environmental and dietary factors may play a more important role than genetic factors in gastrointestinal oncogenesis. [ABSTRACT FROM AUTHOR]

Background & Aims: The potential interaction between family history of liver cancer and HBV infection on liver cancer has not been fully examined. Methods: We conducted a population‐based case‐control study composed of 2011 liver cancer cases and 7933 controls in Jiangsu province, China from 2003 to 2010. Data on major risk or protective factors were collected and HBV/HCV sero‐markers were assayed using blood samples. Semi‐Bayes (SB) adjustments were applied to provide posterior estimates. Results: Both family history of liver cancer (adjusted odds ratios [OR]: 4.32, 95% confidence intervals [CI]: 3.25‐5.73) and hepatitis B surface antigen (HBsAg) positivity (adjusted OR: 9.94, 95% CI: 8.33‐11.87) were strongly associated with liver cancer development. For individuals with different combinations of serological markers, the adjusted ORs were 8.45 (95% CI: 5.16‐13.82) for HBsAg‐ and HBcAb‐positive; 7.57 (95% CI: 4.87‐11.77) for HBsAg‐, HBeAg‐ and HBcAb‐positive; and 3.62 (95% CI: 2.47‐5.31) for HBsAg‐, HBeAb‐ and HBcAb‐positive, compared to all negatives in HBV serological markers. One log increase in HBV DNA level was associated with 17% increased risk (adjusted OR: 1.17, 95% CI: 1.03‐1.32). The SB‐adjusted OR of HBV‐positive individuals with family history of liver cancer was 41.34 (95% posterior interval [PI]: 23.69‐72.12) compared with those HBV‐negative without family history. Relative excess risk due to additive interaction, the attributable proportion and synergy index were 73.13, 0.87 and 8.04 respectively. Adjusted ratio of OR for multiplicative interaction was 2.84 (95% CI: 1.41‐5.75). Conclusions: Super‐additive and super‐multiplicative interactions may exist between family history of liver cancer and HBV infection on the development of liver cancer. [ABSTRACT FROM AUTHOR]

Although tobacco smoking has been reported as a risk factor for liver cancer, few studies have specifically explored the association among Chinese females and the potential interaction between smoking and other risk factors. A population‐based case–control study was conducted and 2,011 liver cancer cases and 7,933 healthy controls were enrolled in Jiangsu, China from 2003 to 2010. Epidemiological data were collected, and serum hepatitis B surface antigen (HBsAg) and anti‐HCV antibody were measured. Unconditional logistic regression was used to examine association and potential interaction, while semi‐Bayes (SB) method was employed to make estimates more conservative. The prevalence of serum HBsAg positivity was 43.2% among cases and 6.5% among controls. The adjusted odds ratios (OR) for ever smoking were 1.62 (95% confidence interval [CI]: 1.33–1.96) among male and 0.82 (95% CI: 0.53–1.26) among female. Age at first cigarette, duration of smoking and pack‐years of smoking were all significantly associated with liver cancer among men. Compared to HBsAg‐negative never smokers, the adjusted ORs were 1.25 (95% CI: 1.03–1.52) for HBsAg‐negative ever smokers, 7.66 (95% CI: 6.05–9.71) for HBsAg‐positive never smokers, and 15.68 (95% CI: 12.06–20.39) for HBsAg‐positive ever smokers. These different odds ratios indicated super‐additive (RERI: 7.77, 95% CI: 3.81–11.73) and super‐multiplicative interactions (ROR: 1.64, 95% CI: 1.17–2.30) between hepatitis B virus (HBV) infection and tobacco smoking. Most associations and interactions detected remained statistically significant after SB adjustments. Tobacco smoking and HBV infection positively interact in the development of liver cancer. [ABSTRACT FROM AUTHOR]