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Coastal habitats, such as salt marshes and dune systems, can protect communities from hazards by reducing coastline exposure. However, these critical habitats and their diverse ecosystem services are threatened by coastal development and the impacts from a changing climate. Ever increasing pressure on coastal habitats calls for coastal climate adaptation efforts that mitigate or adapt to these pressures in ways that maintain the integrity of coastal landscapes. An important challenge for decisionmakers is determining the best mitigation and adaptation strategies that not only protect human lives and property, but also safeguard the ability of coastal habitats to provide a broad suite of benefits. Here, we present a potential pathway for local-scale climate change adaptation planning through the identification and mapping of natural habitats that provide the greatest benefits to coastal communities. The methodology coupled a coastal vulnerability model with a climate adaptation policy assessment in an effort to identify priority locations for nature-based solutions that reduce vulnerability of critical assets using feasible land-use policy methods. Our results demonstrate the critical role of natural habitats in providing the ecosystem service of coastal protection in California. We found that specific dune habitats play a key role in reducing erosion and inundation of the coastline and that several wetland areas help to absorb energy from storms and provide a protective service for the coast of Marin county, California, USA. Climate change and adaptation planning are globally relevant issues in which the scalability and transferability of solutions must be considered. This work outlines an iterative approach for climate adaptation planning at a local-scale, with opportunity to consider the scalability of an iterative science-policy engagement approach to regional, national, and international levels.

People are drawn to the coast for its moderate climate, scenic beauty, cultural and ecological richness, rural expanses, abundant recreational opportunities, vibrant economic activity, and diverse urban communities.’ More than 70% of California residents live and work in coastal counties (U.S. Census Bureau n.d.). Over the last thirty-eight years, the California coastal county population has grown 64%, from about 16.8 million in 1970 to 27.6 million in 2008 (NOEP 2012). Almost 86% of California’s total gross domestic product comes from coastal counties (NOEP 2010).

This chapter summarizes the scope of what is known and not known about climate in the Southwestern United States. There is now more evidence and more agreement among climate scientists about the physical climate and related impacts in the Southwest compared with that represented in the 2009 National Climate Assessment (Karl, Melillo and Peterson 2009). However, there remain uncertainties about the climate system, the complexities within climate models, the related impacts to the biophysical environment, and the use of climate information in decision making.

Using data from five U.S. cohort studies, the authors estimate that 17% of excess mortality among smokers is due to diseases not already established as caused by smoking; for example, renal failure, infections, and intestinal ischemia could potentially be linked to smoking. The 2014 Surgeon General’s report estimates that cigarette smoking causes more than 480,000 deaths each year in the United States. 1 This widely cited estimate of the mortality burden of smoking may be an underestimate, because it considers deaths only from the 21 diseases that have been formally established as caused by smoking (12 types of cancer, 6 categories of cardiovascular disease, diabetes, chronic obstructive pulmonary disease [COPD], and pneumonia including influenza). Associations between smoking and the 30 most common causes of death in the United Kingdom in the Million Women Study suggest that the excess mortality observed among current smokers . . .

In 2020, 146,063 deaths due to pancreatic cancer are estimated to occur in Europe and the United States combined. To identify common susceptibility alleles, we performed the largest pancreatic cancer GWAS to date, including 9040 patients and 12,496 controls of European ancestry from the Pancreatic Cancer Cohort Consortium (PanScan) and the Pancreatic Cancer Case-Control Consortium (PanC4). Here, we find significant evidence of a novel association at rs78417682 (7p12/ TNS3 , P  = 4.35 × 10 −8 ). Replication of 10 promising signals in up to 2737 patients and 4752 controls from the PANcreatic Disease ReseArch (PANDoRA) consortium yields new genome-wide significant loci: rs13303010 at 1p36.33 ( NOC2L , P  = 8.36 × 10 −14 ), rs2941471 at 8q21.11 ( HNF4G , P  = 6.60 × 10 −10 ), rs4795218 at 17q12 ( HNF1B , P  = 1.32 × 10 −8 ), and rs1517037 at 18q21.32 ( GRP , P  = 3.28 × 10 −8 ). rs78417682 is not statistically significantly associated with pancreatic cancer in PANDoRA. Expression quantitative trait locus analysis in three independent pancreatic data sets provides molecular support of NOC2L as a pancreatic cancer susceptibility gene. Genetic variants associated with susceptibility to pancreatic cancer have been identified using genome wide association studies (GWAS). Here, the authors combine data from over 9000 patients and perform a meta-analysis to identify five novel loci linked to pancreatic cancer.

Evidence on the association between vitamin D status and pancreatic cancer risk is inconsistent. This inconsistency may be partially attributable to variation in vitamin D regulating genes. We selected 11 vitamin D-related genes (GC, DHCR7, CYP2R1, VDR, CYP27B1, CYP24A1, CYP27A1, RXRA, CRP2, CASR and CUBN) totaling 213 single nucleotide polymorphisms (SNPs), and examined associations with pancreatic adenocarcinoma. Our study included 3,583 pancreatic cancer cases and 7,053 controls from the genome-wide association studies of pancreatic cancer PanScans-I-III. We used the Adaptive Joint Test and the Adaptive Rank Truncated Product statistic for pathway and gene analyses, and unconditional logistic regression for SNP analyses, adjusting for age, sex, study and population stratification. We examined effect modification by circulating vitamin D concentration (≤50, >50 nmol/L) for the most significant SNPs using a subset of cohort cases (n = 713) and controls (n = 878). The vitamin D metabolic pathway was not associated with pancreatic cancer risk (p = 0.830). Of the individual genes, none were associated with pancreatic cancer risk at a significance level of p<0.05. SNPs near the VDR (rs2239186), LRP2 (rs4668123), CYP24A1 (rs2762932), GC (rs2282679), and CUBN (rs1810205) genes were the top SNPs associated with pancreatic cancer (p-values 0.008-0.037), but none were statistically significant after adjusting for multiple comparisons. Associations between these SNPs and pancreatic cancer were not modified by circulating concentrations of vitamin D. These findings do not support an association between vitamin D-related genes and pancreatic cancer risk. Future research should explore other pathways through which vitamin D status might be associated with pancreatic cancer risk.

Background and objective Survival of patients with pancreatic adenocarcinoma is limited and few prognostic factors are known. We conducted a two-stage genome-wide association study (GWAS) to identify germline variants associated with survival in patients with pancreatic adenocarcinoma. Methods We analysed overall survival in relation to single nucleotide polymorphisms (SNPs) among 1005 patients from two large GWAS datasets, PanScan I and ChinaPC. Cox proportional hazards regression was used in an additive genetic model with adjustment for age, sex, clinical stage and the top four principal components of population stratification. The first stage included 642 cases of European ancestry (PanScan), from which the top SNPs (p≤10−5) were advanced to a joint analysis with 363 additional patients from China (ChinaPC). Results In the first stage of cases of European descent, the top-ranked loci were at chromosomes 11p15.4, 18p11.21 and 1p36.13, tagged by rs12362504 (p=1.63×10−7), rs981621 (p=1.65×10−7) and rs16861827 (p=3.75×10−7), respectively. 131 SNPs with p≤10−5 were advanced to a joint analysis with cases from the ChinaPC study. In the joint analysis, the top-ranked SNP was rs10500715 (minor allele frequency, 0.37; p=1.72×10−7) on chromosome 11p15.4, which is intronic to the SET binding factor 2 (SBF2) gene. The HR (95% CI) for death was 0.74 (0.66 to 0.84) in PanScan I, 0.79 (0.65 to 0.97) in ChinaPC and 0.76 (0.68 to 0.84) in the joint analysis. Conclusions Germline genetic variation in the SBF2 locus was associated with overall survival in patients with pancreatic adenocarcinoma of European and Asian ancestry. This association should be investigated in additional large patient cohorts.

The literature has consistently reported no association between low to moderate alcohol consumption and pancreatic cancer; however, a few studies have shown that high levels of intake may increase risk. Most single studies have limited power to detect associations even in the highest alcohol intake categories or to examine associations by alcohol type. We analyzed these associations using 1,530 pancreatic cancer cases and 1,530 controls from the Pancreatic Cancer Cohort Consortium (PanScan) nested case-control study. Odds ratios (OR) and 95% confidence intervals (95% CI) were calculated using unconditional logistic regression, adjusting for potential confounders. We observed no significant overall association between total alcohol (ethanol) intake and pancreatic cancer risk (OR = 1.38, 95% CI = 0.86-2.23, for 60 or more g/day vs. >0 to <5 g/day). A statistically significant increase in risk was observed among men consuming 45 or more grams of alcohol from liquor per day (OR = 2.23, 95% CI = 1.02-4.87, compared to 0 g/day of alcohol from liquor, P-trend = 0.12), but not among women (OR = 1.35, 95% CI = 0.63-2.87, for 30 or more g/day of alcohol from liquor, compared to none). No associations were noted for wine or beer intake. Overall, no significant increase in risk was observed, but a small effect among heavy drinkers cannot be ruled out.