A Field Report from the Sunken Village Wet Site (35MU4)

During low waters of September a wet site team, sponsored by an international grant from Japan, returned to further record the National Heritage Landmark wet site of Sunken Village (35MU4), Sauvie Island, Portland, Oregon (Figure 1). The one week project (September 16 through 22, 2007) was designed to accurately map the surface features ( especially over a hundred in situ acorn leaching pits and wooden stakes) and surface arti­facts (especially lithic debitage and fauna! remains) as revealed in the limited evaluation of I 060 linear feet (320 metres) of beach before the riprap repair was permitted by the U.S. Corps of Engineers in October of 2006 (Croes, Fagan and Zehendner 2007; a PDF copy of this 2006 field work is available on the web - see References below). The project continues to be co-man­aged through the direct in-put by Cultural Resources Protection Specialists Eirik Thorsgard, Confederated Tribes of the Grand Ronde, and Robert Kentta, Confederated Tribes of Siletz Indi­ans and in consultation with the Confederated Tribes of Warms Springs. A joint team provided the expertise needed to carefully map and record the Sunken Village National Historic Landmark site, consisting of(a) the SPSCC Wet Site Archaeological Inves­tigations and Laboratory team, lead by Dr. Dale Croes, and the SPSCC Computer Aided Drafting Department, lead by Professor Michael Martin, (b) the AINW geoarchaeological and laboratory team, lead by Dr. Michele Punke and Maureen Zehendner, and ( c) the internationally known Wetland Archaeological Team from the National Institute for Cultural Heritage, Nara, Japan, lead by Dr. Akira Matsui. This project was conducted through the sponsorship of a Japanese international grant under the administration of Dr. Akira Matsui, Chief Archaeologist, National Institute for Cultural Heritage, Nara, Japan, as well as support through the SPSCC Anthropology Club, an SPSCC Exceptional Faculty grant, Jean and Ray Auel, and volunteers from Portland State University and the Oregon Archaeological Society. Dr. Matsui brought four Japanese associates to participate in the field work: Dr. Naoto Yamamoto, Dr. Toru Miyao, Dr. Atsushi Iwasaki, and Dr. Tomonori Kanno (Figure 2)

BRCA2 polymorphic stop codon K3326X and the risk of breast, prostate, and ovarian cancers

Background: The K3326X variant in BRCA2 (BRCA2*c.9976A>T; p.Lys3326*; rs11571833) has been found to be associated with small increased risks of breast cancer. However, it is not clear to what extent linkage disequilibrium with fully pathogenic mutations might account for this association. There is scant information about the effect of K3326X in other hormone-related cancers. Methods: Using weighted logistic regression, we analyzed data from the large iCOGS study including 76 637 cancer case patients and 83 796 control patients to estimate odds ratios (ORw) and 95% confidence intervals (CIs) for K3326X variant carriers in relation to breast, ovarian, and prostate cancer risks, with weights defined as probability of not having a pathogenic BRCA2 variant. Using Cox proportional hazards modeling, we also examined the associations of K3326X with breast and ovarian cancer risks among 7183 BRCA1 variant carriers. All statistical tests were two-sided. Results: The K3326X variant was associated with breast (ORw = 1.28, 95% CI = 1.17 to 1.40, P = 5.9x10- 6) and invasive ovarian cancer (ORw = 1.26, 95% CI = 1.10 to 1.43, P = 3.8x10-3). These associations were stronger for serous ovarian cancer and for estrogen receptor–negative breast cancer (ORw = 1.46, 95% CI = 1.2 to 1.70, P = 3.4x10-5 and ORw = 1.50, 95% CI = 1.28 to 1.76, P = 4.1x10-5, respectively). For BRCA1 mutation carriers, there was a statistically significant inverse association of the K3326X variant with risk of ovarian cancer (HR = 0.43, 95% CI = 0.22 to 0.84, P = .013) but no association with breast cancer. No association with prostate cancer was observed. Conclusions: Our study provides evidence that the K3326X variant is associated with risk of developing breast and ovarian cancers independent of other pathogenic variants in BRCA2. Further studies are needed to determine the biological mechanism of action responsible for these associations

Functional mechanisms underlying pleiotropic risk alleles at the 19p13.1 breast-ovarian cancer susceptibility locus

A locus at 19p13 is associated with breast cancer (BC) and ovarian cancer (OC) risk. Here we analyse 438 SNPs in this region in 46,451 BC and 15,438 OC cases, 15,252 BRCA1 mutation carriers and 73,444 controls and identify 13 candidate causal SNPs associated with serous OC (P=9.2 × 10-20), ER-negative BC (P=1.1 × 10-13), BRCA1-associated BC (P=7.7 × 10-16) and triple negative BC (P-diff=2 × 10-5). Genotype-gene expression associations are identified for candidate target genes ANKLE1 (P=2 × 10-3) and ABHD8 (P<2 × 10-3). Chromosome conformation capture identifies interactions between four candidate SNPs and ABHD8, and luciferase assays indicate six risk alleles increased transactivation of the ADHD8 promoter. Targeted deletion of a region containing risk SNP rs56069439 in a putative enhancer induces ANKLE1 downregulation; and mRNA stability assays indicate functional effects for an ANKLE1 3′-UTR SNP. Altogether, these data suggest that multiple SNPs at 19p13 regulate ABHD8 and perhaps ANKLE1 expression, and indicate common mechanisms underlying breast and ovarian cancer risk

Shared heritability and functional enrichment across six solid cancers

Correction: Nature Communications 10 (2019): art. 4386 DOI: 10.1038/s41467-019-12095-8Quantifying the genetic correlation between cancers can provide important insights into the mechanisms driving cancer etiology. Using genome-wide association study summary statistics across six cancer types based on a total of 296,215 cases and 301,319 controls of European ancestry, here we estimate the pair-wise genetic correlations between breast, colorectal, head/neck, lung, ovary and prostate cancer, and between cancers and 38 other diseases. We observed statistically significant genetic correlations between lung and head/neck cancer (r(g) = 0.57, p = 4.6 x 10(-8)), breast and ovarian cancer (r(g) = 0.24, p = 7 x 10(-5)), breast and lung cancer (r(g) = 0.18, p = 1.5 x 10(-6)) and breast and colorectal cancer (r(g) = 0.15, p = 1.1 x 10(-4)). We also found that multiple cancers are genetically correlated with non-cancer traits including smoking, psychiatric diseases and metabolic characteristics. Functional enrichment analysis revealed a significant excess contribution of conserved and regulatory regions to cancer heritability. Our comprehensive analysis of cross-cancer heritability suggests that solid tumors arising across tissues share in part a common germline genetic basis.Peer reviewe

New genetic loci link adipose and insulin biology to body fat distribution.

Body fat distribution is a heritable trait and a well-established predictor of adverse metabolic outcomes, independent of overall adiposity. To increase our understanding of the genetic basis of body fat distribution and its molecular links to cardiometabolic traits, here we conduct genome-wide association meta-analyses of traits related to waist and hip circumferences in up to 224,459 individuals. We identify 49 loci (33 new) associated with waist-to-hip ratio adjusted for body mass index (BMI), and an additional 19 loci newly associated with related waist and hip circumference measures (P < 5 × 10(-8)). In total, 20 of the 49 waist-to-hip ratio adjusted for BMI loci show significant sexual dimorphism, 19 of which display a stronger effect in women. The identified loci were enriched for genes expressed in adipose tissue and for putative regulatory elements in adipocytes. Pathway analyses implicated adipogenesis, angiogenesis, transcriptional regulation and insulin resistance as processes affecting fat distribution, providing insight into potential pathophysiological mechanisms

Shared heritability and functional enrichment across six solid cancers

Quantifying the genetic correlation between cancers can provide important insights into the mechanisms driving cancer etiology. Using genome-wide association study summary statistics across six cancer types based on a total of 296,215 cases and 301,319 controls of European ancestry, here we estimate the pair-wise genetic correlations between breast, colorectal, head/neck, lung, ovary and prostate cancer, and between cancers and 38 other diseases. We observed statistically significant genetic correlations between lung and head/neck cancer (r(g) = 0.57, p = 4.6 x 10(-8)), breast and ovarian cancer (r(g) = 0.24, p = 7 x 10(-5)), breast and lung cancer (r(g) = 0.18, p = 1.5 x 10(-6)) and breast and colorectal cancer (r(g) = 0.15, p = 1.1 x 10(-4)). We also found that multiple cancers are genetically correlated with non-cancer traits including smoking, psychiatric diseases and metabolic characteristics. Functional enrichment analysis revealed a significant excess contribution of conserved and regulatory regions to cancer heritability. Our comprehensive analysis of cross-cancer heritability suggests that solid tumors arising across tissues share in part a common germline genetic basis

Functional mechanisms underlying pleiotropic risk alleles at the 19p13.1 breast-ovarian cancer susceptibility locus

A locus at 19p13 is associated with breast cancer (BC) and ovarian cancer (OC) risk. Here we analyse 438 SNPs in this region in 46,451 BC and 15,438 OC cases, 15,252 BRCA1 mutation carriers and 73,444 controls and identify 13 candidate causal SNPs associated with serous OC (P = 9.2 x 10(-20)), ER-negative BC (P = 1.1 x 10(-13)), BRCA1-associated BC (P = 7.7 x 10(-16)) and triple negative BC (P-diff = 2 x 10(-5)). Genotype-gene expression associations are identified for candidate target genes ANKLE1 (P = 2 x 10(-3)) and ABHD8 (PPeer reviewe

Modelling human choices: MADeM and decision‑making

Research supported by FAPESP 2015/50122-0 and DFG-GRTK 1740/2. RP and AR are also part of the Research, Innovation and Dissemination Center for Neuromathematics FAPESP grant (2013/07699-0). RP is supported by a FAPESP scholarship (2013/25667-8). ACR is partially supported by a CNPq fellowship (grant 306251/2014-0)

Hvordan påvirker sosiale medier unge voksnes fritidsreiser?

I denne oppgaven utforsker jeg hvordan sosiale medier påvirker unge voksne sine valg av fritidsreiser. For å få svar på forskningsspørsmålet mitt ble en kvantitativ forskningsmetode tatt i bruk og en elektronisk spørreundersøkelse ble gjennomført. Dette vil kunne gi et stort utvalg av unge voksne, som er hovedfokus og dermed vil ha relevant erfaring for denne oppgaven. Det er problemstillingen som avgjør hvilket forskningsdesign man bør velge, og metodene og analysene man velger. Disse må derfor ha som mål å finne de svarene vi trenger for å besvare problemstillingen. Undersøkelsen ble lagt ut på Facebook og Instagram, den bestod av 21 spørsmål og jeg mottok 181 besvarelser. Videre i oppgaven går jeg gjennom resultatene fra spørreundersøkelsen. Mesteparten av funnene som kommer fram stemmer bra med hypotesen og gir et solid svar på problemstillingen. De fleste viser seg å være enige i at deres reisevalg blir påvirket av sosiale medier.In this thesis, I explore how social media affects young adults' choices of leisure travel. To get an answer to my research question, a quantitative research method was used and an electronic survey was conducted. This will provide a large selection of young adults, who are the main focus and thus will have relevant experience for this task. It is the problem that determines which research design one should choose, and the methods and analyzes one chooses. These must therefore aim to find the answers we need to answer the problem. The survey was posted on Facebook and Instagram, it consisted of 21 questions and I received 181 answers. Further in the thesis I go through the results from the survey. Most of the findings that emerge agree well with the hypothesis and provide a solid answer to the problem. Most people seem to agree that their travel choices are influenced by social media