Habitat Destruction by Collectors Associated with Decreased Abundance of Rock-Dwelling Lizards

Declines in biodiversity caused by habitat loss have been well documented on large spatial scales, however, effects of habitat loss on small scales have received little attention. Some common methods of reptile collection, primarily for commercial harvest, result in destruction of cracks, crevices, and other cool, moist microhabitats in desert rock outcrops. We developed a method for identifying habitat destruction associated with reptile collecting. We surveyed lightly and heavily disturbed areas near Phoenix, Arizona to determine if microhabitat loss caused by collectors was associated with decreased relative abundance of reptiles. Of four diurnal lizard species studied, relative abundance of two rock-dwelling species was negatively correlated with level of microhabitat destruction, whereas relative abundance of one ground-dwelling species and one habitat generalist species was not. Habitat destruction caused by collectors may have negative effects, not only at the individual level, but at the population and community levels as well. We recommend regulation of commercial trade in reptiles; disallowing collecting activities that cause habitat damage; increased law enforcement; and educational programs directed primarily at novice collectors

Chronic Inflammatory Bowel Disease Risk Factors related to Colorectal Cancer

Patients with inflammatory bowel disease have an increasing risk for colorectal cancer which is believed to begin from no dysplasia progressing to indefinite dysplasia, low-grade dysplasia, high-grade dysplasia and finally to invasive adenocarcinoma, although colorectal cancer can arise without proceeding through each of these steps. As regards to the risk factors predisposing to colorectal cancer in the setting of inflammatory bowel disease, it seems that the risk increases with longer duration and greater anatomic extent of colitis, the degree of inflammation, and the presence of primary sclerosing cholangitis and family history of colorectal cancer. Concerning the mechanisms of carcinogenesis, it is now well established that the molecular alterations responsible for sporadic colorectal cancer, elucidated namely chromosomal instability, microsatellite instability, and hypermethylation, also play a role in colitis-associated colon carcinogenesis. Chemoprevention strategies include the management of medicaments such as aminosalicylates, ursodeoxycholic acid, and possibly folic acid, the exact role of which remains to be elucidated.Keywords: bowel disease, inflammation, patients, dysplasia, cytokines, cancer, smoking, chemoprevention, etc.

Complications, revision fusions, readmissions, and utilization over a 1-year period after bone morphogenetic protein use during primary cervical spine fusions

Nationwide estimates examining Bone Morphogenetic Protein (BMP) use with cervical spine fusions have been limited to perioperative outcomes

Colorectal cancer linkage on chromosomes 4q21, 8q13, 12q24, and 15q22

A substantial proportion of familial colorectal cancer (CRC) is not a consequence of known susceptibility loci, such as mismatch repair (MMR) genes, supporting the existence of additional loci. To identify novel CRC loci, we conducted a genome-wide linkage scan in 356 white families with no evidence of defective MMR (i.e., no loss of tumor expression of MMR proteins, no microsatellite instability (MSI)-high tumors, or no evidence of linkage to MMR genes). Families were ascertained via the Colon Cancer Family Registry multi-site NCI-supported consortium (Colon CFR), the City of Hope Comprehensive Cancer Center, and Memorial University of Newfoundland. A total of 1,612 individuals (average 5.0 per family including 2.2 affected) were genotyped using genome-wide single nucleotide polymorphism linkage arrays; parametric and non-parametric linkage analysis used MERLIN in a priori-defined family groups. Five lod scores greater than 3.0 were observed assuming heterogeneity. The greatest were among families with mean age of diagnosis less than 50 years at 4q21.1 (dominant HLOD = 4.51, α = 0.84, 145.40 cM, rs10518142) and among all families at 12q24.32 (dominant HLOD = 3.60, α = 0.48, 285.15 cM, rs952093). Among families with four or more affected individuals and among clinic-based families, a common peak was observed at 15q22.31 (101.40 cM, rs1477798; dominant HLOD = 3.07, α = 0.29; dominant HLOD = 3.03, α = 0.32, respectively). Analysis of families with only two affected individuals yielded a peak at 8q13.2 (recessive HLOD = 3.02, α = 0.51, 132.52 cM, rs1319036). These previously unreported linkage peaks demonstrate the continued utility of family-based data in complex traits and suggest that new CRC risk alleles remain to be elucidated. © 2012 Cicek et al

Optical scattering and backscattering by organic and inorganic particulates in U.S. coastal waters

We present the results of a study of optical scattering and backscattering of particulates for three coastal sites that represent a wide range of optical properties that are found in U.S. near-shore waters. The 6000 scattering and backscattering spectra collected for this study can be well approximated by a power-law function of wavelength. The power-law exponent for particulate scattering changes dramatically from site to site (and within each site) compared with particulate backscattering where all the spectra, except possibly the very clearest waters, cluster around a single wavelength power-law exponent of −0.94 . The particulate backscattering-to-scattering ratio (the backscattering ratio) displays a wide range in wavelength dependence. This result is not consistent with scattering models that describe the bulk composition of water as a uniform mix of homogeneous spherical particles with a Junge-like power-law distribution over all particle sizes. Simultaneous particulate organic matter (POM) and particulate inorganic matter (PIM) measurements are available for some of our optical measurements, and site-averaged POM and PIM mass-specific cross sections for scattering and backscattering can be derived. Cross sections for organic and inorganic material differ at each site, and the relative contribution of organic and inorganic material to scattering and backscattering depends differently at each site on the relative amount of material that is present

Factors Associated With Outcomes of Patients With Primary Sclerosing Cholangitis and Development and Validation of a Risk Scoring System.

We sought to identify factors that are predictive of liver transplantation or death in patients with primary sclerosing cholangitis (PSC), and to develop and validate a contemporaneous risk score for use in a real-world clinical setting. Analyzing data from 1,001 patients recruited to the UK-PSC research cohort, we evaluated clinical variables for their association with 2-year and 10-year outcome through Cox-proportional hazards and C-statistic analyses. We generated risk scores for short-term and long-term outcome prediction, validating their use in two independent cohorts totaling 451 patients. Thirty-six percent of the derivation cohort were transplanted or died over a cumulative follow-up of 7,904 years. Serum alkaline phosphatase of at least 2.4 × upper limit of normal at 1 year after diagnosis was predictive of 10-year outcome (hazard ratio [HR] = 3.05; C = 0.63; median transplant-free survival 63 versus 108 months; P < 0.0001), as was the presence of extrahepatic biliary disease (HR = 1.45; P = 0.01). We developed two risk scoring systems based on age, values of bilirubin, alkaline phosphatase, albumin, platelets, presence of extrahepatic biliary disease, and variceal hemorrhage, which predicted 2-year and 10-year outcomes with good discrimination (C statistic = 0.81 and 0.80, respectively). Both UK-PSC risk scores were well-validated in our external cohort and outperformed the Mayo Clinic and aspartate aminotransferase-to-platelet ratio index (APRI) scores (C statistic = 0.75 and 0.63, respectively). Although heterozygosity for the previously validated human leukocyte antigen (HLA)-DR*03:01 risk allele predicted increased risk of adverse outcome (HR = 1.33; P = 0.001), its addition did not improve the predictive accuracy of the UK-PSC risk scores. Conclusion: Our analyses, based on a detailed clinical evaluation of a large representative cohort of participants with PSC, furthers our understanding of clinical risk markers and reports the development and validation of a real-world scoring system to identify those patients most likely to die or require liver transplantation.Financial support has been received by National Institute of Health Research (RD-TRC and Birmingham Biomedical Research Centre), Isaac Newton Trust, Addenbrooke’s charitable trust, Norwegian PSC Research Center and PSC Support. GMH is supported by the Lily and Terry Horner Chair in Autoimmune Liver Disease Research, Toronto Centre for Liver Disease, Toronto

Genetic Analysis Workshop 15: gene expression analysis and approaches to detecting multiple functional loci

National Institutes of Health (AR44422, N01-AR-7-2232, 5R01-HL049609-14, IR01-AG021917-01A1); Genome Canada and Associations AFP; Polyarctique-Groupe Taitbout; Rhumatisme et Travail; Arthritis Research Campaign; Unversity of Minnesota; Minnesota Supercomputing Institute; National Institute of General Medical Sciences (R01 GM31575

Characterizing Genetic Risk at Known Prostate Cancer Susceptibility Loci in African Americans

GWAS of prostate cancer have been remarkably successful in revealing common genetic variants and novel biological pathways that are linked with its etiology. A more complete understanding of inherited susceptibility to prostate cancer in the general population will come from continuing such discovery efforts and from testing known risk alleles in diverse racial and ethnic groups. In this large study of prostate cancer in African American men (3,425 prostate cancer cases and 3,290 controls), we tested 49 risk variants located in 28 genomic regions identified through GWAS in men of European and Asian descent, and we replicated associations (at p≤0.05) with roughly half of these markers. Through fine-mapping, we identified nearby markers in many regions that better define associations in African Americans. At 8q24, we found 9 variants (p≤6×10−4) that best capture risk of prostate cancer in African Americans, many of which are more common in men of African than European descent. The markers found to be associated with risk at each locus improved risk modeling in African Americans (per allele OR = 1.17) over the alleles reported in the original GWAS (OR = 1.08). In summary, in this detailed analysis of the prostate cancer risk loci reported from GWAS, we have validated and improved upon markers of risk in some regions that better define the association with prostate cancer in African Americans. Our findings with variants at 8q24 also reinforce the importance of this region as a major risk locus for prostate cancer in men of African ancestry