523 research outputs found

    The continuous plankton recorder survey: A long-term, basin-scale oceanic time series

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    In the 1920s, before the advent of echo sounders, fishery biologists were greatly concerned with assisting the fisherman to locate schools of pelagic fish. One of the approaches they developed was to relate the distribution of the planktonic food organisms to the presence of the schools of predators such as herring (Clupea harengus). The British planktologist, Alister Hardy, who had already carried out extensive studies on the feeding preferences of herring (Hardy, 1926a), initiated a program to examine the fishermen's contention that herring schools avoided 'green', i.e., phytoplankton-rich, water but could be correlated with high concentrations of zooplankton. This practical program was centered on the use of a specially developed instrument, the 'Plankton Indicator', designed to be used by the fisherman to assist in the search for suitable waters. It had limited success in its main aim but, as a collecting device, it embodied several profoundly important features. It was a simple instrument which was robust enough to be deployed and recovered by the crew of commercial vessels (in this case fishing vessels) while they were underway. The Indicator however, was no more than a high speed net which integrated the plankton over the area of sampling, but Hardy had also become interested in describing the patchiness of planktonic populations. He thus developed the Continuous Plankton Recorder (CPR) where he substituted the fixed filter screen of the Indicator by a continually moving length of silk mesh. The screen traversed at constant speed across the path of the incoming water and the trapped organisms were retained in place by sandwiching beneath an additional second mesh screen. Thus, knowing the speed of the towing vessel and the shooting and hauling positions, the spatial patterns of the plankton could be determined. Hardy took the first CPR to the Antarctic where he used it in the Southern Atlantic (Hardy, 1926b) and later deployed it in the North Sea to make some of the earliest contiguous records of plankton patchiness

    Cascading Disturbances in Florida Bay, USA: Cyanobacteria Blooms, Sponge Mortality, And Implications For Juvenile Spiny Lobsters Panulirus Argus

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    Florida Bay, the shallow lagoon separating mainland Florida and the Florida Keys, USA, is experiencing an unprecedented series of ecological disturbances. In 1991, following reports of other ecosystem perturbations, we observed widespread and persistent blooms of cyanobacteria that coincided with the decimation of sponge communities over hundreds of square kilometers. Juvenile Caribbean spiny lobsters Panulirus argus, among other animals, rely on sponges for shelter; the impact of sponge loss on the abundance of lobsters and their use of shelter, in particular, has been dramatic. The loss of sponges on 27 experimental sites in hard bottom habitat in central Florida Bay resulted in the redistribution of juvenile lobsters among the remaining shelters, an influx of lobsters into sites where artificial shelters were present, and a decline in lobster abundances on sites without artificial shelters. Diver surveys of sponge damage at additional sites in central Florida Bay confirmed that the sponge die-off was widespread and its occurrence coincided with areas that had been exposed to the cyanobacteria bloom. This cascade of disturbances has dramatically altered the community structure of affected hard bottom areas and demonstrates the coupled dynamics of this shallow marine ecosystem

    A Phase 3 Trial of 2 Years of Androgen Suppression and Radiation Therapy With or Without Adjuvant Chemotherapy for High-Risk Prostate Cancer: Final Results of Radiation Therapy Oncology Group Phase 3 Randomized Trial NRG Oncology RTOG 9902.

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    PURPOSE: Long-term (LT) androgen suppression (AS) with radiation therapy (RT) is a standard treatment of high-risk, localized prostate cancer (PCa). Radiation Therapy Oncology Group 9902 was a randomized trial testing the hypothesis that adjuvant combination chemotherapy (CT) with paclitaxel, estramustine, and oral etoposide plus LT AS plus RT would improve overall survival (OS). METHODS AND MATERIALS: Patients with high-risk PCa (prostate-specific antigen 20-100 ng/mL and Gleason score [GS] ≥ 7 or clinical stage ≥ T2 and GS ≥ 8) were randomized to RT and AS (AS + RT) alone or with adjuvant CT (AS + RT + CT). CT was given as four 21-day cycles, delivered beginning 28 days after 70.2 Gy of RT. AS was given as luteinizing hormone-releasing hormone for 24 months, beginning 2 months before RT plus an oral antiandrogen for 4 months before and during RT. The study was designed based on a 6% improvement in OS from 79% to 85% at 5 years, with 90% power and a 2-sided alpha of 0.05. RESULTS: A total of 397 patients (380 eligible) were randomized. The patients had high-risk PCa, 68% with GS 8 to 10 and 34% T3 to T4 tumors, and median prostate-specific antigen of 22.6 ng/mL. The median follow-up period was 9.2 years. The trial closed early because of excess thromboembolic toxicity in the CT arm. The 10-year results for all randomized patients revealed no significant difference between the AS + RT and AS + RT + CT arms in OS (65% vs 63%; P=.81), biochemical failure (58% vs 54%; P=.82), local progression (11% vs 7%; P=.09), distant metastases (16% vs 14%; P=.42), or disease-free survival (22% vs 26%; P=.61). CONCLUSIONS: NRG Oncology RTOG 9902 showed no significant differences in OS, biochemical failure, local progression, distant metastases, or disease-free survival with the addition of adjuvant CT to LT AS + RT. The trial results provide valuable data regarding the natural history of high-risk PCa treated with LT AS + RT and have implications for the feasibility of clinical trial accrual and tolerability using CT for PCa

    Bodyweight Perceptions among Texas Women: The Effects of Religion, Race/Ethnicity, and Citizenship Status

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    Despite previous work exploring linkages between religious participation and health, little research has looked at the role of religion in affecting bodyweight perceptions. Using the theoretical model developed by Levin et al. (Sociol Q 36(1):157–173, 1995) on the multidimensionality of religious participation, we develop several hypotheses and test them by using data from the 2004 Survey of Texas Adults. We estimate multinomial logistic regression models to determine the relative risk of women perceiving themselves as overweight. Results indicate that religious attendance lowers risk of women perceiving themselves as very overweight. Citizenship status was an important factor for Latinas, with noncitizens being less likely to see themselves as overweight. We also test interaction effects between religion and race. Religious attendance and prayer have a moderating effect among Latina non-citizens so that among these women, attendance and prayer intensify perceptions of feeling less overweight when compared to their white counterparts. Among African American women, the effect of increased church attendance leads to perceptions of being overweight. Prayer is also a correlate of overweight perceptions but only among African American women. We close with a discussion that highlights key implications from our findings, note study limitations, and several promising avenues for future research

    A missense variant in CST3 exerts a recessive effect on susceptibility to age-related macular degeneration resembling its association with Alzheimer’s disease

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    Age-related macular degeneration (AMD) and Alzheimer’s disease (AD) are degenerative, multifactorial diseases involving age-related accumulation of extracellular deposits linked to dysregulation of protein homeostasis. Here, we strengthen the evidence that an nsSNP (p.Ala25Thr) in the cysteine proteinase inhibitor cystatin C gene CST3, previously confirmed by meta-analysis to be associated with AD, is associated with exudative AMD. To our knowledge, this is the first report highlighting a genetic variant that increases the risk of developing both AD and AMD. Furthermore, we demonstrate that the risk associated with the mutant allele follows a recessive model for both diseases. We perform an AMD-CST3 case–control study genotyping 350 exudative AMD Caucasian individuals. Bringing together our data with the previously reported AMD-CST3 association study, the evidence of a recessive effect on AMD risk is strengthened (OR = 1.89, P = 0.005). This effect closely resembles the AD-CST3 recessive effect (OR = 1.73, P = 0.005) previously established by meta-analysis. This resemblance is substantiated by the high correlation between CST3 genotype and effect size across the two diseases (R2 = 0.978). A recessive effect is in line with the known function of cystatin C, a potent enzyme inhibitor. Its potency means that, in heterozygous individuals, a single functional allele is sufficient to maintain its inhibitory function; only homozygous individuals will lack this form of proteolytic regulation. Our findings support the hypothesis that recessively acting variants account for some of the missing heritability of multifactorial diseases. Replacement therapy represents a translational opportunity for individuals homozygous for the mutant allele

    MiR-137-derived polygenic risk: effects on cognitive performance in patients with schizophrenia and controls

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    Variants at microRNA-137 (MIR137), one of the most strongly associated schizophrenia risk loci identified to date, have been associated with poorer cognitive performance. As microRNA-137 is known to regulate the expression of ~1900 other genes, including several that are independently associated with schizophrenia, we tested whether this gene set was also associated with variation in cognitive performance. Our analysis was based on an empirically derived list of genes whose expression was altered by manipulation of MIR137 expression. This list was cross-referenced with genome-wide schizophrenia association data to construct individual polygenic scores. We then tested, in a sample of 808 patients and 192 controls, whether these risk scores were associated with altered performance on cognitive functions known to be affected in schizophrenia. A subgroup of healthy participants also underwent functional imaging during memory (n=108) and face processing tasks (n=83). Increased polygenic risk within the empirically derived miR-137 regulated gene score was associated with significantly lower performance on intelligence quotient, working memory and episodic memory. These effects were observed most clearly at a polygenic threshold of P=0.05, although significant results were observed at all three thresholds analyzed. This association was found independently for the gene set as a whole, excluding the schizophrenia-associated MIR137 SNP itself. Analysis of the spatial working memory fMRI task further suggested that increased risk score (thresholded at P=10−5) was significantly associated with increased activation of the right inferior occipital gyrus. In conclusion, these data are consistent with emerging evidence that MIR137 associated risk for schizophrenia may relate to its broader downstream genetic effects

    Long Beach Earthquake and Protection Against Future Earthquakes -- Summary of Report by Joint Technical Committee on Earthquake Protection, Dr. Robert A. Millikan, Chairman

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    To the Public of the Pacific Southwest: In response to official requests from many representative technical and civic organizations, the Joint Technical Committee on Earthquake Protection was organized after the earthquake of March 10, 1933 to consider ways and means of minimizing loss of life and property damage in the event of another earthquake of equal or greater intensity. We now present to you, in the form of this summarized report, our belief as to the seismic hazard in this region and our opinion as to the proper balance between the degree of protection to be afforded life and property and the cost of providing such protection. We sincerely hope that the lessons of the Long Beach earthquake will not be forgotten as were the lessons which should have been fixed indelibly in the minds of all by the earthquakes of the past. Joint Technical Committee on Earthquake Protection. Robert A. Millikan, Chairman. June 7-1933

    Genetic variants in novel pathways influence blood pressure and cardiovascular disease risk.

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    Blood pressure is a heritable trait influenced by several biological pathways and responsive to environmental stimuli. Over one billion people worldwide have hypertension (≥140 mm Hg systolic blood pressure or  ≥90 mm Hg diastolic blood pressure). Even small increments in blood pressure are associated with an increased risk of cardiovascular events. This genome-wide association study of systolic and diastolic blood pressure, which used a multi-stage design in 200,000 individuals of European descent, identified sixteen novel loci: six of these loci contain genes previously known or suspected to regulate blood pressure (GUCY1A3-GUCY1B3, NPR3-C5orf23, ADM, FURIN-FES, GOSR2, GNAS-EDN3); the other ten provide new clues to blood pressure physiology. A genetic risk score based on 29 genome-wide significant variants was associated with hypertension, left ventricular wall thickness, stroke and coronary artery disease, but not kidney disease or kidney function. We also observed associations with blood pressure in East Asian, South Asian and African ancestry individuals. Our findings provide new insights into the genetics and biology of blood pressure, and suggest potential novel therapeutic pathways for cardiovascular disease prevention

    A Meta-analysis of Gene Expression Signatures of Blood Pressure and Hypertension

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    Genome-wide association studies (GWAS) have uncovered numerous genetic variants (SNPs) that are associated with blood pressure (BP). Genetic variants may lead to BP changes by acting on intermediate molecular phenotypes such as coded protein sequence or gene expression, which in turn affect BP variability. Therefore, characterizing genes whose expression is associated with BP may reveal cellular processes involved in BP regulation and uncover how transcripts mediate genetic and environmental effects on BP variability. A meta-analysis of results from six studies of global gene expression profiles of BP and hypertension in whole blood was performed in 7017 individuals who were not receiving antihypertensive drug treatment. We identified 34 genes that were differentially expressed in relation to BP (Bonferroni-corrected p<0.05). Among these genes, FOS and PTGS2 have been previously reported to be involved in BP-related processes; the others are novel. The top BP signature genes in aggregate explain 5%–9% of inter-individual variance in BP. Of note, rs3184504 in SH2B3, which was also reported in GWAS to be associated with BP, was found to be a trans regulator of the expression of 6 of the transcripts we found to be associated with BP (FOS, MYADM, PP1R15A, TAGAP, S100A10, and FGBP2). Gene set enrichment analysis suggested that the BP-related global gene expression changes include genes involved in inflammatory response and apoptosis pathways. Our study provides new insights into molecular mechanisms underlying BP regulation, and suggests novel transcriptomic markers for the treatment and prevention of hypertension
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