Does hormone replacement therapy prevent cognitive decline in postmenopausal women?

Q: Evidence-based answer: NO. Hormone replacement therapy (HRT) does not prevent cognitive decline in postmenopausal women—and in fact, it may slightly increase risk (strength of recommendation, A; systematic review, meta-analysis of randomized controlled trials [RCTs], and individual RCT).Madeline Gates, MD; Melissa Beagle, MD, MPH; Lauren Bull, MD; Roxanne Radi, MD, MPH; Corey Lyon, DO (University of Colorado, Family Medicine Residency), Kristen DeSanto, MSLS, MS, RD (University of Colorado, Health Sciences Library), Rick Guthmann, MD, MPH (Advocate Health Care Illinois Masonic Medical Center Program)Includes bibliographical reference

Fragmenting Forests: The Double Edge of Effective Forest Monitoring

The link between ineffective forest monitoring and forest degradation is well known. Under REDD+, monitoring stands to become more important as a means of maintaining incentive. Little attention however has been paid to the possible adverse consequences of forest monitoring. Our research develops a spatially explicit, agent-based model (ABM) of timber extraction in a Congo Basin forest concession to investigate the potential conservation impact of more effective monitoring. We modeled the building of access roads, and logging of legal timber and illegal timber, where illegal timber may be interpreted broadly to include prohibited species, smaller trees, or trees in areas where cutting is not permitted. We investigated road building under (1) random spot monitoring of logging sites and (2) monitoring of logged trunks at checkpoints. Our findings indicate that although more effective monitoring can reduce illegal harvesting, it can also lead to construction of denser road networks and higher levels of forest fragmentation, with an implied loss of biodiversity. These insights are particularly relevant in the context of REDD+, as they suggest that some monitoring strategies may lead to more forest fragmentation, even as they help reduce emissions

Scientific Assessment of Climate Change and Its Effects in Maine

Climate change has already made its presence known in Maine, from shorter winters and warmer summers with ocean heat waves, to stronger storms, new species showing up in our backyards and the Gulf of Maine, aquatic algal blooms, acidic ocean waters that affect shellfish, and new pests and diseases that harm our iconic forests and fisheries. The health of Maine people is also being affected by climate change, from high heat index days driving increased emergency room visits to the ravages of Lyme and other vector-borne diseases. And our economy is feeling the effects, too — with farmers trying to adapt to longer growing seasons but dealing with severe storms and late frosts, aquaculturists already adapting to a more acidic ocean, and winter sports like skiing and snowmobiling being impacted by our shrinking winter season. This is the first report from the Maine Climate Council’s Scientific and Technical Subcommittee, produced by more than 50 scientists from around the State representing Scientific and Technical Subcommittee members, other co-authors, and contributors. This report is part of the 2020 Maine Climate Action Plan. The report summarizes how climate change has already impacted Maine and how it might continue affecting our State in the future

Advanced Technology Large-Aperture Space Telescope (ATLAST): A Technology Roadmap for the Next Decade

The Advanced Technology Large-Aperture Space Telescope (ATLAST) is a set of mission concepts for the next generation of UVOIR space observatory with a primary aperture diameter in the 8-m to 16-m range that will allow us to perform some of the most challenging observations to answer some of our most compelling questions, including "Is there life elsewhere in the Galaxy?" We have identified two different telescope architectures, but with similar optical designs, that span the range in viable technologies. The architectures are a telescope with a monolithic primary mirror and two variations of a telescope with a large segmented primary mirror. This approach provides us with several pathways to realizing the mission, which will be narrowed to one as our technology development progresses. The concepts invoke heritage from HST and JWST design, but also take significant departures from these designs to minimize complexity, mass, or both. Our report provides details on the mission concepts, shows the extraordinary scientific progress they would enable, and describes the most important technology development items. These are the mirrors, the detectors, and the high-contrast imaging technologies, whether internal to the observatory, or using an external occulter. Experience with JWST has shown that determined competitors, motivated by the development contracts and flight opportunities of the new observatory, are capable of achieving huge advances in technical and operational performance while keeping construction costs on the same scale as prior great observatories.Comment: 22 pages, RFI submitted to Astro2010 Decadal Committe

Association of genetic variation with systolic and diastolic blood pressure among African Americans: the Candidate Gene Association Resource study

The prevalence of hypertension in African Americans (AAs) is higher than in other US groups; yet, few have performed genome-wide association studies (GWASs) in AA. Among people of European descent, GWASs have identified genetic variants at 13 loci that are associated with blood pressure. It is unknown if these variants confer susceptibility in people of African ancestry. Here, we examined genome-wide and candidate gene associations with systolic blood pressure (SBP) and diastolic blood pressure (DBP) using the Candidate Gene Association Resource (CARe) consortium consisting of 8591 AAs. Genotypes included genome-wide single-nucleotide polymorphism (SNP) data utilizing the Affymetrix 6.0 array with imputation to 2.5 million HapMap SNPs and candidate gene SNP data utilizing a 50K cardiovascular gene-centric array (ITMAT-Broad-CARe [IBC] array). For Affymetrix data, the strongest signal for DBP was rs10474346 (P= 3.6 × 10−8) located near GPR98 and ARRDC3. For SBP, the strongest signal was rs2258119 in C21orf91 (P= 4.7 × 10−8). The top IBC association for SBP was rs2012318 (P= 6.4 × 10−6) near SLC25A42 and for DBP was rs2523586 (P= 1.3 × 10−6) near HLA-B. None of the top variants replicated in additional AA (n = 11 882) or European-American (n = 69 899) cohorts. We replicated previously reported European-American blood pressure SNPs in our AA samples (SH2B3, P= 0.009; TBX3-TBX5, P= 0.03; and CSK-ULK3, P= 0.0004). These genetic loci represent the best evidence of genetic influences on SBP and DBP in AAs to date. More broadly, this work supports that notion that blood pressure among AAs is a trait with genetic underpinnings but also with significant complexit

Association of genetic variation with systolic and diastolic blood pressure among African Americans: the Candidate Gene Association Resource study.

The prevalence of hypertension in African Americans (AAs) is higher than in other US groups; yet, few have performed genome-wide association studies (GWASs) in AA. Among people of European descent, GWASs have identified genetic variants at 13 loci that are associated with blood pressure. It is unknown if these variants confer susceptibility in people of African ancestry. Here, we examined genome-wide and candidate gene associations with systolic blood pressure (SBP) and diastolic blood pressure (DBP) using the Candidate Gene Association Resource (CARe) consortium consisting of 8591 AAs. Genotypes included genome-wide single-nucleotide polymorphism (SNP) data utilizing the Affymetrix 6.0 array with imputation to 2.5 million HapMap SNPs and candidate gene SNP data utilizing a 50K cardiovascular gene-centric array (ITMAT-Broad-CARe [IBC] array). For Affymetrix data, the strongest signal for DBP was rs10474346 (P= 3.6 × 10(-8)) located near GPR98 and ARRDC3. For SBP, the strongest signal was rs2258119 in C21orf91 (P= 4.7 × 10(-8)). The top IBC association for SBP was rs2012318 (P= 6.4 × 10(-6)) near SLC25A42 and for DBP was rs2523586 (P= 1.3 × 10(-6)) near HLA-B. None of the top variants replicated in additional AA (n = 11 882) or European-American (n = 69 899) cohorts. We replicated previously reported European-American blood pressure SNPs in our AA samples (SH2B3, P= 0.009; TBX3-TBX5, P= 0.03; and CSK-ULK3, P= 0.0004). These genetic loci represent the best evidence of genetic influences on SBP and DBP in AAs to date. More broadly, this work supports that notion that blood pressure among AAs is a trait with genetic underpinnings but also with significant complexity

Analysis of shared heritability in common disorders of the brain

ience, this issue p. eaap8757 Structured Abstract INTRODUCTION Brain disorders may exhibit shared symptoms and substantial epidemiological comorbidity, inciting debate about their etiologic overlap. However, detailed study of phenotypes with different ages of onset, severity, and presentation poses a considerable challenge. Recently developed heritability methods allow us to accurately measure correlation of genome-wide common variant risk between two phenotypes from pools of different individuals and assess how connected they, or at least their genetic risks, are on the genomic level. We used genome-wide association data for 265,218 patients and 784,643 control participants, as well as 17 phenotypes from a total of 1,191,588 individuals, to quantify the degree of overlap for genetic risk factors of 25 common brain disorders. RATIONALE Over the past century, the classification of brain disorders has evolved to reflect the medical and scientific communities' assessments of the presumed root causes of clinical phenomena such as behavioral change, loss of motor function, or alterations of consciousness. Directly observable phenomena (such as the presence of emboli, protein tangles, or unusual electrical activity patterns) generally define and separate neurological disorders from psychiatric disorders. Understanding the genetic underpinnings and categorical distinctions for brain disorders and related phenotypes may inform the search for their biological mechanisms. RESULTS Common variant risk for psychiatric disorders was shown to correlate significantly, especially among attention deficit hyperactivity disorder (ADHD), bipolar disorder, major depressive disorder (MDD), and schizophrenia. By contrast, neurological disorders appear more distinct from one another and from the psychiatric disorders, except for migraine, which was significantly correlated to ADHD, MDD, and Tourette syndrome. We demonstrate that, in the general population, the personality trait neuroticism is significantly correlated with almost every psychiatric disorder and migraine. We also identify significant genetic sharing between disorders and early life cognitive measures (e.g., years of education and college attainment) in the general population, demonstrating positive correlation with several psychiatric disorders (e.g., anorexia nervosa and bipolar disorder) and negative correlation with several neurological phenotypes (e.g., Alzheimer's disease and ischemic stroke), even though the latter are considered to result from specific processes that occur later in life. Extensive simulations were also performed to inform how statistical power, diagnostic misclassification, and phenotypic heterogeneity influence genetic correlations. CONCLUSION The high degree of genetic correlation among many of the psychiatric disorders adds further evidence that their current clinical boundaries do not reflect distinct underlying pathogenic processes, at least on the genetic level. This suggests a deeply interconnected nature for psychiatric disorders, in contrast to neurological disorders, and underscores the need to refine psychiatric diagnostics. Genetically informed analyses may provide important "scaffolding" to support such restructuring of psychiatric nosology, which likely requires incorporating many levels of information. By contrast, we find limited evidence for widespread common genetic risk sharing among neurological disorders or across neurological and psychiatric disorders. We show that both psychiatric and neurological disorders have robust correlations with cognitive and personality measures. Further study is needed to evaluate whether overlapping genetic contributions to psychiatric pathology may influence treatment choices. Ultimately, such developments may pave the way toward reduced heterogeneity and improved diagnosis and treatment of psychiatric disorders