Salt sensitivity: causes, consequences & recent advances

Salt (sodium chloride) is an essential nutrient required to maintain physiological functions. However, for most people daily salt intake far exceeds their physiological need and is habitually greater than recommended upper thresholds. Excess salt intake leads to elevation in blood pressure which drives cardiovascular morbidity and mortality. Indeed, excessive salt intake is estimated to be responsible for ~5 million deaths per year globally. For approximately one-third of otherwise healthy individuals (and >50% of those with hypertension), the effect of salt intake on blood pressure elevation is exaggerated; such people are categorized as ‘salt sensitive’ and salt sensitivity of blood pressure is considered an independent risk factor for cardiovascular disease and death. The prevalence of salt sensitivity is higher in women than in men and, in both, increases with age. This narrative review considers the foundational concepts of salt sensitivity and the underlying effector systems that cause salt-sensitivity. We also consider recent updates in pre-clinical and clinical research that are revealing new modifying factors that determine the blood pressure response to high salt intake

Climate change at the ecosystem scale: a 50-year record in New Hampshire

Observing the full range of climate change impacts at the local scale is difficult. Predicted rates of change are often small relative to interannual variability, and few locations have sufficiently comprehensive long-term records of environmental variables to enable researchers to observe the fine-scale patterns that may be important to understanding the influence of climate change on biological systems at the taxon, community, and ecosystem levels. We examined a 50-year meteorological and hydrological record from the Hubbard Brook Experimental Forest (HBEF) in New Hampshire, an intensively monitored Long-Term Ecological Research site. Of the examined climate metrics, trends in temperature were the most significant (ranging from 0.7 to 1.3 °C increase over 40–50 year records at 4 temperature stations), while analysis of precipitation and hydrologic data yielded mixed results. Regional records show generally similar trends over the same time period, though longer-term (70–102 year) trends are less dramatic. Taken together, the results from HBEF and the regional records indicate that the climate has warmed detectably over 50 years, with important consequences for hydrological processes. Understanding effects on ecosystems will require a diversity of metrics and concurrent ecological observations at a range of sites, as well as a recognition that ecosystems have existed in a directionally changing climate for decades, and are not necessarily in equilibrium with the current climate

Selective serotonin reuptake inhibitors (SSRIs) for stroke recovery.

BACKGROUND: Stroke is the major cause of adult disability. Selective serotonin reuptake inhibitors (SSRIs) have been used for many years to manage depression. Recently, small trials have demonstrated that SSRIs might improve recovery after stroke, even in people who are not depressed. Systematic reviews and meta-analyses are the least biased way to bring together data from several trials. Given the promising effect of SSRIs on stroke recovery seen in small trials, a systematic review and meta-analysis is needed. OBJECTIVES: To determine whether SSRIs improve recovery after stroke, and whether treatment with SSRIs was associated with adverse effects. SEARCH METHODS: We searched the Cochrane Stroke Group Trials Register (August 2011), Cochrane Depression Anxiety and Neurosis Group Trials Register (November 2011), Cochrane Central Register of Controlled Trials (CENTRAL) (The Cochrane Library 2011, Issue 8), MEDLINE (from 1948 to August 2011), EMBASE (from 1980 to August 2011), CINAHL (from 1982 to August 2011), AMED (Allied and Complementary Medicine) (from 1985 to August 2011), PsycINFO (from 1967 to August 2011) and PsycBITE (Pyschological Database for Brain Impairment Treatment Efficacy) (March 2012). To identify further published, unpublished and ongoing trials we searched trials registers, pharmaceutical websites, reference lists, contacted experts and performed citation tracking of included studies. SELECTION CRITERIA: We included randomised controlled trials that recruited stroke survivors (ischaemic or haemorrhagic) at any time within the first year. The intervention was any SSRI, given at any dose, for any period. We excluded drugs with mixed pharmacological effects. The comparator was usual care or placebo. In order to be included, trials had to collect data on at least one of our primary (dependence and disability) or secondary (impairments, depression, anxiety, quality of life, fatigue, healthcare cost, death, adverse events and leaving the trial early) outcomes. DATA COLLECTION AND ANALYSIS: We extracted data on demographics, type of stroke, time since stroke, our primary and secondary outcomes, and sources of bias. For trials in English, two review authors independently extracted data. For Chinese papers, one review author extracted data. We used standardised mean differences (SMD) to estimate treatment effects for continuous variables, and risk ratios (RR) for dichotomous effects, with their 95% confidence intervals (CIs). MAIN RESULTS: We identified 56 completed trials of SSRI versus control, of which 52 trials (4059 participants) provided data for meta-analysis. There were statistically significant benefits of SSRI on both of the primary outcomes: RR for reducing dependency at the end of treatment was 0.81 (95% CI 0.68 to 0.97) based on one trial, and for disability score, the SMD was 0.91 (95% CI 0.60 to 1.22) (22 trials involving 1343 participants) with high heterogeneity between trials (I(2) = 87%; P < 0.0001). For neurological deficit, depression and anxiety, there were statistically significant benefits of SSRIs. For neurological deficit score, the SMD was -1.00 (95% CI -1.26 to -0.75) (29 trials involving 2011 participants) with high heterogeneity between trials (I(2) = 86%; P < 0.00001). For dichotomous depression scores, the RR was 0.43 (95% CI 0.24 to 0.77) (eight trials involving 771 participants) with high heterogeneity between trials (I(2) = 77%; P < 0.0001). For continuous depression scores, the SMD was -1.91 (95% CI -2.34 to -1.48) (39 trials involving 2728 participants) with high heterogeneity between trials (I(2) = 95%; P < 0.00001). For anxiety, the SMD was -0.77 (95% CI -1.52 to -0.02) (eight trials involving 413 participants) with high heterogeneity between trials (I(2) = 92%; P < 0.00001). There was no statistically significant benefit of SSRI on cognition, death, motor deficits and leaving the trial early. For cognition, the SMD was 0.32 (95% CI -0.23 to 0.86), (seven trials involving 425 participants) with high heterogeneity between trials (I(2) = 86%; P < 0.00001). The RR for death was 0.76 (95% CI 0.34 to 1.70) (46 trials involving 3344 participants) with no heterogeneity between trials (I(2) = 0%; P = 0.85). For motor deficits, the SMD was -0.33 (95% CI -1.22 to 0.56) (two trials involving 145 participants). The RR for leaving the trial early was 1.02 (95% CI 0.86 to 1.21) in favour of control, with no heterogeneity between trials. There was a non-significant excess of seizures (RR 2.67; 95% CI 0.61 to 11.63) (seven trials involving 444 participants), a non-significant excess of gastrointestinal side effects (RR 1.90; 95% CI 0.94 to 3.85) (14 trials involving 902 participants) and a non-significant excess of bleeding (RR 1.63; 95% CI 0.20 to 13.05) (two trials involving 249 participants) in those allocated SSRIs. Data were not available on quality of life, fatigue or healthcare costs.There was no clear evidence from subgroup analyses that one SSRI was consistently superior to another, or that time since stroke or depression at baseline had a major influence on effect sizes. Sensitivity analyses suggested that effect sizes were smaller when we excluded trials at high or unclear risk of bias.Only eight trials provided data on outcomes after treatment had been completed; the effect sizes were generally in favour of SSRIs but CIs were wide. AUTHORS' CONCLUSIONS: SSRIs appeared to improve dependence, disability, neurological impairment, anxiety and depression after stroke, but there was heterogeneity between trials and methodological limitations in a substantial proportion of the trials. Large, well-designed trials are now needed to determine whether SSRIs should be given routinely to patients with stroke

Cantar de Mio Cid

Edition and Translation of el Cantar de Mio Cid, a 12th/13th-century epic poem from Castile, Spain. Edition and translation by Matthew Bailey, 2019. This is a pedagogical edition/translation with a short general introduction, notes, and a bibliography of relatively accessible chapters and books. This unit is part of Open Iberia/américa, an online, open-access teaching anthology of texts from the premodern Hispanic world. https://openiberiaamerica.hcommons.org/ This file is the .pdf formatted English version, with introduction and notes in English, and the text in facing medieval Castilian/English translation

Magellan/M2FS Spectroscopy of Galaxy Clusters: Stellar Population Model and Application to Abell 267

We report the results of a pilot program to use the Magellan/M2FS spectrograph to survey the galactic populations and internal kinematics of galaxy clusters. For this initial study, we present spectroscopic measurements for $223$ quiescent galaxies observed along the line of sight to the galaxy cluster Abell 267 ($z\sim0.23$). We develop a Bayesian method for modeling the integrated light from each galaxy as a simple stellar population, with free parameters that specify redshift ($v_\mathrm{los}/c$) and characteristic age, metallicity ($\mathrm{[Fe/H]}$), alpha-abundance ($[\alpha/\mathrm{Fe}]$), and internal velocity dispersion ($\sigma_\mathrm{int}$) for individual galaxies. Parameter estimates derived from our 1.5-hour observation of A267 have median random errors of $\sigma_{v_\mathrm{los}}=20\ \mathrm{km\ s^{-1}}$, $\sigma_{\mathrm{Age}}=1.2\ \mathrm{Gyr}$, $\sigma_{\mathrm{[Fe/H]}}=0.11\ \mathrm{dex}$,$\sigma_{[\alpha/\mathrm{Fe}]}=0.07\ \mathrm{dex}$, and$\sigma_{\sigma_\mathrm{int}}=20\ \mathrm{km\ s^{-1}}$. In a companion paper, we use these results to model the structure and internal kinematics of A267.Comment: 16 pages, 11 figures, accepted for publication in The Astronomical Journa

Failure to Downregulate the Epithelial Sodium Channel Causes Salt Sensitivity in Hsd11b2 Heterozygote Mice

In vivo, the enzyme 11β-hydroxysteroid dehydrogenase type 2 influences ligand access to the mineralocorticoid receptor. Ablation of the encoding gene, HSD11B2, causes the hypertensive syndrome of apparent mineralocorticoid excess. Studies in humans and experimental animals have linked reduced 11β-hydroxysteroid dehydrogenase type 2 activity and salt sensitivity of blood pressure. In the present study, renal mechanisms underpinning salt sensitivity were investigated in Hsd11b2(+/-) mice fed low-, standard-, and high-sodium diets. In wild-type mice, there was a strong correlation between dietary sodium content and fractional sodium excretion but not blood pressure. High sodium feeding abolished amiloride-sensitive sodium reabsorption, consistent with downregulation of the epithelial sodium channel. In Hsd11b2(+/-) mice, the natriuretic response to increased dietary sodium content was blunted, and epithelial sodium channel activity persisted. High-sodium diet also reduced renal blood flow and increased blood pressure in Hsd11b2(+/-) mice. Aldosterone was modulated by dietary sodium in both genotypes, and salt sensitivity in Hsd11b2(+/-) mice was associated with increased plasma corticosterone levels. Chronic administration of an epithelial sodium channel blocker or a glucocorticoid receptor antagonist prevented salt sensitivity in Hsd11b2(+/-) mice, whereas mineralocorticoid receptor blockade with spironolactone did not. This study shows that reduced 11β-hydroxysteroid dehydrogenase type 2 causes salt sensitivity of blood pressure because of impaired renal natriuretic capacity. This reflects deregulation of epithelial sodium channels and increased renal vascular resistance. The phenotype is not caused by illicit activation of mineralocorticoid receptors by glucocorticoids but by direct activation of glucocorticoid receptors

TB88: Descriptive and Comparative Studies of Maine Lakes

This is a descriptive and comparative study of 17 lakes in Maine. The major objectives of this study are (1) to characterize the pelagial zone of the lakes physically, chemically, and biologically, (2) to assess bacterial pollution, (3) to compare the lakes to each other and classify them trophically, and (4) to compare the lakes to others in different geographic regions.https://digitalcommons.library.umaine.edu/aes_techbulletin/1117/thumbnail.jp