- Proceedings of the National Academy of Sciences of the United States of America
- Published about 3 years ago
Salt pollution and human-accelerated weathering are shifting the chemical composition of major ions in fresh water and increasing salinization and alkalinization across North America. We propose a concept, the freshwater salinization syndrome, which links salinization and alkalinization processes. This syndrome manifests as concurrent trends in specific conductance, pH, alkalinity, and base cations. Although individual trends can vary in strength, changes in salinization and alkalinization have affected 37% and 90%, respectively, of the drainage area of the contiguous United States over the past century. Across 232 United States Geological Survey (USGS) monitoring sites, 66% of stream and river sites showed a statistical increase in pH, which often began decades before acid rain regulations. The syndrome is most prominent in the densely populated eastern and midwestern United States, where salinity and alkalinity have increased most rapidly. The syndrome is caused by salt pollution (e.g., road deicers, irrigation runoff, sewage, potash), accelerated weathering and soil cation exchange, mining and resource extraction, and the presence of easily weathered minerals used in agriculture (lime) and urbanization (concrete). Increasing salts with strong bases and carbonates elevate acid neutralizing capacity and pH, and increasing sodium from salt pollution eventually displaces base cations on soil exchange sites, which further increases pH and alkalinization. Symptoms of the syndrome can include: infrastructure corrosion, contaminant mobilization, and variations in coastal ocean acidification caused by increasingly alkaline river inputs. Unless regulated and managed, the freshwater salinization syndrome can have significant impacts on ecosystem services such as safe drinking water, contaminant retention, and biodiversity.
Juxtaglomerular neurons represent one of the largest cellular populations in the mammalian olfactory bulb yet their role for signal processing remains unclear. We used two-photon imaging and electrophysiological recordings to clarify the properties of these cells and their functional organization in the juxtaglomerular space. Juxtaglomerular neurons coded for many perceptual characteristics of the olfactory stimulus such as (1) identity of the odorant, (2) odorant concentration, (3) odorant onset, and (4) offset. The odor-responsive neurons clustered within a narrow area surrounding the glomerulus with the same odorant specificity, with ~80% of responding cells located ≤20 μm from the glomerular border. This stereotypic spatial pattern of activated cells persisted at different odorant concentrations and was found for neurons both activated and inhibited by the odorant. Our data identify a principal glomerulus with a narrow shell of juxtaglomerular neurons as a basic odor coding unit in the glomerular layer and underline the important role of intraglomerular circuitry.
Stabilizing superoxide (O2-) is one of the key issues of sodium-air batteries because the superoxide-based discharge product (NaO2) is more reversibly oxidized to oxygen when compared with peroxide (O22-) and oxide (O2-). Reversibly outstanding performances of sodium-oxygen batteries have been realized with the superoxide discharge product (NaO2) even if sodium peroxide (Na2O2) have been also known as the discharge products. Here we report that the Lewis basicity of anions of sodium salts as well as solvent molecules, both quantitatively represented by donor numbers (DNs), determines the superoxide stability and resultantly the reversibility of sodium-oxygen batteries. A DN map of superoxide stability was presented as a selection guide of salt/solvent pair. Based on sodium triflate (CF3SO3-)/dimethyl sulfoxide (DMSO) as a high-DN-pair electrolyte system, sodium ion oxygen batteries were constructed. Pre-sodiated antimony (Sb) was used as an anode during discharge instead of sodium metal because DMSO is reacted with the metal. The superoxide stability supported by the high DN anion/solvent pair ([Formula: see text] -/DMSO) allowed more reversible operation of the sodium ion oxygen batteries.
Vascular calcification is a risk factor that predicts adverse cardiovascular complications of several diseases including atherosclerosis. Reduced dietary potassium intake has been linked to cardiovascular diseases such as hypertension and incidental stroke, although the underlying molecular mechanisms remain largely unknown. Using the ApoE-deficient mouse model, we demonstrated for the first time to our knowledge that reduced dietary potassium (0.3%) promoted atherosclerotic vascular calcification and increased aortic stiffness, compared with normal (0.7%) potassium-fed mice. In contrast, increased dietary potassium (2.1%) attenuated vascular calcification and aortic stiffness. Mechanistically, reduction in the potassium concentration to the lower limit of the physiological range increased intracellular calcium, which activated a cAMP response element-binding protein (CREB) signal that subsequently enhanced autophagy and promoted vascular smooth muscle cell (VSMC) calcification. Inhibition of calcium signals and knockdown of either CREB or ATG7, an autophagy regulator, attenuated VSMC calcification induced by low potassium. Consistently, elevated autophagy and CREB signaling were demonstrated in the calcified arteries from low potassium diet-fed mice as well as aortic arteries exposed to low potassium ex vivo. These studies established a potentially novel causative role of dietary potassium intake in regulating atherosclerotic vascular calcification and stiffness, and uncovered mechanisms that offer opportunities to develop therapeutic strategies to control vascular disease.
Wearable sensor technologies are essential to the realization of personalized medicine through continuously monitoring an individual’s state of health. Sampling human sweat, which is rich in physiological information, could enable non-invasive monitoring. Previously reported sweat-based and other non-invasive biosensors either can only monitor a single analyte at a time or lack on-site signal processing circuitry and sensor calibration mechanisms for accurate analysis of the physiological state. Given the complexity of sweat secretion, simultaneous and multiplexed screening of target biomarkers is critical and requires full system integration to ensure the accuracy of measurements. Here we present a mechanically flexible and fully integrated (that is, no external analysis is needed) sensor array for multiplexed in situ perspiration analysis, which simultaneously and selectively measures sweat metabolites (such as glucose and lactate) and electrolytes (such as sodium and potassium ions), as well as the skin temperature (to calibrate the response of the sensors). Our work bridges the technological gap between signal transduction, conditioning (amplification and filtering), processing and wireless transmission in wearable biosensors by merging plastic-based sensors that interface with the skin with silicon integrated circuits consolidated on a flexible circuit board for complex signal processing. This application could not have been realized using either of these technologies alone owing to their respective inherent limitations. The wearable system is used to measure the detailed sweat profile of human subjects engaged in prolonged indoor and outdoor physical activities, and to make a real-time assessment of the physiological state of the subjects. This platform enables a wide range of personalized diagnostic and physiological monitoring applications.
Salt sensitivity of blood pressure affects >30% of the hypertensive and >15% of the normotensive population. Variants of the electrogenic sodium bicarbonate cotransporter NBCe2 gene, SLC4A5, are associated with increased blood pressure in several ethnic groups. SLC4A5 variants are also highly associated with salt sensitivity, independent of hypertension. However, little is known about how NBCe2 contributes to salt sensitivity, although NBCe2 regulates renal tubular sodium bicarbonate transport. We hypothesized that SLC4A5 rs10177833 and rs7571842 increase NBCe2 expression and human renal proximal tubule cell (hRPTC) sodium transport and may be a cause of salt sensitivity of blood pressure.
Iron, potassium, zinc, and other minerals might impact the development of premenstrual syndrome (PMS) through multiple mechanisms, but few studies have evaluated these relations. We conducted a case-control study nested within the prospective Nurses' Health Study II (1991-2001). Participants were free from PMS at baseline. After 10 years, 1,057 women were confirmed as PMS cases and 1,968 as controls. Mineral intake was assessed using food frequency questionnaires completed in 1991, 1995, and 1999. After adjustment for calcium intake and other factors, women in the highest quintile of nonheme iron intake had a relative risk of PMS of 0.64 (95% confidence interval (CI): 0.44, 0.92; P for trend = 0.04) compared with women in the lowest quintile. Women in the highest quintile of potassium intake had a relative risk of 1.46 (95% CI: 0.99, 2.15; P for trend = 0.04) compared with women in the lowest quintile. High intake of zinc from supplements was marginally associated with PMS (for intake of ≥25 mg/day vs. none, relative risk = 0.69, 95% CI: 0.46, 1.02; P for trend = 0.05). Intakes of sodium, magnesium, and manganese were unrelated to PMS risk. These findings suggest that dietary minerals may be useful in preventing PMS. Additional studies are needed to confirm these relations.
Fish venoms are often poorly studied, in part due to the difficulty in obtaining, extracting, and storing them. In this study, we characterize the cardiovascular and neurotoxic effects of the venoms from the following six species of fish: the cartilaginous stingrays Neotrygon kuhlii and Himantura toshi, and the bony fish Platycephalus fucus, Girella tricuspidata, Mugil cephalus, and Dentex tumifrons. All venoms (10-100 μg/kg, i.v.), except G. tricuspidata and P. fuscus, induced a biphasic response on mean arterial pressure (MAP) in the anesthetised rat. P. fucus venom exhibited a hypotensive response, while venom from G. tricuspidata displayed a single depressor response. All venoms induced cardiovascular collapse at 200 μg/kg, i.v. The in vitro neurotoxic effects of venom were examined using the chick biventer cervicis nerve-muscle (CBCNM) preparation. N. kuhlii, H. toshi, and P. fucus venoms caused concentration-dependent inhibition of indirect twitches in the CBCNM preparation. These three venoms also inhibited responses to exogenous acetylcholine (ACh) and carbachol (CCh), but not potassium chloride (KCl), indicating a post-synaptic mode of action. Venom from G. tricuspidata, M. cephalus, and D. tumifrons had no significant effect on indirect twitches or agonist responses in the CBCNM. Our results demonstrate that envenoming by these species of fish may result in moderate cardiovascular and/or neurotoxic effects. Future studies aimed at identifying the molecules responsible for these effects could uncover potentially novel lead compounds for future pharmaceuticals, in addition to generating new knowledge about the evolutionary relationships between venomous animals.
Cardiovascular benefits associated with higher dietary K+ versus lower dietary Na+: Evidence from population and mechanistic studies
- American journal of physiology. Endocrinology and metabolism
- Published about 4 years ago
The WHO ranks hypertension the leading global risk factor for disease, specifically, cardiovascular disease. Blood pressure is higher in westernized populations consuming sodium-rich processed foods compared to isolated societies consuming potassium-rich natural foods. Evidence suggests that lowering dietary Na(+) is particularly beneficial in hypertensives who consume a high Na(+) diet. Nonetheless, numerous population studies demonstrate a relationship between higher dietary K(+), estimated from urinary excretion or dietary recall, and lower blood pressure regardless of sodium intake. Interventional studies with potassium supplementation suggest it provides a direct benefit; K(+) may also be a marker for other beneficial components of a “natural” diet. Recent studies in rodent models indicate mechanisms for the potassium benefit: the distal tubule Na(+)- Cl(-) cotransporter (NCC) controls Na(+) delivery downstream to the collecting duct where Na(+) reabsorbed by epithelial Na(+) channels (ENaC) drives K(+) secretion and excretion through K(+) channels in the same region. High dietary K(+) provokes a decrease in the NCC activity to drive more K(+) secretion (and Na(+) excretion, analogous to the actions of a thiazide diuretic) whether Na(+) intake is high or low; low dietary K(+) provokes an increase in NCC activity and Na(+) retention, also independent of dietary Na(+) Taken together, the findings suggest that public health efforts directed towards increasing consumption of natural potassium rich foods would reduce blood pressure and, thus, cardiovascular and kidney disease.