Search

Methane (CH4) is a potent greenhouse gas (GHG) with atmospheric concentrations that have nearly tripled since pre‐industrial times. Wetlands account for a large share of global CH4 emissions, yet the magnitude and factors controlling CH4 fluxes in tidal wetlands remain uncertain. We synthesized CH4 flux data from 100 chamber and 9 eddy covariance (EC) sites across tidal marshes in the conterminous United States to assess controlling factors and improve predictions of CH4 emissions. This effort included creating an open‐source database of chamber‐based GHG fluxes (https://doi.org/10.25573/serc.14227085). Annual fluxes across chamber and EC sites averaged 26 ± 53 g CH4 m−2 year−1, with a median of 3.9 g CH4 m−2 year−1, and only 25% of sites exceeding 18 g CH4 m−2 year−1. The highest fluxes were observed at fresh‐oligohaline sites with daily maximum temperature normals (MATmax) above 25.6°C. These were followed by frequently inundated low and mid‐fresh‐oligohaline marshes with MATmax ≤25.6°C, and mesohaline sites with MATmax >19°C. Quantile regressions of paired chamber CH4 flux and porewater biogeochemistry revealed that the 90th percentile of fluxes fell below 5 ± 3 nmol m−2 s−1 at sulfate concentrations >4.7 ± 0.6 mM, porewater salinity >21 ± 2 psu, or surface water salinity >15 ± 3 psu. Across sites, salinity was the dominant predictor of annual CH4 fluxes, while within sites, temperature, gross primary productivity (GPP), and tidal height controlled variability at diel and seasonal scales. At the diel scale, GPP preceded temperature in importance for predicting CH4 flux changes, while the opposite was observed at the seasonal scale. Water levels influenced the timing and pathway of diel CH4 fluxes, with pulsed releases of stored CH4 at low to rising tide. This study provides data and methods to improve tidal marsh CH4 emission estimates, support blue carbon assessments, and refine national and global GHG inventories. [ABSTRACT FROM AUTHOR]

Voluntary urination ensures that waste is eliminated when safe and socially appropriate, even without a pressing urge. Uncontrolled urination, or incontinence, is a common problem with few treatment options. Normal urine release requires a small region in the brainstem known as Barrington's nucleus (Bar), but specific neurons that relax the urethral sphincter and enable urine flow are unknown. Here we identify a small subset of Bar neurons that control the urethral sphincter in mice. These excitatory neurons express estrogen receptor 1 (BarESR1), project to sphincter-relaxing interneurons in the spinal cord and are active during natural urination. Optogenetic stimulation of BarESR1 neurons rapidly initiates sphincter bursting and efficient voiding in anesthetized and behaving animals. Conversely, optogenetic and chemogenetic inhibition reveals their necessity in motivated urination behavior. The identification of these cells provides an expanded model for the control of urination and its dysfunction.

Rapid point-of-care, antibody-based testing is not currently available for the diagnosis of most autoimmune and infectious diseases. Here we report a simple, robust and ultrafast fluid-phase immunocapture method for clinical measurements of antibody levels. This method employs neodymium magnetic sticks that capture protein A/G-coated paramagnetic beads bound to antibody-luciferase-labeled antigen complexes. We demonstrate the ability to effectively measure specific antibody levels in serum samples from patients with varied infectious or autoimmune disorders, and in the case of Sjögren's syndrome directly in saliva, requiring about a minute per assay. We also show the feasibility of coupling this method with a hand-held luminometer for portable testing. Our method offers the potential to quickly diagnose a multitude of autoimmune and infectious diseases in point-of-care settings.

Henry Miller stated that 'to relieve a full bladder is one of the great human joys'. Urination is critically important in health and ailments of the lower urinary tract cause high pathological burden. Although there have been advances in understanding the central circuitry in the brain that facilitates urination.sup.1-3, there is a lack of in-depth mechanistic insight into the process. In addition to central control, micturition reflexes that govern urination are all initiated by peripheral mechanical stimuli such as bladder stretch and urethral flow.sup.4. The mechanotransduction molecules and cell types that function as the primary stretch and pressure detectors in the urinary tract mostly remain unknown. Here we identify expression of the mechanosensitive ion channel PIEZO2 in lower urinary tract tissues, where it is required for low-threshold bladder-stretch sensing and urethral micturition reflexes. We show that PIEZO2 acts as a sensor in both the bladder urothelium and innervating sensory neurons. Humans and mice lacking functional PIEZO2 have impaired bladder control, and humans lacking functional PIEZO2 report deficient bladder-filling sensation. This study identifies PIEZO2 as a key mechanosensor in urinary function. These findings set the foundation for future work to identify the interactions between urothelial cells and sensory neurons that control urination. PIEZO2 is expressed in the bladder urothelium and sensory neurons innervating the lower urinary tract and is a key mechanosensor for the control of urination., Author(s): Kara L. Marshall [sup.1] , Dimah Saade [sup.2] , Nima Ghitani [sup.3] , Adam M. Coombs [sup.1] , Marcin Szczot [sup.3] , Jason Keller [sup.4] [sup.5] , Tracy Ogata [...]

Dravet syndrome is a severe epileptic encephalopathy, characterized by (febrile) seizures, behavioural problems and developmental delay. Eighty per cent of patients with Dravet syndrome have a mutation in SCN1A , encoding Nav1.1. Milder clinical phenotypes, such as GEFS+ (generalized epilepsy with febrile seizures plus), can also arise from SCN1A mutations. Predicting the clinical phenotypic outcome based on the type of mutation remains challenging, even when the same mutation is inherited within one family. This clinical and genetic heterogeneity adds to the difficulties of predicting disease progression and tailoring the prescription of anti-seizure medication. Understanding the neuropathology of different SCN1A mutations may help to predict the expected clinical phenotypes and inform the selection of best-fit treatments. Initially, the loss of Na+-current in inhibitory neurons was recognized specifically to result in disinhibition and consequently seizure generation. However, the extent to which excitatory neurons contribute to the pathophysiology is currently debated and might depend on the patient clinical phenotype or the specific SCN1A mutation. To examine the genotype-phenotype correlations of SCN1A mutations in relation to excitatory neurons, we investigated a panel of patient-derived excitatory neuronal networks differentiated on multi-electrode arrays. We included patients with different clinical phenotypes, harbouring various SCN1A mutations, along with a family in which the same mutation led to febrile seizures, GEFS+ or Dravet syndrome. We hitherto describe a previously unidentified functional excitatory neuronal network phenotype in the context of epilepsy, which corresponds to seizurogenic network prediction patterns elicited by proconvulsive compounds. We found that excitatory neuronal networks were affected differently, depending on the type of S CN1A mutation, but did not segregate according to clinical severity. Specifically, loss-of-function mutations could be distinguished from missense mutations, and mutations in the pore domain could be distinguished from mutations in the voltage sensing domain. Furthermore, all patients showed aggravated neuronal network responses at febrile temperatures compared with controls. Finally, retrospective drug screening revealed that anti-seizure medication affected GEFS+ patient- but not Dravet patient-derived neuronal networks in a patient-specific and clinically relevant manner. In conclusion, our results indicate a mutation-specific excitatory neuronal network phenotype, which recapitulates the foremost clinically relevant features, providing future opportunities for precision therapies. [ABSTRACT FROM AUTHOR]

Agonists of the vanilloid receptor transient vanilloid potential 1 (TRPV1) are emerging as highly efficacious nonopioid analgesics in preclinical studies. These drugs selectively lesion [TRPV1.sup.+] primary sensory afferents, which are responsible for the transmission of many noxious stimulus modalities. Resiniferatoxin (RTX) is a very potent and selective TRPV1 agonist and is a promising candidate for treating many types of pain. Recent work establishing intrathecal application of RTX for the treatment of pain resulting from advanced cancer has demonstrated profound analgesia in client-owned dogs with osteosarcoma. The present study uses transcriptomics and histochemistry to examine the molecular mechanism of RTX action in rats, in clinical canine subjects, and in 1 human subject with advanced cancer treated for pain using intrathecal RTX. In all 3 species, we observe a strong analgesic action, yet this was accompanied by limited transcriptional alterations at the level of the dorsal root ganglion. Functional and neuroanatomical studies demonstrated that intrathecal RTX largely spares susceptible neuronal perikarya, which remain active peripherally but unable to transmit signals to the spinal cord. The results demonstrate that central chemo-axotomy of the [TRPV1.sup.+] afferents underlies RTX analgesia and refine the neurobiology underlying effective clinical use of TRPV1 agonists for pain control., Introduction Severe chronic pain remains a medically intractable problem with life-altering consequences. While most chronic pain is currently treated with any number of drugs, including opioids, NSAIDs, and calcium channel [...]

Summary: Drainage‐induced encroachment by trees may have major effects on the carbon balance of northern peatlands, and responses of microbial communities are likely to play a central mechanistic role.We profiled the soil fungal community and estimated its genetic potential for the decay of lignin and phenolics (class II peroxidase potential) along peatland drainage gradients stretching from interior locations (undrained, open) to ditched locations (drained, forested).Mycorrhizal fungi dominated the community across the gradients. When moving towards ditches, the dominant type of mycorrhizal association abruptly shifted from ericoid mycorrhiza to ectomycorrhiza at c. 120 m from the ditches. This distance corresponded with increased peat loss, from which more than half may be attributed to oxidation. The ectomycorrhizal genus Cortinarius dominated at the drained end of the gradients and its relatively higher genetic potential to produce class II peroxidases (together with Mycena) was positively associated with peat humification and negatively with carbon‐to‐nitrogen ratio.Our study is consistent with a plant–soil feedback mechanism, driven by a shift in the mycorrhizal type of vegetation, that potentially mediates changes in aerobic decomposition during postdrainage succession. Such feedback may have long‐term legacy effects upon postdrainage restoration efforts and implication for tree encroachment onto carbon‐rich soils globally. See also the Commentary on this article by Parker and Clemmensen, 240: 10–12. [ABSTRACT FROM AUTHOR]

We derive new exact closed-form solutions of magnetohydrodynamics equations, with and without dynamics, which model astrophysical jets and other prolonged plasma configurations. The solutions are obtained in static and dynamic incompressible equilibrium settings, in axial and helical symmetry assumptions, and are given in terms of Whittaker, Coulomb, and Heun special functions. For each symmetry, two distinct families of physical solutions arise, corresponding to two distinct pressure profiles. One pressure profile models plasmas supported by an external pressure and is suitable for the description of plasma configurations in a medium, such as atmosphere. The second profile features higher pressure inside the plasma domain and can model plasmas residing in a vacuum. Examples of static and dynamic solutions in axially and helically symmetric settings, including solutions with boundary current sheets, are presented and discussed. [ABSTRACT FROM AUTHOR]

Northern peatlands store approximately one-third of terrestrial soil carbon. Climate warming is expected to stimulate the microbially mediated degradation of peat soil organic matter (SOM), leading to increasing greenhouse gas (GHG; carbon dioxide, CO2; methane, CH4) production and emission. Porewater dissolved organic matter (DOM) plays a key role in SOM decomposition; however, the mechanisms controlling SOM decomposition and its response to warming remain unclear. The temperature dependence of GHG production and microbial community dynamics were investigated in anoxic peat from a Sphagnum -dominated peatland. In this study, peat decomposition, which was quantified by GHG production and carbon substrate utilization is limited by terminal electron acceptors (TEA) and DOM, and these controls of microbially mediated SOM degradation are temperature-dependent. Elevated temperature led to a slight decrease in microbial diversity, and stimulated the growth of specific methanotrophic and syntrophic taxa. These results confirm that DOM is a major driver of decomposition in peatland soils contains inhibitory compounds, but the inhibitory effect is alleviated by warming. [ABSTRACT FROM AUTHOR]

Abstract.--Soil organic carbon and nitrogen storage represent important ecosystem services provided by salt marshes. To test the importance of vegetation on soil properties, we measured organic carbon, total nitrogen, and [...]

Abstract.--There is a growing interest in managing wetland restoration and conservation projects to maximize carbon sequestration. We measured soil organic carbon storage and methane flux from two southern California salt [...]