Mabel was every inch the superstar as she displayed some edgy new locks while stepping out in London on  Thursday.

Woody networks in agricultural landscapes are known to harbour high intrinsic biodiversity (i.e. diversity of plant species) and functional biodiversity (i.e. ecosystem services that arise from biodiversity). In order to clarify the drivers of intrinsic and functional biodiversity in woody networks, researchers analysed the plant species diversity, pollinator resource value (PRV), and potential edibility value (PEV) of a woody network in northern Belgium. The analysis confirmed that woody elements are a rich source of intrinsic and functional biodiversity and identified several important drivers. From a policy perspective, this research highlights the value of protecting existing woody elements and thoughtfully designing and locating new ones to maximise intrinsic and functional biodiversity in the countryside.

Flea collars, lawn-care products, insect repellant and de-licing products could be harming more than just pests.

The present invention is a solid rinse aid composition and methods of making and using the same. Applicants have surprisingly found that the crystal modifier sodium xylene sulfonate (short chain alkyl benzene or alkyl naphthalene sulfonates) at higher percentage can act as a solidification agent. The solid rinse aid composition generally includes an short chain alkyl benzene or alkyl naphthalene sulfonates solidification agent and an effective amount of a surfactant which can include a sheeting agent component, defoamer component and/or association disruption agent. The solid rinse aid composition may be phosphate-free, aminocarboxylate-free, and GRAS if desired.

A rinse-off composition, such as a shampoo, hair conditioner or shower gel, comprising a rinse-off composition base, lactoyl ethanolamine and at least one compound selected from the group consisting of N-(4-cyanomethylphenyl) p-menthanecarboxamide and N-(2-pyridin-2-ylethyl) p-menthanecarboxamide. The compositions provide a pleasant, long-lasting cooling sensation.

Provided are a method of preparing a chlorohydrin composition and a method of preparing epichlorohydrin by using a chlorohydrin composition prepared by using the method. The method of preparing chlorohydrins in which polyhydroxy aliphatic hydrocarbon is reacted with a chlorination agent in the presence of a catalyst includes performing at least one combination of a series of unit operations comprising a first reaction step, a water removal step, and a second reaction step in this stated order, wherein the method further includes mixing a chlorohydrin concentrate obtained by purifying the reaction mixture discharged from the final reaction step from among the reaction steps and a water-rich layer discharged from the water-removal step and diluting the mixture with water. The method of preparing epichlorohydrin includes contacting the chlorohydrin composition prepared by using the method of preparing a chlorohydrin composition with an alkaline agent.

Cardiac pacing methods for an implantable single chamber pacing system, establish an offset rate for pacing at a predetermined decrement from either a baseline rate (i.e. dictated by a rate response sensor), or an intrinsic rate. Pacing maintains the offset rate until x of y successive events are paced events, at which time the offset rate is switched to the baseline rate for pacing over a predetermined period of time. Following the period, if an intrinsic event is not immediately detected, within the interval of the offset rate, the rate is switched back to baseline for pacing over an increased period of time. Some methods establish a preference rate, between the offset and baseline rates, wherein an additional criterion, for switching from the offset rate to the baseline rate, is established with respect to the preference rate.

A modular, intrinsically-safe power module assembly is provided. The assembly includes a rigid conduit adapter configured to mount to a conduit of a field device. A housing, having an interior, is operably coupled to the rigid conduit adapter and is physically supported by the rigid conduit adapter. At least one non-rechargeable battery is disposed within the housing. Intrinsic safety circuitry is coupled to the at least one non-rechargeable battery, and is coupled to a connector that mates with a cooperative connector in the rigid conduit adapter.

A GRINSCH laser having an asymmetric configuration wherein the optical confinement is weighted more to the n-doped multilayer section than to the p-doped multilayer section. The GRINSCH laser can emit laser light at a wavelength λ=976 nm over a broad area with a beam power of 11.4 W at a 12 A bias current at a temperature of 20° C. Fabry-Perot and distributed Bragg reflector GRINSCH laser configurations are disclosed.

The present invention relates to a composition useful for the diagnosis of diseases associated with aberrant expression of the genes encoding the secreted proteins Futrin 1, 2, 3 and/or 4(=R-Spondin 2, 3, 1 and 4, respectively), e.g. in connection with tumors or diseases of the muscle, kidneys or bones. The present invention also relates to a pharmaceutical composition containing a compound which is capable of modifying (a) the expression of the gene encoding Futrin 1, 2, 3 and/or 4 or (b) the activity of the Futrin 1, 2, 3 and/or 4 protein.

A coffee machine comprises a frothing device, wherein an internal milk channel leading to a frothing chamber is provided into which opens a bypass air inlet for operable air supply to the frothing device. A flexible milk suction line connects the frothing device with a milk supply container. Means are provided for cleaning the frothing device and the milk suction line with rinsing water from a continuous-flow water heater of the coffee machine. A controlled valve arrangement is provided which feeds rinsing water from the continuous-flow water heater to the bypass air inlet of the frothing device. A milk suction end of the milk suction line is directly or indirectly, fluid-conductively connectable with a residual water pan of the coffee machine prior to feeding rinsing water to the bypass air inlet.

An in-depth understanding of immune escape mechanisms in cancer is likely to lead to innovative advances in immunotherapeutic strategies. However, much remains unknown regarding these mechanisms and how they impact immunotherapy resistance. Using several preclinical tumor models as well as clinical specimens, we identified a mechanism whereby CD8+ T cell activation in response to programmed cell death 1 (PD-1) blockade induced a programmed death ligand 1/NOD-, LRR-, and pyrin domain–containing protein 3 (PD-L1/NLRP3) inflammasome signaling cascade that ultimately led to the recruitment of granulocytic myeloid-derived suppressor cells (PMN-MDSCs) into tumor tissues, thereby dampening the resulting antitumor immune response. The genetic and pharmacologic inhibition of NLRP3 suppressed PMN-MDSC tumor infiltration and significantly augmented the efficacy of anti–PD-1 antibody immunotherapy. This pathway therefore represents a tumor-intrinsic mechanism of adaptive resistance to anti–PD-1 checkpoint inhibitor immunotherapy and is a promising target for future translational research.

Review of 'The Case for Nationalism: How It Made Us Powerful, United, and Free' by Rich Lowry

AE Christian
Nov 1, 1997; 38:2264-2272
Articles

Much of our current knowledge of biological chemistry is founded in the structure-function relationship, whereby sequence determines structure that determines function. Thus, the discovery that a large fraction of the proteome is intrinsically disordered, while being functional, has revolutionized our understanding of proteins and raised new and interesting questions. Many intrinsically disordered proteins (IDPs) have been determined to undergo a disorder-to-order transition when recognizing their physiological partners, suggesting that their mechanisms of folding are intrinsically different from those observed in globular proteins. However, IDPs also follow some of the classic paradigms established for globular proteins, pointing to important similarities in their behavior. In this review, we compare and contrast the folding mechanisms of globular proteins with the emerging features of binding-induced folding of intrinsically disordered proteins. Specifically, whereas disorder-to-order transitions of intrinsically disordered proteins appear to follow rules of globular protein folding, such as the cooperative nature of the reaction, their folding pathways are remarkably more malleable, due to the heterogeneous nature of their folding nuclei, as probed by analysis of linear free-energy relationship plots. These insights have led to a new model for the disorder-to-order transition in IDPs termed “templated folding,” whereby the binding partner dictates distinct structural transitions en route to product, while ensuring a cooperative folding.

Much of our current knowledge of biological chemistry is founded in the structure-function relationship, whereby sequence determines structure that determines function. Thus, the discovery that a large fraction of the proteome is intrinsically disordered, while being functional, has revolutionized our understanding of proteins and raised new and interesting questions. Many intrinsically disordered proteins (IDPs) have been determined to undergo a disorder-to-order transition when recognizing their physiological partners, suggesting that their mechanisms of folding are intrinsically different from those observed in globular proteins. However, IDPs also follow some of the classic paradigms established for globular proteins, pointing to important similarities in their behavior. In this review, we compare and contrast the folding mechanisms of globular proteins with the emerging features of binding-induced folding of intrinsically disordered proteins. Specifically, whereas disorder-to-order transitions of intrinsically disordered proteins appear to follow rules of globular protein folding, such as the cooperative nature of the reaction, their folding pathways are remarkably more malleable, due to the heterogeneous nature of their folding nuclei, as probed by analysis of linear free-energy relationship plots. These insights have led to a new model for the disorder-to-order transition in IDPs termed “templated folding,” whereby the binding partner dictates distinct structural transitions en route to product, while ensuring a cooperative folding.

Leipzig : Deuticke, 1898.

London : Elliot Stock, 1886.

Paris : Bailliere, 1896.

Paris : J.-B. Baillière, 1886.

Paris : W. Remquet, 1854.

Marco A. R. Ferreira.

Source: Brazilian Journal of Probability and Statistics, Volume 33, Number 4, 734--744.

Abstract:
We study the limiting behavior of the one-at-a-time Gibbs sampler for the intrinsic conditional autoregressive model with centering on the fly. The intrinsic conditional autoregressive model is widely used as a prior for random effects in hierarchical models for spatial modeling. This model is defined by full conditional distributions that imply an improper joint “density” with a multivariate Gaussian kernel and a singular precision matrix. To guarantee propriety of the posterior distribution, usually at the end of each iteration of the Gibbs sampler the random effects are centered to sum to zero in what is widely known as centering on the fly. While this works well in practice, this informal computational way to recenter the random effects obscures their implied prior distribution and prevents the development of formal Bayesian procedures. Here we show that the implied prior distribution, that is, the limiting distribution of the one-at-a-time Gibbs sampler for the intrinsic conditional autoregressive model with centering on the fly is a singular Gaussian distribution with a covariance matrix that is the Moore–Penrose inverse of the precision matrix. This result has important implications for the development of formal Bayesian procedures such as reference priors and Bayes-factor-based model selection for spatial models.

Zhenhua Lin, Fang Yao.

Source: The Annals of Statistics, Volume 47, Number 6, 3533--3577.

Abstract:
In this work we develop a novel and foundational framework for analyzing general Riemannian functional data, in particular a new development of tensor Hilbert spaces along curves on a manifold. Such spaces enable us to derive Karhunen–Loève expansion for Riemannian random processes. This framework also features an approach to compare objects from different tensor Hilbert spaces, which paves the way for asymptotic analysis in Riemannian functional data analysis. Built upon intrinsic geometric concepts such as vector field, Levi-Civita connection and parallel transport on Riemannian manifolds, the developed framework applies to not only Euclidean submanifolds but also manifolds without a natural ambient space. As applications of this framework, we develop intrinsic Riemannian functional principal component analysis (iRFPCA) and intrinsic Riemannian functional linear regression (iRFLR) that are distinct from their traditional and ambient counterparts. We also provide estimation procedures for iRFPCA and iRFLR, and investigate their asymptotic properties within the intrinsic geometry. Numerical performance is illustrated by simulated and real examples.

Lizhen Lin, Niu Mu, Pokman Cheung, David Dunson.

Source: Bayesian Analysis, Volume 14, Number 3, 907--926.

Abstract:
Gaussian processes (GPs) are very widely used for modeling of unknown functions or surfaces in applications ranging from regression to classification to spatial processes. Although there is an increasingly vast literature on applications, methods, theory and algorithms related to GPs, the overwhelming majority of this literature focuses on the case in which the input domain corresponds to a Euclidean space. However, particularly in recent years with the increasing collection of complex data, it is commonly the case that the input domain does not have such a simple form. For example, it is common for the inputs to be restricted to a non-Euclidean manifold, a case which forms the motivation for this article. In particular, we propose a general extrinsic framework for GP modeling on manifolds, which relies on embedding of the manifold into a Euclidean space and then constructing extrinsic kernels for GPs on their images. These extrinsic Gaussian processes (eGPs) are used as prior distributions for unknown functions in Bayesian inferences. Our approach is simple and general, and we show that the eGPs inherit fine theoretical properties from GP models in Euclidean spaces. We consider applications of our models to regression and classification problems with predictors lying in a large class of manifolds, including spheres, planar shape spaces, a space of positive definite matrices, and Grassmannians. Our models can be readily used by practitioners in biological sciences for various regression and classification problems, such as disease diagnosis or detection. Our work is also likely to have impact in spatial statistics when spatial locations are on the sphere or other geometric spaces.

William W. Seeley
Feb 28, 2007; 27:2349-2356
BehavioralSystemsCognitive

Sebastian Onasch
Apr 15, 2020; 40:3186-3202
Systems/Circuits

Randy L. Buckner
Feb 11, 2009; 29:1860-1873
Neurobiology of Disease

William W. Seeley
Feb 28, 2007; 27:2349-2356
BehavioralSystemsCognitive

Neurons and circuits each with a distinct balance of intrinsic and synaptic conductances can generate similar behavior but sometimes respond very differently to perturbation. Examining a large family of circuit models with non-identical neurons and synapses underlying rhythmic behavior, we analyzed the circuits' response to modifications in single and multiple intrinsic conductances in the individual neurons. To summarize these changes over the entire range of perturbed parameters, we quantified circuit output by defining a global stability measure. Using this measure, we identified specific subsets of conductances that when perturbed generate similar behavior in diverse individuals of the population. Our unbiased clustering analysis enabled us to quantify circuit stability when simultaneously perturbing multiple conductances as a nonlinear combination of single conductance perturbations. This revealed surprising conductance combinations that can predict the response to specific perturbations, even when the remaining intrinsic and synaptic conductances are unknown. Therefore, our approach can expose hidden variability in the balance of intrinsic and synaptic conductances of the same neurons across different versions of the same circuit solely from the circuit response to perturbations. Developed for a specific family of model circuits, our quantitative approach to characterizing high-dimensional degenerate systems provides a conceptual and analytic framework to guide future theoretical and experimental studies on degeneracy and robustness.

SIGNIFICANCE STATEMENT Neural circuits can generate nearly identical behavior despite neuronal and synaptic parameters varying several-fold between individual instantiations. Yet, when these parameters are perturbed through channel deletions and mutations or environmental disturbances, seemingly identical circuits can respond very differently. What distinguishes inconsequential perturbations that barely alter circuit behavior from disruptive perturbations that drastically disturb circuit output remains unclear. Focusing on a family of rhythmic circuits, we propose a computational approach to reveal hidden variability in the intrinsic and synaptic conductances in seemingly identical circuits based solely on circuit output to different perturbations. We uncover specific conductance combinations that work similarly to maintain stability and predict the effect of changing multiple conductances simultaneously, which often results from neuromodulation or injury.

Persistent alterations in neuronal activity elicit homeostatic plastic changes in synaptic transmission and/or intrinsic excitability. However, it is unknown whether these homeostatic processes operate in concert or at different temporal scales to maintain network activity around a set-point value. Here we show that chronic neuronal hyperactivity, induced by M-channel inhibition, triggered intrinsic and synaptic homeostatic plasticity at different timescales in cultured hippocampal pyramidal neurons from mice of either sex. Homeostatic changes of intrinsic excitability occurred at a fast timescale (1–4 h) and depended on ongoing spiking activity. This fast intrinsic adaptation included plastic changes in the threshold current and a distal relocation of FGF14, a protein physically bridging Na_v1.6 and K_v7.2 channels along the axon initial segment. In contrast, synaptic adaptations occurred at a slower timescale (~2 d) and involved decreases in miniature EPSC amplitude. To examine how these temporally distinct homeostatic responses influenced hippocampal network activity, we quantified the rate of spontaneous spiking measured by multielectrode arrays at extended timescales. M-Channel blockade triggered slow homeostatic renormalization of the mean firing rate (MFR), concomitantly accompanied by a slow synaptic adaptation. Thus, the fast intrinsic adaptation of excitatory neurons is not sufficient to account for the homeostatic normalization of the MFR. In striking contrast, homeostatic adaptations of intrinsic excitability and spontaneous MFR failed in hippocampal GABAergic inhibitory neurons, which remained hyperexcitable following chronic M-channel blockage. Our results indicate that a single perturbation such as M-channel inhibition triggers multiple homeostatic mechanisms that operate at different timescales to maintain network mean firing rate.

SIGNIFICANCE STATEMENT Persistent alterations in synaptic input elicit homeostatic plastic changes in neuronal activity. Here we show that chronic neuronal hyperexcitability, induced by M-type potassium channel inhibition, triggered intrinsic and synaptic homeostatic plasticity at different timescales in hippocampal excitatory neurons. The data indicate that the fast adaptation of intrinsic excitability depends on ongoing spiking activity but is not sufficient to provide homeostasis of the mean firing rate. Our results show that a single perturbation such as M-channel inhibition can trigger multiple homeostatic processes that operate at different timescales to maintain network mean firing rate.

A Brown Bear takes a quick dip while hunting for salmon at Anan Creek Bear Observatory in SE Alaska.

QPX7728 is an ultra-broad-spectrum boronic acid beta-lactamase inhibitor that demonstrates inhibition of key serine and metallo beta-lactamases at a nano molar range in biochemical assays with purified enzymes. The broad-spectrum inhibitory activity of QPX7728 observed in biochemical experiments translates into enhancement of the potency of many beta-lactams against strains of target pathogens producing beta-lactamases. The impact of bacterial efflux and permeability on inhibitory potency were determined using isogenic panels of KPC-3 producing isogenic strains of K. pneumoniae and P. aeruginosa and OXA-23-producing strains of A. baumannii with various combinations of efflux and porin mutations. QPX7728 was minimally affected by multi-drug resistance efflux pumps in either Enterobacteriaceae, or in non-fermenters such as P. aeruginosa or A. baumannii. In P. aeruginosa, the potency of QPX7728 was further enhanced when the outer membrane is permeabilized. The potency of QPX7728 in P. aeruginosa is not affected by inactivation of the carbapenem porin OprD. While changes in OmpK36 (but not OmpK35) reduced the potency of QPX7728 (8-16-fold), QPX7728 (4 μg/ml) nevertheless completely reversed KPC-mediated meropenem resistance in strains with porin mutations, consistent with a lesser effect of these mutations on the potency of QPX7728 compared to other agents. The ultra-broad-spectrum beta-lactamase inhibition profile combined with enhancement of the activity of multiple beta-lactam antibiotics with varying sensitivity to the intrinsic resistance mechanisms of efflux and permeability indicate QPX7728 is a useful inhibitor for use with multiple beta-lactam antibiotics.

ABSTRACT

Bacteria that encounter antibiotics can efficiently change their physiology to develop resistance. This intrinsic antibiotic resistance is mediated by multiple pathways, including a regulatory system(s) that activates specific genes. In some Streptomyces and Mycobacterium spp., the WblC/WhiB7 transcription factor is required for intrinsic resistance to translation-targeting antibiotics. Wide conservation of WblC/WhiB7 within Actinobacteria indicates a critical role of WblC/WhiB7 in developing resistance to such antibiotics. Here, we identified 312 WblC target genes in Streptomyces coelicolor, a model antibiotic-producing bacterium, using a combined analysis of RNA sequencing and chromatin immunoprecipitation sequencing. Interestingly, WblC controls many genes involved in translation, in addition to previously identified antibiotic resistance genes. Moreover, WblC promotes translation rate during antibiotic stress by altering the ribosome-associated protein composition. Our genome-wide analyses highlight a previously unappreciated antibiotic resistance mechanism that modifies ribosome composition and maintains the translation rate in the presence of sub-MIC levels of antibiotics.

IMPORTANCE The emergence of antibiotic-resistant bacteria is one of the top threats in human health. Therefore, we need to understand how bacteria acquire resistance to antibiotics and continue growth even in the presence of antibiotics. Streptomyces coelicolor, an antibiotic-producing soil bacterium, intrinsically develops resistance to translation-targeting antibiotics. Intrinsic resistance is controlled by the WblC/WhiB7 transcription factor that is highly conserved within Actinobacteria, including Mycobacterium tuberculosis. Here, identification of the WblC/WhiB7 regulon revealed that WblC/WhiB7 controls ribosome maintenance genes and promotes translation in the presence of antibiotics by altering the composition of ribosome-associated proteins. Also, the WblC-mediated ribosomal alteration is indeed required for resistance to translation-targeting antibiotics. This suggests that inactivation of the WblC/WhiB7 regulon could be a potential target to treat antibiotic-resistant mycobacteria.

Phagocytosis is the key mechanism for host control of Pseudomonas aeruginosa, a motile Gram-negative, opportunistic bacterial pathogen which frequently undergoes adaptation and selection for traits that are advantageous for survival. One such clinically relevant adaptation is the loss of bacterial motility, observed within chronic infections, that is associated with increased antibiotic tolerance and phagocytic resistance. Previous studies using phagocytes from a leukocyte adhesion deficiency type 1 (LAD-I) patient identified CD18 as a putative cell surface receptor for uptake of live P. aeruginosa. However, how bacterial motility alters direct engagement with CD18-containing integrins remains unknown. Here we demonstrate, with the use of motile and isogenic nonmotile deletion mutants of two independent strains of P. aeruginosa and with CRISPR-generated CD18-deficient cell lines in human monocytes and murine neutrophils, that CD18 expression facilitates the uptake of both motile and nonmotile P. aeruginosa. However, unexpectedly, mechanistic studies revealed that CD18 expression was dispensable for the initial attachment of the bacteria to the host cells, which was validated with ectopic expression of complement receptor 3 (CR3) by CHO cells. Our data support that surface N-linked glycan chains (N-glycans) likely facilitate the initial interaction of bacteria with monocytes and cooperate with CD18 integrins in trans to promote internalization of bacteria. Moreover, talin-1 and kindlin-3 proteins promote uptake, but not binding, of P. aeruginosa by murine neutrophils, which supports a role for CD18 integrin signaling in this process. These findings provide novel insights into the cellular determinants for phagocytic recognition and uptake of P. aeruginosa.

Rachel L. Sutcliffe, Shaorong Li, Matthew J. H. Gilbert, Patricia M. Schulte, Kristi M. Miller, and Anthony P. Farrell

We examined cardiac pacemaker rate resetting in rainbow trout following a reciprocal temperature transfer. In the original experiment, performed in winter, 4°C-acclimated fish transferred to 12°C reset intrinsic heart rate after just 1 h (from 56.8±1.2 to 50.8±1.5 bpm); 12°C-acclimated fish transferred to 4°C reset intrinsic heart rate after 8 h (from 33.4±0.7 to 37.7±1.2 bpm). However, in a replicate experiment, performed in the summer using a different brood year, intrinsic heart rate was not reset, even after 10 weeks at a new temperature. Using this serendipitous opportunity, we compared mRNA expression changes of a suite of proteins in sinoatrial node (SAN), atrial and ventricular tissues after both 1 h and longer than 3 weeks for both experimental acclimation groups to identify those changes only associated with pacemaker rate resetting. Of the changes in mRNA expression occurring after more than 3 weeks of warm acclimation and associated with pacemaker rate resetting, we observed downregulation of NKA α1c in the atrium and ventricle, and upregulation of HCN1 in the ventricle. However, in the SAN there were no mRNA expression changes unique to the fish with pacemaker rate resetting after either 1 h or 3 weeks of warm acclimation. Thus, despite identifying changes in mRNA expression of contractile cardiac tissues, there was absence of changes in mRNA expression directly involved with the initial, rapid pacemaker rate resetting with warm acclimation. Importantly, pacemaker rate resetting with thermal acclimation does not always occur in rainbow trout.

Much of our current knowledge of biological chemistry is founded in the structure-function relationship, whereby sequence determines structure that determines function. Thus, the discovery that a large fraction of the proteome is intrinsically disordered, while being functional, has revolutionized our understanding of proteins and raised new and interesting questions. Many intrinsically disordered proteins (IDPs) have been determined to undergo a disorder-to-order transition when recognizing their physiological partners, suggesting that their mechanisms of folding are intrinsically different from those observed in globular proteins. However, IDPs also follow some of the classic paradigms established for globular proteins, pointing to important similarities in their behavior. In this review, we compare and contrast the folding mechanisms of globular proteins with the emerging features of binding-induced folding of intrinsically disordered proteins. Specifically, whereas disorder-to-order transitions of intrinsically disordered proteins appear to follow rules of globular protein folding, such as the cooperative nature of the reaction, their folding pathways are remarkably more malleable, due to the heterogeneous nature of their folding nuclei, as probed by analysis of linear free-energy relationship plots. These insights have led to a new model for the disorder-to-order transition in IDPs termed “templated folding,” whereby the binding partner dictates distinct structural transitions en route to product, while ensuring a cooperative folding.

Yu Liu, Shuhua Qi, Fridtjof Thomas, Brittany L. Correia, Angela P. Taylor, Roy V. Sillitoe, and Detlef H. Heck

Respiration is controlled by central pattern generating circuits in the brain stem, whose activity can be modulated by inputs from other brain areas to adapt respiration to autonomic and behavioral demands. The cerebellum is known to be part of the neuronal circuitry activated during respiratory challenges, such as hunger for air, but has not been found to be involved in the control of spontaneous, unobstructed breathing (eupnea). Here we applied a measure of intrinsic rhythmicity, the CV2, which evaluates the similarity of subsequent intervals and is thus sensitive to changes in rhythmicity at the temporal resolution of individual respiratory intervals. The variability of intrinsic respiratory rhythmicity was reduced in a mouse model of cerebellar ataxia compared to their healthy littermates. Irrespective of that difference, the average respiratory rate and the average coefficient of variation (CV) were comparable between healthy and ataxic mice. We argue that these findings are consistent with a proposed role of the cerebellum in modulating the duration of individual respiratory intervals, which could serve the purpose of coordinating respiration with other rhythmic orofacial movements, such as fluid licking and swallowing.

BACKGROUND AND PURPOSE:

Diffuse intrinsic pontine glioma is a lethal childhood brain cancer with dismal prognosis and MR imaging is the primary methodology used for diagnosis and monitoring. Our aim was to determine whether advanced diffusion, perfusion, and permeability MR imaging metrics predict survival and pseudoprogression in children with newly diagnosed diffuse intrinsic pontine glioma.

For many

I tasked myself with buying no plastic bottles for the year; here's how it's going so far.

Things of Intrinsic Worth is a feature-length documentary which focuses on the ways coal mining is harming the livelihoods of Montana ranchers.

A lot of men don't pay attention to their skin and let it suffer. Just take out a few minutes from your busy schedule and rinse, tone, exfoliate, moisturise daily without fail for a lasting youthful skin, suggest experts. Shubhika Jain, Founder of RAS Luxury Oils, and Megha Asher, Founder of Juicy Chemistry have listed a regime important for men:

1. Use natural homemade scrub: If you use soap to clean your skin, it is one of the biggest mistakes. Soap strips your skin off of nutrients that are necessary. Men need skin exfoliation to remove the dead skin. Using a natural, herbal/home-made scrub can help you remove impurities and other debris that are clogged in the pores along with keeping the skin healthy. Men who shave will find that their cleanser helps ensure the razor has a clean shaving surface to avoid ingrown hairs and razor burn.

2. Always moisturise: Since your skin is tougher and is thicker, it tends to get rough very easily. Hence, it needs its moisture. In addition to that, not all moisturisers are the same. One of the best ways to ensure proper hydration is to use a face oil or a face serum. It is a myth that using oil on an oily face makes it oilier. Actually it is the reverse of that. Super absorbent face oils are like elixirs and help in balancing the sebum production and controlling oil production.

You can also try active plant ingredients like a light aloe vera gel based moisturiser, that works best naturally by hydrating skin and protecting against the damaging, age-accelerating effects of UVA and UVB rays and seal moisture into the skin.

3. Use toner before and after cleansing: Toners keep you refreshed on the go while making your skin look dewy and naturally glowy. They also balance the oil levels in the skin. The toner can be used before and after cleansing the face.

4. Keep a facial scrub handy: Face scrubs help in exfoliating and removing dead skin cells that makes the skin look dull. It helps to prepare the skin for shaving. Scrub 1-3 times a week depending on the skin type for a better looking skin.

5. Applying sunscreen: Men are not as conscious about their sunscreen use as women, but they should be. UV rays lead to accelerated skin aging and can cause skin cancer. It is important to wear a sunscreen if you are going to be outdoors for more than 30 minutes.

One of the most common causes of wrinkles and premature ageing is sun exposure and damage. Using a daily SPF cream will significantly help your skin in the fight against ageing and also decrease the risk of UV-induced skin damage.

6. Use mild and soothing shaving products: Many men shave either daily or every few days. Shaving products should protect and moisturise the skin. They should also be mild and soothing; harsh products can remove the skin's natural lipids which are already under pressure from shaving.

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