Growth rings in tropical trees : role of functional traits, environment, and phylogeny

Acknowledgments Financial support of the Centre National de la Recherche Scientifique (USR 3330), France, and from the Rufford Small Grants Foundation (UK) is acknowledged. We thank the private farmers and coffee plantation companies of Kodagu for providing permissions and logistical support for this project. We are grateful to N. Barathan for assistance with slide preparation and data entry, S. Aravajy for botanical assistance, S. Prasad and G. Orukaimoni for technical inputs, and A. Prathap, S. Shiva, B. Saravana, and P. Shiva for field assistance. The corresponding editor and three anonymous reviewers provided insightful comments that improved the manuscript.Peer reviewedPostprin

Effectiveness of Mechanical Horse-Riding Simulators on Postural Balance in Neurological Rehabilitation: Systematic Review and Meta-Analysis

Mechanical horse-riding simulators consist of a device that mimics the movement of a real horse, generating between 50 and 100 three-dimensional physical movements (forward and back, left and right, up and down). The main objective of this study is to analyze the effectiveness of mechanical horse-riding simulators to improve postural balance in subjects with neurological disorders. The search was conducted during January-March 2019 in PubMed, Physiotherapy Evidence Database (PEDro), Cochrane, Web of Science, CINAHL, and Scopus. The methodological quality of the studies was evaluated through the PEDro scale. A total of seven articles were included in this systematic review, of which four contributed information to the meta-analysis. Statistical analysis showed favorable results for balance in stroke patients, measured by the Berg Balance Scale (standardized mean difference (SMD) = 3.24; 95%; confidence interval (CI): 1.66-4.83). Not conclusive results were found in sitting postural balance, measured using the Gross Motor Function Measure-66 (GMFM-66) Sitting Dimension, in patients with cerebral palsy. Most studies have shown beneficial effects on postural balance compared with conventional physical therapy. However, due to the limited number of articles and their low methodological quality, no solid conclusions can be drawn about the effectiveness of this therapy

Massive Clumps in the NGC 6334 Star Forming Region

We report observations of dust continuum emission at 1.2 mm toward the star forming region NGC 6334 made with the SEST SIMBA bolometer array. The observations cover an area of $\sim 2$ square degrees with approximately uniform noise. We detected 181 clumps spanning almost three orders of magnitude in mass (3\Msun$-6\times10^3$ \Msun) and with sizes in the range 0.1--1.0 pc. We find that the clump mass function $dN/d\log M$ is well fit with a power law of the mass with exponent -0.6 (or equivalently $dN/dM \propto M^{-1.6}$). The derived exponent is similar to those obtained from molecular line emission surveys and is significantly different from that of the stellar initial mass function. We investigated changes in the mass spectrum by changing the assumptions on the temperature distribution of the clumps and on the contribution of free-free emission to the 1.2 mm emission, and found little changes on the exponent. The Cumulative Mass Distribution Function is also analyzed giving consistent results in a mass range excluding the high-mass end where a power-law fit is no longer valid. The masses and sizes of the clumps observed in NGC 6334 indicate that they are not direct progenitors of stars and that the process of fragmentation determines the distribution of masses later on or occurs at smaller spatial scales. The spatial distribution of the clumps in NGC 6334 reveals clustering which is strikingly similar to that exhibited by young stars in other star forming regions. A power law fit to the surface density of companions gives $\Sigma\propto \theta^{-0.62}$.Comment: 16 pages, 11 figures, 4 tables. To appear in the Astrophysical Journa

Music Intervention Approaches for Alzheimer’s Disease: A Review of the Literature

Music interventions have been widely adopted as a potential non-pharmacological therapy for patients with Alzheimer’s disease (AD) to treat cognitive and/or behavioral symptoms of the disease. In spite of the prevalence of such therapies, evidence for their effectiveness report mixed results in the literature. The purpose of this narrative review is to investigate the effectiveness of various intervention strategies (music therapy vs. music listening techniques) and music type used in the intervention (individualized vs. non-individualized music) on cognitive and behavioral outcomes for persons with AD. Databases were searched for studies using either active music therapy or music listening techniques over the last 10 years. These studies were in English, included persons with AD dementia, and whose protocol gathered pre- and post-intervention outcome measures. We initially identified 206 papers which were then reduced to 167 after removing duplicates. Further review yielded 13 papers which were extensively reviewed, resulting in a final sample of six papers. Our analysis of these papers suggested that, regardless of the music intervention approach, individualized music regimens provided the best outcomes for the patient. Furthermore, music listening may act as a relaxation technique and therefore provide a long-term impact for the patient, while active music therapy may acts to engage participants through social interaction and provide acute benefits. Our findings suggest that music techniques can be utilized in various ways to improve behavior and cognition

Suv4-20h Histone Methyltransferases Promote Neuroectodermal Differentiation by Silencing the Pluripotency-Associated Oct-25 Gene

Post-translational modifications (PTMs) of histones exert fundamental roles in regulating gene expression. During development, groups of PTMs are constrained by unknown mechanisms into combinatorial patterns, which facilitate transitions from uncommitted embryonic cells into differentiated somatic cell lineages. Repressive histone modifications such as H3K9me3 or H3K27me3 have been investigated in detail, but the role of H4K20me3 in development is currently unknown. Here we show that Xenopus laevis Suv4-20h1 and h2 histone methyltransferases (HMTases) are essential for induction and differentiation of the neuroectoderm. Morpholino-mediated knockdown of the two HMTases leads to a selective and specific downregulation of genes controlling neural induction, thereby effectively blocking differentiation of the neuroectoderm. Global transcriptome analysis supports the notion that these effects arise from the transcriptional deregulation of specific genes rather than widespread, pleiotropic effects. Interestingly, morphant embryos fail to repress the Oct4-related Xenopus gene Oct-25. We validate Oct-25 as a direct target of xSu4-20h enzyme mediated gene repression, showing by chromatin immunoprecipitaton that it is decorated with the H4K20me3 mark downstream of the promoter in normal, but not in double-morphant, embryos. Since knockdown of Oct-25 protein significantly rescues the neural differentiation defect in xSuv4-20h double-morphant embryos, we conclude that the epistatic relationship between Suv4-20h enzymes and Oct-25 controls the transit from pluripotent to differentiation-competent neural cells. Consistent with these results in Xenopus, murine Suv4-20h1/h2 double-knockout embryonic stem (DKO ES) cells exhibit increased Oct4 protein levels before and during EB formation, and reveal a compromised and biased capacity for in vitro differentiation, when compared to normal ES cells. Together, these results suggest a regulatory mechanism, conserved between amphibians and mammals, in which H4K20me3-dependent restriction of specific POU-V genes directs cell fate decisions, when embryonic cells exit the pluripotent state

FET proteins TAF15 and EWS are selective markers that distinguish FTLD with FUS pathology from amyotrophic lateral sclerosis with FUS mutations

Accumulation of the DNA/RNA binding protein fused in sarcoma as cytoplasmic inclusions in neurons and glial cells is the pathological hallmark of all patients with amyotrophic lateral sclerosis with mutations in FUS as well as in several subtypes of frontotemporal lobar degeneration, which are not associated with FUS mutations. The mechanisms leading to inclusion formation and fused in sarcoma-associated neurodegeneration are only poorly understood. Because fused in sarcoma belongs to a family of proteins known as FET, which also includes Ewing's sarcoma and TATA-binding protein-associated factor 15, we investigated the potential involvement of these other FET protein family members in the pathogenesis of fused in sarcoma proteinopathies. Immunohistochemical analysis of FET proteins revealed a striking difference among the various conditions, with pathology in amyotrophic lateral sclerosis with FUS mutations being labelled exclusively for fused in sarcoma, whereas fused in sarcoma-positive inclusions in subtypes of frontotemporal lobar degeneration also consistently immunostained for TATA-binding protein-associated factor 15 and variably for Ewing's sarcoma. Immunoblot analysis of proteins extracted from post-mortem tissue of frontotemporal lobar degeneration with fused in sarcoma pathology demonstrated a relative shift of all FET proteins towards insoluble protein fractions, while genetic analysis of the TATA-binding protein-associated factor 15 and Ewing's sarcoma gene did not identify any pathogenic variants. Cell culture experiments replicated the findings of amyotrophic lateral sclerosis with FUS mutations by confirming the absence of TATA-binding protein-associated factor 15 and Ewing's sarcoma alterations upon expression of mutant fused in sarcoma. In contrast, all endogenous FET proteins were recruited into cytoplasmic stress granules upon general inhibition of Transportin-mediated nuclear import, mimicking the findings in frontotemporal lobar degeneration with fused in sarcoma pathology. These results allow a separation of fused in sarcoma proteinopathies caused by FUS mutations from those without a known genetic cause based on neuropathological features. More importantly, our data imply different pathological processes underlying inclusion formation and cell death between both conditions; the pathogenesis in amyotrophic lateral sclerosis with FUS mutations appears to be more restricted to dysfunction of fused in sarcoma, while a more global and complex dysregulation of all FET proteins is involved in the subtypes of frontotemporal lobar degeneration with fused in sarcoma patholog