Increased shear in the North Atlantic upper-level jet stream over the past four decades

Earth’s equator-to-pole temperature gradient drives westerly mid-latitude jet streams through thermal wind balance. In the upper atmosphere, anthropogenic climate change is strengthening this meridional temperature gradient by cooling the polar lower stratosphere and warming the tropical upper troposphere acting to strengthen the upper-level jet stream. In contrast, in the lower atmosphere, Arctic amplification of global warming is weakening the meridional temperature gradient acting to weaken the upper-level jet stream. Therefore, trends in the speed of the upper-level jet stream represent a closely balanced tug-of-war between two competing effects at different altitudes. It is possible to isolate one of the competing effects by analysing the vertical shear—the change in wind speed with height—instead of the wind speed, but this approach has not previously been taken. Here we show that, although the zonal wind speed in the North Atlantic polar jet stream at 250 hectopascals has not changed since the start of the observational satellite era in 1979, the vertical shear has increased by 15 per cent (with a range of 11–17 per cent) according to three different reanalysis datasets. We further show that this trend is attributable to the thermal wind response to the enhanced upper-level meridional temperature gradient. Our results indicate that climate change may be having a larger impact on the North Atlantic jet stream than previously thought. The increased vertical shear is consistent with the intensification of shear-driven clear-air turbulence expected from climate change which will affect aviation in the busy transatlantic flight corridor by creating a more turbulent flying environment for aircraft. We conclude that the effects of climate change and variability on the upper-level jet stream are being partly obscured by the traditional focus on wind speed rather than wind shear

Age-Related Changes of Myelin Basic Protein in Mouse and Human Auditory Nerve

Age-related hearing loss (presbyacusis) is the most common type of hearing impairment. One of the most consistent pathological changes seen in presbyacusis is the loss of spiral ganglion neurons (SGNs). Defining the cellular and molecular basis of SGN degeneration in the human inner ear is critical to gaining a better understanding of the pathophysiology of presbyacusis. However, information on age-related cellular and molecular alterations in the human spiral ganglion remains scant, owing to the very limited availably of human specimens suitable for high resolution morphological and molecular analysis. This study aimed at defining age-related alterations in the auditory nerve in human temporal bones and determining if immunostaining for myelin basic protein (MBP) can be used as an alternative approach to electron microscopy for evaluating myelin degeneration. For comparative purposes, we evaluated ultrastructural alternations and changes in MBP immunostaining in aging CBA/CaJ mice. We then examined 13 temporal bones from 10 human donors, including 4 adults aged 38–46 years (middle-aged group) and 6 adults aged 63–91 years (older group). Similar to the mouse, intense immunostaining of MBP was present throughout the auditory nerve of the middle-aged human donors. Significant declines in MBP immunoreactivity and losses of MBP+ auditory nerve fibers were observed in the spiral ganglia of both the older human and aged mouse ears. This study demonstrates that immunostaining for MBP in combination with confocal microscopy provides a sensitive, reliable, and efficient method for assessing alterations of myelin sheaths in the auditory nerve. The results also suggest that myelin degeneration may play a critical role in the SGN loss and the subsequent decline of the auditory nerve function in presbyacusis

Broad-spectrum resistance to Bacillus thuringiensis toxins by western corn rootworm (Diabrotica virgifera virgifera)

The evolution of resistance and cross-resistance threaten the sustainability of genetically engineered crops that produce insecticidal toxins derived from the bacterium Bacillus thuringiensis (Bt). Western corn rootworm, Diabrotica virgifera virgifera LeConte, is a serious pest of maize and has been managed with Bt maize since 2003. We conducted laboratory bioassays with maize hybrids producing Bt toxins Cry3Bb1, mCry3A, eCry3.1Ab, and Cry34/35Ab1, which represent all commercialized Bt toxins for management of western corn rootworm. We tested populations from fields where severe injury to Cry3Bb1 maize was observed, and populations that had never been exposed to Bt maize. Consistent with past studies, bioassays indicated that field populations were resistant to Cry3Bb1 maize and mCry3A maize, and that cross-resistance was present between these two types of Bt maize. Additionally, bioassays revealed resistance to eCry3.1Ab maize and cross-resistance among Cry3Bb1, mCry3A and eCry3.1Ab. However, no resistance or cross-resistance was detected for Cry34/35Ab1 maize. This broad-spectrum resistance illustrates the potential for insect pests to develop resistance rapidly to multiple Bt toxins when structural similarities are present among toxins, and raises concerns about the long-term durability of Bt crops for management of some insect pests

The FKBP52 Cochaperone Acts in Synergy with β-Catenin to Potentiate Androgen Receptor Signaling

FKBP52 and β-catenin have emerged in recent years as attractive targets for prostate cancer treatment. β-catenin interacts directly with the androgen receptor (AR) and has been characterized as a co-activator of AR-mediated transcription. FKBP52 is a positive regulator of AR in cellular and whole animal models and is required for the development of androgen-dependent tissues. We previously characterized an AR inhibitor termed MJC13 that putatively targets the AR BF3 surface to specifically inhibit FKBP52-regulated AR signaling. Predictive modeling suggests that β-catenin interacts with the AR hormone binding domain on a surface that overlaps with BF3. Here we demonstrate that FKBP52 and β-catenin interact directly in vitro and act in concert to promote a synergistic up-regulation of both hormone-independent and -dependent AR signaling. Our data demonstrate that FKBP52 promotes β-catenin interaction with AR and is required for β-catenin co-activation of AR activity in prostate cancer cells. MJC13 effectively blocks β-catenin interaction with the AR LBD and the synergistic up-regulation of AR by FKBP52 and β-catenin. Our data suggest that co-regulation of AR by FKBP52 and β-catenin does not require FKBP52 PPIase catalytic activity, nor FKBP52 binding to Hsp90. However, the FKBP52 proline-rich loop that overhangs the PPIase pocket is critical for synergy

Influência do treinamento da musculatura respiratória e de membros inferiores no desempenho funcional de indivíduos com DPOC

A doença pulmonar obstrutiva crônica (DPOC) caracteriza-se pela obstrução ou limitação crônica do fluxo aéreo, gerando uma desvantagem mecânica, causando fraqueza muscular e recrutamento da musculatura inspiratória acessória. A disfunção muscular esquelética é uma importante manifestação extrapulmonar, que leva à diminuição da capacidade funcional. O objetivo do estudo foi verificar a eficácia de um treinamento da musculatura respiratória e de quadríceps no desempenho funcional de indivíduos com DPOC. De nove indivíduos com idades entre 49 e 76 anos foram avaliadas as pressões respiratórias máximas (por manovacuometria), força muscular de membros inferiores (por repetição máxima), capacidade funcional (pelo teste de caminhada com carga progressiva, shuttle test) e qualidade de vida (pelo questionário de qualidade de vida SF-36), antes e depois da aplicação de protocolo de fortalecimento da musculatura inspiratória, dos músculos quadríceps e abdominais. As sessões de exercícios foram realizadas duas vezes por semana durante dois meses. Foi verificada melhora em todas as vari��veis avaliadas, com diferença significativa na pressão inspiratória máxima (pChronic obstructive pulmonary disease (COPD) is a clinical condition characterized by chronic airflow obstruction or limitation, which generates mechanical disadvantage, causing muscle weakness and recruitment of accessory inspiratory muscles. Skeletal muscle dysfunction is one of the most important extrapulmonary manifestations, leading to decrease in functional capacity. The aim of this study was to verify the effectiveness of respiratory and quadriceps femoris muscle training on functional performance of patients with COPD. Nine subjects aged between 49 and 76 years old were assessed as to maximal respiratory pressures (by spirometry), lower limb muscle strength (by maximal repetition test), functional capacity (by the shuttle walk test) and quality of life (by the SF-36 questionnaire), before and after the protocol of muscle strengthening for inspiratory muscles, quadriceps femoris and abdominal muscles. Exercise program sessions took place twice a week for two months. Results showed improvement in all assessed variables, with significant difference (p<0.05) in maximal inspiratory pressure values. The proposed respiratory and quadriceps muscle training has thus proved beneficial for the functional performance of patients with COPD, suggesting the use of respiratory and peripheral muscle strengthening as co-adjuvant resource in the treatment of these individuals