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PurposeThe aim of this systematic review is to assess the effect of different types of exercise on breast cancer-related lymphedema (BCRL) in order to elucidate the role of exercise in this patient group.MethodsA systematic data search was performed using PubMed (December 2016). The review is focused on the rehabilitative aspect of BCRL and undertaken according to the PRISMA statement with Levels of Evidence (LoE) assessed.Results11 randomized controlled trials (9 with LoE 1a and 2 with LoE 1b) that included 458 women with breast cancer in aftercare were included. The different types of exercise consisted of aqua lymph training, swimming, resistance exercise, yoga, aerobic, and gravity-resistive exercise. Four of the studies measured a significant reduction in BCRL status based on arm volume and seven studies reported significant subjective improvements. No study showed adverse effects of exercise on BCRL.ConclusionThe evidence indicates that exercise can improve subjective and objective parameters in BCRL patients, with dynamic, moderate, and high-frequency exercise appearing to provide the most positive effects.

Autism spectrum disorder (ASD) is a highly heterogeneous disorder, yet transcriptomic profiling of bulk brain tissue has identified substantial convergence among dysregulated genes and pathways in ASD. However, this approach lacks cell-specific resolution. We performed comprehensive transcriptomic analyses on bulk tissue and laser-capture microdissected (LCM) neurons from 59 postmortem human brains (27 ASD and 32 controls) in the superior temporal gyrus (STG) of individuals ranging from 2 to 73 years of age. In bulk tissue, synaptic signaling, heat shock protein-related pathways, and RNA splicing were significantly altered in ASD. There was age-dependent dysregulation of genes involved in gamma aminobutyric acid (GABA) (GAD1 and GAD2) and glutamate (SLC38A1) signaling pathways. In LCM neurons, AP-1-mediated neuroinflammation and insulin/IGF-1 signaling pathways were upregulated in ASD, while mitochondrial function, ribosome, and spliceosome components were downregulated. GABA synthesizing enzymes GAD1 and GAD2 were both downregulated in ASD neurons. Mechanistic modeling suggested a direct link between inflammation and ASD in neurons, and prioritized inflammation-associated genes for future study. Alterations in small nucleolar RNAs (snoRNAs) associated with splicing events suggested interplay between snoRNA dysregulation and splicing disruption in neurons of individuals with ASD. Our findings supported the fundamental hypothesis of altered neuronal communication in ASD, demonstrated that inflammation was elevated at least in part in ASD neurons, and may reveal windows of opportunity for biotherapeutics to target the trajectory of gene expression and clinical manifestation of ASD throughout the human lifespan.

Introduction High-intensity interval training (HIIT) is an appropriate training modality to improve endurance and therefore contributes to physical performance. This review investigates the effect of HIIT on functional performance in cancer patients. We reviewed the relative peak oxygen uptake (relV̇O 2PEAK ) and meta-analytical compared HIIT with moderate intensity continuous training (MICT). Furthermore, we took various training parameters under consideration. Methods A systematic literature search was conducted in Scopus, PubMed, and Cochrane Library databases. For the review, we included randomized controlled trials containing HIIT with cancer patients. From this, we filtered interventions with additional MICT for the meta-analysis. Outcomes of interest were various functional performance assessments and V̇O 2MAX . Results The research yielded 584 records which fit the inclusion criteria, of which 31 studies with n =1555 patients (57.4±8.6 years) could be included in the overall review and 8 studies in the meta-analysis ( n =268, 59.11±5.11 years) regarding relV̇O 2PEAK . Different functional outcomes were found, of which walking distance (+8.63±6.91% meters in 6-min walk test) and mobility (+2.7cm in sit and reach test) improved significantly due to HIIT. In terms of relV̇O 2PEAK , the performance of cancer patients was improved by HIIT (10.68±6.48%) and MICT (7.4±4.29%). HIIT can be favored to increase relV̇O 2PEAK (SMD 0.37; 95% CI 0.09–0.65; I 2 =0%; p =0.009). Effect sizes for relV̇O 2PEAK improvements correlate moderately with total training volume (Spearman’s ρ=0.49; p =0.03), whereas percentage increases do not (Spearman’s ρ=0.24; p =0.14). Conclusion Functional and physical outcomes were positively altered by different HIIT protocols and forms of implementation, whereas a tendency toward more effectiveness of HIIT vs. MICT was found for relV̇O 2PEAK . Future studies should include functional parameters more often, to finally allow a comparison between both training protocols in this regard.

The CAST-CAPP axion haloscope, operating at CERN inside the CAST dipole magnet, has searched for axions in the 19.74  μ eV to 22.47  μ eV mass range. The detection concept follows the Sikivie haloscope principle, where Dark Matter axions convert into photons within a resonator immersed in a magnetic field. The CAST-CAPP resonator is an array of four individual rectangular cavities inserted in a strong dipole magnet, phase-matched to maximize the detection sensitivity. Here we report on the data acquired for 4124 h from 2019 to 2021. Each cavity is equipped with a fast frequency tuning mechanism of 10 MHz/ min between 4.774 GHz and 5.434 GHz. In the present work, we exclude axion-photon couplings for virialized galactic axions down to g a γ γ  = 8 × 10 −14 GeV −1 at the 90% confidence level. The here implemented phase-matching technique also allows for future large-scale upgrades. Haloscopes aim at detecting axions by converting them into photons using high-quality resonant cavities, where the cavity resonance should be tuned with the unknown axion mass. Here, the authors improve exclusion limits using four phase-matched resonant cavities and a fast frequency scanning technique.

The amygdala undergoes aberrant development in autism spectrum disorder (ASD). We previously found that there are reduced neuron numbers in the adult postmortem amygdala from individuals with ASD compared to typically developing controls. The current study is a comprehensive stereological examination of four non-neuronal cell populations: microglia, oligodendrocytes, astrocytes, and endothelial cells, in the same brains studied previously. We provide a detailed neuroanatomical protocol for defining each cell type that may be applied to other studies of the amygdala in neurodevelopmental and psychiatric disorders. We then assess whether cell numbers and average volumes differ between ASD and typically developing brains. We hypothesized that a reduction in neuron numbers in ASD might relate to altered immune function and/or aberrant microglial activation, as indicated by increased microglial number and cell body volume. Overall, average non-neuronal cell numbers and volumes did not differ between ASD and typically developing brains. However, there was evident heterogeneity within the ASD cohort. Two of the eight ASD brains displayed strong microglial activation. Contrary to our original hypothesis, there was a trend toward a positive correlation between neuronal and microglial numbers in both ASD and control cases. There were fewer oligodendrocytes in the amygdala of adult individuals with ASD ages 20 and older compared to typically developing controls. This finding may provide a possible sign of altered connectivity or impaired neuronal communication that may change across the lifespan in ASD.

Aquatic environments serve as a sink for anthropogenic discharges. A significant part of the discharge is tire wear, which is increasingly being released into the environment, causing environmental disasters due to their longevity and the large number of pollutants they contain. Main components of tires are plastic and zinc, which therefore can be used as substitutes for tire abrasion to study the effect on microbial life. We investigate environmentally realistic concentrations of plastic and zinc on a freshwater microeukaryotic community using high-throughput sequencing of the 18S V9 region over a 14-day exposure period. Apart from a generally unchanged diversity upon exposure to zinc and nanoplastics, a change in community structure due to zinc is evident, but not due to nanoplastics. Evidently, nanoplastic particles hardly affect the community, but zinc exposure results in drastic functional abundance shifts concerning the trophic mode. Phototrophic microorganisms were almost completely diminished initially, but photosynthesis recovered. However, the dominant taxa performing photosynthesis changed from bacillariophytes to chlorophytes. While phototrophic organisms are decreasing in the presence of zinc, the mixotrophic fraction initially benefitted and the heterotrophic fraction were benefitting throughout the exposure period. In contrast to lasting changes in taxon composition, the functional community composition is initially strongly imbalanced after application of zinc but returns to the original state.

A bstract We present results of the Relic Axion Dark-Matter Exploratory Setup (RADES), a detector which is part of the CERN Axion Solar Telescope (CAST), searching for axion dark matter in the 34.67 μ eV mass range. A radio frequency cavity consisting of 5 sub-cavities coupled by inductive irises took physics data inside the CAST dipole magnet for the first time using this filter-like haloscope geometry. An exclusion limit with a 95% credibility level on the axion-photon coupling constant of g aγ ≳ 4 × 10 − 13 GeV − 1 over a mass range of 34 . 6738 μ eV < m a < 34 . 6771 μ eV is set. This constitutes a significant improvement over the current strongest limit set by CAST at this mass and is at the same time one of the most sensitive direct searches for an axion dark matter candidate above the mass of 25 μ eV. The results also demonstrate the feasibility of exploring a wider mass range around the value probed by CAST-RADES in this work using similar coherent resonant cavities.

A decrease in the number of functional insulin-producing β-cells contributes to the pathophysiology of type 2 diabetes. Opinions diverge regarding the relative contribution of a decrease in β-cell mass versus an intrinsic defect in the secretory machinery. Here we review the evidence that glucose, dyslipidemia, cytokines, leptin, autoimmunity, and some sulfonylureas may contribute to the maladaptation of β-cells. With respect to these causal factors, we focus on Fas, the ATP-sensitive K+ channel, insulin receptor substrate 2, oxidative stress, nuclear factor-κB, endoplasmic reticulum stress, and mitochondrial dysfunction as their respective mechanisms of action. Interestingly, most of these factors are involved in inflammatory processes in addition to playing a role in both the regulation of β-cell secretory function and cell turnover. Thus, the mechanisms regulating β-cell proliferation, apoptosis, and function are inseparable processes.

Despite substantial progress in reducing the global impact of many non-communicable diseases, including heart disease and cancer, morbidity and mortality due to chronic respiratory disease continues to increase. Many factors have contributed to what must now be considered a public health emergency: failure to limit the sale and consumption of tobacco products, unchecked exposure to environmental pollutants across the life course, and the ageing of the global population (partly as a result of improved outcomes for other conditions). In particular, we advocate for: broader understanding of risk factors (including the devastating effects of global poverty) and the preventive measures necessary to avoid future cases of COPD, disruptive approaches to diagnosis that are not solely based on spirometric airflow limitation but also involve identification of early pathological changes that are more amenable to reversal, classification of the disease into types that share pathophysiological similarities and could lead to novel preventive and therapeutic approaches, and a new approach to the diagnosis and assessment of exacerbations of COPD that focuses on disease mechanisms. An acute worsening of COPD is termed an exacerbation, and such episodes account for a substantial proportion of the attributable cost of the disease and are associated with accelerated lung function loss, prolonged impairments in quality of life, and similar prognosis to many stage III or IV solid organ malignancies.

Epidemiological evidence implicates severe maternal infections as risk factors for neurodevelopmental disorders, such as ASD and schizophrenia. Accordingly, animal models mimicking infection during pregnancy, including the maternal immune activation (MIA) model, result in offspring with neurobiological, behavioral, and metabolic phenotypes relevant to human neurodevelopmental disorders. Most of these studies have been performed in rodents. We sought to better understand the molecular signatures characterizing the MIA model in an organism more closely related to humans, rhesus monkeys (Macaca mulatta), by evaluating changes in global metabolic profiles in MIA-exposed offspring. Herein, we present the global metabolome in six peripheral tissues (plasma, cerebrospinal fluid, three regions of intestinal mucosa scrapings, and feces) from 13 MIA and 10 control offspring that were confirmed to display atypical neurodevelopment, elevated immune profiles, and neuropathology. Differences in lipid, amino acid, and nucleotide metabolism discriminated these MIA and control samples, with correlations of specific metabolites to behavior scores as well as to cytokine levels in plasma, intestinal, and brain tissues. We also observed modest changes in fecal and intestinal microbial profiles, and identify differential metabolomic profiles within males and females. These findings support a connection between maternal immune activation and the metabolism, microbiota, and behavioral traits of offspring, and may further the translational applications of the MIA model and the advancement of biomarkers for neurodevelopmental disorders such as ASD or schizophrenia.