Intramuscular Tenosynovial Massive Mobile Cancer Holding a Novel CSF1CD96 Fusion Transcript

Using a synaptosomal preparation of rat prefrontal cortex devoid of postsynaptic elements, we found that CRF2α and D1R colocalize in synaptic terminals of the rat medial prefrontal cortex and that the simultaneous activation of both receptors also occluded phosphorylation of ERK. These results strengthen the idea that the heteromer CRF2a-D1R is an entity functionally different from each receptor that composes it and suggests that its formation is enhanced by CRF and dopamine co-transmission, as occurs in stress and addiction. This article is protected by copyright. All rights reserved.Litter decomposition plays a key role in nutrient cycling across ecosystems, yet to date, we lack a comprehensive understanding of the non-additive decomposition effects in leaf litter mixing experiments. In order to fill that gap, we compiled 69 individual studies for the purpose of performing two meta-analyses on non-additive effects. We show that a significant synergistic effect (faster decomposition in mixtures than expected) occurs at a global scale, with an average increase of 3-5% in litter mixtures. In particular, low-quality litter in mixtures shows a significant synergistic effect, while additive effects are observed for high-quality species. Additionally, synergistic effects turn into antagonistic effects when soil fauna are absent or litter is in very late stages of decomposition (near-humus). In contrast to temperate and tropical areas, studies in boreal regions show significant antagonistic effects. Our two meta-analyses provide a systematic evaluation of non-additive effects in mixed litter decomposition studies and show that litter quality alters the effects of litter mixing. Our results indicate that nutrient transfer, soil fauna, and inhibitory secondary compounds can influence mixing effects. We also highlight that synergistic and antagonistic effects happen concurrently, and the final litter mixing effect results from the interplay between them. © 2020 The Authors New Phytologist © 2020 New Phytologist Trust.Whether thyroid dysfunction plays a causal role in the development of cancer remains inconclusive. We conducted a two-sample Mendelian randomization study to investigate the associations between genetic predisposition to thyroid dysfunction and 22 site-specific cancers. Single-nucleotide polymorphisms associated with four traits of thyroid function were selected from a genome-wide association meta-analysis with up to 72,167 European-descent individuals. Summary-level data for breast cancer and 21 other cancers were extracted from the Breast Cancer Association Consortium (122,977 breast cancer cases and 105,974 controls) and UK Biobank (367,643 individuals). For breast cancer, a meta-analysis was performed using data from both sources. Genetically predicted thyroid dysfunction was associated with breast cancer, with similar patterns of associations in the Breast Cancer Association Consortium and UK Biobank. The combined odds ratios of breast cancer were 0.94 (0.91-0.98; p = 0.007) per genetically predicted one standard deviation increase in TSH levels, 0.96 (0.91-1.00; p = 0.053) for genetic predisposition to hypothyroidism, 1.04 (1.01-1.07; p = 0.005) for genetic predisposition to hyperthyroidism and 1.07 (1.02-1.12; p = 0.003) per genetically predicted one standard deviation increase in free thyroxine levels. Genetically predicted TSH levels and hypothyroidism were inversely with thyroid cancer; the odds ratios were 0.47 (0.30-0.73; p = 0.001) and 0.70 (0.51-0.98; p = 0.038), respectively. Our study provides evidence of a causal association between thyroid dysfunction and breast cancer (mainly ER-positive tumors) risk. The role of TSH and hypothyroidism for thyroid cancer and the associations between thyroid dysfunction and other cancers need further exploration. © 2020 The Authors. International Journal of Cancer published by John Wiley & Sons Ltd on behalf of UICC.The domesticated marine microalga Diacronema lutheri is of great interest for producing various highly valuable molecules like lipids, particularly long-chain polyunsaturated fatty acids (LC-PUFA). In this study, we investigated the impact of phosphorus (P) and nitrogen (N) starvation on growth, carbon fixation (photosynthetic activity) and partitioning, and membrane lipid remodeling in this alga during batch culture. Our results show that the photosynthetic machinery was similarly affected by P and N stress. click here Under N starvation, we observed a much lower photosynthetic rate and biomass productivity. The degradation and re-use of cellular N-containing compounds contributed to triacylglycerol (TAG) accumulation. On the other hand, P-starved cells maintained pigment content and a carbon partitioning pattern more similar to the control, ensuring a high biomass. Betaine lipids constitute the major compounds of non-plastidial membranes, which are rich in eicosapentaenoic (EPA) and docosahexaenoic (DHA) acids. Under P and N starvations, EPA was transferred from the recycling of membrane polar lipids, most likely contributing to TAG accumulation. This article is protected by copyright. All rights reserved.BACKGROUND Frontal Fibrosing Alopecia (FFA) is a scarring alopecia with unclear pathogenesis and a progressive course. The disease has a major impact on patients' quality of life, lacking effective treatments to halt disease progression. METHODS We profiled lesional and non-lesional scalp biopsies collected in 2017 from FFA patients (n=12) in comparison to scalp biopsies from alopecia areata (AA) (n=8) and control (n=8) individuals to evaluate gene and protein expression including the primary outcome (CXCL9). We determined significant differences between biomarkers by a two-sided Student's t-test adjusting p-values by FDR. RESULTS Significant increases were seen in CD8+ cytotoxic T-cells, CD11c+ dendritic cells, CD103+ and CD69+ tissue-resident memory T-cells/TRM in FFA and AA versus control scalp (p less then 0.05), with corresponding significantly upregulated granzyme B mRNA, particularly in FFA (p less then 0.01). In AA, cellular infiltrates were primarily concentrated at the bulb, while in FFA these were mainly localized at the bulge. FFA demonstrated significant upregulation of Th1/IFN (e.g. IFN-, CXCL9/CXCL10), JAK-STAT pathway (STAT1, JAK3), and fibrosis-related products (vimentin, fibronectin; p less then 0.05 for all), with no concomitant downregulation of hair keratins and the T-regulatory marker, FOXP3, which were decreased in AA. The stem cell markers CD200 and K15 demonstrated significantly reduced expression only in FFA (p less then 0.05). CONCLUSION These data suggest that follicular damage and loss of stem cells in FFA may be mediated through immune attack in the bulge region, with secondary fibrosis and reduced but still detectable stem cells. JAK/STAT-targeting treatments may be able to prevent permanent follicular destruction and fibrosis in early disease stages. This article is protected by copyright. All rights reserved.OBJECTIVE Ovine footrot is a contagious bacterial disease that reduces meat and wool production and can trigger on-farm quarantine in New South Wales. Field diagnosis is based on the prevalence and severity of foot lesions, environmental conditions and flock history. The study evaluated whether a PCR assay or gelatin gel test for virulence in Dichelobacter nodosus isolated from hoof material could aid in the clinical diagnosis of virulent footrot. METHODS A quantitative polymerase chain reaction (qPCR) used for diagnosis of virulent footrot in some Australian states was evaluated on 218 hoof swabs taken from 44 sheep flocks from 36 NSW properties, quantifying both the aprV2 positive and aprB2 positive acidic protease genotypes of D. nodosus. DESIGN The same flocks/swabs were used to evaluate test agreement between the aprV2/B2 qPCR and the gelatin gel test, and a multiple logistic regression was used to identify factors critical for field diagnosis of virulent footrot. RESULTS Only fair to moderate agreement (kappa test) and significant disagreement (McNemar's) was shown between the gelatin gel test and the ratio of aprV2 positive to total D. nodosus. The proportion of aprV2 positive D. nodosus was not significantly different between foot lesions scores of increasing severity. Field diagnosis of virulent footrot was best explained by the prevalence of score 4 and 5 lesions, wet and warm environmental conditions, and recent footrot diagnosis. CONCLUSION Although the apr2 gene could differentiate between benign and virulent strains of D. nodosus, the apr2 qPCR was of minimal use for field diagnosis of virulent footrot, where disease expression relies on host genetics, immunity and environmental conditions. © 2020 Australian Veterinary Association.There is a large and growing interest in non-consumptive effects of predators. Diverse and extensive evidence shows that predation risk directly influences prey traits, such as behaviour, morphology, and physiology, which in-turn, may cause a reduction in prey fitness components (i.e., growth rate, survival, and reproduction). An intuitive expectation is that non-consumptive effects that reduce prey fitness will extend to alter population growth rate and therefore population size. However, our intensive literature search yielded only 10 studies that examined how predator-induced changes in prey traits translate to changes in prey population size. Further, the scant evidence for risk-induced changes on prey population size have been generated from studies that were performed in very controlled systems (mesocosm and laboratory), which do not have the complexity and feedbacks of natural settings. Thus, although likely that predation risk alone can alter prey population size, there is little direct empirical evidntal context interacts with predation risk and prey responses. We highlight the critical need to appreciate risk effects at each level in the chain of events, and that changes at one level cannot be assumed to translate into changes in the next because of the interplay between risk, prey responses, and the environment. The gaps in knowledge we illuminate underscore the need for more evidence to substantiate the claim that predation risk effects extend to prey population size. The lacunae we identify should inspire future studies on the impact of predation risk on population-level responses in free-living animals. This article is protected by copyright. All rights reserved.Cervical spondylotic myelopathy (CSM) is a common cause of disability with few treatments. Aberrant mitochondrial dynamics play a crucial role in the pathogenesis of various neurodegenerative diseases. Thus, regulation of mitochondrial dynamics may offer therapeutic benefit for the treatment of CSM. Muscone, the active ingredient of an odoriferous animal product, exhibits anti-inflammatory and neuroprotective effects for which the underlying mechanisms remain obscure. We hypothesized that muscone might ameliorate inflammatory responses and neuronal damage by regulating mitochondrial dynamics. To this end, the effects of muscone on a rat model of chronic cervical cord compression, as well as activated BV2 cells and injured neurons, were assessed. The results showed that muscone intervention improved motor function compared with vehicle-treated rats. Indeed, muscone attenuated pro-inflammatory cytokine expression, neuronal-apoptosis indicators in the lesion area, and activation of the nod-like receptor family pyrin domain-containing 3 inflammasome, nuclear transcription factor-κB, and dynamin-related protein 1 in Iba1- and βIII-tubulin-labeled cells.