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ZeroNAS: Differentiable Generative Adversarial Networks Look for Zero-Shot Mastering.
In semi-arid environments, the marked contrast in temperature and precipitation over the year strongly shapes ecological communities. The composition of species and their ecological interactions within a community may vary greatly over time. Although intra-annual variations are often studied, empirical information on how plant-bird relationships are structured within and among years, and how their drivers may change over time are still limited. In this study, we analyzed the temporal dynamics of the structure of plant-hummingbird interaction networks by evaluating changes in species richness, diversity of interactions, modularity, network specialization, nestedness, and β-diversity of interactions throughout four years in a Mexican xeric shrubland landscape. We also evaluated if the relative importance of abundance, phenology, morphology, and nectar sugar content consistently explains the frequency of pairwise interactions between plants and hummingbirds across different years. We found that species richness, diversity of interactions, nestedness, and network specialization did vary within and among years. We also observed that the β-diversity of interactions was high among years and was mostly associated with species turnover (i.e., changes in species composition), with a minor contribution of interaction rewiring (i.e., shifting partner species at different times). Finally, the temporal co-occurrence of hummingbird and plant species among months was the best predictor of the frequency of pairwise interactions, and this pattern was consistent within and among years. Our study underscores the importance of considering the temporal scale to understand how changes in species phenologies, and the resulting temporal co-occurrences influence the structure of interaction networks.Psychiatric disorders such as Schizophrenia (SCZ) and Bipolar Disorder (BD) represent an evolutionary paradox, as they exhibit strong negative effects on fitness, such as decreased fecundity and early mortality, yet they persist at a worldwide prevalence of approximately 1%. Molecular mechanisms affecting lifespan, which may be widely common among complex diseases with fitness effects, can be studied by the integrated analysis of data from genome-wide association studies (GWAS) of human longevity together with any disease of interest. Here, we report the first of such studies, focusing on the genetic overlap-pleiotropy-between two psychiatric disorders with shortened lifespan, SCZ and BD, and human parental lifespan (PLS) as a surrogate of life expectancy. Our results are twofold first, we demonstrate extensive polygenic overlap between SCZ and PLS and to a lesser extent between BD and PLS. Second, we identified novel loci shared between PLS and SCZ (n = 39), and BD (n = 8). Whereas most of the identified SCZ (66%) and BD (62%) pleiotropic risk alleles were associated with reduced lifespan, we also detected some antagonistic protective alleles associated to shorter lifespans. In fact, top-associated SNPs with SCZ seems to explain longevity variance explained (LVE) better than many other life-threatening diseases, including Type 2 diabetes and most cancers, probably due to a high overlap with smoking-related pathways. Overall, our study provides evidence of a genetic burden driven through premature mortality among people with SCZ, which can have profound implications for understanding, and potentially treating, the mortality gap associated with this psychiatric disorder.Kawasaki disease has well-described cardiovascular complications. However, the association to autoimmunity and cancer in the long term is not well described. We investigated theses associations using a registry-based matched cohort follow-up study of patients diagnosed with Kawasaki disease. Patients with Kawasaki disease were included and matched 15 to a population control group, matched by birth year, sex and incident month of the Kawasaki disease diagnosis. A total of 820 cases less then  21 years of age were identified. Median age at diagnosis was 3 years. Median follow-up time was 12 years. Patients with KD were at higher risk of being diagnosed with ischaemic heart disease at 10 years (HR 39.94 (95% CI 5.00-319.28)) and 30 years (HR 8.33 (95% CI 3.03-22.91)). The 10-, 20- and 30-year risks of developing autoimmune disorders were HR 4.23 (95% CI 3.01-5.94), HR 3.23 (95% CI 2.44-4.29) and 2.83 (95% CI, 2.17-3.68), all p less then  0.001. DNA Repair inhibitor Cancer risk was increased after 30 years (HR 2.42 (95% CI, 1.09-5.34)). All-cause mortality after 35 years was also significantly increased (HR 3.14 (95% CI, 1.03-9.60)). Children with KD have increased long-term risks of ischaemic heart disease also of autoimmune disease and cancer, as well as an increased all-cause mortality. The surprisingly increased risk of autoimmunity must be investigated further. What is known • Kawasaki disease is characterized by acute vasculitis and inflammation that can affect the coronary arteries. • Anti-inflammatory medicine is effective in the acute stages of the disease. What is new • Children with Kawasaki disease have an increased risk of developing autoimmune disease in the long term. • Kawasaki disease is associated with a slightly increased mortality rate driven by non-cardiovascular causes.We aimed to assess the correlation between clinical findings, serology, endoscopic findings, and histology in children diagnosed with celiac disease. Medical records of children diagnosed with celiac disease (2010-2017) at the Schneider Children's Hospital were reviewed retrospectively. Correlation between serologic measures anti-tissue transglutaminase (anti-tTG)/anti-endomysial antibodies (EMA) and other variables including mucosal damage, endoscopic findings (scalloping of duodenal folds), and clinical findings (abdominal pain, diarrhea, and anemia) was assessed. Out of 686 patients, 432 patients fulfilled the inclusion criteria (females 262, 61%; median age 6.0; interquartile range 4.0-9.0 years). Distribution of histopathology findings was Marsh IIIa 4%, Marsh IIIb 25%, and Marsh IIIc 71% with 313 (73%) patients having anti-tTG titer of ≥ 10 times the upper normal limit. Anti-tTG titer (but not EMA) positively correlated with Marsh grades, scalloping of duodenal folds and anemia. Anti-tTG ≥ 10 times the upper normal limit was associated with Marsh IIIc changes with an adjusted odds ratio of 4.
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