Scaling determination of the nonlinear I-V characteristics for 2D superconducting networks

It is shown from computer simulations that the current-voltage ($I$-$V$) characteristics for the two-dimensional XY model with resistively-shunted Josephson junction dynamics and Monte Carlo dynamics obeys a finite-size scaling form from which the nonlinear $I$-$V$ exponent $a$ can be determined to good precision. This determination supports the conclusion $a=z+1$, where $z$ is the dynamic critical exponent. The results are discussed in the light of the contrary conclusion reached by Tang and Chen [Phys. Rev. B {\bf 67}, 024508 (2003)] and the possibility of a breakdown of scaling suggested by Bormann [Phys. Rev. Lett. {\bf 78}, 4324 (1997)].Comment: 6 pages, to appear in PR

The neuropeptide receptor calcitonin receptor-like (CALCRL) is a potential therapeutic target in acute myeloid leukemia.

Calcitonin receptor-like (CALCRL) is a G-protein-coupled neuropeptide receptor involved in the regulation of blood pressure, angiogenesis, cell proliferation, and apoptosis, and is currently emerging as a novel target for the treatment of migraine. This study characterizes the role of CALCRL in acute myeloid leukemia (AML). We analyzed CALCRL expression in collectively more than 1500 well-characterized AML patients from five international cohorts (AMLCG, HOVON, TCGA, Leucegene, and UKM) and evaluated associations with survival. In the AMLCG analytic cohort, increasing transcript levels of CALCRL were associated with decreasing complete remission rates (71.5%, 53.7%, 49.6% for low, intermediate, high CALCRL expression), 5-year overall (43.1%, 26.2%, 7.1%), and event-free survival (29.9%, 15.8%, 4.7%) (all P < 0.001). CALCRL levels remained associated with all endpoints on multivariable regression analyses. The prognostic impact was confirmed in all validation sets. Genes highly expressed in CALCRLhigh AML were significantly enriched in leukemic stem cell signatures and CALCRL levels were positively linked to the engraftment capacity of primary patient samples in immunocompromised mice. CRISPR- Cas9-mediated knockout of CALCRL significantly impaired colony formation in human myeloid leukemia cell lines. Overall, our study demonstrates that CALCRL predicts outcome beyond existing risk factors and is a potential therapeutic target in AML