One of the major drivers of radiation belt dynamics, electron resonant interaction with whistler-mode chorus waves, is traditionally described using the quasi-linear diffusion approximation. Such a description satisfactorily explains many observed phenomena, but its applicability can be justified only for sufficiently low intensity, long duration waves. Recent spacecraft observations of a large number of very intense lower-band chorus waves (with magnetic field amplitudes sometimes reaching ∼ 1% of the background) therefore challenge this traditional description and call for an alternative approach when addressing the global, long-term effects of the nonlinear interaction of these waves with radiation belt electrons. In this paper, we first use observations from the Van Allen Probes and Time History of Events and Macroscale Interactions during Substorms spacecraft to show that the majority of intense parallel chorus waves consist of relatively short wave packets. Then, we construct a kinetic equation describing the nonlinear resonant interaction of radiation belt electrons with such short and intense wave packets. We demonstrate that this peculiar type of nonlinear interaction produces similar effects as quasi-linear diffusion, that is, a flattening of the electron velocity distribution function within a certain energy/pitch angle range. The main difference is the much faster evolution of the electron distribution when nonlinear interaction prevails. Key Points:• The theory of electron nonlinear interaction with short intense chorus packets is presented • A generalized kinetic equation including nonlinear interactions with short chorus packets is derived • Nonlinear interactions with short wave packets produce essentially similar effects as quasi-linear diffusion but on a much faster timescale Citation:Mourenas, D., Zhang, X.-J., Artemyev, A. V., Angelopoulos, V., Thorne, R. M., Bortnik, J., et al. (2018). Electron nonlinear resonant interaction with short and intense parallel chorus wave packets.

Our epidemiologic studies offer the information about Han Chinese distribution, which provide clues to describe psoriasis in children.

Acute myeloblastic leukemia (AML) is characterized by the accumulation of abnormal myeloblasts (mainly granulocyte or monocyte precursors) in the bone marrow and blood. Though great progress has been made for improvement in clinical treatment during the past decades, only minority with AML achieve long-term survival. Therefore, further understanding mechanisms of leukemogenesis and exploring novel therapeutic strategies are still crucial for improving disease outcome. MicroRNA-100 (miR-100), a small non-coding RNA molecule, has been reported as a frequent event aberrantly expressed in patients with AML; however, the molecular basis for this phenotype and the statuses of its downstream targets have not yet been elucidated. In the present study, we found that the expression level of miR-100 in vivo was related to the stage of the maturation block underlying the subtypes of myeloid leukemia. In vitro experiments further demonstrated that miR-100 was required to promote the cell proliferation of promyelocytic blasts and arrest them differentiated to granulocyte/monocyte lineages. Significantly, we identified RBSP3, a phosphatase-like tumor suppressor, as a bona fide target of miR-100 and validated that RBSP3 was involved in cell differentiation and survival in AML. Moreover, we revealed a new pathway that miR-100 regulates G1/S transition and S-phase entry and blocks the terminal differentiation by targeting RBSP3, which partly in turn modulates the cell cycle effectors pRB/E2F1 in AML. These events promoted cell proliferation and blocked granulocyte/monocyte differentiation. Our data highlight an important role of miR-100 in the molecular etiology of AML, and implicate the potential application of miR-100 in cancer therapy.

Systemic lupus erythematosus (SLE) is an autoimmune disease with heterogeneous clinical manifestations influenced by genetic and environmental factors. Five novel susceptibility genes (TNIP1, SLC15A4, ETS1, RasGRP3 and IKZF1) for SLE have been identified in a recent genome-wide association study of a Chinese Han population. This study investigated their relationships with disease subphenotypes, including renal nephritis, photosensitivity, antinuclear antibody (ANA), age at diagnosis, malar rash, discoid rash, immunological disorder, oral ulcer, hematological disorder, neurological disorder, serositis, arthritis and vasculitis. Significant associations were found for the single nucleotide polymorphism rs10036748 of TNIP1 with photosensitivity (odds ratio (OR) = 0.87, p = 0.01) and vasculitis (OR = 1.18, p = 0.04); rs10847697 of SLC15A4 with discoid rash (OR = 1.18, p = 0.02); rs6590330 of ETS1 with SLE of age at diagnosis <20 years (OR = 1.24, p = 8.91 x 10(-5)); rs13385731 of RasGRP3 with malar rash (OR = 1.20, p = 0.01), discoid rash (OR = 0.78, p = 0.02) and ANA (OR = 0.72, p = 0.004); rs4917014 of IKZF1 with renal nephritis (OR = 1.13, p = 0.02) and malar rash (OR = 0.83, p = 0.00038), respectively. The study suggested that these susceptibility genes might not only play important roles in the development of SLE, but also contribute to the complex phenotypes of SLE.