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The wind effects on the shape of drop size distribution (DSD) and the driving microphysical processes for the DSD shape evolution were investigated using the dataset from the Midlatitude Continental Convective Clouds Experiment (MC3E). The quality-controlled DSD spectra from MC3E were grouped for each of the rainfall events by considering the precipitation type (stratiform vs convective) and liquid water content for the analysis. The DSD parameters (e.g., mass-weighted mean diameter) and the fitted DSD slopes for these grouped spectra showed statistically significant trends with varying wind speed. Increasing wind speeds were observed to modify the DSD shapes by increasing the number of small drops and decreasing the number of large drops, indicating that the raindrop breakup process governs the DSD shape evolution. Both spontaneous and collisional raindrop breakup modes were analyzed to elucidate the process responsible for the DSD shape evolution with varying wind speed. The analysis revealed that the collisional breakup process controls the wind-induced DSD shape. The findings of this study are of importance in DSD parameterizations that are essential to a wide variety of applications such as radar rainfall retrievals and hydrologic models.

Endoplasmic reticulum-associated degradation (ERAD) is an important function for cellular homeostasis. The mechanism of how picornavirus infection interferes with ERAD remains unclear. In this study, we demonstrated that enterovirus 71 (EV71) infection significantly inhibits cellular ERAD by targeting multiple key ERAD molecules with its proteases 2Apro and 3Cpro using different mechanisms. Ubc6e was identified as the key E2 ubiquitin-conjugating enzyme in EV71 disturbed ERAD. EV71 3Cpro cleaves Ubc6e at Q219G, Q260S, and Q273G. EV71 2Apro mainly inhibits the de novo synthesis of key ERAD molecules Herp and VIMP at the protein translational level. Herp differentially participates in the degradation of different glycosylated ERAD substrates α-1 antitrypsin Null Hong Kong (NHK) and the C-terminus of sonic hedgehog (SHH-C) via unknown mechanisms. p97 was identified as a host factor in EV71 replication; it redistributed and co-exists with the viral protein and other known replication-related molecules in EV71-induced replication organelles. Electron microscopy and multiple-color confocal assays also showed that EV71-induced membranous vesicles were closely associated with the endoplasmic reticulum (ER), and the ER membrane molecule RTN3 was redistributed to the viral replication complex during EV71 infection. Therefore, we propose that EV71 rearranges ER membranes and hijacks p97 from cellular ERAD to benefit its replication. These findings add to our understanding of how viruses disturb ERAD and provide potential anti-viral targets for EV71 infection.

In this paper, we are concerned with the stochastic averaging principle for stochastic differential equations (SDEs) with non-Lipschitz coefficients driven by fractional Brownian motion (fBm) of the Hurst parameter [Formula: see text]. We define the stochastic integrals with respect to the fBm in the integral formulation of the SDEs as pathwise integrals and we adopt the non-Lipschitz condition proposed by Taniguchi (1992) which is a much weaker condition with wider range of applications. The averaged SDEs are established. We then use their corresponding solutions to approximate the solutions of the original SDEs both in the sense of mean square and of probability. One can find that the similar asymptotic results are suitable for those non-Lipschitz SDEs with fBm under different types of stochastic integrals.

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