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利用高时空分辨率观测资料、多普勒、风廓线雷达资料和数值预报产品对2015年浙江2次强对流天气进行对比诊断分析.这2次过程差异显著，分别是较大范围短时暴雨和冰雹大风过程.短时暴雨发生在西风槽与位于日本的台风对峙形势下，中低层有低涡切变线，水汽条件好，中尺度云团不断原地生成并滞留；冰雹大风过程发生在副高边缘，东风波西移形势下，0 ℃层高度适宜，风垂直切变弱，风廓线雷达低层水平风速增大.但两者也有共同点，从风廓线雷达的探测数据看，高度及垂直风速均可以较好地体现降水的开始和结束.因此，强对流天气预报中，天气形势、雷达资料和物理量场对区分不同类别强对流天气具有较好的指示意义.

Cellular cholesterol is known to be under homeostatic control in nonsteroidogenic cells, and this intrigued us to understand how such control works in steroidogenic cells that additionally use cholesterol for steroid hormone synthesis. We employed primary culture of rat ovarian granulosa cells to study how steroidogenic cells adapt to acquire sufficient cholesterol to meet the demand of active steroidogenesis under the stimulation of gonadotropin follicle-stimulating hormone (FSH) and cytokine transforming growth factor (TGF)β1. We found that TGFβ1 potentiated FSH to upregulate scavenger receptor class B member I (SR-BI) and LDL receptor (LDLR), both functional in uptaking cholesterol as hHDL3 and hLDL supplementation enhanced progesterone production, and the effect of each lipoprotein was completely or partially blocked by SR-BI selective inhibitor BLT-1. Uptaken cholesterol could also be stored in lipid droplets. Importantly, LDLR and SR-BI responded to sterol with different sensitivity. Giving cells lipoproteins or 25-hydroxycholesterol downregulated Ldlr but not Scarb1; Scarb1 was ultimately downregulated by excessive sterol accumulation under 25-hydroxycholesterol and aminoglutethimide (inhibitor of steroidogenesis) cotreatment. Furthermore, transcription factors sterol regulatory element-binding protein (SREBP)-2 and liver receptor homolog (LRH)-1 crucially mediated Ldlr and Scarb1 differential response to sterol challenge. This study reveals that ovarian granulosa cells retain the cholesterol homeostatic control machinery like nonsteroidogenic cells, although during active steroidogenesis, they utilize SR-BI to evade such feedback control.