Anti-RBL2 monoclonal antibody, clone LBC51

The use of Poisson cluster processes to model rainfall time series at a range of scales now has a history of more than 30 years. Among them, the randomised (also called modified) Bartlett-Lewis model (RBL1) is particularly popular, while a refinement of this model was proposed recently (RBL2; Kaczmarska et al., 2014). Fitting such models essentially relies upon minimising the difference between theoretical statistics of the rainfall signal and their observed estimates. The first statistics are obtained using closed form analytical expressions for statistics of the orders 1 to 3 of the rainfall depths, as well as useful approximations of the wet- dry structure properties. The second are standard estimates of these statistics for each month of the data. This paper discusses two issues that are important for the optimal model fitting of RBL1 and RBL2. The first issue is that, when revisiting the derivation of the analytical expressions for the rainfall depth moments, it appears that the space of possible parameters is wider than has been assumed in past papers. The second issue is that care must be exerted in the way monthly statistics are estimated from the data. The impact of these two issues upon both models, in particular upon the estimation of extreme rainfall depths at hourly and sub-hourly timescales, is examined using 69 years of 5 min and 105 years of 10 min rainfall data from Bochum (Germany) and Uccle (Belgium), respectively.

Novel murine models of retinoblastoma based on Rb gene deletion in concert with inactivation of Rb family members have recently been developed. These new Rb knockout models of retinoblastoma provide excellent tools for pre-clinical studies and for the exploration of the genetics of tumorigenesis driven by RB inactivation. This review focuses on the developmental consequences of Rb deletion in the retina and the genetic interactions between Rb and the two other members of the pocket protein family, p107 (Rbl1) and p130 (Rbl2). There is increasing appreciation that homozygous RB mutations are insufficient for human retinoblastoma. Identifying and understanding secondary gene alterations that cooperate with RB inactivation in tumorigenesis may be facilitated by mouse models. Recent investigation of the p53 pathway in retinoblastoma, and evidence of spatial topology to early murine retinoblastoma are also discussed in this review.