A deterministic simulation model was developed to estimate biological production efficiency and to evaluate goat crossbreeding systems under tropical conditions. The model involves 5 production systems: pure indigenous, first filial generations (F1), backcross (BC), composite breeds of F1 (CMP(F1)), and BC (CMP(BC)). The model first simulates growth, reproduction, lactation, and energy intakes of a doe and a kid on a 1-d time step at the individual level and thereafter the outputs are integrated into the herd dynamics program. The ability of the model to simulate individual performances was tested under a base situation. The simulation results represented daily BW changes, ME requirements, and milk yield and the estimates were within the range of published data. Two conventional goat production scenarios (an intensive milk production scenario and an integrated goat and oil palm production scenario) in Malaysia were examined. The simulation results of the intensive milk production scenario showed the greater production efficiency of the CMP(BC) and CMP(F1) systems and decreased production efficiency of the F1 and BC systems. The results of the integrated goat and oil palm production scenario showed that the production efficiency and stocking rate were greater for the indigenous goats than for the crossbreeding systems.
The effect of parental genotype and paternal heterosis on litter size (LS), total litter birth weight (TLW) and average litter birth weight (ALW) was analysed utilizing data from a crossbreeding programme involving the exotic German Fawn goats and local Katjang goats in Malaysia. In this study, these traits were regarded as traits of the litter to consider the effect of service sire genotype. The results revealed that LS was significantly influenced by the genotype of sire. The genotypes of sire and dam had significant effects on TLW and ALW. Estimates of crossbreeding parameter showed significant and negative influence of paternal heterosis on TLW and ALW while there was no significant effect of paternal heterosis on LS. The results of this study stress the need to reconsider the use of local males in the tropics.
Outbreaks of hand, foot and mouth disease have been documented in Japan since 1963. This disease is primarily caused by the two closely related serotypes of Enterovirus A71 (EV-A71) and Coxsackievirus A16 (CV-A16). Here, we analyse Japanese virologic and syndromic surveillance time-series data from 1982 to 2015. As in some other countries in the Asia Pacific region, EV-A71 in Japan has a 3 year cyclical component, whereas CV-A16 is predominantly annual. We observe empirical signatures of an inhibitory interaction between the serotypes; virologic lines of evidence suggest they may indeed interact immunologically. We fit the time series to mechanistic epidemiological models: as a first-order effect, we find the data consistent with single-serotype susceptible-infected-recovered dynamics. We then extend the modelling to incorporate an inhibitory interaction between serotypes. Our results suggest the existence of a transient cross-protection and possible asymmetry in its strength such that CV-A16 serves as a stronger forcing on EV-A71. Allowing for asymmetry yields accurate out-of-sample predictions and the directionality of this effect is consistent with the virologic literature. Confirmation of these hypothesized interactions would have important implications for understanding enterovirus epidemiology and informing vaccine development. Our results highlight the general implication that even subtle interactions could have qualitative impacts on epidemic dynamics and predictability.
Coffin-Siris syndrome (CSS, MIM#135900) is a congenital disorder characterized by coarse facial features, intellectual disability, and hypoplasia of the fifth digit and nails. Pathogenic variants for CSS have been found in genes encoding proteins in the BAF (BRG1-associated factor) chromatin-remodeling complex. To date, more than 150 CSS patients with pathogenic variants in nine BAF-related genes have been reported. We previously reported 71 patients of whom 39 had pathogenic variants. Since then, we have recruited an additional 182 CSS-suspected patients. We performed comprehensive genetic analysis on these 182 patients and on the previously unresolved 32 patients, targeting pathogenic single nucleotide variants, short insertions/deletions and copy number variations (CNVs). We confirmed 78 pathogenic variations in 78 patients. Pathogenic variations in ARID1B, SMARCB1, SMARCA4, ARID1A, SOX11, SMARCE1, and PHF6 were identified in 48, 8, 7, 6, 4, 1, and 1 patients, respectively. In addition, we found three CNVs including SMARCA2. Of particular note, we found a partial deletion of SMARCB1 in one CSS patient and we thoroughly investigated the resulting abnormal transcripts.