ALBERT

Description: An important challenge facing the New Zealand (NZ) dairy industry is development of production systems that can maintain or increase production and profitability, while reducing impacts on receiving environments including water and air. Using research ‘farmlets’ in Waikato, Canterbury, and Otago (32–200 animals per herd), we assessed if system changes aimed at reducing nitrate leaching can also reduce total greenhouse gas (GHG) emissions (methane and nitrous oxide) and emissions intensity (kg GHG per unit of product) by comparing current and potential ‘improved’ dairy systems. Annual average GHG emissions for each system were estimated for three or four years using calculations based on the New Zealand Agricultural Inventory Methodology, but included key farmlet-specific emission factors determined from regional experiments. Total annual GHG footprints ranged between 10,800 kg and 20,600 kg CO2e/ha, with emissions strongly related to the amount of feed eaten. Methane (CH4) represented 75% to 84% of the total GHG footprint across all modelled systems, with enteric CH4 from lactating cows grazing pasture being the major source. Excreta deposition onto paddocks was the largest source of nitrous oxide (N2O) emissions, representing 7–12% of the total GHG footprint for all systems. When total emissions were represented on an intensity basis, ‘improved’ systems are predicted to generally result in lower emissions intensity. The ‘improved’ systems had lower GHG footprints than the ‘current’ system, except for one of the ‘improved’ systems in Canterbury, which had a higher stocking rate. The lower feed supplies and associated lower stocking rates of the ‘improved’ systems were the key drivers of lower total GHG emissions in all three regions. ‘Improved’ systems designed to reduced N leaching generally also reduced GHG emissions.

Description: Between 2011 and 2016, small-scale farm trials were run across three dairy regions of New Zealand (Waikato, Canterbury, Otago) to compare the performance of typical regional farm systems with farm systems implementing a combination of mitigation options most suitable to the region. The trials ran for at least three consecutive years with detailed recording of milk production and input costs. Nitrate leaching per hectare of the milking platform (where lactating cows are kept) was estimated using either measurements (suction cups), models, or soil mineral nitrogen measurements. Post-trial, detailed farm information was used in the New Zealand greenhouse gas inventory methodology to calculate the emissions from all sources; dairy platform, dairy support land used for wintering non-lactating cows (where applicable) and replacement stock, and imported supplements. Nitrate leaching was also estimated for the support land and growing of supplements imported from off-farm using the same methods as for the platform. Operating profit (NZ$/ha/year), nitrate leaching (kg N/ha/year), and greenhouse gas emissions (t CO2-equivalent/ha/year) were all expressed per hectare of milking platform to enable comparisons across regions. Nitrate leaching mitigations adopted in lower-input (less purchased feed and nitrogen fertiliser) farm systems reduced leaching by 22 to 30 per cent, and greenhouse gas emissions by between nine and 24 per cent. The exception was the wintering barn system in Otago, where nitrate leaching was reduced by 45 per cent, but greenhouse gas emissions were unchanged due to greater manure storage and handling. Important drivers of a lower environmental footprint are reducing nitrogen fertiliser and purchased feed. Their effect is to reduce feed flow through the herd and drive down both greenhouse gas emissions and nitrate leaching. Emission reductions in the lower-input systems of Waikato and Canterbury came at an average loss of profit of approximately NZ$100/t CO2-equivalent (three to five per cent of industry-average profit per hectare).

Description: Uveal melanoma (UM) is the most common primary intraocular malignancy of the eye. It has a high metastatic potential and mainly spreads to the liver. Genetics play a vital role in tumor classification and prognostication of UM metastatic disease. One of the driver genes mutated in metastasized UM is subunit 1 of splicing factor 3b (SF3B1), a component of the spliceosome complex. Recurrent mutations in components of the spliceosome complex are observed in UM and other malignancies, suggesting an important role in tumorigenesis. SF3B1 is the most common mutated spliceosome gene and in UM it is associated with late-onset metastasis. This review summarizes the genetic and epigenetic insights of spliceosome mutations in UM. They form a distinct subgroup of UM and have similarities with other spliceosome mutated malignancies.

Description: Tracheoesophageal Fistula (TOF) is a congenital anomaly for which the cause is unknown in the majority of patients. OA/TOF is a variable feature in many (often mono-) genetic syndromes. Research using animal models targeting genes involved in candidate pathways often result in tracheoesophageal phenotypes. However, there is limited overlap in the genes implicated by animal models and those found in OA/TOF-related syndromic anomalies. Knowledge on affected pathways in animal models is accumulating, but our understanding on these pathways in patients lags behind. If an affected pathway is associated with both animals and patients, the mechanisms linking the genetic mutation, affected cell types or cellular defect, and the phenotype are often not well understood. The locus heterogeneity and the uncertainty of the exact heritability of OA/TOF results in a relative low diagnostic yield. OA/TOF is a sporadic finding with a low familial recurrence rate. As parents are usually unaffected, de novo dominant mutations seems to be a plausible explanation. The survival rates of patients born with OA/TOF have increased substantially and these patients start families; thus, the detection and a proper interpretation of these dominant inherited pathogenic variants are of great importance for these patients and for our understanding of OA/TOF aetiology.