Animal as the Solution II: Phenotyping for Low Milk Urea Nitrogen A1PF Dairy Cows.

The societal pressure on intensive pastoral dairying demands the search for strategies to reduce the amount of N flowing through and excreted by dairy cows. One of the strategies that is being currently explored focuses on the animal as a solution, as there are differences in N metabolism between cows even within the same herd. This work was conducted to explore such an approach in A1PF herds in New Zealand and the possibility of identifying A1PF cows that are divergent for milk urea nitrogen (MUN) concentration through phenotyping as a potential viable strategy to reduce N leaching and emissions from temperate dairy systems.

Birth characteristics and the risk of childhood brain tumors: A case-control study in Ontario, Canada.

Various birth characteristics may influence healthy childhood development, including the risk of developing childhood brain tumors (CBTs). In this study, we aimed to investigate the association between delivery methods, obstetric history, and birth anthropometrics with the risk of CBTs. This study used data from the Childhood Brain Tumour Epidemiology Study of Ontario (CBREO) which included children 0-15 years of age and newly diagnosed with CBTs from 1997 to 2003.

Development of genomic evaluation for methane efficiency in Canadian Holsteins.

Reducing methane (CH) emissions from agriculture, among other sectors, is a key step to reducing global warming. There are many strategies to reduce CH emissions in ruminant animals, including genetic selection, which yields cumulative and permanent genetic gains over generations. A single-step genomic evaluation for methane efficiency (MEF) was officially implemented in April 2023 for the Canadian Holstein breed, aiming to reduce CH emissions without affecting production levels.

Coxsackievirus and adenovirus receptor expression facilitates enteroviral infections to drive the development of pancreatic cancer.

The development of pancreatic cancer requires both, acquisition of an oncogenic mutation in KRAS as well as an inflammatory insult. However, the physiological causes for pancreatic inflammation are less defined. We show here that oncogenic KRas-expressing pre-neoplastic lesion cells upregulate coxsackievirus (CVB) and adenovirus receptor (CAR).