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Greene, K.

Publications and source records attributed to Greene, K..

2 recordsLinked to original sources

A deep learning algorithm for potato tuber hollowheart classification

A novel deep learning algorithm is proposed for hollow heart detection which is an internal tuber defect. Hollow heart is one of many internal defects that decrease the market value of potatoes in the fresh market and food processing sectors. Susceptibility to internal defects like the hollow heart is influenced by genetic and environmental factors so elimination of defect-prone material in potato breeding programs is important. Current methods of evaluation utilize human scoring which is limiting (only collects binary data) relative to the data collection capacity afforded by computer vision or are based upon X-ray transmission techniques that are both expensive and can be hazardous. Automation of defect classification (e.g. hollow heart) from data sets collected using inexpensive, consumer-grade hardware has the potential to increase throughput and reduce bias in public breeding programs. The proposed algorithm consists of ResNet50 as the backbone of the model followed by a shallow fully connected network (FCN). A simple augmentation technique is performed to increase the number of images in the data set. The performance of the proposed algorithm is validated by investigating metrics such as precision and the area under the curve (AUC).

plant biology↗

CD73 maintains hepatocyte metabolic integrity and mouse liver homeostasis in a sex-dependentmanner

Background & AimsMetabolic imbalance and inflammation are common features of chronic liver diseases. Molecular factors controlling these mechanisms represent potential therapeutic targets. One promising target is CD73, the major enzyme that dephosphorylates extracellular adenosine monophosphate (AMP) to form the anti-inflammatory adenosine. In normal liver, CD73 is expressed on pericentral hepatocytes, which are important for long-term liver homeostasis. The aim of this study was to determine if CD73 has non-redundant hepatoprotective functions. Approach & ResultsWe generated mice with a targeted deletion of the CD73-encoding gene (Nt5e) in hepatocytes (CD73-LKO). Deletion of hepatocyte Nt5e resulted in approximately 70% reduction in total liver CD73 protein (p<0.0001). Male and female CD73-LKO mice developed normally during the first 21 weeks, without significant liver phenotypes. Between 21-42 weeks, the CD73-LKO mice developed spontaneous onset liver disease with significant severity in male mice. Notably, middle-aged male CD73-LKO mice displayed hepatocyte swelling and ballooning (p<0.05), inflammation (p<0.01) and variable steatosis. Female CD73-LKO mice had lower serum albumin (p<0.05) and elevated inflammatory markers (p<0.01), but did not exhibit the spectrum of histopathologic changes characteristic of the male mice, potentially due to compensatory induction of adenosine receptors. Serum analysis and proteomic profiling of hepatocytes from male CD73-LKO mice revealed significant metabolic imbalance, with elevated blood urea nitrogen (p<0.0001) and impairments in major metabolic pathways, including oxidative phosphorylation and AMP-activated protein kinase (AMPK) signaling. There was significant hypo-phosphorylation in AMPK substrate in CD73-LKO livers (p<0.0001), while in isolated hepatocytes treated with AMP, soluble CD73 induced AMPK activation (p<0.001). ConclusionsHepatocyte CD73 supports long-term metabolic liver homeostasis through AMPK in a sex-dependent manner. These findings have implications for human liver diseases marked by CD73 dysregulation.

physiology↗