Biology subjects

Ryan, S. D.

Publications and source records attributed to Ryan, S. D..

3 recordsLinked to original sources

bioRxiv2025

Peracetic Acid Efficacy and Decay Kinetics in Poultry Processing under Chiller Conditions

Pathogens on poultry products continue to pose critical public health risks. Despite significant literature examining sanitizer impact on bacterial pathogens during chilling, the mechanisms of sanitizer efficacy in terms of pathogen and organic load, sanitizer levels, and exposure duration are not well understood. To assess these, we report on experimentally-informed-mechanistic-modeling to describe pathogen dynamics during poultry chilling. The shedding and survival of a five-strain cocktail of poultry-plant derived Salmonella enterica serovars, at high and low loads, with exposure to peracetic acid (PAA; 0 - 200 mg{middle dot}L-1) for up to 60 min in 10-L chiller tanks, in the presence or absence of whole chicken carcass/parts, were measured. Process water parameters versus time were simultaneously monitored. Results suggest that total dissolved solids (TDS) predict PAA decay more consistently than chemical oxygen demand (COD). A mathematical model for PAA decay and pathogen shedding/inactivation was developed. This model accurately predicted PAA level changes in the pre/main chiller of a high-speed poultry processing plant in North America. Without PAA, Salmonella shedding from chicken thighs is influenced by rinse time and number of rinses. Without organic load, residual PAA (1 mg{middle dot}L-1) inactivated bacteria given sufficient exposure time, although PAA levels > 5 mg{middle dot}L-1 were essential for rapid inactivation. With organic load, initial PAA concentration (> 40 mg{middle dot}L-1) and exposure time (> 2 min) were critical for bacterial inactivation, with model results connecting process conditions to dominate modes of bacterial inactivation on chicken. The insights from such experimental-modeling studies provide key tools for processors to improve pathogen control during chilling.

microbiology↗

bioRxiv2023

MicroCT-based imaging of microvasculature within the bone tissue

Angiogenesis is essential for skeletal development, bone healing, and regeneration. Improved non-destructive, three-dimensional (3D) imaging of the vasculature within bone tissue benefits many research areas, especially implantology and tissue engineering. X-ray microcomputed tomography (microCT) is a well-suited non-destructive 3D imaging technique for bone morphology. For microCT-based detection of vessels, it is paramount to use contrast enhancement. Limited differences in radiopacity between perfusion agents and mineralized bone make their distinct segmentation problematic and have been a major drawback of this approach. A decalcification step resolves this issue but inhibits the simultaneous assessment of bone microstructure and vascular morphology. The problem of contrasting becomes further complicated in samples with metal implants. This study describes contrast-enhanced microCT-based visualization of vasculature within bone tissue in small and large animal models, also in the vicinity of the metal implants. We present simultaneous microvascular and bone imaging in murine tibia, a murine bone metastatic model, the pulp chamber, gingiva, and periodontal ligaments. In a large animal model (minipig), we perform visualization and segmentation of different tissue types and vessels in the hemimandible containing metal implants. We further demonstrate the potential of dual-energy imaging in distinguishing bone tissue from the applied contrast agents. This work introduces a non-destructive approach for 3D imaging of vasculature within soft and hard tissues near metal implants in a large animal model.

physiology↗

bioRxiv2022

Genetic and pharmacological reduction of CDK14 mitigates synucleinopathy

Parkinsonas disease (PD) is a debilitating neurodegenerative disease characterized by the loss of midbrain dopaminergic neurons (DaNs) and the abnormal accumulation of -Synuclein (-Syn) protein. Currently, no treatment can slow nor halt the progression of PD. Multiplications and mutations of the -Syn gene (SNCA) cause PD-associated syndromes and animal models that overexpress -Syn replicate several features of PD. Decreasing total -Syn levels, therefore, is an attractive approach to slow down neurodegeneration in patients with synucleinopathy. We previously performed a genetic screen for modifiers of -Syn levels and identified CDK14, a kinase of largely unknown function as a regulator of -Syn. To test the potential therapeutic effects of CDK14 reduction in PD, we ablated Cdk14 in the -Syn preformed fibrils (PFF)-induced PD mouse model. We found that loss of Cdk14 mitigates the grip strength deficit of PFF-treated mice and ameliorates PFF-induced cortical -Syn pathology, indicated by reduced numbers of pS129 -Syn-containing cells. In primary neurons, we found that Cdk14 depletion protects against the propagation of toxic -Syn species. We further validated these findings on pS129 -Syn levels in PD patient neurons. Finally, we leveraged the recent discovery of a covalent inhibitor of CDK14 to determine whether this target is pharmacologically tractable in vitro and in vivo. We found that CDK14 inhibition decreases total and pathologically aggregated -Syn in human neurons, in PFF- challenged rat neurons and in the brains of -Syn-humanized mice. In summary, we suggest that CDK14 represents a novel therapeutic target for PD-associated synucleinopathy.

neuroscience↗