skip to main content

Title: Catch More to Catch Less: Estimating Timing Choice as Dynamic Bycatch Avoidance Behavior
Award ID(s):
Author(s) / Creator(s):
; ;
Date Published:
Journal Name:
Environmental and Resource Economics
Page Range / eLocation ID:
953 to 984
Medium: X
Sponsoring Org:
National Science Foundation
More Like this
  1. Background Human papillomavirus (HPV) is the most common sexually transmitted infection in the United States. HPV can cause genital warts and multiple types of cancers in females. HPV vaccination is recommended to youth age 11 or 12 years before sexual initiation to prevent onset of HPV-related diseases. For females who have not been vaccinated previously, catch-up vaccines are recommended through age 26. The extent to which catch-up vaccines are beneficial in terms of disease prevention and cost-effectiveness is questionable given that some women may have been exposed to HPV before receiving the catch-up vaccination. This study aims to examine whether the cutoff age of catch-up vaccination should be determined based on an individual woman’s risk characteristic instead of a one-size-fits-all age 26. Methods We developed a microsimulation model to evaluate multiple clinical outcomes of HPV vaccination for different women based on a number of personal attributes. We modeled the impact of HPV vaccination at different ages on every woman and tracked her course of life to estimate the clinical outcomes that resulted from receiving vaccines. As the simulation model is risk stratified, we used extreme gradient boosting to build an HPV risk model estimating every woman’s dynamic HPV risk over time for the lifetime simulation model. Results Our study shows that catch-up vaccines still benefit all women after age 26 from the perspective of clinical outcomes. Women facing high risk of HPV infection are expected to gain more health benefits compared with women with low HPV risk. Conclusions From a cancer prevention perspective, this study suggests that the catch-up vaccine after age 26 should be deliberately considered. 
    more » « less
  2. Abstract Fibrin polymerization involves thrombin-mediated exposure of knobs on one monomer that bind to holes available on another, leading to the formation of fibers. In silico evidence has suggested that the classical A:a knob-hole interaction is enhanced by surrounding residues not directly involved in the binding pocket of hole a, via noncovalent interactions with knob A. We assessed the importance of extended knob-hole interactions by performing biochemical, biophysical, and in silico modeling studies on recombinant human fibrinogen variants with mutations at residues responsible for the extended interactions. Three single fibrinogen variants, γD297N, γE323Q, and γK356Q, and a triple variant γDEK (γD297N/γE323Q/γK356Q) were produced in a CHO (Chinese Hamster Ovary) cell expression system. Longitudinal protofibril growth probed by atomic force microscopy was disrupted for γD297N and enhanced for the γK356Q mutation. Initial polymerization rates were reduced for all variants in turbidimetric studies. Laser scanning confocal microscopy showed that γDEK and γE323Q produced denser clots, whereas γD297N and γK356Q were similar to wild type. Scanning electron microscopy and light scattering studies showed that fiber thickness and protofibril packing of the fibers were reduced for all variants. Clot viscoelastic analysis showed that only γDEK was more readily deformable. In silico modeling suggested that most variants displayed only slip-bond dissociation kinetics compared with biphasic catch-slip kinetics characteristics of wild type. These data provide new evidence for the role of extended interactions in supporting the classical knob-hole bonds involving catch-slip behavior in fibrin formation, clot structure, and clot mechanics. 
    more » « less