Inequality of Air Quality?: A Study of Air Quality within Housing Price Brackets in Gettysburg, PA

With the rise of cars and other motorized vehicles has come the rise of air pollution, which tends to have disproportionate environmental and health impacts on low-income and communities of color. This study analyzes car presence and air quality on a transect within Gettysburg, PA to determine if there is a relationship between air pollution and vehicle presence, and if there is a difference in air quality between higher price bracket housing compared to campus, commercial, and lower price bracket housing. To test our research questions, we identified nine sampling locations along a transect where we measured air pollutants, including particulate matter (2.5 um and 10 um), VOCs, and NO2, with Flow by Plume Labs and Atmotube Pro air quality monitors. Our hypotheses that car activity will increase the amount of air pollution in Gettysburg and that there will be a greater environmental justice disparity within lower housing price brackets were not supported. The air quality along the transect was not greatly affected by vehicle presence and was consistent with regional conditions, and while measurements of different pollutants changed with location, there was not one clear trend between these two variables. However, there were consistently higher levels of vehicle traffic in the commercial and low-income areas than in the high-income and campus areas. The main limitations of our study were the lack of functionality and accuracy of our air monitors, which reduced the sample size of our data. These results provide room for further study of racial and child health disparities caused by cars and air pollution, as well as the impact of higher traffic levels on the risk of car and pedestrian accidents

The Four Squares of Four Square

A poster presented by Anna Jones, Sophia Sharp, Arden Ensor, Andrew Floyd, Garrett Weakley and Luke Cross for the class Design of Everyday Things.https://scholarworks.moreheadstate.edu/gsp_projects_2019/1016/thumbnail.jp

Dynamic exchange of myosin VI on endocytic structures.

The actin-based molecular motor myosin VI functions in the endocytic uptake pathway, both during the early stages of clathrin-mediated uptake and in later transport to/from early endosomes. This study uses fluorescence recovery after photobleaching (FRAP) to examine the turnover rate of myosin VI during endocytosis. The results demonstrate that myosin VI turns over dynamically on endocytic structures with a characteristic half-life common to both the large insert isoform of myosin VI on clathrin-coated structures and the no-insert isoform on early endosomes. This half-life is shared by the myosin VI-binding partner Dab2 and is identical for full-length myosin VI and the cargo-binding tail region. The 4-fold slower half-life of an artificially dimerized construct of myosin VI on clathrin-coated structures suggests that wild type myosin VI does not function as a stable dimer, but either as a monomer or in a monomer/dimer equilibrium. Taken together, these FRAP results offer insight into both the basic turnover dynamics and the monomer/dimer nature of myosin VI

The Autophagy Receptor TAX1BP1 and the Molecular Motor Myosin VI Are Required for Clearance of Salmonella Typhimurium by Autophagy.

Autophagy plays a key role during Salmonella infection, by eliminating these pathogens following escape into the cytosol. In this process, selective autophagy receptors, including the myosin VI adaptor proteins optineurin and NDP52, have been shown to recognize cytosolic pathogens. Here, we demonstrate that myosin VI and TAX1BP1 are recruited to ubiquitylated Salmonella and play a key role in xenophagy. The absence of TAX1BP1 causes an accumulation of ubiquitin-positive Salmonella, whereas loss of myosin VI leads to an increase in ubiquitylated and LC3-positive bacteria. Our structural studies demonstrate that the ubiquitin-binding site of TAX1BP1 overlaps with the myosin VI binding site and point mutations in the TAX1BP1 zinc finger domains that affect ubiquitin binding also ablate binding to myosin VI. This mutually exclusive binding and the association of TAX1BP1 with LC3 on the outer limiting membrane of autophagosomes may suggest a molecular mechanism for recruitment of this motor to autophagosomes. The predominant role of TAX1BP1, a paralogue of NDP52, in xenophagy is supported by our evolutionary analysis, which demonstrates that functionally intact NDP52 is missing in Xenopus and mice, whereas TAX1BP1 is expressed in all vertebrates analysed. In summary, this work highlights the importance of TAX1BP1 as a novel autophagy receptor in myosin VI-mediated xenophagy. Our study identifies essential new machinery for the autophagy-dependent clearance of Salmonella typhimurium and suggests modulation of myosin VI motor activity as a potential therapeutic target in cellular immunity.FB and DAT thank the Wellcome Trust (www.wellcome.ac.uk) for funding of a University Award to FB (086743), the CIMR Strategic Award (100140) and an equipment grant [093026]. FB also thanks the Medical Research Council UK (www.mrc.ac.uk) for funding of a project grant (MR/K000888/1). JKJ, MA and MB were supported by the Medical Research Council UK (www.mrc.ac.uk) (U105184325).This is the final published version. It first appeared at http://dx.doi.org/10.1371/journal.ppat.100517

See no evil, print no evil: the criminalization of free speech in DMZ

This article examines contemporary notions on free speech and the criminalisation of journalistic expression since 9/11, via discussion of Brian Wood’s DMZ comics (DC Vertigo). Free speech and the importance of a free press are widely accepted notions, yet journalistic and artistic freedom is arguably under attack in our post-9/11 world (Ash, 2016; Article 19, 2007). State responses to global terror threats have criminalised free speech, particularly speech seen as ‘glorifying’ or ‘supporting’ terrorism via anti-terror or restrictive media laws. This article examines these issues via DMZ ’s discussion of a second American civil war in which freedom of the press has all but disappeared, arguing that DMZ ’s ‘War on Terror’ narrative and depiction of controlled news access serve as allegories for contemporary free speech restrictions. DMZ illustrates contemporary concerns about a perceived social problem in its representation of corruption, abuse of power and restrictions on the public’s right to know

The effect of FTO variation on increased osteoarthritis risk is mediated through body mass index : a mendelian randomisation study

Objective: Variation in the fat mass and obesity-associated (FTO) gene influences susceptibility to obesity. A variant in the FTO gene has been implicated in genetic risk to osteoarthritis (OA). We examined the role of the FTO polymorphism rs8044769 in risk of knee and hip OA in cases and controls incorporating body mass index (BMI) information. Methods: 5409 knee OA patients, 4355 hip OA patients and up to 5362 healthy controls from 7 independent cohorts from the UK and Australia were genotyped for rs8044769. The association of the FTO variant with OA was investigated in case/control analyses with and without BMI adjustment and in analyses matched for BMI category. A mendelian randomisation approach was employed using the FTO variant as the instrumental variable to evaluate the role of overweight on OA. Results: In the meta-analysis of all overweight (BMI≥25) samples versus normal-weight controls irrespective of OA status the association of rs8044769 with overweight is highly significant (OR[CIs] for allele G=1.14 [01.08 to 1.19], p=7.5×10−7). A significant association with knee OA is present in the analysis without BMI adjustment (OR[CIs]=1.08[1.02 to 1.14], p=0.009) but the signal fully attenuates after BMI adjustment (OR[CIs]=0.99[0.93 to 1.05], p=0.666). We observe no evidence for association in the BMI-matched meta-analyses. Using mendelian randomisation approaches we confirm the causal role of overweight on OA. Conclusions: Our data highlight the contribution of genetic risk to overweight in defining risk to OA but the association is exclusively mediated by the effect on BMI. This is consistent with what is known of the biology of the FTO gene and supports the causative role of high BMI in OA

The autophagy receptor TAX1BP1 and the molecular motor myosin VI are required for clearance of Salmonella typhimurium by autophagy

Autophagy plays a key role during Salmonella infection, by eliminating these pathogens following escape into the cytosol. In this process, selective autophagy receptors, including the myosin VI adaptor proteins optineurin and NDP52, have been shown to recognize cytosolic pathogens. Here, we demonstrate that myosin VI and TAX1BP1 are recruited to ubiquitylated Salmonella and play a key role in xenophagy. The absence of TAX1BP1 causes an accumulation of ubiquitin-positive Salmonella, whereas loss of myosin VI leads to an increase in ubiquitylated and LC3-positive bacteria. Our structural studies demonstrate that the ubiquitin-binding site of TAX1BP1 overlaps with the myosin VI binding site and point mutations in the TAX1BP1 zinc finger domains that affect ubiquitin binding also ablate binding to myosin VI. This mutually exclusive binding and the association of TAX1BP1 with LC3 on the outer limiting membrane of autophagosomes may suggest a molecular mechanism for recruitment of this motor to autophagosomes. The predominant role of TAX1BP1, a paralogue of NDP52, in xenophagy is supported by our evolutionary analysis, which demonstrates that functionally intact NDP52 is missing in Xenopus and mice, whereas TAX1BP1 is expressed in all vertebrates analysed. In summary, this work highlights the importance of TAX1BP1 as a novel autophagy receptor in myosin VI-mediated xenophagy. Our study identifies essential new machinery for the autophagy-dependent clearance of Salmonella typhimurium and suggests modulation of myosin VI motor activity as a potential therapeutic target in cellular immunity

Patellar cartilage volume of the back leg versus the higher loaded front leg in current elite male english cricket fast bowlers

Patellar cartilage volume of the back leg versus the higher loaded front leg in current elite male english cricket fast bowler

Optineurin links myosin VI to the Golgi complex and is involved in Golgi organization and exocytosis.

Myosin VI plays a role in the maintenance of Golgi morphology and in exocytosis. In a yeast 2-hybrid screen we identified optineurin as a binding partner for myosin VI at the Golgi complex and confirmed this interaction in a range of protein interaction studies. Both proteins colocalize at the Golgi complex and in vesicles at the plasma membrane. When optineurin is depleted from cells using RNA interference, myosin VI is lost from the Golgi complex, the Golgi is fragmented and exocytosis of vesicular stomatitis virus G-protein to the plasma membrane is dramatically reduced. Two further binding partners for optineurin have been identified: huntingtin and Rab8. We show that myosin VI and Rab8 colocalize around the Golgi complex and in vesicles at the plasma membrane and overexpression of constitutively active Rab8-Q67L recruits myosin VI onto Rab8-positive structures. These results show that optineurin links myosin VI to the Golgi complex and plays a central role in Golgi ribbon formation and exocytosis