The Persistent Issue of Fraud in the Public Housing Sector across the United States

The public housing sector and the idea of providing those who need assistance with housing has been around since President Ronald Reagan’s days and even before that, with the New York Housing Act of 1879 (Martens, 2009), when industrial workers faced wretched housing conditions. Public housing in this nation has grown from just being provided for industrial workers and their families in major cities, such as New York and Chicago, to what it is today. Today, public housing is present all across the nation and is found in every state from Indiana to Maryland to California, Florida, Oklahoma, all over. Public housing can be available in very large cities and in smaller towns.Kayla SiddellHonors DiplomaHonors CollegeCunningham Memorial Library, Terre Haute, Indiana State UniversityUndergraduateTitle from document title page. Document formatted into pages: 25

Platelet activation in trauma and other inflammatory conditions

Platelets play critical roles in thrombosis, inflammation, and wound healing, which are essential in response to trauma. These processes are primarily driven through the immunoreceptor tyrosine-based activation motif (ITAM)-containing receptors, glycoprotein VI (GPVI) and C-type lectin-like receptor 2 (CLEC-2). This study aimed to investigate; (i) the effects of Alarmins released following trauma on platelet reactivity and the mechanisms involved; (ii) establish whether soluble GPVI (sGPVI), a platelet activation marker is elevated in trauma and other inflammatory conditions; (iii) determine whether the CLEC-2 ligand, podoplanin, is elevated in inflammatory conditions and (iv) establishing the role of GPVI and platelets in cutaneous wound healing. The nuclear-related Alarmin, histones, induced robust platelet activation both in vitro and in vivo. Histone-induced platelet activation was mediated through GPVI in vitro However, this pathway was found not to underlie histone-induced lowering of platelet count in vivo and is most likely to result from mediators released following vascular damage. GPVI shedding was shown to be induced following activation by thrombin, through a pathway dependent on fibrin generation. sGPVI was found to be a marker for platelet activation during a variety of inflammatory disorders, notably in association with sepsis. Furthermore, GPVI shedding reflects platelet activation by collagen and potentially thrombin-induced fibrin generation

Quantifying Embolism: Label-Free Volumetric Mapping of Thrombus Structure and Kinesis in a Microfluidic System with Optical Holography

Embolization of thrombotic material may lead to acute events such as ischemia and myocardial infarction. The embolus is the physical detachment from a primary thrombus that has developed under fluid shear rates. The physical characteristics (surface area coverage, volume, mass, and packing density) of a thrombus influence the overall flow dynamics of an occluding blood vessel. Here, the effectiveness of holographic quantitative phase microscopy (QPM) in identifying multiple morphological parameters of a thrombus (volume, surface area, and height) formed over collagen‐coated microfluidic channels by exerting a range of shear rates with anticoagulated platelet‐rich plasma (PRP) and whole blood is demonstrated. QPM enables the recording of entire thrombus volumes in real‐time using PRP and observed both growth and contraction trends of thrombi, without need for biochemical labeling. The process of emboli detachment in a microfluidic channel under pathophysiological shear rates (7500 and 12 500 s−1) is quantified. Rapid and direct quantification of an embolizing thrombus can enable the study of events during undesirable vessel occlusion and lead to targeting and early diagnosis of acute coronary and venous events.The authors received funding from the National Health and Medical Research Council of Australia and the Australian Research Council

High contrast imaging and flexible photomanipulation for quantitative in vivo multiphoton imaging with polygon scanning microscope

In this study, we introduce two key improvements that overcome limitations of existing polygon scanning microscopes while maintaining high spatial and temporal imaging resolution over large field of view (FOV). First, we proposed a simple and straightforward means to control the scanning angle of the polygon mirror to carry out photomanipulation without resorting to high speed optical modulators. Second, we devised a flexible data sampling method directly leading to higher image contrast by over 2‐fold and digital images with 100 megapixels (10 240 × 10 240) per frame at 0.25 Hz. This generates sub‐diffraction limited pixels (60 nm per pixels over the FOV of 512 μm) which increases the degrees of freedom to extract signals computationally. The unique combined optical and digital control recorded fine fluorescence recovery after localized photobleaching (r ~10 μm) within fluorescent giant unilamellar vesicles and micro‐vascular dynamics after laser‐induced injury during thrombus formation in vivo. These new improvements expand the quantitative biological‐imaging capacity of any polygon scanning microscope system.Australian Research Council, Grant/Award Number: DE16010084

Fibrin exposure triggers αIIbβ3-independent platelet aggregate formation, ADAM10 activity and glycoprotein VI shedding in a charge-dependent manner

Background Collagen and fibrin engagement and activation of glycoprotein (GP) VI induces proteolytic cleavage of the GPVI ectodomain generating shed soluble GPVI (sGPVI). Collagen‐mediated GPVI shedding requires intracellular signalling to release the sGPVI, mediated by A Disintegrin And Metalloproteinase 10 (ADAM10); however, the precise mechanism by which fibrin induces GPVI shedding remains elusive. Plasma sGPVI levels are elevated in patients with coagulopathies, sepsis, or inflammation and can predict onset of sepsis and sepsis‐related mortality; therefore, it is clinically important to understand the mechanisms of GPVI shedding under conditions of minimal collagen exposure. Objectives Our aim was to characterize mechanisms by which fibrin‐GPVI interactions trigger GPVI shedding. Methods Platelet aggregometry, sGPVI ELISA, and an ADAM10 fluorescence resonance energy transfer assay were used to measure fibrin‐mediated platelet responses. Results Fibrin induced αIIbβ3‐independent washed platelet aggregate formation, GPVI shedding, and increased ADAM10 activity, all of which were insensitive to pre‐treatment with inhibitors of Src family kinases but were divalent cation‐ and metalloproteinase‐dependent. In contrast, treatment of washed platelets with other GPVI ligands, collagen, and collagen‐related peptide caused αIIbβ3‐dependent platelet aggregation and GPVI release but did not increase constitutive ADAM10 activity. Conclusions Fibrin engages GPVI in a manner that differs from other GPVI ligands. Inclusion of polyanionic molecules disrupted fibrin‐induced platelet aggregate formation and sGPVI release, suggesting that electrostatic charge may play a role in fibrin/GPVI engagement. It may be feasible to exploit this property and specifically disrupt GPVI/fibrin interactions whilst sparing GPVI/collagen engagement.Fibrin engages GPVI in a manner that differs from other GPVI ligands. Inclusion of polyanionic molecules disrupted fibrin‐induced platelet aggregate formation and sGPVI release, suggesting that electrostatic charge may play a role in fibrin/GPVI engagement. It may be feasible to exploit this property and specifically disrupt GPVI/fibrin interactions whilst sparing GPVI/collagen engagement.National Health and Medical Research Council of Australia; Australian Research Council; THANZ Science and Education Research Gran