259 research outputs found
Cryoglobulinemic vasculitis
No full textCryoglobulinemic vasculitis is a small- and medium-sized vasculitis characterized by immune complex deposition in various tissues. Cryoglobulins (CGs) are cold precipitable immunoglobulins that redissolve upon heating. Causes of cryoglobulinemia include infections with hepatitis C virus as the leading cause, autoimmune diseases, and lymphoproliferative disorders. Many mechanisms contribute to its pathogenesis, among which there are roles for microorganisms with their molecular mimicry, the rheumatoid factor, and host gene mutations. Other factors reported include adaptive and innate immunity dysregulation, epigenetics, as well as the physicochemical properties of cryoglobulins like hyperviscosity and self-aggregation in type І CG. Clinical manifestations are attributed to hyperviscosity in the monoclonal type І. The mixed types II, III can have cutaneous, musculoskeletal, neurological, renal, cardio-pulmonary, and other organ manifestations. There is an increased risk of malignancy with non-Hodgkin lymphoma being the classical complication. The differential diagnosis includes a wide array of disease entities that need to be considered. Diagnosis requires many modalities: laboratory, imaging, and microscopic. Treatment should be tailored based on disease severity and the underlying cause. Following the successful introduction of direct-acting anti-HCV drugs, autoimmune and lymphoproliferative disorders substituted HCV as the leading cause of CGs. Relapse of Cryoglobulinemic vasculitis was however reported following successful virus eradication
Network Boundary Identification using Local Information
No full textDetection of nodes on the network boundary is necessary for correct operation in many wireless applications. Many virtual coordinate constructions rely on the furthest set of nodes as beacons, and sensing applications may find useful the knowledge of the network edge. In this paper we propose local convex view (lcv) as a means to identify nodes close to the network edge. It is based on the idea that -hulls can capture the shape of a set of points, and motivated by the hypothesis that some structural information relevant to the network is buried within view of many nodes. The lcv differs from most previous methods in that it is a localized algorithm. Nodes using lcv establish neighbourhood coordinates where no location information is available a priori. In those cases where needed information is missing, we adopt a simple probabilistic model to decide the boundary status of a node. We identify two metrics for evaluation, and compare via simulation the performance of lcv against two methods with similar properties. In our experiments we find lcv to be consistent in its performance, and resilient to the impediments facing other methods
Autoinflammatory diseases and the kidney
No full textThe kidney represents an important target of systemic inflammation. Its involvement in monogenic and multifactorial autoinflammatory diseases (AIDs) vary from peculiar and relatively frequent manifestations to some rare but severe features that may end up requiring transplantation. The pathogenetic background is also very heterogeneous ranging from amyloidosis to non-amyloid related damage rooted in inflammasome activation. Kidney involvement in monogenic and polygenic AIDs may present as renal amyloidosis, IgA nephropathy, and more rarely as various forms of glomerulonephritis (GN), namely segmental glomerulosclerosis, collapsing glomerulopathy, fibrillar, or membranoproliferative GN. Vascular disorders such as thrombosis or renal aneurysms and pseudoaneurysms may be encountered in patients with Behcet’s disease. Patients with AIDs should be routinely assessed for renal involvement. Screening with urinalysis, serum creatinine, 24-h urinary protein, microhematuria, and imaging studies should be carried out for early diagnosis. Awareness of drug-induced nephrotoxicity, drug-drug interactions as well as addressing the issue of proper renal adjustment of drug doses deserve a special mention and should always be considered when dealing with patients affected by AIDs. Finally, we will explore the role of IL-1 inhibitors in AIDs patients with renal involvement. Targeting IL-1 may indeed have the potential to successfully manage kidney disease and improve long-term prognosis of AIDs patients
Localised alpha-shape computations for boundary recognition in sensor networks
No full textIntuitively, many wireless and sensing applications benefit from knowledge of network boundaries. Many virtual coordinate constructions rely on the furthest set of nodes as beacons. Network edges may also bound routing holes in the network, regions of failure due to environmental effects, or indicate the need for additional deployment. In this paper we solve the edge detection problem locally using a geometric structure called the alpha-shape (αα-shape). For a disc of radius 1/α1/α, the αα-shape consists of nodes (and joining edges) that sit on the boundary of the discs that contain no other nodes in the network. In the simplest terms a node decides it is on a network boundary by asking the following question: "Do I sit on the boundary of a disc of radius 1/α1/α that contains no other nodes in the network?" We show that using only local communications our algorithm is provably correct. Boundary nodes may further participate to reduce unwanted detail. We show via simulation that our algorithm identifies meaningful boundaries even in networks of low-density and non-uniform distribution
An Analysis of Planarity in Face-Routing
No full textIn this report we investigate the limits of routing according to left- or right-hand rule (LHR). Using LHR, a node upon receipt of a message will forward to the neighbour that sits next in counter-clockwise order in the network graph. When used to recover from greedy routing failures, LHR guarantees success if implemented over planar graphs. This is often referred to as face or geographic routing. In the current body of knowledge it is known that if planarity is violated then LHR is guaranteed only to eventually return to the point of origin. Our work seeks to understand why a non-planar environment stops LHR from making delivery guarantees. Our investigation begins with an analysis to enumerate all node con gurations that cause intersections. A trace over each con guration reveals that LHR is able to recover from all but a single case, the `umbrella' con guration so named for its appearance. We use this information to propose the Prohibitive Link Detection Protocol (PDLP) that can guarantee delivery over non-planar graphs using standard face-routing techniques. As the name implies, the protocol detects and circumvents the `bad' links that hamper LHR. The goal of this work is to maintain routing guarantees while disturbing the network graph as little as possible. In doing so, a new starting point emerges from which to build rich distributed protocols in the spirit of protocols such as CLDP and GDSTR
Prohibitive-link Detection and Routing Protocol
No full textIn this paper we investigate the limits of routing according to left- or righthand rule (LHR). Using LHR, a node upon receipt of a message will forward to the neighbour that sits next in counter-clockwise order in the network graph. When used to recover from greedy routing failures, LHR guarantees success if implemented over planar graphs. We note, however, that if planarity is violated then LHR is only guaranteed to eventually return to the point of origin. Our work seeks to understand why. An enumeration and analysis of possible intersections leads us to propose the Prohibitive-link Detection and Routing Protocol (PDRP) that can guarantee delivery over non-planar graphs. As the name implies, the protocol detects and circumvents the ‘bad' links that hamper LHR. Our implementation of PDRP in TinyOS reveals the same level of service as face-routing protocols despite preserving most intersecting links in the network
The smart safety Shoe: A new type of safety shoe that helps prevent lower back problems and opens the door to a new era of preventive safety footwear
No full textThe smart safety shoe is a concept safety shoe that has been in development as a collaboration between Allshoes safety footwear and TU Delft since 2020. Previous work on the shoe consisted of 2 graduation projects and a student course which resulted in the current concept of an injury preventing safety shoe focused on preventing lower back pain in the logistics sector. The shoe works by using pressure sensors and machine learning to detect unhealthy postures while its wearer has to lift various objects as part of their job (manual handling). This project focused on further developing the concept of the smart safety shoe and evaluating the prototypes from the last two projects. Previous projects provided two different pressure sensor layouts which are evaluated using a high-end pressure sensing insole. A manual handling experiment was set up and performed on 16 different participants from a lab and a warehouse. During testing participants were instructed to perform manual handling while holding 5 different postures. It was possible to train a machine learning model using the various pressure profiles gathered from the experiment. Using this model, the two sensor layouts from the previous projects were evaluated for their ability to detect the 5 predetermined postures. It was found that the latest layout outperformed the previous one and was therefore selected for further development of the smart safety shoe.The integration of various other sensors and actuators was evaluated, and the core functions of the shoe were defined with an indication towards future improvements of the smart safety shoe.The shoe has now been publicly presented by Allshoes and the goal is to have the product on the market by the end of 2025. In order for this to happen further prototyping is needed to create an improved machine learning model based on the selected sensor layout. The shoe shows promising responses from current safety shoe clients. When finally launched it will be part of a new type of protective equipment focused on prevention.Design for Interactio
Erythropoietin mitigated thioacetamide-induced renal injury via JAK2/STAT5 and AMPK pathway
No full textThe kidney flushes out toxic substances and metabolic waste products, and homeostasis is maintained owing to the kidney efforts. Unfortunately, kidney disease is one of the illnesses with a poor prognosis and a high death rate. The current investigation was set out to assess erythropoietin (EPO) potential therapeutic benefits against thioacetamide (TAA)-induced kidney injury in rats. EPO treatment improved kidney functions, ameliorated serum urea, creatinine, and malondialdehyde, increased renal levels of reduced glutathione, and slowed the rise of JAK2, STAT5, AMPK, and their phosphorylated forms induced by TAA. EPO treatment also greatly suppressed JAK2, Phosphatidylinositol 3-kinases, and The Protein Kinase R-like ER Kinase gene expressions and mitigated the histopathological alterations brought on by TAA toxicity. EPO antioxidant and anti-inflammatory properties protected TAA-damaged kidneys. EPO regulates AMPK, JAK2/STAT5, and pro-inflammatory mediator synthesis
Renoprotective Effect of Pitavastatin against TAA-Induced Renal Injury: Involvement of the miR-93/PTEN/AKT/mTOR Pathway
No full textThis research investigated if pitavastatin (Pita) might protect rats' kidneys against thioacetamide (TAA). By altering the PTEN/AKT/mTOR pathway, pitavastatin may boost kidney antioxidant capacity and minimize oxidative damage. Statins have several benefits, including antioxidant and anti-inflammatory characteristics. The principal hypothesis of this study was that Pita can regulate the miR-93/PTEN/AKT/mTOR pathways, which is thought to be responsible for its renoprotective effects. The experiment divided male rats into four groups. Group 1 included untreated rats as the control. Group 2 included rats which received TAA (100 mg/kg intraperitoneally thrice a week for two weeks) to destroy their kidneys. Groups 3 and 4 included rats which received Pita orally at 0.4 and 0.8 mg/kg for 14 days after TAA injections. Renal injury increased BUN, creatinine, and MDA levels and decreased glutathione (GSH) levels. Pitavastatin prevented these alterations. TAA decreased PTEN and increased miR-93, Akt, p-Akt, mTOR, and Stat3 in the kidneys. Pitavastatin also regulated the associated culprit pathway, miR-93/PTEN/Akt/mTOR. In addition, TAA induced adverse effects on the kidney tissue, which were significantly ameliorated by pitavastatin treatment. The findings suggest that pitavastatin can attenuate renal injury, likely by regulating the miR-93/PTEN/Akt/mTOR pathway. This modulation of the pathway appears to contribute to the protective effects of pitavastatin against TAA-induced renal injury, adding to the growing evidence of the pleiotropic benefits of statins in renal health
Erythropoietin Suppresses the Hepatic Fibrosis Caused by Thioacetamide: Role of the PI3K/Akt and TLR4 Signaling Pathways
No full textErythropoietin (EPO) is recognized for its function in erythropoiesis; however, its potential antifibrotic effect against liver fibrosis remains unknown. This study examined whether EPO affects thioacetamide (TAA)-induced liver fibrosis by concentrating on the Toll-like receptor 4 (TLR4) cascade and the phosphatidylinositol 3-kinase (PI3K)/Akt pathway as possible pathways. Male Wistar rats were randomized into four groups, which included: the negative control group, the TAA group (intraperitoneal; TAA 100 mg/kg three times per week for 2 weeks), and EPO-treated groups (150 and 300 IU/kg, i.p.) for 2 weeks after TAA injections. EPO attenuated hepatic fibrosis in a dosage-dependent way, as manifested by the diminution in serum alanine aminotransferase and aspartate aminotransferase activities, as well as the increase in albumin level. EPO inhibited the increase in tissue levels of tumor necrosis factors-α, interleukin-1β, transforming growth factor-β1, and TLR4 and raised tissue levels of PI3K and p-PI3K. EPO antioxidant properties were demonstrated by restoring hepatic glutathione and superoxide dismutase by preventing the accumulation of hepatic malondialdehyde. Further, EPO increased the protein expression of PI3K and Akt and decreased TLR4 protein expression. Immunohistochemically, EPO treatment altered tissue histology and downregulated mitogen-activated protein kinase protein expression. Overall, the research suggested that EPO could prevent TAA-induced hepatic fibrosis through upregulating the PI3K/Akt signaling cascade and downregulation the TLR4 downstream axis
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