Simulation to track 3D location in GSM through NS2 and real life

In recent times the cost of mobile communication has dropped significantly leading to a dramatic increase in mobile phone usage. The widespread usage has led mobiles to emerge as a strong alternative for other applications one of which is tracking. This has enabled law-enforcing agencies to detect overspeeding vehicles and organizations to keep track its employees. The 3 major ways of tracking being employed presently are (a) via GPS [1] (b) signal attenuation property of a packet [3] and (c) using GSM Network [2]. The initial cost of GPS is very high resulting in low usage whereas (b) needs a very high precision measuring device. The paper presents a GSM-based tracking technique which eliminates the above mentioned overheads, implements it in NS2 and shows the limitations of the real life simulation. An accuracy of 97% was achieved during NS2 simulation which is comparable to the above mentioned alternate methods of tracking.Comment: 12 Pages, JGraph-Hoc Journa

Coordination of Mobile Mules via Facility Location Strategies

In this paper, we study the problem of wireless sensor network (WSN) maintenance using mobile entities called mules. The mules are deployed in the area of the WSN in such a way that would minimize the time it takes them to reach a failed sensor and fix it. The mules must constantly optimize their collective deployment to account for occupied mules. The objective is to define the optimal deployment and task allocation strategy for the mules, so that the sensors' downtime and the mules' traveling distance are minimized. Our solutions are inspired by research in the field of computational geometry and the design of our algorithms is based on state of the art approximation algorithms for the classical problem of facility location. Our empirical results demonstrate how cooperation enhances the team's performance, and indicate that a combination of k-Median based deployment with closest-available task allocation provides the best results in terms of minimizing the sensors' downtime but is inefficient in terms of the mules' travel distance. A k-Centroid based deployment produces good results in both criteria.Comment: 12 pages, 6 figures, conferenc

Facial Emotion Recognition

Emotion is a complex conscious that humans experience as a result of interactions with the environment. The project basically takes in the image, recognises the emotion by fragmenting the image with the deep learning technique using CNN. The tools and framework used here are keras and TensorFlow respectively. Here the facial feeling analysis refers to computing system that makes an attempt to mechanically analyse and recognise facial feeling and facial feature changes from visual data. The image being pre-processed helps for aiming a better quality of image and hence the emotion can be detected in a better way. This project can be used in many fields and one such field is mental health care centre. Patients with bipolar disorders should be treated by adhering the emotional behavior of patient and our project helps in doing the same

Patients' Experiences of "Long COVID" in the Community and Recommendations for Improving Services: A Quality Improvement Survey.

INTRODUCTION: "Long COVID" is a multisystem disease that lasts for 4 or more weeks following initial symptoms of COVID-19. In the UK, at least 10% of patient report symptoms at 12 weeks following a positive COVID-19 test. The aims of this quality improvement survey were to explore patients' acute and post-acute "long" COVID-19 symptoms, their experiences of community services and their recommendations for improving these services. METHODS: Seventy patients diagnosed with COVID were randomly selected from 2 large socially and ethnically diverse primary care practices. Of those contactable by telephone, 85% (41/48) agreed to participate in the quality improvement survey. They were interviewed by telephone using a semi-structured questionnaire about community services for COVID-19 patients. Interviews lasted 10 to 15 minutes. RESULTS: Forty-nine percent of patients reported at least 1 post-acute COVID-19 symptom. The most common were severe fatigue (45%), breathlessness (30%), neurocognitive difficulties (such as poor memory), poor concentration and "brain fog" (30%), headaches (20%), and joint pain (20%). Many patients felt isolated and fearful, with scant information about community resources and little safety netting advice. Patients also expected more from primary care with over half (56%) recommending regular phone calls and follow up from healthcare staff as the most important approach in their recovery. CONCLUSIONS: In line with patients' requests for more support, the practices now routinely refer patients with long COVID to an on-site social prescriber who explores how they are getting on, refers them to the GP or practice nurse when required, and sign posts them to support services in the community

Predicting Phenotypic Diversity and the Underlying Quantitative Molecular Transitions

During development, signaling networks control the formation of multicellular patterns. To what extent quantitative fluctuations in these complex networks may affect multicellular phenotype remains unclear. Here, we describe a computational approach to predict and analyze the phenotypic diversity that is accessible to a developmental signaling network. Applying this framework to vulval development in C. elegans, we demonstrate that quantitative changes in the regulatory network can render ~500 multicellular phenotypes. This phenotypic capacity is an order-of-magnitude below the theoretical upper limit for this system but yet is large enough to demonstrate that the system is not restricted to a select few outcomes. Using metrics to gauge the robustness of these phenotypes to parameter perturbations, we identify a select subset of novel phenotypes that are the most promising for experimental validation. In addition, our model calculations provide a layout of these phenotypes in network parameter space. Analyzing this landscape of multicellular phenotypes yielded two significant insights. First, we show that experimentally well-established mutant phenotypes may be rendered using non-canonical network perturbations. Second, we show that the predicted multicellular patterns include not only those observed in C. elegans, but also those occurring exclusively in other species of the Caenorhabditis genus. This result demonstrates that quantitative diversification of a common regulatory network is indeed demonstrably sufficient to generate the phenotypic differences observed across three major species within the Caenorhabditis genus. Using our computational framework, we systematically identify the quantitative changes that may have occurred in the regulatory network during the evolution of these species. Our model predictions show that significant phenotypic diversity may be sampled through quantitative variations in the regulatory network without overhauling the core network architecture. Furthermore, by comparing the predicted landscape of phenotypes to multicellular patterns that have been experimentally observed across multiple species, we systematically trace the quantitative regulatory changes that may have occurred during the evolution of the Caenorhabditis genus

Cysteine oxidation targets peroxiredoxins 1 and 2 for exosomal release through a novel mechanism of redox-dependent secretion

Non-classical protein secretion is of major importance as a number of cytokines and inflammatory mediators are secreted via this route. Current evidence indicates that there are several mechanistically distinct methods of non-classical secretion. We have recently shown that peroxiredoxin (Prdx) 1 and Prdx2 are released by various cells upon exposure to inflammatory stimuli such as LPS or TNF-α. The released Prdx then acts to induce production of inflammatory cytokines. However, Prdx1 and 2 do not have signal peptides and therefore must be secreted by alternative mechanisms as has been postulated for the inflammatory mediators IL-1β and HMGB1. We show here that circulating Prdx1 and 2 are present exclusively as disulphide-linked homodimers. Inflammatory stimuli also induce in vitro release of Prdx1 and 2 as disulfide-linked homodimers. Mutation of cysteines Cys51 or Cys172 (but not Cys70) in Prdx2, and Cys52 or Cys173 (but not Cys71 or Cys83) in Prdx1 prevented dimer formation and this was associated with inhibition of their TNF-α-induced release. Thus, the presence and oxidation of key cysteine residues in these proteins are a prerequisite for their secretion in response to TNF-α and this release can be induced with an oxidant. In contrast, the secretion of the nuclear-associated danger signal HMGB1 is independent of cysteine oxidation, as shown by experiments with a cysteine-free HMGB1 mutant. Release of Prdx1 and 2 is not prevented by inhibitors of the classical secretory pathway; instead, both Prdx1 and 2 are released in exosomes from both HEK cells and monocytic cells. Serum Prdx1 and 2 are also associated with the exosomes. These results describe a novel pathway of protein secretion mediated by cysteine oxidation that underlines the importance of redox-dependent signalling mechanisms in inflammation

Increased capsaicin receptor TRPV1 in skin nerve fibres and related vanilloid receptors TRPV3 and TRPV4 in keratinocytes in human breast pain

BACKGROUND: Breast pain and tenderness affects 70% of women at some time. These symptoms have been attributed to stretching of the nerves with increase in breast size, but tissue mechanisms are poorly understood. METHODS: Eighteen patients (n = 12 breast reduction and n = 6 breast reconstruction) were recruited and assessed for breast pain by clinical questionnaire. Breast skin biopsies from each patient were examined using immunohistological methods with specific antibodies to the capsaicin receptor TRPV1, related vanilloid thermoreceptors TRPV3 and TRPV4, and nerve growth factor (NGF). RESULTS: TRPV1-positive intra-epidermal nerve fibres were significantly increased in patients with breast pain and tenderness (TRPV1 fibres / mm epidermis, median [range] – no pain group, n = 8, 0.69 [0–1.27]; pain group, n = 10, 2.15 [0.77–4.38]; p = 0.0009). Nerve Growth Factor, which up-regulates TRPV1 and induces nerve sprouting, was present basal keratinocytes: some breast pain specimens also showed NGF staining in supra-basal keratinocytes. TRPV4-immunoreactive fibres were present in sub-epidermis but not significantly changed in painful breast tissue. Both TRPV3 and TRPV4 were significantly increased in keratinocytes in breast pain tissues; TRPV3, median [range] – no pain group, n = 6, 0.75 [0–2]; pain group, n = 11, 2 [1-3], p = 0.008; TRPV4, median [range] – no pain group, n = 6, [0–1]; pain group, n = 11, 1 [0.5–2], p = 0.014). CONCLUSION: Increased TRPV1 intra-epidermal nerve fibres could represent collateral sprouts, or re-innervation following nerve stretch and damage by polymodal nociceptors. Selective TRPV1-blockers may provide new therapy in breast pain. The role of TRPV3 and TRPV4 changes in keratinocytes deserve further study

Aurora kinase A drives the evolution of resistance to third-generation EGFR inhibitors in lung cancer.

Although targeted therapies often elicit profound initial patient responses, these effects are transient due to residual disease leading to acquired resistance. How tumors transition between drug responsiveness, tolerance and resistance, especially in the absence of preexisting subclones, remains unclear. In epidermal growth factor receptor (EGFR)-mutant lung adenocarcinoma cells, we demonstrate that residual disease and acquired resistance in response to EGFR inhibitors requires Aurora kinase A (AURKA) activity. Nongenetic resistance through the activation of AURKA by its coactivator TPX2 emerges in response to chronic EGFR inhibition where it mitigates drug-induced apoptosis. Aurora kinase inhibitors suppress this adaptive survival program, increasing the magnitude and duration of EGFR inhibitor response in preclinical models. Treatment-induced activation of AURKA is associated with resistance to EGFR inhibitors in vitro, in vivo and in most individuals with EGFR-mutant lung adenocarcinoma. These findings delineate a molecular path whereby drug resistance emerges from drug-tolerant cells and unveils a synthetic lethal strategy for enhancing responses to EGFR inhibitors by suppressing AURKA-driven residual disease and acquired resistance

Treatment of two postoperative endophthalmitis cases due to Aspergillus flavus and Scopulariopsis spp. with local and systemic antifungal therapy

<p>Abstract</p> <p>Background</p> <p>Endophthalmitis is the inflammatory response to invasion of the eye with bacteria or fungi. The incidence of endophthalmitis after cataract surgery varies between 0.072–0.13 percent. Treatment of endophthalmitis with fungal etiology is difficult.</p> <p>Case Presentation</p> <p><b>Case 1: </b>A 71-year old male diabetic patient developed postoperative endophthalmitis due to <it>Aspergillus flavus</it>. The patient was treated with topical amphotericin B ophthalmic solution, intravenous (IV) liposomal amphotericin-B and caspofungin following vitrectomy.</p> <p><b>Case 2: </b>A 72-year old male cachectic patient developed postoperative endophthalmitis due to <it>Scopulariopsis </it>spp. The patient was treated with topical and IV voriconazole and caspofungin.</p> <p>Conclusion</p> <p><it>Aspergillus </it>spp. are responsible of postoperative fungal endophthalmitis. Endophthalmitis caused by <it>Scopulariopsis </it>spp. is a very rare condition. The two cases were successfully treated with local and systemic antifungal therapy.</p

Gram Negative Bacteria Are Associated with the Early Stages of Necrotizing Enterocolitis

Introduction: Necrotizing enterocolitis (NEC) affects 5–10 % of infants born weighing less than 1500 g. Most models of NEC recapitulate late-stage disease with gut necrosis and elevated inflammatory mediators. Evaluation of NEC at earlier, less lethal stages of disease will allow investigation of initial disease triggers and may advance our understanding of temporal relationships between factors implicated in NEC pathogenesis. In this manuscript, we describe our investigation of early NEC and test the hypothesis that bacteria and inflammatory mediators differ between animals with early NEC and disease fre