Differential Evolution Algorithm with Diversified Vicinity Operator for Optimal Routing and Clustering of Energy Efficient Wireless Sensor Networks

Due to large dimension of clusters and increasing size of sensor nodes, finding the optimal route and cluster for large wireless sensor networks (WSN) seems to be highly complex and cumbersome. This paper proposes a new method to determine a reasonably better solution of the clustering and routing problem with the highest concern of efficient energy consumption of the sensor nodes for extending network life time. The proposed method is based on the Differential Evolution (DE) algorithm with an improvised search operator called Diversified Vicinity Procedure (DVP), which models a trade-off between energy consumption of the cluster heads and delay in forwarding the data packets. The obtained route using the proposed method from all the gateways to the base station is comparatively lesser in overall distance with less number of data forwards. Extensive numerical experiments demonstrate the superiority of the proposed method in managing energy consumption of the WSN and the results are compared with the other algorithms reported in the literature

Filaggrin inhibits generation of CD1a neolipid antigens by house dust mite-derived phospholipase.

Atopic dermatitis is a common pruritic skin disease in which barrier dysfunction and cutaneous inflammation play a role in pathogenesis. Mechanisms underlying the associated inflammation are not fully understood, and while CD1a-expressing Langerhans cells are known to be enriched within lesions, their role in clinical disease pathogenesis has not been studied. Here we observed that house dust mite (HDM) generates neolipid antigens for presentation by CD1a to T cells in the blood and skin lesions of affected individuals. HDM-responsive CD1a-reactive T cells increased in frequency after birth and showed rapid effector function, consistent with antigen-driven maturation. To define the underlying mechanisms, we analyzed HDM-challenged human skin and observed allergen-derived phospholipase (PLA2) activity in vivo. CD1a-reactive T cell activation was dependent on HDM-derived PLA2 and such cells infiltrated the skin after allergen challenge. Filaggrin insufficiency is associated with atopic dermatitis, and we observed that filaggrin inhibits PLA2 activity and inhibits CD1a-reactive PLA2-generated neolipid-specific T cell activity from skin and blood. The most widely used classification schemes of hypersensitivity, such as Gell and Coombs are predicated on the idea that non-peptide stimulants of T cells act as haptens that modify peptides or proteins. However our results point to a broader model that does not posit haptenation, but instead shows that HDM proteins generate neolipid antigens which directly activate T cells. Specifically, the data identify a pathway of atopic skin inflammation, in which house dust mite-derived phospholipase A2 generates antigenic neolipids for presentation to CD1a-reactive T cells, and define PLA2 inhibition as a function of filaggrin, supporting PLA2 inhibition as a therapeutic approach

The role of CD1a-restricted T cells and phospholipase in allergic disease

The skin is an important barrier against a range of different environmental challenges. The skin associated immune system is able to detect breaks in the barrier to initiate a protective immune response. Langerhans cells express a high density of CD1a, which presents lipid antigens to T-cells. However little is known about CD1a-restricted lipid antigens and the role of CD1a-restricted T-cells in inflammatory skin disease. In order to investigate the role of T-cells that react to CD1a presenting lipid in skin disease, wasp and bee venom were studied as an antigen source. Venoms are able to cause allergic hypersensitivity reactions, associated with skin T-cell infiltration, a venom protein-specific T-cell response in allergic individuals and are independent of filaggrin. Using primary antigen presenting cells and target cells lacking surface MHC expression (K562 cells) transfected with CD1a, allowed investigation of polyclonal T-cells responses from unrelated donors. Bee and wasp venoms were shown to induce CD1a-restricted T-cell responses in both peripheral blood and skin. Surprisingly this activity was not contained within the lipid fraction of the venoms, but instead was mediated through the generation of a lipid ligand by venom phospholipase. Furthermore, wasp venom delivery results in the production of phospholipase products in the skin of humans. A significantly increased frequency of IFN-, GM-CSF- and IL-13-producing venom specific CD1a-restricted T-cells was observed in allergic individuals compared to healthy controls. During subcutaneous immunotherapy, frequencies of CD1a-reactive T cells were initially induced, peaking by weeks 5, but then reduced despite escalation of antigen dose. CD1a-reactive T cells were further investigated to characterise their physiological role by generating T cell lines which produced a range of different cytokines, including IL-22 on stimulation with phospholipase and other phospholipase containing allergens. In summary, we identified a novel pathway of skin inflammation where lipids generated by allergen-derived phospholipase can be recognised by CD1a-restricted T cells which produce type 1 and type 2 cytokines and associate with allergic reactivity. These findings have implications for novel therapeutic strategies for allergic disease.</p

The role of CD1a-restricted T cells and phospholipase in allergic disease

The skin is an important barrier against a range of different environmental challenges. The skin associated immune system is able to detect breaks in the barrier to initiate a protective immune response. Langerhans cells express a high density of CD1a, which presents lipid antigens to T-cells. However little is known about CD1a-restricted lipid antigens and the role of CD1a-restricted T-cells in inflammatory skin disease. In order to investigate the role of T-cells that react to CD1a presenting lipid in skin disease, wasp and bee venom were studied as an antigen source. Venoms are able to cause allergic hypersensitivity reactions, associated with skin T-cell infiltration, a venom protein-specific T-cell response in allergic individuals and are independent of filaggrin. Using primary antigen presenting cells and target cells lacking surface MHC expression (K562 cells) transfected with CD1a, allowed investigation of polyclonal T-cells responses from unrelated donors. Bee and wasp venoms were shown to induce CD1a-restricted T-cell responses in both peripheral blood and skin. Surprisingly this activity was not contained within the lipid fraction of the venoms, but instead was mediated through the generation of a lipid ligand by venom phospholipase. Furthermore, wasp venom delivery results in the production of phospholipase products in the skin of humans. A significantly increased frequency of IFNï§-, GM-CSF- and IL-13-producing venom specific CD1a-restricted T-cells was observed in allergic individuals compared to healthy controls. During subcutaneous immunotherapy, frequencies of CD1a-reactive T cells were initially induced, peaking by weeks 5, but then reduced despite escalation of antigen dose. CD1a-reactive T cells were further investigated to characterise their physiological role by generating T cell lines which produced a range of different cytokines, including IL-22 on stimulation with phospholipase and other phospholipase containing allergens. In summary, we identified a novel pathway of skin inflammation where lipids generated by allergen-derived phospholipase can be recognised by CD1a-restricted T cells which produce type 1 and type 2 cytokines and associate with allergic reactivity. These findings have implications for novel therapeutic strategies for allergic disease.</p

Diagnosis of Cervical Cancer based on Ensemble Deep Learning Network using Colposcopy Images

Traditional screening of cervical cancer type classification majorly depends on the pathologist’s experience, which also has less accuracy. Colposcopy is a critical component of cervical cancer prevention. In conjunction with precancer screening and treatment, colposcopy has played an essential role in lowering the incidence and mortality from cervical cancer over the last 50 years. However, due to the increase in workload, vision screening causes misdiagnosis and low diagnostic efficiency. Medical image processing using the convolutional neural network (CNN) model shows its superiority for the classification of cervical cancer type in the field of deep learning. This paper proposes two deep learning CNN architectures to detect cervical cancer using the colposcopy images; one is the VGG19 (TL) model, and the other is CYENET. In the CNN architecture, VGG19 is adopted as a transfer learning for the studies. A new model is developed and termed as the Colposcopy Ensemble Network (CYENET) to classify cervical cancers from colposcopy images automatically. The accuracy, specificity, and sensitivity are estimated for the developed model. The classification accuracy for VGG19 was 73.3%. Relatively satisfied results are obtained for VGG19 (TL). From the kappa score of the VGG19 model, we can interpret that it comes under the category of moderate classification. The experimental results show that the proposed CYENET exhibited high sensitivity, specificity, and kappa scores of 92.4%, 96.2%, and 88%, respectively. The classification accuracy of the CYENET model is improved as 92.3%, which is 19% higher than the VGG19 (TL) model

Bee venom processes human skin lipids for presentation by CD1a.

Venoms frequently co-opt host immune responses, so study of their mode of action can provide insight into novel inflammatory pathways. Using bee and wasp venom responses as a model system, we investigated whether venoms contain CD1-presented antigens. Here, we show that venoms activate human T cells via CD1a proteins. Whereas CD1 proteins typically present lipids, chromatographic separation of venoms unexpectedly showed that stimulatory factors partition into protein-containing fractions. This finding was explained by demonstrating that bee venom-derived phospholipase A2 (PLA2) activates T cells through generation of small neoantigens, such as free fatty acids and lysophospholipids, from common phosphodiacylglycerides. Patient studies showed that injected PLA2 generates lysophospholipids within human skin in vivo, and polyclonal T cell responses are dependent on CD1a protein and PLA2. These findings support a previously unknown skin immune response based on T cell recognition of CD1a proteins and lipid neoantigen generated in vivo by phospholipases. The findings have implications for skin barrier sensing by T cells and mechanisms underlying phospholipase-dependent inflammatory skin disease

Bee venom processes human skin lipids for presentation by CD1a

Venoms frequently co-opt host immune responses, so study of their mode of action can provide insight into novel inflammatory pathways. Using bee and wasp venom responses as a model system, we investigated whether venoms contain CD1-presented antigens. Here, we show that venoms activate human T cells via CD1a proteins. Whereas CD1 proteins typically present lipids, chromatographic separation of venoms unexpectedly showed that stimulatory factors partition into protein-containing fractions. This finding was explained by demonstrating that bee venom–derived phospholipase A2 (PLA2) activates T cells through generation of small neoantigens, such as free fatty acids and lysophospholipids, from common phosphodiacylglycerides. Patient studies showed that injected PLA2 generates lysophospholipids within human skin in vivo, and polyclonal T cell responses are dependent on CD1a protein and PLA2. These findings support a previously unknown skin immune response based on T cell recognition of CD1a proteins and lipid neoantigen generated in vivo by phospholipases. The findings have implications for skin barrier sensing by T cells and mechanisms underlying phospholipase-dependent inflammatory skin disease