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Copyright of Przegląd Elektrotechniczny is the property of Przeglad Elektrotechniczny and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Summary: Background: The outbreak of chilblain‐like lesions (CLL) during the COVID‐19 pandemic has been reported extensively, potentially related to SARS‐CoV‐2 infection, yet its underlying pathophysiology is unclear. Objectives: To study skin and blood endothelial and immune system activation in CLL in comparison with healthy controls and seasonal chilblains (SC), defined as cold‐induced sporadic chilblains occurring during 2015 and 2019 with exclusion of chilblain lupus. Methods: This observational study was conducted during 9–16 April 2020 at Saint‐Louis Hospital, Paris, France. All patients referred with CLL seen during this period of the COVID‐19 pandemic were included in this study. We excluded patients with a history of chilblains or chilblain lupus. Fifty patients were included. Results: Histological patterns were similar and transcriptomic signatures overlapped in both the CLL and SC groups, with type I interferon polarization and a cytotoxic–natural killer gene signature. CLL were characterized by higher IgA tissue deposition and more significant transcriptomic activation of complement and angiogenesis factors compared with SC. We observed in CLL a systemic immune response associated with IgA antineutrophil cytoplasmic antibodies in 73% of patients, and elevated type I interferon blood signature in comparison with healthy controls. Finally, using blood biomarkers related to endothelial dysfunction and activation, and to angiogenesis or endothelial progenitor cell mobilization, we confirmed endothelial dysfunction in CLL. Conclusions: Our findings support an activation loop in the skin in CLL associated with endothelial alteration and immune infiltration of cytotoxic and type I IFN‐polarized cells leading to clinical manifestations. What is already known about this topic?Chilblain‐like lesions have been reported during the COVID‐19 pandemic.They are associated with systemic type I interferon polarization, but the precise pathophysiology is still unclear. What does this study add?We demonstrate cutaneous and systemic immune activation and vascular alteration.Histological patterns were similar and transcriptomic signatures overlapped in chilblain‐like lesions and a comparator group with seasonal chilblains.A systemic immune response was associated with high prevalence of IgA antineutrophil cytoplasmic antibodies and an elevated type I interferon signature.We confirmed endothelial dysfunction in chilblain‐like lesions. What is the translational message?Chilblain‐like lesions and seasonal chilblains seem to share a common pathophysiology.The strong type I interferon response can be explained by a viral trigger.Similar endothelial dysfunctions have been described during mild COVID‐19.Local or systemic anti‐inflammatory treatment could reverse cutaneous manifestations. Linked Comment: S.M. Pilkington and R.E.B. Watson. Br J Dermatol 2021; 185:1090–1091. Plain language summary available online [ABSTRACT FROM AUTHOR]

GLO:F03/01dec21:bjd20647-toc-0001.jpg PHOTO (COLOR): . gl Dear Editor, A range of cutaneous manifestations have been described in association with SARS-CoV-2 infection during the COVID-19 pandemic.1 Among them, chilblain-like lesions (CLL) occurred more frequently than expected. Moreover, specific T-cell response has been less studied, but it has recently been shown that when asymptomatic, patients more frequently display a T-cell response than a humoral response.7 Given that chilblains are described as a later manifestation of COVID-19,1 it is unsurprising that the patients had negative PCR results. Analysis of T-cell responses directed against the spike and/or membrane and/or nucleocapsid proteins in patients with chilblain-like lesions during the COVID-19 pandemic. [Extracted from the article]

Age is a major risk factor for cancer, but how aging impacts tumor control remains unclear. Here, we establish that aging of the immune system, regardless of the age of the stroma and tumor, drives lung cancer progression. Hematopoietic aging enhances emergency myelopoiesis, resulting in the local accumulation of myeloid progenitor-like cells in lung tumors. These cells are a major source of IL-1⍺ that drives the enhanced myeloid response. The age-associated decline of DNMT3A enhances IL-1⍺ production, and disrupting IL-1R1 signaling early during tumor development normalized myelopoiesis and slowed the growth of lung, colonic, and pancreatic tumors. In human tumors, we identified an enrichment for IL-1⍺-expressing monocyte-derived macrophages linked to age, poorer survival, and recurrence, unraveling how aging promotes cancer and offering actionable therapeutic strategies.

Sarcoidosis is a chronic immune disease of unknown origin for which we still lack an immunological framework unifying causal agents, host factors, and natural history of disease. Here, we discuss the initial triggers of disease, and how myeloid cells drive granuloma formation and contribute to immunopathogenesis. We highlight recent advances in our understanding of innate immune memory and propose the hypothesis that maladaptive innate immune training connects previous environmental exposure to granuloma maintenance and expansion. Lastly, we consider how this hypothesis may open novel therapeutic avenues, while corticosteroids remain the front-line treatment., Competing Interests: Declaration of interests The authors have no declaration of interests., (Copyright © 2024 Elsevier Ltd. All rights reserved.)

Through various studies on thermoelectric (TE) materials, thin film configuration gives superior advantages over conventional bulk TEs, including adaptability to curved and flexible substrates. Several different thin film deposition methods have been explored, yet magnetron sputtering is still favorable due to its high deposition efficiency and scalability. Therefore, this study aims to fabricate a bismuth telluride (Bi2Te3) and antimony telluride (Sb2Te3) thin film via the radio frequency (RF) magnetron sputtering method. The thin films were deposited on soda lime glass substrates at ambient temperature. The substrates were first washed using water and soap, ultrasonically cleaned with methanol, acetone, ethanol, and deionized water for 10 min, dried with nitrogen gas and hot plate, and finally treated under UV ozone for 10 min to remove residues before the coating process. A sputter target of Bi2Te3 and Sb2Te3 with Argon gas was used, and pre-sputtering was done to clean the target's surface. Then, a few clean substrates were loaded into the sputtering chamber, and the chamber was vacuumed until the pressure reached 2 x 10 -5 Torr. The thin films were deposited for 60 min with Argon flow of 4 sccm and RF power at 75 W and 30 W for Bi2Te3 and Sb2Te3, respectively. This method resulted in highly uniform n-type Bi2Te3 and p-type Sb2Te3 thin films.

Uric acid is a waste product of the human body where high levels of it or hyperuricemia can lead to gout, kidney disease and other health issues. In this paper, Finite Difference Time Doman (FDTD) simulation method was used to develop a plasmonic optical sensor to detect uric acid with molarity ranging from 0 to 3.0 mM. A hybrid layer of gold-zinc oxide (Au-ZnO) was used in this Kretschmann-based Surface Plasmon Resonance (K-SPR) technique with angular interrogation at 670 nm and 785 nm visible optical wavelengths. The purpose of this study is to observe the ability of the hybrid material as a sensing performance enhancer for differentiating between healthy and unhealthy uric acid levels based on the refractive index values from previous study. Upon exposure to 670 nm wavelength, the average sensitivity of this sensor was found to be 0.028°/mM with a linearity of 98.67 % and Q-factor value of 0.0053 mM - 1 . While at 785 nm, the average sensitivity is equal to 0.0193°/mM with slightly lower linearity at 94.46 % and Q-factor value of 0.0076 mM - 1 . The results have proven the ability of hybrid material Au-ZnO as a sensing performance enhancer for detecting uric acid when compared with bare Au and can be further explored in experimental work., Competing Interests: The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (© 2023 The Authors.)

Background: Coronavirus disease 2019 (COVID-19) is associated with an inflammatory cytokine burst and a prothrombotic coagulopathy. Platelets may contribute to microthrombosis, and constitute a therapeutic target in COVID-19 therapy., Aim: To assess if platelet activation influences mortality in COVID-19., Methods: We explored two cohorts of patients with COVID-19. Cohort A included 208 ambulatory and hospitalized patients with varying clinical severities and non-COVID patients as controls, in whom plasma concentrations of the soluble platelet activation biomarkers CD40 ligand (sCD40L) and P-selectin (sP-sel) were quantified within the first 48hours following hospitalization. Cohort B was a multicentre cohort of 2878 patients initially admitted to a medical ward. In both cohorts, the primary outcome was in-hospital mortality., Results: In cohort A, median circulating concentrations of sCD40L and sP-sel were only increased in the 89 critical patients compared with non-COVID controls: sP-sel 40,059 (interquartile range 26,876-54,678)pg/mL; sCD40L 1914 (interquartile range 1410-2367)pg/mL (P<0.001 for both). A strong association existed between sP-sel concentration and in-hospital mortality (Kaplan-Meier log-rank P=0.004). However, in a Cox model considering biomarkers of immunothrombosis, sP-sel was no longer associated with mortality, in contrast to coagulopathy evaluated with D-dimer concentration (hazard ratio 4.86, 95% confidence interval 1.64-12.50). Moreover, in cohort B, a Cox model adjusted for co-morbidities suggested that prehospitalization antiplatelet agents had no significant impact on in-hospital mortality (hazard ratio 1.05, 95% CI 0.80-1.37; P=0.73)., Conclusions: Although we observed an association between excessive biomarkers of platelet activation and in-hospital mortality, our findings rather suggest that coagulopathy is more central in driving disease progression, which may explain why prehospitalization antiplatelet drugs were not a protective factor against mortality in our multicentre cohort., (Copyright © 2023 Elsevier Masson SAS. All rights reserved.)

Commonly, simultaneous localization and mapping (SLAM) algorithm is developed using high-end sensors. Alternatively, some researchers use low-end sensors due to the lower cost of the robot. However, the low-end sensor produces noisy sensor measurements that can affect the SLAM algorithm, which is prone to error. Therefore, in this paper, a SLAM algorithm, which is a Rao-Blackwellized particle filter (RBPF) integrated with artificial neural networks (ANN) sensor model, is introduced to improve the measurement accuracy of a low-end laser distance sensor (LDS) and subsequently improve the performance of SLAM. The RBPF integrated with the ANN sensor model is experimented with by using the Turtlebot3 mobile robot in simulation and real-world experiments. The experiment is validated by comparing the occupancy grid maps estimated by RBPF integrated with the ANN sensor model and RBPF without ANN. Both the results in simulation and real-world experiments show that the SLAM performance of RBPF integrated with the ANN sensor model is better than the RBPF without ANN. In the real-world experiment results, the performance of the occupied cells integrated with the ANN sensor model is increased by 107.59%. In conclusion, the SLAM algorithm integrated with the ANN sensor model is able to improve the accuracy of the map estimate for mobile robots using low-end LDS sensors.

Host immunity to infection with SARS-CoV-2 is highly variable, dictating diverse clinical outcomes ranging from asymptomatic to severe disease and death. We previously reported reduced type I interferon in severe COVID-19 patients preceded clinical worsening. Further studies identified genetic mutations in loci of the TLR3- or TLR7-dependent interferon-I pathways, or neutralizing interferon-I autoantibodies as risk factors for development of COVID-19 pneumonia. Here we show in patient cohorts with different severities of COVID-19, that baseline plasma interferon α measures differ according to the immunoassay used, timing of sampling, the interferon α subtype measured, and the presence of autoantibodies. We also show a consistently reduced induction of interferon-I proteins in hospitalized COVID-19 patients upon immune stimulation, that is not associated with detectable neutralizing autoantibodies against interferon α or interferon ω. Intracellular proteomic analysis shows increased monocyte numbers in hospitalized COVID-19 patients but impaired interferon-I response after stimulation. We confirm this by ex vivo whole blood stimulation with interferon-I which induces transcriptomic responses associated with inflammation in hospitalized COVID-19 patients, that is not seen in controls or non-hospitalized moderate cases. These results may explain the dichotomy of the poor clinical response to interferon-I based treatments in late stage COVID-19, despite the importance of interferon-I in early acute infection and may guide alternative therapeutic strategies., (© 2022. The Author(s).)

Background: Severe coronavirus disease 2019 (COVID-19) is characterized by impaired type I interferon activity and a state of hyperinflammation leading to acute respiratory distress syndrome. The complement system has recently emerged as a key player in triggering and maintaining the inflammatory state, but the role of this molecular cascade in severe COVID-19 is still poorly characterized., Objective: We aimed at assessing the contribution of complement pathways at both the protein and transcriptomic levels., Methods: To this end, we systematically assessed the RNA levels of 28 complement genes in the circulating whole blood of patients with COVID-19 and healthy controls, including genes of the alternative pathway, for which data remain scarce., Results: We found differential expression of genes involved in the complement system, yet with various expression patterns: whereas patients displaying moderate disease had elevated expression of classical pathway genes, severe disease was associated with increased lectin and alternative pathway activation, which correlated with inflammation and coagulopathy markers. Additionally, properdin, a pivotal positive regulator of the alternative pathway, showed high RNA expression but was found at low protein concentrations in patients with a severe and critical disease, suggesting its deposition at the sites of complement activation. Notably, low properdin levels were significantly associated with the use of mechanical ventilation (area under the curve = 0.82; P = .002)., Conclusion: This study sheds light on the role of the alternative pathway in severe COVID-19 and provides additional rationale for the testing of drugs inhibiting the alternative pathway of the complement system., (Copyright © 2021 American Academy of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved.)

Coordinated local mucosal and systemic immune responses following severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection either protect against coronavirus disease 2019 (COVID-19) pathologies or fail, leading to severe clinical outcomes. To understand this process, we performed an integrated analysis of SARS-CoV-2 spike-specific antibodies, cytokines, viral load and bacterial communities in paired nasopharyngeal swabs and plasma samples from a cohort of clinically distinct patients with COVID-19 during acute infection. Plasma viral load was associated with systemic inflammatory cytokines that were elevated in severe COVID-19, and also with spike-specific neutralizing antibodies. By contrast, nasopharyngeal viral load correlated with SARS-CoV-2 humoral responses but inversely with interferon responses, the latter associating with protective microbial communities. Potential pathogenic microorganisms, often implicated in secondary respiratory infections, were associated with mucosal inflammation and elevated in severe COVID-19. Our results demonstrate distinct tissue compartmentalization of SARS-CoV-2 immune responses and highlight a role for the nasopharyngeal microbiome in regulating local and systemic immunity that determines COVID-19 clinical outcomes., (© 2021. The Author(s).)

Objective: The clinical relevance of antiphospholipid antibodies (aPLs) in COVID-19 is controversial. This study was undertaken to investigate the prevalence and prognostic value of conventional and nonconventional aPLs in patients with COVID-19., Methods: This was a multicenter, prospective observational study in a French cohort of patients hospitalized with suspected COVID-19., Results: Two hundred forty-nine patients were hospitalized with suspected COVID-19, in whom COVID-19 was confirmed in 154 and not confirmed in 95. We found a significant increase in lupus anticoagulant (LAC) positivity among patients with COVID-19 compared to patients without COVID-19 (60.9% versus 23.7%; P < 0.001), while prevalence of conventional aPLs (IgG and IgM anti-β 2 -glycoprotein I and IgG and IgM anticardiolipin isotypes) and nonconventional aPLs (IgA isotype of anticardiolipin, IgA isotype of anti-β 2 -glycoprotein I, IgG and IgM isotypes of anti-phosphatidylserine/prothrombin, and IgG and IgM isotypes of antiprothrombin) was low in both groups. Patients with COVID-19 who were positive for LAC, as compared to patients with COVID-19 who were negative for LAC, had higher levels of fibrinogen (median 6.0 gm/liter [interquartile range 5.0-7.0] versus 5.3 gm/liter [interquartile range 4.3-6.4]; P = 0.028) and C-reactive protein (CRP) (median 115.5 mg/liter [interquartile range 66.0-204.8] versus 91.8 mg/liter [interquartile range 27.0-155.1]; P = 0.019). Univariate analysis did not show any association between LAC positivity and higher risks of venous thromboembolism (VTE) (odds ratio 1.02 [95% confidence interval 0.44-2.43], P = 0.95) or in-hospital mortality (odds ratio 1.80 [95% confidence interval 0.70-5.05], P = 0.24). With and without adjustment for CRP level, age, and sex, Kaplan-Meier survival curves according to LAC positivity confirmed the absence of an association with VTE or in-hospital mortality (unadjusted P = 0.64 and P = 0.26, respectively; adjusted hazard ratio 1.13 [95% confidence interval 0.48-2.60] and 1.80 [95% confidence interval 0.67-5.01], respectively)., Conclusion: Patients with COVID-19 have an increased prevalence of LAC positivity associated with biologic markers of inflammation. However, LAC positivity at the time of hospital admission is not associated with VTE risk and/or in-hospital mortality., (© 2021, American College of Rheumatology.)

The COVID-19 pandemic has spread worldwide, yet the role of antiviral T cell immunity during infection and the contribution of immune checkpoints remain unclear. By prospectively following a cohort of 292 patients with melanoma, half of which treated with immune checkpoint inhibitors (ICIs), we identified 15 patients with acute or convalescent COVID-19 and investigated their transcriptomic, proteomic, and cellular profiles. We found that ICI treatment was not associated with severe COVID-19 and did not alter the induction of inflammatory and type I interferon responses. In-depth phenotyping demonstrated expansion of CD8 effector memory T cells, enhanced T cell activation, and impaired plasmablast induction in ICI-treated COVID-19 patients. The evaluation of specific adaptive immunity in convalescent patients showed higher spike (S), nucleoprotein (N), and membrane (M) antigen-specific T cell responses and similar induction of spike-specific antibody responses. Our findings provide evidence that ICI during COVID-19 enhanced T cell immunity without exacerbating inflammation., (Copyright © 2021 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works. Distributed under a Creative Commons Attribution License 4.0 (CC BY).)

Background: Microvascular, arterial and venous thrombotic events have been largely described during severe coronavirus disease 19 (COVID-19). However, mechanisms underlying hemostasis dysregulation remain unclear., Methods: We explored two independent cross-sectional cohorts to identify soluble markers and gene-expression signatures that discriminated COVID-19 severity and outcomes., Results: We found that elevated soluble (s)P-selectin at admission was associated with disease severity. Elevated sP-selectin was predictive of intubation and death (ROC AUC = 0.67, p = 0.028 and AUC = 0.74, p = 0.0047, respectively). An optimal cutoff value was predictive of intubation with 66% negative predictive value (NPV) and 61% positive predictive value (PPV), and of death with 90% NPV and 55% PPV. An unbiased gene set enrichment analysis revealed that critically ill patients had increased expression of genes related to platelet activation. Hierarchical clustering identified ITG2AB, GP1BB, PPBP and SELPLG to be upregulated in a grade-dependent manner. ROC curve analysis for the prediction of intubation was significant for SELPLG and PPBP (AUC = 0.8, p = 0.046 for both). An optimal cutoff value for PBPP was predictive of intubation with 100% NPV and 45% PPV, and for SELPLG with 100% NPV and 50% PPV., Conclusion: We provide evidence that platelets contribute to COVID-19 severity. Plasma sP-selectin level was associated with severity and in-hospital mortality. Transcriptional analysis identified PPBP/CXCL7 and SELPLG as biomarkers for intubation. These findings provide additional evidence for platelet activation in driving critical COVID-19. Specific studies evaluating the performance of these biomarkers are required., (© 2021. The Author(s).)

The cholinergic system has been proposed as a potential regulator of COVID-19-induced hypercytokinemia. We investigated whole-blood expression of cholinergic system members and correlated it with COVID-19 severity. Patients with confirmed SARS-CoV-2 infection and healthy aged-matched controls were included in this non-interventional study. A whole blood sample was drawn between 9-11 days after symptoms onset, and peripheral leukocyte phenotyping, cytokines measurement, RNA expression and plasma viral load were determined. Additionally, whole-blood expression of native alpha-7 nicotinic subunit and its negative dominant duplicate (CHRFAM7A), choline acetyltransferase and acetylcholine esterase (AchE) were determined. Thirty-seven patients with COVID-19 (10 moderate, 11 severe and 16 with critical disease) and 14 controls were included. Expression of CHRFAM7A was significantly lower in critical COVID-19 patients compared to controls. COVID-19 patients not expressing CHRFAM7A had higher levels of CRP, more extended pulmonary lesions and displayed more pronounced lymphopenia. COVID-19 patients without CHRFAM7A expression also showed increased TNF pathway expression in whole blood. AchE was also expressed in 30 COVID-19 patients and in all controls. COVID-19-induced hypercytokinemia is associated with decreased expression of the pro-inflammatory dominant negative duplicate CHRFAM7A. Expression of this duplicate might be considered before targeting the cholinergic system in COVID-19 with nicotine.

Nutraceuticals from natural sources have shown potential new leads in functional food products. Despite a broad range of health-promoting effects, these compounds are easily oxidized and unstable, making their utilization as nutraceutical ingredients limited. In this study, the encapsulated stingless bees' propolis in liposome was prepared using soy phosphatidylcholine and cholesterol by thin-film hydration technique. Three different formulations of phosphatidylcholine composition and cholesterol prepared by weight ratio was conducted to extract high propolis encapsulation. Physicochemical changes in the result of the encapsulation process are briefly discussed using scanning electron microscopy and Fourier Transform Infrared Spectroscopy. A dynamic light-scattering instrument was used to measure the hydrodynamic diameter, polydispersity index, and zeta potential. The increment of the liposomal size was observed when the concentration of extract loaded increased. In comparing three formulations, F2 (8:1 w/w) presented the best formulation as it yielded small nanoparticles of 275.9 nm with high encapsulation efficiency (66.9%). F1 (6:1 w/w) formed large particles of liposomes with 422.8 nm, while F3 (10:1 w/w) showed low encapsulation efficiency with (by) 38.7%. The liposome encapsulation will provide an effective nanocarrier system to protect and deliver the flavonoids extracted from stingless bees' propolis., Competing Interests: The authors declare no conflict of interest., (© 2021 The Authors.)