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Inflammatory responses in small vessels play an important role in the development of cardiovascular diseases, including hypertension, stroke, and small vessel disease. This involves various complex molecular processes including oxidative stress, inflammasome activation, immune-mediated responses, and protein misfolding, which together contribute to microvascular damage. In addition, epigenetic factors, including DNA methylation, histone modifications, and microRNAs influence vascular inflammation and injury. These phenomena may be acquired during the aging process or due to environmental factors. Activation of proinflammatory signaling pathways and molecular events induce low-grade and chronic inflammation with consequent cardiovascular damage. Identifying mechanism-specific targets might provide opportunities in the development of novel therapeutic approaches. Monoclonal antibodies targeting inflammatory cytokines and epigenetic drugs, show promise in reducing microvascular inflammation and associated cardiovascular diseases. In this article, we provide a comprehensive discussion of the complex mechanisms underlying microvascular inflammation and offer insights into innovative therapeutic strategies that may ameliorate vascular injury in cardiovascular disease. [ABSTRACT FROM AUTHOR]

Muscle wasting is one of the main causes for exercise intolerance and ventilatory inefficiency in patients with heart failure and a strong predictor of frailty and reduced survival. The prevalence of sarcopenia is at least 20% in patients with heart failure. Patients with heart failure often have subclinical systemic inflammation, which may exert sustained effects on skeletal muscle. Besides exercise, nutrition should also be carefully evaluated as an appropriate diet with selected nutraceuticals may be able to stimulate muscle anabolism and inhibit muscle catabolism. This review summarizes the epidemiological and clinical trial evidence supporting the recommendations for the use of nutraceuticals with anti-inflammatory properties in heart failure and provides an overview of the state of the evidence for nutraceutical supplementation to prevent and/or mitigate heart failure muscle wasting.

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Introduction Obesity has became a significant health concern over the past decade. According to a higher body mass index (BMI), obesity enhances the probability of malignancy, type 2 diabetes mellitus, cardiac disorders, and musculoskeletal diseases. Bariatric surgery, a typical and effective surgical intervention for patients with excess body weight with concurrent medical conditions, achieves significant weight loss over a long period. Numerous studies have been conducted on the effectiveness of various bariatric surgery techniques for improving glycemic homeostasis and helping patients lose weight. However, little is known about how bariatric surgery affects the lipid profile. The study aims to determine how patients' altered BMI affects lipid parameters following OAGB/MGB surgery. Methods To achieve this, the longitudinal observational study was conducted from January 2021 to January 2022 among 150 patients scheduled to undergo Anastomosis Gastric Bypass Surgery. The mean age of the patients was 41.7 years, with a standard deviation of 14.7 years (mean±SD: 41.7±14.7). Among the study participants, 56 individuals (37.3%) were male, while 94 (62.7%) were female. Objectives Regarding comorbidities, hypertension was identified as the most prevalent condition among the enrolled patients, affecting 49.3% of them. Results It was observed that the levels of S. Cholesterol and S. Triglyceride showed a significant decrease after one month (Visit-1) of the bypass surgery, with a reduction of 21.8 mg/dl (95% CI=-31.9, -11.6, p=<0.001) and 14 mg/dl (95% CI=-25.5, -2.51, p=0.017), respectively Conclusion OAGB outcome is associated with a healthier lipid profile and enhanced weight management. [ABSTRACT FROM AUTHOR]

Abstract Skin microdialysis (SMD) is a versatile sampling technique that can be used to recover soluble endogenous and exogenous molecules from the extracellular compartment of human skin. Due to its minimally invasive character, SMD can be applied in both clinical and preclinical settings. Despite being available since the 1990s, the technique has still not reached its full potential use as a tool to explore pathophysiological mechanisms of allergic and inflammatory reactions in the skin. Therefore, an EAACI Task Force on SMD was formed to disseminate knowledge about the technique and its many applications. This position paper from the task force provides an overview of the current use of SMD in the investigation of the pathogenesis of chronic inflammatory skin diseases, such as atopic dermatitis, chronic urticaria, psoriasis, and in studies of cutaneous events during type 1 hypersensitivity reactions. Furthermore, this paper covers drug hypersensitivity, UVB-induced- and neurogenic inflammation, and drug penetration investigated by SMD. The aim of this paper is to encourage the use of SMD and to make the technique easily accessible by providing an overview of methodology and applications, supported by standardized operating procedures for SMD in vivo and ex vivo.

Nanopore protein (α-hemolysin) was used to detect sub-nanosized plastic particles leached from a PE-coated paper cup. These sub-nanosized plastic particles can increase the inflammation response of macrophages. [Display omitted] • Nanopore sensing detects sub-nanosized plastics in PE-coated paper cups. • Sub-nanosized plastic particles in paper cups were 1.8 times more detected in boiled water than in room temperature water. • Sub-nanosized and microplastic particles alter cell membrane dynamics. • Sub-nanosized plastic particles can induce inflammatory cell responses. In recent years, there has been growing global concern about environmental pollution, and the increasing use of plastic products has made microplastics a serious environmental pollutant worldwide. Accordingly, the development of microplastic detection methods and research on the harmful effects of microplastics on human health are being actively pursued. In this study, we detected particle leaching from PE-coated paper cups using label-free nanopore sensing to identify and quantify the presence of sub-nanosized plastic particles. Plastic particles leached from the paper cups were classified as < 1 nm and > 1 nm, and their interactions with artificial cell membranes and inflammatory responses in the cells were evaluated. The results demonstrated that in a commonly used paper cup, particles < 1.4 nm were present at a concentration of approximately 1.13 mM in hot water and 0.62 mM in room-temperature water. It was demonstrated that plastic particles < 1 nm could condense the artificial cell membrane, whereas particles > 1 nm could thicken the artificial cell membrane. Furthermore, both size ranges of particles leached from the paper cups triggered an inflammatory response in the cells, with the inflammatory response increasing in proportion to the concentration and treatment time. The detection and analysis revealed the presence of sub-nanosized plastic particles in PE-coated paper cups, which are commonly used in daily life. These particles pose health threats and contribute to environmental pollution. [ABSTRACT FROM AUTHOR]

Muscle wasting is one of the main causes for exercise intolerance and ventilatory inefficiency in patients with heart failure and a strong predictor of frailty and reduced survival. The prevalence of sarcopenia is at least 20% in patients with heart failure. Patients with heart failure often have subclinical systemic inflammation, which may exert sustained effects on skeletal muscle. Besides exercise, nutrition should also be carefully evaluated as an appropriate diet with selected nutraceuticals may be able to stimulate muscle anabolism and inhibit muscle catabolism. This review summarizes the epidemiological and clinical trial evidence supporting the recommendations for the use of nutraceuticals with anti-inflammatory properties in heart failure and provides an overview of the state of the evidence for nutraceutical supplementation to prevent and/or mitigate heart failure muscle wasting. [ABSTRACT FROM AUTHOR]

The immune system interacts with many nominal 'danger' signals, endogenous danger‐associated (DAMP), exogenous pathogen (PAMP) and allergen (AAMP)‐associated molecular patterns. The immune context under which these are received can promote or prevent immune activating or inflammatory mechanisms and may orchestrate diverse immune responses in allergy and cancer. Each can act either by favouring a respective pathology or by supporting the immune response to confer protective effects, depending on acuity or chronicity. In this Position Paper under the collective term danger signals or DAMPs, PAMPs and AAMPs, we consider their diverse roles in allergy and cancer and the connection between these in AllergoOncology. We focus on their interactions with different immune cells of the innate and adaptive immune system and how these promote immune responses with juxtaposing clinical outcomes in allergy and cancer. While danger signals present potential targets to overcome inflammatory responses in allergy, these may be reconsidered in relation to a history of allergy, chronic inflammation and autoimmunity linked to the risk of developing cancer, and with regard to clinical responses to anti‐cancer immune and targeted therapies. Cross‐disciplinary insights in AllergoOncology derived from dissecting clinical phenotypes of common danger signal pathways may improve allergy and cancer clinical outcomes. [ABSTRACT FROM AUTHOR]

Introduction: Apoptosis dysregulation plays a substantial role in the pathophysiology of chronic inflammation and its related symptoms such as edema. Regulation of NF-ĸB activation is involved in apoptosis pattern change. The current study aimed at verifying the effects of local inflammation on edema and changes in apoptotic markers, and investigating the possible role of NF-ĸB in apoptosis pattern change during different stages of complete Freund’s adjuvant (CFA)-induced knee arthritis in rats. Methods: A total of 96 male Wistar rats were divided into different experimental groups. Arthritis was evoked into the right knee articular joint. Changes made in knee edema were assessed by caliper on the days 0, 7, 14, and 21 of the study. Synovial NF-ĸB and levels of apoptotic markers were evaluated during different stages of the study using Western blot technique. Results: CFA injection caused intense edema during the whole study period. Synovial NF-ĸB level increased during the whole study period. The level of apoptotic markers increased during the acute phase of study. But during chronic phase, the apoptosis level decreased. Inh-NF-ĸB administration increased synovial apoptosis during the whole study period. Conclusion: It seems that apoptosis pattern change plays an important role in the progression and modulation of CFA-induced inflammation and its related symptoms. Also, it can be concluded that synovial NF-ĸB had a crucial role in synovial apoptosis change during the study period.

Purpose: Conventionally, keratoconus (KC) has been considered a noninflammatory corneal ectatic disorder. Recent evidence suggests a possible role of inflammation in the pathogenesis of KC. Hence, we analyzed the levels of inflammatory factors in the tear fluid of Indian KC patients. Methods: Tear fluid samples were collected from age- and sex-matched healthy controls and KC patients (with different grades). The levels of the inflammatory factors in tears were analyzed using cytometric bead array (Human Soluble Protein Flex Set System, BD Biosciences) for levels of interleukin-1α (IL-1α), IL-1β, IL-2, IL-4, IL-5, IL-6, IL-8, IL-9, IL-10, IL-12p70, IL-23p40, IL-13, IL-17A, IL-17F, IL-21, interferon-α (IFNα), IFNγ, tumor necrosis factor-α, CCL2/monocyte chemotactic protein-1, CCL4/macrophage inflammatory protein-1β (MIP-1β), MIP-1α, CCL5/RANTES, CXCL10/IP10, ICAM1, CD62E, vascular endothelial growth factor and transforming growth factor β. Results: An increase in Kmax and Kmean, and a decrease in central corneal thickness was observed with increasing grades of KC. Tear analysis showed that most of the tear soluble factors, including cytokines, chemokines, growth factors and cell adhesion molecules were significantly elevated in the KC patients compared to the controls. Conclusion: Our findings suggest that inflammatory factors associated with KC may play a role in its pathogenesis. This opens the potential to explore anti-inflammatory strategies to either halt or delay the progression of KC.

Aim To compare the degree of fibre shedding by six brands of endodontic paper point when used for the paper point technique ( PPT) of working length confirmation. Methodology An in vitro model simulating the clinical use of paper points in PPT was used to assess the degree of fibre shedding of six brands of size 20, .02 taper paper point. Whilst observing the artificial terminal foramen with polarized light microscopy, the number of fibres shed directly (point inserted 1 mm beyond the terminal foramen) and indirectly (point inserted to length then a gutta-percha point inserted) was assessed. The degree of direct fibre shedding as a function of brand was analysed with Fisher's exact test and multiple pairwise comparisons. Indirect fibre shedding was analysed with Kruskal-Wallis and Wilcoxon rank-sum tests. Results All brands shed fibres both directly and indirectly, with a significant influence of brand on the proportion of fibres shed directly ( P < 0.0306) and on the mean number of fibres shed indirectly ( P < 0.0001). Post hoc analysis demonstrated a similar hierarchy of point integrity for both tests with Classic (UnoDent, Witham, UK) shedding significantly more than other brands and SS White (Gloucester, UK) and Antæos® ( VDW, Munich, Germany) shedding the least. Conclusion All brands of paper point may shed cellulose fibres both directly and indirectly with a significant influence of brand on the degree of fibre shedding. Further work should be undertaken to develop biocompatible absorbent dental points. [ABSTRACT FROM AUTHOR]

Introduction: Transforming Growth Factor-Beta 1 (TGF-β1) is a pleiotropic cytokine with potent anti-inflammatory property, which has been considered as an essential risk factor in the inflammatory process of Ischemic Stroke (IS), by involving in the pathophysiological progression of hypertension, atherosclerosis, and lipid metabolisms. -509C/T TGF-β1 gene polymorphism has been found to be associated with the risk of IS. The aim of this meta-analysis was to provide a relatively comprehensive account of the relation between -509C/T gene polymorphisms of TGF-β1 and susceptibility to IS. Methods: A review of literature for eligible genetic association Studies published before October 20, 2014 was conducted in the PubMed, EMBASE, Google Scholar and Trip database. The strength of association was calculated by pooled odds ratios (ORs) with 95% confidence intervals using RevMan 5.3 software. Heterogeneity was examined using Higgins I-squared, Tau-squared, and Chi-squared tests. Results: A total of 2 studies involving 614 cases and 617 controls were found. The overall estimates did not show any significant relation between TGF-β1-509C/T polymorphism and risk of IS under dominant (CC+CT vs. TT: OR=1.01, 95%CI=0.31 to 3.26; P=0.99), recessive (CC vs. CT+TT: OR=0.94, 95%CI=0.47 to 1.90; P=0.87), and allelic models (T vs. C: OR=1.06, 95%CI=0.55 to 2.04; P=0.86). Conclusion: This meta-analysis showed that TGF-β1-509C/T gene polymorphism has no significant association with the susceptibility of IS. Further well-designed prospective studies with larger sample size are needed to confirm these findings.

Background: Hypertension, hyperglycemia, dyslipidemia, overweight, obesity, and tobacco (smoking, chewing, and vaping), together with a pro-inflammatory and procoagulant state, are the main risk factors related to atherosclerotic cardiovascular disease. Objective and methods: A group of experts from the Americas, based on their clinical expertise in cardiology, cardiovascular prevention, and cardiometabolic (CM) diseases, joined together to develop these practical recommendations for the optimal evaluation and treatment of residual CM risk factors in Latin America, using a modified Delphi methodology (details in electronic TSI) to generate a comprehensive CM risk reduction guideline, and through personalized medicine and patient-centered decision, considering the cost-benefit ratio The process was well defined to avoid conflicts of interest that could bias the discussion and recommendations. Results: Residual risk reduction should consider therapeutic options adapted to specific patient needs, based on five treatment objectives: triglyceride-rich lipoproteins, inflammation, impaired glucose metabolism, high blood pressure, and prothrombotic status. Comprehensive control of all CM risk factors should be a priority to deal with this important public health problem and prevent premature deaths. The recommendations in this paper address the evidence-based treatment of CM risk and are intended for clinical application in Latin American countries. [ABSTRACT FROM AUTHOR]

The pandemic of coronavirus disease (COVID)-19 is a global threat, causing high mortality, especially in the elderly. The main symptoms and the primary cause of death are related to interstitial pneumonia. Viral entry also into myocardial cells mainly via the angiotensin converting enzyme type 2 (ACE2) receptor and excessive production of pro-inflammatory cytokines, however, also make the heart susceptible to injury. In addition to the immediate damage caused by the acute inflammatory response, the heart may also suffer from long-term consequences of COVID-19, potentially causing a post-pandemic increase in cardiac complications. Although the main cause of cardiac damage in COVID-19 remains coagulopathy with micro- (and to a lesser extent macro-) vascular occlusion, open questions remain about other possible modalities of cardiac dysfunction, such as direct infection of myocardial cells, effects of cytokines storm, and mechanisms related to enhanced coagulopathy. In this opinion paper, we focus on these lesser appreciated possibilities and propose experimental approaches that could provide a more comprehensive understanding of the cellular and molecular bases of cardiac injury in COVID-19 patients. We first discuss approaches to characterize cardiac damage caused by possible direct viral infection of cardiac cells, followed by formulating hypotheses on how to reproduce and investigate the hyperinflammatory and pro-thrombotic conditions observed in the heart of COVID-19 patients using experimental in vitro systems. Finally, we elaborate on strategies to discover novel pathology biomarkers using omics platforms. [ABSTRACT FROM AUTHOR]

Evidence based medicine should underpin the practice of all orthopaedic surgeons. Spinal pathology should be considered in the differential diagnosis for pain in every upper and lower limbs region and an understanding of spinal anatomy and physiology is vital in the management of the trauma patient. We present ten key articles, which have been selected for their impact within the field. They encompass trauma, degenerative, inflammatory, deformity and emergency spinal disorders. The articles range from level I randomized control trials to level V expert opinion. An understanding of their methodology and key findings should be part of the core knowledge encompassing spinal surgery and will, in particular, be of benefit for those preparing for final professional examinations. [ABSTRACT FROM AUTHOR]

Inflammation is a marker of arterial disease stemming from cholesterol-dependent to -independent molecular mechanisms. In recent years, the role of inflammation in atherogenesis has been underpinned by pharmacological approaches targeting systemic inflammation that have led to a significant reduction in cardiovascular disease (CVD) risk. Although the use of nutraceuticals to prevent CVD has largely focused on lipid-lowering (e.g, red-yeast rice and omega-3 fatty acids), there is growing interest and need, especially now in the time of coronavirus pandemic, in the use of nutraceuticals to reduce inflammatory markers, and potentially the inflammatory CVD burden, however, there is still not enough evidence to confirm this. Indeed, diet is an important lifestyle determinant of health and can influence both systemic and vascular inflammation, to varying extents, according to the individual nutraceutical constituents. Thus, the aim of this Position Paper is to provide the first attempt at recommendations on the use of nutraceuticals with effective anti-inflammatory properties. [ABSTRACT FROM AUTHOR]

The cardiovascular system is significantly affected in coronavirus disease-19 (COVID-19). Microvascular injury, endothelial dysfunction, and thrombosis resulting from viral infection or indirectly related to the intense systemic inflammatory and immune responses are characteristic features of severe COVID-19. Pre-existing cardiovascular disease and viral load are linked to myocardial injury and worse outcomes. The vascular response to cytokine production and the interaction between severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) and angiotensin-converting enzyme 2 receptor may lead to a significant reduction in cardiac contractility and subsequent myocardial dysfunction. In addition, a considerable proportion of patients who have been infected with SARS-CoV-2 do not fully recover and continue to experience a large number of symptoms and post-acute complications in the absence of a detectable viral infection. This conditions often referred to as 'post-acute COVID-19' may have multiple causes. Viral reservoirs or lingering fragments of viral RNA or proteins contribute to the condition. Systemic inflammatory response to COVID-19 has the potential to increase myocardial fibrosis which in turn may impair cardiac remodelling. Here, we summarize the current knowledge of cardiovascular injury and post-acute sequelae of COVID-19. As the pandemic continues and new variants emerge, we can advance our knowledge of the underlying mechanisms only by integrating our understanding of the pathophysiology with the corresponding clinical findings. Identification of new biomarkers of cardiovascular complications, and development of effective treatments for COVID-19 infection are of crucial importance. [ABSTRACT FROM AUTHOR]

For many, Covid-19 is a short-term, mildly debilitating disease. But some people are still struggling with monthly symptoms with persistent inflammation, chronic pain and shortness of breath. The situation of "long-term cowardice" has become so debilitating that it is now common for some to say that they are tired even if they walk a short distance. So far, the focus has been on saving lives from the plague. But now there are growing concerns about people facing the long-term consequences of the COVID epidemic. The fundamental question, with the uncertainty of whether those with chronic goiter, or all those affected, will fully recover is raised. In this paper a smart monitoring model was proposed to keep monitoring the COVID patient's health conditions. The smart method keep on watching the different changes reflected in the body conditions and ensure the changes in the database. In case any emergency is raised, then these smart monitoring tools inform the information to the doctors. This can very much helpful for the patients to communicate with the doctors. [ABSTRACT FROM AUTHOR]

Inflammation is an important driver of atherosclerosis, and the favourable outcomes of the Canakinumab Anti-inflammatory Thrombosis Outcome Study (CANTOS) trial revealed the large potential of anti-inflammatory drugs for the treatment of cardiovascular disease, especially in patients with a pro-inflammatory constitution. However, the complex immune reactions driving inflammation in the vascular wall in response to an atherosclerotic microenvironment are still being unravelled. Novel insights into the cellular processes driving immunity and inflammation revealed that alterations in intracellular metabolic pathways are strong drivers of survival, growth, and function of immune cells. Therefore, this position paper presents a brief overview of the recent developments in the immunometabolism field, focusing on its role in atherosclerosis. We will also highlight the potential impact of immunometabolic markers and targets in clinical cardiovascular medicine. [ABSTRACT FROM AUTHOR]

Purpose: This consensus review article considers the question of whether glucocorticoid (GC) therapy is still relevant in the treatment of rheumatic diseases, with a particular focus on rheumatoid arthritis (RA), and whether its side effects can be adequately managed. Recent basic and clinical research on the molecular, cellular and clinical effects of GCs have considerably advanced our knowledge in this field. An overview of the subject seems appropriate. Methods: This review is the result of a multidisciplinary expert working group, organised by European Society for Clinical and Economic Aspects of Osteoporosis and Osteoarthritis. The recent literature was surveyed and the salient evidence synthetized. Results: The pathophysiological basis of RA (and other inflammatory rheumatic diseases) now strongly implicates the adaptive immune system in addition to innate mechanisms. The molecular effect of GCs and differential GC sensitivity is better understood, although exploiting this knowledge is still in its infancy. The newer treatment strategies of early and aggressive control of RA have gr eatly improved clinical outcomes, but improvements are still possible. Newer targeted anti-inflammatory drugs have made an important impact, yet they too are associated with numerous side effects. Discussion: Short durations of moderate doses of GCs are generally well tolerated and have a positive benefit/risk ratio. Patients should be assessed for fracture risk and bone preserving agents and be prescribed calcium and vitamin D supplementation. Conclusions: Within a strategy of a disease modifying approach to inflammatory disease, combination therapy including a GC is effective approach. [ABSTRACT FROM AUTHOR]

Skin microdialysis (SMD) is a versatile sampling technique that can be used to recover soluble endogenous and exogenous molecules from the extracellular compartment of human skin. Due to its minimally invasive character, SMD can be applied in both clinical and preclinical settings. Despite being available since the 1990s, the technique has still not reached its full potential use as a tool to explore pathophysiological mechanisms of allergic and inflammatory reactions in the skin. Therefore, an EAACI Task Force on SMD was formed to disseminate knowledge about the technique and its many applications. This position paper from the task force provides an overview of the current use of SMD in the investigation of the pathogenesis of chronic inflammatory skin diseases, such as atopic dermatitis, chronic urticaria, psoriasis, and in studies of cutaneous events during type 1 hypersensitivity reactions. Furthermore, this paper covers drug hypersensitivity, UVB‐induced‐ and neurogenic inflammation, and drug penetration investigated by SMD. The aim of this paper is to encourage the use of SMD and to make the technique easily accessible by providing an overview of methodology and applications, supported by standardized operating procedures for SMD in vivo and ex vivo. [ABSTRACT FROM AUTHOR]

Introduction: Stress predisposes organisms to depression and cognitive impairments, and seems to interact with metabolic homeostasis. The inflammatory response and the upregulation of proinflammatory cytokines are some of the consequences related to chronic stress. In this study, we investigated the preventive effect of chronic administration of ibuprofen, as an inhibitor of cyclooxygenases, on the cognitive and behavioral alterations and the weight gain reduction induced by simultaneous chronic restraint stress in rats. Materials and Methods: Male Wistar rats were subjected to chronic restraint stress and injected daily with the variable doses of ibuprofen or vehicle, for 21 consecutive days. Then, all animals were tested with the forced swim test and passive avoidance conditioning. Also, the weight of the animals was recorded before and after the interventions. Ultimately, plasma interleukin 6 (IL-6) levels were measured. Results: Chronic stress increased depressive-like behaviors, impaired learning, and disrupted the normal weight gain. However, the animals that received the highest dose of ibuprofen showed less depressive-like behaviors, a better avoidance memory, and a higher weight gain. However, the level of plasma IL-6 did not differ significantly between the study groups. Conclusion: The administration of ibuprofen prevents the cognitive and behavioral consequences of chronic stress. During the recovery, the plasma levels of IL-6 were not elevated by stress, and the IL-6 levels did not predict the behavioral performance of the stressed animals. The exact mechanisms of the protective effects of ibuprofen against chronic stress need to be further investigated. [ABSTRACT FROM AUTHOR]

Dysregulated lipid metabolism induces an inflammatory and immune response leading to atherosclerosis. Conversely, inflammation may alter lipid metabolism. Recent treatment strategies in secondary prevention of atherosclerosis support beneficial effects of both anti-inflammatory and lipid-lowering therapies beyond current targets. There is a controversy about the possibility that anti-inflammatory effects of lipid-lowering therapy may be either independent or not of a decrease in low-density lipoprotein cholesterol. In this Position Paper, we critically interpret and integrate the results obtained in both experimental and clinical studies on anti-inflammatory actions of lipid-lowering therapy and the mechanisms involved. We highlight that: (i) besides decreasing cholesterol through different mechanisms, most lipid-lowering therapies share anti-inflammatory and immunomodulatory properties, and the anti-inflammatory response to lipid-lowering may be relevant to predict the effect of treatment, (ii) using surrogates for both lipid metabolism and inflammation as biomarkers or vascular inflammation imaging in future studies may contribute to a better understanding of the relative importance of different mechanisms of action, and (iii) comparative studies of further lipid lowering, anti-inflammation and a combination of both are crucial to identify effects that are specific or shared for each treatment strategy. [ABSTRACT FROM AUTHOR]

Abstract In this study, levels of inflammatory protein biomarkers in venous plasma, plasma derived from capillary blood from the earlobe, and capillary plasma stored as dried plasma spots (DPS) were compared. Samples from 12 male individuals were assessed with a panel of 92 inflammation-related proteins using multiplex proximity extension assay. Correlations between sample types varied greatly between analytes. A high correlation of ρ > 0.8 was observed between capillary plasma and DPS for 32 analytes. At this level of correlation, 13 analytes correlated between venous and capillary plasma and 5 analytes in the comparison of venous blood with DPS. Highlights • Measurement of an inflammation protein panel in three sample sources. • Earlobe plasma as a less invasive alternative sample source than venous plasma. • Protein measurement in capillary plasma stored as dried plasma spots (DPS). • Correlation value of ρ > 0.8 between capillary earlobe plasma and DPS for 32 analytes. • Correlation value of ρ > 0.8 between venous and capillary earlobe plasma for 13 analytes. [ABSTRACT FROM AUTHOR]

• Remote dried blood spot (DBS) self-collection in older adults is highly feasible. • Remote DBS yields high-quality spots, sufficient for assaying multiple biomarkers, with high participant adherence. • Inflammatory markers (CRP, IL-6, TNF-α) from self-collected DBS are reliable and valid. Dried blood spots (DBS) provide a minimally invasive method to assess inflammatory markers and can be collected remotely at-home or in-person in the lab. However, there is a lack of methodological information comparing these different collection methods and in older adults. We investigated the feasibility (including adherence, yield, quality, and participant preferences) and measurement properties (reliability, validity) of remotely collected DBS inflammatory markers in older adults. Participants (N = 167, mean age = 72, range: 60–96 years) collected their own DBS (finger prick on filter paper) during three remote interviews over ∼ 6 months. Within 4–5 days on average of their last remote interview, a subset of 41 participants also attended an in-person lab visit that included a researcher-collected DBS sample, venous blood draw, and survey to assess participant preferences of DBS collection. DBS and venous blood were assayed for CRP, IL-6, and TNF-α. Adherence: 98% of expected DBS samples (493 out of 501) were completed and mailed back to the lab. Yield: 97% of DBS samples were sufficient for all assays. Quality: On average, 0.80 fewer optimal spots (60uL of blood that filled the entire circle) were obtained remotely vs. in-person (p = 0.013), but the number of useable or better spots (at least 30-40uL of blood) did not differ (p = 0.89). Preference: A slight majority of participants (54%) preferred in-person DBS collection. Reliability: DBS test–retest reliabilities were good: CRP (ICC = 0.74), IL-6 (ICC = 0.76), and TNF-α (ICC = 0.70). Validity: Inflammatory levels from DBS correlated strongly with levels from venous blood (r = 0.60-0.99) and correlated as expected with sociodemographic and physical health and function variables. Older adults can remotely collect their own DBS to acquire reliable and valid inflammatory data. Remote DBS collection is highly feasible and may allow for inflammatory markers to be assessed in larger, more representative samples than are possible with lab- or clinic-based research designs. [ABSTRACT FROM AUTHOR]

This EAACI position paper aims at providing a state-of-the-art overview on nonallergic rhinitis ( NAR). A significant number of patients suffering from persistent rhinitis are defined as nonallergic noninfectious rhinitis ( NANIR) patients, often denominated in short as having NAR. NAR is defined as a symptomatic inflammation of the nasal mucosa with the presence of a minimum of two nasal symptoms such as nasal obstruction, rhinorrhea, sneezing, and/or itchy nose, without clinical evidence of endonasal infection and without systemic signs of sensitization to inhalant allergens. Symptoms of NAR may have a wide range of severity and be either continuously present and/or induced by exposure to unspecific triggers, also called nasal hyperresponsiveness ( NHR). NHR represents a clinical feature of both AR and NAR patients. NAR involves different subgroups: drug-induced rhinitis, (nonallergic) occupational rhinitis, hormonal rhinitis (including pregnancy rhinitis), gustatory rhinitis, senile rhinitis, and idiopathic rhinitis ( IR). NAR should be distinguished from those rhinitis patients with an allergic reaction confined to the nasal mucosa, also called 'entopy' or local allergic rhinitis ( LAR). We here provide an overview of the current consensus on phenotypes of NAR, recommendations for diagnosis, a treatment algorithm, and defining the unmet needs in this neglected area of research. [ABSTRACT FROM AUTHOR]

In addition to the genetic determinants, inflammation can also be triggered by multiple nongenetic factors including microbiome, toxic compounds, diet, and stress, which affects the epigenome and secretome of tissue microenvironment. Decades of research have shown how the clinical manifestation of inflammation can also be pathological and prime the tissue niche for the progression of myriad complex diseases. [Extracted from the article]

Purpose: The aim of the present study is to comparatively evaluate the anti-inflammatory and antiapoptotic effects of bone marrow and adipose-derived mesenchymal stem cells (MSCs) applied subconjunctivally after alkaline corneal burn. Methods: Thirty-two rats were divided into 4 groups and included in the study (n = 8). While no intervention was made in the control group, a chemical burn was created by applying 4 μL of NaOH soaked in 6 mm filter paper to the right eye of each subject in the other groups under general anesthesia. While only subconjunctival 0.1 mL phosphate-buffered saline (PBS) was injected to in the group 1, 2 × 106 adipose or bone marrow-derived MSC in 0.1 mL PBS was applied subconjunctivally to the subjects in the remaining groups (Group 2 and 3, respectively). Tissue samples were collected for histological analysis on the third day after the burn. Tissue samples were evaluated light microscopically and immunohistochemically stained for interleukin-1 beta (IL-1β), tumor necrosis factor alpha (TNF-α), caspase-3 (Cas-3), and CD68. Results: The IL-1β and TNF-α staining scores and the number of CD68- and Cas-3-positive stained cells were significantly lower in the groups given bone marrow and adipose-derived MSC compared to the alkaline burn group (P < 0.0001, for all parameters). Epithelial IL-1β and TNF-α staining scores were significantly lower in the bone marrow-derived MSC group compared to the adipose-derived MSC group (P < 0.0001, for all parameters). Conclusions: The presented study shows that both bone-marrow and adipose-derived MSCs support wound healing in the corneal tissue and strongly suppress the inflammation occured in the tissue. [ABSTRACT FROM AUTHOR]

Introduction: Apoptosis dysregulation plays a substantial role in the pathophysiology of chronic inflammation and its related symptoms such as edema. Regulation of NF-ĸB activation is involved in apoptosis pattern change. The current study aimed at verifying the effects of local inflammation on edema and changes in apoptotic markers, and investigating the possible role of NF-ĸB in apoptosis pattern change during different stages of complete Freund's adjuvant (CFA)-induced knee arthritis in rats. Methods: A total of 96 male Wistar rats were divided into different experimental groups. Arthritis was evoked into the right knee articular joint. Changes made in knee edema were assessed by caliper on the days 0, 7, 14, and 21 of the study. Synovial NF-ĸB and levels of apoptotic markers were evaluated during different stages of the study using Western blot technique. Results: CFA injection caused intense edema during the whole study period. Synovial NF-ĸB level increased during the whole study period. The level of apoptotic markers increased during the acute phase of study. But during chronic phase, the apoptosis level decreased. Inh-NF-ĸB administration increased synovial apoptosis during the whole study period. Conclusion: It seems that apoptosis pattern change plays an important role in the progression and modulation of CFA-induced inflammation and its related symptoms. Also, it can be concluded that synovial NF-ĸB had a crucial role in synovial apoptosis change during the study period. [ABSTRACT FROM AUTHOR]

Th2 immunity and allergic immune surveillance play critical roles in host responses to pathogens, parasites and allergens. Numerous studies have reported significant links between Th2 responses and cancer, including insights into the functions of IgE antibodies and associated effector cells in both antitumour immune surveillance and therapy. The interdisciplinary field of AllergoOncology was given Task Force status by the European Academy of Allergy and Clinical Immunology in 2014. Affiliated expert groups focus on the interface between allergic responses and cancer, applied to immune surveillance, immunomodulation and the functions of IgE-mediated immune responses against cancer, to derive novel insights into more effective treatments. Coincident with rapid expansion in clinical application of cancer immunotherapies, here we review the current state-of-the-art and future translational opportunities, as well as challenges in this relatively new field. Recent developments include improved understanding of Th2 antibodies, intratumoral innate allergy effector cells and mediators, IgE-mediated tumour antigen cross-presentation by dendritic cells, as well as immunotherapeutic strategies such as vaccines and recombinant antibodies, and finally, the management of allergy in daily clinical oncology. Shedding light on the crosstalk between allergic response and cancer is paving the way for new avenues of treatment. [ABSTRACT FROM AUTHOR]

There is considerable individual variability in vulnerability for developing posttraumatic stress disorder (PTSD); evidence suggests that this variability is related in part to genetic and environmental factors, including adverse early life experience. Interestingly, recent studies indicate that induction of chronic low-grade inflammation may be a common mechanism underlying gene and environment interactions that increase the risk for development of PTSD symptoms, and, therefore, may be a target for novel interventions for prevention or treatment of PTSD. Development of murine models with face, construct, and predictive validity would provide opportunities to investigate in detail complex genetic, environmental, endocrine, and immunologic factors that determine vulnerability to PTSD-like syndromes, and furthermore may provide mechanistic insight leading to development of novel interventions for both prevention and treatment of PTSD symptoms. Here we describe the potential use of the chronic subordinate colony housing (CSC) paradigm in mice as an adequate animal model for development of a PTSD-like syndrome and describe recent studies that suggest novel interventions for the prevention and treatment of PTSD. [ABSTRACT FROM AUTHOR]

Biologic agents (also termed biologicals or biologics) are therapeutics that are synthesized by living organisms and directed against a specific determinant, for example, a cytokine or receptor. In inflammatory and autoimmune diseases, biologicals have revolutionized the treatment of several immune-mediated disorders. Biologicals have also been tested in allergic disorders. These include agents targeting IgE; T helper 2 (Th2)-type and Th2-promoting cytokines, including interleukin-4 ( IL-4), IL-5, IL-9, IL-13, IL-31, and thymic stromal lymphopoietin ( TSLP); pro-inflammatory cytokines, such as IL-1β, IL-12, IL-17A, IL-17F, IL-23, and tumor necrosis factor ( TNF); chemokine receptor CCR4; and lymphocyte surface and adhesion molecules, including CD2, CD11a, CD20, CD25, CD52, and OX40 ligand. In this task force paper of the Interest Group on Biologicals of the European Academy of Allergy and Clinical Immunology, we review biologicals that are currently available or tested for the use in various allergic and urticarial pathologies, by providing an overview on their state of development, area of use, adverse events, and future research directions. [ABSTRACT FROM AUTHOR]

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Purpose: To investigate the therapeutic efficacy of tumor necrosis factor (TNF)-α stimulated gene/protein 6 (TSG-6) in a rat model of corneal alkali injury. Methods: Corneal alkali injury was produced by placing an NaOH-soaked filter paper disk on the central cornea of the right eye of an anesthetized male Lewis (LEW/Crl) rat. Recombinant human TSG-6, or an equal volume of phosphate-buffered saline (PBS), was administered intravenously (IV), by anterior chamber (AC) injection, or as a topical drop. The affected eyes were photographed daily using a dissecting microscope and documented for clinical time course analysis of corneal opacification. Corneal tissue was excised at pre-determined therapeutic endpoints, with subsequent qRT-PCR or histological analyses. Results: The continuous monitoring of corneal alkali injury progression revealed TSG-6 treatments do not show sufficient effectiveness in vivo regardless of IV injection, AC injection, or topical application. Corneal opacification and neovascularization were not diminished, and gene expression was not impacted by these treatments. However, both IV and AC administration of TSG-6 significantly suppressed pro-inflammatory cytokines compared to PBS-treated eyes. Conclusion: We conclude that the therapeutic potential of TSG-6 is insufficient in a rat corneal alkali injury model. [ABSTRACT FROM AUTHOR]

Psoriasis is an immune-mediated inflammatory disease (IMID) which may have a major impact on a patient's life, especially when the disease is moderate to severe. There is evidence that treatment of psoriasis during the first years is conservative and frequently based on topical agents which rarely clear lesions. Treatment with systemic agents including biologics is often undertaken only when topical agents have proved unsuitable, even in patients with moderate to severe disease. However, there is evidence that in other IMIDs (rheumatoid arthritis and Crohn's disease), targeted systemic treatment given early in the treatment pathway may improve long-term patient outcomes. We hypothesize that a patient-centered therapeutic approach, undertaken early in the psoriasis treatment pathway ('early intervention') with the goal of complete clearance, may improve control of cutaneous symptoms and may also modify disease course and burden. Critical points to address when designing an early intervention study would include: the definition of psoriasis disease activity; patient selection; intervention selection; and dosing strategies. [ABSTRACT FROM AUTHOR]

Atherosclerotic plaques prone to rupture may cause acute myocardial infarction (MI) but can also heal without causing an event. Certain common histopathological features, including inflammation, a thin fibrous cap, positive remodelling, a large necrotic core, microcalcification, and plaque haemorrhage are commonly found in plaques causing an acute event. Recent advances in imaging techniques have made it possible to detect not only luminal stenosis and overall coronary atherosclerosis burden but also to identify such adverse plaque characteristics. However, the predictive value of identifying individual adverse atherosclerotic plaques for future events has remained poor. In this Position Paper, the relationship between vulnerable plaque imaging and MI is addressed, mainly for non-invasive assessments but also for invasive imaging of adverse plaques in patients undergoing invasive coronary angiography. Dynamic changes in atherosclerotic plaque development and composition may indicate that an adverse plaque phenotype should be considered at the patient level rather than for individual plaques. Imaging of adverse plaque burden throughout the coronary vascular tree, in combination with biomarkers and biomechanical parameters, therefore holds promise for identifying subjects at increased risk of MI and for guiding medical and invasive treatment. [ABSTRACT FROM AUTHOR]

Background There has been increasing interest in both suicide-specific diagnoses within the psychiatric nomenclature and related biomarkers. Because the Suicide Crisis Syndrome—an emotional crescendo of several interrelated symptoms—seems to be promising for the identification of individuals at risk of suicide, the aim of the present paper is to review the putative biological underpinnings of the Suicide Crisis Syndrome symptoms (entrapment, affective disturbance, loss of cognitive control, hyperarousal, social withdrawal). Methods A PubMed literature search was performed to identify studies reporting a link between each of the 5 Suicide Crisis Syndrome symptoms and biomarkers previously reported to be associated with suicidal outcomes. Results Disturbances in the hypothalamic-pituitary-adrenal axis, with dysregulated corticotropin-releasing hormone and cortisol levels, may be linked to a sense of entrapment. Affective disturbance is likely mediated by alterations in dopaminergic circuits involved in reward and antireward systems as well as endogenous opioids. Loss of cognitive control is linked to altered neurocognitive function in the areas of executive function, attention, and decision-making. Hyperarousal is linked to autonomic dysregulation, which may be characterized by a reduction in both heart rate variability and electrodermal activity. Social withdrawal has been associated with oxytocin availability. There is also evidence that inflammatory processes may contribute to individual Suicide Crisis Syndrome symptoms. Conclusion The Suicide Crisis Syndrome is a complex syndrome that is likely the consequence of distinct changes in interconnected neural, neuroendocrine, and autonomic systems. Available clinical and research data allow for development of empirically testable hypotheses and experimental paradigms to scrutinize the biological substrates of the Suicide Crisis Syndrome. [ABSTRACT FROM AUTHOR]

We have developed a nanomesh based on skin sensors that can detect physiological signals such as electrocardiogram (ECG), pressure, and acoustic detection. Nanomesh sensors have high gas permeability and softness. Owing to the high gas permeability, the nanomesh sensor did not cause inflammation when the sensor was attached to the skin for a week. Furthermore, we developed a wireless ECG monitoring system by combining a nanomesh sensor and a textile‐based wireless module. [ABSTRACT FROM AUTHOR]

A review of the article "The addition of exercise training to a weight-loss program improves clinical control in adults with asthma" by P.D. Freitas is presented.

Purpose: As an autoimmune disease, Vogt‒Koyanagi‒Harada disease (VKHD) is a main type of uveitis in many countries and regions, significantly impacting patient vision. At present, information regarding VKHD is still limited, and further research is needed. We conducted a bibliometric analysis to characterize the overall status, current trends, and current focus of VKHD research. Method: Literature published from 1975 to 2022 was obtained from the Web of Science core collection and analysed with the R-language packages Bibliometrix, VOSviewer, and CiteSpace software. Results: A total of 1050 papers on VKHD were retrieved from 261 journals, and 16,084 references were obtained from the papers in the original search. The average annual number of published articles was approximately 21.9, and the number of publications rapidly increased after 2004. The journal Ocular Immunology and Inflammation published the most papers on VKHD, while the American Journal of Ophthalmology has the highest citation frequency. The leading countries were Japan, China (PRC), and the United States of America (USA). Yang PZ from Chongqing Medical University was the most prolific and cited author. The most frequently cited study discussed revision of VKHD diagnostic criteria. An analysis of the highest frequency keywords showed that most research focused on the treatment, diagnosis, and pathogenesis of VKHD and its relationship with other related diseases. At present, the most urgent research direction is in the relationship between COVID-19 or COVID-19 vaccines and VKHD and the corresponding mechanisms underlying it. Conclusion: Utilizing dynamic and visualization tools, bibliometrics provides a clear depiction of the research history, development trends, and research hotspots in VKHD It serves as a valuable tool for identifying research gaps and areas that necessitate further exploration. Our study revealed potential directions for future VKHD research, including investigating specific molecular mechanisms underlying the disease, exploring the clinical utility of optical coherence tomography angiography and other diagnostic techniques, and conducting clinical research on novel therapeutic drugs. [ABSTRACT FROM AUTHOR]

Background: Spinal cord injury (SCI) is a nervous system disease leading to motor and sensory dysfunction below the injury level, and can result in paralysis. MicroRNAs (miRNAs) play a key role in SCI treatment, and related research provides insights for SCI diagnosis and treatment. Bibliometrics is an important tool for literature statistics and evaluation, objectively summarizing multidimensional information. This study comprehensively overviews the field through bibliometric analysis of miRNA and SCI research, providing contemporary resources for future collaboration and clinical treatment. Materials and methods: In this study, we searched the Web of Science Core Collection (WOSCC) database. After careful screening and data import, we extracted annual publications, citation counts, countries, institutions, authors, journals, highly cited articles, co-cited articles, keywords, and H-index. Bibliometrics and visualization analyses employed VOSviewer, CiteSpace, the R package "bibliometrix," and online analytic platforms. Using Arrowsmith, 1 we determined miRNA-SCI relationships and discussed potential miRNA mechanisms in SCI. Results: From 2008 to 2024, the number of related papers increased annually, reaching 754. The number of yearly publications remained high and entered a period of rapid development. Researchers from 50 countries/regions, 802 institutions, 278 journals, and 3,867 authors participated in the field. Currently, China has advantages in the number of national papers, citations, institutions, and authors. However, it is necessary to strengthen cooperation among different authors, institutions, and countries to promote the production of important academic achievements. The research in the field currently focuses on nerve injury, apoptosis, and gene expression. Future research directions mainly involve molecular mechanisms, clinical trials, exosomes, and inflammatory reactions. Conclusion: Overall, this study comprehensively analyzes the research status and frontier of miRNAs in SCI. A systematic summary provides a complete and intuitive understanding of the relationship between SCI and miRNAs. The presented findings establish a basis for future research and clinical application in this field. [ABSTRACT FROM AUTHOR]