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Artykuły w czasopismach na temat "Inflammation-related factors"
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Limasset, B., F. Michel, R. Rey, G. Guarrigues i A. Crastes De Paulet. "Inflammation-Related Factors in Haemorrhoids". Phlebology: The Journal of Venous Disease 9, nr 1_suppl (styczeń 1994): 30–33. http://dx.doi.org/10.1177/0268355594009001s10.
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Objective: To establish whether eicosanoid production characterizes the inflammatory processes of the haemorrhoidal plexus. Design: Open, single patient group study. Setting: Private practice. Patients: Fourteen patients selected for haemorrhoidectomy. Interventions: Specimens were obtained during either the acute (five patients, group I) or chronic (nine patients, group II) phase of the disease. We assayed the concentrations of prostaglandins E2 (PGE2) and F2α (PGF2α) and of leukotriene B4 (LTB4) in the vascular and mucosal tissues of the anterior and posterior haemorrhoidal plexus. Results: Very high levels of prostaglandins were recorded (up to 1445 <g/g fresh tissue of PGE2 in group I), which were consistently higher in group II than group I ( p <0.05, Wilcoxon distribution free test) for 10 out of 18 parameters measured. Four to 20 times more PGE2 than PGF2α was produced. These two eicosanoids were strongly correlated (0.73–0.93 according to sample). LTB4 production was up to 20 times lower than that of PGE2 (6–10 ng/g, group II; 17–52 ng/g, group I). Conclusions: PGF2α and LTB4 seem to be valuable independent study parameters to be included in the design of protocols investigating the action of anti-inflammatory agents on haemorrhoids.
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Chang, Wen-Jun. "Inflammation-related factors predicting prognosis of gastric cancer". World Journal of Gastroenterology 20, nr 16 (2014): 4586. http://dx.doi.org/10.3748/wjg.v20.i16.4586.
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Reid-Lombardo, Kaye M., Brooke L. Fridley, William R. Bamlet, Julie M. Cunningham, Michael G. Sarr i Gloria M. Petersen. "Inflammation-Related Gene Variants as Risk Factors for Pancreatic Cancer". Cancer Epidemiology Biomarkers & Prevention 20, nr 6 (5.04.2011): 1251–54. http://dx.doi.org/10.1158/1055-9965.epi-11-0264.
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Ravindran, Vinod, i P. P. Anoof. "Traditional and inflammation related cardiovascular risk factors in rheumatoid arthritis". Indian Journal of Rheumatology 9, nr 1 (marzec 2014): 2–3. http://dx.doi.org/10.1016/j.injr.2014.01.009.
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Soto, Ileana, Mark P. Krebs, Alaina M. Reagan i Gareth R. Howell. "Vascular Inflammation Risk Factors in Retinal Disease". Annual Review of Vision Science 5, nr 1 (15.09.2019): 99–122. http://dx.doi.org/10.1146/annurev-vision-091517-034416.
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Inflammation of the blood vessels that serve the central nervous system has been increasingly identified as an early and possibly initiating event among neurodegenerative conditions such as Alzheimer's disease and related dementias. However, the causal relevance of vascular inflammation to major retinal degenerative diseases is unresolved. Here, we describe how genetics, aging-associated changes, and environmental factors contribute to vascular inflammation in age-related macular degeneration, diabetic retinopathy, and glaucoma. We highlight the importance of mouse models in studying the underlying mechanisms and possible treatments for these diseases. We conclude that data support vascular inflammation playing a central if not primary role in retinal degenerative diseases, and this association should be a focus of future research.
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Bilash, S. М., M. M. Koptev, N. I. Vynnyk, O. М. Pronina i L. M. Shylkina. "INFLAMMATION-RELATED MORPHOLOGICAL ALTERATIONS IN THE MICROVASCULATURE". Актуальні проблеми сучасної медицини: Вісник Української медичної стоматологічної академії 21, nr 1 (21.03.2021): 155–59. http://dx.doi.org/10.31718/2077-1096.21.1.155.
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Microvasculature is a complex structural and functional system that regulates blood supply of body organs, provides transcapillary exchange of fluid and supports the tissue homeostasis. The human microvasculature is represented by the system of small vessels: arterioles, capillaries, venules and arteriolovenular anastomoses. The vessels of this complex become flexible in the altered blood flow; they can deposit the blood corpuscles, get affected by spasms and pass plasma only, change their permeability for tissue fluid. Microvasculature is extremely sensitive to the insults of various factors. Microvascular dysfunction coexists or precedes the macrovascular diseases probably due to joint mechanisms of damage to vessels such as oxidative stress and inflammation. Disorders of microcirculation are one of the main components of inflammation. This article is aimed at the analysis of the scientific publications on the study of morphological alterations in the microvasculature in response to inflammation. The bibliosemantic method was used. The findings of current publications on the morphological alterations that occur in the microcirculation in response to inflammation have been investigated. The analysis has shown significant morphological alterations in the microvessels in response to the proinflammatory factors. Inflammatory processes are accompanied by the events of microvascular dysfunction, associated with hyperpermeability of capillaries, destruction of microvascular endothelial barrier, loss of antiadhesive function of endothelium, etc. In response to inflammation, the marked morphofunctional alterations in the microvasculature of the various organs are observed that are dependent on the time course of inflammation. Early onset is manifested mainly by the spasm of the vascular resistance and dilatation of the capacitance vessels. Disorders of blood rheological properties are manifested by stasis, sludge, microthrombosis.
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Philippou, Anastassios. "Systemic Responses of Inflammation-Related Factors Following Eccentric Exercise in Humans". American Journal of Sports Science 6, nr 2 (2018): 32. http://dx.doi.org/10.11648/j.ajss.20180602.11.
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Goldstein, Gregory P., Stephanie A. Leonard, Peiyi Kan, Euna B. Koo, Henry C. Lee i Suzan L. Carmichael. "Prenatal and postnatal inflammation-related risk factors for retinopathy of prematurity". Journal of Perinatology 39, nr 7 (1.04.2019): 964–73. http://dx.doi.org/10.1038/s41372-019-0357-2.
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Bower, Julienne E., i Donald M. Lamkin. "Inflammation and cancer-related fatigue: Mechanisms, contributing factors, and treatment implications". Brain, Behavior, and Immunity 30 (marzec 2013): S48—S57. http://dx.doi.org/10.1016/j.bbi.2012.06.011.
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MOSHFEGHI, DARIUS M., i MARK S. BLUMENKRANZ. "ROLE OF GENETIC FACTORS AND INFLAMMATION IN AGE-RELATED MACULAR DEGENERATION". Retina 27, nr 3 (marzec 2007): 269–75. http://dx.doi.org/10.1097/iae.0b013e31802e3e9b.
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Ong, Kwok-leung, i 王國良. "Genetic variants of obesity- and inflammation-related genes in hypertension: genetic association studiesusing candidate gene approach". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B45200555.
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Mohammed, Zahra M. A. "An investigation of the relationship between tumour and inflammation related factors and survival in patients with primary operable invasive ductal breast cancer". Thesis, University of Glasgow, 2013. http://theses.gla.ac.uk/4720/.
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Saremi, Behnam [Verfasser]. "Characterization of insulin sensitivity and inflammation related factors in dairy cows receiving conjugated linoleic acids (CLA) or a control fat supplement during lactation / Behnam Saremi". Bonn : Universitäts- und Landesbibliothek Bonn, 2013. http://d-nb.info/1043064338/34.
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Hirsso, P. (Päivi). "Alopecia; its prevalence and association with cardiovascular diseases, risk factors and quality of life—cross-sectional population-based studies". Doctoral thesis, University of Oulu, 2007. http://urn.fi/urn:isbn:9789514285226.
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Abstract Alopecia has been suggested to be associated with coronary artery diseases (CAD). However, the mechanism underlying this association has remained unclear. The purpose of the present study was to examine the relationships between metabolic syndrome-related risk factors, cardiovascular diseases (CVD) and alopecia among Finnish population. In addition, health-related quality of life (HRQOL) was studied in respect of alopecia among both genders. The data come from the national Finrisk survey alopecia sub-study (4 066 men aged 25–74 years old) and two community samples of men and women (aged 55 and 63 years) living in the city of Oulu in 2001 and 1998, respectively. The degree of alopecia was assessed using the Norwood-Hamilton classification scale for men and the Ludwig scale for women. This study showed a high prevalence of alopecia in the general male Finnish population varying from 17% to 73% among men aged 25–74 years, and its association with CVD particularly in age-groups older than 55 years. In addition, insulin resistance, as a metabolic syndrome-related risk factor, was associated with alopecia in middle-aged men. Among men younger than 35 years, low-grade inflammation was associated with alopecia, especially combined with central obesity. Further, in middle-aged general Finnish population, obesity associated most closely with low-grade inflammation, which is in line with the findings among young men with alopecia. Compared to subjects with no alopecia, HRQOL dimension scores (RAND-36) were significantly lower in physical functioning, role limitations due to physical health and general health among women with alopecia, and in physical functioning and social functioning among men with alopecia. Regression analyses of HRQOL-related factors revealed that alopecia was associated with role limitations due to physical health in women but not in men. An association between alopecia and CVD was strengthened in this study. In addition, low-grade inflammation and insulin resistance were associated with alopecia, especially with early onset alopecia. In elderly women, alopecia seemed to be associated with morbidity in vascular diseases. In the future, recognition of the risk factors for cardiovascular disease among subjects with alopecia is a challenge for primary health care that may prevent the development of arterial diseasesTiivistelmä Hiustenlähdön yhteys sydän- ja verisuonisairauksiin on ollut tiedossa jo pitkään, mutta yhteyden taustalla olevat patofysiologiset mekanismit ovat edelleenkin epäselviä. Tässä väitöskirjatyössä tutkittiin hiustenlähdön yhteyksiä metaboliseen oireyhtymään ja siihen liittyviin riskitekijöihin suomalaisessa väestössä yleisesti. Lisäksi tutkittiin elämänlaadun yhteyttä hiustenlähtöön 63-vuotiailla miehillä ja naisilla. Tutkimukseen käytettiin kolmea aineistoa; kansallisen Finrisk 2002 tutkimuksen alopecia (hiustenlähtö) alaotos (4066 iältään 25–74-vuotiasta miestä) ja kaksi aineistoa Oulun kaupungista (Oulussa asuneet 55- ja 63-vuotiaat miehet ja naiset vuonna 2001 ja 1998). Hiustenlähdön laajuus määriteltiin miehillä Norwood-Hamiltonin ja naisilla Ludwigin luokitteluasteikon mukaan. Hiustenlähdön esiintyvyys suomalaisessa miesväestössä vaihteli 17 %:sta (25–34-vuotiaat) 73 %:iin (65–74-vuotiaat) ja se näytti liittyvän sydän- ja verisuonisairauksiin 55-vuotiailla ja sitä vanhemmilla miehillä. Lisäksi alentunut insuliiniherkkyys metabolisen oireyhtymän merkkinä oli yhteydessä hiustenlähtöön keski-ikäisillä miehillä. Varhain alkanut hiustenlähtö (alle 35-vuotiaat) liittyi matala-asteiseen tulehdukseen erityisesti keskivartalolihavilla kaljuuntuvilla nuorilla miehillä. Samansuuntainen tulos tuli esille myös väestötutkimuksessa 55-vuotiailla oululaisilla miehillä ja naisilla, jonka mukaan matala-asteinen tulehdus oli yhteydessä erityisesti yleiseen lihavuuteen eikä pelkästään vyötärölihavuuteen. Terveyteen liittyvän elämänlaadun osa-alueiden pisteet (RAND-36) 63-vuotialla hiustenlähdöstä kärsivillä naisilla olivat merkittävästi matalampia kolmella osa-alueella; fyysiset toiminnot, fyysisen terveydentilan aiheuttamat muutokset roolitoiminnoissa ja yleinen terveys. Samanikäisillä kaljuuntuvilla miehillä merkittävästi matalammat terveyteen liittyvät elämänlaadun osakomponentit olivat fyysisten ja sosiaalisten toimintojen alueella. Tilastollisessa regressioanalyysissä ilmeni, että hiustenlähtö selitti fyysisen terveydentilan aiheuttamia rajoituksia roolitoimintoihin erityisesti kaljuuntuvilla naisilla, mutta ei miehillä. Hiustenlähdön yhteys eri sydän- ja verisuonisairauksiin vahvistui tässä tutkimuksessa. Varhainen hiustenlähtö on ilmeisesti merkki sekä matala-asteisesta tulehduksesta että alentuneesta insuliiniherkkyydestä. Myös naisilla hiustenlähtö näyttäisi liittyvän suurempaan sairastavuuteen. Terveydenhuollon tulisi jatkossa tarkemmin paneutua sydän- ja verisuonisairauksien riskin kartoittamiseen hiustenlähdöstä kärsivien potilaiden kohdalla
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Sawaya, Melissa. "Chronic Inflammation and The Risk of Prostate Cancer : Role of Infections, Calculi, COX-2 gene and their GxE Interaction". Electronic Thesis or Diss., université Paris-Saclay, 2024. http://www.theses.fr/2024UPASR018.
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Introduction : L'inflammation chronique a été suggérée comme un facteur contribuant à la carcinogenèse prostatique. Divers facteurs liés à l’inflammation, tels que les infections, les calculs rénaux et biliaires, ainsi que la susceptibilité génétique impliquant des gènes de l’inflammation comme COX-2, ont été étudiés, mais les résultats restent souvent contradictoires ou limités. Peu d’études ont également examiné l’impact de ces facteurs sur l’agressivité du cancer. Objectifs : 1) Étudier le rôle des infections, 2) des calculs et le cancer de la prostate ; 3) Analyser l'influence des SNPs du gène COX-2 et l’interaction gènes-environnement sur le risque de cancer de la prostate. Méthodes : Les données de l'étude EPICAP, une étude cas- témoins en population menée dans le département de l'Hérault en France, ont été utilisées pour analyser les infections et les calculs, avec 819 cas et 879 témoins. Des informations ont été collectées sur l’historique de ces facteurs, ainsi que sur les scores de Gleason pour différents grades de cancer. Pour l'analyse génétique, les données sur le gène COX-2 provenant des 732 cas et 783 témoins ayant des données obtenues à partir d'échantillons de sang ou de salive, ont été utilisées après contrôle qualité, avec un total de 20 SNPs analysés. Résultats : Aucune association significative n’a été observée entre les infections sexuellement ou non sexuellement transmissibles (bactériennes ou virales) et le risque de cancer de la prostate. Les calculs rénaux, en particulier en présence d'un antécédent de pyélonéphrite, et les calculs biliaires, notamment chez les individus avec une hypertriglycéridémie, ont été associés à un risque accru de cancer de la prostate. Des associations significatives ont été observées entre plusieurs SNPs du gène COX-2 et le cancer de la prostate, avec l'allèle A du rs4648261 lié aux cancers de haut grade. Les interactions entre les variations génétiques du COX-2 et les facteurs environnementaux comme les infections et les calculs n'ont pas eu d'influence significative sur le risque de cancer de la prostate. Conclusion : Ces résultats soulignent le rôle important des processus inflammatoires dans la carcinogenèse prostatique et mettent en lumière la nécessité de poursuivre les recherches sur les facteurs liés à l'inflammation. Il est important d'étudier la durée d'exposition à ces facteurs et l'efficacité des traitements pour mieux comprendre l’impact de l’inflammation chronique sur le risque de cancer. Les résultats génétiques, basés sur une approche préliminaire par SNP, suggèrent des associations potentielles qui nécessitent des recherches supplémentaires pour être confirmées et approfondies. Enfin, étant donné l'importance du cancer de la prostate agressif et son pronostic souvent défavorable, il est essentiel que les futures recherches se concentrent sur les facteurs génétiques et environnementaux qui l'influencent, afin de mieux comprendre les mécanismes sous-jacents et d'élaborer des stratégies de prévention et de traitement plus efficacesChronic inflammation has been suggested to contribute to prostate carcinogenesis. Inflammation-related risk factors, such as infections, kidney and gallbladder stones, and genetic susceptibility involving inflammatory genes like COX-2, have been studied, but results are often contradictory or limited. Few studies have considered how these factors impact the aggressiveness of the cancer as well. Objectives: 1) Study the role of infections and calculi in the occurrence of prostate cancer 2) Study the role of COX-2 SNPs and the GxE interaction and Prostate Cancer. Methods: Data from the EPICAP, a population-based case-control study carried out in the department of Herault in France, was used for the analysis of infections and calculi, including 819 cases & 879 controls. Information was collected on the history of these factors along with Gleason scores for various grades of cancer. For genetic analysis, EPICAP provided data on the COX-2 gene, including 732 cases and 783 controls derived from blood or saliva samples, after quality control checks, with 20 SNPs analyzed in total. Results: No significant associations between sexually and non- sexually transmitted infections (STIs) whether bacterial or viral and the risk of prostate cancer. Kidney stones, particularly with a history of pyelonephritis, and gallbladder stones, especially in individuals with hypertriglyceridemia, were associated with an increased risk of prostate cancer. Significant associations were observed between several SNPs in the COX-2 gene and prostate cancer, with the A allele of rs4648261 linked to high-grade cancer. Interactions between COX-2 genetic variations and environmental factors like infections and stones did not significantly influence prostate cancer risk. Conclusion: The findings underscore the significant role of inflammatory processes in prostate carcinogenesis and highlight the need for further research into inflammation- related factors. Investigating the duration of these factors and the effectiveness of treatments is crucial to see how chronic inflammation can impact cancer risk. The genetic results based on a preliminary SNP-by-SNP approach, indicate potential associations that require further investigation to confirm and expand upon these findings. Finally, given the importance of aggressive PC and its associated poor prognosis, future research should specifically explore the genetic and environmental factors influencing it and understand the underlying mechanisms for better preventions strategies and more effective treatments
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Dern, Kathryn V. "Evaluation of the Effects of Therapeutic Digital Hypothermia on Lamellar Signaling in Sepsis Related Laminitis". The Ohio State University, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=osu1492639420006617.
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Farjood, Farhad. "Effect of Physical Stimuli on Angiogenic Factor Expression in Retinal Pigment Epithelial Cells". DigitalCommons@USU, 2019. https://digitalcommons.usu.edu/etd/7457.
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Age-related macular degeneration (AMD) is a major cause of blindness in adults. Abnormal growth of blood vessels in the eye during the course of AMD causes damage to the retina, resulting in irreversible blindness. The goal of this research was to determine whether physical pressure on retinal cells can contribute to the increased blood vessel formation. To replicate the tears in the cell layers, a micropatterning method was used as a means of detaching cells from each other. Two new devices were also developed to mimic slow and fast increases in mechanical pressure on cell layers of the eye. After detaching cells from each other and adding mechanical stress to cells, the levels of angiogenic proteins secreted by retinal cells were measured. The results showed that both cell-cell detachment and mechanical stress can increase the secretion of angiogenic proteins. After adding mechanical stress, we also added the secreted proteins to blood vessel cells and observed an increase in blood vessel formation, indicating that mechanical stress can independently induce angiogenesis. These results suggest that physical stimuli in the eye can contribute to the aberrant blood vessel formation in AMD.
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Touhami, Sara. "L’hypoxie et l’inflammation sous-rétinienne dans le contexte de la dégénérescence maculaire liée à l’âge". Thesis, Sorbonne université, 2018. http://www.theses.fr/2018SORUS553.
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L'hypoxie pourrait être un facteur causal dans la dégénérescence maculaire liée à l'âge, caractérisée par une infiltration anormale de phagocytes mononucléés (PMs) dans l’espace sous rétinien (ESR). Nous avons précédemment montré que le facteur H du complément (CFH) inhibe l'élimination des PMs dépendant de la thrombospondine 1 (TSP-1). Ici, nous montrons que l'hypoxie (10%O2) augmente l'infiltration de ces cellules et inhibe la résolution de l'inflammation sous-rétinienne après impacts lasers chez la souris. In vitro, l'hypoxie (2%) retarde l'élimination des monocytes humains (Mo) en coculture avec l'épithélium pigmentaire rétinien (EPR), habituellement immuno-suppresseur. In vivo, l’hypoxie diminue la quantité d’ARNm de Tsp-1 et augmente celle du Cfh et du Tnfα dans les Mo qui participent à l'inflammation dans l’ESR. Contrairement aux animaux wild type, l’hypoxie n’a aucun effet sur l’infiltration exagérée des PMs observée chez les souris normoxiques Thbs1-/-, mais diminue leur accumulation chez les souris normoxiques Cfh-/-. L’injection intravitréenne d'un anticorps bloquant le CFH ou de la protéine recombinante TSP-1 permet d’inverser l'effet pathogène de l'hypoxie. Le TNFα provoque la dédifférenciation de l’EPR in vitro, diminuant son immunosuppressivité, ce qui pourrait participer à la perpétuation de l'accumulation des Mo dans l’ESR. Nos résultats démontrent que l'hypoxie perturbe l'immunosuppression sous-rétinienne TSP-1-dépendante, augmente l'expression du TNFα par les Mo et favorise la pérennisation d’une inflammation pathogène dans l’ESR. Nous montrons que l'effet de l'hypoxie peut être contré par une inhibition locale du CFH ou l’administration de TSP-1Hypoxia is suspected to be one of the essential triggers in the pathogenesis of age related macular degeneration, characterized by abnormal mononuclear phagocyte (MP) infiltration. We recently showed that the inhibition of the TSP-1 (thrombospondin 1) dependent physiological elimination of MPs by complement factor H (CFH) plays an important role in subretinal MP accumulation. Here, we showed that ambient 10%O2 hypoxia increased subretinal MP infiltration and inhibited inflammation resolution after laser-induced subretinal injury, compared to normoxia (20,9%O2) in mice. In vitro, hypoxia (2%) delayed the elimination of human primary Monocytes (Mo) in coculture with immune-suppressive retinal pigment epithelium (RPE). In vivo, 10% hypoxia decreased Tsp-1 and increased Cfh and Tnfα mRNA expression in Mo that participate in the subretinal inflammation. Interestingly, contrary to wildtype animals, hypoxic ambient air had no effect on the exaggerated subretinal MP infiltration observed in normoxic Thbs1-/-mice, but diminished MP accumulation in normoxic Cfh-/-mice. Intravitreal injections of a CFH blocking antibody or recombinant TSP-1 completely reversed the pathogenic effect of hypoxia. In vitro, exogenous TNFα caused RPE cell dedifferenciation, decreasing their immunosuppressivity, which likely perpetuates Mo accumulation in the subretinal space. Together, our results demonstrate that systemic hypoxia disturbs TSP-1-dependent subretinal immune suppression, increases TNFα expression by Mo and promotes pathogenic subretinal inflammation. We show that the pathogenic effect of hypoxia can be therapeutically countered by local recombinant TSP1 or CFH inhibition
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Puurunen, J. (Johanna). "Androgen secretion and cardiovascular risk factors in women with and without PCOS:studies on age-related changes and medical intervention". Doctoral thesis, Oulun yliopisto, 2015. http://urn.fi/urn:isbn:9789526208091.
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Abstract Polycystic ovary syndrome (PCOS) is the most common endocrine disorder in women of reproductive age. The main features of the syndrome include menstrual irregularities and hyperandrogenism. In addition to symptoms related to fertility, some women also suffer from an unfavourable metabolic profile including impaired glucose tolerance, dyslipidaemia and low-grade chronic inflammation. In the present studies we aimed to investigate the role of age on adrenal and ovarian androgen secretion in 79 women with PCOS and 98 healthy women, with special focus on the menopause. Furthermore, we studied the effects of combined hormonal contraceptives (CHCs) administered orally, transdermally and vaginally (n=42, healthy women, 9 weeks) and atorvastatin treatment (n=28, women with PCOS, 6 months) on androgen levels and metabolic factors. Androgen secretion capacity was analysed by using adrenal and ovarian stimulation tests and glucose tolerance by using oral and intravenous glucose tolerance tests. Furthermore, chronic inflammation was assessed via assay of C-reactive protein and pentraxin-3. Basal and stimulated adrenal and ovarian androgen production was elevated and levels remained higher in women with PCOS compared with healthy women even after the menopause. Furthermore, women with PCOS presented with enhanced insulin resistance and chronic inflammation, which persisted beyond menopausal transition. During CHC treatment, the route of administration was insignificant, and all treatments impaired insulin sensitivity and increased chronic inflammation. In women with PCOS, treatment with atorvastatin improved chronic inflammation and the lipid profile as expected, but worsened glucose tolerance and did not affect testosterone levels. Regardless of strict exclusion criteria, where only relatively healthy women with PCOS were recruited, the results showed that enhanced androgen secretion and unfavourable metabolic alterations associated with PCOS persist through menopausal transition. The findings emphasize the importance of monitoring glucose metabolism during the use of CHCs, especially in women with known risks of type 2 diabetes. Atorvastatin treatment exacerbates insulin resistance in women with PCOS and therefore the treatment should only be considered after individual risk assessment of cardiovascular disease and not just because of PCOSTiivistelmä Monirakkulainen munasarjaoireyhtymä (PCOS) on hedelmällisessä iässä olevien naisten yleisin hormonaalinen ongelma. Tyypillisiä PCOS:n oireita ovat munarakkuloiden epäsäännöllisestä kypsymisestä johtuvat kuukautiskierron häiriöt ja miessukuhormonien eli androgeenien liikatuotanto. Hedelmällisyyttä heikentävien oireiden lisäksi PCOS:än liittyy aineenvaihdunnan ongelmia, kuten heikentynyttä sokerinsietoa sekä taipumus rasva-aineenvaihdunnan häiriöihin ja krooniseen tulehdukseen. Tutkimuksessa selvitettiin ikääntymisen ja vaihdevuosien vaikutuksia lisämunuais- ja munasarjaperäiseen androgeenieritykseen 79 PCOS-naisella ja 98 terveellä naisella. Lisäksi tutkittiin eri yhdistelmäehkäisyvalmisteiden antoreittien (suu, iho, emätin) (n=42, terveet naiset, 9 viikkoa) ja atorvastatiinihoidon (n=28, PCOS-naiset, 6 kuukautta) vaikutuksia androgeenitasoihin ja aineenvaihdunnallisiin muuttujiin. Androgeenieritystä tutkittiin lisämunuaisten ja munasarjojen stimulaatiotesteillä ja sokeriaineenvaihdunnan muutoksia suun kautta ja suonensisäisesti tehtävillä sokerirasituskokeilla. Tulehduksellista tilaa mitattiin määrittämällä C-reaktiivisen proteiinin ja pentraksiini-3:n pitoisuuksia. Lisämunuaisten ja munasarjojen androgeenieritys oli PCOS-naisilla lisääntynyt terveisiin naisiin verrattuna, ja ero säilyi vaihdevuosi-iän jälkeen. PCOS-naisilla esiintyi myös enemmän heikentynyttä sokerinsietoa ja kroonista tulehdusta vielä vaihdevuosi-iän jälkeenkin. Hormonaalinen yhdistelmäehkäisy heikensi insuliiniherkkyyttä sekä pahensi pitkäaikaista tulehdusta annostelureitistä riippumatta. Atorvastatiinihoito puolestaan paransi pitkäaikaista tulehdusta sekä rasva-aineenvaihduntaa PCOS-naisilla, mutta huononsi sokerinsietoa ja insuliiniherkkyyttä eikä sillä ollut vaikutusta testosteronitasoihin. Koska poissulkukriteerit olivat tiukat, tutkimuksiin valikoitui varsin terveitä PCOS-naisia. Siitä huolimatta osoittautui, että PCOS:än liittyvä lisääntynyt androgeenituotanto sekä epäedulliset aineenvaihdunnan muutokset jatkuvat vielä vaihdevuosi-iän jälkeen. Hormonaalisen yhdistelmäehkäisyn käytön aikana olisi hyvä seurata sokeriaineenvaihdunnan muutoksia erityisesti niillä naisilla, joilla on kohonnut riski sairastua aikuistyypin diabetekseen. Atorvastatiinihoito huonontaa PCOS-naisilla insuliiniherkkyyttä, minkä vuoksi hoito tulisi aloittaa vain yksilöllisen riskiarvion perusteella
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Pretorius, Rachelle Ann. "Body composition and systematic low-grade inflammation in children : the PLAY study / Rachelle A. Pretorius". Thesis, North-West University, 2006. http://hdl.handle.net/10394/1096.
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Background: Obesity-related diseases are arising as a major problem among children. inflammation
has recently been identified to play an important role in the relationship between obesity.- as well as
stunting-related diseases.
Objectives: The aim of this study was to assess the association between serum tumour necrosis factor-alpha
(TNF-α), interleukin-6 (IL-6) and C-reactive protein (CRP) concentrations and a variety of
cardiometabolic and anthropometric indices of children in a township outside Potchefstroom, South
Africa.
Methods: Blood samples of 115 girls and 78 boys (mean age 15.6 ± 1.35) in the Physical Activity in
the Young (PLAY) study were cross-sectionally analysed. Trained fieldworkers collected the
demographic, Tanner growth stage and habitual physical activity information. Physiologists measured
the children’s blood pressure. Anthropometric measurements were taken by. trained post-graduate
students with level 1 or 2 qualifications in anthropometrics. A standard test battery was administered
by trained postgraduate students in Human Movement Science to assess muscular strength. flexibility
and endurance of the children. Blood samples were collected, centrifuged and stored frozen until
further analyses.
Results: Stunted girls had a significantly higher serum TNF-α concentration than the non-stunted girls
(p=0.03). The factor analyses showed that the inflammatory. status clustered with the height for age-z-scores
(HAZ) scores and the waist-hip-ratio (WHR). The HAZ-score of the over-fat boys (- 1.46) was
significantly smaller than the lean boys (- 1.14, p=0.0 1). whereas the over-fat girls had a trend for a
smaller HAZ-score (-1.07) than the lean girls (-0.89). No significant differences were found between
the over-fat and the lean children-s inflammatory status. TNF-α and CRP levels tended to be higher in
the over-fat children than in lean children. The girls' scrum IL-6 and CRP concentrations correlated
significantly with their body mass index (BMI) and WHR (p<0.05 )and their TNF-α and IL-6
concentrations correlated significantly with their WHR (p<0.01 and p<0.05, respectively).
Conclusion: In comparison to the non-stunted girls, stunted girls had a statistically significantly higher
TNF-α concentration. Unusual fat distribution that is found in over-fat and stunted children may be
associated with low-grade inflammation in children. More research is needed on these associations with
markers of inflammation in a long-term longitudinal study.Thesis (M.Sc. (Nutrition))--North-West University, Potchefstroom Campus, 2007.
Książki na temat "Inflammation-related factors"
1
1949-, Breit Samuel N., i Wahl Sharon M, red. TGF-Ý and related cytokines in inflammation. Basel: Birkhäuser, 2001.
Znajdź pełny tekst źródła
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TGF-beta and Related Cytokines in Inflammation (Progress in Inflammation Research). Birkhauser, 2001.
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O’Riordan, Stephen MP, i Antoinette Moran. Cystic fibrosis-related diabetes. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780198702948.003.0008.
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This chapter on CFRD reviews the ever-evolving topic and provides up-to-date information on how to diagnose and manage cystic fibrosis-related diabetes CFRD in the acute and chronic setting. The treatments necessary to treat and prolong life in CF, including their unique dietary requirements, must always be followed as a first priority, with diabetes care adjusted accordingly. Early intervention with insulin has been shown to reverse clinical deterioration, even in those with mild diabetes. Newly emerging treatments for CF which have the potential to restore defective chloride channels may have implications for the development and treatment of CFRD. Whilst CFRD shares features of both type 1 and type 2 diabetes, there are important differences which necessitate a unique approach to diagnosis and management. Factors specific to CF that variably affect glucose metabolism include chronic respiratory infection and inflammation, increased energy expenditure, malnutrition, glucagon deficiency, and gastrointestinal abnormalities.
4
Stanworth, Simon, i Stuart McKechnie. Pathophysiology of disordered coagulation. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0269.
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Imbalances in the regulation of haemostasis may manifest as bleeding (depletion of pro-coagulant factors) or thrombosis (deficiency of anti-coagulants). Disordered haemostasis is common in critically-ill patients and may result from infection, trauma, haemorrhage, inflammation, organ dysfunction (notably renal and liver dysfunction), or drug therapy. Complex patterns of coagulopathy where both bleeding and prothrombotic tendencies co-exist are well recognized in critical illness. The limitations of standard laboratory coagulation tests to predict bleeding risk, including activated partial thromboplastin time and prothrombin time, are well recognized. These assays were developed for diagnosis of inherited bleeding disorders or for monitoring of anticoagulant therapy. This has led to increased interest in global haemostatic tests, such as viscoelastic and thrombin generation tests. Thromboembolism is an important cause of morbidity and mortality in critically-ill patients. While inherited causes of bleeding appear to be often related to single gene abnormalities, thrombotic tendencies appear to reflect more complex interactions between inherited and acquired factors. Many interactions exist between coagulation pathways and inflammation. Systemic inflammation triggers widespread activation of coagulation, with pro-inflammatory cytokines activating pro-coagulant pathways and downregulating anticoagulant pathways. A net result of this interaction between inflammatory and coagulation pathways in sepsis is thrombin generation, intravascular fibrin deposition and a consumptive coagulopathy.
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Segall, Liviu, i Adrian Covic. Immune-mediated tubulointerstitial nephritis. Redaktor Adrian Covic. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0093_update_001.
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Immune-mediated tubulointerstitial nephritides (TINs) are generally encountered in the context of systemic or extrarenal autoimmune diseases, such as sarcoidosis, Sjögren syndrome, systemic lupus erythematosus, inflammatory bowel disease, TIN and uveitis (TINU) syndrome, and immunoglobulin G4-related disease. The pathogenesis of these TINs is complex and more or less unclear; it usually involves leucocyte activation, autoantibodies, immune complex deposition, complement activation, and release of inflammatory cytokines and growth factors. Tubulointerstitial inflammation most commonly has a chronic pattern, although acute forms of TIN may also occur. Furthermore, inflammation may be granulomatous (as in sarcoidosis or Crohn’s disease) or non-granulomatous. Immunofluorescence staining can sometimes reveal immune complex deposits and even antitubular basement membrane autoantibodies. Systemic immunosuppressive therapies are almost always required to prevent progression to irreversible interstitial fibrosis, tubular atrophy, and end-stage renal disease.
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Twisk, Jos, i Isabel Ferreira. Physical activity, physical fitness, and cardiovascular health. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199232482.003.0025.
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The incidence of morbidity and mortality related to CVD is rather low in a paediatric population. Studies investigating the relationship between physical activity, physical fitness, and cardiovascular health in children and adolescents are therefore mostly limited to CVD risk factors as outcome measures. For this reason, this chapter will focus on the association of physical activity and physical fitness with CVD risk factors in children and adolescents. These risk factors can be divided into the so-called traditional CVD risk factors; that is, lipoproteins [total cholesterol, low-density lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL) cholesterol, triglycerides (TG)], blood pressure, body fatness, and diabetes, and ‘new’ CVD risk factors; that is, other lipoproteins [lipoprotein(a) (Lp(a)), apolipoprotein (apo)B, and apoA-1], coagulation and inflammation markers [fibrinogen, C-reactive protein (CRP)], homocysteine, and heart rate variability.
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Jay, Taylor R., Shane M. Bemiller, Lee E. Neilson, Paul J. Cheng-Hathaway i Bruce T. Lamb. Neuroinflammation and Neurodegenerative Diseases. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190233563.003.0004.
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Neuroinflammation has long been associated with many neurodegenerative diseases (NDDs). Immune-related genetic and environmental risk factors have recently been identified for NDDs, suggesting that neuroinflammation can play an active role in modifying NDD pathologies. Immune cells that underlie this neuroinflammatory response can have both beneficial and detrimental roles in NDDs. These cells can engage in clearance of debris and provide important survival factors to neighboring neurons. However, these cells can also release inflammatory molecules that promote oxidative stress and excitotoxic damage in surrounding neurons, and aberrantly clear healthy cells and structures from the brain. In turn, the cells within the brain play important roles in determining the phenotype and function of these immune cells, and changes in the interaction among these cells in the context of disease can lead to detrimental immune cell activation. There has been recent interest in developing inflammation-related biomarkers to help diagnose NDDs and immune-targeted therapeutics.
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Charlson, Robert W., i Matthew S. Robbins. Migraine and Other Headache Disorders. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0047.
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In recent years, the characterization of the neurobiology of migraine and other headache disorders has been driven by the search to better understand several key factors: genetics, the role of neuromodulators such as calcitonin gene-related peptide (CGRP), processes including central and peripheral sensitization, neurogenic inflammation, central pain networks, and areas of activation demonstrated by advancing functional neuroimaging techniques. Yet the ultimate causes of migraine remain unknown. Nonetheless, recent work has advanced our understanding of this complex disorder, and pointed toward a future where these modalities may provide an integrated understanding of its pathophysiology and provide specific treatment targets.
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Abhishek, Abhishek, i Michael Doherty. Pathophysiology of calcium pyrophosphate deposition. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.003.0049.
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Calcium pyrophosphate (CPP) dihydrate crystals form extracellularly. Their formation requires sufficient extracellular inorganic pyrophosphate (ePPi), calcium, and pro-nucleating factors. As inorganic pyrophosphate (PPi) cannot cross cell membranes passively due to its large size, ePPi results either from hydrolysis of extracellular ATP by the enzyme ectonucleotide pyrophosphatase/phosphodiesterase 1 (also known as plasma cell membrane glycoprotein 1) or from the transcellular transport of PPi by ANKH. ePPi is hydrolyzed to phosphate (Pi) by tissue non-specific alkaline phosphatase. The level of extracellular PPi and Pi is tightly regulated by several interlinked feedback mechanisms and growth factors. The relative concentration of Pi and PPi determines whether CPP or hydroxyapatite crystal is formed, with low Pi/PPi ratio resulting in CPP crystal formation, while a high Pi/PPi ratio promotes basic calcium phosphate crystal formation. CPP crystals are deposited in the cartilage matrix (preferentially in the middle layer) or in areas of chondroid metaplasia. Hypertrophic chondrocytes and specific cartilage matrix changes (e.g. high levels of dermatan sulfate and S-100 protein) are related to CPP crystal deposition and growth. CPP crystals cause inflammation by engaging with the NALP3 inflammasome, and with other components of the innate immune system, and is marked with a prolonged neutrophilic inflitrate. The pathogenesis of resolution of CPP crystal-induced inflammation is not well understood.
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Chung, Melissa, i Warren Lo. Pediatric Stroke. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0106.
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A variety of congenital and genetic disorders not seen frequently in adults may be responsible for stroke in infants and children. Stroke in newborn infants is as common as stroke in elderly individuals due to risk factor such as congenital heart disease, thrombophilia associated with polycythemia in neonates and genetic disorders, high estrogen impact from the mother during pregnancy, and inflammation due to infections. Stroke can also be caused by genetic disorders such as Ehleers-Danlos syndrome, Sturge-Weber syndrome, and vasculopathies such as lupus and fibromuscular dysplasia. Arterial dissection may be related to trauma and athletic injuries. Some drugs used to treat cancer such as asparaginase can also cause strokes, and infants and children can also present with venous sinus thrombosis associated with critical illness and dehydration.
Części książek na temat "Inflammation-related factors"
1
Yeung, Wendy Wing Shan, Maurice Kwok Chung Ho i Yung Hou Wong. "Functional Impacts of Signal Integration: Regulation of Inflammation-Related Transcription Factors by Heterotrimeric G Proteins". W From Molecular to Modular Tumor Therapy, 161–89. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-90-481-9531-2_9.
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Reindl, Judith, Ana Margarida Abrantes, Vidhula Ahire, Omid Azimzadeh, Sarah Baatout, Ans Baeyens, Bjorn Baselet i in. "Molecular Radiation Biology". W Radiobiology Textbook, 83–189. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-18810-7_3.
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AbstractVarious exogeneous and endogenous factors constantly cause damages in the biomolecules within a cell. For example, per day, 10,000–100,000 molecular lesions occur in DNA per cell. The molecule modifications that are formed disturb the structure and function of the affected molecules. The purpose of this chapter is to introduce the damages to biomolecules caused by radiation, the associated repair pathways, and the effect on the cellular function. Special interest lies on the damages induced to DNA, the carrier of the human genome, and the consequence to genomic integrity, cell death, and cell survival. Additionally, related effects regarding inflammation and immunity, epigenetic factors, and omics are discussed. The chapter concludes with an explanation of the molecular factors of cellular hyper-radiosensitivity and induced radiation resistance.
3
Yucel, Zeliha, i E. Berrin Yuksel. "The Genetics of Diabetic Neuropathy". W Current Perspective on Diabetes Mellitus in Clinical Sciences, 423–36. Istanbul: Nobel Tip Kitabevleri, 2023. http://dx.doi.org/10.69860/nobel.9786053359111.39.
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Diabetic neuropathy, a common complication of diabetes mellitus (DM), involves nerve damage resulting from prolonged exposure to high blood sugar levels. Genetic factors play a crucial role in influencing susceptibility to this condition. Variations in genes related to nerve structure and function, inflammatory responses, and metabolic processes have been implicated in diabetic neuropathy. For instance, polymorphisms in the gene encoding protein kinase C beta (PKC-β) contribute to increased vulnerability by promoting oxidative stress and inflammation in nerve tissues. Similarly, genetic variations in the aldose reductase gene (AKR1B1), involved in the polyol pathway, may disrupt glucose metabolism and contribute to nerve damage. Furthermore, genes regulating neurotrophic factors like nerve growth factor (NGF) and those affecting mitochondrial function and oxidative stress responses also influence neuropathy risk. Understanding these genetic underpinnings not only enhances our knowledge of diabetic neuropathy’s pathophysiology but also opens avenues for personalized therapeutic strategies aimed at mitigating its impact. Continued research into the interplay of genetic predisposition and environmental factors promises further insights into preventing and managing this debilitating complication effectively.
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Ali, Rania Alhaj, Hussein Halabi i Hani Almoallim. "Cardiovascular Diseases and Rheumatology". W Skills in Rheumatology, 353–81. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-15-8323-0_16.
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AbstractThe prevalence of various cardiovascular diseases (CVD) in the different rheumatologic disorders is a very important topic. Each disease has a number of unique manifestations despite the fact that an overlap is present due to shared common risk factors, which may be related to the longer life expectancy of the recent therapeutic advances. A growing understanding of the role of inflammation and immune system in the initiation and progression of atherosclerosis as well as the early detection of cardiovascular manifestations is due to the availability and use of sophisticated noninvasive cardiac and vascular diagnostic technology. Such discipline results in the detection of cardiac manifestation unique to each rheumatologic disorder. This was not possible previously due to short life expectancy, limited therapeutic interventions, vague understanding of pathological process for each disease, and the limited diagnostic resources.
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Gamble, Jennifer R., Pu Xia i Mathew A. Vadas. "The transforming growth factor family and the endothelium". W TGF-β and Related Cytokines in Inflammation, 41–64. Basel: Birkhäuser Basel, 2001. http://dx.doi.org/10.1007/978-3-0348-8354-2_3.
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Maswood, Navin, i Don M. Gash. "Biology of glial cell-line derived neurotrophic factor". W TGF-β and Related Cytokines in Inflammation, 157–72. Basel: Birkhäuser Basel, 2001. http://dx.doi.org/10.1007/978-3-0348-8354-2_7.
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Georgiou, Georgios K., i Evangelos Briasoulis. "Peri-operative Shift in Angiogenesis-Related Factors in Breast Cancer Patients". W Perioperative Inflammation as Triggering Origin of Metastasis Development, 55–81. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-57943-6_3.
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Karalezli, Ilknur. "Cancer and Pathogenesis". W Oncological Rehabilitation a Handbook for Healthcare Professionals, 1–18. Istanbul: Nobel Tip Kitabevleri, 2024. http://dx.doi.org/10.69860/nobel.9786053358893.1.
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Cancer assessment is of paramount importance as it encompasses understanding the nature of cancer, risk evaluation, prevention strategies, and health management. A tumor denotes an abnormal proliferation of cells lacking functional purpose and without the potential to metastasize to adjacent cells, organs, or distant parts of the body; hence, not all tumors are malignant, with benign tumors exhibiting non-invasive characteristics. The etiology of benign tumors remains somewhat elusive; however, genetic predispositions, poor dietary choices, exposure to radiation or toxins, occupational stress, infections, or inflammation are known factors contributing to their development. Consequently, cells capable of metastasis must be clearly distinguished from others, a crucial factor influencing treatment modalities. As epigenetic mechanisms exert direct control over gene expression, research in this field has witnessed a surge. While certain epigenetic mechanisms silence genes by converting chromatin into heterochromatin, others activate genes by transforming them into euchromatin. Chromatin modification mechanisms facilitating epigenetic alterations encompass DNA methylation, nucleosome reorganization, histone methylation, modulation of nucleosome density, regulation of nuclear architecture, among others. These mechanisms are under scrutiny in cancer research, aided by advancements in technology, to unravel their role in oncogenic processes. Oncogenes play crucial roles in both the initiation and progression of human carcinogenesis, converting healthy cells into cancerous ones. Alongside oncoproteins or tumor suppressor gene products, they contribute to the development of human cancers by stimulating proliferation, disrupting cell cycle regulation, or inhibiting apoptosis. These mechanisms also influence the duration of disease-related survival. Molecular biomarkers utilized in decision-making processes within oncology are categorized as prognostic or predictive, with ongoing efforts to understand their significance in elucidating cancer mechanisms. Prognostic biomarkers enable the classification of cancer based on the risk of disease progression or mortality, facilitating tailored treatment strategies for individual patients. Such biomarkers serve as indicators of patient survival, reflecting the intrinsic aggressiveness of the tumor. Hence, early diagnosis holds pivotal importance in the cancer trajectory. In solid tumors, clinically significant molecular biomarkers aid in delineating the mechanisms underlying cancer initiation, progression, and response to treatment, thereby influencing therapeutic success. The objective of this chapter is to underscore that understanding cancer mechanisms can pave the way for enhanced early diagnosis and treatment. There exist crucial connections between research, technological advancements, and the formulation of innovative approaches in the diagnosis and treatment of oncological malignancies. Leveraging current knowledge to develop novel strategies holds significant promise in extending survival rates.
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Fikri, Erjan, Ahmad Razi Maulana Alnaz i Fini Meirisa Alnaz. "Endothelial Dysfunction in Appendicitis". W Endothelial Dysfunction - A Novel Paradigm. IntechOpen, 2023. http://dx.doi.org/10.5772/intechopen.107480.
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In an inflammation, including appendicitis, vascular adequacy is required to supply anti-inflammatory substances and nutrition due to inflamed tissue remodeling. Normal tissue has balanced tissue regeneration and tissue destruction from apoptosis. While in inflammation, inflammatory substances tend to cause tissue destruction and lead to necrosis. This requires the tissue to increase cell regeneration to maintain tissue homeostasis in the appendix, induced mainly by oxygenation, nutrition, growth factors, and mainly anti-inflammatory substances that are obtained with vascular adequacy. This process needs active vascularization that can be achieved with neovascularization to ensure good vascularization to the tissue lacking from vascular damage. The ability of neovascularization is mainly related to growth factors acting in the endothelium and inducing neovascularization process. This mechanism is impaired in the process of inflammation by inflammatory substances causing endothelial dysfunction. As stated that vascular adequacy is related to growth factors such as vascular endothelial growth factors (VEGF) that may differ from one person to another, external and internal factors plays role in affecting individualized difference in adapting to inflammatory process, the expression of the VEGF may be a novel distinction to cut-off requirements of inflammation process in appendicitis would be self-limiting or continue to cause tissue necrosis and perforating appendicitis that urges surgical treatment to encounter the unstoppable inflammatory process in the appendix.
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Castanheiro Esteves Carias, Eduarda, Roberto Calças Marques i Ana Paula Andrade da Silva. "Vascular Calcification and Cardiovascular Risk in Chronic Kidney Disease: A Problem That Is Here to Stay". W Cardiovascular Risk Factors [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.99886.
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Cardiovascular disease is the primary cause of morbidity and mortality in chronic kidney disease (CKD) population, particularly in end stage renal disease (ESRD). This could be explained in part due to the presence of traditional cardiovascular risk factors, such as older age, hypertension, dyslipidemia and diabetes, but is also associated with nontraditional cardiovascular risk factors related to CKD, like inflammation, anemia, abnormal calcium and phosphate metabolism and extracellular fluid volume overload, which may contribute to intimal or medial wall arterial calcification. Vascular calcification (VC) is a dynamic process, resulting from the dysregulation of the balance of molecules that promote and those that inhibit this course. It is important for clinicians to both acknowledge and recognize the pathways and risk factors of VC in order to improve cardiovascular health in CKD patients. This chapter will focus on the biology of VC, the association with CKD, risk factor modification, screening and prevention of VC and cardiovascular disease in CKD patients.
Streszczenia konferencji na temat "Inflammation-related factors"
1
Chen, C. T. Christopher, Alexandra DiTullio i Xianghua Deng. "Gelatinase B (MMP-9) Modulates Joint Inflammation and Cartilage Degradation After Overload Injury". W ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176466.
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Osteoarthritis is the leading cause for disability in the U.S. Primary osteoarthritis occurs progressively with age due to a variety of factors, while secondary osteoarthritis is usually the result of a sports or accident-related joint injury. Several recent studies found that degraded matrix in synovial fluid was surged within days after initial injury along with the elevation of matrix degradative enzymes, including matrix metalloproteinases (MMPs) and aggrecanases [1]. The elevation of degraded matrix could last for up to a decade, although it is not clear whether these degradative events are related to joint inflammation, the chronic presence of which is the hallmark of rheumatoid arthritis and often leads to joint degeneration.
2
Al Joujou, Abeer, i Shahed Kuraitby. "A Management of Severe Papillary Denture Stomatitis with A Double Treatment of Nystatin Mouthwash and Diode Laser. A Case Report". W 5th International Conference on Biomedical and Health Sciences, 444–47. Cihan University-Erbil, 2024. http://dx.doi.org/10.24086/biohs2024/paper.1111.
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The inflammation of the oral mucosa beneath the denture base is known as denture stomatitis, prosthetic stomatitis, denture sore mouth, and inflammatory papillary hyperplasia.[1] It is characterized by inflammation and erythema of the oral mucosa tissues that are covered by the denture.[2] With a prevalence ranging from 15% to over 70%, it is the most common issue among denture wearers.[3]Denture stomatitis is a complex condition with an intricate etiology that remains poorly understood. However, several factors contribute to its development, including inadequate denture hygiene, continuous and nocturnal denture wearing, accumulation of plaque on dentures, poorly fitting dentures, and denture-related trauma. These factors create an environment that promotes the colonization of Candida on both the oral mucosa and denture surfaces, ultimately leading to stomatitis. Although most cases of this disorder are asymptomatic, some individuals may experience clinical manifestations such as alterations in the color and texture of the mucous membranes, dry mouth, breathing difficulties, a burning sensation, halitosis, and painful symptoms.
3
Liu, Xihan, Beihua Kong, Kun Song i Jin Peng. "EP076/#303 Immune and inflammation-related factors alteration as a biomarker for predicting prognosis and responsiveness to PD-1 monoclonal antibody in patients with recurrent cervical cancer". W IGCS 2022 Annual Meeting Abstracts. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/ijgc-2022-igcs.167.
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Soroceanu, Radu-Petru, Ioana Silistraru, Anamaria Ciubara, Doina Azoicai, Daniel Timofte, Liviu Răzvan Platon, Bogdan Ciuntu i Mădălina Maxim. "OBESITY AND DEPRESSION INTERTWINED – A NARRATIVE REVIEW". W The European Conference of Psychiatry and Mental Health "Galatia". Archiv Euromedica, 2023. http://dx.doi.org/10.35630/2022/12/psy.ro.18.
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Both pathologies—obesity and depression—have high prevalence rates and have serious negative effects on the public's health. In recent meta-analyses, clinical trials, and epidemiological studies, they have been observed in people of all races. Both obesity and major depression are risk factors related to one another. In this paper, we suggest an overview of the two interconnected biological processes, including genetic influences and changes to the systems in charge of energy synthesis and consumption (hypothalamic-pituitary-adrenal axis, and inflammation, neuroendocrine regulators, and gut microbiota). Additionally, we look into how people perceive their bodies and social stigma, as well as the potential benefits of physical activity and weight-loss surgery on comorbid conditions and quality of life.
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Liu, Xiao-Ling. "DECIPHERING THE GENETIC LINKS BETWEEN PSYCHOLOGICAL STRESS, AUTOPHAGY, AND DERMATOLOGICAL HEALTH: INSIGHTS FROM BIOINFORMATICS, SINGLE-CELL ANALYSIS, AND MACHINE LEARNING IN PSORIASIS AND ANXIETY DISORDERS". W BioClina 2024 – International Conference on Biological & Clinical Studies, 21-22 June, Singapore. Global Research & Development Services, 2024. http://dx.doi.org/10.20319/icrlsh.2024.8687.
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The relationship between psychological stress, altered skin immunity, and autophagy-related genes (ATGs) is currently unclear. Psoriasis is a chronic skin inflammation of unclear etiology that is characterized by persistence and recurrence. Immune dysregulation and emotional disturbances are recognized as significant risk factors. Emerging clinical evidence suggests a possible connection between anxiety disorders, heightened immune system activation, and altered skin immunity, offering a fresh perspective on the initiation of psoriasis. The aim of this study was to explore the potential shared biological mechanisms underlying the comorbidity of psoriasis and anxiety disorders. Psoriasis and anxiety disorders data were obtained from the GEO database. A list of 3254 ATGs was obtained from the public database. Differentially expressed genes (DEGs) were obtained by taking the intersection of DEGs between psoriasis and anxiety disorder samples and the list of ATGs. Five machine learning algorithms used screening hub genes. The ROC curve was performed to evaluate diagnostic performance. Then, GSEA, immune infiltration analysis, and network analysis were carried out. The Seurat and Monocle algorithms were used to depict T-cell evolution. Cellchat was used to infer the signaling pathway between keratinocytes and immune cells. Four key hub genes were identified as diagnostic genes related to psoriasis autophagy. Enrichment analysis showed that these genes are indeed related to T cells, autophagy, and immune regulation, and have good diagnostic efficacy validated. Using single-cell RNA sequencing analysis, we expanded our understanding of key cellular participants, including inflammatory keratinocytes and their interactions with immune cells. We found that the CASP7 gene is involved in the T-cell development process, and correlated with γδ T cells, warranting further investigation. We found that anxiety disorders are related to increased autophagy regulation, immune dysregulation, and inflammatory response, and are reflected in the onset and exacerbation of skin inflammation. The hub gene is involved in the process of immune signaling and immune regulation. The CASP7 gene, which is related with the development and differentiation of T cells, deserves further study. Potential biomarkers between psoriasis and anxiety disorders were identified, which are expected to aid in the prediction of disease diagnosis and the development of personalized treatments.
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Pizarro, Jorge, Byron Vásquez, Willan Steven Mendieta Molina i Remigio Hurtado. "Hepatitis predictive analysis model through deep learning using neural networks based on patient history". W 13th International Conference on Applied Human Factors and Ergonomics (AHFE 2022). AHFE International, 2022. http://dx.doi.org/10.54941/ahfe1001449.
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First of all, one of the applications of artificial intelligence is the prediction of diseases, including hepatitis. Hepatitis has been a recurring disease over the years as it seriously affects the population, increasing by 125,000 deaths per year. This process of inflammation and damage to the organ affects its performance, as well as the functioning of the other organs in the body. In this work, an analysis of variables and their influence on the objective variable is made, in addition, results are presented from a predictive model.We propose a predictive analysis model that incorporates artificial neural networks and we have compared this prediction method with other classification-oriented models such as support vector machines (SVM) and genetic algorithms. We have conducted our method as a classification problem. This method requires a prior process of data processing and exploratory analysis to identify the variables or factors that directly influence this type of disease. In this way, we will be able to identify the variables that intervene in the development of this disease and that affect the liver or the correct functioning of this organ, presenting discomfort to the human body, as well as complications such as liver failure or liver cancer. Our model is structured in the following steps: first, data extraction is performed, which was collected from the machine learning repository of the University of California at Irvine (UCI). Then these data go through a variable transformation process. Subsequently, it is processed with learning and optimization through a neural network. The optimization (fine-tuning) is performed in three phases: complication hyperparameter optimization, neural network layer density optimization, and finally dropout regularization optimization. Finally, the visualization and analysis of results is carried out. We have used a data set of patient medical records, among the variables are: age, sex, gender, hemoglobin, etc. We have found factors related either indirectly or directly to the disease. The results of the model are presented according to the quality measures: Recall, Precision and MAE.We can say that this research leaves the doors open to new challenges such as new implementations within the field of medicine, not only focused on the liver, but also being able to extend the development environment to other applications and organs of the human body in order to avoid risks possible, or future complications. It should be noted that the future of applications with the use of artificial neural networks is constantly evolving, the application of improved models such as the use of random forests, assembly algorithms show a great capacity for application both in biomedical engineering and in focused areas to the analysis of different types of medical images.
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Costa, Guilherme Albuquerque de Araujo, Mariana Silva Regadas i Myrela Murad Sampaio. "Hemorrhagic stroke (ICH): A consequence of thromboembolic events resulting from COVID-19". W XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.364.
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Introduction: The COVID-19 pandemic has been alarming the world since its first outbreak in December 2019. In this scenario, the presence of aggravating factors such as the elevation of the D-dimer and the reduction of the angiotensin-converting enzyme 2 (ACE2) during the clinical course of the disease, collaborated in the appearance of thromboembolic events derived from inflammatory processes and extensive intravascular coagulation, contributing to the emergence of diseases such as Hemorrhagic Stroke (ICH), leading the patient to have a worse clinical prognosis and a consecutive worsening of their health. Objective: To investigate occurrences of ICH derived from thromboembolic effects resulting from COVID-19. Methods: We selected 43 articles published between 2020 and 2021 on the PubMed platforms, SciELO portal, CAPES Journal and Google Scholar in order to conduct an integrative review within this database. Results: The elevated D-dimer was widely cited as a favorable factor for thromboembolic events due to the influence of excessive inflammatory processes, hypoxia and intravascular dissemination of coagulation, contributing to the development of ICH, given its greater association with disorders such as ischemic strokes, considering only these parameters. However, the reduction in ACE2 and the occurrence of cytokine storms end up causing increased inflammation and blood pressure, increasing the risk of stroke due to the rupture of capillaries sensitized by the action of thromboembolic effects and becoming a risk to the life and prognosis of patients infected with SARS-CoV2, especially in groups of individuals with a greater predisposition to the development of thromboembolic and hypertensive events related to COVID-19.
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Silva, Alexandre Almeida da, Lucas Cruz Furtado i Júlio César Claudino dos Santos. "Gut-microbiome-brain-axis: the crosstalk between the vagus nerve, alpha-synuclein and the brain in Parkinson’s disease". W XIV Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2023. http://dx.doi.org/10.5327/1516-3180.141s1.783.
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Introduction: The vagus nerve, the main component of the parasympathetic nervous system, is involved in the regulation of immune response, digestion, heart rate, and control of mood. It can detect microbiota metabolites through its afferents, transferring this gut information to the central nervous system. Preclinical and clinical studies have shown the important role played by the gut microbiome and gut-related factors in disease development and progression, as well as treatment responses. Objectives: To describe and discuss the close link between the microbiome, the gut and the brain in Parkinson’s disease. Methods: This is a critical review of the literature on the microbiome, gut, and brain in Parkinson’s disease. Results: The gut microbiota has been demonstrated to be a pivotal contributor to the promotion of health. Emerging data has indicated that, up to 20 years before the onset of motor symptoms, an alteration in the gut microbiome may be present in Parkinson’s disease patients. This dysbiosis of the gut may lead to increased intestinal permeability and inflammation, as well as Lewis body formation, and can also cause neuroinflammation and decreased neurotransmitter production in the central nervous system. Conclusion: More studies are needed to better understand the underlying biology and how this axis can be modulated for the patient’s benefit.
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Grubač, Siniša, Marko Cincović, Jože Starič, Marinković Došenović, Biljana Delić-Vujanović i Jasna Prodanov-Radulović. "The relationship of the metabolism of iron, organic matter and phlebotomy with the erythropoiesis of ruminants". W Zbornik radova 26. medunarodni kongres Mediteranske federacije za zdravlje i produkciju preživara - FeMeSPRum. Poljoprivredni fakultet Novi Sad, 2024. http://dx.doi.org/10.5937/femesprumns24012g.
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Erythropesis is the process of making red blood cells and it is related to numerous factors in the body. Iron is important because of its role in the process of making hemoglobin. In addition to the mentioned iron, it is an indirect indicator of inflammation and is regulated at the systemic and cellular level, so its lack speaks of the overall health status of individuals. Fe deficiency in the body takes place through three phases. In the first phase, there is emptying of tissue depots, but its total amount in the circulation increases, then follows the second phase or the phase of real deficit with decreasing concentration of serum iron and hemoglobin, and the third phase is the phase in which the significance of iron deficit is clinically seen. Iron deficiency disrupts all aspects of erythropoiesis. Therefore, first the iron reserves are used up, then with the decrease of transported iron, erythropoiesis changes, and when the availability of this iron is completely reduced, anemia will occur due to iron deficiency. Lipid metabolism also plays a very important role in the functioning of hematopoietic stem cells. Fatty acid oxidation is the main catabolic pathway by which energy is produced in hematopoietic stem cells. Long-chain fatty acids are activated in the cytosol and transported to the mitochondria by the transport system. In them, beta oxidation takes place through several known stages, creating acetyl coenzyme A, which starts the cycle of tricarboxylic acids. Deletion of the gene for regulation of fatty acid oxidation causes hematopoiesis stem cells to lose their potential to reconstruct and maintain themselves. Due to the importance of lipolysis in ruminants and the fact that stem cells are found in the lipidrich niches of bone marrow, we will also consider the relationship between bone marrow adipocytes and hematopoiesis. Chronic phlebotomy in rams or Fe deficiency due to inflammation and fatty liver in cows lead to specific changes in red blood cell and blood metabolites. All of the above shows that it is necessary to know the metabolic flows in order to better understand erythropoiesis in ruminants.
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Stocchino, Alessandro, Domenico Palombo, Bianca Pane i Giovanni Spinella. "In Vivo Echo-PIV Measurements of the Flow Within Abdominal Aortic Aneurisms (AAA)". W ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19331.
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The incidence of Abdominal Aortic Aneurysms (AAA) varies between 3% and 6% of the elder population, especially men over sixty years of age. Moreover, familiarity, smoking and peripherical atherosclerosis are known to be important risk factors. In the United States AAA ruptures cause about 9000 deaths every year. About 33000 elective surgical treatments per year are performer with a mortality of 1400–2800 patients. The percentage of success of surgical treatment remains strictly related to the diagnosis of the stage of the AAA. Mortality rate for elective surgical intervention (asymptomatic aneurysms) is 5%. On the contrary mortality rate for emergency surgical intervention is about 70% [1]. Selection of candidates to surgery is still based on measurement of aortic diameter, with a threshold size of 55 mm. The rate of AAA rupture increases from 21% to 46% for diameters between 50 and 70 mm. The main diagnostic tool currently adopted is the CT that allows for obtaining precise information regarding the dimensions and the morphology of the aneurysm and possible proximal extension (juxarenal, infrarenal, thorac-abdominal) and distal (iliac and hypogastric) of the aneurysm, intramural thrombus. Since rupture occurs when the aneurysm wall fails to withstand the forces acting on it, in vivo data on AAA wall pathology could identify patients at risk of rupture. End-stage aneurysm disease and especially aneurysm rupture are characterized by extensive inflammation of the arterial wall. Although the stimulus for this enhanced infiltration is not known, recent insights into the pathophysiology of aneurysm formation, growth, and rupture indicate a close relationship between increased mechanical stress and the activation of infiltrated lymphocytes and macrophages [2]. This increased inflammatory activity results in the progressive breakdown of the aortic wall, aneurysm dilatation and, ultimately, rupture. A further complication is represented by the mechanical actions exerted on the arterial wall by the internal blood flow. The blood flow is strongly influenced by the presence of an AAA, which modifies significantly the geometry of the aorta. Shear stresses and pressure are important factors to understand the formation and evolution of an AAA. Another important aspect is related to the formation of the thrombus that is thought to be relevant for the wall degeneration, see [3] for a comprehensive review of these topics.
Raporty organizacyjne na temat "Inflammation-related factors"
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Yu, Mei, Pengyu Wang, Binbin Li, Qiaoling Ruan, Jingzi ZhangBao, Lei Wu, Xiaoshuang Zhang, Zhaolin Liu i Fang Huang. NRSF Negatively Regulates Microglial Pro-Inflammatory Activation. Progress in Neurobiology, maj 2024. http://dx.doi.org/10.60124/j.pneuro.2024.20.02.
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Microglial activation contributes to neurological disorders like Parkinson’s disease (PD), and modulating this activation is a potential therapeutic approach. The neuron-restrictive silencer factor (NRSF) functions as a negative regulator of gene transcription through epigenetic modifications. While previous research has primarily examined the role of NRSF in neuronal differentiation and injury, emerging evidence indicates that NRSF also plays a significant role in maintaining the phenotype of glial cells. In this study, we explored the role and underlying mechanisms of NRSF in lipopolysaccharide (LPS)-induced pro-inflammatory or interleukin-4 (IL4)-induced anti-inflammatory phenotype of microglial activation. Following LPS stimulation, the nuclear localization of NRSF increased in BV2 microglial cells, primary mouse microglia, and microglia within the substantia nigra of PD mice. Knockdown of NRSF enhanced the expression of inflammation-related factors induced by LPS via the mitogen-activated protein kinase-extracellular signal-regulated kinase (MAPK-ERK) and nuclear factor-κB (NF-κB) p65 signalling pathways in BV2 cells. Moreover, the culture medium from LPS-treated NRSF knockdown BV2 cells exerted greater toxic effects on human neuroblastoma SH-SY5Y cells compared to the control. However, NRSF knockdown exerted inconsistent effects on the expression of anti-inflammatory-related genes in IL4-treated BV2 cells. Our findings suggest that NRSF knockdown promotes microglial pro-inflammatory activation.
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Zhao, Zepeng, Fengyuan Zhang i Yijin Li. The Relationship Between Il-1 RN intron 2 (VNTR) rs2234663 Gene Polymorphism and The Progression of Periodontitis: A systematic Review and Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, marzec 2023. http://dx.doi.org/10.37766/inplasy2023.3.0100.
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Review question / Objective: The aim of this systematic review and meta-analysis of case-control studies is to find out the association of IL-1 RN intron 2 (VNTR) rs2234663 Gene Polymorphism and the occurrence and progression of periodontitis(including chronic periodontitis, aggressive periodontitis and early-onset periodontitis). Condition being studied: Periodontitis is one of the most common ailments affecting the teeth, leading to the destruction of the supporting and surrounding tooth structure. Periodontitis is originally a disease originating from the gingival tissue which if left untreated results in penetration of inflammation to the deeper tissues, altering the bone homeostasis causing tooth loss. Periodontal disease has a multifactorial origin. The main culprit identified in periodontitis is the bacterial biofilm growing on the tooth surfaces. The deleterious effects of periodontopathogens are not limited to the periodontium, but they also exude their ill effects on the systemic health of the patients. While the host response determines the progression of the disease, genetics, environmental factors, systemic health of the patient, lifestyle habits and various social determinants also play a role. Interleukin-1 receptor antagonist encoded by this gene IL-1RN is a member of the interleukin 1 cytokine family. This protein inhibits the activities of interleukin 1, alpha (IL1A) and interleukin 1, beta (IL1B), and modulates a variety of interleukin 1 related immune and inflammatory responses, particularly in the acute phase of infection and inflammation. We aim to study their association by conducting a meta-analysis.
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Liu, Yangjun, Wei Xie, Zbigniew Ossowski, Juan Li, Juan Yang, Yiming Luo, Xia Wu i Liying Liu. Physical activity, abdominal obesity and inflammatory response in the elderly: a systematic review and meta-analysis of randomized-controlled trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, marzec 2023. http://dx.doi.org/10.37766/inplasy2023.3.0051.
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Review question / Objective: The purpose of this study was to explore the effects of physical activity (i.e., type of exercise, FITT criteria, control group, other interventions) on abdominal obesity and inflammatory response in elderly? The study method was a randomized controlled trial. Condition being studied: An increasing number of studies have demonstrated that chronic inflammation is closely associated with the initiation and progression of a broad range of age-related diseases, such as cardiovascular disease, cancer, diabetes, Alzheimer’s disease, and other neurodegenerative diseases and is an independent risk factor for mortality in healthy adults. Moreover, there is strong evidence that the development of age-related diseases is linked to low-grade elevation of circulating inflammatory mediators. Therefore, future interventional researches should focus on preserving overall homeostatic balance and controlling inflammatory status in the aging patient.