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Journal articles on the topic 'Pentraxina 3'

Author: Grafiati
Published: 4 June 2021
Last updated: 11 March 2023

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1

El Wakeel, Maged A., Rania N. Sabry, Ghada M. El-kassas, Shereen A. Abd El-Gaffar, Wael H. El batal, Essam M. Galal, Ashraf Azmy, and Eman Awadallah. "Pentraxin 3: A Potential Novel Predictor for Neonatal Pulmonary Hypertension." Open Access Macedonian Journal of Medical Sciences 7, no. 15 (August 14, 2019): 2424–27. http://dx.doi.org/10.3889/oamjms.2019.638.

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BACKGROUND: Persistent pulmonary hypertension of the newborn (PPHN) is a serious neonatal problem which has a high mortality rate even with advanced modes of mechanical ventilation. Pentraxin 3 is one of the long pentraxins, which plays an essential role in regulation of cell proliferation and angiogenesis. AIM: This study aims to assess serum pentraxin 3 levels in neonates with pulmonary arterial hypertension and compare them in those who have other congenital heart diseases and healthy neonates. Also, we intended to evaluate serum levels of CRP as a mediator of inflammation in the studied groups. METHODS: The study is a case-control study. Cases were recruited from El Galaa Teaching Hospital, classified into three groups; each group had thirty cases. The first one: cases with pulmonary hypertension (PHT), the second one: cases with congenital heart diseases (CHD) without pulmonary hypertension and the third group included healthy neonates. All participants were subjected to full history taking and full clinical examination. Diagnosis of congenital heart disease and pulmonary hypertension was made according to echocardiographic findings by pediatric cardiologist using echocardiography machine. Laboratory investigations included measurement of serum pentraxin 3, Routine CBC, CRP. RESULTS: This study found that the mean serum pentraxin 3 in PHT neonates was significantly higher than that of the control and CHD neonates (p ≤ 0.001, p = 0.02 respectively). Also, the mean Pentraxin3 of the CHD neonates was significantly higher than that of the control (p = 0.06). Also, the mean CRP of the PHT neonates was significantly higher than that of the control (p = 0.01). Regression analysis showed that Pentraxin3 was the main predictor of PAP (P = 0.01). CONCLUSION: Serum pentraxin 3 is significantly elevated in neonates with pulmonary hypertension, so measurement of pentraxin 3 levels in neonates may be valuable as a predictor for pulmonary hypertension in neonates.
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2

Kunes, P., Z. Holubcova, M. Kolackova, and J. Krejsek. "Pentraxin 3(PTX 3): An Endogenous Modulator of the Inflammatory Response." Mediators of Inflammation 2012 (2012): 1–10. http://dx.doi.org/10.1155/2012/920517.

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Inflammatory or anti-inflammatory? That is the question as far as the acute-phase response and its mediators, the pentraxins, are concerned. Only some ten years ago, the classical or short pentraxin C-reactive protein and the newly discovered long pentraxin PTX3 were considered to exert most of the detrimental effects of acute inflammation, whether microbial or sterile in origin. However, accumulating evidence suggests an at least dichotomous, context-dependent outcome attributable to the pentraxins, if not a straightforward anti-inflammatory nature of the acute-phase response. This paper is focused on the inherent effects of pentraxin 3 in inflammatory responses, mainly in coronary artery disease and inAspergillus fumigatusinfection. Both are examples of inflammatory reactions in which PTX3 is substantially involved; the former sterile, the latter infectious in origin. Apart from different inducing noxae, similarities in the pathogenesis of the two are striking. All the same, the introductory question still persists: is the ultimate impact of PTX3 in these conditions inflammatory or anti-inflammatory, paradoxical as the latter might appear? We try to provide an answer such as it emerges in the light of recent findings.
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3

Alieva, Amina M., Natalia V. Teplova, Maxim A. Batov, Kira V. Voronkova, Ramiz K. Valiev, Lidia M. Shnakhova, Tatiana V. Pinchuk, Alik M. Rakhaev, Marina R. Kalova, and Igor G. Nikitin. "Pentraxin-3 – a promising biological marker in heart failure: literature review." Consilium Medicum 24, no. 1 (January 15, 2022): 53–59. http://dx.doi.org/10.26442/20751753.2022.1.201382.

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According to many studies, inflammation plays a very significant role in the pathogenesis of heart failure. Many studies have demonstrated an increase in circulating levels of inflammatory markers and cytokines such as C-reactive protein, tumor necrosis factor-a (TNF-a), and interleukins. C-reactive protein is produced in the liver in response to stimulation by various cytokines, mainly interleukin-6, and is a member of the pentraxin superfamily. Pentraxin-3, which is a long pentraxin, has a C-terminal domain of pentraxin similar to the classic short pentraxins, but differs from them in the presence of an unrelated long N-terminal domain. Various cell types can produce pentraxin-3 when exposed to primary inflammatory signals such as interleukin-1, tumor necrosis (TNF-a), oxidized low density lipoprotein, and microbial fragments (eg, lipopolysaccharide, lipoarabinomannans). Data in experimental animal models have demonstrated that pentraxin-3 can play cardioprotective and atheroprotective roles through its influence on the inflammatory process. Pentraxin-3 has been studied in several clinical protocols as a potential biomarker for cardiovascular disease.
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4

Lucarelli, G., G. S. Netti, F. Spadaccino, G. Castellano, M. Gigante, C. Divella, M. T. Rocchetti, et al. "La Pentraxina 3 (PTX3) Modula l’immunoflogosi nel microambiente tumorale ed è un fattore prognostico in pazienti con carcinoma renale a cellule chiare." European Urology Open Science 20 (October 2020): S63—S64. http://dx.doi.org/10.1016/s2666-1683(20)35398-2.

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5

Bonacina, Fabrizia, Andrea Baragetti, Alberico Luigi Catapano, and Giuseppe Danilo Norata. "Long Pentraxin 3: Experimental and Clinical Relevance in Cardiovascular Diseases." Mediators of Inflammation 2013 (2013): 1–10. http://dx.doi.org/10.1155/2013/725102.

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Pentraxin 3 (PTX3) is an essential component of the humoral arm of innate immunity and belongs, together with the C-reactive protein (CRP) and other acute phase proteins, to the pentraxins' superfamily: soluble, multifunctional, pattern recognition proteins. Pentraxins share a common C-terminal pentraxin domain, which in the case of PTX3 is coupled to an unrelated long N-terminal domain. PTX3 in humans, like CRP, correlates with surrogate markers of atherosclerosis and is independently associated with the risk of developing vascular events. Studies addressing the potential physiopathological role of CRP in the cardiovascular system were so far inconclusive and have been limited by the fact that the sequence and regulation have not been conserved during evolution between mouse and man. On the contrary, the conservation of sequence, gene organization, and regulation of PTX3 supports the translation of animal model findings in humans. While PTX3 deficiency is associated with increased inflammation, cardiac damage, and atherosclerosis, the overexpression limits carotid restenosis after angioplasty. These observations point to a cardiovascular protective effect of PTX3 potentially associated with the ability of tuning inflammation and favor the hypothesis that the increased levels of PTX3 in subjects with cardiovascular diseases may reflect a protective physiological mechanism, which correlates with the immunoinflammatory response observed in several cardiovascular disorders.
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6

Introna, M., VV Alles, M. Castellano, G. Picardi, L. De Gioia, B. Bottazzai, G. Peri, et al. "Cloning of mouse ptx3, a new member of the pentraxin gene family expressed at extrahepatic sites." Blood 87, no. 5 (March 1, 1996): 1862–72. http://dx.doi.org/10.1182/blood.v87.5.1862.1862.

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Abstract Pentraxins, which include C reactive protein (CRP) and serum amyloid P component (SAP), are prototypic acute phase reactants that serve as indicators of inflammatory reactions. Here we report genomic and cDNA cloning of mouse ptx3 (mptx3), a member of the pentraxin gene family and characterize its extrahepatic expression in vitro and in vivo. mptx3 is organized into three exons on chromosome 3: the first (43 aa) and second exon (175 aa) code for the signal peptide and for a protein portion with no high similarity to known sequences the third (203 aa) for a domain related to classical pentraxins, which contains the “pentraxin family signature.” Analysis of the N terminal portion predicts a predominantly alpha helical structure, while the pentraxin domain of ptx3 is accommodated comfortably in the tertiary structure fold of SAP. Normal and transformed fibroblasts, undifferentiated and differentiated myoblasts, normal endothelial cells, and mononuclear phagocytes express mptx3 mRNA and release the protein in vitro on exposure to interleukin-1beta (IL-1beta) and tumor necrosis factor (TNF)alpha. mptx3 was induced by bacterial lipopolysaccharide in vivo in a variety of organs and, most strongly, in the vascular endothelium of skeletal muscle and heart. Thus, mptx3 shows a distinct pattern of in vivo expression indicative of a significant role in cardiovascular and inflammatory pathology.
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Introna, M., VV Alles, M. Castellano, G. Picardi, L. De Gioia, B. Bottazzai, G. Peri, et al. "Cloning of mouse ptx3, a new member of the pentraxin gene family expressed at extrahepatic sites." Blood 87, no. 5 (March 1, 1996): 1862–72. http://dx.doi.org/10.1182/blood.v87.5.1862.bloodjournal8751862.

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Pentraxins, which include C reactive protein (CRP) and serum amyloid P component (SAP), are prototypic acute phase reactants that serve as indicators of inflammatory reactions. Here we report genomic and cDNA cloning of mouse ptx3 (mptx3), a member of the pentraxin gene family and characterize its extrahepatic expression in vitro and in vivo. mptx3 is organized into three exons on chromosome 3: the first (43 aa) and second exon (175 aa) code for the signal peptide and for a protein portion with no high similarity to known sequences the third (203 aa) for a domain related to classical pentraxins, which contains the “pentraxin family signature.” Analysis of the N terminal portion predicts a predominantly alpha helical structure, while the pentraxin domain of ptx3 is accommodated comfortably in the tertiary structure fold of SAP. Normal and transformed fibroblasts, undifferentiated and differentiated myoblasts, normal endothelial cells, and mononuclear phagocytes express mptx3 mRNA and release the protein in vitro on exposure to interleukin-1beta (IL-1beta) and tumor necrosis factor (TNF)alpha. mptx3 was induced by bacterial lipopolysaccharide in vivo in a variety of organs and, most strongly, in the vascular endothelium of skeletal muscle and heart. Thus, mptx3 shows a distinct pattern of in vivo expression indicative of a significant role in cardiovascular and inflammatory pathology.
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8

Nagai, Kei, Atsushi Ueda, Chie Saito, Asako Zempo-Miyaki, and Kunihiro Yamagata. "Annual Decline in Pentraxin 3 Is a Risk of Vascular Access Troubles in Hemodialysis Patients." International Journal of Nephrology 2014 (2014): 1–7. http://dx.doi.org/10.1155/2014/297954.

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Pentraxin 3 (PTX3), a multifunctional modulator of the innate immunoinflammatory response, is higher in patients undergoing hemodialysis than healthy control. Our study focused on annual change in PTX3 levels in patients with chronic hemodialysis, because regularly undergoing hemodialysis for many years modifies vascular inflammatory status. To demonstrate whether annual change in PTX3 is associated with vascular events, we measured blood levels of pentraxins (PTX3 and high-sensitivity C-reactive protein (hsCRP)) at baseline and in the next year in 76 hemodialysis patients and observed 20 patients with vascular access troubles during follow-up years. The annual decline in PTX3, but not hsCRP, is a significant risk of the incidence of vascular access trouble that is a critical and specific complication for hemodialysis patients (hazard ratio; 0.732 per +1 ng/mL/year in PTX3,*P=0.039). This study is the first to focus on the annual change of pentraxins in a hemodialysis cohort.
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9

Lech, M., C. Rommele, and H. J. Anders. "Pentraxins in nephrology: C-reactive protein, serum amyloid P and pentraxin-3." Nephrology Dialysis Transplantation 28, no. 4 (December 14, 2012): 803–11. http://dx.doi.org/10.1093/ndt/gfs448.

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10

Szymkowiak, Martyna, Piotr Surmiak, and Małgorzata Baumert. "Pentraxin 3 – possible uses in neonatology and paediatrics." Pediatria i Medycyna Rodzinna 16, no. 3 (October 30, 2020): 247–50. http://dx.doi.org/10.15557/pimr.2020.0045.

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Pentraxin 3 (PTX3) is a multifunctional acute phase protein belonging to the family of long pentraxins, which is synthesised in numerous cells of the body under the influence of proinflammatory factors and locally at the site of inflammation. Under physiological conditions, PTX3 is stored in neutrophil granules, where there is a constant pool of glycoproteins. Increased pentraxin 3 levels in blood serum are observed as early as 1 hour after a damaging stimulus. Elevation of PTX3 serum levels can be used to diagnose fertility disorders in women as well as in pregnancy pathology, women at risk of pre-eclampsia, gestational diabetes, premature rupture of membrane and preterm delivery. The biological function of PTX3 is not fully understood, especially in the population of newborns and children. So far, no reference values for PTX3 levels in newborns and children have been developed. This protein can be used as a marker of pulmonary hypertension in newborns as well as to assess the degree of respiratory failure in premature infants. In older children, it is useful in the assessment of the severity of meningococcal disease and sepsis as well as in the treatment of childhood asthma. There are studies available in which blood levels of PTX3 significantly correlate with the severity of kidney damage in Henoch–Schönlein macular degeneration in children, and the evaluation of this protein in urine is used to detect renal parenchymal destruction after pyelonephritis.
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Golconda, Umamaheshwari, Richard Sobonya, and Stephen Klotz. "Do Pentraxins Bind to Fungi in Invasive Human Gastrointestinal Candidiasis?" Journal of Fungi 4, no. 3 (September 17, 2018): 111. http://dx.doi.org/10.3390/jof4030111.

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Tissue from 13 autopsy cases with invasive gastrointestinal candidiasis was studied for the binding of the pentraxins, C-reactive protein (CRP), pentraxin 3 (PTX3), and serum amyloid P component (SAP) to fungal surfaces. Invasive candidal infection was demonstrated using a hematoxylin and eosin stain and a Gomori methenamine silver stain (GMS). Immunohistochemistry was performed with CRP and PTX3 monoclonal antibodies and did not demonstrate CRP or PTX3 bound to fungi (0 of 13 cases), although CRP was extensively deposited on human tissue. A polyclonal antibody to SAP showed that SAP was bound to fungi in 12 of 13 cases. Although all three pentraxins have been reported to bind to fungi or bacteria, only SAP was bound to filamentous and yeast forms of Candida in human tissue, as detected by immunohistochemistry. SAP was abundantly present on fungi and may have affected the host innate immune response to the invading fungi.
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12

Kathariya, Rahul, Hansa Jain, Dnyneshwari Gujar, Archana Singh, Himanshu Ajwani, and Devendra Mandhyan. "Pentraxins as Key Disease Markers for Periodontal Diagnosis." Disease Markers 34, no. 3 (2013): 143–51. http://dx.doi.org/10.1155/2013/259273.

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Periodontal diseases are characterized by a complex set of biologic interactions between a diverse and dynamic microbial ecosystem and the host’s multifaceted and responsive immune and inflammatory machinery. Such interactions between microbial pathogens and various host response systems play a critical role in the development and progression of periodontal disease via the release of inflammatory and immune mediators. Advances in periodontal disease diagnostic are moving toward methods whereby periodontal risk can be identified and quantified by detecting such inflammatory mediators in its sequential pathophysiology. Pentraxins (PTXs) are classical mediators of inflammation and markers of acute-phase reaction. They are a super family of multifunctional molecules characterized by multimeric structure, divided into “short” PTXs and “long” PTXs. C-reactive protein (CRP) and pentraxin-3 (PTX3) are prototypic molecules of the short and long PTX family, respectively. Evidence suggests that PTXs acts as a non-redundant component of the humoral arm of innate immunity, downstream of, and complementary to, cellular recognition, as well as a tuner of inflammation. CRP is a cheaper biomarker and more readily available in everyday clinical practice compared with other inflammatory markers, on the other hand, PTX3 is believed to be the true independent indicator of disease activity and could have clinical implication in diagnosing the “at site” inflammatory status of the periodontal disease. These pentraxins are sensitive and specific in the diagnosis and prognosis of chronic diseases. Thus the pentraxins could be used as preferred biomarkers in periodontal disease diagnosis.
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13

Gursu, M., S. Ozturk, Z. Aydin, S. Karadag, Y. Doventas, M. Koldas, S. Uzun, A. Sumnu, and R. Kazancioglu. "Is Pentraxin-3 Stronger Than C-Reactive Protein to Determine Inflammation in Peritoneal Dialysis Patients?" European Journal of Inflammation 10, no. 3 (September 2012): 289–95. http://dx.doi.org/10.1177/1721727x1201000305.

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Pentraxin-3 (PTX-3) is the prototype of long pentraxins and is produced by many tissues and organs including vascular endothelial cells in response to pro-inflammatory signals. It is thought to be an independent indicator of disease activity. We analyzed the correlation of PTX-3 with other markers of inflammation in peritoneal dialysis (PD) patients. Non-diabetic patients on chronic PD program who meet the dialysis adequacy criteria and who had no active infectious/inflammatory disease were included. Demographic and clinical parameters were recorded as well as hsCRP, fibrinogen, interleukin-6 (IL-6) and PTX-3 levels; and the correlation between them were studied. Twenty-five patients (mean age: 45.7±12.5 years; female/male ratio: 16/9) were included. Mean PTX-3 level was 2.16±2.76ng/ml. PTX-3 was found to be correlated positively with only IL-6 among inflammatory markers (r=0.827; p<0.001) but not with hsCRP. With linear regression model, IL-6 was the only independent determinant of PTX-3 levels. PTX-3 may be a more valuable marker of inflammation than CRP in patients on PD.
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Battal, Fatih, Özgül Emel Bulut, Şule Yıldırım, Hakan Aylanç, Nazan Kaymaz, and Sema Uysal. "Serum Pentraxin 3 Concentration in Neonatal Sepsis." Journal of Pediatric Infectious Diseases 14, no. 05 (May 24, 2019): 219–22. http://dx.doi.org/10.1055/s-0039-1688930.

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Objective Neonatal sepsis is one of the most important causes of neonatal morbidity and mortality. Symptoms and signs of neonatal sepsis can be silent; therefore, laboratory investigation is necessary in cases of doubt or if there are risk factors. Early diagnosis is important for early intervention and treatment. The most valuable method for diagnosis is blood culture; however, false positivity due to contamination or false negativity despite ongoing fatal bacterial infections can be seen. Pentraxin 3 is a prototype of the long pentraxin family. It has some differences from C-reactive protein (CRP) in terms of gene organization and localization and production site. It is effective in the early phase of inflammation and it is detected as an early marker of sepsis in adults. The aim of this study was to investigate whether pentraxin 3 can be used as a marker in neonatal sepsis. Materials and Methods Thirty newborns with suspected sepsis with antenatal history or the presence of clinical signs of sepsis, such as hypo/hyperthermia, feed intolerance, lethargy, hypotonia, irregular cardiac rhythms, bradycardia, cyanosis, apnea, respiratory distress, or metabolic acidosis, were enrolled in the study as a case group, and 28 healthy newborns were included as a control group. Serum pentraxin 3, procalcitonin, CRP, and hemogram in the study group and serum procalcitonin and pentraxin in the control group were examined. Results Serum pentraxin 3 (pg/mL) and serum procalcitonin (ng/mL) levels were 2,273.82 ± 1,260.75 and 0.86 ± 0.52 in the case group and 957.41 ± 268.00 and 0.19 ± 0.18 in the control group (p < 0.001 for both), respectively. Conclusion The present study showed that serum pentraxin 3 levels may be a useful marker in the diagnosis of neonatal sepsis.
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Roy, Nitai, Katsuki Ohtani, Yoshihiko Hidaka, Yoshiro Amano, Yasuyuki Matsuda, Kenichiro Mori, Insu Hwang, Norimitsu Inoue, and Nobutaka Wakamiya. "Three pentraxins C-reactive protein, serum amyloid p component and pentraxin 3 mediate complement activation using Collectin CL-P1." Biochimica et Biophysica Acta (BBA) - General Subjects 1861, no. 2 (February 2017): 1–14. http://dx.doi.org/10.1016/j.bbagen.2016.11.023.

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Nabrdalik, Katarzyna, Artur Chodkowski, Wojciech Bartman, Andrzej Tomasik, Hanna Kwiendacz, Tomasz Sawczyn, Michał Kukla, Władysław Grzeszczak, and Janusz Gumprecht. "Pentraxin 3 and atherosclerosis among type 2 diabetic patients." Open Life Sciences 12, no. 1 (April 24, 2017): 92–98. http://dx.doi.org/10.1515/biol-2017-0010.

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AbstractType 2 diabetes is contemporarily a major social and epidemiological problem and among others is a strong risk factor for cardiovascular diseases. Pentraxin 3, a potential early biomarker of atherosclerosis, is an acute-phase reactant produced by the peripheral tissues where the inflammation takes place. In this study we examined a group of patients with type 2 diabetes with and without cardiovascular complications compared to persons with normal glucose tolerance (patients with cardiovascular complications and healthy volunteers). Plasma pentraxin 3 concentration as well as some basic biochemical blood analysis were performed. Moreover, transcranial and carotid Doppler ultrasound examination as well as transthoracic echocardiography were performed. It turned out that there was an association of plasma pentraxin 3 concentration and carotid atherosclerosis found in the control group of patients with cardiovascular complications but with normal glucose tolerance. In the group of patients with type 2 diabetes and cardiovascular complications we have found an association of plasma pentraxin 3 concentration with diastolic left ventricular dysfunction. Additionally, in the group of patients with type 2 diabetes without cardiovascular disease plasma pentraxin 3 concentration was associated with elevated urinary albumin creatinine ratio. Further studies, on a larger group of patients, are required to confirm these observations.
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Aygun, O., and R. Yildiz. "Evaluation of thrombomodulin and pentraxin-3 as diagnostic biomarkers in calves with sepsis." Veterinární Medicína 63, No. 7 (July 25, 2018): 313–20. http://dx.doi.org/10.17221/159/2017-vetmed.

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Early diagnosis and treatment of sepsis in patients are crucial for their survival and can help reduce mortality rates. Novel biomarkers, such as thrombomodulin and pentraxin-3, have been used as diagnostic, prognostic and mortality indicators in patients with sepsis. Plasma thrombomodulin is a vascular endothelial membrane-bound glycoprotein and pentraxin-3 is an acute-phase protein. In the present study, thrombomodulin and pentraxin-3 levels were determined in calves with sepsis, to determine their diagnostic values as well as usefulness as indicators of health status. To this end, 20 neonatal calves with sepsis (G1) and ten healthy neonatal calves (G2) were used. Additionally, group G1 was also divided into two groups consisting of surviving (G1-S; n = 9) and non-surviving calves (G1-NS; n = 11). A single blood sample was collected from all the calves and the prepared serum samples were used to measure thrombomodulin and pentraxin-3 levels using bovine-specific ELISA kits. The serum concentrations of thrombomodulin and pentraxin-3 were found to be significantly higher (P &lt; 0.01) in the G1 group than in G2. Thrombomodulin and pentraxin-3 levels were also found to be higher in the G1-NS group than in G1-S but the difference was not significant. We conclude that thrombomodulin and pentraxin-3 may have some diagnostic value in calves with sepsis. Furthermore, these findings may also help in understanding the pathogenesis of sepsis in neonatal calves. Further studies are required to determine the importance of thrombomodulin and pentraxin-3 as diagnostic and prognostic biomarkers in calves with sepsis and to evaluate the concentrations of these biomarkers also in other disease states.
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Zhu, Min, Hongli Yu, Ying Sun, and Wenli Yu. "Pentraxin-3 in the Spinal Dorsal Horn Upregulates Nectin-1 Expression in Neuropathic Pain after Spinal Nerve Damage in Male Mice." Brain Sciences 12, no. 5 (May 15, 2022): 648. http://dx.doi.org/10.3390/brainsci12050648.

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Purpose: Neuropathic pain often originates from nerve injury or diseases of the somatosensory nervous system. However, its specific pathogenesis remains unclear. The requirement for excitatory synaptic plasticity in pain-related syndromes has been demonstrated. A recent study reported that pentraxin-3 is important in glutamatergic synaptic formation and function. Meanwhile, nectin-1 mediates synaptogenesis in neurological disorders. The present study aimed to evaluate whether pentraxin-3 and nectin-1 modulate spinal nerve damage-related neuropathic pain in male mice. Methods: L4 spinal nerve ligation (SNL) in male mice was performed to induce experimental neuropathic pain. Mechanical allodynia and heat hyperalgesia following SNL were based on paw withdrawal (PW) threshold and PW latency, respectively. Spinal pentraxin-3 levels and nectin-1 expression following SNL were examined. Pentraxin-3 and nectin-1 knockdown models were established by the shRNA method. These models were used with a recombinant pentraxin-3 cell model to investigate the underlying mechanisms of SNL. Results: The SNL operation generated persistent decreases in mechanical PW threshold and thermal PW latency, with subsequent long-lasting elevations in spinal pentraxin-3 and nectin-1 expression levels. Pentraxin-3 knockdown reduced SNL-associated neuropathic pain behaviors as well as nectin-1 amounts in the spinal dorsal horn. Nectin-1 deficiency impaired mechanical allodynia and thermal hyperalgesia following spinal nerve injury. The application of recombinant pentraxin-3 in the spinal cord triggered an acute nociception phenotype and induced spinal overexpression of nectin-1. The intrathecal knockdown of nectin-1 prevented exogenous pentraxin-3-evoked pain hypersensitivity. Conclusions: The findings suggest spinal pentraxin-3 is required for SNL-triggered neuropathic pain via nectin-1 upregulation in male mice.
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Zhang, Jun, Haili Wang, Boming Xia, and Lun Dong. "Brief overview of Pentraxin 3." American Journal of Emergency Medicine 38, no. 8 (August 2020): 1692. http://dx.doi.org/10.1016/j.ajem.2020.01.018.

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Kontny, Frederic, Thomas Andersen, Thor Ueland, Axel Åkerblom, Tatevik G. Lakic, Annika E. Michelsen, Pål Aukrust, et al. "Pentraxin-3 vs C-reactive protein and other prognostic biomarkers in acute coronary syndrome: A substudy of the Platelet Inhibition and Patients Outcomes (PLATO) trial." European Heart Journal: Acute Cardiovascular Care 9, no. 4 (April 24, 2019): 313–22. http://dx.doi.org/10.1177/2048872619846334.

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Aims: We investigated the dynamics, associations with patient characteristics, other biomarkers, and clinical outcomes of pentraxin 3 in acute coronary syndrome. Methods and results: In multivariate analyses, pentraxin 3 measured in 5154 patients randomised in the Platelet Inhibition and Patients Outcomes (PLATO) trial (NCT00391872) was compared with leukocytes, high-sensitivity C-reactive protein, interleukin-6, cystatin C, N-terminal prohormone brain natriuretic peptide, high-sensitivity troponin T and growth differentiation factor 15 concerning prediction of clinical outcome. Pentraxin 3 peaked earlier than high-sensitivity C-reactive protein and was more strongly correlated with N-terminal prohormone brain natriuretic peptide and high-sensitivity troponin T than with high-sensitivity C-reactive protein. The frequency of cardiovascular death, spontaneous myocardial infarction or stroke by quartiles of pentraxin 3 at admission was 6.1%, 7.3%, 9.7% and 10.7%, respectively ( p<0.0001). The hazard ratio per 50% increase of pentraxin 3 was 1.13 (95% confidence interval: 1.07–1.19), p<0.0001. This association remained significant after stepwise adjustments for leukocytes/high-sensitivity C-reactive protein (1.09 (1.02–1.15)), p=0.009, interleukin-6 (1.07 (1.01–1.14)), p=0.026, and cystatin C (1.07 (1.00–1.13)), p=0.044, but not after adjustment for N-terminal prohormone brain natriuretic peptide, high-sensitivity troponin T and growth differentiation factor 15. Admission pentraxin 3 was also associated with several of the individual endpoint components (cardiovascular death/spontaneous myocardial infarction; p=0.008, cardiovascular death; p=0.026, and spontaneous myocardial infarction; p=0.017), but not with stroke. Pentraxin 3 measured in the chronic phase (i.e. at one month) was still predictive of the composite endpoint in univariate analysis (1.12 (1.04–1.20) per 50% increase) p=0.0024, but not after adjustment for the other biomarkers. Conclusion: Admission level of pentraxin 3 is a modestly stronger predictor than high-sensitivity C-reactive protein and interleukin-6, but not than N-terminal prohormone brain natriuretic peptide or high-sensitivity troponin T, concerning cardiovascular outcome in acute coronary syndrome. Pentraxin 3 is more strongly correlated with N-terminal prohormone brain natriuretic peptide and high-sensitivity troponin T than with high-sensitivity C-reactive protein.
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Inoue, Kenji. "The Cardioprotective Role of Pentraxin 3." Journal of Atherosclerosis and Thrombosis 22, no. 4 (2015): 335–37. http://dx.doi.org/10.5551/jat.ed011.

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Hill, A. L., D. A. Lowes, N. R. Webster, C. C. Sheth, N. A. R. Gow, and H. F. Galley. "Regulation of pentraxin-3 by antioxidants." British Journal of Anaesthesia 103, no. 6 (December 2009): 833–39. http://dx.doi.org/10.1093/bja/aep298.

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Lannergård, Anders, Fredrik Rosenström, Erik Normann, and Anders Larsson. "Serum pentraxin 3 concentrations in neonates." Upsala Journal of Medical Sciences 119, no. 1 (January 17, 2014): 62–64. http://dx.doi.org/10.3109/03009734.2013.878770.

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Zhang, Yingze, and John F. McDyer. "Pentraxin 3 in Primary Graft Dysfunction." American Journal of Respiratory and Critical Care Medicine 186, no. 6 (September 15, 2012): 475–77. http://dx.doi.org/10.1164/rccm.201207-1158ed.

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Korzonek-Szlacheta, Ilona, Bartosz Hudzik, Aleksander Danikiewicz, Janusz Szkodzinski, Andrzej Lekston, Mariusz Gąsior, and Barbara Zubelewicz-Szkodzinska. "Pentraxin-3 and coronary artery disease." Experimental Gerontology 102 (February 2018): 1–2. http://dx.doi.org/10.1016/j.exger.2017.11.016.

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Larsson, Anders, Maria Palm, Johanna Helmersson, and Ove Axelsson. "Pentraxin 3 Values During Normal Pregnancy." Inflammation 34, no. 5 (September 18, 2010): 448–51. http://dx.doi.org/10.1007/s10753-010-9252-x.

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Baumert, Małgorzata, Piotr Surmiak, Martyna Szymkowiak, and Agnieszka Janosz. "The Assessment of Pentraxin 3: A Novel Biomarker in Early Detection of Infection in Newborns." BioMed Research International 2021 (June 30, 2021): 1–8. http://dx.doi.org/10.1155/2021/6638622.

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Introduction. As the clinical manifestation of neonatal infection is nonspecific and characterised by varied clinical features, it is highly problematic to establish an early diagnosis. Recently, hopes have been raised by the new acute-phase protein—pentraxin 3 (PTX3). PTX3 belongs to the family of long pentraxins, which is synthesized in numerous cells like endothelial cells, macrophages, and monocytes infiltrating sites of inflammation. Material and Methods. In our research, we have enrolled 29 newborns with infection as the study group and 47 healthy ones as the control group, as well as their mothers. The C-reactive protein (CRP), procalcitonin (PCT), and PTX3 levels were determined in venous blood samples from all investigated neonates and their mothers. Moreover, PTX3 concentrations were assessed in the umbilical cord. Results. There were statistically significant differences in PTX3 levels between healthy and sick newborns both in the umbilical cord ( p = 0.02 ) and venous blood ( p = 0.01 ). The highest PTX3 concentrations were observed in children with infection in the presence of premature rupture of membranes (PROM). PTX3 concentrations in this group were significantly higher compared to those in healthy children without PROM. We observed elevated PCT levels in newborns with infection. No differences in CRP levels in 12 hours of life were noticed between the investigated groups. A comparison of ROC curves for PTX3 and PCT concentrations revealed similar sensitivity and specificity in the prediction of infection in neonates. Conclusions. Serum PTX3 is an important and specific biomarker of early infection. It is already elevated in the umbilical cord, so measuring PTX3 concentration might be useful in the early prediction of infection in newborns.
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Ceylan, Mustafa, Omer Faruk Bayraktutan, Sinan Becel, Ömer Atis, Ahmet Yalcin, and Dilcan Kotan. "Serum levels of pentraxin-3 and other inflammatory biomarkers in migraine: Association with migraine characteristics." Cephalalgia 36, no. 6 (August 4, 2015): 518–25. http://dx.doi.org/10.1177/0333102415598757.

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Background Several studies have been conducted on the inflammatory aspects of migraine. Pentraxins are a novel and important part of innate immunity as a superfamily of acute phase proteins. In our study, we aimed to demonstrate the relationship between migraine and the serum levels of pentraxin-3 (PTX-3), C-reactive protein (CRP), fibrinogen and D-dimer. Methods We recruited 30 migraine patients (in both the attack and interictal period) and 30 healthy controls. Serum samples were obtained from all participants, and a brain MRI performed in the last six months was assessed regarding the presence of deep white matter lesions. Comparisons between the attack, interictal and control groups regarding the serum levels of PTX-3, CRP, fibrinogen and D-dimer were performed. The association between serum PTX-3 levels and migraine characteristics (disease duration, headache frequency, MRI findings, aura, family history, attack duration, and MIDAS score) was also assessed. Results We found higher serum levels of fibrinogen and PTX-3 in migraine attack patients compared with the interictal and control groups ( p = 0.03 and p < 0.001, respectively). Subgroup analysis also showed that patients with a disease duration of more than five years and with an attack duration of more than 12 hours have lower serum levels of PTX-3 than patients who have a relatively new diagnosis and have relatively short-lasting migraine attacks ( p = 0.042 and p = 0.038, respectively). Conclusions PTX-3 and fibrinogen exhibit different serum levels in patients undergoing a migraine attack compared with the interictal group and the controls. Participants with longer attacks and disease durations have lower serum levels of PTX-3, suggesting that inflammatory processes change along with disease progression.
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El-Kassas, Ghada M., Maged A. El Wakeel, Mona A. Elabd, Alyaa H. Kamhawy, Mohamed Abdel Atti, Shereen A. Abd El-Gaffar, Salwa Kamal Hanafy, and Eman Awadallah. "Vitamin D Status in Neonatal Pulmonary Infections: Relationship to Inflammatory Indicators." Open Access Macedonian Journal of Medical Sciences 7, no. 23 (December 14, 2019): 3970–74. http://dx.doi.org/10.3889/oamjms.2019.592.

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AIM: The study aimed to evaluate serum vitamin D concentrations among neonates with pneumonia. METHODS: This case-control study enrolled 33 neonates with pneumonia in addition to 30 healthy controls. CBC, CRP, Serum vitamin D and Pentraxin 3 levels were measured for all participants. RESULTS: There was significant difference between patients and controls regarding Hemoglobin levels, TLC and CRP (p value < 0.01, = 0.002, < 0.01 respectively). Patients with pneumonia showed significant lower levels of Vit. D (9 ± 2.1) compared to controls (14.1 ± 2.8), P value < 0.01. However, patient group had significant higher levels of Pentraxin 3 (29.1 ± 4.8) compared with controls (12.6 ± 3), P value < 0.01. Moreover, mechanically ventilated patients revealed significant lower vit D (7.7 ± 1.8) and higher pentraxin 3 (32.2 ± 2.6) compared to patients on free oxygen (9.1 ± 2.1, 26.4 ± 3.7 respectively), P value = 0.05, 0.02 respectively. Regarding hospital stay, it had significant positive correlation with serum pentraxin 3 (r = 0.6, P value < 0.01) and significant negative correlation with serum vit D (r = -0.4, P value = 0.04). Finally a significant negative correlation between serum levels of vitamin D and Pentraxin 3 was found (r = -0.4, P value = 0.01). CONCLUSION: Lower concentration of serum vitamin D may be significantly associated with neonatal pneumonia. It also can predict the need for mechanical ventilation and duration of hospital stay in neonatal pneumonia. Similarly, higher levels of Pentraxin 3 may be used as an indicator for mechanical ventilation need and a longer hospital stay in neonates with pneumonia.
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Petterson, Stine Asferg, Mia Dahl Sørensen, and Bjarne Winther Kristensen. "Expression Profiling of Primary and Recurrent Glioblastomas Reveals a Reduced Level of Pentraxin 3 in Recurrent Glioblastomas." Journal of Neuropathology & Experimental Neurology 79, no. 9 (August 13, 2020): 975–85. http://dx.doi.org/10.1093/jnen/nlaa088.

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Abstract Glioblastomas (GBM) are highly infiltrative tumors and despite intensive treatment tumor recurrence is inevitable. The immune microenvironment in recurrent GBM is poorly characterized, but it is potentially influenced by therapeutic interventions with surgery, radiotherapy, and chemotherapy. The aim of this study was to obtain a deeper insight in the immune microenvironment in primary and recurrent GBM. Primary and recurrent glioblastoma samples from 18 patients were identified and expression profiling of 770 myeloid innate immune-related markers was performed. Leukemia inhibitory factor and pentraxin 3 were expressed at lower levels in recurrent tumors. Using in silico data and immunohistochemical staining, this was validated for pentraxin 3. Both high leukemia inhibitory factor and pentraxin 3 expression appeared to be associated with shorter survival in primary and recurrent GBM using in silico data. In primary GBM, gene set analysis also showed higher expression of genes involved in metabolism, extracellular matrix remodeling and complement activation, whereas genes involved in T cell activation and checkpoint signaling were expressed at higher levels in recurrent GBM. The reduced level of pentraxin 3 in recurrent glioblastomas and the gene set analysis results suggest an altered microenvironment in recurrent GBM that might be more active.
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Augusto, Jean-François, Caroline Poli, Céline Beauvillain, Jean-François Subra, Sebastien Jaillon, Gilles Renier, Alain Chevailler, Xavier Puéchal, Yves Delneste, and Pascale Jeannin. "Anti-pentraxin antibodies in autoimmune systemic diseases: Focus on anti-pentraxin-3 autoantibodies." International Reviews of Immunology 36, no. 3 (May 4, 2017): 145–53. http://dx.doi.org/10.1080/08830185.2017.1284210.

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Barazzoni, R., M. Zanetti, M. Giuricin, S. Palmisano, M. R. Cattin, E. Moretti, G. Guarnieri, and N. De Manzini. "PP219-SUN GASTRIC BY-PASS DIFFERENTIALLY MODULATES CIRCULATING SHORT AND LONG PENTRAXINS – HIGHER PLASMA PENTRAXIN-3 AFTER GASTRIC BY-PASS-INDUCED WEIGHT LOSS." Clinical Nutrition 32 (September 2013): S105—S106. http://dx.doi.org/10.1016/s0261-5614(13)60264-2.

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Turkmen, O., S. Mollaoglu, G. Goynumer, and B. Isbilen. "Plasma pentraxin 3 levels in preeclamptic patients." Clinical and Experimental Obstetrics & Gynecology 42, no. 2 (April 10, 2015): 220–23. http://dx.doi.org/10.12891/ceog1825.2015.

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Dickerson, Faith, Cassie Stallings, Andrea Origoni, Emily Katsafanas, Lucy AB Schweinfurth, Christina LG Savage, Sunil Khushalani, and Robert Yolken. "Pentraxin 3 is reduced in bipolar disorder." Bipolar Disorders 17, no. 4 (November 25, 2014): 409–14. http://dx.doi.org/10.1111/bdi.12281.

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Agilli, Mehmet, and Fevzi Nuri Aydin. "Evaluation of pentraxin-3 in POEMS syndrome." Journal of Neuroimmunology 278 (January 2015): 136. http://dx.doi.org/10.1016/j.jneuroim.2014.12.015.

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Razvina, Olga, Shuying Jiang, Koichi Matsubara, Riuko Ohashi, Go Hasegawa, Takashi Aoyama, Kenji Daigo, Tatsuhiko Kodama, Takao Hamakubo, and Makoto Naito. "Differential expression of pentraxin 3 in neutrophils." Experimental and Molecular Pathology 98, no. 1 (February 2015): 33–40. http://dx.doi.org/10.1016/j.yexmp.2014.11.009.

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Guo, Tang-Meng, Li Ke, Xiu-E. Zhang, Ling Li, Li-Juan Xiong, and Bei Cheng. "Reply: Pentraxin-3 and coronary artery disease." Experimental Gerontology 103 (March 2018): 87. http://dx.doi.org/10.1016/j.exger.2018.01.004.

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Angeli, Fabio, Enrica Angeli, Monica Trapasso, and Paolo Verdecchia. "Pentraxin-3 and the pathogenesis of preeclampsia." Hypertension Research 43, no. 9 (May 14, 2020): 979–81. http://dx.doi.org/10.1038/s41440-020-0466-5.

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Menon, P. S. N. "Childhood Obesity, Metabolic Syndrome and Pentraxin-3." Indian Journal of Pediatrics 82, no. 1 (December 13, 2014): 3–4. http://dx.doi.org/10.1007/s12098-014-1644-8.

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Iwagaitsu, Shiho, and Taio Naniwa. "Improvement of Arterial Wall Lesions in Parallel with Decrease of Plasma Pentraxin-3 Levels in a Patient with Refractory Takayasu Arteritis after Treatment with Tocilizumab." Case Reports in Rheumatology 2017 (2017): 1–5. http://dx.doi.org/10.1155/2017/4580967.

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A 19-year-old Japanese woman with active Takayasu arteritis despite multiple conventional immunosuppressive therapies with glucocorticoids in combination with intravenous cyclophosphamide, azathioprine, or infliximab with methotrexate and tacrolimus was successfully treated by switching from infliximab to intravenous tocilizumab. Worsening of claudication of the legs and elevated acute phase reactants, including plasma pentraxin-3 levels, were observed during combination therapy with infliximab. Computed tomography demonstrated increased wall thickening with contrast enhancement in the preexisting lesion of the descending aorta and the femoral arteries. After switching from infliximab to tocilizumab, plasma pentraxin-3 levels gradually decreased to the normal range in parallel with the improvement of claudication. Follow-up computed tomographic scans confirmed the marked improvement of these arterial lesions. Moreover, plasma pentraxin-3 level was increased in response to the worsening of claudication that occurred just after switching to a subcutaneous tocilizumab injection. Measurements of plasma pentraxin-3 might be useful for evaluation of the vascular wall inflammation and therapeutic efficacy even during biologic therapy targeting tumor necrosis factor α and interleukin-6.
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Rauten, Anne Marie, Isabela Silosi, Stefan Ioan Stratul, Liliana Foia, Adrian Camen, Vasilica Toma, Daniel Cioloca, Valeriu Surlin, Petra Surlin, and Maria Bogdan. "Expression of Pentraxin 3 and Thrombospondin 1 in Gingival Crevicular Fluid during Wound Healing after Gingivectomy in Postorthodontic Patients." Journal of Immunology Research 2016 (2016): 1–7. http://dx.doi.org/10.1155/2016/4072543.

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Background. Wound healing is a tissue repair process after an injury, and two of its main components are inflammation and angiogenesis, in which course a cascade of mediators is involved. The aim of this research was to evaluate the involvement of Pentraxin 3 and Thrombospondin 1 in wound healing after periodontal surgery (gingivectomy) for gingival overgrowth during orthodontic treatment with or without magnification devices, by assessing their levels in GCF.Methods. From 19 patients with gingival overgrowth as a result of fixed orthodontic treatment, the overgrown gingiva was removed by gingivectomy, from one half of the mandibular arch without magnification and from the other under magnification. Pentraxin 3 and Thrombospondin 1 were determined from gingival crevicular fluid by ELISA tests.Results. Statistically significant differences (p<0.05) and correlations between levels of the two biomarkers were analyzed. Statistically significant differences were established between levels of the two biomarkers at different time points, with significant positive correlation at the point of 24 hours.Conclusions. Within the limitations of this study, the results seem to sustain the involvement of Pentraxin 3 and Thrombospondin 1 in the processes of inflammation and angiogenesis in wound healing of patients with postorthodontic gingivectomy. The dynamics of Pentraxin 3 and Thrombospondin 1 levels could suggest a reduced inflammation and a faster angiogenesis using microsurgery.
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Mahmudov, R. M., V. S. Mammadov, and L. R. Mirzakhanova. "Association of blood level of inflammatory mediators and morphology of coronary artery stenosis in patients with stable angina." Kazan medical journal 95, no. 3 (June 15, 2014): 331–34. http://dx.doi.org/10.17816/kmj1507.

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Aim. To study the association of morphology of coronary artery disease and pentraxin-3, tumor necrosis factor α blood levels in patients with stable angina who undergo coronary artery bypass surgery. Methods. The study included 92 patients aged 44-73 years with stable angina of II-III functional class. The coronary artery disease type was classified by AHA/ACC criteria: type A - concentric stenosis with flat plague and plague length less than 10 mm, type B - eccentric stenosis or blunt-edged stenosis with moderate calcinosis or signs of mural trombosis, with length not exceeding 200 mm, type C - stenosis with plague length over 20 mm, plague ulceration, marked calcinosis, diffuse lesions, chronic coronary artery occlusion. Pentraxin-3, tumor necrosis factor α blood levels were measured by ELISA in all patients before the surgery, 8 and 24 hours after the surgery. Results. There was a relation found between the type of stenosis and pentraxin-3 and tumor necrosis factor α blood levels. In patients with С type stenosis, pentraxin-3 blood level was 4 times higher (p 0.001) 24 hours after the coronary artery bypass surgery compared to patients with A type stenosis, and by 1.8 and 1.3 times higher compared to patients with В1 and В2 stenosis type, accordingly. Conclusion. There was a close relation revealed between the morphology of coronary artery stenosis and pentraxin-3 and tumor necrosis factor α blood levels in patients with stable angina.
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Lee, Kyong-No, Kyo Hoon Park, Yu Mi Kim, Iseop Cho, and Tae Eun Kim. "Prediction of emergency cerclage outcomes in women with cervical insufficiency: The role of inflammatory, angiogenic, and extracellular matrix-related proteins in amniotic fluid." PLOS ONE 17, no. 5 (May 10, 2022): e0268291. http://dx.doi.org/10.1371/journal.pone.0268291.

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Objective We aimed to determine whether various novel inflammatory, angiogenic, and extracellular matrix-related mediators in amniotic fluid (AF) can independently predict emergency cerclage outcomes in women with acute cervical insufficiency (CI). Methods This was a retrospective cohort study conducted among 50 singleton pregnant women (18–25 weeks) who underwent emergency cerclage for CI and were subjected to amniocentesis. The AF samples were assayed for endoglin, endostatin, haptoglobin, insulin-like growth factor-binding protein (IGFBP)-3, -4, kallistatin, lumican, macrophage colony-stimulating factor (M-CSF), pentraxin 3, p-selectin, receptor for advanced glycation end products (RAGE), resistin, transforming growth factor beta-induced (TGFBI), and vitamin D-binding protein (VDBP) levels. Interleukin (IL)-6 levels in the AF were also measured for comparison with potential biomarkers assessed in this study. The primary endpoint was spontaneous preterm delivery (SPTD) at <34 weeks following emergency cerclage. Results The AF levels of pentraxin 3, RAGE, and resistin were significantly higher in women who had SPTD at <34 weeks after cerclage placement (pentraxin-3: P = 0.003; RAGE: P = 0.041; and resistin; P = 0.002). In multivariate analysis, elevated AF levels of pentraxin 3 (P = 0.007) and resistin (P = 0.006), but not those of RAGE (P = 0.069), were independently associated with the occurrence of SPTD at <34 weeks after cerclage, following adjustment for baseline clinical variables (e.g., cervical dilation). The area under the curve (AUC) values of AF pentraxin 3, RAGE, and resistin for the prediction of SPTD at <34 weeks were 0.749, 0.669, and 0.770, respectively, which were similar to those of AF IL-6. However, in univariate analyses, no differences in the AF levels of endoglin, endostatin, haptoglobin, IGFBP-3, IGFBP-4, kallistatin, lumican, p-selectin, TGFBI, and VDBP were found to be associated with SPTD at <34 weeks after cerclage placement. Conclusions In women with acute CI, the AF levels of pentraxin 3, RAGE, and resistin could be useful novel biomarkers for predicting SPTD following emergency cerclage. However, the clinical utility of these new biomarkers should be validated in larger multicenter studies.
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Mairuhu, Albert T. A., Giuseppe Peri, Tatty E. Setiati, C. Erik Hack, Penelopie Koraka, Augustinus Soemantri, Albert D. M. E. Osterhaus, et al. "Elevated plasma levels of the long pentraxin, pentraxin 3, in severe dengue virus infections." Journal of Medical Virology 76, no. 4 (2005): 547–52. http://dx.doi.org/10.1002/jmv.20397.

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Inoue, Kenji, Tatsuhiko Kodama, and Hiroyuki Daida. "Pentraxin 3: A Novel Biomarker for Inflammatory Cardiovascular Disease." International Journal of Vascular Medicine 2012 (2012): 1–6. http://dx.doi.org/10.1155/2012/657025.

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Numerous studies have recently examined the role of pentraxin 3 (PTX3) in clinical situations. The pentraxin family includes C-reactive protein (CRP); however, unlike CRP, PTX3 is expressed predominantly in atherosclerotic lesions that involve macrophages, neutrophils, dendritic cells, or smooth muscle cells. Interestingly, PTX3 gene expression in human endothelial cells is suppressed to a greater extent by pitavastatin than the expression of 6,000 other human genes that have been examined, suggesting that PTX3 may be a novel biomarker for inflammatory cardiovascular disease. The expression and involvement of PTX3 in cardiovascular diseases are discussed in this paper, along with the characteristics of PTX3 that make it a suitable biomarker; namely, that the physiological concentration is known and it is independent of other risk factors. The results discussed in this paper suggest that further investigations into the potential novel use of PTX3 as a biomarker for inflammatory cardiovascular disease should be undertaken.
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Tornyigah, Bernard, Samuel Odarkwei Blankson, Rafiou Adamou, Azizath Moussiliou, Lauriane Rietmeyer, Patrick Tettey, Liliane Dikroh, et al. "Specific Combinations of Inflammatory, Angiogenesis and Vascular Integrity Biomarkers Are Associated with Clinical Severity, Coma and Mortality in Beninese Children with Plasmodium Falciparum Malaria." Diagnostics 12, no. 2 (February 18, 2022): 524. http://dx.doi.org/10.3390/diagnostics12020524.

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Malaria-related deaths could be prevented if powerful diagnostic and reliable prognostic biomarkers were available to allow rapid prediction of the clinical severity allowing adequate treatment. Using quantitative ELISA, we assessed the plasma concentrations of Procalcitonin, Pentraxine-3, Ang-2, sTie-2, suPAR, sEPCR and sICAM-1 in a cohort of Beninese children with malaria to investigate their potential association with clinical manifestations of malaria. We found that all molecules showed higher levels in children with severe or cerebral malaria compared to those with uncomplicated malaria (p-value < 0.005). Plasma concentrations of Pentraxine-3, Procalcitonin, Ang-2 and the soluble receptors were significantly higher in children with coma as defined by a Blantyre Coma Score < 3 (p < 0.001 for Pentraxine-3, suPAR, and sTie-2, p = 0.004 for PCT, p = 0.005 for sICAM-1, p = 0.04 for Ang-2). Moreover, except for the PCT level, the concentrations of Pentraxine-3, suPAR, sEPCR, sICAM-1, sTie-2 and Ang-2 were higher among children who died from severe malaria compared to those who survived (p = 0.037, p = 0.035, p < 0.0001, p= 0.0008, p = 0.01 and p = 0.02, respectively). These findings indicate the ability of these molecules to accurately discriminate among clinical manifestations of malaria, thus, they might be potentially useful for the early prognostic of severe and fatal malaria, and to improve management of severe cases.
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Bilgin, Huseyin, Murat Haliloglu, Ali Yaman, Pinar Ay, Beliz Bilgili, Mustafa Kemal Arslantas, Filiz Ture Ozdemir, Goncagul Haklar, Ismail Cinel, and Lutfiye Mulazimoglu. "Sequential Measurements of Pentraxin 3 Serum Levels in Patients with Ventilator-Associated Pneumonia: A Nested Case-Control Study." Canadian Journal of Infectious Diseases and Medical Microbiology 2018 (2018): 1–8. http://dx.doi.org/10.1155/2018/4074169.

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Purpose. The main purpose of this study was to investigate the dynamics of pentraxin 3 (PTX3) compared with procalcitonin (PCT) and C-reactive protein (CRP) in patients with suspicion of ventilator-associated pneumonia (VAP). Materials and Methods. We designed a nested case-control study. This study was performed in the Surgical Intensive Care Unit of a tertiary care academic university and teaching hospital. Ninety-one adults who were mechanically ventilated for >48 hours were enrolled in the study. VAP diagnosis was established among 28 patients following the 2005 ATS/IDSA guidelines. Results. The median PTX3 plasma level was 2.66 ng/mL in VAP adults compared to 0.25 ng/mL in non-VAP adults (p<0.05). Procalcitonin and CRP levels did not significantly differ. Pentraxin 3, with a 2.56 ng/mL breakpoint, had 85% sensitivity, 86% specificity, 75% positive predictive value, and 92.9% negative predictive value for VAP diagnosis (AUC = 0.78). Conclusions. With the suspicion of VAP, a pentraxin 3 plasma breakpoint of 2.56 ng/mL could contribute to the decision of whether to start antibiotics.
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Górka-Dynysiewicz, Joanna, and Jolanta Zuwała-Jagiełło. "Pentraxin 3 and its role in tissue repair." Farmacja Polska 76, no. 2 (March 15, 2020): 65–72. http://dx.doi.org/10.32383/farmpol/118530.

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Mantovani, A. "Pentraxin-3 in COPD: innocent bystander or amplifier?" European Respiratory Journal 39, no. 4 (March 31, 2012): 795–96. http://dx.doi.org/10.1183/09031936.00198111.

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Imai, Naofumi, Shinichi Nishi, Kazuhiro Yoshita, Yumi Ito, Yutaka Osawa, Kaori Takahashi, Yuki Nakagawa, Kazuhide Saito, Kota Takahashi, and Ichiei Narita. "Pentraxin-3 expression in acute renal allograft rejection." Clinical Transplantation 26 (June 29, 2012): 25–31. http://dx.doi.org/10.1111/j.1399-0012.2012.01641.x.

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