Journal articles on the topic 'Growth factors – Pathophysiology'
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1
Koutsilieris, Michael. "Pathophysiology of uterine leiomyomas." Biochemistry and Cell Biology 70, no. 5 (May 1, 1992): 273–78. http://dx.doi.org/10.1139/o92-043.
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Uterine leiomyomas is the most common benign neoplasia in women, one of the most frequent causes of infertility in reproductive years, and the leading cause for hysterectomy. The pathophysiology of uterine leiomyomas is uncertain. Therefore, therapeutic approaches have been primarily empirical. It is now well documented that growth factors control the functional and possibly the histological integrity of several tissues. Recently the presence of growth substances in uterine tissues suggested that the role of sex steroid hormones in the pathophysiology of leiomyomas may be mediated by substances influencing the proliferation of smooth muscle cells and fibroblasts. This report summarizes the data related to the pathophysiology of leiomyomas, which indicate a possible role of growth factors in uterine leiomyomas.Key words: leiomyomas, growth factors, uterus, smooth muscle cells, fibroblasts.
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Lee, Robert M. K. W., Gary K. Owens, Timothy Scott-Burden, Richard J. Head, Michael J. Mulvany, and Ernesto L. Schiffrin. "Pathophysiology of smooth muscle in hypertension." Canadian Journal of Physiology and Pharmacology 73, no. 5 (May 1, 1995): 574–84. http://dx.doi.org/10.1139/y95-073.
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Structural changes of the arteries in hypertension are determined by the unique genetics of the animals and by various growth promoters and growth inhibitors. Vascular smooth muscle cell growth promoting factors include fibroblast growth factor, platelet-derived growth factor, and vasoactive peptides such as norepinephrine, angiotensin II, and endothelin. Endothelial cells secrete three types of growth inhibiting factors. These are heparin – heparan sulfate, transforming growth factor β, and nitric oxide. The effect of sympathetic innervation on vascular growth is probably dependent on its interaction with the rennin–angiotensin system. In the mesenteric vascular bed, the elevated resistance in the arterial system is present in both the macroarteries and in the more distal microarteries and veins. Changes in resistance arteries include hypertrophy and reduction in outer diameter (remodelling). In the resistance arteries from human essential hypertensives, remodelling is the predominant finding. Long-term treatment with an angiotensin I converting enzyme inhibitor but not with a β-blocker was effective in reversing this type of vascular change. Studies have suggested that in addition to angiotensin II, endothelin may play a role in vascular remodelling of resistance arteries.Key words: hypertension, vascular, remodelling, smooth muscle, growth factors.
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Scott-Burden, Timothy, Alfred W. A. Hahn, Fritz R. Bühler, and Thérèse J. Resink. "Vasoactive Peptides and Growth Factors in the Pathophysiology of Hypertension." Journal of Cardiovascular Pharmacology 20 (1992): S55—S64. http://dx.doi.org/10.1097/00005344-199206201-00011.
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Scott-Burden, Timothy, Alfred W. A. Hahn, Fritz R. Bühler, and Thérèse J. Resink. "Vasoactive Peptides and Growth Factors in the Pathophysiology of Hypertension." Journal of Cardiovascular Pharmacology 20 (December 1992): S55—S64. http://dx.doi.org/10.1097/00005344-199212001-00011.
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Hortobágyi, Tibor, János Bencze, Balázs Murnyák, Mahan C. Kouhsari, László Bognár, and György Marko-Varga. "Pathophysiology of meningioma growth in pregnancy." Open Medicine 12, no. 1 (July 13, 2017): 195–200. http://dx.doi.org/10.1515/med-2017-0029.
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AbstractMeningioma is among the most frequent brain tumours predominantly affecting elderly women. Epidemiological studies have shown that at the age of fertility the incidence is relatively low. The biological behaviour of meningioma in pregnancy is different from other meningiomas. The possible explanation is rooted in the complex physiological changes and hormonal differences during pregnancy. The increased meningioma growth observed in pregnancy is presumably the result of endocrine mechanisms. These include increase in progesterone, human placental lactogen (hPL) and prolactin (PRL) serum levels. In contrast, levels of pituitary hormones such as follicle stimulating hormone (FSH), luteinizing hormone (LH) and human chorionic gonadotropin (hCG) produced by the placenta are decreasing in the mother prior to childbirth. Besides, vascular factors also play a crucial role. Peritumoral brain edema (PTBE), with well-known causative association with vascular endothelial growth factor (VEGF), can often be seen both with imaging and in the surgical specimens. Our aim is to assess published research on this topic including diagnostic and therapeutic guidelines, and to provide a clinically useful overview on the pathophysiology and biological behaviour of this rare complication of pregnancy.
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Cho, Chul-Hyun, Kwang-Soon Song, Beom-Soo Kim, Du Hwan Kim, and Yun-Mee Lho. "Biological Aspect of Pathophysiology for Frozen Shoulder." BioMed Research International 2018 (2018): 1–8. http://dx.doi.org/10.1155/2018/7274517.
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It is fairly well understood that frozen shoulder involves several stages, which reflect the series of process from capsular inflammation and fibrosis to spontaneous resolution of this fibrosis. However, the underlying pathophysiologic process remains poorly determined. For this reason, management of frozen shoulder remains controversial. Determining the pathophysiological processes of frozen shoulder is a pivotal milestone in the development of novel treatment for patients with frozen shoulder. This article reviews what is known to date about the biological pathophysiology of frozen shoulder. Although articles for the pathophysiology of frozen shoulder provide inconsistent and inconclusive results, they have suggested both inflammation and fibrosis mediated by cytokines, growth factors, matrix metalloproteinases, and immune cells. Proinflammatory cytokines and growth factors released from immune cells control the action of fibroblast and matrix remodeling is regulated by the matrix metalloproteinases and their inhibitors. To improve our understanding of the disease continuum, better characterizing the biology of these processes at clearly defined stages will be needed. Further basic studies that use standardized protocols are required to more narrowly identify the role of cytokines, growth factors, matrix metalloproteinases, and immune cells. The results of these studies will provide needed clarity into the control mechanism of the pathogenesis of frozen shoulder and help identify new therapeutic targets for its treatment.
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Achrol, Achal S., Raphael Guzman, Marco Lee, and Gary K. Steinberg. "Pathophysiology and genetic factors in moyamoya disease." Neurosurgical Focus 26, no. 4 (April 2009): E4. http://dx.doi.org/10.3171/2009.1.focus08302.
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Moyamoya disease is an uncommon cerebrovascular condition characterized by progressive stenosis of the bilateral internal carotid arteries with compensatory formation of an abnormal network of perforating blood vessels providing collateral circulation. The etiology and pathogenesis of moyamoya disease remain unclear. Evidence from histological studies, proteomics, and endothelial progenitor cell analyses suggests new theories underlying the cause of vascular anomalies, including moyamoya disease. Familial moyamoya disease has been noted in as many as 15% of patients, indicating an autosomal dominant inheritance pattern with incomplete penetrance. Genetic analyses in familial moyamoya disease and genome-wide association studies represent promising strategies for elucidating the pathophysiology of this condition. In this review, the authors discuss recent studies that have investigated possible mechanisms underlying the etiology of moyamoya disease, including stem cell involvement and genetic factors. They also discuss future research directions that promise not only to offer new insights into the origin of moyamoya disease but to enhance our understanding of new vessel formation in the CNS as it relates to stroke, vascular anomalies, and tumor growth.
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Burgess, Adriane, Teresa S. Johnson, Amanda Simanek, Theodore Bell, and Sandra Founds. "Maternal ABO Blood Type and Factors Associated With Preeclampsia Subtype." Biological Research For Nursing 21, no. 3 (March 14, 2019): 264–71. http://dx.doi.org/10.1177/1099800419833782.
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Background: The pathophysiology of preeclampsia remains unclear. The disorder is heterogeneous, and the pathophysiology may vary by subtype. Identification of relevant biomarkers will help to better elucidate the pathophysiologic basis of each preeclampsia subtype. Blood type may be a biomarker that allows risk identification for preeclampsia. Objective: The purpose of this study was to investigate the associations among maternal ABO blood type and preeclampsia subtype and fetal growth restriction (FGR). Method: Medical records of 126 women with early-onset preeclampsia (≤33 6/7 weeks’ gestation), 126 women with late-onset preeclampsia (≥34 0/7 weeks’ gestation), and 259 controls who gave birth between January 2012 and June 2016 were retrospectively abstracted from a large suburban tertiary referral center in South Central Pennsylvania for this hospital-based case–control study. Results: Women with AB blood type had >3 times the odds of late-onset preeclampsia (odds ratio [ OR] = 3.35, 95% confidence interval (CI) = [1.02, 11.05]) compared to those with O blood type. Among women with early-onset preeclampsia, those with B blood type had 5 times the odds of having a growth-restricted fetus than did women with O blood type ( OR = 5.44, 95% CI [1.65, 17.94]). Discussion: Our findings suggest that AB blood type may be an important risk factor for late-onset preeclampsia and that among women with early-onset preeclampsia, those with B blood type have increased odds of FGR. These findings warrant further study in women and their offspring to identify the pathophysiologic processes that may link ABO blood type, preeclampsia subtype, and FGR.
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Homburg, R. "Involvement of growth factors in the pathophysiology of polycystic ovary syndrome." Gynecological Endocrinology 12, no. 6 (January 1998): 391–97. http://dx.doi.org/10.3109/09513599809012841.
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Hill-Kapturczak, Nathalie, Tambi Jarmi, and Anupam Agarwal. "Growth Factors and Heme Oxygenase-1: Perspectives in Physiology and Pathophysiology." Antioxidants & Redox Signaling 9, no. 12 (December 2007): 2197–208. http://dx.doi.org/10.1089/ars.2007.1798.
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Mathé, G. "Hormones and/or growth factors in prostate hypertrophy, pathophysiology and treatment." Biomedicine & Pharmacotherapy 49, no. 7-8 (January 1995): 317–18. http://dx.doi.org/10.1016/0753-3322(96)82657-6.
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Huang, Chenyu, and Rei Ogawa. "Keloidal pathophysiology: Current notions." Scars, Burns & Healing 7 (January 2021): 205951312098032. http://dx.doi.org/10.1177/2059513120980320.
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Introduction: Keloids are pathological scars that are notorious for their chronic and relentless invasion into adjacent healthy skin, with commonly seen post-therapeutic recurrence after monotherapies. Methods: An English literature review on keloid pathophysiology was performed by searching the PubMed, Embase and Web of Science databases, to find out the up-to-date relevant articles. The level of evidence was evaluated based on the included studies with the highest level of evidence first. Results: Keloid morphology, signs, symptoms and the histopathological changes that occur in the local cells and extracellular matrix components are described. The theories on the pathophysiology of keloidogenesis that have been proposed to date are also covered; these include endocrinological, nutritional, vascular, and autoimmunological factors. In addition, we describe the local mechanical forces (and the mechanosignalling pathways by which these forces shape keloid cell activities) that promote keloid formation and determine the direction of invasion of keloids and the body sites that are prone to them. Conclusion: A better understanding of this pathological entity, particularly its mechanobiology, will aid the development of new diagnostic and therapeutic strategies for use in the clinic to prevent, reduce or even reverse the growth of this pathological scar. Lay Summary Keloids are skin scars that are famous for their chronic invasion into healthy skin, with commonly seen recurrence after surgeries. Cells such as lymphocytes, macrophages, mast cells and endothelial cells are involved in keloid growth. Particularly, endocrinological, nutritional, vascular, autoimmunological and mechanical factors actively take part in keloid progression.
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Tarr, Joanna M., Kirti Kaul, Mohit Chopra, Eva M. Kohner, and Rakesh Chibber. "Pathophysiology of Diabetic Retinopathy." ISRN Ophthalmology 2013 (January 15, 2013): 1–13. http://dx.doi.org/10.1155/2013/343560.
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Diabetes is now regarded as an epidemic, with the population of patients expected to rise to 380 million by 2025. Tragically, this will lead to approximately 4 million people around the world losing their sight from diabetic retinopathy, the leading cause of blindness in patients aged 20 to 74 years. The risk of development and progression of diabetic retinopathy is closely associated with the type and duration of diabetes, blood glucose, blood pressure, and possibly lipids. Although landmark cross-sectional studies have confirmed the strong relationship between chronic hyperglycaemia and the development and progression of diabetic retinopathy, the underlying mechanism of how hyperglycaemia causes retinal microvascular damage remains unclear. Continued research worldwide has focussed on understanding the pathogenic mechanisms with the ultimate goal to prevent DR. The aim of this paper is to introduce the multiple interconnecting biochemical pathways that have been proposed and tested as key contributors in the development of DR, namely, increased polyol pathway, activation of protein kinase C (PKC), increased expression of growth factors such as vascular endothelial growth factor (VEGF) and insulin-like growth factor-1 (IGF-1), haemodynamic changes, accelerated formation of advanced glycation endproducts (AGEs), oxidative stress, activation of the renin-angiotensin-aldosterone system (RAAS), and subclinical inflammation and capillary occlusion. New pharmacological therapies based on some of these underlying pathogenic mechanisms are also discussed.
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Wang, Nanping. "PPAR-δin Vascular Pathophysiology." PPAR Research 2008 (2008): 1–10. http://dx.doi.org/10.1155/2008/164163.
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Peroxisome proliferator-activated receptors belong to the superfamily of ligand-dependent nuclear receptor transcription factors, which include three subtypes: PPAR-α,β/δ, andγ. PPAR-δ, play important roles in the regulation of cell growth and differentiation as well as tissue wound and repair. Emerging evidence has also demonstrated that PPAR-δis implicated in lipids and glucose metabolism. Most recently, the direct effects of PPAR-δon cardiovascular processes such as endothelial function and angiogenesis have also been investigated. Therefore, it is suggested that PPAR-δmay have critical roles in cardiovascular pathophysiology and is a potential target for therapeutic intervention of cardiovascular disorders such as atherosclerosis.
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Keskinov, A. A., M. R. Shurin, V. M. Bukhman, and Z. S. Shprakh. "PATHOPHYSIOLOGY OF DENDRITIC CELLS IN CANCER." Russian Journal of Biotherapy 15, no. 4 (December 30, 2016): 25–33. http://dx.doi.org/10.17650/1726-9784-2016-15-4-25-33.
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Immune system plays a crucial role in tumor growth process. It exerts cancer surveillance function via innate and adaptive immune mechanisms, nonetheless tumor may exploit various immune cells to escape specific immune response. Dendritic cells are the primary antigen presenting cells, which mediate immune response against cancer cells. Dendritic cells are capable of processing and presenting tumor antigens to T cells, which results in tumor-specific T cell- mediated response. However, adoptive therapy with dendritic cells demonstrates poor clinical outcomes. Among a variety of factors, the impact of tumor microenvironment on dendritic cells may be the primary one. Therefore, tumor-derived factors, which lead to dendritic cells malfunction, may be the key target for improving dendritic cell - based therapy. Meanwhile, recovery of dendritic cell functions in cancer patients remains one of primary aims for cancer immunotherapy. This review outlines main types of tumor-induced dendritic cells dysfunctions in cancer.
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Ma, Shenghong, Zhipeng Meng, Rui Chen, and Kun-Liang Guan. "The Hippo Pathway: Biology and Pathophysiology." Annual Review of Biochemistry 88, no. 1 (June 20, 2019): 577–604. http://dx.doi.org/10.1146/annurev-biochem-013118-111829.
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The Hippo pathway was initially discovered in Drosophila melanogaster as a key regulator of tissue growth. It is an evolutionarily conserved signaling cascade regulating numerous biological processes, including cell growth and fate decision, organ size control, and regeneration. The core of the Hippo pathway in mammals consists of a kinase cascade, MST1/2 and LATS1/2, as well as downstream effectors, transcriptional coactivators YAP and TAZ. These core components of the Hippo pathway control transcriptional programs involved in cell proliferation, survival, mobility, stemness, and differentiation. The Hippo pathway is tightly regulated by both intrinsic and extrinsic signals, such as mechanical force, cell–cell contact, polarity, energy status, stress, and many diffusible hormonal factors, the majority of which act through G protein–coupled receptors. Here, we review the current understanding of molecular mechanisms by which signals regulate the Hippo pathway with an emphasis on mechanotransduction and the effects of this pathway on basic biology and human diseases.
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Karmpaliotis, Dimitrios, Ioanna Kosmidou, Edward P. Ingenito, Kailin Hong, Atul Malhotra, Mary E. Sunday, and Kathleen J. Haley. "Angiogenic growth factors in the pathophysiology of a murine model of acute lung injury." American Journal of Physiology-Lung Cellular and Molecular Physiology 283, no. 3 (September 1, 2002): L585—L595. http://dx.doi.org/10.1152/ajplung.00048.2002.
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Capillary leakage and alveolar edema are hallmarks of acute lung injury (ALI). Neutrophils and serum macromolecules enter alveoli, promoting inflammation. Vascular endothelial growth factor (VEGF) causes plasma leakage in extrapulmonary vessels. Angiopoietin (Ang)-1 and -4 stabilize vessels, attenuating capillary leakage. We hypothesized that VEGF and Ang-1 and -4 modulate vessel leakage in the lung, contributing to the pathogenesis of ALI. We examined a murine model of lipopolysaccharide (LPS)-induced ALI. C57BL/6 and 129/J mice were studied at baseline and 24, 48, and 96 h after single or multiple doses of aerosolized LPS. Both strains exhibited time- and dose-dependent increases in inflammation and a deterioration of lung mechanics. Bronchoalveolar lavage (BAL) protein levels increased significantly, suggesting capillary leakage. Increased BAL neutrophil and total protein content correlated with time-dependent increased tissue VEGF and decreased Ang-1 and -4 levels, with peak VEGF and minimum Ang-1 and -4 expression after 96 h of LPS challenge. These data suggest that changes in the balance between VEGF and Ang-1 and -4 after LPS exposure may modulate neutrophil influx, protein leakage, and alveolar flooding during early ALI.
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Csósza, G., K. Karlócai, G. Losonczy, V. Müller, and Z. Lázár. "Growth factors in pulmonary arterial hypertension: Focus on preserving right ventricular function." Physiology International 107, no. 2 (June 2020): 177–94. http://dx.doi.org/10.1556/2060.2020.00021.
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AbstractPulmonary arterial hypertension (PAH) is a rare and progressive disease, characterized by increased vascular resistance leading to right ventricle (RV) failure. The extent of right ventricular dysfunction crucially influences disease prognosis; however, currently no therapies have specific cardioprotective effects. Besides discussing the pathophysiology of right ventricular adaptation in PAH, this review focuses on the roles of growth factors (GFs) in disease pathomechanism. We also summarize the involvement of GFs in the preservation of cardiomyocyte function, to evaluate their potential as cardioprotective biomarkers and novel therapeutic targets in PAH.
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Bobircă, Anca, Ana Dumitrache, Cristina Alexandru, Anca Florescu, George Ciobotaru, Florin Bobircă, Romina-Marina Sima, Cristian Poalelungi, Mihai Bojincă, and Ioan Ancuța. "Pathophysiology of Placenta in Antiphospholipid Syndrome." Physiologia 2, no. 3 (August 17, 2022): 66–79. http://dx.doi.org/10.3390/physiologia2030007.
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Antiphospholipid syndrome (APS) is an autoimmune disorder characterized by clinical manifestations caused by arterial or venous thrombosis and pregnancy conditions such as recurrent miscarriage, fetal death, or premature birth in the presence of antiphospholipid antibodies. The obstetrical manifestations are strongly related to the placental alterations. The aim of this review is to summarize the latest data on pathophysiology of obstetrical APS, emphasizing the disturbance of the placentation process. Due to a lack of extravillous trophoblasts to properly reconstruct the spiral arteries, APS causes hypoxic or ischemic injury or high-speed blood flow that damages the placenta. This results in decreased or interrupted maternal blood flow to the placenta and a lack of nutrients for the fetus. Antiphospholipid antibodies can lower the proliferation and infiltration of the extravillous trophoblasts. The placental mal-perfusion causes the release of antiangiogenic substances such as soluble fms-like tyrosine kinase-1 and soluble endoglin. Placental growth factor and vascular endothelial growth factor (VEGF) may be sequestered by sFlt1 and blocked from binding to trophoblast and endothelial cell VEGF receptors, inhibiting their proangiogenic effects. Preeclampsia is the clinical result from a lack of angiogenic factors needed for endothelial vascular homeostasis due to an excess of sFlt1 in the maternal circulation.
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Erusalimsky, Jorge D. "Vascular endothelial senescence: from mechanisms to pathophysiology." Journal of Applied Physiology 106, no. 1 (January 2009): 326–32. http://dx.doi.org/10.1152/japplphysiol.91353.2008.
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Most mitotically competent mammalian cell types can react to stress by undergoing a phenotypically distinctive and permanent form of growth arrest called “cellular senescence.” This response has been extensively characterized in cell culture and more recently it has been found to occur also in vivo in a number of tissues. In this review I will present the case for the occurrence of senescence in the vascular endothelium. I will also discuss the mechanisms and factors that modulate endothelial cell replicative capacity and the onset of senescence. Finally, I will examine the senescent phenotype and its possible consequences for the development and progression of vascular diseases.
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Kytikova, O. Yu, T. P. Novgorodtseva, M. V. Antonyuk, and T. A. Gvozdenko. "The role of neurotrophic growth factors in the pathophysiology of bronchial asthma associated with obesity." Bulletin of Siberian Medicine 20, no. 1 (April 12, 2021): 158–67. http://dx.doi.org/10.20538/1682-0363-2021-1-158-167.
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Sanju, S. "MICRO AND NANOPARTICLES FOR THE DELIVERY OF GROWTH FACTORS IN DIABETIC WOUNDS." Journal of Medical pharmaceutical and allied sciences 10, no. 5 (October 15, 2021): 3552–59. http://dx.doi.org/10.22270/jmpas.v10i5.1470.
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Diabetic wound (DW) is one of the leading complications of diabetes patients with a long history. It also puts an economic burden on people recovering from injuries to manage medication. The critical factors in the treatment of DW are infection, inflammation, and low oxygen level. Since these non-healing injuries are linked to the extended recovery process, current treatments are studied only for a short period. The areas covered in this article are an overview of DM, Pathophysiology of DW, stages of wound healing (Hemostasis, Inflammation, Proliferation, Maturation), the role of growth factor in diabetic wound healing, advantages of micro and nanoparticles over other drug delivery systems and micro and nanoparticles for the delivery of growth factors with different studies.
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Polverini, P. J. "The Pathophysiology of Angiogenesis." Critical Reviews in Oral Biology & Medicine 6, no. 3 (July 1995): 230–47. http://dx.doi.org/10.1177/10454411950060030501.
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The formation of new capillary blood vessels, a process termed "angiogenesis", is one of the most pervasive and fundamentally essential biological processes encountered in mammalian organisms. Angiogenesis is an important event in a variety of physiological settings, such as embryonic development, chronic inflammation, and wound repair. It is a process that is tightly regulated in both time and space. Angiogenesis is driven by a cocktail of growth factors and pro-angiogenic cytokines and is tempered by an equally diverse group of inhibitors of neovascularization. Angiogenesis is also central to the etiology and pathogenesis of a number of pathological processes that include, among others, solid tumors, diseases of the eye, and chronic inflammatory disorders such as rheumatoid arthritis, psoriasis, and periodontitis. Based on recent work from several laboratories, it is now eminently clear that most if not all angiogenesis and vasoproliferative-dependent disease processes are not only a consequence of the unrestricted production of normal or aberrant forms of pro-angiogenic mediators but also the result of a relative deficiency in angiogenic-inhibitory molecules. In this review, I will describe how these multifunctional mediator systems function to coordinate and regulate the angiogenic response, and how disruption in the molecular controls that regulate the production of pro-angiogenic and angiostatic mediators leads to aberrant angiogenesis and disease. The implications of these findings in the development of novel therapeutic strategies for the treatment of diseases characterized by disregulated angiogenesis will also be discussed.
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Kapustin, Roman V., Alexandra R. Onopriychuk, Olga N. Arzhanova, Victoria O. Polyakova, and Elena N. Alekseyenkova. "Pathophysiology of placenta and fetus in diabetes mellitus." Journal of obstetrics and women's diseases 67, no. 6 (December 15, 2018): 79–92. http://dx.doi.org/10.17816/jowd67679-92.
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Currently, there is a steady increase in the incidence of diabetes mellitus (DM) in the global population, which causes an increase in maternal and perinatal mortality. Children born to mothers with DM have a high risk of not only congenital abnormalities, but also cardiovascular and metabolic disorders in later life. Fetal growth is determined by both the metabolic and nutritional status of the mother, and the placental nutrient transfer capacity. Pregnancy complicated by DM is associated not only with overgrowth of the fetus, but also with the excess deposition of metabolites in the placenta. The role of disorders of carbohydrate metabolism, obesity and other factors in relation to the function of the placenta and fetal growth remains not fully understood. This review provides an overview of the literature on the placental complex status in pregnancy complicated by obesity, as well as pre-gestational and gestational types of DM. The focus is on three key substrates in these conditions: glucose, lipids, and amino acids, and their influence on placental metabolic activity and on the fetus. Improved knowledge of morphology and understanding of changes in the function of the placenta that lead to abnormal growth of the fetus will allow for the development of new therapeutic approaches to improve the outcomes of pregnancy, maternal and child health.
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Akwii, Racheal G., Md S. Sajib, Fatema T. Zahra, and Constantinos M. Mikelis. "Role of Angiopoietin-2 in Vascular Physiology and Pathophysiology." Cells 8, no. 5 (May 17, 2019): 471. http://dx.doi.org/10.3390/cells8050471.
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Angiopoietins 1–4 (Ang1–4) represent an important family of growth factors, whose activities are mediated through the tyrosine kinase receptors, Tie1 and Tie2. The best characterized are angiopoietin-1 (Ang1) and angiopoietin-2 (Ang2). Ang1 is a potent angiogenic growth factor signaling through Tie2, whereas Ang2 was initially identified as a vascular disruptive agent with antagonistic activity through the same receptor. Recent data demonstrates that Ang2 has context-dependent agonist activities. Ang2 plays important roles in physiological processes and the deregulation of its expression is characteristic of several diseases. In this review, we summarize the activity of Ang2 on blood and lymphatic endothelial cells, its significance in human physiology and disease, and provide a current view of the molecular signaling pathways regulated by Ang2 in endothelial cells.
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Ahn, Soo Hyun, Stephany P. Monsanto, Caragh Miller, Sukhbir S. Singh, Richard Thomas, and Chandrakant Tayade. "Pathophysiology and Immune Dysfunction in Endometriosis." BioMed Research International 2015 (2015): 1–12. http://dx.doi.org/10.1155/2015/795976.
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Endometriosis is an estrogen-dependent, chronic, proinflammatory disease prevalent in 10% of women of reproductive age worldwide. Characterized by the growth of endometrium-like tissue in aberrant locations outside of the uterus, it is responsible for symptoms including chronic pelvic pain, dysmenorrhea, and subfertility that degrade quality of life of women significantly. In Canada, direct and indirect economic cost of endometriosis amounts to 1.8 billion dollars, and this is elevated to 20 billion dollars in the United States. Despite decades of research, the etiology and pathophysiology of endometriosis still remain to be elucidated. This review aims to bring together the current understanding regarding the pathogenesis of endometriosis with specific focus on mechanisms behind vascularization of the lesions and the contribution of immune factors in facilitating lesion establishment and development. The role of hormones, immune cells, and cytokine signaling is highlighted, in addition to discussing the current pharmaceutical options available for management of pain symptoms in women with endometriosis.
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Fang, Yao-Ching, Ling-Fei Wei, Chaur-Jong Hu, and Yong-Kwang Tu. "Pathological Circulating Factors in Moyamoya Disease." International Journal of Molecular Sciences 22, no. 4 (February 8, 2021): 1696. http://dx.doi.org/10.3390/ijms22041696.
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Moyamoya disease (MMD) is a cerebrovascular disease that presents with vascular stenosis and a hazy network of collateral formations in angiography. However, the detailed pathogenic pathway remains unknown. Studies have indicated that in addition to variations in the of genetic factor RNF213, unusual circulating angiogenetic factors observed in patients with MMD may play a critical role in producing “Moyamoya vessels”. Circulating angiogenetic factors, such as growth factors, vascular progenitor cells, cytokines, inflammatory factors, and other circulating proteins, could promote intimal hyperplasia in vessels and excessive collateral formation with defect structures through endothelial hyperplasia, smooth muscle migration, and atypical neovascularization. This study summarizes the hypothesized pathophysiology of how these circulating factors affect MMD and the interactive modulation between them.
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Rocha, Natalia Pessoa, João Paulo Sampaio Ferreira, Paula Luciana Scalzo, Izabela Guimarães Barbosa, Mariana Soares de Souza, Paulo Pereira Christo, Helton José Reis, and Antonio Lucio Teixeira. "Circulating levels of neurotrophic factors are unchanged in patients with Parkinson's disease." Arquivos de Neuro-Psiquiatria 76, no. 5 (May 2018): 310–15. http://dx.doi.org/10.1590/0004-282x20180035.
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ABSTRACT There is great evidence linking neurotrophic factor (NF) dysfunction with Parkinson's disease (PD) pathophysiology. This study was conducted to evaluate plasma levels of NFs and their possible associations with clinical symptoms in PD. For this purpose, 40 PD patients and 25 controls were subjected to a clinical evaluation and peripheral blood draw. Plasma levels of brain-derived neurotrophic factor (BDNF), pro-BDNF, neurotrophin 3, neurotrophin 4, nerve growth, glial cell line-derived neurotrophic factor and ciliary neurotrophic factor were measured by enzyme-linked immunosorbent assay. There was no significant difference between PD patients and controls regarding the plasma levels of the evaluated NFs. In addition, NF levels were not associated with disease duration, degree of motor or functional impairment, cognitive performance or severity of depressive symptoms. In conclusion, although NFs may play relevant roles in the pathophysiology of PD, the circulating levels of these molecules are not necessarily changed in patients with PD.
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Yadav, Monu, Ishu Sardana, Amarjeet Sharma, Nidhi Sharma, Kalpana Nagpal, and Paramjeet Malik. "Emerging Pathophysiological Targets of Psoriasis for Future Therapeutic Strategies." Infectious Disorders - Drug Targets 20, no. 4 (October 16, 2020): 409–22. http://dx.doi.org/10.2174/1871526519666190617162701.
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Psoriasis is a chronic autoimmune skin disorder which involves complex interactions between genes, keratinocytes, T-cells and inflammatory cells. It affects 2-3% population worldwide. Molecular biology and cellular immunology of psoriasis, when linked with biotechnology and genetic studies can help researchers to understand the pathophysiology of psoriasis. T-cells activation, keratinocyte hyperproliferation, and angiogenesis are the core mechanisms entailed in the development of psoriasis lesion. Investigators are trying to overcome the challenges of complex pathophysiology pathways involved in this disorder. The different possible hypotheses for its pathophysiology such as growth factors, enzymes, inflammation, and genetic factors mediated pathophysiology have been described in the present review paper in detail. Clinically available drugs only control the symptoms of psoriasis but are not effective for the treatment of the disorder completely and are also associated with some side effects such as itching, renal disorders, hematologic, nonmelanoma skin cancer, pulmonary, gastrointestinal toxicity, etc. This paper made an effort to understand the pathophysiological targets, discuss the research done so far and the treatments available for the effective management of psoriasis.
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Simińska, Donata, Klaudyna Kojder, Dariusz Jeżewski, Ireneusz Kojder, Marta Skórka, Izabela Gutowska, Dariusz Chlubek, and Irena Baranowska-Bosiacka. "The Pathophysiology of Post-Traumatic Glioma." International Journal of Molecular Sciences 19, no. 8 (August 19, 2018): 2445. http://dx.doi.org/10.3390/ijms19082445.
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Malignant glioma is a brain tumor with a very high mortality rate resulting from the specific morphology of its infiltrative growth and poor early detection rates. The causes of one of its very specific types, i.e., post-traumatic glioma, have been discussed for many years, with some studies providing evidence for mechanisms where the reaction to an injury may in some cases lead to the onset of carcinogenesis in the brain. In this review of the available literature, we discuss the consequences of breaking the blood–brain barrier and consequences of the influx of immune-system cells to the site of injury. We also analyze the influence of inflammatory mediators on the expression of genes controlling the process of apoptosis and the effect of chemical mutagenic factors on glial cells in the brain. We present the results of experimental studies indicating a relationship between injury and glioma development. However, epidemiological studies on post-traumatic glioma, of which only a few confirm the conclusions of experimental research, indicate that any potential relationship between injury and glioma, if any, is indirect.
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Sopova, Kateryna, Katerina Gatsiou, Konstantinos Stellos, and Christoph Laske. "Dysregulation of Neurotrophic and Haematopoietic Growth Factors in Alzheimer’s Disease: From Pathophysiology to Novel Treatment Strategies." Current Alzheimer Research 11, no. 1 (January 31, 2014): 27–39. http://dx.doi.org/10.2174/1567205010666131120100743.
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Martel-Pelletier, Johanne. "10 CYTOKINES, PROTEASES AND GROWTH FACTORS IN THE PATHOPHYSIOLOGY OF OSTEOARTHRITIS:WHAT ARE THEIR LEVELS OF GUILT?" Osteoarthritis and Cartilage 14 (2006): S4—S5. http://dx.doi.org/10.1016/s1063-4584(07)60430-0.
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Nazarenko, L. G., and O. V. Demina. "Placement of the placenta: issues of etiology, pathophysiology, diagnosis (Clinical lecture)." HEALTH OF WOMAN, no. 8(144) (October 31, 2019): 7–11. http://dx.doi.org/10.15574/hw.2019.144.7.
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In modern obstetrics, there is an increase in the frequency of pathological conditions, combined with the sign of abnormal syvasive of the placenta, the spectrum of which includes placenta accreta, placenta increta, placenta percreta. The most favored definition is placenta accreta, in international sources of information – placenta accreta spectrum. This pathology is the leading cause of life-threatening hemorrhage, which often requires blood transfusion, hysterectomy. The issues of prediction and diagnosis are relevant. Contemporary ideas about the etiology and pathogenesis of placental growth are covered, risk factors as a basis for clinical prognosis are substantiated and specified. The basic elements of diagnostics of placental growth in the observation of the pregnant woman are presented. The necessity of prenatal hospitalization and delivery in conditions of providing modern technologies of blood circulation, surgical help, highly professional multidisciplinary team is emphasized. Key words: placenta, growth, caesarean section, prognosis, diagnosis.
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Wong, Siu Him Janus, Kwong Yuen Chiu, and Chun Hoi Yan. "Review Article: Osteophytes." Journal of Orthopaedic Surgery 24, no. 3 (December 2016): 403–10. http://dx.doi.org/10.1177/1602400327.
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An osteophyte is a fibrocartilage-capped bony outgrowth that is one of the features of osteoarthritis. This study reviewed the types, risk factors, pathophysiology, clinical presentations, and medical and surgical treatment of osteophytes. Extraspinal osteophytes are classified as marginal, central, periosteal, or capsular, whereas vertebral osteophytes are classified as traction or claw. Risk factors for development of osteophytes include age, body mass index, physical activity, and other genetic and environmental factors. Transforming growth factor β plays a role in the pathophysiology of osteophyte formation. Osteophytes can cause pain, limit range of motion, affect quality of life, and cause multiple symptoms at the spine. Medical treatment involves the use of bisphosphonates and other non-steroidal anti-inflammatory agents. Surgical treatment in the form of cheilectomy for impingement syndromes during joint replacement is recommended.
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Clement, Dominique, John Ramage, and Raj Srirajaskanthan. "Update on Pathophysiology, Treatment, and Complications of Carcinoid Syndrome." Journal of Oncology 2020 (January 21, 2020): 1–11. http://dx.doi.org/10.1155/2020/8341426.
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Carcinoid syndrome (CS) develops in patients with hormone-producing neuroendocrine neoplasms (NENs) when hormones reach a significant level in the systemic circulation. The classical symptoms of carcinoid syndrome are flushing, diarrhoea, abdominal pain, and wheezing. Neuroendocrine neoplasms can produce multiple hormones: 5-hydroxytryptamine (serotonin) is the most well-known one, but histamine, catecholamines, and brady/tachykinins are also released. Serotonin overproduction can lead to symptoms and also stimulates fibrosis formation which can result in development of carcinoid syndrome-associated complications such as carcinoid heart disease (CaHD) and mesenteric fibrosis. Transforming growth factor beta (TGF-β) is one of the main factors in developing fibrosis, but platelet-derived growth factor (PDGF), basic fibroblast growth factor (FGF2), and connective tissue growth factor (CTGF or CCN2) are also related to fibrosis development. Treatment of CS focuses on reducing serotonin levels with somatostatin analogues (SSA’s). Telotristat ethyl and peptide receptor radionuclide therapy (PRRT) have recently become available for patients with symptoms despite being established on SSA’s. Screening for CaHD is advised, and early intervention prolongs survival. Mesenteric fibrosis is often present and associated with poorer survival, but the role for prophylactic surgery of this is unclear. Depression, anxiety, and cognitive impairment are frequently present symptoms in patients with CS but not always part of their care plan. The role of antidepressants, mainly SSRIs, is debatable, but recent retrospective studies show evidence for safe use in patients with CS. Carcinoid crisis is a life-threatening complication of CS which can appear spontaneously but mostly described during surgery, anaesthesia, chemotherapy, PRRT, and radiological procedures and may be prevented by octreotide administration.
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Aryal, Bibek, Munekazu Yamakuchi, Toshiaki Shimizu, Jun Kadono, Akira Furoi, Kentaro Gejima, Teruo Komokata, Teruto Hashiguchi, and Yutaka Imoto. "Deciphering Platelet Kinetics in Diagnostic and Prognostic Evaluation of Hepatocellular Carcinoma." Canadian Journal of Gastroenterology and Hepatology 2018 (June 27, 2018): 1–9. http://dx.doi.org/10.1155/2018/9142672.
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Liver pathophysiology can, directly and indirectly, impose morphological or biochemical abnormalities of the platelets. Conversely, platelets are also able to regulate the promitogenic and profibrotic signals on liver pathobiology. Platelet contribution to the liver pathophysiology is typically facilitated by the platelet-derived growth factors that are sequestered in different subsets of alpha and dense granules, and the release of these growth factors is synchronized according to the stage and type of liver disease or injury. Thus, platelets harbor clinically relevant information with potential diagnostic and prognostic implications in liver diseases. Hepatocellular carcinoma (HCC) largely influences the platelet kinetics, and a growing body of evidence has recognized its association with HCC occurrence or prognosis. This narrative review summarizes the progress made on implicating platelet as a diagnostic and prognostic tool for HCC; the review also dissects the contradictory results from earlier studies and reflects how combining platelet-based information may enable more reliable test for diagnostic and prognostic evaluation of HCC.
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Tchernof, André, and Jean-Pierre Després. "Pathophysiology of Human Visceral Obesity: An Update." Physiological Reviews 93, no. 1 (January 2013): 359–404. http://dx.doi.org/10.1152/physrev.00033.2011.
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Excess intra-abdominal adipose tissue accumulation, often termed visceral obesity, is part of a phenotype including dysfunctional subcutaneous adipose tissue expansion and ectopic triglyceride storage closely related to clustering cardiometabolic risk factors. Hypertriglyceridemia; increased free fatty acid availability; adipose tissue release of proinflammatory cytokines; liver insulin resistance and inflammation; increased liver VLDL synthesis and secretion; reduced clearance of triglyceride-rich lipoproteins; presence of small, dense LDL particles; and reduced HDL cholesterol levels are among the many metabolic alterations closely related to this condition. Age, gender, genetics, and ethnicity are broad etiological factors contributing to variation in visceral adipose tissue accumulation. Specific mechanisms responsible for proportionally increased visceral fat storage when facing positive energy balance and weight gain may involve sex hormones, local cortisol production in abdominal adipose tissues, endocannabinoids, growth hormone, and dietary fructose. Physiological characteristics of abdominal adipose tissues such as adipocyte size and number, lipolytic responsiveness, lipid storage capacity, and inflammatory cytokine production are significant correlates and even possible determinants of the increased cardiometabolic risk associated with visceral obesity. Thiazolidinediones, estrogen replacement in postmenopausal women, and testosterone replacement in androgen-deficient men have been shown to favorably modulate body fat distribution and cardiometabolic risk to various degrees. However, some of these therapies must now be considered in the context of their serious side effects. Lifestyle interventions leading to weight loss generally induce preferential mobilization of visceral fat. In clinical practice, measuring waist circumference in addition to the body mass index could be helpful for the identification and management of a subgroup of overweight or obese patients at high cardiometabolic risk.
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Pollan, Charlene. "Retinopathy of Prematurity: An Eye Toward Better Outcomes." Neonatal Network 28, no. 2 (March 2009): 93–101. http://dx.doi.org/10.1891/0730-0832.28.2.93.
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Retinopathy of prematurity (ROP) results from the abnormal growth of blood vessels in the vascular bed supporting the developing retina. Estimated to cause up to 500 new cases of blindness in the U.S. each year, ROP affects primarily infants born at less than 1,500 g. Although its etiology is not well understood, ROP is thought to occur as a result of a complex interaction between oxygen and vascular growth factors. This article briefly reviews the history of ROP, discusses its pathophysiology, and addresses the risk factors and strategies for prevention.
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Bersano, Anna, Stephanie Guey, Gloria Bedini, Sara Nava, Dominique Hervé, Peter Vajkoczy, Turgut Tatlisumak, et al. "Research Progresses in Understanding the Pathophysiology of Moyamoya Disease." Cerebrovascular Diseases 41, no. 3-4 (2016): 105–18. http://dx.doi.org/10.1159/000442298.
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Background: The pathogenesis of moyamoya disease (MMD) is still unknown. The detection of inflammatory molecules such as cytokines, chemokines and growth factors in MMD patients' biological fluids supports the hypothesis that an abnormal angiogenesis is implicated in MMD pathogenesis. However, it is unclear whether these anomalies are the consequences of the disease or rather causal factors as well as these mechanisms remain insufficient to explain the pathophysiology of MMD. The presence of a family history in about 9-15% of Asian patients, the highly variable incidence rate between different ethnic and sex groups and the age of onset support the role of genetic factors in MMD pathogenesis. However, although some genetic loci have been associated with MMD, few of them have been replicated in independent series. Recently, RNF213 gene was shown to be strongly associated with MMD occurrence with a founder effect in East Asian patients. However, the mechanisms leading from RNF213 mutations to MMD clinical features are still unknown. Summary: The research on pathogenic mechanism of MMD is in its infancy. MMD is probably a complex and heterogeneous disorder, including different phenotypes and genotypes, in which more than a single factor is implicated. Key Message: Since the diagnosis of MMD is rapidly increasing worldwide, the development of more efficient stratifying risk systems, including both clinical but also biological drivers became imperative to improve our ability of predict prognosis and to develop mechanism-tailored interventions.
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Lipunov, A. R., I. M. Afanasov, E. S. Vorobeva, A. B. Chuhnina, M. G. Gladkova, A. V. Kibardin, and V. A. Mitish. "Molecular systems for targeted delivery and controlled release of growth factors for chronic wound treatment." Wounds and wound infections. The prof. B.M. Kostyuchenok journal 5, no. 3 (May 28, 2020): 6–15. http://dx.doi.org/10.25199/2408-9613-2018-5-3-6-15.
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Growth factors (GFs) are endogenous signaling proteins, that regulate cell migration, proliferation and differentiation in tissue regeneration. GFs’ concentrations in chronic wounds are pathologically reduced. This leads to a disruption of the healing process and makes chronic wounds treatment more complicated. There are drugs currently used in clinical practice, that contain GFs in a free form. However, their efficiency for chronic wounds treatment is limited, as GFs are quickly degraded in a proteolytic environment of chronic wounds. In order to overcome this limitation biocompatible molecular systems for targeted delivery and controlled release are proposed, such as: micro- and nanoparticles, hydrogels, scaffolds. GFs roles in the healing process, chronic wounds pathophysiology and molecular systems for GFs targeted delivery and controlled release are reviewed.
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Shieh, Jae-Hung, Tsann-Long Su, Jason Shieh, and Malcolm A. S. Moore. "Derivation and Drug Screening of Growth Factors- and Stroma-Dependent Human Multiple Myeloma Cells." Blood 120, no. 21 (November 16, 2012): 5020. http://dx.doi.org/10.1182/blood.v120.21.5020.5020.
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Abstract Abstract 5020 Multiple myeloma (MM) is the second most common hematological malignancy in the U. S. MM is treatable but not curable with a median survival of 5–7 years with advanced treatment. There are several established human MM cell lines that grow in the absence of any cytokine dependence or stromal interaction. However, most primary MM patient specimens are difficult to maintain or to expand in vitro for pathophysiology investigation and drug screening. To address this issue, we systemically evaluated effects of various culture parameters on the growth of primary MM cells. A serum-free MS-5 cell (a murine bone marrow stromal cell line) co-culture system containing cytokine cocktail is capable of expanding purified CD138+ cells from primary MM specimens in vitro. Optimal expansion of the MM CD138+ cells requires a combination of stromal cells, human interleukin (IL-6) and human hepatocyte growth factors (hHGF). These MM cells can be maintained and repeatedly recovered following cryopreservation. The in vitro effect of five novel alkylating agents (BO-1055, −1090, 1099, −1393 and −1509) was evaluated for an inhibition of proliferation of the MM cells, and on human mesenchymal stem cells (hMSC), murine MSC (MS-5 cells and Op9 cells), human bone marrow derived endothelial cells (BMEC), and human cord blood (CB) CD34+ cells, as well as for a week 5 Cobblestones area forming cells (CAFC; an in vitro surrogate assay for hematopoietic stem cells) assay with CB CD34+ cells. BO-1055 shows a promising therapeutic window between the MM cells and other normal tissues. For the MM cells, IC50 was ∼1. 02 μM. In contrast, IC50 of BMEC, MSC, CB CD34+ cells and CAFC was >10, >25, 8, and >5 μM, respectively. Therefore, our stromal culture system supports human primary MM cells and closely recapitulates the growth of MM cells in their niche in vivo. We also identified a novel BO-1055 molecule that inhibits primary MM cells but is well-tolerated by other normal tissues. This in vitro stromal co-culture system provides a powerful tool to dissect the pathophysiology of human MM, and to screen new drugs for MM therapy. Disclosures: No relevant conflicts of interest to declare.
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Mitre, Mariela, Abigail Mariga, and Moses V. Chao. "Neurotrophin signalling: novel insights into mechanisms and pathophysiology." Clinical Science 131, no. 1 (December 1, 2016): 13–23. http://dx.doi.org/10.1042/cs20160044.
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Neurotrophins, such as brain-derived neurotrophic factor (BDNF), are prominent regulators of neuronal survival, growth and differentiation during development. While trophic factors are viewed as well-understood but not innovative molecules, there are many lines of evidence indicating that BDNF plays an important role in the pathophysiology of many neurodegenerative disorders, depression, anxiety and other psychiatric disorders. In particular, lower levels of BDNF are associated with the aetiology of Alzheimer's and Huntington's diseases. A major challenge is to explain how neurotrophins are able to induce plasticity, improve learning and memory and prevent age-dependent cognitive decline through receptor signalling. This article will review the mechanism of action of neurotrophins and how BDNF/tropomyosin receptor kinase B (TrkB) receptor signaling can dictate trophic responses and change brain plasticity through activity-dependent stimulation. Alternative approaches for modulating BDNF/TrkB signalling to deliver relevant clinical outcomes in neurodegenerative and neuropsychiatric disorders will also be described.
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Patel, Rutu M., and Digvijaysinh G. Rana. "ROLE OF INSULIN-LIKE GROWTH FACTOR IN DEPRESSION: A REVIEW." International Research Journal of Pharmacy 12, no. 3 (April 6, 2021): 6–10. http://dx.doi.org/10.7897/2230-8407.1203124.
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Depression is a disorder of unknown origin and it involves disturbance of many physiological processes. There are many mechanisms in depression including alterations in neurotrophic factors. It has been suggested in this review that an impairment of synaptic plasticity in specific areas of central nervous system, specifically in hippocampus can be an important factor in the pathophysiology of depression. Further, an abnormal neural plasticity may be related to alterations in the level of neurotrophic factors. In context with this, it can be suggested that there can be a connection between occurrences of depression with the disturbance of neurotrophic factors, raising great attention in the recent years. In the present review, it has been tried to explain the significance of insulin-like growth factor in depression by presenting the several important topics such as neurotrophic factors in depression, insulin like growth factor in central nervous system, insulin like growth factor receptor in depression, neurotrophic role of insulin like growth factor and correlation between insulin like growth factor and brain serotonin levels.
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Anderson, KC, RM Jones, C. Morimoto, P. Leavitt, and BA Barut. "Response patterns of purified myeloma cells to hematopoietic growth factors." Blood 73, no. 7 (May 15, 1989): 1915–24. http://dx.doi.org/10.1182/blood.v73.7.1915.1915.
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Abstract Tumor cells were isolated from the bone marrow of seven patients with multiple myeloma and from the peripheral blood of three patients with plasma cell leukemia using Ficoll-Hypaque (FH) density sedimentation followed by immune rosette depletion of T, myeloid, monocytoid, and natural killer (NK) cells. Enrichment to greater than or equal to 93% plasma cells was confirmed with Wright's-Giemsa staining, with intracytoplasmic immunoglobulin staining, and with staining using monoclonal antibodies (MoAbs) directed at B, T, myeloid, monocytoid, and myeloma antigens in indirect immunofluorescence assays. Myeloma cells neither proliferated nor secreted Ig in response to G/M-CSF, G- CSF, M-CSF, interleukin-1 alpha (IL-1 alpha), interleukin-1 beta (IL-1 beta), interleukin-2 (IL-2), or interleukin-4 (IL-4). Significant proliferation (SI greater than or equal to 3.0) was induced by interleukin-6 (IL-6) in six of ten patients (SI of 31 and 43 in two cases); and to interleukin-3 (IL-3) and interleukin-5 (IL-5), independently, in two patients each. Peak proliferation to IL-5 or IL-6 and to IL-3 occurred in cells pulsed with 3[H] thymidine at 24 and 48 hours, respectively; and proliferation to combinations of factors did not exceed that noted to IL-6 alone; Ig secretion was not documented under any culture conditions. Three myeloma-derived cell lines similarly studied demonstrated variable responses. The heterogeneity in the in vitro responses of myeloma cells and derived cell lines to exogenous growth factors enhances our understanding of abnormal plasma cell growth and may yield insight into the pathophysiology of plasma cell dyscrasias.
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Anderson, KC, RM Jones, C. Morimoto, P. Leavitt, and BA Barut. "Response patterns of purified myeloma cells to hematopoietic growth factors." Blood 73, no. 7 (May 15, 1989): 1915–24. http://dx.doi.org/10.1182/blood.v73.7.1915.bloodjournal7371915.
Full textAbstract:
Tumor cells were isolated from the bone marrow of seven patients with multiple myeloma and from the peripheral blood of three patients with plasma cell leukemia using Ficoll-Hypaque (FH) density sedimentation followed by immune rosette depletion of T, myeloid, monocytoid, and natural killer (NK) cells. Enrichment to greater than or equal to 93% plasma cells was confirmed with Wright's-Giemsa staining, with intracytoplasmic immunoglobulin staining, and with staining using monoclonal antibodies (MoAbs) directed at B, T, myeloid, monocytoid, and myeloma antigens in indirect immunofluorescence assays. Myeloma cells neither proliferated nor secreted Ig in response to G/M-CSF, G- CSF, M-CSF, interleukin-1 alpha (IL-1 alpha), interleukin-1 beta (IL-1 beta), interleukin-2 (IL-2), or interleukin-4 (IL-4). Significant proliferation (SI greater than or equal to 3.0) was induced by interleukin-6 (IL-6) in six of ten patients (SI of 31 and 43 in two cases); and to interleukin-3 (IL-3) and interleukin-5 (IL-5), independently, in two patients each. Peak proliferation to IL-5 or IL-6 and to IL-3 occurred in cells pulsed with 3[H] thymidine at 24 and 48 hours, respectively; and proliferation to combinations of factors did not exceed that noted to IL-6 alone; Ig secretion was not documented under any culture conditions. Three myeloma-derived cell lines similarly studied demonstrated variable responses. The heterogeneity in the in vitro responses of myeloma cells and derived cell lines to exogenous growth factors enhances our understanding of abnormal plasma cell growth and may yield insight into the pathophysiology of plasma cell dyscrasias.
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Poppema, Sibrand. "Immunobiology and Pathophysiology of Hodgkin Lymphomas." Hematology 2005, no. 1 (January 1, 2005): 231–38. http://dx.doi.org/10.1182/asheducation-2005.1.231.
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Abstract Classical Hodgkin lymphoma (HL) is characterized by the presence of Reed-Sternberg (RS) cells, which are transformed post-germinal center B cells destined for apoptosis since they have not undergone successful immunoglobulin gene rearrangement. Several mechanisms, including latent infection by Epstein-Barr virus (EBV), allow these cells to survive. It is remarkable that many of the signaling pathways that promote survival are shared between the EBV-induced proteins, such as EBNA1, LMP1, and LMP2, and other molecules that are upregulated in RS cells. A key role is played by the presence of constitutive nuclear factor (NF)-κB, which is induced by LMP1, as well as by CD30, CD40, tumor necrosis factor (TNF)-α, and Notch1 interactions, and results in the upregulation of at least 45 genes including chemokines, cytokines, receptors, apoptotic regulators, intracellular signaling molecules, and transcription factors. The other characteristic of classical HL is the presence of an extensive inflammatory infiltrate. Key features of this infiltrate are that it comprises Th2 and T regulatory cells and generally lacks Th1 cells, CD8 cytotoxic T cells, and natural killer (NK) cells. The RS cells appear to induce this infiltrate by the secretion of Th2 type chemokines such as TARC and MDC. The RS cells also produce cytokines that inhibit Th1 responses, as interleukin (IL)-10 and transforming growth factor (TGF)-β express CD95 ligand, which induces apoptosis of activated Th1 and CD8 T cells. Other important mechanisms that allow the RS cells to escape an effective anti-EBV immune response include the downregulation of HLA class I in EBV-negative cases or the presence of a polymorphism in HLA class I in EBV-positive cases that allow escape from CD8-mediated cytotoxicity. On the other hand, expression of HLA-G allows the escape from NK cells that would normally recognize the HLA class I-negative RS cells. Overall, the cellular infiltrate in HL appears to play a decisive role in allowing the RS cells to survive by providing an environment that suppresses cytotoxic immune responses and providing cellular interactions and cytokines that support the growth and survival of RS cells. Future therapeutic strategies could focus directly on the NF-κB activation, on various receptors to ligand interactions, on the chemokine and cytokine network, or on the induction of effective anti-EBV latent protein immune responses.
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Rosner, Jack, Pablo Avalos, Frank Acosta, John Liu, and Doniel Drazin. "The Potential for Cellular Therapy Combined with Growth Factors in Spinal Cord Injury." Stem Cells International 2012 (2012): 1–11. http://dx.doi.org/10.1155/2012/826754.
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Any traumatic spinal cord injury (SCI) may cause symptoms ranging from pain to complete loss of motor and sensory functions below the level of the injury. Currently, there are over 2 million SCI patients worldwide. The cost of their necessary continuing care creates a burden for the patient, their families, and society. Presently, few SCI treatments are available and none have facilitated neural regeneration and/or significant functional improvement. Research is being conducted in the following areas: pathophysiology, cellular therapies (Schwann cells, embryonic stem cells, induced pluripotent stem cells, mesenchymal stem cells, olfactory ensheathing cells), growth factors (BDNF), inhibitory molecules (NG2, myelin protein), and combination therapies (cell grafts and neurotrophins, cotransplantation). Results are often limited because of the inhibitory environment created following the injury and the limited regenerative potential of the central nervous system. Therapies that show promise in small animal models may not transfer to nonhuman primates and humans. None of the research has resulted in remarkable improvement, but many areas show promise. Studies have suggested that a combination of therapies may enhance results and may be more effective than a single therapy. This paper reviews and discusses the most promising new SCI research including combination therapies.
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Ware, Lorraine B., and Michael A. Matthay. "Keratinocyte and hepatocyte growth factors in the lung: roles in lung development, inflammation, and repair." American Journal of Physiology-Lung Cellular and Molecular Physiology 282, no. 5 (May 1, 2002): L924—L940. http://dx.doi.org/10.1152/ajplung.00439.2001.
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A growing body of evidence indicates that the epithelial-specific growth factors keratinocyte growth factor (KGF), fibroblast growth factor (FGF)-10, and hepatocyte growth factor (HGF) play important roles in lung development, lung inflammation, and repair. The therapeutic potential of these growth factors in lung disease has yet to be fully explored. KGF has been best studied and has impressive protective effects against a wide variety of injurious stimuli when given as a pretreatment in animal models. Whether this protective effect could translate to a treatment effect in humans with acute lung injury needs to be investigated. FGF-10 and HGF may also have therapeutic potential, but more extensive studies in animal models are needed. Because HGF lacks true epithelial specificity, it may have less potential than KGF and FGF-10 as a targeted therapy to facilitate lung epithelial repair. Regardless of their therapeutic potential, studies of the unique roles played by these growth factors in the pathogenesis and the resolution of acute lung injury and other lung diseases will continue to enhance our understanding of the complex pathophysiology of inflammation and repair in the lung.
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Feldo, Marcin, Magdalena Wójciak-Kosior, Ireneusz Sowa, Janusz Kocki, Jacek Bogucki, Tomasz Zubilewicz, Jan Kęsik, and Anna Bogucka-Kocka. "Effect of Diosmin Administration in Patients with Chronic Venous Disorders on Selected Factors Affecting Angiogenesis." Molecules 24, no. 18 (September 12, 2019): 3316. http://dx.doi.org/10.3390/molecules24183316.
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Diosmin is a natural compound with a wide range of biological activity, e.g., it improves lymphatic drainage, supports microcirculation, and increases venous tone, and venous elasticity, hence, it is applied in the pharmacotherapy of chronic venous disorders (CVD). The aim of this study was to assess the correlation between diosmin administration (2 × 600 mg daily) in patients suffering from CVD and the levels of selected factors influencing angiogenesis, which are involved in CVD pathophysiology. Thirty-five CVD patients were examined. Levels of plasma tumor necrosis factor alpha (TNF alpha), vascular endothelial growth factor (VEGF-A and VEGF-C); angiostatin, interleukin 6 (IL-6), fibroblast growth factor 2 (FGF2); and plasminogen (PLG) were measured with an Elisa assay before and after three months of diosmin administration. The clinical symptoms of CVD were monitored using ultrasound images, echo Doppler assay, visual analogue scale (VAS), and measurement of the leg circumference. The average content of TNF alpha, VEGF-C, VEGF-A IL-6, and FGF2 decreased after the therapy with diosmin in a significant manner; with p < 0.001, p < 0.05, p < 0.05, p < 0.01, and p < 0.01, respectively, and a significant (p < 0.05) increase in the plasma angiostatin level after the three-month treatment was found. A significant (p < 0.05) decrease in edema and the average leg circumference of the patients was observed after the therapy. Diosmin influences the angiogenic and inflammatory mechanisms involved in the pathophysiology of edema presented in patients with a different class of CVD.
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Mora, Zuamí Villagrán-de la, María Esther Macías-Rodríguez, Jenny Arratia-Quijada, Yesica Sughey Gonzalez-Torres, Karla Nuño, and Angélica Villarruel-López. "Clostridium perfringens as Foodborne Pathogen in Broiler Production: Pathophysiology and Potential Strategies for Controlling Necrotic Enteritis." Animals 10, no. 9 (September 22, 2020): 1718. http://dx.doi.org/10.3390/ani10091718.
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Clostridium perfringens (Cp.) is the cause of human foodborne desease. Meat and poultry products are identified as the main source of infection for humans. Cp. can be found in poultry litter, feces, soil, dust, and healthy birds’ intestinal contents. Cp. strains are known to secrete over 20 identified toxins and enzymes that could potentially be the principal virulence factors, capable of degrading mucin, affecting enterocytes, and the small intestine epithelium, involved in necrotic enteritis (NE) pathophysiology, also leading to immunological responses, microbiota modification and anatomical changes. Different environmental and dietary factors can determine the colonization of this microorganism. It has been observed that the incidence of Cp-associated to NE in broilers has increased in countries that have stopped using antibiotic growth promoters. Since the banning of such antibiotic growth promoters, several strategies for Cp. control have been proposed, including dietary modifications, probiotics, prebiotics, synbiotics, phytogenics, organic acids, and vaccines. However, there are aspects of the pathology that still need to be clarified to establish better actions to control and prevention. This paper reviews the current knowledge about Cp. as foodborne pathogen, the pathophysiology of NE, and recent findings on potential strategies for its control.