Relevant bibliographies by topics / Biological markers

Academic literature on the topic 'Biological markers'

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Published: 4 June 2021
Last updated: 29 July 2024

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Journal articles on the topic "Biological markers"

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Vine, M. F. "Biological Markers: Their Use in Quantitative Assessments." Advances in Dental Research 8, no. 1 (June 1994): 92–99. http://dx.doi.org/10.1177/08959374940080011601.

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Biological markers can be conceptualized in terms of categories of markers that form a continuum representing a sequence of events from exposure to disease. These categories include markers of internal dose, biologically effective dose, early response, and disease. Outside of this sequence are susceptibility factors that can act at any point along the way to modify the effects of external exposures on disease outcomes. Examples of the use of these different types of markers in epidemiologic research are provided. There are many factors that one must consider when selecting a biological marker for use in an epidemiologic study. These factors include: the objectives of the study, the availability and specificity of potential markers, the feasibility of measuring the markers in various biological media, the invasiveness of the techniques necessary to measure the markers, the amount of biological specimen needed for analysis, the time to appearance of the markers in the biological media, the persistence of the markers in biological media, the variability of marker levels within and between individuals, the stability of markers in storage, as well as the cost, sensitivity, specificity, and reliability of the assays used to measure the markers. Each of these characteristics is discussed. The usefulness of biological markers in an epidemiologic study depends on the objectives of the study and whether the properties of the markers fulfill the objectives of the study in a feasible and cost-effective manner.
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Hermanussen, Michael. "Biological and Cultural Markers of Environmental Pressure." Anthropologischer Anzeiger 68, no. 4 (September 1, 2011): ix—x. http://dx.doi.org/10.1127/0003-5548/2011/editorial.

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Mahakkanukrauh, Pasuk. "Biological Markers Associated Osteoarthritis." Medicine & Health 12, no. 1 (2017): 18–26. http://dx.doi.org/10.17576/mh.2017.1201.03.

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Gottfries, C. G. "Biological markers in dementia." Nordisk Psykiatrisk Tidsskrift 42, no. 2 (January 1988): 147–53. http://dx.doi.org/10.3109/08039488809103220.

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Waalkes, T. Phillip. "Biological Markers: An Overview." Laboratory Medicine 16, no. 5 (May 1, 1985): 276–78. http://dx.doi.org/10.1093/labmed/16.5.276.

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Cowen, P. J. "Biological markers in depression." Current Opinion in Psychiatry 2, no. 1 (February 1989): 106–9. http://dx.doi.org/10.1097/00001504-198902000-00025.

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Copolov, David, and Jeremy Crook. "Biological Markers and Schizophrenia." Australian & New Zealand Journal of Psychiatry 34, no. 2_suppl (December 2000): S108—S112. http://dx.doi.org/10.1080/000486700230.

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Bunney, Jr., William E., Blynn Garland-Bunney, and Sarju B. Patel. "Biological Markers in Depression." Psychopathology 19, no. 2 (1986): 72–78. http://dx.doi.org/10.1159/000285136.

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Lerner, Alan J., Robert P. Friedland, and Peter J. Whitehouse. "Uses of Biological Markers." Alzheimer Disease & Associated Disorders 6, no. 4 (1992): 197–200. http://dx.doi.org/10.1097/00002093-199206040-00001.

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WHITFIELD, J. B. "Biological markers of alcoholism." Drug and Alcohol Review 10, no. 2 (April 1991): 127–35. http://dx.doi.org/10.1080/09595239100185191.

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Dissertations / Theses on the topic "Biological markers"

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Nordqvist, Sarah. "Biological Markers of Fertility." Doctoral thesis, Uppsala universitet, Obstetrik & gynekologi, 2014. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-234067.

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Infertility affects 15 % of couples, which corresponds to 60 - 80 million worldwide. The microenvironments in which the oocyte, embryo and fetus mature are vital to the establishment and development of a healthy pregnancy. Different biological systems, such as angiogenesis, the immune system and apoptosis need to be adequately regulated for pregnancy to occur and progress normally. The overall aim of this thesis was to investigate the impact of Histidine-rich glycoprotein (HRG) and Src homology 2 domain-containing adapter protein B (SHB) on human female fertility. HRG is a plasma protein that regulates angiogenesis, the immune system, coagulation/fibrinolysis and apoptosis, by building complexes with various ligands. The impact of HRG on fertility is studied here for the first time. HRG is present in follicular fluid, the Fallopian tube, endometrium, myometrium and placenta. HRG distribution within embryo nuclei depends on developmental stage. Blastocysts express and secrete HRG. The HRG C633T single nucleotide polymorphism (SNP) appears to affect the chance of pregnancy and, correspondingly, parameters associated with pregnancy in IVF. Additionally, this HRG genotype may increase the risk in IVF of only developing embryos unfit for transfer. SHB is an adaptor protein involved in intracellular signaling complexes that regulate angiogenesis, the immune system and cell proliferation/apoptosis. Shb knockout mice have altered oocyte/follicle maturation and impaired embryogenesis. The impact of three SHB polymorphisms (rs2025439, rs13298451 and rs7873102) on human fertility is studied for the first time. The SNP prevalences did not differ between infertile and fertile women. BMI, gonadotropin dosages, the percentage of immature oocytes, the number of fertilized oocytes, the percentage of good-quality embryos and the day of embryo transfer seems to be affected by SHB genotype. In conclusion, HRG and SHB appear to influence female fertility. They are potential biomarkers that might be used for predicting pregnancy chance in infertile women. Knowledge of these genotypes may improve patient counseling and individualization of treatment.
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Bont, Judith Maria de. "Biological Markers in Pediatric Brain Tumors." [S.l.] : Rotterdam : [The Author] ; Erasmus University [Host], 2008. http://hdl.handle.net/1765/13263.

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Godschalk, Roger Wilhelmus Laurentius. "Biological markers for exposure to polycyclic aromatic hydrocarbons." Maastricht : Maastricht : Universiteit Maastricht ; University Library, Maastricht University [Host], 1999. http://arno.unimaas.nl/show.cgi?fid=6862.

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Azari, Mansur Rezazadeh. "Biological markers of occupational exposure to nitrogen oxides." Thesis, University of Newcastle Upon Tyne, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.261238.

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Bur, H. (Hamid). "Biological prognostic and predictive markers in Hodgkin lymphoma." Doctoral thesis, Oulun yliopisto, 2018. http://urn.fi/urn:isbn:9789526219455.

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Abstract Hodgkin lymphoma (HL) is among a heterogeneous group of lymphomas. Over 80% of all patients can be cured with chemo- and radiotherapy. HL has become a model to study long-term effects of radio- and chemotherapy, because of the excellent prognosis. There are a significant number of patients who suffer or die because of the treatment-related long-term toxicity. The aim of this work was to discover new possible biological factors to predict poor prognosis and offer new aspects to individualize patient treatment in a convenient manner in HL. The retrospective study involved HL patients uniformly treated in 1997–2015. Immunohistochemistry was used to determine the expression of various biological markers, including oxidative stress markers 8-hydroxydeoxyguanosine (8-OHdG) and nitrotyrosine and the antioxidant enzymes manganese superoxide dismutase (MnSOD) as well as peroxiredoxins (Prx II, Prx III, Prx V, Prx VI) in HL patient samples. Using immunohistochemistry, we also evaluated expression of hypoxia-inducible factors (HIF-1α, HIF-2α), prolyl hydroxylase domain enzymes (PHD1, PHD2, PHD3), the epigenetic regulator lysine (K)-specific demethylase 4 (KDM4A, KDM4B, KDM4D) as well as sirtuins (SIRT1, SIRT4, SIRT6), the DNA-repair proteins Human Rap1 interacting factor 1 (Rif1) and O6-alkylguanine DNA alkyltransferase (MGMT) from representative classical Hodgkin lymphoma (cHL) patient samples. Low-level expression of 8-OHdG was associated with poorer relapse-free survival (RFS) in advanced-stage HL and a high extent of MnSOD predicted early relapse in the whole HL cohort. Strong expression of PHD1, KDM4B and KDM4D predicted dismal RFS in radiotherapy-treated cHL patients. The results also showed that strong expression of HIF-1α, SIRT6 and Rif1, and SIRT6 together with Rif1, were associated with prolonged RFS, especially in advanced-stage radiotherapy-treated cHL patients. In multivariate analysis, PHD1, MnSOD, 8-OHdG and Rif1 separately and together with SIRT6 were statistically significant predictors of RFS. The results reflect the significance of the studied biomarkers in HL, especially in radiotherapy-treated patients. This might be beneficial when individualizing treatment strategies, avoiding overtreatment and controlling long-term treatment-related toxicity. Further research, however, is needed to confirm these preliminary findings
Tiivistelmä Hodgkinin lymfooma (engl. HL) kuuluu heterogeeniseen imukudossyöpien eli lymfoomen ryhmään. Yli 80 % lymfoomapotilaista voidaan parantaa solunsalpaaja- ja sädehoidon avulla. Hyvän ennusteen takia HL- tutkimuksen tärkeä painopiste on säde- ja solunsalpaajahoidon pitkän ajan haittavaikutukset. Huomattava määrä potilaista kärsii tai jopa kuolee hoitoon liittyvistä pitkäaikaishaitoista johtuen. Tämän tutkimuksen tarkoituksena oli löytää uusia mahdollisia biologisia tekijöitä, jotka ennakoisivat taudin huonoa ennustetta ja samalla antaa uusia näkökulmia HL potilaiden hoidon yksilöllistämiseen. Tämä retrospektiivinen tutkimus käsitti vuosina 1997-2015 samanlaisesti hoidettuja Hodgkinin lymfooma -potilaita. Immunohistokemiallisilla värjäyksillä määritettiin biologisten merkkiaineiden, mukaan lukien oksidatiivisen stressin markkereiden 8- hydroksideoksiguanosiinin (8-OHdG) ja nitrotyrosiinin, sekä antioksidanttientsyymien mangaanisuperoksidi-dismutaasin (MnSOD) sekä peroksiredoksiinien (Prx II, Prx III, Prx V, Prx VI) ilmentymistä HL -potilasnäytteissä. Määrittelimme myös immunohistokemiallisilla värjäyksillä epigeneettisten säätelijöiden lysiinin spesifisen demetylaasientsyymin 4 (KDM4A, KDM4B, KDM4D) sekä sirtuiinien (SIRT1, SIRT4, SIRT6), hypoksiaa indusoivien tekijöiden (HIF-1α, HIF-2α), prolyylihydroksylaasientsyymien (PHD1, PHD2, PHD3) ja DNA:ta korjaavien proteiinien Rap1 vaikuttuvan tekijä 1 (Rif1) ja O6-metyyliguaniini-DNA metyylitransferaasin (MGMT) ilmentymistä edustavissa klassista Hodgkinin lymfoomaa sairastavien potilaiden (engl. cHL) näytteissä. Heikko 8-OHdG värjäytyminen ennusti ennenaikaista taudin uusiutumaa levinneessä HL:ssa ja korkea MnSOD ilmaantuvuus ennusti ennenaikaista taudin uusiutumaa koko HL -ryhmässä. Sädehoidetuilla cHL potilailla voimakas PHD1, KDM4B ja KDM4D värjäytyminen ennusti ennenaikaista taudin uusiutumaa. Tulokset osoittivat myös, että erityisesti sädehoidetuilla levinneen taudin cHL potilailla voimakas HIF-1α, SIRT6, Rif1 ja SIRT6 yhdessä Rif1:n kanssa oli yhteydessä pidentyneeseen uusiutumavapaaseen aikaan. Monimuuttuja-analyysissä PHD1, MnSOD, 8-OHdG ja Rif1 itsenäisenä ja yhdessä SIRT6 kanssa ennustivat tilastollisesti merkitsevästi taudin ennenaikaista uusiutumaa. Tulokset osoittavat näiden eri biomarkkereiden merkittävyyden HL:ssä, erityisesti sädehoitoa saaneilla potilailla. Tuloksista voi olla hyötyä, kun hoitokäytäntöjä yksilöidään, mikä voisi helpottaa välttämään liiallista hoitoa ja hallitsemaan pitkäaikaisiin hoitoihin liittyviä haittoja. Näiden alustavien havaintojen vahvistamiseksi tarvitaan kuitenkin lisätutkimuksia
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Thomas, Jim. "Biological markers in sediments with respect to geological time." Thesis, University of Bristol, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.279796.

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Gupta, Jayanta. "Genetic and Biological Markers of Atopic Dermatitis in Children." University of Cincinnati / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1204843640.

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Akiki, Zeina. "Biological Markers For Chronic Obstructive Pulmonary Disease And Asthma." Thesis, Université Paris-Saclay (ComUE), 2016. http://www.theses.fr/2016SACLS081/document.

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L’étude des marqueurs biologiques dans la broncho-pneumopathie chronique obstructive (BPCO) et l'asthme, deux maladies respiratoires chroniques affectant des millions de personnes dans le monde, pourrait améliorer leur diagnostic, leur traitement et leur prévention.Cette thèse comprend deux parties. La première visait à évaluer l'association entre un marqueur spécifique des poumons, la protéine surfactant D (SP-D) sérique, et la BPCO, et à trouver un seuil de SP-D capable de discriminer les patients BPCO des témoins. Elle a été réalisée dans le cadre d’une étude cas-témoin au Liban incluant des patients BPCO (n=90), des asthmatiques (n=124) et des témoins (n=180). La deuxième partie visait à évaluer les associations chez les adultes des marqueurs de l’inflammation systémique (protéine C-réactive ultra-sensible, hs-CRP (n=252), et des cytokines (n=283)) et des marqueurs de dommages dus au stress oxydant (8-isoprostanes 8-IsoPs (n=258) du condensat de l’air exhalé) avec les phénotypes de l’asthme.Elle a été réalisée dans le cadre de l'étude épidémiologique longitudinale Française des facteurs génétiques et environnementaux de l'asthme (EGEA).Les résultats ont montré que les niveaux de SP-D sériques étaient associés positivement avec la BPCO et des seuils des niveaux de SP-D chez ces patients ont été identifiés avec d'excellentes valeurs discriminantes. Dans EGEA, aucune association n'a été trouvée entre les niveaux de hs-CRP sériques et le contrôle de l’asthme. Des profils de cytokines sériques (identifiés par analyse en composante principale) avec des niveaux élevés d’interleukine(IL)-1Ra et d’IL-10 ont été associés avec moins de crises d'asthme et un risque plus faible d'un mauvais contrôle de l'asthme sept ans plus tard. Les résultats des analyses préliminaires sur les associations entre les niveaux de 8-IsoPs et les phénotypes de l'asthme sont également présentés.Globalement, ces résultats ont montré l'utilité d'étudier les marqueurs biologiques en lien avec la BPCO et l'asthme
Studying the biological markers in chronic obstructive pulmonary disease (COPD) and asthma, two chronic respiratory diseases affecting millions of individuals around the world, could improve their diagnosis, their treatment and their prevention.This thesis includes two parts. The first aimed to assess the association between a lung-specific biomarker, serum Surfactant Protein D (SP-D), and COPD, and to find cut-off points able to discriminate COPD patients from controls using SP-D levels. It was performed in a case-control study in Lebanon including COPD (n=90) and asthma patients (n=124) and controls (n=180). The second part aimed to assess the cross-sectional and longitudinal associations in adults for systemic inflammatory biomarkers (high sensitivity C reactive protein hs-CRP (n=252) and cytokines (n=283) as well as biomarkers of damage due to oxidative stress (8-Isoprostanes 8-IsoPs (n=258) from the exhaled breath condensate) and asthma outcomes.It was performed in the French longitudinal epidemiological study on the genetics and environmental factors of asthma (EGEA).Results showed that serum SP-D levels were positively associated with COPD and thresholds for SP-D levels in these patients were identified with excellent discriminant values. In EGEA, no association was found between serum hs-CRP levels and asthma control. Serum cytokine profiles (identified by principal component analysis) with high levels of interleukin (IL)-1Ra and IL-10 were associated with less asthma attacks and lower risk of poor asthma control in adults seven years later. The results of the preliminary analyses on the associations between the levels of 8-IsoPs and asthma outcomes are also presented.Overall, these results have shown the usefulness of studying the biological markers related to COPD and asthma
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PIAZZA, FABRIZIO. "Biological markers of vascular damage in Alzheimer’s disease patients." Doctoral thesis, Università degli Studi di Milano Bicocca, 2008. http://hdl.handle.net/10281/33165.

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Alzheimer's disease (AD) represents the most common type of dementia, accounting for 50% of the total amount of cognitive impairment, while vascular dementia (VD) accounts for approximately 20% of the cases. AD has traditionally been considered a neurodegenerative condition in which vascular dysfunction plays a marginal role. On the other hand, VD is thought to be caused by a subacute or chronic reduction in cerebral blood flow (CBF) leading to neuronal dysfunction and death. However, it is not clear if these two major causes of dementia also share pathogenetic mechanisms. Many evidences point out a vascular pathogenetic involvement in its etiology. The recent finding that Abeta has also harmful effects on vessels indicates that vascular damage could be involved in the pathogenesis of AD, thus explaining how AD and VD are not always distinct entities but overlap by varying degrees. Abeta peptide, which plays a central role in AD, not only exerts harmful effects on the vessel walls increasing the risk of silent hemorrhagic/ischemic strokes, but it also facilitates the ultrastructural degeneration of the vessels, reducing vessels’ diameters, cerebral blood flow and energetic metabolism. Conversely, vascular damage which results in hypoxia/ischemia, inflammation, microglia activation and oxidative stress, can influence APP processing, modulating the expression of enzymes responsible for Abeta production. These mechanisms have been described in animal models, while few independent observations have been performed in humans. Classical neuropathological markers of AD are: (i) deposits of amyloid β (Abeta) in brain tissue (neuritic plaques), as well as within the wall of cerebral blood vessels; (ii) microglia activation; (iii) dystrophic neuronal processes in proximity and within Abeta plaques; (iv) progressive loss of synapses and neurons; and (v) severe structural damage of cerebral blood vessels. Nonetheless, many vascular risk factors have been also associated to AD, i.e. ApoE-e4 genotype, diabetes and hyperinsulinemia, high systolic blood pressure in midlife to late life and low diastolic blood pressure in late life, smoking, stroke, traumatic brain injury, elevated serum homocysteine (Hcy) levels, hypercholesterolemia and atherosclerosis. Furthermore, there are many evidences of peripheral haemostatic abnormalities, in particular platelets alterations, Von Willebrand Factor and Activated Factor VII, and increased level of thrombomodulin and E-selectin in AD, suggesting that an endothelial dysfunction may be involved in AD pathogenesis. Based on these evidences, a possible hypothesis is that Abeta induces endothelial injury, thus promoting ischemic damage, which may in turn affect APP processing and Abeta production. This reciprocal interaction may provide an explanation to the pathogenetic link between these two conditions. In this contest, elevated plasma levels of Homocysteine (Hcy), also know as Hyperhomocysteinemia (HHcy), is one of the strongest independent risk factors for vascular and cerebrovascular disorders and it has been associated to the risk of develop AD in elderly people. Recently, our group has published evidences of elevated plasma levels of Hcy in AD, correlated with folate deficiencies. Moreover, we have demonstrated that Post Methionine Load (PML) test is able to reveal twice as many HHcy AD subjects with respect to the fasting analysis, suggesting PML as useful test in detecting AD patients who may have the chance of an early folate treatment. Since vascular lesions often coexist with Abeta deposits in AD, and aberrant Abeta deposition in the intima may be pathologically important, it is possible that this phenomena is not only the consequence of the AD-related aberrant APP processing but may represent the early trigger of Amyloid deposition, in response to the primary endothelial damage. Moreover, after Abeta or hypoxia exposure, the endothelium undergoes changes which trigger the inflammatory response, as demonstrated in cerebral small vessel disease where there is histopathological evidence of endothelial cell activation. The increased vascular permeability is one of the features of endothelial cell activation, and it is thought that entry of serum proteins, such as coagulation and/or inflammatory mediators, into the vascular wall and perivascular neural parenchyma may sustain toxic effects. Indeed the blood-brain barrier (BBB) microvasculature, plays a crucial role in the regulation of cerebral blood flow (CBF) and may also play a pivotal role in AD pathogenesis by regulating the entry into brain parenchyma of a plethora of circulating molecules and xenobiotics, also triggering inflammation and oxidative stress. Cerebral endothelium could be of clinical relevance to investigate BBB permeability, indicating early endothelial perturbation as a consequence of hypoxia or Abeta deposition, events involved in inflammatory and oxidative cerebrovascular activity. Indeed, it has been previously demonstrated that proinflammatory cytokines alter the expression and processing of Abeta precursor protein, and fibrillar Abeta itself in turn promotes the production of proinflammatory cytokines by microglial and monocytic cell lines. Microglia is the major component of the intrinsic brain immune system and its pivotal role in cerebral inflammation-like responses could trigger and sustain neurodegenerative events. However, clinical observations on the potential role of inflammation in AD have yielded inconsistent results. Whereas several community-based studies have linked antiinflammatory interventions to a lowered risk of developing AD, a randomized, placebo-controlled clinical trial failed to demonstrate a beneficial effect of nonsteroidal anti-inflammatory drugs (NSAIDs) on the progression of disease. It is noteworthy that, in the brain, perivascular macrophages and microglia that participate in intraparenchymal inflammation are derived from circulating macrophages. Previous studies have reported higher CSF levels of TNF-alpha than serum levels in AD patients, strengthening the hypothesis of a pivotal role of BBB and microglia activity in the pathogenetic mechanisms of AD. Activated microglia may also be involved in mechanisms of impaired glial glutamate uptake and reduced expression of glutamate transporters, or increased free radicals and nitric oxide synthesis in brain parenchyma. Central nervous system is particularly exposed to free radical injury, given its high metal content, which can catalyze the formation of oxygen free radicals, and the relatively low content of antioxidant defenses. Indeed, several studies show markers of oxidative damage (lipid peroxidation, protein oxidation, DNA oxidation and glycosidation markers) in brain areas affected by neurodegenerative disorders. Our group published several works demonstrating a link between oxidative stress and excitotoxicity in AD, and described peripheral markers of these mechanisms, that may be analyzed in patients as possible diagnostic and therapeutic tools. On the other hand, hypoxia and stroke could influence Abeta processing, as demonstrated by the hypoxia-inducible factor1 alpha (HIF-1alpha) regulation of BACE promoter or increased production of Abeta after stroke, which may increase caspase 3 cleavage of the GGA3 protein carrier resulting in decreased degradation of BACE. Studies of the effect of vascular risk factors on Abeta processing could help to elucidate whether vascular disease has only an additive effect on cognitive performance or it is also intrinsic to the pathogenesis of AD. We have recently analyzed some markers of vascular damage, in particular we have demonstrated that mean plasma levels of TF (Tissue Factor) and TFPI (TF Pathway Inhibitor) are both correlated with Hcy and they are significantly higher in AD and MCI patients than in healthy subjects (Piazza 2007). Moreover, the measurement of immunologically defined "circulating endothelial cells" (CECs) has been used to assess vascular integrity and the amount of microparticles (MP) has been reported elevated in a number of conditions where vascular dysfunction, thrombosis and inflammation are relevant. However, the identification of relevant biological markers for the state of brain microvessels in demented patients is still lacking. Such biomarkers, together with known risk factors common to AD and VD, can be used to better understand the involvement of cerebrovascular implications in the pathophysiology of dementia, with possible therapeutic interventions. In conclusion, it is possible that the initial endothelial damage in AD brains can trigger Abeta deposits which, in turn, may fuel monocytes infiltration through damaged BBB and microglia activation. Abeta deposits and inflammation can lead to the production of superoxide radicals, exacerbating endothelial injury. Moreover, all these processes can support previous findings of the generalized peripheral and CNS oxidative stress that typically defines AD.
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Engelbrecht, Albertus Hermanus. "Biological markers for major depressive disorder in children and adolescents." Thesis, Cape Technikon, 1986. http://hdl.handle.net/20.500.11838/1481.

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Thesis (Masters Diploma (Technology)--Cape Technikon, Cape Town, 1986
Child psychiatrists have become increasingly aware of the existence. of affective disorders in prepubertal and pubertal patients. This has led to the investigation of possible biological factors contributing to the disorders. Due to the lack of availability of human brain material, different parameters have been investigated in the periphery in order to obtain information regarding the aetiology of major depressive disorder. The neurotransmitters, NA, 5-HT and DA have been implicated in depression. Levels of the metabolites of these transmitters have been measured in plasma, urine and CSF of adult depressed patients. Two other peripheral "tools" used in the study of major depressive disorder are blood platelets and lymphocytes. The former contain cr 2 -adrenoceptors and imipramine binding sites (indicative of 5-HT uptake into the platelet) and the latter S-adrenoceptors. Platelets have been widely used as a model for indirectly evaluating changes in central cr2-adrenoceptor and imipramine binding whereas lymphocytes have been used to measure changes in S-adrenoceptor binding and activity in adults with major depressive disorder.
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Books on the topic "Biological markers"

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S, Hulka Barbara, Wilcosky Timothy C, and Griffith Jack D, eds. Biological markers in epidemiology. New York: Oxford University Press, 1990.

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Boller, François, Robert Katzman, André Rascol, Jean-Louis Signoret, and Yves Christen, eds. Biological Markers of Alzheimer’s Disease. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-46690-8.

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International Cancer Research Data Bank., Cancer Information Dissemination and Analysis Center (CIDAC) for Carcinogenesis and Cancer Biology., and National Cancer Institute (U.S.), eds. Biological markers of carcinogen exposure. [Bethesda, Md.]: U. S. Dept. of Health and Human Services, Public Health Service, National Institutes of Health, National Cancer Institute, International Cancer Research Data Bank ; Washington, D.C. : for sale by the Supt. of Docs., U. S. G.P.O., 1989.

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Nela, Pivac, ed. Peripheral biological markers in alcoholism. New York: Nova Science Publishers, 2008.

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François, Boller, and Fondation IPSEN pour la recherche thérapeutíque., eds. Biological markers of Alzheimer's disease. Berlin: Springer-Verlag, 1989.

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Van Venrooij, W. J., and R. N. Maini, eds. Manual of Biological Markers of Disease. Dordrecht: Springer Netherlands, 1996. http://dx.doi.org/10.1007/978-94-011-5444-4.

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van Venrooij, W. J., and R. N. Maini, eds. Manual of Biological Markers of Disease. Dordrecht: Springer Netherlands, 1996. http://dx.doi.org/10.1007/978-94-011-1670-1.

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1930-, Johns R. B., ed. Biological markers in the sedimentary record. Amsterdam: Elsevier, 1986.

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van, Venrooij W. J., and Maini R. N, eds. Manual of biological markers of disease. Dordrecht: Kluwer Academic Publishers, 1996.

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Venrooij, Martin A. M. van, 1934- and Maini R. N, eds. Manual of biological markers of disease. Dordrecht: Kluwer Academic Publishers, 1993.

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Book chapters on the topic "Biological markers"

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Wideman, Timothy H., Michael J. L. Sullivan, Shuji Inada, David McIntyre, Masayoshi Kumagai, Naoya Yahagi, J. Rick Turner, et al. "Biological Markers." In Encyclopedia of Behavioral Medicine, 225. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-1005-9_100180.

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Rea, William S., Irl L. Extein, and Mark S. Gold. "Biological Markers." In Issues in Diagnostic Research, 161–78. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-1265-9_6.

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Samuelson, Stephen D., and George Winokur. "Biological Markers." In Research in Psychiatry, 235–63. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4899-0688-5_9.

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Maes, Michael. "Biological Markers of Fibromyalgia." In Somatoform Disorders, 111–21. Tokyo: Springer Japan, 1999. http://dx.doi.org/10.1007/978-4-431-68500-5_11.

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Connor, T. J., and B. E. Leonard. "Biological Markers of Depression." In Antidepressants: Past, Present and Future, 117–48. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-642-18500-7_4.

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Helander, A. "Biological markers in alcoholism." In Addiction Mechanisms, Phenomenology and Treatment, 15–32. Vienna: Springer Vienna, 2003. http://dx.doi.org/10.1007/978-3-7091-0541-2_2.

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Rosman, Alan S., and Charles S. Lieber. "Biological Markers of Alcoholism." In Medical and Nutritional Complications of Alcoholism, 531–63. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3320-7_18.

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Johnson, Natalie G., and Naim Kadoglou. "Microbiology and Biological Markers." In Idiopathic Granulomatous Mastitis, 37–44. Cham: Springer Nature Switzerland, 2023. http://dx.doi.org/10.1007/978-3-031-30391-3_6.

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Perera, Frederica P. "Biological Markers in Risk Assessment." In Carcinogen Risk Assessment, 123–38. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4684-5484-0_10.

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Thung, Stephen F., and Alan M. Peaceman. "Biological Markers of Preterm Delivery." In Handbook of Clinical Laboratory Testing During Pregnancy, 35–54. Totowa, NJ: Humana Press, 2004. http://dx.doi.org/10.1007/978-1-59259-787-1_3.

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Conference papers on the topic "Biological markers"

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Coreţchi, Liuba, Mariana Gincu, Viktoria K. Sakara, Igor Opalco, Anna Mishina, Irina-Anca Popescu, Ion Bahnarel, Ludmila Bejenari, and Sergiu Gladun. "Biological markers of ionizing radiation." In XIth International Congress of Geneticists and Breeders from the Republic of Moldova. Scientific Association of Geneticists and Breeders of the Republic of Moldova, Institute of Genetics, Physiology and Plant Protection, Moldova State University, 2021. http://dx.doi.org/10.53040/cga11.2021.028.

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D'yachuk, I. S., and E. R. Fajzullin. "Cytokines as biological markers of oncopathologies." In Scientific dialogue: Medical issues. ЦНК МОАН, 2019. http://dx.doi.org/10.18411/spc-15-05-2019-17.

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Rodriguez Gonzalez-Moro, Jose Miguel, Pilar de Lucas-Ramos, Zoraida Verde Rello, Jose Luis Izquierdo Alonso, Jose Mª Bellón Cano, and Catalina Santiago Dorrego. "Cardiovascular Biological Risk Markers In Patients With COPD." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a2618.

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Casas, Maribel, Ana Belén, Lea Maitre, Mariona Bustamante, Diana Clemente, Valérie Siroux, Alicia Abellan, et al. "Is childhood asthma associated with biological aging markers?" In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa5435.

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Будаш, Д. С., and С. А. Бабанов. "Biological markers and mathematical modeling in occupational lung diseases." In The second international scientific Forum "Health and Safety at the Workplace". Encyclopedix, 2018. http://dx.doi.org/10.31089/978-985-7153-46-6-2018-1-2-267-272.

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Psallidas, Ioannis, Nikolaos Kanellakis, Marie-Laetitia Thezenas, Philip Charles, John Corcoran, Rob Hallifax, Ambika Talwar, et al. "Biological markers of successful pleurodesis for malignant pleural effusion." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.oa495.

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Picard, P., J. Y. Borg, M. Vasse, D. Boudhabhay, J. Soria, J. P. Fillastre, C. Soria, T. Hannedouche, M. Godin, and M. Monconduit. "BIOLOGICAL PRETHROMBOTIC MARKERS AND COAGULATION INHIBITORS IN NEPHROTIC SYNDROME." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643051.

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Nephrotic syndrome (NS) has long been recognized as a clinical prethrombotic state, because of severe thrombo-embolic complications. But underlying mechanisms are still poorly defined. In 56 untreated nephrotic adult patients (most of them without renal failure), we investigate in vivo coagulation activation by measuring 0 plasmatic specific fibrin degradation products (FbDP) (immuno-enzymological assay using a monoclonal anti D-neo antibody) and (2) the ratio of factor VII coagulant activity (V11c) to factor VII:Anti gen (VII;Ag) tested by an ELISA method. We examined coagulation inhibitors in plasmas and urines (antithrombin III—AT III, heparin cofactor II-HC II by amidolytic and laurell methods; protein C-PC by an ELISA assay ;free and bound protein S—PS:Ag by laurell assays). In few patients we also determinecjfribronectin and t-PA inhibitor.Results in plasma are submitted and expressed as mean ± DS and compared (t test) with controls (C) without nephropathySignificantly elevated activated factor VII and FbDP levels show an “in vivo activation” of coagulation in NS. Plasmatic fibronectin, HC II, PC:frg, and tPA-I levels are alsp significantly elevated and roughly paralleled fibrinogen (6,25 ± 2,9 g/1) and other acute-phase proteins measurements. Significant amounts of AT 111:Ag were present in about half tested urines, but in a degraded form with low or absent heparin cofactor activity. Mean plasmatic AT III concentration was in normal range, but three of the 4 patients with a thrombotic disease had the lowest values of AT III and the highest fibrinogen levels.We could demonstrate a biological prethrombotic state in NS and suggest the way of identifying patients with high risk of thrombosis.
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Orlov, A. V. "Real-time Detection of Molecular Markers in Complex Biological Matrices." In 2022 International Conference Laser Optics (ICLO). IEEE, 2022. http://dx.doi.org/10.1109/iclo54117.2022.9839990.

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Li, R. H., L. Carfi, Y. H. Lv, Y. S. Xia, C. Wu, Y. W. Yu, M. W. Qiu, W. C. Zhao, and P. G. Guo. "Association analysis of MFLP markers with bacterial wilt resistance in tobacco." In International Conference on Environmental Science and Biological Engineering. Southampton, UK: WIT Press, 2014. http://dx.doi.org/10.2495/esbe140381.

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Guo, Yue. "Advances in esophageal cancer-specific tumor markers and immunotherapy." In Third International Conference on Biological Engineering and Medical Science (ICBioMed2023), edited by Alan Wang. SPIE, 2024. http://dx.doi.org/10.1117/12.3012834.

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Reports on the topic "Biological markers"

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Kennel, S. (Biological markers for tumors). Office of Scientific and Technical Information (OSTI), January 1989. http://dx.doi.org/10.2172/5469723.

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Shugart, L. R. Biological (molecular and cellular) markers of toxicity. Office of Scientific and Technical Information (OSTI), October 1990. http://dx.doi.org/10.2172/6441197.

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McCarthy, J. Biological (molecular and cellular) markers of toxicity. Office of Scientific and Technical Information (OSTI), October 1989. http://dx.doi.org/10.2172/5346682.

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McCarthy, J. Biological (molecular and cellular) markers of toxicity. Office of Scientific and Technical Information (OSTI), April 1990. http://dx.doi.org/10.2172/6943031.

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Perera, Frederica P. Biological Markers of Environmental Carcinogens in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 1998. http://dx.doi.org/10.21236/adb248851.

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Shugart, L. Biological (molecular and cellular) markers of toxicity. [Oryzias latipes]. Office of Scientific and Technical Information (OSTI), April 1991. http://dx.doi.org/10.2172/5797375.

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Ruibal, Alvaro. Tumor markers have biological functions that we should know. CEACAM1 as an example. Science Repository OÜ, October 2018. http://dx.doi.org/10.31487/j.aco.2018.01.001.

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Shugart, L. R., S. J. D'Surney, C. Gettys-Hull, and M. S. Greeley, Jr. Biological (molecular and cellular) markers of toxicity. Final report, September 15, 1988 - September 14, 1991. Office of Scientific and Technical Information (OSTI), December 1991. http://dx.doi.org/10.2172/7044713.

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Barefoot, Susan F., Bonita A. Glatz, Nathan Gollop, and Thomas A. Hughes. Bacteriocin Markers for Propionibacteria Gene Transfer Systems. United States Department of Agriculture, June 2000. http://dx.doi.org/10.32747/2000.7573993.bard.

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The antibotulinal baceriocins, propionicin PLG-1 and jenseniin G., were the first to be identified, purified and characterized for the dairy propionibaceria and are produced by Propionibacterium thoenii P127 and P. thoenii/jensenii P126, respectively. Objectives of this project were to (a) produce polyclonal antibodies for detection, comparison and monitoring of propionicin PLG-1; (b) identify, clone and characterize the propionicin PLG-1 (plg-1) and jenseniin G (jnG) genes; and (3) develop gene transfer systems for dairy propionibacteria using them as models. Polyclonal antibodies for detection, comparison and monitoring of propionicin PLG-1 were produced in rabbits. Anti-PLG-1 antiserum had high titers (256,000 to 512,000), neutralized PLG-1 activity, and detected purified PLG-1 at 0.10 mg/ml (indirect ELISA) and 0.033 mg/ml (competitive indirect ELISA). Thirty-nine of 158 strains (most P. thoenii or P. jensenii) yielded cross-reacting material; four strains of P. thoenii, including two previously unidentified bacteriocin producers, showed biological activity. Eight propionicin-negative P127 mutants produced neither ELISA response nor biological activity. Western blot analyses of supernates detected a PLG-1 band at 9.1 kDa and two additional protein bands with apparent molecular weights of 16.2 and 27.5 kDa. PLG-1 polyclonal antibodies were used for detection of jenseniin G. PLG-1 antibodies neutralized jenseniin G activity and detected a jenseniin G-sized, 3.5 kDa peptide. Preliminary immunoprecipitation of crude preparations with PLG-1 antibodies yielded three proteins including an active 3-4 kDa band. Propionicin PLG-1 antibodies were used to screen a P. jensenii/thoenii P126 genomic expression library. Complete sequencing of a cloned insert identified by PLG-1 antibodies revealed a putative response regulator, transport protein, transmembrane protein and an open reading frame (ORF) potentially encoding jenseniin G. PCR cloning of the putative plg-1 gene yielded a 1,100 bp fragment with a 355 bp ORF encoding 118 amino acids; the deduced N-terminus was similar to the known PLG-1 N-terminus. The 118 amino acid sequence deduced from the putative plg-1 gene was larger than PLG-1 possibly due to post-translational processing. The product of the putative plg-1 gene had a calculated molecular weight of 12.8 kDa, a pI of 11.7, 14 negatively charged residues (Asp+Glu) and 24 positively charged residues (Arg+Lys). The putative plg-1 gene was expressed as an inducible fusion protein with a six-histidine residue tag. Metal affinity chromatography of the fused protein yielded a homogeneous product. The fused purified protein sequence matched the deduced putative plg-1 gene sequence. The data preliminarily suggest that both the plg-1 and jnG genes have been identified and cloned. Demonstrating that antibodies can be produced for propionicin PLG-1 and that those antibodies can be used to detect, monitor and compare activity throughout growth and purification was an important step towards monitoring PLG-1 concentrations in food systems. The unexpected but fortunate cross-reactivity of PLG-1 antibodies with jenseniin G led to selective recovery of jenseniin G by immunoprecipitation. Further refinement of this separation technique could lead to powerful affinity methods for rapid, specific separation of the two bacteriocins and thus facilitate their availability for industrial or pharmaceutical uses. Preliminary identification of genes encoding the two dairy propionibacteria bacteriocins must be confirmed; further analysis will provide means for understanding how they work, for increasing their production and for manipulating the peptides to increase their target species. Further development of these systems would contribute to basic knowledge about dairy propionibacteria and has potential for improving other industrially significant characteristics.
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Crisosto, Carlos, Susan Lurie, Haya Friedman, Ebenezer Ogundiwin, Cameron Peace, and George Manganaris. Biological Systems Approach to Developing Mealiness-free Peach and Nectarine Fruit. United States Department of Agriculture, 2007. http://dx.doi.org/10.32747/2007.7592650.bard.

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Peach and nectarine production worldwide is increasing; however consumption is flat or declining because of the inconsistent eating quality experienced by consumers. The main factor for this inconsistent quality is mealiness or woolliness, a form of chilling injury that develops following shipping periods in the global fruit market today. Our research groups have devised various postharvest methods to prolong storage life, including controlled atmosphere and delayed storage; however, these treatments only delay mealiness. Mealiness texture results from disruption of the normal ripening process involving disassembly of cell wall material, and creates a soft fruit texture that is dry and grainy instead of juicy and smooth. Solving this problem is a prerequisite for increasing the demand for fresh peach and nectarine. Two approaches were used to reveal genes and their associated biochemical processes that can confer resistance to mealiness or wooliness. At the Volcani Center, Israel, a nectarine cultivar and the peach cultivar (isogenetic materials) from which the nectarine cultivar spontaneously arose, and at the Kearney Agricultural Center of UC Davis, USA, a peach population that segregates for quantitative resistance to mealiness was used for dissecting the genetic components of mealiness development. During our project we have conducted research integrating the information from phenotypic, biochemical and gene expression studies, proposed possible candidate genes and SNPs-QTLs mapping that are involved in reducing peach mealiness susceptibility. Numerous genes related to ethylene biosynthesis and its signal transduction, cell wall structure and metabolism, stress response, different transcription factor families were detected as being differentially accumulated in the cold-treated samples of these sensitive and less sensitive genotypes. The ability to produce ethylene and keep active genes involved in ethylene signaling, GTP-binding protein, EIN-3 binding protein and an ethylene receptor and activation of ethyleneresponsive fruit ripening genes during cold storage provided greater resistance to CI. Interestingly, in the functional category of genes differentially expressed at harvest, less chilling sensitive cultivar had more genes in categories related to antioxidant and heat sock proteins/chaperones that may help fruit to adapt to low temperature stress. The specific objectives of the proposed research were to: characterize the phenotypes and cell wall components of the two resistant systems in response to mealiness- inducing conditions; identify commonalities and specific differences in cell wall proteins and the transcriptome that are associated with low mealiness incidence; integrate the information from phenotypic, biochemical, and gene expression studies to identify candidate genes that are involved in reducing mealiness susceptibility; locate these genes in the Prunus genome; and associate the genes with genomic regions conferring quantitative genetic variation for mealiness resistance. By doing this we will locate genetic markers for mealiness development, essential tools for selection of mealiness resistant peach lines with improved fruit storability and quality. In our research, QTLs have been located in our peach SNPs map, and proposed candidate genes obtained from the integrated result of phenotypic, biochemical and gene expression analysis are being identified in our QTLs as an approach searching for consistent assistant markers for peach breeding programs.
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