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Journal articles on the topic 'Biological markers'

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Author: Grafiati

Published: 4 June 2021

Last updated: 29 July 2024

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1

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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2

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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3

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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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11

Copolov, David, and Jeremy Crook. "Biological Markers and Schizophrenia." Australian & New Zealand Journal of Psychiatry 34, no. 1_suppl (February 2000): A108—A112. http://dx.doi.org/10.1177/000486740003401s16.

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Objective The delivery of biological markers for schizophrenia would greatly assist preventative strategies by identifying at-risk individuals who could then be monitored and treated in a manner with a view to minimising subsequent morbidity. This paper aims to present a selection of biological measures that may indicate risk of schizophrenia. Method A selective and brief review is provided of intensively studied putative markers, including enlarged cerebral ventricles, dopamine D2 receptor density, amphetamine-stimulated central nervous system dopamine release, plasma homovanillic acid and smooth pursuit eye tracking dysfunction. Results A number of biological measures have been reported to be correlated with schizophrenia. Conclusions Presently, none of these measures has satisfactory performance characteristics in terms of predictive validity, noninvasiveness, ease of testing and low cost that would enable their widespread use. However, a few have potential for further investigation and development.

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12

Rousseau, Jean-Charles, and Pierre D. Delmas. "Biological markers in osteoarthritis." Nature Clinical Practice Rheumatology 3, no. 6 (June 2007): 346–56. http://dx.doi.org/10.1038/ncprheum0508.

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13

Zetterberg, Henrik. "Psychosis and biological markers." Lancet Psychiatry 4, no. 1 (January 2017): 3–5. http://dx.doi.org/10.1016/s2215-0366(16)30407-2.

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14

Cowen, P. J., and A. J. Wood. "Biological markers of depression." Psychological Medicine 21, no. 4 (November 1991): 831–36. http://dx.doi.org/10.1017/s0033291700029834.

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15

Thrusfield, Michael. "Biological markers in epidemiology." Preventive Veterinary Medicine 21, no. 3 (December 1994): 273. http://dx.doi.org/10.1016/0167-5877(94)90025-6.

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16

Schuckit, Marc A. "Biological markers in alcoholism." Progress in Neuro-Psychopharmacology and Biological Psychiatry 10, no. 2 (January 1986): 191–99. http://dx.doi.org/10.1016/0278-5846(86)90073-4.

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17

Copolov, David, and Jeremy Crook. "Biological markers and schizophrenia." Australian and New Zealand Journal of Psychiatry 34, (Suppl.) (November 2000): S108—S112. http://dx.doi.org/10.1046/j.1440-1614.2000.00778.x.

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18

Humphries, S. "Biological Markers in Epidemiology." Journal of Epidemiology & Community Health 45, no. 2 (June 1, 1991): 173. http://dx.doi.org/10.1136/jech.45.2.173-a.

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19

Whelan, GREG. "Biological markers of alcoholism." Australian and New Zealand Journal of Medicine 22, no. 2 (April 1992): 209–13. http://dx.doi.org/10.1111/j.1445-5994.1992.tb02815.x.

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20

Kietzmann, M. "Biological markers in immunotoxicology." Toxicon 31, no. 8 (August 1993): 1065. http://dx.doi.org/10.1016/0041-0101(93)90267-m.

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21

Rousseau, J. Ch, and P. Garnero. "Biological markers in osteoarthritis." Bone 51, no. 2 (August 2012): 265–77. http://dx.doi.org/10.1016/j.bone.2012.04.001.

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22

Silva, P., N. J. Slevin, P. Sloan, H. Valentine, D. Ryder, P. Price, C. M. L. West, and J. J. Homer. "Use of multiple biological markers in radiotherapy-treated head and neck cancer." Journal of Laryngology & Otology 124, no. 6 (April 14, 2010): 650–58. http://dx.doi.org/10.1017/s0022215110000228.

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AbstractObjective:Management of patients with head and neck squamous cell carcinoma is often based on clinical parameters, with little appreciation of the underlying tumour biology. Single biological marker studies fail to acknowledge the complexity of these tumours. Our aim was to define a profile of biological markers associated with outcome.Design:This retrospective study involved consecutive patients with oropharyngeal squamous cell carcinoma treated with primary radiotherapy between 1996 and 2001. Pre-treatment biopsies were used to study the immunohistochemical expression of nine biological markers. Markers were chosen to reflect biologically relevant pathways.Results:Following analysis of nine markers, a profile of two markers was derived (carbonic anhydrase 9 and major vault protein), the co-expression of which conferred a significantly poor probability of locoregional control. The prognostic effect of these biomarkers in combination was greater than their effect individually.Conclusion:Biomarker profiles can be established which highlight large differences in locoregional control. Identifying tumours that express both carbonic anhydrase 9 and major vault protein may facilitate patient selection for more aggressive treatment.

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23

Andriushkova, Natalia G., Volodymyr P. Shyrobokov, Nataliia S. Turchyna, Valentyna V. Melnyk, Olena V. Kuzminska, and Ludmyla V. Dolinchuk. "RESEARCH OF BIOLOGICAL PROPERTIES OF ENTEROVIRUS STRAINS ASSOCIATED WITH ISCHEMIC STROKE." Wiadomości Lekarskie 73, no. 3 (2020): 423–27. http://dx.doi.org/10.36740/wlek202003102.

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Introduction: The research of biological properties of enteroviruses associated with ischemic stroke (IS) allows us to identify their intratypic differences. The aim: to identify genetic markers of strains of enteroviruses associated with IS. Materials and methods: 11 strains of enteroviruses isolated from the serum of patients with IS were identified in the virus neutralization test. Genetic markers of isolated strains (Abent, marker S, marker rct40) were determined. Results: Eleven strains of enteroviruses were isolated from the serum of patients with IS. Eight viruses: Coxsackie B viruses (serotypes 2, 3, 4) and ECHO viruses (serotypes 6, 9, 27 (two strains), 29) were identified in these strains. Other three strains of enteroviruses were unidentified. Different combinations of genetic markers were found. Seven strains of enteroviruses (Coxsackie B2, B3, ECHO 6, ECHO 9, ECHO 27 (two strains) and one unidentified virus) had virulence markers: Abent–, rct40+ and S−. Three strains (Coxsackie B4, ECHO 29, one unidentified virus) had markers: Abent–, rct40+, S+. Another one unidentified virus had markers: Abent+, rct40+, S –. Conclusions: All 11 isolates of enteroviruses associated with IS had rct40+ marker, 10 of the 11 isolates had marker Abent– and 8 of 11 isolates had marker S–. The research of genetic markers allows to perform typic and intratypic differentiation of strains of enteroviruses associated with the IS.

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24

Kurz, Alexander, Matthias Riemenschneider, and Anders Wallin. "Potential Biological Markers for Cerebrovascular Disease." International Psychogeriatrics 15, S1 (July 2003): 89–97. http://dx.doi.org/10.1017/s1041610203009025.

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Cerebrovascular diseases can causes cognitive impairment and dementia by loss of neurons and synaptic connections, destruction of axons, and demyelinization. Biological markers including genetic tests, brain imaging techniques, and biochemical assays in the CSF are valuable for the identification and quantification of cerebrovascular diseases. Genetic tests may be used to detect mutations that cause hereditary cerebral amyloid angiopathies or cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL). Structural CT and MR imaging is routinely used to visualize and quantify infarcts and white-matter changes. Functional SPET and PET imaging can demonstrate focal and remote effects of vascular lesions on cerebral blood flow and metabolism. Biochemical imaging using proton MRS is a nonspecific marker for neuronal and axonal damage. Among biochemical markers in the CSF, tau protein, phospho-tau, and beta amyloid protein are helpful to differentiate vascular dementia from Alzheimer's disease.

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25

Schneider, Lon S. "Biological Markers in Geriatric Depression." Psychiatric Annals 20, no. 2 (February 1, 1990): 83–91. http://dx.doi.org/10.3928/0048-5713-19900201-07.

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26

Łoś, Kacper, and Napoleon Waszkiewicz. "Biological Markers in Anxiety Disorders." Journal of Clinical Medicine 10, no. 8 (April 17, 2021): 1744. http://dx.doi.org/10.3390/jcm10081744.

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Anxiety disorders are one of the most commonly reported disorders in psychiatry, causing a high medical and socio-economic burden. Recently, there has been a soaring interest in the biological basis of anxiety disorders, which is reflected in an increasing number of articles related to the topic. Due to the ambiguity of the diagnosis and a large number of underdiagnosed patients, researchers are looking for laboratory tests that could facilitate the diagnosis of anxiety disorders in clinical practice and would allow for the earliest possible implementation of appropriate treatment. Such potential biomarkers may also be useable in monitoring the efficacy of pharmacological therapy for anxiety disorders. Therefore this article reviews the literature of potential biomarkers such as components of saliva, peripheral blood, cerebrospinal fluid (CSF), and neuroimaging studies. There are promising publications in the literature that can be useful. The most valuable and promising markers of saliva are cortisol, lysozyme, and α-amylase (sAA). In the blood, in turn, we can distinguish serotonin, brain-derived serum neurotrophic factor (BDNF), cortisol, and microRNA. Structural changes in the amygdala and hippocampus are promising neuroimaging markers, while in CSF, potential markers include oxytocin and 5-Hydroxyindoleacetic acid (5-HIAA). Unfortunately, research in the field of biomarkers is hampered by insufficient knowledge about the etiopathogenesis of anxiety disorders, the significant heterogeneity of anxiety disorders, frequent comorbidities, and low specificity of biomarkers. The development of appropriate biomarker panels and their assessment using new approaches may have the prospective to overcome the above-mentioned obstacles.

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27

Goldstein, Bernard D. "Biological Markers and Risk Assessment." Drug Metabolism Reviews 28, no. 1-2 (January 1996): 225–33. http://dx.doi.org/10.3109/03602539608994002.

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28

Andreas Lutterotti, Thomas Berger, and Markus Reindl. "Biological Markers for Multiple Sclerosis." Current Medicinal Chemistry 14, no. 18 (August 1, 2007): 1956–65. http://dx.doi.org/10.2174/092986707781368478.

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29

Rousseau, Jean-Charles, Roland Chapurlat, and Patrick Garnero. "Soluble biological markers in osteoarthritis." Therapeutic Advances in Musculoskeletal Disease 13 (January 2021): 1759720X2110403. http://dx.doi.org/10.1177/1759720x211040300.

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In recent years, markers research has focused on the structural components of cartilage matrix. Specifically, a second generation of degradation markers has been developed against type II collagen neoepitopes generated by specific enzymes. A particular effort has been made to measure the degradation of minor collagens III and X of the cartilage matrix. However, because clinical data, including longitudinal controlled studies, are very scarce, it remains unclear whether they will be useful as an alternative to or in combination with current more established collagen biological markers to assess patients with osteoarthritis (OA). In addition, new approaches using high-throughput technologies allowed to detect new types of markers and improve the knowledge about the metabolic changes linked to OA. The relative advances coming from phenotype research are a first attempt to classify the heterogeneity of OA, and several markers could improve the phenotype characterization. These phenotypes could improve the selection of patients in clinical trials limiting the size of the studies by selecting patients with OA characteristics corresponding to the metabolic pathway targeted by the molecules evaluated. In addition, the inclusion of rapid progressors only in clinical trials would facilitate the demonstration of efficacy of the investigative drug to reduce joint degradation. The combination of selective biochemical markers appears as a promising and cost-effective approach to fulfill this unmet clinical need. Among the various potential roles of biomarkers in OA, their ability to monitor drug efficacy is probably one of the most important, in association with clinical and imaging parameters. Biochemical markers have the unique property to detect changes in joint tissue metabolism within a few weeks.

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30

Lemal, Richard, Olivier Tournilhac, and Jacques-Olivier Bay. "Biological markers in haematological malignancies." Bulletin du Cancer 101, S1 (June 2014): 7–11. http://dx.doi.org/10.1684/bdc.2014.1974.

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31

CUNNINGHAM, E. P., and C. M. MEGHEN. "Biological identification systems: genetic markers." Revue Scientifique et Technique de l'OIE 20, no. 2 (August 1, 2001): 491–99. http://dx.doi.org/10.20506/rst.20.2.1284.

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32

Frese, A., and S. Evers. "Biological Markers of Cervicogenic Headache." Cephalalgia 28, no. 1_suppl (July 2008): 21–23. http://dx.doi.org/10.1111/j.1468-2982.2008.01613.x.

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Upper cervical pain is frequent in different primary headaches and not sufficient evidence for cervicogenic headache (CH). Biological markers should help to differentiate CH from other headache disorders. In most cases, imaging techniques of the cervical spine are not helpful for the diagnosis of CH. Symptoms and signs of neck involvement, such as a mechanical precipitation of attacks, a restriction in range of motion of the cervical spine, and the existence of ipsilateral neck, shoulder, or arm pain, seem to be reasonably valid for the diagnosis of CH, but its reliability and validity should be confirmed in larger studies. Positive diagnostic blockades of cervical structures or its nerve supply are not specific for CH. Neurophysiological investigations give some insight into the pathophysiological mechanisms of CH but are not diagnostic. In CH, calcitonin gene-related peptide levels do not differ between the symptomatic and the asymptomatic side, between the jugular and the cubital blood, and between days with and without headache. There is no evidence for an activation of the trigeminovascular system in CH. It can be concluded that CH is not just a migraine variant triggered by neck dysfunction but a functional entity.

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33

Ott, Jurg. "Linkage Analysis with Biological Markers." Human Heredity 45, no. 3 (1995): 169–74. http://dx.doi.org/10.1159/000154280.

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34

Gallo, Maria F., Markus J. Steiner, Marcia M. Hobbs, Lee Warner, Denise J. Jamieson, and Maurizio Macaluso. "Biological Markers of Sexual Activity." Sexually Transmitted Diseases 40, no. 6 (June 2013): 447–52. http://dx.doi.org/10.1097/olq.0b013e31828b2f77.

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35

Neugroschl, Judith, and Kenneth L. Davis. "Biological Markers in Alzheimer Disease." American Journal of Geriatric Psychiatry 10, no. 6 (November 2002): 660–77. http://dx.doi.org/10.1097/00019442-200211000-00005.

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36

Riechelmann, H., T. Deutschle, E. Friemel, H.-J. Gross, and M. Bachem. "Biological markers in nasal secretions." European Respiratory Journal 21, no. 4 (April 2003): 600–605. http://dx.doi.org/10.1183/09031936.03.00072003.

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37

Posternak, Michael A. "Biological Markers of Atypical Depression." Harvard Review of Psychiatry 11, no. 1 (January 2003): 1–7. http://dx.doi.org/10.1097/00023727-200301000-00001.

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38

Post, Stephen G., and Joseph M. Foley. "Biological Markers and Truth-Telling." Alzheimer Disease & Associated Disorders 6, no. 4 (1992): 201–4. http://dx.doi.org/10.1097/00002093-199206040-00002.

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39

Wolff, Kim. "Biological markers of drug use." Psychiatry 5, no. 12 (December 2006): 439–41. http://dx.doi.org/10.1053/j.mppsy.2006.10.012.

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40

Wolff, Kim, and E. Jane Marshall. "Biological markers of alcohol use." Psychiatry 5, no. 12 (December 2006): 437–38. http://dx.doi.org/10.1053/j.mppsy.2006.10.013.

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41

Johnson, Ralph H. "Biological Markers in Tort Litigation." Statistical Science 3, no. 3 (August 1988): 367–70. http://dx.doi.org/10.1214/ss/1177012839.

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42

Posternak, Michael A. "Biological Markers of Atypical Depression." Harvard Review of Psychiatry 11, no. 1 (January 2003): 1–7. http://dx.doi.org/10.1080/10673220303941.

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43

Bangerter, L., and S. Zarit. "BIOLOGICAL MARKERS IN FAMILY RESEARCH." Innovation in Aging 1, suppl_1 (June 30, 2017): 11. http://dx.doi.org/10.1093/geroni/igx004.038.

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44

Svennerholm, L. "Biological Markers in Alzheimer's Disease." International Psychogeriatrics 3, S1 (March 1991): 29–41. http://dx.doi.org/10.1017/s1041610205001110.

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Clinical and neuropathological examinations have shown that Alzheimer's disease is not a single entity. An early onset form with predominant parietal symptoms (type I) can be differentiated from a late onset form with mainly general cognitive symptoms and only mild parietal symptoms (type II). In CSF of patients with Alzheimer's disease type I there are signs of reduced blood-CSF barrier function and the metabolites of serotonin and dopamine are reduced in early stages, while in patients with type II there is often a diminished blood-CSF barrier function and in later stages there are reduced monoamine metabolites. Studies of membrane lipids of the brain have shown that myelin lipids are reduced in type II while gangliosides are markedly reduced in type I. Based on this finding a method has been developed for the assay of gangliosides in CSF. An increase of ganglioside GM1 seems to be a hallmark for Alzheimer's disease, type I.

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45

Hock, C. "Biological Markers of Alzheimer’s Disease." Neurobiology of Aging 19, no. 2 (March 1998): 149–51. http://dx.doi.org/10.1016/s0197-4580(98)00010-4.

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46

Klunk, W. E. "Biological Markers of Alzheimer’s Disease." Neurobiology of Aging 19, no. 2 (March 1998): 145–47. http://dx.doi.org/10.1016/s0197-4580(98)00013-x.

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47

Nedic Erjavec, Gordana, Marina Sagud, Matea Nikolac Perkovic, Dubravka Svob Strac, Marcela Konjevod, Lucija Tudor, Sandra Uzun, and Nela Pivac. "Depression: Biological markers and treatment." Progress in Neuro-Psychopharmacology and Biological Psychiatry 105 (March 2021): 110139. http://dx.doi.org/10.1016/j.pnpbp.2020.110139.

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48

Bailey, Peter. "Biological Markers in Alzheimer's Disease." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 34, S1 (March 2007): S72—S76. http://dx.doi.org/10.1017/s0317167100005618.

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abstractBiomarkers are required to improve our diagnostic sensitivity and specificity and to monitor the biological activity of the Alzheimer’s disease (AD) in terms of the burden of neural involvement and the tempo of disease progression. Biomarkers will initially supplement our more traditional neuropsychological and imaging markers but may eventually evolve into useful surrogate endpoints in AD research. These markers may also provide important mechanistic clues to the pharmacological action of anti-dementia compounds. At this point, the combination of elevated cerebrospinal fluid phosphorylated TAU (CSF p-TAU) proteins and low CSF A²1-42are the only biomarkers with the sensitivity and specificity to serve as useful diagnostic biomarkers capable of distinguishing AD from other dementias in the early stages. Advances in non CSF tests is urgently required. Markers assessing the progression of disease do not necessarily require the same high disease specificity as diagnostic markers, but need to be sensitive to changes in disease state. At present, candidate markers fall under four main biological rationales: 1. Specific markers of AD neuropathology; 2. Non-specific markers of neural degeneration; 3. Markers of oxidative stress; 4. Markers of neural inflammation. It is foreseeable that a panel of such markers might prove advantageous. It will be important to develop “non-invasive “ markers utilizing readily obtainable tissue samples such as serum or urine to monitor disease progression (or hopefully regression). Repeated sampling would allow for comparison with traditional neuropsychological and imaging measures. The assays themselves will need to be reproducible, reliable and relatively inexpensive. Unfortunately, these biomarkers are in the formative stages of testing and results at present are inconclusive. To facilitate biomarker development in the future it would be highly advantageous to begin to collect and store biological specimens as an adjunct to current research in AD.

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49

Bruyn, G. W. "Biological markers of Alzheimer's disease." Journal of the Neurological Sciences 96, no. 1 (April 1990): 127. http://dx.doi.org/10.1016/0022-510x(90)90067-w.

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50

DeFeudis, Francis V. "Biological markers of alzheimer's disease." Neurochemistry International 17, no. 4 (January 1990): 635–37. http://dx.doi.org/10.1016/0197-0186(90)90057-z.

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