Journal articles: 'Somatic Marker Hypothesi'

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Trajkovski, Miroslava. "On the somatic marker hypothesis." Theoria, Beograd 58, no. 2 (2015): 65–72. http://dx.doi.org/10.2298/theo1502065t.

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The somatic marker hypothesis is the hypothesis of the neural mechanism which is spontaneously triggered in the process of decision making. It is about bodily changes that accompany certain ideas we relate to the prospects of our choices. The somatic marker is the feeling of these changes occurring before the decision is made. In the paper I deal with the hypothesis of Antonio Damasio and his associates which is related to the perceptual theory of emotions that claims that the feeling of bodily changes precedes the feeling of emotion.

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Dunn, Barnaby D., Tim Dalgleish, and Andrew D. Lawrence. "The somatic marker hypothesis: A critical evaluation." Neuroscience & Biobehavioral Reviews 30, no. 2 (January 2006): 239–71. http://dx.doi.org/10.1016/j.neubiorev.2005.07.001.

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Leland, Jonathan W., and Jordan Grafman. "Experimental tests of the Somatic Marker hypothesis." Games and Economic Behavior 52, no. 2 (August 2005): 386–409. http://dx.doi.org/10.1016/j.geb.2004.09.001.

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Wagenmakers, Eric-Jan, and Sander Nieuwenhuis. "Damasio's error? De somatic-marker-hypothese onder vuur." Neuropraxis 9, no. 6 (December 2005): 159–63. http://dx.doi.org/10.1007/bf03079064.

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Maia, Tiago V., and James L. McClelland. "The somatic marker hypothesis: still many questions but no answers." Trends in Cognitive Sciences 9, no. 4 (April 2005): 162–64. http://dx.doi.org/10.1016/j.tics.2005.02.006.

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Kallenberg, Brad J. "Teaching Engineering Ethics by Conceptual Design: The Somatic Marker Hypothesis." Science and Engineering Ethics 15, no. 4 (April 10, 2009): 563–76. http://dx.doi.org/10.1007/s11948-009-9129-2.

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Bechara, Antoine, and Antonio R. Damasio. "The somatic marker hypothesis: A neural theory of economic decision." Games and Economic Behavior 52, no. 2 (August 2005): 336–72. http://dx.doi.org/10.1016/j.geb.2004.06.010.

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Nishitsutsumi, Yu. "Does the “Iowa Gambling Task” Really Verify the Somatic Marker Hypothesis?" Kagaku tetsugaku 43, no. 1 (2010): 31–44. http://dx.doi.org/10.4216/jpssj.43.1_31.

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Batson, C. Daniel, Connie L. Engel, and Scott R. Fridell. "Value Judgments: Testing the Somatic-Marker Hypothesis Using False Physiological Feedback." Personality and Social Psychology Bulletin 25, no. 8 (August 1999): 1021–32. http://dx.doi.org/10.1177/01461672992511009.

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Cantarella, Simona, Carola Hillenbrand, Luke Aldridge-Waddon, and Ignazio Puzzo. "Preliminary evidence on the somatic marker hypothesis applied to investment choices." Journal of Neuroscience, Psychology, and Economics 11, no. 4 (December 2018): 228–38. http://dx.doi.org/10.1037/npe0000097.

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Suzuki, Atsunobu, Akihisa Hirota, Noriyoshi Takasawa, and Kazuo Shigemasu. "Application of the somatic marker hypothesis to individual differences in decision making." Biological Psychology 65, no. 1 (December 2003): 81–88. http://dx.doi.org/10.1016/s0301-0511(03)00093-0.

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Jiménez-Rodríguez, Alejandro, Luis Fernando Castillo, and Manuel González. "Studying the mechanisms of the Somatic Marker Hypothesis in Spiking Neural Networks (SNN)." ADCAIJ: Advances in Distributed Computing and Artificial Intelligence Journal 1, no. 2 (July 1, 2013): 35–42. http://dx.doi.org/10.14201/adcaij2012123542.

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In this paper, a mechanism of emotional bias in decision making is studied using Spiking Neural Networks to simulate the associative and recurrent networks involved. The results obtained are along the lines of those proposed by A. Damasio as part of the Somatic Marker Hypothesis, in particular, that, in absence of emotional input, the decision making is driven by the rational input alone. Appropriate representations for the Objective and Emotional Values are also suggested, provided a spike representation (code) of the information.

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Schmitt, William A., Chad A. Brinkley, and Joseph P. Newman. "Testing Damasio's somatic marker hypothesis with psychopathic individuals: Risk takers or risk averse?" Journal of Abnormal Psychology 108, no. 3 (August 1999): 538–43. http://dx.doi.org/10.1037/0021-843x.108.3.538.

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Lösel, Friedrich, and Martin Schmucker. "Psychopathy, Risk Taking, and Attention: A Differentiated Test of the Somatic Marker Hypothesis." Journal of Abnormal Psychology 113, no. 4 (2004): 522–29. http://dx.doi.org/10.1037/0021-843x.113.4.522.

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Bechara, A., H. Damasio, D. Tranel, and A. R. Damasio. "The Iowa Gambling Task and the somatic marker hypothesis: some questions and answers." Trends in Cognitive Sciences 9, no. 4 (April 2005): 159–62. http://dx.doi.org/10.1016/j.tics.2005.02.002.

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Carter, Sid, and Marcia Smith Pasqualini. "Stronger autonomic response accompanies better learning: A test of Damasio's somatic marker hypothesis." Cognition and Emotion 18, no. 7 (November 2004): 901–11. http://dx.doi.org/10.1080/02699930341000338.

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Cabrera, Daniel, Claudio Cubillos, Enrique Urra, and Rafael Mellado. "Framework for Incorporating Artificial Somatic Markers in the Decision-Making of Autonomous Agents." Applied Sciences 10, no. 20 (October 21, 2020): 7361. http://dx.doi.org/10.3390/app10207361.

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The somatic marker hypothesis proposes that when a person faces a decision scenario, many thoughts arise and different “physical consequences” are fleetingly observable. It is generally accepted that affective dimension influences cognitive capacities. Several proposals for including affectivity within artificial systems have been presented. However, to the best of our knowledge, a proposal that considers the incorporation of artificial somatic markers in a disaggregated and specialized way for the different phases that make up a decision-making process has not been observed yet. Thus, this research work proposes a framework that considers the incorporation of artificial somatic markers in different phases of the decision-making of autonomous agents: recognition of decision point; determination of the courses of action; analysis of decision options; decision selection and performing; memory management. Additionally, a unified decision-making process and a general architecture for autonomous agents are presented. This proposal offers a qualitative perspective following an approach of grounded theory, which is suggested when existing theories or models cannot fully explain or understand a phenomenon or circumstance under study. This research work represents a novel contribution to the body of knowledge in guiding the incorporation of this biological concept in artificial terms within autonomous agents.

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Poppa, Tasha, and Antoine Bechara. "The somatic marker hypothesis: revisiting the role of the ‘body-loop’ in decision-making." Current Opinion in Behavioral Sciences 19 (February 2018): 61–66. http://dx.doi.org/10.1016/j.cobeha.2017.10.007.

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North, N. "Decision making in patients with spinal cord damage: afferent feedback and the somatic marker hypothesis." Neuropsychologia 39, no. 5 (2001): 521–24. http://dx.doi.org/10.1016/s0028-3932(00)00107-x.

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Le Roith, Derek, Carolyn Bondy, Shoshana Yakar, Jun-Li Liu, and Andrew Butler. "The Somatomedin Hypothesis: 2001." Endocrine Reviews 22, no. 1 (February 1, 2001): 53–74. http://dx.doi.org/10.1210/edrv.22.1.0419.

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Abstract Since the original somatomedin hypothesis was conceived, a number of important discoveries have allowed investigators to modify the concept. Originally somatic growth was thought to be controlled by pituitary GH and mediated by circulating insulin-like growth factor-I (IGF-I, somatomedin C) expressed exclusively by the liver. With the discovery that IGF-I is produced by most, if not all, tissues, the role of autocrine/paracrine IGF-I vs. the circulating form has been hotly debated. Recent experiments using transgenic and gene-deletion technologies have attempted to answer these questions. In the liver-specific igf-1 gene-deleted mouse model, postnatal growth and development are normal despite the marked reduction in circulating IGF-I and IGF-binding protein levels; free IGF-I levels are normal. Thus, the normal postnatal growth and development in these animals may be due to normal free IGF-I levels (from as yet unidentified sources), although the role of autocrine/paracrine IGF-I has yet to be determined.

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Mardaga, Solange, and Michel Hansenne. "Personality and Skin Conductance Responses to Reward and Punishment." Journal of Individual Differences 33, no. 1 (January 2012): 17–23. http://dx.doi.org/10.1027/1614-0001/a000057.

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For several years now, the somatic aspect of emotions has been regarded as a major factor in the decision-making process. A large body of literature has investigated this issue, within the somatic marker hypothesis perspective, using the classical Iowa Gambling Task (IGT). Many studies reported an influence of clinical and differential factors, including personality, on IGT performance. On the other hand, personality appears to modulate the emotional responses as a function of valence (i.e., responses to rewards vs. punishments). The present study investigated whether the influence of personality on the decision-making process might be mediated by differential emotional responsiveness. Skin conductance levels were recorded in 32 subjects while performing the IGT. The results showed that novelty seeking (NS) modulated the skin conductance responses to feedback, and both NS and harm avoidance (HA) influenced anticipative response development. We also found that NS tended to modulate the final score, beyond the influence of beneficial anticipative autonomic responses. The present data partially support the hypothesis that personality-related differential emotional responsiveness may modulate somatic marker development in a decision-making situation. On the other hand, personality influence on the performance was not entirely explained by these emotional differences.

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Wines, D. R., and S. Henikoff. "Somatic instability of a Drosophila chromosome." Genetics 131, no. 3 (July 1, 1992): 683–91. http://dx.doi.org/10.1093/genetics/131.3.683.

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Abstract A mitotically unstable chromosome, detectable because of mosaic expression of marker genes, was generated by X-ray mutagenesis in Drosophila. Nondisjunction of this chromosome is evident in mitotic chromosome preparations, and premature sister chromatid separation is frequent. The mosaic phenotype is modified by genetic elements that are thought to alter chromatin structure. We hypothesize that the mitotic defects result from a breakpoint deep in the pericentric heterochromatin, within or very near to the DNA sequences essential for centromere function. This unique chromosome may provide a tool for the genetic and molecular dissection of a higher eukaryotic centromere.

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Adamson, H. D. "CODES AND CONSEQUENCES: CHOOSING LINGUISTIC VARIETIES.Carol Myers-Scotton (Ed.). Oxford: Oxford University Press, 1998. Pp. x + 219. $24.95 paper." Studies in Second Language Acquisition 22, no. 2 (June 2000): 287. http://dx.doi.org/10.1017/s0272263100262062.

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The phenomenon of styleswitching has been important in the study of L1 and L2 language use. Labov's early studies correlated formal style with attention paid to speech, a notion echoed in Krashen's monitor model. Giles' accommodation theory and Bell's audience design theory claim that speakers styleswitch in order to accommodate to the speech of their audience. Several SLA scholars have found evidence for accommodation in L2 speech as well. Such correlational studies have been criticized for lacking a clear foundation in cognitive theory. In this volume Myers-Scotton describes her Markedness Model (MM), which grounds styleswitching (including codeswitching) in the cognitive theory of somatic markers (Damasio, 1994). Because speech styles are distinguished mainly by the frequency at which certain features (such as dropping a consonant from a cluster) appear, variationists have sought to identify a cognitive mechanism that could account for the apparent fine-tuning of feature frequencies. However, it is not clear from the discussion in this volume whether the somatic marker hypothesis provides such a mechanism.

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Ishii, Ryouhei, and Leonides Canuet. "Heartbeat evoked potentials: A new possible clinical biomarker for depression based on the somatic marker hypothesis." Clinical Neurophysiology 123, no. 10 (October 2012): 1899–900. http://dx.doi.org/10.1016/j.clinph.2012.03.002.

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Colombetti, Giovanna. "The Somatic Marker Hypotheses, and What the Iowa Gambling Task Does and Does not Show." British Journal for the Philosophy of Science 59, no. 1 (March 1, 2008): 51–71. http://dx.doi.org/10.1093/bjps/axm045.

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Wright, Rebecca J., and Tim Rakow. "Don’t sweat it: Re-examining the somatic marker hypothesis using variants of the Balloon Analogue Risk Task." Decision 4, no. 1 (January 2017): 52–65. http://dx.doi.org/10.1037/dec0000055.

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Vanheule, Stijn, Mattias Desmet, and Reitske Meganck. "What the Heart Thinks, the Tongue Speaks: A Study on Depression and Lexical Choice." Psychological Reports 104, no. 2 (April 2009): 473–81. http://dx.doi.org/10.2466/pr0.104.2.473-481.

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The present study examined symptom-specificity in depression, testing the hypothesis that affective, cognitive, and somatic dimensions in depressive symptoms, as measured with the Beck Depression Inventory–II, cohere, respectively, with the use of affective-, cognitive-, and somatic-related words in natural language, as measured with the Linguistic Inquiry and Word Count. Based on questionnaire and interview data from 32 mental health outpatients, analyses indicate scores for affective depressive symptoms correlate significantly with affective word use, cognitive depressive symptoms are related to cognitively oriented word use combined with affective word use, and the presence of somatic depressive symptoms correlates significantly with words referring to physical states and functions. These results indicate that different facets of depression have specific correlates and that natural word use serves as a psychological marker. From a psychometric point of view, this study substantiates the concurrent validity of the Linguistic Inquiry and Word Count (LIWC2001) categories under study and the Beck Depression Inventory-II subscales for affective, cognitive, and somatic symptoms.

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Heyes, C. M. "Theory of mind and other domain-specific hypotheses." Behavioral and Brain Sciences 24, no. 6 (December 2001): 1143–45. http://dx.doi.org/10.1017/s0140525x01270149.

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The commentators do not contest the target article's claim that there is no compelling evidence of theory of mind in primates, and recent empirical studies further support this view. If primates lack theory of mind, they may still have other behavior control mechanisms that are adaptive in complex social environments. The Somatic Marker Mechanism (SMM) is a candidate, but the SMM hypothesis postulates a much weaker effect of natural selection on social cognition than the theory of mind hypothesis (on inputs to cognitive mechanisms, not on the mechanisms themselves), and there is currently no evidence that it is specific to social stimuli or to primates. “Two Guesser” training would make the goggles test too chauvinistic, and in its current form the goggles problem could not be solved by physical matching because, while wearing goggles, an individual cannot see itself seeing.

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Хаптанова, Valentina Khaptanova, Ильин, Vladimir Ilin, Гольменко, Aleksandr Golmenko, Выговский, and Evgeniy Vygovskiy. "THE HYPOTHESIS OF THE INTERDEPENDENCE OF THE INCIDENCE OF MEDICAL PROFESSIONALS AND THE SYNDROME OF PROFESSIONAL-PSYCHOLOGICAL DISADAPTATION." Бюллетень Восточно-Сибирского научного центра Сибирского отделения Российской академии медицинских наук 1, no. 6 (December 20, 2016): 39–43. http://dx.doi.org/10.12737/23732.

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The impaired adaptation is a dynamic condition, structurally comprising the combination of independent components: the syndrome of professional-psychological disadaptation (SPPD) (psychological component), morbidity (somatic component), and psychosomatics, including the interaction of the above components. Thus, a psychological compo-nent is the initial phase, and a somatic one, to a more marked degree, leading to further disruptions in the increase of psychological disorders and morbidity, i.e. disadaptation. The study found that the highest rates of the syndrome of professional psychological disadaptatiion are noted in the group with work experience of 0–5 years. The cause is a long period of not working in their specialty, which leads to a decrease in self-regulation, psychological defenses, general theoretical and practical professional level.Preventive work in the organization should focus on psychological trainings, refresher courses or the introduction of mentoring.

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Kralovics, Robert, Soon-Siong Teo, Sai Li, Alexandre Theocharides, Andreas S. Buser, Andre Tichelli, and Radek C. Skoda. "Acquisition of the V617F mutation of JAK2 is a late genetic event in a subset of patients with myeloproliferative disorders." Blood 108, no. 4 (August 15, 2006): 1377–80. http://dx.doi.org/10.1182/blood-2005-11-009605.

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AbstractAn acquired gain-of-function mutation in the Janus kinase 2 (JAK2-V617F) is frequently found in patients with myeloproliferative disorders (MPDs). To test the hypothesis that JAK2-V617F is the disease-initiating mutation, we examined whether all cells of clonal origin carry the JAK2-V617F mutation. Using allele-specific polymerase chain reaction (PCR) assays for the JAK2 mutation and for the X-chromosomal clonality markers IDS and MPP1, we found that the percentage of granulocytes and platelets with JAK2-V617F was often markedly lower than the percentage of clonal granulocytes determined by IDS or MPP1 clonality assays in female patients. Using deletions of chromosome 20q (del20q) as an autosomal, X-chromosome–independent clonality marker, we found a similar discrepancy between the percentage of cells carrying JAK2-V617F and del20q. Our results suggest that in a proportion of patients with MPDs, JAK2-V617F occurs on the background of clonal hematopoiesis caused by a somatic mutation in an as-yet-unknown gene.

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Wang, RR C., X. M. Li, and N. J. Chatterton. "Loss of heterozygosity and accelerated genotype fixation in rice hybrids." Genome 42, no. 5 (October 1, 1999): 789–96. http://dx.doi.org/10.1139/g99-061.

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Loss of heterozygosity is reported in rice hybrids of a particular heritage. Hybrids derived from a plant selected from the Chinese rice cultivar 'Zhongxin No. 1' exhibited somatic variations as evidenced by having both segregating and uniform panicle rows in F2 progenies. F3 plants from uniform F2 rows were found to be homozygous for all 14 RAPD (random amplified polymorphic DNA) markers, of which two co-dominant markers were located on chromosome 2 and five other markers were on five different chromosomes. RAPD markers unique to either parent were present or absent in all F2 plants within some panicle rows, yet segregated in a Mendelian manner in other panicle rows. The molecular data suggest that somatic cells in these hybrids do not always contain both parental homologues of some chromosomes. These findings support the hypothesis that somatic chromosome pairing and recombination lead to loss of heterozygosity and non-identical daughter cells following mitosis. Sequential mitotic assortment of chromosome homologues of a plant's genome can lead to homozygous or nearly homozygous somatic cells that eventually develop into reproductive cells. As a result of this unique mechanism in rice hybrids derived from Zhongxin No. 1, uniform or less-segregating progenies can be identified from F2 or F3 panicle rows at a much higher frequency than normally expected. This phenomenon can be utilized to shorten the breeding cycle of rice, or other crops when plants containing gene(s) for mitotic pairing are identified, or when the genes are isolated from rice and effectively transferred into other crops.Key words: LOH, in vivo somatic variation, homozygous F2, RAPD, apomixis.

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Toschi, P., D. Iuso, D. A. Anzalone, M. Czernik, G. Ptak, and P. Loi. "343 DIRECT EXPRESSION OF PLURIPOTENCY MARKERS IN CULTURED SOMATIC CELLS BY SMALL REPROGRAMMING MOLECULES." Reproduction, Fertility and Development 27, no. 1 (2015): 260. http://dx.doi.org/10.1071/rdv27n1ab343.

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The differentiate state of the cell may be reversed by a process called reprogramming. To date, a totipotent status is conferred to a somatic cell by nuclear transfer (SCNT) and a condition of pluripotency is conferred by induced expression of defined factors (iPSC). While the restoration of full totipotency by SCNT is rarely achieved, pluripotency by Yamanaka's factors (Oct4, c-myc, Sox-2, Klf4) is inducible, although with low efficiency, in a large set of cell in different animal models. However, the isolation of iPSC requires complex technical skills and time-consuming protocols. In our laboratory we have observed that the simple expansion of fibroblasts in culture switches on pluripotency markers such as Oct4 and Nanog (Anzalone et al. 2015 Reprod. Fertil. Dev. IETS Abstract 344). CHIR99021 is a small molecule, targeting the Wnt/β-catenin signalling pathway, which is used for stem cell culture (Li et al. 2009). CHIR99021 acts as selective inhibitor of both isoform of GSK3 α/β regulating cellular proliferation and differentiation. In this work we tested the hypothesis that the exposure to a small reprogramming molecule (CHIR99021) induces pluripotency marker expression in primary cultures of somatic cells. Sheep and mouse primary fibroblasts cultured in low oxygen and induced to enter GO (low serum, 0.5% FBS for 5 days, <3% cell proliferation in our conditions) were treated with different CHIR concentrations (from 2.5 to 5 µM) for different time periods (from 1 to 5 days) in order to test the proper concentration and to exclude any cytotoxic effects. Nuclear reprogramming was assessed in treated and control cells by analysing β-catenin and oct4, nanog, sox2, klf4, and c-myc expression by immuno-detection and PCR. We found that CHIR interferes with β-catenin pathway in both sheep and mouse fibroblast in a time- and dose-dependent manner; the best results were obtained using 3 µM of CHIR for 3 days. Western blot analysis confirmed that CHIR treatment leads to an increased cellular level of β-catenin; furthermore, pluripotency marker expression (protein and mRNA) was increased (P = 0.023 nonparametric Mann-Whitney test) in CHIR-treated cells compared to controls. These observations, confirmed in both the experimental models, indicate that treatment with a small molecule inhibitor interfering with glucose metabolism induces the expression of pluripotency marker in somatic cells.

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Proskuryakov, S. Ya, A. G. Konoplyannikov, Yu G. Verkhovskii, L. P. Ulyanova, and A. F. Tsyb. "Where intestinal epithelial stem cells are localized? About molecular markers." Biomeditsinskaya Khimiya 57, no. 4 (2011): 359–73. http://dx.doi.org/10.18097/pbmc20115704359.

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Using stem cells as an example the review considers a new history and methodology of search for stem cells (SC), found in tissues of adult Homo sapiens and Drosophila melanogaster organisms. These studies of SC resulted in several original hypotheses explaining their unusual features. Impressive progress recently achieved in this direction (2008-2010) is associated with employment of new methods of somatic recombination for long-term registration of various strains of differentiated cells, early and distant SC progeny. 1) Although anatomic localization of intestinal epithelium cells lacking marked morphological and biochemical differentiation markers (the lower third of intestinal and colon crypts) is known for about 40 years results of their experimental identification, isolation and detection of their functional characteristics still represent the subject for discussions. Particularly, it remains unclear, which SC are involved in crypt regeneration: the same as those involved into homeostatic renewal or their various subpopulations or early SC progenies acquired stem features by reprogramming? 2) In addition, most detected biochemical markers of potential SC are common for SC from other tissues of embryonic and mature organisms so it is possible to apply method developed for intestinal epithelium for their isolation. 3) Data on induction of intestinal epithelium polyps and neoplasias by mutations in genes encoding SC markers and identification of biochemical characteristics of potential SC in these tumors support the hypothesis of stem tumor cell origination from normal SC or their earliest progeny. In general, facts considered in this review may be useful for both development of optimal methods for the use of SC in cell therapy (as the source of humoral factors), regenerative medicine (as the source of differentiated cells for restoration of injured tissue), and also for targeted search of antitumor drugs (SC as the target) and preparations modifying genetic and epigenetic reactions of SC to genotoxic and stress treatments.

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Wu, Jiande, Tarun Mamidi, Lu Zhang, and Chindo Hicks. "Integrating Germline and Somatic Mutation Information for the Discovery of Biomarkers in Triple-Negative Breast Cancer." International Journal of Environmental Research and Public Health 16, no. 6 (March 23, 2019): 1055. http://dx.doi.org/10.3390/ijerph16061055.

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Recent advances in high-throughput genotyping and the recent surge of next generation sequencing of the cancer genomes have enabled discovery of germline mutations associated with an increased risk of developing breast cancer and acquired somatic mutations driving the disease. Emerging evidence indicates that germline mutations may interact with somatic mutations to drive carcinogenesis. However, the possible oncogenic interactions and cooperation between germline and somatic alterations in triple-negative breast cancer (TNBC) have not been characterized. The objective of this study was to investigate the possible oncogenic interactions and cooperation between genes containing germline and somatic mutations in TNBC. Our working hypothesis was that genes containing germline mutations associated with an increased risk developing breast cancer also harbor somatic mutations acquired during tumorigenesis, and that these genes are functionally related. We further hypothesized that TNBC originates from a complex interplay among and between genes containing germline and somatic mutations, and that these complex array of interacting genetic factors affect entire molecular networks and biological pathways which in turn drive the disease. We tested this hypothesis by integrating germline mutation information from genome-wide association studies (GWAS) with somatic mutation information on TNBC from The Cancer Genome Atlas (TCGA) using gene expression data from 110 patients with TNBC and 113 controls. We discovered a signature of 237 functionally related genes containing both germline and somatic mutations. We discovered molecular networks and biological pathways enriched for germline and somatic mutations. The top pathways included the hereditary breast cancer and role of BRCA1 in DNA damage response signaling pathways. In conclusion, this is the first large-scale and comprehensive analysis delineating possible oncogenic interactions and cooperation among and between genes containing germline and somatic mutations in TNBC. Genetic and somatic mutations, along with the genes discovered in this study, will require experimental functional validation in different ethnic populations. Functionally validated genetic and somatic variants will have important implications for the development of novel precision prevention strategies and discovery of prognostic markers in TNBC.

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Maia, T. V., and J. L. McClelland. "A reexamination of the evidence for the somatic marker hypothesis: What participants really know in the Iowa gambling task." Proceedings of the National Academy of Sciences 101, no. 45 (October 22, 2004): 16075–80. http://dx.doi.org/10.1073/pnas.0406666101.

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Pannett, Anna A. J., and Rajesh V. Thakker. "Somatic Mutations in MEN Type 1 Tumors, Consistent with the Knudson “Two-Hit” Hypothesis." Journal of Clinical Endocrinology & Metabolism 86, no. 9 (September 1, 2001): 4371–74. http://dx.doi.org/10.1210/jcem.86.9.7844.

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MEN type 1 is an autosomal dominant disorder characterized by the combined occurrence of tumors of the parathyroids, anterior pituitary, and pancreatic islet cells. The MEN1 gene, which is located on chromosome 11q13, consists of 10 exons and encodes a 610-amino acid protein named MENIN. The observation of LOH involving 11q13 in MEN type 1 tumors and the inactivating germline mutations found in patients suggest that the MEN1 gene acts as a tumor suppressor, in keeping with the “two-hit” model of hereditary cancer. The second hit in MEN type 1 tumors typically involves large chromosomal deletions that include 11q13. However, this only represents one mechanism by which the second hit may occur, and the other mechanisms, such as intragenic deletions or point mutations that inactivate the gene, have not been reported in MEN type 1 tumors. We have therefore undertaken studies to search for such mutations in six MEN type 1 tumors (four parathyroid tumors, one insulinoma, and one lipoma) that did not have LOH at 11q13 as assessed using the flanking markers D11S480, D11S1883 and PYGM centromerically and D11S449 and D11S913 telomerically. This revealed four somatic mutations, which consisted of two missense mutations and two frameshift mutations in two parathyroid tumors, one insulinoma, and one lipoma. Thus, our results, which represent the first small intragenic somatic mutations reported in MEN type 1 tumors, provide further evidence that the role of the MEN1 gene is consistent with that of a tumor suppressor gene, as postulated by Knudson’s “two-hit” hypothesis.

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Xu, N., S. Paul, J. Bennewitz, N. Reinsch, G. Thaller, F. Reinhardt, C. Kühn, et al. "Confirmation of quantitative trait loci for somatic cell score on bovine chromosome 18 in the German Holstein." Archives Animal Breeding 49, no. 2 (October 10, 2006): 111–19. http://dx.doi.org/10.5194/aab-49-111-2006.

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Abstract. Fifty-one half-sib families with 2768 sires were selected for this study to confirm a quantitative trait locus (QTL) detected within a previous project initiated by the German Cattle Breeders Federation (ADR). The data based on a granddaughter design were divided into two parts and were analysed using linear models and paternal half sib regression methods. The results strongly support the hypothesis that the chromosomal region around marker TGLA227 at the telomeric end of chromosome 18 harbours a QTL for somatic cell score (SCS) in the German Holstein population. Using a two-QTL model the analysis showed evidence for another QTL for SCS in that region on chromosome 18. Further fine mapping studies should be carried out to decide on the two QTL hypothesis.

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Garson, Kenneth, and Barbara C. Vanderhyden. "Epithelial ovarian cancer stem cells: underlying complexity of a simple paradigm." REPRODUCTION 149, no. 2 (February 2015): R59—R70. http://dx.doi.org/10.1530/rep-14-0234.

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The lack of significant progress in the treatment of epithelial ovarian cancer (EOC) underscores the need to gain a better understanding of the processes that lead to chemoresistance and recurrence. The cancer stem cell (CSC) hypothesis offers an attractive explanation of how a subpopulation of cells within a patient's tumour might remain refractory to treatment and subsequently form the basis of recurrent chemoresistant disease. This review examines the literature defining somatic stem cells of the ovary and fallopian tube, two tissues that give rise to EOC. In addition, considerable research has been reviewed, that has identified subpopulations of EOC cells, based on marker expression (CD133,CD44,CD117,CD24, epithelial cell adhesion molecule,LY6A,ALDH1and side population (SP)), which are enriched for tumour initiating cells (TICs). While many studies identified eitherCD133orCD44as markers useful for enriching for TICs, there is little consensus. This suggests that EOC cells may have a phenotypic plasticity that may preclude the identification of universal markers defining a CSC. The assay that forms the basis of quantifying TICs is the xenograft assay. Considerable controversy surrounds the xenograft assay and it is essential that some of the potential limitations be examined in this review. Highlighting such limitations or weaknesses is required to properly evaluate data and broaden our interpretation of potential mechanisms that might be contributing to the pathogenesis of ovarian cancer.

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Dziubka, Kazimierz. "A Postmodern Public Man and His Mental-Cultural Markers." World Political Science 13, no. 2 (December 20, 2017): 273–301. http://dx.doi.org/10.1515/wps-2017-0006.

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AbstractThe article aims to describe the fundamental principles of the postmodern concepts of public life viewed from the perspective of neuroscience and cognitive science. Considering the fact that both systems of theories are focused on the psychobiological aspects of human mind and body, and in consequence they both endeavor to understand and explain the relations between brain, mind, and social environment (sphere), I decided to use this particular assumption as a starting point to analyse categories such as: public man, public sphere, space of life, modern and postmodern normative patterns, and heuristic paradigms of relationships between Nature, Society, and Culture. As a leading cognitive and interpretative approach I selected the theory of mental and cultural markers, based on somatic marker hypothesis presented by Antonio R. Damasio and the first-person ontology developed by John R. Searle. Ultimately, both concepts support a more extensive and complex approach in explaining direction of contemporary public debate and associated with it expectations to reorganize people’s life in terms of their physical and spiritual needs. The crucial role of the aforementioned changes has the embodied self – a source of unique and everyday experiences that stimulate the thoughts and emotions of men.

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Aubin-Horth, Nadia, and Julian J. Dodson. "Impact of differential energy allocation in Atlantic salmon (Salmo salar) precocious males on otolithsomatic size proportionality: a longitudinal approach." Canadian Journal of Fisheries and Aquatic Sciences 59, no. 10 (October 1, 2002): 1575–83. http://dx.doi.org/10.1139/f02-124.

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We studied juvenile Atlantic salmon (Salmo salar) males that become precociously mature or not at age-1+ to test the hypothesis that differential energy allocation affects the relationship between otolith size and fish size and to validate the use of a back-calculation method to estimate size over 30 weeks. We used a longitudinal approach by repeatedly measuring marked fish and obtaining corresponding otolith radius measurements. Differential energy allocation of mature males did not affect the proportionality ratio between otolith and somatic size. Short-term otolith growth varied with short-term somatic growth, but only weakly with temperature. Some correlation coefficients of the covariation of otolith growth estimated over a longer time interval with somatic growth were significantly greater than the short-term estimate. For mature and immature males, back-calculated lengths accurately estimated the observed individual length on practically all occasions. These results indicate that back-calculation can be used to estimate size for Atlantic salmon with different energy allocation patterns. Variable strength of coupling of otolith and somatic growth depending on time interval suggests that these processes are completed on different time scales.

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Moncada, Ximena, Frédérique Pelsy, Didier Merdinoglu, and Patricio Hinrichsen. "Genetic diversity and geographical dispersal in grapevine clones revealed by microsatellite markers." Genome 49, no. 11 (November 2006): 1459–72. http://dx.doi.org/10.1139/g06-102.

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Intravarietal genetic diversification associated with geographical dispersal of a vegetatively propagated species was studied using grapevine Vitis vinifera L. ‘Cabernet Sauvignon’ as a model. Fifty-nine clonal samples obtained from 7 countries (France, Chile, Spain, Australia, Hungary, USA, and Italy) were analyzed using 84 microsatellite markers. Eighteen polymorphic microsatellite loci (21.4%) were detected, finding 22 different genotypes in the population analyzed with a genetic similarity of over 97%. The presence of chimeric clones was evidenced at locus VMC5g7 by means of a segregation analysis of descendants by self-pollination of a triallelic Chilean clone and by somatic embryogenesis analysis, showing a mutation in L2 cell layer. Only 2 clones (obtained from France and Australia) presented the ancestral genotype, and the most divergent genotype was exhibited by another French clone, which had accumulated 5 somatic mutations. The 2 largest populations considered (from France and Chile) showed a clear divergency in the polymorphisms detected. These antecedents enabled the tracing of geographical dispersal with a phylogenetic hypothesis supporting France as the center of origin of diversification of Cabernet Sauvignon. The results obtained could help to explain diversification processes in other grapevine cultivars. The possibility that this kind of genetic variability occurs in other vegetatively propagated species is discussed, focusing on possible fingerprinting applications.

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Steenbergen, Laura, Lorenza S. Colzato, and María J. Maraver. "Vagal signaling and the somatic marker hypothesis: The effect of transcutaneous vagal nerve stimulation on delay discounting is modulated by positive mood." International Journal of Psychophysiology 148 (February 2020): 84–92. http://dx.doi.org/10.1016/j.ijpsycho.2019.10.010.

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Marsit, Carmen J., E. Andres Houseman, Heather H. Nelson, and Karl T. Kelsey. "Genetic and Epigenetic Tumor Suppressor Gene Silencing Are Distinct Molecular Phenotypes Driven by Growth Promoting Mutations in Nonsmall Cell Lung Cancer." Journal of Cancer Epidemiology 2008 (2008): 1–8. http://dx.doi.org/10.1155/2008/215809.

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Both genetic and epigenetic alterations characterize human nonsmall cell lung cancer (NSCLC), but the biological processes that create or select these alterations remain incompletely investigated. Our hypothesis posits that a roughly reciprocal relationship between the propensity for promoter hypermethylation and a propensity for genetic deletion leads to distinct molecular phenotypes of lung cancer. To test this hypothesis, we examined promoter hypermethylation of 17 tumor suppressor genes, as a marker of epigenetic alteration propensity, and deletion events at the 3p21 region, as a marker of genetic alteration. To model the complex biology between these somatic alterations, we utilized an item response theory model. We demonstrated that tumors exhibiting LOH at greater than 30% of informative alleles in the 3p21 region have a significantly reduced propensity for hypermethylation. At the same time, tumors with activatingKRASmutations showed a significantly increased propensity for hypermethylation of the loci examined, a result similar to what has been observed in colon cancer. These data suggest that NSCLCs have distinct epigenetic or genetic alteration phenotypes acting upon tumor suppressor genes and that mutation of oncogenic growth promoting genes, such asKRAS, is associated with the epigenetic phenotype.

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Moreno, Aurora, and José Ramón Alameda. "Cognitive Mechanisms Underlying Risky Decision-Making. A Study of Patients with Alzheimer’s Dementia." European Journal of Investigation in Health, Psychology and Education 2, no. 2 (June 15, 2012): 67–76. http://dx.doi.org/10.1989/ejihpe.v2i2.15.

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Patients with mild dementia of Alzheimer’s type (DAT) use to present problems in decision making. Several studies have analyzed the cognitive functions in the process of decision making, especially in situations under ambiguity. One approach is the somatic marker hypothesis from the Iowa Gambling Task (IGT) and the Gambling Index (IG). One problem is the lack of specificity from IGT indicators, for this reason some hypotheses have been proposed in order to solve these deficiencies, i.e. the Prospective Valence Learning (PVL). In this study, we apply the IGT to 10 patients and 10 control subjects. We analyze the PVL parameter: loss aversion parameter (λ), shape parameter (α), recency parameter (A), consistency (c) and task development in function of advantageous choices. Our results show that control subjects’ performance is better than DAT´, nevertheless, in the first stages there are not differences, these appear in the two last blocks. Whit the PVL parameters we obtain differences in α and c, and, to a lesser extent, in λ. According to PVL parameters, DAT patients can be described as sensible at loss subjects who are more influenced by immediate choice and a very low level of consistence, what implies the use of random choice strategies.

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Moreno, Aurora, and José Ramón Alameda. "Cognitive Mechanisms Underlying Risky Decision-Making. A Study of Patients with Alzheimer’s Dementia." European Journal of Investigation in Health, Psychology and Education 2, no. 2 (June 15, 2012): 67–76. http://dx.doi.org/10.3390/ejihpe2020006.

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Patients with mild dementia of Alzheimer’s type (DAT) use to present problems in decision making. Several studies have analyzed the cognitive functions in the process of decision making, especially in situations under ambiguity. One approach is the somatic marker hypothesis from the Iowa Gambling Task (IGT) and the Gambling Index (IG). One problem is the lack of specificity from IGT indicators, for this reason some hypotheses have been proposed in order to solve these deficiencies, i.e. the Prospective Valence Learning (PVL). In this study, we apply the IGT to 10 patients and 10 control subjects. We analyze the PVL parameter: loss aversion parameter (λ), shape parameter (α), recency parameter (A), consistency (c) and task development in function of advantageous choices. Our results show that control subjects’ performance is better than DAT´, nevertheless, in the first stages there are not differences, these appear in the two last blocks. Whit the PVL parameters we obtain differences in α and c, and, to a lesser extent, in λ. According to PVL parameters, DAT patients can be described as sensible at loss subjects who are more influenced by immediate choice and a very low level of consistence, what implies the use of random choice strategies.

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Beer, Jennifer S. "Current Emotion Research in Social Neuroscience: How does emotion influence social cognition?" Emotion Review 9, no. 2 (January 31, 2017): 172–80. http://dx.doi.org/10.1177/1754073916650492.

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Neuroscience investigations of emotional influences on social cognition have been dominated by the somatic marker hypothesis and dual-process theories. Taken together, these lines of inquiry have not provided strong evidence that emotional influences on social cognition rely on neural systems which code for bodily signals of arousal nor distinguish emotional reasoning from other modes of reasoning. Recent findings raise the possibility that emotionally influenced social cognition relies on two stages of neural changes: once when emotion is elicited and a different set of changes at the time of social cognitive judgment. These findings suggest that affect infusion models may be a fruitful framework for bridging neuroscience and psychological understanding of the role of emotion in social cognition.

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Carmena, M., C. Gonzalez, J. Casal, and P. Ripoll. "Dosage dependence of maternal contribution to somatic cell division in Drosophila melanogaster." Development 113, no. 4 (December 1, 1991): 1357–64. http://dx.doi.org/10.1242/dev.113.4.1357.

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Most mitotic mutants in Drosophila do not lead to lethality in early development despite the highly abnormal chromosome behaviour that they elicit. This has been explained as being the effect of maternally provided wild-type products. We have tested this hypothesis by studying cuticular clones derived from cells in which there has been loss of a marked Y chromosome due to chromosome nondisjunction in individuals homozygous for the mutation abnormal spindle who are progeny of heterozygous mothers. We have found that the size and frequency of these clones are higher than in control flies. Furthermore, by analysing flies whose female parents have different doses of the asp+ gene, we have found that there is a correlation between the amount of maternally contributed asp+ product and the frequency and size of cuticular clones. We have also estimated the time in development when the first mitotic mistakes take place, i.e. the time when maternal products are no longer sufficient to carry out normal cell division.

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Enatescu, Ileana, Raluka Kalinovic, Catalina Giurgi-Oncu, Vladimir Poroch, Ioan Sorin Stratulat, Gabriela Vlad, Oana Neda-Stepan, et al. "Study on the Role of Inflammatory Markers and Type D Personality on Symptom Profiles and Severity in Patients with Major Depressive Disorder." Applied Sciences 10, no. 16 (August 13, 2020): 5615. http://dx.doi.org/10.3390/app10165615.

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The high rates of chronicity and recurrences account for the limited efficacy of current antidepressants, conceived based on the current neurobiological hypotheses, in reaching the full clinical and functional remission of major depressed (MDD) patients. We aimed to analyze the role of pro-inflammatory markers, C-reactive protein (CRP) and interleukin-6 (IL-6), respectively, and type D personality (TDP) on the depressive symptoms measured by the 17-item Hamilton Depression Rating Scale (HAM-D). The processed data are part of a prospective 8-weeks follow-up study conducted in 50 subjects with MDD referred to ‘Eduard Pamfil’ Psychiatric Clinic Timisoara. The presence of elevated pro-inflammatory markers in MDD patients with TDP has been significantly associated with higher somatic anxiety (p = 0.005) and somatic symptoms-general (p = 0.016) mean rank scores compared to their counterparts without significant inflammation. The combination of increased CRP and IL-6 levels were significantly correlated with higher impaired insight (p = 0.026) mean rank scores, additionally. The presence of a significant level of IL-6 has shown a significant effect of size (p = 0.023) on the severity of major depression at baseline. On the contrary, type D personality has not influenced the severity of depressive symptoms (p > 0.05). Inflammatory markers significantly impact the clinical profiles and symptoms severity of MDD patients.

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Martin, T., S. F. Duffy, D. A. Carson, and T. J. Kipps. "Evidence for somatic selection of natural autoantibodies." Journal of Experimental Medicine 175, no. 4 (April 1, 1992): 983–91. http://dx.doi.org/10.1084/jem.175.4.983.

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Natural autoantibodies are primarily immunoglobulin M (IgM) antibodies that bind to a variety of self-antigens, including self-IgG. Accounting for a large proportion of the early B cell repertoire, such polyspecific autoantibodies are speculated to contribute to the homeostasis and/or competence of the primary humoral immune system. Recent studies indicate that the leukemia cells from most patients with chronic lymphocytic leukemia (CLL) also express such IgM autoantibodies. Similarly, the leukemia cells from many CLL patients react with murine monoclonal antibodies (mAbs) specific for crossreactive idiotypes (CRIs) associated with human IgM autoantibodies. In particular, leukemic cells frequently react with G6, a mAb specific for an Ig heavy chain (H chain)-associated CRI, and/or with 17.109, a mAb that defines a kappa light chain (L chain)-associated CRI. Generated against IgM rheumatoid factor (RF) paraproteins, G6 and 17.109 each recognize a major CRI that is present in many IgM RF paraproteins. Furthermore, over 90% of the IgM paraproteins found to bear both H and L chain-associated CRIs also are found to have RF activity. Molecular characterization of these CRIs demonstrates that each is a serologic marker for expression of a highly conserved Ig V gene. As such, the frequent production of IgM polyspecific autoantibodies in CLL simply may reflect the frequent use of such highly conserved autoantibody-encoding Ig V genes with little or no somatic mutation. To test this hypothesis, we generated murine transfectomas to pair the 17.109-reactive kappa L chain of SMI, a 17.109/G6-reactive CLL population, with the Ig H chain of SMI or other G6-reactive leukemia cells or tonsillar lymphocytes. Cotransfection of vectors encoding the Ig H and L chains of SMI generated transfectomas that produce IgM kappa RF autoantibodies reactive with human IgG1 and IgG4. In contrast to G6/17.109-reactive IgM kappa RF Waldenstrom's paraproteins, the SMI IgM kappa also reacts with several other self-antigens, including myoglobin, actin, and ssDNA. However, cotransfection of the SMI L chain with a vector encoding any one of 10 different G6-reactive Ig H chains generated transfectomas that produce IgM kappa antibodies without detectable polyspecific autoantibody activity. These results indicate that polyspecific antiself-reactivity of G6/17.019-reactive Ig is dependent on the somatically generated Ig third complementarity determining region. Collectively, these studies imply that selection may be responsible for the frequent expression of polyspecific autoantibodies in CLL and early B cell ontogeny.

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Al Amri, Waleed S., Diana E. Baxter, Andrew M. Hanby, Lucy F. Stead, Eldo T. Verghese, James L. Thorne, and Thomas A. Hughes. "Identification of candidate mediators of chemoresponse in breast cancer through therapy-driven selection of somatic variants." Breast Cancer Research and Treatment 183, no. 3 (July 30, 2020): 607–16. http://dx.doi.org/10.1007/s10549-020-05836-7.

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Abstract Purpose More than a third of primary breast cancer patients are treated with cytotoxic chemotherapy, typically without guidance from predictive markers. Increased use of neoadjuvant chemotherapy provides opportunities for identification of molecules associated with treatment response, by comparing matched tumour samples before and after therapy. Our hypothesis was that somatic variants of increased prevalence after therapy promote resistance, while variants with reduced prevalence cause sensitivity. Methods We performed systematic analyses of matched pairs of cancer exomes from primary oestrogen receptor-positive/HER2-negative breast cancers (n = 6) treated with neoadjuvant epirubicin/cyclophosphamide. We identified candidate genes as mediators of chemotherapy response by consistent subclonal changes in somatic variant prevalence through therapy, predicted variant impact on gene function, and enrichment of specific functional pathways. Influence of candidate genes on breast cancer outcome was tested using publicly available breast cancer expression data (n = 1903). Results We identified 14 genes as the strongest candidate mediators of chemoresponse: TCHH, MUC17, ARAP2, FLG2, ABL1, CENPF, COL6A3, DMBT1, ITGA7, PLXNA1, S100PBP, SYNE1, ZFHX4, and CACNA1C. Genes contained somatic variants showing prevalence changes in up to 4 patients, with up to 3 being predicted as damaging. Genes coding for extra-cellular matrix components or related signalling pathways were significantly over-represented among variants showing prevalence changes. Expression of 5 genes (TCHH, ABL1, CENPF, S100PBP, and ZFHX4) was significantly associated with patient survival. Conclusions Genomic analysis of paired pre- and post-therapy samples resulting from neoadjuvant therapy provides a powerful method for identification of mediators of response. Genes we identified should be assessed as predictive markers or targets in chemo-sensitization.

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Journal articles on the topic 'Somatic Marker Hypothesi'

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