9 results on '"Marissa Cross"'
Search Results
2. Heightened activity in social reward networks is associated with adolescents’ risky sexual behaviors
- Author
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Kristen L. Eckstrand, Sophia Choukas-Bradley, Arpita Mohanty, Marissa Cross, Nicholas B. Allen, Jennifer S. Silk, Neil P. Jones, and Erika E. Forbes
- Subjects
Neurophysiology and neuropsychology ,QP351-495 - Abstract
Adolescent sexual risk behavior can lead to serious health consequences, yet few investigations have addressed its neurodevelopmental mechanisms. Social neurocircuitry is postulated to underlie the development of risky sexual behavior, and response to social reward may be especially relevant. Typically developing adolescents (N = 47; 18M, 29F; 16.3 ± 1.4 years; 42.5% sexual intercourse experience) completed a social reward fMRI task and reported their sexual risk behaviors (e.g., lifetime sexual partners) on the Youth Risk Behavior Survey (YRBS). Neural response and functional connectivity to social reward were compared for adolescents with higher- and lower-risk sexual behavior. Adolescents with higher-risk sexual behaviors demonstrated increased activation in the right precuneus and the right temporoparietal junction during receipt of social reward. Adolescents with higher-risk sexual behaviors also demonstrated greater functional connectivity between the precuneus and the temporoparietal junction bilaterally, dorsal medial prefrontal cortex, and left anterior insula/ventrolateral prefrontal cortex. The greater activation and functional connectivity in self-referential, social reward, and affective processing regions among higher sexual risk adolescents underscores the importance of social influence underlying sexual risk behaviors. Furthermore, results suggest an orientation towards and sensitivity to social rewards among youth engaging in higher-risk sexual behavior, perhaps as a consequence of or vulnerability to such behavior. Keywords: Sexual risk, Sexual behavior, Adolescence, Social reward, Peers, Affective neuroscience
- Published
- 2017
- Full Text
- View/download PDF
3. Social and Non-social Reward Processing and Depressive Symptoms Among Sexual Minority Adolescents
- Author
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Kristen L. Eckstrand, Luis E. Flores Jr., Marissa Cross, Jennifer S. Silk, Nicholas B. Allen, Kati L. Healey, Michael P. Marshal, and Erika E. Forbes
- Subjects
depression ,adolescence ,social reward ,LGBT ,fMRI ,Neurosciences. Biological psychiatry. Neuropsychiatry ,RC321-571 - Abstract
Sexual minority adolescents (SMA) are more likely to suffer from depression, putatively through experiences of social stress and victimization interfering with processing of social reward. Alterations in neural reward networks, which develop during adolescence, confer risk for the development of depression. Employing both social and monetary reward fMRI tasks, this is the first neuroimaging study to examine function in reward circuitry as a potential mechanism of mental health disparities between SMA and heterosexual adolescents. Eight SMA and 38 heterosexual typically developing adolescents completed self-report measures of depression and victimization, and underwent fMRI during monetary and peer social reward tasks in which they received positive monetary or social feedback, respectively. Compared with heterosexual adolescents, SMA had greater interpersonal depressive symptoms and exhibited blunted neural responses to social, but not monetary, reward in socioaffective processing regions that are associated with depressive symptoms. Specifically, compared with heterosexual adolescents, SMA exhibited decreased activation in the right medial prefrontal cortex, left anterior insula (AI), and right temporoparietal junction (TPJ) in response to being liked. Lower response in the right TPJ was associated with greater interpersonal depressive symptoms. These results suggest that interpersonal difficulties and the underlying substrates of response to social reward (perhaps more so than response to monetary reward) may confer risk for development of depressive symptoms in SMA.
- Published
- 2019
- Full Text
- View/download PDF
4. Leukocyte cytokine responses in adult patients with mitochondrial DNA defects
- Author
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Kalpita R. Karan, Caroline Trumpff, Marissa Cross, Kristin M. Englestad, Anna L. Marsland, Peter McGuire, Michio Hirano, and Martin Picard
- Subjects
Lipopolysaccharides ,Mitochondrial Diseases ,Interleukin-6 ,DNA, Mitochondrial ,Article ,Dexamethasone ,Drug Discovery ,Leukocytes ,Animals ,Cytokines ,Humans ,Molecular Medicine ,Glucocorticoids ,Genetics (clinical) - Abstract
Patients with oxidative phosphorylation (OxPhos) defects causing mitochondrial diseases appear particularly vulnerable to infections. Although OxPhos defects modulate cytokine production in vitro and in animal models, little is known about how circulating leukocytes of patients with inherited mitochondrial DNA (mtDNA) defects respond to acute immune challenges. In a small cohort of healthy controls (n=21) and patients (n=12) with either the m.3243A>G mutation or single, large-scale mtDNA deletions, we examined: i) cytokine responses (IL-6, TNF-α, IL-1β) in response to acute lipopolysaccharide (LPS) exposure, and ii) sensitivity to the immunosuppressive effects of glucocorticoid signaling (dexamethasone) on cytokine production. In dose-response experiments to determine the half-maximal effective LPS concentration (EC50), relative to controls, leukocytes from patients with mtDNA deletions showed 74 - 79% lower responses for IL-6 and IL-1β (pIL-6=0.031, pIL-1β=0.009). Moreover, IL-6 response to LPS in presence of GC was also blunted in cells from patients with mtDNA deletions (pIL-6=0.006), but not in leukocytes from patients with the m.3243A>G mutation. Overall, these ex vivo data provide preliminary evidence that some systemic OxPhos defects may compromise immune cytokine responses and glucocorticoid sensitivity. Further work in larger cohorts is needed to define the nature of immune dysregulation in patients with mitochondrial disease, and their potential implications for disease phenotypes.
- Published
- 2022
5. OxPhos Dysfunction Causes Hypermetabolism and Reduces Lifespan in Cells and in Patients with Mitochondrial Diseases
- Author
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Gabriel Sturm, Kalpita R Karan, Anna Monzel, Balaji S Santhanam, Tanja Taivassalo, Céline Bris, Sarah A Ware, Marissa Cross, Atif Towheed, Albert Higgins-Chen, Meagan J McManus, Andres Cardenas, Jue Lin, Elissa S Epel, Shamima Rahman, John Vissing, Bruno Grassi, Morgan Levine, Steve Horvath, Ronald G Haller, Guy Lenaers, Douglas C Wallace, Marie-Pierre St-Onge, Saeed Tavazoie, Vincent Procaccio, Brett A Kaufman, Erin L Seifert, Michio Hirano, and Martin Picard
- Subjects
Mitochondrial DNA ,Mitochondrial disease ,Hypermetabolism ,medicine ,Integrated stress response ,Oxidative phosphorylation ,Epigenetics ,Hayflick limit ,Biology ,Bioinformatics ,medicine.disease ,Telomere - Abstract
Patients with primary mitochondrial diseases present with fatigue and multi-system disease, are often lean, and die prematurely, but the mechanistic basis for this clinical picture remains unclear. Integrating data from 17 cohorts of patients with mitochondrial diseases (n=690), we find that clinical mitochondrial disorders increase resting energy expenditure, a state termed hypermetabolism. In a longitudinal cellular model of primary patient-derived fibroblasts from multiple donors, we show that genetic and pharmacological disruptions of oxidative phosphorylation (OxPhos) similarly trigger increased energy consumption in a cell-autonomous manner, despite near-normal OxPhos coupling efficiency. Hypermetabolism is associated with mtDNA instability, activation of the integrated stress response, increased extracellular secretion of age-related cytokines and metabokines including GDF15, as well as an accelerated rate of telomere erosion and epigenetic aging, and a reduced Hayflick limit. Together with these dynamic measures, we have generated a longitudinal RNASeq and DNA methylation resource dataset, which reveals conserved, energetically demanding, genome-wide recalibrations in response to OxPhos dysfunction. The increased energetic cost of living, or hypermetabolism, in cells and organisms with OxPhos defects has important biological and clinical implications.
- Published
- 2021
6. Heightened activity in social reward networks is associated with adolescents’ risky sexual behaviors
- Author
-
Nicholas B. Allen, Arpita Mohanty, Neil P. Jones, Erika E. Forbes, Jennifer S. Silk, Marissa Cross, Sophia Choukas-Bradley, and Kristen L. Eckstrand
- Subjects
Male ,Ventrolateral prefrontal cortex ,Adolescent ,Sexual Behavior ,Cognitive Neuroscience ,Temporoparietal junction ,Affective neuroscience ,Article ,050105 experimental psychology ,Developmental psychology ,03 medical and health sciences ,Social support ,Risk-Taking ,0302 clinical medicine ,Reward ,medicine ,Humans ,0501 psychology and cognitive sciences ,Prefrontal cortex ,Social influence ,lcsh:QP351-495 ,05 social sciences ,Social Support ,Youth Risk Behavior Survey ,Sexual intercourse ,lcsh:Neurophysiology and neuropsychology ,medicine.anatomical_structure ,Adolescent Behavior ,Female ,Psychology ,psychological phenomena and processes ,030217 neurology & neurosurgery - Abstract
Adolescent sexual risk behavior can lead to serious health consequences, yet few investigations have addressed its neurodevelopmental mechanisms. Social neurocircuitry is postulated to underlie the development of risky sexual behavior, and response to social reward may be especially relevant. Typically developing adolescents (N = 47; 18M, 29F; 16.3 ± 1.4 years; 42.5% sexual intercourse experience) completed a social reward fMRI task and reported their sexual risk behaviors (e.g., lifetime sexual partners) on the Youth Risk Behavior Survey (YRBS). Neural response and functional connectivity to social reward were compared for adolescents with higher- and lower-risk sexual behavior. Adolescents with higher-risk sexual behaviors demonstrated increased activation in the right precuneus and the right temporoparietal junction during receipt of social reward. Adolescents with higher-risk sexual behaviors also demonstrated greater functional connectivity between the precuneus and the temporoparietal junction bilaterally, dorsal medial prefrontal cortex, and left anterior insula/ventrolateral prefrontal cortex. The greater activation and functional connectivity in self-referential, social reward, and affective processing regions among higher sexual risk adolescents underscores the importance of social influence underlying sexual risk behaviors. Furthermore, results suggest an orientation towards and sensitivity to social rewards among youth engaging in higher-risk sexual behavior, perhaps as a consequence of or vulnerability to such behavior. Keywords: Sexual risk, Sexual behavior, Adolescence, Social reward, Peers, Affective neuroscience
- Published
- 2017
7. Social and Non-social Reward Processing and Depressive Symptoms Among Sexual Minority Adolescents
- Author
-
Erika E. Forbes, Kristen L. Eckstrand, Nicholas B. Allen, Kati L. Healey, Marissa Cross, Michael P. Marshal, Jennifer S. Silk, and Luis E. Flores
- Subjects
Cognitive Neuroscience ,Temporoparietal junction ,Interpersonal communication ,lcsh:RC321-571 ,03 medical and health sciences ,Behavioral Neuroscience ,0302 clinical medicine ,5. Gender equality ,medicine ,Prefrontal cortex ,lcsh:Neurosciences. Biological psychiatry. Neuropsychiatry ,Depression (differential diagnoses) ,Original Research ,030304 developmental biology ,Social stress ,0303 health sciences ,LGBT ,fMRI ,social reward ,SMA ,Mental health ,Sexual minority ,Neuropsychology and Physiological Psychology ,medicine.anatomical_structure ,depression ,adolescence ,Psychology ,psychological phenomena and processes ,030217 neurology & neurosurgery ,Clinical psychology - Abstract
Sexual minority adolescents (SMA) are more likely to suffer from depression, putatively through experiences of social stress and victimization interfering with processing of social reward. Alterations in neural reward networks, which develop during adolescence, confer risk for the development of depression. Employing both social and monetary reward fMRI tasks, this is the first neuroimaging study to examine function in reward circuitry as a potential mechanism of mental health disparities between SMA and heterosexual adolescents. Eight SMA and 38 heterosexual typically developing adolescents completed self-report measures of depression and victimization, and underwent fMRI during monetary and peer social reward tasks in which they received positive monetary or social feedback, respectively. Compared with heterosexual adolescents, SMA had greater interpersonal depressive symptoms and exhibited blunted neural responses to social, but not monetary, reward in socioaffective processing regions that are associated with depressive symptoms. Specifically, compared with heterosexual adolescents, SMA exhibited decreased activation in the right medial prefrontal cortex, left anterior insula (AI), and right temporoparietal junction (TPJ) in response to being liked. Lower response in the right TPJ was associated with greater interpersonal depressive symptoms. These results suggest that interpersonal difficulties and the underlying substrates of response to social reward (perhaps more so than response to monetary reward) may confer risk for development of depressive symptoms in SMA.
- Published
- 2019
8. 4.20 Heightened Activity in Social Reward Networks Is Associated With Adolescents’ Risky Sexual Behaviors
- Author
-
Jennifer S. Silk, Marissa Cross, Neil P. Jones, Kristen L. Eckstrand, Sophia Choukas-Bradley, Nicholas B. Allen, and Erika E. Forbes
- Subjects
Psychiatry and Mental health ,Reward dependence ,Sexual behavior ,Developmental and Educational Psychology ,Psychology ,Social psychology - Published
- 2017
9. The cytotoxic effects of estradiol-17 beta, catecholestradiols and methoxyestradiols on dividing MCF-7 and HeLa cells
- Author
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J.C. Seegers, Casper H. van Aswegen, Mona-Liza Aveling, Willem S. Joubert, Marissa Cross, and Francois Koch
- Subjects
Metabolite ,Fluorescence spectrometry ,Biology ,Hydroxylation ,Biochemistry ,HeLa ,chemistry.chemical_compound ,Endocrinology ,Tubulin ,Mitotic Index ,Cytotoxic T cell ,Humans ,Metaphase ,Benzoflavones ,Quinalizarin ,Estradiol ,biology.organism_classification ,Molecular biology ,Immunohistochemistry ,Estrogens, Catechol ,chemistry ,Cell culture ,Multipolar spindles ,Cell Division ,HeLa Cells - Abstract
In this study the cytotoxic effects of high concentrations (greater than or equal to 1 x 10(-6) M) of estradiol-17 beta (E2), 2-/4-hydroxyestradiol-17 beta (2-/4-OHE2) and 2-/3-/4-methoxyestradiol-17 beta (2-/3-/4-MeOE2) were determined on dividing MCF-7 and HeLa cells. The 2-MeOE2 metabolite followed by 2-OHE2 and E2 (in this order) proved to be extremely toxic to dividing MCF-7 and HeLa cells. The cytotoxic effect on these cells comprised uneven chromosome distribution. Indirect immunofluorescent studies, in which monoclonal anti-alpha-tubulin antibodies were used, showed that these compounds (2-MeOE2 greater than 2-OHE2 greater than E2) at high concentrations caused abnormal and fragmented polar formations as well as disorientated microtubule arrangement in the dividing MCF-7 and HeLa cells. The 4-OHE2 and 3-/4-MeOE2 metabolites had little or no cytotoxic effects on dividing cells. The large number of abnormal metaphases seen in HeLa cells exposed to 2-MeOE2 suggested that this metabolite may be the ultimate cytotoxic compound. The reduction in the number of HeLa cells with abnormal metaphase configurations after exposure to 2-OHE2 plus quinalizarin (an inhibitor of catechol-O-methyltransferase) indicated that the production of 2-MeOE2 is necessary for the formation of abnormal spindles in metaphase. Quinalizarin treatment in the presence of 2-MeOE2 had no effect on the large number of abnormal metaphases. We therefore conclude that neither E2 nor 2-OHE2, but a high concentration of 2-MeOE2 is responsible for abnormal spindle formation. In additional experiments the number of normal and abnormal dividing HeLa cells were greatly reduced when simultaneously exposed to E2 and 2-/4-hydroxylase-inhibitor alpha-naphthoflavone.
- Published
- 1989
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