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Roger K. Pitman - One of the best experts on this subject based on the ideXlab platform.
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Subtle neurologic compromise as a Vulnerability Factor for combat-related posttraumatic stress disorder: results of a twin study.
Archives of general psychiatry, 2006Co-Authors: Tamara V. Gurvits, Linda J. Metzger, Natasha B. Lasko, Paul A. Cannistraro, Alexandra S. Tarhan, Mark W. Gilbertson, Scott P. Orr, Anna M. Charbonneau, Michelle M. Wedig, Roger K. PitmanAbstract:Previous studies have demonstrated subtle neurologic dysfunction in chronic posttraumatic stress disorder (PTSD) manifest as increased neurologic soft signs (NSSs). The origin of this dysfunction is undetermined. To resolve competing origins of increased NSSs in PTSD, namely, preexisting Vulnerability Factor vs acquired PTSD sign. Case-control study of identical twins. A Veterans Affairs and academic medical center (ambulatory). A convenience sample of male Vietnam veteran twins with (n = 25) and without (n = 24) PTSD and their combat-unexposed identical (monozygotic) co-twins. Neurologic examination for 45 NSSs. Average scores for 45 NSSs, each scored on an ordinal scale from 0 to 3, masked to diagnosis and combat exposure status. There was a significant between-pair main effect of PTSD diagnosis (as determined in the combat-exposed twin) on average NSS score in the absence of a significant combat exposure main effect or diagnosis x exposure interaction. Combat veterans with PTSD had significantly higher NSS scores than combat veterans without PTSD. The "high-risk," unexposed co-twins of the former also had significantly higher NSS scores than the "low-risk," unexposed co-twins of the latter. This result could not be explained by age, number of potentially traumatic lifetime noncombat events, alcoholism, or the presence of a comorbid affective or anxiety disorder. The average NSS score in unexposed co-twins was not significantly associated with combat severity in combat-exposed twins. These results replicate previous findings of increased NSSs in Vietnam combat veterans with PTSD. Furthermore, results from their combat-unexposed identical co-twins support the conclusion that subtle neurologic dysfunction in PTSD is not acquired along with the trauma or PTSD but rather represents an antecedent familial Vulnerability Factor for developing chronic PTSD on exposure to a traumatic event.
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subtle neurologic compromise as a Vulnerability Factor for combat related posttraumatic stress disorder results of a twin study
Archives of General Psychiatry, 2006Co-Authors: Tamara V. Gurvits, Linda J. Metzger, Natasha B. Lasko, Paul A. Cannistraro, Alexandra S. Tarhan, Mark W. Gilbertson, Scott P. Orr, Anna M. Charbonneau, Michelle M. Wedig, Roger K. PitmanAbstract:Context Previous studies have demonstrated subtle neurologic dysfunction in chronic posttraumatic stress disorder (PTSD) manifest as increased neurologic soft signs (NSSs). The origin of this dysfunction is undetermined. Objective To resolve competing origins of increased NSSs in PTSD, namely, preexisting Vulnerability Factor vs acquired PTSD sign. Design Case-control study of identical twins. Setting A Veterans Affairs and academic medical center (ambulatory). Participants A convenience sample of male Vietnam veteran twins with (n = 25) and without (n = 24) PTSD and their combat-unexposed identical (monozygotic) co-twins. Interventions Neurologic examination for 45 NSSs. Main Outcome Measure Average scores for 45 NSSs, each scored on an ordinal scale from 0 to 3, masked to diagnosis and combat exposure status. Results There was a significant between-pair main effect of PTSD diagnosis (as determined in the combat-exposed twin) on average NSS score in the absence of a significant combat exposure main effect or diagnosis × exposure interaction. Combat veterans with PTSD had significantly higher NSS scores than combat veterans without PTSD. The “high-risk,” unexposed co-twins of the former also had significantly higher NSS scores than the “low-risk,” unexposed co-twins of the latter. This result could not be explained by age, number of potentially traumatic lifetime noncombat events, alcoholism, or the presence of a comorbid affective or anxiety disorder. The average NSS score in unexposed co-twins was not significantly associated with combat severity in combat-exposed twins. Conclusions These results replicate previous findings of increased NSSs in Vietnam combat veterans with PTSD. Furthermore, results from their combat-unexposed identical co-twins support the conclusion that subtle neurologic dysfunction in PTSD is not acquired along with the trauma or PTSD but rather represents an antecedent familial Vulnerability Factor for developing chronic PTSD on exposure to a traumatic event.
Michael R. Irwin - One of the best experts on this subject based on the ideXlab platform.
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preexisting mild sleep disturbance as a Vulnerability Factor for inflammation induced depressed mood a human experimental study
Translational Psychiatry, 2016Co-Authors: Hyong Jin Cho, Naomi I. Eisenberger, Richard G. Olmstead, Elizabeth C Breen, Michael R. IrwinAbstract:Sleep disturbance and depression are common, particularly in females, and sleep disturbance is a well-known risk Factor for depression. Systemic inflammation has been suggested as a potential mechanism of this association. This study examined whether preexisting sleep disturbance acted as a Vulnerability Factor for depressed mood induced by an inflammatory challenge in healthy females vs males. In a randomized double-blind placebo-controlled design, volunteers aged 18-50 (N = 111; 67 females) were assigned to placebo or low-dose endotoxin. Before substance administration, sleep disturbance was assessed using the Pittsburgh Sleep Quality Index and dichotomized using median split (⩾ 3 vs < 3). Self-reported depressed mood (profile of mood states) and circulating proinflammatory cytokines (interleukin-6, tumor necrosis Factor-α) were repeatedly assessed over 6 h. Among females, moderation of depressed mood by sleep disturbance was significant even after adjustment for covariates (X(2) = 12.73, df = 6, P < 0.05). There was a robust time-by-condition interaction in females with sleep disturbance (X(2) = 26.22, df = 6, P < 0.001), but not in females without sleep disturbance (X(2) = 8.65, df = 6, P = 0.19). Although cytokines increased equally in all females, the correlations between cytokines and depressed mood were significantly stronger in females with sleep disturbance. Among males, no moderating effect of sleep disturbance was observed. Inflammation-induced depressed mood was considerably more severe among females reporting mild sleep disturbance compared with those reporting no sleep disturbance, suggesting that even mild sleep disturbance may increase Vulnerability for inflammation-induced depression in females. Furthermore, sleep disturbance appears to increase the Vulnerability to depression by augmenting affective sensitivity to cytokines rather than by enhancing cytokine responses to inflammatory challenge in females.
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Mild sleep disturbance as a Vulnerability Factor for inflammation-induced depressed mood in women: An experimental study
Brain Behavior and Immunity, 2015Co-Authors: Hyong Jin Cho, Naomi I. Eisenberger, Steve W. Cole, Richard G. Olmstead, A. Avidan, Michael R. IrwinAbstract:Sleep disturbance and depression are major public health burdens, particularly in women, and sleep disturbance is a well-known risk Factor for depression. Systemic inflammation has been suggested as a potential mechanism of this association. This study examined whether self-reported sleep disturbance acted as a Vulnerability Factor for inflammation-induced depression among healthy women. Healthy women aged 18–50 (N = 67) were randomly assigned to receive either placebo or low-dose endotoxin (0.8 ng/kg). Self-reported depressed mood was repeatedly assessed over 6 h. Participants exposed to endotoxin, compared with placebo, showed greater increases in depressed mood over time according to mixed-effects model regression (X2 = 28.35, df = 6, p = 0.0001). To examine whether sleep disturbance enhances depressive responses to endotoxin, moderation was tested for sleep disturbance assessed using the Pittsburgh Sleep Quality Index (PSQI) as a binary variable using median split (PSQI global score ≥3 vs.
Stewart A. Shankman - One of the best experts on this subject based on the ideXlab platform.
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reactivity to uncertain threat as a familial Vulnerability Factor for alcohol use disorder
Psychological Medicine, 2016Co-Authors: Stephanie M. Gorka, Danelle Hee, Lynne Lieberman, Vijay A. Mittal, Kinh Luan Phan, Stewart A. ShankmanAbstract:Background When sober, problematic drinkers display exaggerated reactivity to threats that are uncertain (U-threat). Since this aversive affective state can be alleviated via acute alcohol intoxication, it has been posited that individuals who exhibit heightened reactivity to U-threat at baseline are motivated to use alcohol as a means of avoidance-based coping, setting the stage for excessive drinking. To date, however, no study has attempted to characterize the dispositional nature of exaggerated reactivity to U-threat and test whether it is a Vulnerability Factor or exclusively a disease marker of problematic alcohol use. Method The current investigation utilized a family study design to address these gaps by examining whether (1) reactivity to U-threat is associated with risk for problematic alcohol use, defined by family history of alcohol use disorder (AUD) and (2) reactivity to U-threat is correlated amongst adult biological siblings. A total of 157 families, and 458 individuals, participated in the study and two biological siblings completed a threat-of-shock task designed to probe reactivity to U-threat and predictable threat (P-threat). Startle potentiation was collected as an index of aversive responding. Results Within biological siblings, startle potentiation to U-threat [intraclass correlation (ICC) = 0.35] and P-threat (ICC = 0.63) was significantly correlated. In addition, independent of an individuals’ own AUD status, startle potentiation to U-threat, but not P-threat, was positively associated with risk for AUD (i.e. AUD family history). Conclusion This suggests that heightened reactivity to U-threat may be a familial Vulnerability Factor for problematic drinking and a novel prevention target for AUD.
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Reactivity to uncertain threat as a familial Vulnerability Factor for alcohol use disorder.
Psychological medicine, 2016Co-Authors: Stephanie M. Gorka, Danelle Hee, Lynne Lieberman, Vijay A. Mittal, Kinh Luan Phan, Stewart A. ShankmanAbstract:When sober, problematic drinkers display exaggerated reactivity to threats that are uncertain (U-threat). Since this aversive affective state can be alleviated via acute alcohol intoxication, it has been posited that individuals who exhibit heightened reactivity to U-threat at baseline are motivated to use alcohol as a means of avoidance-based coping, setting the stage for excessive drinking. To date, however, no study has attempted to characterize the dispositional nature of exaggerated reactivity to U-threat and test whether it is a Vulnerability Factor or exclusively a disease marker of problematic alcohol use. The current investigation utilized a family study design to address these gaps by examining whether (1) reactivity to U-threat is associated with risk for problematic alcohol use, defined by family history of alcohol use disorder (AUD) and (2) reactivity to U-threat is correlated amongst adult biological siblings. A total of 157 families, and 458 individuals, participated in the study and two biological siblings completed a threat-of-shock task designed to probe reactivity to U-threat and predictable threat (P-threat). Startle potentiation was collected as an index of aversive responding. Within biological siblings, startle potentiation to U-threat [intraclass correlation (ICC) = 0.35] and P-threat (ICC = 0.63) was significantly correlated. In addition, independent of an individuals' own AUD status, startle potentiation to U-threat, but not P-threat, was positively associated with risk for AUD (i.e. AUD family history). This suggests that heightened reactivity to U-threat may be a familial Vulnerability Factor for problematic drinking and a novel prevention target for AUD.
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blunted neural response to rewards as a Vulnerability Factor for depression results from a family study
Journal of Abnormal Psychology, 2015Co-Authors: Anna Weinberg, Huiting Liu, Greg Hajcak, Stewart A. ShankmanAbstract:Depressive disorders are associated with significant economic and public health burdens as well as increased morbidity. Yet, perhaps due to the heterogeneous nature of the disease, prevention and intervention efforts are only moderately efficacious. A better understanding of core mechanisms of depressive disorders might aid in the development of more targeted intervention, and perhaps help identify individuals at risk. One mechanism that may be particularly important to depressive phenotypes is reward insensitivity. Examination of neurobiological correlates of reward-processing, which should relate more directly to the neuropathology of depression, may be helpful in identifying liability for the disorder. To that end, we used a family study design to examine whether a neural response to rewards is a familial risk Factor for depression in a sample of probands with a wide range of internalizing psychopathology, as well as their biological siblings. Event-related potentials were recorded during a simple forced-choice gambling paradigm, in which participants could either win or lose small amounts of money. Lower levels of positive affect in probands predicted a reduced neural response to rewards in siblings, even over and above the sibling's own level of positive and negative affect. Additionally, the neural response to rewards was familial (i.e., correlated among siblings). Combined, these analyses suggest that a blunted neural response to rewards may be useful in identifying individuals vulnerable to depressive illnesses.
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Is risk-taking propensity a familial Vulnerability Factor for alcohol use? An examination in two independent samples.
Journal of psychiatric research, 2015Co-Authors: Stephanie M. Gorka, Huiting Liu, Daniel N. Klein, Stacey B. Daughters, Stewart A. ShankmanAbstract:Research indicates that increased risk-taking propensity (RTP) is associated with higher alcohol use. There is also some evidence to suggest that it is not just a state Factor or 'scar,' but instead a Vulnerability Factor. If this is the case, increased RTP should be evident in healthy individuals that are at risk for alcohol use. To date, few studies have examined whether RTP is a familial Vulnerability Factor and thus, the aim of the current study was to test whether RTP aggregates within families and if increased RTP is evident in biological family members at risk for alcohol use. Sample 1 included 87 biological, adult sibling pairs and Sample 2 included 111 biological mother and adolescent dyads (total N = 396). All participants completed a behavioral measure of RTP and were assessed for alcohol use. Results in both samples were strikingly consistent. In Sample 1, RTP was correlated among siblings and greater frequency of proband alcohol use predicted greater sibling RTP, over and above sibling alcohol use. In Sample 2, RTP was correlated among mothers and their offspring and greater maternal alcohol use problems predicted greater adolescent RTP over and above adolescent substance use. Together, these findings suggest that RTP may be a familial Vulnerability Factor for alcohol use as it aggregates within families and is increased in relatives of individuals with higher levels of alcohol use.
Simha Sethumadhavan - One of the best experts on this subject based on the ideXlab platform.
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ISCA - Side-channel Vulnerability Factor: a metric for measuring information leakage
ACM SIGARCH Computer Architecture News, 2012Co-Authors: John Demme, Robert Martin, Adam Waksman, Simha SethumadhavanAbstract:There have been many attacks that exploit side-effects of program execution to expose secret information and many proposed countermeasures to protect against these attacks. However there is currently no systematic, holistic methodology for understanding information leakage. As a result, it is not well known how design decisions affect information leakage or the Vulnerability of systems to side-channel attacks. In this paper, we propose a metric for measuring information leakage called the Side-channel Vulnerability Factor (SVF). SVF is based on our observation that all side-channel attacks ranging from physical to microarchitectural to software rely on recognizing leaked execution patterns. SVF quantifies patterns in attackers' observations and measures their correlation to the victim's actual execution patterns and in doing so captures systems' Vulnerability to side-channel attacks. In a detailed case study of on-chip memory systems, SVF measurements help expose unexpected vulnerabilities in whole-system designs and shows how designers can make performance-security trade-offs. Thus, SVF provides a quantitative approach to secure computer architecture.
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Side-channel Vulnerability Factor: A metric for measuring information leakage
Proceedings - International Symposium on Computer Architecture, 2012Co-Authors: John Demme, Robert Martin, Adam Waksman, Simha SethumadhavanAbstract:There have been many attacks that exploit side-effects of program execution to expose secret information and many proposed countermeasures to protect against these attacks. However there is currently no systematic, holistic method- ology for understanding information leakage. As a result, it is not well known how design decisions affect informa- tion leakage or the Vulnerability of systems to side-channel attacks. In this paper, we propose a metric for measuring information leakage called the Side-channel Vulnerability Fac- tor (SVF). SVF is based on our observation that all side- channel attacks ranging from physical to microarchitectural to software rely on recognizing leaked execution patterns. SVF quantifies patterns in attackers’ observations and mea- sures their correlation to the victim’s actual execution pat- terns and in doing so captures systems’ Vulnerability to side-channel attacks. \\ In a detailed case study of on-chip memory systems, SVF measurements help expose unexpected vulnerabilities in whole-system designs and shows how designers can make performance-security trade-offs. Thus, SVF provides a quantitative approach to secure computer architecture.
Tamara V. Gurvits - One of the best experts on this subject based on the ideXlab platform.
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Subtle neurologic compromise as a Vulnerability Factor for combat-related posttraumatic stress disorder: results of a twin study.
Archives of general psychiatry, 2006Co-Authors: Tamara V. Gurvits, Linda J. Metzger, Natasha B. Lasko, Paul A. Cannistraro, Alexandra S. Tarhan, Mark W. Gilbertson, Scott P. Orr, Anna M. Charbonneau, Michelle M. Wedig, Roger K. PitmanAbstract:Previous studies have demonstrated subtle neurologic dysfunction in chronic posttraumatic stress disorder (PTSD) manifest as increased neurologic soft signs (NSSs). The origin of this dysfunction is undetermined. To resolve competing origins of increased NSSs in PTSD, namely, preexisting Vulnerability Factor vs acquired PTSD sign. Case-control study of identical twins. A Veterans Affairs and academic medical center (ambulatory). A convenience sample of male Vietnam veteran twins with (n = 25) and without (n = 24) PTSD and their combat-unexposed identical (monozygotic) co-twins. Neurologic examination for 45 NSSs. Average scores for 45 NSSs, each scored on an ordinal scale from 0 to 3, masked to diagnosis and combat exposure status. There was a significant between-pair main effect of PTSD diagnosis (as determined in the combat-exposed twin) on average NSS score in the absence of a significant combat exposure main effect or diagnosis x exposure interaction. Combat veterans with PTSD had significantly higher NSS scores than combat veterans without PTSD. The "high-risk," unexposed co-twins of the former also had significantly higher NSS scores than the "low-risk," unexposed co-twins of the latter. This result could not be explained by age, number of potentially traumatic lifetime noncombat events, alcoholism, or the presence of a comorbid affective or anxiety disorder. The average NSS score in unexposed co-twins was not significantly associated with combat severity in combat-exposed twins. These results replicate previous findings of increased NSSs in Vietnam combat veterans with PTSD. Furthermore, results from their combat-unexposed identical co-twins support the conclusion that subtle neurologic dysfunction in PTSD is not acquired along with the trauma or PTSD but rather represents an antecedent familial Vulnerability Factor for developing chronic PTSD on exposure to a traumatic event.
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subtle neurologic compromise as a Vulnerability Factor for combat related posttraumatic stress disorder results of a twin study
Archives of General Psychiatry, 2006Co-Authors: Tamara V. Gurvits, Linda J. Metzger, Natasha B. Lasko, Paul A. Cannistraro, Alexandra S. Tarhan, Mark W. Gilbertson, Scott P. Orr, Anna M. Charbonneau, Michelle M. Wedig, Roger K. PitmanAbstract:Context Previous studies have demonstrated subtle neurologic dysfunction in chronic posttraumatic stress disorder (PTSD) manifest as increased neurologic soft signs (NSSs). The origin of this dysfunction is undetermined. Objective To resolve competing origins of increased NSSs in PTSD, namely, preexisting Vulnerability Factor vs acquired PTSD sign. Design Case-control study of identical twins. Setting A Veterans Affairs and academic medical center (ambulatory). Participants A convenience sample of male Vietnam veteran twins with (n = 25) and without (n = 24) PTSD and their combat-unexposed identical (monozygotic) co-twins. Interventions Neurologic examination for 45 NSSs. Main Outcome Measure Average scores for 45 NSSs, each scored on an ordinal scale from 0 to 3, masked to diagnosis and combat exposure status. Results There was a significant between-pair main effect of PTSD diagnosis (as determined in the combat-exposed twin) on average NSS score in the absence of a significant combat exposure main effect or diagnosis × exposure interaction. Combat veterans with PTSD had significantly higher NSS scores than combat veterans without PTSD. The “high-risk,” unexposed co-twins of the former also had significantly higher NSS scores than the “low-risk,” unexposed co-twins of the latter. This result could not be explained by age, number of potentially traumatic lifetime noncombat events, alcoholism, or the presence of a comorbid affective or anxiety disorder. The average NSS score in unexposed co-twins was not significantly associated with combat severity in combat-exposed twins. Conclusions These results replicate previous findings of increased NSSs in Vietnam combat veterans with PTSD. Furthermore, results from their combat-unexposed identical co-twins support the conclusion that subtle neurologic dysfunction in PTSD is not acquired along with the trauma or PTSD but rather represents an antecedent familial Vulnerability Factor for developing chronic PTSD on exposure to a traumatic event.
