On March 23, 2010, President Barack Obama signed the Affordable Care Act (ACA) into law. Implicat... more On March 23, 2010, President Barack Obama signed the Affordable Care Act (ACA) into law. Implications of the ACA on mental health care for 9.7 million military active-duty, reserve, and family members and 22.2 million veterans, as well as 1.3 uninsured veterans, is reviewed in light of a major crisis. The authors trace historical roots of the ACA to the World War II generation and efforts to transform the mental health care system by implementing hard-won war trauma lessons. The authors posit 9 principles reflected in the ACA that represent unfulfilled generational war trauma lessons and potential transformation of the military and national mental health care systems.
Background: After extensive review of official military records, government investigations, and n... more Background: After extensive review of official military records, government investigations, and news media accounts, the authors provide the first-ever examination of repetitive mental health crises after every major American war since the 20 th century. Method: Compelling evidence of generational crises is established using direct testimony from credible first-hand sources, clearly indicating that over the past century American society has continued to replicate preventable mental health crises. Results: This has largely been caused by repetitive failure to learn from and improve upon lessons learned about the psychiatric effects of war. The authors identify ten super ordinate " foundational lessons " essential to meeting wartime needs. Conclusion: Antiquated medical dualism, dysfunctional organizational structure, and leadership ambivalence toward mental health services are believed to promulgate a culture of mental health stigma, discrimination, and disparity. The key to transforming military mental healthcare and ending the cycle is to adopt a contemporary holistic mind-body approach emphasizing full-parity with medical services.
An integrative neurobehavioral model for " compassion stress injury " is offered to explain the "... more An integrative neurobehavioral model for " compassion stress injury " is offered to explain the " double-edge sword " of empathy and inherent vulnerability of helping professionals and care-givers. One of the most strikingly robust, yet largely invisible scientific findings to emerge over the past decade is identifying the neurophysiological mechanisms enabling human beings to understand and feel what another is feeling. The compelling convergence of evidence from multidisciplinary lines of primary research and studies of paired-deficits has revealed that the phenomenon of human beings witnessing the pain and suffering of others is clearly associated with activation of neural structures used during first-hand experience. Moreover, it is now evident that a large part of the neural activation shared between self-and other-related experiences occurs automatically, outside the observer's conscious awareness or control. However, it is also well established that full blown human empathic capacity and altruistic behavior is regulated by neural pathways responsible for flexible consciously controlled actions of the observer. We review the history, prevalence, and etiological models of " compassion stress injury " such as burnout, secondary traumatic stress, vicarious traumatization, compassion fatigue, and empathic distress fatigue, along with implications of the neurobehavioral approach in future research.
A contiguous physical map was constructed from the Harvey ras-1 (HRAS1) gene to the 11p telomere.... more A contiguous physical map was constructed from the Harvey ras-1 (HRAS1) gene to the 11p telomere. The contig spans approximately 500 kb and is minimally composed of a telomere-containing YAC and P1 and cosmid clones. Included in the contig are 11 sequence-tagged sites derived from P1 and cosmid ends. Three genes were placed on the contig in the following order: telomere–ribonuclease/angiogenin inhibitor (RNH)–Harveyras-1(HRAS1)–HRAS1-related complex (HRC). Two novel tetranucleotide repeats (heterozygosity of 66 and 68%) and a complex CA repeat (heterozygosity of 78%) were isolated and characterized.
Page 1. Examining the Absence of a Gender EfSect on Abortion Attitudes: Is There Really No DifSer... more Page 1. Examining the Absence of a Gender EfSect on Abortion Attitudes: Is There Really No DifSerence? Bradley R. Hertel and Mark C. Russell, Virginia Polyiechnic Institute and State University Earlier research on attitudes ...
Journal of Strength and Conditioning Research, 2015
This study investigated changes in indices of acid-base balance during 120 minutes of simulated s... more This study investigated changes in indices of acid-base balance during 120 minutes of simulated soccer match-play that included a 30 min extra-time (ET) period. Eight English Premier League academy soccer players participated in a simulated soccer match that required varying intensities of intermittent exercise including 15 m sprints and soccer dribbling throughout. Blood samples were obtained prior to (i.e., baseline, pre-exercise) and throughout exercise (i.e., 15, 30, 45, 60, 75, 90, 105, 120 min), and at half-time. Sprint speeds over 15 m reduced in ET compared to the first (-0.39 ± 0.37 m[BULLET OPERATOR]s, -7 ± 6%, p = 0.021) but not the second half (-0.18 ± 0.25 m[BULLET OPERATOR]s, -3 ± 4%, p = 0.086). At 105 min, blood lactate concentrations reduced compared to the opening 30 min (-0.9 to -1.2 mmol·l, p < 0.05). Blood pH (-0.03 to -0.04 units), base excess (-0.95 to -1.48 mmol·l) and bicarbonate concentrations (-0.9 ± 0.8 mmol·l) were depressed at 120 min compared to 105 min, baseline and half-time (all p < 0.05). There were no significant correlations between changes in acid-base balance and sprint speed (all p > 0.05). Although the perturbations in acid-base balance during ET were statistically significant, the decreases in blood pH, lactate, base excess, and bicarbonate concentrations may not represent metabolic acidosis or impairments in buffering capacity that are likely to explain reduced physical performance. Further research is warranted to investigate mechanisms of fatigue during ET and to develop interventions that attenuate decrements in performance.
The Romano-Ward Long QT syndrome (RWLQTS) has been linked to 11p15.5 in several large families bu... more The Romano-Ward Long QT syndrome (RWLQTS) has been linked to 11p15.5 in several large families but demonstrates genetic heterogeneity, since in other families the RWLQTS phenotype is not linked to 11p15. To date, no recombinants between the H-Ras-1 locus and RWLQTS in families linked to 11p15 have been published. In a large family, we demonstrate linkage of RWLQTS to marker D11S932 on chromosome 11p15.4 with a LOD score of 3.14 (θ=0;90% penetrance). An unaffected individual and her two unaffected offspring inherited the affected haplotype for the H-ras-1 region telomeric to D11S932. All three have QTc measurements of ⤠0.40 seconds and no history of syncope, making the diagnosis of RWLQTS extremely unlikely. This suggests that, although the gene for the RWlQTS is linked to 11p15 in this family, a recombination event may have occurred that separated the RWLQTS gene from the affected H-ras-1 region haplotype. To investigate a possible telomeric recombination event, cosmids telomeric to H-ras-1 were isolated. A highly polymorphic, complex CA/CT repeat marker (78% heterozygosity) was characterized and its location telomeric to H-ras-1 verified by interphase FISH. The same three unaffected individuals had the affected allele for this marker, ruling our recombination telomeric to H-ras-1 but proximal to the new marker. As the most telemeric marker on 11p to date, this marker will aid the physical and genetic mapping of the 11p telomere. The potential recombination event in this family apparently excludes H-ras-1 as a candidate gene and may aid the localization of the RWLQTS gene linked to 11p15.5. However, it remains a possibility that another genetic locus on 11p15, in addition to the one near the H-ras-1 gene, can cause the RWLQTS phenotype. This is the first report of recombination between H-ras-1 and RWLQTS in a family linked to 11p15.
On March 23, 2010, President Barack Obama signed the Affordable Care Act (ACA) into law. Implicat... more On March 23, 2010, President Barack Obama signed the Affordable Care Act (ACA) into law. Implications of the ACA on mental health care for 9.7 million military active-duty, reserve, and family members and 22.2 million veterans, as well as 1.3 uninsured veterans, is reviewed in light of a major crisis. The authors trace historical roots of the ACA to the World War II generation and efforts to transform the mental health care system by implementing hard-won war trauma lessons. The authors posit 9 principles reflected in the ACA that represent unfulfilled generational war trauma lessons and potential transformation of the military and national mental health care systems.
Background: After extensive review of official military records, government investigations, and n... more Background: After extensive review of official military records, government investigations, and news media accounts, the authors provide the first-ever examination of repetitive mental health crises after every major American war since the 20 th century. Method: Compelling evidence of generational crises is established using direct testimony from credible first-hand sources, clearly indicating that over the past century American society has continued to replicate preventable mental health crises. Results: This has largely been caused by repetitive failure to learn from and improve upon lessons learned about the psychiatric effects of war. The authors identify ten super ordinate " foundational lessons " essential to meeting wartime needs. Conclusion: Antiquated medical dualism, dysfunctional organizational structure, and leadership ambivalence toward mental health services are believed to promulgate a culture of mental health stigma, discrimination, and disparity. The key to transforming military mental healthcare and ending the cycle is to adopt a contemporary holistic mind-body approach emphasizing full-parity with medical services.
An integrative neurobehavioral model for " compassion stress injury " is offered to explain the "... more An integrative neurobehavioral model for " compassion stress injury " is offered to explain the " double-edge sword " of empathy and inherent vulnerability of helping professionals and care-givers. One of the most strikingly robust, yet largely invisible scientific findings to emerge over the past decade is identifying the neurophysiological mechanisms enabling human beings to understand and feel what another is feeling. The compelling convergence of evidence from multidisciplinary lines of primary research and studies of paired-deficits has revealed that the phenomenon of human beings witnessing the pain and suffering of others is clearly associated with activation of neural structures used during first-hand experience. Moreover, it is now evident that a large part of the neural activation shared between self-and other-related experiences occurs automatically, outside the observer's conscious awareness or control. However, it is also well established that full blown human empathic capacity and altruistic behavior is regulated by neural pathways responsible for flexible consciously controlled actions of the observer. We review the history, prevalence, and etiological models of " compassion stress injury " such as burnout, secondary traumatic stress, vicarious traumatization, compassion fatigue, and empathic distress fatigue, along with implications of the neurobehavioral approach in future research.
A contiguous physical map was constructed from the Harvey ras-1 (HRAS1) gene to the 11p telomere.... more A contiguous physical map was constructed from the Harvey ras-1 (HRAS1) gene to the 11p telomere. The contig spans approximately 500 kb and is minimally composed of a telomere-containing YAC and P1 and cosmid clones. Included in the contig are 11 sequence-tagged sites derived from P1 and cosmid ends. Three genes were placed on the contig in the following order: telomere–ribonuclease/angiogenin inhibitor (RNH)–Harveyras-1(HRAS1)–HRAS1-related complex (HRC). Two novel tetranucleotide repeats (heterozygosity of 66 and 68%) and a complex CA repeat (heterozygosity of 78%) were isolated and characterized.
Page 1. Examining the Absence of a Gender EfSect on Abortion Attitudes: Is There Really No DifSer... more Page 1. Examining the Absence of a Gender EfSect on Abortion Attitudes: Is There Really No DifSerence? Bradley R. Hertel and Mark C. Russell, Virginia Polyiechnic Institute and State University Earlier research on attitudes ...
Journal of Strength and Conditioning Research, 2015
This study investigated changes in indices of acid-base balance during 120 minutes of simulated s... more This study investigated changes in indices of acid-base balance during 120 minutes of simulated soccer match-play that included a 30 min extra-time (ET) period. Eight English Premier League academy soccer players participated in a simulated soccer match that required varying intensities of intermittent exercise including 15 m sprints and soccer dribbling throughout. Blood samples were obtained prior to (i.e., baseline, pre-exercise) and throughout exercise (i.e., 15, 30, 45, 60, 75, 90, 105, 120 min), and at half-time. Sprint speeds over 15 m reduced in ET compared to the first (-0.39 ± 0.37 m[BULLET OPERATOR]s, -7 ± 6%, p = 0.021) but not the second half (-0.18 ± 0.25 m[BULLET OPERATOR]s, -3 ± 4%, p = 0.086). At 105 min, blood lactate concentrations reduced compared to the opening 30 min (-0.9 to -1.2 mmol·l, p < 0.05). Blood pH (-0.03 to -0.04 units), base excess (-0.95 to -1.48 mmol·l) and bicarbonate concentrations (-0.9 ± 0.8 mmol·l) were depressed at 120 min compared to 105 min, baseline and half-time (all p < 0.05). There were no significant correlations between changes in acid-base balance and sprint speed (all p > 0.05). Although the perturbations in acid-base balance during ET were statistically significant, the decreases in blood pH, lactate, base excess, and bicarbonate concentrations may not represent metabolic acidosis or impairments in buffering capacity that are likely to explain reduced physical performance. Further research is warranted to investigate mechanisms of fatigue during ET and to develop interventions that attenuate decrements in performance.
The Romano-Ward Long QT syndrome (RWLQTS) has been linked to 11p15.5 in several large families bu... more The Romano-Ward Long QT syndrome (RWLQTS) has been linked to 11p15.5 in several large families but demonstrates genetic heterogeneity, since in other families the RWLQTS phenotype is not linked to 11p15. To date, no recombinants between the H-Ras-1 locus and RWLQTS in families linked to 11p15 have been published. In a large family, we demonstrate linkage of RWLQTS to marker D11S932 on chromosome 11p15.4 with a LOD score of 3.14 (θ=0;90% penetrance). An unaffected individual and her two unaffected offspring inherited the affected haplotype for the H-ras-1 region telomeric to D11S932. All three have QTc measurements of ⤠0.40 seconds and no history of syncope, making the diagnosis of RWLQTS extremely unlikely. This suggests that, although the gene for the RWlQTS is linked to 11p15 in this family, a recombination event may have occurred that separated the RWLQTS gene from the affected H-ras-1 region haplotype. To investigate a possible telomeric recombination event, cosmids telomeric to H-ras-1 were isolated. A highly polymorphic, complex CA/CT repeat marker (78% heterozygosity) was characterized and its location telomeric to H-ras-1 verified by interphase FISH. The same three unaffected individuals had the affected allele for this marker, ruling our recombination telomeric to H-ras-1 but proximal to the new marker. As the most telemeric marker on 11p to date, this marker will aid the physical and genetic mapping of the 11p telomere. The potential recombination event in this family apparently excludes H-ras-1 as a candidate gene and may aid the localization of the RWLQTS gene linked to 11p15.5. However, it remains a possibility that another genetic locus on 11p15, in addition to the one near the H-ras-1 gene, can cause the RWLQTS phenotype. This is the first report of recombination between H-ras-1 and RWLQTS in a family linked to 11p15.
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Papers by Mark C Russell