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Office of Neuroscience Research > Resources and Facilities > WUSTL Neuroscience Publications for the week

WUSTL Neuroscience Publications for the week

 

The publications below include authors at Washington University and were identified by Scopus search.  These are the most current publications.  For previous lists, visit the WUSTL Neuroscience publications archive.

June 11, 2018 

1) 

Voet, S.a b , Mc Guire, C.a b c d , Hagemeyer, N.e , Martens, A.a b , Schroeder, A.f g , Wieghofer, P.e n , Daems, C.h , Staszewski, O.e , Walle, L.V.a i , Jordao, M.J.C.e , Sze, M.a b , Vikkula, H.-K.a b , Demeestere, D.a b , Van Imschoot, G.a b , Scott, C.L.a b , Hoste, E.a b , Gonçalves, A.a b j , Guilliams, M.a b , Lippens, S.a b j , Libert, C.a b , Vandenbroucke, R.E.a b , Kim, K.-W.k o , Jung, S.k , Callaerts-Vegh, Z.l , Callaerts, P.h , De Wit, J.f g , Lamkanfi, M.a i , Prinz, M.e m , Van Loo, G.a b
A20 critically controls microglia activation and inhibits inflammasome-dependent neuroinflammation
(2018) Nature Communications, 9 (1), art. no. 2036, . 


a VIB Center for Inflammation Research, Ghent, Belgium
b Department of Biomedical Molecular Biology, Ghent University, Ghent, Belgium
c VIB Center for Medical Biotechnology, Ghent, Belgium
d Department of Biochemistry and Microbiology, Ghent University, Ghent, Belgium
e Institute of Neuropathology, Faculty of Medicine, University of Freiburg, Freiburg, Germany
f VIB Center for Brain and Disease Research, Leuven, Belgium
g Department of Neurosciences, KU Leuven, Leuven, Belgium
h Department of Human Genetics, KU Leuven, Leuven, Belgium
i Department of Internal Medicine, Ghent University, Ghent, Belgium
j VIB Bio-Imaging Core, Ghent, Belgium
k Department of Immunology, Weizmann Institute of Science, Rehovot, Israel
l Laboratory of Biological Psychology, KU Leuven, Leuven, Belgium
m BIOSS Centre for Biological Signalling Studies, University of Freiburg, Freiburg, Germany
n Institute of Anatomy, University of Leipzig, Leipzig, Germany
o Department of Pathology and Immunology, Washington University of Medicine, St. Louis, MO, United States


Abstract
Microglia, the mononuclear phagocytes of the central nervous system (CNS), are important for the maintenance of CNS homeostasis, but also critically contribute to CNS pathology. Here we demonstrate that the nuclear factor kappa B (NF-κB) regulatory protein A20 is crucial in regulating microglia activation during CNS homeostasis and pathology. In mice, deletion of A20 in microglia increases microglial cell number and affects microglial regulation of neuronal synaptic function. Administration of a sublethal dose of lipopolysaccharide induces massive microglia activation, neuroinflammation, and lethality in mice with microglia-confined A20 deficiency. Microglia A20 deficiency also exacerbates multiple sclerosis (MS)-like disease, due to hyperactivation of the Nlrp3 inflammasome leading to enhanced interleukin-1β secretion and CNS inflammation. Finally, we confirm a Nlrp3 inflammasome signature and IL-1β expression in brain and cerebrospinal fluid from MS patients. Collectively, these data reveal a critical role for A20 in the control of microglia activation and neuroinflammation. © 2018 The Author(s).


Document Type: Article
Source: Scopus

 

2) 

Liau, L.M.a , Ashkan, K.b , Tran, D.D.c , Campian, J.L.d , Trusheim, J.E.e , Cobbs, C.S.f , Heth, J.A.g , Salacz, M.h , Taylor, S.h , D'Andre, S.D.i , Iwamoto, F.M.j , Dropcho, E.J.k , Moshel, Y.A.l , Walter, K.A.m , Pillainayagam, C.P.n , Aiken, R.o , Chaudhary, R.p , Goldlust, S.A.q , Bota, D.A.r , Duic, P.s , Grewal, J.bg , Elinzano, H.t , Toms, S.A.t , Lillehei, K.O.u , Mikkelsen, T.v , Walpert, T.v , Abram, S.R.w , Brenner, A.J.x , Brem, S.y , Ewend, M.G.z , Khagi, S.z , Portnow, J.aa , Kim, L.J.ab , Loudon, W.G.ac , Thompson, R.C.ad , Avigan, D.E.ae , Fink, K.L.af , Geoffroy, F.J.ag , Lindhorst, S.ah , Lutzky, J.ai , Sloan, A.E.aj , Schackert, G.ak , Krex, D.ak , Meisel, H.-J.al , Wu, J.am , Davis, R.P.an , Duma, C.ao , Etame, A.B.ap , Mathieu, D.aq , Kesari, S.ar , Piccioni, D.ar , Westphal, M.as , Baskin, D.S.at , New, P.Z.at , Lacroix, M.au , May, S.-A.av , Pluard, T.J.aw , Tse, V.ax , Green, R.M.ay , Villano, J.L.az , Pearlman, M.ba , Petrecca, K.bb , Schulder, M.bc , Taylor, L.P.bd , Maida, A.E.bf , Prins, R.M.a , Cloughesy, T.F.a , Mulholland, P.be , Bosch, M.L.bf
First results on survival from a large Phase 3 clinical trial of an autologous dendritic cell vaccine in newly diagnosed glioblastoma
(2018) Journal of Translational Medicine, 16 (1), art. no. 142, p. 1. 


a University of California Los Angeles (UCLA) David Geffen School of Medicine, Jonsson Comprehensive Cancer Center, Los Angeles, CA, United States
b King's College London School of Medical Education, London, United Kingdom
c University of Florida, Gainesville, FL, United States
d Washington University, St. Louis, MO, United States
e Abbott Northwestern Hospital, Minneapolis, MN, United States
f Swedish Neuroscience Institute, Swedish Medical Center, Seattle, WA, United States
g University of Michigan Medical School, Ann Arbor, MI, United States
h University of Kansas Cancer Center, Kansas City, KS, United States
i Sutter Institute for Medical Research, Sacramento, CA, United States
j Columbia University Medical Center, New York, NY, United States
k Indiana University Simon Cancer Center, Indianapolis, IN, United States
l Overlook Medical Center, Summit, NJ, United States
m University of Rochester Medical Center, Rochester, NY, United States
n Rush University Medical Center, Rochester, United States
o Rutgers Cancer Institute, New Brunswick, NJ, United States
p University of Cincinnati Medical Center, Cincinnati, OH, United States
q Hackensack University Medical Center, Hackensack, NJ, United States
r UC Irvine Medical Center, Irvine, CA, United States
s Winthrop-University Hospital, Mineola, NY, United States
t Rhode Island Hospital, Providence, RI, United States
u University of Colorado Hospital, Aurora, CO, United States
v Henry Ford Health System, Detroit, MI, United States
w St. Thomas Research Institute, Nashville, TN, United States
x University of Texas Health Science Center, San Antonio, TX, United States
y University of Pennsylvania Perelman School of Medicine, Philadelphia, PA, United States
z University of North Carolina, Chapel Hill, NC, United States
aa City of Hope National Medical Center, Duarte, CA, United States
ab Thomas Jefferson University, Philadelphia, PA, United States
ac St. Joseph Hospital, Newport Beach, CA, United States
ad Vanderbilt University, Nashville, TN, United States
ae Beth Israel Deaconess Medical Center, Boston, MA, United States
af Baylor University Medical Center, Dallas, TX, United States
ag Illinois CancerCare, Peoria, IL, United States
ah Medical University of South Carolina, Charleston, SC, United States
ai Mount Sinai Comprehensive Cancer Center, Miami, FL, United States
aj University Hospitals Case Medical Center, Cleveland, OH, United States
ak University Hospital Carl-Gustav-Carus of Technical University, Dresden, Germany
al BG-Klinikum Bergmannstrost, Halle, Germany
am Tufts University School of Medicine, Boston, MA, United States
an Stony Brook University, Stony Brook, NY, United States
ao Hoag Cancer Center, Newport Beach, CA, United States
ap H. Lee Moffit Cancer Center and Research Institute, Tampa, FL, United States
aq CHUS-Hopital Fleurimont, Sherbrooke University, Sherbrooke, QC, Canada
ar UCSD Health System, UC San Diego, San Diego, CA, United States
as Neurochirurgische Klinik University Clinic Hamburg-Eppendorf, Hamburg, Germany
at Houston Methodist, Houston, TX, United States
au Geisinger Health System, Danville, PA, United States
av Klinikum Chemnitz GGMBH, Chemnitz, Germany
aw Saint Luke's Cancer Institute, Kansas City, MO, United States
ax Kaiser Permanente Northern California, Redwood City, CA, United States
ay Kaiser Permanente Southern California, Los Angeles, CA, United States
az University of Kentucky College of Medicine, Lexington, KY, United States
ba Colorado Neurological Institute, Englewood, CO, United States
bb Montreal Neurological Institute and Hospital, McGill University, Montreal, Canada
bc Northwell Hofstra School of Medicine, Lake Success, NY, United States
bd University of Washington, Department of Neurology, Alvord Brain Tumor Center, Seattle, WA, United States
be University College Hospitals, London, United Kingdom
bf Northwest Biotherapeutics Inc., Bethesda, MD, United States
bg NYU Winthrop Hospital, Mineola, NY, United States


Abstract
Background: Standard therapy for glioblastoma includes surgery, radiotherapy, and temozolomide. This Phase 3 trial evaluates the addition of an autologous tumor lysate-pulsed dendritic cell vaccine (DCVax®-L) to standard therapy for newly diagnosed glioblastoma. Methods: After surgery and chemoradiotherapy, patients were randomized (2:1) to receive temozolomide plus DCVax-L (n = 232) or temozolomide and placebo (n = 99). Following recurrence, all patients were allowed to receive DCVax-L, without unblinding. The primary endpoint was progression free survival (PFS); the secondary endpoint was overall survival (OS). Results: For the intent-to-treat (ITT) population (n = 331), median OS (mOS) was 23.1 months from surgery. Because of the cross-over trial design, nearly 90% of the ITT population received DCVax-L. For patients with methylated MGMT (n = 131), mOS was 34.7 months from surgery, with a 3-year survival of 46.4%. As of this analysis, 223 patients are ≥ 30 months past their surgery date; 67 of these (30.0%) have lived ≥ 30 months and have a Kaplan-Meier (KM)-derived mOS of 46.5 months. 182 patients are ≥ 36 months past surgery; 44 of these (24.2%) have lived ≥ 36 months and have a KM-derived mOS of 88.2 months. A population of extended survivors (n = 100) with mOS of 40.5 months, not explained by known prognostic factors, will be analyzed further. Only 2.1% of ITT patients (n = 7) had a grade 3 or 4 adverse event that was deemed at least possibly related to the vaccine. Overall adverse events with DCVax were comparable to standard therapy alone. Conclusions: Addition of DCVax-L to standard therapy is feasible and safe in glioblastoma patients, and may extend survival. © 2018 The Author(s).


Author Keywords
Dendritic cell;  Glioblastoma;  Immunotherapy;  Vaccine


Document Type: Article
Source: Scopus

 

3) 

Hirbe, A.C.a , Zhang, X.a , Dahiya, S.b , Godec, A.a , Chrisinger, J.b , Tao, Y.c , Luo, J.c , Gutmann, D.H.d
β-III-spectrin immunohistochemistry as a potential diagnostic tool with high sensitivity for malignant peripheral nerve sheath tumors
(2018) Neuro-Oncology, 20 (6), pp. 858-862. 


a Division of Medical Oncology, Department of Medicine, Washington University School of Medicine, Box 8076, 660 S Euclid Avenue, St Louis, MO, United States
b Department of Pathology and Immunology, Washington University School of Medicine, St Louis, MO, United States
c Siteman Cancer Center Biostatistics Shared Resource, Division of Public Health Sciences, Department of Surgery, Washington University School of Medicine, St. Louis, MO, United States
d Department of Neurology, Washington University School of Medicine, St Louis, MO, United States


Author Keywords
MPNSTs;  sarcomas;  β-III-spectrin


Document Type: Letter
Source: Scopus

 

4) 

Lissemore, J.I.a , Bhandari, A.a , Mulsant, B.H.b c , Lenze, E.J.d , Reynolds, C.F., IIIe , Karp, J.F.e f , Rajji, T.K.a b c , Noda, Y.a b , Zomorrodi, R.a b , Sibille, E.b c g , Daskalakis, Z.J.a b c , Blumberger, D.M.a b c
Reduced GABAergic cortical inhibition in aging and depression
(2018) Neuropsychopharmacology, pp. 1-8. Article in Press. 


a Temerty Centre for Therapeutic Brain Intervention, Centre for Addiction and Mental Health, Toronto, ON, Canada
b Department of Psychiatry, University of Toronto, Toronto, ON, Canada
c Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health, Toronto, ON, Canada
d Healthy Mind Lab, Department of Psychiatry, Washington University School of Medicine, St Louis, MO, United States
e Department of Psychiatry, Western Psychiatric Institute and Clinic of University of Pittsburgh Medical Center, Pittsburgh, PA, United States
f Geriatric Research, Education, and Clinical Center, Pittsburgh, PA, United States
g Department of Psychiatry and Pharmacology and Toxicology, University of Toronto, Toronto, ON, Canada


Abstract
The neurobiology underlying depression in older adults is less extensively evaluated than in younger adults, despite the putative influence of aging on depression neuropathology. Studies using transcranial magnetic stimulation (TMS), a neurophysiological tool capable of probing inhibitory and excitatory cortical neurotransmission, have identified dysfunctional GABAergic inhibitory activity in younger adults with depression. However, GABAergic and glutamatergic cortical neurotransmission have not yet been studied in late-life depression (LLD). Here, we used single- and paired-pulse TMS to measure cortical inhibition and excitation in 92 LLD patients and 41 age-matched healthy controls. To differentiate the influence of age and depression, we also compared these TMS indices to those of 30 younger depressed adults and 30 age- and sex-matched younger healthy adults. LLD patients, older healthy adults, and younger depressed adults demonstrated significantly lower GABAA receptor-mediated cortical inhibition than younger healthy controls. By contrast, no significant differences in cortical inhibition were observed between older adults with and without depression. No significant differences in GABAB receptor-mediated inhibition or cortical excitation were found between the groups. Altogether, these findings suggest that reduced cortical inhibition may be associated with both advancing age and depression, which (i) supports the model of depression as a disease of accelerated aging, and (ii) prompts future investigation into diminished GABAergic neurotransmission in late-life as a biological predisposing factor to the development of depression. Given that cortical neurophysiology was similar in depressed and healthy older adults, future prospective studies need to establish the relative influence of age and depression on cortical inhibition deficits. © 2018 American College of Neuropsychopharmacology


Document Type: Article in Press
Source: Scopus

 

5) 

Griffith, J.L., Wong, M.
The mTOR pathway in treatment of epilepsy: A clinical update
(2018) Future Neurology, 13 (2), pp. 49-58. 


Department of Neurology, Washington University, School of Medicine, St. Louis, MO, United States


Abstract
Nearly a third of patients with epilepsy have seizures refractory to current medical therapies. In the search for novel drug targets, the mTOR pathway has emerged as key in the regulation of neuronal function, growth and survival, and other cellular processes related to epileptogenesis. Hyperactivation of the mTOR pathway has been implicated in tuberous sclerosis complex and other 'mTORopathies', clinical syndromes associated with cortical developmental malformations and drug-resistant epilepsy. Recently published clinical trials of mTOR inhibitors in tuberous sclerosis complex have shown that these drugs are effective at decreasing seizure frequency. Future studies may establish whether mTOR inhibitors can provide effective treatment for patients with diverse genetic and acquired epilepsies, including preventative, disease-modifying therapies. © 2018 2018 Future Medicine Ltd.


Author Keywords
epilepsy;  everolimus;  mTOR;  rapamycin;  seizure;  tuberous sclerosis


Document Type: Article
Source: Scopus

 

6) 

Guilliams, K.P.d , Fields, M.E.a , Ragan, D.K.d , Eldeniz, C.b , Binkley, M.M.c , Chen, Y.d , Comiskey, L.S.d , Doctor, A.a , Hulbert, M.L.a , Shimony, J.S.b , Vo, K.D.b , McKinstry, R.C.b , An, H.b , Lee, J.-M.b d , Ford, A.L.d
Red cell exchange transfusions lower cerebral blood flow and oxygen extraction fraction in pediatric sickle cell anemia
(2018) Blood, 131 (9), pp. 1012-1021. Cited 2 times.


a Department of Pediatrics, Washington University School of Medicine, St. Louis, MO, United States
b Mallinckrodt Institute of Radiology, Washington University School of Medicine, St. Louis, MO, United States
c Department of Mechanical Engineering and Material Science, Washington University in St. Louis, St. Louis, MO, United States
d Department of Neurology, Washington University School of Medicine, 600 South Euclid Ave, Campus Box 8111, St. Louis, MO, United States


Abstract
Blood transfusions are the mainstay of stroke prevention in pediatric sickle cell anemia (SCA), but the physiology conferring this benefit is unclear. Cerebral blood flow (CBF) and oxygen extraction fraction (OEF) are elevated in SCA, likely compensating for reduced arterial oxygen content (CaO2). We hypothesized that exchange transfusions would decrease CBF and OEF by increasing CaO2, thereby relieving cerebral oxygen metabolic stress. Twenty-one children with SCA receiving chronic transfusion therapy (CTT) underwent magnetic resonance imaging before and after exchange transfusions. Arterial spin labeling and asymmetric spin echo sequences measured CBF and OEF, respectively, which were compared pre- and posttransfusion. Volumes of tissue with OEF above successive thresholds (36%, 38%, and 40%), as a metric of regional metabolic stress, were compared pre- and posttransfusion. Transfusions increased hemoglobin (Hb; from 9.1 to 10.3 g/dL; P < .001) and decreased Hb S (from 39.7% to 24.3%; P < .001). Transfusions reduced CBF (from 88 to 82.4 mL/100 g per minute; P 5 .004) and OEF (from 34.4% to 31.2%; P < .001). At all thresholds, transfusions reduced the volume of peak OEF found in the deep white matter, a location at high infarct risk in SCA (P < .001). Reduction of elevated CBF and OEF, both globally and regionally, suggests that CTT mitigates infarct risk in pediatric SCA by relieving cerebral metabolic stress at patient- and tissue-specific levels. © 2018 by The American Society of Hematology.


Document Type: Article
Source: Scopus

 

7) 

Snyder-Warwick, A.K.a , Satoh, A.b c d , Santosa, K.B.a , Imai, S.-i.b d , Jablonka-Shariff, A.a
Hypothalamic Sirt1 protects terminal Schwann cells and neuromuscular junctions from age-related morphological changes
(2018) Aging Cell, . Article in Press. 


a Division of Plastic Surgery Department of Surgery Washington University School of Medicine St. Louis, MO USA
b Department of Developmental Biology Washington University School of Medicine St. Louis, MO USA
c Sleep and Aging Regulation Research Project Team National Center for Geriatrics and Gerontology Obu, Aichi Japan
d Project for Elucidating and Controlling Mechanisms of Aging and Longevity Japan Agency for Medical Research and Development Tokyo Japan


Abstract
Neuromuscular decline occurs with aging. The neuromuscular junction (NMJ), the interface between motor nerve and muscle, also undergoes age-related changes. Aging effects on the NMJ components-motor nerve terminal, acetylcholine receptors (AChRs), and nonmyelinating terminal Schwann cells (tSCs)-have not been comprehensively evaluated. Sirtuins delay mammalian aging and increase longevity. Increased hypothalamic Sirt1 expression results in more youthful physiology, but the relationship between NMJ morphology and hypothalamic Sirt1 was previously unknown. In wild-type mice, all NMJ components showed age-associated morphological changes with ~80% of NMJs displaying abnormalities by 17 months of age. Aged mice with brain-specific Sirt1 overexpression (BRASTO) had more youthful NMJ morphologic features compared to controls with increased tSC numbers, increased NMJ innervation, and increased numbers of normal AChRs. Sympathetic NMJ innervation was increased in BRASTO mice. In contrast, hypothalamic-specific Sirt1 knockdown led to tSC abnormalities, decreased tSC numbers, and more denervated endplates compared to controls. Our data suggest that hypothalamic Sirt1 functions to protect NMJs in skeletal muscle from age-related changes via sympathetic innervation. © 2018 The Anatomical Society and John Wiley & Sons Ltd.


Author Keywords
Aging;  Neuromuscular junction;  NMJ;  Sirt1;  Sirtuin;  Terminal Schwann cell


Document Type: Article in Press
Source: Scopus
Access Type: Open Access

 

8) 

Morris, S.M., Gutmann, D.H.
A genotype–phenotype correlation for quantitative autistic trait burden in neurofibromatosis 1
(2018) Neurology, 90 (8), pp. 377-379. 


Washington University School of Medicine, St. Louis, MO, United States


Document Type: Article
Source: Scopus

 

9) 

Zhou, W.a , Anastasio, M.A.b
Learning the ideal observer for SKE detection tasks by use of convolutional neural networks (Cum Laude Poster Award)
(2018) Progress in Biomedical Optics and Imaging - Proceedings of SPIE, 10577, art. no. 1057719, . 


a Department of Electrical and Systems Engineering, Washington University in St. Louis, St. Louis, MO, United States
b Department of Biomedical Engineering, Washington University in St. Louis, St. Louis, MO, United States


Abstract
It has been advocated that task-based measures of image quality (IQ) should be employed to evaluate and optimize imaging systems. Task-based measures of IQ quantify the performance of an observer on a medically relevant task. The Bayesian Ideal Observer (IO), which employs complete statistical information of the object and noise, achieves the upper limit of the performance for a binary signal classification task. However, computing the IO performance is generally analytically intractable and can be computationally burdensome when Markov-chain Monte Carlo (MCMC) techniques are employed. In this paper, supervised learning with convolutional neural networks (CNNs) is employed to approximate the IO test statistics for a signal-known-exactly and background-known-exactly (SKE/BKE) binary detection task. The receiver operating characteristic (ROC) curve and the area under the ROC curve (AUC) are compared to those produced by the analytically computed IO. The advantages of the proposed supervised learning approach for approximating the IO are demonstrated. © 2018 SPIE.


Author Keywords
Bayesian Ideal Observer;  convolutional neural networks;  signal detection theory;  Supervised learning


Document Type: Conference Paper
Source: Scopus

 

10) 

Greeson, J.M.a , Zarrin, H.b , Smoski, M.J.c d , Brantley, J.G.d e , Lynch, T.R.f , Webber, D.M.g , Hall, M.H.h , Suarez, E.C.d e , Wolever, R.Q.i j k
Mindfulness Meditation Targets Transdiagnostic Symptoms Implicated in Stress-Related Disorders: Understanding Relationships between Changes in Mindfulness, Sleep Quality, and Physical Symptoms
(2018) Evidence-based Complementary and Alternative Medicine, 2018, art. no. 4505191, . 


a Department of Psychology, College of Science and Mathematics, Rowan University, 201 Mullica Hill Road, Glassboro, NJ, United States
b Thomas Jefferson University, 130 S. 9th Street, Philadelphia, PA, United States
c Department of Psychology and Neurosciences, Duke University, DUMC, Box 3026, Durham, NC, United States
d Department of Psychiatry and Behavioral Sciences, Duke University School of Medicine, Box 3022, Durham, NC, United States
e Duke Integrative Medicine, Duke University Medical Center, 3475 Erwin Road, Durham, NC, United States
f School of Psychology, University of Southampton Highfield Campus, Shackleton Building (B44), Southampton, United Kingdom
g Department of Pathology and Immunology, Washington University School of Medicine, 660 S. Euclid Ave., St. Louis, MO, United States
h Departments of Psychiatry Psychology and Clinical and Translational Science, University of Pittsburgh School of Medicine, 3811 O'Hara Street, Pittsburgh, PA, United States
i Osher Center for Integrative Medicine at Vanderbilt, Department of Physical Medicine and Rehabilitation, Vanderbilt University Medical Center, 3401 West End, Nashville, TN, United States
j Department of Psychiatry and Behavioral Sciences, Vanderbilt University Medical Center, Nashville, TN, United States
k Vanderbilt University School of Nursing, Nashville, TN, United States


Abstract
Mindfulness-Based Stress Reduction (MBSR) is an 8-week meditation program known to improve anxiety, depression, and psychological well-being. Other health-related effects, such as sleep quality, are less well established, as are the psychological processes associated with therapeutic change. This prospective, observational study (n=213) aimed to determine whether perseverative cognition, indicated by rumination and intrusive thoughts, and emotion regulation, measured by avoidance, thought suppression, emotion suppression, and cognitive reappraisal, partly accounted for the hypothesized relationship between changes in mindfulness and two health-related outcomes: sleep quality and stress-related physical symptoms. As expected, increased mindfulness following the MBSR program was directly correlated with decreased sleep disturbance (r=-0.21, p=0.004) and decreased stress-related physical symptoms (r=-0.38, p<0.001). Partial correlations revealed that pre-post changes in rumination, unwanted intrusive thoughts, thought suppression, experiential avoidance, emotion suppression, and cognitive reappraisal each uniquely accounted for up to 32% of the correlation between the change in mindfulness and change in sleep disturbance and up to 30% of the correlation between the change in mindfulness and change in stress-related physical symptoms. Results suggest that the stress-reducing effects of MBSR are due, in part, to improvements in perseverative cognition and emotion regulation, two "transdiagnostic" mental processes that cut across stress-related disorders. © 2018 Jeffrey M. Greeson et al.


Document Type: Article
Source: Scopus