scholarly journals Timing in the absence of supraspinal input III: Regularly spaced cutaneous stimulation prevents and reverses the spinal learning deficit produced by peripheral inflammation.

2011 ◽  
Vol 125 (1) ◽  
pp. 37-45 ◽  
Author(s):  
Kyle M. Baumbauer ◽  
James W. Grau
Keyword(s):  
Peripheral Inflammation ◽  
Learning Deficit ◽  
Cutaneous Stimulation ◽  
Spinal Learning

Lipopolysaccharide induces a spinal learning deficit that is blocked by IL-1 receptor antagonism

2007 ◽  
Vol 21 (6) ◽  
pp. 748-757 ◽  
Author(s):  
Erin E. Young ◽  
Kyle M. Baumbauer ◽  
Audrea Elliot ◽  
Robin L. Joynes
Keyword(s):  
Learning Deficit ◽  
Receptor Antagonism ◽  
Spinal Learning

The neonatal injury-induced spinal learning deficit in adult rats: Central mechanisms.

2008 ◽  
Vol 122 (3) ◽  
pp. 589-600 ◽  
Author(s):  
Erin E. Young ◽  
Kyle M. Baumbauer ◽  
Jessica E. Hillyer ◽  
Ann Marie Patterson ◽  
Kevin C. Hoy ◽  
...  
Keyword(s):  
Learning Deficit ◽  
Adult Rats ◽  
Spinal Learning ◽  
Neonatal Injury

PERIPHERAL INFLAMMATION AND DYNORPHIN RELEASE IN THE RAT SPINAL CORD

Analgesia ◽  
1995 ◽  
Vol 1 (4) ◽  
pp. 687-690
Author(s):  
R.C. RILEY ◽  
Z.Q. ZHAO ◽  
A.W. DUGGAN
Keyword(s):  
Spinal Cord ◽  
Peripheral Inflammation ◽  
Rat Spinal Cord ◽  
Dynorphin Release

Vitamin-D-Free Regimen Intensifies the Spatial Learning Deficit in Alzheimer's Disease

2011 ◽  
Vol 121 (1) ◽  
pp. 16-24 ◽  
Author(s):  
Mohsen Taghizadeh ◽  
Abolghassem Djazayery ◽  
Mahmoud Salami ◽  
Mohammad Reza Eshraghian ◽  
Sayyed Alireza Talaei Zavareh
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Vitamin D ◽  
Spatial Learning ◽  
Learning Deficit

Redefining peripheral inflammation signature in schizophrenia based on the real-world FACE-SZ cohort

2021 ◽  
pp. 110335
Author(s):  
G. Fond ◽  
P.L. Sunhary de Verville ◽  
R. Richieri ◽  
D. Etchecopar-Etchart ◽  
T. Korchia ◽  
...  
Keyword(s):  
Real World ◽  
Peripheral Inflammation ◽  
The Real

scholarly journals The influence of comorbid depression and overweight status on peripheral inflammation and cortisol levels

2021 ◽  
pp. 1-8
Author(s):  
Anna P. McLaughlin ◽  
Naghmeh Nikkheslat ◽  
Caitlin Hastings ◽  
Maria A. Nettis ◽  
Melisa Kose ◽  
...  
Keyword(s):  
Logistic Regression ◽  
Significant Risk ◽  
Normal Weight ◽  
Cortisol Awakening Response ◽  
Peripheral Inflammation ◽  
Comorbid Depression ◽  
Diurnal Cortisol ◽  
Overweight Status ◽  
Multivariable Logistic Regression ◽  
Cortisol Levels

Abstract Background Depression and overweight are each associated with abnormal immune system activation. We sought to disentangle the extent to which depressive symptoms and overweight status contributed to increased inflammation and abnormal cortisol levels. Methods Participants were recruited through the Wellcome Trust NIMA Consortium. The sample of 216 participants consisted of 69 overweight patients with depression; 35 overweight controls; 55 normal-weight patients with depression and 57 normal-weight controls. Peripheral inflammation was measured as high-sensitivity C-Reactive Protein (hsCRP) in serum. Salivary cortisol was collected at multiple points throughout the day to measure cortisol awakening response and diurnal cortisol levels. Results Overweight patients with depression had significantly higher hsCRP compared with overweight controls (p = 0.042), normal-weight depressed patients (p < 0.001) and normal-weight controls (p < 0.001), after controlling for age and gender. Multivariable logistic regression showed that comorbid depression and overweight significantly increased the risk of clinically elevated hsCRP levels ⩾3 mg/L (OR 2.44, 1.28–3.94). In a separate multivariable logistic regression model, overweight status contributed most to the risk of having hsCRP levels ⩾3 mg/L (OR 1.52, 0.7–2.41), while depression also contributed a significant risk (OR 1.09, 0.27–2). There were no significant differences between groups in cortisol awakening response and diurnal cortisol levels. Conclusion Comorbid depression and overweight status are associated with increased hsCRP, and the coexistence of these conditions amplified the risk of clinically elevated hsCRP levels. Overweight status contributed most to the risk of clinically elevated hsCRP levels, but depression also contributed to a significant risk. We observed no differences in cortisol levels between groups.

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