scholarly journals The impact of dietary tarragon (Artemisia dracunculus) on serum apelin, brain-derived neurotrophic factor, cardiac troponin concentrations and histopathology of liver tissue in laying hens housed at different stocking densities

2020 ◽  
Vol 65 (No. 6) ◽  
pp. 269-279
Author(s):  
B Bayraktar ◽  
E Tekce ◽  
H Kaya ◽  
M Karaalp ◽  
E Turunc

Due to its association with several other stress factors (poultry house gases, inadequate ventilation, heat, cold and poor hygiene), the high stocking density is a major stress factor that adversely affects the health and performance of poultry and the quality of the poultry products. Therefore, this experimental study was aimed at analysing the impact of different doses of dietary tarragon (Artemisia dracunculus) on the serum apelin, plasma brain-derived neurotrophic factor (p-BDNF), and cardiac troponin I (cTnI) concentrations, and the correlation between these indicators in laying hens housed at different stocking densities. The aim of this study is to investigate the effects of adding tarragon in different ratios to laying hen rations in the 2<sup>nd</sup> ovulation period on the cTnI, apelin, and BDNF hormone concentrations and the liver histopathology. The experiment was carried out over a period of eight weeks, with 192 Lohman Brown commercial hybrids at 50 weeks of age. Eight groups (four replicates each), composed of laying hens of equal body weight, which were housed at stocking densities of 580 cm<sup>2</sup>/hen and 810 cm<sup>2</sup>/hen and received 0, 1, 5 and 10 mmol/kg of tarragon (Artemisia dracunculus) in the feed, were established. At the end of the trial, 96 of the housed egg-laying hens (3 birds in each subgroup, a total of 12 birds in each group) were randomly selected and blood samples were taken from the vena subcutanea ulnaris. The samples collected were analysed for the apelin, p-BDNF, and cTnI contents. The analysis results demonstrated that tarragon supplementation had no effect on the serum apelin, p-BDNF and cTnI concentrations (P &gt; 0.05). The Sub-Groups ST1, ST1.2, and ST6 presented with severe hyperaemia of the sinusoidal, portal and acinar blood vessels, whilst the hyperaemia of these blood vessels was moderate in Sub-Group ST12. Apelin, BDNF, and cTnI can act as protective factors against negative consequences of stress (e.g., stocking density or heat stress).

2010 ◽  
Vol 214 (1) ◽  
pp. 319-328 ◽  
Author(s):  
Bernet M. Elzinga ◽  
Marc L. Molendijk ◽  
Richard C. Oude Voshaar ◽  
Boudewijn A. A. Bus ◽  
Jos Prickaerts ◽  
...  

2017 ◽  
Vol 30 (1) ◽  
pp. 125-141 ◽  
Author(s):  
Alexandria Meyer ◽  
Greg Hajcak ◽  
Elizabeth Hayden ◽  
Haroon I. Sheikh ◽  
Shiva M. Singh ◽  
...  

AbstractThe error-related negativity (ERN) is a negative deflection in the event-related potential occurring when individuals make mistakes, and is increased in children with internalizing psychopathology. We recently found that harsh parenting predicts a larger ERN in children, and recent work has suggested that variation in the brain-derived neurotrophic factor (BDNF) gene may moderate the impact of early life adversity. Parents and children completed measures of parenting when children were 3 years old (N = 201); 3 years later, the ERN was measured and diagnostic interviews as well as dimensional symptom measures were completed. We found that harsh parenting predicted an increased ERN only among children with a methionine allele of the BDNF genotype, and evidence of moderated mediation: the ERN mediated the relationship between parenting and internalizing diagnoses and dimensional symptoms only if children had a methionine allele. We tested this model with externalizing disorders, and found that harsh parenting predicted externalizing outcomes, but the ERN did not mediate this association. These findings suggest that harsh parenting predicts both externalizing and internalizing outcomes in children; however, this occurs through different pathways that uniquely implicate error-related brain activity in the development of internalizing disorders.


2019 ◽  
Vol 148 ◽  
pp. 40-49 ◽  
Author(s):  
Anna M. Rosenhauer ◽  
Linda Q. Beach ◽  
Elizabeth C. Jeffress ◽  
Brittany M. Thompson ◽  
Katharine E. McCann ◽  
...  

2013 ◽  
Vol 93 (12) ◽  
pp. 1707-1716 ◽  
Author(s):  
Cameron S. Mang ◽  
Kristin L. Campbell ◽  
Colin J.D. Ross ◽  
Lara A. Boyd

Recovery of motor function after stroke involves relearning motor skills and is mediated by neuroplasticity. Recent research has focused on developing rehabilitation strategies that facilitate such neuroplasticity to maximize functional outcome poststroke. Although many molecular signaling pathways are involved, brain-derived neurotrophic factor (BDNF) has emerged as a key facilitator of neuroplasticity involved in motor learning and rehabilitation after stroke. Thus, rehabilitation strategies that optimize BDNF effects on neuroplasticity may be especially effective for improving motor function poststroke. Two potential poststroke rehabilitation strategies that consider the importance of BDNF are the use of aerobic exercise to enhance brain function and the incorporation of genetic information to individualize therapy. Converging evidence demonstrates that aerobic exercise increases BDNF production and consequently enhances learning and memory processes. Nevertheless, a common genetic variant reduces activity-dependent secretion of the BDNF protein. Thus, BDNF gene variation may affect response to motor rehabilitation training and potentially modulate the effects of aerobic exercise on neuroplasticity. This perspective article discusses evidence that aerobic exercise promotes neuroplasticity by increasing BDNF production and considers how aerobic exercise may facilitate the acquisition and retention of motor skills for poststroke rehabilitation. Next, the impact of the BDNF gene val66met polymorphism on motor learning and response to rehabilitation is explored. It is concluded that the effects of aerobic exercise on BDNF and motor learning may be better exploited if aerobic exercise is paired more closely in time with motor training. Additionally, information about BDNF genotype could provide insight into the type and magnitude of effects that aerobic exercise may have across individuals and potentially help guide an individualized prescription of aerobic exercise to enhance motor rehabilitation poststroke.


2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Jesus Montero-Marin ◽  
Laura Andrés-Rodríguez ◽  
Mattie Tops ◽  
Juan V. Luciano ◽  
Mayte Navarro-Gil ◽  
...  

Abstract Fibromyalgia (FM) is a disabling syndrome characterized by chronic pain associated with fatigue. Its pathogenesis is unknown, but alterations in central sensitization, involving an imbalance of brain-derived neurotrophic factor (BDNF) and inflammatory biomarkers, appear to be implicated. The aim of this study was to evaluate the impact of attachment-based compassion therapy (ABCT) on levels of BDNF, the inflammatory markers TNF-α, IL-6, IL-10, and the C-reactive protein (CRP), analysing whether biomarkers play a mediating/moderating role in improvements in FM functional status. Thirty-four female patients with FM participated in a RCT and were assigned to ABCT or relaxation therapy. Blood extractions were conducted at baseline and post-intervention, with self-report assessments of functional status (FIQ) at baseline, post-intervention and 3-month follow-up. A pro-inflammatory composite was obtained by summing up IL-6, TNF-α and CRP normalized values. Non-parametric tests, analysis of variance and regression models were used to evaluate treatment and mediation/moderation. Compared to relaxation therapy, ABCT showed significant improvements in FIQ and decreases in BDNF, CRP, and pro-inflammatory composite. Changes in BDNF had a mediating role in FIQ. ABCT seems to reduce BDNF and appears to have anti-inflammatory effects in FM patients. Reductions in BDNF could be a mechanism of FM functional status improvement. Clinical Trial Registration:http://ClinicalTrials.gov, identifier NCT02454244. Date: May 27th, 2015.


2017 ◽  
Vol 6 (12) ◽  
pp. 108 ◽  
Author(s):  
Jessica Miller ◽  
Siné McDougall ◽  
Sarah Thomas ◽  
Jan Wiener

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