No abstract available.
Amniotic Fluid* ; beta-Endorphin* ; Female

No abstract available.
beta-Endorphin* ; Cardiopulmonary Bypass* ; Thiopental*

No abstract available.
beta-Endorphin* ; Exercise* ; Pain Threshold* ; Plasma*

Lameness is one of the most painful conditions that affects dairy cattle. This study was conducted to evaluate clinical signs and plasma concentration of several pain and stress biomarkers after oligofructose-induced lameness in dairy heifers. Lameness was induced using an oligofructose overload model in 12 non-pregnant heifers. Clinical parameters and blood samples were obtained at 48 and 24 h and at 6, 12, 24, 36 and 48 h after induction of lameness. Clinical parameters included heart rate, respiratory rate, ruminal frequency and lameness score. Plasma biomarkers included cortisol, haptoglobin, norepinephrine, beta-endorphin and substance P. Differences were observed in all parameters between control and treated heifers. The plasma concentration of biomarkers increased significantly in treated animals starting 6 h after induction of lameness, reaching maximum levels at 24 h for cortisol, 48 h for haptoglobin, 6 h for norepinephrine, 12 h for substance P and at 24 h for beta-endorphin. Overall, our results confirm that lameness associated pain induced using the oligofructose model induced changes in clinical parameters and plasma biomarkers of pain and stress in dairy heifers.
Animals ; beta-Endorphin ; Biological Markers ; Cattle ; Haptoglobins ; Heart Rate ; Hydrocortisone ; Norepinephrine ; Plasma ; Respiratory Rate ; Substance P

We built the hypothesis that the hypertrophic callus formation is mediated by beta-endorphin that stimulates secretion of GH and increase circulation growth factor activity in head injury patient. We classified 4 groups such as 5 normal person(control), group I;5 patients with only fracture, group II;5 patients with fracture and head injury, group III; 5 patients with only head injury, group IV. We obtained the samples of serum from each group at 0, 2, 4, 6, 8 weeks after trauma and assessed the serum level of GH, GHRH, somatostatin. The serum level of GH was statisticallyu higher in group III, IV than group I, II. There was not significant difference in serum level of GHRH. The serum level of somatostatin was higher in group II, III, IV than group I, but there was no statistical significance in each group. GH has a important role in hypertrophic callus formation in severe head injury patients, but there was no evidence that the mechanism is mediated by beta-EndorphinGHRH & somatostatin-GH-GF-1, beta-FGF axis. There may be a another mechanism in increasing GH that was stimulated by beta-endorphin in thalamus and lateral ventricle, and it should be necessary for further evaluation of it.
Axis, Cervical Vertebra ; beta-Endorphin ; Bony Callus ; Craniocerebral Trauma* ; Head* ; Humans ; Lateral Ventricles ; Somatostatin ; Thalamus

BACKGROUND: This study aimed to investigate the effect of strenuous exercise on β-endorphine (β-END) level in fibromyalgia (FM) patients compared to healthy subjects. METHODS: We enrolled 30 FM patients and 15 healthy individuals. All study participants underwent a treadmill exercise test using modified Bruce protocol (M.Bruce). The goal of the test was achieving at least 70% of the predicted maximal heart rate (HRMax). The serum levels of β-END were measured before and after the exercise program. Measurements were done while heart rate was at least 70% of its predicted maximum. RESULTS: The mean ± the standard deviation (SD) of exercise duration in the FM and control groups were 24.26 ± 5.29 and 29.06 ± 3.26 minutes, respectively, indicating a shorter time to achieve the goal heart rate in FM patients (P < 0.003). Most FM patients attained 70% HRMax at lower stages (stage 2 and 3) of M.Bruce compared to the control group (70% versus 6.6%, respectively; P < 0.0001). Compared to healthy subjects, FM patients had lower serum β-END levels both in baseline and post-exercise status (Mean ± SD: 122.07 ± 28.56 µg/ml and 246.55 ± 29.57 µg/ml in the control group versus 90.12 ± 20.91 µg/ml and 179.80 ± 28.57 µg/ml in FM patients, respectively; P < 0.001). CONCLUSIONS: We found that FM patients had lower levels of β-END in both basal and post-exercise status. Exercise increased serum the β-END level in both groups but the average increase in β-END in FM patients was significantly lower than in the control group.
beta-Endorphin* ; Exercise Test ; Fibromyalgia* ; Healthy Volunteers ; Heart Rate ; Humans ; Plasma*

BACKGROUND: This study aimed to investigate the effect of strenuous exercise on β-endorphine (β-END) level in fibromyalgia (FM) patients compared to healthy subjects. METHODS: We enrolled 30 FM patients and 15 healthy individuals. All study participants underwent a treadmill exercise test using modified Bruce protocol (M.Bruce). The goal of the test was achieving at least 70% of the predicted maximal heart rate (HRMax). The serum levels of β-END were measured before and after the exercise program. Measurements were done while heart rate was at least 70% of its predicted maximum. RESULTS: The mean ± the standard deviation (SD) of exercise duration in the FM and control groups were 24.26 ± 5.29 and 29.06 ± 3.26 minutes, respectively, indicating a shorter time to achieve the goal heart rate in FM patients (P < 0.003). Most FM patients attained 70% HRMax at lower stages (stage 2 and 3) of M.Bruce compared to the control group (70% versus 6.6%, respectively; P < 0.0001). Compared to healthy subjects, FM patients had lower serum β-END levels both in baseline and post-exercise status (Mean ± SD: 122.07 ± 28.56 µg/ml and 246.55 ± 29.57 µg/ml in the control group versus 90.12 ± 20.91 µg/ml and 179.80 ± 28.57 µg/ml in FM patients, respectively; P < 0.001). CONCLUSIONS: We found that FM patients had lower levels of β-END in both basal and post-exercise status. Exercise increased serum the β-END level in both groups but the average increase in β-END in FM patients was significantly lower than in the control group.
beta-Endorphin* ; Exercise Test ; Fibromyalgia* ; Healthy Volunteers ; Heart Rate ; Humans ; Plasma*

Adult ; Altitude ; Arteries ; metabolism ; Calcitonin Gene-Related Peptide ; blood ; Humans ; beta-Endorphin ; blood

OBJECTIVES: The present study was performed to evaluate the change in releasing action of hypothalamus-pituitary-adrenal axis after alcohol abstinence in patients with alcohol dependence, and to identify the etiologic mechanism of alcohol dependence indirectly. METHODS: Plasma beta-endorphin, cortisol and ACTH level was measured in 14 alcohol dependent patients and in 14 healthy persons after 7 days and 28 days of alcohol abstinence at 08: 00h and 12: 00h, twice a day. RESULTS: 1) There was no significant difference in plasma beta-endorphin, cortisol and ACTH level measured at 08: 00h and 12: 00h between patients and control group after 7days of alcohol withdrawal. 2) Plasma beta-endorphin level measured at 08: 00h in patients was significantly elevated comparing with control group after 28days of alcohol withdrawal. But, there was no significant difference in plasma beta-endorphin level measured at 12: 00h and in plasma cortisol and ACTH level measured at both 08: 00h and 12: 00h between two groups after 28days of alcohol withdrawal. 3) In the patient group, there was no significant difference between patients after 7days and 28 days of alcohol withdrawal in plasma beta-endorphin, cortisol and ACTH level measured at 08: 00h and ACTH level measured at 12: 00h. But, beta-endorphin and cortisol level measured at 12: 00h were significantly lowered in patients after 28days of alcohol withdrawal than after 7days of withdrawal. 4) In decreasing rate of beta-endorphin production from 08: 00h to 12: 00h, there was significant difference between patients and controlled group after 28days of alcohol withdrawal. CONCLUSION: In alcohol dependent patients, lower level of beta-endorphin and increased reducing rate in diurnal variation of beta-endorphin after alcohol withdrawal are evident, which in turn may elevate craving for alcohol intake, and there findings support the opioid compensation theory in the development of alcohol dependence.
Adrenocorticotropic Hormone* ; Alcohol Abstinence ; Alcoholism ; Axis, Cervical Vertebra ; beta-Endorphin* ; Compensation and Redress ; Humans ; Hydrocortisone* ; Plasma*

This study was designed to investigate the contribution of prostaglandins to the maintenance of inflammatory pain. Inflammation was induced by intraplantar (i.pl.) injection of carrageenan in right hindpaw in rats. Indomethacin (non-selective COX inhibitor) was administered i.pl. 1 h after the carrageenan injection, and paw withdrawal latency (PWL) responding to noxious heat was measured. &beta;-endorphin (&beta;-END) and μ-opioid receptor (MOR) expressed in the inflamed site were examined by using immunocytochemistry, ELISA and RT-PCR techniques. The results showed that indomethacin dose-dependently increased PWL to the levels that were above the baseline on the day 2 and 3, referred to as hypoalgesia. The hypoalgesia was abolished by a local injection of the non-selective opioid receptor inhibitor naloxone methiodide. The number of &beta;-END-positive cells, the content of &beta;-END and the expression of MOR mRNA in the inflammatory site of inflammation model rats were all significantly increased by indomethacin. These results reveal a novel mechanism of prostaglandins for the inhibition of inflammation-induced endogenous opioid activity. This study provides further evidence that inhibition of prostaglandins in inflamed site could be a promising therapy for inflammatory pain.
Analgesics, Opioid ; Animals ; Carrageenan ; Indomethacin ; Inflammation ; Naloxone ; Pain ; Prostaglandins ; Rats ; Receptors, Opioid ; beta-Endorphin