Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two trials (winter and summer) were conducted to determine effects of fasting and transportation and adrenocorticotropic hormone (ACTH) administration on the amount and source of weight lost by feeder steers. Sixteen steers, in each of two experiments, were adapted to metabolism stalls for 10 d, were fed medium-quality hay at 2.1% of BW for 3 d, and then were subjected to either fasting alone or fasting plus transit for 48 h. In Exp. 1 steers were randomly assigned to treatments. In Exp. 2 steers were blocked by age (OLD or YOUNG) and assigned to treatments. Fecal and urinary excretions accounted for 65 and 38% of the total weight lost in Exp. 1 and 2, respectively. Fasting plus transit did not consistently increase the amount of weight lost compared with fasting alone but increased (P less than .01) plasma glucose concentrations. Injection of ACTH before either fasting alone or fasting plus transit increased (P less than .05) the amount of weight lost as feces. Steers in the OLD group lost more weight during transit and fasting but regained the lost weight faster (P less than .01) during the recovery period than did steers in the YOUNG group. Injecting YOUNG steers with ACTH before fasting alone or fasting plus transit increased plasma fibrinogen (P less than .10) and serum glucose (P less than .05) concentrations more than ACTH injections in OLD steers. Although fasting and transit elicit mobilization of body nutrients and resulted in a loss of BW, these effects were quickly reversed during the poststress period.
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PMID:The effect of fasting, transit plus fasting, and administration of adrenocorticotropic hormone on the source and amount of weight lost by feeder steers of different ages. 165 94

Administration of the pituitary hormone alpha-melanocyte-stimulating hormone (alpha-MSH) to mice was found to inhibit a number of IL-1 and TNF-inducible biologic responses in situ. The ability of either IL-1 or TNF to cause fever, enhance plasma levels of acute phase proteins, and increase the numbers of peripheral blood neutrophils was inhibited by the simultaneous peripheral administration of this neuropeptide. In addition, alpha-MSH reversed the depressive influences of IL-1 or TNF on the effector phase of contact hypersensitivity (CH) responses in animals given an adoptive transfer of primed lymphocytes from hapten-sensitized donors. Intracerebral injection of nanogram quantities of alpha-MSH inhibited the ability of peripherally administered IL-1 or TNF to induce both fever and neutrophilia without affecting the increase in plasma levels of serum amyloid P and fibrinogen. Also, nanogram quantities of alpha-MSH given intracerebrally to normal mice did not reverse the depressed CH responses observed after peripheral IL-1 or TNF administration. These findings suggest that both fever and neutrophilia are linked to the direct action of IL-1 or TNF on the brain. This was supported by the observation that an intracerebral injection of IL-1 or TNF in low doses increased core body temperature and circulating neutrophil numbers without affecting plasma levels of acute phase proteins or CH responsiveness. Our results provide additional support for the hypothesis that bidirectional control exists between elements of the neuroendocrine and immune systems.
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PMID:Neuropeptide regulation of inflammatory and immunologic responses. The capacity of alpha-melanocyte-stimulating hormone to inhibit tumor necrosis factor and IL-1-inducible biologic responses. 283 10

Ninety patients aged 41 to 68 years with the chronic patterns of coronary heart disease (CHD) were examined for the content of triiodothyronine (T3), total T4 and free thyroxine (FT4), thyrotropic hormone (TTH), adrenocorticotropic hormone (ACTH), and insulin. At the same time the patients were examined with the aid of the glucose tolerance test, determination of blood concentration of cholesterol, triglyceride, high density lipoprotein cholesterol, fibrinogen and soluble fibrin. The patients with CHD showed a decrease in the basal level of T3, T4, FT4 and elevation of TTH, ACTH and insulin in blood. A correlation was found between the basal of insulin and thyroid hormones and lipid metabolism in CHD patients. It was shown that thyroid hypofunction, unmarked clinically but detectable by the lowering of the content of thyroid hormones and rise of thyrotropic hormone in blood of CHD patients, might promote the development of hyperinsulinemia.
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PMID:[Relation between blood levels of thyroid hormones and insulin and lipid metabolism and the clinical course of chronic forms of ischemic heart disease]. 300 47

The purpose of this investigation is to study the ability of antibodies to penetrate sections of LR-WHITE resin. The methods used in this study were the following: (1) Reembedding of sections labeled with immunogold (1 nm) and peroxidase/DAB/gold chloride, (2) tilting of ultrathin sections treated with immunogold (1 nm), (3) immunolabeling of cylindrical structures embedded in LR-WHITE, (4) application of primary and secondary antibodies on opposite sides of ultrathin sections. Fibrin and human pituitary tissue was embedded in LR-WHITE and treated with anti-fibrinogen or anti-ACTH respectively (ACTH = Adrenocorticotropic hormone). No indication of antibody penetration into the section were found with either of the methods, contrary to findings in earlier publications. The significance of this result is that antigens cannot be demonstrated in the interior of LR-WHITE sections with post-embedding techniques. Furthermore, LR-WHITE resin may be used for quantitative immunoelectron microscopy, and the resin may be used for double immunogold labeling since the application of immunoreagents on opposite sides of the sections is completely safe.
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PMID:Antibody penetration into LR-White sections. 785 Mar 51

We have investigated whether parotin subunit (PS) and its partial synthetic peptide (P-10.2: TDDTAIVLLK), possess interleukin 1 (IL-1)-like activities, and act on cell lines other than lymphocytes. When Chang liver cells were cultured with P-10.2, PS or IL-1, P-10.2 and PS augmented the growth of Chang liver cells. On the other hand, IL-1 enhanced the growth of Change liver cells at 1 day of the initial culture and subsequently failed to enhance during at least 4-day incubation. Next, effects of P-10.2 and PS on the growth of Alexander cells and MH134 were investigated. The proliferation of Alexander cells was inhibited with P-10.2 or PS but not with IL-1. P-10.2 inhibited the growth of MH134 at day 1 and 3, while the growth of MH134 was shown not to be inhibited with PS and IL-1 at day 1, but rather suppressed them at day 3. These results suggest that P-10.2 augments the growth of non-malignant liver cells (Chang liver cells) but inhibits that of hepatoma cells (Alexander cells and MH134). P-10.2 enhanced fibrinogen and hepatoglobin secretion from Chang liver cells. In addition to their liver cell activation, P-10.2 and PS stimulated ACTH and beta-endorphin secretion from AtT-20 cells.
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PMID:Parotin subunit and its synthetic peptide possess interleukin 1-like activity and exert stimulating effects on liver cells and brain cells. 805 82

The purpose of the present study was to determine if opioid agonism (beta-endorphin) and antagonism (Naloxone) exert rheological and cardiovascular effects in normal humans and in patients with essential hypertension. Eight hypertensive patients were matched for age, sex, and body habitus (body mass index, waist to hip ratio) with eight normotensive healthy subjects. In all subjects, heart rate and blood pressure (continuous automatic recording), blood and plasma viscosity, fibrinogen, hematocrit, and platelet aggregation to ADP were evaluated during an infusion of human synthetic beta-endorphin (0.5 mg/h). On a different day and in randomized order, the subjects were submitted to another beta-endorphin infusion preceded by an i.v. naloxone bolus (5 mg in 5 min). beta-Endorphin and naloxone failed to significantly alter heart rate or blood pressure in both normotensive and hypertensive subjects. In hypertensive patients, beta-endorphin significantly increased blood viscosity and ADP-induced platelet aggregation, but only the former effect was naloxone-sensitive. In normotensive subjects, beta-endorphin caused a transient but significant decrease of platelet aggregation that was reversed by naloxone. These data suggest that beta-endorphin may play some role in the inhibitory control of platelet aggregation in normal subjects. An altered responsiveness of some rheological determinants to beta-endorphin seems to be present in human hypertension.
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PMID:Hemorheological and cardiovascular responses to beta-endorphin and naloxone in healthy subjects and in patients with essential hypertension. 807 68

The performance of many biomaterials in hemocompatibility tests is altered when blood is drawn from stressed subjects. A salient physiological response during stress is one in which hormones are released into plasma by the hypothalamo-pituitary-adrenal axis. We investigated the influence of basal and stress levels of epinephrine and beta-endorphin on the conformation of fibrinogen (Fbg), both in saline solution (under physiological conditions) and after its adsorption to polyethylene (PE), by FT-IR spectroscopy. Moreover, as Fbg is one of the major mediators of platelet adhesion, the behavior of platelets in contact with PE was also evaluated as a function of the two different hormone concentrations. Epinephrine was found to affect Fbg conformation and to increase platelet adhesion to PE at stress level. Basal and stress levels of beta-endorphin did not significantly affect the Fbg conformation and only induced adhesion of isolated platelets to the PE surface. A direct relationship was therefore found between Fbg conformation and platelet behavior. The response of platelets was affected by the stress status of donors through the influence of epinephrine on Fbg conformation.
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PMID:Fibrinogen conformation and platelet reactivity in relation to material-blood interaction: effect of stress hormones. 1460 74

Platelets play a critical role in homeostasis and blood clotting at sites of vascular injury, and also in various ways in innate immunity and inflammation. Platelets are one of the first cells to accumulate at an injured site, and local release of their secretome at some point initiate an inflammatory cascade that attracts leukocytes, activates target cells, stimulates vessel growth and repair. The level of exogenous ATP in the body may be increased in various inflammatory and shock conditions, primarily as a consequence of nucleotide release from platelets, endothelium and blood vessel cells. An increase of ATP release has been described during inflammation and this compound presents proinflammatory properties. ADP is a nucleotide known to induce changes in platelets shape and aggregation, to promote the exposure of fibrinogen-binding sites and to inhibit the stimulation of adenylate cyclase. Adenosine, the final product of the nucleotide hydrolysis, is a vasodilator and an inhibitor of platelet aggregation. There is a group of ecto-enzymes responsible for extracellular nucleotide hydrolysis named ectonucleotidases, which includes the NTPDase (nucleoside triphosphate diphosphohydrolase) family, the NPP (nucleoside pyrophosphatase/phosphodiesterase) family and an ecto-5'-nucleotidase. Therefore, we have aimed to investigate the effect of lipopolysaccharide endotoxin from Escherichia coli on ectonucleotidases in platelets from adult rats in order to better understand the role of extracellular adenine nucleotides and nucleosides in the maintenance of blood homeostasis in inflammatory processes. LPS administered in vitro was not able to alter the ATP, ADP, AMP and rho-Nph-5'-TMP hydrolysis of platelets from untreated rats in all concentrations tested (25-100 microg/ml). There was a significant decrease in ATP, ADP, AMP and rho-Nph-5'-TMP hydrolysis in rat platelets after 48 hours of LPS exposure (2 mg/Kg, i.p.). ATP and ADP hydrolysis has been reduced about 28% whereas it has been observed a significant 30% and 26% decrease on AMP and rho-Nph-5'-TMP hydrolysis. Platelet aggregation and platelet number have shown a significant decrease in LPS-treated rats (40% and 55%, respectively) when compared to control group. These results suggest that changes observed in platelet count and, consequently, in nucleotidase activities from circulatory system could alter extracellular nucleotide and nucleoside levels, which might modulate the inflammatory process.
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PMID:Endotoxemia alters nucleotide hydrolysis in platelets of rats. 1923 49

Familial Mediterranean fever (FMF) is an autoinflammatory disorder and is characterized by self-limited attacks of inflammation. Although mutations in the gene coding for pyrin are responsible for the inflammation seen in attacks, the question of whether the failure to mount an appropriate cortisol response to inflammation has any additive effects allowed us to plan this study. The aim was to determine the interactions between the neuroendocrine and immune system in patients with FMF and investigate the role of the neuroendocrine system in the acute inflammation process. Demographic characteristics, disease activity, mutation analysis, and duration of the disease were defined in 15 FMF patients (7 female, 8 male; mean age +/- SD: 9.1 +/- 4.2 years). The diagnosis was based on Tel-Hashomer criteria. Ten healthy volunteers and 21 active juvenile idiopathic arthritis (JIA) patients formed the control groups. Furthermore, 10 of these 15 patients with FMF were also studied during the attack-free period. Erythrocyte sedimentation rate (ESR) C-reactive protein (CRP), fibrinogen, adrenocorticotropic hormone (ACTH), cortisol, insulin-like growth factor-1 (IGF)-1, IGF binding protein (BP)-3, urinary cortisol levels, interleukin (IL)-1beta, IL-6, and tumor necrosis factor (TNF)-a were evaluated in FMF patients with attack and during the attack-free period. Although the median levels of ACTH (12.7 pg/ml) and cortisol (12 ug/dl) at 08:00 a.m. were lower in FMF patients during attack than in the attack-free period, these differences did not reach statistical significance. On the other hand, the median levels of ACTH were significantly lower during attack than in the healthy control group (p < 0.05). Median levels of IGF-1 (118.5 ng/ml) were significantly lower during FMF attack than in the attack-free period (p < 0.05). There was a negative correlation between IGF-1 and CRP (r = -0.47). The median level of IL-6 was 18.1 pg/dl during FMF attack and was significantly higher than in the attack-free period and in the healthy control group (p < 0.05). There was a negative correlation between cortisol level at 08:00 am and IL-6 (r = -0.45). When we compared JIA with FMF patients during attack, inappropriately low secretion of adrenal cortisol and ACTH and low urine cortisol levels were more pronounced in JIA than FMF Although it is more prominent in chronic inflammation, the neuroendocrine immune system seems to be impaired in relation to acute inflammation in FMF.
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PMID:Neuroendocrine immune system in familial Mediterranean fever. 2142 90

We report the case of a 7-month-old boy who developed hypofibrinogenemia (66.6 mg/dL; reference value, 170-405 mg/dL) during adrenocorticotropic hormone (ACTH) therapy for infantile spasms. Although the patient showed no clinical signs of a bleeding diathesis, we recommend that plasma fibrinogen levels should be monitored during ACTH therapy, which should be discontinued when fibrinogen levels fall below hemostatic levels (60.0mg/dL) or when bleeding tendencies are recognized.
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PMID:Hypofibrinogenemia caused by adrenocorticotropic hormone for infantile spasms: a case report. 2473 83


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