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Aim: The major target of this research is to examine whether there is any connection between the levels of vitamin D and anti-inflammatory mediators in patients with fibromyalgia syndrome (FMS). Materials and Methods: The study contains 30 FMS diagnosed and 25 healthy female individuals and the determination of FMS was made according to the standards of 2010 American College of Rheumatology (ACR). Vitamin D, vitamin D receptor (VDR), vitamin D binding protein (VDBP) levels, and anti-inflammatory cytokine (IL-4, IL-10, TGF-β) levels in the serum of patients with FMS and healthy individuals were measured using enzyme-linked immunosorbent assay (ELISA). Results: The concentrations of vitamin D, VDR, and VDBP were determined to be higher in healthy controls than in patients with FMS (p<0.001). Correlating with this, IL-4, IL-10, and TGF-β levels were measured remarkably higher in the healthy group than in the FMS patients (p<0.001). Conclusion: Low vitamin D levels may cause a decrease in anti-inflammatory cytokine levels and their immunosuppressive effect in FMS. [ABSTRACT FROM AUTHOR]

Background The aim of this study was to determine the effectiveness of cortisol, interleukin (IL)-6, C-reactive protein (CRP), and white blood cell (WBC) count as inflammatory markers to evaluate the postoperative inflammatory response associated with various abdominal surgical procedures in rats. Methods Wistar albino rats (N=152) were randomly assigned to 7 groups: control, hepatectomy, splenectomy, nephrectomy, colectomy, gastrectomy, and sham. Apart from the control group, each group was then divided into 3 subgroups: 6th, 24th and 48th h. Thus, a total of 19 groups were defined, each including 8 rats. At the 6th, 24th and 48th h following the surgical procedures blood samples from each rat were collected. The plasma concentrations of IL- 6, cortisol, CRP, and WBC were measured. Results Both the surgery category and the elapsed time after the surgery had a significant effect on IL-6 levels (P<0.0001). Blood CRP levels were primarily determined by the surgery category (P<0.0001). Neither surgery nor the elapsed time had a significant effect on the cortisol levels. The elapsed time after surgery was the major factor that influenced the differences in WBC count among the surgery groups (P<0.0001). Conclusions Our results cumulatively indicate that the levels of IL-6, CRP, and cortisol and WBC count change at different time points after several abdominal surgical procedures. Cortisol level is not related to the type of surgical procedure or the elapsed time, while WBC count decreases with the elapsed time. None of the changes in the markers investigated in this study is specifically related to the category of abdominal surgical procedure. [ABSTRACT FROM AUTHOR]

Severe hemorrhage lowers arterial pressure by suppressing sympathetic activity. This study tested the hypothesis that the decompensatory phase of hemorrhage is mediated by the ventrolateral periaqueductal gray (vlPAG), a region importantly involved in the autonomic and behavioral responses to stress and trauma. Neuronal activity in the vlPAG was inhibited with either lidocaine or cobalt chloride 5 min before hemorrhage (2.5 ml/100 g body wt) was initiated in conscious, unrestrained rats. Bilateral injection of lidocaine (0.5 [micro]l of a 2% or 1 [micro]l of a 5% solution) into the caudal vlPAG delayed the onset and reduced the magnitude of the hypotension produced by hemorrhage significantly. In contrast, inactivation of the dorsolateral PAG with lidocaine was ineffective. Cobalt chloride (5 mM; 0.5 [micro]l), which inhibits synaptic transmission but not axonal conductance, also attenuated hemorrhagic hypotension significantly. Microinjection of lidocaine or cobalt chloride into the vlPAG of normotensive, nonhemorrhaged rats did not influence cardiovascular function. These data indicate that the vlPAG plays an important role in the response to hemorrhage. hemorrhage; cardiovascular regulation; lidocaine; cobalt

Background Helicobacter pylori is associated with gastrointestinal diseases such as gastritis, peptic ulcers, malignancy and lymphoma, and extra-gastrointestinal conditions. H. pylori infection is negatively associated with children's growth. Chronic inflammation of the stomach that results in the loss of appetite and, dysregulation of neuroendocrine hormones such as leptin, and ghrelin are the probable reasons of this negative association. The objective of this study is to determine the serum levels of leptin, ghrelin, and IGF-1 in H. pylori-infected children and their relations with growth. Materials and methods A hundred and sixty-one school children aged between 6 and 14 years were selected randomly from five primary schools representing a cross section of population. Demographic and sociocultural characteristics, and anthropometric measurements were recorded. Serum H. pylori IgG, insulin-like growth factor-1, leptin, and ghrelin levels were measured in all children. The children were grouped according to the nutritional status and Helicobacter pylori seropositivity. Nutritional indices were compared among groups in association with serum leptin, ghrelin, and insulin-like growth factor-1 levels. Results H. pylori IgG positivity was found in 34.2%, and 14.9% of children were malnourished. H. pylori seropositivity was significantly higher in older ages (10.32 ± 2.26 vs 9.53 ± 2.36 years, p = .036), and body weight and height Z scores were significantly lower in H. pylori-seropositive children (−0.33 ± 1.08 vs 0.04 ± 1.26, p = .044 and 0.13 ± 0.92 vs 0.23 ± 0.91, p = .018 respectively). H. pylori seropositivity was found to be an independent risk factor for shorter body height ( p = .01). Serum leptin, ghrelin, and IGF-1 levels were not associated with H. pylori IgG seropositivity (0.35 vs 0.55 ng/mL, p = .3; 3267.4 ± 753.0 vs 2808.3 ± 911.4 pg/mL, p = .06; 470 ± 176 vs 521 ± 179 ng/mL, p = .32, respectively). Conclusions Children infected with H. pylori are prone to short stature. This effect seems to be independent of neuroendocrine hormones. [ABSTRACT FROM AUTHOR]

1. In the present study, we aimed to determine the involvement of brain thromboxane A2 (TXA2) in blood pressure decreases evoked by acute and/or graded haemorrhage in rats. 2. Sprague-Dawley rats were used throughout the study. Acute haemorrhage was achieved by withdrawing a total volume or 2.1 and 2.5 mL blood/100 g bodyweight over a period of 10 min. A microdialysis study was performed in a hypothalamic area to measure extracellular TXA2 levels. Graded haemorrhage was conducted successively by withdrawing carotid arterial blood (0.55 mL/100 g bodyweight) over a 10 s period four times (S1-S4) at 5 min intervals. Furegrelate (125, 250 and 500 µg), a TXA2 synthase inhibitor, was injected intracerebroventricularly (i.c.v.) 60 min before acute or graded haemorrhage was initiated. U-46619 (0.5, 1 and 2 µg, i.c.v.), a synthetic TXA2 analogue, was administered 5 min before acute haemorrhage (2.1 mL/100 g bodyweight). 3. Acute haemorrhage produced a severe and long-lasting decrease in blood pressure and had a tendency to increase heart rate. Both haemorrhage protocols (2.1 or 2.5 mL/100 g) generated similar approximate twofold increases in extracellular hypothalamic TXA2 levels. Intracerebroventricular furegrelate (250 µg) pretreatment completely blocked the TXA2 increases induced by acute haemorrhage. Furegrelate administration (100, 250 and 500 µg, i.c.v.) attenuated the fall in arterial pressure evoked by acute haemorrhage and caused significant increases in heart rate at all doses injected. 4. Graded haemorrhage progressively lowered arterial pressure and increased plasma vasopressin and adrenaline levels in the last period. Furegrelate-injected rats were greatly resistant to the hypotensive effect of haemorrhage for all degrees of blood removed. Plasma adrenaline and vasopressin levels were significantly elevated in furegrelate-pretreated rats compared with the saline-treated group during S2-S3 and S4, respectively. U-46619 administration caused small but statistically significant decreases in arterial pressure induced by haemorrhage. 4. The results show that acute hypotensive haemorrhage increases extracellular hypothalamic TXA2 levels. The increase in brain endogenous TXA2 levels involves a decrease in blood pressure evoked by haemorrhage because the blockade of TXA2 synthesis by furegrelate pretreatment attenuated the haemorrhagic hypotension. Increases in plasma adrenaline and vasopressin levels may mediate this effect. [ABSTRACT FROM AUTHOR]

In the present study, both the effects of intracerebroventricular (i.c.v.) injection of cytidine-5′-diphosphate choline (CDP-choline) on plasma vasopressin levels and the choline involvement of these effects were investigated. I.c.v. administration of CDP-choline (0.5, 1.0 and 2.0 μmol) increased plasma vasopressin levels dose- and time-dependently. I.c.v. injection of equimolar dose of choline (1 μmol) produced similar vasopressin response. However equimolar dose of cytidine (1 μmol; i.c.v.), the other hydrolysis product of CDP-choline, did not affect plasma vasopressin levels. Pretreatment of rats with hemicholinium-3, neuronal high affinity choline uptake inhibitor (20 μg; i.c.v.) blocked the vasopressin response to i.c.v. CDP-choline (1 μmol). Pretreatment of rats with mecamylamine (50 μg; i.c.v.), a nonselective nicotinic receptor antagonist, abolished the increase in plasma vasopressin induced by CDP-choline while atropine (10 μg; i.c.v.), nonselective muscarinic receptor antagonist, failed to change the response. In conclusion, intracerebroventricularly injected CDP-choline can increase plasma vasopressin levels by activating central nicotinic cholinergic receptors through the activation of presynaptic cholinergic mechanisms. [ABSTRACT FROM AUTHOR]