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Objective: To determine the prevalence of nocturnal polyuria (NP) in patients with spinal cord injury (SCI) during three different particular phases, and investigate the impact of injury level and injury type on the prevalence of NP. Design: A cross-sectional study. Setting: Neurogenic Bladder Study Group from six different rehabilitation centers across the country. Participants: 40 patients with SCI. Outcome measures: Patients were divided into three groups according to mobilization phase; 1st group included patients confined to bed (n =14), 2nd group included patients sitting on a wheelchair (n =19) and 3rd group included patients standing with an assistive ambulation device (n =7). NP was assessed by nocturnal polyuria index (NPi) and nocturnal urine production (NUP) indexes. Results: No significant difference was found between the groups (P=0.312 for NPi and P=0.763 for NUP) in terms of the presence of NP according to their mobilization phase. The night and 24-hour urine volumes showed no significant difference between the groups (P=0.907 and P=0.395 respectively). The NPi and NUP values did not show a significant difference between male and female patients (P=0.826, P=0.364 respectively), patients with the injury level of ?T6 and

Phoenixin (PNX) and nesfatin-1 are localised in the hypothalamus and the pituitary gland. Moreover, the most of the PNX-expressing neurons in the hypothalamus also co-express nesfatin-1. These outcomes may suggest that there is an interaction between PNX and nesfatin-1, at least in terms of neuroendocrine-mediated regulations. Hence, the study was planned to find out the effects of centrally delivered PNX and nesfatin-1 on male sex hormones or to show the interactive association of intracerebroventricularly (ICV) injected PNX+nesfatin-1 combination on the release of male hormones. PNX and nesfatin-1, single or together, were delivered ICV to different male Wistar Albino rat groups. Both PNX and nesfatin-1 induced a significant enhancement in plasma FSH, LH and testosterone without inducing any alteration in plasma GnRH in the rats. The central combinatorial treatment of both the neuropeptides produced a more potent rise in male plasma hormone levels than treating with single neuropeptide. In summary, our preliminary data show that centrally delivered PNX and nesfatin-1 can affect plasma male hormone levels. Moreover, that the combinatorial treatment with both the neuropeptides in male rats leading to a more potent effect on the plasma male hormone levels might suggest that both these neuropeptides act synergistically in terms of regulation of male HPGA.

The current study was designed to determine the effect of centrally chronic-administrated histamine and histaminergic receptors antagonist on the hypothalamic cyclooxygenase (COX) and lipoxygenase (LOX) enzymes amount. Studies were performed in male Sprague–Dawley rats. Histamine (100 nmol), histaminergic H1 receptor antagonist chlorpheniramine (100 nmol), histaminergic H2 receptor antagonist ranitidine (100 nmol) or histaminergic H3/H4 receptor antagonist thioperamide (100 nmol) was injected intracerebroventricularly for 7 days. Central chronic histamine treatment caused an increase in all three enzymes amount in the hypothalamus. Histaminergic receptors antagonist chronic-treatments with chlorpheniramine, ranitidine and thioperamide produced to decrease in hypothalamic COX-1 amount and to increase in hypothalamic COX-2 and LOX amounts. In conclusion, our findings show that the central histaminergic system has a potential for effect the central COX and LOX pathways. This could be interpreted that central histaminergic and central COX and LOX pathways have an interaction to regulate in many central nervous system functions.

Nesfatin-1 is an anorexic nucleobindin-2 -derived peptide and it has directly and centrally effect on the heart. The current study was designed to determine the effect of centrally and peripherally administered nesfatin-1 on electrocardiography (ECG) of healthy both fasted rats for 12 h and satiated rats fed ad libitum. In order to record ECG, the electrodes were placed limbs of at lead II under ketamine (50 mg/kg; im) and xylazine (20 mg/kg; im) anesthesia mix. Centrally administered different doses of nesfatin-1 (100 and 200 pmol; icv) resulted in dose- and time-dependently a statistically significant increase (p

Rheumatoidarthritis (RA) is an inflammatory autoimmune disease that causes chronic painand joint destruction. T cells activation has an important role in RApathogenesis. Activation of T lymphocytes requires the co-stimulatory signalsprovided by antigen-presenting cells. T-cell activation without co-stimulationresults in anergy. In this study, to inhibit the activation of T lymphocytesformed in the experimental arthritis, tolerogenic dendritic cells were aimed tobe obtained by the genetical modification of dendritic cells with CTLA4-KDEL overexpression in endoplasmicreticulum. Then, RA created animals treated with tolDCs and the effect oftreatment on blood parameters were investigated.Forthis purpose, mouse collagen induced arthritis model was used. The mice witharthritis were intraarticularly treated with modified tolDCs. It was observedthat the treatment group significantly reversed the increase in the jointthickness and the increase in the number of white blood cells, especially withthe increase in neutrophils when compared with control groups.Asa result, genetically modified tolDCs reduced the clinical symptoms ofexperimental arthritis and also reversed the changes in blood parameters due toexperimental arthritis in mice., Rheumatoid arthritis (RA) is an inflammatory autoimmune disease that causes chronic pain and joint destruction. T cells activation has an important role in RA pathogenesis. Activation of T lymphocytes requires the co-stimulatory signals provided by antigen-presenting cells. T-cell activation without co-stimulation results in anergy. In this study, to inhibit the activation of T lymphocytes formed in the experimental arthritis, tolerogenic dendritic cells were aimed to be obtained by the genetical modification of dendritic cells with CTLA4-KDEL overexpression in endoplasmic reticulum. Then, RA created animals treated with tolDCs and the effect of treatment on blood parameters were investigated.For this purpose, mouse collagen induced arthritis model was used. The mice with arthritis were intraarticularly treated with modified tolDCs. It was observed that the treatment group significantly reversed the increase in the joint thickness and the increase in the number of white blood cells, especially with the increase in neutrophils when compared with control groups.As a result, genetically modified tolDCs reduced the clinical symptoms of experimental arthritis and also reversed the changes in blood parameters due to experimental arthritis in mice.