Antibody response of sheep to simultaneous vaccination of foot-and-mouth disease, peste des petits ruminants, sheep pox and goat pox, and bluetongue vaccines.

There are many infectious animal diseases in T urkey and generally, vaccination is the primarly control strategy to combat them. However, it is difficult to apply all vaccines in a definite period in the field due to limitations of the labor and finance. Rapid vaccination and effective use of labor can be possible with the help of simultaneous vaccine administrations. The study aims to show the effects of simultaneous foot-and-mouth disease (FMD), peste des petits ruminants (PPR), sheep pox and goat pox (SGP), and bluetongue (BT) vaccine administration on the antibody response of sheep. For this aim, 30 sheep were divided into one experiment and 5 control groups. Blood samples were collected in each group at 0, 30 and 60 days post-vaccination (DPV). Immune response was measured with virus neutralization test (VNT) and, liquid phase blocking ELISA (LPBE) for FMDV; VNT for BTV and PPR. A live virus challenge study was performed to determine the immune response of SGP vaccine. As a result, antibody titers for each vaccine agent decreased on 60 DPV with the simultaneous vaccination except FMD. The difference between means of antibody titer decrease with single and simultaneous vaccinations is significant especially for BTV and PPR vaccines at 60DPV (p<0.05). Briefly, this decreasing immune response of three live vaccines can be explained with the development of the interference, administration of these vaccines from the same injection site, the effect of cytokines, especially IL-10 effect of SGP vaccine. It was concluded that four vaccines can not be used simultaneously in sheep.

No relationship between lipoprotein-associated phospholipase A2, proinflammatory cytokines, and neopterin in Alzheimer's disease.

OBJECTIVE: Lipoprotein-associated phospholipase A2 (Lp-PLA2) is a reported risk factor for dementia. However, the relationship between Alzheimer's disease (AD) and Lp-PLA2 is still debatable and, to the best of our knowledge, no study has evaluated the associations between levels of Lp-PLA2, proinflammatory cytokines, and neopterin in AD. METHODS: In total, 59 patients with AD and 38 non-demented individuals were included in the case-control study. Fasting serum concentrations of interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), neopterin, and Lp-PLA2 were determined using ELISA. The associations between AD and each of the variables were analyzed by logistic regression. RESULTS: The median Lp-PLA2 levels in AD and controls were similar (P=0.29, not significant). Median serum neopterin and IL-6 levels were significantly higher in patients with AD than in controls (P=0.0001 and P=0.03, respectively). In regression analyses, median neopterin levels, a lower level of education, and female gender were significantly associated with AD when compared with controls (OR, 31.44, 95% CI 3.59-275.28, P=0.002; OR, 4.35, 95% CI 1.13-16.61, P=0.032; OR, 7.25, 95% CI 1.88-28.00, P=0.004, respectively). CONCLUSION: In contrast to previous evidence suggesting its role in dementia and AD, Lp-PLA2 enzyme levels were higher in the controls, and no relationship between Lp-PLA2 and either proinflammatory cytokines or neopterin was identified in AD. Elevated neopterin levels may be considered inflammatory markers of AD.

Is obesity a possible modifier of periodontal disease as a chronic inflammatory process? A case-control study.

BACKGROUND AND OBJECTIVE: This cross-sectional case-control study was conducted to provide a comparative evaluation of clinical periodontal measurements, together with serum levels of certain bioactive peptides and inflammatory cytokines, in relation to obesity. For this purpose, clinical periodontal measurements and the levels of serum leptin, adiponectin, interleukin-6 (IL-6), C-reactive protein and soluble intercellular adhesion molecule-1 of obese female individuals and their nonobese counterparts were compared. MATERIAL AND METHODS: Sixty obese (body mass index (BMI) > 30) and 31 nonobese (BMI < 30) female subjects were recruited for the present study. Before any periodontal intervention, serum samples were obtained and full-mouth clinical periodontal measurements were recorded at six sites per tooth. ELISA was used for the biochemical analysis. Data were tested statistically. RESULTS: Clinical attachment level was significantly higher in the obese group compared with the nonobese control group (p < 0.05). Serum levels of leptin and IL-6 were significantly higher in the obese group (p < 0.05). BMI correlated with the serum levels of inflammatory molecules (p < 0.05), but not with clinical periodontal parameters, in the obese group. CONCLUSION: In conclusion, obesity does not seem to have a prominent effect on clinical periodontal parameters but it does have many correlations with circulating inflammatory molecules. As suggested in the literature, increased levels of leptin and IL-6 in the obese group might be one explanation for a possible relationship between obesity and periodontal disease. A prospective study is warranted to clarify, in greater detail, the effects of obesity on periodontal health.

Association of osteopontin and tumor necrosis factor-α levels with insulin resistance in obese patients with obstructive sleep apnea syndrome.

OBJECTIVE: The aims of this study were to compare the tumor necrosis factor (TNF)-α and osteopontin levels, to identify the relationship between insulin resistance (IR) and osteopontin levels in obese patients with and without obstructive sleep apnea syndrome (OSAS). METHOD: The study population included 62 obese patients (35 males, 27 females) with OSAS and was compared with 26 obese patients (16 males, 10 females) without OSAS as a control group. Polysomnographic evaluation, spirometric tests and arterial blood gas sampling were performed on the obese patients with OSAS. Plasma levels of TNF-α and osteopontin were measured by enzyme-linked immunosorbent assays during the process. IR was estimated using the homeostasis model assessment (HOMA). RESULTS: Mean plasma levels of fasting glucose, insulin, HOMA, liver function test, hematocrit, leukocyte, TSH, free T4, fibrinogen, TNF-α, and osteopontin were similar in the 2 groups. In patients with OSAS, mean osteopontin levels were positively correlated with mean fasting insulin levels (r=0.306, p=0.01), HOMA (r=0.299, p=0.01), apnea-hypopnea index (r=0.377, p=0.03) and Epworth Sleepiness Scale (r=0.299, p=0.01). However, mean TNF-α levels were negatively correlated with Epworth Sleepiness Scale (r=-0.298, p=0.01) in the patients with OSAS. CONCLUSIONS: It was observed that TNF-α and osteopontin levels showed no difference between obese patients with and without OSAS. However, osteopontin levels increased with fasting insulin, IR, OSAS severity, and daytime sleepiness.

Thermogenic response and leptin levels rise after recovery of the euthyroid state.

OBJECTIVE: The aims of the study were to compare: a) the thermogenic responses in subclinical hypothyroidism (SH) and euthyroid state; b) the relationship between thermogenic response and leptin level. METHODS: Thirty women diagnosed with SH (mean age 39.9+/-4.1 yr; body mass index 23.2+/-2.5 kg/m(2)) were enrolled in the study. Thyroid function tests, leptin, and lipid profiles were measured during SH and after stable euthyroidism was recovered. Thermogenic response was measured by Water Immersion Calorimetry during SH and after the euthyroid state was attained. RESULTS: The mean level of thermogenic response was found to be 1.45+/-0.43 kcal/kg*h in women with SH. It changed to 1.54+/-0.77 kcal/kg*h (p=0.01) in the euthyroid state; the change was statistically significant. Mean level of leptin was found to be 7.22+/-2.6 ng/ml in SH; and 15.8+/-8.0 ng/ml in the euthyroid state. There was a positive correlation between leptin and free T(3) (r=0.460, p=0.009) levels in SH. There were positive correlations between leptin level and fat mass in SH (r=0.820, p=0.01) and in the euthyroid state (r=0.700, p=0.03). CONCLUSIONS: No correlations were found between thermogenic response and leptin levels in SH and in the euthyroid state. Thermogenic response and leptin levels rose after the euthyroid state was recovered.

The effects of local and sustained release of fibroblast growth factor on wound healing in esophageal anastomoses.

BACKGROUND/PURPOSE: Postsurgical complications, such as anastomotic leaks in patients with esophageal atresia, have remained unchanged during the last 3 decades. Growth factors enhance healing in several wound-healing models. Therefore, an experimental study was used to evaluate the effects of local and sustained release of basic fibroblast growth factor (FGF) on wound healing in esophageal anastomoses. MATERIALS AND METHODS: Twenty-four male Wistar albino rats, which were subjected to a 1-cm segmental resection of the abdominal esophagus followed by end-to-end anastomosis, were allocated into 3 groups. Group I, the control group, had no gelatin film applied to the anastomosis. In group II (gelatin film without FGF) and group III (gelatin film with FGF), anastomoses were covered with unloaded and 2.55 mug FGF-loaded gelatin films, respectively. On postoperative day 7, bursting pressures, histopathologic collagen deposition, and tissue hydroxyproline concentrations of the anastomoses were then analyzed and compared. RESULTS: Mean bursting pressures, mean submucosal and muscular collagen deposition scores, and mean tissue hydroxyproline concentrations differed significantly between groups. Mean bursting pressures were 22.5 +/- 3.1 mm Hg in group I, 29 +/- 1.6 mm Hg in group II, and 63.2 +/- 6.8 mm Hg in group III (P < .001). Mean submucosal collagen deposition scores (group I: 0.7 +/- 0.2, group II: 0.7 +/- 0.1, group III: 1.5 +/- 0.2; P = .02) and mean muscular collagen deposition scores (group I: 0.8 +/- 0.2, group II: 0.8 +/- 0.1, group III: 1.8 +/- 0.1; P = .01) were significantly higher in FGF animals than the other in the other 2 groups. Mean tissue hydroxyproline concentrations were 2.4 +/- 0.5 microg/mg in group I, 3.9 +/- 0.4 microg/mg in group II, and 6.0 +/- 1.0 microg/mg in group III (P = .007). CONCLUSION: Local and sustained release of FGF enhanced wound healing in esophageal anastomoses in this animal model.

Dehydroepiandrosterone and human adipose tissue.

OBJECTIVE: The aim of this study was to investigate whether DHEA alters the proliferation and differentiation of human sc and visceral adipose cells in primary cultures. METHOD: Sc and omental adipose tissue was obtained from 10 female donors aged 36+/-3.6 yr with a body mass index (BMI) of 33+/-3.21 kg/m2. Stromal vascular cells were isolated and cultured using modified procedures described by Entenmann and Hauner. For the proliferation assay, stromal-vascular cells from sc and visceral adipose tissue cultures were fed with proliferation media containing 0, 25 or 100 microM DHEA for 3 days. At the end of this treatment period, two type cultures were prepared for determining their metabolic activity using the sulforhodamine B staining procedure. RESULTS: The metabolic activity of proliferating human visceral adipose tissue was higher than sc adipose tissue. The activity of proliferating human visceral tissue cultures decreased more than the sc tissue as the level of DHEA in the cultures was increased. CONCLUSIONS: These data suggest that DHEA predominantly influences the proliferation and differentiation of human omental adipose tissue.

Effects of sibutramine on thermogenesis in obese patients assessed via immersion calorimetry.

Glucose utilization studies show that sibutramine-induced thermogenesis is mediated via selective sympathetic activation of brown adipose tissue. The goal of the present study was to use a new calorimetry method in which resting metabolic rate is enhanced to evaluate the effects of sibutramine treatment on thermogenesis. Sixty obese women were included in the study. Subjects were divided into 2 equal groups-the placebo and sibutramine treatment groups. The sibutramine group was given sibutramine 10 mg daily for 12 wk. At baseline and at the end of the 12-wk treatment period, thermogenic measurements were taken with the use of water immersion calorimetry. Subjects were examined at weeks 4, 8, and 12 of treatment to identify adverse effects. Body mass index, measured at 31.5+/-2.05 kg/m2 in the placebo group, decreased to 30.4+/-2.94 kg/m(2) after 12 wk (P=.07). In the sibutramine group, it decreased from 33.5+/-4.1 kg/m(2) to 30.9+/-4.8 kg/m(2) (P<.05). In the sibutramine group, mean thermogenic response changed from a baseline value of 1.27+/-0.29 kcal/kg/h to 1.44+/-0.13 kcal/kg/h after 12 wk of treatment. In the placebo group, the baseline value was 1.56+/-0.27 kcal/kg/h; it changed to 1.33+/-0.36 kcal/kg/h at the end of 12 wk. The findings of this study suggest that sibutramine treatment promotes thermogenesis, thus facilitating weight loss. Calorimetry enhances resting metabolism through more efficient heat transfer from the body.