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1.
Ahmet Celik Mehmet Balin Mehmet Ali Kobat Kenan Erdem Adil Baydas Musa Bulut Yakup Altas Suna Aydin Suleyman Aydin 《Cardiovascular therapeutics》2013,31(3):174-178
The pathophysiology of cardiac syndrome X (CSX) is still unclear, but most patients with CSX have endothelial dysfunction. It has been shown that adropin uniquely effects the regulation of endothelial function. The purpose of the study was to evaluate the role of adropin in CSX. Eighty‐six consecutive cardiac syndrome X‐diagnosed patients and 86 age‐sex matched healthy subjects were enrolled into the study. Serum adropin levels, nitrite/nitrate levels were measured in each subject. The adropin levels were significantly lower in patients with CSX than healthy subjects (1.7 ± 0.8 ng/mL and 3.4 ± 1.8 ng/mL, respectively; P < 0.001). The BMI values of patients with CSX were significantly higher than control subjects (28.1 ± 2.4 kg/m2 and 26.0 ± 3.7 kg/m2, respectively; P < 0.001). Plasma nitrite/nitrate levels were lower in patients with CSX than control subjects (15.9 ± 1.6 μmol/L vs. 25.4 ± 2.8 μmol/L, respectively; P < 0.001), and they have a significantly positive correlation with plasma adropin levels (r = 0.463, P < 0.001). In the multiple linear regression analysis, nitrite/nitrate levels, BMI, and adropin were found to be independent risk factors for CSX. A ROC curve is used to identify the ability of adropin levels to predict the cardiac syndrome X. The area under the ROC curve was 0.854 for adropin levels (P = 0.0001). The sensitivity and specificity values of adropin levels were 90.7 and 70.9%, respectively (cut‐off value 2.73). In conclusion, lower serum adropin levels were associated with CSX. Adropin is an independent risk factor for CSX. 相似文献
2.
Effect of melatonin and vitamin E on diabetes-induced learning and memory impairment in rats 总被引:6,自引:0,他引:6
Previous studies indicate that diabetes mellitus might be accompanied by a certain erosion of brain function such as cognitive impairment. The aim of this study was to examine and compare the effects of melatonin and vitamin E on cognitive functions in diabetic rats. Diabetes was induced in male albino rats via intraperitoneal streptozotocin injection. Learning and memory behaviors were investigated using a spatial version of the Morris water maze test. The levels of lipid peroxidation and glutathione were detected in hippocampus and frontal cortex. The diabetic rats developed significant impairment in learning and memory behaviors as indicated by the deficits in water maze tests as compared to control rats. Furthermore, lipid peroxidation levels increased and glutathione concentration decreased in diabetic rats. Treatment with melatonin and vitamin E significantly ameliorated learning and memory performance. Furthermore, both antioxidants reversed lipid peroxidation and glutathione levels toward their control values. These results suggest that oxidative stress may contribute to learning and memory deficits in diabetes and further suggest that antioxidant melatonin and vitamin E can improve cognitive impairment in streptozotocin-induced diabetes. 相似文献
3.
The purpose of this study was to determine the possible effect of genetic factors on Bolton tooth-size discrepancy. Subjects who applied for orthodontic treatment and their siblings (106 females and 78 males) were included in the study. The ages of the subjects ranged from 13 to 21 years. The siblings were grouped according to gender: male-male (24 pairs), female-female (38 pairs) and male-female (30 pairs). Mesio-distal tooth size was measured using a pair of dividers with fine tips, and Bolton anterior and overall ratios were calculated. The effect of heritability on Bolton ratios was studied by means of Harvey's mixed model least-squared and maximum likelihood computer program (LSMLMW) model type II.Statistical analysis showed that heritability was effective on Bolton tooth-size discrepancy in all groups except the male-female group. Siblings of the same gender showed high heritability for anterior and overall ratios, but no statistically significant difference was observed in the siblings of different gender. 相似文献
4.
Thinner containing 60-70% toluene is a neurotoxic mixture, which is widely used as an aromatic industrial solvent. This product has been shown to cause functional and structural changes in the central nervous system. Thinner generates reactive oxygen species and the toxic effects relating to these reactants. We have investigated the effect of exposure to high concentrations (3000 ppm) of thinner for 45 days (1 h/day) on cognitive function and the levels of neural cell adhesion molecules (NCAM) and lipid peroxidation products in the hippocampus, cortex and cerebellum of rats. Thinner exposure caused a significant increase in lipid peroxidation products (malondialdehyde and 4-hydroxyalkenals) in all brain regions. Levels of NCAM 140 and NCAM 180 kDa were significantly decreased in the hippocampus and cortex of the thinner-exposed group. Furthermore, thinner-exposed rats showed cognitive deficits in passive avoidance and Morris water maze tasks. These cognitive deficits may be due to both elevated oxidative stress and changes in synaptic plasticity. Almost all studied parameters were reversed in animals which were allowed to recover from thinner inhalation, suggesting that the effects of exposure to thinner, at least for 1 h/day for 45 days, are reversible. 相似文献
5.
Ramazan Bal Giyasettin Baydas 《Journal of the Association for Research in Otolaryngology》2009,10(2):281-293
Electrophysiological studies from mice in vitro have suggested that octopus cells of the mammalian ventral cochlear nucleus
(VCN) are anatomically and biophysically specialized for detecting the coincident firing of a population of auditory nerve
fibers. Recordings from cats in vivo have shown that octopus cells fire rapidly and with exceptional temporal precision as
they convey the timing of that coincidence to higher auditory centers. The current study addresses the question whether the
biophysical properties of octopus cells that have until now been examined only in mice, are shared by octopus cells in cats.
Whole-cell patch-clamp recordings confirm that octopus cells in brain slices from kittens share the anatomical and biophysical
features of octopus cells in mice. As in mice, octopus cells in kittens have large cell bodies and thick dendrites that extend
in one direction. Voltage changes produced by depolarizing and hyperpolarizing current injection were small and rapid. Input
resistances and membrane time constants in octopus cells of 16-day-old kittens were 15.8 ± 1.5 MΩ (n = 16) and 1.28 ± 0.3 ms (n = 16), respectively. Octopus cells fired only a single action potential at the onset of a depolarizing current pulse; suprathreshold
stimuli were greater than 1.8 nA. A tetrodotoxin (TTX)-sensitive sodium conductance (g
Na) was responsible for the generation of the action potentials. Octopus cells displayed outward rectification that lasted for
the duration of the depolarizing pulses. Hyperpolarizations produced by the injection of current exhibited a depolarizing
sag of the membrane potential toward the resting value. A 4-aminopyridine (4-AP) and α-dendrotoxin (α-DTX)-sensitive, low-voltage-activated
potassium conductance (g
KL) and a ZD7288-sensitive, mixed-cation conductance (g
h) were partially activated at rest, giving the octopus cells low input resistances and, as a consequence, brief time constants.
In 7-day-old kittens, action potentials were taller and broader, input resistances higher, and both inward and outward rectification
was weaker than in 16-day-old kittens. Also as in mice, stellate cells of the VCN fired trains of action potentials with constant
interspike intervals when they were depolarized (n = 10) and bushy cells of the VCN fired only a single action potential at the onset of depolarizations (n = 6). In conclusion, the similarity of octopus cells in mice and kittens suggests that the anatomical and biophysical specializations
that allow octopus cells to detect and convey synchronous firing among auditory nerve fibers are common to all mammals. 相似文献
6.
OBJECTIVE: To evaluate the skeletal effects of nonsurgical rapid maxillary expansion (RME) on craniofacial structures with bone scintigraphy in young adult female subjects. MATERIALS AND METHODS: The material of the present study consists of scintigraphic records taken from 17 early adult females treated with RME. All patients had a bilateral posterior crossbite, transverse maxillary deficiency, deep palatal vault, and dental crowding at the beginning of the treatment. The age range of the patients was 16.1 to 18.8 years, and the mean age was 17.3 +/- 0.86 years. Bone scintigraphy records were obtained before RME (T1), during the splitting of the midpalatal suture (T2), and after the end of active widening period (T3). Repeated measure analysis of variance was used to assess the differences between the periods. In addition, Bonferroni multiple comparison tests were applied to the measurements at which F values were found to be statistically significant. RESULTS: According to the statistical analysis, significant activity changes were found in all regions studied and in all slices. The metabolic activity in all regions showed significant increases up to the separation of the midpalatal suture (T1-T2), whereas the metabolic activity exhibited a remarkable decrease (T2-T3) after the opening of the midpalatal suture. CONCLUSIONS: Scintigraphic records revealed an increase in the regions of interest scores during RME in all regions and all slices. Therefore, it can be speculated that RME has had not only dental effects but also skeletal effects on young adult patients. 相似文献
7.
We aimed to study the effects of gingko biloba extract (EGb) on oxidative stress, astrocyte maturation and cognitive disfunction in offspring of hyperhomocysteinemic rats. Hyperhomocysteinemia was induced in the pregnant rats by administration of methionine (1 gr/kg body weight) dissolved in drinking water throughout pregnancy. One group of animals has received same amount of methionine plus 100 mg/kg/day EGb during pregnancy. On the postnatal day 1, half of the pups from all groups were sacrificed to study the lipid peroxidation (LPO) in different subfractions of brain. Other half of pups were tested in Morris water maze to assess differences in learning and memory performance at the 75 days of age. Maternal hyperhomocysteinemia significantly increased LPO levels especially in mitochondrial subfraction of fetal pup brains. EGb significantly prevented this LPO inrease. Methionine administration to animals reduced glial fibrillary acidic protein (GFAP) expression in pup brains significantly. EGb administration improved GFAP expression significantly. Offspring of hyperhomocysteinemic animals had poor long term spatial memory performance on Morris water maze and EGb administration had no effect on impaired spatial memory. In conclusion, maternally induced hyperhomocysteinemia significantly increased oxidative stress, decreased expression of GFAP and impaired learning performance. Copyright © 2011 John Wiley & Sons, Ltd. 相似文献
8.
Sema T. Koz Nevhayat T. Gouwy Nevgul Demir Viktor S. Nedzvetsky Ebru Etem Giyasettin Baydas 《International journal of developmental neuroscience》2010
Maternal hyperhomocysteinemia is associated with a number of complications such as preeclampsia syndrome, thromboembolic events, repeated miscarriages, abruptio placentae, in utero fetal death, intrauterine fetal growth restriction and fetal neural tube defects. However, little is known about the mechanism of homocysteine on the degeneration of fetal brain. Thus, our study is aimed to investigate the effects of maternal hyperhomocysteinemia on oxidative stress and apoptosis in pup brain. Hyperhomocysteinemia was induced in female rats by way of administrating methionine dissolved in water at a dose of 1 g/kg body weight throughout the pregnancy. After delivery, level of lipid peroxidation (LPO; as malondialdehyde + 4-hydroxyalkenals) was determined in various fractions of pub brains. Furthermore, DNA fragmentation, levels of Bcl-2 protein and p53 mRNA expression were determined to evaluate apoptosis. Significant elevation was found in the levels of LPO in subcellular fractions of pup brains delivered from hyperhomocysteinemic mothers. DNA fragmentation, a hallmark of apoptosis was observed in the brain of pups of homocysteine group while significant reduction was seen in the levels of anti-apoptotic Bcl-2 levels. In addition, maternal hyperhomocysteinemia increased cerebral p53 mRNA expression above the control value. As a conclusion, we demonstrate and suggest that the pups of hyperhomocysteinemic mothers have an increased oxidative stress in brain tissues. The increased oxidative stress appears to cause apoptosis and cell death. These results may be significant to understand chronic pathology of the complications of hyperhomocysteinemia and congenital malformations of fetuses. 相似文献
9.
Moderate hyperhomocysteinemia is a risk factor for neurodegenerative diseases and complications during pregnancy. Increased homocysteine levels during pregnancy may elevate developmental risk on fetal brain structure and function. However, little is known about the mechanism of action of homocysteine on the degeneration of the fetal brain. Hence in this study, we examined the effects of maternal hyperhomocysteinemia on oxidative stress and apoptosis in brain tissues and investigated whether administration of melatonin to the mother would prevent homocysteine-induced oxidative cerebral damage in pups. Hyperhomocysteinemia was induced in female rats by administration of methionine at a dose of 1 g/kg body weight dissolved in drinking water during pregnancy. Some animals received methionine plus 10 mg/kg/day melatonin subcutaneously throughout pregnancy. After delivery, the level of lipid peroxidation (malondialdehyde + 4-hydroxyalkenals) was determined in different subfractions of pup brains. Furthermore, DNA fragmentation, levels of Bcl-2 protein and p53 mRNA expression were determined to evaluate apoptosis. Significant elevation was found in the levels of lipid peroxidation in subcellular fractions of the brain of pups of hyperhomocysteinemic dams. Increased DNA fragmentation and p53 mRNA expression was observed in the brain of pups of homocysteine-treated rats, while a significant reduction was seen in the levels of anti-apoptotic Bcl-2 levels. Melatonin administration prevented markers of oxidative stress and biochemical signs of apoptosis. In conclusion, therapeutic administration of melatonin protects against the induction of oxidative stress and neural tissue injury and might prevent congenital malformations of fetal brain caused by maternal hyperhomocysteinemia. 相似文献
10.
AIM: To investigate the effect of gabapentin on neural [neuron-specific enolase (NSE)] and glial markers [glial fibrillary acidic protein (GFAP) and S100B] in different brain regions of diabetic rats. METHODS: Diabetes was induced by a single intraperitoneal injection of streptozotocine (50 mg/kg body weight). Rats in one diabetic group received gabapentin (50 mg.kg(-1).d(-1)) and rats in the other diabetic group received vehicle only for 6 weeks. The levels of GFAP, S100B, and NSE were determined by immunoblotting in the hippocampus, cortex, and cerebellum. Lipid peroxidation (LPO as malondialdehyde+ 4-hydroxyalkenals) and glutathione (GSH) levels were also determined in the same brain parts. RESULTS: Total and degraded GFAP content and S100B protein expression in different areas of brain tissues significantly increased in diabetic rats compared to control rats. Similarly, NSE levels were also significantly elevated in hyperglycemic rats. In addition, there was a significant increase in LPO levels in the diabetic rat brain compared to control rat brains. Pretreatment with gabapentin prevented the upregulation of GFAP, S100B, and NSE in all brain regions of diabetic rats. The level of LPO was reduced, but not completely halted, by treatment with gabapentin. CONCLUSION: These results suggest that diabetes causes glial and neuronal injury, possibly as a result of elevated oxidative stress, and that gabapentin protects neurons and glial cells. Thus, we predict that gabapentin treatment will attenuate the hippo-campal and cortical neurodegeneration observed during diabetes mellitus in rats. 相似文献