[Changes in cognitive function in patients with diabetes mellitus]. / A kognitív funkciók változásai cukorbetegségben.

Patients with diabetes are approximately 1.5 times more likely to experience cognitive decline than individuals without diabetes mellitus. Most of the data suggest that patients with diabetes have reduced performance in numerous domains of cognitive function. In patients with type 1 diabetes, specific and global deficits involving speed of psychomotor efficiency, information processing, mental flexibility, attention, and visual perception seem to be present, while in patients with type 2 diabetes an increase in memory deficits, a reduction in psychomotor speed, and reduced frontal lobe (executive) functions have been found. The complex pathophysiology of changes in the central nervous system in diabetes has not yet been fully elucidated. It is important to consider the patient's age at the onset of diabetes, the glycemic control status, and the presence of diabetic complications. Neurological consequences of diabetes appear parallel to those observed in the aging brain. Neuroimaging studies highlight several structural cerebral changes, cortical and subcortical atrophy, beside increased leukoaraiosis that occurs in association with diabetes. There is supporting evidence from many hypotheses to explain the pathophysiology of cognitive decline associated with diabetes. The main hypotheses pointing to the potential, implied mechanisms involve hyperglycemia, hypoglycemia, microvascular disease, insulin resistance, hyperinsulinism, hyperphosphorylation of tau protein, and amyloid-ß deposition.

The effect of regular exercise on development of sarcoma tumor and oxidative damage in mice liver.

Regular exercise has the capability of decreasing the incidence and progress of certain cancers. Murine sarcoma, (S-180) cells were transplanted to control (TC), exercise trained (10 week, 1 hour day, 5 times/ week) mice, which had the swimming training terminated at the time of transplantation (ETT), and also to a group of mice that continued to exercise during tumor bearing (ETC). Continuous exercise decreased the size of tumor by about 50%. The accumulation of reactive carbonyl groups (RCD), were not significantly different for any group. The oxidative modification of proteins in the liver of the animals decreased in the exercise- trained non-tumor bearing group compared with control or tumor-bearing groups. No significant alteration was detected in the level of mutant p53. The data indicate that regular exercise retards the development of sarcoma solid tumors and it seems unlikely that massive uncompensated oxidative stress takes place in the tumor. Key pointsRegular exercise has a capability to reduce the inci-dence and progress of certain cancers.Free radicals could act as a promoters and suppres-sors of cancers.Exercise can suppress the development of Sarcoma, but the underlying mechanisms are not known.

Hemorheological, morphological, and oxidative changes during ischemia-reperfusion of latissimus dorsi muscle flaps in a canine model.

Although ischemia-reperfusion (I/R) strongly influences muscle flap survival in reconstructive surgery, there is limited knowledge about its relation to hemorheological parameters and oxidative stress markers in flaps. In the present study we investigated these changes during I/R of latissimus dorsi muscle (LDM) flaps in beagle dogs. In four animals LDM flaps were prepared bilaterally. The right side served as control, while the left side's vascular pedicle was clamped for 60 minutes, and a 60-minute reperfusion was allowed afterward. Blood samples (0.5 ml each) were taken from the pedicle's vein bilaterally before and after the ischemia, and at the 5th, 15th, 30th, 45th, and 60th minutes of the reperfusion, for hematological and erythrocyte aggregation tests. In muscle biopsies, taken before and after I/R, histological investigations and tests for measuring gluthation-peroxidase (GSH-PX) activity, glutathione (GSH) and carbonyl concentrations, and thiobarbituric acid reactive substances (TBARS) content were carried out. In I/R side leukocyte count increased during the reperfusion with a peak at the 30th minute. Hematocrit continuously increased from the 15th minute. In the first 5 minutes of the reperfusion, erythrocyte aggregation increased, than tented to be normalized. In muscle homogenates GSH-PX activity did not change markedly, GSH content slightly decreased, carbonyl and TBARS content increased during reperfusion. A 1-hour ischemia and reperfusion of LDM flaps caused local changes of leukocyte distribution and erythrocyte aggregation, supposedly due to the metabolic and inflammatory reactions. Oxidative damage during reperfusion was also demonstrated.

The beneficial effects of nettle supplementation and exercise on brain lesion and memory in rat.

Regular swimming and phytotherapeutic supplementation are assumed to alleviate the severity of neurodegeneration leading to dementia. The effect of swimming training and that of enriched lab chow containing 1% (w/w) dried nettle (Urtica dioica) leaf on the prevention of severity of brain injury caused by N-methyl-d-aspartate (NMDA) lesion in Wistar rats were investigated. Nettle supplementation and regular swimming exercise seem to improve the adverse effect of brain injury caused by NMDA lesion assessed by passive avoidance test and open-field test. Nettle supplementation decreases the level of reactive oxygen species, measured by electron paramagnetic resonance, and the DNA-binding activity of NF-kappaB. The data reveal that nettle supplementation has an effective antioxidant role, down-regulates the inflammatory transcription factors and could also promote learning performance in the brain. Regular swimming increases the concentration of reactive species in the cerebellum and alters the activity of transcription factors toward inflammation. The additive effect of the two treatments was more profound in the down-regulation of inflammatory transcription processes in NMDA lesion.

[Gender differences in the neurocognitive components of depression]. / A depresszió neurokognitív összetevoinek és nemi külonbségeinek vizsgálata.

UNLABELLED: The clinical symptoms of major depression are paralleled by typical neurocognitive deficits. Our aim was to investigate the gender differences in neurocognitive impairment in patients with major depressive disorder. METHODS: 96 patients with acute major depressive disorder meeting DSM-IV criteria participated in our study. Depression was assessed by the Montgomery-Asberg Depression Rating Scale, the Hamilton Depression Scale and the Beck Depression Inventory. We measured neurocognitive functions associated with verbal learning and memory (Rey Auditive Verbal Learning Test), visual reconstruction and recall (Rey-Osterreith Complex Figure Test), selective attention, executive functions and inhibitory control (Trail Making Test, Stroop Test). RESULTS: Depressive patients performed significantly worse than controls in all tests. We found no gender differences in any of the tests in the control group. Depressed women performed significantly worse on tests of cognitive interference threshold compared to depressed men (Stroop III). Depressed women performed significantly worse compared to depressed men in the test of visual recall (Rey-Osterreith Complex Figure Test). CONCLUSION: Depressed patients performed worse in all tests of neurocognitive function compared to healthy controls. Depressed women performed significantly worse compared to depressed men in tests of visuospatial recall and cognitive interference. In the light of neuroimaging studies our results suggest that in the background of gender differences we observed in depressed patients lateralisation of hippocampal function may play an important role.

[Markers of cognitive vulnerability in major depression]. / Kognitív vulnerabilitás markerek major depresszióban.

Neuropsychological deficits have been reported in patients with major depressive disorder in a lot of lectures. The aim of the present study was to measure the neurocognitive functions of major depressive patients and healthy controls, and identify some vulnerability marker of the disease. Seventy-one patients with major depressive disorder were compared to thirty healthy control subjects on tasks from Trail Making Test, Stroop Test, Rey Verbal Auditory Learning Test and Rey-Osterreich Figure Test. Patients with depression relative to controls were significantly impaired on tasks of attention, executive function, memory and psychomotor speed, but not in visuo-spatial function. These findings suggest deficits in cognitive function as, attention, visual and verbal memory and learning, as vulnerability marker for major depressive disorder. The second important finding, the better result of the visual perception and short memory in depressed patient, was caused by intact hippocampal function. The functional importance of this result is the connection of the neuronal network and signs of depression.

Evidence of nitric oxide produced by the internal mammary artery graft in venous drainage of the recipient coronary artery.

BACKGROUND: The endothelium of the internal mammary artery produces nitric oxide in greater quantity than other vessels employed in revascularization of the ischemic myocardium. The aim of this study was to measure the concentration of stable metabolite (nitrite) of the endothelium-derived nitric oxide in the venous drainage (anterior interventricular vein) of the recipient coronary artery, which was the left anterior descending branch. The sampling was carried out before and after anastomosis completion. METHODS: Nitrite levels in the anterior interventricular vein, before and after anastomosis completion, in the left internal mammary artery free flow, and in the subclavian vein were measured. Fluroscopy after 4-hydroxycoumarin nitrozation was utilized to measure nitrite content of blood samples in 50 consecutive, partly heparinized patients undergoing off-pump coronary bypass surgery. Nitrate content of all samples was removed by Cadmium pearls. RESULTS: One hundred and sixty-four samples taken from 41 patients were feasable to analyze. A significant increase of nitric oxide (nitrite) level was found in the anterior interventricular vein, when comparing concentrations measured before and after the anastomosis between the left internal mammary artery and the left anterior descending artery. Mean values in the anterior inteventricular vein before and after anastomosis completion were as follows: 44.8 microMol (SD 4.9) and 70.7 microMol (SD 8.1), respectively. CONCLUSIONS: The increased production of nitric oxide by the internal mammary arterial graft may provide a perpetual vasodilatory response and partially protect the distal coronary vessel from atherosclerosis.

The effects of moderate, strenuous, and overtraining on oxidative stress markers and DNA repair in rat liver.

Physical exercise above a certain load has been suggested as being a cause of oxidative stress. We have tested whether training with moderate (MT), strenuous (ST), or over (OT) load can cause alterations in the activities of antioxidant enzymes, lipid peroxidation, protein oxidation, DNA damage, or activity of 8-oxoG-DNA glycosylase (OGG1) in rat liver. The levels of corticosterone decreased in all exercising groups but the differences were not significant. Adrenocorticotrophin hormone (ACTH) levels decreased, not significantly, in MT and OT compared to C. Activity levels of antioxidant enzymes did not change significantly in the liver. The levels of reactive carbonyl derivative (RCD) content decreased in the liver of exercising animals, and the differences reached significance between control and moderately trained groups. The changes in the levels of lipid peroxidation (LIPOX) were not significant, but were lower in the exercised groups. The 8-hydroxydeoxyguanosine (8-OHdG) levels increased in the OT group, and the activity of OGG1 measured from crude cell extracts tended to increase in MT and ST. The findings of this study imply that overtraining induces oxidative damage to nuclear DNA, but not to liver lipids and proteins.

The effect of exercise and nettle supplementation on oxidative stress markers in the rat brain.

Chronic swimming training and phytotherapeutic supplementation are assumed to alleviate oxidative damage, and support cell survival in the brain. The effect of forced, chronic swimming training, and enriched lab chow containing 1% (w/w) dried nettle (Urtica dioica) leaf were investigated for oxidative stress, inflammation and neurotrophic markers in Wistar rat brains. The rats were divided into groups subjected to swimming training (6 weeks) or to nettle supplementation (8 weeks) or to a combination of these two treatments. The level of oxidative stress was measured by electron spin resonance (EPR), and by the concentration of carbonylated proteins. Nettle supplementation resulted in a decreased concentration of free radicals in both cerebellum and frontal lobe. Swimming, however, did not influence significantly the oxidative damage nor was it reflected in the carbonyl content. The protein content of nerve growth factor (NGF), and brain-derived neurotrophic factors (BDNF) was evaluated by E-Max ImmunoAssay in the cerebellum. No changes occurred either with exercise or nettle diet treatments. On the other hand, nuclear factor kappa B (NF-kappaB) binding activity to DNA increased with the combined effect of swimming training and nettle diet, while the activator protein1 (AP-1) DNA binding activity showed a more profound elevation in the nettle treated animals. The amount of c-Jun decreased by swimming training. In conclusion, the results suggest that both exercise and nettle influenced physiological brain functions. Nettle supplementation reduces the free radical concentration and increases the DNA binding of AP-1 in the brain. Nettle was found to be an effective antioxidant and possible antiapoptotic supplement promoting cell survival in the brain. Exercise, as a downregulator of c-Jun and in combined group as an upregulator of NF-kappaB, may play also a role in antiapoptotic processes, which is important after brain injury.

[Analysis of the stable metabolite of endothelium-derived nitric oxide of internal mammary artery bypass grafts at the venous drainage system of the recipient coronary artery. Morphologic implications and consequences]. / Az arteria mammaria interna bypass graft endotheliuma által termelt nitrogén-monoxid stabil metabolitjának mérése a recipiens coronariaág gyújtóeres rendszerében. Morfológiai vonatkozások és következmények.

INTRODUCTION: The internal mammary artery's endothelium continuously produces nitric oxide in a large quantity resulting in local and downstream vasodilatation, inhibition of platelet aggregation and in the tunica media prevents smooth muscle cell proliferation. OBJECTIVE: The aim of this study was to measure the concentration of the internal mammary artery bypass graft's endothelium derived nitric oxide's stable metabolite, (nitrite) at the venous drainage site (great cardiac vein) of the recipient coronary artery (left anterior descending), and to prove that the change of the biochemical milieu provides morphological stability (vasodilation and lack of atherosclerosis) in the recipient coronary artery based on recoronarographies. METHOD: Authors investigated the levels of endothelium derived nitric oxide in intraoperative settings of 50 off pump, partly heparinized coronary bypass surgery cases sampling from the internal mammary free cut end flow (81.2 +/- 12.1 mumol/l), the great cardiac vein (anterior interventricular vein) prior and after arterial bypass graft completion and in the systemic circulation (42.9 +/- 7.1 mumol/l), The stable metabolite concentration measurement was carried out with the modified Takafumi Ohta method utilizing fluoroscopy. Out of the 200 samples 164 were feasible to analyze. RESULTS: A significant increase was found in the great cardiac vein, comparing concentrations measured prior and after IMA anastomosis completion: 46.7 +/- 11.4 mumol/l, and 71.12 +/- 13.1 mumol/l, respectively (p < 0.05). CONCLUSION: Based on these findings, due to the continuous protective (vasodilatative and antiatherogen) effect of the IMA provided EDNO, the recipient artery shows no pathological changes in time. This was proved by studying recoronarographies of 103 patients--with prior coronary bypass surgery in 5-12 years using the IMA, and with new symptomatology. Out of 87 functioning IMA to LAD grafts, 85 LAD showed no atherosclerotic changes, while in the same patients' other coronary systems significant, de novo stenotic lesions had developed.