Immunoglobulin-G and creatinine levels in rabbits in altitude adaptation.

The changes of immunoglobulin-G and creatinine levels in mid-altitude were investigated in rabbits. The animals living at sea level were exposed to 2240 m altitude for 22 days period. When compared with sea level values; immunoglobulin-G levels were significantly low. Serum creatinine level decreased significantly in the 2nd day, then reached the sea level amount on the 12th day. On the 22nd day a significant increase was observed. It was concluded that the decrease in immunoglobulin-G values may be due to the depression of protein synthesis. The increase in plasma creatinine level would be explained by the decrease in urine.     

Focus: Preventive Medicine: Pre-Participation Screening of Athletes: Primary Health Care Physicians’ Knowledge,Experience, and Approach in Turkey

Pre-participation screening (PPS) is crucial for assessing the competitive athletes since their risk of sudden death is higher than non-athletes. In Turkey, PPS is performed at the primary health care setting by primary care physicians (PCPs) who are family medicine specialists (FMSs) or general practitioners (GPs). Although there are national guidelines, there is no legal regulation for this process. This study aims to evaluate PCPs’ knowledge, experience, and approach about PPS. We prepared an online survey for PCPs and used non-probabilistic sampling. PPS attitudes and practices were analyzed and compared according to factors such as experience, education, and being GP or FMS. Of the 214 PCPs included in the study, 39.3% were female. The mean age was 44.9 years (SD:8.88). The average work experience was 7.9 years. Most participants were aware of their authorization to perform PPS (89.7%) and had previously prepared it (90.2%). However, 6.5% of them felt confident in performing PPS. Only 13.1% were aware of the guidelines. Almost 25% of the participants stated being informed about the subject at some part of their career, but this did not affect the confidence or referral decisions. In addition to medical history and physical examination, further testing was considered necessary by 96.3% of the participants. Significantly more tests were ordered by GPs than FMSs (p=0.026 and p=0.011, respectively). The accurate referral decision ratio was 59.3%, without difference between FMSs and GPs (p=0.216). We found that awareness of the guidelines was low among PCPs who lack confidence in PPS. These factors collectively increased the tendency for unnecessary further testing and referral. Therefore, the PPS implementation into medical school and residency curriculums and national legal regulation for the process is a necessity in Turkey.     

Acute adriamycin-induced cardiotoxicity is exacerbated by angiotension II

Adriamycin (ADR) increases the production of reactive oxygen species (ROS), which diminishes mitochondrial function. Angiotensin-II stimulates mitochondrial ROS generation. The aim of the study was to examine whether angiotensin converting enzyme (ACE) or renin inhibitors protect against ADR-induced mitochondrial function impairment. Rats were divided into five groups as control, ADR, co-treatment ADR with captopril, co-treatment ADR with aliskiren, co-treatment ADR with both captopril and aliskiren. Left ventricular function and blood pressures were assessed at the end of treatment period. Mitochondrial membrane potential (MMP) and ATP levels were determined. ADR treatment decreased the left ventricular pressure and increased the left ventricular end-diastolic pressure. ADR decreased MMP and ATP levels in myocyte mitochondria due to increasing oxidative stress. ADR decreased MMP and ATP levels due to increased oxidative stress in the heart. Inhibitors of ACE and renin caused the elevation of the decreased of MMP and ATP levels. The pathologic changes in electrocardiogram, blood pressure and left ventricular function were decreased by inhibition of Ang-II production. We concluded that inhibitors of angiotensin II are effective against ADR cardiotoxicity via the restoration of MMP and ATP production and prevention of mitochondrial damage in vivo.     

Tumour necrosis factor alpha, lipid peroxidation and NO* are increased and associated with decreased free-radical scavenging enzymes in patients with Weill-Marchesani syndrome

AIM: Weill-Marchesani syndrome (WMS) is a rare systemic disorder with both autosomal recessive and dominant inheritances. Accumulation of reactive oxygen species such as O2*-, H2O2 and OH* causes lipid peroxidation (LPO), whereas antioxidant enzymes (superoxide dismutase (SOD), glutathione peroxidase (GSHPx)) mediate defence against oxidative stress. Excess tumour necrosis factor (TNF)-alpha and NO* react with O2*- and cause further antioxidant depletion with an increase in mutation frequency by H2O2. This study investigated the levels of SOD, GSHPx, catalase (CAT), TNF-alpha, NO and LPO in patients with WMS. METHODS: A group of 10 WMS patients (four males, six females; age, 26.5+/-19.0 years) and 10 age-matched and sex-matched controls (five males, five females; age, 27.3+/-18.2 years) were included. Serum TNF-alpha levels were determined by a spectrophotometer technique using immulite chemiluminescent immunometric assay. Malondialdehyde (MDA) was determined in plasma; CAT in red blood cells (RBCs), and SOD and GSHPx in both plasma and RBCs. Total serum NO* levels were evaluated by Griess reaction. RESULTS: Mean levels of TNF-alpha (8.3+/-0.6 pg/ml) in WMS patients were significantly (p<0.001) higher than controls (4.3+/-0.2 pg/ml). Plasma MDA levels in patients and controls were 5.4+/-0.8 and 1.8+/-0.6 micromol/l, respectively, and the difference was significant (p=0.0002). SOD and GSHPx activities were significantly lower in both RBCs and plasma of WMS than in controls (RBC-SOD, 3981.9+/-626.6 versus 5261.6+/-523.0 U/g haemoglobin (Hb), p=0.0005; plasma-SOD, 529.4+/-49.3 versus 713.4+/-55.7 U/g protein, p=0.0002; RBC-GSHPx, 682.7+/-42.0 versus 756.5+/-47.6 U/g Hb, p=0.0011; plasma-GSHPx, 107.3+/-15.0 versus 131.4+/-19.7 U/g protein, p=0.0113). In addition, serum NO (NO*-2 + NO*-3) levels were also significantly (p = 0.0002) increased in WMS patients (54.4+/-5.7 versus 26.9+/-6.7 micromol/l). RBC-CAT levels were similar between groups (125.6+/-21.3 versus 131.0+/-21.5 k/g Hb, p = 0.8798). CONCLUSIONS: The elevated LPO, TNF-alpha and NO* with decreased antioxidant enzyme activities indicated impaired antioxidative defence mechanisms with an oxidative injury and cell toxicity in WMS patients. The use of multiple antioxidants and free radical scavengers might be helpful in this genetic disorder.     

Molecular analysis of 16 Turkish families with DHPR deficiency using denaturing gradient gel electrophoresis (DGGE)

Dihydropteridine reductase (DHPR) catalyses the conversion of quinonoid dihydrobiopterin (qBH2) to tetrahydrobiopterin (BH4), which serves as the obligatory cofactor for the aromatic amino acid hydroxylases. DHPR deficiency, caused by mutations in the QDPR gene, results in hyperphenylalaninemia and deficiency of various neurotransmitters in the central nervous system, with severe neurological symptoms as a consequence. We have studied, at the clinical and molecular levels, 17 patients belonging to 16 Turkish families with DHPR deficiency. The patients were detected at neonatal screening for hyperphenylalaninemia or upon the development of neurological symptoms. To identify the disease causing molecular defects, we developed a sensitive screening method that rapidly scans the entire open reading frame and all splice sites of the QDPR gene. This method combines PCR amplification and "GC-clamping" of each of the seven exonic regions of QDPR, resolution of mutations by denaturing gradient gel electrophoresis (DGGE), and identification of mutations by direct sequence analysis. A total of ten different mutations were identified, of which three are known (G23D, Y150C, R221X) and the remaining are novel (G17R, G18D, W35fs, Q66R, W90X, S97fs and G149R). Six of these mutations are missense variants, two are nonsense mutations, and two are frameshift mutations. All patients had homoallelic genotypes, which allowed the establishment of genotype-phenotype associations. Our findings suggest that DGGE is a fast and efficient method for detection of mutations in the QDPR gene, which may be useful for confirmatory DNA-based diagnosis, genetic counselling and prenatal diagnosis in DHPR deficiency.     

Relationship between hemorheology and Glu(298)Asp polymorphism of endothelial nitric oxide synthase gene in patients with coronary artery disease

This study aimed to investigate the relationship between endothelial nitric oxide synthase Glu(298)Asp gene polymorphism and hemorheological parameters. Red blood cell (RBC) deformability, aggregation were measured using an ectacytometry, whole blood, plasma viscosities were determined by a viscometer. Restriction fragment length polymorphism was used to detect polymorphism. Plasma nitrite, nitrate concentrations were determined by Griess method. The genotype distribution of the control group was as follows: 50 (67.5%) GG, 21 (28.4%) GT, 3 (4.1%) TT. A 48 (57.8%) of the patients with CAD had GG, 28 (33.7%) GT, 7 (8.5%) of them TT genotype. RBC aggregation index of CAD patients with G allele was higher and t½ lower compared to controls carrying the same allele. The amplitude of RBC aggregation of healthy subjects with T allele, who are under increased cardiovascular risk was lower compared to control subjects with G allele. The results of this study indicate that, alterations in RBC aggregation seem to be a consequence of CAD, more than being a preexisting cause. Additionally, some compensatory mechanisms by causing decrements in RBC aggregation, may help regulation of circulation in healthy individuals with high cardiovascular risk.     

Neurofeedback Intervention in Fibromyalgia Syndrome; a Randomized,Controlled, Rater Blind Clinical Trial

We designed a randomized, rater blind study to assess the efficacy of EEG Biofeedback (Neurofeedback-NFB) in patients with fibromyalgia syndrome (FMS). Eighteen patients received twenty sessions of NFB-sensory motor rhythm (SMR) treatment (NFB group) during 4 weeks, and eighteen patients were given 10 mg per day escitalopram treatment (control group) for 8 weeks. Visual Analog Scales for pain and fatigue, Hamilton and Beck Depression and Anxiety Inventory Scales, Fibromyalgia Impact Questionnaire and Short Form 36 were used as outcome measures which were applied at baseline and 2nd, 4th, 8th, 16th, 24th weeks. Mean amplitudes of EEG rhythms (delta, theta, alpha, SMR, beta1 and beta2) and theta/SMR ratio were also measured in NFB group. All post-treatment measurements showed significant improvements in both of the groups (for all parameters p < 0.05). NFB group displayed greater benefits than controls (for all parameters p < 0.05). Therapeutic efficacy of NFB was found to begin at 2nd week and reached to a maximum effect at 4th week. On the other hand, the improvements in SSRI treatment were also detected to begin at 2nd week but reached to a maximum effect at 8th week. No statistically significant changes were noted regarding mean amplitudes of EEG rhythms (p > 0.05 for all). However, theta/SMR ratio showed a significant decrease at 4th week compared to baseline in the NFB group (p < 0.05). These data support the efficacy of NFB as a treatment for pain, psychological symptoms and impaired quality of life associated with fibromyalgia.     

Sleep stage and obstructive apneaic epoch classification using single-lead ECG

Background  

Polysomnography (PSG) is used to define physiological sleep and different physiological sleep stages, to assess sleep quality and diagnose many types of sleep disorders such as obstructive sleep apnea. However, PSG requires not only the connection of various sensors and electrodes to the subject but also spending the night in a bed that is different from the subject's own bed. This study is designed to investigate the feasibility of automatic classification of sleep stages and obstructive apneaic epochs using only the features derived from a single-lead electrocardiography (ECG) signal.