Remzi Yigiter

Is increased red cell distribution width (RDW) indicating the inflammation in Alzheimer's disease (AD)?

Increasing evidence indicates that inflammation has a substantial role in the pathogenesis and progression of AD. RDW, a measure of heterogeneity in the size of circulating erythrocytes, is associated with inflammatory markers in many numerous diseases. Present study was undertaken to assess the interrelationships between RDW and AD. A total of 197 patients with AD (male/female: 96/101, mean age 76.2 ± 6.9) and 133 patients as controls with normal cognitive function (male/female: 72/61, mean age 71.68 ± 5.3) were enrolled in this cross-sectional study. RDW values of all participants were measured. Mini-Mental State Examination (MMSE) and clock drawing tests were performed for cognitive assessment. DSM-IV and NINCDS-ADRDA criteria were used for diagnosis of AD. The mean RDW values were significantly higher in AD group (13.93 ± 1.1 vs. 13.24 ± 1.2; p<0.001) and also a negative moderate correlation between RDW and MMSE was identified (r: -0.453; p<0.001). After adjusting for confounders, RDW has the strongest association with AD (odd ratio (OR) 1.51, CI=1.10-2.07). In present study RDW levels were significantly increased in patients with AD. Whereas elevated RDW value is usually considered as a novel biomarker of inflammation, the results of our study may support the role of inflammation in pathophysiology of AD. Furthermore the correlation of RDW with poorer cognition status suggests that it may be used as a marker of AD severity.

Gene expression profiles of autophagy-related genes in multiple sclerosis

Multiple sclerosis (MS) is an imflammatory disease of central nervous system caused by genetic and environmental factors that remain largely unknown. Autophagy is the process of degradation and recycling of damaged cytoplasmic organelles, macromolecular aggregates, and long-lived proteins. Malfunction of autophagy contributes to the pathogenesis of neurological diseases, and autophagy genes may modulate the T cell survival. We aimed to examine the expression levels of autophagy-related genes. The blood samples of 95 unrelated patients (aged 17-65years, 37 male, 58 female) diagnosed as MS and 95 healthy controls were used to extract the RNA samples. After conversion to single stranded cDNA using polyT priming: the targeted genes were pre-amplified, and 96×78 (samples×primers) qRT-PCR reactions were performed for each primer pair on each sample on a 96.96 array of Fluidigm BioMark™. Compared to age- and sex-matched controls, gene expression levels of ATG16L2, ATG9A, BCL2, FAS, GAA, HGS, PIK3R1, RAB24, RGS19, ULK1, FOXO1, HTT were significantly altered (false discovery rate<0.05). Thus, altered expression levels of several autophagy related genes may affect protein levels, which in turn would influence the activity of autophagy, or most probably, those genes might be acting independent of autophagy and contributing to MS pathogenesis as risk factors. The indeterminate genetic causes leading to alterations in gene expressions require further analysis.

Cryptogenic stroke in two cases with left atrial band: coincidence or cause?

Congenital left atrial band (LAB) has been reported previously. However, clinical significance of the LAB has not been clearly defined. Although LAB is generally known as a benign entity, it has been reported to be associated with Chiaris network, patent foramen ovale, mitral valve prolapse, mitral regurgitation, and supraventricular arrhythmias. In this case report we report LAB in a 34-year-old male and 56-year-old female with cryptogenic stroke. To our knowledge, the association of LAB with cardioembolic events has not been reported previously. Lack of other potential risk factors of cardioembolic stroke and normal laboratory examinations lead us to suggest that LAB might be the cause of cardioembolism in the present two cases. In conclusion, in cases with ischaemic stroke, especially the ones with undetermined aetiology, LAB should be kept in mind as a potential cause of cardioembolism.

The Effect of Circadian Melatonin Levels on Inflammation and Neurocognitive Functions Following Coronary Bypass Surgery

PURPOSE In this study, the relationship between the plasma levels of melatonin and intercellular adhesion molecule-1 (ICAM-1), which plays role in several intercellular interactions including inflammatory and immune responses, and early neurocognitive functions associated with ischaemia-reperfusion injury during open heart surgery is examined. METHODS Forty patients who were to undergo elective coronary artery bypass grafting (CABG) were divided into two groups, those who underwent their operations at 8 AM (group I; n = 20) and those who underwent their operations at 1 PM (group II; n = 20). Blood samples were collected prior to surgery (S1), when the aortic cross clamp was removed (S2) and 4 (S3) and 24 h after the surgery (S4). Neuropsychiatric assessment was conducted one day before and seven days after surgery. RESULTS Melatonin levels measured during and after surgery were also significantly higher in Group 1. ICAM-1 levels were significantly lower in Group 1 at S2 and S3. Significant deterioration was observed in postoperative neurocognitive function compared with preoperative functions in Group 2 more than Group 1. CONCLUSION We hypothesise that the greater preservation of neurocognitive functions in the morning patients is associated with elevated melatonin levels, which reduce the damage from ischaemia-reperfusion injury.

Investigation of the Rho-kinase 2 gene Thr431Asn polymorphism in migraine

BACKGROUND Migraine has a complex etiology determined by genetic and environmental factors, but the molecular mechanisms and genetics of this disease have not yet been fully clarified. AIM This case/control study was designed to analyze the genotype distributions and allele frequencies for the Rho-kinase 2 (ROCK2) gene Thr431Asn polymorphism among the migraine patients. MATERIALS AND METHODS A total of 155 migraine patients and 155 healthy age and sex matched controls were included in this study. Genomic deoxyribonucleic acid from migraine patients and controls was analyzed by real-time polymerase chain reaction. RESULTS Neither genotype distributions nor the allele frequencies for the Thr431Asn polymorphism showed a significant difference between the groups. In addition, there were no marked differences in genotype and allele frequencies for the migraine without aura and migraine with aura subgroups when compared with control group. CONCLUSION This is the first study to show that the ROCK2 gene Thr431Asn polymorphism is not a risk factor for the migraine in the Turkish population.

Decreased HDAC1 Gene Expression in Patients with Alzheimer's Disease

Abstract One of the commonest neurodegenerative diseases, Alzheimer’s disease (AD), is characterized by progressive decline in memory and cognitive functions with inexorable neurodegeneration in brain. Histone-tail acetylation have been known to be associated with some crucial neurologic functions, thus, the enzymes regulating this events such as HDAC1 are associated with such neurodegenerative diseases like AD. The research objective was to document the levels of HDAC1 expression in peripheral lymphocytes harvested from patients clinically diagnosed with AD. Fifty patients diagnosed with AD, and 49 age-and sex-matched controls were recruited to the study. Total RNA was extracted, cDNA was synthesized, and HDAC1 expressions were tested using quantitative real-time polymerase chain reaction (qRT-PCR). HDAC1 expression was found significantly attenuated in patients with AD compared with the controls (p>0.001). The research data suggested that lower expression levels of HDAC1 may have an impact in the etiology or disease course of AD.

Colchicine treatment in children with familial Mediterranean fever: is it a risk factor for neuromyopathy?

BACKGROUND We cared for a 17-year-old adolescent with familial Mediterranean fever under colchicine treatment. Because of the increased creatinine kinase level (3937 U/L) observed in this individual, we planned to assess all pediatric patients with familial Mediterranean fever under colchicine treatment to detect any resultant neuromyopathy. METHODS The study included 88 children with familial Mediterranean fever who were receiving colchicine. The patient with myopathy was not included in the study. Serum creatinine kinase levels were measured and nerve conduction studies were carried out in all patients. RESULTS The study included 88 patients (47 female, 53.4%) with an average age of 10.1 ± 3.35 years. The average period of colchicine use was 28.25 ± 17.66 months. Side effects of colchicine were detected in 10 patients (11%)--as diarrhea in eight patients, leukopenia in one patient, and hair loss in one patient. Nerve conduction studies determined incidental carpal tunnel syndrome in only one patient. CONCLUSIONS Our study did not suggest an elevated risk of neuromyopathy associated with the use of colchicine for familial Mediterranean fever.

Electrophysiologic assessment of the subclinical changes in facial functions after parotidectomy.

Objective: Our objective was to evaluate whether there was a subclinical change in the functions of the facial nerve after parotidectomy. Methods: Facial nerve functions of 21 patients who had parotidectomy between January 1999 and December 2003 were assessed using electromyography (EMG) at least 5 years after the surgery. Results: There was no significant difference between both sides of the face in the EMG amplitudes (P > 0.05) except for the amplitudes obtained from the site of nasolabial sulcus (P < 0.05). In the patients who underwent total parotidectomy, the EMG amplitudes were significantly different for both sides of the face (P < 0.05). No significant difference was found in the comparison of other measurements performed by EMG. Conclusions: Tumor histopathologic type (benign or malignant) and type of parotidectomy (superficial or total) do not cause a subclinical dysfunction of the facial nerve after parotidectomy in the patients who also have clinically normal facial functions. The only exception to this contention is the subclinical dysfunction in nasal branches of the facial nerve in total parotidectomy cases.