Dicle University

About: Dicle University is a education organization based out in Diyarbakır, Turkey. It is known for research contribution in the topics: Population & Catalysis. The organization has 3007 authors who have published 6368 publications receiving 94797 citations. The organization is also known as: Dicle Üniversitesi & Zanîngeha Dîcleyê.

Molecular investigations of Hepatozoon species in dogs and developmental stages of Rhipicephalus sanguineus

Abstract: The occurrence and distribution of Hepatozoon species in stray dogs, and the developmental stages of Rhipicephalus sanguineus detached from the same dogs in Diyarbakir Province, Turkey is reported. A total of 328 ticks, including 133 adults (55 males and 75 females consist of 63 partially engorged and 15 fully engorged) and 195 nymphs (91 partially engorged and 104 fully engorged) were detached from the dogs. Fully engorged nymphs and females were incubated at 27 °C and relative humidity of 85 % to molt to adult stage and recover eggs. The ticks were pooled according to sex and developmental stage. No Hepatozoon gamonts were found, whereas, by PCR, 15.87 % (10/63) of the dogs were infected with Hepatozoon canis. Of the 68 tick pools tested, 14 (20.58 %) pools were infected with Hepatozoon spp., an overall maximum likelihood estimation of prevalence of 4.9 % (95 % confidence intervals (CI) = 2.85–7.93 %) per 100 ticks. Maximum likelihood estimation of the infection rate varied by tick sex and developmental categories, ranging from 1.75 % (95 % CI = 0.11–8.11 %) in fed males to 6.81 % (95 % CI = 2.07–17.46 %) in unfed females. One amplicon from a fed adult female was 99 % identical to the sequence for Hepatozoon felis. The remaining sequences isolated from both dogs and ticks shared 99–100 % similarity with the corresponding H. canis isolates. This is the first detection of H. canis and H. felis in the tick R. sanguineus in Turkey.

Complement activation in acute coronary syndromes

Abstract: The complement system is part of the host defence response. However, considerable evidence suggests that complement plays an important role in the pathophysiology of ischemic heart disease. The aim of this study was to evaluate complement activation in patients with all forms of acute coronary syndromes (ACS) and to examine the relationship between the degree of complement activation and myocardial injury. The study population included 152 subjects (26 females): 82 with ACS (35 acute myocardial infarction (AMI), 22 non-Q wave MI (NQMI), 25 unstable angina (UAP)) (Group A), 35 stable angina (SA) (Group B), and 35 healty control subjects (Group C). Complement 3 (C3), Complement 4 (C4), C-reactive protein (CRP), troponin I (TnI) as well as creatine kinase MB (CK-MB) were evaluated. Patients' blood samples were taken on admission (day 1) and after 2, 3 and 7 days in group A. However, only one measurement was performed in the groups B and C. Plasma C3 and C4 peak levels were significantly higher in patients with AMI (141±29 and 35±11 mg/dl) and NQMI (136±13 and 35±7 mg/dl) than in patients with SA (128±14 and 27±10 mg/dl) and the control subjects (114±22 and 22±7 mg/dl) (p 0.05). However, plasma levels of C3 and C4 were significantly different between days in patients with AMI and NQMI (p<0.0001). Plasma C3 and C4 levels in ACS showed a relationship with peak CK-MB and Tn I levels (p<0.01). Plasma CRP level in ACS showed positive correlation with C3 (p<0.01) and C4 (p<0.001). In this study, we determined that plasma C3 and C4 levels were elevated in ACS and SA. Although C3 and C4 were higher in ACS and SA, the systemic levels of inflammatory markers in patients with SA and UAP were lower than those found in the AMI and NQMI groups. The relationship between C3, C4 levels and ACS further suggests that the complement activation is related to necrosis within the myocardium.

Novel Alu retrotransposon insertion leading to Alström syndrome

Abstract: Alstrom syndrome is a clinically complex disorder characterized by childhood retinal degeneration leading to blindness, sensorineural hearing loss, obesity, type 2 diabetes mellitus, cardiomyopathy, systemic fibrosis, and pulmonary, hepatic, and renal failure. Alstrom syndrome is caused by recessively inherited mutations in the ALMS1 gene, which codes for a putative ciliary protein. Alstrom syndrome is characterized by extensive allelic heterogeneity, however, founder effects have been observed in some populations. To date, more than 100 causative ALMS1 mutations have been identified, mostly frameshift and non-sense alterations resulting in termination signals in ALMS1. Here, we report a complex Turkish kindred in which sequence analysis uncovered an insertion of a novel 333 basepair Alu Ya5 SINE retrotransposon in the ALMS1 coding sequence, a previously unrecognized mechanism underlying the mutations causing Alstrom syndrome. It is extraordinarily rare to encounter the insertion of an Alu retrotransposon in the coding sequence of a gene. The high frequency of the mutant ALMS1 allele in this isolated population suggests that this recent retrotransposition event spreads quickly, and may be used as a model to study the population dynamics of deleterious alleles in isolated communities.