Browsing by Author "Solak M."

Now showing 1 - 8 of 8
  • No Thumbnail Available
    Item
    Evaluation of non-invasive clinical samples in chronic Chlamydial prostatitis by using In situ hybridization
    (Informa Healthcare, 1997) Gümüş B.; Sengil A.Z.; Solak M.; Fistik T.; Alibey E.; Çakmak E.A.; Yeter M.
    Seventy-eight non-invasive prostate specimens collected from patients with chronic non-bacterial prostatitis were evaluated by in situ hybridization (IH) for evidence of Chlamydia trachomatis. Intracellular Chlamydia bodies were detected in 18 of 78 cases (20.6%). Homogeneous blue- black bodies in the cellular cytoplasm were accepted as in situ positive. Chlamydial antigen detected by enzyme immuno assay (EIA) was positive in 12 cases (13.7%), but only nine of them were positive by IH. Our study confirms previous reports implicating C. trachomatis as an aetiological agent in chronic non-bacterial prostatitis, and underscores the applicability of DNA probes for detection and identification of C. trachomatis in prostatic materials.
  • No Thumbnail Available
    Item
    A new susceptibility gene in patients with schizophrenia?
    (1998) Gölge M.; Mehles A.; Lemke I.; Lustig M.; Solak M.; Bagci H.; Schnakenberg E.; Schloot W.
    We have investigated the polymorphic N-acetyltransferase 2 gene (NAT2) from male patients with schizophrenia and controls of Caucasian origin. The diagnosis of schizophrenia is followed according to the DSM III-R characteristics. Since purified NAT enzyme (EC 2.3.1.5) is said to be involved in serotonm metabolism we identified six point mutations of the NAT2 gene leading to eight different alleles and 36 possible genotypes. From patients with schizophrenia, 43.5% were slow acetylators compared to 56.2% of controls, indicating that rapid acetylators could have a higher risk to develop schizophrenia. In addition, we have analyzed the human serotonin-N-acetyltransferase (aa-NAT, EC 2.3.1.87). The aa-NAT, the rate-limiting enzyme in melatonin synthesis, catalyzes the step from serotonin to N-acetylserotonin and controls the night/day rhythm in melatonin production. Since there are some studies of serotonin receptor genes in schizophrenia published in the last years, there haven't been any researches about the relevance of a possible genetic polymorphism of serotonin acetylation. The human serotonin-NAT gene spans 2.550 bp and contains four exons and three introns and is located on chromosome 17q25. The four exons have been separately amplified, isolated, and finally sequenced. As a result of sequencing, we found two point mutations, which are located at positions 2164 (G→A; Ala→Thr) and 2247 (C→T; silent) in the fourth exon of the AA-NAT gene. Furthermore, to detect these point mutations in a great number of patients we have developed a simple PCR/RFLP assay.
  • No Thumbnail Available
    Item
    Effects of sevoflurane on the cell division and levels of sister cromatid exchange; [Sevofluran hucre bolunmesi ve kardes kromatid degisimi duzeyleri uzerine etkisi]
    (1999) Solak M.; Erincler T.; Luleci E.; Gul R.; Luleci N.; Fistik T.; Tutan A.
    In this study, the mitotic index (MI) and Sister Cromatid Exchange (SCE) levels were investigated to identify the mutagenic and carcinogenic effects of sevoflurane (sevorane). The data of 20 patients in ASA I-II were studied. All of the patients received an anaesthesia induction with anaesthesia mask and 'tidal volume method. 8 % sevoflurane in 100 % oksigen was used to the induction of anaesthesia and 0.1 mg/kg vecuronium for neuromuscular block and intratracheal intubation. Anaesthesia continued with 2-2.5 sevoflurane, in 60 % N2O and 40 % O2 . Three mL venous blood samples taken before (as controls) 60 minutes, 24 hours and 5 days after the sevoflurane induction, were examined according to the periferic blood culture assay with conventional cytogenetic methods. On the metaphase plaques which obtained in this way, the levels of MI and SCE were examined. As a result, a significant decrease of MI has been found in the test objects at the first 60 minutes of sevoflurane anaesthesia compared to controls (p<0.001). But this depression was smaller after 24 hours (p<0.01) and reversible after 5 days (p>0.05). SCE increased significantly at the first 60 minutes of anaesthesia (p<0.001) was also smaller after 24 hours (p<0.01) and returned to normal levels after 5 days (p>0.05). As conclusion; It has been revealed the effects of sevoflurane on cellular replication and on DNA at the cellular level were repaired in a short period of time. Thus, it has been suggested that sevoflurane had no permanent effect on genetic material of healthy individuals.
  • No Thumbnail Available
    Item
  • No Thumbnail Available
    Item
    Effects of sevofluran on cell division and levels of sister chromatid exchange; [Die wirkung von sevofluran auf zellteilung, mitose-index (MI) und austausch der schwesterchromatide (sister chromatide exchange SCE)]
    (2005) Lüleci N.; Sakarya M.; Topçu I.; Lüleci E.; Erinçler T.; Solak M.
    Objective: Purpose of the study was to investigate the mitotic index (MI) and sister chromatid exchange (SCE) levels to identify the mutagenic and carcinogenic effects of sevoflurane (sevoflurane). Methods: 42 non-smoking male and female turkish patients of ASA-risk I and II were included. The patients received an anaesthesia induction with 8% sevoflurane in 100% oxygen ("tidal volume methode") and 0,1 mg/kg BW vecuronium for neuromuscular block and endotracheal intubation. Anaesthesia was maintained with 2.0-2.5 sevoflurane in 60% N2O and 40% O2. Four 5 ml venous blood samples werde taken: before induction (control), 60 minutes, 24 hours and 5 days after sevoflurane anesthesia. Samples were prepared according to the periferic blood culture assay, modified by Morhead and co-workers, and levels of MI and SCE were examined. Results: 60 minutes after sevoflurane-anaesthesia a significant decrease of MI was found compared to controls (p < 0.01). This depression was lower after 24 hours (p < 0.05) and reversible after 5 days. SCE increased significantly during 60 minutes of anaesthesia (p < 0.001), was also lower after 24 hours (5.6 ± 2.4 vs. 4.4 ± 1.7) and returned to normal levels after 5 days (p > 0.05). Conclusion: The application of sevoflurane for anaesthesia may influence the cell division in humans and may have a mutagenic effect on DNA at the cell level, which is reversible.
  • No Thumbnail Available
    Item
    Analysis of the dermatoglyphics in Turkish patients with Klinefelter's syndrome
    (2008) Sirri Cam F.; Gul D.; Tunca Y.; Fistik T.; Ozdemir Erdogan M.; Yildiz H.; Erdem S.; Solak M.
    The word "dermatoglyphics" indicates study of epidermal ridge configuration on palms, soles and fingertips. This investigation was aimed to analyze dermatoglyphic patterns in Klinefelter's syndrome (KS) patients. The study cohort consisted of 57 cases and 25 controls. The prints were taken by using the ink method. Fingertip patterns, triradial counts, a-t-d angle and a-b ridge count were studied. There were significant differences in radial loops and whorls (p < 0.05), and there were very highly significant differences in arches (p < 0.001) in KS patients as compared to controls. Dermatoglyphic patterns at the hypothenar area (p < 0.05), and areas between at the I. interdigital and thenar sites (p < 0.001) have been found to be significantly different in KS patients compared to controls. Total ridge counts (TRC), a-b, a-t-d angels were not different in the two groups (p > 0.05). A definite correlation between the dermatoglyphic patterns and the KS has been shown. © Journal compilation © 2008 Hereditas.
  • No Thumbnail Available
    Item
    Comprehensive analysis of a large-scale screen for MEFV gene mutations: Do they truly provide a "heterozygote advantage" in Turkey?
    (2011) Berdeli A.; Mir S.; Nalbantoglu S.; Kutukculer N.; Sozeri B.; Kabasakal Y.; Cam S.; Solak M.
    Familial Mediterranean fever (FMF) is a hereditary autoinflammatory disorder characterized by episodes of inflammation in the absence of high-titer autoantibodies or antigen-specific T cells. The Mediterranean fever (MEFV) gene located on chromosome 16p13.3, which encodes the 781-amino-acid protein pyrin, is the causative gene for this monogenic Mendelian disease. This study presents the molecular analysis of an MEFV gene mutation screen of 5518 Turkish individuals with clinical diagnoses of FMF. Patients were genetically diagnosed using the FMF StripAssay and DNA sequencing analysis. Contrary to the results achieved by the FMF StripAssay, DNA sequencing analysis identified large-scale coding and noncoding novel sequence variants, together with a significant group (76%) of individuals who were receiving colchicine and had a single heterozygous mutation, despite the recessive inheritance of FMF. In conclusion, sequence analysis, unlike other routine laboratory techniques, may enable screening for a broad range of nucleotide variations and may prevent less common, population-restricted, novel sequence variants from being overlooked. © 2011, Mary Ann Liebert, Inc.
  • No Thumbnail Available
    Item
    Investigation of Genetic Changes in Three Families with Bipolar Disease
    (S. Karger AG, 2024) Çolak-Geniş E.; Özdemir Erdoǧan M.; Çam F.S.; Aydemir Ö.; Akin F.; Gerik-Celebi H.B.; Solak M.
    Introduction: Bipolar disorder (BD) is a serious psychiatric disorder characterized by mood swings (depressive and manic phases) that can strongly affect the quality of life of patients and their families. The lifetime prevalence of BD in the general population is 1%. The pathogenesis of BD is unknown; however, comprehensive epidemiological studies have shown that both genetic and environmental factors play a role. Within the scope of the current project, we aim to determine the genetic change responsible for the emergence of the disease and to make a genotype-phenotype correlation. Methods: In this study, we evaluated single nucleotide gene variants in three families (n = 6 patients) with bipolar disorder using whole-exome sequencing. Results: Seven genes (TMTC1, DGKH, STARD9, ITIH1, MARCKS, CSMD1, and ADRA2B) were identified as possibly associated with BPD. In addition, two novel variants were presented in the TMTC1 (c.1214T>G) and STARD9 (c.8288C>G) genes. Conclusion: Prospective studies in larger patient groups are required to determine the role of these genes in the etiology of the disease and their potential in diagnosis and treatment. To the best of our knowledge, this is the first methodically comprehensive study conducted in our country and cancontribute to the identification of genes that may be associated with BD and the etiopathogenesis of the disease. © 2024 S. Karger AG, Basel.