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Background/aim: Increased susceptibility to infections is a serious problem in diabetics. Impairment in the energy metabolism of the immune system is the main source of the problem. Early diagnosis of the impairment in energy metabolism is crucial. Our study aimed to investigate the energy metabolism in leukocytes in patient groups such as prediabetics and patients newly diagnosed with type 2 diabetes mellitus. Materials and methods: Our study included 21 newly diagnosed type 2 diabetic patients (NDDP), 30 prediabetic patients, and 22 adult volunteers. 75 g oral glucose tolerance test (OGTT) was applied to all patients included in the study. Blood samples were taken after 9-16 h of fasting and fasting blood glucose (FBG), postprandial blood glucose (PBG) levels, total cholesterol (TC), triglyceride (TG), highdensity lipoprotein (HDL), fasting serum insulin, and hemoglobin A1c (HbA1c) levels were evaluated. After the cells were completely lysed, citrate levels from the released mononuclear leukocyte cells (MNC) content were manually studied, and lactate levels were applied to the autoanalyzer with the lactate kit. Lactate and citrate results were calculated as μg/mL. Statistical comparisons were done using Chi-square test, Mann-Whitney U test and student’s t test, and P < 0.05 values were accepted as significant. Results: A significant difference was found between the controls and the other groups (newly diagnosed diabetic patients (NDDP), impaired fasting glucose (IFG), and impaired glucose tolerance (IGT)) in terms of FBG levels (P < 0.001, P < 0.001 and P < 0.001, respectively). IFG and IGT patients had significantly higher PBG levels compared to the control group (P = 0.009 and P < 0.001, respectively). There was a significant difference between the IFG and IGT patients in terms of insulin levels (P = 0.019). There was a significant relationship between FBG levels and lactate production only in the NDDP group (r = 0.610, P = 0.003) Conclusion: The metabolic effects of hyperglycemia on leukocytes is in direction of anaerobic glycolysis. The increased anaerobic pathway is closely related to blood glucose levels and insulin resistance.

Sometimes fingerprint-like features are found in a material. The exciting discovery poses new challenges on how to use the features to build an object authentication protocol that could tell customers and retailers equipped with a mobile device whether a good is authentic or fake. We are exactly in this situation with Cholesteric Spherical Reflectors (CSRs), tiny spheres of liquid crystals with which we can tag or coat objects. They are being proposed as a potential game-changer material in anti-counterfeiting due to their unique optical properties. In addition to the problem of processing images and extracting the minutiæ embedded in a CSR, one major challenge is designing cryptographically secure authentication protocols. The authentication procedure has to handle unstable input data; it has to measure the distance between some reference data stored at enrollment and noisy input provided at authentication. We propose a cryptographic authentication protocol that solves the problem, and that is secure against semi-honest and malicious adversaries. We prove that our design ensures data privacy even if enrolled data are leaked and even if servers and provers are actively curious. We implement and benchmark the protocol in Python using the Microsoft SEAL library through its Python wrapper PySEAL.

Innovative pharma-genomics and personalized medicine services are now possible thanks to the availability for processing and analysis of a large amount of genomic data. Operating on such databases, is possible to test for predisposition to diseases by searching for genomic variants on whole genomes as well as on exomes, which are collections of protein coding regions called exons. Genomic data are therefore shared amongst research institutes, public/private operators, and third parties, creating issues of privacy, ethics, and data protection because genome data are strictly personal and identifying. To prevent damages that could follow a data breach—a likely threat nowadays—and to be compliant with current data protection regulations, genomic data files should be encrypted, and the data processing algorithms should be privacy-preserving. Such a migration is not always feasible: not all operations can be implemented straightforwardly to be privacypreserving; a privacy-preserving version of an algorithm may not be as accurate for the purpose of biomedical analysis as the original; or the privacy-preserving version may not scale up when applied to genomic data processing because of inefficiency in computation time. In this work, we demonstrate that at least for a wellknown genomic data procedure for the analysis of copy number variants called copy number variations (CNV) a privacy-preserving analysis is possible and feasible. Our algorithm relies on Homomorphic Encryption, a cryptographic technique to perform calculations directly on the encrypted data. We test our implementation for performance and reliability, giving evidence that it is practical to study copy number variations and preserve genomic data privacy. Our proof-of-concept application successfully and efficiently searches for a patient’s somatic copy number variation changes by comparing the patient gene coverage in the whole exome with a healthy control exome coverage. Since all the genomics data are securely encrypted, the data remain protected even if they are transmitted or shared via an insecure environment like a public cloud. Being this the first study for privacy-preserving copy number variation analysis, we demonstrate the potential of recent Homomorphic Encryption tools in genomic applications.

In this paper we present effect of the chaotic crossover operator with different chaotic maps on the metaheuristic search algorithm Breeding Swarms algorithm which is the Particle Swarm Optimization’s one of the genetic algorithm hybrid form. Some of the many optimization problems could have too many local extrema. Most of the time optimization algorithms could stuck on these extrema therefore these algorithms could have trouble with finding global extremum. To avoiding local extrema and conduct better search on search space, a chaotic number generator is used on Breeding Swarms algorithm’s most of the random procedures. To test efficiency and randomness of the chaotic crossover operator, different chaotic maps are used on the Breeding Swarm algorithm. Test and performance evaluations are conducted on Multimodal and unimodal benchmark functions. This new approach showed us that modified Breeding Swarms algorithm yielded slightly better results than Particle Swarm Optimization and original Breeding Swarms algorithms on tested benchmark functions.

Introduction: Patients with polycystic ovary syndrome (PCOS) are in the risk group for early-onset cardiovascular disease. There are few studies evaluating physiological and inflammatory cardiovascular risk factors in PCOS. Our study aimed to measure carotid intima-media thickness (IMT) in PCOS cases and to assess the effects of metformin, ethinyl estradiol/cyproterone acetate (EE/CA) and metformin + EE/ CA combination therapy on carotid IMT, insulin resistance, C-reactive protein (CRP), apelin and adiponectin. Methods: Basal carotid IMT, insulin resistance [Homeostasis model assessment insulin resistance (HOMA-IR)], apelin, adiponectin, and CRP values were evaluated in 60 women with PCOS and 43 healthy volunteers between the ages of 18 and 45. After baseline evaluation, patients were divided into metformin (n=20), EE/CA (n=20) and metformin + EE/CA (n=20) treatment groups. Treatment regimens were administered for six months. At the end of the treatment, the same parameters were reevaluated. Results: Compared with the control group, CRP (p=0.003), HOMA-IR (p=0.004) and IMT (p=0.049) were significantly higher, and adiponectin (p=0.002) and apelin (p=0.031) levels were significantly lower in patients with PCOS. At the end of the six-month treatment, the adiponectin level in the metformin (p=0.012) and metformin + EE/CA groups (p=0.012), and the apelin level in the metformin (p=0.024), EE/CA (p=0.024) and metformin + EE/CA groups (p=0.024) were significantly higher. There was no statistically significant change in CRP level in all treatment groups (p>0.05). There was no statistically significant change in carotid IMT value in all treatment groups (p>0.05). Conclusion: According to these results, we can say that women with PCOS have subclinical atherosclerosis and that metformin treatment has a positive effect on subclinical atherosclerosis. Amaç: Polikistik over sendromu (PKOS) erken dönemde ortaya çıkan kardiyovasküler hastalık için risk grubundadır. PKOS’de, fizyolojik ve enflamatuvar kardiyovasküler risk faktörlerini değerlendiren az sayıda çalışma vardır. Çalışmamızın amacı, PKOS olgularında karotis intima media kalınlığını (İMK) ve ayrıca metformin, etinil estradiol/siproteron asetat (EE/SA) ve metformin + EE/SA kombinasyon tedavisinin karotis İMK, insülin direnci, C-reaktif protein (CRP), apelin ve adiponektin üzerine etkilerini değerlendirmektir. Yöntemler: Çalışmamıza katılan 18-45 yaş arasındaki 60 PKOS’li kadında ve 43 sağlıklı gönüllü kadında bazal karotis İMK, insülin direnci [Homeostasis model assessment insulin resistance (HOMA-IR)], apelin, adiponektin ve CRP değerlendirmeleri yapıldı. Bazal değerlendirmeden sonra, hastalar metformin (n=20), EE/SA (n=20) ve metformin + EE/SA (n=20) tedavi gruplarına ayrıldı. Tedavi rejimleri 6 ay boyunca uygulandı. Tedavi sonunda aynı parametreler tekrar değerlendirildi. Bulgular: Kontrol grubuyla karşılaştırıldığında PKOS’li olguların CRP (p=0,003), HOMA-IR (p=0,004), İMK (p=0,049) değerleri istatistiksel olarak anlamlı derecede daha yüksek, adiponektin (p=0,002), apelin (p=0,031) düzeyleri kontrol grubundan istatistiksel olarak daha düşük saptandı. Altı aylık tedavinin sonunda adiponektin seviyesi metformin (p=0,012) ve metformin + EE/SA grubunda (p=0,012), apelin seviyesi ise metformin grubu (p=0,024), EE/SA grubu (p=0,024), ve metformin + EE/SA grubunda (p=0,024) anlamlı olarak yüksek saptandı. Üç tedavi grubunda da CRP seviyesinde istatistiksel olarak anlamlı değişim yoktu (p>0,05). Üç tedavi grubunda da karotis İMK değerinde istatistiksel olarak anlamlı değişim yoktu (p>0,05). Sonuç: Bu sonuçlara göre PKOS’de subklinik aterosklerozun varlığını ve metformin tedavisinin subklinik ateroskleroz üzerine olumlu etki gösterdiğini söyleyebiliriz.

WOS: 000432704800022 Klinefelter syndrome (KS) is the most common chromosomal disorder in men characterized by clinical features of hypogonadism and infertility. About 90% of cases have classically 47, XXY karyotype and the remaining have additional X or Y chromosomes, high grade aneuploidies or X chromosome structural abnormalities. Portal vein aneurysms are very rare. Reported cases are increasing due to use of modern imaging techniques in clinic practise. Here we report a 19-year-old man with KS who was admitted with complaints of abdominal pain, nausea and vomiting. Further investigations revealed 23 mm anechoic, saccular expansion in the left branch of the portal vein. It is well known that KS is associated with venous thromboembolic diseases including portal venous thrombosis, but association with portal vein aneurysm has not been previously reported. Klinefelter sendromu (KS), hipogonadizm ve infertilite ile karakterize, erkeklerde en yaygın görülen kromozomal bozukluktur. Olguların yaklaşık % 90'ında klasik 47,XXY karyotipi, geri kalanlarında ise ek X veya Y kromozomu, yüksek dereceli anöploidler veya X kromozomu yapısal anomalileri bulunmaktadır. Portal ven anevrizmaları çok nadirdir. Klinik pratikte modern görüntüleme tekniklerinin kullanımı ile birlikte, bildirilen vaka sayıları artmaktadır. Burada karın ağrısı, bulantı ve kusma şikayetleri ile başvuran 19 yaşındaki KS'li bir erkek hasta sunmaktayız. Yapılan incelemelerde; portal venin sol dalında 23 mm'lik, anekoik, sakküler genişleme saptanmıştır. KS'nin portal ven trombozu da dahil olmak üzere venöz tromboembolik hastalıklarla ilişkili olduğu iyi bilinmektedir; ancak portal ven anevrizması ile ilişkisi daha önce bildirilmemiştir.

WOS: 000417410900008 Acromegaly is caused by the uncontrolled hypersecretion of growth hormone (GH) and secondary increases of insulin-like growth factor-1. More than 95% of patients with acromegaly have a growth hormone-secreting pituitary adenoma. Ectopic GH or growth hormone releasing hormone (GHRH)-secreting tumors are rare cause of acromegaly. Pituitary adenomas that cause the hypersecretion of GH are nearly always visible on magnetic resonance imaging. Rarely, patients without an ectopic source may have normal pituitary imaging. In managing this rare circumstance, exploring pituitary or medical treatment with a somatostatin analog might be useful. We describe a patient with acromegaly with no pituitary adenoma and no evidence of ectopic source, who was treated with long-acting octreotide.

This study aimed to identify PYGM mutations in patients with McArdle disease from Turkey by next generation sequencing (NGS). Genomic DNA was extracted from the blood of the McArdle patients (n = 67) and unrelated healthy volunteers (n = 53). The PYGM gene was sequenced with NGS and the observed mutations were validated by direct Sanger sequencing. A diagnostic algorithm was developed for patients with suspected McArdle disease. A total of 16 deleterious PYGM mutations were identified, of which 5 were novel, including 1 splice-site donor, 1 frame-shift, and 3 non-synonymous variants. The p.Met1Val (27-patients/11-families) was the most common PYGM mutation, followed by p.Arg576* (6/4), c.1827+7A>G (5/4), c.772+2_3delTG (5/3), p.Phe710del (4/2), p.Lys754Asnfs (2/1), and p.Arg50* (1/1). A molecular diagnostic flowchart is proposed for the McArdle patients in Turkey, covering the 6 most common PYGM mutations found in Turkey as well as the most common mutation in Europe. The diagnostic algorithm may alleviate the need for muscle biopsies in 77.6% of future patients. A prevalence of any of the mutations to a geographical region in Turkey was not identified. Furthermore, the NGS approach to sequence the entire PYGM gene was successful in detecting a common missense mutation and discovering novel mutations in this population study. (C) 2017 Elsevier B.V. All rights reserved.

In disorders of sexual differentiation, sexual development may not be in accordance with chromosomal structure. 46,XX male syndrome is one of these kind of situations of which most of the patients are in normal male phenotype at birth. These patients are diagnosed while investigating for gynecomastia during puberty or infertility at older ages. One of the comorbidities of testosterone deficiency is metabolic syndrome. Recent studies have demonstrated a strong relationship between hypogonadism and metabolic syndrome. A 42-year-old male patient was admitted to our outpatient clinic with the complaint of gynecomastia. Based on laboratory tests results, he was diagnosed with hypergonadotropic hypogonadism accompanied by metabolic syndrome. Chromosomal analysis showed 46,XX SRY (+) genotype. Turk Jem 2014; 1: 28-30

Although the association between adiponectin gene polymorphisms and insulin resistance has been investigated in many studies, there are only a few studies, which have investigated adiponectin gene polymorphisms in patients with polycystic ovary syndrome (PCOS). The objectives of this study were to determine the frequency of T45G polymorphisms localised in exon 2 of the adiponectin gene in a Turkish population with PCOS and to determine the association of T45G polymorphisms with insulin resistance and serum adiponectin levels in PCOS.Ninety-six patients with PCOS and 93 healthy control subjects were included in the study. Insulin resistance was estimated via HOMA-IR. Serum adiponectin levels were measured by ELISA. For determination of adiponectin gene polymorphisms, PCR was performed with appropriate primers after genomic DNA was obtained from the peripheral blood of the patients and control subjects.Adiponectin levels were low in patients with PCOS than control subjects. There was no significant statistical difference between the PCOS and control groups with respect to the frequency of polymorphisms and the genotype distribution. Adiponectin gene polymorphisms were not associated with the anthropometric parameters, hyperandrogenism and adiponectin levels in PCOS. However, the fasting insulin level and insulin resistance were significantly higher and more frequent, respectively, in the polymorphic group compared to the other genotypes among patients with PCOS.The risk of PCOS, hyperandrogenism in patients with PCOS and low serum adiponectin levels cannot be directly attributed to T45G adiponectin gene polymorphisms in exon 2, rather these polymorphisms may be associated with insulin resistance and hyperinsulinemia in PCOS.

Objectives We aimed to evaluate the oxidant/antioxidant status of thyroid tissue in patients with multinodular goiter, papillary carcinoma and to compare with their nonpathologic tissues. Methods We studied 41 patients with multinodular goiter who underwent surgical treatment. The patients were divided into three groups according to clinical diagnosis. Malondialdehyde, selenium, total superoxide dismutase and glutathione peroxidase of thyroid tissue samples were determined in 14 toxic multinodular goiters, 18 non-toxic multinodular goiters, and 9 papillary carcinomas. Result Superoxide dismutase and glutathione peroxidase and selenium were found lower but malondialdehyde was higher in both nodule and cancerous tissues compared with those of control ones. The level of malondialdehyde in non-toxic multinodular goiters group was higher than toxic multinodular goiters group in nodule tissues. Conclusions It can be stated that the lipid peroxidation is increased and enzymatic free radical defense system was significantly impaired in patients with both multinodular goiters and papillary carcinomas.

Type 1 diabetes mellitus (T1DM) is an autoimmune disease characterized by progressive destruction of islet β-cells (Atkinson and MacLaren 1994). It apparently arises from T-cell dependent destruction of β-cells in genetically susceptible individuals (Eisenbarth 2005). The cytokines secreted by CD4 T helper type 1 and 2 (Th1 and Th2) cells may play a crucial role in the pathogenesis of T1DM (Almawi et al. 1999). Cytokines can be classified into two groups: Th1 (proinflammatory) cytokines such as TNF-α and interleukin 1, and Th2 (anti-inflammatory) cytokines such as interleukin 10 and interleukin 4 (Keen 2002). Although the exact roles that Th1 and Th2 cells play in IDDM pathogenesis remain to be established, it was suggested that Th1 cytokines promote, whereas Th2 cytokines protect from the diabetes progression (Rapoport et al. 1993; Pennline et al. 1994). It is thought that the onset and progression of T1DM results from an altered balance between Th1 and Th2 cells (Almawi et al. 1999). IL-10 is a pleiotropic Th2 cytokine that is usually considered to have a role in the downregulation of cell mediated and cytotoxic inflammatory responses, thus being a potent anti-inflammatory mediator. It has been suggested that Th2 induced component of anti-β cell immunity is mediated principally by IL-10 (Lee et al. 1994, 1996; Pakala et al. 1997). Approximately 75% of the variation in IL-10 production appears to be genetically determined (Westendorp et al. 1997). The gene encoding IL-10 has been mapped to chromosome 1q. Several polymorphic sites within the promoter region have been described, including two microsatellite polymorphisms and three biallelic polymorphisms at

PubMed: 19337008 Aim: This study was designed in order to examine the relationship between Calpain 10 [single-nucleotide polymorphism (SNP) 19,43,44,63] gene polymorphisms and clinical and hormonal characteristics in women with polycystic ovary syndrome (PCOS). Materials and methods: One hundred and seven patients with PCOS and 114 healthy subjects were included in this study. Serum levels of sex steroids were measured for each individual. Insulin resistance (IR) was evaluated by the homeostasis model assessment (HOMA) and quantitative insulin-sensitivity check index (QUICKI) methods. Insulin and glucose responses to the oral glucose tolerance test (OGTT) were analyzed by calculating the areas under the curve for insulin (AUCI) and glucose by the trapezoidal methods. We used PCR and restriction fragment length polymorphism technique to examine Calpain 10 SNP 19,43,44, and 63 polymorphisms. Results: Allele distribution of Calpain 10 SNP 44 gene polymorphism was observed as significantly different between the groups. Calpain 10 SNP 44 TC genotype was found to be increased in PCOS subjects (69.15%) compared to the control subjects (50%). However, when compared to control subjects, patients with PCOS had similar Calpain 10 SNP 19, Calpain 10 SNP 43, and SNP 63 gene polymorphisms. When compared with normal Calpain 10 gene SNP 44 allele in PCOS subjects, subjects with PCOS having Calpain 10 gene SNP 44 allele polymorphism had higher free testosterone, androstenedione, DHEA-S, and fasting insulin levels. Also, PCOS women with Calpain 10 gene SNP 44 allele polymorphism had high Ferriman-Gallwey (F-G) score, acne, prevalence of menstrual disturbances, waist-hip ratio, HOMA-IR, AUCI levels and low QUICKI levels. Conclusion: The findings show that Calpain 10 gene SNP 44 allele polymorphism may have a role in PCOS pathogenesis. However, larger-scale studies are needed in this field. © 2009, Editrice Kurtis.