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Objectives: We aimed to evaluate oxidative stress [8-hydroxydeoxyguanosine (8-OHdG), malondialdehyde (MDA)] endothelial damage [asymmetric dimethylarginine (ADMA)] and markers of cellular inflammation [interleukin 6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), neopterin (NP) and high-sensitivity C-reactive protein (hsCRP)] in patients with diabetic nephropathy (DN) and non-diabetic nephropathy who were being administered hemodialysis treatment because of chronic renal failure. Methods: In determining 8-OHdG, IL-6 and TNF-alpha levels, Enzyme-Linked Immuno-Sorbent Assay method was used. Serum MDA, ADMA and NP levels were determined by using high performance liquid chromatography (HPLC). And hs-CRP values were measured with nephelometric method. Results: Serum 8-OHdG and MDA levels were found statistically to have increased when compared with those of the control group in patients groups after dialysis. However, serum ADMA and neopterin levels were observed statistically to have decreased when compared with those of the control group in patients groups after dialysis. But, decreases on ADMA and neopterin levels are still much higher than those of control. IL-6 and TNF-alpha levels were found to have increased when compared with those of control group in patients groups before dialysis. Conclusion: The oxidative stress in patients with DN, who were being treated with hemodialysis due to chronic renal failure, was higher than that of non-DN patients who were being treated with hemodialysis. In contrast with this, inflammation occurring in non-DN patients was found to have been higher than that of in patients with DN.

Rheumatoid arthritis (RA) is an inflammatory multisystem disease of unknown etiology characterized by chronic destructive synovitis. It and #8217;s prevalence is about 1% all over the world. Serologic markers are also important beside some clinical situations upon RA diagnosis. Today, the most commonly used laboratory test is rheumatoid factor (RF) in patients with suspected RA. RF is sensitive but not a specific biomarker for diagnosing RA. Early diagnosis of RA is essential to prevent of progressive joint damage. In recent years, anticyclic citrullinated peptide/protein antibody (anti-CCP) attracts the attention as a remarkable biomarker for early diagnosis. Anti-CCP which is a family of anti-citrullinated protein antibodies (ACPA) family, showed quite satisfactory specificity in the diagnosis of RA. Due to the prescence of ACPA was included to 2010 RA diagnostic criteria, in a manner of speaking, importance of anti-CCP was registered. [TAF Prev Med Bull 2014; 13(1.000): 83-88]

An overdose of acetaminophen (APAP) produces acute tubular necrosis. The aim of this study was to observe the effects of hyperbaric oxygen (HBO) only and combined with N-acetylcysteine (NAC) on inflammatory cytokines in kidney. Thirty-two male Sprague-Dawley rats were divided into four groups: sham, control (APAP), NAC, and NAC + HBO. In the APAP, NAC, and NAC + HBO groups, renal injury was induced by oral administration of 1 g/kg APAP. The NAC group received NAC (100 mg/kg/day). NAC + HBO group received NAC (100 mg/kg/day) intraperitoneally and HBO underwent at 2.8 ATA pressure with 100 % oxygen inhalation for 90 min every 12 h for 5 days. Rats in the sham group received distilled water only by gastric tube. All animals were killed on 6 days after APAP or distilled water administration. Creatinine, urea, neopterin, tumor necrosis factor-α (TNF-α), and interleukin (IL)-6 levels were measured in sera. There was a significant increase in serum creatinine and urea levels in the control group compared to the sham group (in both, p = 0.001). NAC and NAC + HBO significantly decreased serum neopterin, TNF-α, and IL-6 levels compared to control group. APAP administration caused tubular necrosis in the renal. NAC and NAC + HBO treatments significantly reduced APAP-induced renal damage. The results of this study showed that renal dysfunction in APAP toxicity was attenuated by the use of HBO and NAC treatments. The combination of NAC and HBO treatments might be recommended as an effective treatment modality for APAP-induced nephrotoxicity.

Acetaminophen (APAP) is an analgesic and antipyretic agent. In overdoses, it is associated with nephrotoxicity. We examined the potential protective effects of N-acetylcysteine (NAC) and NAC + ozone therapy (OT) combination against APAP-induced nephrotoxicity.Thirty-two male Sprague-Dawley rats were divided into four groups: sham, control (APAP), NAC, and NAC + OT. In the APAP, NAC, and NAC + OT groups, kidney injury was induced by oral administration of 1 g/kg APAP. The NAC group received NAC (100 mg/kg/day). NAC + OT group received NAC (100 mg/kg/day) and ozone/oxygen mixture (0.7 mg/kg/day) intraperitoneally for 5 days immediately after APAP administration. All animals were killed at 5 days after APAP administration. Renal tissues and blood samples were obtained for biochemical and histopathological analyses. Neopterin, tumor necrosis factor-α (TNF-α), interleukin (IL)-6 and IL-10 levels were measured in sera. Malondialdehyde (MDA) levels and glutathione peroxidase (GPx) activities were determined in renal homogenates.NAC and NAC + OT significantly decreased MDA and TNF-α levels and increased IL-10 levels and GPx activities. Serum neopterin and IL-6 levels were not different among all groups. APAP administration caused tubular necrosis in the kidney. The degrees of renal necrosis of the APAP group were higher than the other groups. Renal injury in rats treated with combination of NAC and OT were found to be significantly less than the other groups.Our results showed that NAC and OT prevented renal injury in rats and reduced inflammation. These findings suggest that combination of NAC and OT might improve renal damages because of both oxidative stress and inflammation.

The aim of this study was to investigate the protective effects of taurine (Tau) on experimental acute pancreatitis (AP) in a rat model by measuring cytokines and oxidant stress markers. Forty rats were randomly divided into four groups: sham, AP, Tau and AP + Tau. AP was induced with sodium taurocholate. No treatment was given to the AP. All rats were killed 5 days later. Pancreatic tissues of rats and blood samples were obtained. Tau treatment significantly decreased serum amylase activity ( p < 0.001), total injury score ( p < 0.001), malondialdehyde levels ( p < 0.001) and myeloperoxidase (MPO) activity ( p < 0.001). There was no significant difference between the Tau and AP + Tau groups in serum and pancreatic tumor necrosis factor-α, interleukin (IL)-1β and IL-6 levels ( p = 1.000). Histopathologic scores in the AP + Tau and Tau groups were significantly lower compared with the AP group (both p < 0.001). These results showed that Tau reduces lipid peroxidation, amylase and MPO activities and the concentrations of proinflammatory cytokines secondary to AP and also increases superoxide dismutase and glutathione peroxidase activities in rats with sodium taurocholate-induced AP. It also has a marked ameliorative effect at histopathologic lesions. With these effects, Tau protects the cells from oxidative damage, reduces inflammation and promotes regression of pancreatic damage.

Objective: The aim of our study was to investigate the relationship between Nitric Oxide, ADMA, homocysteine in endotoxin-induced human umblical vein endothelial cell cultures. Methods: For this reason two groups are formed (n=12). Control group consists of HUVEC cultures without any treatment. LPS group is treated with 10μg/mL endotoxin (E.coli 0111: B4).The measurement of NO levels is perfomed by spectrophotometric measurement of nitrite and nitrate. ADMA and Homocysteine levels are measured using HPLC with fluorescence detection. Results: The results of our study showed that there was a significant increase of NO, ADMA and Homocysteine in endotoxemia (p

Overdose of acetaminophen (APAP) can lead to severe liver injury in humans and experimental animals. Pentraxin-3 (PTX-3) is produced and released by several cell types. In this study, we aimed to evaluate whether PTX-3 is a potential biomarker in the identification of APAP-induced liver injury.Thirty adult male Wistar rats were randomly divided into three groups: control, APAP-1 and APAP-2 groups. APAP-1 (1 g/kg) and APAP-2 (2 g/kg) group rats were given APAP by gastric tube. Liver tissues and blood samples were obtained for biochemical and histopathological analysis. Biochemical parameters, plasma and liver PTX-3 levels and degree of liver necrosis were measured in all groups.APAP treatments caused necrosis in liver and accompanied by elevated liver PTX-3 levels after 48 h. In APAP-1 and APAP-2 groups when compared with control group (7.5±3.3 ng/mg protein), mean liver PTX-3 concentrations were 14.1±3.0 (p=0.032) and 28.5±8.2 (p0.001) ng/mg protein, respectively. All rats (100%) in the APAP-2 group had the degree 3 liver necrosis. However 10%, 40% and 50% of rats had the degree 1, the degree 2 and the degree 3 liver necrosis in the APAP-1 group, respectively. The degrees of liver necrosis of the APAP-1 and APAP-2 groups were higher than the group of control (p0.001 and p0.001, respectively).PTX-3 may have a role in the APAP-induced liver injury in the rats. The elevated liver PTX-3 in the APAP-induced hepatic necrosis might be a marker of acute histological liver damage. Further prospective studies are necessary to clarify the prognostic value of liver PTX-3 for prediction of histological hepatic necrosis in the APAP-induced liver injury.

Mitochondrial respiratory chains consist of approximately 100 structural proteins. Thirteen of these structural proteins are encoded by mitochondrial DNA (mtDNA), and the others by nuclear DNA (nDNA). Mutation in any of the mitochondrial structural-protein related genes, regardless of whether they are in the nDNA or mtDNA, might cause mitochondrial disorders. In the recent past, new nuclear genes required for assembly, maintenance, and translation of respiratory chain proteins have been found. Mutation in these genes might also cause mitochondrial disorders (MD). NFU1 gene is one of such genes and has a role in the assembly of iron-sulfur cluster (ISC). ISCs are included in a variety of metalloproteins, such as the ferredoxins, as well as in enzymatic reactions and have been first identified in the oxidation-reduction reactions of mitochondrial electron transport. It is important to be aware of NFU1 gene mutations that may cause severe mitochondrial respiratory chain defects, mitochondrial encephalomyopathies and death, early in life.

Diabetic nephropathy (DN) is a major manifestation of microangiopathy in patients with Diabetes Mellitus (DM). Inflammation is one of the major factors in the formation of endothelial dysfunction. Endothelial dysfunction is a major contributor to the complications of DM. The aim of the present study was to investigate the possible relationship between inflammation, endothelial dysfunction and proteinuria in patients with diabetic nephropathy.Plasma TNF-α and IL-6, pro-inflammatory cytokines, concentrations were measured in 25 patients with DN and in 30 diabetic control subjects. Also, we evaluated the markers of endothelial dysfunction such as flow mediated dilatation (FMD), nitrate-mediated dilatation (NMD) and carotid intima-media thickness (CIMT).TNF-α, IL-6 and high-sensitivity C-reactive protein concentrations were significantly higher (p = 0.012, p = 0.006 and p0.001, respectively) in the patients with DN than the controls. And, urinary protein concentrations were significantly higher (p0.001) but eGFR levels were significantly lower (p0.001) in the patients with DN. FMD was significantly lower in DN patients (p0.001). We have observed that FMD correlated negatively with body mass index (r = -0.424, p0.05). And there was also a positive correlation between TNF-α and urinary protein concentrations in the patients with DN (p0.05).TNF-α, IL-6, hsCRP and urinary protein concentrations are higher in the DN patients. There were no correlations among pro-inflammatory cytokines concentrations and markers of vascular endotelial disfunction. These findings did not show vascular endothelial dysfunction, but may indicate glomerular endothelial dysfunction.

Aim: In this study, we aimed to measure malondialdehyde levels by two different methods and compare these methods. Material and Methods; Serum malondialdehyde levels of 60 volunteers were measured with thiobarbituric acid test and high pressure liquid chromatography after derivatization of malondialdehyde with 2,4 dinitrophenylhydrazine and these two methods were compared. Results A statistically significant difference (p

Introduction: In large dosages, acetaminophen (APAP) produces acute kidney necrosis in most mammalian species. High neopterin levels have been accepted as strong indicators for the clinical severity of some diseases. In this study, we aimed to evaluate whether neopterin is a biomarker in the identification of APAP-induced nephrotoxicity. Materials and Methods: Thirty adult male Wistar rats were randomly divided into three groups: control, APAP-1, and APAP-2 groups. APAP-1 and APAP-2 group rats were given a single dose of 1 and 2 g/kg body weight of APAP by gastric tube, respectively. Kidney tissues and blood samples were obtained for biochemical and histopathological analyses. Biochemical parameters, serum and kidney neopterin levels, and the grade of tubular injury were compared in the control, APAP-1, and APAP-2 group animals. Results: APAP treatments caused tubular necrosis in the kidney and increase in serum creatinine concentrations accompanied by elevated serum and kidney neopterin levels. In the rats of groups APAP-1 and APAP-2 when compared with that of the control group (109.1 pmol/mg protein), median kidney neopterin concentrations were 162.1 (p = 0.089) and 222.2 (p < 0.001) pmol/mg protein, respectively. The grade of tubular injury of the APAP-1 and APAP-2 groups was higher than the group of control (both p < 0.001). Conclusions: Serum and kidney neopterin levels could be sensible alternative to evaluate the risk to have nephrotoxicity because of APAP overdose. The elevated serum and kidney neopterin in the APAP-induced tubular necrosis might be a marker of acute histological kidney injury.

Dear Editor, In a recent issue of Annals of Neurosciences, we read with great interest the article by Kasarpalkar and colleagues entitled “Brain-Derived Neurotrophic Factor in children with Autism Spectrum Disorder” in which the investigators reported that the protective effect of brain derived neurotrophic factor (BDNF) due to relatively higher levels in mild phenotypes of autism compared to severe autism and its possible diagnostic role in autism spectrum disorders.1 However, we think that some points should be discussed. BDNF is signaling protein that involved in the central regulation of energy homeostasis. Maffioletti and colleagues reported that serum preparation procedure is quite important issue to present robust methodology while measuring serum BDNF.2 BDNF level is presumably affected from duration of the clotting procedure due to being stored in thrombocytes. They observed progression on serum BDNF concentrations, which reached 38% of the plateau value after 10 min, 91.8% after 30 min, and 100% after 1 hour. Therefore, they recommended the minimum clotting duration for a correct serum BDNF dosage as 1 hour. However, in this study, the authors stated that serum samples were separated immediately after blood was collected. We think that standardization of clotting process is highly important to prevent misinterpretation of serum BDNF levels. Previous studies suggested that certain diseases such as epilepsy, allergic rhinitis and atopic dermatitis could likely affect BDNF levels.3 In addition, medications such as aspirin and corticosteroids, and dietary supplements such as vitamin E, vitamin A, vitamin B12, folic acid, zinc, omega-3 fatty acids, and ginkgo biloba extracts can influence BDNF levels.4-6 In this regard, without defining these contributing factors, interpreting the results is problematic. The authors did not express any of above contributors. In conclusion, clarifying these concerns will certainly provide a clearer picture when interpreting serum BDNF levels among participants.

We have read with a great interest the published article by Aoki and colleagues entitled ‘Increase of nerve growth factor levels in the human herniated intervertebral disc: can annular rupture trigger discogenic back pain?’ [1]. The authors suggest that nerve growth factor (NGF) increases in herniated discs, and may play an important role in the generation of discogenic pain. However, we think some points should be discussed. NGF is a polypeptide that plays an important role for cells belonging to the nervous, endocrine, and immune systems [2]. We think the study group in which the authors evaluated tissue NGF levels is not well defined. Namely, they should state whether the patients have one of following diseases, which could probably affect NGF levels: neuropsychiatric diseases such as epilepsy, depression, schizophrenia, migraine and primary headache; and eating disorders or cardiometabolic diseases such as atherosclerosis, metabolic syndrome and type 2 diabetes mellitus [3]. In addition to these diseases, obesity is also shown to affect NGF levels [4]. In this regard, the above diseases should be taken into account while designing a study group, and the body mass index of participants has to be thought of as another confounding variable and included in multiple regression analysis like age and sex are. Besides the above confounders, supplements such as vitamin D analogs, zinc, vitamin B12, vitamin A, omega 3 fatty acid or herbal medicines and some drugs such as estrogen, glucocorticoids, acetyl-l-carnitine and antipsychotics also have to be denoted regarding whether the participants use these medications or not because they are affecting factors for NGF [5]. In conclusion, explanation of these concerns will certainly provide clearer information for the readers.

Thanks are due to Dr. Ucak and colleagues for their valuable research evaluating the levels of serum ghrelin in patients with psoriasis [1]. However, we wish to make some comments on methodology of their study. Ghrelin is a hormone secreted mainly by stomach. Some types of antipsychotics, antidepressants, corticosteroids, bromocriptine, and anti-TNF-α therapy drugs were suggested to affect serum ghrelin levels [2, 3]. Also, dietary food supplements such as vitamin D and free fatty acids could affect these levels [4]. In this respect, the authors should define whether the participants use these kinds of drugs and dietary supplements or not. In addition, several studies revealed that certain diseases such as functional dyspepsia, celiac disease, cachexia, inflammatory bowel disease, asthma, ankylosing spondylitis, coronary artery disease, iron deficiency anemia, hepatocellular cancer, chronic liver disease, chronic renal disease, epilepsy, and Helicobacter pylori infection could affect serum ghrelin [5, 6]. The authors did not mention these contributing diseases in their paper. Ucak and colleagues stated that they questioned the patients' alcohol and cigarette smoking habits. As known, serum ghrelin levels are associated with alcohol intake and smoking [7, 8]. In this regard, a regression analysis could be applied for these variables to examine whether they affect serum ghrelin levels. Therefore, interpretation of results with its current form seems problematic. In conclusion, we believe that the study of Ucak et al. contributes important data to medical literature and could lead other researchers to design a study. However clarifying above concerns will provide clearer picture to the readers.

In this article, an interference caused by hemoglobin H (Hb H), during the measurement of hemoglobin A1c (HbA1c) with ion exchange high pressure liquid chromatography (HPLC) method, was presented in blood sample of a 20-year-old male patient. HbA1c measurement was performed with Agilent 1200 HPLC system using a commercial Recipe HbA1c ion-exchange column. Hemoglobin electrophoresis was performed with Interlab G26 agarose electrophoresis automated compact system. HbA1c level was 18.2% and HbA0 level was 81.5% with ion-exchange HPLC method. Patient's fasting serum glucose was assessed before HbA1c measurement and the result was 165 mg/dL (9.16 mmol/L). On the other hand, the result of HbA0 was 87.9%, Hb H was 10.8% and Hb A2 was 1.3% with electrophoresis. Whole blood test values were within reference ranges except MCV. MCV value was 79.6 fL. It is important to keep in mind that HbA1c level might be considered falsely high with ion-exchange HPLC method because of Hb H containing sample.

In a recent issue of Acta Orthopaedica et Traumatologica Turcica, we read with great interest the article by Zehir et al. entitled ‘Red cell distribution width and mortality in patients with hip fracture treated with partial prosthesis’.[1] They evaluated the outcome of patients with hip fracture treated with partial hip replacement, and investigated the relationship between red cell distribution width (RDW) and mortality in patients who underwent partial hip replacement surgery. They concluded that there was a significant correlation between elevated RDW level and mortality. We believe that these findings will act as a guide for further studies, and we thank the authors for their contribution to the literature. However, we think that some points should be discussed., sayımı tahlilinde ana parametrelerden biri ve aneminin ayırıcı tanısında kullanılır. Son zamanlarda çok sayıda araştırmada RDW ile birçok hastalık durumlarının ölüm oranı arasında doğrudan bir ilişki olduğu sonucuna varılmıştır.[1] Hatta yüksek RDW değerleri genel popu- lasyonda daha yüksek mortalite ile ilişkili bulunmuştur. [2] Fakat bu hastalık durumlarındaki artmış mortalite ile RDW yukselmesi mekanizması arasında direk bir ilişki kurulamamıştır ama hastanın yaşından, beslenme düzeyinden ve eritrositlerdeki kronik enflamasyondan süphelenilmiştir. Çok değişkenli analizler göstermiştir ki; artmış RDW düzeyine neden olan patofizyoloji anemi durumuna bakılmaksızın, akut ve kronik hastalık durumlarının sonuçlarını etkileyebilir. RDW birden fazla patolojik sürecin bir bütünleştirici belirteci olarak görünmektedir.[3] Bu durum RDW değerinin hastalık durumlarının şiddeti ile ilişkili ve prognoz ile korele olduğunu açıklayabilir. RDW kalça kırığı cerrahisi olan hastalar için hazır, objektif ve ucuz bir testtir. Hasta daha acil servisteyken prognoz ve mortalite hakkında fikir verebilir. Gelecekte kalça kırığı hastalarının risk

We have read the published paper by Singh et al. [1] with great interest. In their study, the authors evaluated the outcome of video-assisted thoracic surgery (VATS) in 9 patients (males = 6, females = 3) with clinicoradiological diagnosis of tubercular spondylitis of the dorsal spine. But they said “We performed video-assisted thoracoscopic surgery in 9 patients (males = 6, females = 7) with tubercular spondylitis of the dorsal spine at our centre from January 2009 to December 2011” in Patients and Method section.

Dear Editor, We read with great interest the recent article by Tapper et al. [1]. The authors aimed to determine the clinical predictors of advanced histology in the referral population. In multivariate logistic regression analyses, they have demonstrated that body mass index (BMI) ≥30 kg/m2, female gender, and aspartate aminotransferase (AST) >40 IU/L were associated with a non-alcoholic fatty liver disease (NAFLD) activity score >4. They have also shown that AST-to-platelet ratio index (APRI) >1 was the most significant predictor of advanced fibrosis. Additionally, they have suggested that patients with suspected NAFLD should be routinely evaluated for advanced liver disease, including non-invasive indices of fibrosis such as APRI, and serious consideration given to liver biopsy. Understanding the value of non-invasive indices of fibrosis such as APRI in patients with NAFLD, we consider this large, retrospective study to be very important; however, we have some questions that should be mentioned as contributory factors. The authors mentioned exclusion criteria: patients with viral hepatitis, alcoholic liver disease, haemochromatosis, Wilson disease, drug-induced liver injury and autoimmune hepatitis were excluded from the study. We wonder whether patients with pancreatobiliary disease and platelet disorders were also excluded from the study. Elevated AST levels might be the result of the pancreatobiliary disease, even in the absence of obvious liver disease [2]. Therefore, amylase, alkaline phosphatase, gamma-glutamyl transferase, bilirubin results and platelet count should also be included in this study. APRI has an important disadvantage because of the use of upper limits of normal (ULN) for aminotransferases. There is no standardization between laboratories [3]. It was shown that ULN for AST ranged from 26–49 IU/L according to gender, BMI and serum cholesterol in the control population [4]. On the other hand, in another study, it was reported that serum aminotransferase activities were significantly higher in men than in women in a control population [5]. In conclusion, we think APRI results could cause confusing interpretations for the staging of advanced fibrosis in the patients with NAFLD. We need further studies to better understand the relationship between APRI results and fibrosis in patients with NAFLD.