Serum Cingulin levels are increased in children with autism spectrum disorder.

Background: Autism spectrum disorder (ASD) is a group of neurodevelopmental disorders in which the underlying pathogenesis and etiologic factors are not fully understood. The blood brain barrier (BBB) ​​plays a critical role in central nervous system defense by limiting access to circulating solutes, macromolecules, and cells that can negatively affect neuronal activity. The loss of BBB integrity is likely to be seen as a common pathologic finding for many psychiatric disorders such as schizophrenia, ASD, and mood disorders. In this study, we aimed to investigate whether serum Cingulin levels are associated with ASD. Subjects and Methods: A total of 40 treatment-naive children with ASD and 40 healthy controls were included in the present study. The Schedule for Affective Disorders and Schizophrenia for School-Aged Children, Present and Lifetime Version-DSM-5 (K-SADS-PL-DSM-5) has been used to screen healthy controls for psychiatric disorders by a psychiatrist after a physical examination by a paediatrician. The clinical severity of the ASD symptoms has been assessed by the Childhood Autism Rating Scale (CARS). Venous blood samples were collected and serum Cingulin levels were measured. Results: When the ASD and control groups were compared, CARS and Cingulin values of the patient group were statistically higher than the healthy group. There is a statistically positive correlation between CARS and Cingulin values. Discussion: To the best of our knowledge, this study is a first in the literature conducted about the serum Cingulin levels, which is a component of BBB, among patients with ASD. Our findings demonstrate that serum Cingulin levels are meaningfully higher in ASD group compared to the healthy control group. It has been also indicated that there has been a meaningful relationship between serum Cingulin levels and ASD symptom severity.

Increased serum levels of tumour necrosis factor-like weak inducer of apoptosis in children with autism spectrum disorder.

Introduction: A previous study has evaluated the association between serum tumour necrosis factor-like weak apoptosis inducer (TWEAK) levels and autism spectrum disorder (ASD). In line with this investigation, the present study aimed to measure serum TWEAK levels to determine whether their eventual alteration might have etiopathogenetic significance in children with ASD. Methods: A total of 40 treatment-naive children with ASD and 40 healthy children as controls were included in the present study. The Schedule for Affective Disorders and Schizophrenia for School-Aged Children-Present and Lifetime Version, DSM-5 was used by a psychiatrist to screen the healthy controls for psychiatric disorders after a physical examination by a paediatrician. The clinical severity of the ASD symptoms was assessed by the Childhood Autism Rating Scale. Venous blood samples were collected, and serum TWEAK levels were measured. Results: This study included 80 children in total, with 40 (50.0%) in the patient group and 40 (50.0%) in the healthy control group. Thirty four (85.0%) of the participants in the patient group, and 31 (77.5%) in the healthy control group, were male, and the remainder were female. The distribution of the gender ratio was statistically similar between groups (p = 0.568). The volunteers were between 36 and 59 months old. The average age in the patient group was 46.0 ± 6.5, while that in the healthy control group was 45.2 ± 6.7. The ages were also statistically similar between groups (p = 0.615). The TWEAK values of the patient group were found to be statistically higher than those of the healthy control group (p < 0.001). Discussion: This study examined whether serum TWEAK levels were related to ASD in childhood. Our findings indicate that children with ASD have higher TWEAK levels when compared to other children. The findings further indicate that serum TWEAK levels could be related to ASD etiopathogenesis independent of ASD symptom severity.

The effect of long term nicotine exposure on endothelial function in rats.

Nicotine is one of the main chemicals in the cigarettes responsible for addiction formation. Many researches investigating the effects of nicotine on coronary heart disease and atherosclerosis have been published. The robustness of endothelial cells is very important in the development of atherosclerosis. The aim of this study is to evaluate the effect of nicotine exposure on the indicators of endothelial function either by examining the vascular reactivity of aorta taken from rats exposed to nicotine during prenatal (starting by the mating period) and postnatal periods (6 weeks after delivery), or by determining the protein expression of nitric oxide synthase (NOS) enzymes, NADPH oxidase (Nox) and nitrotyrosine. Chronic nicotine exposure at 6 mg/L in drinking water produced a significant decrease in phenylephrine contractility of thoracic aortic rings compared to control and low dose exposure group (0.4 mg/L, p < 0.001). Endothelium-dependent relaxations to acetylcholine increased dose-dependently while no changes were observed in endothelium-independent relaxations to sodium nitroprusside and protein expressions in rat thoracic aorta. It has been concluded that long term nicotine exposure does not have serious effects on endothelial vasodilator response directly and does not change protein expression of NOS or Nox enzymes. However, more studies should be done for the exact mechanisms responsible for the effect of nicotine on endothelial function.

Diagnostic Value of Inflammatory Factors in Patients with Gallbladder Cancer, Dysplasia, and Cholecystitis.

BACKGROUND: Involving pre-sampled patients with cholecystitis, dysplasia, and adenocarcinoma, the present study aimed to compare the neutrophil/lymphocyte (NLR), monocyte/lymphocyte (MLR), platelet/lymphocyte (PLR) ratios, and plateletcrit (PCT), mean platelet volume (MPV), and platelet distribution width (PDW) values and to determine their prognostic importance. METHODS: The present study involved 187 cholecystectomy specimens that were diagnosed as cholecystitis, dysplasia, and adenocarcinoma. Preoperative neutrophil, monocyte, lymphocyte, and platelet counts, NLR, MLR, and PLR ratios, and PCT, MPV, and PDW levels of the same patient groups were retrospectively recorded. RESULTS: In the present study, the cut-off values for dysplasia of NLR, PLR, and MLR were found as 1.61, 81.45, and .19, whereas those for cancer of NLR, PLR, and MLR were 2.65, 182.69, and .35, respectively. The NLR, PLR, and MLR values of the chronic cholecystitis and chronic calculous cholecystitis groups were statistically significantly lower than those of the chronic active calculous cholecystitis group (P < .01). The NLR and MLR values of the non-cancer and non-dysplasia groups were statistically lower than those of the cancer and dysplasia groups (P < .05). CONCLUSION: According to the results of the present study, using additional imaging methods, acute-phase cholecystitis can be distinguished using preoperative neutrophil and monocyte counts, and NLR, PLR, and MLR cut-off values can be used to distinguish dysplasia, which is the antecedent of gallbladder cancer. It is thought that this might provide patients with an advantage in terms of early treatment and survival.

Fecal neopterin level determination: can be a useful screening test for colorectal polyps?

BACKGROUND: Colorectal cancer (CRC) is a leading cause of cancer death worldwide. The main precursor lesion leading to CRC is the adenomatous colorectal polyp (CP). Nowadays, there is no recognized perfect screening test of CP and CRC. Neopterin is an important marker of cellular inflammation. In this study, we aimed to evaluate comparatively immunochromatographic fecal occult blood test (iFOBT) and fecal neopterin levels (FNLs) in patients with CP and controls. METHODS: One hundred eleven patients diagnosed with CP and 68 individuals with negative colonoscopy were included in the study. iFOBT and FNLs were assessed in patients and controls. RESULTS: FNLs and iFOBT positivity were significantly higher in patients with CP than in controls (17.15 ± 3.55 µmol/L/g vs. 12.25 ± 2.19 µmol/L/g, P = 0.00 and 46.8% vs. 14.8%, P = 0.00, respectively). FNLs were significantly higher in cases with adenomatous polyps than in hyperplastic polyps (P = 0.002). FNL ≥14.00 µmol/L/g was the best cutoff value to differentiate between patients with CP from controls (P = 0.000). A multiple logistic regression analysis showed that high FNL was positively correlated with presence, number, diameter of CPs, and presence of adenoma (P < 0.005). The sensitivity of high FNL for CP was 81.1%, which was superior to iFOBT positivity (47.7%, P < 0.001). DISCUSSION: FNL level is significantly increased in CPs. The FNL exhibited increased sensitivity for identifying CP and adenomatous lesions compared with iFOBT. FNL determination could have as a new screening and diagnostic test for CP.

Can neopterin be a useful immune biomarker for differentiating gastric intestinal metaplasia and gastric atrophy from non-atrophic non-metaplastic chronic gastritis? / ¿Puede la neopterina ser un biomarcador inmunológico para diferenciar la metaplasia intestinal gástrica y la atrofia gástrica de la gastritis crónica no atrófica y no metaplásica?

Introduction: Helicobacter pylori (H. pylori) is closely related to pre-neoplastic lesions such as gastric atrophy (GA), gastric intestinal metaplasia (GIM) and eventually gastric cancer (GC). The diagnosis of GIM and GA is usually based on endoscopic and histopathological features. Nowadays, there are no recognized good serological markers of GIM and GA. Neopterin is an important marker of cellular inflammation. In this study, we aimed to comparatively evaluate C-reactive protein (CRP) and neopterin levels in patients with GIM, GA and chronic gastritis, and to show the increased serum neopterin levels in GIM and GA according to non-atrophic and non-metaplastic chronic gastritis. Patients and methods: 98 patients with GIM and 68 patients with GA and 70 patients with non-atrophic non-metaplastic gastritis were included in the study. CRP and neopterin levels were assessed in patients and controls. Results: CRP and neopterin levels were significantly higher in patients with GIM and GA than in controls (p<0.05 and p<0.001, respectively). A multiple logistic regression analysis showed that high levels of serum neopterin were positively correlated with GIM and GA. According to the ROC curve analysis, the best cut-off value to differentiate between patients with GIM and/or GA from controls was ≥10.15nmol/l (p<0.001) for serum neopterin levels and ≥1.95mg/l (p<0.001) for serum CRP levels. Discussion: CRP and neopterin levels are significantly increased in GIM and GA. Neopterin may be a useful biomarker and diagnostic test for detecting GIM and GA in clinical practice. CRP levels may be helpful for this observation

Introducción: Helicobacter pylori (H. pylori) está estrechamente relacionado con lesiones preneoplásicas, como la atrofia gástrica (AG), metaplasia intestinal gástrica (MIG) y finalmente cáncer gástrico (CG). El diagnóstico de MIG y AG generalmente se basa en características endoscópicas e histopatológicas. Hoy día, no hay buenos marcadores serológicos reconocidos de MIG y AG. La neopterina es un marcador importante de inflamación celular. En este estudio, nuestro objetivo fue evaluar comparativamente la proteína C-reactiva (PCR) y los niveles de neopterina en pacientes con MIG, AG y gastritis crónica, y mostrar el aumento del nivel sérico de neopterina en MIG y AG sobre la base de gastritis crónica no atrófica y no metaplásica. Pacientes y métodos: Se incluyó en el estudio a 98 pacientes con MIG, 68 pacientes con AG y 70 pacientes con gastritis no atrófica y no metaplásica. Se evaluaron los niveles de PCR y neopterina en pacientes y controles. Resultados: Los niveles de PCR y neopterina fueron considerablemente más altos en los pacientes con MIG y AG que en los controles (p<0,05 y p<0,001, respectivamente). Un análisis de regresión logística múltiple mostró que el elevado nivel de neopterina sérica se correlacionó positivamente con MIG y AG. Según el análisis de la curva ROC, el mejor valor de corte para diferenciar entre pacientes con MIG y/o AG y controles fue ≥10,15nmol/l (p<0,001) para el nivel de neopterina sérica y ≥1,95mg/l (p<0,001) para el nivel de PCR en suero. Discusión: Los niveles de PCR y neopterina aumentan considerablemente en MIG y AG. La neopterina puede ser un biomarcador útil y una prueba de diagnóstico para detectar MIG y AG en el entorno clínico. Los niveles de PCR pueden ser útiles para esta observación

Can neopterin be a useful immune biomarker for differentiating gastric intestinal metaplasia and gastric atrophy from non-atrophic non-metaplastic chronic gastritis?

INTRODUCTION: Helicobacter pylori (H. pylori) is closely related to pre-neoplastic lesions such as gastric atrophy (GA), gastric intestinal metaplasia (GIM) and eventually gastric cancer (GC). The diagnosis of GIM and GA is usually based on endoscopic and histopathological features. Nowadays, there are no recognized good serological markers of GIM and GA. Neopterin is an important marker of cellular inflammation. In this study, we aimed to comparatively evaluate C-reactive protein (CRP) and neopterin levels in patients with GIM, GA and chronic gastritis, and to show the increased serum neopterin levels in GIM and GA according to non-atrophic and non-metaplastic chronic gastritis. PATIENTS AND METHODS: 98 patients with GIM and 68 patients with GA and 70 patients with non-atrophic non-metaplastic gastritis were included in the study. CRP and neopterin levels were assessed in patients and controls. RESULTS: CRP and neopterin levels were significantly higher in patients with GIM and GA than in controls (p<0.05 and p<0.001, respectively). A multiple logistic regression analysis showed that high levels of serum neopterin were positively correlated with GIM and GA. According to the ROC curve analysis, the best cut-off value to differentiate between patients with GIM and/or GA from controls was ≥10.15nmol/l (p<0.001) for serum neopterin levels and ≥1.95mg/l (p<0.001) for serum CRP levels. DISCUSSION: CRP and neopterin levels are significantly increased in GIM and GA. Neopterin may be a useful biomarker and diagnostic test for detecting GIM and GA in clinical practice. CRP levels may be helpful for this observation.

Effect of nicotine on RANKL and OPG and bone mineral density.

AIM: The signaling pathway OPG/RANK/RANKL is a key in maintaining the balance between the activity of osteoblasts and osteoclasts in order to prevent bone loss. In this study, our aim was to assess the effects of long-term nicotine exposure on plasma RANKL and OPG levels, tissue RANKL and OPG immunoreactivities, and bone mineral density (BMD) scores in rats. MATERIALS AND METHODS: Thirty-six Swiss Albino rats weighing 70 ± 10 g were divided into three groups. While the controls (n = 12) were only given normal drinking water, for low-dose nicotine (LDN) group (n = 12) 0.4 mg/kg/day; for high-dose nicotine (HDN) group (n = 12), 6.0 mg/kg/day nicotine was added to drinking water for a year. At the end of 12th month, BMD scores were measured using an X-ray absorptiometry and bone turnover was assessed by measuring plasma RANKL and OPG levels and RANKL and OPG immunoreactivities in tail vertebrae of the rats. RESULTS: There was no statistically significant difference in BMD scores of lumbar spine and femoral regions of the nicotine groups in comparison to controls. Plasma OPG levels were found to be significantly higher in HDN group, in comparison to the controls and LDN groups (p = .001) unlike plasma RANKL levels. Tissue RANKL and OPG immunoreactivities decreased significantly in the LDN and HDN groups (p < .001, p < .01, respectively). CONCLUSIONS: The results of this study show that nicotine is not primarily responsible for the decrease in BMD frequently seen in smokers. Measuring plasma RANKL and OPG levels did not reflect tissue immunoreactivities.

The effect of long-term nicotine exposure on bone mineral density and oxidative stress in female Swiss Albino rats.

PURPOSE: To evaluate the effect of long-term low or high-dose nicotine exposure on bone mass via measuring bone mineral density (BMD) and oxidant-antioxidant status markers. METHODS: Thirty-five female Swiss Albino rats weighing 70 ± 10 g were divided as the control group (n = 12), low-dose nicotine group (n = 12) and high-dose nicotine group (n = 11). While the control group was given only normal drinking water, the low-dose nicotine group had 0.4 mg/kg per day and the high-dose nicotine group, 6.0 mg/kg per day of nicotine added to their water for the period of 1 year. BMD was determined with X-ray absorptiometry of lumbar vertebra, corpus femoris, proximal and distal femur. To evaluate oxidant-antioxidant status malondialdehyde (MDA) levels, superoxide dismutase (SOD) and catalase (CAT) activities were determined. RESULTS: When comparing the nicotine groups and controls, neither BMD nor oxidant-antioxidant status markers showed any statistically significant difference. In comparison to the controls, 12 months of high-dose oral nicotine exposure did not have a significant effect on BMD and low-dose nicotine exposure led to a statistically insignificant increase in BMD. CONCLUSIONS: Contrary to common belief, the results of this study show that nicotine is not responsible for the decrease in BMD leading to osteoporosis frequently seen in smokers. However, there is a need to explore the other harmful materials in tobacco which may be responsible for the alterations seen in BMD of smokers.

The effect of long term nicotine exposure on nicotine addiction and fetal growth.

OBJECTIVE: To investigate the effect of nicotine exposure starting before coitus and continuing during pregnancy and lactation period on delivery rate, fetal growth and nicotine addiction in rats. MATERIAL AND METHODS: Ten female Swiss Albino rats were divided into 2 groups as the nicotine group (NG) (n=5), and the control group (n=5), conceived by adding 2 male rats to each group. While the control group was given only normal drinking water, 0.4 mg/kg body weight (BW)/day nicotine was given to the NG in drinking water. After delivery, the BWs of pups were recorded weekly for 6 weeks and their drinking water preferences were assessed. Meanwhile, pups of the NG continued to receive 0.4 mg/kg/day nicotine for 12 months while the controls continued with normal drinking water. RESULTS: At the end of the 6(th) week, it was determined that 30 (69%) rats out of 43 in the NG and only 7 rats (20%) out of 35 in the control group preferred the nicotine added drinking water (p<0.05). No significant difference was observed between control and NGs in post-natal birth weights and BWs recorded for 6 weeks. On the contrary, a significant decrease (p< 0.05) was observed in the BWs of NG at the end of 12 months nicotine exposure. CONCLUSION: Use of maternal nicotine in pregnancy and lactation periods, even at a low dose, may be effective in nicotine addiction development although it may not affect delivery rate, and BWs of pups after delivery and during six weeks follow up in the lactation period.