Search

Introduction: The ghrelin system, which generates the appetite hormone, is harmed by obesity, a problem of worldwide public health. An efficient way to cure obesity is through bariatric surgery. This randomized controlled study's objective was to assess preoperative diet-related DNA methylation of Ghrelin (GHRL) levels in patients undergoing bariatric surgery. Methods: The 50 patients who volunteered to participate in the trial were randomly divided into two groups. The study group followed the very low-calorie diet for 2 weeks. The control group did not follow any diet. The physiological parameters, weight, and DNA methylation levels of the patients were assessed. Results: The percentage of excess weight loss (EWL) in the control and study groups was determined as 47.1% and 51.5%, respectively. The study group's GHRL percentage of methylated reference was 76.8%, whereas the control group's was 67.3%. It was concluded that the EWL and GHRL gene DNA methylation of the diet-treated study group were significantly higher than the control group (p < 0.05). Conclusion: According to the findings, the pre-op diet had a favorable effect on the patient's behavior modification. It has also been shown to increase postoperative weight loss and DNA methylation of the Ghrelin gene. The ghrelin gene has been muted by methylation, making hunger regulation more manageable. [ABSTRACT FROM AUTHOR]

Copyright of Ümraniye Pediatri Dergisi is the property of KARE Publishing and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Istanbul Medical Journal is the property of Galenos Yayinevi Tic. LTD. STI and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective: Histopathological changes in the kidney in type 1 diabetes mellitus (T1DM) begin before detection of microalbuminuria. Therefore, there is interest in finding a better biomarker for the early detection of diabetic kidney injury. The aim of this present study was to determine whether urinary indicators of fibrosis are detectable early in the development of T1DM in children and if they may predict progressive renal injury. Methods: Urinary matrix metalloproteinase 2 and 9 (MMP2 and MMP9), tissue inhibitor of metalloproteinase 1 and 2 (TIMP1 and TIMP2) and transforming growth factor-β1 (TGF-β1) were assessed in 33 patients with T1DM with normal renal functions and in 24 healthy controls. Microalbuminuria was not present in the patient group with the exception of three patients. The results were adjusted to urine creatinine (Cr) and the differences between patients and controls were evaluated. These measurements were repeated after one year and the results were compared with the first year results. Results: Urine MMP2/Cr, MMP9/Cr, TIMP1/Cr, TIMP2/Cr, TGF-β1/Cr were not different between the patient and control groups (p>0.05). There were also no significant differences between the first and second year results for these biomarkers (p>0.05). None of these parameters were correlated with hemoglobin A1c, body mass index and duration of T1DM. Interestingly, all parameters were negatively correlated to age of onset of T1DM (p<0.05) Conclusion: Our findings suggest that urinary biomarkers of fibrosis do not show an increase in diabetic children without microalbuminuria. The results also indicate that the risk of early fibrosis may increase as age of onset of T1DM decreases. [ABSTRACT FROM AUTHOR]

Kisspeptin (KP), a hypothalamic peptide, is known as an important marker for neuroendocrine regulation during the human reproduction process. The unexplained infertility (UI) group comprised 30 patients, polycystic ovary syndrome (PCOS) group comprised 29 patients and the male factor infertility (MFI) group comprised 27 patients. An observational cohort study was conducted. The basic characteristics of the study population, BMI, and serum FSH, LH, E2, AMH, KP, TSH, and PRL levels and antral follicle count (AFC) on the 3rd menstruation day were evaluated. The mean KP level was 281.98 ± 73.9 ng/ml in the UI group, 525.49 ± 164.17 ng/ml in the PCOS group, and 354.313 ± 111.38 ng/ml in the MFI group (p < .001). KP levels were significantly higher in the PCOS group than in the UI and MFI groups (p < .001 for both). AUC was 83% (95% CI: 73%-93%), with 375.15 (pg/ml) as the cutoff value in the PCOS group with 83% sensitivity and 79% specificity. UI may be treated by KP injection therapies and higher levels of KP may be a reliable marker for AFC and diagnosis of PCOS. Clinical Trials registration number: NCT03018314 [ABSTRACT FROM AUTHOR]

Copyright of Turkish Journal of Physical Medicine & Rehabilitation / Turkiye Fiziksel Tip ve Rehabilitasyon Dergisi is the property of Turkish Society of Physical Medicine & Rehabilitation and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of the Turkish-German Gynecological Association is the property of Galenos Yayinevi Tic. LTD. STI and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Introduction: Acromegaly is a systemic disease that causes multiple metabolic disorders caused by an excess of growth hormone. The excess of growth hormone affects the secretion of adipokines in fat tissue, leading to metabolic disorders. Visfatin is also an adipokine synthesized in visceral fat tissue, and plays a role in systemic inflammation. In this study, we evaluated the effect of acromegaly on serum visfatin levels and the parameters that may be associated with it. Method: 53 acromegaly patients (37 females/16 males) in acromaegaly gruop and 34 patient (22 females/12 males) in the control group with normal IGF1 and BH with similar age and body mass index (BMI) were included in our study. The waist and hip circumference, fasting blood glucose, insulin, HbA1c, lipid profile, BH, IGF1 and visfatin levels were compared among the groups. Epicardial fat tissue was examined by echocardiography. Serum visfatin levels were measured by micro ELISA. Correlation analysis was performed. Result: The visfatin levels in the acromegaly group were significantly higher than the control group (p<0.001). In addition, HbA1c values were higher in the acromegaly group (p=0.007), while other parameters were similar between the groups (Table 1). In the correlation analysis of all groups, there was a significant positive correlation between visfatin levels and HbA1c, IGF1 and BH levels (p=0.02, p=0.03, p=0.02, respectively). Conclusion: In acromegalic patients, visfatin levels increase with IGF1 and GH levels. In addition, glucose metabolism impairment also increases visfatin levels. This adipokine may also be effective in systemic inflammation in acromegaly. The results of our studies with more patients should be verified. [ABSTRACT FROM AUTHOR]

AbstractWhen the studies are evaluated, immunomodulatory effect of MSCs, administration in critically ill patients, obstacle situations in use and side effects, pulmonary fibrosis prevention, which stem cells and their products, regeneration effect, administration route, and dosage are listed under the main heading like. The effect of MSC administration on DNA repair genes in COVID-19 infection is unknown. Our aim is to determine the effect of mesenchymal stem cells (MSCs) therapy applied in critically ill patients with coronavirus infection on DNA repair pathways and genes associated with those pathways. Patients (n = 30) divided into two equal groups. Group-1: Patients in a critically ill condition, Group-2: Patients in critically ill condition and transplanted MSCs. The mechanism was investigated in eleven genes of five different pathways; Base excision repair: PARP1, Nucleotide excision repair (NER): RAD23B and ERCC1, Homologous recombinational repair (HR): ATM, RAD51, RAD52 and WRN, Mismatch repair (MMR): MLH1, MSH2, and MSH6, Direct reversal repair pathway: MGMT. It was found that MSCs application had a significant effect on 6 genes located in 3 different DNA damage response pathways. These are NER pathway genes; RAD23 and ERCC1, HR pathway genes; ATM and RAD51, MMR pathway genes; MSH2 and MSH6 (p < 0.05). Two main points were shown. First, as a result of cellular damage in critical patients with COVID-19, DNA damage occurs and then DNA repair pathways and genes are activated in reaction to this situation. Second, administration of MSC to patients with COVID-19 infection plays a positive role by increasing the expression of DNA repair genes located in DNA damage pathways. [ABSTRACT FROM AUTHOR]

Objective: Endocrine abnormalities may represent the only clinical manifestation of primary mitochondrial disorders. This study aimed to evaluate the endocrinological characteristics of mitochondrial disease in our cohort., Methods: A total of twenty-six pediatric patients diagnosed with mitochondrial disease were categorized on the basis of their specific genetic abnormalities. The auxologic data, pubertal development, and, based on their clinical symptoms, hormonal profiles were obtained., Results: Twelve of the cohort of 26 patients (46%) were female. In 15 of the patients (57.6%), their mitochondrial disease (MD) was caused by nuclear DNA mutations (nDNA group). Four patients had Leigh syndrome, 2 patients had LHON syndrome, 2 patients had MELAS, and 1 patient had KSS clinical phenotype. The median age at diagnosis was 2.91 (0.59-16.8) years, and the median age at first endocrinologic evaluation was 4.62 (1.26-18) years. The mean height SDS was -1.34 ± 2.12, and the mean BMI SDS was -0.82 ± 1.96 for all patients. Of the 26 patients, 6 (23%) had a range of hormonal deficits. Ovarian insufficiency, central adrenal insufficiency, central hypothyroidism, diabetes mellitus, and critical illness-related adrenal insufficiency were all observed. Three of the patients were initially monitored in the endocrine clinic for hormone deficiencies but it was later determined that the hormonal abnormalities were caused by underlying mitochondrial disease., Conclusion: Individuals diagnosed with mitochondrial disease, particularly those with specific genetic abnormalities, are considered a high-risk group for developing hormonal deficits. Endocrine diseases could be one of the primary mitochondrial disorders' early warning symptoms.

Background/aim: The purpose of this study is to compare the diagnostic value of hepcidin level with the white blood cell (WBC), C-reactive protein (CRP), procalcitonin (PCT), and interleukin-6 (IL-6) levels in pediatric sepsis and septic shock. Materials and methods: A cohort of 89 individuals were divided into four groups: a healthy control group (HCG, n = 28), pediatric intensive care unit control group (PICUCG, n = 17), sepsis group (SG, n = 23), and septic shock group (SSG, n = 21). WBC, CRP, PCT, IL-6, and hepcidin levels were studied in the PICUCG, SG, and SSG, while hepcidin and IL-6 levels were studied in the HCG. Results: In distinguishing the SG and SSG from the HCG, hepcidin sensitivity and specificity were found to be 100%. Distinguishing between the PICUCG and the SG, hepcidin sensitivity was calculated as 95.6% and specificity was calculated as 100%. The sensitivity of WBC, CRP, and PCT was lower than that of hepcidin, but the sensitivity of IL-6 was higher than that of hepcidin. While the specificity of PCT and IL-6 was the same as hepcidin, the specificity of WBC and CRP was lower than that of hepcidin. Conclusion: Hepcidin is a more reliable indicator than WBC and CRP levels in distinguishing children with sepsis and septic shock from healthy children and nonseptic pediatric ICU patients.

Objective: To identify biochemical factors that serve as predictors for the metabolic syndrome (MetS) in patients with polycystic ovary syndrome (PCOS) and to investigate the value of adipocytokines in the prediction of metabolic syndrome., Material and Methods: A total of 91 pre-menopausal women with PCOS diagnosed according to the Rotterdam consensus criteria were recruited as study subjects. Waist circumference, blood pressure, body mass index (BMI), fasting glucose, serum lipids, insulin, FSH, LH, E2, total testosteron, homeostatic model assessment-insulin resistance (HOMA-IR), serum leptin and adiponectin levels were evaluated for all patients., Results: Of the 91 women with PCOS, 15 patients met the criteria for MetS. Body weight, BMI, waist circumference, systolic blood pressure, diastolic blood pressure, fasting glucose, total cholesterol, triglyceride, and VLDL concentrations were significantly higher and HDL was significantly lower in women with PCOS+MetS compared with those with PCOS only. However, the level of LDL, FSH, LH, E2 and total testesterone was not significantly different between these two groups. Women with PCOS+MetS had significantly higher levels of leptin and HOMA-IR, and significantly lower levels of adiponectin compared to the women with PCOS only. In the multiple logistic regression model, the association between HOMA-IR and leptin, and MetS remained statistically significant (p=0.001 and 0.018), while the association between adiponectin and MetS was no longer statistically significant., Conclusion: Aside from the biochemical markers such as glucose, cholesterol and triglyceride, adipose tissue factors and insulin resistance are valuable parameters in the prediction of MetS in patients with PCOS.