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An Evaluation of Oxidative Stress With Thiol/Disulfide Homeostasis in Patients With Persistent Allergic Rhinitis.
Göker, AE, Alagöz, MH, Kumral, TL, Karaketir, S, Yilmazer, AB, Tutar, B, Ahmed, EA, Biçer, C, Uyar, Y
Ear, nose, & throat journal. 2022;(1):NP13-NP17
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Abstract
BACKGROUND We evaluated the efficacy of medical treatment on thiol-disulfide balance despite ongoing allergic stimulation. METHODS The research design was a prospective observational study that included 35 persistent allergic rhinitis (AR) patients. All patients who were diagnosed with persistent AR were included. A skin prick test was applied to all patients, and the Sino-nasal Outcome Test-22 was used to evaluate sinonasal symptoms. Thiol/disulfide homeostasis balance parameters were measured using a novel automatic and spectrophotometric method and compared statistically. Serum total thiol (TT), native thiol (SH), disulphide (SS), disulphide/native thiol (SS/SH), disulphide/total thiol (SS/TT), and native thiol/total thiol (SH/TT) ratios were measured after the second month of the treatment. RESULTS The 35 patients included 20 (58%) females and 15 (42%) males. The mean age of the patients was 33.17 ± 9.9 years. Disulphide, SS/SH, and SS/TT ratios decreased significantly after the treatment (P < .05), while SH and SH/TT increased significantly (P < .05). The mean SH measurement increased significantly in the second month (P = .001), but TT mean measurements showed no difference after the treatment (P = .058). The mean SS measurements, on the other hand, decreased significantly in the second month (P = .003). CONCLUSION Thiol/disulfide homeostasis may be used as a marker to evaluate the efficacy of persistent AR treatments. After the treatment, the increase in SH levels suggested the decrease in oxidative stress, even though allergen exposure continued.
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Disruption of fasting and post-load glucose homeostasis are largely independent and sustained by distinct and early major beta-cell function defects: a cross-sectional and longitudinal analysis of the Relationship between Insulin Sensitivity and Cardiovascular risk (RISC) study cohort.
Mengozzi, A, Tricò, D, Nesti, L, Petrie, J, Højlund, K, Mitrakou, A, Krebs, M, Mari, A, Natali, A, ,
Metabolism: clinical and experimental. 2020;:154185
Abstract
BACKGROUND/AIMS: Uncertainty still exists on the earliest beta-cell defects at the bases of the type 2 diabetes. We assume that this depends on the inaccurate distinction between fasting and post-load glucose homeostasis and aim at providing a description of major beta-cell functions across the full physiologic spectrum of each condition. METHODS In 1320 non-diabetic individuals we performed an OGTT with insulin secretion modeling and a euglycemic insulin clamp, coupled in subgroups to glucose tracers and IVGTT; 1038 subjects underwent another OGTT after 3.5 years. Post-load glucose homeostasis was defined as mean plasma glucose above fasting levels (δOGTT). The analysis was performed by two-way ANCOVA. RESULTS Fasting plasma glucose (FPG) and δOGTT were weakly related variables (stβ = 0.12) as were their changes over time (r = -0.08). Disruption of FPG control was associated with an isolated and progressive decline (approaching 60%) of the sensitivity of the beta-cell to glucose values within the normal fasting range. Disruption of post-load glucose control was characterized by a progressive decline (approaching 60%) of the slope of the full beta-cell vs glucose dose-response curve and an early minor (30%) decline of potentiation. The acute dynamic beta-cell responses, neither per se nor in relation to the degree of insulin resistance appeared to play a relevant role in disruption of fasting or post-load homeostasis. Follow-up data qualitatively and quantitatively confirmed the results of the cross-sectional analysis. CONCLUSION In normal subjects fasting and post-load glucose homeostasis are largely independent, and their disruption is sustained by different and specific beta-cell defects.
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[The effect of low dose ionizing radiation exposure on dynamic thiol-disulfide homeostasis and ischemia modified albumin levels: an observational study].
Arıcan, S, Dertli, R, Baktik, S, Hacibeyoglu, G, Erol, A, Ulukaya, SO, Goger, E, Erel, Ö
Brazilian journal of anesthesiology (Elsevier). 2020;(3):233-239
Abstract
BACKGROUND The primary objective of this study was to investigate the effect of low dose ionizing radiation exposure on thiol/disulfide homeostasis and ischemia modified albumin levels. The secondary objective is to compare thiol/disulfide homeostasis and ischemia modified albumin levels among the personnel exposed to low dose ionizing radiation in anesthesia application areas, in and out of the operation room. METHODS The study included a total of 90 volunteers aged between 18 and 65 years old, with 45 personnel working in a setting with potential for radiation exposure (Exposed Group) and 45 personnel in a setting without radiation exposure (Control Group). Their native thiol, total thiol, disulphide, albumine and IMA levels were measured. Exposed group included personnel who were exposed to radiation outside the operating room – Operation room (−) Group and inside the operating room – Operation room (+) Group. RESULTS Albumin, native and total thiol levels were significantly lower in the participants exposed to radiation in the anesthesia application area; no statistically significant difference was found in terms of disulfide and ischemia modified albumin levels. In the Operation room (−) Group exposed to radiation, native thiol and total thiol values were significantly lower compared to the Operation room (+) Group. CONCLUSION Awareness of being in danger of oxidative stress should be established in personnel exposed to radiation in the anesthesia application area following low dose ionizing radiation exposure, and the necessary measures should be taken.
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Overfeeding-associated hyperglycemia and injury-response homeostasis in critically ill neonates.
Tian, T, Coons, J, Chang, H, Chwals, WJ
Journal of pediatric surgery. 2018;(9):1688-1691
Abstract
BACKGROUND Injury severity induces a proportionate acute metabolic stress response, associated with increased risk of hyperglycemia. We hypothesized that excess caloric delivery (overfeeding) during high stress states would increase hyperglycemia and disrupt response homeostasis. METHODS Gestational age, daily weight, total daily caloric intake, serum C-reactive protein (CRP), prealbumin, and blood glucose concentrations in all acutely-injured premature NICU infants requiring TPN over the past 3years were reviewed. Injury severity was based on CRP and patients were divided into high (CRP ≥50mg/L) versus low (CRP <50mg/L) stress groups. Glycemic variability was used to measure disruption of homeostasis. RESULTS Overall sample included N=563 patient days (37 patients; 42 episodes). High stress group pre-albumin levels negatively correlated with CRP levels (R=-0.62, p<0.005). A test of equal variance demonstrated significantly increased high stress glycemic variability (Ha:ratio>1, Pr(F>f)=0.0353). When high stress patients were separated into high caloric intake (≥70kg/kcal/day) versus low caloric intake (<70kg/kcal/day), maximum serum glucose levels were significantly higher with overfeeding (230.33±55.81 vs. 135.71±37.97mg/dL, p<0.004). CONCLUSION Higher injury severity induces increased disruption of response homeostasis in critically ill neonates. TPN-associated overfeeding worsens injury-related hyperglycemia in more severely injured infants. TYPE OF STUDY Retrospective study. LEVEL OF EVIDENCE Level II.
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Altered serum copper homeostasis suggests higher oxidative stress and lower antioxidant capability in patients with chronic hepatitis B.
Huang, Y, Zhang, Y, Lin, Z, Han, M, Cheng, H
Medicine. 2018;(24):e11137
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Abstract
Copper homeostasis can be altered by inflammation. This study aimed to investigate the alteration of serum copper homeostasis and to explore its clinical significance in patients with chronic hepatitis B (CHB).Thirty-two patients with CHB and 10 aged- and sex-matched healthy controls were recruited. Analyses included serum levels of total copper (TCu), copper ions (Cu), small molecule copper (SMC), ceruloplasmin (CP), Cu/Zn superoxide dismutase 1 (SOD1), urinary copper, and the activities of serum CP and SOD1.The serum TCu and urinary copper levels in patients with CHB were significantly higher than the controls (P = .04 and .003), while the serum Cu was lower than the controls (P = .0002). CP and SOD1 activities in the serum were significantly lower in patients with CHB compared to controls (P = .005) despite higher serum concentrations. In addition, serum alanine aminotransferase inversely correlated with serum CP activity (P = .0318, r = -0.4065).Serum copper homeostasis was altered in this cohort of patients with CHB. The results suggest increased oxidative stress and impaired antioxidant capability in patients with CHB, in addition to necroinflammation. These results may provide novel insights into the diagnosis and treatment of patients with CHB.
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Status of vitamin D and parameters of calcium homeostasis in renal transplant recipients in Nepal: a cross sectional study.
Timalsina, S, Sigdel, MR, Baniya, S, Subedee, S
BMC nephrology. 2018;(1):290
Abstract
BACKGROUND Vitamin D, apart from being an important part of the "calcium-vitamin D-parathyroid hormone" endocrine axis, has diverse range of "non-calcemic" biological actions. A high prevalence of vitamin D deficiency has been observed in renal transplant recipients (RTRs) worldwide. This study aimed to determine the prevalence of hypovitaminosis D in Nepalese RTRs and interrelations between serum 25-hydroxyvitamin D [25(OH) D] and other biochemical parameters. METHODS A total of 80 adult RTRs visiting a university hospital were enrolled in this cross sectional study. Serum 25(OH) D and intact parathyroid hormone (iPTH) were measured using Enhanced Chemiluminiscent Immunoassay. The RTR population was categorized into recent transplant recipients (≤1 year) and long term recipients (> 1 year). The vitamin D status was defined as per NKF/KDOQI guidelines. SPSS version 20.0 was used to analyze the data. Appropriate statistical tests were applied to compare variables between groups and establish correlation. P < 0.05 was considered to be statistically significant. RESULTS The mean age of the recipients was 38.11 ± 11.47 years (68 males, 85.0%). Chronic glomerulonephritis was the leading cause of CKD. The two RTR groups (recent and long term) didn't differ in demographic and biochemical characteristics. 83.75% of the recipients had PTH levels above the upper limit of the recommended range for their stage of CKD. 57.5% had hypocalcemia and none of the recipients had hypercalcemia. The median serum 25(OH) D was 24.15 ng/ml (8.00-51.50 ng/ml). Only 27.5% had sufficient vitamin D status whereas 53.8% were vitamin D insufficient and 18.8% were vitamin D deficient, the distribution almost comparable in the 2 transplant group. The serum 25(OH) D was not significantly affected by the time post-transplant, gender and sunlight avoidance. There was a significant negative correlation between serum 25(OH) D and iPTH (Pearson's r = - 0.35, P = 0.001), but not so with the graft function. CONCLUSION There is a high prevalence of vitamin D insufficiency in RTRs. The deficiency status is not corrected despite of nutritional improvement and normalization of GFR post-transplantation and likely exacerbates secondary hyperparathyroidism. Vitamin D supplementation coupled with sensible sun exposure could be important strategies in optimization of the vitamin D status in this population.
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Arterial hypoxaemia and its impact on coagulation: significance of altered redox homeostasis.
Fall, L, New, KJ, Evans, KA, Bailey, DM
Journal of clinical pathology. 2015;(9):752-4
Abstract
AIMS: Arterial hypoxaemia stimulates free radical formation. Cellular studies suggest this may be implicated in coagulation activation though human evidence is lacking. To examine this, an observational study was designed to explore relationships between systemic oxidative stress and haemostatic responses in healthy participants exposed to inspiratory hypoxia. RESULTS Activated partial thromboplastin time and international normalised ratio were measured as routine clinical biomarkers of coagulation and ascorbate free radical (A(•-)) as a direct global biomarker of free radical flux. Six hours of hypoxia activated coagulation, and increased formation of A(•-), with inverse correlations observed against oxyhaemoglobin saturation. CONCLUSIONS This is the first study to address the link between free radical formation and coagulation in vivo. This 'proof-of-concept' study demonstrated functional associations between hypoxaemia and coagulation that may be subject to redox activation of the intrinsic pathway. Further studies are required to identify precisely which intrinsic factors are subject to redox activation.
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Indirect effects of decompression surgery on glycemic homeostasis in patients with type 2 diabetes mellitus and lumbar spinal stenosis.
Kim, HJ, Lee, KW, Cho, HG, Kang, KT, Chang, BS, Lee, CK, Yeom, JS
The spine journal : official journal of the North American Spine Society. 2015;(1):25-33
Abstract
BACKGROUND CONTEXT Lumbar spinal stenosis (LSS) patients with diabetes mellitus (DM) are presumed to experience difficulty when performing regular daily exercise, although such exercise is of paramount importance for glucose homeostasis and control. Therefore, decompression surgery, which can help patients perform regular physical activity, would have indirect positive effects on blood glucose control in LSS patients with DM. PURPOSE To evaluate the indirect effects of spinal surgery on hemoglobin A(1c) (HbA(1c)) levels in the patient with Type 2 DM and LSS. STUDY DESIGN Prospectively collected observational cohort data. PATIENT SAMPLE Patients with degenerative LSS and DM. OUTCOME MEASURES The fasting total cholesterol (TC), fasting blood glucose (FBG), and HbA1c levels and visual analog scale (VAS) for back pain, VAS for leg pain, and Oswestry Disability Index (ODI). METHODS According to the treatment methods, 31 and 37 patients were allocated to the surgical and conservative treatment groups, respectively. The HbA(1c), TC, and FBG levels and the ODI and VAS for back/leg pain were recorded for all patients before surgical and conservative treatments. At the first and second follow-up assessments after surgical or conservative treatment, the data were reassessed for all patients. RESULTS In both groups, the VAS for back/leg pain and the ODI scores significantly decreased after surgical or conservative treatment. In the surgical treatment group, the HbA(1c) levels were significantly decreased at the first and second assessments after surgery, whereas the conservative treatment group did not show significant reductions in HbA(1c) levels at the first and second follow-up assessments. In both groups, the FBG levels did not differ between the initial and follow-up assessments. The TC levels were significantly decreased at the second follow-up assessment, only in the surgical treatment group. The amount of ODI score reduction correlated positively with the degree of HbA(1c) level reduction at the first follow-up assessment. CONCLUSIONS The present study demonstrates the reduction in HbA(1c) level in patients with DM and LSS after decompression surgery with or without fusion. We believe this reduction in the HbA(1c) level may be a result of increased physical activity, subsequent to successful surgical decompression of the cauda equina.
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Integration of Peripheral and Glandular Regulation of Triiodothyronine Production by Thyrotropin in Untreated and Thyroxine-Treated Subjects.
Hoermann, R, Midgley, JE, Larisch, R, Dietrich, JW
Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme. 2015;(9):674-80
Abstract
The objective of the study was to evaluate the roles of central and peripheral T3 regulation. In a prospective study involving 1,796 patients, the equilibria between FT3 and TSH were compared in untreated and L-T4-treated patients with varying functional states, residual thyroid secretory capacities and magnitudes of TSH stimulation. T3 concentrations were stable over wide variations in TSH levels (from 0.2 to 7 mU/l) and endogenous T4 production in untreated patients, but unbalanced in L-T4-treated athyreotic patients where T3 correlated with exogenous T4 supply. T3 stability was related to TSH-stimulated deiodinase activity by clinical observation, as predicted by theoretical modelling. Deiodinase activity in treated patients was reduced due to both diminished responsiveness to TSH and lack of thyroidal capacity. Deiodinase activity was increased in high thyroid volume, compared to lower volumes in euthyroid patients (<5 ml, p<0.001). While deiodinase differed between euthyroid and subclinically hypothyroid patients in high volume, 26.7 nmol/s (23.6, 29.2), n=214 vs. 28.9 nmol/s (26.7, 31.5), n=20, p=0.02, it was equivalent between the 2 functional groups in low volume, 23.3 nmol/s (21.3, 26.1), n=117 vs. 24.6 nmol/s (22.2, 27.5), n=38, p=0.22. These findings suggest that the thyroid gland and peripheral tissues are integrated in the physiological process of T3 homeostasis in humans via a feed-forward TSH motif, which coordinates peripheral and central regulatory mechanisms. Regulatory and capacity deficiencies collectively impair T3 homeostasis in L-T4-treated patients.