Study on the role of CCM3 gene and lead exposure induced neurotoxicity through neurovascular units.

This study aimed to determine the toxic effects of vascular CCM3 gene deficiency and lead (Pb) exposure on the nervous system. Lentiviral transfection was performed to generate a stable strain of brain microvascular endothelial cells with low CCM3 expression. MTT assay assessed the survival rate of cells exposed to Pb, determining the dose and duration of Pb exposure in vitro. Proteomic analysis was performed on the differentially expressed proteins in bEnd3 and HT22 cells and flow cytometry was used to detect cell apoptosis. Finally, urine samples from pregnant and postpartum women were subjected to ICP-MS to detect Pb levels and HPLC to detect neurotransmitter metabolites. Based on the proteomic analysis of bEnd3 (CCM3-/-) cells co-cultured with HT22 cells, it was determined that HT22 cells and CCM3 genes interfered with bEnd3 cell differential proteins,2 including apoptosis and ferroptosis pathways. Electron microscopy observation, ICP-MS iron ion loading detection, and WB determination of protein GPX4 expression confirmed that HT22 cells undergo apoptosis, while bEnd3 cells undergo multiple pathways of iron death and apoptosis regulation. Furthermore, a linear regression model showed the interaction between maternal urine Pb levels, the rs9818496 site of the CCM3 SNP in peripheral blood DNA, and the concentration of the neurotransmitter metabolite 5-HIAA in maternal urine (F=4.198, P < 0.05). bEnd3 cells with CCM3 gene deficiency can induce HT22 cell apoptosis through iron death and apoptosis pathways under Pb exposure in a combined cell culture Pb exposure model, and CCM3 gene deficiency in endothelial cells and Pb exposure interacts with neural cell HT22. Epidemiological studies on maternal and newborn infants further confirmed the interaction between urine Pb levels in mothers and the SNP rs9818496 site of the CCM3 gene in peripheral blood DNA.

Treatment of lidocaine on subacute thyroiditis via restraining inflammatory factor expression and inhibiting pyroptosis pathway.

BACKGROUND: To explore the role of lidocaine on subacute thyroiditis (SAT) and the molecular mechanism. METHODS: SAT models were constructed by infecting adenovirus to thyroid follicular epithelial cells. Cells were randomly divided into five groups: model group, low lidocaine, middle lidocaine, high lidocaine, and a control group. Thyroid secretion related factors TG and TPO, T3 and T4 were separately determined by reverse transcription-polymerase chain reaction (RT-PCR) and radioimmunoassay. Flow cytometry was used to determine thyroid follicular epithelial cell apoptosis situation. RT-PCR and Western blot analysis were used to determine the expression of inflammatory cytokines and pyroptosis related factors interleukin (IL)-1α, IL-6, THF-α, ELAVL1, NLR family pyrin domain containing 3 (NLRP3), caspase-1, and IL-1ß. RESULTS: Lidocaine decreased the relative level of TG, TPO, T3, and T4 in adenovirus-infected thyroid follicular epithelial cells. All levels of concentrations, including low, middle, and high, of lidocaine, significantly decreased the apoptosis rate of adenovirus-infected cells. Lidocaine dramatically reduced the protein expression of IL-1α, IL-6, THF-α, ELAVL1, NLRP3, caspase-1, and IL-1ß in adenovirus-infected thyroid follicular epithelial cells. CONCLUSION: Lidocaine can improve SAT through inhibiting expression of inflammatory factors and the pyroptosis pathway.

Heterozygous Mutations of the DUOXA2 and DUOX2 Genes in Dizygotic Twins with Congenital Hypothyroidism.

BACKGROUND: The mutations in the dual oxidase maturation factor 2 (DUOXA2) and dual oxidase 2 (DUOX2) genes have been identified in patients with congenital hypothyroidism (CH). This study reports a set of dizygotic twins with CH due to the mutations in the DUOX2/DUOXA2 system. METHODS: The dizygotic twins, a boy and a girl, both aged 7 years, were born to euthyroid nonconsanguineous parents; they were diagnosed with CH at neonatal screening and were enrolled in this study. The DUOXA2, DUOX2, paired box 8 (PAX8), thyroid peroxidase (TPO), and thyrotropin receptor (TSHR) genes were considered for mutation screening. Genomic DNA was extracted from peripheral blood leukocytes, and Sanger sequencing was used to screen for the mutations in the exon fragments. Family members of the patients were also enrolled and evaluated. RESULTS: The fraternal twins each harbored a single heterozygous mutation, including c.738C>G (p.Y246X) in the boy inherited from the paternal DUOXA2 allele and c.2654G>A (p.R885Q) in the girl from the maternal DUOX2 allele. The two mutations have been previously reported. The boy showed enlarged thyroid lobes and a little calcification in the left lobe, while the girl's thyroid gland was severely underdeveloped and the girl had obvious complications due to irregular treatment. The germline mutations from this family were consistent with an autosomal recessive inheritance pattern. No mutations in the PAX8, TPO, and TSHR genes were detected in this study. CONCLUSIONS: The inactivating mutations in the DUOXA2 (p.Y246X) and DUOX2 (p.R885Q) genes were identified in a set of dizygotic twins with CH. The girl was more severe in several aspects than her brother. The similar genetic defect resulted in very different outcomes.

A comparative study of urinary levels of multiple metals and neurotransmitter correlations between GDM and T2DM populations.

OBJECTIVE: The pathogenesis of GDM and T2DM are closely related to various metals in vivo, and changes in the concentration of these metal exposures can lead to neuropathy through the DNA damage pathway caused by the accumulation of ROS. METHOD: Urine samples were analyzed for heavy metals and trace elements by ICP-MS, neurotransmitter metabolites by HPLC, 8-OH-dG by HPLC-MS and metabolomics by UPLC-MS. RESULT: Cd and Hg were risk factors for T2DM. There was a positive correlation between 8-OH-dG and neurotransmitter metabolites in both two populations. For GDM, the metabolite with the largest down-regulation effect was desloratadine and the largest up-regulation effect was D-glycine. That tyrosine and carbon metabolites were upregulated in the GDM population and downregulated in the T2DM population. CONCLUSION: The BMI, urinary Cd and Hg endo-exposure levels correlated with elevated blood glucose, and the latter may cause changes in the DNA damage marker 8-OH-dG in both study populations and trigger common responses to neurological alterations changes in the neurotransmitter. Tyrosine, carbonin metabolites, alanine, aspartate, and glutamate were signature metabolites that were altered in both study populations. These indicators and markers have clinical implications for monitoring and prevention of neurological injury in patients with GDM and T2DM.

Assessment of the platelet parameters and serum butyrylcholinesterase activity in type 1 diabetes patients with ketoacidosis.

The potential roles of serum butyrylcholinesterase (BChE) activity and platelet indices in type 1 diabetes (T1D) remain uncertain. We aimed to investigate the correlation among the platelet indices, serum BChE activity, and diabetic ketoacidosis (DKA). Sixty-one T1D patients, 29 patients with DKA, and 30 age- and sex-matched controls were enrolled. Mean platelet volume (MPV), platelet distribution width (PDW), and serum BChE activity were measured and evaluated at admission and after the treatment. The serum BChE activity was significantly lower in patients with DKA at admission to the hospital compared with non-DKA and control subjects; however, plasma glucose level, HbA1c level, MPV and PDW were significantly higher. Serum BChE activity, variables related to glycemic control, and platelet parameters were higher in non-DKA patients than in controls. Serum BChE activity was correlated with the serum HCO3 level (r = 0.375, p < 0.05) and plasma glucose level (r = -0.387, p < 0.05). Receiver operating characteristic curve analyses showed no difference between serum BChE activity and the platelet parameters with respect to the ability to reflect DKA. Logistic regression showed that increased PDW can act as a risk marker for the presence of DKA. Serum BChE activity and the platelet parameters returned to normal along with the plasma glucose levels when metabolic acidosis was well controlled. Serum BChE activity and the platelet parameters were significantly correlated with DKA. Measurement of PDW can provide complementary information and a risk biomarker reflecting the presence of DKA.

Suppression of long non-coding RNA TNRC6C-AS1 protects against thyroid carcinoma through DNA demethylation of STK4 via the Hippo signalling pathway.

OBJECTIVES: Thyroid carcinoma (TC) represents a malignant neoplasm affecting the thyroid. Current treatment strategies include the removal of part of the thyroid; however, this approach is associated with a significant risk of developing hypothyroidism. In order to adequately understand the expression profiles of TNRC6C-AS1 and STK4 and their potential functions in TC, an investigation into their involvement with Hippo signalling pathway and the mechanism by which they influence TC apoptosis and autophagy were conducted. METHODS: A microarray analysis was performed to screen differentially expressed lncRNAs associated with TC. TC cells were employed to evaluate the role of TNRC6C-AS1 by over-expression or silencing means. The interaction of TNRC6C-AS1 with methylation of STK4 promoter was evaluated to elucidate its ability to elicit autophagy, proliferation and apoptosis. RESULTS: TNRC6C-AS1 was up-regulated while STK4 was down-regulated, where methylation level was elevated. STK4 was verified as a target gene of TNRC6C-AS1, which was enriched by methyltransferase. Methyltransferase's binding to STK4 increased expression of its promoter. Over-expressed TNRC6C-AS1 inhibited STK4 by promoting STK4 methylation and reducing the total protein levels of MST1 and LATS1/2. The phosphorylation of YAP1 phosphorylation was decreased, which resulted in the promotion of SW579 cell proliferation and tumorigenicity. CONCLUSION: Based on our observations, we subsequently confirmed the anti-proliferative, pro-apoptotic and pro-autophagy capabilities of TNRC6C-AS1 through STK4 methylation via the Hippo signalling pathway in TC.

Association of Serum Angiopoietin-Like Protein 8 With Albuminuria in Type 2 Diabetic Patients: Results From the GDMD Study in China.

Background: Hyperglycemia, insulin resistance and hypertriglyceridesmia are risk factors for albuminuria in type 2 diabetes. Angiopoietin-like Protein 8(ANGPTL8) is a newly identified liver-derived hormone related to these risk factors. Hence, we aimed to explore the relationship between ANGPTL8 and albuminuria in type 2 diabetes. Methods: Serum ANGPTL8 levels were determined in groups of control (n = 50) and type 2 diabetic patients with normoalbuminuria (A1, n = 100), microalbuminuria (A2, n = 45), and macroalbuminuria (A3, n = 33). Results: Serum levels of ANGPTL8 and triglycerides were significantly increased in type 2 diabetic patients with albuminuria as compared with controls (P < 0.001). ANGPTL8 levels were positively correlated with triglycerides, duration of diabetes, and urine albumin-to-creatinine ratio (ACR) and negatively correlated with estimated glomerular filtration rate in type 2 diabetic patients with A2 and A3 (all P < 0.05). Logistic regression analysis indicated that ANGPTL8 had higher odds of having A2 (OR = 2.52, 95% CI 1.16-5.48, P = 0.019) and A3 (OR = 4.89, 95% CI 2.10-11.39, P < 0.001) in type 2 diabetes. Mediation analysis indicated that triglycerides might act as a partial mediator in the relationship between ANGPTL8 and ACR. Conclusions: Triglycerides might partially mediate the correlation between ANGPTL8 and ACR. Our data provide the evidence for a strong link between ANGPTL8 and albuminuria, indicating that ANGPTL8 may be a new biomarker for diabetic kidney disease in type 2 diabetes. TRIAL REGISTRATION NUMBER: ChiCTR-EPC-14005273.

Association of plasma dipeptidyl peptidase-4 activity with non-alcoholic fatty liver disease in nondiabetic Chinese population.

OBJECTIVE: The pathogenesis of non-alcoholic fatty liver disease (NAFLD) is attributed to a "multi-hits hypothesis" involving insulin resistance, oxidative stress and inflammation. Dipeptidyl peptidase-4 (DPP4) was identified as a novel adipokine capable of enhancing the"multi-hits". Hence, we investigated the association between plasma DPP4 activity and NAFLD in nondiabetic Chinese population. DESIGN AND METHODS: We performed a cross-sectional study using data from 1105 subjects (36-79years) in Guilin between 2015 and 2016. Plasma DPP4 activity, homeostatic model assessment of insulin resistance (HOMA-IR), oxidative stress parameters, and inflammatory markers were measured in all participants. NAFLD and its severity were diagnosed by ultrasound after the exclusion of alcohol abuse and other liver diseases. RESULTS: Participants in the highest quartile of DPP4 activity had higher HOMA-IR, nitrotyrosine, 8-iso-PGF2a, interleukin-6, CRP, alanine aminotransferase, aspartate aminotransferase and γ-glutamyltransferase compared with those in the lowest quartile (all P<0.05). Plasma DPP4 activity gradually increased across the groups according to the ultrasonographic severity of steatosis (P<0.001 for the trend). In the highest DPP4 quartile, NAFLD risk was higher (odds ratio 1.88; 95% CI 1.04-3.37) than in the lowest quartile after adjustment for confounders. The risk for NAFLD increased more with higher levels of DPP4 activity, HOMA-IR, nitrotyrosine, 8-iso-PGF2a, interleukin-6 and CRP. CONCLUSIONS: Plasma DPP4 activity is significantly associated with NAFLD. The underlying mechanisms may be partly attributed to the interactions between insulin resistance, oxidative stress, inflammation, and DPP4.

Improvement of therapeutic effects of mesenchymal stem cells in myocardial infarction through genetic suppression of microRNA-142.

Transplanted mesenchymal stem cells (MSCs) have been shown to contribute to myocardial repair after myocardial infarction (MI), primarily through production and secretion some growth factors and cytokines related to cell survival and regeneration. Further improvement of the therapeutic potential of MSCs appears to be an attractive strategy for MI treatment. CXC chemokine receptor (CXCR) 7 is the receptor for stromal cell-derived factor-1 (SDF-1), an important chemokine that is essential for tissue repair and angiogenesis. SDF-1/CXCR7 axis plays a critical role in the mobilization, recruitment and function of MSCs during tissue regeneration. Here, we depleted miR-142 that targets CXCR7 in MSCs cells through expression of antisense of miR-142, resulting in enhanced expression of CXCR7 in these miR-142-depleted MSCs (md-MSCs). In vitro, presence of md-MSCs reduced hypoxia-induced cardiac muscle cell apoptosis in a more pronounced manner than MSCs. In vivo, compared to transplantation of MSCs, transplantation of md-MSCs further enhanced cardiac re-vascularization and further improved cardiac functions after MI in mice. Together, our data suggest that depletion of miR-142 in MSCs may improve their therapeutic effects on MI.

Coexistence of resistance to thyroid hormone and ectopic thyroid: ten-year follow-up.

Resistance to thyroid hormone (RTH) coexisting with ectopic thyroid is rare. Here we report a case of RTH with ectopic thyroid. A ten-year-old girl had been misdiagnosed as congenital hypothyroidism and treated with levothyroxine since she was born. Ten-year follow-up showed that the elevated thyrotropin was never suppressed by levothyroxine and no signs indicating hyperthyroidism or hypothyroidism despite elevated FT3 and FT4 levels. Therefore the girl developed no defects in physical and cognitive development. Pituitary adenoma was excluded by magnetic resonance imaging. Ultrasonography did not find the thyroid gland in the normal place, while the thyroid scan found a large lingual thyroid gland. The octreotide inhibition test showed a reduction in thyrotropin by 41.98%. No mutation was detected in the thyroid hormone receptor (THR) ß, THRα, thyrotropin receptor (TSHR), and GNAS1 genes. To our knowledge, it is an interesting RTH case coexisting with lingual thyroid.

Increased Dipeptidyl Peptidase-4 Activity Is Associated With High Prevalence of Depression in Middle-Aged and Older Adults: A Cross-Sectional Study.

OBJECTIVE: Obesity, inflammation, and decreased neuropeptide Y (NPY) are risk factors for depression. Dipeptidyl peptidase-4 (DPP4), a newly identified adipokine, has been proved to promote inflammation and NPY degradation. Hence, we aimed to investigate the association between plasma DPP4 activity and depression symptoms in middle-aged and older adults. METHODS: We cross-sectionally assessed 1,335 Chinese adults aged 45-76 years recruited from the Medical Examination Center, Guilin, China, between 2013 and 2014. The main outcome measures were plasma DPP4 activity, inflammatory markers, and NPY. Depression symptoms were determined by the score on the 9-item Patient Health Questionnaire (PHQ-9). Each of the 9 depression items of the PHQ-9 correspond to 1 of the DSM-IV diagnostic criteria for symptoms of major depressive disorder. RESULTS: Subjects in the highest quartile of DPP4 activity had higher body mass index (BMI), interleukin-6 (IL-6), high-sensitivity C-reactive protein (hs-CRP), and PHQ-9 score compared with subjects in the lowest quartile (P < .05). Compared to patients without depression symptoms, patients with depression symptoms had higher BMI, waist-to-hip ratio, IL-6, hs-CRP, and DPP4 activity (P < .05). DPP4 activity was associated positively with IL-6, hs-CRP, and PHQ-9 score and negatively with NPY after adjustment for potential confounders (P < .05). The risk for depression symptoms increased with higher levels of DPP4 activity and inflammation and lower levels of NPY. CONCLUSIONS: Increased DPP4 activity is independently associated with depression symptoms in middle-aged and older adults. The mechanisms might be partly explained by mutual influence among inflammation, NPY, and DPP4. These observations raise further interest in DPP4 activity for the potential effect on inflammation and NPY metabolism, as a risk biomarker, or even a possible therapeutic target for depression. TRIAL REGISTRATION: Chinese Clinical Trial Registry (ChiCTR-EPC-14005273).

Plasma DPP4 Activities Are Associated With Osteoporosis in Postmenopausal Women With Normal Glucose Tolerance.

CONTEXT: Inflammation, insulin resistance, dyslipidemia, and glucagon-like peptide-1 (GLP-1) are risk factors for osteoporosis. Dipeptidyl peptidase-4 (DPP4) is a newly identified adipokine related to these risk factors. OBJECTIVE: To investigate the association between plasma DPP4 activities and osteoporosis. DESIGN, SETTING, AND PATIENTS: This was a cross-sectional study conducted in Guilin, China. A total of 744 postmenopausal women with normal glucose tolerance were studied. MAIN OUTCOME MEASURES: Plasma DPP4 activity, inflammatory markers, blood lipids, homeostatic model assessment of insulin resistance (HOMA-IR), active GLP-1, bone turnover markers, and bone mineral density (BMD) were measured in all participants. RESULTS: Participants in the highest quartile of DPP4 activity had higher triglyceride, total cholesterol, HOMA-IR, IL-6, high-sensitivity C-reactive protein (hs-CRP), C-terminal telopeptide of type I collagen, and osteocalcin and lower BMD (lumbar spine and femoral neck) and active GLP-1 compared with participants in the lowest quartile (P < .05). DPP4 activities were associated positively with triglyceride, total cholesterol, HOMA-IR, IL-6, hs-CRP, C-terminal telopeptide of type I collagen, and osteocalcin and negatively with active GLP-1 and BMD (P < .05). In the highest DPP4 quartile, osteoporosis risk was significantly higher (odds ratio, 3.01; 95% confidence interval, 1.66-5.43) than in the lowest quartile after adjustment for potential confounders. The risk for osteoporosis increased more with higher levels of DPP4 activity, HOMA-IR, IL-6, and hs-CRP (P < .05), but not with higher levels of triglyceride and total cholesterol or lower levels of active GLP-1. CONCLUSIONS: This study shows that increased DPP4 activities are independently associated with osteoporosis. The mechanisms may be partly explained by the effect of DPP4 on inflammation and insulin resistance.

Influence of obstructive sleep apnea on serum butyrylcholinesterase activity and ischemia-modified albumin levels.

OBJECTIVE: To investigate the effect of obstructive sleep apnea and continuous positive airway pressure treatment on serum butyrylcholinesterase activity and ischemia-modified albumin levels. METHODS: Thirty-two patients with obstructive sleep apnea and 30 age- and sex-matched controls were enrolled and underwent a diagnostic polysomnogram. The serum butyrylcholinesterase activity, ischemia-modified albumin levels, metabolic parameters, and polysomnography scores were detected and evaluated. Nine patients were studied before and after treatment with continuous positive airway pressure. RESULTS: The serum ischemia-modified albumin levels were significantly higher and the butyrylcholinesterase activity was significantly lower in patients with obstructive sleep apnea than in the controls (p<0.001). The continuous positive airway pressure treatment decreased the modified albumin levels and elevated the buthrylcholinesterase activity (p=0.019 and p=0.023, respectively). The modified albumin levels were positively correlated with the apnea-hypopnea index (r=0.462, p=0.008) at baseline. Elevated ischemia-modified albumin levels can be more accurate than butyrylcholinesterase activity at reflecting the presence of obstructive sleep apnea. Receiver operating characteristic curves revealed a significant difference between the areas under the curve 0.916 for ischemia-modified albumin and 0.777 for butyrylcholinesterase (z=2.154, p=0.031). CONCLUSION: The elevated ischemia-modified albumin level was significantly associated with obstructive sleep apnea and was more sensitive than butyrylcholinesterase activity in reflecting obstructive sleep apnea. The continuous positive airway pressure treatment helped to ameliorate the imbalance.

Ischemia-modified albumin in patients with hyperthyroidism and hypothyroidism.

BACKGROUND: The relationship between ischemia-modified albumin (IMA) and thyroid dysfunction remains uncertain. This study aimed to investigate the influence of overt hypothyroidism (Oho), overt hyperthyroidism (Ohe), and their treatments on serum IMA levels. METHODS: A total of 35 untreated patients with Ohe, 35 untreated patients with Oho, and 35 control subjects were enrolled in the study. C-reactive protein (CRP), homocysteine (Hcy), IMA, and lipid profiles were measured and evaluated before and after treatment. RESULTS: CRP, Hcy, and IMA levels and lipid profiles were higher in patients with Oho than in euthyroid or Ohe subjects (p<0.05). Basal IMA levels were reduced after treatments in all patients (p<0.05). In Ohe patients, serum IMA levels were positively correlated with free triiodothyronine (r=0.424, p=0.011) and free thyroxine (r=0.567, p<0.001) levels. In Oho patients, serum IMA levels were inversely correlated with free triiodothyronine (r=-0.555, p=0.001) and free thyroxine (r=-0.457, p=0.006) but positively correlated with anti-thyroid peroxidase antibody, C-reactive protein, and homocysteine levels (p<0.05). Linear regression analyses showed that free triiodothyronine was the most important factor affecting serum IMA levels in Ohe (ß=0.694, p=0.019) and in Oho (ß=-0.512, p=0.025). CONCLUSIONS: IMA levels are increased in patients with thyroid dysfunction, particularly in overt hypothyroidism. Thyroid dysfunction has a significant impact on the oxidative stress status.

Coexistence of resistance to thyroid hormone and ectopic thyroid: ten-year follow-up

SUMMARY Resistance to thyroid hormone (RTH) coexisting with ectopic thyroid is rare. Here we report a case of RTH with ectopic thyroid. A ten-year-old girl had been misdiagnosed as congenital hypothyroidism and treated with levothyroxine since she was born. Ten-year follow-up showed that the elevated thyrotropin was never suppressed by levothyroxine and no signs indicating hyperthyroidism or hypothyroidism despite elevated FT3 and FT4 levels. Therefore the girl developed no defects in physical and cognitive development. Pituitary adenoma was excluded by magnetic resonance imaging. Ultrasonography did not find the thyroid gland in the normal place, while the thyroid scan found a large lingual thyroid gland. The octreotide inhibition test showed a reduction in thyrotropin by 41.98%. No mutation was detected in the thyroid hormone receptor (THR) β, THRα, thyrotropin receptor (TSHR), and GNAS1 genes. To our knowledge, it is an interesting RTH case coexisting with lingual thyroid.

Influence of obstructive sleep apnea on serum butyrylcholinesterase activity and ischemia-modified albumin levels

OBJECTIVE: To investigate the effect of obstructive sleep apnea and continuous positive airway pressure treatment on serum butyrylcholinesterase activity and ischemia-modified albumin levels. METHODS: Thirty-two patients with obstructive sleep apnea and 30 age- and sex-matched controls were enrolled and underwent a diagnostic polysomnogram. The serum butyrylcholinesterase activity, ischemia-modified albumin levels, metabolic parameters, and polysomnography scores were detected and evaluated. Nine patients were studied before and after treatment with continuous positive airway pressure. RESULTS: The serum ischemia-modified albumin levels were significantly higher and the butyrylcholinesterase activity was significantly lower in patients with obstructive sleep apnea than in the controls (p<0.001). The continuous positive airway pressure treatment decreased the modified albumin levels and elevated the buthrylcholinesterase activity (p = 0.019 and p = 0.023, respectively). The modified albumin levels were positively correlated with the apnea-hypopnea index (r = 0.462, p = 0.008) at baseline. Elevated ischemia-modified albumin levels can be more accurate than butyrylcholinesterase activity at reflecting the presence of obstructive sleep apnea. Receiver operating characteristic curves revealed a significant difference between the areas under the curve 0.916 for ischemia-modified albumin and 0.777 for butyrylcholinesterase (z = 2.154, p = 0.031). CONCLUSION: The elevated ischemia-modified albumin level was significantly associated with obstructive sleep apnea and was more sensitive than butyrylcholinesterase activity in reflecting obstructive sleep apnea. The continuous positive airway pressure treatment helped to ameliorate the imbalance. .