Association between preoperative lipid profiles and new‐onset diabetes after transplantation in Chinese kidney transplant recipients: A retrospective cohort study

BackgroundThis study investigated the association between the preoperative lipid profiles and new‐onset diabetes after transplantation (NODAT) in Chinese kidney transplant recipients (KTRs).MethodsIn this study, of 1140 KTRs registered between January 1993 and March 2018 in Zhongshan Hospital, Fudan University, 449 were enrolled. Clinical data, obtained through a chart review of the patient records in the medical record system, were evaluated, and NODAT was diagnosed based on the American Diabetes Association guidelines. Multivariate Cox regression analysis was conducted to determine whether the preoperative lipid profiles in KTRs were independently associated with NODAT incidence. The preoperative lipid profiles were analyzed as continuous variables and grouped into tertiles. Smooth curve fitting was used to confirm the linear associations.ResultsDuring a median follow‐up of 28.03 (interquartile range 12.00–84.23) months, 104 of the 449 (23.16%) participants developed NODAT. The multivariate model analysis, adjusted for all potential covariates, showed that increased values of the following parameters were associated with NODAT (hazard ratio, 95% confidence interval): preoperative total cholesterol (TC; 1.25, 1.09–1.58, p = 0.0495), low‐density lipoprotein cholesterol (LDL‐C; 1.33, 1.02–1.75, p = 0.0352), non‐high‐density lipoprotein cholesterol (non‐HDL‐C; 1.41, 1.09–1.82, p = 0.0084), TC/HDL‐C (1.28, 1.06–1.54, p = 0.0109), and non‐HDL‐C/HDL‐C (1.26, 1.05–1.52, p = 0.0138). However, the association between the preoperative triglyceride, HDL‐C, or TG/HDL‐C and NODAT was not significant.ConclusionsPreoperative TC, LDL‐C, non‐HDL‐C, TC/HDL‐C, and non‐HDL‐C/HDL‐C were independent risk factors for NODAT.     

Association between aldehyde dehydrogenase 2 gene rs671 G>A polymorphism and alcoholic liver cirrhosis in southern Chinese Hakka population

BackgroundAlcoholic liver cirrhosis (ALC) endangering people''s health. The association between aldehyde dehydrogenase 2 (ALDH2) gene polymorphisms and ALC is not clear. To analyze the relationship between ALDH2 and ALC among Hakka population in southern China.MethodsA total of 292 ALC patients and 278 controls were included in the study. The ALDH2 gene rs671 polymorphism was analyzed by polymerase chain reaction (PCR)‐gene chip. Relevant information and medical records of these participants were collected.ResultsThe ALC patients had higher percentage of smoking, lower prevalence of hypertension, higher level of alanine aminotransferase (ALT), aspertate aminotransferase (AST), alkaline phosphatase (ALP), gamma‐glutamyltransferase (GGT), total bile acid (TBA), total bilirubin (Tbil), and direct bilirubin (Dbil), lower level of total cholesterol (TC), high‐density lipoprotein‐cholesterol (HDL‐C), and low‐density lipoprotein‐cholesterol (LDL‐C) than controls. The proportions of the G/A genotype (p = 0.017), G/A plus A/A genotype (p = 0.023) and A allele (p = 0.031) were significantly higher in ALC patients than that of controls. ALC patients with G/A genotype had higher TC, HDL‐C, and Apo‐A1 than those with G/G genotype, while with A allele had higher HDL‐C, and Apo‐A1 than those with G allele. Logistic regression analysis indicated that ALDH2 SNP rs671 G/A plus A/A genotypes (A allele carriers) (OR 2.030, 95% CI 1.109–3.715, p = 0.022) in the dominant model was the risk factor for ALC.Conclusions ALDH2 A allele (G/A + A/A genotypes) increased the risk of developing ALC among Hakka people in southern China. The results should enrich the relevant data and provide valuable information for the future related research.     

JNK pathway‐associated phosphatase in acute ischemic stroke patients: Its correlation with T helper cells,clinical properties,and recurrence risk

ObjectiveJKAP modifies T‐cell immune response and inflammation, also involves in cardia‐cerebrovascular disease etiology. This study intended to explore JKAP''s relation with T‐helper 1 (Th1), T‐helper 17 (Th17) cell levels, clinical properties, and recurrence‐free survival (RFS) in acute ischemic stroke (AIS) patients.MethodsA total of 155 AIS patients were analyzed. Serum JKAP, interferon‐gamma (IFN‐γ), and interleukin‐17A (IL‐17A) were detected by ELISA; then blood Th1 and Th17 cells were quantified by flow cytometry. Besides, 30 healthy subjects were enrolled as controls to detect JKAP, Th1, and Th17 cells.ResultsJKAP level was lower (p < 0.001), Th1 cells were not differed (p = 0.068), but Th17 cells were elevated in AIS patients versus controls (p < 0.001). Meanwhile, JKAP was negatively correlated with Th1 cells (p = 0.038), Th17 cells (P<0.001), IFN‐γ (p = 0.002), and IL‐17A (p < 0.001) in AIS patients. JKAP was negatively associated with the National Institutes of Health Stroke Scale (NIHSS) score (p < 0.001), but Th17 cells (p = 0.001), IFN‐γ (p = 0.035), and IL‐17A (p = 0.008) levels were positively associated with NIHSS score. Additionally, accumulating RFS was numerically longer in patients with JKAP Quantile (Q) 4 than patients with JKAP Q1–Q3 (p = 0.068), and numerically better in patients with JKAP Q3–Q4 than patients with JKAP Q1–Q2 (p = 0.069), but without statistical significance.ConclusionJKAP correlates with lower Th1 and Th17 cell percentages as well as milder disease severity.     

Longitudinal change of serum inter‐alpha‐trypsin inhibitor heavy chain H4, and its correlation with inflammation,multiorgan injury,and death risk in sepsis

BackgroundInter‐alpha‐trypsin inhibitor heavy chain H4 (ITIH4) inhibits infection‐induced inflammation and multiorgan injury through several methods. The present study aimed to estimate the association of serum ITIH4 with inflammatory cytokines, multiorgan injury, and death risk in sepsis patients.MethodsSerum samples were collected to detect ITIH4 by enzyme‐linked immunosorbent assay in 127 sepsis patients at admission (baseline), day (D)1, D3, and D7 after admission, as well as in 30 healthy controls (HCs). Additionally, 28‐day mortality was recorded in sepsis patients.ResultsITIH4 was reduced in sepsis patients versus HCs (median [interquartile range]: 147.9 [78.2–208.8] vs. 318.8 [237.2–511.4] ng/ml) (p < 0.001). In sepsis patients, ITIH4 was associated with the absence of cardiovascular and cerebrovascular disease history (p = 0.021). Additionally, ITIH4 was negatively correlated with tumor necrosis factor‐α (p < 0.001), interleukin (IL)‐1β (p < 0.001), IL‐6 (p = 0.019), IL‐17A (p = 0.002), and C‐reactive protein (p = 0.001), but positively related to IL‐10 (p = 0.007). Moreover, ITIH4 was also inversely associated with Acute Physiology and Chronic Health Evaluation II score (p = 0.002), Sequential Organ Failure Assessment (SOFA) score (p < 0.001), SOFA‐respiratory system score (p = 0.023), and SOFA‐renal system score (p = 0.007). Interestingly, ITIH4 gradually increased from baseline to D7 (p < 0.001); besides, ITIH4 at baseline (p = 0.009), D1 (p = 0.002), D3 (p < 0.001), and D7 (p = 0.015) were all decreased in sepsis deaths versus sepsis survivors.ConclusionSerum ITIH4 is raised from baseline to D7 after disease onset, and it reflects the reduction of systemic inflammation, disease severity, and 28‐day mortality for sepsis. However, further verification is required.     

The potency of common proinflammatory cytokines measurement for revealing the risk and severity of anxiety and depression in psoriasis patients

ObjectiveProinflammatory cytokines mediate anxiety and depression in various ways, such as immunity, inflammation, and the hypothalamic–pituitary–adrenal axis. This study intended to further explore the linkage of common proinflammatory cytokine levels with anxiety and depression in psoriasis patients.MethodsTotally, 150 psoriasis patients and 50 healthy controls (HCs) were included; the serum samples were collected, then common proinflammatory cytokines were measured by ELISA. Hospital Anxiety and Depression Scale (HADS) was assessed.ResultsHADS‐anxiety (HADS‐A) score, HADS‐depression (HADS‐D) score, TNF‐α, IL‐1β, IL‐6, IL‐12, IL‐17A, and IL‐23 were all increased in psoriasis patients compared to HCs (all p < 0.05). In psoriasis patients, TNF‐α (p = 0.001), IL‐12 (p = 0.035), and IL‐17A (p < 0.001), but not IL‐1β (p = 0.255), IL‐6 (p = 0.248), and IL‐23 (p = 0.216), were positively linked to HADS‐A score. Meanwhile, TNF‐α (p = 0.007) and IL‐17A (p = 0.007) were enhanced in psoriasis patients with anxiety in contrast to those without anxiety; whereas IL‐1β (p = 0.178), IL‐6 (p = 0.360), IL‐12 (p = 0.239), and IL‐23 (p = 0.450) were not different. TNF‐α (p < 0.001), IL‐1β (p = 0.013), Il‐17A (p < 0.001), and IL‐23 (p = 0.023), but not IL‐6 (p = 0.143) and IL‐12 (p = 0.158), were positively linked to HADS‐D score. Concurrently, TNF‐α (p = 0.015), IL‐17A (p < 0.001), and IL‐23 (p = 0.017) were climbed in psoriasis patients with depression by comparison to those without depression; whereas IL‐1β (p = 0.113), IL‐6 (p = 0.237), IL‐12 (p = 0.660) did not differ.ConclusionTNF‐α, IL‐17A, and IL‐23 increments reflect anabatic anxiety and depression in psoriasis patients, uncovering the potency of proinflammatory cytokines measurement for monitoring or even preventing psoriasis patients'' anxiety and depression.     

Circulating brain‐derived neurotrophic factor dysregulation and its linkage with lipid level,stenosis degree,and inflammatory cytokines in coronary heart disease

BackgroundBrain‐derived neurotrophic factor (BDNF) regulates the lipid metabolism, atherosclerosis plaque formation, and inflammatory process, while the study about its clinical role in coronary heart disease (CHD) is few. The present study intended to explore the expression of BDNF and its relationship with stenosis, inflammation, and adhesion molecules in CHD patients.MethodsAfter serum samples were obtained from 207 CHD patients, BDNF, tumor necrosis factor‐alpha (TNF‐α), interleukin (IL)‐1β, IL‐6, IL‐8, IL‐17A, vascular cell adhesion molecule‐1 (VCAM‐1), and intercellular adhesion molecule‐1 (ICAM‐1) levels were determined using ELISA. Then, the BDNF level was also examined in 40 disease controls (DCs) and 40 healthy controls (HCs), separately.ResultsBDNF was lower in CHD patients than in DCs and HCs (median (95% confidential interval) value: 5.6 (3.5–9.6) ng/mL vs. 10.7 (6.1–17.0) ng/mL and 12.6 (9.4–18.2) ng/mL, both p < 0.001). BDNF could well distinguish CHD patients from DCs (area under the curve [AUC]: 0.739) and HCs (AUC: 0.857). BDNF was negatively associated with triglyceride (p = 0.014), total cholesterol (p = 0.037), and low‐density lipoprotein cholesterol (p = 0.008). BDNF was negatively associated with CRP (p < 0.001), TNF‐α (p < 0.001), IL‐1β (p = 0.008), and IL‐8 (p < 0.001). BDNF was negatively related to VCAM‐1 (p < 0.001) and ICAM‐1 (p = 0.003). BDNF was negatively linked with the Gensini score (p < 0.001).ConclusionBDNF reflects the lipid dysregulation, inflammatory status, and stenosis degree in CHD patients.     

Diagnostic value of total testosterone and free androgen index measured by LC–MS/MS for PCOS and insulin resistance

BackgroundThe objective of the study was to explore the clinical significance of steroid hormones in the diagnosis of PCOS and PCOS‐related insulin resistance through liquid chromatography–mass spectrometry/mass spectrometry (LC–MS/MS) and chemiluminescent immunoassay (CLIA).MethodsThe study included 114 patients with PCOS and 100 controls. Steroid hormone levels in serum were measured using LC–MS/MS and CLIA. The Bland–Altman method was used to check the consistency between the two methods. The diagnostic value of the LC–MS/MS method for female hyperandrogenemia and PCOS was evaluated.ResultsWomen with PCOS were younger than controls on average (p < 0.001). PCOS patients had higher luteal hormone (LH, p < 0.001), insulin (p = 0.002), estradiol (E2, p < 0.001), total testosterone (TT, p < 0.001), free androgen index (FAI, p = 0.021), dehydroepiandrosterone sulfate (DHEA, p = 0.021), insulin resistance index (HOMA‐IR) (p = 0.034), and fasting glucose (p = 0.017) levels than controls as measured by CLIA. The diagnostic value of TT was the best, and the area under the AUC curve was 0.766. Women with PCOS had higher androstenedione (A2, p < 0.001), FAI (p < 0.001), TT (p < 0.001), and 17‐hydroxyprogesterone (17‐OHP, p < 0.001) levels than controls as measured by LC–MS/MS. The ROC curve showed that the diagnostic efficacy of A2, TT, and 17‐OHP was 0.830, 0.851, and 0.714, respectively. The consistency of TT detected by LC–MS/MS and CLIA was poor according to the Bland–Altman method. Detected TT by LC–MS/MS had the highest diagnostic efficiency for PCOS. The diagnostic power of the LC–MS/MS results for PCOS‐related insulin resistance was analyzed. The results showed that the FAI had the highest diagnostic power, with an ROC curve of 0.798.ConclusionLC–MS/MS is more sensitive and accurate than CLIA in the determination of serum TT and FAI. TT is more effective for the diagnosis of PCOS, whereas FAI is more valuable in the diagnosis of insulin resistance.     

Clinical value of YKL‐40 in patients with polymyositis/dermatomyositis: A cross‐sectional study and a systematic review

IntroductionWe performed a cross‐sectional study to investigate the clinical usefulness of YKL‐40 in patients with dermatomyositis (DM) and conducted a systematic review to summarize the clinical value of YKL‐40 in patients with polymyositis (PM)/DM.Materials and methodsA cross‐sectional study and a systematic review were performed to study the clinical value of YKL‐40 in patients with PM/DM. Serum YKL‐40 level was detected using enzyme‐linked immunosorbent assay, and its association with clinical and laboratory parameters was analyzed. In the systematic review, electronic databases of OVID Embase, OVID Medline, and web of science were searched to collect studies that reported clinical use of YKL‐40 in patients with PM/DM.ResultsIn the cross‐sectional study, serum YKL‐40 level was higher in patients with DM than in healthy controls (median [interquartile range]: 84.09 [52.72–176.4] ng/ml versus 27.37 [12.30–53.58] ng/ml, p < 0.0001). Serum levels of YKL‐40 were associated with the course of DM (r = −0.469, p < 0.001), CRP (r = 0.303, p = 0.043), CK (r = 0.263, p = 0.037), and global disease activity (r = 0.628, p < 0.001). The area under the ROC curve was 0.835 (95% confidence interval 0.751–0.920). In the systematic review, a total of four studies were included with moderate to high quality. Serum level of YKL‐40 has the possibility for diagnosing PM/DM, identifying PM/DM patients with interstitial lung disease (ILD) or rapid progress ILD, and predicting death.ConclusionSerum YKL‐40 level is a possible useful biomarker for PM/DM diagnosis and may be used to predict prognosis.     

Association of plasma bone morphogenetic protein‐4 levels with arterial stiffness in hypertensive patients

BackgroundArterial stiffness interacts with hypertension, becoming an early marker of hypertension‐mediated target organ damage. This study aimed to assess the association between plasma concentrations of bone morphogenetic protein‐4 (BMP‐4) and arterial stiffness during hypertension.MethodsUsing cardio‐ankle vascular index (CAVI) to determine arterial stiffness status, 204 individuals with essential hypertension were classified into two groups, high CAVI (abnormal) group (n = 94) and low (normal) CAVI group (n = 110). Data were collected including clinical characteristics and laboratory measurements. Plasma levels of BMP‐4 were tested by using ELISA analysis.ResultsPlasma levels of BMP‐4 were substantially greater in high CAVI group than that in low CAVI group [38.51 (31.79–50.83) pg/mL vs. 31.15 (29.38–32.37) pg/mL; p < 0.001]. As shown by spearman correlation analysis, BMP‐4 concentrations were correlated with CAVI values in hypertensive individuals (r = 0.406, p < 0.001). After adjustment for potential confounders, elevated BMP‐4 levels were related with high CAVI (OR, 1.070; 95% CI, 1.003–1.108; p < 0.001). The best BMP‐4 cutoff value for identifying high CAVI, as determined by ROC curve analysis, was 33.34 pg/mL (AUC, 0.751; 95% CI, 0.683–0.818; p < 0.001).ConclusionPlasma levels of BMP‐4 are increased in hypertensive individuals with high CAVI. Elevated BMP‐4 levels are strongly correlated with higher CAVI values, implying a predictive value of BMP‐4 in arterial stiffness during hypertension.     

Circulating long non‐coding RNA Coromarker expression correlated with inflammation,coronary artery stenosis,and plaque vulnerability in patients with coronary artery disease

BackgroundThe aim of the study was to assess the correlation between circulating long non‐coding RNA (lncRNA) OTTHUMT00000387022 (named Coromarker) expression and disease severity, inflammatory cytokine levels, and plaque vulnerability in patients with coronary artery disease (CAD).MethodsA total of 134 participants who received coronary angiography were enrolled and classified them as CAD patients (N = 89) and controls (N = 45). Blood samples were obtained from all subjects. Quantitative polymerase chain reaction was used to evaluate Coromarker expression. The enzyme‐linked immunosorbent test was used to measure inflammatory cytokines including high sensitivity C reactive protein (hsCRP), interleukin (IL)‐1β (IL‐1β), IL‐6, NOD‐like receptor protein 3 (NLRP3), and markers of coronary plaque stability including matrix metallopeptidase 9 (MMP‐9) and soluble CD40 ligand (sCD40L). The severity of coronary stenosis was determined from the Gensini Score.ResultsLncRNA Coromarker expression was elevated to a greater extent in CAD patients than in control subjects before and after adjustments for age/gender (both p < 0.001); it was an independent predictor of CAD risk (area under curve: 0.824, 95% CI: 0.732–0.915). Additionally, Coromarker expression was significantly associated with Gensini Score (r = 0.574, p < 0.001), hsCRP (r = 0.221, p = 0.015), IL‐1β (r = 0.351, p < 0.001), IL‐6 (r = 0.286, p < 0.01), and NLRP3 levels (r = 0.312, p < 0.001). Coromarker expression was found to be linked with MMP‐9 (r = 0.260, p < 0.01) and sCD40L (r = 0.441, p < 0.001).ConclusionCirculating lncRNA Coromarker expression correlates with increased disease severity and inflammation as well as plaque vulnerability in patients with CAD.     

Cautions on the laboratory indicators of COVID‐19 patients on and during admission

BackgroundDifferent disease severities of COVID‐19 patients could be reflected on clinical laboratory findings.MethodsIn this single‐centered retrospective study, demographic, clinical, and laboratory indicators on and during admission were compared among 74 participants with mild, moderate, critical severe, or severe classification. Risk factors associated with disease severity were analyzed by multivariate analyses. The AUC and 95% CI of the ROC curve were calculated.ResultsThe most common manifestations of these patients were fever and cough. Critical severe or severe group owned the longest length of stay (23 (19,31), p < 0.001). After multivariate logistic regression, independent influence factors on admission for severity of disease were CK‐MB (OR 0.674; 95% CI 0.489–0.928; p = 0.016), LDH (OR 1.111 or 1.107; 95% CI 1.026–1.204 or 1.022–1.199; p = 0.009 or 0.013), normal T‐BIL (OR 4.58 × 10⁻⁸; 95% CI 3.05 × 10⁻⁹–6.88 × 10⁻⁷; p < 0.001), LYM% (OR 0.008; 95% CI 0–0.602; p = 0.029), and normal ESR (OR 0.016; 95% CI 0–0.498; p = 0.019). Factors during hospitalization were normal T‐BIL (OR 8.56 × 10⁻⁹; 95% CI 8.30 × 10⁻¹⁰–8.83 × 10⁻⁸; p < 0.001), LYM (OR 0.068; 95% CI 0.005–0.934; p = 0.044), albumin (OR 0.565; 95% CI 0.327–0.977; p = 0.041), and normal NEU% (OR 0.013; 95% CI 0.000–0.967; p = 0.048). Combined indicators of AUC were 0.860 (LYM, LDH, and normal ESR on admission, p < 0.001) and 0.750 (CK‐MB, LDH, and normal T‐BIL during hospitalization, p = 0.020) when predicting for severe or critical severe patients.ConclusionTo pay close attention to the progression of COVID‐19 and take measures promptly, we should be cautious of the laboratory indicators when patients on admission especially CK‐MB, LDH, LYM%, T‐BIL as well as ESR; and T‐BIL, LYM, albumin, NEU% with the process of disease.     

The longitudinal changes of serum JKAP and IL‐17A,and their linkage with anxiety,depression, and cognitive impairment in acute ischemic stroke patients

BackgroundOur previous study discovers that Jun N‐terminal kinase pathway‐associated phosphatase (JKAP) is dysregulated and negatively links with the disease severity in acute ischemic stroke (AIS) patients. This study intended to further evaluate the linkage of JKAP and interleukin (IL)‐17A with anxiety, depression, and cognitive impairment in AIS patients.MethodsSerum JKAP and IL‐17A levels in 120 AIS patients at admission, 1st (D1), 3rd (D3), 7th (D7) day after admission, and from 20 controls, were detected by ELISA. Hospital Anxiety and Depression Scale (HADS) and Mini‐Mental State Examination (MMSE) were assessed in AIS patients at discharge.ResultsJKAP (p < 0.001) was reduced, but IL‐17A (p < 0.001) was increased in AIS patients versus controls, and negatively correlated with each other in AIS patients (p = 0.014). In AIS patients, JKAP was reduced from baseline to D1 and then increased to D7 (p < 0.001), while IL‐17A exhibited an opposite trend (p < 0.001). Notably, JKAP at D3 was negatively linked with HADS‐anxiety score (p = 0.044), then decreased JKAP at D3 (p = 0.017) and D7 (p = 0.037) related to increased anxiety occurrence. However, JKAP was not linked to HADS‐depression score or depression occurrence. Besides, JKAP at multiple time points were positively associated with MMSE score (all p < 0.05); decreased JKAP at D3 (p = 0.017) and D7 (p = 0.026) related to raised cognitive impairment occurrence.ConclusionJKAP initially decreases then shows an increasing trend after disease onset, and its decrement relates to elevated IL‐17A, anxiety and cognitive impairment in AIS patients.     

Serum HDAC4 level in rheumatoid arthritis: Longitudinal change during treatment and correlation with clinical outcomes

ObjectiveHistone deacetylase 4 (HDAC4) modulates immunity, inflammation, and osteoblast differentiation to engage in rheumatoid arthritis (RA) etiology. This study aimed to evaluate the HDAC4 longitudinal change and its relationship with clinical features and outcomes in RA patients.MethodsEighty‐three RA patients were enrolled. Their serum HDAC4 level was detected by ELISA at baseline (W0), week (W) 4, W12, and W24 after treatment. RA patients were divided into response or non‐response, low disease activity (LDA) or non‐LDA, remission or non‐remission patients according to their treatment outcomes at W24. Meanwhile, serum HDAC4 was detected by ELISA in 20 osteoarthritis patients and 20 healthy controls (HCs).ResultsHDAC4 level was reduced in RA patients compared with HCs (p < 0.001) and osteoarthritis patients (p = 0.009). HDAC4 was negatively related to some of the disease activity indexes such as C‐reactive protein (p = 0.003), tender joint count (p = 0.025), and disease activity score based on 28 joints (p = 0.013) in RA patients; it was also negatively correlated with TNF‐α (p = 0.003), IL‐6 (p = 0.022), and IL‐17A (p = 0.015). However, the HDAC4 level was not related to different treatment histories or current initiating treatment regimens (all p < 0.05). After treatment, HDAC4 was gradually elevated along with the time (p < 0.001). Interestingly, HDAC4 level at W12 (p = 0.041) and W24 (p = 0.012) was higher in response patients versus non‐response patients, and its level at W24 was higher in LDA patients versus non‐LDA patients (p = 0.019), and in remission patients versus non‐remission patients (p = 0.039).ConclusionHDAC4 gradually increases during treatment and its elevation estimates good treatment outcomes in RA patients.     

Blood Th17 cells and IL‐17A as candidate biomarkers estimating the progression of cognitive impairment in stroke patients

BackgroundT helper (Th) cells regulate immunity and inflammation to engage in cognitive impairment in several neurological diseases, while their clinical relevance in stroke patients is not clear. The current study intended to assess the relationship of Th1 cells, Th17 cells, interferon‐gamma (IFN‐γ), and interleukin (IL)‐17A with cognitive function in stroke patients.MethodsOne hundred twenty stroke patients and 40 controls were enrolled in this muticenter study. Th1 and Th17 cells in peripheral blood were assessed by flow cytometry; meanwhile, IFN‐γ and IL‐17A in serum were detected by enzyme‐linked immunosorbent assay. Cognitive function of stroke patients was evaluated by Mini‐Mental State Examination (MMSE) score at enrollment (baseline), year 1, year 2, and year 3.ResultsTh1 cells (p = 0.037) and IFN‐γ (p = 0.048) were slightly increased, while Th17 cells (p < 0.001) and IL‐17A (p < 0.001) were greatly elevated in stroke patients compared with controls. Th17 cells (r _s = −0.374, p < 0.001) and IL‐17A (r _s = −0.267, p = 0.003) were negatively correlated with MMSE score at baseline, but Th1 cells and IFN‐γ were not. Meanwhile, Th17 cells (p = 0.001) and IL‐17A (p = 0.024) were increased in patients with cognitive impairment compared to those without cognitive impairment. Notably, Th17 cells were positively associated with 1‐year (r _s = 0.331, p < 0.001), 2‐year (r _s = 0.261, p = 0.006), and 3‐year (r _s = 0.256, p = 0.011) MMSE decline; IL‐17A was positively correlated with 1‐year (r _s = 0.262, p = 0.005), 2‐year (r _s = 0.193, p = 0.045), but not 3‐year MMSE decline. However, both Th1 cells and IFN‐γ were not linked with MMSE decline.ConclusionTh17 cells and IL‐17A estimate the progression of cognitive impairment in stroke patients.     

Serum HDL cholesterol uptake capacity in subjects from the MASHAD cohort study: Its value in determining the risk of cardiovascular endpoints

BackgroundThe efficiency of high‐density lipoprotein (HDL) to efflux cholesterol contributes to the reverse cholesterol transport (RCT) pathway as one of HDL’s proposed functions and depends on the ability of HDL to uptake cholesterol. We aimed to investigate cholesterol uptake capacity (CUC) by a newly developed assay in samples from the MASHAD (Mashhad Stroke and Heart Atherosclerotic Disorders) cohort study.MethodThe study population comprised 153 individuals developed CVD diagnosed by a specialist cardiologist, over 6 years of follow‐up, and 350 subjects without CVD. We used a modified CUC method to evaluate the functionality of HDL in serum samples.ResultThe CUC assay was highly reproducible with values for inter‐ and intra‐assay variation of 13.07 and 6.65, respectively. The mean serum CUC was significantly lower in the CVD group compared to control (p = 0.01). Although, there were no significant differences in serum HDL‐C between the groups and there was no significantly association with risk of progressive CVD. Multivariate logistic regression analysis showed that there was a significantly negative association between CUC and risk of CVD after adjustment for confounding parameters (OR = 0.57, 95% CI = 0.38–0.87, p = 0.009). The CUC was also inversely and independently associated with the risk of CVD event using Cox proportional hazards models analysis (HR = 0.62; 95% CI = 0.41–0.94, p = 0.02). We determined the optimum cutoff value of 1.7 a.u for CUC in the population. Furthermore, the CUC value was important in determining the CVD risk stratification derived from data mining analysis.ConclusionsReduced HDL functionality, as measured by CUC, appears to predict CVD in population sample from north‐eastern Iran.     

Association between squamous cell carcinoma antigen level and EGFR mutation status in Chinese lung adenocarcinoma patients

BackgroundTo investigate the association between squamous cell carcinoma antigen (SCCAg) level and epidermal growth factor receptor (EGFR) mutation status in Chinese lung adenocarcinoma patients.MethodsWe retrospectively analyzed 293 patients with lung adenocarcinoma, divided into EGFR mutant group (n = 178) and EGFR wild‐type group (n = 115). The general data and laboratory parameters of the two groups were compared. We used univariable and multivariable logistic regression to analyze the association between SCCAg level and EGFR mutation. Generalized additive model was used for curve fitting, and a hierarchical binary logistic regression model was used for interaction analysis.ResultsSquamous cell carcinoma antigen level in the EGFR wild‐type group was significantly higher than that in the mutant group (p < 0.001). After adjusting for confounding factors, we found that elevated SCCAg was associated with a lower probability of EGFR mutation, with an OR of 0.717 (95% CI: 0.543–0.947, p = 0.019). For the tripartite SCCAg groups, the increasing trend of SCCAg was significantly associated with the decreasing probability of EGFR mutation (p for trend = 0.015), especially for Tertile 3 versus Tertile 1 (OR = 0.505; 95% CI: 0.258–0.986; p = 0.045). Curve fitting showed that there was an approximate linear negative relationship between continuous SCCAg and EGFR mutation probability (p = 0.020), which was first flattened and then decreased (p < 0.001). The association between the two was consistent among different subgroups, suggesting no interaction (all p > 0.05).ConclusionThere is a negative association between SCCAg level and EGFR mutation probability in Chinese lung adenocarcinoma patients.