The correlation between professional quality of life and mental health outcomes among hospital personnel during the Covid-19 pandemic in Taiwan.

PURPOSE: This study investigated the association between professional quality of life, working context, and mental health outcomes among hospital personnel in Taiwan during the worldwide upsurge in COVID-19 cases. PATIENTS AND METHODS: We recruited 503 hospital personnel to whom we administered online questionnaires containing items from the Professional Quality of Life (ProQoL) scale, which covers compassion satisfaction (CS), burnout (BO) and compassion fatigue (CF), the Depression, Anxiety and Stress Scale (DASS-21) and questions on work-related variables. Data were collected from 13 July to 19 August 2020. RESULTS: The participants generally reported moderate CS and BO and low CF. Overall prevalence of mild-to-extremely-severe stress, anxiety and depression was 24.5%, 39.6% and 31.2%, respectively. Multiple logistic regression revealed that moderate-to-high BO and CF correlated with increased risks of mild-to-extremely-severe stress (OR = 4.17 and 2.23, respectively), anxiety (OR = 4.86 and 2.81, respectively) and depression (OR = 5.83 and 3.01, respectively), while moderate-to-high CS correlated with reduced risks of stress (OR = 0.53) and depression (OR = 0.45) only. There were CS and BO differences in groups categorized by marital status and profession. Anxiety increased linearly by seniority <10, 10-19 and ≥20 years (p for trend <0.05). CONCLUSION: In conclusion, the subscales of ProQOL, BO and CF appeared to be associated with increased risks of stress, anxiety and depression among hospital personnel during the COVID-19 epidemic. A long-term contingency program may be needed to adjust work context variables and support emotional well-being of these workers.

The hOGG1 Ser326Cys gene polymorphism and the risk of coronary ectasia in the Chinese population.

Oxidative stress (OS) is related to vascular inflammation possibly, contributing to the development of coronary ectasia (CE). Base excision repair (BER) and nucleotide excision repair are the main DNA repair pathways that can help to remove 8-hydroxydeoxyguanine (8-OHdG), a marker of OS. Human 8-oxoguanine DNA glycosylase 1 (hOGG1) is a key enzyme of the BER pathway and catalyzes the removal of 8-OHdG. The aim of our study was to investigate the association between hOGG1 Ser326Cys gene polymorphism and CE in a Chinese population. Five-hundred forty-seven patients who underwent diagnostic coronary angiography in a tertiary medical center were recruited. The angiographic definition of CE is the diameter of the ectatic segment being more than 1.5 times larger compared with an adjacent healthy reference segment. The gene polymorphisms were analyzed by polymerase chain reaction. The urine 8OHdG concentration was measured using a commercial ELISA kit. The distribution of hOGG1 Ser326Cys genotypes was significantly different between CE and non-CE groups (p = 0.033). The odds ratio of CE development for the Ser to the Cys variant was 1.55 (95% confidence interval (CI), 1.04-2.31, p = 0.033). Both univariate and logistic regression analysis showed a significant association of hOGG1 Ser326Cys polymorphism in the dominant model with CE development (p = 0.009 and 0.011, respectively). Urine 8-OHdG levels were significantly higher in subjects carrying the hOGG1 Ser variant than in those with the Cys/Cys genotype (p < 0.03). In conclusion, our study suggests that the hOGG1 Ser326Cys gene variant might play a role in susceptibility to the development of CE.

Matrix metalloproteinase-1 mitral expression and -1607 1G/2G gene promoter polymorphism in mitral chordae tendinae rupture.

Understanding the pathogenesis of mitral chordae tendinae rupture (MCTR) is essential for identification of risk factors. Mitral matrix metalloproteinase (MMP) triggers the signal cascade that instigates cardiac fibrosis, which may be a predisposing factor in MCTR. We investigated associations among MMP1 expression, MMP1 -1607 1G/2G polymorphism and mitral chordae tendinae rupture (MCTR). This study enrolled 185 patients (group A) receiving mitral valve replacement. Group A included 65 patients with MCTR and 120 controls without MCTR. MMP1 was assessed on a semiquantitative scale (0-3) by immunohistochemical staining. For genetic association study, another 227 subjects were recruited for group B, including 75 with MCTR and 152 controls. The gene polymorphisms were analyzed by polymerase chain reaction. In group A, MCTR patients had a higher MMP1 expression compared to controls (P < 0.001). Binary regression analysis showed the variation in the MCTR patients was independently explained by MMP1 (P = 0.027). Hypertension and MMP1 staining had a synergistic effect on the MCTR occurrence (P < 0.001). In group B, MMP1 -1607 1G allele was increased in patients with MCTR compared to controls (P = 0.014). The odds ratio for the 1G/1G genotype to the 2G/2G genotype was 3.22 (P = 0.009). Univariate and logistic regression analysis showed an independent association between MCTR and MMP1 -1607 1G/2G polymorphism (P = 0.028 and 0.032, respectively). Since MMP1 mitral expression and -1607 1G/2G polymorphism were associated with MCTR independently of other baseline characteristics, MMP1 may play a role in the individual susceptibility to MCTR.

The Gly460Trp polymorphism of alpha-adducin gene as a predictor of renal function decline over 4 years of follow-up in an apparently healthy Chinese population.

There were conflict data between alpha-adducin Gly460Trp genetic variant and changes of renal function. We conducted a prospective study to investigate the influence of alph-adducin Gly460Trp polymorphism on the quantitative changes of renal function. Of 1500 people screened, 112 non-diabetic normotensive elderly Chinese were recruited and received biochemistry examination at the baseline, at the second and fourth year follow-up. Serum creatinine and calculated renal parameter, using Modification of Diet in Renal Disease (MDRD) Study, were used to evaluate renal function and their progression. Genotyping was performed by polymerase chain reaction-restriction fragment length polymorphism. Age was 71.9 ± 3.7 years (range 60-81). Serum creatinine and MDRD glomerular filtration rate (GFR) were significantly worsened at the 2 and 4-year follow-up (all P < 0.001). The magnitude of 4-year decline of MDRD GFR was significantly higher in subjects carrying the a-adducin Gly460Trp G-allele than TT genotype (P = 0.045). The multivariate analyses showed that a-adducin Gly460Trp (P = 0.034), baseline MDRD GFR (P < 0.001), diastolic blood pressure (P = 0.021) and body weight (P = 0.022) could independently predict 4-year change of MDRD GFR. This longitudinal study showed that the aging process was associated with decline of renal function in the healthy elderly. The alpha-adducin Gly460Trp gene polymorphism might modulate these changes in the Chinese. This provides further knowledge essential in the assessment of renal disease and determination of renal function in the older subjects.

The 8-oxoguanine glycosylase I (hOGG1) Ser326Cys variant affects the susceptibility to multi-vessel disease in Taiwan coronary artery disease patients.

8-hydroxydeoxyguanosine, the key lesion of oxidative DNA damage, contributes to the development of coronary artery disease (CAD). In humans, 8-hydroxydeoxyguanosine is repaired by the enzyme 8-oxoguanine glycosylase I (hOGG1). We investigated the association between the hOGG1 Ser(326)Cys polymorphism and the presence and the severity of CAD in a Taiwan population. Genotypes of the hOGG1 Ser(326)Cys polymorphism were determined from 1397 participants enrolled in this study (378 CAD patients and 1019 controls). CAD severity was indicated both by number of vessels affected (single-vessel disease, SVD vs. multi-vessel disease, MVD), and by individual diffuse score. Real-time polymerase chain reaction was used to determine genotype, using allele-specific TaqMan probes. We found that presence of the hOGG1 Ser(326)Cys polymorphism was associated with a significantly increased risk of CAD and multi-vessel disease when assuming a dominant model of inheritance (OR: 1.52 [95%:1.082~2.133], p=0.015; OR: 2.26 [95%:1.232~4.156], p=0.007). This result was confirmed by multivariate analysis, after adjustment for age, gender, body-mass index, diabetes hypertension, hypercholesterolemia and smoking (OR: 1.78 [95%:1.127~2.806], p<0.005; OR: 2.44 [95%:1.276~4.651], p<0.001). In the present study, hOGG1 Ser(326)Cys polymorphism is a novel genetic marker to be independently associated with the development and severity of CAD in Taiwanese population.

Functional vascular endothelial growth factor gene polymorphisms and diabetes: effect on coronary collaterals in patients with significant coronary artery disease.

BACKGROUND: Vascular endothelial growth factor (VEGF) plays a pivotal role in angiogenesis. This study tested the association between functional VEGF +405 C>G (rs2010963), -2578C>A (rs699947) polymorphisms, and coronary collaterals in patients with coronary artery disease (CAD). METHOD: The collateral scoring system developed by Rentrop was used to classify 393 patients according to their collaterals as either "poor" (grades 0 and 1) or "good" (grades 2 and 3). Gene polymorphisms were analyzed by TaqMan assay. RESULTS: The frequency of +405C and -2578A alleles was higher in the good collaterals group (p=0.007 and 0.005, respectively). For the +405C>G allele, the odds ratio (OR) of good collaterals for CC to GG genotype was 2.54 (p=0.003). For the -2578A allele, the OR of good collaterals for AA to CC genotype was 2.31 (p=0.038). Univariate and logistic regression analysis found 2 polymorphisms in the additive model for associations with collateral development: +405C>G (p=0.005 and 0.010) and -2578C>A (p=0.006 and 0.006). The VEGF +405C>G polymorphism and DM revealed an interactive effect on collateral development (p=0.027). CONCLUSIONS: The VEGF +405C>G and -2578C>A polymorphisms might be novel genetic factors affecting collateral development in Chinese patients.

Vascular endothelial growth factor polymorphisms and extent of coronary atherosclerosis in Chinese population with advanced coronary artery disease.

BACKGROUND: Vascular endothelial growth factor (VEGF) is important in atherosclerotic development. We examined two VEGF polymorphisms, including +405 C/G (rs2010963) and -2578C/A (rs699947), to assess their relation to the extent of coronary atherosclerosis. METHODS: We recruited 398 patients with advanced coronary artery disease (CAD). Angiographic "clinical vessel score" (CVS, 1-3 vessels) and "diffuse score" (DS, 0-11.5) were used to evaluate the extent of coronary atherosclerosis. CVS are further categorized into single- (SVD) and multi-vessel disease (MVD: 2 and 3 vessels). Genotyping was performed by TaqMan assay. RESULTS: The frequency of +405 C/G genotype was correlated with CVS and DS (P = 0.016 and 0.016, respectively). The +405C allele frequency was significantly increased in patients with MVD (P = 0.020). The odds ratio (OR) for the CC to the GG genotype was 2.92 (95% confidence interval (CI): 1.31-6.55, P = 0.007). Univariate and logistic regression analysis showed a significant independent association of +405 C/G genotype with SVD/MVD (P = 0.010 and 0.015, respectively) in the recessive model. Furthermore, there is a synergistic effect of CC genotype and diabetes on the occurrence of MVD (P = 0.001 for interaction). There is also a significant independent association of +405 C/G genotype in the recessive model with DS in the uni- and multivariate regression analysis (P = 0.013 and 0.005, respectively). No association was found between VEGF -2578C/A polymorphism and both atherosclerotic parameters. CONCLUSIONS: The VEGF +405C/G polymorphism is a novel genetic factor to influence the extent of coronary atherosclerosis in the Chinese CAD population.

Elevated serum retinol-binding protein 4 concentrations are associated with renal dysfunction and uric acid in type 2 diabetic patients.

BACKGROUND: While some studies have reported that retinol-binding protein 4 (RBP4) might induce insulin resistance, other studies have demonstrated that the presence of albuminuria in diabetic patients and increased uric acid are related to insulin resistance. Therefore, this study attempted to further investigate the relationship among serum RBP4, serum uric acid, and the severity of albuminuria in diabetic patients. METHODS: A total of 95 type 2 diabetic patients and 16 healthy subjects participated in this study. Diabetic patients were classified into normoalbuminuria, microalbuminuria and macroalbuminuria groups according to their urine albumin-to-creatinine ratio (ACR). Serum RBP4 was measured by an enzyme-linked immunosorbent assay (ELISA). RESULTS: Serum RBP4 was significantly elevated in type 2 diabetic patients with normoalbuminuria (43.4 +/- 14.9 microg/mL), microalbuminuria (57.3 +/- 24.2 microg/mL) and macroalbuminuria (64.7 +/- 27.6 microg/mL) as compared with control patients (32.6 +/- 10.0 microg/mL). Serum RBP4 was also significantly elevated in type 2 diabetic patients with microalbuminuria or macroalbuminuria as compared with the normoalbuminuric group. Serum RBP4 in diabetic subjects was positively correlated with triglycerides, uric acid and ACR, and negatively correlated with low-density lipoprotein cholesterol and estimated glomerular filtration rate (eGFR; with age and gender adjustment in each parameter). Multiple stepwise linear regression analysis showed that uric acid and eGFR remained significantly associated with serum RBP4. CONCLUSIONS: Both eGFR and uric acid are significant determinants of serum RBP4, suggesting that the impaired renal clearance of early diabetic nephropathy affects RBP4 and indirectly supporting the hypothesized link among metabolic syndrome, uric acid and insulin resistance.

Thiazolidinedione addition reduces the serum retinol-binding protein 4 in type 2 diabetic patients treated with metformin and sulfonylurea.

Retinol-binding protein 4 (RBP4) has been found to induce insulin resistance and to be increased in type 2 diabetes. Thiazolidinediones (TZDs) can improve insulin sensitivity through the activation of peroxisome proliferators-activated receptor-gamma (PPAR-gamma) and have been suggested as an adjunct to metformin (MF) and sulfonylurea (SU) in type 2 diabetes in a consensus statement from the ADA and EASD. Therefore, we investigated whether TZD could affect serum RBP4 level in type 2 diabetes already treated with MF and/or SU. Eighty-one type 2 diabetic patients were divided into 2 groups: (1) TZD group (n = 55): Pioglitazone 30 mg/day was given as an add-on medication; (2) SU group (n = 26): Gliclazide MR 30-120 mg or glimepiride 2-8 mg/day was prescribed. The average period of study was 97.1 days. Serum RBP4 and adiponectin were measured by enzyme-linked immunosorbent assay and radioimmunoassay, respectively. The addition of pioglitazone (TZD group) markedly decreased homeostasis model assessment of insulin resistance (HOMA-IR) (P = 0.021) compared with the SU group (P = 0.688). The change of RBP4 in the TZD group (-3.87 +/- 11.27 microg/mL) significantly differed from that in the SU group (2.52 +/- 8.24 microg/mL, P < 0.012). The increase of adiponectin in the TZD group (11.49 +/- 7.85 microg/mL) was apparently higher than that in the SU group (1.54 +/- 5.62 microg/mL, P < 0.001). Despite the change of glycosylated hemoglobin (HbA1c) did not differ (-0.77 +/- 1.3 vs -0.50 +/- 1.7, P = 0.446), the addition of pioglitazone could significantly lower serum RBP4 and HOMA-IR values, whereas an increased dosage of sulfonylurea agents did not alter HOMA-IR, RBP4, or adiponectin in type 2 diabetic patients who had been treated with metformin and/or sulfonylurea.

Decreased insulin secretion and insulin sensitivity are associated with liver function in subjects with fasting glucose between 100 and 109 mg/dL in Taiwanese population.

OBJECTIVE: In 2003, the American Diabetes Association recommended that the lower limit for the diagnosis of impaired fasting glucose (IFG) should be reduced from 110 to 100 mg/dL in the analysis of the associated risk factors of IFG. It has been proposed that liver dysfunction may contribute to the development of type 2 diabetes. A primary aim was to investigate the relationship between liver enzyme and insulin resistance (IR) in IFG group. The secondary aim was to investigate IR and beta-cell function assessed by homeostasis model assessment (HOMA-IR and HOMA-%B, respectively) in subjects with fasting plasma glucose (FPG) between 100 and 109 mg/dL. METHODS: We enrolled 284 subjects whose medical history and physical examination required tests to screen for metabolic abnormalities. In addition, we also excluded all factors affecting glucose or insulin metabolism. According to the FPG level, they were divided into the following groups: group A, FPG < 100 mg/dL; group B, FPG = 100 to 109 mg/dL; group C, FPG = 110 to 125 mg/dL. RESULTS: Group B as compared with group A had significant increase of HOMA-IR and decrease of HOMA-%B. Among the whole population, the fasting insulin level, the fasting glucose, HbA1c, HOMA-IR, alanine aminotransferase, gamma-glutamyltranspeptidase, aspartate aminotransferase, and the diastolic blood pressure all increased significantly as the glycemic status progressed, whereas HOMA-%B levels decreased significantly as the glycemic status progressed. The lipid profile, alkaline phosphatase, and systolic blood pressure did not differ significantly among 3 different glycemic classifications. CONCLUSIONS: Study results indicate that, first, there was a significant decrease of insulin sensitivity and insulin secretion in subjects with fasting glucose from 100 to 109 mg/dL compared with subjects with normal fasting glucose. Second, alanine aminotransferase, aspartate aminotransferase, and gamma-glutamyltranspeptidase were associated with IR as the glycemic status progressed in the IFG group.

SUMO4 M55V variant is associated with diabetic nephropathy in type 2 diabetes.

OBJECTIVE-SUMO4 mRNA was recently found to be mainly expressed in the kidney, and the methionine-to-valine substitution at codon 55 (M55V) variant of SUMO4 may induce higher nuclear factor-kappaB (NF-kappaB) activity. Because NF-kappaB is known to mediate the development of diabetic nephropathy, we examined the association between the SUMO4 M55V variant and the severity of diabetic nephropathy. RESEARCH DESIGN AND METHODS-We recruited a total of 430 patients with type 2 diabetes. The M55V (rs237025, 163A-->G) polymorphism of SUMO4 was genotyped by real-time PCR, and urine albumin concentration was measured by radioimmunoassay. RESULTS-The frequencies of SUMO4 AA, GA, and GG were 52.6, 40.7, and 6.7%, respectively, in the normoalbuminuric group; 45.5, 47.3, and 7.1% in the microalbuminuric group; and 36.9, 46.2, and 16.9% in the macroalbuminuric group. We detected a significant linear trend for SUMO4 genotype between the macroalbuminuric and normoalbuminuric groups. The mean urine albumin-to-creatinine ratio (42.3 +/- 108.82 mg/mmol) in the GG group was significantly higher than in the AA (14.9 +/- 51.49 mg/mmol) and GA (17.0 +/- 43.74 mg/mmol) groups. Multivariate logistic regression analysis showed the SUMO4 M55V variant to be independently associated with the severity of diabetic nephropathy. CONCLUSIONS-This study indicates that the SUMO4 gene M55V variant is associated with severity of diabetic nephropathy in patients with type 2 diabetes.

The hOGG1 Ser326Cys gene polymorphism is associated with decreased insulin sensitivity in subjects with normal glucose tolerance.

Increased oxidative stress has been observed to contribute the development of insulin resistance. Oxidative stress is known to increase the conversion of deoxyguanosine (dG) to 8-hydroxy-2'-deoxyguanosine (8-OHdG). Human 8-oxoguanine glycosylase (hOGG1) is the key component responsible for the removal of 8-OHdG from oxidatively damaged DNA. The repair activity of the hOGG1 Ser326Cys gene variant has been demonstrated to be lower than that of the hOGG1 Ser/Ser genotype. Therefore, the possible association of the hOGG1 Ser326Cys gene variant with insulin sensitivity was investigated in 279 normal glucose-tolerant subjects without history of cancer. Allele frequency was 21.5% for the Ser/Ser genotype (n = 60), 45.9% for the Ser/Cys genotype (n = 128), and 32.6% for the Cys/Cys genotype (n = 91). Subjects carrying the Cys/Cys genotype had significantly lower insulin sensitivity levels, assessed by homeostasis model assessment-insulin resistance (HOMA-IR), compared with the Ser/Ser and Ser/Cys genotypes (P < 0.001 and P < 0.001, respectively). In a multiple linear regression analysis, the Cys/Cys genotype was a significant determinant of HOMA-IR, independent of age, sex, body mass index, fasting plasma cholesterol, triglyceride, HDL cholesterol, LDL cholesterol, or hypertension. The present study indicates that the hOGG1 gene Cys/Cys variant is associated with a significant decrease in insulin sensitivity in subjects with normal glucose tolerance.