Age- and gender-adjusted estimated glomerular filtration rate definition reveals hyperfiltration as a risk factor for renal function deterioration in type 2 diabetes.

AIM: To assess the role of hyperfiltration for diabetic kidney disease (DKD) progression. MATERIALS AND METHODS: A retrospective observational cohort study enrolled type 2 diabetes (T2D) patients with an initial estimated glomerular filtration rate (eGFR) of 60 mL/min/1.73m2 or higher. Patients were categorized into two groups: hyperfiltration (eGFR exceeding the age- and gender-specific 95th percentile values from a prior national cohort study) and normofiltration. Rapid DKD progression was defined as an eGFR decline of more than 5 mL/min/1.73m2/year. We used a linear mixed effect model and Cox regression with time-varying covariate model to compare eGFR changes and identify factors associated with rapid DKD progression. RESULTS: Of the enrolled 7563 T2D patients, 7.2% had hyperfiltration. The hyperfiltration group exhibited a higher rate of eGFR decline compared with the normofiltration group (-2.0 ± 0.9 vs. -1.1 ± 0.9 mL/min/1.73m2/year; P < .001). During an average follow-up period of 4.65 ± 3.86 years, 24.7% of patients with hyperfiltration experienced rapid DKD progression, compared with 15.7% of patients with normofiltration (P < .001). Cox regression analyses identified that initial hyperfiltration was a significant determinant of rapid DKD progression, with a hazard ratio of 1.66 (95% confidence interval: 1.41-1.95; P < .001). When combined with albuminuria, the risk of progression was further compounded (hazard ratio 1.76-3.11, all P < .001). CONCLUSIONS: In addition to using the current Kidney Disease: Improving Global Outcomes CGA classification system, considering glomerular hyperfiltration status can improve the accuracy of predicting DKD progression.

Transcription factor 21 rs12190287 polymorphism is related to stable angina and ST elevation myocardial infarction in a Chinese Population.

Background: Transcription factor 21 (TCF21, epicardin, capsuling, pod-1) is expressed in the epicardium and is involved in the regulation of cell fate and differentiation via epithelial-mesenchymal transformation during development of the heart. In addition, TCF21 can suppress the differentiation of epicardial cells into vascular smooth muscle cells and promote cardiac fibroblast development. This study aimed to explore whether TCF21 gene (12190287G/C) variants affect coronary artery disease risk. Methods: We enrolled 381 patients who had stable angina, 138 with ST elevation myocardial infarction (STEMI), and 276 healthy subjects. Genotyping of rs12190287 of the TCF21 gene was performed. Results: Higher frequencies of the CC genotype were found in the patients with stable angina/STEMI than in the healthy controls. After adjusting for diabetes mellitus, hypertension, age, sex, smoking, body mass index and hyperlipidemia, the patients with the CC genotype of the TCF21 gene were associated with 2.49- and 9.19-fold increased risks of stable angina and STEMI, respectively, compared to the patients with the GG genotype. Furthermore, TCF21 CC genotypes showed positive correlations with both stable angina and STEMI, whereas TCF21 GG genotypes exhibited a negative correlation with STEMI. Moreover, the stable angina and STEMI patients with the CC genotype had significantly elevated high-sensitivity C-reactive protein levels than those with the GG genotype. In addition, significant associations were found between type 2 diabetes mellitus, hypertension, and hyperlipidemia with TCF21 gene polymorphisms (p for trend < 0.05). Conclusion: TCF21 gene polymorphisms may increase susceptibility to stable angina and STEMI.

Residual risk of cardiovascular complications in statin-using patients with type 2 diabetes: the Taiwan Diabetes Registry Study.

BACKGROUND: The residual risks of atherosclerotic cardiovascular disease in statin-treated patients with diabetes remain unclear. This study was conducted to identify factors associated with these residual risks in patients with no prior vascular event. METHODS: Data on 683 statin-using patients with type 2 diabetes mellitus (T2DM) from the Taiwan Diabetes Registry were used in this study. Patients aged < 25 or > 65 years at the time of diabetes diagnosis and those with diabetes durations ≥ 20 years were excluded. The United Kingdom Prospective Diabetes Study risk engine (version 2.01; https://www.dtu.ox.ac.uk/riskengine/ ) was used to calculate 10-year residual nonfatal and fatal coronary heart disease (CHD) and stroke risks. Associations of these risks with physical and biochemical variables, including medication use and comorbidity, were examined. RESULTS: The 10-year risks of nonfatal CHD in oral anti-diabetic drug (OAD), insulin and OAD plus insulin groups were 11.8%, 16.0%, and 16.8%, respectively. The 10-year risks of nonfatal stroke in OAD, insulin and OAD plus insulin groups were 3.0%, 3.4%, and 4.3%, respectively. In the multivariate model, chronic kidney disease (CKD), neuropathy, insulin use, calcium-channel blocker (CCB) use, higher body mass indices (BMI), low-density lipoprotein (LDL), fasting glucose, log-triglyceride (TG), and log-alanine transaminase (ALT) levels were associated with an increased CHD risk. The residual risk of stroke was associated with CKD, neuropathy, CCB use, and lower LDL cholesterol levels, higher BMI and diastolic blood pressure. CONCLUSION: This study indicated that insulin was probably a residual risk factor of CHD but not stroke, and that there was a possible presence of obesity paradox in patients with T2DM on statin therapy. In addition to lowering TG and normalizing fasting glucose levels, lower LDL cholesterol level is better for reduction of risk of CHD on statin therapy. On the other hand, lower LDL cholesterol level could potentially be related to higher risk of stroke among populations receiving statin therapy. These findings suggest potential therapeutic targets for residual cardiovascular risk reduction in patients with T2DM on statin therapy.

Behavioral and Psychological Factors in Buffering Diabetes-related Disability Development.

BACKGROUND: Diabetes is associated with disability development. Healthy behaviors and psychosocial support can help patients manage their disease. PURPOSE: To examine the role of various behavioral and psychological factors in buffering the effect of diabetes on disability development over time in Taiwanese adults. METHODS: Data on 5,131 adults aged ≥50 years were obtained from the Taiwan Longitudinal Study on Aging. A cohort sequential multilevel design was employed to analyze the association between behavioral and psychosocial factors and the risk of disability over a 11-year period. RESULTS: In patients with diabetes, having social support and exercising more than six times a week were associated with 4% and 49% reductions in the risk of disability, respectively (ßdiabetes*socialsupport = -0.285, p = .006; ßdiabetes*exercise3 = -2.612, p = .007). Exercising more than six times a week had an additional significant protective effect against disability development per year (ßdiabetes*exercises3*age = -0.241, p = .038). Depression did not significantly interact with diabetes. However, a trajectory analysis revealed that individuals who had both diabetes and depression had the highest disability score from middle age among all participants. CONCLUSIONS: Engaging in frequent exercise is the most influential factor for reducing the risk of disability in patients with diabetes. Social support provides an additional benefit for disability prevention in individuals with diabetes.

Diabetes can lead to several diseases that affect the heart, vessels, brain, kidneys, and nerves. These diseases can cause disabilities in people with diabetes. Disabilities among people with diabetes lead to higher death rates, depression, and poor life quality. All these have become a great burden to our public health care system. Several past studies let us know healthy behaviors and good social support have positive effects on reducing complications of diabetes. Healthy behaviors, such as healthy diets, regular exercises, and proper stress management. Good social support and participation are known to reduce dementia in people with diabetes. However, it remains unclear about interactions and exact associations among all these factors. This study was designed to find out how health behaviors and social support help people with diabetes reduce the risks of disabilities. By analyzing data from Taiwan Longitudinal Study on Aging, we found that exercising more than six times a week reduced disability risk the most for people with diabetes. Social support, although not as effective as exercising, provided additional positive effects to reducing disability risks of people with diabetes.

Loss of ficolin-3 expression is associated with poor prognosis in patients with hepatocellular carcinoma.

Background: Ficolin-3 (FCN3) is a well-known circulating pattern recognition molecule which plays a role in host immune responses to cancer via activation of the lectin complement pathway. Nevertheless, the clinical significance of FCN3 in patients with hepatocellular carcinoma (HCC) is unclear. Methods: Eighty-seven HCC patients who received hepatectomy at our hospital were included. Immunohistochemical staining was used to assess the FCN3 expression in both tumorous and non-tumorous tissues from the patients, who were classified into high and low expression groups. Differences in clinicopathological characteristics between the two groups were then analyzed. Results: Survival was significantly associated with FCN3 immunohistochemical score (p for trend = 0.048). Kaplan-Meier analysis revealed a higher overall survival rate in the patients with a high FCN3 expression than in those with a low FCN3 expression (p=0.031). A high FCN3 expression in tumor tissue was independently associated with better overall survival (p=0.042). However, multivariate analysis showed that FCN3 expression was not an independent risk factor for overall survival. Conclusion: Our findings suggest that FCN3 is significantly related to the prognosis of HCC. FCN3 may be a prognostic marker in patients with HCC.

Elevated plasma leptin levels are associated with vascular access dysfunction in patients on maintenance hemodialysis.

BACKGROUND: Inflammation has been associated with vascular access (VA) dysfunction. The adipocytokine leptin can directly induce pro-inflammatory T helper 1 immune responses and the pathogenesis of chronic inflammation. We explored the association between plasma leptin and VA dysfunction in patients on maintenance hemodialysis (HEMO). METHODS: A total of 344 consecutive patients who received anastomosis for VA at a single HEMO center between June 1, 2010 and December 31, 2021 were screened. Of these patients, 267 met the inclusion criteria and were included. ELISA was used to measure circulating levels of leptin. RESULTS: The VA dysfunction group had a higher leptin level than the patent VA group. A higher concentration of leptin was independently and significantly associated with an elevated risk of VA dysfunction. Multiple logistic regression analysis showed that leptin, female sex, and hypertension were independently associated with VA dysfunction, even after adjusting for known biomarkers. We then evaluated the ability of leptin, female sex, and hypertension to predict the risk of VA dysfunction, and the area under the curve (AUC) for leptin was 0.626 (p = 0.0001). When leptin, female sex, and hypertension were added to this multivariate model, the AUC increased to 0.679 (p = 0.001) for leptin and hypertension, and 0.690 for leptin, hypertension, and female sex (p = 0.004). In addition, plasma leptin levels were associated with sex, body mass index, and hemoglobin. CONCLUSIONS: In addition to the association between leptin and VA dysfunction, hypertension and female sex independently predicted VA dysfunction in patients with HEMO.

Plasma levels and tissue expression of liver-type fatty acid-binding protein in patients with breast cancer.

BACKGROUND: Liver-type fatty acid-binding protein (L-FABP) is widely expressed in hepatocytes and plays a role in lipid metabolism. It has been demonstrated to be overexpressed in different types of cancer; however, few studies have investigated the association between L-FABP and breast cancer. The aim of this study was to assess the association between plasma concentrations of L-FABP in breast cancer patients and the expression of L-FABP in breast cancer tissue. METHOD: A total of 196 patients with breast cancer and 57 age-matched control subjects were studied. Plasma L-FABP concentrations were measured using ELISA in both groups. The expression of L-FABP in breast cancer tissue was examined using immunohistochemistry. RESULT: The patients had higher plasma L-FABP levels than the controls (7.6 ng/mL (interquartile range 5.2-12.1) vs. 6.3 ng/mL (interquartile range 5.3-8.5), p = 0.008). Multiple logistic regression analysis showed an independent association between L-FABP and breast cancer, even after adjusting for known biomarkers. Moreover, the rates of pathologic stage T2+T3+T4, clinical stage III, positive HER-2 receptor status, and negative estrogen receptor status were significantly higher in the patients with an L-FABP level greater than the median. Furthermore, the L-FABP level gradually increased with the increasing stage. In addition, L-FABP was detected in the cytoplasm, nuclear, or both cytoplasm and nuclear of all breast cancer tissue examined, not in the normal tissue. CONCLUSIONS: Plasma L-FABP levels were significantly higher in the patients with breast cancer than in the controls. In addition, L-FABP was expressed in breast cancer tissue, which suggests that L-FABP may be involved in the pathogenesis of breast cancer.

[Holistic Person-Centered Care for Individuals With Type 2 Diabetes Mellitus].

In 2022, the American Diabetes Association and the European Association for the Study of Diabetes emphasized that type 2 diabetes care is a person-centered holistic care concept. This article summarizes the concepts of holistic care for individuals with type 2 diabetes and proposes a complete model of the six-layer whole-person care circle for individuals with type 2 diabetes. This model treats individuals with type 2 diabetes as the core of care and adopts their specific needs, preferences, and values to design individualized care plans. The overall goal of care is to maintain quality of life and to avoid or delay complications. Management methods must be holistic. Based on people and comprehensive considerations, six circles of care are listed. The first layer is caregivers, taking into account the influence of the family and the community on the individual. The second layer is multi-professional and multi-disciplinary team care, which provides support to individuals with diabetes. The third layer emphasizes the need for the following thirteen principles in diabetes care: monitoring and screening for complications, behavior modification for healthy habits, monitoring and continuous assessment, reducing the risk of hypoglycemia, effective implementation and care organization, considering underlying physiological conditions, avoiding therapeutic inertia, considering social determinants of health, psychological factors, structured diabetes education, language proficiency, shared decision-making, and considering regional healthcare institutions and related resources. The fourth layer is the decision cycle of care, which applies the principles of care and conducts continuous and dynamic case management based on the decision cycle. The fifth layer is the healthcare network through which health providers provide hospital, long-term care, and primary clinics/ primary network care referrals based on the needs of individual with diabetes. The sixth layer leverages the chronic care model to construct a supportive healthcare system comprising organizational support, clinical information systems, delivery system design, decision support, self-management support, and community resources. This proposed model may provide a reference for constructing healthcare systems to care for patients with type 2 diabetes.

Fibroblast growth factor 21 is associated with widening QRS complex and prolonged corrected QT interval in patients with stable angina.

BACKGROUND: Fibroblast growth factor 21 (FGF21) is produced by cardiac cells, may acts in an autocrine manner, and was suggested to has a cardioprotective role in atherosclerosis. Wide QRS complex and heart rate-corrected QT interval (QTc interval) prolongation are associated to dangerous ventricular arrhythmias and cardiovascular disease mortality. Yet, the role of FGF21 in cardiac arrhythmia has never been studied. The aim of the study was to investigate the relationship between plasma FGF21 and the QRS duration and QTc interval in patients with stable angina. METHODS: Three hundred twenty-one consecutive stable angina patients were investigated. Plasma FGF21 was measured through ELISA, and each subject underwent 12-lead electrocardiography. RESULTS: FGF21 plasma levels were positively associated with the QRS duration (ß = 0.190, P = 0.001) and QTc interval (ß = 0.277, P < 0.0001). With increasing FGF21 tertiles, the patients had higher frequencies of wide QRS complex and prolonged QTc interval. After adjusting for patients' anthropometric parameters, the corresponding odd ratios (ORs) for wide QRS complex of the medium and high of FGF21 versus the low of FGF21 were 1.39 (95% CI 0.51-3.90) and 4.41 (95% CI 1.84-11.59), respectively, and p for trend was 0.001. Furthermore, multiple logistic regression analysis also showed the corresponding odd ratios (ORs) for prolonged QTc interval of the medium and high of FGF21 versus the low of FGF21 were 1.02 (95% CI 0.53-1.78) and 1.93 (95% CI 1.04-3.60) respectively with the p for trend of 0.037. In addition, age- and sex-adjusted FGF21 levels were positively associated with fasting glucose, HbA1c, creatinine, and adiponectin, but negatively associated with albumin, and the estimated glomerular filtration rate. CONCLUSIONS: This study indicates that plasma FGF21 is associated with wide QRS complex and prolonged corrected QT interval in stable angina patients, further study is required to investigate the role of plasma FGF21 for the underlying pathogenesis.

Association of plasma fatty acid-binding protein 3 with estimated glomerular filtration rate in patients with type 2 diabetes mellitus.

Background: Fatty acid-binding protein 3 (FABP3) located in renal mesangial and distal tubular cells, and had been shown to be a sensitive marker of renal injury, potentially be a mediator in pathogenesis of chronic kidney disease (CKD). Our previous study revealed that plasma FABP1 and FABP2 were independently associated with CKD, however, little is known about the relationship between plasma FABP3 level and CKD. The aim of this study was therefore to evaluate the plasma levels of FABP3 at different stages of estimated glomerular filtration rate (eGFR) in patients with type 2 diabetes mellitus (T2DM). Methods: A total of 334 subjects with T2DM who enrolled in a disease management program were included in this study and stratified according to eGFR. Plasma FABP3 concentrations were measured by an enzyme-linked immunosorbent assay. Results: FABP3 levels increased in parallel with the eGFR level. Increasing concentrations of FABP3 were independently and significantly associated with eGFR stage G2-G4. Age- and sex-adjusted FABP3 levels were positively associated with uric acid, urinary albumin-to-creatinine ratio, FABP1, FABP2, and fatty liver index, but negatively associated with eGFR and hemoglobin. Conclusion: Our results indicate that circulating FABP3 in patients with T2DM is associated with eGFR, which suggests that increased plasma FABP3 may be involved in the pathogenesis of CKD.

Interactive effect of obesity and cognitive function decline on the risk of chronic kidney disease progression in patients with type 2 diabetes mellitus: a 9.1-year cohort study.

Background: Obesity and cognitive function decline are independent risk factors for chronic kidney disease (CKD). However, few studies have examined the combined effects of obesity status and cognitive function on change in CKD risk. We aimed to evaluate the association between obesity status, cognitive function and CKD risk change in patients with type 2 diabetes mellitus (T2DM). Methods: Data on 3399 T2DM patients were extracted from a diabetes disease management program between 2006 and 2018. Univariate and multivariate analyses were used to assess the association between obesity, cognitive decline, and CKD risk change. Three indexes, including the relative excess risk of interaction (RERI), attributable proportion of interaction (API), and synergy index (SI), were used to analyze interactions. CKD risk was classified according to the KDIGO 2012 CKD definition. Results: In multivariate analysis, the hazard ratio (HR, 95%Cis) for CKD risk progression was 1.34 (1.12-1.61) times higher in the moderate and severely obese patients compared with the normal weight patients, and 1.34 (1.06-1.67) times higher in the patients with a Mini-Mental State Examination (MMSE) score ≤18 compared to those with an MMSE score ≥24. There was a synergistic interaction between moderate and severe obesity and MMSE score ≤18 on CKD risk progression (SI=4.461; 95% CI: 1.998-9.962), and the proportion of CKD risk progression caused by this interaction was 52.7% (API=0.527; 95% CI: 0.295-0.759). However, normal weight and MMSE score ≥24 were not beneficial on CKD risk improvement in the patients with a moderate risk and very high-risk stage of CKD. Conclusion: There may be a synergistic interaction between obesity and cognitive function decline, and the synergistic interaction may increase the risk of CKD progression.

Low plasma growth/differentiation factor 1 levels are associated with liver fibrosis in patients with stable angina.

BACKGROUND: Growth differentiation factor 1 (GDF1) is a member of the transforming growth factor-ß (TGF-ß) superfamily and a protective mediator against the development of post-infarction cardiac remodeling by negatively regulating MEK-ERK1/2 and Smad signaling pathways in the heart. The TGF-ß/SMAD pathway has been shown to play a key role in the development of hepatic fibrosis. In addition, fatty liver disease has been associated with reduced MEK/ERK1/2 signaling. However, no previous study has investigated the association between GDF1 and liver fibrosis. Therefore, the aim of this study was to investigate the association between plasma GDF1 and liver fibrosis in patients with stable angina. METHODS: We included 327 consecutive patients with stable angina. ELISA was used to measure circulating levels of GDF1, and the fibrosis-4 index was used to assess liver fibrosis. RESULTS: The advanced liver fibrosis group had lower median plasma GDF1 levels than those with minimal liver fibrosis. There was a significant negative association between GDF1 plasma level and fibrosis-4 index (r = -0.135, p = 0.019). A lower concentration of GDF1 was significantly and independently associated with an increased risk of liver fibrosis when concentration was analyzed as a continuous variable and by tertile. In addition, fibrosis-4 index, aspartate aminotransferase (AST)-to-platelet ratio index, and AST/alanine aminotransferase ratio were significantly associated with GDF1 concentration. CONCLUSIONS: Our results indicated an association between low plasma GDF1 and liver fibrosis in the enrolled patients. Further investigations into the role of plasma GDF1 in the pathogenesis of liver fibrosis are warranted.

Effects of different blood pressures and their long-term variability on the development of diabetic kidney disease in patients with type 2 diabetes mellitus.

AIM: To explore the relationship between long-term variabilities in different blood pressure variables and diabetic kidney disease (DKD) in patients with type 2 diabetes. DESIGN: A retrospective study. METHODS: This study included 3050 patients with type 2 diabetes whose metabolic parameters were regularly checked. Intrapersonal means and standard deviations (SDs) of all recorded systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial pressure (MAP), and pulse pressure (PP) measurements were calculated. Subjects were divided into four groups: Q1 (SBP-Mean < 130, SBP-SD < 11.06); Q2 (SBP-Mean < 130, SBP-SD ≥ 11.06); Q3 (SBP-Mean ≥ 130, SBP-SD < 11.06); Q4 (SBP-Mean ≥ 130, SBP-SD ≥ 11.06). Similarly, based on whether the PP-Mean was higher or lower than 80 mmHg (average PP-Mean) and the PP-SD was higher or lower than 6.48 mmHg (average PP-SD), the involved patients were redivided into Q1'~ Q4' groups. RESULTS: Adjusted for age, sex and diabetes duration, results revealed that the SBP-Mean, SBP-SD, PP-Mean and PP-SD were risk factors for DKD. Meanwhile, patients in the Q4 group had the highest DKD prevalence (HR = 1.976, p < .001), while Q1 group had the lowest. In addition, patients in the Q3 group (HR = 1.614, P < .001) had a higher risk of DKD than those in the Q2 group (HR = 1.408, P < .001). After re-stratification by PP-Mean and PP-SD, patients in the Q4' group had the highest risk of DKD (HR = 1.370, p < .001), while those in the Q1' group had the lowest risk. Patients in the Q3' group (HR = 1.266, p < .001) had a higher risk of DKD than those in the Q2' group (HR = 1.212, p < .001).

Determinants of fear of falling in older adults with diabetes.

OBJECTIVES: To identify the important determinants of FoF among older adults with diabetes in endocrine clinics based on demographic and illness characteristics, physical function and capability, psychosocial and cognitive factors. METHODS: A cross-sectional study was conducted on 240 older adults with Type 2 diabetes who were recruited by convenience sampling. Self-reported questionnaires, medical records as well as physical function and capability tests were used to collect the data. Multiple linear regression was used to identify the important determinants of FoF. RESULT: Diabetes distress, sarcopenia levels, TUG results, and HbA1c levels were significant determinants of FoF. These determinants uniquely explained 14%, 9%, 4%, and 2% of the variance in FoF respectively. CONCLUSION: Beside sarcopenia and dynamic balance being known as significantly associated with FoF in a general older population, diabetes distress and HbA1c levels should also be considered in designing interventions to improve FoF among older adults with diabetes.

Circulating hepassocin level in patients with stable angina is associated with fatty liver and renal function.

Background: Chronic kidney disease (CKD) is a major risk factor for coronary artery disease and it is often associated with hepatic steatosis. Hepassocin (also known as hepatocyte-derived fibrinogen related protein or fibrinogen-like 1) is a novel hepatokine that causes hepatic steatosis and induces insulin resistance. However, the role of hepassocin in renal function status remains unclear. Our objective was to investigate the association of plasma hepassocin level with fatty liver and renal function status in patients with stable angina. Methods: Plasma hepassocin levels were determined by enzyme-linked immunosorbent assays in 395 consecutive patients with stable angina. Renal function was defined as an estimated glomerular filtration rate (eGFR). Fatty liver was defined by ultrasonography and fibrosis-4 (FIB-4) index. Results: With increasing hepassocin tertiles, patients had higher prevalence of fatty live, an increased waist-to-hip ratio, and neutrophil count, monocyte count, and FIB-4 index, higher levels of uric acid, blood urine nitrogen and higher sensitivity C-reactive protein. They also had incrementally lower eGFR, serum hemoglobin and albumin levels. In multiple linear stepwise regression analysis, only eGFR was significantly independent negatively associated with plasma hepassocin levels. Conclusion: Our results indicate that circulating hepassocin in patients with stable angina is associated with fatty liver and renal function, which suggests that increased plasma hepassocin may be involved in the pathogenesis of fatty liver and CKD.

Elevated plasma fatty acid-binding protein 3 is related to prolonged corrected QT interval and reduced ejection fraction in patients with stable angina.

Background: Higher concentrations of plasma fatty acid-binding protein 3 (FABP3) play a role in the development of cardiovascular events, cerebrovascular deaths, and acute heart failure. However, little is known about the relationship between plasma FABP3 level and prolonged QT interval and reduced ejection fraction (EF). This study aimed to investigate the relationship between plasma FABP3 level and prolonged corrected QT (QTc) interval and reduced EF in patients with stable angina. Inflammatory cytokine and adipocytokine levels were also measured to investigate their associations with plasma FABP3. Methods: We evaluated 249 consecutive patients with stable angina. Circulating levels of FABP3 were measured by ELISA. In addition, 12-lead ECG and echocardiography recordings were obtained from each patient. Results: Multiple regression analysis showed that high-density lipoprotein cholesterol, high sensitivity C-reactive protein (hs-CRP), white blood cell (WBC) count, visfatin, adiponectin, FABP4, heart rate, QTc interval, left atrial diameter, left ventricular mass index, end-systolic volume, end-systolic volume index, fractional shortening, and EF were independently associated with FABP3 (all p<0.05). Patients with an abnormal QTc interval had a higher median plasma FABP3 level than those with a borderline and normal QTc interval. With increasing FABP3 tertiles, the patients had higher frequencies of abnormal QTc interval, left ventricular systolic dysfunction, and all-cause mortality, incrementally lower EF, higher WBC count, and higher levels of hs-CRP, visfatin, adiponectin, and FABP4. Conclusion: This study indicates that plasma FABP3 may act as a surrogate parameter of prolonged QTc interval and reduced EF in patients with stable angina, partially through the effects of inflammation or cardiomyocyte injury. Further studies are required to elucidate whether plasma FABP3 plays a role in the pathogenesis of QTc prolongation and reduced EF.

Elevated plasma level of neutrophil gelatinase-associated lipocalin (NGAL) in patients with breast cancer.

Background: Neutrophil gelatinase­associated lipocalin (NGAL), also known as lipocalin 2, siderocalin, 24p3 or uterocalin, plays a key role in inflammation and in different types of cancer. In this study, we investigated whether plasma NGAL levels were altered in patients with breast cancer. The relationship between plasma NGAL levels and pretreatment hematologic profile was also explored. Methods: Plasma NGAL concentrations were measured using ELISA in breast cancer patients and control subjects. A total of 75 patients with breast cancer and 65 age- and body mass index-matched control subjects were studied. All of the study subjects were female. Results: Plasma NGAL level was found to be elevated in the patients with breast cancer compared to the control subjects (94.3 ng/mL (interquartile range 39.3-207.6) vs. 55.0 ng/mL (interquartile range 25.8-124.7), p = 0.007). Multiple logistic regression analysis revealed that NGAL was independently associated with breast cancer, even after adjusting for known biomarkers. Furthermore, NGAL level was elevated in the breast cancer patients who were negative progesterone receptor status, had a histologic grade ≥ 2, clinical stage III, and pathologic stage T2+T3+T4. In addition, NGAL level was significantly correlated with white blood cell (WBC) count, monocyte count, neutrophil count, and platelet count (all p < 0.01). Moreover, WBC count, neutrophil count, monocyte count, lymphocyte count, platelet count, and NGAL level gradually increased as the stage progressed. Conclusions: Increased plasma NGAL levels were associated with breast cancer independently of risk factors, and were correlated with inflammatory biomarkers. These results suggest that NGAL may act through inflammatory reactions to play an important role in the pathogenesis of breast cancer.

Risk factors of falls and the gender differences in older adults with diabetes at outpatient clinics.

AIMS: To explore the risk factors of falls and the gender differences based on demographic and disease characteristics, physical capability, and fear of falling in older adults with diabetes visiting outpatient clinics in Taiwan. DESIGN: Cross-sectional design. METHODS: A total of 485 patients with type 2 diabetes aged between 65 and 80 years were recruited from three endocrine outpatient clinics in Taiwan. Demographic and disease characteristics, fall history in the previous one year and fear of falling were collected by a self-reported questionnaire. Calf circumference, handgrip strength, one-leg standing and time up-and-go tests were all performed to assess the physical capability of participants. Data were collected from May 2019 to May 2020. RESULTS: Female gender (OR = 1.75), handgrip strength (OR = 2.43) and fear of falling (OR = 3.38) were important risk factors of falls overall, although fear of falling (OR = 4.69) was the only important risk factor of falls in males, while handgrip strength (OR = 3.48) and fear of falling (OR = 2.86) were important risk factors of falls in females. The sensitivity of simultaneous screening handgrip strength and fear of falling were 85.7, 86.4 and 86.2 in males, females and older adults overall with diabetes, respectively. CONCLUSION: Fear of falling was an important risk factor of falls in both genders, especially in males. Handgrip strength was an important risk factor of falls specifically for females. By simultaneously screening fear of falling and handgrip strength, risk of falls in older adults with diabetes at outpatient clinics could be identified in a more timely manner. Impact Nurses could periodically and simultaneously assess fear of falling and handgrip strength of older adults with diabetes at outpatient clinics. For those are identified at risk of falls on either fear of falling or handgrip strength, nurses could provide corresponding interventions to reduce the fear of falling or improve muscle strength to prevent such falls.

Pathways of diabetes distress, decisional balance, self-efficacy and resilience to quality of life in insulin-treated patients with type 2 diabetes: A 9-month prospective study.

AIMS AND OBJECTIVES: To construct a path model addressing influences of diabetes distress, self-efficacy of injecting insulin, resilience and decisional balance of injecting insulin to quality of life (QoL) in insulin-treated patients with type 2 diabetes (T2DM). BACKGROUND: Insulin regimens more negatively impact QoL than oral medication treatments in patients with T2DM. Understanding the factors and influencing pathways associated with subsequent QoL will help nurses design timely interventions to improve QoL of insulin-treated T2DM patients. DESIGN: A 9-month prospective design was employed in this study. METHODS: Self-reported questionnaires were used to collect data from 185 insulin-treated T2DM patients. At baseline, diabetes distress and self-efficacy of injecting insulin were collected, while QoL, resilience and decisional balance of injecting insulin were collected 9 months later. Data were collected from February 2017 to February 2018. Structural equation modelling was used for analysis. This study was conducted based on the STROBE. RESULTS: Low baseline diabetes distress and high 9-month decisional balance of injecting insulin directly associated with high 9-month QoL. High baseline self-efficacy of injecting insulin and high 9-month resilience directly associated with high 9-month decisional balance of insulin injection and indirectly associated with high 9-month QoL. High baseline diabetes distress directly and indirectly associated with poor 9-month QoL. CONCLUSIONS: Diabetes distress, self-efficacy of injecting insulin, resilience and decisional balance of injecting insulin play different roles in associating with QoL in insulin-treated T2DM patients. RELEVANCE TO CLINICAL PRACTICE: Nurses could provide educational programs focusing on enhancing decisional balance of injecting insulin to improve QoL in insulin-treated patients. Improving self-efficacy of injecting insulin and resilience could be promising strategies to improve the decisional balance of injecting insulin. More timely assessment of diabetes distress and intervention might be powerful strategies to improve subsequent QoL in these patients.

FABP1 and FABP2 as markers of diabetic nephropathy.

Background: Diabetes mellitus is the leading cause of diabetic nephropathy and a major public health issue worldwide. Approximately 20-30% of patients with type 2 diabetes mellitus (T2DM) have renal impairment. Fatty acid-binding protein 1 (FABP1) is expressed in renal proximal tubule cells and released into urine in response to hypoxia caused by decreased peritubular capillary blood flow, and FABP2 is responsible for the transport of free fatty acids in the intestinal endothelium cells. There is increasing evidence that FABP1 and FABP 2 play a role in the development and progression of chronic kidney disease. The aim of this study was to investigate the relation of circulating FABP1 and FABP2 levels to nephropathy in patients with T2DM. Methods: For this study, 268 subjects with T2DM who were enrolled in a disease management program were stratified according to urinary microalbumin and serum creatinine measurements. The plasma FABP1 and FABP2 concentrations were examined by enzyme-linked immunosorbent assay. Demographic and potential metabolic confounding factors were analyzed with logistic regression to calculate the effects of FABP1 and FABP2 levels on diabetic nephropathy. Results: The FABP1 and FABP2 levels increased in parallel with the advancement of diabetic nephropathy. Increasing concentrations of FABP1 and FABP2 were independently and significantly associated with diabetic nephropathy. Multiple logistic regression analysis revealed FABP1 and FABP2 as an independent association factor for diabetic nephropathy, even after full adjustment of known biomarkers. Furthermore, receiver operating characteristic curve analysis showed that a FABP1 level of >33.8 ng/mL and a FABP2 level of >2.8 ng/mL were associated with diabetic nephropathy. Conclusion: Our results suggest that FABP1 and FABP2 may be novel biomarkers of diabetic nephropathy.