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Many adults with diabetes mellitus are unaware worldwide. The study objectives aimed to evaluate the risk of dialysis within 5 years of diagnosis between patients with newly diagnosed diabetes with and without diabetes-related complications. A retrospective longitudinal nationwide cohort study was conducted. Patients diagnosed with diabetes between 2005 and 2013 were followed up until 2018. They were categorized based on the presence or absence of complications, the number of complications, and the diabetes complications severity index (DCSI) scores. Dialysis outcomes were determined through the Registry of Catastrophic Illness from the National Health Insurance Research Database. Among the analyzed patients, 25.38% had complications at diagnosis. Patients with complications at diagnosis had a significantly higher risk of dialysis within 5 years (adjusted hazard ratio: 9.55, 95% confidence interval CI 9.02–10.11). Increasing DCSI scores and the number of complications were associated with higher dialysis risks. Patients with one complication had a 7.26-times higher risk (95% CI 6.83–7.71), while those with ≥ 3 complications had a 36.12-times higher risk (95% CI 32.28–40.41). In conclusion, newly diagnosed diabetes patients with complications face an increased risk of dialysis within 5 years. The severity and number of complications are directly linked to the risk of dialysis within this timeframe. [ABSTRACT FROM AUTHOR]

Tumor necrosis factor receptor-associated factor-interacting protein with a forkhead-associated domain (TIFA), a key regulator of inflammation, may be involved in the pathogenesis of pulmonary arterial hypertension (PAH). A total of 48 PAH patients (age 50.1 ± 13.1 years, 22.9% men), 25 hypertensive subjects, and 26 healthy controls were enrolled. TIFA protein expression in peripheral blood mononuclear cells (PBMCs) and plasma interleukin (IL)-1β and tumor necrosis factor (TNF)-α were measured. Pulmonary arterial hemodynamics were derived from right heart catheterization. PAH patients had the highest expression of TIFA, TNF-α, and IL-1β. TIFA protein expression was significantly associated with IL-1β (r = 0.94; P < 0.001), TNF-α (r = 0.93; P < 0.001), mean pulmonary artery pressure (r = 0.41; P = 0.006), and pulmonary vascular resistance (r = 0.41; P = 0.007). TIFA protein expression could independently predict the presence of PAH (odds ratio [95% confidence interval per-0.1 standard deviation]: 1.72 [1.37–2.16]; P < 0.001) and outperformed echocardiographic estimation. Ex vivo silencing of TIFA protein expression in PBMCs led to the suppression of the cellular expression of IL-1β and TNF-α. IL-1β and TNF-α mediated 80.4% and 56.6% of the causal relationship between TIFA and PAH, respectively, supporting the idea that TIFA protein is involved in the pathogenesis of PAH. [ABSTRACT FROM AUTHOR]

Acoustic cardiography can provide simultaneous electrocardiography and acoustic cardiac data to assess the electronic and mechanical heart functions. The aim of this study was to assess whether changes in acoustic cardiographic parameters (ACPs) before and after hemodialysis (HD) are associated with overall and cardiovascular (CV) mortality in HD patients. A total of 162 HD patients was enrolled and ACPs were measured before and after HD, including left ventricular systolic time (LVST), systolic dysfunction index (SDI), third (S3) and fourth (S4) heart sounds, and electromechanical activation time (EMAT). During a follow-up of 2.9 years, 25 deaths occurred with 16 from CV causes. Multivariate analysis showed that high △SDI (per 1; hazard ratio [HR], 2.178; 95% confidence interval [CI], 1.189–3.990), high △EMAT (per 1%; HR, 2.218; 95% CI 1.382–3.559), and low △LVST (per 1 ms; HR, 0.947; 95% CI 0.912–0.984) were independently associated with increased overall mortality. In addition, high △EMAT (per 1%; HR, 2.141; 95% CI 1.117–4.102), and low △LVST (per 1 ms; HR, 0.777; 95% CI 0.637–0.949) were associated with increased CV mortality. In conclusion, the changes in ACPs before and after HD may be a useful clinical marker and stronger prognostic marker of overall and CV mortality than ACPs before HD. [ABSTRACT FROM AUTHOR]

The aim of this study was to investigate the associations between sibling history, parental history and simultaneous sibling and parental history of diabetes, and the presence of the metabolic syndrome (MetS) and its components. Our study comprised 5000 participants from Taiwan Biobank until April, 2014. The participants were stratified into four groups according to sibling and/or parental family history (FH) of DM. MetS was defined as having 3 of the following 5 abnormalities based on the standard of the NCEP ATP III and modified criteria for Asians. The prevalence of MetS and its traits was estimated and compared among the four familial risk strata. Multivariate logistic regression analysis showed participants with sibling FH of DM [vs. no FH of DM; odds ratio (OR) 1.815; 95% confidence interval (CI) 1.293 to 2.548; p = 0.001], participants with parental FH of DM (vs. no FH of DM; OR 1.771; 95% CI 1.468 to 2.135; p < 0.001), and participants with simultaneous sibling and parental FH of DM (vs. no FH of DM; OR 2.961; 95% CI 2.108 to 4.161; p < 0.001) were significantly associated with MetS. A synergistic effect of sibling FH of DM and parental FH of DM on the association of MetS was also observed. In a nationally representative sample of Taiwan adults, a simultaneous sibling and parental history of diabetes shows a significant, independent association with MetS and its components, except for abdominal obesity. The association highlights the importance of obtaining stratified FH information in clinical practice and may help to identify individuals who should be targeted for screening and early prevention of MetS. [ABSTRACT FROM AUTHOR]

Dyslipidemia is common in patients with chronic kidney disease (CKD), however the relationship between dyslipidemia and mortality in patients with moderate to severe CKD remains controversial. Non-high-density lipoprotein (HDL) cholesterol has been reported to be a more accurate predictor of clinical outcomes than conventional lipid measurements. Hence, the aim of this study was to investigate associations between non-HDL cholesterol and the risk of overall and cardiovascular mortality in patients with CKD stage 3–5. We enrolled 429 pre-dialysis patients with stage 3 to 5 CKD from May 2006 to January 2010. The patients were divided into four groups according to quartiles of non-HDL cholesterol. The patients were followed until death or until January 2020. During a median 11.6 years of follow-up, there were 78 (18.2%) deaths overall and 32 (7.5%) cardiovascular deaths. In adjusted models, the patients in quartile 1 (hazard ratio [HR] 3.368; 95% confidence interval [CI] 1.388–8.176; p = 0.007), quartile 3 (HR 3.666; 95% CI 1.486–9.044; p = 0.005), and quartile 4 (HR 2.868; 95% CI 1.136–7.240; p = 0.026) of non-HDL cholesterol had a higher risk of overall mortality (vs. quartile 2). In addition, the patients in quartile 1 (HR 19.503; 95% CI 2.185–174.0925 p = 0.008), quartile 3 (HR 28.702; 95% CI 2.990–275.559; p = 0.004), and quartile 4 (HR 11.136; 95% CI 1.126–110.108; p = 0.039) had a higher risk of cardiovascular mortality (vs. quartile 2). Our study showed a U-shaped relationship between non-HDL cholesterol and the risk of overall and cardiovascular mortality in patients with CKD stage 3–5. Assessing non-HDL cholesterol may help to identify subjects at high-risk of adverse outcomes. [ABSTRACT FROM AUTHOR]

In this work, a high-density hydrogen (HDH) treatment is proposed to reduce interface traps and enhance the efficiency of the passivated emitter rear contact (PERC) device. The hydrogen gas is compressed at pressure (~ 70 atm) and relatively low temperature (~ 200 °C) to reduce interface traps without changing any other part of the device's original fabrication process. Fourier-transform infrared spectroscopy (FTIR) confirmed the enhancement of Si–H bonding and secondary-ion mass spectrometry (SIMS) confirmed the SiN/Si interface traps after the HDH treatment. In addition, electrical measurements of conductance-voltage are measured and extracted to verify the interface trap density (Dit). Moreover, short circuit current density (Jsc), series resistance (Rs), and fill factor (F.F.) are analyzed with a simulated light source of 1 kW M−2 global AM1.5 spectrum to confirm the increase in cell efficiency. External quantum efficiency (EQE) is also measured to confirm the enhancement in conversion efficiency between different wavelengths. Finally, a model is proposed to explain the experimental result before and after the treatment. [ABSTRACT FROM AUTHOR]

Front-side metallization of a Si wafer was carried out using electroless deposition of nickel-phosphorus (Ni-P) catalyzed by polyvinylpyrrolidone-capped palladium nanoclusters (PVP-nPd). A 3-[2-(2-Aminoethylamino)ethylamino] propyl-trimethoxysilane (ETAS) layer was covalently bonded on the Si surface as bridge linker to the Pd cores of PVP-nPd clusters for improving adhesion between the Ni-P layer and the Si surface. To investigate the effects of an interfacial ETAS layer on the Ni silicide formation at the Ni-P/Si contact, the Ni-P-coated Si samples were thermally annealed via rapid thermal annealing (RTA) from 500°C to 900°C for 2 min. To compare with the ETAS sample, the sputtered Ni layer on Si and electroless Ni-P layer on ion-Pd-catalyzed Si (both are standard processes) were also investigated. The microstructural characterizations for the Ni-P or Ni layer deposited on the Si wafer were performed using x-ray diffractometer, scanning electron microscopy, and transmission electron microscopy. Our results showed that the ETAS layer acted as a barrier to slow the atomic diffusion of Ni toward the Si side. Although the formation of Ni silicides required a higher annealing temperature, the adhesion strength and contact resistivity measurements of annealed Ni-P/Si contacts showed satisfactory results, which were essential to the device performance and reliability during thermal annealing. [ABSTRACT FROM AUTHOR]

Membrane electroporation (MEP) induces a drastic change in membrane conductance and permeability. However, the underlying mechanisms by which MEP-induced currents ( I) are generated or resealed remain unclear. In this study, we investigated how the fluctuations of I might be elicited in different types of cells, including pituitary GH cells, NG108-15 neuronal cells, and RAW 264.7 macrophages. We applied the detrended fluctuation analysis (DFA) to analyze the current signals in response to large hyperpolarizations. The DFA exponents from the current signals at 10 s preceding the start of the initial I ( I) in GH cells exhibited two components (short time lag [α] and long time lag [α]) with a crossover threshold of about 7 ms. The α value was 0.46 ± 0.04 ( n = 7), whereas the α value with 0.62 ± 0.05 ( n = 7) indicated the presence of long-term correlations of current signals. However, during maximal I, the slope of double logarithmic plot was linear and estimated to be 0.99 ± 0.02 ( n = 8) with no clear crossover. Upon changes in membrane polarization, neither short- nor long-range correlation was altered. Chloroquine (CQ), a lysosomotropic agent, decreased the I amplitude with an IC value of 46 μM; however, it had no effects on the scaling exponents of I or I. Although CQ or membrane polarization altered the amplitudes of I, no changes in correlation properties of this current were detected. The scaling exponents derived from I exhibit long-range correlations in these different types of cells, indicating there is a correlated character of the electropore dynamics that may be allowed to predict the MEP process. [ABSTRACT FROM AUTHOR]

Icilin is recognized as a chemical agonist of nociceptors and can activate TRPM8 channels. However, whether this agent has any effects on immune cells remains unknown. In this study, the effects of icilin on ion currents were investigated in RAW 264.7 murine macrophage-like cells. Icilin (1-100 μM) increased the amplitude of nonselective (NS) cation current (INS) in a concentration-dependent manner with an EC50 value of 8.6 μM. LaCl3 (100 μM) or capsazepine (30 μM) reversed icilin-induced INS; however, neither apamin (200 nM) nor iberiotoxin (200 nM) had any effects on it. In cell-attached configuration, when the electrode was filled with icilin (30 μM), a unique population of NS cation channels were activated with single-channel conductance of 158 pS. With the use of a long-lasting ramp pulse protocol, increasing icilin concentration produced a left shift in the activation curve of NS channels, with no change in the slope factor of the curve. The probability of channel opening enhanced by icilin was increased by either elevated extracellular Ca2+ or application of ionomycin (10 μM), while it was reduced by BAPTA-AM (10 μM). Icilin-stimulated activity is associated with an increase in mean open time and a reduction in mean closed time. Under current-clamp conditions, icilin caused membrane depolarization. Therefore, icilin interacts with the TRPM8-like channel to increase INS and depolarizes the membrane in these cells. [ABSTRACT FROM AUTHOR]

The hyperpolarization-activated cation current ( I h) in rat pituitary lactotrophs (GH3 cells) was characterized. Tramadol-induced block of this current was investigated. Effects of various related compounds on I h in GH3 cells were also compared. Tramadol caused a time- and concentration-dependent reduction in the amplitude of I h with an IC50 value of 13.6 μM. ZD7288 (30 μM), CsCl (2 mM), and propofol (30 μM) were effective in suppressing the amplitude of I h. 2′,5′-dideoxyadenosine (100 μM) suppressed I h, while sp-cAMPS (100 μM) had no effect on it. Tramadol (10 μM) shifted the activation curve of I h to a more negative potential by approximately −20 mV, although no change in the slope factor was observed. Under current-clamp configuration, tramadol (10 μM) could reduce the firing frequency of action potentials. Intracellular Ca2+ measurements revealed its ability to reduce spontaneous Ca2+ oscillations in GH3 cells. The results suggests that during cell exposure to tramadol used at clinically relevant concentration, the tramadol-mediated inhibition of I h could be direct and mediated via a non-opioid mechanism and would be one of the ionic mechanisms underlying reduced cell excitability. [ABSTRACT FROM AUTHOR]

Vascular calcification and cardiomegaly are highly prevalent in chronic kidney disease (CKD) patients. However, the association of the combination of aortic arch calcification (AoAC) and cardio-thoracic ratio (CTR) with clinical outcomes in patients with CKD is not well investigated. This study investigated whether the combination of AoAC and CTR is associated with poor clinical outcomes in CKD stages 3–5 patients. We enrolled 568 CKD patients, and AoAC and CTR were determined by chest radiography at enrollment. Rapid renal progression was defined as estimated glomerular filtration rate (eGFR) decline over 3 ml/min/1.73 m2 per year. Both AoAC score and CTR were significantly associated with rapid renal progression. High CTR was correlated with increased risk for cardiovascular mortality. We stratified the patients into four groups according to the median AoAC score of 4 and CTR of 50%. Those with AoAC ≥ 4 and CTR ≥ 50% (vs. AoAC score < 4 and CTR < 50%) were associated with eGFR decline over 3 ml/min/1.73 m2/year and cardiovascular mortality. AoAC and CTR were independently associated with eGFR slope. In conclusion, the combination of increased AoAC and cardiomegaly was associated with rapid renal progression and increased cardiovascular mortality in patients with CKD stage 3–5 patients. We suggest that evaluating AoAC and CTR on chest plain radiography may be a simple and inexpensive method for detecting CKD patients at high risk for adverse clinical outcomes. [ABSTRACT FROM AUTHOR]