Prevalence and Characteristics of Isolated Nighttime Masked Uncontrolled Hypertension in Treated Patients.

Background and Objectives: We evaluated the prevalence and characteristics of isolated nighttime masked uncontrolled hypertension (IN-MUCH) in treated patients. Materials and Methods: Participants aged 20 years or older who were on antihypertensive medication underwent three-day office blood pressure (BP) and 24 h ambulatory BP measurements. Hypertension phenotypes were classified as controlled hypertension (CH), isolated daytime masked uncontrolled hypertension (ID-MUCH), IN-MUCH, and daytime and nighttime masked uncontrolled hypertension (DN-MUCH). Results: Among 701 participants, 544 had valid BP data and controlled office BP (<140/90 mmHg). The prevalence of IN-MUCH was 34.9%, with a higher prevalence of men and drinkers than in those with CH. Patients with IN-MUCH had higher office systolic BP (SBP) and diastolic BP (DBP) than those with CH. The prevalence of IN-MUCH was 37.6%, 38.5%, and 27.9% in patients with optimal, normal, and high-normal office BP levels, respectively. Among IN-MUCH patients, 51.6% exhibited isolated uncontrolled DBP and 41.1% uncontrolled SBP and DBP. Younger age (p = 0.043), male sex (p = 0.033), and alcohol consumption (p = 0.011) were more prevalent in patients with isolated uncontrolled DBP than in those with uncontrolled SBP and DBP. Age and alcohol consumption were positively associated, whereas high-normal office BP exhibited a negative association with IN-MUCH. Conclusions: The IN-MUCH was significantly more prevalent in patients with normal or optimal office BP, posing treatment challenges. Further investigation is needed to determine whether differentiation between isolated uncontrolled DBP and combined uncontrolled SBP and DBP is necessary for prognostic assessment of IN-MUCH.

Impact of etiology on force and kinetics of left ventricular end-stage failing human myocardium.

BACKGROUND: Heart failure (HF) is associated with highly significant morbidity, mortality, and health care costs. Despite the significant advances in therapies and prevention, HF remains associated with poor clinical outcomes. Understanding the contractile force and kinetic changes at the level of cardiac muscle during end-stage HF in consideration of underlying etiology would be beneficial in developing targeted therapies that can help improve cardiac performance. OBJECTIVE: Investigate the impact of the primary etiology of HF (ischemic or non-ischemic) on left ventricular (LV) human myocardium force and kinetics of contraction and relaxation under near-physiological conditions. METHODS AND RESULTS: Contractile and kinetic parameters were assessed in LV intact trabeculae isolated from control non-failing (NF; n = 58) and end-stage failing ischemic (FI; n = 16) and non-ischemic (FNI; n = 38) human myocardium under baseline conditions, length-dependent activation, frequency-dependent activation, and response to the ß-adrenergic stimulation. At baseline, there were no significant differences in contractile force between the three groups; however, kinetics were impaired in failing myocardium with significant slowing down of relaxation kinetics in FNI compared to NF myocardium. Length-dependent activation was preserved and virtually identical in all groups. Frequency-dependent activation was clearly seen in NF myocardium (positive force frequency relationship [FFR]), while significantly impaired in both FI and FNI myocardium (negative FFR). Likewise, ß-adrenergic regulation of contraction was significantly impaired in both HF groups. CONCLUSIONS: End-stage failing myocardium exhibited impaired kinetics under baseline conditions as well as with the three contractile regulatory mechanisms. The pattern of these kinetic impairments in relation to NF myocardium was mainly impacted by etiology with a marked slowing down of kinetics in FNI myocardium. These findings suggest that not only force development, but also kinetics should be considered as a therapeutic target for improving cardiac performance and thus treatment of HF.

Association between household income and pulse pressure: data from the Korean National Health and Nutrition Examination Survey.

PURPOSE: There has been limited evidence for the association between socioeconomic status (SES) and arterial stiffness. This study was performed to investigate the association between household income and brachial pulse pressure (PP) in the general Korean population. MATERIALS AND METHODS: This study was based on data acquired in the 2018 Korea National Health and Nutrition Examination Survey (2018 KNHANES). A total of 13004 subjects at the age of 20 years or older analysed. The information on monthly household income was obtained through the questionnaire, and was stratified into 5 groups for each quintile. Brachial blood pressure (BP) was measured 3 times, and the average of the second and third measured BPs were used. PP was calculated as the difference between systolic and diastolic BPs. RESULTS: A lower household income was associated with a higher prevalence of cardiovascular risk factors. As household income increased, PP decreased proportionally (p < .001). In multiple linear regression analysis, household income (per quintile) was independently associated with PP even after controlling for potential confounders (ß = -.125, p < .001). Multiple binary logistic regression analysis showed that the increased household income level was significantly associated lower probability having higher PP (≥ 43.5 mmHg) even after controlling for multiple covariates (the lowest vs. the highest household income; odds ratio, 0.48; 95% confidence interval, .41-.55; p < .001). CONCLUSION: Low household income was associated with higher PP. This provides additional evidence for the association between low SES and high arterial stiffness.

Association of the Serum Osteoprotegerin Level With Target Organ Damage in Patients at High Risk of Coronary Artery Disease.

BACKGROUND: There is little data as to whether osteoprotegerin (OPG) is associated with target organ damage (TOD), so we evaluated the association in patients at high risk of coronary artery disease (CAD).Methods and Results:A total of 349 patients who underwent invasive coronary angiography (ICA) for suspected CAD were prospectively recruited. During the index admission, 6 TOD parameters were collected: extent of CAD, glomerular filtration rate (GFR), left ventricular mass index (LVMI), E/e', brachial-ankle pulse wave velocity (baPWV), and ankle-brachial index (ABI). Serum OPG levels were measured using enzyme-linked immunosorbent assay. The OPG level was significantly higher in patients with ≥1 TOD parameter than in those without (314±186 vs. 202±74 pg/mL, P<0.001). For each TOD parameter, the serum OPG level was significantly higher in patients with TOD than in those without (P<0.05 for each) except for ABI. In correlation analysis, OPG was significantly associated with GFR, LVMI, E/e', baPWV and ABI (P<0.05 for each). The OPG concentration increased proportionally with increasing TOD (P<0.001). Higher OPG concentrations (≥198 pg/mL) was significantly associated with the presence of TOD (odds ratio 3.22; 95% confidence interval 1.51-6.85; P=0.002) even after controlling for potential confounders. CONCLUSIONS: Serum OPG level was significantly associated with a variety of TOD in patients undergoing ICA. OPG may be a useful marker for TOD and in the risk stratification of patients at high risk of CAD.

Impact of heart rate on cross-bridge cycling kinetics in failing and nonfailing human myocardium.

The force-frequency relationship (FFR) is an important regulatory mechanism that increases the force-generating capacity as well as the contraction and relaxation kinetics in human cardiac muscle as the heart rate increases. In human heart failure, the normally positive FFR often becomes flat, or even negative. The rate of cross-bridge cycling, which has been reported to affect cardiac output, could be potentially dysregulated and contribute to blunted or negative FFR in heart failure. We recently developed and herein use a novel method for measuring the rate of tension redevelopment. This method allows us to obtain an index of the rate of cross-bridge cycling in intact contracting cardiac trabeculae at physiological temperature and assess physiological properties of cardiac muscles while preserving posttranslational modifications representative of those that occur in vivo. We observed that trabeculae from failing human hearts indeed exhibit an impaired FFR and a reduced speed of relaxation kinetics. However, stimulation frequencies in the lower spectrum did not majorly affect cross-bridge cycling kinetics in nonfailing and failing trabeculae when assessed at maximal activation. Trabeculae from failing human hearts had slightly slower cross-bridge kinetics at 3 Hz as well as reduced capacity to generate force upon K+ contracture at this frequency. We conclude that cross-bridge kinetics at maximal activation in the prevailing in vivo heart rates are not majorly impacted by frequency and are not majorly impacted by disease.NEW & NOTEWORTHY In this study, we confirm that cardiac relaxation kinetics are impaired in filing human myocardium and that cross-bridge cycling rate at resting heart rates does not contribute to this impaired relaxation. At high heart rates, failing myocardium cross-bridge rates are slower than in nonfailing myocardium.

Increased cross-bridge recruitment contributes to transient increase in force generation beyond maximal capacity in human myocardium.

Cross-bridge attachment allows force generation to occur, and rate of tension redevelopment (ktr) is a commonly used index of cross-bridge cycling rate. Tension overshoots have been observed briefly after a slack-restretch ktr maneuver in various species of animal models and humans. In this study, we set out to determine the properties of these overshoots and their possible underlying mechanism. Utilizing human cardiac trabeculae, we have found that tension overshoots are temperature-dependent and that they do not occur at resting states. In addition, we have found that myosin cross-bridge cycle is vital to these overshoots as inhibition of the cycle results in the blunting of the overshoots and the magnitude of the overshoots are dependent on the level of myofilament activation. Lastly, we show that the number of cross-bridges transiently increase during tension overshoots. These findings lead us to conclude that tension overshoots are likely due to a transient enhancement of the recruitment of myosin heads into the cross-bridge cycling, regulated by the myocardium, and with potential physiological significance in determining cardiac output. NEWS AND NOTEWORTHY: We show that isolated human myocardium is capable of transiently increasing its maximal force generation capability by increasing cross-bridge recruitment following slack-restretch maneuver. This process can potentially have important implications and significance in cardiac contraction in vivo.

Etiology-dependent impairment of relaxation kinetics in right ventricular end-stage failing human myocardium.

BACKGROUND: In patients with end-stage heart failure, the primary etiology often originates in the left ventricle, and eventually the contractile function of the right ventricle (RV) also becomes compromised. RV tissue-level deficits in contractile force and/or kinetics need quantification to understand involvement in ischemic and non-ischemic failing human myocardium. METHODS AND RESULTS: The human population suffering from heart failure is diverse, requiring many subjects to be studied in order to perform an adequately powered statistical analysis. From 2009-present we assessed live tissue-level contractile force and kinetics in isolated myocardial RV trabeculae from 44 non-failing and 41 failing human hearts. At 1 Hz stimulation rate (in vivo resting state) the developed active force was not different in non-failing compared to failing ischemic nor non-ischemic failing trabeculae. In sharp contrast, the kinetics of relaxation were significantly impacted by disease, with 50% relaxation time being significantly shorter in non-failing vs. non-ischemic failing, while the latter was still significantly shorter than ischemic failing. Gender did not significantly impact kinetics. Length-dependent activation was not impacted. Although baseline force was not impacted, contractile reserve was critically blunted. The force-frequency relation was positive in non-failing myocardium, but negative in both ischemic and non-ischemic myocardium, while the ß-adrenergic response to isoproterenol was depressed in both pathologies. CONCLUSIONS: Force development at resting heart rate is not impacted by cardiac pathology, but kinetics are impaired and the magnitude of the impairment depends on the underlying etiology. Focusing on restoration of myocardial kinetics will likely have greater therapeutic potential than targeting force of contraction.

Role of intermediate phase for stable cycling of Na7V4(P2O7)4PO4 in sodium ion battery.

Sodium ion batteries offer promising opportunities in emerging utility grid applications because of the low cost of raw materials, yet low energy density and limited cycle life remain critical drawbacks in their electrochemical operations. Herein, we report a vanadium-based ortho-diphosphate, Na7V4(P2O7)4PO4, or VODP, that significantly reduces all these drawbacks. Indeed, VODP exhibits single-valued voltage plateaus at 3.88 V vs. Na/Na(+) while retaining substantial capacity (>78%) over 1,000 cycles. Electronic structure calculations reveal that the remarkable single plateau and cycle life originate from an intermediate phase (a very shallow voltage step) that is similar both in the energy level and lattice parameters to those of fully intercalated and deintercalated states. We propose a theoretical scheme in which the reaction barrier that arises from lattice mismatches can be evaluated by using a simple energetic consideration, suggesting that the presence of intermediate phases is beneficial for cell kinetics by buffering the differences in lattice parameters between initial and final phases. We expect these insights into the role of intermediate phases found for VODP hold in general and thus provide a helpful guideline in the further understanding and design of battery materials.

Multimodality Molecular Imaging of Cardiac Cell Transplantation: Part I. Reporter Gene Design, Characterization, and Optical in Vivo Imaging of Bone Marrow Stromal Cells after Myocardial Infarction.

Purpose To use multimodality reporter-gene imaging to assess the serial survival of marrow stromal cells (MSC) after therapy for myocardial infarction (MI) and to determine if the requisite preclinical imaging end point was met prior to a follow-up large-animal MSC imaging study. Materials and Methods Animal studies were approved by the Institutional Administrative Panel on Laboratory Animal Care. Mice (n = 19) that had experienced MI were injected with bone marrow-derived MSC that expressed a multimodality triple fusion (TF) reporter gene. The TF reporter gene (fluc2-egfp-sr39ttk) consisted of a human promoter, ubiquitin, driving firefly luciferase 2 (fluc2), enhanced green fluorescent protein (egfp), and the sr39tk positron emission tomography reporter gene. Serial bioluminescence imaging of MSC-TF and ex vivo luciferase assays were performed. Correlations were analyzed with the Pearson product-moment correlation, and serial imaging results were analyzed with a mixed-effects regression model. Results Analysis of the MSC-TF after cardiac cell therapy showed significantly lower signal on days 8 and 14 than on day 2 (P = .011 and P = .001, respectively). MSC-TF with MI demonstrated significantly higher signal than MSC-TF without MI at days 4, 8, and 14 (P = .016). Ex vivo luciferase activity assay confirmed the presence of MSC-TF on days 8 and 14 after MI. Conclusion Multimodality reporter-gene imaging was successfully used to assess serial MSC survival after therapy for MI, and it was determined that the requisite preclinical imaging end point, 14 days of MSC survival, was met prior to a follow-up large-animal MSC study. (©) RSNA, 2016 Online supplemental material is available for this article.

Multimodality Molecular Imaging of Cardiac Cell Transplantation: Part II. In Vivo Imaging of Bone Marrow Stromal Cells in Swine with PET/CT and MR Imaging.

Purpose To quantitatively determine the limit of detection of marrow stromal cells (MSC) after cardiac cell therapy (CCT) in swine by using clinical positron emission tomography (PET) reporter gene imaging and magnetic resonance (MR) imaging with cell prelabeling. Materials and Methods Animal studies were approved by the institutional administrative panel on laboratory animal care. Seven swine received 23 intracardiac cell injections that contained control MSC and cell mixtures of MSC expressing a multimodality triple fusion (TF) reporter gene (MSC-TF) and bearing superparamagnetic iron oxide nanoparticles (NP) (MSC-TF-NP) or NP alone. Clinical MR imaging and PET reporter gene molecular imaging were performed after intravenous injection of the radiotracer fluorine 18-radiolabeled 9-[4-fluoro-3-(hydroxyl methyl) butyl] guanine ((18)F-FHBG). Linear regression analysis of both MR imaging and PET data and nonlinear regression analysis of PET data were performed, accounting for multiple injections per animal. Results MR imaging showed a positive correlation between MSC-TF-NP cell number and dephasing (dark) signal (R(2) = 0.72, P = .0001) and a lower detection limit of at least approximately 1.5 × 10(7) cells. PET reporter gene imaging demonstrated a significant positive correlation between MSC-TF and target-to-background ratio with the linear model (R(2) = 0.88, P = .0001, root mean square error = 0.523) and the nonlinear model (R(2) = 0.99, P = .0001, root mean square error = 0.273) and a lower detection limit of 2.5 × 10(8) cells. Conclusion The authors quantitatively determined the limit of detection of MSC after CCT in swine by using clinical PET reporter gene imaging and clinical MR imaging with cell prelabeling. (©) RSNA, 2016 Online supplemental material is available for this article.

Experimental demonstration of highly sensitive optical sensor based on grating-assisted light coupling between strip and slot waveguides.

An optical sensor based on grating-assisted light coupling between a strip waveguide and a slot waveguide is demonstrated (the sensor was proposed and analyzed in [Opt. Express21, 5897-5909 (2013)]. The wavelength at which the light is strongly coupled between two waveguides is used to the measure the external medium's refractive index. The sensor was fabricated with silicon nitride waveguides and obvious grating induced band-rejection and band-pass characteristics were observed. The measured sensitivity of the fabricated sensor was -756.1 nm/RIU. Furthermore, by covering the strip waveguide with the silicon dioxide cladding, the sensitivity was measured to be as large as -1970 nm/RIU, which was 2.6 times enhanced. The experimental results agreed well with the calculated sensitivity values.

Insights into length-dependent regulation of cardiac cross-bridge cycling kinetics in human myocardium.

Cross-bridge cycling kinetics play an essential role in the heart's ability to contract and relax. The rate of tension redevelopment (ktr) slows down as a muscle length is increased in intact human myocardium. We set out to determine the effect of rapid length step changes and protein kinase A (PKA) and protein kinase C-ßII (PKC-ßII) inhibitors on the ktr in ultra-thin non-failing and failing human right ventricular trabeculae. After stabilizing the muscle either at L90 (90% of optimal length) or at Lopt (optimal length), we rapidly changed the length to either Lopt or L90 and measured ktr. We report that length-dependent changes in ktr occur very rapidly (in the order of seconds or faster) in both non-failing and failing muscles and that the length at which a muscle had been stabilized prior to the length change does not significantly affect ktr. In addition, at L90 and at Lopt, PKA and PKC-ßII inhibitors did not significantly change ktr. Our results reveal that length-dependent regulation of cross-bridge cycling kinetics predominantly occurs rapidly and involves the intrinsic properties of the myofilament rather than post-translational modifications that are known to occur in the cardiac muscle as a result of a change in muscle/sarcomere length.

Left ventricular long axis function assessed during cine-cardiovascular magnetic resonance is an independent predictor of adverse cardiac events.

BACKGROUND: Left ventricular pump function requires a complex interplay involving myocardial fibers orientated in the longitudinal, oblique and circumferential directions. Long axis dysfunction appears to be an early marker for a number of pathological states. We hypothesized that mitral annular plane systolic excursion (MAPSE) measured during cine-cardiovascular magnetic resonance (CMR) reflects changes in long axis function and may be an early marker for adverse cardiovascular outcomes. The aims of this study were therefore: 1) To assess the feasibility and reproducibility of MAPSE measurements during routine cine-CMR; and 2) To assess whether MAPSE, as a surrogate for long axis function, is a predictor of major adverse cardiovascular events (MACE). METHODS: Four hundred consecutive patients undergoing CMR were prospectively enrolled. MAPSE was measured in the 4-chamber cine view. Patients were prospectively followed for major adverse cardiac events (MACE) - death, non-fatal myocardial infarction, hospitalization for heart failure or unstable angina, and late revascularization. Cox proportional hazards regression modeling was used to identify factors independently associated with MACE. Net reclassification improvement (NRI) was calculated to assess whether addition of MAPSE resulted in improved risk reclassification of MACE. RESULTS: Seventy-two MACE occurred during a median follow-up of 14.5 months. By Kaplan-Meier analysis, patients with lateral MAPSE <1.11 cm (median) experienced significantly higher incidence of MACE than patients with a MAPSE ≥1.11 cm (p = 0.027). After adjustment for established clinical risk factors which were univariate predictors (age, diabetes, hypertension, NYHA class, LV mass), lateral MAPSE remained a significant independent predictor of MACE (HR = 4.384 per cm decrease or 1.344 per 2 mm decrease; p = 0.020). Incorporation of lateral MAPSE into this risk model resulted in a net reclassification improvement (NRI) of 0.18 (p = 0.006). CONCLUSIONS: Reduced long axis function assessed with lateral MAPSE during cine-CMR is an independent predictor of MACE.

Hierarchical Cu pillar electrodes for electrochemical CO2 reduction to formic acid with low overpotential.

To achieve high performance of electrochemical CO2 reduction, a series of Cu pillar electrodes (Cu-2.5 h, Cu-5 h) were fabricated by using an electrodeposition method, and then their catalytic activities and reaction mechanisms were investigated. The series of Cu pillar electrodes exhibited improved electrocatalytic activities toward CO2 reduction to formic acid (HCOOH) as Cu pillars on electrodes developed. The Cu-5 h electrode performed well with a 28% Faradaic efficiency for formic acid at -0.5 V (vs. RHE). X-ray diffraction (XRD) analysis indicated that the enhanced catalytic activities were primarily attributable to the increased (111) facet, which is energetically favourable for the production of HCOOH. Also, ultraviolet photoelectron spectroscopy (UPS) and in situ electrochemical impedance spectroscopy (EIS) results suggested that the series of Cu pillar structure electrodes improved the electron transfer to adsorbed CO2 due to the decreased work function of the Cu pillar structure.

Ascites analysis by a microfluidic chip allows tumor-cell profiling.

Ascites tumor cells (ATCs) represent a potentially valuable source of cells for monitoring treatment of ovarian cancer as it would obviate the need for more invasive surgical biopsies. The ability to perform longitudinal testing of ascites in a point-of-care setting could significantly impact clinical trials, drug development, and clinical care. Here, we developed a microfluidic chip platform to enrich ATCs from highly heterogeneous peritoneal fluid and then perform molecular analyses on these cells. We evaluated 85 putative ovarian cancer protein markers and found that nearly two-thirds were either nonspecific for malignant disease or had low abundance. Using four of the most promising markers, we prospectively studied 47 patients (33 ovarian cancer and 14 control). We show that a marker set (ATCdx) can sensitively and specifically map ATC numbers and, through its reliable enrichment, facilitate additional treatment-response measurements related to proliferation, protein translation, or pathway inhibition.

Highly Efficient, Selective, and Stable CO2 Electroreduction on a Hexagonal Zn Catalyst.

Electrocatalytic CO2 conversion into fuel is a prospective strategy for the sustainable energy production. However, still many parts of the catalyst such as low catalytic activity, selectivity, and stability are challenging. Herein, a hierarchical hexagonal Zn catalyst showed highly efficient and, more importantly, stable performance as an electrocatalyst for selectively producing CO. Moreover, we found that its high selectivity for CO is attributed to morphology. In electrochemical analysis, Zn (101) facet is favorable to CO formation whereas Zn (002) facet favors the H2 evolution during CO2 electrolysis. Indeed, DFT calculations showed that (101) facet lowers a reduction potential for CO2 to CO by more effectively stabilizing a (.) COOH intermediate than (002) facet. This further suggests that tuning the crystal structure to control (101)/(002) facet ratio of Zn can be considered as a key design principle to achieve a desirable product from Zn catalyst.

The Frank-Starling mechanism involves deceleration of cross-bridge kinetics and is preserved in failing human right ventricular myocardium.

Cross-bridge cycling rate is an important determinant of cardiac output, and its alteration can potentially contribute to reduced output in heart failure patients. Additionally, animal studies suggest that this rate can be regulated by muscle length. The purpose of this study was to investigate cross-bridge cycling rate and its regulation by muscle length under near-physiological conditions in intact right ventricular muscles of nonfailing and failing human hearts. We acquired freshly explanted nonfailing (n = 9) and failing (n = 10) human hearts. All experiments were performed on intact right ventricular cardiac trabeculae (n = 40) at physiological temperature and near the normal heart rate range. The failing myocardium showed the typical heart failure phenotype: a negative force-frequency relationship and ß-adrenergic desensitization (P < 0.05), indicating the expected pathological myocardium in the right ventricles. We found that there exists a length-dependent regulation of cross-bridge cycling kinetics in human myocardium. Decreasing muscle length accelerated the rate of cross-bridge reattachment (ktr) in both nonfailing and failing myocardium (P < 0.05) equally; there were no major differences between nonfailing and failing myocardium at each respective length (P > 0.05), indicating that this regulatory mechanism is preserved in heart failure. Length-dependent assessment of twitch kinetics mirrored these findings; normalized dF/dt slowed down with increasing length of the muscle and was virtually identical in diseased tissue. This study shows for the first time that muscle length regulates cross-bridge kinetics in human myocardium under near-physiological conditions and that those kinetics are preserved in the right ventricular tissues of heart failure patients.

Latent process genes for cell differentiation are common decoders of neurite extension length.

A latent process involving signal transduction and gene expression is needed as a preparation step for cellular function. We previously found that nerve growth factor (NGF)-induced cell differentiation has a latent process, which is dependent on ERK activity and gene expression and required for subsequent neurite extension. A latent process can be considered as a preparation step that decodes extracellular stimulus information into cellular functions; however, molecular mechanisms of this process remain unknown. We identified Metrnl, Dclk1 and Serpinb1a as genes that are induced during the latent process (LP) with distinct temporal expression profiles and are required for subsequent neurite extension in PC12 cells. The LP genes showed distinct dependency on the duration of ERK activity, and they were also induced during the latent process of PACAP- and forskolin-induced cell differentiation. Regardless of neurotrophic factors, expression levels of the LP genes during the latent process (0-12 hours), but not phosphorylation levels of ERK, always correlated with subsequent neurite extension length (12-24 hours). Overexpression of all LP genes together, but not of each gene separately, enhanced NGF-induced neurite extension. The LP gene products showed distinct spatial localization. Thus, the LP genes appear to be the common decoders for neurite extension length regardless of neurotrophic factors, and they might function in distinct temporal and spatial manners during the latent process. Our findings provide molecular insight into the physiological meaning of the latent process as the preparation step for decoding information for future phenotypic change.

Influence of Socioeconomic Status on the Presence of Obstructive Coronary Artery Disease and Cardiovascular Outcomes in Patients Undergoing Invasive Coronary Angiography.

This retrospective study investigated the impact of socioeconomic status (SES) on patients at high risk of cardiovascular disease, focusing on obstructive coronary artery disease (CAD) presence and long-term cardiovascular outcomes in individuals undergoing invasive coronary angiography (ICA). Analyzing data from 9530 patients categorized by health insurance type (medical aid beneficiaries (MABs) as the low SES group; national health insurance beneficiaries (NHIBs) as the high SES group), this research explores the relationship between SES and outcomes. Despite a higher prevalence of cardiovascular risk factors, the MAB group exhibited similar rates of obstructive CAD compared to the NHIB group. However, over a median 3.5-year follow-up, the MAB group experienced a higher incidence of composite cardiovascular events, including cardiac death, acute myocardial infarction, coronary revascularization, and ischemic stroke, compared with the NHIB group (20.2% vs. 16.2%, p < 0.001). Multivariable Cox regression analysis, adjusting for potential confounders, revealed independently worse clinical outcomes for the MAB group (adjusted odds ratio 1.28; 95% confidence interval 1.07-1.54; p = 0.006). Despite comparable CAD rates, this study underscores the fact that individuals with low SES encounter an elevated risk of composite cardiovascular events, emphasizing the association between socioeconomic disadvantage and heightened susceptibility to cardiovascular disease, even among those already at high risk.

Precursor Ink Engineering to Implement Vacuum Extraction Method for Scalable Production of Perovskite Solar Cells.

Engineering perovskite precursor ink to widen the processing window is crucial to obtaining uniform, compact, and pinhole-free perovskite films at scale using industrially relevant solution coating techniques. Here, we introduce a ternary solvent system and systematically investigate the impacts of coordinating solvents, N-methyl-2-pyrrolidone (NMP) and N,N'-dimethylpropyleneurea (DMPU), on the physical properties of the slot-die-coated perovskite films and on the corresponding device performance. Tailoring NMP and DMPU concentrations in the precursor ink allows us to control the perovskite intermediate phase formation and widen the processing window, enabling the reproducible production of perovskite films with high photoelectrical quality at scale. Using the optimized precursor ink, we demonstrate slot-die-coated perovskite minimodules with power conversion efficiencies of 19 and 16% on 56 and 100 cm2 substrates, respectively.