Wavelength-Controlled Photoconductance Polarity Switching via Harnessing Defects in Doped PdSe2 for Artificial Synaptic Features.

Optoelectronic synapses are currently drawing significant attention as fundamental building blocks of neuromorphic computing to mimic brain functions. In this study, a two-terminal synaptic device based on a doped PdSe2 flake is proposed to imitate the key neural functions in an optical pathway. Due to the wavelength-dependent desorption of oxygen clusters near the intrinsic selenide vacancy defects, the doped PdSe2 photodetector achieves a high negative photoresponsivity of -7.8 × 103 A W-1 at 473 nm and a positive photoresponsivity of 181 A W-1 at 1064 nm. This wavelength-selective bi-direction photoresponse endows an all-optical pathway to imitate the fundamental functions of artificial synapses on a device level, such as psychological learning and forgetting capability, as well as dynamic logic functions. The underpinning photoresponse is further demonstrated on a flexible platform, providing a viable technology for neuromorphic computing in wearable electronics. Furthermore, the p-type doping results in an effective increase of the channel's electrical conductivity and a significant reduction in power consumption. Such low-power-consuming optical synapses with simple device architecture and low-dimensional features demonstrate tremendous promise for building multifunctional artificial neuromorphic systems in the future.

Polarization-Resolved Near-Infrared PdSe2 p-i-n Homojunction Photodetector.

Constructing high-quality homojunctions plays a pivotal role for the advancement of two-dimensional transition metal sulfide (TMDC) based optoelectronic devices. Here, a lateral PdSe2 p-i-n homojunction is constructed by electrostatic doping. Electrical measurements reveal that the homojunction diode exhibits a strong rectifying characteristic with a rectification ratio exceeding 104 and an ideality factor approaching 1. When functioning in photovoltaic mode, the device achieves a high responsivity of 1.1 A/W under 1064 nm illumination, with a specific detectivity of 1.3 × 1011 Jones and a high linearity of 45 dB. Benefiting from the lateral p-i-n structure, the junction capacitance is significantly reduced, and an ultrafast response (3/6 µs) is obtained. Additionally, the photodiode has the capability of polarization distinction due to the unique in-plane anisotropic structure of PdSe2, exhibiting a dichroic ratio of 1.6 at a 1064 nm wavelength. This high-performance polarization-sensitive near-infrared photodetector exhibits great potential in the next-generation optoelectronic applications.

Centimeter-Scale PdS2 Ultrathin Films with High Mobility and Broadband Photoresponse.

2D materials with mixed crystal phase will lead to the nonuniformity of performance and go against the practical application. Therefore, it is of great significance to develop a valid method to synthesize 2D materials with typical stoichiometry. Here, 2D palladium sulfides with centimeter scale and uniform stoichiometric ratio are synthesized via controlling the sulfurization temperature of palladium thin films. The relationship between sulfurization temperature and products is investigated in depth. Besides, the high-quality 2D PdS2 films are synthesized via sulfurization at the temperature of 450-550 °C, which would be compatible with back-end-of-line processes in semiconductor industry with considering of process temperature. The PdS2 films show an n-type semiconducting behavior with high mobility of 10.4 cm2 V-1 s-1 . The PdS2 photodetector presents a broadband photoresponse from 450 to 1550 nm. These findings provide a reliable way to synthesizing high-quality and large-area 2D materials with uniform crystal phase. The result suggests that 2D PdS2 has significant potential in future nanoelectronics and optoelectronic applications.

Phase-Selective Synthesis of Ultrathin FeTe Nanoplates by Controllable Fe/Te Atom Ratio in the Growth Atmosphere.

Phase controllable synthesis of 2D materials is of significance for tuning related electrical, optical, and magnetic properties. Herein, the phase-controllable synthesis of tetragonal and hexagonal FeTe nanoplates has been realized by a rational control of the Fe/Te ratio in a chemical vapor deposition system. Using density functional theory calculations, it has been revealed that with the change of the Fe/Te ratio, the formation energy of active clusters changes, causing the phase-controllable synthesis of FeTe nanoplates. The thickness of the obtained FeTe nanoplates can be tuned down to the 2D limit (2.8 nm for tetragonal and 1.4 nm for hexagonal FeTe). X-ray diffraction pattern, transmission electron microscopy, and high resolution scanning transmission electron microscope analyses exhibit the high crystallinity of the as-grown FeTe nanoplates. The two kinds of FeTe nanoflakes show metallic behavior and good electrical conductivity, featuring 8.44 × 104 S m-1 for 9.8 nm-thick tetragonal FeTe and 5.45 × 104 S m-1 for 7.6 nm-thick hexagonal FeTe. The study provides an efficient and convenient route for tailoring the phases of FeTe nanoplates, which benefits to study phase-sensitive properties, and may pave the way for the synthesis of other multiphase 2D nanosheets with controllable phases.

The role of intestinal microbiota in cardiovascular disease.

Accumulating evidence has indicated that intestinal microbiota is involved in the development of various human diseases, including cardiovascular diseases (CVDs). In the recent years, both human and animal experiments have revealed that alterations in the composition and function of intestinal flora, recognized as gut microflora dysbiosis, can accelerate the progression of CVDs. Moreover, intestinal flora metabolizes the diet ingested by the host into a series of metabolites, including trimethylamine N-oxide, short chain fatty acids, secondary bile acid and indoxyl sulfate, which affects the host physiological processes by activation of numerous signalling pathways. The aim of this review was to summarize the role of gut microbiota in the pathogenesis of CVDs, including coronary artery disease, hypertension and heart failure, which may provide valuable insights into potential therapeutic strategies for CVD that involve interfering with the composition, function and metabolites of the intestinal flora.

Molecular biomarkers in cardiac hypertrophy.

Cardiac hypertrophy is characterized by an increase in myocyte size in the absence of cell division. This condition is thought to be an adaptive response to cardiac wall stress resulting from the enhanced cardiac afterload. The pathogenesis of heart dysfunction, which is one of the primary causes of morbidity and mortality in elderly people, is often associated with myocardial remodelling caused by cardiac hypertrophy. In order to well understand the potential mechanisms, we described the molecules involved in the development and progression of myocardial hypertrophy. Increasing evidence has indicated that micro-RNAs are involved in the pathogenesis of cardiac hypertrophy. In addition, molecular biomarkers including vascular endothelial growth factor B, NAD-dependent deacetylase sirtuin-3, growth/differentiation factor 15 and glycoprotein 130, also play important roles in the development of myocardial hypertrophy. Knowing the regulatory mechanisms of these biomarkers in the heart may help identify new molecular targets for the treatment of cardiac hypertrophy.

Non-coding RNA involvement in the pathogenesis of diabetic cardiomyopathy.

In recent years, the incidence of diabetes has been increasing rapidly, which seriously endangers human health. Diabetic cardiomyopathy, an important cardiovascular complication of diabetes, is characterized by myocardial fibrosis, ventricular remodelling and cardiac dysfunction. It has been documented that mitochondrial dysfunction, oxidative stress, inflammatory response, autophagy, apoptosis, diabetic microangiopathy and myocardial fibrosis are implicated in the pathogenesis of diabetic cardiomyopathy. With the development of molecular biology technology, accumulating evidence demonstrates that non-coding RNAs (ncRNAs) are critically involved in the molecular mechanisms of diabetic cardiomyopathy. In this review, we summarize the pathological roles of three types of ncRNAs (microRNA, long ncRNA and circular RNA) in the progression of diabetic cardiomyopathy, which may provide valuable insights into the pathogenesis of diabetic cardiovascular complications.

Novel mouse models of oculopharyngeal muscular dystrophy (OPMD) reveal early onset mitochondrial defects and suggest loss of PABPN1 may contribute to pathology.

Oculopharyngeal muscular dystrophy (OPMD) is a late onset disease caused by polyalanine expansion in the poly(A) binding protein nuclear 1 (PABPN1). Several mouse models have been generated to study OPMD; however, most of these models have employed transgenic overexpression of alanine-expanded PABPN1. These models do not recapitulate the OPMD patient genotype and PABPN1 overexpression could confound molecular phenotypes. We have developed a knock-in mouse model of OPMD (Pabpn1+/A17) that contains one alanine-expanded Pabpn1 allele under the control of the native promoter and one wild-type Pabpn1 allele. This mouse is the closest available genocopy of OPMD patients. We show that Pabpn1+/A17 mice have a mild myopathic phenotype in adult and aged animals. We examined early molecular and biochemical phenotypes associated with expressing native levels of A17-PABPN1 and detected shorter poly(A) tails, modest changes in poly(A) signal (PAS) usage, and evidence of mitochondrial damage in these mice. Recent studies have suggested that a loss of PABPN1 function could contribute to muscle pathology in OPMD. To investigate a loss of function model of pathology, we generated a heterozygous Pabpn1 knock-out mouse model (Pabpn1+/Δ). Like the Pabpn1+/A17 mice, Pabpn1+/Δ mice have mild histologic defects, shorter poly(A) tails, and evidence of mitochondrial damage. However, the phenotypes detected in Pabpn1+/Δ mice only partially overlap with those detected in Pabpn1+/A17 mice. These results suggest that loss of PABPN1 function could contribute to but may not completely explain the pathology detected in Pabpn1+/A17 mice.

Diagnostic and prognostic value of biomarkers in acute myocardial infarction.

The incidence of acute myocardial infarction (AMI) has been increasing rapidly in recent years, seriously endangering human health. Cardiac biomarkers play critical roles in the diagnosis and prognosis of AMI. Troponin is a highly sensitive and specific biomarker for AMI diagnosis and can independently predict adverse cardiac events. Other biomarkers such as N-terminal B-type natriuretic peptide and C reactive protein are also valuable predictors of cardiovascular prognosis. Recently, several novel biomarkers have been identified for the diagnosis and risk assessment in patients with AMI. A multibiomarker approach can potentially enhance the diagnostic accuracy and provide more information for the early risk stratification of AMI. In this review, we will summarise the biomarkers discovered in recent years and focus on their diagnostic and prognostic value for patients with AMI.

Significant reduction of peripheral blood interleukin-35 and CD4+EBI3+ T cells, which are negatively correlated with an increase in the plasma IL-17 and cTnI level, in viral myocarditis patients.

INTRODUCTION: Viral myocarditis (VMC) has become an increasingly common heart disease that endangers human health. In the present study, the plasma interleukin-35 (IL-35) level and the percentage of CD4+EBI3+ T cells in VMC patients were detected to investigate the significance of changes in these parameters in the plasma of VMC patients and their association with the disease. MATERIAL AND METHODS: ELISA was performed to detect the plasma IL-35 level and the percentage of peripheral blood CD4+EBI3+ T cells in 40 VMC patients and in 20 healthy individuals. Moreover, the plasma IL-17 levels in the VMC patients and in the healthy individuals were detected using an ELISA, and the cardiac Troponin-I (cTnI) levels were detected using a chemiluminescent microparticle immunoassay to compare the differences in the groups. RESULTS: Plasma IL-35 level and the percentage of CD4 + EBI3 + T cells in acute phase VMC patients was lower than that in the healthy control group and the convalescent phase VMC patients. Additionally, the plasma IL-35 level in the VMC patients exhibited a negative correlation with the levels of cTnI and IL-17. The percentage of CD4+EBI3+ T cells also showed a negative correlation with the levels of cTnI and IL-17. CONCLUSIONS: The plasma IL-35 level and the percentage of CD4+EBI3+ T cells in VMC patients was reduced, and the amount of the decrease was associated with the severity of the disease. These results suggest that IL-35 and CD4+EBI3+ T might play important roles in the progression of VMC and could be used as indictors of the disease.

Prognostic Significance of Right Bundle Branch Block for Patients with Acute Myocardial Infarction: A Systematic Review and Meta-Analysis.

BACKGROUND: The aim of the current meta-analysis was to assess the effect of right bundle branch block (RBBB) on mortality outcome in patients with acute myocardial infarction (AMI). MATERIAL/METHODS: Embase, PubMed, and Cochrane databases were searched through January 2015 using the keywords "RBBB", "mortality", "AMI", "Coronary Heart Disease", and "cardiovascular". An odds ratio (OR) of RBBB on mortality endpoints was calculated using random-effects models. RESULTS: RBBB was associated with significantly increased overall mortality in patients with AMI. The OR of RBBB for deaths was 1.56 [95% confidence interval (CI), 1.44 to 1.68, p<0.001]. Moreover, RBBB showed a considerable effect on both in-hospital mortality (OR: 1.94, 95% CI: 1.60 to 2.37, p=0.002) and long-term mortality (OR: 1.49, 95% CI: 1.37 to 1.62, p<0.001). CONCLUSIONS: RBBB is associated with an increased risk of all-cause mortality and indicates a poorer prognosis in patients with AMI.

Independent prognostic value of left atrial function by two-dimensional speckle tracking imaging in patients with non -ST-segment-elevation acute myocardial infarction.

BACKGROUND: The objective of this study is to evaluate left atrial(LA) function and its prognostic value by two-dimensional speckle tracking echocardiography (STE) in patients with non-ST-segment-elevation acute myocardial infarction (NSTEAMI). METHODS: Global longitudinal LA S/SR data obtained by 2D speckle imaging with automated software (Echo PAC, GE Medical). RESULTS: Clinical variables and angiographic, echocardiographic, and STE parameters were studied in 65 patients with NSTEAMI (51 males and 14 females; mean age of 60.7 ± 9.8 years) who underwent elective PCI. The final study population consisted of 51 individuals (43 males and 8 females; mean age of 62.9 ± 11.1 years) and a 12 ± 3 months follow-up was performed. A total of 22 combined cardiovascular events(20 patients) occurred. With the use of Univariable Cox regression, all parameters were evaluated in the prediction of cardiac events, ischemic events, and/or cardiac death. According to ROC analysis, baseline mean global left atrial SRs (ROC area 0.82, p = 0.001) and baseline mean global left atrial SRe (ROC area 0.68, p = 0.036) were the only predictive variables. CONCLUSIONS: In patients with NSTEAMI, we found that the novel global strain parameter of left atrial function is a valuable predictor of combined cardiovascular events over conventional echocardiography and may therefore be an important clinical tool for risk stratification in the acute phase of NSTEAMI.

Serum Soluble Semaphorin 4D is Associated with Left Atrial Diameter in Patients with Atrial Fibrillation.

BACKGROUND: The aim of this study was to evaluate the serum soluble semaphorin 4D (sSema4D) in patients with atrial fibrillation and to investigate the relationship of serum sSema4D with left atrial diameter (LAD). MATERIAL AND METHODS: We studied a total of 113 patients who were subdivided into paroxysmal and non-paroxysmal (included persistent and permanent) atrial fibrillation groups, respectively. Another 55 subjects without atrial fibrillation were enrolled as the healthy control group. Serum levels of soluble semaphorin 4D (Sema4D) were measured in all subjects using the enzyme-labeled immunosorbent assay method. We also evaluated the coagulation parameters and left atrial diameters. RESULTS: Patients with paroxysmal and non-paroxysmal atrial fibrillation had significantly higher sSema4D level compared with controls (8.50±2.19 ng/mL and 9.30±2.28 ng/mL vs. 6.56±1.27 ng/ml, P<0.05). Serum sSema4D concentrations were elevated in patients with non-paroxysmal atrial fibrillation compared to those with paroxysmal atrial fibrillation (P<0.001). The level of sSema4D was positively correlated with LAD (r=0.606, P<0.001). Multivariate logistic regression analysis revealed that serum sSema4D, LAD, male sex, heart rate, hypertension, and coronary artery disease were associated with atrial fibrillation (P<0.05). CONCLUSIONS: Serum sSema4D levels are increased in patients with atrial fibrillation and are independently associated with atrial remodeling.

Serum adropin level in patients with stable coronary artery disease.

OBJECTIVES: Adropin is a newly identified secreted protein implicated in the regulation of insulin sensitivity and vascular endothelial function. Recent studies have shown that lower serum adropin level is related to acute myocardial infarction and coronary atherosclerosis. The primary objective of this study was to ascertain the association of serum adropin level with stable coronary artery disease (SCAD). METHODS: We prospectively recruited a cohort of patients with SCAD and similar sample size subjects without coronary artery disease as controls. Their serum adropin levels were measured, and the severity of coronary atherosclerosis in SCAD patients was quantified with the syntax score. RESULTS: A total of 116 patients with SCAD and 116 control subjects without coronary artery disease were recruited. Patients with SCAD had lower serum adropin levels when compared with the controls (59.2±19.3 versus 70.0±18.2 pg/mL, P<0.001). The multiple logistic regression revealed that low serum adropin level was a significant predictor of SCAD (AOR 0.976, 95% CI 0.960-0.992; p=0.003). Through the gamma regression model, it was further revealed that serum adropin level is significantly associated with syntax score (coefficient: -0.134, 95% CI: -0.212- -0.056; p=0.001). CONCLUSIONS: Low serum adropin level is a significant predictor of SCAD. It is also associated with syntax score, thus indicating the close relationship between adropin and coronary atherosclerosis.

[Correlation of serum adropin level with coronary artery disease].

OBJECTIVE: To explore the correlation of serum adropin level with coronary artery disease (CAD). METHODS: According to coronary angiography, 356 consecutive patients with chest complaints from January 2011 to July 2012 were divided into 2 groups of CAD (n = 264, with CAD) and control (n = 92, without CAD). The serum adropin level and other CAD related metabolic parameters were measured and SYNTAX score was calculated. RESULTS: Serum adropin level was significantly lower in group CAD than that in control group ((56 ± 15) vs (83 ± 10) ng/L, P < 0.01).Serum adropin levels in high, mild, low SYNTAX score group were (60 ± 22),(56 ± 12),(54 ± 10) ng/L respectively, and there was no significant difference among 3 groups(P = 0.116). Multivariate regression analysis revealed that adropin was an independent risk factor for CAD (OR = 0.849, 95%CI:0.817-0.882, P < 0.01). CONCLUSIONS: Lower serum adropin level is significantly associated with CAD. Thus it indicates a possible role of adropin in the prevention of CAD.

Study on the Preparation and Properties of Vegetation Lightweight Porous Concrete.

The objective of this study is to formulate vegetated light porous concrete (VLPC) through the utilization of various cementing materials, the design of porosity, and the incorporation of mineral additives. Subsequently, the study aims to assess and analyze key properties, including the bulk density, permeability coefficient, mechanical characteristics, and alkalinity. The findings indicate a linear decrease in the volume weight of VLPC as the designed porosity increases. While higher design porosity elevates the permeability coefficient, the measured effective porosity closely aligns with the design values. The examined VLPC exhibits a peak compressive strength of 17.7 MPa and a maximum bending strength of 2.1 MPa after 28 days. Notably, an escalation in porosity corresponds to a decrease in both the compressive and the bending strength of VLPC. Introducing mineral additives, particularly silicon powder, is shown to be effective in enhancing the strength of VLPC. Furthermore, substituting slag sulfonate cement for ordinary cement significantly diminishes the alkalinity of VLPC, resulting in a pH below 8.5 at 28 days. Mineral additives also contribute to a reduction in the pH of concrete. Among them, silica fume, fly ash, fly ash + slag powder, and slag powder exhibit a progressively enhanced alkaline reduction effect.

The Mechanical Performance and Reaction Mechanism of Slag-Based Organic-Inorganic Composite Geopolymers.

A series of organic-inorganic composite geopolymer paste samples were prepared with slag-based geopolymer and three types of hydrophilic organic polymers, i.e., PVA, PAA, and CPAM, by ordinary molding and pressure-mixing processes. The reaction mechanism between slag-based geopolymer and organic polymers was studied by FT-IR, NMR, and SEM techniques. The experimental results showed that the slag-based geopolymer with the addition of 3% PVA presented the highest 28-day flexural strength of 19.0 MPa by means of a pressure-mixing process and drying curing conditions (80 °C, 24 h) compared with the geopolymers incorporating PAA and CPAM. A more homogeneous dispersion morphology was also observed by BSE and SEM for the 3% PVA-incorporated slag-based geopolymer. The FT-IR testing results confirmed the formation of a C-O-Si (Al) bond between PVA and the slag-based geopolymer. The deconvolution of the Q3 and Q2(1Al) species obtained by 29Si NMR testing manifested the addition of PVA and increased the length of the silicon backbone chain in the geopolymer. These findings confirmed that a composite geopolymer with high toughness can be produced based on the interpenetrating network structure formed between organic polymers and inorganic geopolymer.

Layer-dependent ultrafast carrier dynamics of PdSe2 investigated by photoemission electron microscopy.

For atomically thin two-dimensional materials, variations in layer thickness can result in significant changes in the electronic energy band structure and physicochemical properties, thereby influencing the carrier dynamics and device performance. In this work, we employ time- and energy-resolved photoemission electron microscopy to reveal the ultrafast carrier dynamics of PdSe2 with different layer thicknesses. We find that for few-layer PdSe2 with a semiconductor phase, an ultrafast hot carrier cooling on a timescale of approximately 0.3 ps and an ultrafast defect trapping on a timescale of approximately 1.3 ps are unveiled, followed by a slower decay of approximately tens of picoseconds. However, for bulk PdSe2 with a semimetal phase, only an ultrafast hot carrier cooling and a slower decay of approximately tens of picoseconds are observed, while the contribution of defect trapping is suppressed with the increase of layer number. Theoretical calculations of the electronic energy band structure further confirm the transition from a semiconductor to a semimetal. Our work demonstrates that TR- and ER-PEEM with ultrahigh spatiotemporal resolution and wide-field imaging capability has great advantages in revealing the intricate details of ultrafast carrier dynamics of nanomaterials.

Glycolytic enzyme PFKL governs lipolysis by promoting lipid droplet-mitochondria tethering to enhance ß-oxidation and tumor cell proliferation.

Lipid droplet tethering with mitochondria for fatty acid oxidation is critical for tumor cells to counteract energy stress. However, the underlying mechanism remains unclear. Here, we demonstrate that glucose deprivation induces phosphorylation of the glycolytic enzyme phosphofructokinase, liver type (PFKL), reducing its activity and favoring its interaction with perilipin 2 (PLIN2). On lipid droplets, PFKL acts as a protein kinase and phosphorylates PLIN2 to promote the binding of PLIN2 to carnitine palmitoyltransferase 1A (CPT1A). This results in the tethering of lipid droplets and mitochondria and the recruitment of adipose triglyceride lipase to the lipid droplet-mitochondria tethering regions to engage lipid mobilization. Interfering with this cascade inhibits tumor cell proliferation, promotes apoptosis and blunts liver tumor growth in male mice. These results reveal that energy stress confers a moonlight function to PFKL as a protein kinase to tether lipid droplets with mitochondria and highlight the crucial role of PFKL in the integrated regulation of glycolysis, lipid metabolism and mitochondrial oxidation.

Overexpression of APRIN inhibits differentiation and proliferation and promotes apoptosis in P19 embryonal carcinoma cells.

We have previously demonstrated that androgen-induced proliferation inhibitor (APRIN) expression was upregulated in ventricular septum tissues from patients with ventricular septal defect (VSD). The present study was designed to investigate the effects of APRIN on P19 cell differentiation, proliferation and apoptosis. In this study, we established a stable APRIN-overexpressing P19 embryonal carcinoma cell line that can differentiate into myocardial cells when treated with 1 % dimethyl sulfoxide. Our data showed that mRNA expressions of myocardial cell differentiation-related genes (such as cTnT, α-MHC, GATA4, and MEF2C) in the APRIN-overexpressing P19 cells were downregulated compared to the empty-vector controls. Our findings also indicated that P19 cells overexpressing APRIN had a reduced growth rate and a decreased S phase of the cell cycle. Moreover, the apoptotic rate in P19 cells overexpressing APRIN was significantly higher than that in the controls. In conclusion, our study demonstrates that overexpression of APRIN inhibits differentiation and proliferation and promotes apoptosis in P19 cells, suggesting that APRIN may be involved in the pathogenesis of VSD.