Coexpression networks implicate human midfetal deep cortical projection neurons in the pathogenesis of autism.

Autism spectrum disorder (ASD) is a complex developmental syndrome of unknown etiology. Recent studies employing exome- and genome-wide sequencing have identified nine high-confidence ASD (hcASD) genes. Working from the hypothesis that ASD-associated mutations in these biologically pleiotropic genes will disrupt intersecting developmental processes to contribute to a common phenotype, we have attempted to identify time periods, brain regions, and cell types in which these genes converge. We have constructed coexpression networks based on the hcASD "seed" genes, leveraging a rich expression data set encompassing multiple human brain regions across human development and into adulthood. By assessing enrichment of an independent set of probable ASD (pASD) genes, derived from the same sequencing studies, we demonstrate a key point of convergence in midfetal layer 5/6 cortical projection neurons. This approach informs when, where, and in what cell types mutations in these specific genes may be productively studied to clarify ASD pathophysiology.

Ultrafast universal fabrication of configurable porous silicone-based elastomers by Joule heating chemistry.

Silicone-based elastomers (SEs) have been extensively applied in numerous cutting-edge areas, including flexible electronics, biomedicine, 5G smart devices, mechanics, optics, soft robotics, etc. However, traditional strategies for the synthesis of polymer elastomers, such as bulk polymerization, suspension polymerization, solution polymerization, and emulsion polymerization, are inevitably restricted by long-time usage, organic solvent additives, high energy consumption, and environmental pollution. Here, we propose a Joule heating chemistry method for ultrafast universal fabrication of SEs with configurable porous structures and tunable components (e.g., graphene, Ag, graphene oxide, TiO2, ZnO, Fe3O4, V2O5, MoS2, BN, g-C3N4, BaCO3, CuI, BaTiO3, polyvinylidene fluoride, cellulose, styrene-butadiene rubber, montmorillonite, and EuDySrAlSiOx) within seconds by only employing H2O as the solvent. The intrinsic dynamics of the in situ polymerization and porosity creation of these SEs have been widely investigated. Notably, a flexible capacitive sensor made from as-fabricated silicone-based elastomers exhibits a wide pressure range, fast responses, long-term durability, extreme operating temperatures, and outstanding applicability in various media, and a wireless human-machine interaction system used for rescue activities in extreme conditions is established, which paves the way for more polymer-based material synthesis and wider applications.

Post-transcriptional regulation of mouse neurogenesis by Pumilio proteins.

Despite extensive studies on mammalian neurogenesis, its post-transcriptional regulation remains under-explored. Here we report that neural-specific inactivation of two murine post-transcriptional regulators, Pumilio 1 (Pum1) and Pum2, severely reduced the number of neural stem cells (NSCs) in the postnatal dentate gyrus (DG), drastically increased perinatal apoptosis, altered DG cell composition, and impaired learning and memory. Consistently, the mutant DG neurospheres generated fewer NSCs with defects in proliferation, survival, and differentiation, supporting a major role of Pum1 and Pum2 in hippocampal neurogenesis and function. Cross-linking immunoprecipitation revealed that Pum1 and Pum2 bind to thousands of mRNAs, with at least 694 common targets in multiple neurogenic pathways. Depleting Pum1 and/or Pum2 did not change the abundance of most target mRNAs but up-regulated their proteins, indicating that Pum1 and Pum2 regulate the translation of their target mRNAs. Moreover, Pum1 and Pum2 display RNA-dependent interaction with fragile X mental retardation protein (FMRP) and bind to one another's mRNA. This indicates that Pum proteins might form collaborative networks with FMRP and possibly other post-transcriptional regulators to regulate neurogenesis.

Exploring the role of CBLB in acute myocardial infarction: transcriptomic, microbiomic, and metabolomic analyses.

BACKGROUND: Specific alterations in gut microbiota and metabolites have been linked to AMI, with CBLB potentially playing an essential role. However, the precise interactions remain understudied, creating a significant gap in our understanding. This study aims to address this by exploring these interactions in CBLB-intervened AMI mice using transcriptome sequencing, 16 S rDNA, and non-targeted metabolite analysis. METHODS: To probe the therapeutic potential and mechanistic underpinnings of CBLB overexpression in AMI, we utilized an integrative multi-omics strategy encompassing transcriptomics, metabolomics, and 16s rDNA sequencing. We selected these particular methods as they facilitate a holistic comprehension of the intricate interplay between the host and its microbiota, and the potential effects on the host's metabolic and gene expression profiles. The uniqueness of our investigation stems from utilizing a multi-omics approach to illuminate the role of CBLB in AMI, an approach yet unreported to the best of our knowledge. Our experimental protocol encompassed transfection of CBLB lentivirus-packaged vectors into 293T cells, followed by subsequent intervention in AMI mice. Subsequently, we conducted pathological staining, fecal 16s rDNA sequencing, and serum non-targeted metabolome sequencing. We applied differential expression analysis to discern differentially expressed genes (DEGs), differential metabolites, and differential microbiota. We performed protein-protein interaction analysis to identify core genes, and conducted correlation studies to clarify the relationships amongst these core genes, paramount metabolites, and key microbiota. RESULTS: Following the intervention of CBLB in AMI, we observed a significant decrease in inflammatory cell infiltration and collagen fiber formation in the infarcted region of mice hearts. We identified key changes in microbiota, metabolites, and DEGs that were associated with this intervention. The findings revealed that CBLB has a significant correlation with DEGs, differential metabolites and microbiota, respectively. This suggests it could play a pivotal role in the regulation of AMI. CONCLUSION: This study confirmed the potential of differentially expressed genes, metabolites, and microbiota in AMI regulation post-CBLB intervention. Our findings lay groundwork for future exploration of CBLB's role in AMI, suggesting potential therapeutic applications and novel research directions in AMI treatment strategies.

Multi-omics analysis identifies potential mechanisms by which high glucose accelerates macrophage foaming.

Atherosclerotic morbidity is significantly higher in the diabetic population. Hyperglycemia, a typical feature of diabetes, has been proven to accelerate foam cell formation. However, the molecular mechanisms behind this process remain unclear. In this study, LPS and IFN-γ were used to convert THP-1-derived macrophages into M1 macrophages, which were then activated with ox-LDL in either high glucose or normal condition. We identified lipids within macrophages by Oil red O staining and total cholesterol detection. The genes involved in lipid absorption, efflux, inflammation, and metabolism were analyzed using qRT-PCR. The mechanisms of high glucose-induced foam cell formation were further investigated through metabolomics and transcriptomics analysis. We discovered that high glucose speed up lipid accumulation in macrophages (both lipid droplets and total cholesterol increased), diminished lipid efflux (ABCG1 down-regulation), and aggravated inflammation (IL1B and TNF up-regulation). Following multi-omics analysis, it was determined that glucose altered the metabolic and transcriptional profiles of macrophages, identifying 392 differently expressed metabolites and 293 differentially expressed genes, respectively. Joint pathway analysis suggested that glucose predominantly disrupted the glycerolipid, glycerophospholipid, and arachidonic acid metabolic pathways in macrophages. High glucose in the glyceride metabolic pathway, for instance, suppressed the transcription of triglyceride hydrolase (LIPG and LPL), causing cells to deposit excess triglycerides into lipid droplets and encouraging foam cell formation. More importantly, high glucose triggered the accumulation of pro-atherosclerotic lipids (7-ketocholesterol, lysophosphatidylcholine, and glycerophosphatidylcholine). In conclusion, this work elucidated mechanisms of glucose-induced foam cell formation via a multi-omics approach.

Integrated analysis of miRNA-mRNA regulatory network and functional verification of miR-338-3p in coronary heart disease.

Coronary heart disease is a cardiovascular disease with high morbidity and mortality. Although great progress has been made in treatment, the prognosis is still very poor. Therefore, this project aims to screen potential diagnostic markers and therapeutic targets related to the progression of coronary heart disease. A total of 94 overlapping differentially expressed mRNAs and 70 differentially expressed miRNAs were identified from GSE20681, GSE12288, GSE49823, and GSE105449. Through a series of bioinformatics methods and experiment, we obtained 5 core miRNA-mRNA regulatory pairs, and selected miR-338-3p/RPS23 for functional analysis. Moreover, we found that RPS23 directly targets miR-338-3p by dual luciferase assay, western, and qPCR. And the expression of miR-338-3p and RPS23 is negatively correlated. The AUC value of miR-338-3p is 0.847. Downregulation of miR-338-3p can significantly inhibit the proliferation and migration of HUVEC. On the contrary, overexpression of miR-338-3p promoted the proliferation and migration of HUVEC. In addition, the interference of RPS23 expression can reverse the regulation of miR-338-3p on HUVEC proliferation. In conclusion, miR-338-3p/RPS23 may be involved in the progression of coronary heart disease, and miR-338-3p may be a diagnostic biomarker and therapeutic target for coronary heart disease.

Metallic Sandwiched-Aerogel Hybrids Enabling Flexible and Stretchable Intelligent Sensor.

Flexible strain sensors have been widely investigated with their rapid development in human-machine interfaces, soft robots, and medical care monitoring. Here, we report a new in situ catalytic strategy toward the fabrication of metallic aerogel hybrids, which are composed of vanadium nitride (VN) nanosheets decorated with well-defined vertically aligned carbon nanotube arrays (VN/CNTs) for the first time. In this architecture, the two-dimensional VN nanosheets as the main bone structure are favorable for the flexible devices due to their excellent structural compatibility during the repetitive deforming process. In addition, the sandwiched aerogel hybrids form highly conductive 3D network, affording outstanding sensitivity for the strain-responsive behaviors. Further, the VN/CNTs-based flexible strain sensors are successfully fabricated, showing a high gauge factor of 386 within a small strain of 10%, fast response, and extraordinary durability. The monitoring of physical signals and an actual real-time human-machine controlling system based on the sensors are also presented.

Reciprocal Connections Between Cortex and Thalamus Contribute to Retinal Axon Targeting to Dorsal Lateral Geniculate Nucleus.

The dorsal Lateral Geniculate Nucleus (dLGN) is the primary image-forming target of the retina and shares a reciprocal connection with primary visual cortex (V1). Previous studies showed that corticothalamic input is essential for the development of thalamocortical projections, but less is known about the potential role of this reciprocal connection in the development of retinal projections. Here, we show a deficit of retinal innervation in the dLGN around E18.5 in Tra2ß conditional knockout (cKO) "cortexless" mice, an age when apoptosis occurs along the thalamocortical tract and in some dLGN neurons. In vivo electrophysiology experiments in the dLGN further confirmed the loss of functional retinal input. Experiments with N-methyl-d-aspartic acid-induced V1 lesion as well as Fezf2 cKO mice confirmed that the disruption of connections between the dLGN and V1 lead to abnormal retinal projections to the dLGN. Interestingly, retinal projections to the ventral Lateral Geniculate Nucleus (vLGN) and Superior Colliculus (SC) were normal in all 3 mice models. Finally, we show that the cortexless mice had worse performance than control mice in a go-no go task with visual cues. Our results provide evidence that the wiring of visual circuit from the retina to the dLGN and V1 thereafter is coordinated at a surprisingly early stage of circuit development.

Factors Influencing Stent Restenosis After Percutaneous Coronary Intervention in Patients with Coronary Heart Disease: A Clinical Trial Based on 1-Year Follow-Up.

BACKGROUND This study observed the incidence of in-stent restenosis (ISR) after percutaneous coronary intervention (PCI) and discusses the risk factors of ISR based on clinical data, coronary angiography, and stent features, to provide a theoretical basis for the prevention and treatment of ISR. MATERIAL AND METHODS We selected 1132 cases who received stent implantation at the Shaanxi People's Hospital from June 2014 to June 2016 and were followed up by coronary angiography within 1 year. Based on coronary angiography, the cases were divided into ISR and non-ISR groups. ISR was defined as a reduction in lumen diameter by over 50% after PCI. The ISR group consisted of 93 cases and the non-ISR group consisted of 1039 cases. Medical history, biochemical indicators, features of coronary artery lesions, and stent status were analyzed retrospectively. Risk factors of ISR were identified by univariate and multivariate logistic regression analyses. RESULTS Among 1132 cases, 93 cases had ISR, with the overall incidence of 8.21%. Univariate and multivariate logistic regression analyses indicated that postoperative hypersensitive C-reactive protein (hs-CRP) levels (OR=2.309, 1.579-3.375 mg/L), postoperative homocysteine (HCY) levels (OR=2.202, 1.268-3.826 µmol/L), history of diabetes (OR=1.955,1.272-3.003), coronary bifurcation lesions (OR=3.785, 2.246-6.377), and stent length (OR=1.269, 1.179-1.365 mm) were independent risk factors of ISR after PCI (P<0.05). CONCLUSIONS Elevated hs-CRP and HCY levels after PCI, history of diabetes, coronary bifurcation lesions, and greater stent length were associated with a higher risk of ISR. Patients with a higher risk of ISR should receive routine follow-up and intense medication management after PCI to control the risk factors and to reduce ISR.

Microparticles from Patients with the Acute Coronary Syndrome Impair Vasodilatation by Inhibiting the Akt/eNOS-Hsp90 Signaling Pathway.

OBJECTIVES: Endothelial dysfunction is involved in the development of the acute coronary syndrome (ACS). Plasma microparticles(MPs) from other diseases have been demonstrated to initiate coagulation and endothelial dysfunction.However, whether MPs from ACS patients impair vasodilatation and endothelial function remains unclear. METHODS: Patients(n = 62) with ACS and healthy controls (n = 30) were recruited for MP isolation. Rat thoracic aortas were incubated with MPs from ACS patients or healthy controls to determine the effects of MPs on endothelial-dependent vasodilatation,the phosphorylation of Akt and endothelial nitric oxide synthase (eNOS), the interaction of eNOS with heat shock protein 90 (Hsp90), and nitric oxide (NO) and superoxide anion(O 2 ­ ) production. The origin of MPs was assessed by flow cytometry. RESULTS: MP concentrations were increased in patients with ACS compared with healthy controls. They were positively correlated with the degree of coronary artery stenosis. MPs from ACS patients impair endothelial-dependent vasodilatation, decrease both Akt and eNOS phosphorylation,decrease the interaction between eNOS and Hsp90,and decrease NO production but increase O 2 ­ generation in rat thoracic aortas. Endothelial-derived MPs and platelet-derived MPs made up nearly 75% of MPs. CONCLUSIONS: Our data indicate that MPs from ACS patients negatively affect endothelial-dependent vasodilatation via Akt/eNOS-Hsp90 pathways.

Highly sensitive detection of cancer antigen human epidermal growth factor receptor 2 using novel chicken egg yolk immunoglobulin.

Human epidermal growth factor receptor 2 (HER2) is an important biomarker that plays a crucial role in therapeutic decision-making for breast cancer patients. Ensuring the accuracy and reproducibility of HER2 assays by enzyme-linked immunosorbent assay (ELISA), western blot and immunohistochemistry (IHC) requires high sensitive and specific antibodies. Immunoglobulin Y (IgY) is a kind of avian antibody usually isolated from chicken egg yolks. Generation and use of IgY is of increasing interest in a wide variety of applications within the life sciences. In this study, IgY antibodies against two different truncated proteins of the extracellular domain (ECD) of human HER2 were produced, their sensitivity and specificity were evaluated. Specific IgYs were produced by hens immunized with the ECD proteins of human HER2 in long-standing immunization response and were isolated from yolks with a purity of 90% by water dilution, salt precipitations and ultrafiltration. The anti-HER2 IgYs were analytically validated for specificity by ELISA, western blot, immunocytochemistry and IHC. The IgYs bound desired targets in cells and fixed tissues and showed high affinity to HER2. The results demonstrated the viability of detection of HER2 with IgYs and showed promise for the using of IgYs in strict clinical validation.

Allitridin reduces I Kr current by disrupting the trafficking of human ether-à-go-go-related gene channels.

OBJECTIVES: To investigate the effects of allitridin on human ether-à-go-go-related gene (hERG) channels. METHODS: We used whole-cell patch clamping and laser confocal scanning microscopy to evaluate the effects of allitridin on hERG currents and the membrane expression of the hERG protein expressed in HEK 293 cells. RESULTS: The amplitude of IKr showed a concentration-dependent decrease with increasing allitridin concentration. Additionally, alterations in the gating properties of hERG channels were also confirmed. Allitridin does not alter the voltage- and time-dependent activation of hERG channels, the gating properties of hERG channel inactivation over time or the recovery from inactivation, but allitridin does cause alterations in the steady-state inactivation and the deactivation of hERG channels. We further evaluated the influence of allitridin on membrane expression of the hERG protein. Images of allitridin-treated cells showed a reduction in hERG protein on the membrane and retention in the cytoplasm. CONCLUSIONS: To the best of our knowledge this is the first study to show that allitridin reduces the IKr current by impairing the trafficking of hERG channels. The results may demonstrate that allitridin could be a promising candidate for the prevention and treatment of arrhythmia-related diseases.

TBR1 directly represses Fezf2 to control the laminar origin and development of the corticospinal tract.

The corticospinal (CS) tract is involved in controlling discrete voluntary skilled movements in mammals. The CS tract arises exclusively from layer (L) 5 projection neurons of the cerebral cortex, and its formation requires L5 activity of Fezf2 (Fezl, Zfp312). How this L5-specific pattern of Fezf2 expression and CS axonal connectivity is established with such remarkable fidelity had remained elusive. Here we show that the transcription factor TBR1 directly binds the Fezf2 locus and represses its activity in L6 corticothalamic projection neurons to restrict the origin of the CS tract to L5. In Tbr1 null mutants, CS axons ectopically originate from L6 neurons in a Fezf2-dependent manner. Consistently, misexpression of Tbr1 in L5 CS neurons suppresses Fezf2 expression and effectively abolishes the CS tract. Taken together, our findings show that TBR1 is a direct transcriptional repressor of Fezf2 and a negative regulator of CS tract formation that restricts the laminar origin of CS axons specifically to L5.

Identification of necroptosis-related diagnostic biomarkers in coronary heart disease.

Background: The implication of necroptosis in cardiovascular disease was already recognized. However, the molecular mechanism of necroptosis has not been extensively studied in coronary heart disease (CHD). Methods: The differentially expressed genes (DEGs) between CHD and control samples were acquired in the GSE20681 dataset downloaded from the GEO database. Key necroptosis-related DEGs were captured and ascertained by bioinformatics analysis techniques, including weighted gene co-expression network analysis (WGCNA) and two machine learning algorithms, while single-gene gene set enrichment analysis (GSEA) revealed their molecular mechanisms. The diagnostic biomarkers were selected via receiver operating characteristic (ROC) analysis. Moreover, an analysis of immune elements infiltration degree was carried out. Authentication of pivotal gene expression at the mRNA level was investigated in vitro utilizing quantitative real-time PCR (qRT-PCR). Results: A total of 94 DE-NRGs were recognized here, among which, FAM166B, NEFL, POLDIP3, PRSS37, and ZNF594 were authenticated as necroptosis-related biomarkers, and the linear regression model based on them presented an acceptable ability to different sample types. Following regulatory analysis, the ascertained biomarkers were markedly abundant in functions pertinent to blood circulation, calcium ion homeostasis, and the MAPK/cAMP/Ras signaling pathway. Single-sample GSEA exhibited that APC co-stimulation and CCR were more abundant, and aDCs and B cells were relatively scarce in CHD patients. Consistent findings from bioinformatics and qRT-PCR analyses confirmed the upregulation of NEFL and the downregulation of FAM166B, POLDIP3, and PRSS37 in CHD. Conclusion: Our current investigation identified 5 necroptosis-related genes that could be diagnostic markers for CHD and brought a novel comprehension of the latent molecular mechanisms of necroptosis in CHD.

miR-200a-3p overexpression alleviates diabetic cardiomyopathy injury in mice by regulating autophagy through the FOXO3/Mst1/Sirt3/AMPK axis.

Objective: Hyperglycemia and insulin resistance or deficiency are characteristic features of diabetes. Diabetes is accompanied by cardiomyocyte hypertrophy, fibrosis and ventricular remodeling, and eventually heart failure. In this study, we established a diabetic cardiomyopathy (DCM) mouse model to explore the role and mechanism of miR-200a-3p in DCM. Methods: We used db/db mice to simulate the animal model of DCM and the expression of miR-200a-3p was then examined by RT-qPCR. Tail vein injection of mice was done with rAAV-miR-200a-3p for 8 weeks, and cardiac function was assessed by cardiac ultrasound. The levels of myocardial tissue injury, fibrosis, inflammation, apoptosis and autophagy in mice were detected by histological staining, TUNEL and other molecular biological experiments. Results: miR-200a-3p expression levels were significantly decreased in the myocardium of DCM mice. Diabetic mice developed cardiac dysfunction and presented pathological changes such as myocardial injury, myocardial interstitial fibrosis, cardiomyocyte apoptosis, autophagy, and inflammation. Overexpression of miR-200a-3p expression significantly ameliorated diabetes induced-cardiac dysfunction and myocardial injury, myocardial interstitial fibrosis, cardiomyocyte apoptosis, and inflammation, and enhanced autophagy. Mechanistically, miR-200a-3p interacted with FOXO3 to promote Mst1 expression and reduce Sirt3 and p-AMPK expression. Conclusion: In type 2 diabetes, increased miR-200a-3p expression enhanced autophagy and participated in the pathogenic process of cardiomyopathy throug7 Mst1/Sirt3/AMPK axis regulation by its target gene FOXO3. This conclusion provides clues for the search of new gene targeted therapeutic approaches for diabetic cardiomyopathy.

Association of dietary cholesterol and dyslipidemia in Chinese health examinees.

BACKGROUND: The association between dietary cholesterol consumption and dyslipidemia is still in controversy. The study aims to evaluate whether dietary cholesterol intake associated with dyslipidemia and its components in Chinese health examinees. METHODS: A large-scale cross-sectional study was conducted among health examinees of in Shaanxi province. Totally of 8358 participants (3677 male and 4681 female) were included. Dietary cholesterol intake was assessed by validated food frequency questionnaire. Multivariable regression and restricted cubic spline models were used to capture the linear and non-linear association between dietary cholesterol and dyslipidemia. RESULTS: A total of 2429 (29.1%) subjects were newly diagnosed of dyslipidemia, the prevalence was 29.2% in male and 27.7% in female. Mean intake of dietary cholesterol was 213.7 mg/day. After adjusting for all potential confounders including demographics information and lifestyles, higher cholesterol consumption was related to lower risk of dyslipidemia, the ORs (95% CIs) across Q2 to Q4 group were 0.87 (0.60-1.26), 0.80 (0.55-1.18) and 0.61 (0.41-0.91) in female. With further controlling for nutrients principal components, a null association was observed between dietary cholesterol and dyslipidemia and serum lipids, regardless of gender. Results of restricted cubic splines showed that the risk of dyslipidemia decreased slowly until around 300 mg/day in men and 200 mg/day in women, although the non-linear association was not significant. CONCLUSIONS: The study suggested that dietary cholesterol consumption was not associated with dyslipidemia or serum lipids in Chinese health examinees, although a decreased risk was observed before the threshold points.

Efficacy and safety of drug-coated balloon combined with cutting balloon for side branch of true coronary bifurcation lesions: Study protocol for a multicenter, prospective, randomized controlled trial.

Background: Coronary bifurcation lesions are common of percutaneous coronary intervention (PCI), and the optimal interventional therapy strategy is still a matter of debate and remains a challenge for interventional cardiologists. The provisional stenting technique is still a preferred method for most bifurcation lesions, but restenosis of the side branch (SB) occurs in approximately 17-19% of cases. Therefore, the dilemma of reducing SB restenosis still exists, and further research on strategies to reduce restenosis for SB is necessary. Drug-coated balloon (DCB) can reduce clinical events in small vessel disease and in-stent restenosis. The efficacy and safety of DCB for SB of true coronary bifurcation lesions have not been fully investigated. A randomized comparison of DCB combined with cutting balloon angioplasty vs. cutting balloon angioplasty for SB has never been published. Methods and design: The purpose of this study is to explore the superiority of DCB combined with cutting balloon vs. cutting balloon angioplasty for SB after main vessel (MV) drug-eluting stent implantation of true coronary bifurcation lesions. This study is a multicenter, prospective, randomized controlled trial including 140 patients with true coronary bifurcation lesions. Patients will be randomized in a 1:1 manner to receive either DCB combined with cutting balloon or cutting balloon angioplasty for SB after MV drug-eluting stent implantation. The primary endpoint is the evaluation of late lumen loss (LLL) of SB at the 9-month follow-up. The secondary endpoints include procedural success during initial hospitalization, LLL of MV at the 9-month follow-up, binary angiographic restenosis in MV and SB at the 9-month follow-up, the proportion of patients with a final post-PCI quantitative flow ratio result ≤ 0.80 for SB at the 9-month follow-up, and major adverse cardiac events during the 24-month follow-up. Conclusions: This clinical trial will provide evidence as to whether DCB combined with cutting balloon for SB of true coronary bifurcation lesions is a superior treatment approach. Trial Registration Number: ChiCTR2000040475. Dissemination: The results of this clinical trial will be published in a peer-reviewed journal.

Artificial Intelligence Assisted Topographic Mapping System for Endoscopic Submucosal Dissection Specimens.

Background: Endoscopic submucosal dissection (ESD), a minimally invasive surgery used to treat early gastrointestinal malignancies, has been widely embraced around the world. The gross reconstruction of ESD specimens can facilitate a more precise pathological diagnosis and allow endoscopists to explore lesions thoroughly. The traditional method of mapping is time-consuming and inaccurate. We aim to design a topographic mapping system via artificial intelligence to perform the job automatically. Methods: The topographic mapping system was built using computer vision techniques. We enrolled 23 ESD cases at the Peking Union Medical College Hospital from September to November 2019. The reconstruction maps were created for each case using both the traditional approach and the system. Results: Using the system, the time saved per case ranges from 34 to 3,336 s. Two approaches revealed no significant variations in the shape, size, or tumor area. Conclusion: We developed an AI-assisted system that would help pathologists complete the ESD topographic mapping process rapidly and accurately.

The Alteration of HDL in Patients with AMI Inhibited Angiogenesis by Blocking ERK1/2 Activation.

Objective: High-density lipoprotein (HDL) was found vasoprotective, but numbers of patients with acute myocardial infarction (AMI) have normal or even high levels of pathological HDL (pHDL). So, we investigate the mechanism of pHDL in AMI patients on angiogenesis. Methods: HDL with normal levels from healthy subjects (nHDL, control group, n = 20) and patients with AMI (pHDL, experimental groups, n = 30) were obtained by super high speed centrifugation. Then, effects of HDL on proliferation, migration, angiogenesis, and expression of ERK1/2 and its phosphorylation in human umbilical vein endothelial cells (HUVEC) with or without PD98059 (inhibitor of ERK1/2) preincubation were detected. Results: Compared with the control group (nHDL), HDL from the experimental group (pHDL) significantly inhibited the phosphorylation of ERK1/2, proliferation, migration, and angiogenesis of HUVEC (P < 0.05), while these effects of HDL could substantially be blocked by preincubation of PD98059 (P < 0.05). Conclusion: HDL in AMI patients affects angiogenesis by inhibiting ERK1/2 activation free from HDL levels.

3D Printed Flexible Strain Sensors: From Printing to Devices and Signals.

The revolutionary and pioneering advancements of flexible electronics provide the boundless potential to become one of the leading trends in the exploitation of wearable devices and electronic skin. Working as substantial intermediates for the collection of external mechanical signals, flexible strain sensors that get intensive attention are regarded as indispensable components in flexible integrated electronic systems. Compared with conventional preparation methods including complicated lithography and transfer printing, 3D printing technology is utilized to manufacture various flexible strain sensors owing to the low processing cost, superior fabrication accuracy, and satisfactory production efficiency. Herein, up-to-date flexible strain sensors fabricated via 3D printing are highlighted, focusing on different printing methods based on photocuring and materials extrusion, including Digital Light Processing (DLP), fused deposition modeling (FDM), and direct ink writing (DIW). Sensing mechanisms of 3D printed strain sensors are also discussed. Furthermore, the existing bottlenecks and future prospects are provided for further progressing research.