Miracle-dz/UniFAR-FTUs huggingface dataset:
Study on the surface characteristic of PTFE after atmospheric plasma treatment

This paper discuss the preliminary result for surface characteristic of polytetrafloroethylene (PTFE) after atmospheric plasma treatment. An atmospheric pressure plasma system has been assembled and the effect of helium plasma treatment on PTFE surfaces was studied by scanning electron microscope (SEM). The contact angle of PTFE surface after helium plasma treatment were measured and recorded. Results showed that the contact angle of sample decreased with the increase of helium plasma treatment time. Also, relative increment of surface hydrophilicity could be optimized by the plasma conditions. Based on the preliminary findings, atmospheric plasma with helium as a working gas treatment on the PTFE surfaces improved the surface hydrophilicity and increased the surface area of the sample.
Increased expression of the HDAC9 gene is associated with antiestrogen resistance of breast cancers

Estrogens play a pivotal role in breast cancer etiology, and endocrine therapy remains the main first line treatment for estrogen receptor‐alpha (ERα)‐positive breast cancer. ER are transcription factors whose activity is finely regulated by various regulatory complexes, including histone deacetylases (HDACs). Here, we investigated the role of HDAC9 in ERα signaling and response to antiestrogens in breast cancer cells. Various Michigan Cancer Foundation‐7 (MCF7) breast cancer cell lines that overexpress class IIa HDAC9 or that are resistant to the partial antiestrogen 4‐hydroxy‐tamoxifen (OHTam) were used to study phenotypic changes in response to ER ligands by using transcriptomic and gene set enrichment analyses. Kaplan–Meier survival analyses were performed using public transcriptomic datasets from human breast cancer biopsies. In MCF7 breast cancer cells, HDAC9 decreased ERα mRNA and protein expression and inhibited its transcriptional activity. Conversely, HDAC9 mRNA was strongly overexpressed in OHTam‐resistant MCF7 cells and in ERα‐negative breast tumor cell lines. Moreover, HDAC9‐overexpressing cells were less sensitive to OHTam antiproliferative effects compared with parental MCF7 cells. Several genes (including MUC1, SMC3 and S100P) were similarly deregulated in OHTam‐resistant and in HDAC9‐overexpressing MCF7 cells. Finally, HDAC9 expression was positively associated with genes upregulated in endocrine therapy‐resistant breast cancers and high HDAC9 levels were associated with worse prognosis in patients treated with OHTam. These results demonstrate the complex interactions of class IIa HDAC9 with ERα signaling in breast cancer cells and its effect on the response to hormone therapy.
Activation of the macroautophagy pathway by Yersinia enterocolitica promotes intracellular multiplication and egress of yersiniae from epithelial cells

The virulence strategy of pathogenic Yersinia spp. involves cell‐invasive as well as phagocytosis‐preventing tactics to enable efficient colonisation of the host organism. Enteropathogenic yersiniae display an invasive phenotype in early infection stages, which facilitates penetration of the intestinal mucosa. Here we show that invasion of epithelial cells by Yersinia enterocolitica is followed by intracellular survival and multiplication of a subset of ingested bacteria. The replicating bacteria were enclosed in vacuoles with autophagy‐related characteristics, showing phagophore formation, xenophagy, and recruitment of cytoplasmic autophagosomes to the bacteria‐containing compartments. The subsequent fusion of these vacuoles with lysosomes and concomitant vesicle acidification were actively blocked by Yersinia. This resulted in increased intracellular proliferation and detectable egress of yersiniae from infected cells. Notably, deficiency of the core autophagy machinery component FIP200 impaired the development of autophagic features at Yersinia‐containing vacuoles as well as intracellular replication and release of bacteria to the extracellular environment. These results suggest that Y. enterocolitica may take advantage of the macroautophagy pathway in epithelial cells to create an autophagosomal niche that supports intracellular bacterial survival, replication, and, eventually, spread of the bacteria from infected cells.
A Population-Based Study of Effects of Genetic Loci on Orofacial Clefts

Prior genome-wide association studies for oral clefts have focused on clinic-based samples with unclear generalizability. Prior samples were also small for investigating effects by cleft type and exclusively studied isolated clefts (those occurring without other birth defects). We estimated the effects of 17 top loci on cleft types in both isolated and nonisolated cases in the largest consortium to date of European-descent population-based studies. Our analytic approach focused on a mother-child dyad case-control design, but it also allowed analyzing mother-only or child-only genotypes to maximize power. Our total sample included 1,875 cases with isolated clefts, 459 cases with nonisolated clefts, and 3,749 controls. After correcting for multiple testing, we observed significant associations between fetal single-nucleotide polymorphisms (SNPs) at IRF6, PAX7, 8q21.3, 8q24, KIAA1598-VAX1, and MAFB and isolated cleft lip only (CLO) and cleft lip and palate (CLP). Significant associations were observed between isolated CLO and fetal SNPs near TPM1 and NOG1 and between CLP and fetal SNPs at ABCA4-ARHGAP29, THADA, FOXE1, and SPRY2. Overall, effects were similar for isolated CLO and CLP, except for ABCA4-ARHGAP29. A protective effect was observed for the fetal NOG1 SNP on cleft palate only, opposite in direction to the effect on CLO. For most fetal SNPs, a dose-response allelic effect was observed. No evidence of parent-of-origin or maternal genome effects was observed. Overall, effect direction and magnitude were similar between isolated and nonisolated clefts, suggesting that several loci are modifiers of cleft risk in both isolated and nonisolated forms. Our results provide reliable estimates of the effects of top loci on risks of oral clefts in a population of European descent.
Open source HLS tools: A stepping stone for modern electronic CAD

This paper presents a comprehensive survey on commonly used High-Level synthesis (HLS) tools that are available as open source. The HLS tools considered in this paper include Bambu, GAUT, Icarus Verilog, LegUp, and MyHDL. This paper also presents the process steps involved in each tool in detail and the major issues and challenges that are to be addressed in these tools in order to make the tools to become the most suitable choice for modern electronic system design.
Crystal structure of ATP sulfurylase from Saccharomyces cerevisiae, a key enzyme in sulfate activation

ATP sulfurylases (ATPSs) are ubiquitous enzymes that catalyse the primary step of intracellular sulfate activation: the reaction of inorganic sulfate with ATP to form adenosine‐5′‐phosphosulfate (APS) and pyrophosphate (PPi). With the crystal structure of ATPS from the yeast Saccharomyces cerevisiae, we have solved the first structure of a member of the ATP sulfurylase family. We have analysed the crystal structure of the native enzyme at 1.95 Å resolution using multiple isomorphous replacement (MIR) and, subsequently, the ternary enzyme product complex with APS and PPi bound to the active site. The enzyme consists of six identical subunits arranged in two stacked rings in a D3 symmetric assembly. Nucleotide binding causes significant conformational changes, which lead to a rigid body structural displacement of domains III and IV of the ATPS monomer. Despite having similar folds and active site design, examination of the active site of ATPS and comparison with known structures of related nucleotidylyl transferases reveal a novel ATP binding mode that is peculiar to ATP sulfuryl‐ases.
Assessment of CSP-based two-stage channel selection approach and local transformation-based feature extraction for classification of motor imagery/movement EEG data

Abstract The main idea of brain-computer interfaces (BCIs) is to facilitate the lives of patients having difficulties to move their muscles due to a disorder of their motor nervous systems but healthy cognitive functions. BCIs are usually electroencephalography (EEG)-based, and the success of the BCIs relies on the precision of signal preprocessing, detection of distinctive features, usage of suitable classifiers and selection of effective channels. In this study, a two-stage channel selection and local transformation-based feature extraction are proposed for the classification of motor imagery/movement tasks. In the first stage of the channel selection, the channels were combined according to the neurophysiological information about brain functions acquired from the literature, then averaged and a single channel was formed. In the second stage, selective channels were specified with the common spatial pattern-linear discriminant analysis (CSP-LDA)-based sequential channel removal. After the channel selection phase, the feature extraction was carried out with local transformation-based methods (LTBM): local centroid pattern (LCP), one-dimensional-local gradient pattern (1D-LGP), local neighborhood descriptive pattern (LNDP) and one-dimensional-local ternary pattern (1D-LTP). The distinctions and deficiencies of these methods were compared with other methods in the literature and the classification performances of the k-nearest neighbor (k-NN) and the support vector machines (SVM) were evaluated. As a result, the proposed methods yielded the highest average classification accuracies as 99.34%, 95.95%, 98.66% and 99.90% with the LCP, 1D-LGP, LNDP and 1D-LTP when using k-NN, respectively. The two-stage channel selection and 1D-LTP method showed promising results for recognition of motor tasks. The LTBM will contribute to the development of EEG-based BCIs with the advantages of high classification accuracy, easy implementation and low computational complexity.
Behavioural Plasticity by Eastern Grey Kangaroos in Response to Human Behaviour

Simple Summary Many species of wildlife live in landscapes they share with people. Some exploit resources and protection provided by close proximity to people, while others learn to avoid people all together. In this study, we sought to test whether individuals from a population of eastern grey kangaroos altered grouping and spacing behaviour in response to human presence, depending upon whether the intent and actions of those people were benign or harmful. Under harmful conditions, kangaroos failed to form larger groups when far from cover, however, this typical antipredator grouping behaviour persisted when human disturbances were benign. These differences in grouping and spacing behaviour suggest that kangaroos can exhibit bidirectional behavioural plasticity at fine scales, a trait that may confer adaptive advantages when sharing landscapes with humans. Abstract Sharing landscapes with humans is an increasingly fraught challenge for wildlife across the globe. While some species benefit from humans by exploiting novel opportunities (e.g., provision of resources or removal of competitors or predators), many wildlife experience harmful effects, either directly through persecution or indirectly through loss of habitat. Consequently, some species have been shown to be attracted to human presence while others avoid us. For any given population of a single species, though, the question of whether they can recognise and change their response to human presence depending on the type of human actions (i.e., either positive or negative) has received little attention to date. In this study, we chose to examine the behavioural plasticity within a single population of eastern grey kangaroos (Macropus giganteus) to both positive and negative human activity. Within a relatively small and contiguous landscape, we identified areas where kangaroos experience a combination of either low and high frequencies of benign and harmful human disturbances. From six sampling sessions over five months, we found that density and group sizes were higher where humans acted benignly towards them, and that these groups had higher representations of sub-adults and juveniles than where humans had harmful intentions. Importantly, we found that the vital antipredator strategy of increasing group size with distance from cover was not detectable at sites with low and high levels of harm. Our findings suggest that these kangaroos are recognising and adjusting their behavioural response to humans at fine spatial scales, a plasticity trait that may be key to the survival of these species in human dominated landscapes.
Influence of Local Myocardial Infarction on Endothelial Function, Neointimal Progression, and Inflammation in Target and Non-Target Vascular Territories in a Porcine Model of Acute Myocardial Infarction

Background Patients with acute myocardial infarction (AMI) have worse clinical outcomes than those with stable coronary artery disease despite revascularization. Non-culprit lesions of AMI also involve more adverse cardiovascular events. This study aimed to investigate the influence of AMI on endothelial function, neointimal progression, and inflammation in target and non-target vessels. Methods In castrated male pigs, AMI was induced by balloon occlusion and reperfusion into the left anterior descending artery (LAD). Everolimus-eluting stents (EES) were implanted in the LAD and left circumflex (LCX) artery 2 days after AMI induction. In the control group, EES were implanted in the LAD and LCX in a similar fashion without AMI induction. Endothelial function was assessed using acetylcholine infusion before enrollment, after the AMI or sham operation, and at 1 month follow-up. A histological examination was conducted 1 month after stenting. Results A total of 10 pigs implanted with 20 EES in the LAD and LCX were included. Significant paradoxical vasoconstriction was assessed after acetylcholine challenge in the AMI group compared with the control group. In the histologic analysis, the AMI group showed a larger neointimal area and larger area of stenosis than the control group after EES implantation. Peri-strut inflammation and fibrin formation were significant in the AMI group without differences in injury score. The non-target vessel of the AMI also showed similar findings to the target vessel compared with the control group. Conclusion In the pig model, AMI events induced endothelial dysfunction, inflammation, and neointimal progression in the target and non-target vessels.
Effect of Fatigue Three-Needle acupuncture therapy in a patient with cancer-related fatigue

Rationale: Cancer-related fatigue (CRF) is a persistent, subjective sense of tiredness or exhaustion experienced by cancer patients. Acupuncture is a safe and feasible optional method for adjunctive treatment for CRF. However, the therapeutic effect of the Fatigue Three-Needle acupuncture therapy in patients with CRF has not been well-investigated. Patient concerns: A 53-year-old woman had been experiencing fatigue since the radical resection of sigmoid colon cancer 2 years ago, for which she underwent traditional Chinese medicine treatment. Diagnosis: After some review, she was diagnosed with CRF. Although she underwent traditional Chinese medicine treatment, she continued experiencing fatigue symptoms. Interventions: When she visited our hospital, she was treated with the Fatigue Three-Needle for 3 sessions a week, 30 minutes per session. Outcomes: After 4 weeks of treatment, the patient felt refreshed and relieved from the fatigue. Lessons: The finding from this case provides further evidence for the therapeutic benefits of the Fatigue Three-Needle therapy for patients with CRF, suggesting that acupuncture treatment with the Fatigue Three-Needle is an effective option for patients with CRF.
Mining and validating the expression pattern and prognostic value of acetylcholine receptors in non-small cell lung cancer

Abstract Acetylcholine receptors (AChRs), including nicotinic acetylcholine receptors (nAChRs) and muscarinic acetylcholine receptors (mAChRs), are highly expressed in bronchial epithelial cells. We used The Cancer Genome Atlas (TCGA) data set to evaluate the expression pattern and prognostic value of the AChR gene family in non-small cell lung cancer (NSCLC). The mined data was validated by quantitative real-time polymerase chain reaction (qRT-PCR) and immunohistochemistry (IHC). The survival analysis of TCGA data set showed that only CHRNA7 in the AChR gene family affected prognosis in both lung adenocarcinoma and lung squamous cell carcinoma. Furthermore, qRT-PCR proved that CHRNA7 was significantly upregulated in tumor tissues compared with matched normal tissues at mRNA level (P = .001). The expression level of &agr;7 nAChR (encoded by CHRNA7) in 141 patients was measured by IHC and a high expression of &agr;7 nAChR was associated with unfavorable prognosis (P = .008). Multivariate analysis showed that &agr;7 nAChR was an independent prognostic factor (HR = 2.041; 95% CI 1.188-3.506; P = .007). &agr;7 nAChR was upregulated in NSCLC and was associated with unfavorable prognosis. This gene may be a potential target for lung cancer treatment.
Epigallocatechin gallate reduces vascular inflammation in db/db mice possibly through an NF-κB-mediated mechanism.

SCOPE Hyperglycemia-induced vascular inflammation resulting in the adhesion of monocytes to endothelium is a key event in the pathogenesis of atherosclerosis in diabetes. We investigated whether epigallocatechin gallate (EGCG), a major catechin found in green tea, reduces vascular inflammation in diabetes. METHODS AND RESULTS Human aortic endothelial cells (HAEC) were pretreated with green tea catechins before the addition of high glucose (25 mM) for 72 h. EGCG at physiologically achievable concentration (1 μM) significantly inhibited high glucose induced adhesion of monocytes to HAEC both in static and under flow conditions. EGCG also reduced nuclear factor κB (NF-κB) regulated transcriptional activity in ECs. Six-week-old diabetic db/db mice were fed a diet containing 0% or 0.1% EGCG for 8 weeks. ECs were isolated from aortic vessels of db/db, db/db-EGCG, and control db/+ mice. EGCG supplementation greatly suppressed diabetes-increased monocytes adhesion to ECs, which is associated with reduced circulating levels of chemokines, and reduced secretions of chemokines and adhesion molecules by aortic ECs from db/db-EGCG mice. EGCG treatment reduced nuclear translocation of NF-κB p65 in aortic vessels, decreased blood pressure and serum concentrations of cholesterol and triglycerides in db/db-EGCG mice. CONCLUSION EGCG may have a direct protective effect against vascular inflammation in diabetes.
Clinical Targeted Next-Generation sequencing Panels for Detection of Somatic Variants in Gliomas

Purpose Targeted next-generation sequencing (NGS) panels for solid tumors have been useful in clinical framework for accurate tumor diagnosis and identifying essential molecular aberrations. However, most cancer panels have been designed to address a wide spectrum of pan-cancer models, lacking integral prognostic markers that are highly specific to gliomas. Materials and Methods To address such challenges, we have developed a glioma-specific NGS panel, termed “GliomaSCAN,” that is capable of capturing single nucleotide variations and insertion/deletion, copy number variation, and selected promoter mutations and structural variations that cover a subset of intron regions in 232 essential glioma-associated genes. We confirmed clinical concordance rate using pairwise comparison of the identified variants from whole exome sequencing (WES), immunohistochemical analysis, and fluorescence in situ hybridization. Results Our panel demonstrated high sensitivity in detecting potential genomic variants that were present in the standard materials. To ensure the accuracy of our targeted sequencing panel, we compared our targeted panel to WES. The comparison results demonstrated a high correlation. Furthermore, we evaluated clinical utility of our panel in 46 glioma patients to assess the detection capacity of potential actionable mutations. Thirty-two patients harbored at least one recurrent somatic mutation in clinically actionable gene. Conclusion We have established a glioma-specific cancer panel. GliomaSCAN highly excelled in capturing somatic variations in terms of both sensitivity and specificity and provided potential clinical implication in facilitating genome-based clinical trials. Our results could provide conceptual advance towards improving the response of genomically guided molecularly targeted therapy in glioma patients.
Casein kinase 1 family regulates PRR5 and TOC1 in the Arabidopsis circadian clock

Significance The mechanisms of eukaryotic circadian clocks rely on transcriptional-translational feedback loops (TTFLs), but components of TTFLs from different phylogenetic lineages are thought to be evolutionarily diverse. Posttranslational modification is also required for clock function, but those within the plant clock are less studied, likely due to genetic redundancy. Here, we identified a small synthetic molecule that lengthened the Arabidopsis circadian period. Using an affinity probe, we found that the molecule inhibited multiple members of the casein kinase I (CK1) family, which is also essential in animal, fungal, and algal clocks. The CK1 family modulated plant-specific clock-associated transcriptional repressors. With other studies, our results established the prominent role of CK1 family to control circadian clocks among vastly divergent phylogenetic lineages. The circadian clock provides organisms with the ability to adapt to daily and seasonal cycles. Eukaryotic clocks mostly rely on lineage-specific transcriptional-translational feedback loops (TTFLs). Posttranslational modifications are also crucial for clock functions in fungi and animals, but the posttranslational modifications that affect the plant clock are less understood. Here, using chemical biology strategies, we show that the Arabidopsis CASEIN KINASE 1 LIKE (CKL) family is involved in posttranslational modification in the plant clock. Chemical screening demonstrated that an animal CDC7/CDK9 inhibitor, PHA767491, lengthens the Arabidopsis circadian period. Affinity proteomics using a chemical probe revealed that PHA767491 binds to and inhibits multiple CKL proteins, rather than CDC7/CDK9 homologs. Simultaneous knockdown of Arabidopsis CKL-encoding genes lengthened the circadian period. CKL4 phosphorylated transcriptional repressors PSEUDO-RESPONSE REGULATOR 5 (PRR5) and TIMING OF CAB EXPRESSION 1 (TOC1) in the TTFL. PHA767491 treatment resulted in accumulation of PRR5 and TOC1, accompanied by decreasing expression of PRR5- and TOC1-target genes. A prr5 toc1 double mutant was hyposensitive to PHA767491-induced period lengthening. Together, our results reveal posttranslational modification of transcriptional repressors in plant clock TTFL by CK1 family proteins, which also modulate nonplant circadian clocks.