Miracle-dz/UniFAR-FTUs huggingface dataset:
Thermally Conductive Graphene-Polymer Composites: Size, Percolation, and Synergy Effects

The rapidly increasing device densities in electronics dictate the need for efficient thermal management. If successfully exploited, graphene, which possesses extraordinary thermal properties, can be commercially utilized in polymer composites with ultrahigh thermal conductivity (TC). The total potential of graphene to enhance TC, however, is restricted by the large interfacial thermal resistance between the polymer mediated graphene boundaries. We report a facile and scalable dispersion of commercially available graphene nanoplatelets (GnPs) in a polymer matrix, which formed composite with an ultrahigh TC of 12.4 W/m K (vs 0.2 W/m K for neat polymer). This ultrahigh TC was achieved by applying high compression forces during the dispersion that resulted in the closure of gaps between adjacent GnPs with large lateral dimensions and low defect densities. We also found strong evidence for the existence of a thermal percolation threshold. Finally, the addition of electrically insulating boron-nitride nanopart.
CD‐g‐CS nanoparticles for enhanced antibiotic treatment of Staphylococcus xylosus infection

Staphylococcus xylosus (S. xylosus)‐induced cow mastitis is an extremely serious clinical problem. However, antibiotic therapy does not successfully treat S. xylosus infection because these bacteria possess a strong biofilm formation ability, which significantly reduces the efficacy of antibiotic treatments. In this study, we developed ceftiofur‐loaded chitosan grafted with β‐cyclodextrins (CD‐g‐CS) nanoparticles (CT‐NPs) using host–guest interaction. These positively charged nanoparticles improved bacterial internalization, thereby significantly improving the effectiveness of antibacterial treatments for planktonic S. xylosus. Moreover, CT‐NPs effectively inhibited biofilm formation and eradicated mature biofilms. After mammary injection in a murine model of S. xylosus‐induced mastitis, CT‐NPs significantly reduced bacterial burden and alleviated inflammation, thereby achieving optimized therapeutic efficiency for S. xylosus infection. In conclusion, this treatment strategy could improve the efficiency of antibiotic therapeutics and shows great potential in the treatment of S. xylosus infections.
The Economic Impact of Extensor Tendon Lacerations of the Hand in the United States

Purpose Extensor tendon lacerations (ETLs) are a common and debilitating injury for thousands of Americans annually. No study has attempted to estimate their economic impact. The objective of this study was to estimate the economic impact of ETLs in America. Methods The cost of ETLs to society was estimated using a validated prevalence-based cost of illness model. The primary cohort was defined as all patients with complete ETLs in the United States undergoing surgical repair and, secondarily, the imputed number of patients requiring reoperation within 1 year. For these groups, both direct and indirect costs (lost income, missed workdays, and disability payments) were measured. Results The total annual direct medical costs amounted to $14,095.28 per injury and 100,000 population. The total annual indirect labor costs were found to range between $80,842.90 and $150,136.82 per injury and 100,000 population. Hence, the estimated total costs of ETLs are $307 million per year in the United States alone and could be as high as $531 million annually depending on the effects of worker absenteeism on the core production–based industries. Conclusions Extensor tendon lacerations incur a significant economic burden to our health care system and are more costly when compared with many other common hand conditions. Specifically, indirect costs are the major contributor toward the total cost these injuries incur on society, accounting for an upward of 91% of the total cost. These results suggest efforts be focused on improving rehabilitation protocols and treatments. Level of Evidence Level II—economic and decision analyses.
The Use of Herbal Therapy to Improve the Quality of Life among Cancer Patients in the Southern Region of Peninsular Malaysia

Objective: To investigate the impact of herbal therapy on the quality of life (QoL) among cancer patients and to evaluate the relationship of QoL with age, gender, cancer stage, cancer type, and history of conventional treatment. Methodology: A prospective study was targeted on cancer patients receiving herbal therapy from a Traditional and Complementary Medicine (T&CM) clinic in a public hospital from 1st January 2016 to 31st August 2018. The European Organization for Research and Treatment of Cancer Quality of Life Questionnaire (EORTCQLQ-C30) was distributed to the patients prior to herbal therapy (baseline) and after the sixth and twelfth week of herbal therapy. Socio-demographic and clinical data were collected and analyzed using SPSS version 16. Results: The majority of the patients were females (60.0%) and were from the Chinese ethnic group (77.4%) with a mean age of 58.72 ± 12.17 years. Approximately 42.4% of patients were in advanced cancer stages at the time of study and 60.7% of patients had undergone radiotherapy before receiving herbal therapy. The most commonly prescribed herbs were Bai Hua She She Cao (90.6%) and Zhen Ren Huo Ming Yin (57.6%). Significant differences in mean score were observed in global health status, overall functional scales, and symptom scales after the sixth and twelfth week of receiving herbal therapy. QoL in terms of global health status and overall functional scales improved with higher scores while symptom scales recorded a lower score after twelve weeks of receiving herbal therapy in the T&CM clinic. Herbal therapy has a significant effect (p < 0.05) on the improvement of QoL of cancer patients. However, gender, cancer stage, cancer type, age, history of radiotherapy, and history of chemotherapy has no effect (p > 0.05). Conclusion: Herbal therapy did improve the QoL of cancer patients in the southern region of Peninsular Malaysia.
Design, Synthesis, and Antitumor Activity of Novel Dispiro[oxindole-cyclohexanone]-pyrrolidines.

BACKGROUND Spirooxindoles are privileged scaffolds in medicinal chemistry and were identified through Wang's pioneering work as inhibitors of MDM2-p53 interactions. OBJECTIVE To design and synthesize 2,6-diarylidenecyclohexanones and dispiro[oxindole-cyclohexanone]-pyrrolidines of potential antitumor effect. METHOD Dispiro[oxindole-cyclohexanone]-pyrrolidines 6a-h were synthesized in a regioselective manner via 1,3-dipolar cycloaddition reaction of 2,6-diarylidenecyclohexanones 3a-h, isatin, and sarcocine. Compounds 6a-h were alkylated to give (7-10) a,b. All compounds were evaluated in vitro for their antitumor activity and cytotoxic selectivity against breast cancer cell lines (MCF-7, and MDA-MB-231), breast fibrosis cell line (MCF10a) and placental cancer cell line (JEG-3). Molecular modeling inside the MDM2 binding site was performed using AutoDock4.2. RESULTS Synthesized compounds showed antitumor activity comparable to tamoxifen, and compounds 3a,b,f,g, and 9a,b showed selective cytotoxicity against tumor cells but reduced toxicity toward MCF-10a cells. Molecular modelling shows that both classes of synthesized compounds are predicted to fit the deep hydrophobic cleft on the surface of MDM2 and mimic the interactions between p53 and MDM2. CONCLUSION The synthesized compounds have antitumor activity against MCF-7, MDA-MB-231, and JEG-3. Few compounds showed a selective cytotoxic effect and may have the potential to inhibit MDM2 and stimulate p53. Future medicinal chemistry optimization and mechanistic study will be conducted to enhance the inhibition effect of identified compounds and elucidate their mechanism of action.
The Role of GIP in the Regulation of GLP-1 Satiety and Nausea

Gastric inhibitory peptide (GIP) is best known for its role as an incretin hormone in control of blood glucose concentrations. As a classic satiation signal, however, the literature illustrates a mixed picture of GIP involvement with an at best weak anorectic response profile being reported for GIP receptor (GIPR) signaling. Not surprisingly, the pursuit of exploiting the GIP system as a therapeutic target for diabetes and obesity has fallen behind that of the other gastrointestinal-derived incretin, glucagon-like peptide 1 (GLP-1). However, recent discoveries highlighted here support potential therapeutic advantages of combinatorial therapies targeting GIP and GLP-1 systems together, with perhaps the most surprising finding that GIPR agonism may have antiemetic properties. As nausea and vomiting are the most common side effects of all existing GLP-1 pharmacotherapies, the ability for GIP agonism to reduce GLP-1–induced illness behaviors but retain (if not enhance) weight loss and glycemic control may offer a new era in the treatment of obesity and diabetes.
Glutathione and its dependent enzymes’ modulatory responses to neonicotinoid insecticide sulfoxaflor induced oxidative damage in zebrafish in vivo

The use of neonicotinoid insecticides has progressively increased worldwide when compared with other insecticide groups. Due to this increase, non-target animal species such as fish are exposed to neonicotinoids from different sources, so they can be accumulated at trophic levels and cause various toxic effects by reaching humans. There are limited studies related to the toxic effects of neonicotinoid sulfoximine insecticides including sulfoxaflor on non-target species. The purpose of the present study was to evaluate the effects of sulfoxaflor on GSH-related antioxidants and to determine oxidative stress-producing effect of sulfoxaflor in the gill of zebrafish (Danio rerio). For this purpose, three sublethal concentrations of sulfoxaflor 0.87 mg/L (2.5% of 96 h LC50), 1.75 mg/L (5% of 96 h LC50), 3.51 mg/L (10% of 96 h LC50) of sulfoxaflor were exposed to zebrafish for 24, 48, and 96 h. GSH related antioxidants were evaluated by analyzing tGSH levels and GPx, GR, GST specific enzyme activities in the gill of zebrafish. The oxidative damage of sulfoxaflor on gill cells was determined by measuring TBARS levels. The results of this study demonstrated that sulfoxaflor activated GSH related antioxidants by increasing tGSH levels, GPx, GR enzyme activities and by diminishing GST enzyme activity in the gill of zebrafish. Sulfoxaflor also caused oxidative damage in the gill of zebrafish by increasing lipid peroxidation. In conclusion, this study indicated that sulfoxaflor led to oxidative stress and activation of GSH related antioxidants in the gill of zebrafish.
Lower limb rehabilitation robotics: The current understanding and technology.

BACKGROUND With the increasing rate of ambulatory disabilities and rise in the elderly population, advance methods to deliver the rehabilitation and assistive services to patients have become important. Lower limb robotic therapeutic and assistive aids have been found to improve the rehabilitation outcome. OBJECTIVE The article aims to present the updated understanding in the field of lower limb rehabilitation robotics and identify future research avenues. METHODS Groups of keywords relating to assistive technology, rehabilitation robotics, and lower limb were combined and searched in EMBASE, IEEE Xplore Digital Library, Scopus, Web of Science and Google Scholar database. RESULTS Based on the literature collected from the databases we provide an overview of the understanding of robotics in rehabilitation and state of the art devices for lower limb rehabilitation. Technological advancements in rehabilitation robotic architecture (sensing, actuation and control) and biomechanical considerations in design have been discussed. Finally, a discussion on the major advances, research directions, and challenges is presented. CONCLUSIONS Although the use of robotics has shown a promising approach to rehabilitation and reducing the burden on caregivers, extensive and innovative research is still required in both cognitive and physical human-robot interaction to achieve treatment efficacy and efficiency.
Role of Complement Component 3 in Early Erythrolysis in the Hematoma After Experimental Intracerebral Hemorrhage

Supplemental Digital Content is available in the text. Background and Purpose: Early erythrolysis occurs within the hematoma following intracerebral hemorrhage (ICH), and the release of erythrocyte cytoplasmic proteins such as hemoglobin and Prx2 (peroxiredoxin 2) can cause brain injury. Complement activation can induce erythrolysis. This study determined the function of complement component 3 (C3) in erythrolysis in hematoma and brain injury after ICH in mice. Methods: This study has 3 parts. First, ICH was induced in adult male C3-sufficient and deficient mice and animals were euthanized on days 1, 3, 7, and 28 for immunohistochemistry after magnetic resonance imaging and behavioral testing. Second, C3-sufficient and deficient mice with ICH were euthanized on day 1 for Western blot analysis. Third, C3-sufficient mice received injections of PBS and Prx2. Mice underwent both magnetic resonance imaging and behavioral tests on day 1 and were then euthanized. Brains were harvested for immunohistochemistry and Fluoro-Jade C staining. Results: Erythrolysis occurred in the hematoma in C3-sufficient and deficient mice on day 3 following ICH. C3-deficient mice had less erythrolysis, brain swelling, and neuronal degeneration in the acute phase and less brain atrophy in the chronic phase. There were fewer neurological deficits on days 3, 7, and 28 in C3-deficient mice. C3-deficient mice also had less extracellular Prx2 release. Moreover, Prx2 induced brain edema and brain injury and recruited macrophage scavenger receptor-1- and CD4-positive cells following ICH in mice. Conclusions: C3-deficient mice had less severe erythrolysis and brain injury following ICH compared with C3-sufficient mice. Prx2 released after erythrolysis can cause brain damage and neuroinflammation in mice.
Determinants of Ligand-Functionalized DNA Nanostructure–Cell Interactions

Synthesis of ligand-functionalized nanomaterials with control over size, shape, and ligand orientation facilitates the design of targeted nanomedicines for therapeutic purposes. DNA nanotechnology has emerged as a powerful tool to rationally construct two- and three-dimensional nanostructures, enabling site-specific incorporation of protein ligands with control over stoichiometry and orientation. To efficiently target cell surface receptors, exploration of the parameters that modulate cellular accessibility of these nanostructures is essential. In this study, we systematically investigate tunable design parameters of antibody-functionalized DNA nanostructures binding to therapeutically relevant receptors, including the programmed cell death protein 1, the epidermal growth factor receptor, and the human epidermal growth factor receptor 2. We show that, although the native affinity of antibody-functionalized DNA nanostructures remains unaltered, the absolute number of bound surface receptors is lower compared to soluble antibodies due to receptor accessibility by the nanostructure. We explore structural determinants of this phenomenon to improve efficiency, revealing that receptor binding is mainly governed by nanostructure size and DNA handle location. The obtained results provide key insights in the ability of ligand-functionalized DNA nanostructures to bind surface receptors and yields design rules for optimal cellular targeting.
An investigation of iconic language development in four datasets

Abstract Iconic words imitate their meanings. Previous work has demonstrated that iconic words are more common in infants’ early speech, and in adults’ child-directed speech (e.g., Perry et al., 2015; 2018). This is consistent with the proposal that iconicity provides a benefit to word learning. Here we explored iconicity in four diverse language development datasets: a production corpus for infants and preschoolers (MacWhinney, 2000), comprehension data for school-aged children to young adults (Dale & O'Rourke, 1981), word frequency norms from educational texts for school aged children to young adults (Zeno et al., 1995), and a database of parent-reported infant word production (Frank et al., 2017). In all four analyses, we found that iconic words were more common at younger ages. We also explored how this relationship differed by syntactic class, finding only modest evidence for differences. Overall, the results suggest that, beyond infancy, iconicity is an important factor in language acquisition.
Micro RNA-148a Targets Bcl-2 in Patients with Non-Small Cell Lung Cancer

Objective: Lung cancer is one of the most prevalent cancers and the leading cause of cancer-related deaths worldwide. MicroRNAs regulate more than 60% of human genes, including tumor suppressor genes and oncogenes. Accordingly, they can affect cancer risk. This study aimed to evaluate the role of serum miR-148a as a non-invasive biomarker in non-small cell lung cancer (NSCLC) patients and to assess the correlation between miR-148a and Bcl-2, as one of its target proteins. Materials and Methods: A total of 50 newly diagnosed NSCLC cases and 30 apparently healthy controls were recruited in this study. MiR-148a level was measured by TaqMan- Real time RT-PCR assay and Bcl-2 level was measured by ELISA. Results: Significant lower expression of serum miR-148a and higher serum Bcl-2 levels were observed in NSCLC patients as compared to the control group (p <0.001 each). A statistically significant inverse correlation was also evident between miR-148a and Bcl-2. Lower miR-148a gene expression level and higher Bcl-2 concentration were found to be associated with advanced tumor stage, lymph node involvement and distant metastasis. Conclusion: MiR-148a could be a possible biomarker for NSCLC and by targeting Bcl-2, it may offer a novel approach for treatment.
Predicting their past: Machine language learning can discriminate the brains of chimpanzees with different early-life social rearing experiences.

Early life experiences, including separation from caregivers, can result in substantial, persistent effects on neural, behavioral, and physiological systems as is evidenced in a long-standing literature and consistent findings across species, populations, and experimental models. In humans and other animals, differential rearing conditions can affect brain structure and function. We tested for whole brain patterns of morphological difference between 108 chimpanzees reared typically with their mothers (MR; N = 54) and those reared decades ago in a nursery with peers, human caregivers, and environmental enrichment (NR; N = 54). We applied support vector machine (SVM) learning to archival MRI images of chimpanzee brains to test whether we could, with any degree of significant probability, retrospectively classify subjects as MR and NR based on variation in gray matter within the entire brain. We could accurately discriminate MR and NR chimpanzee brains with nearly 70% accuracy. The combined brain regions discriminating the two rearing groups were widespread throughout the cortex. We believe this is the first report using machine language learning as an analytic method for discriminating nonhuman primate brains based on early rearing experiences. In this sense, the approach and findings are novel, and we hope they stimulate application of the technique to studies on neural outcomes associated with early experiences. The findings underscore the potential for infant separation from caregivers to leave a long-term mark on the developing brain.
Silencing of the chemokine CXC receptor 4 (CXCR4) hampers cancer progression and increases cisplatin (DDP)-sensitivity in clear cell renal cell carcinoma (ccRCC)

ABSTRACT Aberrant expression of the chemokine CXC receptor 4 (CXCR4) is closely associated with cancer progression and drug-resistance in multiple cancers, and we first investigated the role of CXCR4 in regulating cancer pathogenesis and cisplatin (DDP)-resistance in clear cell renal cell carcinoma (ccRCC) in the present study. Here, we identified that CXCR4 acted as an oncogene to promote cancer progression and genetically silencing of CXCR4 increased cisplatin (DDP)-sensitivity in ccRCC in vitro and in vivo. Functionally, analysis from the clinical and cellular data indicated that CXCR4 was significantly upregulated in ccRCC tissues and cells, compared to their normal counterparts. Next, the loss-of-function experiments validated that knock-down of CXCR4 suppressed cell proliferation, invasion, migration and epithelial-mesenchymal transition (EMT) in ccRCC cells, while CXCR4 overexpression had opposite effects on the above cellular functions. Consistently, the xenograft tumor-bearing mice models were established, and the results supported that knock-down of CXCR4 inhibited tumor growth and the expression levels of Ki67 protein in vivo. In addition, the ccRCC cells were exposed to DDP treatment, and we surprisingly found that upregulation of CXCR4 increased DDP-resistance in ccRCC cells, and conversely, CXCR4 ablation sensitized ccRCC cells to DDP stimulation. Taken together, we concluded that CXCR4 ablation hindered cancer progression and enhanced DDP-sensitivity in ccRCC, and the present study identified a novel therapeutic biomarker for ccRCC. GRAPHICAL ABSTRACT
Contribution of Mitochondria to Insulin Secretion by Various Secretagogues

Significance: Mitochondria determine glucose-stimulated insulin secretion (GSIS) in pancreatic β-cells by elevating ATP synthesis. As the metabolic and redox hub, mitochondria provide numerous links to the plasma membrane channels, insulin granule vesicles (IGVs), cell redox, NADH, NADPH, and Ca2+ homeostasis, all affecting insulin secretion. Recent Advances: Mitochondrial redox signaling was implicated in several modes of insulin secretion (branched-chain ketoacid [BCKA]-, fatty acid [FA]-stimulated). Mitochondrial Ca2+ influx was found to enhance GSIS, reflecting cytosolic Ca2+ oscillations induced by action potential spikes (intermittent opening of voltage-dependent Ca2+ and K+ channels) or the superimposed Ca2+ release from the endoplasmic reticulum (ER). The ATPase inhibitory factor 1 (IF1) was reported to tune the glucose sensitivity range for GSIS. Mitochondrial protein kinase A was implicated in preventing the IF1-mediated inhibition of the ATP synthase. Critical Issues: It is unknown how the redox signal spreads up to the plasma membrane and what its targets are, what the differences in metabolic, redox, NADH/NADPH, and Ca2+ signaling, and homeostasis are between the first and second GSIS phase, and whether mitochondria can replace ER in the amplification of IGV exocytosis. Future Directions: Metabolomics studies performed to distinguish between the mitochondrial matrix and cytosolic metabolites will elucidate further details. Identifying the targets of cell signaling into mitochondria and of mitochondrial retrograde metabolic and redox signals to the cell will uncover further molecular mechanisms for insulin secretion stimulated by glucose, BCKAs, and FAs, and the amplification of secretion by glucagon-like peptide (GLP-1) and metabotropic receptors. They will identify the distinction between the hub β-cells and their followers in intact and diabetic states. Antioxid. Redox Signal. 36, 920–952.