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We address the link between communication accommodation and compliance gaining in momentary, mediated encounters, using Goffman’s theory of interaction ritual as a conceptual bridge. We report an online experiment of compliance-gaining conversations with 915 dyads of strangers recruited from Amazon M-Turk. The extent to which two strangers accommodated each other’s non-content linguistic features predicted their behavioral compliance—monetary donation to a charity. This accommodation–compliance link was (a) observed, to some extent, in both conversationalists in the dyads, albeit moderated by seeker–target role differentiation, (b) partially mediated by perceived warmth and competence, and (c) was robust against alternative mechanisms including compliance-gaining strategies, personalities, and demographics. We discuss implications regarding communication-induced influence in mediated conversations and related interpersonal communication processes in general. Lay Summary How can a fleeting online interaction bring about compliance, especially for prosocial causes such as charity donation? This article finds that compliance is increased when there is a legacy of cooperative interactions (i.e., successful interaction rituals) on the part of all conversation partners—not just the one who seeks compliance. Such interaction can be identified when the individuals start to coordinate and accommodate each other’s language use (e.g., using similar expressions or adopting similar linguistic styles). The research shows that since online conversations often rely on text-based communication that lacks other channels with which to signal cooperative interactions, coordinated language plays an important role in gaining compliance.

This study is aimed at exploring the release of bound polyphenols (BP) from insoluble dietary fiber (IDF) and its mechanism by solid-state fermentation (SSF) via Trichoderma viride. The results indicated that BP released by SSF (5.55 mg GAE/g DW) was significantly higher than by alkaline hydrolysis. In addition, 39 polyphenols and catabolites were detected, and the related biotransformation pathways were speculated. Quantitative analysis showed that SSF released more ferulic acid, p-coumaric acid, and organic acids, which led to advances in antioxidant, α-amylase, and α-glucosidase inhibitory activities. Furthermore, structural characteristics (scanning electron microscopy, X-ray diffraction, thermos gravimetric analysis, and Fourier transform infrared spectroscopy) and dynamic changes of carbohydrate-hydrolyzing enzymes indicated that the destruction of hemicellulose and the secretion of xylanase were vital for releasing BP. Overall, this study demonstrated that SSF was beneficial to release BP from IDF, which could provide insight into utilizing agricultural byproducts in a more natural and economical way.

Epigenetics alternation of non-genetic variation and genome-wide association study proven allelic variants may associate with insulin secretion in type 2 diabetes (T2D) development. We analyzed promoter DNA methylation array to evaluate the associated with increased susceptibility to T2D (30 cases, 10 controls) and found 1,091 gene hypermethylated in promoter regions. We performed the association study of T2D and found 698 single nucleotide polymorphisms in exon and promoter sites by using 2,270 subjects (560 cases, 1,710 controls). A comparison of DNA hypermethylation and gene silencing of mouse T2D results in our T2D patients' results showed that the 5'-nucleotidase, cytosolic II (NT5C2) and fucosyltransferase 8 (FUT8) genes were strongly associated with increased susceptibility to T2D. DNA hypermethylation in promoter regions reduced NT5C2 gene expression, but not FUT8 in T2D patients. NT5C2 protein expression was decreased in pancreatic β-cells from T2D mice. Transient transfection NT5C2 into RIN-m5F cells down-regulated DNA methyltransferase I (DNMT1) expression and up-regulation of the insulin receptor. Moreover, NT5C2 knockdown induced in DNMT1 overexpression and insulin receptor inhibition. Taken together, these results showed that NT5C2 epigenetically regulated insulin receptor in patients and mice with T2D, and maybe provide for T2D therapy strategy.

This paper proposes that artificial agents’ underperformance in interpersonal influence situations can be explained by stereotypical perceptions of such agents’ lack of capacity to act and accomplish goals (i.e., agency), triggered by their non-human identity. In two experiments of text-based conversations ( N = 305 and 309), the identity of a human advice giver was manipulated to be either a human or a chatbot. The chatbot identity resulted in less perceived agency of the giver, which then mediated the identity’s effects on the advice seeker’s (a) perceived advice effectiveness and (b) intention to follow advice after the conversation, as well as (c) adherence to advice and (d) trouble relief after a week. A positive correlation between perceived agency of the artificial agent and the seeker’s self-efficacy was identified as part of this mediation. In contrast, perceived emotional capacity (i.e., experience), despite a discrepancy between the two identities, had non-significant mediating effects.

Background: Magnetic resonance imaging (MRI) provides objective information about brain structural atrophy in patients with Alzheimer’s disease (AD). This multi-structural atrophic information, when integrated as a single differential index, has the potential to further elevate the accuracy of AD identification from normal control (NC) compared to the conventional structure volumetric index. Objective: We herein investigated the performance of such an MRI-derived AD index, AD-Resemblance Atrophy Index (AD-RAI), as a neuroimaging biomarker in clinical scenario. Method: Fifty AD patients (19 with the Amyloid, Tau, Neurodegeneration (ATN) results assessed in cerebrospinal fluid) and 50 age- and gender-matched NC (19 with ATN results assessed using positron emission tomography) were recruited in this study. MRI-based imaging biomarkers, i.e., AD-RAI, were quantified using AccuBrain®. The accuracy, sensitivity, specificity, and area under the ROC curve (AUC) of these MRI-based imaging biomarkers were evaluated with the diagnosis result according to clinical criteria for all subjects and ATN biological markers for the subgroup. Results: In the whole groups of AD and NC subjects, the accuracy of AD-RAI was 91%, sensitivity and specificity were 88% and 96%, respectively, and the AUC was 92%. In the subgroup of 19 AD and 19 NC with ATN results, AD-RAI results matched completely with ATN classification. AD-RAI outperforms the volume of any single brain structure measured. Conclusion: The finding supports the hypothesis that MRI-derived composite AD-RAI is a more accurate imaging biomarker than individual brain structure volumetry in the identification of AD from NC in the clinical scenario.

The liver is a key player for maintaining glucose homeostasis. Excessive hepatic glucose production is considered to be a key for the onset of type 2 diabetes. The primary function of heme oxygenase-1 (HO1) is to catalyze the degradation of heme into biliverdin, ferrous iron, and carbon monoxide. Previous studies have demonstrated that the degradation of heme by HO1 in the liver results in mitochondrial dysfunction and drives insulin resistance. In this study, by overexpressing HO1 in hepatocytes and mice, we showed that HO1 promotes gluconeogenesis in a Foxo1-dependent manner. Importantly, HO1 overexpression increased the generation of ferrous iron in the liver, which further activates nuclear factor-κB and phosphorylates Foxo1 at Ser273 to enhance gluconeogenesis. We further assessed the role of HO1 in insulin-resistant liver-specific knockout of IRS1 and IRS2 genes (L-DKO) mice, which exhibit upregulation of HO1 in the liver and hepatic ferrous iron overload. HO1 knockdown by shRNA or treatment of iron chelator rescued the aberrant gluconeogenesis in L-DKO mice. In addition, we found that systemic iron overload promotes gluconeogenesis by activating the hepatic protein kinase A→Foxo1 axis. Thus, our results demonstrate the role of HO1 in regulating hepatic iron status and Foxo1 to control gluconeogenesis and blood glucose.

Graphical abstract, Ovatodiolide is a bioactive cembrane-type diterpenoid isolated from Anisomeles indica (L.) Kuntze. It has been proven that ovatodiolide is anti-inflammatory, anti-tumorigenic, anti-melanogenic and attenuates asthma by regulating signaling pathways. The aim of this study was to evaluate the safety of ovatodiolide by conducting genotoxicity tests and 28-day oral toxicity tests in rats. Genotoxicity assays were conducted by using a bacterial reverse mutation test and mammalian chromosomal aberration test to assess whether ovatodiolide causes reverse mutations and mutagenicity with or without metabolism activation. For the in vivo mammalian erythrocyte micronucleus test, mice were administered a single dose of 0, 250, 500 or 1000 mg/kg b.w. ovatodiolide by single gavage. In the acute oral toxicity test, rats were given a single dose of ovatodiolide 1000 mg/kg b.w. by single gavage. In the 28-day oral toxicity test, groups were divided into a control, ovatodiolide 10, 25 and 50 mg/kg b.w. The results showed that there was no mutagenicity in the bacterial reverse mutation test or the mammalian chromosomal aberration test with or without S9 fraction. Ovatodiolide did not produce an increase in micronucleated reticulocytes in the micronucleus test. The results revealed that the acute oral toxicity of ovatodiolide is over 1000 mg/kg b.w. in rats. Moreover, 10, 25 and 50 mg/kg b.w. of ovatodiolide did not cause a significant effect in rats. According to the results of the genotoxicity and oral toxicity studies in rats, ovatodiolide did not produce any adverse effects, and the tested doses can serve as clinical references.

Asthma is one of the most common childhood chronic diseases worldwide. Subcutaneous immunotherapy (SCIT) is commonly used in the treatment of house dust mite (HDM)‑related asthma in children. However, the therapeutic mechanism of SCIT in asthma remains unclear. The present study aimed to investigate the molecular biomarkers associated with HDM‑related asthma in asthmatic children prior and subsequent to SCIT treatment compared with those in healthy children via proteomic analysis. The study included a control group (30 healthy children), ‑Treatment group (30 children with HDM‑related allergic asthma) and +Treatment group (30 children with HDM‑related allergic asthma treated with SCIT). An isobaric labeling with relative and absolute quantification‑based method was used to analyze serum proteome changes to detect differentially expressed proteins, while functional enrichment and protein‑protein interaction network analysis were used to select candidate biomarkers. A total of 72 differentially expressed proteins were detected in the ‑Treatment, +Treatment and control groups. A total of 33 and 57 differentially expressed proteins were observed in the ‑Treatment vs. control and +Treatment vs. control groups, respectively. Through bioinformatics analysis, 5 candidate proteins [keratin 1 (KRT1), apolipoprotein B (APOB), fibronectin 1, antithrombin III (SERPINC1) and α‑1‑antitrypsin (SERPINA1)] were selected for validation by western blotting; among them, 4 proteins (KRT1, APOB, SERPINC1 and SERPINA1) showed robust reproducibility in asthma and control samples. This study illustrated the changes in proteome regulation following SCIT treatment for asthma. The 4 identified proteins may serve as potential biomarkers prior and subsequent to SCIT treatment, and help elucidate the molecular regulation mechanisms of SCIT to treat HDM‑related asthma.

Epigenetics alternation of non-genetic variation and genome-wide association study proven allelic variants may associate with insulin secretion in type 2 diabetes (T2D) development. We analyzed promoter DNA methylation array to evaluate the associated with increased susceptibility to T2D (30 cases, 10 controls) and found 1,091 gene hypermethylated in promoter regions. We performed the association study of T2D and found 698 single nucleotide polymorphisms in exon and promoter sites by using 2,270 subjects (560 cases, 1,710 controls). A comparison of DNA hypermethylation and gene silencing of mouse T2D results in our T2D patients’ results showed that the 5′-nucleotidase, cytosolic II (NT5C2) and fucosyltransferase 8 (FUT8) genes were strongly associated with increased susceptibility to T2D. DNA hypermethylation in promoter regions reduced NT5C2 gene expression, but not FUT8 in T2D patients. NT5C2 protein expression was decreased in pancreatic β-cells from T2D mice. Transient transfection NT5C2 into RIN-m5F cells down-regulated DNA methyltransferase I (DNMT1) expression and up-regulation of the insulin receptor. Moreover, NT5C2 knockdown induced in DNMT1 overexpression and insulin receptor inhibition. Taken together, these results showed that NT5C2 epigenetically regulated insulin receptor in patients and mice with T2D, and maybe provide for T2D therapy strategy.

The major aim of the present study was to determine the effects of quercetin, a well-known flavonoid, on attenuating cisplatin (CDDP)-induced fat loss and the possible mechanisms. Tumor-bearing nude mice and tumor-free BALB/c mice were administrated with CDDP alone or in combination with quercetin by a diet containing 0.1% or 1% quercetin (LQ or HQ) or by intraperitoneal injection (IQ) to determine the effects of quercetin on the anticancer effect of CDDP or CDDP-induced fat loss. The effects of quercetin on fat accumulation in CDDP-exposed 3T3-L1 cells were also determined. We first showed that HQ and IQ significantly enhanced the anticancer effect of CDDP by upregulating p53- and p21-associated pathways, while tended to attenuate CDDP-induced fat loss in tumor-bearing nude mice. The study in 3T3-L1 cells showed that CDDP decreased the fat accumulation accompanied by strong upregulation of the expression of six genes which are associated with fat metabolism, while quercetin completely suppressed such an effect. The tumor-free BALB/c mice study consistently showed a protective effect of HQ on CDDP-induced body weight and epididymal fat loss. HQ also increased the fat levels in liver and muscle tissues. In epididymal fat tissues, HQ consistently attenuated CDDP-induced changes in fat metabolism-associated gene expression. However, CDDP alone or in combination with HQ did not affect the food intake. This study demonstrates that quercetin possesses the potential to suppress CDDP-induced fat loss may partly through the regulation of the fat metabolism-associated gene expression.

Muon-induced single event upset (SEU) is predicted to increase with technology scaling. Although previous works investigated the dependencies of muon-induced SEU cross sections on energy, voltage, and technology, the angle of incidence of terrestrial muons is not always perpendicular to the chip surface. Consequently, the impact of the angle of incidence of muons on SEUs should be evaluated. This study conducts negative muon irradiation tests on bulk and fully depleted silicon on insulator static random access memories at two angles of incidence: 0° (vertical) and 45° (tilted). The tilted incidence drifts the muon energy peak to a higher energy as expected. However, the SEU characteristics in the bulk device between the vertical and tilted incidences, including the voltage dependences of the SEU cross sections and multiple cells upset patterns, are similar despite the unexpected impact on the SEU cross section at an operating voltage of 0.4 V.

Negative and positive muon irradiation tests of static random access memories (SRAMs) were performed at Muon Science Innovation Channel (MuSIC) of Research Center for Nuclear Physics (RCNP), Osaka University. The muon-induced single event upset (SEU) cross sections for 65-nm bulk SRAMs were measured. The SRAM device was irradiated by the muon beams with average momenta ranging from 37.8 to 41.0 MeV/c at the beam exit. The incident muon fluence was measured using a one-by-one muon detection system with a plastic scintillator by taking advantage of the direct current (dc) muon beam and reliable absolute values of SEU cross sections were obtained. In addition to the measurement of the SEU cross sections, we measured muonic X-rays from the irradiated device to investigate the relation between the measured SEU cross section and the emission rate of muonic X-rays associated with the stopping position of the muons as a function of incident muon momentum. The result suggested that negative muons have a significant effect on SEUs by the emission of secondary light ions via negative muon capture reaction when negative muons stop near sensitive volumes (SVs) in SRAMs.

Food protein-derived bioactive peptides, particularly antihypertensive peptides, are important constituents of functional foods or nutraceuticals. Most antihypertensive are identified as the inhibitors of angiotensin converting enzyme (ACE), a key enzyme responsible for the generation of angiotensin II (Ang II), which is a vasoconstricting peptide. Hence, ACE has long been used as a universal target to identify antihypertensive peptides. Angiotensin converting enzyme 2 (ACE2), is a homolog of ACE but uses Ang II as its key substrate to produce angiotensin (1-7), exerting vasodilatory activity via the mas receptor (MasR). Therefore, ACE2 functions in the opposite way as ACE and is an emerging novel target for cardiovascular therapy. The potential of food protein-derived bioactive peptides in targeting ACE2 has been rarely explored. While, recently we found that IRW, an egg white ovotransferrin-derived antihypertensive peptide, reduced blood pressure in spontaneously hypertensive rats via the ACE2/Ang (1-7)/MasR axis, indicating a new mechanism of food protein-derived bioactive peptides in reducing blood pressure. The objectives of this review are to summarize the functions of the ACE2/Ang (1-7)/MasR axis and to examine its potential roles in the actions of food protein-derived antihypertensive peptides. The interaction between antihypertensive peptides and the ACE2/Ang (1-7)/MasR axis will also be discussed.

Oxidative stress is an important contributing factor for inflammation. Piper methysticum, also known as Kava-kava, is a shrub whose root extract has been consumed as a drink by the pacific islanders for a long time. Flavokawain A (FKA) is a novel chalcone derived from the kava plant that is known to have medicinal properties. This study was aimed at demonstrating the antioxidant molecular mechanisms mediated by FKA on lipopolysaccharide- (LPS-) induced inflammation in BALB/c mouse-derived primary splenocytes. In vitro data show that the nontoxic concentrations of FKA (2-30 μM) significantly suppressed the proinflammatory cytokine (TNF-α, IL-1β, and IL-6) release but induced the secretion of interleukin-10 (IL-10), an anti-inflammatory cytokine. It was also shown that FKA pretreatment significantly downregulated the LPS-induced ROS production and blocked the activation of the NFκB (p65) pathway leading to the significant suppression of iNOS, COX-2, TNF-α, and IL-1β protein expressions. Notably, FKA favored the nuclear translocation of Nrf2 leading to the downstream expression of antioxidant proteins HO-1, NQO-1, and γ-GCLC via the Nrf2/ARE signaling pathway signifying the FKA’s potent antioxidant mechanism in these cells. Supporting the in vitro data, the ex vivo data obtained from primary splenocytes derived from the FKA-preadministered BALB/c mice (orally) show that FKA significantly suppressed the proinflammatory cytokine (TNF-α, IL-1β, and IL-6) secretion in control-, LPS-, or Concanavalin A- (Con A-) stimulated cells. A significant decrease in the ratios of pro- and anti-inflammatory cytokines (IL-6/IL-10; TNF-α/IL-10) showed that FKA possesses strong anti-inflammatory properties. Furthermore, BALB/c mice induced with experimental pancreatitis using cholecystokinin- (CCK-) 8 showed decreased serum lipase levels due to FKA pretreatment. We conclude that with its potent antioxidant and anti-inflammatory properties, chalcone flavokawain A could be a novel therapeutic agent in the treatment of inflammation-associated diseases.

Background Taraxacum species (commonly known as dandelion) used as herbal medicine have been reported to exhibit an antiproliferative effect on hepatoma cells and antitumor activity in non-small-cell lung cancer cells. Although several investigations have demonstrated the safety of Taraxacum officinale, the safety of tissue-cultured plants of T. formosanum has not been assessed so far. Therefore, the present study examines the safety of the water extract of the entire plant of tissue cultured T. formosanum based on acute and subacute toxicity tests in rats, as well as the Ames tests. Results No death or toxicity symptoms were observed in the acute and subacute tests. The results of the acute test revealed that the LD50 (50% of lethal dose) value of the T. formosanum water extract for rats exceeded 5 g/kg bw. No abnormal changes in the body weight, weekly food consumption, organ weight, or hematological, biochemical, and morphological parameters were observed in the subacute toxicity test. Thus, the no observed adverse effect level (NOAEL) of T. formosanum water extract was estimated to be higher than 2.0 g/kg. Finally, the results of the Ames test revealed that T. formosanum water extract was not genotoxic at any tested concentration to any of five Salmonella strains. Conclusions The water extract of tissue-cultured T. formosanum was non-toxic to rats in acute and subacute tests and exhibited no genotoxicity to five Salmonella strains. How to cite: Tsai WC, Chang HC, Tseng YH, et al. Toxicity evaluation of water extract of tissue-cultured Taraxacum formosanum by acute, subacute administration, and Ames test. Electron J Biotechnol 2020;45. https://doi.org/10.1016/j.ejbt.2020.04.001

Vascular oxidative stress, inflammatory response, and proliferation are crucial mediators of vascular dysfunction which contribute to the pathology of hypertension. A tripeptide, LRW (Leu-Arg-Trp), was characterized from pea protein legumin, and its previously studied isomer IRW (Ile-Arg-Trp) was reported to exhibit antihypertensive activity via activation of angiotensin-converting enzyme 2. The objective of the current study was to explore the effects of LRW on vascular stress in vascular smooth muscle cells (VSMCs) under angiotensin II (Ang II)-induced cellular stress. LRW treatment could decrease Ang II-triggered superoxide production, inflammation, and proliferation in VSMCs. The abovementioned advantageous effects appeared to involve the upregulation of the ACE2-Ang-(1-7)-MasR axis and modulation of the nuclear factor-κB pathway. These findings specified the prospective role of LRW as a functional food ingredient or nutraceutical in the prevention of cardiovascular diseases, particularly hypertension and vascular damage.

Food protein-derived bioactive peptides have been recognized as a promising candidate for the development of functional foods or nutraceuticals. Peptides exhibiting antioxidant, anti-proliferative and anti-hypertensive activities have been characterized from corn proteins while the knowledge on the presence of immunomodulatory peptides in corn proteins is limited. The objective of this study was to identify the immunomodulatory peptides from corn proteins using interleukin 6 (IL-6) in human macrophage-like U937 cells as the marker. Results indicated that zein protein hydrolysate digested by thermolysin showed a high yield of peptides with potent activity, which was then used for further fractionation by RP-HPLC. We identified five peptides using LC–MS/MS, among which, peptide FLPFNQL showed the highest activity reducing IL-6 production by 57.7% ± 6.1%.

Although the safety of commercial genetically modified (GM) soybeans has been well evaluated and GM soybeans are legally sold under government management, some consumers still have concerns about their safety. The objective of this study was to evaluate the safety of commercial GM soybeans sold in markets as a food source. In the present study, two commercial GM (GM-1 and -2) soybeans and one non-GM soybean were randomly purchased and subjected to a whole food toxicity assessment. Rats (SD), male and female, were divided into six groups (10/sex/group). Two dosages of 1 g/kg/day and 5 g/kg/day of soybeans were selected for the low- and high-dose groups. Rats were administered the soybeans via daily oral fed for 90 days. The results indicate that the body weight, organ weight, biochemistry, hematology, and urology showed no biologically adverse effects. At necropsy, no significant differences between organ weights were noted between the non-GM- and GM soybeans-treated groups. Moreover, no gross or histopathological lesions were observed in the high-dosage (5 g/kg/day) fed groups of the non-GM and GM soybean fed rats. In conclusion, this food safety assessment revealed that commercial GM soybeans are substantially equivalent to non-GM soybeans in rats.

Documenting the emergent social representations of COVID-19 in public communication is necessary for critically reflecting on pandemic responses and providing guidance for global pandemic recovery policies and practices. This study documents the dynamics of changing social representations of the COVID-19 pandemic on one of the largest Chinese social media, Weibo, from December 2019 to April 2020. We draw on the social representation theory (SRT) and conceptualize topics and topic networks as a form of social representation. We analyzed a dataset of 40 million COVID-19 related posts from 9.7 million users (including the general public, opinion leaders, and organizations) using machine learning methods. We identified 12 topics and found an expansion in social representations of COVID-19 from a clinical and epidemiological perspective to a broader perspective that integrated personal illness experiences with economic and sociopolitical discourses. Discussions about COVID-19 science did not take a prominent position in the representations, suggesting a lack of effective science and risk communication. Further, we found the strongest association of social representations existed between the public and opinion leaders and the organizations' representations did not align much with the other two groups, suggesting a lack of organizations' influence in public representations of COVID-19 on social media in China.

Spent hens are egg-laying chicken reaching the end of their egg-laying cycle and are seen as a by-product to the egg industry. A spent hen muscle protein hydrolysate prepared by food-grade thermoase PC10F (SPH-T) has previously shown antihypertensive potential. In the present work, we further investigated its antihypertensive effect and underlying mechanisms in spontaneously hypertensive rats. There are three groups: untreated, low dose (250 mg SPH-T/kg/day body weight), and high dose (1,000 mg SPH-T/kg/day body weight). Oral administration of SPH-T over a period of 20 days reduced systolic blood pressure by 25.7 mm Hg (p0.001) and 11.9 mm Hg (p0.05), respectively, for the high- and low-dose groups. The high-dose treatment decreased the circulating level of angiotensin II (from 25.0 to 5.7 pg/ml) while increased angiotensin-converting enzyme 2 (ACE2) (from 1.3 to 3.3 IU/ml) and angiotensin (1-7) (from 37.0 to 70.1 pg/ml) significantly (p0.05). Furthermore, the high-dose group doubled the aortic expression of ACE2 while reduced the expression of angiotensin (Ang) II type 1 receptor (by 35%). Circulating inflammatory cytokines including tumor necrosis factor alpha and monocyte chemoattractant protein-1 as well as vascular inflammatory proteins including inducible nitric oxide synthase and vascular cell adhesion molecule-1 were attenuated by ∼15%-50% by the treatment; nitrosative stress (35%) and type I collagen synthesis (50%) in the aorta were also attenuated significantly (p0.05). Moreover, SPH-T possessed an umami taste (no obvious bitter taste) as analyzed by electronic tongue. PRACTICAL APPLICATION: Hypertension is a global health concern, afflicting more than 20% of adults worldwide. Uncovering the antihypertensive effect of spent hen protein hydrolysate underpinned its functional food nutraceutical applications for the prevention and treatment of hypertension.

Additional file 2 : Table S1. Extracted radiomics features

Background: Osteosarcoma (OS) is the most common primary malignancy of the bone and is notoriously resistant to radiation therapy. High-dose cytotoxic chemotherapy and surgical resection have improved the survival rate and prognosis of patients with OS. Nonetheless, treatment challenges remain when the tumor cannot be removed by surgery. Boron neutron capture therapy (BNCT) provides high linear energy transfer (LET) radiation, and its internal targeted characteristics make BNCT a novel therapy for removing OS and reducing radiation damage to adjacent healthy tissues. Methods: In this study, a UMR-106-grafted OS rat model was developed, and boric acid (BA) was used as the boron drug for BNCT. The pharmacokinetics of BA, following intravenous injection, were evaluated to determine the optimal time window for neutron irradiation. OS-bearing rats were irradiated by an epithermal neutron beam at Tsing Hua Open-Pool Reactor (THOR). The therapeutic efficacy of and tissue response after BNCT were evaluated by radiographic and histopathological observations. Results: OS-bearing rats were irradiated by neutrons in the first hour following the intravenous injection of BA. The prescription-absorbed doses in the tumor regions were 5.8 and 11.0 Gy. BNCT reduced the body weight of the tumor-bearing rats, but they recovered after a few days. The BA-mediated BNCT effectively controlled the orthotopic OS tumor, reduced osteolysis, and induced bone healing. Autoradiography and histological analysis confirmed that the BA retention region is consistent with the calcification region in OS tissue. Conclusion: BA is specifically retained in OS, and the BA-mediated BNCT can significantly reduce the tumor burden and osteolysis in OS-bearing rats.

Systemic sclerosis associated with lung interstitial lung disease (SSc-ILD) is the most common cause of death among patients with SSc. Mesenchymal stem cell (MSCs) transplantations had been treated by SSc patients that showed in the previous case report. The therapeutic mechanisms and effects of MSCs on SSc-ILD are still obscure. In this study, we investigated the therapeutic effects and mechanisms of treatment of BM-MSC derived from C57BL/6 on the topoisomerase I (TOPO I) induced SSc-ILD-like mice model. The mice were immunized with a mixture of recombinant human TOPO I in PBS solution (500 U/mL) and completed Freund's adjuvant [CFA; 1:1 (volume/volume)] twice per week for 9 weeks. On week 10, the mice were sacrificed to analyze the related pathological parameters. Lung and skin pathologies were analyzed using histochemical staining. CD4 T-helper (T

Head and neck squamous cell carcinoma (HNSCC) is a relatively common malignancy, characterized by lethal morbidity. Herein, we attempted to investigate the autophagy/apoptosis activities of the submerged fermented broths of Antrodia salmonea (AS) in HNSCC Twist-overexpressing (OECM-1 and FaDu-Twist) cells. AS (0-150 μg/mL) effectively reduced cell viability, colony formation, and downregulated Twist expression in OECM-1 and FaDu-Twist cells compared to FaDu cells. AS- induced apoptosis was mainly associated with activation of caspase-3, PARP cleavage, increased expression of VDAC-1 and disproportionation of Bax/Bcl-2. Annexin V/PI staining suggested late apoptosis induction by AS treatment. AS exhibits enhanced autophagy process mediated via LC3-I/II accumulation, increased acidic vesicular organelles (AVOs) formation and p62/SQSTM1 expression feeding into the apoptotic program. However, pre-treatment with autophagy blockers 3-MA and CQ significantly diminished AS-induced cell death. Additionally, suppression of AS-induced ROS release by treatment with antioxidant N-acetylcysteine (NAC) resulted in reduction of apoptotic and autophagic cell death. In vivo studies strengthened the above observations and showed that AS effectively reduced the tumor volume and tumor weight in OECM-1-xenografted nude mice. This study discovered that Antrodia salmonea exhibits a novel anti-cancer mechanism which could be harnessed as a new potent drug for HNSCC treatment.

The changing technological landscape has brought about new forms of groups and grouping that span across computing and communication devices, space, time, institutions, cultures, realities (physical, virtual, and augmented), and intelligence (natural and artificial intelligence). This chapter utilizes a series of publication and keyword analyses to identify trends in group and technology research in the fields of communication, management, and computer-supported cooperative work (CSCW) between 2008 and 2019. The results reveal prominent research areas, and recent shifts and emergent questions in the study of groups and technology, highlighting a complex entanglement of technology with collaborative social practices. The chapter concludes with a discussion of novel key areas and trends suggested by the analyses, with the goal of contributing toward a research agenda for future study of groups and technology.

Lupus nephritis (LN) is a chronic autoimmune disease, leading to progressive renal dysfunction. MicroRNAs (miRNAs) contribute to LN pathophysiology. Nevertheless, the potential mechanisms of miR-145 in LN remain unclear. Here, we investigated the contribution of miR-145 to LN progression.qRT-PCR analysis determined miR-145 and CSF1 expression. Western blot tested CSF1, JAK2, p-JAK2, STAT3, p-STAT3, cleaved caspase3, Bax and Bcl-2 expression. Dual luciferase reporter assay confirmed the interaction between miR-145 and CSF1. ELISA assay detected the secretion of inflammatory molecules. Flow cytometric analysis determined cell cycle and apoptosis. MTT was conducted to test cell viability. The LN mouse model was constructed for in vivo experiments. HE and Masson staining examined the kidney pathologic changes.MiR-145 was down-regulated in LN patients and LPS-induced HRMCS, whereas CSF1 was up-regulated. Moreover, miR-145 overexpression inhibited HRMCS cell apoptosis and inflammatory damage. Besides, miR-145 was found to directly target CSF1. Additionally, knockdown of CSF1 inhibited HRMCS cell apoptosis and inflammatory damage by inactivating the JAK/STAT signaling pathway. Furthermore, miR-145 inhibited inflammatory damage and cell apoptosis of HRMCS by down-regulating CSF1. Finally, we verified that miR-145 suppressed LN development in vivo.Our data reveals that miR-145 regulates LN progression via CSF1 mediated JAK/STAT signaling pathway, and miR-145 may be a new therapeutic target for LN treatment.

Preschoolers are within their critical time in motion development; while muscles are the fundamental units in motion control and by monitoring activated intensity and duration of muscles, preschooler's motor ability which would disclose their potential pathogenesis quality can be objectively and quantitatively assessed. Although a large number of studies were available on this issue, questions still being there: what are the patterns and characteristics of lower limb muscles when they are facing with the curve walking(CW) tasks; and then how individual muscle or muscle groups coordinated while turning curves. Our purpose of this study is first to portray the patterns and characteristics of lower limb muscles of healthy preschoolers while CW and then to insight their muscles' coordination mechanism and "neuro-musculo-skeletal" feedback during motion.35 healthy preschoolers and 35 healthy adults' lower limbs surface electromyography (sEMG) were collected while left and right CW and four muscle groups (Tibialis Anterior, Lateral Gastrocnemius, Rectus Femoris, and Biceps Femoris) were recorded. sEMG variables such as Muscle Activation Time, Total Duration of Activity Time, Average Muscle Activation Rate and Average Rate of Change were calculated. Paired sample t-test was used to explore the differences of sEMG variables between preschoolers and adults when turning curves.Preschoolers would adjust the gait by changing the activation time and activation rate to fulfill the curve turning tasks; but they also showed variations in coordination mechanism when contrasting with the adults group. Those findings in preschoolers would support to build muscles' coordination mechanism and further insight to neuro-muscular skeletal feedback regulation.Although preschoolers performed good enough to switching gait from normal walking to CW, but gaps in their abilities were still apparent when compared to adults. Hence, with the help of highly recognizable muscle coordination mechanism in CW, motor dysfunction in lower limbs of preschool children can be effectively identified.

Although clinical trials of food-protein-derived peptides in the management of hypertension have been published, the results are controversial, which compelled us to conduct a meta-analysis to evaluate the pooled effect of peptide intervention. In this study, we searched for studies published between 2010 and 2021 and selected 12 eligible studies for a meta-analysis. The pooled effect of peptide intervention for systolic blood pressure (SBP) and diastolic blood pressure (DBP) was −3.28 mmHg (95% CI: −4.54, −2.03, p < 0.001) and −1.82 mmHg (95% CI: −3.46, −0.18, p = 0.03), respectively. Sub-group analyses showed that the reduction in BP in participants with higher basal BP (>140/85 mmHg) was greater (p = 0.007 for SBP and p = 0.01 for DBP), and the effect was stronger in Asian participants as compared with non-Asian participants (p = 0.01 for SBP and p = 0.04 for DBP). In addition, the effect of peptide intervention was more pronounced on SBP in participant groups with a lower ratio of male to female (≤0.5) as well as in participants with a mean age ≥50 years old. In conclusion, food-protein-derived antihypertensive peptides can significantly reduce BP in prehypertensive and hypertensive patients. Findings from this study could provide guidance for the design of clinical trials of antihypertensive peptides.

Although pulmonary fibrosis (PF) is considered a rare disease, the incidence thereof has increased steadily in recent years, while a safe and effective cure remains beyond reach. In this study, the potential of tocotrienol-rich fractions (TRF) and carotene to alleviate PF was explored. PF was induced in Sprague-Dawley rats via a single intratracheal bleomycin (BLM) (5 mg/kg) instillation. These rats were subsequently treated with TRF, carotene, pirfenidone (Pir) and nintedanib (Nin) for 28 days via gavage administration, whereafter histopathological performance, biochemical functions and molecular alterations were studied in the lung tissues. Our results showed that TRF, carotene, Nin and Pir all ameliorated PF by reducing inflammation and resisting oxidative stress to varying degrees. The related mechanisms involved the TGF-β1/Smad, PI3K/Akt and NF-κB signaling pathways. Ultimately, our findings revealed that, when combined with TRF, the therapeutic effects of Nin and Pir on PF were enhanced, indicating that TRF may, indeed, provide promising potential for use in combination therapy in the treatment of PF.