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The new development pattern is a strategic choice to reshape China's new advantages in international cooperation and competition. It is based on China's current development stage, changes in the environment, and other factors. Located deep within China's interior, Xinjiang is a crucial region for the development of the western region and the Belt and Road Initiative. Its agricultural resources are exported to numerous foreign nations. In the context of the new development pattern, this paper first examines the foreign trade issues in Xinjiang. Second, this paper analyzes the current state of Sino-Kazakhstani trade, in particular the current state of trade in agricultural products. In addition, the growth potential of Xinjiang's agricultural international trade is analyzed utilizing the gravity model and fuzzy algorithm. Finally, countermeasures for the mode of development of Xinjiang's international trade are proposed. [ABSTRACT FROM AUTHOR]

It remains a substantial challenge to balance treatment efficacy and toxicity in geriatric patients with multiple myeloma (MM), primarily due to the dynamic nature of frailty. Here, we conducted a prospective study to evaluate the feasibility and benefits of dynamic frailty-tailored therapy (DynaFiT) in elderly patients. Patients with newly diagnosed MM (aged ≥ 65 years) received eight induction cycles of bortezomib, lenalidomide, and dexamethasone (daratumumab was recommended for frail patients), with treatment intensity adjusted according to longitudinal changes in the frailty category (IMWG-FI) at each cycle. Of 90 patients, 33 (37%), 16 (18%), and 41 (45%) were fit, intermediate fit, and frail at baseline, respectively. Of 75 patients who had geriatric assessment at least twice, 28 (37%) experienced frailty category changes at least once. At analysis, 15/26 (58%) frail patients improved (27% became fit and 31% became intermediate fit), 4/15 (27%) intermediate fit patients either improved or deteriorated (two for each), and 6/30 (20%) fit patients deteriorated. During induction, 34/90 (38%) patients discontinued treatment, including 10/33 (30%) fit, 4/16 (25%) intermediate fit, and 20/41 (49%) frail; 14/40 (35%) frail patients discontinued treatment within the first two cycles, mainly because of non-hematologic toxicity (mostly infections). For fit, intermediate-fit, and frail patients, the overall response rate was 100%, 93%, and 73%, respectively; one-year overall survival was 90%, 75%, and 54%, respectively. Therefore, the individualized DynaFiT is feasible and promising for heterogeneous elderly patients. [ABSTRACT FROM AUTHOR]

Pulmonary arterial hypertension (PAH) is characterized by impaired regulation of pulmonary hemodynamics and vascular growth. Alterations of metabolism and bioenergetics are increasingly recognized as universal hallmarks of PAH, as metabolic abnormalities are identified in lungs and hearts of patients, animal models of the disease, and cells derived from lungs of patients. Mitochondria are the primary organelle critically mediating the complex and integrative metabolic pathways in bioenergetics, biosynthetic pathways, and cell signaling. Here, we review the alterations in metabolic pathways that are linked to the pathologic vascular phenotype of PAH, including abnormalities in glycolysis and glucose oxidation, fatty acid oxidation, glutaminolysis, arginine metabolism, one-carbon metabolism, the reducing and oxidizing cell environment, and the tricarboxylic acid cycle, as well as the effects of PAH-associated nuclear and mitochondrial mutations on metabolism. Understanding of the metabolic mechanisms underlying PAH provides important knowledge for the design of new therapeutics for treatment of patients. [ABSTRACT FROM AUTHOR]

Diagnosing Meckel's diverticulum in emergency conditions remains challenging, especially in adult cases for acute abdominal complaints. Here, retrospective analysis of computed tomography (CT) findings in such conditions was performed. Retrospective analysis of fifteen adults (sixteen CT scans) with a final diagnosis of Meckel's diverticulum who underwent a CT scan for acute abdominal complaints was performed. Nine patients received an intravenous (IV) contrast–enhanced CT scan; four of these were CT enteroclysis with oral contrast (mannitol). The accuracy of CT diagnosis was compared with pathological results. The overall accuracy of CT for diagnosing Meckel's diverticulum is 56.2% (9/16) in our cohort. The accuracy of non-IV contrast CT and IV contrast CT is 25% (4/16) and 77.8% (7/9). All patients undergoing oral contrast (mannitol)–enhanced CT promptly received correct diagnosis. Meckel's diverticulum localized mostly to the right quadrant, presenting with spherical/oblong morphology or blind-ended tubular aspects. Meckel's diverticulum contained liquid and gas-like substances, and sometimes enteroliths. Inflammatory infiltrates were present in 9 cases, one with concomitant appendicitis. Obstruction was observed in 6 patients. CT is valuable for identifying Meckel's diverticulum, especially in conjunction with contrast imaging and with good bowel preparation. An outpouching, blind-ended digestive structure from the distal small bowel is an alarm signal for Meckel's diverticulum. [ABSTRACT FROM AUTHOR]

Osteoarthritis (OA) is a degenerative joint disease characterized by joint pain, stiffness, and function degeneration with high incidence. Recent studies have been inspired based on the association between microRNAs (miRs) and therapeutic research of OA. Hence, the present study evaluates the effects of miR‐138 on chondrocyte proliferation, differentiation, and apoptosis through the WNT/β‐catenin signaling pathway in mice with OA by binding to NIMA‐related kinase 2 (NEK2). Appropriate dataset was selected from the Gene Expression Omnibus database, and differentially expressed genes and potential miRNAs that could regulate NEK2 were explored. A mouse model of OA was established. The expressions of miR‐138, NEK2, β‐catenin, GSK3β, Bcl‐2, Bcl‐2‐associated X protein (Bax), p53, MMP‐13, Col2, and Aggrecan and the phosphorylation levels of β‐catenin were determined by the reverse transcription quantitative polymerase chain reaction and Western blot analysis. The 3‐(4,5‐dimethyl‐2‐thiazolyl)‐2,5‐diphenyl‐2H‐tetrazolium bromide (MTT) assay and flow cytometry were employed to detect cell proliferation and apoptosis, respectively. The potential functional role of NEK2 was revealed to be related to the WNT/β‐catenin signaling pathway, and miR‐138 was the putative regulator of NEK2. miR‐138 expression was downregulated while expressions of NEK2 and β‐catenin as well as the phosphorylation levels of β‐catenin were upregulated in mice with OA. The chondrocytes treated with miR‐138 mimic and siRNA‐NEK2 exhibited reduced expressions of NEK2, β‐catenin, MMP‐13, Bax, and p53 and elevated expressions of Col2, Aggrecan, and Bcl‐2 as well as phosphorylation levels of β‐catenin along with enhanced chondrocytes' proliferation and suppressed cell apoptosis. Overexpression of miR‐138 induces cell survival and reduces WNT/β‐catenin signaling of OA chondrocytes through NEK2. © 2019 IUBMB Life, 71(9):1355–1366, 2019 [ABSTRACT FROM AUTHOR]

Long non-coding RNA (lncRNA)-NEF is a newly discovered lncRNA, which exhibits an inhibitory function on the metastasis of hepatocellular carcinoma, while its involvement in other types of malignancy are unknown. In the present study, tumor and adjacent healthy tissues were obtained from patients with non-small-cell lung cancer (NSCLC), and blood was obtained from patients with NSCLC and healthy individuals. Expression levels of lncRNA-NEF in tumor tissue samples, healthy tissue samples and serum were detected by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Receiver operating characteristic curve analysis and survival curve analysis were performed to evaluate the diagnostic and prognostic value of serum lncRNA-NEF for NSCLC. The effects of lncRNA-NEF overexpression in NSCLC cell lines on tumor cell proliferation, glucose uptake, glucose transporter 1 (GLUT1) protein expression and mRNA expression were investigated by Cell Counting kit-8 assay, glucose uptake assay, western blot analysis and RT-qPCR, respectively. It was identified that lncRNA-NEF was downregulated in NSCLC tissues, compared with healthy controls, and the serum level of lncRNA-NEF was negatively associated with primary tumor stage. Therefore, serum lncRNA-NEF may be a sensitive diagnostic and prognostic marker for NSCLC. Overexpression of lncRNA-NEF inhibited NSCLC cell proliferation and glucose uptake, and downregulated GLUT1 expression. Therefore, it can be concluded that lncRNA-NEF can target glucose transportation to inhibit the proliferation of NSCLC cells. [ABSTRACT FROM AUTHOR]

Aims: Arginine metabolism via inducible nitric oxide synthase (iNOS) and arginase 2 (ARG2) is higher in asthmatics than in healthy individuals. We hypothesized that a sub-phenotype of asthma might be defined by the magnitude of arginine metabolism categorized on the basis of high and low fraction of exhaled nitric oxide (FENO). Methods: To test this hypothesis, asthmatics (n = 52) were compared to healthy controls (n = 51) for levels of FENO, serum arginase activity, and airway epithelial expression of iNOS and ARG2 proteins, in relation to clinical parameters of asthma inflammation and airway reactivity. In parallel, bronchial epithelial cells were evaluated for metabolic effects of iNOS and ARG2 expression in vitro. Results: Asthmatics with high FENO (≥ 35 ppb; 44% of asthmatics) had higher expression of iNOS (P = 0.04) and ARG2 (P = 0.05) in the airway, indicating FENO is a marker of the high arginine metabolic endotype. High FENO asthmatics had the lowest FEV1% (P < 0.001), FEV1/FVC (P = 0.0002) and PC20 (P < 0.001) as compared to low FENO asthmatics or healthy controls. Low FENO asthmatics had near normal iNOS and ARG2 expression (both P > 0.05), and significantly higher PC20 (P < 0.001) as compared to high FENO asthmatics. In vitro studies to evaluate metabolic effects showed that iNOS overexpression and iNOS+ARG2 co-expression in a human bronchial epithelial cell line led to greater reliance on glycolysis with higher rate of pyruvate going to lactate. Conclusions: The high FENO phenotype represents a large portion of the asthma population, and is typified by greater arginine metabolism and more severe and reactive asthma. [ABSTRACT FROM AUTHOR]

[Display omitted] • A colorimetric and fluorescent chemosensor for Cu2+ based on internal charge transfer (ICT) was synthesized. • A visually dramatic color change from light green to orange, which can be used for qualitative determination of Cu2+. • Reliable detection of Cu2+ at concentrations ranging from 5.0 × 10−7 to 1.1 × 10−5 M with detection limit of 1.2 × 10−7 M was realized. A colorimetric and fluorescent chemosensor (CS1) for Cu2+ based on the mechanism of internal charge transfer (ICT) has been successfully designed and prepared by simple condensation of 4_(diethylamino)salicylaldehyde and oxalyl dihydrazide. Cu2+ in solution (DMSO/H 2 O = 7:3, v/v) by 5 mM NaAc–HAc at pH 7.0 was determined through dual channels: (1) "naked-eye" observation, a visually dramatic color change from light green to orange, which can be used for qualitative determination of Cu2+; (2) spectrofluorometry, which can quantificationally assay Cu2+. It provides a simple-to-use platform for reliable detection of Cu2+ at concentrations ranging from 5.0 × 10−7 to 1.1 × 10−5 M with detection limit of 1.2 × 10−7 M, which is nearly 2 × 102 times lower than the maximum allowable level of inorganic Cu2+ in drinking water (1.3 ppm, ∼20 µM) permitted by the EPA (Environmental Protection Agency), and the sensing detection of Cu2+ ions was reversible. [ABSTRACT FROM AUTHOR]

Asthma, a chronic inflammatory airway disease, is typified by high levels of TH2-cytokines and excessive generation of reactive nitrogen and oxygen species, which contribute to bronchial epithelial injury and airway remodeling. While immune function plays a major role in the pathogenesis of the disease, accumulating evidence suggests that altered cellular metabolism is a key determinant in the predisposition and disease progression of asthma. Further, several studies demonstrate altered mitochondrial function in asthmatic airways and suggest that these changes may be systemic. However, it is unknown whether systemic metabolic changes can be detected in circulating cells in asthmatic patients. Platelets are easily accessible blood cells that are known to propagate airway inflammation in asthma. Here we perform a bioenergetic screen of platelets from asthmatic and healthy individuals and demonstrate that asthmatic platelets show a decreased reliance on glycolytic processes and have increased tricarboxylic acid cycle activity. These data demonstrate a systemic alteration in asthma and are consistent with prior reports suggesting that oxidative phosphorylation is more efficient asthmatic individuals. The implications for this potential metabolic shift will be discussed in the context of increased oxidative stress and hypoxic adaptation of asthmatic patients. Further, these data suggest that platelets are potentially a good model for the monitoring of bioenergetic changes in asthma. [ABSTRACT FROM AUTHOR]

Also, there were no significant differences between patients with either 2-5% or 5-20% CPCs and those with >= 20% CPCs in PFS and OS ( I P i > 0.05). Compared to patients with < 2% CPCs, median PFS and OS of patients with 2-20% CPCs were 11.2 months (vs 18.8 months, I P i = 0.0001; Fig. [Extracted from the article]

A chitosan plate assay was employed to screen for chitosanase-producing bacterial strains and isolate 141 was found to exhibit high activity. Characterization of this isolate revealed that it belonged to Mitsuaria (designated as Mitsuaria sp. 141). The encoded chitosanase ( choA) gene was then cloned by PCR and the deduced amino acid sequence showed 98% identity to a formerly described Mitsuaria chitosanitabida 3001 ChoA (McChoA). Surprisingly, the ChoA encoded by Mitsuaria sp. 141 (MsChoA) appeared to have a much higher optimum temperature compared to McChoA. Site-directed mutagenesis was then employed to generate five MschoA mutant genes encoding MsChoA K204Q, R216K, T222N, R216K/T222N, or K204Q/R216K/T222N. All the ChoA mutants exhibited a much lower specific activity and a lower optimum temperature. The results confirmed that the substitution of three non-conserved amino acids accounts for the major reduction of the enzyme activity in MsChoA. Furthermore, the MschoA gene was cloned for over-expression in Pichia pastoris after coding sequence optimization. One of the P. pastoris transformants with Mut phenotype was found to produce 1,480.2 ± 340.9 U ChoA mL of cell culture by high-cell-density fermentation. This represents the highest yield of recombinant ChoA production that has ever been reported thus far. The recombinant P. pastoris strain should therefore be well suited for industrial-scale production of chitosanase. [ABSTRACT FROM AUTHOR]

Abstract: The airway mucosal epithelium is the first site of virus contact with the host, and the main site of infection and inflammation. Nitric oxide (NO) produced by the airway epithelium is vital to antiviral inflammatory and immune defense in the lung. Multiple mechanisms function coordinately to support high-level basal NO synthesis in healthy airway epithelium and further induction of NO synthesis in the infected airway of normal hosts. Hosts deficient in NO synthesis, such as those patients with cystic fibrosis, have impaired antiviral defense and may benefit from therapies to augment NO levels in the airways. [Copyright &y& Elsevier]

Dear Editor, Leukoencephalopathy is a term given to any disorder that affects the white matter in the CNS [[1]]. On August 19, the brain MRI revealed patchy T2/fluid-attenuated inversion recovery (FLAIR) hyperintense signal in bilateral frontal and parietal white matter, centrum semiovale, and corona radiate (Fig. Whereas daratumumab-associated AEs involving CNS are relatively rare (e.g., only one case of progressive multifocal leukoencephalopathy reported thus far in the trials involving daratumumab) [[2]], DRL has been reported in at least three cases [[3]], showing DRL as a late AE after long-term use of daratumumab (Supplemental Table S1). [Extracted from the article]

Pulmonary arterial endothelial cells (PAEC) are mechanistically linked to origins of pulmonary arterial hypertension (PAH). Here, global proteomics and phosphoproteomics of PAEC from PAH (n = 4) and healthy lungs (n = 5) were performed using LC-MS/MS to confirm known pathways and identify new areas of investigation in PAH. Among PAH and control cells, 170 proteins and 240 phosphopeptides were differentially expressed; of these, 45 proteins and 18 phosphopeptides were located in the mitochondria. Pathologic pathways were identified with integrative bioinformatics and human protein-protein interactome network analyses, then confirmed with targeted proteomics in PAH PAEC and non-targeted metabolomics and targeted high-performance liquid chromatography of metabolites in plasma from PAH patients (n = 30) and healthy controls (n = 12). Dysregulated pathways in PAH include accelerated one carbon metabolism, abnormal tricarboxylic acid (TCA) cycle flux and glutamate metabolism, dysfunctional arginine and nitric oxide pathways, and increased oxidative stress. Functional studies in cells confirmed abnormalities in glucose metabolism, mitochondrial oxygen consumption, and production of reactive oxygen species in PAH. Altogether, the findings indicate that PAH is typified by changes in metabolic pathways that are primarily found in mitochondria. [ABSTRACT FROM AUTHOR]

Mitochondrial dysfunction has emerged to be associated with a broad spectrum of diseases, and there is an increasing demand for accurate detection of mitochondrial DNA (mtDNA) variants. Whole genome sequencing (WGS) has been the dominant sequencing approach to identify genetic variants in recent decades, but most studies focus on variants on the nuclear genome. Whole genome sequencing is also costly and time consuming. Sequencing specifically targeted for mtDNA is commonly used in the diagnostic settings and has lower costs. However, there is a lack of pairwise comparisons between these two sequencing approaches for calling mtDNA variants on a population basis. In this study, we compared WGS and mtDNA-targeted sequencing (targeted-seq) in analyzing mitochondrial DNA from 1499 participants recruited into the Severe Asthma Research Program (SARP). Our study reveals that targeted-sequencing and WGS have comparable capacity to determine genotypes and to call haplogroups and homoplasmies on mtDNA. However, there exists a large variability in calling heteroplasmies, especially for low-frequency heteroplasmies, which indicates that investigators should be cautious about heteroplasmies acquired from different sequencing methods. Further research is highly desired to improve variant detection methods for mitochondrial DNA. [ABSTRACT FROM AUTHOR]

Soft modular biomimetic robots, driven by flexible actuators, are extensively used in various fields due to their excellent flexibility, environmental adaptability, and isomorphism. However, existing flexible modules typically possess no more than two degrees of freedom for structural limitations. This paper proposes a biomimetic robot module supported by a spring and actuated by water hydraulic artificial muscles (WHAMs). Combining the mechanical properties of WHAMs and spring, the static model of the soft module was established by force balance method. Moreover, the contraction force coefficient and contraction ratio coefficient of WHAMs were identified through the static characteristics test. The rod length coefficient and stress coefficient of the spring were also identified through the spring bending test. The errors between the experimental results and the model are analyzed and discussed, uncovering the main reasons. The influence of spring pre-compression, spring elasticity coefficient, initial working pressure of WHAM, and the installation distance of WHAM on the motion space of module were analyzed and discussed. This work serves as a guide for the structural design of flexible modules to meet specific requirements and lays the foundation for future research on integrated flexible biomimetic robots driven by WHAMs. [Display omitted] • Mechanical modeling of spring subjected to simultaneous axial load and bending moment. • Mechanical modeling of unidirectional deflection of modules based on symmetric variation of working pressure of WHAMs. • The effect of relevant factors on module movement is analyzed. [ABSTRACT FROM AUTHOR]

Abstract: The regulation of nitric oxide synthase 2 (NOS2) in airway epithelial cells plays a key role in the innate host response to a wide variety of microbial agents and also participates in the generation of pathologic airway inflammation. Among the important signalling cascades that direct NOS2 gene expression are nuclear factor κB (NFκB) and interferon-γ (IFNγ)/signal transducer and activator of transcription 1 (STAT-1). Previous studies suggest activator protein-1 (AP-1), in particular c-Fos component of AP-1, influences NOS2 expression. We investigated the effect of c-Fos modulation using RNA interference siRNA on NOS2 gene expression. A549 cells stably transfected with a plasmid overexpressing a c-Fos siRNA construct (FOSi) resulted in a decrease of NOS2 protein inducibility by IFN γ. In contrast, classical IFN γ inducible signal transduction pathways interferon regulated factor-1 (IRF-1) and pSTAT-1 were activated at a similar magnitude in FOSi and control cells. DNA–protein binding assays showed that c-Fos binding was present in wild type cells, but reduced in FOSi clones. FOSi clones had activation of NFκB detectable by DNA–protein binding assays, which may have contributed to a decrease of NOS2 expression. Overall, these studies indicate that c-Fos is a requisite and specific component for inducible NOS2 expression. [Copyright &y& Elsevier]

Pulmonary arterial hypertension (PAH) is an insidious disease characterized by severe remodeling of the pulmonary vasculature caused in part by pathologic changes of endothelial cell functions. Although heterogeneity of endothelial cells across various vascular beds is well known, the diversity among endothelial cells in the healthy pulmonary vascular bed and the pathologic diversity among pulmonary arterial endothelial cells (PAEC) in PAH is unknown and previously unexplored. Here single-cell RNA sequencing technology was used to decipher the cellular heterogeneity among PAEC in the human pulmonary arteries isolated from explanted lungs from three patients with PAH undergoing lung transplantation and three healthy donor lungs not utilized for transplantation. Datasets of 36,368 PAH individual endothelial cells and 36,086 healthy cells were analyzed using the SeqGeq bioinformatics program. Total population differential gene expression analyses identified 629 differentially expressed genes between PAH and controls. Gene Ontology and Canonical Ingenuity analysis revealed pathways that are known to be involved in pathogenesis, as well as unique new pathways. At the individual cell level, dimensionality reduction followed by density based clustering revealed the presence of eight unique PAEC clusters that were typified by proliferative, angiogenic or quiescent phenotypes. While control and PAH harbored many similar subgroups of endothelial cells, PAH had greater proportions of angiogenic and proliferative subsets. These findings identify that only specific subgroups of PAH PAEC have gene expression different than healthy PAEC, and suggest these subpopulations lead to the pathologic functions leading to remodeling. [ABSTRACT FROM AUTHOR]

Pulmonary arterial hypertension (PAH) is an insidious disease characterized by severe remodeling of the pulmonary vasculature caused in part by pathologic changes of endothelial cell functions. Although heterogeneity of endothelial cells across various vascular beds is well known, the diversity among endothelial cells in the healthy pulmonary vascular bed and the pathologic diversity among pulmonary arterial endothelial cells (PAEC) in PAH is unknown and previously unexplored. Here single-cell RNA sequencing technology was used to decipher the cellular heterogeneity among PAEC in the human pulmonary arteries isolated from explanted lungs from three patients with PAH undergoing lung transplantation and three healthy donor lungs not utilized for transplantation. Datasets of 36,368 PAH individual endothelial cells and 36,086 healthy cells were analyzed using the SeqGeq bioinformatics program. Total population differential gene expression analyses identified 629 differentially expressed genes between PAH and controls. Gene Ontology and Canonical Ingenuity analysis revealed pathways that are known to be involved in pathogenesis, as well as unique new pathways. At the individual cell level, dimensionality reduction followed by density based clustering revealed the presence of eight unique PAEC clusters that were typified by proliferative, angiogenic or quiescent phenotypes. While control and PAH harbored many similar subgroups of endothelial cells, PAH had greater proportions of angiogenic and proliferative subsets. These findings identify that only specific subgroups of PAH PAEC have gene expression different than healthy PAEC, and suggest these subpopulations lead to the pathologic functions leading to remodeling. [ABSTRACT FROM AUTHOR]

The sex discordance in COVID-19 outcomes has been widely recognized, with males generally faring worse than females and a potential link to sex steroids. A plausible mechanism is androgen-induced expression of TMPRSS2 and/or ACE2 in pulmonary tissues that may increase susceptibility or severity in males. This hypothesis is the subject of several clinical trials of anti-androgen therapies around the world. Here, we investigated the sex-associated TMPRSS2 and ACE2 expression in human and mouse lungs and interrogated the possibility of pharmacologic modification of their expression with anti-androgens. We found no evidence for increased TMPRSS2 expression in the lungs of males compared to females in humans or mice. Furthermore, in male mice, treatment with the androgen receptor antagonist enzalutamide did not decrease pulmonary TMPRSS2. On the other hand, ACE2 and AR expression was sexually dimorphic and higher in males than females. ACE2 was moderately suppressible with enzalutamide administration. Our work suggests that sex differences in COVID-19 outcomes attributable to viral entry are independent of TMPRSS2. Modest changes in ACE2 could account for some of the sex discordance. [ABSTRACT FROM AUTHOR]

Background: Antiphospholipid syndrome (APS) is an acquired pre-thrombotic autoimmune condition, which produces autoantibodies called antiphospholipid antibodies (APL) against phospholipid-binding plasma proteins. The diagnosis of APS requires at least one of Sapporo standard clinical manifestations and one laboratory criteria (persistently medium/high titer anticardiolipin antibodies, and/or medium/high titer anti-β2-glycoprotein I antibodies, and/or a positive lupus anticoagulant test). Gastrointestinal lesions are rarely reported in APS patients. APS cases with recurrent abdominal pain as the first clinical manifestation are even rarer.Case Presentation: This report describes an APS case with recurrent abdominal pain as the first clinical manifestation of antiphospholipid syndrome. The patient has a history of two miscarriages. Computed tomography of the abdomen confirmed mesenteric thrombosis and intestinal obstruction while laboratory tests for serum antiphospholipid and anti-β2-glycoprotein I antibodies were positive. This led to the diagnosis of APS.Conclusions: This paper provides useful information on gastrointestinal manifestations and APS, also including a brief literature review about possible gastrointestinal symptoms of APS. [ABSTRACT FROM AUTHOR]

Acute lung injury (ALI) is a severe lung disease with high mortality rate. Research has highlighted that the immune response to ALI is associated with significant changes in the expression of several microRNAs (miRNAs) in the lungs. In our research, we speculated that miR-124 moderated the severity of ALI through comprehensive suppression of the mitogen-activated protein kinase (MAPK) signaling pathway activation by targeting MAPK14. A mouse model of ALI was established by array of experiments. The expression of MAPK14 and miR-124 was assessed in the tissues of ALI mice and the expression of inflammatory cytokines in ALI mice was determined. The expression of the related kinases in the MAPK signaling pathway and key cytokines in the pro-inflammatory response were assessed by a series of experiments. Immunohistochemistry and TUNEL staining were adopted to detect lung tissue cell proliferation and apoptosis in mice with ALI. MiR-124 was poorly expressed and MAPK14 was highly expressed in tissues of ALI mice. Overexpression of miR-124 or silence of MAPK14 alleviated the symptoms of ALI by down-regulating inflammatory cytokines expression, which could intrinsically suppress the expression of associated proteins in the MAPK signaling pathway and the downstream pro-inflammatory response factors, promote proliferation and inhibit apoptosis of lung tissue cells. Overexpression of MAPK14 inverted the phenotypic changes induced by overexpressing miR-124. These results indicated that miR-124 could alleviate the symptoms of ALI by inhibiting the activation of MAPK signaling pathway via subsequent targeting of MAPK14. Additionally, miR-124 may serve as a useful biomarker to alleviate the severity of septic shock-induced lung injury. • Our study reported the function of miR-124 in ALI. • miR-124 was poorly expressed and MAPK14 was highly expressed in ALI mice. • miR-124 inactivates MAPK signaling pathway by targeting MAPK14 to relieve ALI. • miR-124 promotes proliferation and inhibits apoptosis of cells by suppressing MAPK14. • Our study provides a theoretical basis for the treatment of acute lung injury. [ABSTRACT FROM AUTHOR]

The roles of long non-coding RNA (lncRNA) FENDRR in non-small cell lung cancer (NSCLC) cells progression have never been revealed. As cancer stem cells (CSCs) act important roles in tumor progression, here, we focused on FENDRR roles in NSCLC cell stemness. We found that lncRNA FENDRR expression was significantly decreased in lung cancer tissues and cells, especially in NSCLC cells. Then we constructed NSCLC cells with FENDRR stable overexpression and revealed that FENDRR overexpression attenuated the stemness of NSCLC cells, evident by decreased stemness markers expression and capacity of cell spheroid formation. Mechanistically, we found that FENDRR could directly and specifically bind to the 3′ untranslated region (3′UTR) of multidrug resistance gene 1 (MDR1), hinder the binding of RNA binding protein HuR to MDR1 3′UTR and thus decrease MDR1 expression. Finally, we demonstrated that FENDRR exerted its effects on NSCLC cell stemness through the HuR/MDR1 axis. Our results suggest that FENDRR attenuates NSCLC cell stemness through inhibiting the HuR/MDR1 axis. [ABSTRACT FROM AUTHOR]

• The eutectic region strength of SAC305 solder decreases with aging by nanoindentation analysis. • The dual-phase RVE CPFEM can simulate aging effect of SAC305 solder. • The simulated strain "hot zones" by DP CPFEM are consistent with SEM-DIC calculation. Because typical solder joints undergo thermal aging during use, models simulating the behaviors of solder under mechanical stress must accurately reflect the changes in properties caused by thermal aging effects. The uniaxial deformation of SAC305 (96.5Sn–3.0Ag–0.5Cu wt.%) solder under different aging conditions indicates that the mechanical properties of solder are weakened with aging. In this study, the nanoindentation method was used to evaluate the effect of aging on the mechanical properties of the β-Sn dendritic regions and eutectic regions of SAC305. Based on this evaluation, a dual-phase (DP) representative volume element (RVE) crystal plasticity finite-element method (CPFEM) model was developed to simulate the thermal aging effects of SAC305 solder. In situ tensile tests performed with scanning electron microscopy (SEM) showed that the tensile deformation was concentrated in the β-Sn dendritic regions of the solder. The DP CPFEM model was established based on the microstructures shown by electron backscatter diffraction (EBSD) analysis performed during the in situ tensile tests. This model was used to verify the accuracy of the DP CPFEM in simulating the deformation localization by comparison with the strain field distribution observed via SEM–digital image correlation (DIC) technology. The developed DP CPFEM model allows the prediction of the potential failure locations of a microscale solder joint. [Display omitted] [ABSTRACT FROM AUTHOR]

High levels of arginine metabolizing enzymes, including inducible nitric oxide synthase (iNOS) and arginase (ARG), are typical in asthmatic airway epithelium; however, little is known about the metabolic effects of enhanced arginine flux in asthma. Here, we demonstrated that increased metabolism sustains arginine availability in asthmatic airway epithelium with consequences for bioenergetics and inflammation. Expression of iNOS, ARG2, arginine synthetic enzymes, and mitochondrial respiratory complexes III and IV was elevated in asthmatic lung samples compared with healthy controls. ARG2 overexpression in a human bronchial epithelial cell line accelerated oxidative bioenergetic pathways and suppressed hypoxia-inducible factors (HIFs) and phosphorylation of the signal transducer for atopic Th2 inflammation STAT6 (pSTAT6), both of which are implicated in asthma etiology. Arg2-deficient mice had lower mitochondrial membrane potential and greater HIF-2α than WT animals. In an allergen-induced asthma model, mice lacking Arg2 had greater Th2 inflammation than WT mice, as indicated by higher levels of pSTAT6, IL-13, IL-17, eotaxin, and eosinophils and more mucus metaplasia. Bone marrow transplants from Arg2-deficient mice did not affect airway inflammation in recipient mice, supporting resident lung cells as the drivers of elevated Th2 inflammation. These data demonstrate that arginine flux preserves cellular respiration and suppresses pathological signaling events that promote inflammation in asthma. [ABSTRACT FROM AUTHOR]

"All data associated with this study are available in the main text or the Supplementary materials." now reads: "All raw mRNA-seq data files are available on NCBI's Gene Expression Omnibus (GEO), accessible using the following link https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE185479." Correction to: I Scientific Reports i https://doi.org/10.1038/s41598-021-94163-y, published online 19 July 2021 The original version of this Article omitted an URL to all of the raw single-cell omics data in Data availability section. [Extracted from the article]

Abstract: Reactive oxygen species have been implicated in the pathogenesis of asthma and, in atopic asthmatics, endogenous superoxide dismutase (SOD) enzyme levels are known to decrease. This suggests that replacing a failed endogenous SOD enzyme system with a mimetic of the endogenous enzyme would be beneficial and protective. In this study we demonstrate that removal of superoxide by the SOD mimetic (SODm) M40403 reduces the respiratory and histopathological lung abnormalities due to ovalbumin (OA) aerosol in a model of allergic asthma-like reaction in sensitized guinea pigs. Both respiratory abnormalities and bronchoconstriction in response to OA challenge are nearly absent in naïve animals, while they sharply became severe in sensitized animals. In addition, OA aerosol induced a reduction of MnSOD activity which was paralleled with bronchiolar lumen reduction, pulmonary air space hyperinflation, mast cell degranulation, eosinophil infiltration, bronchial epithelial cell apoptosis, increase in myeloperoxidase activity, malonyldialdehyde production and 8-hydroxy-2′-deoxyguanosine formation in the lung tissue, as well as elevation of PGD2 in the bronchoalveolar lavage fluid. Treatment with M40403 restored the levels of MnSOD activity and significantly reduced all the above parameters. In summary, our findings support the potential therapeutic use of SOD mimetics in asthma and anaphylactic reactions and account for a critical role for superoxide in acute allergic asthma-like reaction in actively sensitized guinea pig. [Copyright &y& Elsevier]

• A new unified constitutive model is proposed to describe the thermomechanical response of solder. • The model is capable of predicting the in-phase (IP) and out-phase (OP) hysteresis loop of solder under thermomechanical symmetrical loading very well. • The model can accurately simulate the thermo-mechanical ratcheting behavior under IP, OP, and isothermal loading conditions. To describe the mechanical properties of SAC305 under comprehensive loading conditions, a new model was proposed based on the internal variable theory. The tensile property of SAC305 can be normalized by dividing the stress with the saturated stress. The flow law and kinematic hardening rule can be determined by relating the property to the evolution of internal variables. Since SAC305 had no obvious yield stress, strain hardening/softening was simulated by the evolution of drag stress. The model can be used to accurately simulate the hysteresis loop and ratcheting tests at constant temperature. However, the unified model greatly overpredicted the ratcheting strain associated with thermomechanical ratcheting. Thus, a correlation term for the rate of temperature change must be introduced to adjust the back stress with changing temperature. Therefore, the modulus of back stress will be less than that of saturated stress during the entire loading process. By correlating with the kinematic hardening rule, the model could be used to simulate the thermo-mechanical ratcheting behavior, and the results were well in agreement with experimental results. Image, graphical abstract [ABSTRACT FROM AUTHOR]

The article presents information on a hypothesis which studies that phenotype of Primary Pulmonary Hypertension (PPH) edothelial cells in angiogenesis causes Primary Pulmonary Hypertension (PPH) disease. The article authors say that they developed hypothesis to substantiate that PPH cells in angiogenesis causes PPH . For this research they isolated and characterized Primary Pulmonary Artery Endothelial Cells (PAECs) from control and PPH lungs. The article author says that in the absence of growth factors, PPH PAECs have is three times greater in PPH patients.