Comparison of Direct Pars Repair Techniques for Spondylolysis in Young Patients: Pedicle Screw Hook System versus Pedicle Screw Rod.

Background: Lumbar spondylolysis (LS) poses a potential threat, and there is a need to evaluate and compare the effectiveness of direct pars repair techniques. Objective: To assess and compare the clinical and radiographic outcomes of direct pars repair techniques using the pedicle screw hook system (PSHS) and the pedicle screw rod system (PSRS) in young symptomatic patients with lumbar spondylolysis. Methods: A retrospective study was conducted to compare clinical and radiological data in young symptomatic LS patients after surgery. Records of 45 post-surgery LS patients with a minimum 24-month follow-up (January 2014 to June 2019) were reviewed. A total of 26 patients underwent PSHS, and 19 had PSRS. Treatment outcomes were analyzed using the visual analog pain scale (VAS), Oswestry disability index (ODI), MacNab criteria, lumbar fusion status, and Pfirrmann grading standards. Patient baseline characteristics were also compared between the two groups. Results: No disc degeneration was observed in either PSHS or PSRS groups at 24 months postoperatively, according to the Pfirrmann grading scale. The PSRS group outperformed the PSHS group in operative time, intraoperative blood loss, postoperative drainage, length of hospital stays, ODI, VAS values at 3 months postoperatively, and fusion status at 6 months postoperatively. No notable differences were observed in other parameters during the 24-month follow-up period, and no significant surgical complications were recorded. Conclusions: Direct pars repair techniques using PSHS and PSRS yielded satisfactory clinical and radiographic results in young patients with symptomatic LS. PSRS, compared to PSHS, demonstrated greater effectiveness in young individuals with LS and promoted early recovery.

Exogenous Application of Amino Acids Alleviates Toxicity in Two Chinese Cabbage Cultivars by Modulating Cadmium Distribution and Reducing Its Translocation.

Plants communicate underground by secreting multiple amino acids (AAs) through their roots, triggering defense mechanisms against cadmium (Cd) stress. However, the specific roles of the individual AAs in Cd translocation and detoxification remain unclear. This study investigated how exogenous AAs influence Cd movement from the roots to the shoots in Cd-resistant and Cd-sensitive Chinese cabbage cultivars (Jingcui 60 and 16-7 cultivars). The results showed that methionine (Met) and cysteine (Cys) reduced Cd concentrations in the shoots of Jingcui 60 by approximately 44% and 52%, and in 16-7 by approximately 43% and 32%, respectively, compared to plants treated with Cd alone. However, threonine (Thr) and aspartic acid (Asp) did not show similar effects. Subcellular Cd distribution analysis revealed that AA supplementation increased Cd uptake in the roots, with Jingcui 60 preferentially storing more Cd in the cell wall, whereas the 16-7 cultivar exhibited higher Cd concentrations in the organelles. Moreover, Met and Cys promoted the formation of Cd-phosphate in the roots of Jingcui 60 and Cd-oxalate in the 16-7 cultivar, respectively. Further analysis showed that exogenous Cys inhibited Cd transport to the xylem by downregulating the expression of HMA2 in the roots of both cultivars, and HMA4 in the 16-7 cultivar. These findings provide insights into the influence of exogenous AAs on Cd partitioning and detoxification in Chinese cabbage plants.

Exogenous IL-25 ameliorates airway neutrophilia via suppressing macrophage M1 polarization and the expression of IL-12 and IL-23 in asthma.

BACKGROUND: Severe asthma is associated with substantial mortality and has unmet therapeutic need. A subset of severe asthma is characterized by neutrophilic airway inflammation. Classically activated (or M1) macrophages which express IL-12 and IL-23 are associated with airway neutrophilia in asthma. Exogenous IL-25 was reported to suppress intestinal inflammation in animal models of inflammatory bowel diseases via suppressing IL-12 and IL-23 production. We hypothesize that IL-25 ameliorates airway neutrophilia via inhibiting macrophage M1 polarization and the expression of IL-12 and IL-23 in asthma. METHODS: In a mouse model of neutrophil-dominant allergic airway inflammation, the effect of mouse recombinant IL-25 on airway inflammation were assessed by H&E staining and bronchoalveolar lavage (BAL) cell counting. The percentage of M1 macrophages in lung tissue and BAL cells were analyzed by flow cytometry. Quantitative PCR and immunostaining were performed to measure the expression of Il12, Il23, and inflammatory cytokines. Mechanistic experiments were performed in primary culture of macrophages from mouse lungs. The expression of IL-12, IL-23 and IL-25 in sputum was analyzed in a cohort of severe asthma and subjects with eosinophilic or non-eosinophilic asthma. RESULTS: Intranasal administration of IL-25 markedly decreased the number of neutrophils in BAL cells in a murine model of neutrophil-dominant allergic airway inflammation. Moreover, exogenous IL-25 decreased the number of M1 macrophages, and reduced the expression of IL-12, IL-23 in the lungs of the mouse model. Exogenous IL-25 also inhibited the expression of inflammatory cytokines IL-1ß, IFN-γ, TNF-α and IL-17 A. In vitro, IL-25 suppressed IL-12 and IL-23 expression in lipopolysaccharide (LPS)-stimulated primary culture of mouse pulmonary macrophages. Mechanistically, IL-25 inhibited LPS-induced c-Rel translocation to nucleus via STAT3-dependent signaling. In a cohort of severe asthma, IL-25 protein levels in sputum were significantly lower than control subjects. The transcript levels of IL-12 and IL-23 were increased whereas IL-25 transcripts were decreased in sputum cells from subjects with non-eosinophilic asthma compared to eosinophilic asthma. CONCLUSIONS: IL-25 expression is downregulated in subjects with severe or non-eosinophilic asthma. Exogenous IL-25 ameliorates airway neutrophilia, at least in part, via inhibiting macrophage M1 polarization and the expression of IL-12 and IL-23.

Special tea products featuring functional components: Health benefits and processing strategies.

The functional components in tea confer various potential health benefits to humans. To date, several special tea products featuring functional components (STPFCs) have been successfully developed, such as O-methylated catechin-rich tea, γ-aminobutyric acid-rich tea, low-caffeine tea, and selenium-rich tea products. STPFCs have some unique and enhanced health benefits when compared with conventional tea products, which can meet the specific needs and preferences of different groups and have huge market potential. The processing strategies to improve the health benefits of tea products by regulating the functional component content have been an active area of research in food science. The fresh leaves of some specific tea varieties rich in functional components are used as raw materials, and special processing technologies are employed to prepare STPFCs. Huge progress has been achieved in the research and development of these STPFCs. However, the current status of these STPFCs has not yet been systematically reviewed. Here, studies on STPFCs have been comprehensively reviewed with a focus on their potential health benefits and processing strategies. Additionally, other chemical components with the potential to be developed into special teas and the application of tea functional components in the food industry have been discussed. Finally, suggestions on the promises and challenges for the future study of these STPFCs have been provided. This paper might shed light on the current status of the research and development of these STPFCs. Future studies on STPFCs should focus on screening specific tea varieties, identifying new functional components, evaluating health-promoting effects, improving flavor quality, and elucidating the interactions between functional components.

Cadherin-26 Amplifies Airway Epithelial IL-4 Receptor Signaling in Asthma.

Activation of IL-4R (IL-4 receptor) signaling in airway epithelial cells leads to airway hyperresponsiveness and mucus overproduction in asthma. CDH26 (cadherin-26), a cadherin implicated in the polarization of airway epithelial cells, is upregulated in asthma. However, the role of CDH26 in asthma remains unknown. In this study, we demonstrated that Cdh26 deficiency significantly reduced airway mucus overproduction, airway hyperresponsiveness, and airway eosinophilia in a murine model of allergic airway disease. Interestingly, allergen-induced Il-4Rα upregulation in airway epithelium was markedly reduced in Cdh26-/- mice. In cultured human bronchial epithelial cells, CDH26 knockdown inhibited IL-13, a ligand for IL-4R; induced IL-4Rα and IL-13Rα1 (IL-13 receptor α1) upregulation; and suppressed downstream Jak1 (Janus kinase 1) and Stat6 (signal transducer and activator of transcription 6) phosphorylation. Moreover, CDH26 knockdown inhibited IL-13-induced MUC5AC and eosinophilic chemokine expression. These results suggest that CDH26 plays a key role in epithelial IL-4R signaling activation and downstream effectors. In contrast, CDH26 overexpression amplified IL-13-activated IL-4R signaling in BEAS-2B cells. In the airway epithelium of patients with asthma, IL-4Rα expression was elevated, and CDH26 was the only cadherin that was upregulated among 11 cadherin family members. CDH26 expression was strongly correlated with epithelial IL-4Rα and MUC5AC expression, sputum eosinophilia, and fractional exhaled nitric oxide in patients with asthma. Taken together, we identified CDH26 as a key regulator of epithelial IL-4R signaling in asthma and a potential therapeutic target for IL-4R-mediated allergic diseases.

Epithelial microRNA-30a-3p targets RUNX2/HMGB1 axis to suppress airway eosinophilic inflammation in asthma.

BACKGROUND: Type 2-high asthma is a prominent endotype of asthma which is characterized by airway eosinophilic inflammation. Airway epithelial cells play a critical role in the pathogenesis of asthma. Our previous miRNA profiling data showed that miR-30a-3p was downregulated in bronchial epithelial cells from asthma patients. We hypothesize that epithelial miR-30a-3p plays a role in asthma airway inflammation. METHODS: We measured miR-30a-3p expression in bronchial brushings of asthma patients (n = 51) and healthy controls (n = 16), and analyzed the correlations between miR-30a-3p expression and airway eosinophilia. We examined whether Runt-related transcription factor 2 (RUNX2) was a target of miR-30a-3p and whether RUNX2 bound to the promoter of high mobility group box 1 (HMGB1) by using luciferase reporter assay and chromatin immunoprecipitation (ChIP)-PCR. The role of miR-30a-3p was also investigated in a murine model of allergic airway inflammation. RESULTS: We found that miR-30a-3p expression were significantly decreased in bronchial brushings of asthma patients compared to control subjects. Epithelial miR-30a-3p expression was negatively correlated with parameters reflecting airway eosinophilia including eosinophils in induced sputum and bronchial biopsies, and fraction of exhaled nitric oxide in asthma patients. We verified that RUNX2 is a target of miR-30a-3p. Furthermore, RUNX2 bound to the promoter of HMGB1 and upregulated HMGB1 expression. RUNX2 and HMGB1 expression was both enhanced in airway epithelium and was correlated with each other in asthma patients. Inhibition of miR-30a-3p enhanced RUNX2 and HMGB1 expression, and RUNX2 overexpression upregulated HMGB1 in BEAS-2B cells. Intriguingly, airway overexpression of mmu-miR-30a-3p suppressed Runx2 and Hmgb1 expression, and alleviated airway eosinophilia in a mouse model of allergic airway inflammation. CONCLUSIONS: Epithelial miR-30a-3p could possibly target RUNX2/HMGB1 axis to suppress airway eosinophilia in asthma.

Study of Compound Sanqi Nanoparticles for Local Infection of Hydrocephalus Patients after Neurosurgery Medium Craniocerebral Injury.

Panax notoginseng is the dried root and rhizome of Panax notoginseng, which has the effect of lowering blood lipid, lowering blood pressure and promoting blood circulation to remove blood stasis. At present, the research on Panax notoginseng is mainly focused on its pharmacological action and its compound preparation, but the research on the granule of Panax notoginseng is less. This paper mainly studied the clinical study of compound notoginseng nanoparticles in the treatment of local infection in patients with hydrocephalus after medium craniocerebral injury in neurosurgery. The purpose of this article is to investigate the effects of compound notoginseng nanoparticles on serum TNF-α, IL-2 and IL-6 in rats with craniocerebral injury and to verify the protective effect of compound notoginseng nanoparticles on the body after craniocerebral injury. In this paper, 90 patients admitted to a hospital in this city were divided into a control group, model group and compound notoginseng nanoparticle group. According to the Zealonga method, the neurological function deficit score of experimental rats in each group was evaluated. The levels of TNF-α, IL-2 and IL-6 in the serum of the three groups were observed 1, 3 and 5 days after treatment. RESULTS: Compared with serum TNF-α, IL-2 and IL-6 of the three groups, there were significant differences in the main effects of time and intervention (P < 0.05). CONCLUSIONS: Compound notoginseng nanoparticles can reduce the contents of TNF-α and IL-6 in serum and increase the expression of IL-2 in rats with craniocerebral injury.

Decreased eosinophil counts and elevated lactate dehydrogenase predict severe COVID-19 in patients with underlying chronic airway diseases.

BACKGROUND: Several predictors of COVID-19 severity have been reported. However, chronic airway inflammation characterised by accumulated lymphocytes or eosinophils may affect the pathogenesis of COVID-19. METHODS: In this retrospective cohort study, we reviewed the medical records of all patients with laboratory-confirmed COVID-19 with chronic bronchitis, chronic obstructive pulmonary disease (COPD) and asthma admitted to the Sino-French New City Branch of Tongji Hospital, a large regional hospital in Wuhan, China, from 26 January to 3 April. The Tongji Hospital Ethics Committee approved this study. RESULTS: There were 59 patients with chronic bronchitis, COPD and asthma. When compared with non-severe patients, severe patients were more likely to have decreased lymphocyte counts (0.6×109/L vs 1.1×109/L, p<0.001), eosinopaenia (<0.02×109/L; 73% vs 24%, p<0.001), increased lactate dehydrogenase (LDH) (471.0 U/L vs 230.0 U/L, p<0.001) and elevated interleukin 6 level (47.4 pg/mL vs 5.7 pg/mL, p=0.002) on admission. Eosinopaenia and elevated LDH were significantly associated with disease severity in both univariate and multivariate regression models including the above variables. Moreover, eosinophil count and LDH level tended to return to normal range over time in both groups after treatment and severe patients recovered slower than non-severe patients, especially in eosinophil count. CONCLUSIONS: Eosinopaenia and elevated LDH are potential predictors of disease severity in patients with COVID-19 with underlying chronic airway diseases. In addition, they could indicate disease progression and treatment effectiveness.

Increased epithelial galectin-13 expression associates with eosinophilic airway inflammation in asthma.

BACKGROUND: Airway eosinophilic inflammation is a central feature in asthma which is mainly driven by type 2 response. The expression of galectin-13 was up-regulated in a parasitic infection model which is also characterized by type 2 immune response. We hypothesized that galectin-13 may be involved in airway eosinophilic inflammation in asthma. OBJECTIVE: To unveil the role of galectin-13 in asthma airway inflammation. METHODS: We measured galectin-13 expressions in bronchial brushings, sputum, and plasma of asthma patients (n = 54) and healthy controls (n = 15), and analysed the correlations between galectin-13 expression and airway eosinophilia. We used human bronchial epithelial cell line 16HBE to investigate the possible mechanism by which galectin-13 participates in eosinophilic inflammation. RESULTS: The expression of galectin-13 was markedly increased in subjects with asthma compared to controls. Epithelial galectin-13 mRNA levels in asthmatic subjects were strongly correlated with eosinophilic airway inflammation (the percentage of sputum eosinophils, the number of eosinophils in bronchial submucosa and FeNO) and the expression of Th2 signature genes (CLCA1, POSTN and SERPINB2). Inhaled corticosteroid (ICS) treatment reduced plasma galectin-13 levels, and baseline plasma galectin-13 levels reflect the response to ICS treatment. In cultured 16HBE cells, knockdown of galectin-13 suppressed IL-13-stimulated MCP-1 and eotaxin-1 expression by inhibiting the activation of EGFR and ERK. CONCLUSIONS & CLINICAL RELEVANCE: Galectin-13 is a novel marker for airway eosinophilia in asthma, and may contribute to allergic airway eosinophilic inflammation by up-regulating the expression of MCP-1 and eotaxin-1. Plasma galectin-13 levels may be useful for predicting responses to ICS treatment.

microRNA-218-5p plays a protective role in eosinophilic airway inflammation via targeting δ-catenin, a novel catenin in asthma.

BACKGROUND: microRNA (miR)-218-5p is involved in cigarette smoke-induced airway inflammation. In our earlier asthma epithelial miRNA profiling data, miR-218-5p was the top 2 down-regulated miRNA. We hypothesize that miR-218-5p plays a role in asthma airway inflammation. OBJECTIVE: To unveil the role of miR-218-5p and its target gene in asthma airway inflammation. METHODS: We measured miR-218-5p expression in bronchial brushings of asthma patients (n = 50) and healthy controls (n = 15), and analysed the correlations between miR-218-5p expression and airway eosinophilia. We examined whether CTNND2 was a target of miR-218-5p, and the expression of 12 catenin family members in bronchial brushings, in cultured human bronchial epithelial (HBE) cells and BEAS-2B cells. We explored the role of miR-218-5p-CTNND2 pathway using a murine model of allergic airway inflammation. RESULTS: Epithelial miR-218-5p expression was significantly decreased and negatively correlated with eosinophils in induced sputum and bronchial biopsies, and other type 2 biomarkers in asthma patients. We verified that CTNND2 (encoding δ-catenin) was a target of miR-218-5p. Remarkably, CTNND2 was the most significantly up-regulated catenin compared with the other 11 catenin family members in bronchial brushings of asthma patients, IL-13-stimulated HBE and BEAS-2B cells. Moreover, epithelial CTNND2 expression positively correlated with airway eosinophilia in asthma. Airway mmu-miR-218-5p expression was also decreased, and Ctnnd2 expression was increased in a murine model of allergic airway inflammation. Intriguingly, mmu-miR-218-5p overexpression suppressed airway hyperresponsiveness, eosinophilic airway inflammation and Ctnnd2 up-regulation in the mouse model. Finally, perturbation of miR-218-5p or CTNND2 expression significantly altered chemokine CCL26 expression in the cell cultures and the mouse model. CONCLUSIONS AND CLINICAL RELEVANCE: Epithelial miR-218-5p plays a protective role in eosinophilic airway inflammation via targeting CTNND2, a novel catenin in asthma, and suppressing chemokine CCL26 expression.

Combined use of tranexamic acid and rivaroxaban in posterior lumbar interbody fusion safely reduces blood loss and transfusion rates without increasing the risk of thrombosis-a prospective, stratified, randomized, controlled trial.

PURPOSE: This prospective, stratified, randomized, single-blind, placebo-controlled multicentre study investigated the safety and effectiveness of reducing blood loss and preventing venous thromboembolism (VTE) during posterior lumbar interbody fusion (PLIF) in patients with stenosis or spondylolisthesis using the combination of tranexamic acid (TXA) and rivaroxaban. METHODS: The Autar score was evaluated in patients after admission. Patients with an Autar score ≤ 10 were randomized to group A or B. Group A was the placebo-controlled group. Patients in group B were treated with 1 g TXA via intravenous injection and 1 g TXA for external use. Patients with an Autar score > 10 were randomized to group C or D. Patients in group C were treated with 10-mg rivaroxaban qd for 35 days after surgery. Patients in group D received the same treatment as those in group B intra-operatively and as those in group C post-operatively. RESULTS: A total of 599 patients from eight hospitals participated in this clinical trial. The total blood loss, intra-operative blood loss, and drainage volume were reduced by the administration of TXA (group A vs group B, P < 0.01; group C vs group D, P < 0.01), and the blood transfusion rate was also decreased (group A vs group B, P < 0.01; group C vs group D, P < 0.01). There were no significant differences (P > 0.05) in the VTE incidence rates among group A and group B. In patients with high-risk thrombosis, the number of patients with VTE was only three and seven after the application of rivaroxaban. Epidural haematoma was not discovered in any patients in our trial. CONCLUSION: The combined application of tranexamic acid and rivaroxaban significantly reduced the amount of blood loss and the transfusion rate during PLIF surgery and avoided an increase in the probability of thrombosis and the occurrence of epidural haematoma. TRIAL REGISTRATION NUMBER AND DATE OF REGISTRATION: ChiCTR-1800016430 2018-06-01.

Epithelial SERPINB10, a novel marker of airway eosinophilia in asthma, contributes to allergic airway inflammation.

Serine peptidase inhibitor, clade B, member 10 (SERPINB10) expression is increased in IL-13-stimulated human bronchial epithelial cells and in a murine model of allergic airway inflammation. However, the role of SERPINB10 in asthma remains unknown. We examined the association between epithelial SERPINB10 expression and airway eosinophilia in subjects with asthma and the role of Serpinb10 in allergic airway inflammation in an animal model. Epithelial SERPINB10 mRNA and protein expression were markedly increased in subjects with asthma ( n = 60) compared with healthy controls ( n = 25). Epithelial SERPINB10 mRNA levels were significantly correlated with airway hyperresponsiveness (AHR) and three parameters reflecting airway eosinophilia including the percentage of sputum eosinophils, the number of eosinophils in bronchial submucosa, and fraction of exhaled nitric oxide in subjects with asthma. Moreover, epithelial SERPINB10 expression was strongly correlated with the epithelial gene signature ( CLCA1, POSTN, and SERPINB2) for type 2 status. In normal human bronchial epithelial cells cultured at air-liquid interface, knockdown of SERPINB10 suppressed IL-13-stimulated periostin (encoded by POSTN) and CCL26 (eotaxin-3) expression by inhibiting the activation of p38 MAPK. Epithelial CCL26 mRNA levels were correlated with SERPINB10 expression in subjects with asthma. Airway knockdown of Serpinb10 alleviated AHR, airway eosinophilia and the expression of periostin and Ccl26 in a murine model of allergic airway disease. Taken together, epithelial SERPINB10 is a novel marker for airway eosinophilia in asthma. Epithelial SERPINB10 contributes to allergic airway eosinophilic inflammation, at least in part, by regulating the expression of periostin and CCL26.

Decreased epithelial and sputum miR-221-3p associates with airway eosinophilic inflammation and CXCL17 expression in asthma.

Airway eosinophilic inflammation is a key feature of type 2 high asthma. The role of epithelial microRNA (miR) in airway eosinophilic inflammation remains unclear. We examined the expression of miR-221-3p in bronchial brushings, induced sputum, and plasma from 77 symptomatic, recently diagnosed, steroid-naive subjects with asthma and 36 healthy controls by quantitative PCR and analyzed the correlation between miR-221-3p expression and airway eosinophilia. We found that epithelial, sputum, and plasma miR-221-3p expression was significantly decreased in subjects with asthma. Epithelial miR-221-3p correlated with eosinophil in induced sputum and bronchial biopsies, fraction of exhaled nitric oxide, blood eosinophil, epithelial gene signature of type 2 status, and methacholine provocative dosage required to cause a 20% decline in forced expiratory volume in the first second in subjects with asthma. Sputum miR-221-3p also correlated with airway eosinophilia and was partially restored after inhaled corticosteroid treatment. Inhibition of miR-221-3p expression suppressed chemokine (C-C motif) ligand (CCL) 24 (eotaxin-2), CCL26 (eotaxin-3), and periostin (POSTN) expression in BEAS-2B bronchial epithelial cells. We verified that chemokine (C-X-C motif) ligand (CXCL) 17, an anti-inflammatory chemokine, is a target of miR-221-3p, and epithelial CXCL17 expression significantly increased in asthma. CXCL17 inhibited CCL24, CCL26, and POSTN expression via the p38 MAPK pathway. Airway overexpression of miR-221-3p exacerbated airway eosinophilic inflammation, suppressed CXCL17 expression, and enhanced CCL24, CCL26, and POSTN expression in house dust mite-challenged mice. Taken together, epithelial and sputum miR-221-3p are novel biomarkers for airway eosinophilic inflammation in asthma. Decreased epithelial miR-221-3p may protect against airway eosinophilic inflammation by upregulating anti-inflammatory chemokine CXCL17.

MicroRNA-645 promotes metastasis of osteosarcoma via targeting tumor suppressor NM23 nucleoside diphosphate kinase 2.

Osteosarcoma is the most common non-hematological primary bony malignancy in children and young adults with tumor metastasis being a common event at diagnosis. Understanding the pathogenesis of metastatic osteosarcoma may help identify potential therapeutic targets. In this study, we found that the level of microRNA-645 (miR-645) in osteosarcoma tumor tissues was significantly increased compared with their paired non-tumorous tissues, and was associated with histologic grade, TNM staging, lymph metastasis and distant metastasis. Knockdown of miR-645 caused a remarkable inhibition of migration of osteosarcoma U2OS cells. Furthermore, miR-645 inhibited NME2 (nucleoside diphosphate kinase 2) expression through directly binding to its 3' untranslated region. In human osteosarcoma tissues, we also found that NME2 was significantly decreased in tumor tissues, and its level was negatively correlated with miR-645. In addition, silencing NME2 attenuated the decreased cell migration by knockdown of miR-645, suggesting that it was involved in the miR-645 induced cell migration of osteosarcoma cells. Taken together, we found that miR-645 was up-regulated in osteosarcoma tissues and could promote osteosarcoma cell migration through directly inhibiting the tumor suppressor NME2. Our data provide novel insight into the role of miR-645 in osteosarcoma and indicate that miR-645 might be a potential therapeutic target of osteosarcoma.

Design and Analysis of a Data Fusion Scheme in Mobile Wireless Sensor Networks Based on Multi-Protocol Mobile Agents.

Sensors are increasingly used in mobile environments with wireless network connections. Multiple sensor types measure distinct aspects of the same event. Their measurements are then combined to produce integrated, reliable results. As the number of sensors in networks increases, low energy requirements and changing network connections complicate event detection and measurement. We present a data fusion scheme for use in mobile wireless sensor networks with high energy efficiency and low network delays, that still produces reliable results. In the first phase, we used a network simulation where mobile agents dynamically select the next hop migration node based on the stability parameter of the link, and perform the data fusion at the migration node. Agents use the fusion results to decide if it should return the fusion results to the processing center or continue to collect more data. In the second phase. The feasibility of data fusion at the node level is confirmed by an experimental design where fused data from color sensors show near-identical results to actual physical temperatures. These results are potentially important for new large-scale sensor network applications.

Environmental impacts and production performances of organic agriculture in China: A monetary valuation.

Organic agriculture has developed rapidly in China since the 1990s, driven by the increasing domestic and international demand for organic products. Quantification of the environmental benefits and production performances of organic agriculture on a national scale helps to develop sustainable high yielding agricultural production systems with minimum impacts on the environment. Data of organic production for 2013 were obtained from a national survey organized by the Certification and Accreditation Administration of China. Farming performance and environmental impact indicators were screened and indicator values were defined based on an intensive literature review and were validated by national statistics. The economic (monetary) values of farming inputs, crop production and individual environmental benefits were then quantified and integrated to compare the overall performances of organic vs. conventional agriculture. In 2013, organically managed farmland accounted for approximately 0.97% of national arable land, covering 1.158 million ha. If organic crop yields were assumed to be 10%-15% lower than conventional yields, the environmental benefits of organic agriculture (i.e., a decrease in nitrate leaching, an increase in farmland biodiversity, an increase in carbon sequestration and a decrease in greenhouse gas emissions) were valued at 1921 million RMB (320.2 million USD), or 1659 RMB (276.5 USD) per ha. By reducing the farming inputs, the costs saved was 3110 million RMB (518.3 million USD), or 2686 RMB (447.7 USD) per ha. The economic loss associated with the decrease in crop yields from organic agriculture was valued at 6115 million RMB (1019.2 million USD), or 5280 RMB (880 USD) per ha. Although they were likely underestimated because of the complex relationships among farming operations, ecosystems and humans, the production costs saved and environmental benefits of organic agriculture that were quantified in our study compensated substantially for the economic losses associated with the decrease in crop production. This suggests that payment for the environmental benefits of organic agriculture should be incorporated into public policies. Most of the environmental impacts of organic farming were related to N fluxes within agroecosystems, which is a call for the better management of N fertilizer in regions or countries with low levels of N-use efficiency. Issues such as higher external inputs and lack of integration cropping with animal husbandry should be addressed during the quantification of change of conventional to organic agriculture, and the quantification of this change is challenging.

Co-delivery of indomethacin and uricase as a new strategy for inflammatory diseases associated with high uric acid.

Uric acid is the final metabolite in humans. High level of uric acid chronically induces urate deposition, aggravates kidney damage, and concomitantly causes an increase in inflammatory factors. Alleviating acute inflammation and decreasing uric acid levels are the key points in the treatment of inflammatory diseases associated with high uric acid. However, a drug delivery system that combines anti-inflammatory and uric acid reduction functions at the same time remains a challenge to be settled. Here, we designed a nanocrystal-based co-delivery platform, IND Nplex, characterized by loading of indomethacin (IND) and uricase. Compared with free IND or uricase, IND Nplex possessed a better anti-inflammatory effect by restraining the release of inflammation-related factors in vitro. In addition, pharmacokinetic and biodistribution studies revealed that IND Nplex significantly prolonged the retention time in vivo and was more concentrated in the kidney. In acute gouty arthritis model rats, IND Nplex markedly relieved ankle joint swelling and mitigated synovial inflammation. In acute kidney injury model rats, IND Nplex indicated better biocompatibility and significant amelioration of renal fibrosis. Moreover, IND Nplex showed the effect of anti-inflammatory and improved renal function via determination of inflammatory factors and biochemical markers in the serum and kidney. In conclusion, these results indicate that IND Nplex exerts anti-inflammatory activity and uric acid-lowering effect and could become a promising candidate for the treatment of uric acid-related diseases.

Amino acid application inhibits root-to-shoot cadmium translocation in Chinese cabbage by modulating pectin methyl-esterification.

The exogenous application of amino acids (AAs) generally alleviates cadmium (Cd) toxicity in plants by altering their subcellular distribution. However, the physiological mechanisms underlying AA-mediated cell wall (CW) sequestration of Cd in Chinese cabbage remain unclear. Using two genotypes of Chinses cabbage, Jingcui 60 (Cd-tolerant) and 16-7 (Cd-sensitive), we characterized the root structure, subcellular distribution of Cd, CW component, and related gene expression under the Cd stress. Cysteine (Cys) supplementation led to a reduction in the Cd concentration in the shoots of Jingcui 60 and 16-7 by 65.09 % and 64.03 %, respectively. Addition of Cys alleviated leaf chlorosis in both cultivars by increasing Cd chelation in the root CW and reducing its distribution in the cytoplasm and organelles. We further demonstrated that Cys supplementation mediated the downregulation of PMEI1 expression and improving the activity of pectin methyl-esterase (PME) by 17.98 % and 25.52 % in both cultivars, respectively, compared to the Cd treatment, resulting in an approximate 12.00 %-14.70 % increase in Cd retention in pectin. In contrast, threonine (Thr) application did not significantly alter Cd distribution in the shoots of either cultivar. Taken together, our results suggest that Cys application reduces Cd root-to-shoot translocation by increasing Cd sequestration in the root CW through the downregulation of pectin methyl-esterification.

CuI-catalyzed aerobic oxidative α-aminaton cyclization of ketones to access aryl or alkenyl-substituted imidazoheterocycles.

CuI-catalyzed aerobic oxidative synthesis of imidazoheterocycles has been achieved. Four hydrogen atoms were removed in one step. This protocol was compatible with a broad range of functional groups, and it has been also successfully extended to unsaturated ketones, bringing about the formation of alkenyl-substituted imidazoheterocycles, which were difficult to prepare by previous means. Preliminary mechanistic studies indicated that this reaction was most likely to proceed through a catalytic Ortoleva-King reaction. By using this method, the marketed drug Zolimidine could be prepared with 90% yield on a gram scale from commercially available materials.