RÉSUMÉ
Objective@#To evaluate the dietary risk of neonicotinoid insecticides in market-sold vegetables in Guangzhou City, so as to provide insights into ensuring food safety for residents.@*Methods@#Forty-five samples of 21 kinds of vegetables were collected from supermarkets and farmer's markets in Guangzhou City from June to September in 2022, and 10 kinds of neonicotinoid insecticides were determined using liquid chromatography-mass spectrometry (LC-MS). The vegetable consumption was obtained through the survey of food consumption and nutrients intake of residents in Guangzhou City. The dietary risk was evaluated by calculating daily exposure and non-carcinogenic risk quotients of neonicotinoid insecticides. @*Results@#A total of 27 samples of vegetables were detected with neonicotinoid insecticides, and the detection rate was 60.00%. Among 10 kinds of neonicotinoid insecticides, 6 kinds were identified, including clothianidin, thiamethoxam, imidacloprid, acetamiprid, dinotefuranand and nitenpyram. The detection rates of clothianidin, thiamethoxam and imidacloprid were relatively high (26.67%, 11.11% and 6.67%), and some samples exceeded the standard, with the rate of 4.44%, 2.22% and 2.22%, respectively. The total exposure of neonicotinoid pesticides (IMIRPF) was 3 053.00 ng/g, and the contents and IMIRPF of imidacloprid were the highest in roots and tubers. The daily exposure of imidacloprid, acetamiprid, dinotefuran, clothianidin, thiamethoxam and nitenpyram was 34.58, 3.85, 1.20, 6.87, 7.19 and 0.86 ng/(kg·d). Non-carcinogenic risk quotients of imidacloprid, acetamiprid, dinotefuran, clothianidin, thiamethoxam and nitenpyram was 5.76×10-4, 0.55×10-4, 0.06×10-4, 0.69×10-4, 0.90×10-4 and 0.02×10-4, respectively, which was lower than 1; and the sum of non-carcinogenic risk quotients was 7.98×10-4, which was lower than 1. @*Conclusions@#The dietary risk of neonicotinoid pesticides is low in 21 kinds of market-sold vegetables in Guangzhou City; however, the contents of neonicotinoid insecticides in some vegetable samples exceed the standard. The supervision of vegetable markets should be strengthened.
RÉSUMÉ
Osteoporosis (OP), a common systemic metabolic bone disease, is characterized by low bone mass, increasing bone fragility and a high risk of fracture. At present, the clinical treatment of OP mainly involves anti-bone resorption drugs and anabolic agents for bone, but their long-term use can cause serious side effects. The development of stem cell therapy and regenerative medicine has provided a new approach to the clinical treatment of various diseases, even with a hope for cure. Recently, the therapeutic advantages of the therapy have been shown for a variety of orthopedic diseases. However, these stem cell-based researches are currently limited to animal models; the uncertainty regarding the post-transplantation fate of stem cells and their safety in recipients has largely restricted the development of human clinical trials. Nevertheless, the feasibility of mesenchymal stem cells to treat osteoporotic mice has drawn a growing amount of intriguing attention from clinicians to its potential of applying the stem cell-based therapy as a new therapeutic approach to OP in the future clinic. In the current review, therefore, we explored the potential use of mesenchymal stem cells in human OP treatment.
Sujet(s)
Animaux , Souris , Ostéoporose/thérapie , Résorption osseuse , Cellules souches mésenchymateusesRÉSUMÉ
Sepsis is the systemic inflammatory response caused by infection. Cardiac dysfunction is an acknowledged result of sepsis.Shengjiang Powder, a prescribed traditional Chinese medicine, showed anti-infection and antipyretic functions in ourprevious study. In this study, we established a septic rat model via cecal ligation puncture (CLP) to evaluate the effects ofShengjiang Powder on sepsis and the involvement of P38 mitogen activated protein kinase (P38-MAPK) signaling. The 10main ingredients of Shengjiang Powder were identified by LC–MS. The results of this study indicated that ShengjiangPowder at a concentration of 3.0 g/kg with SB203580 (an inhibitor of P38-MAPK) could improve myocardial injury,ameliorate the histopathological abnormalities, decrease apoptosis and upregulate proliferating cell nuclear antigen (PCNA)levels in myocardial tissues. Further, cytokine mRNA expression levels (tumor necrosis factor - alpha, TNF-a and interleukin 6, IL-6) were decreased by Shengjiang Powder and SB203580 in the myocardial tissues. Furthermore, the p-P38protein level in myocardial tissues was upregulated in septic rats but decreased upon treatment with Shengjiang Powder andSB203580; however, the relative protein level of P38 showed no significant changes. Collectively, Shengjiang Powdershowed a myocardial protective effect on rats with CLP-induced sepsis.
RÉSUMÉ
Abstract Introduction: Hepatic ischemia-reperfusion injury is a common pathophysiological process in liver surgery. Whether Propofol can reduce myocardial ischemia-reperfusion injury induced by hepatic ischemia-reperfusion injury in rats, together with related mechanisms, still needs further studies. Objective: To investigate if propofol would protect the myocardial cells from apoptosis with hepatic ischemia-reperfusion injury. Methods: Male Sprague-Dawley rats (n = 18) were randomly allocated into three groups: Sham Group (Group S, n = 6), Hepatic Ischemia-reperfusion Injury Group (Group IR, n = 6) and Propofol Group (Group P, n = 6). Group S was only subjected to laparotomy. Group IR was attained by ischemia for 30 min and reperfusion for 4 h. Group P was subjected identical insult as in Group IR with the administration of propofol started 10 min before ischemia with 120 mg.kg−1, following by continuous infusion at 20 mg.kg−1.h−1. Cell apoptosis was examined by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling assay. Endoplasmic reticulum Ca2+-ATPase2 (SERCA2) and cysteine-containing aspartic acid cleaved-caspase3 (cleaved-caspase3) were assayed by western blot and Altimeter polymerase chain reaction. Results: Apoptosis rate was increased, with mRNA and protein of SERCA2 down-regulated and cleaved-caspase3 up-regulated in Group IR compared with Group S (p < 0.01). Apoptosis rate was decreased, with mRNA and protein of SERCA2 up-regulated and cleaved-caspase3 down-regulated in Group P compared with Group IR (p < 0.01). Conclusions: Propofol can reduce hepatic ischemia-reperfusion injury-induced myocardial cell apoptosis, meanwhile, can up-regulate mRNA and protein of SERCA2 in rats.
Resumo Introdução: A lesão hepática por isquemia-reperfusão é um processo fisiopatológico comum em cirurgias hepáticas. Mais estudos ainda são necessários para avaliar se o propofol pode reduzir a lesão de isquemia-reperfusão miocárdica induzida pela lesão de isquemia-reperfusão hepática em ratos, juntamente com os mecanismos que estão relacionados. Objetivo: Investigar se propofol protege as células do miocárdio da apoptose com a lesão hepática por isquemia-reperfusão. Métodos: Ratos machos da raça Sprague-Dawley (n = 18) foram alocados aleatoriamente em três grupos: Grupo Sham (Grupo S, n = 6), Grupo Lesão Hepática por Isquemia-reperfusão (Grupo IR, n = 6) e Grupo Propofol (Grupo P, n = 6). O Grupo S foi submetido apenas à laparotomia. O grupo IR foi submetido à isquemia por 30 min e reperfusão por 4 h. O grupo P foi submetido à mesma isquemia do grupo IR, com a administração de 120 mg.kg-1 de propofol iniciada 10min antes da isquemia, seguida de infusão contínua a 20 mg.kg-1.h-1. A apoptose celular foi examinada por meio do ensaio de marcação de terminações dUTP pela deoxinucleotidil transferase. Retículo endoplasmático Ca2+-ATPase2 (SERCA2) e caspase-3 do ácido aspártico contendo cisteína (caspase-3 clivada) foram avaliados com o ensaio western blot e reação em cadeia da polimerase. Resultados: A taxa de apoptose foi maior com mRNA e proteína de SERCA2 regulados para baixo e caspase-3 clivada suprarregulada no Grupo IR, em comparação com o Grupo S (p < 0,01). A taxa de apoptose foi menor com mRNA e proteína de SERCA2 suprarregulada e caspase-3 clivada sub-regulada no Grupo P, em comparação com o Grupo IR (p < 0,01). Conclusões: O propofol pode reduzir a apoptose de células miocárdicas induzida por lesão hepática por isquemia-reperfusão. Entretanto, pode suprarregular o mRNA e a proteína de SERCA2 em ratos.
Sujet(s)
Animaux , Mâle , Rats , Lésion d'ischémie-reperfusion/prévention et contrôle , Propofol/administration et posologie , Apoptose/effets des médicaments et des substances chimiques , Anesthésiques intraveineux/administration et posologie , Myocytes cardiaques/effets des médicaments et des substances chimiques , Myocytes cardiaques/physiologie , Sarcoplasmic Reticulum Calcium-Transporting ATPases/biosynthèse , Sarcoplasmic Reticulum Calcium-Transporting ATPases/effets des médicaments et des substances chimiques , Foie/vascularisation , Répartition aléatoire , Propofol/pharmacologie , Rat Sprague-Dawley , Anesthésiques intraveineux/pharmacologieRÉSUMÉ
ABSTRACT LOB (lateral organ boundaries)-domain proteins define a family of plant-specific transcription factors involved in developmental process from embryogenesis to seed production. They play a crucial role in shaping the plant architecture through coordinating cell fate at meristem to organ boundaries. Identification of LBD genes from Brassica rapa genome, and analysis of phylogeny,gene structure, chromosome location, phylogenetic and tissue expression pattern analysis of LBD family genes in Chinese cabbage will be useful to the functions identification of plant LBD genes. Based on Brassica rapa genome database and bioinformatic method, Chinese cabbage LBD family genes were identified and the genes were sequenced. A phylogenetic tree was created using the MEGA5 program. Gene structure and chromosomes location were done by MapDraw, GSDS and Clustal X. Expression pattern of LBD genes at different development stages was analyzed based on RNA-seq. A total of 62 LBD genes were identified and could be classified into two classes and four subclasses according to the gene structure and conserved domain phylogeny relationship. Distribution mapping showed that the predicted LBDs were unevenly localized on all the 10 chromosomes, suggesting that they have an extensive distribution on the Brassica rapa chromosomes. Most of the LBD genes had differential expression pattern and showed highly diverse tissue-specific expression and functional diversity. To our knowledge, this is the first report of a genome wide analysis of the Brassica rapa LBD gene family, which would provide valuable information for understanding the classification and putative functions of the gene family.
RÉSUMÉ
Long non-coding RNAs (lncRNAs) play an important role in the pathogenesis of cardiovascular diseases, especially in myocardial infarction and ischemia/reperfusion (I/R). However, the underlying molecular mechanism remains unclear. In this study, we determined the role and the possible underlying molecular mechanism of lncRNA-ROR in myocardial I/R injury. H9c2 cells and human cardiomyocytes (HCM) were subjected to either hypoxia/reoxygenation (H/R), I/R or normal conditions (normoxia). The expression levels of lncRNA-ROR were detected in serum of myocardial I/R injury patients, H9c2 cells, and HCM by qRT-PCR. Then, levels of lactate dehydrogenase (LDH), malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GSH-PX) were measured by kits. Cell viability, apoptosis, apoptosis-associated factors, and p38/MAPK pathway were examined by MTT, flow cytometry, and western blot assays. Furthermore, reactive oxygen species (ROS) production was determined by H2DCF-DA and MitoSOX Red probes with flow cytometry. NADPH oxidase activity and NOX2 protein levels were measured by lucigenin chemiluminescence and western blot. Results showed that lncRNA-ROR expression was increased in I/R patients and in H/R treatment of H9c2 cells and HCM. Moreover, lncRNA-ROR significantly promoted H/R-induced myocardial injury via stimulating release of LDH, MDA, SOD, and GSH-PX. Furthermore, lncRNA-ROR decreased cell viability, increased apoptosis, and regulated expression of apoptosis-associated factors. Additionally, lncRNA-ROR increased phosphorylation of p38 and ERK1/2 expression and inhibition of p38/MAPK, and rescued lncRNA-ROR-induced cell injury in H9c2 cells and HCM. ROS production, NADPH oxidase activity, and NOX2 protein levels were promoted by lncRNA-ROR. These data suggested that lncRNA-ROR acted as a therapeutic agent for the treatment of myocardial I/R injury.
Sujet(s)
Humains , Ischémie myocardique/métabolisme , Lésion de reperfusion myocardique/métabolisme , ARN long non codant/métabolisme , Apoptose , Technique de Western , Survie cellulaire , Glutathione peroxidase/métabolisme , Hydro-lyases/métabolisme , Malonaldéhyde/métabolisme , Ischémie myocardique/génétique , Lésion de reperfusion myocardique/génétique , Myocytes cardiaques , Réaction de polymérisation en chaine en temps réel , ARN long non codant/génétique , Transduction du signal , Superoxide dismutase/métabolisme , TransfectionRÉSUMÉ
Bone is a unique tissue which could regenerate completely after injury rather than heal itself with a scar. Compared with other tissues the difference is that, during bone repairing and regeneration, after the inflammatory phase the mesenchymal stem cells (MSCs) are recruited to the injury site and differentiate into either chondroblasts or osteoblasts precursors, leading to bone repairing and regeneration. Besides these two precursors, the MSCs can also differentiate into adipocyte precursors, skeletal muscle precursors and some other mesodermal cells. With this multiline-age potentiality, the MSCs are probably used to cure bone injury and other woundings in the near future. Here we will introduce the recent developments in understanding the mechanism of MSCs action in bone regeneration and repairing.
Sujet(s)
Humains , Animaux , Ostéogenèse/physiologie , Régénération osseuse/physiologie , Différenciation cellulaire/physiologie , Chondrogenèse/physiologie , Transplantation de cellules souches mésenchymateuses , Cellules souches mésenchymateuses/physiologie , Ostéoblastes/physiologie , Chondrocytes/physiologieRÉSUMÉ
As a precursor, pimelic acid plays an important role in biotin biosynthesis pathway of Bacillus subtilis. Fermentations supplemented with pimelic acid could improve the production of biotin, however, with a disadvantage-high cost. So it is necessary to improve the biosynthesis of pimelic acid via genetic engineering in B. subtilis. In this study, we constructed a recombinant B. subtilis strain for improving the synthesis of pimelic acid, in which a maltose-inducible Pglv promoter was inserted into the upstream of the cistron bioI-orf2-orf3 and, meanwhile, flanked by the tandem cistrons via a single crossover event. The copy number of the integrant was amplified by high-concentration resistance screen and increased to 4-5 copies. The production of pimelic acid from multiple copies integrant was about 4 times higher than that from single copy (1017.13 ug/ml VS. 198.89 μg/ml). And when induced by maltose the production of pimelic acid was about 2 times of that under non-induction conditions (2360.73 μg/ml VS. 991.59 ug/ml). Thus, these results demonstrated that the production of pimelic acid was improved obviously through reconstructed B. subtilis. It also suggested that our expression system provided a convenient source of pimelic acid that would potentially lower the cost of production of biotin from engineered B. subtilis.