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At present, the research and innovation of packaging materials are in a period of rapid development. Starch, a sustainable, low-cost, and abundant polymer, can develop environmentally friendly packaging alternatives, and it possesses outstanding degradability and reproducibility in terms of improving environmental issues and reducing oil resources. However, performance limitations, such as less mechanical strength and lower barrier properties, limit the application of starch in the packaging industry. The properties of starch-based films can be improved by modifying starch, adding reinforcing groups, or blending with other polymers. It is of significance to study starch as an active and intelligent packaging option for prolonging shelf life and monitoring the extent of food deterioration. This paper reviews the development of starch-based films, the current methods to enhance the mechanical and barrier properties of starch-based films, and the latest progress in starch-based activity, intelligent packaging, and food applications. The potential challenges and future development directions of starch-based films in the food industry are also discussed.
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Chronic diseases, especially cardiovascular diseases (CVD), have become one of the main causes affecting human health. Hypertension is a prominent representative of CVD. The formation and development of hypertension is closely related to people's daily diet. A large number of studies have shown that excessive intake of salt (NaCl) could increase the risk of hypertension. In recent years, more and more investigations have focused on other cations that may be contained in edible salt, exploring whether they have an effect on hypertension and the underlying mechanism. This article focuses on the relationship between four metal elements (potassium, calcium, magnesium, and zinc) and hypertension, by discussing the main metabolic pathway, the impact of diet intake on blood pressure, and especially the regulation mechanisms on blood pressure in detail. At the same time, some opinions and suggestions are put forward, combined with the current hot topics "salt reduction" and "salt substitution".
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Enfermedades Cardiovasculares , Hipertensión , Cationes , Ingestión de Alimentos , Humanos , Sodio , Cloruro de Sodio , Cloruro de Sodio Dietético/efectos adversosRESUMEN
Endothelial dysfunction is an initial and essential step in vascular-remodeling diseases, including atherosclerosis and neointima formation. During vascular remodeling, activated endothelial cells can release pro-inflammatory factors that promote phenotypic switching of vascular smooth muscle cells (VSMCs) to the proliferative phenotype. We previously reported that MEK1/2 inhibitor, U0126, has a protective effect on the development of atherosclerosis and vascular calcification. However, the effect of MEK1/2 inhibitors on neointimal formation and the underlying mechanism is not fully understood. We determined that MEK1/2 inhibitor reduced carotid artery ligation-induced neointimal formation, while increased collagen and elastin levels and vascular integrality. Mechanistically, MEK1/2 inhibitor or ERK1/2 siRNA increased miR-126-3p level in endothelial cells, thereby inhibiting expression of regular of G-protein signaling 16 (RGS16), a miR-126-3p target gene, to activate the C-X-C motif chemokine ligand 12 (CXCL12)/C-X-C motif chemokine receptor 4 (CXCR4) signaling pathway. Accordingly, miR-126-3p was also increased by U0126 in serum and carotid artery. RGS16 was inhibited while CXCR4 and CXCL12 was increased by U0126 in neointimal areas, especially in the endothelium. Moreover, similar results were observed in atherosclerotic plaques of high-fat diet-fed apolipoprotein E deficiency (apoE-/-) mice. In addition, vascular cell adhesion molecule 1 (VCAM-1), another miR-126-3p target gene, was reduced by U0126 in the neointimal areas, resulting reduced monocytes/macrophages accumulation. Taken together, our results indicate that MEK1/2 inhibitor can reduce neointima formation by activating endothelial miR-126-3p production to facilitate endothelium repair while reduce monocyte adhesion/infiltration.
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Aterosclerosis , MicroARNs , Quinasas de Proteína Quinasa Activadas por Mitógenos/antagonistas & inhibidores , Inhibidores de Proteínas Quinasas/farmacología , Animales , Aterosclerosis/genética , Quimiocina CXCL12/metabolismo , Células Endoteliales/metabolismo , Ligandos , Ratones , MicroARNs/genética , MicroARNs/metabolismo , Neointima/genética , Neointima/metabolismo , Receptores CXCR4/metabolismo , Transducción de SeñalRESUMEN
The bioactive lipid sphingosine 1-phosphate (S1P) is implicated in many pivotal processes for the physiological and pathological actions via activating five types of G-protein-coupled S1P receptors (S1PR1-5). The role of S1P in renal cell carcinoma (RCC) and its receptor subtype specific mediating mechanism are poorly studied. So we focus on the regulatory role of S1P in RCC progression and the receptor subtypes involved in S1P-induced actions, intending to further clarify a novel therapeutic target for RCC. Analysis of The Cancer Genome Atlas (TCGA) databases showed that the patients with high expression of S1PR3 had significantly worse overall than with low expression. We further demonstrated that S1P could promote proliferation, migration, and epithelial-mesenchymal transition (EMT) of renal cancer cells in vitro, and the actions were enhanced with the increase of S1PR3 expression. Meanwhile, the results in animal experiments also showed that S1PR3 could accelerate tumorigenesis and metastasis of RCC. Our study also clarified the mechanism for S1P induced cell proliferation is mediated by S1PR3/Gi/p38/Akt/p65/cyclin D1-CDK4 pathway and the main pathway for migration is S1PR3/Gi/q/ERK/p38/p65. In addition, S1PR3 was involved in epidermal growth factor (EGF)-induced actions by enhancing protein expression, not by transactivation of epidermal growth factor receptor (EGFR). These results also further supported our conclusion that the carcinogenic role of S1P/S1PR3 axis. Thus, our findings provide that S1PR3 may be a promising small molecular therapeutic target for S1PR3 expressed cancers.
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Carcinoma de Células Renales , Neoplasias Renales , Animales , Carcinoma de Células Renales/genética , Receptores ErbB/genética , Femenino , Humanos , Neoplasias Renales/genética , Masculino , FN-kappa B , Receptores de Esfingosina-1-Fosfato/metabolismoRESUMEN
BACKGROUND: Dexmedetomidine (DEX) has a pharmacological profile that should allow rapid recovery and prevent undesirable outcomes such as pulmonary complications. METHODS: This large retrospective study compared the beneficial effects of perioperative infusion of DEX with propofol on the postoperative outcome after coronary artery bypass graft surgery. We reviewed patients' medical notes at Luoyang Central Hospital from 1st January 2012 to 31st December 2019. All continuous variables, if normally distributed, were presented as mean ± SD; Otherwise, the non-normally distributed data and categorical data were presented as median (25-75 IQR) or number (percentage). The Mann-Whitney U test and Chi-square test were used to evaluate the difference of variables between the DEX and propofol groups. Multivariate logistic regression analysis was performed on the main related and differential factors in the perioperative period. RESULTS: A total of 1388 patients were included in the study; of those, 557 patients received propofol infusion, and 831 patients received dexmedetomidine. DEX significantly reduced postoperative pulmonary complications compared with propofol, 7.82% vs 13.29%; P < 0.01, respectively. When compared with propofol, DEX significantly shortened the duration of mechanical lung ventilation, 18 (13,25) hours vs 21 (16,37) hours; P < 0.001, the length of stay in the intensive care unit, 51 (42,90) vs 59 (46,94.5) hours; P = 0.001 and hospital stay, 20 (17,24) vs 22 (17,28) days; P < 0.001, respectively. The incidences of postoperative wound dehiscence and infection were significantly reduced with DEX compared with propofol groups, 2.53% vs 6.64%; P < 0.001, respectively. Interestingly, patients receiving DEX had significantly shorter surgical time compared to propofol; 275 (240,310) vs 280 (250,320) minutes respectively (P = 0.005) and less estimated blood loss (P = 0.001). CONCLUSION: Perioperative infusion of dexmedetomidine improved the desirable outcomes in patients who had coronary artery bypass graft surgery compared with propofol.
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Puente de Arteria Coronaria/métodos , Dexmedetomidina/farmacología , Hipnóticos y Sedantes/farmacología , Complicaciones Posoperatorias/epidemiología , Propofol/farmacología , Anciano , China/epidemiología , Estudios de Cohortes , Femenino , Humanos , Tiempo de Internación/estadística & datos numéricos , Masculino , Persona de Mediana Edad , Respiración Artificial/estadística & datos numéricos , Estudios RetrospectivosRESUMEN
Current studies have demonstrated that significant increased LPA levels to be observed in ascites in patients with ovarian cancer. Although several studies have shown that Lysophosphatidic acid (LPA) related to the progression of ovarian cancer, which LPA receptors (LPARs) and G-coupled protein subtypes mediated in LPA actions have not been clearly elucidated. This study aimed to clarify the roles of LPA and it is subtype-specific LPARs mediating mechanisms in ovarian cancer integrated using bioinformatic analysis and biological experimental approaches. The big data analysis shown that LPA3 was the only differentially expressed LPA receptor among the six LPARs in ovarian cancer and further verified in immunohistochemistry of tissue microarrays. Also found that LPA3 was also highly expressed in ovarian cancer tissue and ovarian cancer cells. Importantly, LPA significantly promoted the proliferation and migration of LPA3-overexpressing ovarian cancer cells, while the LPA-induced actions blocked by Ki16425, a LPAR1/3 antagonist treated, and LPA3-shRNA transfected. In vivo study indicated that the LPA3-overexpressing cell-derived tumors metastasis, tumors volume, and tumors mass were apparently increased in xenografted nude mice. In addition, we also observed that LPA3 was differential high expression in ovarian cancer tissue of the patients. Our studies further confirmed the LPA3/Gi/MAPKs/NF-κB signals were involved in LPA-induced oncogenic actions in ovarian cancer cells. Our findings indicated that the LPA3 might be a novel precise therapeutic target and potential biomarker for ovarian cancer.
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Biomarcadores de Tumor/genética , Regulación Neoplásica de la Expresión Génica , Lisofosfolípidos/genética , Neoplasias Ováricas/genética , Neoplasias Ováricas/patología , Receptores del Ácido Lisofosfatídico/genética , Animales , Diferenciación Celular , Línea Celular Tumoral , Movimiento Celular , Proliferación Celular , Progresión de la Enfermedad , Femenino , Proteínas de Unión al GTP/metabolismo , Humanos , Inmunohistoquímica , Lisofosfolípidos/metabolismo , Ratones Endogámicos BALB C , Ratones Desnudos , Metástasis de la Neoplasia , Neoplasias Ováricas/metabolismo , Receptores del Ácido Lisofosfatídico/metabolismo , Transducción de SeñalRESUMEN
Rosa roxburghii Tratt. is an important commercial horticultural crop endemic to China, which is recognized for its extremely high content of L-ascorbic acid (AsA). To understand the mechanisms underlying AsA overproduction in fruit of R. roxburghii, content levels, accumulation rate, and the expression of genes putatively in the biosynthesis of AsA during fruit development have been characterized. The content of AsA increased with fruit weight during development, and AsA accumulation rate was found to be highest between 60 and 90 days after anthesis (DAA), with approximately 60% of the total amount being accumulated during this period. In vitro incubating analysis of 70DAA fruit flesh tissues confirmed that AsA was synthesized mainly via the L-galactose pathway although L-Gulono-1, 4-lactone was also an effective precursor elevating AsA biosynthesis. Furthermore, in transcript level, AsA content was significantly associated with GDP-L-galactose phosphorylase (RrGGP2) gene expression. Virus-induced RrGGP2 silencing reduced the AsA content in R. roxburghii fruit by 28.9%. Overexpressing RrGGP2 increased AsA content by 8-12-fold in tobacco leaves and 2.33-3.11-fold in tomato fruit, respectively, and it showed enhanced resistance to oxidative stress caused by paraquat in transformed tobacco. These results further justified the importance of RrGGP2 as a major control step to AsA biosynthesis in R. roxburghii fruit.
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As a tool for modifying the genome, gene editing technology has developed rapidly in recent years, especially in the past two years. With the emergence of new gene editing technologies, such as transposon editing tools, numerous advancements have been made including precise editing of the genome, double base editing, and pilot editing. This report focuses on the development of gene editing tools in recent years, elaborates the progress made in classic editing tools, base editor and other new editing tools, and provides insights into challenges and opportunities.
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Sistemas CRISPR-Cas , Edición Génica , Sistemas CRISPR-Cas/genética , TecnologíaRESUMEN
Atherosclerosis is a major pathology for cardiovascular diseases (CVDs). Clinically, the intermittent fasting (IF) has been observed to reduce the risk of CVDs. However, the effect of IF on the development of atherosclerosis has not been fully elucidated. Herein, we determined the protection of IF against high-fat diet-induced atherosclerosis in pro-atherogenic low-density lipoprotein receptor deficient (LDLR-/-) mice and the potentially involved mechanisms. The LDLR-/- mice were scheduled intermittent fasting cycles of 3-day HFD feeding ad libitum and 1 day fasting, while the mice in the control group were continuously fed HFD. The treatment was lasted for 7 weeks (â¼12 cycles) or 14 weeks (â¼24 cycles). Associated with the reduced total HFD intake, IF substantially reduced lesions in the en face aorta and aortic root sinus. It also increased plaque stability by increasing the smooth muscle cell (SMC)/collagen content and fibrotic cap thickness while reducing macrophage accumulation and necrotic core areas. Mechanistically, IF reduced serum total and LDL cholesterol levels by inhibiting cholesterol synthesis in the liver. Meanwhile, HFD-induced hepatic lipid accumulation was attenuated by IF. Interestingly, circulating Ly6Chigh monocytes but not T cells and serum c-c motif chemokine ligand 2 levels were significantly reduced by IF. Functionally, adhesion of monocytes to the aortic endothelium was decreased by IF via inhibiting VCAM-1 and ICAM-1 expression. Taken together, our study indicates that IF reduces atherosclerosis in LDLR-/- mice by reducing monocyte chemoattraction/adhesion and ameliorating hypercholesterolemia and suggests its potential application for atherosclerosis treatment.
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BACKGROUND: The long noncoding RNA (lncRNA) nuclear-enriched abundant transcript 1 (NEAT1) has been implicated in many tumors risk including gastric cancer. However, the association of single nucleotide polymorphisms (SNPs) at NEAT1 with gastric cancer risk has not been studied. The aim of this study was to investigate the association between SNPs in NEAT1 and gastric cancer susceptibility. METHODS: In this study, four SNPs in lncRNA NEAT1 were selected for genotyping in 484 gastric cancer patients and 484 controls in Chinese Han population. Quantitative real-time PCR (qRT-PCR) was conducted to evaluate the potential function of rs3825071. Attributable risk percentage (ARP) and population attributable risk percentage (PARP) were used to assess the epidemiological effect. RESULTS: In the dominant model (GG), the genotypes AG + AA of rs3825071 and rs7943779 were associated with an increased risk of gastric cancer (OR = 1.72, 95%CI = 1.27-2.32 and OR = 1.63, 95%CI = 1.19-2.22). Individuals harboring ≥ 3 risk alleles have higher risk of gastric cancer (OR = 1.88, 95% CI = 1.26-2.80, P = 0.002). ARP and PARP associated with gastric cancer were 42.53% and 10.88% for rs3825071, and were 33.78% and 6.26% for rs7943779, respectively. Furthermore, compared with the genotype GG of rs3825071, the genotypes AG and AA had higher expression of NEAT1. CONCLUSIONS: We found that the genetic variations in NEAT1 were significantly associated with risk of gastric cancer. The G > A variant of rs3825071 may confer gastric cancer susceptibility by changed biological effects to increase the expression of NEAT1.
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ARN Largo no Codificante , Neoplasias Gástricas , Estudios de Casos y Controles , China , Predisposición Genética a la Enfermedad , Humanos , Polimorfismo de Nucleótido Simple/genética , ARN Largo no Codificante/genética , Neoplasias Gástricas/genéticaRESUMEN
Owing to their characteristic structures, metal-organic frameworks (MOFs) are considered as the leading candidate for drug-delivery materials. However, controlling the synthesis of MOFs with uniform morphology and high drug-loading/release efficiencies is still challenging, which greatly limits their applications and promotion. Herein, a multifunctional MOF-based drug-delivery system (DDS) with a controlled pore size of 100-200 nm for both therapeutic and bioimaging purposes was successfully synthesized in one step. Fe-MOF-based microcapsules were synthesized through a competitive coordination method, which was profited from the intrinsic coordination characteristics of the Fe element and the host-guest supramolecular interactions between Fe3+ and polyoxometalates anions. This as-synthesized macroporous DDS could greatly increase the drug-loading/release rate (77%; 83%) and serve as a magnetic resonance (MR) contrast agent. Because an Fe-containing macroporous DDS presents ultrahigh drug loading/release, the obtained 5-FU/Fe-MOF-based microcapsules displayed good biocompatibility, extremely powerful inhibition of tumor growth, and satisfactory MR imaging capability. Given all these advantages, this study integrates high therapeutic effect and diagnostic capability via a simple and effective morphology-controlling strategy, aiming at further facilitating the applications of MOFs in multifunctional drug delivery.
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Antimetabolitos Antineoplásicos/farmacología , Sistemas de Liberación de Medicamentos , Fluorouracilo/farmacología , Hierro/química , Estructuras Metalorgánicas/química , Animales , Antimetabolitos Antineoplásicos/química , Línea Celular , Proliferación Celular/efectos de los fármacos , Supervivencia Celular/efectos de los fármacos , Portadores de Fármacos/química , Liberación de Fármacos , Ensayos de Selección de Medicamentos Antitumorales , Fluorouracilo/química , Humanos , Estructuras Metalorgánicas/síntesis química , Ratones , Ratones Desnudos , Neoplasias Experimentales/tratamiento farmacológico , Neoplasias Experimentales/patología , Tamaño de la Partícula , Porosidad , Propiedades de SuperficieRESUMEN
Recently, the widespread use of antibiotics is becoming a serious worldwide public health challenge, which causes antimicrobial resistance and the occurrence of superbugs. In this context, MnO2 has been proposed as an alternative approach to achieve target antibacterial properties on Streptococcus mutans (S. mutans). This requires a further understanding on how to control and optimize antibacterial properties in these systems. We address this challenge by synthesizing δ-MnO2 nanoflowers doped by magnesium (Mg), sodium (Na), and potassium (K) ions, thus displaying different bandgaps, to evaluate the effect of doping on the bacterial viability of S. mutans. All these samples demonstrated antibacterial activity from the spontaneous generation of reactive oxygen species (ROS) without external illumination, where doped MnO2 can provide free electrons to induce the production of ROS, resulting in the antibacterial activity. Furthermore, it was observed that δ-MnO2 with narrower bandgap displayed a superior ability to inhibit bacteria. The enhancement is mainly attributed to the higher doping levels, which provided more free electrons to generate ROS for antibacterial effects. Moreover, we found that δ-MnO2 was attractive for in vivo applications, because it could nearly be degraded into Mn ions completely following the gradual addition of vitamin C. We believe that our results may provide meaningful insights for the design of inorganic antibacterial nanomaterials.
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Background: Family history may inform individuals that they are at risk of gastric cancer (GC). However, it is too extensive to conduct intensive screening strategies for all individuals with family history of GC instead of average-risk screening. To establish more precise prevention strategies, accurate risk estimates are necessary for individuals with family history of GC. Methods: We searched PubMed, EMBASE and Cochrane for all relevant studies from their inception to May 21, 2020, for cohort and case-control studies investigating the association between family history of GC and its risk. Relative risk (RR) and 95% confidence interval (CI) were pooled from studies using random-effects or fixed effects. Results: The RR of GC was 2.08 (95% CI=1.86-2.34) in individuals with family history of GC according to twenty-nine case-control studies and 1.83 (95%CI=1.67-2.01) from six cohort studies. The increased risk was higher in individuals with sibling history of GC than those with parental history of GC (RR=3.18, 95% CI=2.12-4.79 vs. RR=1.66, 95% CI=1.46-1.89, P=0.021). For individuals with 2 or more first-degree relatives (FDRs) with GC, the RR was 2.81(95% CI=1.89-3.99). Subjects with both family history and Helicobacter pylori (H. pylori) infection confer a higher risk of GC (RR = 4.03, 95%CI=2.46-6.59). Conclusion: The RR of GC among FDRs is lower than in previous studies. However, the risk of GC is markedly increased in individuals having a sibling with GC, more than 2 FDRs with GC. Intensified screening and eradication therapy for H. pylori could be considered for these individuals.
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Hypertension and triglyceride-glucose (TyG) index are both closely associated with insulin resistance, respectively, while the role of TyG index and the association between TyG index and obesity on hypertension risk remain unclear. This study aimed to examine the association and interactive effect of TyG index and obesity on hypertension risk. There was a population-based cross-sectional survey in Henan, China. Multivariate logistic regression analysis was performed to estimate the association between TyG index and the risk of prehypertension and hypertension. The area under curves (AUC) of TyG index and joint indicators (TyG index and obesity indices) was calculated to assess the predictive ability of hypertension. The additive interaction was computed to evaluate the interactive effect between TyG index and obesity. Compared with the lowest TyG quartile, participants in the highest quartile had an increased risk of prehypertension (odds ratio (OR): 1.69, 95% confidence interval (CI): 1.18-2.44) and hypertension (OR: 2.53, 95% CI: 1.80-3.57). The AUCs of joint indicators were significantly higher than TyG index in predicting hypertension (all P < 0.01). Presence of higher TyG index enhanced the ORs of waist-to-height ratio (WHtR) and percent body fat (PBF) from 3.50 (95% CI: 2.55-4.80) to 6.51 (95% CI: 4.81-8.82), and from 3.88 (95% CI: 2.78-5.42) to 7.09 (95% CI: 5.11-9.84) with significant additive interaction on hypertension, respectively. Increased TyG index was significantly associated with a higher risk of prehypertension and hypertension in Chinese adults. Besides, our results also demonstrated the interactions of TyG index and WHtR and PBF on hypertension risk.
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Glucosa , Hipertensión , Adulto , Glucemia , China/epidemiología , Estudios Transversales , Humanos , Hipertensión/diagnóstico , Hipertensión/epidemiología , Obesidad/complicaciones , Obesidad/epidemiología , Factores de Riesgo , TriglicéridosRESUMEN
Diarrhea is considered to be associated with microbial dysbiosis caused by infection of pathogens but poorly understood. We herein characterized the colonic microbiota of diarrheal early-weaning piglets infected with porcine circovirus type 2 (PCV2) and Campylobacter. Campylobacter infection significantly decreased species richness and Shannon diversity index of colonic microbiota together with a significant increase in the proportion of Campylobacter and Enterobacteriaceae, whereas no significant difference on the above indexes was observed in piglets infected with PCV2 compared with healthy piglets. PCV2 and Campylobacter infection could disturb the homeostasis of colonic microbiota through deterioration of ecological network within microbial community, and specially Campylobacter performed as a module hub in ecological networks. The microbial dysbiosis caused metabolic dysfunction and led to a remarkable reduction in production of short chain fatty acids, following by a higher pH level in colon cavity. Campylobacter infection disturbed the function of colonic tract barrier observed in terms of significant lower relative expression of claudin-1, occluding, and zonula occludens protein-1 genes, and PCV2 infection induced intestinal inflammation together with a higher permeability of colon. Generally, these results suggested that PCV2 and Campylobacter infection could induce microbial dysbiosis and metabolic dysfunction, and cause intestinal disorder, all of which finally were associated to contribute to the diarrhea of early-weaning piglets.
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Calorie restriction (CR) ameliorates various diseases including cardiovascular disease. However, its protection and underlying mechanisms against atherosclerosis remain un-fully elucidated. In this study, we fed apoE deficient (apoE-/-) mice in Control group a high-fat diet (HFD, 21% fat plus 0.5% cholesterol) or in CR group a CR diet (CRD, 2% fat plus 0.5% cholesterol, â¼40% calorie restriction and same levels of cholesterol, vitamins, minerals and amino acids as in HFD). After 16 weeks feeding, compared with HFD, CRD substantially reduced atherosclerosis in mice. CRD increased SMC and collagen content but reduced macrophage content, necrotic core and vascular calcification in lesion areas. Mechanistically, CRD attenuated bodyweight gain, improved lipid profiles but had little effect on macrophage lipid metabolism. CRD also inhibited expression of inflammatory molecules in lesions. Taken together, our study demonstrates CRD effectively reduces atherosclerosis in apoE-/- mice, suggesting it as a potent and reproducible therapy for atherosclerosis management.
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Apolipoproteínas E/genética , Aterosclerosis/dietoterapia , Aterosclerosis/etiología , Restricción Calórica , Animales , Aterosclerosis/genética , Aterosclerosis/patología , Dieta Alta en Grasa/efectos adversos , Masculino , Ratones , Placa Aterosclerótica/dietoterapia , Placa Aterosclerótica/etiología , Placa Aterosclerótica/genética , Placa Aterosclerótica/patología , Factores ProtectoresRESUMEN
Powdery mildew (PM) is considered a major cause of yield losses and reduced quality in cucumber worldwide, but the molecular basis of PM resistance remains poorly understood. A segment substitution line, namely, SSL508-28, was developed with dominant PM resistance in the genetic background of PM-susceptible cucumber inbred line D8. The substituted segment contains 860 genes. An iTRAQ-based comparative proteomic technology was used to map the proteomes of PM-inoculated and untreated (control) D8 and SSL508-28. The number of differentially regulated proteins (DRPs) in SSL508-28 was almost three times higher than that in D8. Fourteen DRPs were located in the substituted segment interval. Comparative gene expression analysis revealed that nodulin-related protein 1 (NRP1) may be a good candidate for PM resistance. Gene Ontology enrichment analysis showed that DRPs functioning in tetrapyrrole biosynthetic process, sulfur metabolic process and cell redox homeostasis were specifically enriched in the resistant line SSL508-28. DRPs categorized in the KEGG term photosynthesis increased in both lines upon PM infection, suggesting that the strategies used by cucumber may be different from those used by other crops to react to PM attacks at the initial stage. The measurement of hydrogen peroxide and superoxide anion production and net photosynthetic rate were consistent with the changes in protein abundance, suggesting that the proteomic results were reliable. There was a poor correlation between DRPs measured by iTRAQ and the corresponding gene expression changes measured by RNA-seq with the same experimental design. Taken together, these findings improve the understanding of the molecular mechanisms underlying the response of cucumber to PM infection.
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BACKGROUND: Moyamoya disease belongs to rare diseases which are arousing public awareness of its importance in China. In order to investigate the clinical features of inpatients diagnosed Moyamoya disease, the study was conducted to collect clinical information data of subjects on demographic information and clinical characteristics in Henan, China. METHODS: The data of 198 cases of Moyamoya disease from 56 tertiary hospitals in Henan province from January 2003 to June 2015 were collected retrospectively. Analysis was performed based on demographic, clinical and radiological characteristics of the patients. RESULTS: The mean onset age was 44.03±14.45 years old. Unilateral limb weakness (36.4%) was the most common physical examination. Primary clinical manifestation was headache and dizziness (50.3%). Cranial CT showed cerebral infarction was mainly located in the frontal lobe (27.4%). MRA and DSA showed lesions mainly located in the middle cerebral artery (30.3% and 18.7%). CONCLUSIONS: Clinical manifestations of Moyamoya disease varied. Early diagnosis was necessary to reduce the misdiagnosis rate of this disease. Symptoms, radiological characteristics, and lesion localization characteristics should be fully considered, especially for indicators with a certain onset age, headache and dizziness, lesion located in the frontal lobe of middle cerebral artery.
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Enfermedad de Moyamoya/diagnóstico , Adolescente , Adulto , Anciano , Niño , Preescolar , China , Femenino , Humanos , Masculino , Persona de Mediana Edad , Estudios Retrospectivos , Adulto JovenRESUMEN
Five Mn(i) photo-activated carbon monoxide-releasing molecules (photo-CORMs) with benzimidazole coligands, namely [MnBr(CO)3L1] (1, L1 = 2-(2-pyridyl)benzimidazole), [Mn(CO)2L1(PPh3)2](ClO4) (2), [MnBr(CO)3L2] (3, L2 = 2,2'-bisbenzimidazole), [MnBr(CO)3L3]·CH3OH (4, L3 = 2,6-bis(benzimidazole-2'-yl)pyridine) and fac-[MnBr(CO)3L4] (5, L4 = 2,4-bis(benzimidazole-2'-yl) pyridine) were synthesized by reactions of MnBr(CO)5 with complexes L1-L4, respectively, and characterized via single crystal X-ray diffraction, elemental analysis, 1H-NMR, 13C-NMR, IR, UV-vis and fluorescence spectroscopy. The CO-release properties of 1-5 were investigated using the myoglobin assay and CO detection, and the results show that all of the complexes could release CO rapidly upon exposure to 365 nm UV light. Comparing their half-lives of CO release, we found that increasing the degree of unsaturation and conjugation of the ligand frame could be advantageous for prolonging the time of CO-release, and that the luminescence intensity of 1-5 could gradually be enhanced. The cellular fluorescence imaging tests demonstrate that these Mn(i) photo-CORMs can be taken up by human liver cells (HL-7702) and liver cancer cells (SK-Hep1), and exhibit good capabilities for bioimaging. A cell viability assay for SK-Hep1 shows that the anticancer activity of 3 is better than that of other complexes.