DNA-modified Prussian blue nanozymes for enhanced electrochemical biosensing.

Prussian blue nanoparticles exhibit the potential to be employed in bioanalytical applications due to their robust stability, peroxidase-like catalytic functionality, straightforward synthesis, and biocompatibility. An efficient approach is presented for the synthesis of nucleic acid-modified Prussian blue nanoparticles (DNA-PBNPs), utilizing nanoparticle porosity to adsorb nucleic acids (polyT). This strategic adsorption leads to the exposure of nucleic acid sequences on the particle surface while retaining catalytic activity. DNA-PBNPs further couple with functional nucleic acid sequences and aptamers through complementary base pairing to act as transducers in biosensors and amplify signal acquisition. Subsequently, we integrated a copper ion-dependent DNAzyme (Cu2+-DNAzyme) and a vascular endothelial growth factor aptamer (VEGF aptamer) onto screen-printed electrodes to serve as recognition elements for analytes. Significantly, our approach leverages DNA-PBNPs as a superior alternative to traditional enzyme-linked antibodies in electrochemical biosensors, thereby enhancing both the efficiency and adaptability of these devices. Our study conclusively demonstrates the application of DNA-PBNPs in two different biosensing paradigms: the sensitive detection of copper ions and vascular endothelial growth factor (VEGF). These results indicate the promising potential of DNA-modified Prussian blue nanoparticles in advancing bioanalytical sensing technologies.

Network Pharmacology and Experimental Verification Reveal the Regulatory Mechanism of Chuanbeimu in Treating Chronic Obstructive Pulmonary Disease.

Background: Chronic obstructive pulmonary disease (COPD) is a common respiratory disorder in pulmonology. Chuanbeimu (CBM) is a traditional Chinese medicinal herb for treating COPD and has been widely utilized in clinical practice. However, the mechanism of CBM in the treatment of COPD remains incompletely understood. This study aims to investigate the underlying therapeutic mechanism of CBM for COPD using network pharmacology and experimental approaches. Methods: Active ingredients and their targets were obtained from the Traditional Chinese Medicine Systems Pharmacology database. COPD-associated targets were retrieved from the GeneCards database. The common targets for CBM and COPD were identified through Venn diagram analysis. Protein-protein interaction (PPI) networks and disease-herb-ingredient-target networks were constructed. Subsequently, the results of the network pharmacology were validated by molecular docking and in vitro experiments. Results: Seven active ingredients and 32 potential targets for CBM were identified as closely associated with COPD. The results of the disease-herb-ingredient-target network and PPI network showed that peimisine emerged as the core ingredient, and SRC, ADRB2, MMP2, and NOS3 were the potential targets for CBM in treating COPD. Molecular docking analysis confirmed that peimisine exhibited high binding affinity with SRC, ADRB2, MMP2, and NOS3. In vitro experiments demonstrated that peimisine significantly upregulated the expression of ADRB2 and NOS3 and downregulated the expression of SRC and MMP2. Conclusion: These findings indicate that CBM may modulate the expression of SRC, ADRB2, MMP2, and NOS3, thereby exerting a protective effect against COPD.

Hsa_circ_0008833 promotes COPD progression via inducing pyroptosis in bronchial epithelial cells.

Purpose: Chronic obstructive pulmonary disease (COPD) is a common respiratory disorder. Pyroptosis represents a distinctive form of inflammatory cell death that is mediated through the activation of Caspase-1 and inflammasomes. CircRNAs have emerged as a novel class of biomolecules with implications in various human diseases. This study aims to investigate the circRNAs profile of in COPD progression and identify pivotal circRNAs associated with the development of this disease. Methods: he expression profiles of circRNAs in peripheral blood mononuclear cells of COPD patients were assessed by circRNA microarray. Furthermore, flag-labeled vectors were constructed to assess the potential protein-coding capacity of has-circ-0008833. 16HBE cells were stably transfected with lentivirus approach, and cell proliferation and death were assessed to clarify the functional roles of has-circ-0008833 and its encoded protein circ-0008833aa. Additionally, western blot analysis was furthered performed to determine the level of Caspase-1, IL-18, IL-1ß, NLRP3, ASC, and cleaved GSDMD regulated by has-circ-0008833 and circ-0008833-57aa. Results: Initially, we screened the expression profiles of human circRNAs in peripheral blood mononuclear cells of COPD patients, and found that has-circ-0008833 exhibited a significant increase in COPD mononuclear cells. Subsequently, we demonstrated that has-circ-0008833 carried an open reading frame (ORF), which encoded a functional protein, referred to as circ-0008833-57aa. By employing gain-of-function approaches, our results suggested that both circ-0008833 and circ-0008833-57aa inhibited proliferation, but accelerated the rate of 16HBE cell death. Finally, we discovered that circ-0008833 and circ-0008833-57aa promoted the expression of Caspase-1, IL-18, IL-1ß, NLRP3, ASC, and cleaved GSDMD in 16HBE cells. Conclusions: Upregulation of circ-0008833 might promote COPD progression by inducing pyroptosis of bronchial epithelial cells through the encoding of a 57-amino acid peptide.

Correction: A super-high brightness and excellent colour quality laser-driven white light source enables miniaturized endoscopy.

Correction for 'A super-high brightness and excellent colour quality laser-driven white light source enables miniaturized endoscopy' by Shuxing Li et al., Mater. Horiz., 2023, 10, 4581-4588, https://doi.org/10.1039/D3MH01170D.

The Study of the Influence of IL5RA Variants on Chronic Obstructive Pulmonary Disease.

Chronic obstructive pulmonary disease (COPD) is a complex disease, and its pathogenesis is influenced by genetic factors. This study aimed to evaluate the role of IL5RA genetic variation in the risk of COPD. In this study, 498 patients with COPD and 498 normal controls were recruited. Subsequently, five SNPs (rs3804795, rs2290610, rs13097407, rs334782, and rs3856850) in the IL5RA gene were genotyped. Logistic analysis examined the association of five single nucleotide polymorphisms (SNPs) in IL5RA with the risk of COPD under various genetic models. Furthermore, the association between IL5RA and susceptibility to COPD was comprehensively analyzed with stratification based on age, sex, smoking, and alcohol consumption. Our study showed that IL5RA rs13097407 reduced susceptibility to COPD (OR = 0.43, p < 0.001, p (FDR)< 0.001). On the other hand, rs3856850 was associated with an increased risk of COPD (OR = 1.71, p = 0.002, p (FDR) = 0.002). Interestingly, the effect of IL5RA SNPs on susceptibility to COPD was found to be influenced by factors such as sex and smoking. IL5RA gene variants were significantly associated with susceptibility to COPD.

Research into the mechanism of intervention of Wenjing decoction in endometriosis based on network pharmacology and molecular docking technology.

BACKGROUND: Endometriosis (EMs) is a frequent disease in women and is the principal cause of infertility and dysmenorrhea. Due to its high recurrence rate and serious complications, more research on EMs is needed. We used network pharmacology and molecular docking technology to predict the key active components, targets, and signaling pathways of Wen Jing decoction (WJD) in the treatment of EMs. METHODS: The components and targets of WJD were collected and identified using the Traditional Chinese Medicine Systems Pharmacology Database and BATMAN-TCM. The EMs targets were obtained from GeneCards, OMIM, TTD, Kyoto encyclopedia of genes and genomes (KEGG) and GAD Databases; the Venny diagram was used to analyze the overlap between the targets of WJD and EMs; use Cytoscape 3.8.2 software to build a drug active ingredient-target protein interaction network; after downloading the data from the String online database, Cytoscape 3.8.2 software was used to draw the intersection target protein-protein interaction network diagram. Finally, microbiotic information mapping was used to analyze gene ontology function enrichment and KEGG pathway enrichment. Molecular docking was used to predict the binding affinity of the components of WJD to the targets of EMs. RESULTS: Seventy-eight active ingredients of WJD were screened, corresponding to 108 targets, 2626 EMs-related targets and 124 intersection targets. The results of gene ontology functional enrichment analysis showed that WJD could affect 709 biological processes, 131 molecular functions and 54 cell composition. The enrichment analysis of KEGG pathway yielded 185 pathways. The treatment of EMs by WJD has the characteristics of multiple targets and multiple pathways. Molecular docking with the AutoDock Vina platform found that 5 active ingredients of WJD were successfully docked with 6 common targets. CONCLUSION: Based on network pharmacology and molecular docking, WJD was found to act on EMs through multi-targets and related signaling pathways.

PARP-1 improves leukemia outcomes by inducing parthanatos during chemotherapy.

Previous chemotherapy research has focused almost exclusively on apoptosis. Here, a standard frontline drug combination of cytarabine and idarubicin induces distinct features of caspase-independent, poly(ADP-ribose) polymerase 1 (PARP-1)-mediated programmed cell death "parthanatos" in acute myeloid leukemia (AML) cell lines (n = 3/10 tested), peripheral blood mononuclear cells from healthy human donors (n = 10/10 tested), and primary cell samples from patients with AML (n = 18/39 tested, French-American-British subtypes M4 and M5). A 3-fold improvement in survival rates is observed in the parthanatos-positive versus -negative patient groups (hazard ratio [HR] = 0.28-0.37, p = 0.002-0.046). Manipulation of PARP-1 activity in parthanatos-competent cells reveals higher drug sensitivity in cells that have basal PARP-1 levels as compared with those subjected to PARP-1 overexpression or suppression. The same trends are observed in RNA expression databases and support the conclusion that PARP-1 can have optimal levels for favorable chemotherapeutic responses.

A super-high brightness and excellent colour quality laser-driven white light source enables miniaturized endoscopy.

A laser-driven white light source promises intrinsic advantages for miniaturized endoscopic illumination. However, it remains a great challenge to simultaneously achieve high brightness and excellent colour rendition due to the shortage of highly efficient and thermally robust red-emitting laser phosphor converters. Here, we designed CaAlSiN3:Eu@Al (CASN@Al) converters with neglectable efficiency loss by tightly bonding all-inorganic phosphor films on an aluminium substrate. A layer-by-layer phosphor converter (LuAG/CASN@Al), i.e., stacking a green-emitting Lu3Al5O12:Ce (LuAG) layer on CASN@Al, was constructed to enhance light conversion efficiency and reduce reabsorption loss under blue laser excitation, which thus produces an excellent white light source with a luminous efficacy of 258 lm W-1 and a colour rendering index of 91. A miniaturized endoscopy with a coupling efficiency twice that of the commercial white LEDs was demonstrated by using the laser-driven white light and showed a central illuminance as high as 52 730 lx, more vivid images and long-term reliability.

Liver abscess complicated with multiple organ invasive infection caused by hematogenous disseminated hypervirulent Klebsiella pneumoniae: A case report.

Hypervirulent Klebsiella pneumoniae (hvKp) causes increasing infections in healthy individuals from the community. In severe cases, it can cause multiple organ infection with invasive metastasis of blood sources, seriously threatening the patients' life. Rapid and accurate diagnosis of the pathogen becomes the key to timely antibiotic treatment to improve the prognosis. This article reports a case of liver abscess complicated with multiple organ invasive infection caused by hematogenous-disseminated hvKp. K. pneumoniae was identified by culture and metagenomic next-generation sequencing (mNGS) using blood and liver abscess drainage fluid. The isolates from the two samples were subsequently identified with high homology (99.999%) by whole genome sequencing. In addition, multiple virulence genes were detected in the two isolates and the string test was positive, indicating hvKp with hypermucoviscosity phenotype. Multiple antibiotic treatments were given. The conditions of the patient were stable but the temperature remained high. Surgical drainage treatment was performed, and the patient's body temperature immediately dropped to normal. He finally recovered after 6 months of follow-up. mNGS using body fluids can facilitate the rapid diagnosis of pathogens. For hvKp infection, choosing a better antibiotic therapy and receiving surgical drainage can significantly improve the prognosis of the patient.

Suggestive evidence of genetic association of IL23R polymorphisms with chronic obstructive pulmonary disease risk in the Chinese population.

BACKGROUND: Chronic obstructive pulmonary disease (COPD) is a worldwide public health problem. Previous genetic association studies have identified several susceptibility loci in the interleukin genes that may participate in the nosogenesis of COPD. This study aimed to evaluate the relationship between IL23R loci and COPD susceptibility in the Chinese population. METHODS: Agena MassARRAY technology was applied to genotype five single nucleotide polymorphisms (SNPs) in the IL23R gene in 498 COPD patients and 498 healthy people. The association between IL23R SNPs and COPD risk was calculated by logistic regression analysis, with odds ratios and 95% confidence intervals. The false-positive report probability analysis was noteworthy for evaluating the significant results. Also, haplotype analysis was performed among IL23R variants, and multifactor dimensionality reduction analysis was performed to assess the SNP-SNP interactions to predict the risk of COPD. RESULTS: Overall analysis showed that rs7517847 had a significant association with an increased risk of COPD. Age-stratified analysis revealed that rs7517847 was significantly related to an increased risk of COPD in people aged over 68 years old. Sex-stratified analysis illustrated a significant association between rs2295359 and rs7517847 and COPD risk in the female population. The significant association of COPD risk with IL23R SNPs was assessed by false-positive report probability values. Additionally, we observed that the haplotypes AAC and GGA formed by rs2201841, rs12743974 and rs10889677 were associated with a reduced risk of COPD (p = 0.009, p = 0.026). Also, the five-loci interaction model formed by rs2295359, rs7517847, rs2201841, rs12743974 and rs10889677 became the best predictor of COPD, with 10/10 cross-validation consistency and 52.4% testing balance accuracy. CONCLUSION: The research indicated a remarkable association between IL23R variants and COPD susceptibility in the Chinese population. Larger samples and functional research are required to ascertain the relationship between IL23R variants and COPD susceptibility.

Association of paternal rejection with externalizing problems of adolescents: A moderated mediation model.

Despite evidence suggesting the role of the parent-child relationship in externalizing problems, few studies have examined the direct and indirect association of father rejection and externalizing problems. This research examines the mediation effect of peer victimization in the association of paternal rejection with externalizing problems in adolescents. Besides, it explores the moderating effect of impulsivity on this association. In total, 2,116 pupils completed anonymous questionnaires about paternal rejection, peer victimization, externalizing problems, and impulsivity. Sex, age, paternal and maternal education, and per capita income were set as covariates. The results revealed that peer victimization mediated the relationship between paternal rejection and externalizing problems in adolescents. Impulsivity played a moderating role not only in the relationship between paternal rejection and externalizing problems but also in the link between peer victimization and externalizing problems. Specifically, paternal rejection predicted greater externalizing problems only for adolescents with high-level impulsivity, and peer victimization was predictive of greater externalizing problems only for adolescents with high levels of impulsivity. The findings highlight that paternal rejection and peer victimization have a potential, long-lasting influence on the psychological well-being of adolescents, particularly for adolescents high in impulsivity.

Selective activation of cannabinoid receptor 2 regulates Treg/Th17 balance to ameliorate neutrophilic asthma in mice.

BACKGROUND: The cannabinoid receptor 2 (CNR2) plays a critical role in relieving asthma, with the mechanism still unclear. We aimed to investigate the mechanism of the CNR2 agonist (ß-caryophyllene, ß-Car) in regulating the balance of regulatory T cells (Treg) and T helper cell 17 (Th17) and thus its role in asthma. METHODS: The study group of 50 pathogen-free female BALB/c mice were randomly divided at 6-8 weeks old into five groups of Control, Asthma, Asthma + ß-Car (10 mg/kg), Asthma + ß-Car + SR144528 (specific CNR2 antagonist, 3 mg/kg), and Asthma + ß-Car + CMD178 (inhibitor of Treg cell, 10 mg/kg). ELISA was conducted to evaluate the main inflammatory cytokines [interleukin (IL)-6, IL-8, and tumor necrosis factor-α], and those secreted by Treg (transforming growth factor-ß and IL-10), and Th17 (IL-17A and IL-22). Markers of Treg and Th17 cells were assessed by flow cytometry. In vitro, the CD4+ T cells were sorted and directed to differentiate to Treg and Th17 cells. The expression levels of CNR2, STAT5 and JNK1/2 were investigated by western blot and immunofluorescence assay. RESULTS: ß-Car relieved neutrophilic asthma severity in mice by elevating the marker genes' expression of Treg and inhibiting those of Th17, causing an increased proportion of Treg to Th17. ß-Car also promoted the directed differentiation of CD4+ T cells into Treg, but not Th17. Activation of the CNR2 regulated the Treg/Th17 balance and relieved neutrophilic asthma possibly through promotion of phosphorylation of STAT5 and JNK1/2. CONCLUSIONS: The effect of the selective CNR2 agonist activating STAT5 and JNK1/2 signaling was to change the Treg/Th17 balance and reduce the inflammatory reaction, thus ameliorating neutrophilic asthma in a mouse model.

Characteristics and outcomes of patients with COVID-19 in Hainan, South China.

ABSTRACT: As an international tourist center, Hainan province includes both imported and local COVID-19 cases. This study aimed to investigate the clinical characteristics and outcomes of COVID-19 patients in Hainan, China.COVID-19 patients hospitalized in Hainan affiliated Hospital of Hainan Medical University in January to March 2020 were retrospectively assessed. Routine blood tests, blood gas analyses, and computed tomography imaging were performed within 24 hours. Virus nucleic acid was detected every other day. The patients were divided into local resident and traveler groups, and differences in clinical data as well as leukocyte, lymphocyte, and neutrophil levels were analyzed.A total of 70 patients aged 51.23 ±â€Š13.54 years were assessed, including 16 local residents and 54 travelers. Of these, 55 cases (78.6%) had fever, 47 (67.1%) had cough and sputum, and 9 (12.9%) had chest dyspnea; 60 and 10 cases were mild/common and severe/critical, respectively. Sex, basic diseases, smoking history and drinking history, Charlson Comorbidity Index, symptoms, time of onset to admission, clinical severity, white blood cell count, lymphocyte count, neutrophil count, oxygen inhalation, mechanical ventilation, glucocorticoid therapy, treatment, admission to ICU, hospital stay, and mortality were similar between the 2 groups.The warm and humid climate of Hainan does not seem to significantly affect patient features and outcomes from COVID-19. Unnecessary travel to tourist areas should be avoided.

LncRNA NEAT1 promotes airway smooth muscle cell inflammation by activating the JAK3/STAT5 pathway through targeting of miR-139.

Background Asthma is a chronic inflammatory heterogeneous respiratory disease. Previous studies showed that the lncRNA NEAT1 (nuclear paraspeckle assembly transcript 1) might play an important role in the pathogenesis of asthma, but its potential mechanism in airway smooth muscle cell (ASMC) inflammation remains largely unknown and needs further investigation.Methods We performed cellular immunofluorescence to identify the features of ASMCs and detected the expression levels of lncRNA NEAT1, miR-139, TNF-α, IL-6, IL-8 and IL-1ß by quantitative real-time PCR (Q-PCR) and ELISA. Western blotting (WB) was used to measure the protein expression of the related genes, and bioinformatics as well as dual luciferase assays were used to validate the interaction between lncRNA NEAT1 and miR-139 and the interaction between miR-139 and the 3'-UTR of JAK3.Results The expression of lncRNA NEAT1 was increased in the ASMCs of asthma patients, but miR-139 was decreased. Overexpression of lncRNA NEAT1 promoted the expression of the inflammatory cytokines such as TNF-α, IL-6, IL-8 and IL-1ß in ASMCs. LncRNA NEAT1 was able to target miR-139 to activate the JAK3/STAT5 signaling pathway and induced the expression of these inflammatory cytokines in ASMCs. Overexpression of miR-139 or suppression of the JAK3/STAT5 signaling pathway reversed the inflammatory effect of lncRNA NEAT1.Conclusion LncRNA NEAT1 played a pivotal role in ASMC inflammation and exerted its function through the miR-139/JAK3/STAT5 signaling network.

LncRNA OIP5­AS1 aggravates house dust mite­induced inflammatory responses in human bronchial epithelial cells via the miR­143­3p/HMGB1 axis.

Bronchial asthma poses a serious threat to human health. Previous studies have documented the role of long non­coding RNAs (lncRNAs) in asthma. However, the molecular mechanism underlying bronchial asthma remains unclear. The aim of the present study was to evaluate the role of the lncRNA Opa­interacting protein 5 antisense RNA1 (OIP5­AS1) in the house dust mite­induced inflammatory response in human bronchial epithelial cells. BEAS­2B cells were treated with Dermatophagoides pteronyssinus peptidase 1 (Der p1) to establish an in vitro model of asthma. OIP5­AS1 expression levels increased in BEAS­2B cells following Der p1 treatment, while microRNA (miR)­143­3p was downregulated. Additionally, the levels of the pro­inflammatory factors tumor necrosis factor­α, interleukin (IL)­6 and IL­8 were measured, and apoptosis was evaluated following OIP5 silencing. OIP5­AS1 knockdown reduced the inflammatory response and apoptosis in BEAS­2B cells. Furthermore, using dual luciferase reporter assays and co­transfection experiments, it was demonstrated that the function of OIP5­AS1 was mediated by miR­143­3p. miR­143­3p overexpression attenuated the Der p1­induced inflammatory response and apoptosis of BEAS­2B cells by targeting high mobility group box 1 (HMGB1). In summary, OIP5­AS1 exacerbated Der p1­induced inflammation and apoptosis in BEAS­2B cells by targeting miR­143­3p via HMGB1.

Mannan oligosaccharide supplementation in diets of sow and (or) their offspring improved immunity and regulated intestinal bacteria in piglet1.

The objectives of the current study were to explore the effects of mannan oligosaccharide (MOS) supplementation in the diets of sow and (or) their offspring on intestinal bacteria, intestinal and systemic inflammation in the piglet. A total of 60 multiparous sows (4 ± 1 parity; Landrace × Yorkshire) were fed either control diet (sCON, n = 30) or a diet containing 400 mg kg-1 MOS (sMOS, n = 30) from day 86 of gestation until weaning (day 20 of postpartum). On day 7 of age, offspring (Duroc × Landrace Yorkshire) were assigned within sow treatments and fed control diet (pCON) or diet containing 800 mg kg-1 MOS (pMOS) for 28 d (end at 35 d of age), resulting in four piglet diet groups (n = 15 litters per diet group): sCON-pCON, sCON-pMOS, sMOS-pCON, and sMOS-pMOS. Results found that piglet diet MOS increased or tend to increase Lactobacillus amount in the ileum digesta (P < 0.01) and jejunum digesta (P = 0.07), respectively; while tend to decrease Escherichia coli amount in jejunum digesta (P =0.06) and cecum digesta (P = 0.08). Both sow and piglet diets add MOS (sMOS-pMOS) increased Lactobacillus amount but decreased E. coli amount in jejunum digesta (P < 0.05) compared with the sCON-pCON diet group. In addition, sow diet MOS (rather than piglet diet MOS) increased sIgA content in piglet jejunum mucosa compared with control (P = 0.04). Sow diet MOS decreased toll-like receptor 2 (TLR2), toll-like receptor 4 (TLR4), and interleukin 8 (IL-8) mRNA levels (P < 0.05) and tended to decrease nuclear factor-κB p65 (NF-κB p65) mRNA level (P = 0.07) in piglet intestinal lymphatic. The interaction effects between sow and piglet diets were found on the mRNA levels of NF- κB p65 (P = 0.03) and IL-8 (P = 0.02) in piglet jejunum. Finally, the sow diet MOS decreased proinflammatory cytokines IL-2 (P < 0.01) and IL-4 (P < 0.01) concentrations in piglet serum. Piglets diet MOS decreased the contents of IL-2 (P = 0.03), IL-4 (P = 0.01) and interferon (IFN)-γ (P < 0.01) while increased anti-inflammatory cytokine IL-10 (P < 0.01) content in serum. The interaction effects between sows and piglet diets on IL-4 (P = 0.02), IL-10 (P < 0.01), and IFN-γ (P = 0.08) were observed. In conclusion, sow and/or piglet diet MOS could improve intestinal microbiota, enhance intestinal mucosal immune competence, and suppress intestinal and systemic inflammation in the piglet.

Resistant Maltodextrin Ameliorates Altered Hepatic Lipid Homeostasis via Activation of AMP-Activated Protein Kinase in a High-Fat Diet-Fed Rat Model.

Many studies have shown that resistant maltodextrin (RMD) possesses blood cholesterol lowering and anti-obesity effects. In order to investigate the effect of RMD on lipid metabolism in the liver, rats were fed with a high-fat (HF) diet for 7 weeks to induce hyperlipidemia and fatty liver. Normal control rats were fed with a normal diet. HF-diet-fed rats were treated with 5% RMD for 8 weeks. The results showed that the increased plasma aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities, the increased hepatic triglyceride and total cholesterol levels, and fatty liver in HF-diet-fed rats were significantly decreased after supplementation with RMD. Supplementation with RMD significantly (1) induced AMP-activated protein kinase (AMPK) phosphorylation; (2) inhibited the activities of acetyl-CoA carboxylase (ACC), fatty acid synthase (FAS), and HMG-CoA reductase (HMGCR); (3) suppressed the protein expression of peroxisome proliferator activated receptor (PPAR)-γ; (4) increased ß-oxidation of fatty acids by increasing the protein expression carnitine palmitoyl transferase 1α (CPT-1α) in the livers of HF-diet-fed rats. Taken together, supplementation of RMD was capable of inhibiting lipogenic enzyme activities and inducing fatty acid ß-oxidation through increasing AMPK activation, thereby reducing lipid accumulation in the liver.

[Preliminary application of injectable calcium phosphate cement/poly (lactic-co-glycolic acid) microspheres for extraction site preservation].

OBJECTIVE: To investigate the feasibility of extraction site preservation using injectable calcium phosphate cement (CPC) combine with poly (lactic-co-glycolic acid) (PLGA) microspheres. METHODS: Immediate extraction defects models were created in canine mandibles, and the defects were filled with CPC/PLGA (experimental group, E) , Bio-Oss (positive control, P), non-treatment (blank control, B) respectively. Dogs were sacrificed after 4, 8, 12 weeks post operation. Statistical analysis were conducted using SPSS 19. RESULTS RESULTS: of radiological observation showed that there were not significantly different between groups in 4 and 8 week (P > 0.05). After 12 week,E (114.9 ± 8.4) were not significantly different compared with P (117.4 ± 12.1) (P > 0.05) , both were significantly higher than B (95.0 ± 12.6) (P < 0.05) . Histology examination showed that at 4 week following surgery, the result of newly formed bone was as follow, P[ (87.5 ± 1.5) %] > B[(78.7 ± 2.7)%] > E[(69.2 ± 1.8)%] (P < 0.05). At 8, 12 week, results of P[(94.0 ± 2.3)% and (93.5 ± 1.9) %] and E[ (94.7 ± 1.1) % and (96.0 ± 0.9) %] were better than those of B[ (76.8 ± 3.0)% and (87.0 ± 2.4)%] (P < 0.05). CONCLUSIONS: The effect of CPC/PLGA repair immediate alveolar ridge defects is the same as that of Bio-Oss, and CPC/PLGA can be used as a material in extraction site preservation.