UDP glycosyltransferase (UGT) is a terminal modifying enzyme for the formation of flavonoid glycosides. In this study, we obtained two glycosyltransferase genes, CtUGT25 and CtUGT18, which are closely related to the synthesis of safflower flavonoids, through the Pierce correlation analysis of the expression of glycosyltransferase genes in the safflower corolla transcriptome database at different developmental stages with the contents of the major constituents of safflower metabolome database, and bioinformatically analyzed the gene and protein sequences of the two genes. Expression pattern analysis revealed that CtUGT25 was mainly expressed in the corolla, with the highest expression on day 3 of flowering stage; CtUGT18 was mainly expressed in the root, with the highest expression on day 1 of flowering stage. Functional validation was verified in safflower by Agrobacterium-mediated pollen-tube pathway transgenesis method, demonstrating that CtUGT25 promoted the accumulation of kaempferol-3-O-glucoside and hydroxysafflor yellow A (HSYA), and CtUGT18 promoted the accumulation of kaempferol-3-O-glucoside and orientin, both of which may be the glycosyl-modifying enzymes for the synthesis of safflower flavonoids. Meanwhile, in vitro experiments demonstrated the catalytic activity of CtUGT25 protein on naringenin, quercetin, apigenin, kaempferol, luteoin, 2-hydroxynaringenin and galangin. This study serves as reference for future advancements in regulating the quality of safflower using molecular biotechnology, particularly focuses on the industrial production of safflower exclusive component HSYA. Additionally, it offers valuable insights for researching related genes in other plants.

As a serious cardiovascular disease, atherosclerosis (AS) causes chronic inflammation and oxidative stress in the body and poses a threat to human health. Lipoprotein-associated phospholipase A2 (Lp-PLA2) is a member of the phospholipase A2 (PLA2) family, and its elevated levels have been shown to contribute to AS. Lp-PLA2 is closely related to a variety of lipoproteins, and its role in promoting inflammatory responses and oxidative stress in AS is mainly achieved by hydrolyzing oxidized phosphatidylcholine (oxPC) to produce lysophosphatidylcholine (lysoPC). Moreover, macrophage apoptosis within plaque is promoted by localized Lp-PLA2 which also promotes plaque instability. This paper reviews those researches of Chinese medicine in treating AS via reducing Lp-PLA2 levels to guide future experimental studies and clinical applications related to AS.
Humans ; 1-Alkyl-2-acetylglycerophosphocholine Esterase ; Medicine, Chinese Traditional ; Atherosclerosis/drug therapy* ; Lipoproteins ; Plaque, Atherosclerotic ; Biomarkers

Objective: This study aimed to identify internal ribosome entry sites (IRESs) in the open reading frame (ORF) of the Coxsackievirus B3 (CVB3) genome. Methods: The sequences of P1, P2, or P3 of the CVB3 genome or the truncated sequences from each antithymocyte globulin (ATG) to the end of the P1, P2, or P3 gene were inserted into the pEGFP-N1 vector. After transfection, possible IRES-dependent green fluorescent protein (GFP)-fused proteins were detected by anti-GFP western blotting. The sequences of possible IRESs were inserted into specific Fluc/Rluc bicistronic vectors, in which the potential IRESs were determined according to the Fluc/Rluc activity ratio. Expression of Fluc and Rluc mRNA of the bicistronic vector was detected by RT-qPCR. Results: After transfection of full length or truncated sequences of the P1, P2, or P3 plasmids, six GFP-fused protein bands in P1, six bands in P2 and nine bands in P3 were detected through western blotting. Two IRESs in VP2 (1461-1646 nt) and VP1 (2784-2983 nt) of P1; one IRES in 2C (4119-4564 nt) of P2; and two IRESs in 3C (5634-5834 nt) and 3D (6870-7087 nt) of P3 were identified according to Fluc/Rluc activity ratio. The cryptic promoter was also excluded by RT-qPCR. Conclusion Five IRESs are present in the CVB3 coding region.
Internal Ribosome Entry Sites/genetics* ; Open Reading Frames ; RNA, Messenger/genetics*

BACKGROUND: Thyroid transcription factor-1 (TTF-1) has been widely studied in non-small cell lung cancer, which is considered as an independent prognostic factor in patiens with non-small cell lung cancer. However, there are few studies on the prognostic value of TTF-1 in small cell lung cancer (SCLC). The purpose of this study was to explore the relationship between the expression state of TTF-1 and the sensitivity to first-line chemotherapy and prognosis in patients with SCLC. METHODS: A retrospective analysis was made on 234 patients with SCLC who were diagnosed and treated in The Affiliated Hospital of Qingdao University and received platinum-based chemotherapy. The clinical characteristics, treatment and survival of the patients were followed up. Chi χ² test and Logistic regression model were used to analyze the relationship between TTF-1 expression and chemotherapy response rate. Kaplan-Meier method and Cox proportional hazard regression model were used to analyze the effect of TTF-1 expression on survival time of patients. RESULTS: Among the 234 patients, the positive expression of TTF-1 was 188 cases (80.3%), and the negative expression of TTF-1 was 46 cases (19.7%). The objective response rate (ORR) of first-line chemotherapy in patients with positive expression of TTF-1 was higher than that in patients with negative expression of TTF-1 (70.7% vs 47.8%) (χ²=8.681, P=0.003). Logistic regression multivariate analysis showed that the expression state of TTF-1 was an independent predictor of ORR in first-line chemotherapy (OR=0.216, 95%CI: 0.076-0.615, P=0.004), however this difference was only reflected in LS-SCLC. The median progression free survival (PFS) of patients with negative expression of TTF-1 was shorter than that of patients with positive expression (6.9 months vs 9.0 months) (χ²=9.357, P=0.002). The median OS in TTF-1 negative group was shorter than that in TTF-1 positive group (13.3 months vs 20.1 months)(χ²=12.082, P=0.001). CONCLUSIONS TTF-1 expression is an independent predictor of first-line chemotherapy response rate and survival in patients with SCLC, and may become a biomarker to predict the efficacy and prognosis of SCLC.

OBJECTIVE This study aimed to investigate the role and mechanism of Astragaloside IV (AS-IV)in rats with myocardial infarction.METHODS The myocardial infarction model was established by ligation of the left anterior descending artery. The rats were randomly divided into sham, DMSO, model group, AS-IV and CID755673 groups. The rats were sacrificed 4 weeks later, and segmental heart samples were used for hematoxylin and eosin staining and masson staining. The expression of PKD1, HDAC5 and VEGF were analyzed using immunohistochemistry, reverse transcription poly-merase chain reaction and western blot. RESULTS Compared with the sham operation and DMSO groups,morphology of myocardium in model group was disordered,accompanied with necrotic myocar-dial cells and obvious collagen tissues. After treatment with AS-IV, the morphology of myocardium was obviously improved, and the number of new blood vessels increased significantly. However, after treatment with CID755673, the myocardial tissue of rats became disordered again, the necrotic cells increased, and some vessels closed. The expression levels of PKD1, HDAC5 and VEGF mRNA and protein in myocardial tissue of model group were significantly lower than the other four groups(P<0.05), whereas these levels in the AS-IV group were significantly higher than those in the other four groups (P<0.01). Additionally, the CID755673 group had significantly higher levels of PKD1, HDAC5 and VEGF mRNA and protein than the sham group, DMSO group and model group (P<0.05). CONCLUSION AS-IV may partly promote the angiogenesis of myocardial tissue in rats with myocardial infarction via the PKD1-HDAC5-VEGF pathway.

AIM:To investigate the angiogenic effect and mechanisms of astragaloside IV(AS-IV)in rats with myocardial infarction via protein kinase D 1(PKD1)-histone deacetylase 5(HDAC5)-vascular endothelial growth factor (VEGF)signaling pathway.METHODS:The classic model of myocardial infarction by ligation of the left anterior de-scending coronary artery was replicated,and the rats were randomly divided into model group,AS-IV group,and AS-IV+CID755673(PKD1 inhibitor)group.The sham operation control group and DMSO control group were also set up.All the rats were given intravenous injection via caudal vein.The rats were sacrificed 4 weeks later,and segmental heart samples were used for HE staining and Masson staining.The expression of PKD1,HDAC5 and VEGF was analyzed by immunohis-tochemistry,RT-PCR and and Western blot.RESULTS:Compared with sham operation group and DMSO group,the myo-cardium in model group showed disordered arrangement, accompanied with necrotic myocardial cells and obvious fibrosis tissue.After treatment with AS-IV,the morphological changes of myocardium were obviously improved,and the number of new blood vessels increased significantly.However,after treatment with AS-IV+CID755673,the myocardial tissues of the rats became disordered again,with increased necrotic cells and some closed vessels.The mRNA and protein expression of PKD1,HDAC5 and VEGF in myocardial tissue in model group was significantly lower than that in sham operation and DMSO groups(P<0.05).The expression in AS-IV group was significantly higher than that in model group(P<0.01), while that in AS-IV+CID755673 group was significantly lower than that in AS-IV group(P<0.05).CONCLUSION:AS-IV promotes the angiogenesis of myocardial tissues in the rats after myocardial infarction partly by regulating the PKD 1-HDAC5-VEGF signaling pathway.

OBJECTIVETo screen the differentially expressed miRNAs and their target genes in adipogenic differentiation of human bone marrow mesenchymal stem cells (hMSCs) to better understand the mechanism for regulating the balance between osteoblast and adipocyte differentiation.

METHODSCultured hMSCs were induced for adipogenic differentiation, and at 0, 7, 14, and 21 days of induction, the cells were examined for miRNA and mRNA expression profiles using miRNA chip and transcriptome sequencing (RNA-seq) techniques. Correlation analysis was carried out for the miRNAs and mRNAs of potential interest. The databases including TargetScan, PicTar and miRanda were used to predict the target genes of the differentially expressed miRNA.

RESULTSThe expression of miR-140-5p was down-regulated and leukemia inhibitory factor receptor (LIFR) expression increased progressively during adipogenic differentiation of hMSCs, showing a negative correlation between them. Target gene prediction using the 3 databases identified LIFR as the target gene of miR-140-5p.

CONCLUSIONmiRNA-140-5p may play an important role by regulating its target gene LIFR during adipogenic differentiation of hMSCs.

Adipocytes ; cytology ; Adipogenesis ; Cell Differentiation ; Cells, Cultured ; Down-Regulation ; Humans ; Leukemia Inhibitory Factor Receptor alpha Subunit ; metabolism ; Mesenchymal Stromal Cells ; cytology ; MicroRNAs ; genetics ; Oligonucleotide Array Sequence Analysis ; Osteoblasts ; cytology ; RNA, Messenger ; Transcriptome

To understand the potential causes of laboratory-acquired infections and to provide possible solutions that would protect laboratory personnel, samples from a viral laboratory were screened to determine the main sources of contamination with six subtypes of Rhinovirus. Rhinovirus contamination was found in the gloves, cuffs of protective wear, inner surface of biological safety cabinet (BSC) windows, and trash handles. Remarkably, high contamination was found on the inner walls of the centrifuge and the inner surface of centrifuge tube casing in the rotor. Spilling infectious medium on the surface of centrifuge tubes was found to contribute to contamination of centrifuge surfaces. Exposure to sodium hypochlorite containing no less than 0.2 g/L available chlorine decontaminated the surface of the centrifuge tubes from Rhinovirus after 2 min.
Equipment Contamination ; statistics & numerical data ; Humans ; Laboratories, Hospital ; manpower ; standards ; statistics & numerical data ; Occupational Exposure ; analysis ; statistics & numerical data ; Virus Diseases ; virology ; Viruses ; genetics ; growth & development ; isolation & purification

Performance evaluation system of 13 research institutions funded by the South Korean government was introduced in terms of policy and management.The situation of Korea Institute of Oriental Medicine performance evaluation in 2012 was presented.A reference has been provided for further improving science and technology evaluation system of China.

OBJECTIVETo investigate the molecular genetic abnormalities of N-myc and C-myc, and their clinical pathological implications in pediatric neuroblastic tumors (NTs).

METHODSAbnormalities of N-myc were detected by interphase fluorescence in situ hybridization (FISH) technique in 246 cases of NTs, including neuroblastoma (NB,188 cases), ganglioneuroblastoma (GNB, 52 cases), ganglioneuroma (GN, 6 cases), and their association with the histological typing of the tumors and prognosis was analyzed. Abnormalities of C-myc were detected by FISH in 133 cases of NTs.

RESULTSOf the 246 cases of NTs, N-myc amplification was only found in 27 cases (11.0%, 27/246) of NB, but not in any cases of GNB or GN (P < 0.05). 89.0% (219/246) N-myc non-amplification were found in NTs, and it included N-myc gain in 175 cases (71.1%, 175/246) and normal N-myc in 44 cases (17.9%, 44/246). Univariate analysis indicated significantly (P = 0.012) poorer outcome in patients with N-myc amplification than N-myc non-amplification. However no significant difference was observed between N-myc gain cases and normal N-myc cases (P = 0.057). C-myc gain was found in 74 of 133 cases (55.6%) of NTs; no C-myc amplification or translocation was detected. Forty percent (6/15) of cases with N-myc amplification and 57.6% (68/118) of cases with N-myc non-amplification were accompanied by C-myc gain. The difference between N-myc amplification and non-amplification with C-myc gain was not significant (P > 0.05). Univariate analysis indicated that the outcome difference was not statistically significant between C-myc gain cases and normal C-myc cases (P = 0.357).

CONCLUSIONSThe incidence of N-myc amplification only found in NB is low in pediatric NTs in China. Patients with N-myc amplification predict poorer outcome. No amplification or translocation of C-myc is detected in NTs, whereas C-myc gain is relatively common in NTs. There is no obvious association between N-myc amplification and C-myc gain.

Adrenal Gland Neoplasms ; genetics ; pathology ; Child ; Child, Preschool ; Female ; Follow-Up Studies ; Ganglioneuroblastoma ; genetics ; pathology ; Ganglioneuroma ; genetics ; pathology ; Gene Amplification ; Genes, myc ; Humans ; In Situ Hybridization, Fluorescence ; Infant ; Male ; Mediastinal Neoplasms ; genetics ; pathology ; Neuroblastoma ; genetics ; pathology ; Survival Rate