Exploring the anti-glioma mechanism of the active components of Cortex Periplocae based on network pharmacology and iTRAQ proteomics in vitro.

BACKGROUND: The active components of Cortex Periplocae (CP) exert antitumor properties in many cancers. However, little is known about their effects on glioma or the related underlying mechanisms. OBJECTIVES: The study investigated the underlying mechanism of CP in treating glioma. MATERIAL AND METHODS: The U251 and TG905 cells were treated with an ethanol extract from CP. Cell proliferation was detected using Cell Counting Kit-8 (CCK-8) and a colony formation assay. The flow cytometric analysis was applied to explore the induction of cell cycle arrest and apoptosis. The expression levels of cell cycleand apoptosis-associated proteins were measured with western blot. A network pharmacology method was performed to predict the potential mechanism underlying the effects of the active components of CP on glioma. Then, isobaric tags for relative and absolute quantitation (iTRAQ)-based quantitative proteomics analysis was used to verify the differentially expressed proteins and pathways in order to reveal the underlying mechanisms. Furthermore, to determine the iTRAQ results, 6 candidate proteins were chosen for quantification using parallel reaction monitoring (PRM). RESULTS: The CP extract inhibited the proliferation of U251 and TG905 cells and induced cell cycle arrest and apoptosis. There are 16 active compounds of CP. The antitumor mechanism of CP may be related to the apoptosis pathway, p53 signaling pathway, PI3K-AKT pathway, or transcriptional misregulation in cancer pathway. Six proteins (HSP90AB1, TOP2A, ATP1A1, TGFß1, ATP1B1, and TYMS) were determined to be key factors involved in regulating CP in glioma. CONCLUSIONS: Our research revealed the underlying mechanism of CP in treating glioma using integrated network pharmacology and iTRAQ-based quantitative proteomics technology.

LPS induces SGPP2 to participate metabolic reprogramming in endothelial cells.

Sepsis often causes organ dysfunction and is manifested in increased endothelial cell permeability in blood vessels. Early-stage inflammation is accompanied by metabolic changes, but it is unclear how the metabolic alterations in the endothelial cells following lipopolysaccharide (LPS) stimulation affect endothelial cell function. In this study, the effects of 1 µg/ml of LPS on the metabolism of human umbilical vein endothelial cells (HUVECs) were investigated, and the metabolic changes after LPS stimulation were explained from the perspective of mRNA expression, chromatin openness and metabolic flux. We found changes in the central metabolism of endothelial cells after LPS stimulation, such as enhanced glycolysis function, decreased mitochondrial membrane potential, and increased production of reactive oxygen species (ROS). Sphingolipid metabolic pathways change at the transcriptome level, and sphingosine-1-phosphatase 2 (SGPP2) was upregulated in LPS-stimulated endothelial cells and zebrafish models. Overexpression of SGPP2 improved cell barrier function, enhanced mitochondrial respiration capacity, but also produced oxidative respiration chain uncoupling. In addition, SGPP2 overexpression inhibited the degradation of HIF-1α protein. The molecular and biochemical processes identified in this study are not only beneficial for understanding the metabolic-related mechanisms of LPS-induced endothelial injury, but also for the discovery of general therapeutic targets for inflammation and inflammation-related diseases.

Driver mutations in ADGRL3 are involved in the evolution of ependymoma.

Although there have been recent advances in the molecular pathology of ependymomas, little is known about the underlying molecular evolution during its development. Here, we assessed the clinical, pathological and molecular evolutionary process of ependymoma recurrence in a 9-year-old patient who had seven recurrences of supratentorial ependymoma and died from intracranial multiregional recurrences at the age of 19 years old. Whole-genome sequencing (WGS) of 7 tumor samples (1 primary and 6 subsequent recurrent tumors) was performed to elucidate the mutation landscape and identify potential driver mutations for tumor evolution. The genetic profiles of the seven tumor specimens showed significant heterogeneity and suggested a highly branched evolutionary pattern. The mutational signatures and chromothripsis changed with treatments. Strikingly, adhesion G protein-coupled receptor L3 (ADGRL3, also known as Latrophilins 3, LPNH3) was found to be consistently mutated during the entire disease process. However, Sanger sequencing of other 78 ependymoma patients who underwent surgery at our institution showed no genetic alteration of ADGRL3, as found in the present case. The mRNA levels of ADGRL3 were significantly lower in ependymomas (n = 36), as compared with normal brain tissue (n = 3). Grade III ependymomas had the lowest ADGRL3 expression. Moreover, ependymomas with lower mRNA level of ADGRL3 had shorter overall survival. Our findings, therefore, demonstrate a rare evolutionary process of ependymoma involving ADGRL3.

Astragalus Polysaccharides Improve Cisplatin Resistance by Inhibiting EMT of Lung Adenocarcinoma A549/DDP Cells Transplanted into Nude Mice / 中国实验方剂学杂志

ObjectiveTo investigate the inhibitory effect of Astragalus polysaccharide （APS） on epithelial-mesenchymal transition （EMT） induced by transforming growth factor-β1 （TGF-β1） in cisplatin （DDP）-resistant lung adenocarcinoma cell line A549/DDP cells transplanted into nude mice and the molecular mechanism in improving DDP resistance. MethodBALB/c nude mice were randomly divided into a blank group， a model group， a DDP group， and a combination group （APS combined with DDP）. A549/DDP cells were infected with TGF-β1-overexpressed lentiviral vector and the negative control. The infected cells were inoculated subcutaneously in nude mice. The A549/DDP cells with TGF-β1 gene overexpression were inoculated into all groups except the control group with negative TGF-β1 gene overexpression. The drug intervention was performed eight days after cell inoculation. The mice in the combination group received intragastric administration of APS （0.3 g·kg-1·d-1） and intraperitoneal injection of cisplatin （0.003 5 g·kg-1）， and those in the cisplatin group received intraperitoneal injection of cisplatin （0.003 5 g·kg-1）. After 32 days of cell inoculation， the nude mice were killed and the tumor tissues and lungs were collected. The tumor weight was recorded and the inhibition rate was calculated. The number of metastatic nodules of the lung tumor on the whole slide was counted under the microscope. Immunohistochemistry， Western blot， and real-time fluorescence-based quantitative polymerase chain reaction （Real-time PCR） were used to detect the protein and gene expression of EMT molecular markers α-catenin and N-cadherin， and tumor drug resistance markers human lung resistance protein （LRP）， multidrug resistance-associated protein （MRP）， and P-glycoprotein （P-gp） in the transplanted tumor. ResultCompared with the blank group， the model group showed increased tumor weight and metastatic nodules of the lung tumor （P<0.05）， decreased protein and mRNA expression of α-catenin （P<0.05）， and elevated protein and mRNA expression of N-cadherin， LRP， MRP， and P-gp （P<0.05）. Compared with the model group and the cisplatin group， the combination group showed reduced tumor weight and metastatic nodules of the lung tumor （P<0.05）， increased protein and mRNA expression of α-catenin （P<0.05）， and decreased protein and mRNA expression of N-cadherin， LRP， MRP， and P-gp （P<0.05）. ConclusionAPS can inhibit the growth and metastasis of the transplanted tumor of lung adenocarcinoma and improve cisplatin resistance， which may be related to the inhibition of EMT of tumor cells.

Clinical effects of botulinum toxin A intradermal injection in treatment of erythematotelangiectatic rosacea / 中华医学美学美容杂志

Objective:To evaluate the efficacy and safety of intradermal injection of botulinum toxin A (BTX-A) in the treatment of erythematotelangiectatic rosacea.Methods:From January 2019 to December 2020, 30 patients with erythematotelangiectatic rosacea were treated in the Department of Dermatology at Xijing Hospital, Fourth Military Medical University. There were 26 females and 4 males, the age range from 23 to 42 years, with the average (30.9±5.7) years. Patients were randomly divided into two groups and given intradermal injection of botulinum toxin A. In detail, 0.25 U and 0.5 U was injected at each point in the low and high concentration group of BTX-A. The clinician erythema assessment (CEA) scores were recorded before treatment and at 2, 4, 8 and 12 weeks after treatment. The standard grading system scores for rosacea were recorded before treatment and at 12 weeks after treatment.Results:Both treatments could significantly reduce CEA scores, but the declined degree was more significant ( P<0.05), the onset time was shorter and the duration of efficacy was longer in the high concentration group. The scores of flushing, persistent erythema, burning sensation, stinging sensation and the total score of the standard grading system for rosacea after treatment in both two groups were significantly lower than those before treatment (high concentration group: t=5.00, 5.93, 4.10, 2.74, 12.37; low concentration group: t=6.17, 4.12, 2.87, 2.81, 7.88; P<0.05), and the improvement in high concentration group was significantly more than that in low concentration group ( t=2.02, 2.31, 2.15, 2.56, P<0.05). There was no significant difference in the overall effective rate between the two treatments ( P>0.05). Conclusions:Intradermal injection of BTX-A is safe and effective in the treatment of rosacea. Compared with the low concentration group, the efficacy is better, the onset time is shorter and the duration of efficacy is longer in the high concentration group.

Identification and Validation of a Seizure-Free-Related Gene Signature for Predicting Poor Prognosis in Lower-Grade Gliomas.

BACKGROUND: Lower-grade gliomas (LGGs) patients presented seizure-free have a worse survival than those presented with seizures. However, the current knowledge on its potential value in LGGs remains scarce. PURPOSE: This study aimed to identify a novel gene signature associated with seizures-free for predicting poor prognosis for LGGs patients. MATERIALS AND METHODS: The RNA expression and clinical information of LGGs patients were downloaded from the Cancer Genome Atlas database. Differentially expressed genes (DEGs) were screened out between LGGs patients presented seizures-free and seizures. The novel gene signature was constructed by Lasso and multivariate regression analyses for predicting prognosis in LGGs. Its prognostic value was assessed and validated by Kaplan-Meier analyses and receiver operating characteristic (ROC) curves. Multivariate regression analysis was applied to identify the independent prognostic value of the gene signature. Furthermore, bioinformatics analysis was performed to elucidate the molecular mechanisms. RESULTS: A total of 253 DEGs were screened out between LGG patients presented with seizures and free of seizures. A 5-gene signature (HIST1H4F, HORMAD2, LILRA3, PRSS33, and TBX20 genes) was constructed from these 253 DEGs. Kaplan-Meier analyses and ROC curves assessed and validated the good performance of the 5-gene signature in differentiating and predicting prognosis of high- and low-risk patients. Multivariate regression analysis determined the independent prognostic value of the 5-gene signature. According to bioinformatics analysis, DEGs were mainly enriched in biological processes related to positive regulation of transcription from RNA polymerase II promoter, G-protein coupled receptor signaling pathway, and pathways of cytokine-cytokine receptor interaction, chemokine signaling pathway. CONCLUSION: Our findings suggested that the 5-gene signature might serve as a potential prognostic biomarker and provide guidance for the personalized LGGs management.

Effect of Astragalus Polysaccharide on EMT of A549/DDP Lung Adenocarcinoma Xenograft： An Exploration Based on PI3K/Akt Signaling Pathway / 中国实验方剂学杂志

Objective:To investigate the effect of Astragalus polysaccharide （APS） on transforming growth factor-<italic>β</italic>₁ （TGF-<italic>β</italic>₁）-induced epithelial mesenchymal transition （EMT） of A549/DDP lung adenocarcinoma xenograft and its potential molecular mechanism. Method:BALB/c nude mice were randomly divided into the non-loading group （A549/DDP cells not loaded with TGF-<italic>β</italic>₁）， model group， cisplatin group， and combined group （A549/DDP cells overexpressing TGF-<italic>β</italic>₁）. Mice in the combined group were treated with intragastric administration of APS （0.3 g·kg^-1·d^-1） and intraperitoneal injection of cisplatin （0.003 5 g·kg^-1）， while those in the cisplatin group only received intraperitoneal injection of cisplatin （0.003 5 g·kg^-1）. After drug intervention， the nude mice were sacrificed and the xenograft and lung were harvested， followed by the weighing of tumor and the calculation of the inhibition rate. The number of tumors metastasizing to the lung was counted under the microscope. The pathological features of tumors and their metastasis to the lung tumor were observed by hematoxylin-eosin （HE） staining. The protein and mRNA expression levels of EMT molecular markers E-cadherin， Vimentin， <italic>α</italic>-smooth muscle actin （<italic>α</italic>-SMA）， and phosphatidylinositol 3-kinase/protein kinase B （PI3K/Akt） in the xenograft were detected by immunohistochemistry， Western blot， and Real-time polymerase chain reaction （Real-time PCR）. Result:Compared with the non-loading group， the model group exhibited increased tumor weight and pulmonary metastatic nodules （<italic>P</italic><0.05）， sparse tumor cell junctions， long spindle cells， massive metastatic nodules in the lung， down-regulated E-cadherin protein and mRNA expression， and up-regulated Vimentin and <italic>α</italic>-SMA protein and mRNA expression and p-PI3K and p-Akt protein expression （<italic>P</italic><0.05）. Compared with the model group and cisplatin group， the combined group displayed decreased tumor weight and pulmonary metastatic nodules （<italic>P<</italic>0.05）， tight tumor cell junctions， round or oval cells， no obvious lung metastasis， up-regulated E-cadherin protein and mRNA expression （<italic>P</italic><0.05）， and down-regulated Vimentin and <italic>α</italic>-SMA protein and mRNA expression （<italic>P</italic><0.05） and p-PI3K and p-Akt protein expression （<italic>P</italic><0.05）. There was no significant difference in PI3K or Akt protein expression among groups. Conclusion:APS has a certain inhibitory effect against EMT in lung adenocarcinoma A549/DDP cells， which may be related to the inhibition of activated PI3K/Akt protein expression.

Downregulation of circular RNA hsa_circ_0000735 boosts prostate cancer sensitivity to docetaxel via sponging miR-7.

BACKGROUND: One of the main reasons for the failure of prostate cancer (PCa) treatment is the generation of chemoresistance. Circular RNA hsa_circ_0000735 (hsa_circ_0000735) is connected with the progression of cancer. Nevertheless, the role and regulatory mechanism of hsa_circ_0000735 in the resistance of PCa to docetaxel (DTX) are unclear. METHODS: Expression levels of hsa_circ_0000735 and miR-7-5p (miR-7) in tissue samples and cells were examined via quantitative real-time polymerase chain reaction (qRT-PCR). The DTX sensitivity, viability, colony formation, cell cycle progression, and apoptosis of DTX-resistant PCa cells were determined via Cell Counting Kit-8 (CCK-8), cell colony formation, or flow cytometry assays. The levels of multidrug resistance protein 1 (MDR1) protein, cyclinD1, and B cell lymphoma 2 (bcl-2) were detected by western blotting. The interaction between hsa_circ_0000735 and miR-7 was verified via dual-luciferase reporter, RNA immunoprecipitation (RIP), and RNA pull-down assays. The role of hsa_circ_0000735 in vivo was validated through tumor formation experiments. RESULTS: Hsa_circ_0000735 was upregulated and miR-7 was downregulated in DTX-resistant PCa tissues and cells. High hsa_circ_0000735 expression had a shorter overall survival. Both hsa_circ_0000735 knockdown and miR-7 mimic boosted DTX sensitivity, constrained viability, colony formation, cell cycle progression, and fostered apoptosis of DTX-resistant PCa cells. Also, hsa_circ_0000735 silencing elevated DTX sensitivity and repressed tumor growth in PCa in vivo. Mechanistically, hsa_circ_0000735 served as a sponge for miR-7. MiR-7 inhibition overturned hsa_circ_0000735 silencing-mediated impacts on DTX sensitivity and the malignant behaviors of DTX-resistant PCa cells. CONCLUSION: Hsa_circ_0000735 downregulation boosted PCa sensitivity to DTX and reduced tumor growth via sponging miR-7, providing a promising prognostic biomarker and therapeutic target for PCa.

Role of BCL2L10 in regulating buffalo (Bubalus bubalis) oocyte maturation.

It has been reported that BCL2L10 is abundantly and specifically expressed in adult human and mouse oocytes and played a very important role in oocytes maturation and early embryonic development. This study is to investigate the expression pattern of BCL2L10 in buffalo ovaries and its effect on the in vitro maturation of buffalo oocytes, so as to dissect mechanism of oocytes maturation and provide theoretical guidance for improvement of the in vitro maturation of buffalo oocytes. The results showed that BCL2L10 gene was enriched in ovary and the expression of BCL2L10 was oocyte specific and up-regulated during oocyte maturation. BCL2L10 protein and mRNA were detectable in buffalo early embryos, upregulated at 2-cell to 8-cell stages and down-regulated in the later stages. Knockdown of BCL2L10 by RNA interference resulted in a significant decrease in the maturation rate (33.5%) and cleavage rate (37.52%) of buffalo oocytes coupled with up-regulation of apoptosis-related gene Caspase-9. We concluded that BCL2L10 is a candidate associated with buffalo oocyte maturation.

Dual function of MAZ mediated by FOXF2 in basal-like breast cancer: Promotion of proliferation and suppression of progression.

Myc-associated zinc finger protein (MAZ) is a transcription factor with C2H2-type zinc-finger motifs that can bind GC-rich cis-elements. MAZ activates the transcription of some cancer-related genes and represses that of others, suggesting that changes in MAZ expression may play different roles in the development and progression of different types or subtypes of cancers depending on its target genes. However, the functions and mechanisms of MAZ in regulating the carcinogenesis and progression of breast cancer have remained unclear. In the current study, we show that MAZ performs dual function in basal-like breast cancer (BLBC): suppression of aggressiveness and promotion of proliferation. Forkhead box F2 (FOXF2) is a novel transcription target of MAZ and mediates the functions of MAZ. The MAZ mRNA level, particularly in combination with the FOXF2 mRNA level, may serve as a prognostic marker for BLBC patients. Our results indicate that the dual function of the MAZ-FOXF2 axis reflect the pleiotropic nature of multifunctional transcription factors in regulating the different stages of cancer development and progression, which could lead to the complexity of cancer diagnosis and treatment.

Palladium-Catalyzed Cleavage of α-Allenylic Aryl Ether toward Pyrazolemethylene-Substituted Phosphinyl Allenes and Their Transformations via Alkenyl C-P(O) Cleavage.

A palladium-catalyzed two-component coupling of allenylphosphine oxides with conjugated N-tosylhydrazones is revealed. For the first time, the cleavage of α-allenylic aryl ether toward pyrazolemethylene-substituted phosphinyl allenes enabled facile synthesis of combined motifs with pyrazole and allene. Moreover, the obtained adducts could be easily transformed to potential bioactive multifunctionalized phosphinates via a novel alkenyl C-P(O) cleavage.

Mineralocorticoid Receptor Deficiency in Macrophages Inhibits Atherosclerosis by Affecting Foam Cell Formation and Efferocytosis.

Mineralocorticoid receptor (MR) has been considered as a potential target for treating atherosclerosis. However, the cellular and molecular mechanisms are not completely understood. We aim to explore the functions and mechanisms of macrophage MR in atherosclerosis. Atherosclerosis-susceptible LDLRKO chimeric mice with bone marrow cells from floxed control mice or from myeloid MR knock-out (MRKO) mice were generated and fed with high cholesterol diet. Oil red O staining showed that MRKO decreased atherosclerotic lesion area in LDLRKO mice. In another mouse model of atherosclerosis, MRKO/APOEKO mice and floxed control/APOEKO mice were generated and treated with angiotensin II. Similarly, MRKO inhibited the atherosclerotic lesion area in APOEKO mice. Histological analysis showed that MRKO increased collagen coverage and decreased necrosis and macrophage accumulation in the lesions. In vitro results demonstrated that MRKO suppressed macrophage foam cell formation and up-regulated the expression of genes involved in cholesterol efflux. Furthermore, MRKO decreased accumulation of apoptotic cells and increased effective efferocytosis in atherosclerotic lesions. In vitro study further revealed that MRKO increased the phagocytic index of macrophages without affecting their apoptosis. In conclusion, MRKO reduces high cholesterol- or angiotensin II-induced atherosclerosis and favorably changes plaque composition, likely improving plaque stability. Mechanistically, MR deficiency suppresses macrophage foam cell formation and up-regulates expression of genes related to cholesterol efflux, as well as increases effective efferocytosis and phagocytic capacity of macrophages.

Study of anti-aging protective effect of catalpol on cultured cortical neurons from rats / 中国药理学通报

Aim To investigate the anti-aging effect of catalpol on normal cortical neurons and its possible mechanism. Methods Primary cultured cortical neu-rons from 24 h newly born rats were dissociated and cultured. The cells were divided into normal group, catalpol (0. 1 mg · L - 1 )group,catalpol (1 mg · L - 1 )group and catalpol (10 mg·L - 1 )group. Neu-rons were cultured for 13d,and the cell morphology was observed by microscope. Cell activity was detected by MTT assay. p-S6 and Map-2 of 13d neurons were detected by immunofluorescence to reveal cell viability and the axon growth. GAP-43,p-S6,PI3K,p-PI3K, Akt,p-Akt,mTOR and p-mTOR protein expression of 13d neurons were detected by Western blot. Results Compared with normal group,different concentrations of catalpol could delay the aging of neurons,promote their survival and increase cell viability. The nμmber of p-S6 positive cells increased. Different concentra-tions of catalpol could promote axon growth. GAP-43, p-S6,PI3K,p-PI3K,Akt,p-Akt,mTOR and p-mTOR protein expression of 13d neurons increased. Conclusions Catalpol has anti-aging effects on cere-bral cortical neurons,and its mechanism may be relat-ed to regulating PI3K/ Akt/ mTOR signaling pathway and enhancing neuronal growth activity.

Spermatogenesis-associated proteins at different developmental stages of buffalo testicular seminiferous tubules identified by comparative proteomic analysis.

The testicular seminiferous tubules contain Sertoli cells and different types of spermatogenic cells. They provide the microenvironment for spermatogenesis, but the precise molecular mechanism of spermatogenesis is still not well known. Here, we have employed tandem mass tag coupled to LC-MS/MS with the high-throughput quantitative proteomics technology to explore the protein expression from buffalo testicular seminiferous tubules at three different developmental stages (prepuberty, puberty, and postpuberty). The results show 304 differentially expressed proteins with a ≥2-fold change, and bioinformatics analysis indicates that 27 of these may be associated with spermatogenesis. Expression patterns of seven selected proteins were verified via Western blot and quantitative RT-PCR analysis, and further cellular localizations of these proteins by immunohistochemical or immunofluorescence analysis. Taken together, the results provide potential molecular markers of spermatogenesis and provide a rich resource for further studies on male reproduction regulation.

DNA Methylation Affects the SP1-regulated Transcription of FOXF2 in Breast Cancer Cells.

FOXF2 (forkhead box F2) is a mesenchyme-specific transcription factor that plays a critical role in tissue homeostasis through the maintenance of epithelial polarity. In a previous study, we demonstrated that FOXF2 is specifically expressed in basal-like breast cancer (BLBC) cells and functions as an epithelial-mesenchymal transition suppressor. FOXF2 deficiency enhances the metastatic ability of BLBC cells through activation of the epithelial-mesenchymal transition program, but reduces cell proliferation. In this study, we demonstrate that CpG island methylation of the FOXF2 proximal promoter region is involved in the regulatory mechanism of the subtype-specific expression of FOXF2 in breast cancer cells. DNMT1, DNMT3A, and DNMT3B commonly or individually contributed to this DNA methylation in different breast cancer cells. SP1 regulated the transcriptional activity of FOXF2 through direct binding to the proximal promoter region, whereas this binding was abrogated through DNA methylation. FOXF2 mediated the SP1-regulated suppression of progression and promotion of proliferation of non-methylated BLBC cells. Thus, we conclude that the subtype-specific expression and function of FOXF2 in breast cancer cells are regulated through the combined effects of DNA methylation and SP1 transcriptional regulation.

[Clinicopathological significance of gastric mucosal infection with coccoid Helicobacter pylori].

OBJECTIVE: To study the detection method of coccoid helicobacter pylori (HP) and to investigate the significance of pure coccoid HP infection of gastric mucous membrane. METHODS: A total of 171 gastric biopsy specimens were reviewed by HE stain, and the presence, density and tissue distribution of HP were investigated by sliver stain and immunohistochemistry(S-P method). RESULTS: The rates of mucosal erosion and active inflammation with the presence of pure coccoid HP infection were 36.0% (9/25) and 44.0% (11/25), respectively, both higher than those without HP infection (13.5%, 10/74; 24.3%, 18/74), while lower than those infected with spiral HP (72.1%, 49/68; 79.4%, 54/68). The quantity of interstitial lymphocyte and inflammation severity were also higher than those without HP infection, while lower than those with spiral HP infection. CONCLUSIONS: Pure coccoid HP causes human gastritis, similar to that of spiral HP infection but at a lesser degree. Further studies are important to confirm its clinical significance.

Dense assembly of Gd2O3:0.05X3+ (X = Eu, Tb) nanorods into nanoscaled thin-films and their photoluminescence properties.

This paper presents a simple and effective oil-water interfacial self-assembly strategy to fabricate monolayer and bilayer nanofilms of densely packed Gd2O3:0.05X(3+) (X = Eu, Tb) nanorods with characteristic luminescence properties. In this process, Gd2O3:0.05X(3+) (X = Eu, Tb) nanotubes synthesized by a hydrothermal method are dispersed in deionized water; then, a certain amount of n-hexane is added to produce a hexane-water interface. With n-butanol added as initiator, the nanotubes are gradually trapped at the interface to form a densely packed nanofilm. A monolayer nanofilm of densely packed Gd2O3:0.05Eu(3+) nanorods is obtained after annealing. In addition, the bilayer nanofilm composed of Gd2O3:0.05X(3+) (X = Eu, Tb) nanorods still retains the luminescence properties of each monolayer nanofilm. Moreover, the adhesion of the film on the substrate is very strong, which is extremely beneficial for its future applications.

The study of differences between eye acupuncture therapy and body acupuncture therapy on tumor necrosis factor-αexpression in rats with acute cerebral ischemia reperfusion / 中国生化药物杂志

Objective To observe the effects of eye acupuncture and body acupuncture on tumor necrosis factor-α(TNF-α) expression in the cerebral cortex of rats after ischemia-reperfusion injury,in order to investigate the differences in therapeutic function between eye acupuncture and body acupuncture against acute cerebral ischemia-reperfusion injury. Method 48 Rats established by suture method were randomly divided into control group,sham operation group,model group,eye-acupuncture in point area group,eye-acupuncture outside point area group and body acupuncture group. After reperfusion 24 h,the neurophysical behaviours were accessed by ZeaLonga neurophysical impairment marks;the levels of plasma TNF-αwere determined by ELISA method;the expression of ischemic cerebral cortex TNF-αmRNA was measured by RT-PCR method;the expression of ischemic cerebral cortex TNF-αprotein was detected by western blot. Results After reperfusion 24 h,compared with control group,neurologic impairment marks of eye-acupuncture therapy in point area group and body acupuncture group both decreased obviously (P<0.01),however there were no significant differences between the eye-acupuncture in point area group and body acupuncture group;the levels of plasma TNF-αin rat cerebral cortex after the eye acupuncture therapy and body acupuncture therapy were obviously decreased (P<0.01),however there were no significant differences between the eye-acupuncture in point area group and body acupuncture group; the expressions of TNF-α mRNA and protein in rat cerebral cortex after the eye acupuncture therapy and body acupuncture therapy were also obviously down-regulated (P<0.01),however there were no significant differences between the eye-acupuncture in point area group and body acupuncture group.Conclusion The eye and body acupuncture therapy show the same effects on treating cerebral ischemia reperfusion. The mechanisms of these two therapies may be related to up regulating TNF-αexpression in rat cerebral cortex with ischemia-reperfusion injury.

Effect of Buzhong Yiqi Decoction serum on cell cycle of A 549/DDP cell / 中国生化药物杂志

Objective To study the effect of Buzhong Yiqi Decoction serum on cell cycle of A549/DDP cell. Methods A549/DDP cells and splenocytes cells were cultured in vitro and divided randomly into three groups:control group, Buzhong Yiqi Decoction group and splenocyte group. A 549/DDP cells were stimulated by different concentrations of Buzhong Yiqi Decoction serum and spleen cells, the direct killing effect on cells were measured by MTT method, cell apoptosis were detected by lfow cytometric analysis and the apoptotic body were observed by immunolfuorescence method. Results MTT results showed that cell growth were inhibited by Buzhong Yiqi Decoction serum in contrast with control groups, and the effect was same as spleen cells, and both treated groups had similar effects. Marked apoptotic peak and the apoptotic body were seen by lfow cytometric analysis and lfuorescence microscope in both two groups. Conclusion Buzhong Yiqi Decoction could inhibit the proliferation of A549/DDP cells in vitro and induced cell apoptosis, which is the similar as spleen cells.