MicroRNA-34a inhibits the proliferation and promotes the apoptosis of non-small cell lung cancer H1299 cell line by targeting TGFßR2.

MicroRNAs (MiRNAs) are small non-coding RNA molecules which act as important regulators of post-transcriptional gene expression by binding 3'-untranslated region (3'-UTR) of target messenger RNA (mRNA). In this study, we analyzed miRNA-34a (miR-34a) as a tumor suppressor in non-small cell lung cancer (NSCLC) H1299 cell line. The expression level of miR-34a in four different NSCLC cell lines, H1299, A549, SPCA-1, and HCC827, was significantly lower than that in the non-tumorigenic bronchial epithelium cell line BEAS-2B. In human NSCLC tissues, miR-34a expression level was also significantly decreased in pT2-4 compared with the pT1 group. Moreover, miR-34a mimic could inhibit the proliferation and triggered apoptosis in H1299 cells. Luciferase assays revealed that miR-34a inhibited TGFßR2 expression by targeting one binding site in the 3'-UTR of TGFßR2 mRNA. Quantitative real-time PCR (qRT-PCR) and Western blot assays verified that miR-34a reduced TGFßR2 expression at both mRNA and protein levels. Furthermore, downregulation of TGFßR2 by siRNA showed the same effects on the proliferation and apoptosis as miR-34a mimic in H1299 cells. Our results demonstrated that miR-34a could inhibit the proliferation and promote the apoptosis of H1299 cells partially through the downregulation of its target gene TGFßR2.

Global trends in colorectal cancer and metabolic syndrome research: a bibliometric and visualization analysis.

Numerous studies have demonstrated a robust correlation between metabolic syndrome (MetS) and colorectal cancer (CRC). Nonetheless, no systematic analysis or visualization of relevant publications has been conducted via bibliometrics. This research, centred on 616 publications obtainable through the Web of Science Core Collection (WoSCC), employed CiteSpace software and VOSviewer software for correlation analyses of authors, journals, institutions, countries, keywords, and citations. The findings indicate that the Public Library of Science had the highest number of publications, while the United States, China, and South Korea were the most contributory nations. Recent years have seen the mechanisms linking Metabolic Syndrome with Colorectal Cancer, including diet, obesity, insulin resistance, and intestinal flora, remain a burgeoning research area. Furthermore, bariatric surgery appears to be a promising new area of study. This paper presents the initial bibliometric and visualization analysis of research literature concerning CRC and MetS which examines research trends and hotspots.

Mucins 1-shRNA inhibit the proliferation and HIF-1alpha protein expression on human cholangiocarcinoma cells.

To explore the effects of Mucins (MUC)1-shRNA on the proliferation and hypoxia inducible factor (HIF)-1alpha expression of human cholangiocarcinoma (CCA) QBC939 cells in vitro. MUC1-shRNA was constructed and transfected with Lipofectamine™ 2000 into cultured CCA cells. MUC1 mRNA and protein expression levels were determined by RT-PCR and Western blot, respectively. The cellular proliferation and HIF-1alpha expression of QBC939 cells were evaluated by the MTT assay and Western blot, respectively. After transfection, the expression levels of MUC1 mRNA and protein in the experimental group decreased significantly in QBC939 (P < 0.01). The proliferation of MUC1 shRNA-transfected group was 0.30 ± 0.05, 38.32 ± 1.43%, 15.18 ± 1.32%, and there were remarkable differences when compared with the control groups (P < 0.05). Significant inhibition of HIF-1alpha protein expression in MUC1 shRNA-transfected group was also discovered (P < 0.05). MUC1-shRNA could inhibit proliferation and significantly weaken HIF-1alpha protein expression of QBC939 cells, suggesting its potential as a therapeutic target of CCA.

Efficacy and Safety of Sevelamer Carbonate in Chinese Nondialysis Chronic Kidney Disease Patients with Hyperphosphatemia: A Randomized, Double-Blind, Parallel-Group Study.

Introduction: Previous studies suggested that sevelamer carbonate is well tolerated with a favorable efficacy and safety profile in both dialysis and nondialysis patients in Europe; however, the efficacy remains controversial, and few studies have examined sevelamer carbonate therapy in other ethnic nondialysis CKD patients. This study assessed the efficacy and safety of sevelamer carbonate in Chinese nondialysis CKD patients with hyperphosphatemia. Methods: The multicenter, randomized, double-blind, parallel-group, placebo-controlled, and phase 3 clinical trial enrolled 202 Chinese nondialysis CKD patients with serum phosphorus ≥1.78 mmol/L. Patients were randomly assigned 1:1 to receive sevelamer carbonate (2.4-12 g per day) or placebo for 8 weeks. The primary outcome was the change in serum phosphorous between baseline and week 8. Results: Totally 482 Chinese patients were screened and 202 were randomized (sevelamer carbonate, n = 101; placebo, n = 101). The mean serum phosphorous decreased significantly in patients treated with sevelamer carbonate compared with placebo (-0.22 ± 0.47 vs. 0.05 ± 0.44 mmol/L, p < 0.0001). Significantly (p < 0.0001), decreases of serum total cholesterol, low-density lipoprotein cholesterol, and calcium-phosphorus (Ca × P) product levels from baseline to week 8 were shown in sevelamer carbonate group compared with placebo group. Serum intact parathyroid hormone was not significantly changed in the sevelamer carbonate group (p = 0.83). Patients in the sevelamer carbonate group experienced similar adverse events as the placebo group. Conclusion: Sevelamer carbonate is an effective and well-tolerated phosphate binder in advanced nondialysis CKD Chinese patients with hyperphosphatemia.

Systematic review and meta-analysis of Chinese herbal formula Tongxie Yaofang for diarrhea-predominant irritable bowel syndrome: Evidence for clinical practice and future trials.

Introduction: Diarrhea-predominant irritable bowel syndrome (IBS-D) significantly decreases the quality of life of patients and their families, and affects patients' mental health. No specific western medications are available. Ancient classical Chinese medical texts have recognized Tongxie Yaofang (TXYF) as a therapy for diarrhea which is widely used in clinical practice. Standard TXYF prescription (S-TXYF) is composed of four herbal medicines: Atractylodes macrocephala Koidz. [Asteraceae; Rhizoma Atractylodis Macrocephalae.], Paeonia lactiflora Pall. [Ranunculaceae; Paeoniae Radix Alba], Citrus × aurantium L. [Rutaceae; Citri Reticulatae Pericarpium] and Saposhnikovia divaricata (Turcz. ex Ledeb.) Schischk. [Umbelliferae; Saposhnikoviae Radix]. This review aimed to evaluate the therapeutic effects and safety of S-TXYF for IBS-D. Methods: Eight English and Chinese electronic databases were searched from their inception to 25 December 2021 for randomized controlled trials (RCTs) comparing S-TXYF with placebo, western medications or no treatment for IBS-D. The primary outcome was the global improvement of IBS-D symptoms. Data were analyzed using Cochrane's Revman 5.4 software. Evidence certainty was assessed using the online GRADEpro tool for the primary outcome. Results: Eleven RCTs involving 985 adults with IBS-D were included. For global improvement of symptoms, S-TXYF was superior to western medication and placebo (moderate evidence by GRADE). Regarding the improvement of stool consistency, stool frequency and abdominal pain, S-TXYF was significantly effective than placebo. In addition, S-TXYF was superior to western medication on improving the quality of life and relieving anxiety. Six trials reported adverse events: five of them reported (non-serious) adverse events occurred in both groups, and one trial reported that 3 cases with adverse events (constipation, elevation in liver-enzyme, nausea) occurred in S-TXYF group and 3 cases with adverse events (abdominal distension, nausea) occurred in placebo group. Conclusion: Although current results showed that S-TXYF may have potential to treat IBS-D and its use appears to be safe, no a clear and confirmed conclusion can be drawn from our review as the overall inadequate design of the included trials reviewed. So more rigorous trials are warranted to establish confirmed evidence on its benefits and safety.

Step by Step Golgi-Cox Staining for Cryosection.

Golgi staining, though invented hundreds of years ago, is still a reliable method to study the cytoarchitecture of the brain. Almost all published Golgi staining protocols and methods were used for microtome, and rarely applied in cryosection, which restricted the application of this technique. Currently, several commercial Golgi-stain kits are available for both vibratome section and cryosection, but these kits are costly, and it is still challenging for researchers to obtain significant results. In the present study, we described a protocol of Golgi-Cox Staining for Cryosection, with the modified cryosection protection solution based on the Golgi-Cox method, which makes cryosection easy to apply in the section of the Golgi-Cox impregnated tissue. Our methods provide a low-cost and simple option for Golgi staining, and it will facilitate researchers to obtain useful Golgi staining results for neuronal architecture studies.

Capability analysis and improvement research of surgical equipment management capability based on maturity assessment model / 中国医学装备

Objective:To construct a maturity assessment model of surgical equipment management capability and improve the quality of surgical equipment management.Methods:According to the composition form and operation status of the equipment,A maturity model framework for the management capability of surgical hand equipment was constructed,and a maturity evaluation system was developed from five levels:resource allocation,environmental guarantee,information basis,technical support and management performance.The cloud model evaluation strategy was adopted to evaluate the maturity in four levels:Level A,Level B,level C and level D,and a path for improving the maturity of management capability was developed.1 621 surgical equipment in clinical use in hospitals were selected and divided into control mode and observation mode according to different management modes.The conventional management mode was adopted in the control mode,and the priority management mode based on maturity assessment model was adopted in the observation mode.Compared the maturity level of device management capability,the score value of management index and the recognition degree of device management in the two management modes.Results:In observation mode,3.33%(54/1 621)and 7.28%(118/1 621)rated as grade A and Grade B were lower than those in control mode,while 60.76%(985/1 621)and 28.62%(464/1 621)rated as grade C and grade D were higher than those in control mode.The difference was statistically significant(x2=132.402,x2=411.692,x2=120.166,x2=269.033;P<0.05).The index scores of surgical equipment management resource allocation,operation environment guarantee,network information foundation,engineering technical support and operation and maintenance management performance were(90.98±5.21)points,(89.21±3.91)points,(91.40±4.09)points,(90.15±3.64)points and(91.57±3.37)points,respectively scores were higher than those in the control mode,and the difference was statistically significant(t=3.334,t=4.943,t=2.252,t=6.015,t=4.400;P<0.05).Engineers,nurses,doctors and related department managers involved in the management of equipment use were(87.63±4.12)%,(91.18±3.76)%,(96.65±3.04)%and(89.58±4.02)%,respectively,which were higher than those in the control mode.The difference was statistically significant(t=5.376,t=4.761,t=4.526,t=4.482;P<0.05).Conclusion:The maturity assessment model of surgical equipment management capability can improve the quality of surgical equipment management and operation,improve the level of equipment service,and has important value for the improvement of hospital management quality.

Brain-Derived Neurotrophic Factor Precursor in the Hippocampus Regulates Both Depressive and Anxiety-Like Behaviors in Rats.

Depression and anxiety are two affective disorders that greatly threaten the mental health of a large population worldwide. Previous studies have shown that brain-derived neurotrophic factor precursor (proBDNF) is involved in the development of depression. However, it is still elusive whether proBDNF is involved in anxiety, and if so, which brain regions of proBDNF regulate these two affective disorders. The present study aims to investigate the role of proBDNF in the hippocampus in the development of depression and anxiety. Rat models of an anxiety-like phenotype and depression-like phenotype were established by complete Freund's adjuvant intra-plantar injection and chronic restraint stress, respectively. Both rat models developed anxiety-like behaviors as determined by the open field test and elevated plus maze test. However, only rats with depression-like phenotype displayed the lower sucrose consumption in the sucrose preference test and a longer immobility time in the forced swimming test. Sholl analysis showed that the dendritic arborization of granule cells in the hippocampus was decreased in rats with depression-like phenotype but was not changed in rats with anxiety-like phenotype. In addition, synaptophysin was downregulated in the rats with depression-like phenotype but upregulated in the rats with anxiety-like phenotype. In both models, proBDNF was greatly increased in the hippocampus. Intra-hippocampal injection anti-proBDNF antibody greatly ameliorated the anxiety-like and depressive behaviors in the rats. These findings suggest that despite some behavioral and morphological differences between depression and anxiety, hippocampal proBDNF is a common mediator to regulate these two mental disorders.

Simvastatin inhibits tissue factor and plasminogen activator inhibitor-1 secretion by peripheral blood mononuclear cells in patients with primary nephrotic syndrome.

BACKGROUND: Tissue factor (TF) and plasminogen activator inhibitor-1 (PAI-1) activity and/or expression are upregulated in nephrotic syndrome. Despite extensive research on antithrombotic effect of statins, little is known about their effects on TF and PAI-1 expression in peripheral blood mononuclear cells in patients with primary nephrotic syndrome(PNS). METHODS: PBMCs were isolated by gradient centrifugation from 25 individuals with PNS and 25 healthy subjects. TF and PAI-1 mRNA were detected by RT-PCR. The activities of TF and PAI-1 were determined with ELISA and chromogenic substrate method, respectively. The patients with PNS were then treated with simvastatin 40 mg/day for 2 weeks. The activities of TF, PAI-1 and TF, PAI-1 mRNA of PBMCs were also measured. RESULTS: Compared with controls, patients with PNS had increased TF, PAI-1 secretion by PBMCs at baseline (70.4 +/- 15.6 ng/l vs. 32.7 +/- 8.2 ng/l; 15.9 +/- 2.4 (x10(3) AU/l) vs. 3.9 +/- 1.5(x10(3) AU/l), P<0.01) and after stimulated by LPS (10 ng/mL) (89.2 +/- 13.4 ng/l vs. 49.5 +/- 10.3 ng/l; 23.8 +/- 3.3 (x10(3) AU/l) vs. 8.1 +/- 2.1, P<0.01). The simvastatin treatment resulted in a significant effect in decreasing TF and PAI-1 (69.1 +/- 14.6 ng/l vs. 89.2 +/- 13.4 ng/l; 16.5 +/- 4.8 (x10(3) AU/l) vs. 23.8 +/- 3.3 (x10(3) AU/l), P<0.05) secretion in PBMCs. Increased TF and PAI-1 mRNA expression in PBMCs from PNS (1.034 +/- 0.043 and 0.982 +/- 0.056, respectively) as compared to the control (0.221 +/- 0.015 and 0.221 +/- 0.015, respectively) (p<0.01). two-week simvastatin treatment resulted in significant decrease of TF (0.535 +/- 0.028, p<0.01) and PAI-1 mRNA (0.602 +/- 0.037, p<0.01). CONCLUSION: TF and PAI-1 mRNA expression and activities in PBMCs were increased in PNS. Simvastatin reduced TF and PAI-1 expression and activity in PBMCs. These effects may partially be relevant to the clinical benefits of statins in the treatment of PNS.

[Genetic analysis and mapping of the rice leafy-hull mutant Oslh].

Oslh (lh=leafy hull), in the japonica cultivar 9522 background, a mutant of Oryza sativa L. spp. japonica cv. 9522 identified from an M(2) population, was mutagenized by irradiation with (60)Co gamma-ray. The Oslh mutant plants flowered about 15 days later than the wild-type plants (Fig.1e). The paleas, lemmas and lodicules of the flowers of Oslh mutant were transformed into leaf-like structures (Fig.1b, d). Genetic analysis of the F(2) progeny from a cross between the Oslh mutant and wild-type japonica cv. 9522 revealed that the Oslh mutant arouse from a single recessive nuclear gene mutation of the cv. 9522. To map the Oslh locus, an F(2) population generated by crossing between Oslh (japonica) mutant and Guangluai4 (indica) was analyzed. The Oslh locus was mapped to the long arm of rice chromosome 3, between a SSR marker RM5475 and an InDel marker GY305, 2.9 and 1.5 cM away from these two markers respectively (Fig.4). These results are useful for further cloning and functional analysis of the OsLH gene.

[Effect of indomethacin on fibronectin and plasminogen activator inhibitor-1 in cultured human peritoneal mesothelial cells].

OBJECTIVE: To determine the effect of indomethacin on high concentration glucose and lipopolysaccharide (LPS) induced fibronectin (FN) and plasminogen activator inhibitor-1 (PAI-1) secretion in cultured human peritoneal mesothelial cells. METHODS: Mesothelial cells were isolated from human omental specimens by trypsin disaggregation and incubated by 2.5% glucose or LPS together with different concentrations of indomethacin. Enzyme-linked immunosorbent assay determined the quantity of FN and PAI-1 in the cultured supernatants. RESULTS: Compared with the control group, the levels of FN and PAI-1 in the cultured supernatants were increased significantly exposuring to high concentration glucose and LPS (P <0.01). The different concentrations of indomethacin decreased FN and PAI-1 secretion in the 2.5% glucose or the LPS group within 24 h (P < 0.05). CONCLUSION: Indomethacin can inhibit the synthesis and secretion of extracellular matrix in human peritoneal mesothelial cells, which may be effective in the gene therapy for peritoneal fibrosis.

Tanshinones suppress AURKA through up-regulation of miR-32 expression in non-small cell lung cancer.

Tanshinone is the liposoluble constituent of Salia miltiorrhiza, a root used in traditional herbal medicine which is known to possess certain health benefits. Although it is known that tanshinones, including tanshinone I (T1), tanshinone IIA (T2A), and cryptotanshinone (CT), can inhibit the growth of lung cancer cells in vitro, the mechanism under which they act is still unclear. AURKA, an oncogene, encodes a serine-threonine kinase which regulates mitotic processes in mammalian cells. Here, we reported that tanshinones mediate AURKA suppression partly through up-regulating the expression of miR-32. We found that tanshinones could inhibit cell proliferation, promote apoptosis, and impede cell-cycle progression, thus performing an antineoplastic function in non-small cell lung cancer (NSCLC). Additionally, we demonstrated that tanshinones attained these effects in part by down-regulating AURKA, corroborating previous reports. Our results showed that in NSCLC, similar effects were obtained with knock-down of the AURKA gene by siRNA. We also verified that AURKA was the direct target of miR-32. Collectively, our results demonstrated that tanshinones could inhibit NSCLC by suppressing AURKA via up-regulating the expressions of miR-32 and other related miRNAs.

AEG-1 participates in high glucose-induced activation of Rho kinase and epithelial-mesenchymal transition in proximal tubular epithelial cells.

OBJECTIVE: To prove whether astrocyte elevated gene-1 (AEG-1) plays a role in high glucose-stimulated Rho kinase activation and epithelial-mesenchymal transition (EMT) in human renal tubular epithelial (HK-2) cells. METHODS: The protein levels of AEG-1, alpha-smooth muscle actin, E-cadherin and MYPT1 were determined by Western blot. RESULTS: AEG-1 protein level was upregulated in HK-2 cells stimulated with high glucose. AEG-1 siRNA downregulated Rho kinase protein expression and blocked high glucose-induced EMT. CONCLUSIONS: Our results show that AEG-1 acts a key role in high glucose-induced activation of Rho kinase and EMT in HK-2 cells.

[Subclassification of seronegative type 1 diabetic subjects with HLA-DQ genotypes].

OBJECTIVE: To reveal the relationship between disease phenotype and HLA-DQ genotype in autoantibody-negative type 1 diabetics and to explore whether HLA-DQ genotypes can reclassify seronegative type 1 diabetic patients. METHODS: Sixty-one diabetics with unprovoked ketosis or ketoacidosis at presentation were tested for glutamic acid decarboxylase antibody (GAD-Ab), tyrosine phosphatase antibody (IA2-Ab), thyroglobulin antibody (TGA), thyroid peroxidase antibody (TPO-Ab) and HLA-DQ genotype. GAD-Ab and IA2-Ab were measured with radioligand assay. TGA and TPO-Ab were evaluated using RIA. Sequence-based genotyping (SBT) was used to determine the alleles of HLA-DQA1 and DQB1. Autoantibody negative patients were subdivided into group A (with type 1 diabetes susceptible alleles) and group B (without type 1 diabetes susceptible alleles). Clinical characteristics, including age, sex, mode of presentation, body mass index (BMI), islet beta-cell function and current treatment were compared between the autoantibody-positive and autoantibody-negative patients and between group A and B. RESULTS: Among the 61 patients, 29 (47.5%) were negative for all the antibodies tested, while 31 (50.8%) were positive for one or more antibodies tested. 5 (8.2%) were positive for all those 4 antibodies. As for genetic analysis, 18 of the 29 seronegative patients carried 1-4 HLA-DQ risk alleles, while the other 11 did not carry any type 1 diabetes susceptible alleles tested. As compared with the autoantibody-negative patients, younger age at onset, less obesity, severer degree of diabetic ketoacidosis (DKA) and lower C peptide were found in the autoantibody-positive ones. As compared with group B, less obesity [BMI: (22.4 +/- 4.4) kg/m(2) vs (25.8 +/- 3.7) kg/m(2), P = 0.03], severer degree of DKA [CO(2)CP: (16.3 +/- 7.1) mmol/L vs (19.2 +/- 2.0) mmol/L, P = 0.01; pH: 7.26 +/- 0.20 vs 7.34 +/- 0.06, P = 0.03], and lower C peptide [fasting C peptide: (254.6 +/- 189.4) pmol/L vs (458.7 +/- 274.1) pmol/L, P = 0.06] were observed in group A. During follow-up, 73% (8/11) patients in group B discontinued insulin therapy and maintained acceptable glycemic control by either diet or oral hypoglycemic agents (OHA), while only 28% (5/18) of the patients in group A discontinued and maintained control with OHA (28% vs 73%, P < 0.01). Among those who kept on using insulin, group A patients required higher insulin dosage than those of group B [(0.43 +/- 0.16) U x kg(-1) x d(-1) vs (0.24 +/- 0.18) U x kg(-1) x d(-1), P = 0.07]. CONCLUSIONS: Autoantibody-negative diabetics, if with susceptible HLA-DQ genotypes, presented more type 1A-like features, implying possible existence of as yet unidentified immunologic abnormalities in these patients. HLA-DQ risk genotypes may reclassify seronegative type 1 diabetics. Those who are autoantibody negative but carry susceptible HLA-DQ genotypes, should not be diagnosed as type 1B diabetes.

Insulin-producing acinar cells in adult human pancreas.

OBJECTIVE: The aim of this study was to characterize cells expressing insulin and amylase in adult human pancreas. METHODS: We applied serial section and immunohistochemistry to pancreas samples from 5 adult nondiabetic subjects (2 men and 3 women;mean age, 65.8 years; random plasma glucose level, 5.1 mM). Cells expressing insulin and amylase were captured by immunofluorescence and confocal miscroscopy. RESULTS: We found a widespread occurrence of insulin-producing cells in exocrine acini and amylase-reactive acinar cells in well-formed islets. The insulin-producing cells in exocrine acini predominantly formed single and double cell units though cell clusters, and islands occurred. Acini containing insulin-producing cells outnumbered the islets with a factor of approximately 5. Confocal microscopy and double immunostaining identified acinar A-cells coexpressing both amylase and insulin. CONCLUSIONS: The acinar A-cells represent a distinct category of pancreatic cell populations and might be possible endogenous progenitors of insulin-producing cells in normal and abnormal metabolic homeostasis.

miR-150, p53 protein and relevant miRNAs consist of a regulatory network in NSCLC tumorigenesis.

microRNAs (miRNAs) are a class of non-coding small RNAs that act as negative regulators of gene expression by binding to the 3'-untranslated region (3'-UTR) of target mRNAs. Tumor protein p53, a transcriptional factor, plays an important role in the progression of tumorigenesis. miR-150 was the only miRNA predicted to target 3'-UTR of p53 by Targetscan. In order to investigate the function of miR-150, p53 and relevant miRNAs in non-small cell lung cancer (NSCLC), we constructed two expression vectors of p53 (pcDNA3.1-p53 and pcDNA3.1-p53-3'-UTR) and two report vectors (pGL3-p53-3'-UTR and pGL3-p53-3'-mUTR). The activity of luciferase transfected with miR-150 mimics was lower by 30% when compared to that of the miRNA-negative control (miRNA-NC). Moreover, the p53 protein was downregulated by at least 50% when miR-150 mimics were cotransfected with pcDNA3.1-p53-3'-UTR when compared to miRNA-NC. We also determined the expression of miR-150 and p53 in NSCLC patient tissue samples. The expression of miR-150 in T2 stage tissue samples was higher than that in T1 stage tissue samples. The corresponding target gene p53 was correlated with miR-150 expression. In the present study, we further analyzed the cell cycle distribution. The cells transfected with pcDNA3.1-p53 were significantly arrested in the G1 phase when compared to the control cells. When miR-150 mimics were cotransfected with pcDNA3.1-p53-3'-UTR, the percentage of cells in the G1 phase was significantly lower by 4% when compared to miRNA-NC. To identify miRNAs that are regulated by the p53 protein, qRT-PCR was performed after pcDNA3.1-p53 transfection. miR-34a, miR-184, miR-181a and miR-148 were upregulated significantly. However, there was no distinct difference in the expression of miR-10a, miR-182 and miR-34c. Our results showed that miR-150 targets the 3'-UTR of p53, and p53 protein promotes the expression of miRNAs which affect cell cycle progression. These findings suggest that miR-150, p53 protein and relevant miRNAs are members of a regulatory network in NSCLC tumorigenesis.

Research on prescription screening of Acteoside solid lipid nanoparticles / 药物评价研究

Objective To explore the impacts of different excipients on physical and chemical properties of Acteoside solid lipid nanoparticles (Acteoside-SLN),and make experimental evidence for the study of prescription SLN.Methods Emulsification-evaporation was appropriate for the preparation of Acteoside-SLN.Single variable method was used for fumbling the effects of Compritol 888 ATO,glyceryl monostearate,soy lecithin,Myrj52 and other accessories on the physicochemical properties including nanoparticles particle size,encapsulation efficiency and characterization dispersity (PDI) of Acteoside-SLN.Transmission electron microscope was used to observe the morphology of Acteoside-SLN and the structure of Acteoside in SLN was measured by XRD.Results With the increasing of the amount of Compritol 888 ATO,the particle size of nanoparticles decreased significantly,encapsulation efficiency decreased slightly,PDI increased;With the increasing of amount of glycerol monostearate,particle size increased obviously,encapsulation efficiency decreased slightly,and PDI decreased;With the increasing of the amount of lecithin,particles size increased significantly,encapsulation efficiency decreased,and PDI decreased;With the increasing of Myrj52 amount,the nanoparticles particle size decreased,encapsulation rate and PDI increased slightly.The appearance of Acteoside-SLN was presented uniform spherically.Acteoside was wrapped in SLN in a molecular dispersion state.Conclusion Various additives have a greater impact on physicochemical properties of Acteoside-SLN,and inspiration for prescription screening of SLN is supplied by this study.

[Effects of saline-alkali and drought stress on seed germination and TvNHX1 expression of Tripolium vulgare].

By applying 40-400 mmol x L(-1) NaCl, 20-200 mmol x L(-1) NaHCO3, and 5%-30% PEG, this paper studied the effects of saline-alkali and drought stress on the seed germination and Na+/H+ antiporter gene (TvNHX1) expression of Tripolium vulgare. 40-160 mmol x L(-1) NaCl, 20 mmol x L(-1) NaHCO3, and 5%-10% PEG-6000 had less effects on the seed germination; while > or = 240 mmol x L(-1) NaCl decreased the seed germination rate, root length, and shoot length (P < 0.05), > or = 50 mmol x L(-1) NaHCO3 decreased the seed germination rate (P < 0.05), 130 mmol x L(-1) NaHCO3 decreased the seed germination potential, root length, and shoot length (P < 0.05), and > or = 15% PEG delayed the seed germination. TvNHX1 transcripts were basically constitutive at germination stage, but their expression increased distinctly at 160 mmol x L(-1) NaCl, 100 mmol x L(-1) NaHCO3, and 10% PEG. Under salt and drought stress, the expression of TvNHX1 changed in-phase with the phenotype change of germinated seeds, suggesting that TvNHX1 play important roles in the tolerance of T. vulgare against adversity stress.

Connective tissue growth factor and fibronectin secretion in renal tubular epithelial cells induced by TGF-beta1: suppressive effects of troglitazone.

Although some studies have suggested that troglitazone could retard the progression of glomerulosclerosis, its effects on renal tubulointerstitial fibrosis have not been completely clarified. The aim of this study was to investigate the effects of troglitazone on the secretion of connective tissue growth factor (CTGF) and fibronectin (FN) in human renal proximal tubular epithelial (HK-2) cells induced by transforming growth factor-beta1 (TGF-beta1). The mRNA of CTGF and FN were measured by semi-quantitative RT-PCR. CTGF and FN protein were detected by Western blot and ELISA, respectively. Our results revealed that troglitazone could inhibit CTGF and FN expression in a dose-dependent manner in human renal proximal tubular epithelial cells induced by TGF-beta1, which may be one of the mechanisms of troglitazone contributing to retard the progression of renal tubulointerstitial fibrosis.