Tenecteplase Plus Butyphthalide for Stroke Within 4.5-6 Hours of Onset (EXIT-BT): a Phase 2 Study.

To date, the benefit of intravenous thrombolysis is confined to within 4.5 h of onset for acute ischemic stroke (AIS) without advanced neuroimaging selection. The current trial aimed to investigate the safety and efficacy of intravenous tenecteplase (TNK) plus Dl-3-n-Butylphthalide (NBP) in AIS within 4.5 to 6 h of onset. In this randomized, multicenter trial, eligible AIS patients were randomly assigned to receive intravenous TNK (0.25 mg/kg) plus NBP or NBP within 4.5 to 6 h of onset. The primary endpoint was symptomatic intracranial hemorrhage (sICH). Secondary endpoints included excellent functional outcome defined as a modified Rankin Scale score of 0 to 1 at 90 days. 100 patients diagnosed by non-contrast CT (NCCT) were enrolled, including 50 in TNK group and 50 in control group. sICH occurred in 2.0% (1/50) in TNK group and 0.0% (0/49) in control group with no difference (unadjusted P = 0.998). The proportion of excellent functional outcome was 77.6% (38/49) in TNK group and 69.4% (34/49) in control group with non-significance (absolute difference 8.2%, P = 0.36). A significant decrease in NIHSS score at 24 h (P = 0.004) and more early neurological improvement (20.4% vs 4.1%; P = 0.026) was observed in TNK vs control group, but there was no difference in other secondary outcomes. This phase 2 study suggests that intravenous TNK with adjuvant NBP seems safe, feasible and may improve early neurological function in AIS patients within 4.5 to 6 h of symptom onset selected using NCCT.Clinical Trials Registration: This trial was registered with ClinicalTrials.gov (NCT05189509).

Multidrug-resistant organisms in intensive care units and logistic analysis of risk factors.

BACKGROUND: Intensive care unit (ICU) patients are critically ill and have low immunity. They will undergo various trauma medical procedures during diagnosis and treatment. The use of high-dose hormones and broad-spectrum antibiotics will increase the incidence of nosocomial infection in ICU patients. Therefore, it is necessary to explore the causes of nosocomial infection in ICU and provide basis for the prevention and control of nosocomial infection in ICU. AIM: To explore major pathogens of nosocomial infection in ICUs, methods of detection and drug resistance trends. METHODS: Risk factors of multidrug-resistant infection were analyzed to provide a basis for clinical rational use of antimicrobial drugs in the ICU. These findings were used to standardize rational use of antimicrobial agents. BD PhoenixTM100 automatic bacterial identification analyzer was used to for cell identification in specimens collected from the ICU between January 2016 and December 2019. Drug sensitivity tests were carried out and drug resistance trends were analyzed using the optical disc diffusion method. Odds ratios and corresponding 95%CI of independent variables were calculated using a logistic regression model. Backward elimination (trend = 0.1) was used as an inclusion criterion for multivariate analysis. All data were analyzed using SPSS version 22.0, and P < 0.05 was considered statistically significant. RESULTS: We collected 2070 samples from ICU patients between January 2016 and December 2019. Sample types comprised sputum (1139 strains, 55.02%), blood (521 strains, 25.17%), and drainage fluid (117 strains, 5.65%). A total of 1051 strains of major pathogens, including Acinetobacter baumannii, Escherichia coli (E. coli), Pseudomonas aeruginosa (P. aeruginosa), Klebsiella pneumoniae (K. pneumoniae) and Staphylococcus aureus, were detected, with a detection rate of 35.97% (378/1051). Most of these strains were resistant to antibiotics. Detection rate of E. coli was 21.79% (229/1051), and it was generally sensitive to many antimicrobial drugs. Detection rate of P. aeruginosa was 24.74% (260/1051), and showed low sensitivity to most antibiotics. Detection rate of K. pneumoniae was 9.42% (99/1051), which was generally resistant to multiple antimicrobial drugs and resistant forms. K. pneumoniae was resistant to imipenem for approximate 4 years, and showed a 19.9% (19/99) and 20.20% (20/99) rate of meropenem resistance. Logistic analysis showed that mechanical ventilation and ureteral intubation were risk factors for multidrug-resistant bacterial infections. CONCLUSION: This study showed a high incidence of ICU infections. Mechanical ventilation and urine tube intubation were risk factors for infection with multidrug-resistant bacteria.

Use of Retroauricular Flaps to Reconstruct Defects of the Helical Rim and Adjuvant Intralesional Corticosteroids after Resection of Large Keloids.

BACKGROUND: The optimal treatment for large helical rim keloids remains unclear. AIMS: The authors evaluated patient outcomes when retro auricular flaps were used to reconstruct helical rim defects and adjuvant intralesional corticosteroids were prescribed after resection of large keloids. MATERIALS AND METHODS: The authors evaluated 7 females with 12 large keloids of the helical rim (5 patients had lesions in both ears). All patients were aged 18 to 33 years. The authors used retro auricular flaps to reconstruct the helical rim defects and prescribed adjuvant intralesional corticosteroids after resection. The lesion area ranged from 2.5 × 2.0 to 3.5 × 3.5 cm2. The flap size ranged from 2.5 × 3.0 to 3.5 × 4.5 cm2. The flaps and wound bases received 3 steroid injections at approximately 1, 2, and 3 months postoperatively. RESULTS: No flap necrosis or complications were noted. The postoperative esthetic results were satisfactory in 8 patients and excellent in 4. All patients were followed up for 14 to 28 months (median, 20.6 months). No recurrence was noted, although 3 patients exhibited mild scarring of the wound flap base. CONCLUSIONS: A retro auricular flap is safe and effective for reconstructing helical rim defects; adjuvant intralesional corticosteroids prevent scarring of the flap wound base after resection of large keloids.

Blockage of ETS homologous factor inhibits the proliferation and invasion of gastric cancer cells through the c-Met pathway.

BACKGROUND: Gastric cancer (GC) is one of the most common and deadliest types of cancer worldwide due to its delayed diagnosis and high metastatic frequency, but its exact pathogenesis has not been fully elucidated. ETS homologous factor (EHF) is an important member of the ETS family and contributes to the pathogenesis of multiple malignant tumors. To date, whether EHF participates in the development of GC via the c-Met signaling pathway remains unclear. AIM: To investigate the role and mechanism of EHF in the occurrence and development of GC. METHODS: The expression of EHF mRNA in GC tissues and cell lines was measured by quantitative PCR. Western blotting was performed to determine the protein expression of EHF, c-Met, and its downstream signal molecules. The EHF expression in GC tissues was further detected by immunohistochemical staining. To investigate the role of EHF in GC oncogenesis, small interfering RNA (siRNA) against EHF was transfected into GC cells. The cell proliferation of GC cells was determined by Cell Counting Kit-8 and colony formation assays. Flow cytometry was performed following Annexin V/propidium iodide (PI) to identify apoptotic cells and PI staining to analyze the cell cycle. Cell migration and invasion were assessed by transwell assays. RESULTS: The data showed that EHF was upregulated in GC tissues and cell lines in which increased expression of c-Met was also observed. Silencing of EHF by siRNA reduced the proliferation of GC cells. Inhibition of EHF induced significant apoptosis and cell cycle arrest in GC cells. Cell migration and invasion were significantly inhibited. EHF silencing led to c-Met downregulation and further blocked the Ras/c-Raf/extracellular signal-related kinase 1/2 (Erk1/2) pathway. Additionally, phosphatase and tensin homolog was upregulated and glycogen synthase kinase 3 beta was deactivated. Moreover, inactivation of signal transducer and activator of transcription 3 was detected following EHF inhibition, leading to inhibition of the epithelial-to-mesenchymal transition (EMT). CONCLUSION: These results suggest that EHF plays a key role in cell proliferation, invasion, apoptosis, the cell cycle and EMT via the c-Met pathway. Therefore, EHF may serve as an antineoplastic target for the diagnosis and treatment of GC.

Histone acetyltransferase p300/CBP inhibitor C646 blocks the survival and invasion pathways of gastric cancer cell lines.

The histone acetyltransferases (HATs) adenovirus E1A-associated protein (p300) and CREB binding protein (CBP) serve as coactivators during a diverse assortment of cellular processes. In the present study, p300 and CBP were highly expressed in 5 gastric cancer (GC) cell lines (SGC­7901, MKN45, MGC-803, BGC-823 and KATO III) compared with human normal gastric epithelial cell line (GES-1). C646, a selective inhibitor of p300 and CBP, inhibited cell viability and cell cycle and promoted cell apoptosis in all 5 GC cell lines. In addition, C646 suppressed the migration and invasion capability of the GC cell lines, except for the middle-differentiated SGC-7901 cell line. Furthermore, we detected the differential expression of corresponding oncogenic signalling molecules, such as c-Met, Akt, Bcl-2, Bax, cyclin D1, MMP7 and MMP9, in GC cells following C646 treatment. In conclusion, our results suggest that C646 inhibits the acetylation of histone H3 via inactivation of p300 and CBP, resulting in antineoplastic effects toward GC cells. Thus, the selective HAT inhibitor C646 could be a promising antitumour reagent for GC treatment.

An inhibitor of the acetyltransferases CBP/p300 exerts antineoplastic effects on gastrointestinal stromal tumor cells.

Gastrointestinal stromal tumors (GISTs) are the most common mesenchymal neoplasm featured by activated mutations of KIT and PDGFRA. Although overall survival rates have greatly improved by the development of receptor tyrosine kinase inhibitors, most patients ultimately acquire resistance due to secondary mutations of KIT or PDGFRA. Inhibition of the histone acetyltransferases (HATs) CREB­binding protein (CBP) and p300 results in antineoplastic effects in various cancers. To determine whether CBP/p300 can serve as an antineoplastic target for GISTs, specific short interfering RNA sequences and the selective HAT inhibitor C646 were administered to GIST882 cells. Cell viability, apoptosis and the cell cycle were analysed using the Cell Counting Kit-8, a caspase-3/7 activity assay or Annexin V-fluorescein isothiocyanate/propidium iodide (PI) staining and PI staining. Gene and protein expression levels were measured by quantitative real-time polymerase chain reaction and western blotting, respectively. Transcriptional blockage of CBP, rather than p300, resulted in suppression of cell proliferation. Interestingly, both CBP and p300 depletion enhanced caspase-3/7 activity. A lack of CBP and p300 caused ETS translocation variant 1 (ETV1) downregulation and KIT inhibition in GIST cells. Nevertheless, the absence of CBP, not p300, leads to extracellular signal-regulated kinase 1/2 inactivation and c-Jun NH2-terminal kinase activation, suggesting a more crucial role for CBP than p300 in cell proliferation and survival. Furthermore, proliferation of GIST cells was reduced by administration of C646, a selective HAT inhibitor for CBP/p300. Apoptosis induction and cell cycle arrest were detected after exposure to C646, indicating that its antitumor activities were supported by its antiproliferative and proapoptotic effects. Additionally, C646 treatment attenuated ETV1 protein expression and inactivated KIT-dependent pathways. Taken together, the present study suggests that CBP/p300 may serve as novel antineoplastic targets and that use of the selective HAT inhibitor C646 is a promising antitumor strategy for GISTs.

Comparison of endoscopic resection and gastrectomy for the treatment of early gastric cancer: a meta-analysis.

BACKGROUND: Endoscopic resection methods, including endoscopic mucosal resection and endoscopic submucosal dissection, have become standard treatment modalities for patients with early gastric cancer (EGC) and absolute indications, with en bloc resection being more frequent with the latter. Endoscopic resection, however, has been associated with higher recurrence and metachronous cancer rates than gastrectomy. This meta-analysis compared the efficacy and safety of endoscopic resection and gastrectomy for EGC. METHODS: PubMed, EMBASE and Web of Science were electronically searched for relevant studies comparing endoscopic resection and gastrectomy for EGC from 1976 through March 2015. The primary endpoints were en bloc resection and histologically complete resection rates. The secondary endpoints were duration of hospital stay and rates of complications, recurrence, metachronous cancer and overall survival. RESULTS: This meta-analysis enrolled 10 studies with 2070 patients: 993 patients who underwent endoscopic resection and 1077 who underwent gastrectomy. Endoscopic resection was associated with shorter hospital stay (standardized mean difference -2.02; 95 % confidence interval [CI] -2.64 to -1.39) and lower complication rate (relative risk [RR] 0.41; 95 % CI 0.22-0.76) than gastrectomy. However, endoscopic resection was associated with lower rates of en bloc resection (odds ratio [OR] 0.05; 95 % CI 0.02-0.16) and histologically complete resection (OR 0.04; 95 % CI 0.01-0.11) and higher rates of recurrence (RR 5.23; 95 % CI 2.43-11.27) and metachronous cancer (RR 5.22; 95 % CI 2.40-11.34) than gastrectomy. Overall survival rate (OR 1.18; 95 % CI 0.76-1.82) was similar. CONCLUSIONS: Endoscopic resection is minimally invasive and as effective as surgery, suggesting that the former be considered standard treatment for EGC. It should be recommended as standard treatment for EGC with indications. Additional randomized controlled trials from more countries are required.

[Physiological response of the distribution of non-structural carbohydrates to water stress in wheat].

In this paper, the spring wheat (cv. Xihan No. 2) was taken as research material to investigate the dynamic changes of the non-structural carbohydrates (NSC) in flag leaves, stems and leaf sheaths and activities of carbon-metabolizing enzymes (SSS, GBSS) in grains during wheat development process under various water stresses by water stress and re-watering treatment methods. The results indicated that various water stresses had no significant effects on the sucrose contents in flag leaves, stems, leaf sheaths and other organs of wheat. With the increase of water stress, the content of starch in flag leaves was significantly increased within 12-18 d after flowering. Water stress shortened the starch accumulation period in stems and sheaths after flowering and inhibited the transformation and distribution of starch in wheat stems. The accumulation of starch in sheath also gradually increased, which was early terminated under moderate water stress. At the beginning of the water stress, the contents of NSC in vegetative organs were listed as: flag leaves > stems > leaf sheaths. With the increase of water stresses, the NSC contents in vegetative organs were listed as: stems > flag leaves > leaf sheaths. We could conclude that the changes in main NSC (sugar, starch) distribution and carbon-metabolism enzyme activities was a kind of physiological regulation response of wheat to water stresses.

Succinate dehydrogenase-deficient gastrointestinal stromal tumors.

Most gastrointestinal stromal tumors (GISTs) are characterized by KIT or platelet-derived growth factor alpha (PDGFRA) activating mutations. However, there are still 10%-15% of GISTs lacking KIT and PDGFRA mutations, called wild-type GISTs (WT GISTs). Among these so-called WT GISTs, a small subset is associated with succinate dehydrogenase (SDH) deficiency, known as SDH-deficient GISTs. In addition, GISTs that occur in Carney triad and Carney-Stratakis syndrome represent specific examples of SDH-deficient GISTs. SDH-deficient GISTs locate exclusively in the stomach, showing predilection for children and young adults with female preponderance. The tumor generally pursues an indolent course and exhibits primary resistance to imatinib therapy in most cases. Loss of succinate dehydrogenase subunit B expression and overexpression of insulin-like growth factor 1 receptor (IGF1R) are common features of SDH-deficient GISTs. In WT GISTs without succinate dehydrogenase activity, upregulation of hypoxia-inducible factor 1α may lead to increased growth signaling through IGF1R and vascular endothelial growth factor receptor (VEGFR). As a result, IGF1R and VEGFR are promising to be the novel therapeutic targets of GISTs. This review will update the current knowledge on characteristics of SDH-deficient GISTs and further discuss the possible mechanisms of tumorigenesis and clinical management of SDH-deficient GISTs.

[The influence of oil heat treatment on wood decay resistance by Fourier infrared spectrum analysis].

Wood preservative treatment can improve defects of plantation wood such as easy to corrupt and moth eaten. Among them heat-treatment is not only environmental and no pollution, also can improve the corrosion resistance and dimension stability of wood. In this test Poplar and Mongolian Seoteh Pine was treated by soybean oil as heat-conducting medium, and the heat treatment wood was studied for indoor decay resistance; wood chemical components before and after treatment, the effect of heat treatment on wood decay resistance performance and main mechanism of action were analysed by Fourier infrared spectrometric. Results showed that the mass loss rate of poplar fell from 19.37% to 5% and Mongolian Seoteh Pine's fell from 8.23% to 3.15%, so oil heat treatment can effectively improve the decay resistance. Infrared spectrum analysis shows that the heat treatment made wood's hydrophilic groups such as hydroxyl groups in largely reduced, absorbing capacity decreased and the moisture of wood rotting fungi necessary was reduced; during the heat treatment wood chemical components such as cellulose, hemicellu lose were degraded, and the nutrient source of wood rotting fungi growth necessary was reduced. Wood decay fungi can grow in the wood to discredit wood is because of that wood can provide better living conditions for wood decay fungi, such as nutrients, water, oxygen, and so on. The cellulose and hemicellulose in wood is the main nutrition source of wood decay fungi. So the oil heat-treatment can reduce the cellulose, hemicellulose nutrition source of wood decay fungi so as to improve the decay resistance of wood.

[Spatial distribution, mechanism and management strategies of carbon source and sink of urban residential area: a case in Guanzhong Region, China].

Urban residential area is an important component of urban ecosystem. Its carbon process will have an important impact on carbon cycle and carbon balance of urban ecosystem. In this paper, the data of CO2 emission and absorption in Guanzhong area were collected by case ana-lysis, literature consulting and questionnaires and surveys to analyze its sources and the spatial distribution characteristics. The results showed that building materials production and renovation of residential area had the most CO2 emission, and building materials had much larger CO2 emission compared with everyday means of subsistence. Only 40% -52% of total carbon emission occurred within the residential area, while the rest was in the peripheral area. The spatial distance variation of carbon source, the spatial differences of carbon component and the spatial distribution by spheres and zoning were observed. As for CO2 absorption, only 9%-17% CO2 emission could be absorbed in the residential area, and the others had to be imposed to the outer space, showing hierarchical grading rules and spatial variation. Some space management techniques and intervention measures were put forward.

Chemoradiotherapy followed by surgery could improve the efficacy of treatments in patients with resectable esophageal carcinoma.

BACKGROUND: The effectiveness of chemoradiotherapy followed by surgery (CRTS) in patients with resectable esophageal carcinoma remains controversial. We performed a systematic review of the literature with meta-analysis. METHODS: Electronic databases were used to identify published studies between January 1992 and April 2012. Pooled relative risk (RR) with 95% confidence interval (95% CI) was utilized to estimate the strength of the association between CRTS and surgery alone (SA) survival of the resectable esophageal carcinoma patients. Heterogeneity and publication bias were also assessed in the present study. RESULTS: The final analysis of 2755 resectable esophageal carcinoma cases from 21 randomized controlled trials (RCTs) are presented. Compared to the SA group, the 1, 3- and 5-year survival rates were significantly higher in the CRTS group (all P < 0.05); the 3- and 5-year survival rates for the Eastern patients, Western patients, patients undergoing concurrent chemoradiotherapy, patients with squamous cell carcinoma, patients undergoing High-dose radiotherapy (≥ 40 Gy), and patients given either "cisplatin + Fluorouracil" or "cisplatin + paclitaxel" chemotherapy were significantly higher in the CRTS group (all P < 0.05). There were no statistical significances in the 3- and 5-year survival rates for patients undergoing sequential chemoradiotherapy or patients with adenocarcinoma between the two groups (all P > 0.05). Compared to the RCTS group, the surgery rate in the SA group was higher (P < 0.05), while the CRTS group had significantly higher radical resection rate, R0 resection rate and lower postoperative local recurrence rate (all P < 0.05). The differences in postoperative complication incidence, post-operative distant metastasis and postoperative mortality rate were not statistically significant between the two groups (all P > 0.05). CONCLUSION: CRTS can significantly improve the survival and surgical conditions of patients with resectable esophageal carcinoma.

[Mechanical ventilation in acute respiratory distress syndrome].

The goal of mechanically ventilating patients with acute respiratory distress syndrome (ARDS) is to ensure adequate oxygenation and minimal ventilator-associated lung injury. Non-invasive ventilation should be cautiously used in patients with ARDS. Protective ARDS mechanical ventilation strategies with low tidal volumes can reduce mortality. Driving pressure is the most reasonable parameter to optimize tidal volume. Available evidence does not support the routine use of higher positive end expiratory pressure (PEEP) in patients with ARDS. The optimal level of PEEP may be titrated by the inflection point obtained from static pressure-volume curve. Promising therapies include prone position ventilation, high frequency oscillatory ventilation and extracorporeal membrane oxygenation as salvage treatment. While mechanically ventilating, it is also important for ARDS patients to maintain spontaneous breathing via assisted ventilation mode such as bilevel positive airway pressure, pressure support ventilation and neurally adjusted ventilation assist. Exogenous surfactant, inhaled nitric oxide, bronchodilators, airway pressure release ventilation and partial liquid ventilation are not recommended therapies.

[Mechanism for promoting repair of renal ischemia reperfusion injury by mesenchymal stem cells].

OBJECTIVE: Preclinical studies have demonstrated that exogenous mesenchymal stem cells (MSCs) may ameliorate kidney damage and enhance repair of renal ischemia reperfusion injury (IRI). This review will focus on the mechanism for accelerating repair of renal IRI by MSCs. Several chemokine receptors such as CXCR4 and CD44 are related to MSCs trafficking to post-ischemic kidney. MSCs differentiate into tubular epithelial cells, which is not the predominant mechanism for repair of the damaged kidney. Instead, MSCs exert their therapeutic effect mainly through paracrine action via a variety of cytokines and microvesicles, and the paracrine actions of infused MSCs work to activate intrinsic kidney cells, promote angiogenesis, inhibit oxidative stress and reduce apoptosis, inflammation and renal fibrosis.

[Primary culture and identification of rat glomerular podocytes].

OBJECTIVE: To establish an easy and feasible method for primary culture and identification of rat glomerular podocytes. METHODS: Glomeruli from Sprague-Dawley (SD) rats weighing 60-100 gram were isolated by the method of different size combination of screen. Isolated glomeruli were appropriately digested with 2 g/L type IV collagenase and cultured in 25 cm2 plastic flask coated with rat tail collagen in K1-3T3 medium with ITS-X (containing insulin-transferrin-selenium). Subculture of primary cultured epithelial cells was performed at 9-10 days after implantation of collagenase digested glomeruli. Podocytes were identified by the morphology study with scanning electron microscope and inverted microscope, as well as the immunohistochemistry staining (SP methods) study for the expression of keratin, desmin and Wilms' tumor suppressor-1 (WT-1). RESULTS: Epithelial cells outgrowth from isolated glomeruli appeared after 3 days primary culture and grew to confluence with cobblestone-appearance at 9-10 days. These cobblestone cells were subcultured at this point and gradually conversed into large, flat arborized cells with well-developed processes and microvilli. These arborized cells were negative expression with desmin staining and showed positive expression of cytokeratin and WT-1, which indicated that they were podocytes. CONCLUSION: Implantating collagenase digested-glomeruli is an easy and feasible method for primary culture of rat glomerular podocytes. WT-1 may serve as a good marker to identify rat glomerular podocytes.

Correlation between DNase I hypersensitive site distribution and gene expression in HeLa S3 cells.

Mapping DNase I hypersensitive sites (DHSs) within nuclear chromatin is a traditional and powerful method of identifying genetic regulatory elements. DHSs have been mapped by capturing the ends of long DNase I-cut fragments (>100,000 bp), or 100-1200 bp DNase I-double cleavage fragments (also called double-hit fragments). But next generation sequencing requires a DNA library containing DNA fragments of 100-500 bp. Therefore, we used short DNA fragments released by DNase I digestion to generate DNA libraries for next generation sequencing. The short segments are 100-300 bp and can be directly cloned and used for high-throughput sequencing. We identified 83,897 DHSs in 2,343,479 tags across the human genome. Our results indicate that the DHSs identified by this DHS assay are consistent with those identified by longer fragments in previous studies. We also found: (1) the distribution of DHSs in promoter and other gene regions of similarly expressed genes differs among different chromosomes; (2) silenced genes had a more open chromatin structure than previously thought; (3) DHSs in 3'untranslated regions (3'UTRs) are negatively correlated with level of gene expression.

MicroRNA miR-886-5p inhibits apoptosis by down-regulating Bax expression in human cervical carcinoma cells.

OBJECTIVE: MicroRNA (miRNA) plays an essential role in the progression of a variety of cancers, but its role in cervical cancer progression is not well defined. We aimed to test whether special miRNAs and their target mRNAs contribute to cervical cancer progression. METHODS: The expression profiles of 1145 microRNAs in cervical squamous cell carcinomas (CSCC) and adjacent non-tumor tissues were investigated using an Illumina microRNA microarray platform. Differentially expressed miRNAs were validated by RT-PCR. Downstream target validation was performed for miR-886-5p. RESULTS: We found that the expression levels of seven miRNAs differed significantly between CSCC tissues and adjacent non-tumor tissues. Forced expression of one miRNA, miR-886-5p, over-expressed in CSCC tissues lowered expression of the pro-apoptotic protein Bax, reduced apoptosis and promoted cell proliferation in H8, an HPV16-immortalized human cervical squamous epithelial cell line. Knockdown of miR-886-5p increased Bax protein and apoptotic cell death in cells of the cervical squamous carcinoma cell line, SiHa. CONCLUSION: MicroRNA miR-886-5p inhibits apoptosis of cervical cancer cells by down-regulating the production of Bax.

[Study on fixation mechanism of CuAz preservatives in bamboo by ATR-FTIR].

The fixation mechanism of CuAz preservatives in bamboo was studied with bamboo as the experimental material in the present paper. The purpose of the study is to understand the interaction between preservatives and bamboo, provide a theoretical basis for the design and optimization of preservatives formula and for improving preservative treatment. The chemical combination between preservatives and bamboo components was analysed by ATR Fourier transform infrared spectroscopy (ATR-FTIR), and the results show that the infrared spectra of lignin after treatment changed significantly. The lignin characteristic peaks (1,510 cm(-1)) changed obviously. Lignin phenolic hydroxyl was involved in the lignin-copper complex formation. Holocellulose's spectra after treatment changed little, with just a change in hemicellulose carboxyl and hemicellulose acyl-oxygen bond (CO-O) stretching vibration.

[Construction of VEGF recombinant plasmid pcDNA/V and its expression in model rats with acute myocardial ischemia].

The cDNA encoding human Vascular Endothelial Growth Factor 165 (VEGF165) was amplified using RT-PCR from human tonsil tissue and cloned into eukaryotic expression vector pcDNA3.1 (+). The recombinant plasmid pcDNA/V was transferred into 293 cells mediated by liposome and the cells stably expressing VEGF were selected under the pressure of G418. ELISA and Western blotting demonstrated that the eukaryotic expression vector pcDNA/V was successfully constructed and its corresponding protein could be expressed efficiently in vitro. Chick Charioallantoic Membrane (CAM) bioassay showed that recombinant protein has biological activity of hVEGF. Model rats with acute myocardial ischemia were used to further study the expression of VEGFin vivo. The model rats were divided randomly into three groups: control group, pcDNA3.1 (+) group and pcDNA/V group. 50microL naked plasmid DNA or saline was intramyocardially injected at three sites into the border zone of infarction. The hearts of rats were excised and fixed histologically, then the infarction sizes were studied by immunohistochemical staining and electron microscope after four weeks. Immunohistochemical staining for VEGF appeared to be negative in control and pcDNA3.1 (+) groups. In pcDNA/V group, myocardial cells in infarction border zone showed positive staining for VEGF in cytoplasm. Ultrastructural anaylsis showed that there were visible hyperplasia of vascular endothilium in pcDNA/V group. The control and pcDNA3.1 (+) groups showed less capillary hyperplasia. In this study, VEGF165 gene was successfully cloned and its protein expressed in vitro and in vivo was of bioactivity, which provides a basis for the further study of biological functions of human VEGF.