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For flames with very low burning speed, the flame propagation is affected by buoyancy. Flame front evolution and laminar flame parameter evaluation methods of buoyancy-affected flame have been proposed. The evolution and propagation process of a center ignited expanding ammonia/air flame has been analyzed by using the methods. The laminar flame parameters of ammonia/air mixture under different equivalence ratio (ER) and initial pressure have been studied. At barometric pressure, with the increase of ER, the laminar burning velocity (LBV) of ammonia/air mixture undergoes a first increase and then decrease process and reaches its maximum value of 7.17 cm/s at the ER of 1.1, while the Markstein length increases monotonously. For ammonia/air flames with ER less than unity, the flame velocity shows a decreasing trend with stretch rate, resulting in the propensity to flame instability, but no cellular structure was observed in the process of flame propagation. As the initial pressure increases, the LBV decreases monotonously as well as the Markstein length. The flame thicknesses of ammonia/air mixtures decrease with initial pressure and are much thicker than those of hydrogen flames, which makes a stronger stabilizing effect of curvature on the flame front. The most enhancement of LBV is contributed by the dehydrogenation reaction of NH3 with OH. The NO concentration decreases significantly with the increase of ER.

Purpose: Increasing evidence has revealed that nicotinamide N-methyltransferase (NNMT) is a key factor influencing the prognosis of tumors. The present study aimed to investigate the role of NNMT in glioma and to elucidate the associated functional mechanisms. Methods: Clinical samples were analyzed by immunohistochemical staining and Western blotting to evaluate NNMT expression in glioma and normal brain tissues. The correlation between NNMT expression and glioma was analyzed using the Cancer Genome Atlas (TCGA) database. Additionally, NNMT was knocked down in two types of glioma cells, U87 and U251, to evaluate the invasive ability of these cells. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to validate NNMT knockdown in the cells. Furthermore, ELISA was used to determine the balance between nicotinamide adenine dinucleotide and nicotinamide adenine dinucleotide hydrogen (NAD/NADH ratio), which verified the altered methylation patterns in the cells. The glioma xenograft mouse models were used to verify the regulatory role of NNMT, GAP43, and SIRT1. Results: Analysis based on our clinical glioma samples and TCGA database revealed that overexpression of NNMT was associated with poor prognosis of patients. Knockdown of NNMT reduced the invasive ability of glioma cells, and downregulation of its downstream protein GAP43 occurred due to altered cellular methylation caused by NNMT overexpression. Gene Set Enrichment Analysis confirmed that NNMT modulated the NAD-related signaling pathway and showed a negative association between NNMT and SIRT1. Moreover, the regulatory roles of NNMT, GAP43, and SIRT1 were confirmed in glioma xenograft mouse models. Conclusion: Overexpression of NNMT causes abnormal DNA methylation through regulation of the NAD/NADH ratio, which in turn leads to the downregulation of GAP43 and SIRT1, eventually altering the biological behavior of tumor cells.

Background. Emerging evidence reveals that long noncoding RNAs (lncRNAs) play important roles in the pathogenesis of sepsis. However, the detailed regulatory mechanisms of lncRNAs or whether certain lncRNA could serve as a biomarker in the septic colon remains unclear. The aim of this study was to investigate the profiles of lncRNAs and mRNAs in the septic colon through whole-transcriptome RNA sequencing and to reveal the associated regulatory mechanism. Method and Result. We established a mouse model of sepsis by cecal ligation and puncture (CLP). Colon samples were collected upon CLP or sham surgery after 24 h. Whole-transcriptome RNA sequencing was performed to profile the relative expressions of lncRNAs and mRNAs. 808 lncRNAs and 1509 mRNAs were differentially found in the septic group compared with the sham group. Bioinformatics analysis including Gene Ontology (GO) analysis and Kyoto Encyclopedia of Genes and Genomes pathway analysis (KEGG) was performed to predict the potential functions of these RNAs. GO analysis showed that the altered lncRNAs were enriched and involved in multiple immune responses, which may be a response to sepsis stress. KEGG analysis indicated that upregulated lncRNAs were significantly enriched in the p53 signaling pathway, NF-κB signaling pathway, and HIF-1 signaling pathway. Downregulated lncRNAs were mostly found to be involved in tight junction, leukocyte transendothelial migration, and HIF-1 signaling pathway. Conclusion. Our results indicate that these altered lncRNAs and mRNAs may have crucial roles in the pathogenesis of sepsis. This study could contribute to extending the understanding of the function of lncRNAs in sepsis, which may help in searching for new diagnostic biomarkers and therapeutic targets to treat sepsis.

Curcumin (CM) is a natural polyphenolic compound with multiple biomedical functions. However, clinical applications face more challenges due to its low dissolution rate and poor bioavailability. Mi...

Formic acid is a representative small molecule acid in lignocellulosic hydrolysate that can inhibit the growth of Saccharomyces cerevisiae cells during alcohol fermentation. However, the mechanism of formic acid cytotoxicity remains largely unknown. In this study, RNA-Seq technology was used to study the response of S. cerevisiae to formic acid stress at the transcriptional level. Scanning electron microscopy and Fourier transform infrared spectroscopy were conducted to observe the surface morphology of yeast cells. A total of 1504 genes were identified as being differentially expressed, with 797 upregulated and 707 downregulated genes. Transcriptomic analysis showed that most genes related to glycolysis, glycogen synthesis, protein degradation, the cell cycle, the MAPK signaling pathway, and redox regulation were significantly induced under formic acid stress and were involved in protein translation and synthesis amino acid synthesis genes were significantly suppressed. Formic acid stress can induce oxidative stress, inhibit protein biosynthesis, cause cells to undergo autophagy, and activate the intracellular metabolic pathways of energy production. The increase of glycogen and the decrease of energy consumption metabolism may be important in the adaptation of S. cerevisiae to formic acid. In addition, formic acid can also induce sexual reproduction and spore formation. This study through transcriptome analysis has preliminarily reveal the molecular response mechanism of S. cerevisiae to formic acid stress and has provided a basis for further research on methods used to improve the tolerance to cell inhibitors in lignocellulose hydrolysate.

Various inhibitors are produced during the hydrolysis of lignocellulosic biomass that can interfere with the growth of yeast cells and the production of bioethanol. Formic acid is a common weak acid inhibitor present in lignocellulosic hydrolysate that has toxic effects on yeast cells. However, the mechanism of the response of Saccharomyces cerevisiae to formic acid is not fully understood. In this study, liquid chromatography-mass spectrometry (LC-MS) was used to investigate the effects of formic acid treatment on cell metabolites of S. cerevisiae. Treatment with different concentrations of formic acid significantly inhibited the growth of yeast cells, reduced the yield of ethanol, prolonged the cell fermentation cycle, and increased the content of malondialdehyde. Principal component analysis and orthogonal partial least squares discriminant analysis showed that 55 metabolites were significantly altered in S. cerevisiae after formic acid treatment. The metabolic relevance of these compounds in the response of S. cerevisiae to formic acid stress was investigated. Formic acid can cause oxidative stress, inhibit protein synthesis, and damage DNA in S. cerevisiae, and these are possible reasons for the inhibition of S. cerevisiae cell growth. In addition, the levels of several aromatic amino acids identified in the cells of formic acid-treated yeast were increased; the biosynthesis of nucleotides was slowed, and energy consumption was reduced. These mechanisms may help to improve the tolerance of yeast cells to formic acid. The results described herein highlight our current understanding of the molecular mechanism of the response of S. cerevisiae to formic acid. The study will provide a theoretical basis for research on the tolerance mechanisms of S. cerevisiae.

Glioblastoma is a highly aggressive brain tumor characterized by high recurrence and poor prognosis. Vitexin has shown activities against esophageal, liver, lung, colorectal, and ovarian cancers; however, there is little knowledge on the activity of vitexin against glioblastoma. This study was therefore designed with aims to examine the effects of vitexin on proliferation, invasion, and apoptosis of human U251 glioblastoma cells and explore the underlying molecular mechanisms using mRNA sequencing and molecular docking. Vitexin was found to inhibit cell proliferation, colony formation, and invasion and promote apoptosis in U251 cells. mRNA sequencing identified 499 differentially expressed genes in vitexin-treated U251 cells relative to controls, including 154 upregulated genes and 345 downregulated genes. Gene ontology (GO) term enrichment analysis revealed that the upregulated genes were most significantly enriched in intrinsic apoptotic signaling pathway and the downregulated genes were most significantly enriched in positive regulation of cell development and positive regulation of locomotion relating to biological processes, endoplasmic reticulum lumen and side of membrane relating to cellular components, and receptor ligand activity and receptor regulator activity relating to molecular functions. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis revealed that the upregulated genes were involved in the pathways of transcriptional misregulation in cancer and the downregulated genes were involved in FoxO and JAK/STAT signaling pathways. Western blotting assay revealed that vitexin treatment resulted in reduced p-JAK1, p-JAK3, and p-STAT3 protein expression in U251 cells relative to untreated controls, and molecular docking predicted that vitexin had docking scores of –8.8, –10.8, and –10.5 kJ/mol with STAT3, JAK1, and JAK2, respectively. The results of the present study demonstrate that vitexin inhibits the proliferation and invasion and induces the apoptosis of glioblastoma U251 cells through suppressing the JAK/STAT3 signaling pathway, and vitexin may be a promising potential agent for the chemotherapy of glioblastoma.

Object: To investigate the effects of Oleanolic acid (OA) on proliferation, apoptosis, migration, and invasion of human glioma cell U251, as well as IKK-β and MAPK signaling pathways.Methods: The binding of OA to IKK-β and MAPK signaling pathway essential proteins IKK-β, MAPK3, and MAPK4 was analyzed by molecular docking technique. U251 cells were treated with different concentrations of OA. The proliferation and apoptosis rates of U251 cells were detected by CCK-8 assay, MTT assay, cell cloning assay, and AnnexinⅤ FITC/PI double staining assay. Transwell chamber assay was used to detect migration and invasion of U251 cells. Western blot was used to detect and analyze the expression levels of CYP17A1, IKK-β, PTGS2 and MAPK3/4 protein in U251 cells after OA treatment. Finally, the transcriptome sequencing method was used to detect the differentially expressed genes in the two groups, and the GO and KEGG enrichment analysis were performed.Results: The results of molecular docking showed that OA could stably bind to IKK-β, MAPK3, and MAPK4 proteins. OA could not only effectively inhibit the proliferation and induce apoptosis of U251 cells (P < 0.05), but also significantly inhibit the invasion of U251 cells (P < 0.005). Western blot assay confirmed that OA could dramatically inhibit the protein expression levels of CYP17A1, IKK-β, PTGS2, MAPK3, and MAPK4 in U251 cells (P < 0.01). A total of 446 significantly differentially expressed genes were detected in transcriptome sequencing, of which 96 were up-regulated genes and 350 were down-regulated genes. These genes are mainly involved in processes such as inflammation, metabolism, immunity, and regulation of cell growth.Conclusions: OA may inhibit the proliferation, migration, and invasion of glioma U251 cells by binding key molecules of the IKK-β signaling pathway and essential target proteins of MAPK3 and MAPK4 in the MAPK signaling pathway.

Formic acid is a representative small molecule acid cell inhibitor in lignocellulosic hydrolysate, which can inhibit the growth of yeast cells in the process of alcohol fermentation. However, the mechanism of formic acid cytotoxicity remains largely unknown. This study aimed to study the cytotoxicity of formic acid stress to Saccharomyces cerevisiae. We evaluated the effects of formic acid on growth metabolism and cell morphology of yeast cells, and comprehensively and systematically analyzed the molecular mechanism of formic acid stress tolerance through transcriptome technology. The results showed that when the concentration of formic acid was 1.8 g/L, the growth of yeast cells was significantly inhibited, the cell surface was wrinkled, and the adhesion between cells was observed, and the cell wall and cell membrane of yeast were destroyed by changing the structure of proteins and carbohydrates, resulting in cell damage. Transcriptome sequencing results showed that formic acid stress inhibited protein biosynthesis, induced oxidative stress, resulted in autophagy, impaired intracellular ATP production and increased consumption, and then impaired normal physiological and metabolic functions of cells. Yeast cells provide sufficient ATP by accelerating glucose metabolism, enhancing electron transport and ATP synthesis more energy to resist formic acid stress, and reduce the expression of genes related to energy metabolism such as intracellular amino acids to achieve an energy-saving strategy, In addition, it can also induce sexual reproduction and spore formation to improve cell tolerance to formic acid. This study initially revealed the molecular response mechanism of S. cerevisiae under formic acid stress, and provided a scientific basis for further research on methods to improve the tolerance of cell inhibitors in lignocellulose hydrolysate.

ObjectTo investigate the effects of Oleanolic acid (OA) on proliferation, apoptosis, migration, and invasion of human glioma cell U251, as well as IKK-β and MAPK signaling pathways.MethodsThe binding of OA to IKK-β and MAPK signaling pathway essential proteins IKK-β, MAPK3, and MAPK4 was analyzed by molecular docking technique. U251 cells were treated with different concentrations of OA. The proliferation and apoptosis rates of U251 cells were detected by CCK-8 assay, MTT assay, cell cloning assay, and AnnexinⅤ FITC/PI double staining assay. Transwell chamber assay was used to detect migration and invasion of U251 cells. Finally, Western blotting was used to detect the protein expression levels of IKK-β, MAPK3, and MAPK4 in U251 cells treated with OA.ResultsThe results of molecular docking showed that OA could stably bind to IKK-β, MAPK3, and MAPK4 proteins. OA could not only effectively inhibit the proliferation and induce apoptosis of U251 cells (P β, MAPK3, and MAPK4 in U251 cells (P β signaling pathway and essential target proteins of MAPK3 and MAPK4 in the MAPK signaling pathway.

Pituitary tumor is among the most common types of brain tumor, and the underlying molecular mechanism of this disease is still obscure. Here we found downregulation of SIRT1 in tumor tissues of pituitary tumor patients by real-time PCR and immunohistochemistry staining. In vitro studies reveal that upregulation of SIRT1 suppresses pituitary tumor cell line growth, and vice versa. We also find that enzymatic activity of SIRT1 is required for its cellular function. Mechanism study uncovers that SIRT1 negatively regulates PTTG1 expression by deacetylation of H3K9ac at promoter region of PTTG1. Moreover, H3K9ac level at PTTG1 promoter is an essential regulatory element for PTTG1 expression. Thus SIRT1/H3K9ac/PTTG1 axis contributes to pituitary tumor formation and may provide further potential therapeutic opportunity.

Curcumin (CM) has multiple pharmacological activities including anti-fungal activity, but its clinical application is limited due to low solubility in aqueous media, poor bioavailability and extensive first pass metabolism. We aimed to resolve the limitation and enhance antifungal activity of CM using nanotechnology. Using silk fibroin (SF) as a carrier, we fabricated curcumin-silk fibroin nanoparticles (CM-SF NPs) by solution enhanced dispersion of supercritical CO₂ (SEDS) technique. The characterization of CM-SF NPs was analyzed using scanning electron microscopy (SEM), fourier transform infrared spectroscopy (FTIR), differential scanning calorimeter (DSC) and thermo gravimetric apparatus (TGA). Following characterization of the NPs, we evaluated the antifungal activity of CM-SF NPs against Candida albicans in vitro and in vivo. A SF-based drug delivery system (CM-SF NPs, 85 ± 15 nm) was established by SEDS. Compared to original CM, water solubility of CM-SF NPs was improved, and its antifungal activity was enhanced. The natural compound-loaded SF nanoparticles may be a promising therapeutic candidate for fungal infection.

As a carbon free fuel and a hydrogen-energy carrier, ammonia is expected to be one of the promising energy carriers and to be widely used in industries. In this study, the parameters of ammonia/oxygen flame, such as laminar flame speed, the Markstein length, laminar flame thickness, and critical radius of flame instability onset have been investigated experimentally and numerically. A spherical ammonia /oxygen flame propagated in a constant volume chamber and a high speed digital Schilieren photograph system were used in the study. The influences of initial pressure and equivalence ratio on flame propagation have been investigated. It was found that the maximum laminar flame speed in ammonia/oxygen mixture is 1.09 m/s. The flame thickness decreases with the initial pressure increase. Generally, Markstein length increases with the increasing of equivalence ratio while it decreases with the increasing of initial pressure. The minimum critical radius in ammonia/oxygen is 1.8 cm. And the critical radius decreases with the increase of initial pressure. The mechanisms of flame instability in ammonia/oxygen mixture were analyzed, and the stabilize effect of flame stretch in ammonia/oxygen have been observed.

Improving quality of areca nut is a critical problem for manufacturers. A steam experimental explosion device has been developed. An areca nut processing technology was optimized by using the orthogonal experiment method. In which, the processing parameters including pressure, processing time and temperature, were taken by three factors. Each factor selected three levels and nine groups of orthogonal experiments were carried out. The volume expansion rate of the sample was taken as evaluation standard; the best treatment scheme is obtained through optimization. The experimental results showed that the equipment shortened soaking time of normal process, orthogonal experiment reduced the number of experiments, and orthogonal experiment accelerated the application speed. Products will meet the use requirements of customers.

Purpose A spinal extradural arachnoid cyst (SEAC) is a rare condition with unclear etiology. Herein, we report a series of symptomatic SEACs to illustrate features of SEACs in adults, surgical management, and outcomes. Methods A total of 34 consecutive patients who underwent microsurgical treatment were retrospectively reviewed. Patient characteristics were recorded in each case, including presenting symptoms, imaging findings, neurologic status, a surgical procedure performed and follow-up. Results There were 19 (56%) male and 15 (44%) female patients, with the ages ranging from 16 to 71 years (average 45 years). The lesions were located in the cervical segment (n = 4, 12%), thoracic segment (n = 6, 18%), thoracolumbar segment (n = 10, 29%) and lumbar segment (n = 14, 41%). Clinical presentations included back pain (n = 18, 53%), sensory deficits (n = 14, 41%), weakness (n = 4, 12%) and gait ataxia (n = 4, 12%), with a mean duration of symptoms of 17 months. The lesion was hypointense with the spinal cord on T1-weighted images and hyperintense on T2-weighted images and showed no homogeneous enhancement after contrast medium injection. Communication between the cyst and subarachnoid space was found in 23 patients and the cyst was resected after fistula ligation. Postoperatively, patients were followed up for an average of 80 months. The patients’ symptoms dramatically improved and follow-up radiological images showed a complete disappearance of the cyst in all patients. No recurrence was observed in the dural repair group. Conclusion Patients with symptomatic SEAC present with obvious and persistent symptoms. Complete microsurgical cyst removal with the closure of the dural defect is the standard treatment procedure with good results and a low recurrence rate.

Eighteen derivatives of pentacyclic triterpene carboxylic acids (Maslinic acid, Corosolic acid and Asiatic acid) have been prepared by coupling the piperazine complex of l -amino acids at the C-28 site of the parent compounds. The α-glucosidase inhibitory activities of the pristine derivatives were evaluated in vitro. The results indicated that the inhibitory activity of some compounds (15e IC50 = 591 μM, 16e IC50 = 423 μM) was closed to that of the reference acarbose (IC50 = 347 μM) in ethanol-water system. In addition, compound 16e (IC50 = 380 μM) showed superior inhibitory activity than acarbose (IC50 = 493 μM) in the measurement system with DMSO as solvent. The comparison of two different solvent systems showed that the derivatives had better α-glucosidase inhibitory activity in the DMSO system than that of in ethanol-water system. Regrettably, all of the as-synthesized derivatives exhibited inferior α-glucosidase inhibitory activities than those of the parent compounds in both test solvent systems. Furthermore, the result of enzyme kinetics demonstrated that the inhibition mechanism of compound 16e was noncompetitive inhibition with the inhibition constant Ki = 552 μM.

Curcumin (CM) has multiple pharmacological activities including anti-fungal activity, but its clinical application is limited due to low solubility in aqueous media, poor bioavailability and extensive first pass metabolism. We aimed to resolve the limitation and enhance antifungal activity of CM using nanotechnology. Using silk fibroin (SF) as a carrier, we fabricated curcumin-silk fibroin nanoparticles (CM-SF NPs) by solution enhanced dispersion of supercritical CO₂ (SEDS) technique. The characterization of CM-SF NPs was analyzed using scanning electron microscopy (SEM), fourier transform infrared spectroscopy (FTIR), differential scanning calorimeter (DSC) and thermo gravimetric apparatus (TGA). Following characterization of the NPs, we evaluated the antifungal activity of CM-SF NPs against Candida albicans

A disintegrin and metalloproteinase domain-containing protein 10 (ADAM10) is a metalloproteinase known to modulate the progression of several types of tumor. However, the role played by ADAM10 in pituitary adenomas is currently unknown, and what factors orchestrate the activation of ADAM10 in this kind of tumor is also unclear. Here, we found that SRC kinase is an ADAM10-interacting partner and that SRC kinase activity is required for this interaction. As a new positive regulator promoting the shedding activity of ADAM10, SRC could compete with calmodulin 1 (CALM1) for ADAM10 binding in a mutually exclusive manner. Strikingly, the interaction between ADAM10 and CALM1 is regulated by SRC activity. Furthermore, we proved that the cytoplasmic region of ADAM10 is required for the shedding activity of ADAM10 upon SRC activation. As a proof-of-concept, we discovered that the combination of ADAM10 and SRC inhibitors can inhibit cell proliferation and migration to a great extent. Thus, our findings shed light on a novel therapeutic strategy to block the tumorigenesis and migration of pituitary adenoma.

PURPOSE Prolactinoma (prolactin-secreting pituitary adenoma) is one of the most common estrogen-related functional pituitary tumors. As an agonist of the dopamine D2 receptor, bromocriptine is used widely to inhibit prolactinoma progression. On the other hand, it is not always effective in clinical application. Although a dopamine D2 receptor deficiency contributes to the impaired efficiency of bromocriptine therapy to some extent, it is unknown whether there some other underlying mechanisms leading to bromocriptine resistance in prolactinoma treatment. That is the main point addressed in this project. MATERIALS AND METHODS Human prolactinoma samples were used to analyze the S-phase kinase associated protein 2 (SKP2) expression level. Nutlin-3/adriamycin/cisplatin-treated GH3 and MMQ cells were used to analyze apoptosis in SKP2 overexpression or knockdown cells. SKP2 expression and the interaction partners of SKP2 were also detected after a bromocriptine treatment in 293T. Apoptosis was analyzed in C25 and bromocriptine-treated GH3 cells. RESULTS Compared to normal pituitary samples, most prolactinoma samples exhibit higher levels of SKP2 expression, which could inhibit apoptosis in a p53-dependent manner. In addition, the bromocriptine treatment prolonged the half-life of SKP2 and resulted in SKP2 overexpression to a greater extent, which in turn compromised its pro-apoptotic effect. As a result, the bromocriptine treatment combined with C25 (a SKP2 inhibitor) led to the maximal apoptosis of human prolactinoma cells. CONCLUSION These findings indicated that SKP2 inhibition sensitized the prolactinoma cells to bromocriptine and helped promote apoptosis. Moreover, a combined treatment of bromocriptine and C25 may contribute to the maximal apoptosis of human prolactinoma cells.

Combining two bioactive moieties by covalent bond into a novel single hybrid biological entity in view of the principle of active splicing, twenty-two C28-modified derivatives of pentacyclic dihydroxytriterpene carboxylic acids with saturated nitrogen heterocycle segments (i.e. 1-deoxynojirimycin or piperazines) have been synthesized. The inhibitory activities of all final target compounds on α-glucosidase were evaluated in vitro. The results of α-glucosidase inhibition assay indicate that some derivatives (e.g. 4b: IC50 = 1468.4 µM; 12b: IC50 = 499.6 µM 12c: IC50 = 768.5 µM, 13c: IC50 = 819.2 µM) show superior inhibitory activity in α-glucosidase than that of the precursor maslinic acid (IC50 = 2540.6 µM) or corosolic acid (IC50 = 1363.7 µM), in which compound 12b (IC50 = 499.6 µM) possesses stronger inhibitory activity than that of acarbose (IC50 = 606 µM). In addition, the result of enzyme kinetics study reveals that the inhibitory mechanism of the compound 12b is non-competitive inhibition and the inhibition constant Ki is 570 µM. The binding interaction between compounds with α-glucosidase are predicted by molecular docking simulation.

Human adenovirus (Adv) infection is responsible for most community-acquired pneumonia in infants and children, which results in significant morbidity and mortality in children every year. MicroRNAs (miRNAs) are associated with viral replication and host immune response. Knowing the miRNA expression profile will help understand the role of miRNAs in modulating the host response to adenovirus infection and possibly improve the diagnosis of adenovirus-infected pneumonia. In our study, total RNA extracted from whole blood of adenovirus-infected pneumonia children and healthy controls were analyzed by small RNA deep sequencing. Expression profiles of whole blood microRNAs were altered and distinctly different in adenovirus-infected children. The top 3 upregulated miRNA (hsa-miR-127-3p, hsa-miR-493-5p, and hsa-miR-409-3p) were identified in adenovirus-infected children and provided a clear distinction between infected and healthy individuals. Potential host target genes were predicated and validated by qRT-PCR to study the impact of microRNAs on the host genes. Most of the target genes were involved in the MAPK signaling pathway and innate immune response. These highly upregulated microRNAs may have crucial roles in Adv pathogenesis and are potential biomarkers for adenovirus-infected pneumonia.

Gliomas are the most common form of primary brain tumor in the adult central nervous system. Altered expression and prognostic value of transmembrane protein 97 (TMEM97) has been recently reported in different types of human tumors. However, the association of TMEM97and glioma is poorly defined. Here, we reported that TMEM97 was significantly increased in glioma tissues compared to non-tumorous brain tissues. Furthermore, TMEM97 levels were progressively increased with increasing histologic tumor grade in glioma. Higher TMEM97 expression level was correlated with shorter survival time of patients with glioma. Downregulation of TMEM97 through RNA interference inhibited cell proliferation and G1/S transition in two glioma cell lines, U87 and U373. More importantly, TMEM97 silencing induced a significant decrease in the expression of G1/S transition key regulators, cyclin D1, cyclin E, CDK2, and CDK4. Additionally, downregulation of TMEM97 in glioma cells notably repressed cell migration and cell invasion. Further analysis suggested that the decreased invasion was associated with alterations in EMT markers, including E-cadherin, β-catenin, and Twist. Since expression of TMEM97 seems to be associated with the oncogenic potential of glioma, and suppression of its expression can inhibit cancer cell growth and metastasis, TMEM97 may be a potential therapeutic target in human glioma.

Deflagration to detonation transitions (DDTs) in JP-10 mist/air mixtures have been studied in a horizontal multiphase combustion and explosion tube with inner diameter of 199mm and length of 32.8m. The mist/air mixtures were generated by injecting liquid samples into the experimental tube. Experiments were performed at 298k and 101kPa with equivalence ratio ranged from 0.51 to 2.09. The coupling process of deflagration wave with leading shock wave and low-velocity self-sustained detonation were observed in JP-10 mist/air mixture with a concentration of 142.86g/m3, and the average velocity of the self-sustained detonation wave is 510m/s, which is as low as 26% of C-J value. The low-velocity detonation in JP-10 mist/air mixture can be explained by the low-volatile property of JP-10 liquid and boundary condition. The leanest and richest critical detonable concentrations were studied. The detonation structure was studied by using pressure sensors array mounted in the wave structure test section. A single-head spin detonation wave front was observed and the cellular structure resulting from the spinning movement of the triple point was analyzed.

The human glutamate receptor delta 2 gene (GRID2) shares 90% homology with the orthologous mouse gene. The mouse Grid2 gene is involved with functions of the cerebellum and spontaneous mutation of Grid2 leads to a spinocerebellar ataxia-like phenotype. To investigate whether such mutations occur in humans, we screened for mutations in the coding sequence of GRID2 in 24 patients with familial or sporadic spinocerebellar ataxia and in 52 normal controls. We detected no point mutations or insertion/deletion mutations in the 16 exons of GRID2. However, a polymorphic 4 nucleotide deletion (IVS5-121_-118 GAGT) and two single nucleotide polymorphisms (c.1251G>T and IVS14-63C>G) were identified. The frequency of these polymorphisms was similar between spinocerebellar ataxia patients and normal controls. These data indicate that spontaneous mutations do not occur in GRID2 and that the incidence of spinocerebellar ataxia in humans is not associated with GRID2 mutation or polymorphisms.

We have found that in the presence of hydroxylamine, the heme prosthetic group of the heme protein adsorbed at the mercury electrode surface reacts with mercury ion produced by the electrochemical oxidation of mercury and is quantitatively converted into the mercury protoporphyrin IX group using single-sweep polarography. As a result, the small redox peak P(0) of the heme prosthetic group at about -0.46 V (vs SCE) disappears and a large new reduction peak P of mercury protoporphyrin IX group at -0.89 V comes out in a pH 9.6 NaHCO(3)-Na(2)CO(3) solution. Peak P is extremely sensitive to heme protein concentration. On the basis of the reduction peak P, a unique electrochemical method for heme protein assays is constructed. For the cytochrome c determination, the peak height is linearly proportional to the concentration in the range of 0.005-15 mg L(-1) (correlation coefficient 0.999). The detection limit is 0.003 mg L(-1). In contrast with peak P(0), the detection limit of cytochrome c is only 0.6 mg L(-1). The voltammograms of heme proteins in the absence and presence of hydroxylamine can serve as a reliable qualitative analytical method. The chemical reaction is peculiar to the heme prosthetic group. Without hydroxylamine it cannot occur. Thereby the method is highly specific and free from interference. The performance takes only a few minutes. These advantages make the method attractive for heme protein detecting.

Gliomas are the most common and aggressive type of primary adult brain tumor. Although high expression and prognostic value of TMEM45A has been recently reported in various types of human tumors, the association of TMEM45A expression and glioma is still unknown. Here, we reported that TMEM45A was significantly overexpressed in glioma tissues compared to non-tumorous brain tissues. Furthermore, TMEM45A mRNA levels were gradually increased with the increasing severity of histological grade of glioma. Moreover, high TMEM45A expression level was correlated with short survival time of glioma patients. Down-regulation of TMEM45A in two glioma cell lines, U251 and U373 by transected with TMEM45A siRNA resulted in a significant reduction of cell proliferation and G1-phase arrest. Additionally, we found that suppressing of TMEM45A expression in glioma cells remarkably suppressed cell migration and cell invasion. More importantly, TMEM45A siRNA treatment significantly down-regulated the proteins promoting cell cycles transition (Cyclin D1, CDK4 and PCNA) and cell invasion (MMP-2 and MMP-9), which indicted a possible mechanism underlying its functions on glioma. In summary, our study suggests that TMEM45A may work as an oncogene and a new effective therapeutic target for glioma treatment.

1 Twenty-one cases out of 272 patients of acute organophosphates poisoning were diagnosed as intermediate syndrome (IMS) with a prevalence at 7.7%. The responsible OP insecticides included parathion, omethoate and some OP containing pesticide mixtures. IMS occurred mainly in severe OP poisoning patients who recovered from the acute cholinergic crisis at 7-75 h after the onset of acute poisoning. 2 Muscular weakness appeared in the following three categories of muscles: (1) neck flexors and proximal limb muscles; (2) muscles innervated by motor cranial nerves and/or (3) respiratory muscles. Blood acetylcholinesterase activity was persistently inhibited. Electroneuromyography (ENMG) with repetitive nerve stimulation (RNS) at frequencies of 20 Hz or 30 Hz in seven patients showed decrements of common muscle action potentials during the presence of myasthenia in five patients and became normal when their muscle strength recovered. 3 Mild IMS recovered within 2-7 days and had a favorable prognosis. Severe IMS patients with respiratory paralysis needed immediate endotracheal intubation and mechanical ventilation. Recovery of weakness of the respiratory muscles and proximal limb muscles took longer, the slowest being 30 days. Four of the patients died of respiratory paralysis and the fatality rate was 19%. 4 The mechanism of IMS remains to be further investigated. The RNS/ENMG changes indicate a post-synaptic block at the neuromuscular junctions. 5 In order to promote the recognition of this syndrome, we proposed to name the syndrome as Intermediate Myasthenia Syndrome (IMS).

The problems of conditional entropy's definition and the formula to compute conditional entropy are analyzed from various perspectives. Examples are given to prove the conclusion that conditional entropy never be increased is not absolute, thus the representation that information is to decrease uncertainty in the definition of information is not absolutely correct. In most conditions the reduction of uncertainty is just a byproduct by the aim of reliability. It is more important to increase the reliability of information than to reduce the uncertainty of information.

Man-in-the-middle attack on the BB84 protocol is presented. The man in the middle can intercept the message from the sender and send his message to the receiver in every step of the BB84 protocol. The attack can be analogously used on other quantum key distribution schemes. Some methods are suggested to defense against the attack by discovering the attack or handicapping the attack, and the security of BB84 Protocol is analyzed.

To provide a reference for clinically curing organophosphrous compounds Poisoning. A high performance liquid chromatography method has been developed for determination of pralidoxime chloride in rat plasma. BECKMAN ODS C18 column, Waters Model 510 HPLC pump and 996 photodiode Detector were used. The mobile phase consisted of 7.5% acetonitrile and 92.5% (20nmol/L NaH2PO4, 0.2% C8H17SO3 Na, pH3.0, adjusted by H3PO4 Solution) the flow rate was 1.0mol/min. detection wavelength was set at 296. The samples were pretreated with acetonitrite. The results show a good liner correlation between pralidoxime chloride concentration(from 1.0 - 5.0 microg/ml) and absorption intensity. The detection limit is 0.5 microg/ml with signal to noise ratio of 2. The intra-assay and inter-assay coefficients of variation were 1.35% and 2.73%. The recoveries for plasma were in ranges of 76% - 84%.

The mechanism of striatal damage induced by 3-nitropropionic acid (3-NPA) was studied in rats by neuropathological and neurochemical methods. Neuronal shrinkage with astrogliosis was observed in striatum after local injection of 0.5-5 μmol 3-NPA. Decortications involving dorsal and lateral aspects of frontal cortex or both frontal and parietal cortices significantly decreased the severity of striatal injuries induced by 3-NPA. This result suggests that corticostriatal projections play an important role in the development of striatal damage. No significant increase of glutamate and aspartate in striatal dialysates was observed, which indicated that 3-NPA may affect the postsynaptical sites and make the striatal neurons more vulnerable to endogenous levels of glutamate. Both of these findings suggested that 3-NPA produces indirect excitotoxic lesion to striatum. An increase of dopamine found in striatal dialysates may also be related to the occurrence of striatal damage.

While heavy exposure to inorganic lead is capable of inducing symptomatic neuropathy in man, the subclinical neuropathy due to low levels of occupational lead exposure remains to be proved. The reported results of electroneurographic studies on lead workers, however, have been controversial. In this study, 40 lead smeltery workers and 50 non-exposed referents were investigated. The air concentrations of lead at worksites were 0.25 to 42.5 mg/m3. The geometric means of PbB, PbU and δ-ALAU in lead exposed group were 40.03 μg/dl, 71 μg/l and 4.68 mg/l respectively, which were significantly higher (P < 0.001) than those (7.01 μg/dl, 6.0 μg/l and 1.81 mg/l respectively) in the reference group. There were no clinical symptoms or signs of nerve damage in either group. Alcoholism and diabetes were excluded in both groups. Nerve conduction velocity was measured by a DISA 1500 electromyograph in both groups. Eleven electroneurographic parameters, including motor nerve conduction velocity (MCV) and distal latency (DML) of median, ulnar and peroneal nerves as well as sensory nerve conduction velocity (SCV) and distal latency (DSL) of median, ulnar and sural nerves, showed statistically significant differences between the two groups. However, the results of electroneurographic measurements of each individual in the lead-exposed group were all within the normal range. There was no correlation between the bloodlead levels and the neurophysiological measurements except for the median MCV. No correlation was seen between the median MCV and the exposure duration. A reduction in MCVs of median and ulnar nerves and sural SCV was unexpectedly seen in eight lead workers after chelation therapy with CaEDTA, although their mean PbB decreased from 42.08 to 27.92 μg/dl. No consistent findings in nerve conduction were found at these exposure levels.

Renal function was studied in 40 workers chronically exposed to lead at a smelter. The geometric means of lead were 40 (range 24.0 - 63.0) micrograms/dl in blood and 47 (range 19 - 115) micrograms/g creatinine or 71 (range 20 - 250) micrograms/l in urine, respectively. There were no significant differences between the lead-exposed group and a control group in the concentrations of beta 2-microglobulin in serum, urinary total protein and IgG, whereas the level of beta 2-microglobulin in urine was significantly higher in the lead-exposed group (p less than 0.01). No individual lead worker showed abnormally increased level of urinary beta 2-microglobulin. The significance of increased excretion of beta 2-microglobulin on the basis of the group remains to be elucidated.