超级微波消解-电感耦合等离子体发射光谱（ICP-OES）法测定土壤中18种元素

为提高土壤多元素同时检测的效率,采用超级微波消解-电感耦合等离子体发射光谱法测定土壤中钾、钠、钙、镁、铜、铁、锰、锌、磷、硫、硼、砷、镉、铬、铅、钴、镓、锂等18种元素含量。比较了超级微波消解、常规微波消解和电热板消解的处理效果,采用超级微波消解法对样品进行前处理,并优化了消解条件。在最优条件下,各元素的检出限在0.05~20 mg/kg,加标回收率在86.2%~107.5%,RSD在0.1%~3.0%,方法准确度及精密度可以满足多元素同时测定的需求,且该方法具有简单、快速、成本低、用酸量少、重现性好等特点。     

Determination of carbonate content in barite ore by headspace gas chromatography

This paper reports a method for determining the carbonate content in barite ore using headspace gas chromatography. Based on the acidification reaction, the carbonate in the barite ore was converted to CO₂ in a closed headspace vial. When the carbonate content was significant, the pressure caused changes in the CO₂ and O₂ signals and affected the measurement accuracy. It was found that carbonate content is proportional to the intensity ratio of the CO₂ to O₂ signals. Thus, the carbonate content in barite ore can be measured indirectly using a theoretical model. The results showed that the carbonate in 3 g of barite ore sample with a particle size of 74 μm could react completely with a hydrochloric acid solution (2 mol/L) at 65°C for 5 min. The method described herein had good precision (relative standard deviation < 4.14%) and accuracy (relative differences < 6.12%). Further, the limit of quantification was 0.07 mol/L. Owing to its simplicity and speed, this method can be used for the batch determination of carbonate content in barite ore.     

Synthesis of PEGylated hyaluronic acid for loading dichloro(1,2-diaminocyclohexane)platinum(Ⅱ)(DACHPt) in nanoparticles for cancer treatment

Dichloro(1,2-diaminocyclohexane)platinum(II)(DACHPt), a cisplatin(CDDP) analog, has shown lower toxicity than CDDP and no cross-resistance with CDDP in many CDDP-resistant cancers. PEGylated hyaluronan(m PEG-HA) is an m PEG conjugated with hyaluronan biodegradable polymer which is a naturally occurring biopolymer in the interstitium, is primarily cleared by the lymphatic system. m PEGhyaluronan–DACHPt(PEG-HA–Pt) conjugate could circulate long-term in the bloodstream and increase DACHPt concentration in the tumor site and decrease systemic toxicity. m PEG-HA conjugates with the range of 1%–5% substitution were synthesized, and the structures were confirmed by1 H NMR and IR. The particle size of DACHPt incorporated with m PEG-HA was about 86 nm and the loading content and efficiency were about 19%(w/w) and 86%, respectively. The synthesized m PEG-HA with different PEG substitution degrees presented non toxicity, and the cell viability of DACHPt loaded in m PEG-HA nanoparticles increased with increasing doses of DACHPt. DACHPt release from nanoparticles slightly decreased with increasing PEG substitution degree from 1% to 5% at 37 8C, pH 7.4 PBS solution. The DACHPt loaded in m PEG-HA nanoparticles significantly inhibited the growth of A549 xenografts in nude mice when compared to the DACHPt loaded in HA nanoparticles and the control group after 4 weeks treatment(p 0.01 compared with control). The body weight change curve shows that the mice weight loss was less than 5% by treating with both DACHPt loaded in m PEG-HA and HA nanoparticles. In conclusion, a novel DACHPt loaded m PEG-HA delivery system was developed with sustained release and increased platinum concentration in the tumor.     

聚吡咯/纳米SiO_2复合材料的制备及氧化性能

采用化学氧化法制备聚吡咯/纳米Si O2(PPy/n Si O2)复合材料,通过扫描电子显微镜和红外光谱对其进行表征,并将其应用到对苯二酚的氧化反应中.结果表明,PPy/n Si O2复合材料中,PPy较均匀地负载在纳米Si O2表面.在弱酸性介质中,PPy/n Si O2对对苯二酚具有很好的氧化性能.反应2 h内,对苯二酚的氧化过程符合表观一级反应动力学.结合紫外-可见光谱法分析表明,聚吡咯通过与对苯二酚之间的氢键相互作用形成聚吡咯活性中间体,将对苯二酚氧化为对苯醌,聚吡咯具有氧化剂和催化剂的双重功能.     

Analyses of the TCR repertoire of MHC class II-restricted innate CD4+ T cells

Analysis of the T-cell receptor (TCR) repertoire of innate CD4⁺ T cells selected by major histocompatibility complex (MHC) class II-dependent thymocyte–thymocyte (T-T) interaction (T-T CD4⁺ T cells) is essential for predicting the characteristics of the antigens that bind to these T cells and for distinguishing T-T CD4⁺ T cells from other types of innate T cells. Using the TCR^mini Tg mouse model, we show that the repertoire of TCRα chains in T-T CD4⁺ T cells was extremely diverse, in contrast to the repertoires previously described for other types of innate T cells. The TCRα chain sequences significantly overlapped between T-T CD4⁺ T cells and conventional CD4⁺ T cells in the thymus and spleen. However, the diversity of the TCRα repertoire of T-T CD4⁺ T cells seemed to be restricted compared with that of conventional CD4⁺ T cells. Interestingly, the frequency of the parental OT-II TCRα chains was significantly reduced in the process of T-T interaction. This diverse and shifted repertoire in T-T CD4⁺ T cells has biological relevance in terms of defense against diverse pathogens and a possible regulatory role during peripheral T-T interaction.     

Serum exosomal microRNAs as novel biomarkers for hepatocellular carcinoma

Recent studies have shown that circulating microRNAs are a potential biomarker in various types of malignancies. The aim of this study was to investigate the feasibility of using serum exosomal microRNAs as novel serological biomarkers for hepatocellular carcinoma (HCC) in patients with chronic hepatitis B (CHB). We measured the serum exosomal microRNAs and serum circulating microRNAs in patients with CHB (n=20), liver cirrhosis (LC) (n=20) and HCC (n=20). Serum exosomal microRNA was extracted from 500 μl of serum using an Exosome RNA Isolation kit. The expression levels of microRNAs were quantified by real-time PCR. The expression levels of selected microRNAs were normalized to Caenorhabditis elegans microRNA (Cel-miR-39). The serum levels of exosomal miR-18a, miR-221, miR-222 and miR-224 were significantly higher in patients with HCC than those with CHB or LC (P<0.05). Further, the serum levels of exosomal miR-101, miR-106b, miR-122 and miR-195 were lower in patients with HCC than in patients with CHB (P=0.014, P<0.001, P<0.001 and P<0.001, respectively). There was no significant difference in the levels of miR-21 and miR-93 among the three groups. Additionally, the serum levels of circulating microRNAs showed a smaller difference between HCC and either CHB or LC. This study suggests that serum exosomal microRNAs may be used as novel serological biomarkers for HCC.     

Epstein–Barr virus latent genes

Latent Epstein–Barr virus (EBV) infection has a substantial role in causing many human disorders. The persistence of these viral genomes in all malignant cells, yet with the expression of limited latent genes, is consistent with the notion that EBV latent genes are important for malignant cell growth. While the EBV-encoded nuclear antigen-1 (EBNA-1) and latent membrane protein-2A (LMP-2A) are critical, the EBNA-leader proteins, EBNA-2, EBNA-3A, EBNA-3C and LMP-1, are individually essential for in vitro transformation of primary B cells to lymphoblastoid cell lines. EBV-encoded RNAs and EBNA-3Bs are dispensable. In this review, the roles of EBV latent genes are summarized.     

β-TrCP1 degradation is a novel action mechanism of PI3K/mTOR inhibitors in triple-negative breast cancer cells

An F-box protein, β-TrCP recognizes substrate proteins and destabilizes them through ubiquitin-dependent proteolysis. It regulates the stability of diverse proteins and functions as either a tumor suppressor or an oncogene. Although the regulation by β-TrCP has been widely studied, the regulation of β-TrCP itself is not well understood yet. In this study, we found that the level of β-TrCP1 is downregulated by various protein kinase inhibitors in triple-negative breast cancer (TNBC) cells. A PI3K/mTOR inhibitor PI-103 reduced the level of β-TrCP1 in a wide range of TNBC cells in a proteasome-dependent manner. Concomitantly, the levels of c-Myc and cyclin E were also downregulated by PI-103. PI-103 reduced the phosphorylation of β-TrCP1 prior to its degradation. In addition, knockdown of β-TrCP1 inhibited the proliferation of TNBC cells. We further identified that pharmacological inhibition of mTORC2 was sufficient to reduce the β-TrCP1 and c-Myc levels. These results suggest that mTORC2 regulates the stability of β-TrCP1 in TNBC cells and targeting β-TrCP1 is a potential approach to treat human TNBC.