抗菌肽CGA-N12对腹腔注射热带念珠菌小鼠的治疗作用

CGA-N12为嗜铬粒蛋白A的N端65-76位氨基酸组成的衍生肽,前期研究表明,CGA-N12具有特异性抗念珠菌活性,尤其对临床病原真菌热带念珠菌拮抗活性最强。为研究CGA-N12体内抗真菌活性,建立了热带念珠菌深部感染小鼠模型,分别用每日15mg/kg和30mg/kg的CGA-N12对小鼠进行治疗,并设每日15mg/kg伊曲康唑治疗对照组和感染对照组。通过测定治疗后小鼠存活率、体重变化、肾脏载菌量,以及组织器官病理变化,判断CGA-N12对小鼠的治疗效果。结果表明,每日15 mg/kg和30mg/kg的CGA-N12治疗14d后与感染对照组相比,小鼠肾脏载菌量分别降低97.6%和99.1%,小鼠存活率分别提高40%和45%,体重分别增加1.3g和5.9g,免疫器官指数均显著增加,而与治疗对照组差异不显著。病理切片观察,每日15mg/kg和30mg/kg的CGA-N12对组织器官的病变均有明显改善,并且没有出现伊曲康唑治疗后产生的肝小叶血管内皮细胞增生和肾出血现象。结果表明,CGA-N12对热带念珠菌深部感染小鼠具有治疗作用。     

Quantitative determination of 12-hydroxyeicosatetraenoic acids by chiral liquid chromatography tandem mass spectrometry in a murine atopic dermatitis model

Atopic dermatitis, one of the most important skin diseases, is characterized by both skin barrier impairment and immunological abnormalities. Although several studies have demonstrated the significant relationship between atopic dermatitis and immunological abnormalities, the role of hydroxyeicosatetraenoic acids (HETE) in atopic dermatitis remains unknown. To develop chiral methods for characterization of 12-HETE enantiomers in a 1-chloro-2,4-dinitrochlorobenzene (DNCB)-induced atopic dermatitis mouse model and evaluate the effects of 12-HETE on atopic dermatitis, BALB/c mice were treated with either DNCB or acetone/olive oil (AOO) to induce atopic dermatitis, after which 12(R)- and 12(S)-HETEs in the plasma, skin, spleen, and lymph nodes were quantified by chiral liquid chromatography-tandem mass spectrometry. 12(R)- and 12(S)-HETEs in biological samples of DNCB-induced atopic dermatitis mice increased significantly compared with the AOO group, reflecting the involvement of 12(R)- and 12(S)-HETEs in atopic dermatitis. These findings indicate that 12(R)- and 12(S)-HETEs could be a useful guide for understanding the pathogenesis of atopic dermatitis.     

马铃薯新品种‘天薯12号’

‘天薯12号’是以自育品系‘天97-8-98’为母本,‘庄薯3号’为父本杂交选育而成,2014年通过甘肃省农作物品种审定委员会审定。该品种从出苗至块茎成熟126 d左右,属晚熟品种。薯块椭圆形,黄皮黄肉,芽眼浅而紫。单株块茎数4.1个,平均单薯质量105 g,大中薯率87.4%,产量在1 500 kg/667m2以上。块茎干物质含量23.14%,淀粉17.47%,维生素C 176.2 mg/kg,粗蛋白2.53%,还原糖0.159%。抗马铃薯晚疫病、环腐病等主要病害。‘天薯12号’适于甘肃天水、临夏、定西、平凉、陇南等地种植。     

雷州刚果12号桉W5无性系林分蓄积量与胸径树高密度及其之间关系的探讨

采用雷州林业局2002年森林二类调查的刚果12号桉W5无性系林分1071块样地中279块样地材料，进行蓄积量与胸径、树高、密度及其之间关系的探讨分析。分析结果表明：胸径是影响林分蓄积量的主要因素，其次是树高与密度；树高与胸径关系密切，呈正相关，但两者的生长随着造林密度的加大而显著下降。因此，进行W5无性系林分密度试验，提出合理的造林密度，是提高其单位面积蓄积量的关键。     

Bubble distribution of Cr12N high-pressure solidification ingot

There are a number of bubbles when Cr12N stainless steel is smelted. But its number is smaller and smaller with the increasing of solidification pressure. When the melting pressure is 0.6 MPa and the solidification pressure increases from 1.0 to 1.6 MPa, the average number of bubbles decreases from 46.37 to 9.46 per square millimeter. Bubble number is reduced by 20.4%. The number of bubbles whose diameters are greater than 20 μm is reduced to 17.4%, while the number of bubbles whose diameters are less than 5μm increases by 37.7%. With 0.3 MPa melting pressure and 1.6 MPa solidification pressure, the average bubble size content near the lower surface is 23.9% of that near the upper surface. Average bubble size content at the edge is 25.9% of that at the center. According to the actual nitrogen content in steel ingot calculated by the established mathematical model, no bubbles of high nitrogen steel ingot may be obtained when melting pressure is 0.6 MPa and solidification pressure increases to 1.8 MPa.     

Ethanol extract of propolis protects macrophages from oxidized low-density lipoprotein-induced apoptosis by inhibiting caspase-12

AIM: To investigate the inhibitory effect of ethanol extract of propolis (EEP) on oxidized low-density lipoprotein (ox-LDL)-induced macrophage apoptosis and the underlying molecular mechanisms. METHODS: RAW264.7 macrophages were pretreated with EEP (7.5, 15 and 30 mg/L), 4-phenylbutyric acid (PBA, 5 mmol/L) or diphenyleneiodonium (DPI, 5 μmol/L) for 1 h and then treated with ox-LDL (100 mg/L) or tunicamycin (TM, 4 mg/L) for 24 h. The cell viability and apoptosis were determined by MTT assay and Annexin V-FITC apoptosis detection kit, respectively. The activity of superoxide dismutase (SOD), and the levels of reactive oxygen species (ROS) and malondialdehyde (MDA) in the cells were measured. The protein levels of caspase-12, a proapoptotic molecule under endoplasmic reticulum stress (ERS), were examined by Western blot analysis. RESULTS: Like PBA (an ERS inhibitor), EEP protected RAW264.7 macrophages from ox-LDL-induced injury in a dose-dependent manner, as assessed by the increased cell viability and the decreased apoptotic rate. The decrease in cell viability and increase in apoptotic rate induced by TM, an ERS inducer, were also attenuated by EEP. Moreover, EEP suppressed ox-LDL-induced oxidative stress as revealed by the decreased generation of ROS and MDA as well as elevated SOD activity, which were similar to DPI, an oxidative stress inhibitor. Furthermore, EEP significantly suppressed ox-LDL- or TM-induced activation of caspase-12. Similar results were observed in the cells pretreated with PBA or DPI and then treated with ox-LDL. CONCLUSION: EEP may protect RAW264.7 macrophages from ox-LDL-induced apoptosis and the mechanism is at least partially involved in the ability of EEP to suppress oxidative stress and subsequent activation of caspase-12.     

Insulin resistance selectively alters cell-surface glucose transporters but not their total protein expression in equine skeletal muscle

Background: Insulin resistance (IR) has been widely recognized in humans, and more recently in horses, but its underlying mechanisms are still not well understood. The translocation of glucose transporter 4 (GLUT4) to the cell surface is the limiting step for glucose uptake in insulin‐sensitive tissues. Although the downstream signaling pathways regulating GLUT translocation are not well defined, AS160 recently has emerged as a potential key component. In addition, the role of GLUT12, one of the most recently identified insulin‐sensitive GLUTs, during IR is unknown. Hypothesis/Objectives: We hypothesized that cell‐surface GLUT will be decreased in muscle by an AS160‐dependent pathway in horses with IR. Animals: Insulin‐sensitive (IS) or IR mares (n = 5/group). Methods: Muscle biopsies were performed in mares classified as IS or IR based on results of an insulin‐modified frequently sampled IV glucose tolerance test. By an exofacial bis‐mannose photolabeled method, we specifically quantified active cell‐surface GLUT4 and GLUT12 transporters. Total GLUT4 and GLUT12 and AS160 protein expression were measured by Western blots. Results: IR decreased basal cell‐surface GLUT4 expression (P= .027), but not GLUT12, by an AS160‐independent pathway, without affecting total GLUT4 and GLUT12 content. Cell‐surface GLUT4 was not further enhanced by insulin stimulation in either group. Conclusions and Clinical Importance: IR induced defects in the skeletal muscle glucose transport pathway by decreasing active cell‐surface GLUT4.     

转基因耐除草剂大豆A2704-12定性PCR检测方法研究

本研究建立了转基因耐除草剂大豆A2704-12定性PCR检测方法.根据A2704-12转化体外源插入片段5'端与大豆基因组连接区序列设计特异性引物,以大豆内源基因Lectin为内标,从A2704-12转化体中特异性扩增出239 by大小的特异性目的片段.同时对该方法特异性和灵敏度进行测试,结果显示:该方法能检测出A27...     

Inhibitory effect of quercetin on apoptosis of PC12 cells induced by rotenone

AIM: To observe the effects and mechanisms of quercetin on the apoptosis of PC12 cells induced by rotenone. METHODS: PC12 cells were used in the study. Quercetin at the concentration of 300 μmol/L was added into the PC12 cells cultured in DMEM-F12 medium with 10% fetal calf serum. The morphological changes of the cells were observed under fluorescence microscope. The apoptotic rate was determined by flow cytometry assay. The protein levels of Bax and Bcl-2 were determined by Western blotting, and the mitochondrial membrane potential was measured by ratiometric probe JC-1.RESULTS: In the cells treated with rotenone+quercetin, the morphology of the cells was significantly improved, and the apoptotic rate was decreased to 6.7%, significantly lower than that in the cells treated with rotenone alone (P<0.01). The expression of Bcl-2 was up-regulated and Bax was down-regulated in rotenone+quercetin group (P<0.01), while the mitochondrial membrane potential was also increased (P<0.01) as compared to those in rotenone group.CONCLUSION: Pretreatment of quercetin inhibits the development of apoptosis in PC12 cells induced by rotenone. One of the mechanisms may be correlated with up-regulating the expression of Bcl-2 and down-regulating the expression of Bax, thus maintaining mitochondrial membrane potential.