微波辅助合成4-苯基氨基-7-氨基喹唑啉

以2-氨基-4-硝基苯甲酸和甲酰胺为原料,经Niementowski、氯代、烃化反应合成4-苯基氨基-7-硝基喹唑啉盐酸盐,再经铁粉还原得4-苯基氨基-7-氨基喹唑啉。目标化合物的结构经1HNMR、IR、MS谱表征。前三步反应采用微波辐助合成,大大缩短了反应时间,提高了反应速率和收率。     

5-(4'-甲基联苯-2-基)-1H-四唑的合成研究进展

5-(4-甲基联苯-2-基)-1H-四唑是血管紧张素Ⅱ受体拮抗剂的关键原料,综述其合成方法的研究进展.     

对甲基苯甲醛改性煤沥青的工艺研究

以对甲基苯甲醛(4-methyl benzaldehyde,简称4-MB)为改性剂,在对甲苯磺酸(PTS)的作用下对煤沥青(coal tar pitch)进行了改性。采用偏光显微镜研究了4-MB改性煤沥青的光学组织;考察了4-MB用量,反应温度和反应时间对改性沥青的软化点、密度、残炭率的影响。结果表明,在同一反应条件下,随4-MB用量的增加,改性沥青的密度、软化点、残炭率先显著提高后稍有降低。随着反应温度的提高及反应时间的延长,改性沥青的密度、软化点、残炭率先明显提高,后增加不大。可通过添加不同的4-MB用量或调节反应温度控制改性沥青的中间相小球的数量和球径的大小,从而改善得到较好的光学组织。     

带倾斜回转工作台的四坐标后置处理方法

针对带倾斜回转工作台的四坐标数控加工的后置处理,提出了一种非正交多轴联动数控机床的逆运动学求解方法。基于矢量绕任意轴线的旋转变换,建立了非正交情况下四坐标机床各运动坐标同刀位数据之间的映射关系,从而实现了机床平动坐标和转动坐标的计算。该方法同样适用于非正交情况下五坐标机床的逆运动学求解。利用刀具同加工表面相切的控制方式,给出了实际加工中进刀及退刀过程的构造方法。本文方法稳定可靠,并已成功应用于工程实际中。     

3-氨基-1,2,4-三氮唑自组装膜对Cu-Ni合金缓蚀作用及吸附机理研究

利用3-氨基-1,2,4-三氮唑(ATA)金属处理剂在Cu-Ni合金表面制备了自组装单分子膜(SAMs),用电化学方法研究ATA SAMs对Cu-Ni合金的缓蚀作用及其吸附行为.结果表明, ATA分子易在Cu-Ni合金表面形成稳定的ATA SAMs,抑制了Cu-Ni合金的阳极氧化过程,改变了电极表面双电层结构,使零电荷电位正移,固/液界面双电层电容明显降低,有良好的缓蚀效果,这与交流阻抗和极化曲线得到的结论一致.同时研究表明ATA的吸附行为符合Langmuir吸附等温式,吸附机理是典型的化学吸附.     

TiB2含量对B4C-TiB2-Al复合材料组织与力学性能的影响

通过在B4C-TiB2预烧体中真空熔渗Al制备了B4C-TiB2-Al复合材料,研究了TiB2含量对复合材料显微组织和力学性能的影响.结果表明: B4C-TiB2-Al复合材料主要由B4C,TiB2,Al和Al3BC等相组成;随着TiB2含量的增加,复合材料的HRA硬度逐渐降低,抗弯强度逐渐增大,断裂韧性先增大后稍微降低,当TiB2含量为40%(质量分数)时,复合材料的气孔率、硬度HRA、抗弯强度和断裂韧性分别为1.32%,80.3,559.4 MPa和7.83 MPa·m1/2;延性Al的加入,裂纹的偏转和分叉、B4C和TiB2晶粒的细化以及B4C基体和TiB2晶粒热膨胀的不匹配,是造成材料断裂韧性提高的主要原因;随着Al渗入量的增加,复合材料断口中金属撕裂棱及韧窝的比例增加.     

磺化硅胶催化合成2-叔丁基对甲基苯酚

以4-甲基苯酚、叔丁醇为原料,磺化硅胶(SSA)为催化剂,合成了2-叔丁基对甲基苯酚。并获得了较佳合成条件:酚醇摩尔比1:1,催化剂用量为(以对甲苯酚质量计)11.75%,反应时间为3 h,反应温度80℃。产物的平均收率为89.4%,酚的选择性大于92%。该催化剂具有较高的催化活性,可回收重复利用。     

CTLA4-Linked Autoimmunity in the Pathogenesis of Endometriosis and Related Infertility: A Systematic Review

Several studies, although with conflicting results, have sought to determine the concentration of soluble CTLA4 antigens in peripheral blood plasma and peritoneal fluid in patients with endometriosis-related infertility. A systematic review was performed according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) through a search of the following databases: MEDLINE, EMBASE, Global Health, The Cochrane Library, Health Technology Assessment Database and Web of Science, and Clinical Trials research register. We included observational or prospective human and animal studies with any features related to endometriosis and/or infertility studies involving CTLA4-related pathogenesis published in English. The results of studies in which the size and characteristics of the observed groups were not stated were excluded. From the initial pool of 73 publications identified and screened, we finally included 5 articles to summarize the most recent knowledge about CTLA4-linked autoimmunity in the pathogenesis of endometriosis and related infertility. Evidence from clinical studies shows that CTLA4-based autoimmunity is involved in the maintenance of chronic inflammation in the peritoneal environment, with pre-clinical evidence of anti-CTLA antibodies as a potential novel target therapy for endometriosis. However, CTLA4 gene analyses do not support findings of CTLA4-linked autoimmunity as a primary determinant of the pathogenesis of endometriosis. These findings underlie the role of complex interactions within the family of immune checkpoint molecules involved. Further studies are needed to investigate the clinical relevance of anti-CTLA target therapy, taking into account the potential adverse events and repercussions of novel immunologic therapy modalities. However, with the general scarcity of studies investigating this topic, the clinical importance of CTLA4 autoimmunity still remains unclear.     

TRPV4 Promotes Metastasis in Melanoma by Regulating Cell Motility through Cytoskeletal Rearrangement

The abnormal expression of Transient Receptor Potential cation channel subfamily V member 4 (TRPV4) is closely related to the progression of multiple tumors. In addition, TRPV4 is increasingly being considered a potential target for cancer therapy, especially in tumor metastasis prevention. However, the biological correlation between TRPV4 and tumor metastasis, as well as the specific role of TRPV4 in malignant melanoma metastasis, is poorly understood. In this study, we aimed to examine the role of TRPV4 in melanoma metastasis through experiments and clinical data analysis, and the underlying anticancer mechanism of Baicalin, a natural compound, and its inhibitory effect on TRPV4 with in vivo and in vitro experiments. Our findings suggested that TRPV4 promotes metastasis in melanoma by regulating cell motility via rearranging the cytoskeletal, and Baicalin can inhibit cancer metastasis, whose mechanisms reverse the recruitment of activated cofilin to leading-edge protrusion and the increasing phosphorylation level of cortactin, which is provoked by TRPV4 activation.     

Elevated Expression of CCN3 in Articular Cartilage Induces Osteoarthritis in Hip Joints Irrespective of Age and Weight Bearing

Osteoarthritis (OA) occurs not only in the knee but also in peripheral joints throughout the whole body. Previously, we have shown that the expression of cellular communication network factor 3 (CCN3), a matricellular protein, increases with age in knee articular cartilage, and the misexpression of CCN3 in cartilage induces senescence-associated secretory phenotype (SASP) factors, indicating that CCN3 promotes cartilage senescence. Here, we investigated the correlation between CCN3 expression and OA degenerative changes, principally in human femoral head cartilage. Human femoral heads obtained from patients who received total hip arthroplasty were categorized into OA and femoral neck fracture (normal) groups without significant age differences. Gene expression analysis of RNA obtained from femoral head cartilage revealed that CCN3 and MMP-13 expression in the non-weight-bearing part was significantly higher in the OA group than in the normal group, whereas the weight-bearing OA parts and normal cartilage showed no significant differences in the expression of these genes. The expression of COL10A1, however, was significantly higher in weight-bearing OA parts compared with normal weight-bearing parts, and was also higher in weight-bearing parts compared with non-weight-bearing parts in the OA group. In contrast, OA primary chondrocytes from weight-bearing parts showed higher expression of CCN3, p16, ADAMTS4, and IL-1β than chondrocytes from the corresponding normal group, and higher ADAMTS4 and IL-1β in the non-weight-bearing part compared with the corresponding normal group. Acan expression was significantly lower in the non-weight-bearing group in OA primary chondrocytes than in the corresponding normal chondrocytes. The expression level of CCN3 did not show significant differences between the weight-bearing part and non-weight-bearing part in both OA and normal primary chondrocytes. Immunohistochemical analysis showed accumulated CCN3 and aggrecan neoepitope staining in both the weight-bearing part and non-weight-bearing part in the OA group compared with the normal group. The CCN3 expression level in cartilage had a positive correlation with the Mankin score. X-ray analysis of cartilage-specific CCN3 overexpression mice (Tg) revealed deformation of the femoral and humeral head in the early stage, and immunohistochemical analysis showed accumulated aggrecan neoepitope staining as well as CCN3 staining and the roughening of the joint surface in Tg femoral and humeral heads. Primary chondrocytes from the Tg femoral head showed enhanced expression of Ccn3, Adamts5, p16, Il-6, and Tnfα, and decreased expression of Col2a1 and -an. These findings indicate a correlation between OA degenerative changes and the expression of CCN3, irrespective of age and mechanical loading. Furthermore, the Mankin score indicates that the expression level of Ccn3 correlates with the progression of OA.