超声微波协同萃取垂柳叶中α-葡萄糖苷酶抑制剂的研究

研究了超声微波协同萃取垂柳叶中α-葡萄糖苷酶抑制剂的方法。在单因素实验的基础上,通过正交实验确定了最佳提取工艺为:微波功率150W,料液比1∶18g/mL,时间270s,乙醇浓度70%。在此条件下,α-葡萄糖苷酶抑制率达到77.85%。与其他提取方法相比,超声微波协同萃取在提取效果上具有明显的优势。与其他植物原料相比,垂柳叶提取物对α-葡萄糖苷酶具有较强的抑制活性。      

大孔树脂纯化血管紧张素酶抑制肽VLPVPR的工艺优化

考察大孔树脂(AB8,D101,DM130,HPD100B,HPD826)对血管紧张素酶抑制肽VLPVPR的吸附性能及纯化效果,确立纯化VLPVPR的较优工艺。结果表明,HPD100B最适于VLPVPR的纯化。最优纯化工艺为:温度20℃,pH9.8,上样流速为3mL/(cm2·min),上样量达到180mL,洗脱液乙醇溶液浓度为60%,洗脱流速为0.25mL/(cm2·min),洗脱体积为45mL。此条件下,VLPVPR的解吸率达93.1%,纯度为28.8%,血管紧张素酶抑制率IC50为4.1μmol/L。      

新型凝胶泡沫材料阻化性能实验研究

为研究新型凝胶泡沫对煤体阻化作用的效能与影响,基于程序升温实验,对凝胶泡沫处理前后的不同粒径煤样组进行实验,分析煤样升温过程中的耗氧速率、CO与CH₄气体体积分数及其产生率,以及凝胶泡沫对煤样的阻化率。研究结果表明：煤的粒径不同,其耗氧速率也不同,经新型凝胶泡沫处理煤样的CO、CH₄气体的体积分数及其产生率均明显低于未经处理的煤样;在100 ℃时,粒径小于0.9 mm煤样的阻化率为59.23%,粒径3~5 mm煤样的阻化率为61.69%,粒径6~10 mm煤样的阻化率为65.63%,各粒径煤样受凝胶泡沫的阻化影响顺序为大粒径> 中粒径> 小粒径;新型凝胶泡沫材料能有效延缓煤的氧化过程、抑制煤氧复合反应、延迟煤体蓄热进程,对防治煤自燃具有十分积极的作用。     

玻璃包覆FeCoSiB微丝包覆层化学去除方法

以玻璃包覆FeCoSiB合金微丝为对象,研究了氢氟酸含量和反应温度对包覆层去除过程的影响,以及缓蚀剂对Fe-CoSiB芯丝的保护效果.结果表明:在反应温度为25℃的条件下,当所采用的HF质量分数从10%增加到40%时,玻璃包覆层去除速度从0.005μm·s^-1提高至0.076μm·s^-1;在HF质量分数为40%的条件下,当反应温度从10℃升高到45℃时,玻璃包覆层去除速度从0.033μm·s^-1提高到0.234μm·s^-1;反应温度为20~25℃时,用质量分数40%的氢氟酸溶液去除厚度范围为7.5~9.0μm高硼硅玻璃包覆层的最佳时间为150s;硫氰酸钠及硫氰酸钠+乌洛托品作为缓蚀剂均可显著抑制氢氟酸溶液对芯丝的腐蚀,硫氰酸钠+乌洛托品还可有效减少金属吸氢,有利于防止芯丝力学性能的劣化.

     

新型青铜器缓蚀剂的研制及其应用效果

近年来,青铜器保护方法由一般的清除粉状锈转向高效缓蚀剂的应用,并成为研究热点.介绍了加速青铜器腐蚀的多孔氧电极机理,提出了加入氧还原反应抑制剂改进缓蚀剂的新思路.采用电化学Tafel曲线法进行腐蚀电流的测试并对缓蚀效果作出定量的评价.结果表明,在传统的苯骈三氮唑(BTA)中添加钝化促进剂后缓蚀效率可由原来的68.39%提高到97.81%,已对郑州博物馆2批文物进行了保护试验,至今未见新锈生成.对青铜盆残片保护前后腐蚀电流的测试结果分别为2.636×10-9 A和1.687×10-10A,缓蚀效率为93.6%.该缓蚀剂已成功应用于焊丝等表面铜层的抗变色处理.     

The Effect of Sodium-Dependent Glucose Cotransporter 2 Inhibitor Tofogliflozin on Neurovascular Coupling in the Retina in Type 2 Diabetic Mice

We investigated the effect of tofogliflozin, a sodium-dependent glucose cotransporter 2 inhibitor (SGLT2i), on retinal blood flow dysregulation, neural retinal dysfunction, and the impaired neurovascular coupling in type 2 diabetic mice. Tofogliflozin was added to mouse chow to deliver 5 mg/kg/day and 6-week-old mice were fed for 8 weeks. The longitudinal changes in the retinal neuronal function and blood flow responses to systemic hyperoxia and flicker stimulation were evaluated every 2 weeks in diabetic db/db mice that received tofogliflozin (n =6) or placebo (n = 6) from 8 to 14 weeks of age. We also evaluated glial activation and vascular endothelial growth factor (VEGF) expression by immunofluorescence. Tofogliflozin treatment caused a sustained decrease in blood glucose in db/db mice from 8 weeks of the treatment. In tofogliflozin-treated db/db mice, both responses improved from 8 to 14 weeks of age, compared with vehicle-treated diabetic mice. Subsequently, the electroretinography implicit time for the oscillatory potential was significantly improved in SGLT2i-treated db/db mice. The systemic tofogliflozin treatment prevented the activation of glial fibrillary acidic protein and VEGF protein expression, as detected by immunofluorescence. Our results suggest that glycemic control with tofogliflozin significantly improved the impaired retinal neurovascular coupling in type 2 diabetic mice with the inhibition of retinal glial activation.     

Therapeutic Strategies for Disseminated Intravascular Coagulation Associated with Aortic Aneurysm

Aortic aneurysms are sometimes associated with enhanced-fibrinolytic-type disseminated intravascular coagulation (DIC). In enhanced-fibrinolytic-type DIC, both coagulation and fibrinolysis are markedly activated. Typical cases show decreased platelet counts and fibrinogen levels, increased concentrations of fibrin/fibrinogen degradation products (FDP) and D-dimer, and increased FDP/D-dimer ratios. Thrombin-antithrombin complex or prothrombin fragment 1 + 2, as markers of coagulation activation, and plasmin-α₂ plasmin inhibitor complex, a marker of fibrinolytic activation, are all markedly increased. Prolongation of prothrombin time (PT) is not so obvious, and the activated partial thromboplastin time (APTT) is rather shortened in some cases. As a result, DIC can be neither diagnosed nor excluded based on PT and APTT alone. Many of the factors involved in coagulation and fibrinolysis activation are serine proteases. Treatment of enhanced-fibrinolytic-type DIC requires consideration of how to control the function of these serine proteases. The cornerstone of DIC treatment is treatment of the underlying pathology. However, in some cases surgery is either not possible or exacerbates the DIC associated with aortic aneurysm. In such cases, pharmacotherapy becomes even more important. Unfractionated heparin, other heparins, synthetic protease inhibitors, recombinant thrombomodulin, and direct oral anticoagulants (DOACs) are agents that inhibit serine proteases, and all are effective against DIC. Inhibition of activated coagulation factors by anticoagulants is key to the treatment of DIC. Among them, DOACs can be taken orally and is useful for outpatient treatment. Combination therapy of heparin and nafamostat allows fine-adjustment of anticoagulant and antifibrinolytic effects. While warfarin is an anticoagulant, this agent is ineffective in the treatment of DIC because it inhibits the production of coagulation factors as substrates without inhibiting activated coagulation factors. In addition, monotherapy using tranexamic acid in cases of enhanced-fibrinolytic-type DIC may induce fatal thrombosis. If tranexamic acid is needed for DIC, combination with anticoagulant therapy is of critical importance.     

Theranostic Interpolation of Genomic Instability in Breast Cancer

Breast cancer is a diverse disease caused by mutations in multiple genes accompanying epigenetic aberrations of hazardous genes and protein pathways, which distress tumor-suppressor genes and the expression of oncogenes. Alteration in any of the several physiological mechanisms such as cell cycle checkpoints, DNA repair machinery, mitotic checkpoints, and telomere maintenance results in genomic instability. Theranostic has the potential to foretell and estimate therapy response, contributing a valuable opportunity to modify the ongoing treatments and has developed new treatment strategies in a personalized manner. “Omics” technologies play a key role while studying genomic instability in breast cancer, and broadly include various aspects of proteomics, genomics, metabolomics, and tumor grading. Certain computational techniques have been designed to facilitate the early diagnosis of cancer and predict disease-specific therapies, which can produce many effective results. Several diverse tools are used to investigate genomic instability and underlying mechanisms. The current review aimed to explore the genomic landscape, tumor heterogeneity, and possible mechanisms of genomic instability involved in initiating breast cancer. We also discuss the implications of computational biology regarding mutational and pathway analyses, identification of prognostic markers, and the development of strategies for precision medicine. We also review different technologies required for the investigation of genomic instability in breast cancer cells, including recent therapeutic and preventive advances in breast cancer.     

Effects of PCSK-9 Inhibition by Alirocumab Treatments on Biliary Cirrhotic Rats

Hyperlipidemia and oxidative stress with elevated oxidized low-density lipoprotein (ox-LDL) exacerbate hepatic inflammation and fibrosis. The plasma level of low-density lipoprotein (LDL) is controlled by proprotein convertase subtilisin/kexin 9 (PCSK9). Alirocumab is a monoclonal antibody that decreases LDL via inhibiting PCSK9 function. Apart from lipid-lowering effects, alirocumab exerts anti-inflammation, anti-angiogenesis and anti-oxidant effects. This study aims to investigate the impact of alirocumab treatment on common bile duct ligation (BDL)-induced biliary cirrhotic rats. After a 4-week treatment of alirocumab, the hemodynamic data, blood biochemistry, ox-LDL level, oxidative stress markers, severity of hepatic encephalopathy and abnormal angiogenesis of BDL rats were measured and compared to the control group. BDL rats presented cirrhotic pictures and elevated ammonia, total cholesterol, LDL and ox-LDL levels compared to the control group. Alirocumab decreased plasma levels of total cholesterol, LDL, and oxidative stress markers; however, it did not affect the hemodynamics, liver and renal biochemistry, and the plasma levels of ammonia and ox-LDL. The motor activities, portal-systemic collaterals and mesenteric vascular density were not significantly different between alirocumab-treated and control groups. In addition, it did not affect hepatic inflammation, intrahepatic angiogenesis, liver fibrosis and free cholesterol accumulation in the liver of BDL rats. In conclusion, PCSK9 inhibition by alirocumab treatment ameliorates hyperlipidemia and systemic oxidative stress in biliary cirrhotic rats. However, it does not affect the plasma level of ox-LDL, intrahepatic inflammation and fibrosis. In addition, PCSK9 inhibition has a neutral effect on abnormal angiogenesis and hepatic encephalopathy in biliary cirrhotic rats.     

The Role of Metalloproteinases and Their Tissue Inhibitors on Ocular Diseases: Focusing on Potential Mechanisms

Eye diseases are associated with visual impairment, reduced quality of life, and may even lead to vision loss. The efficacy of available treatment of eye diseases is not satisfactory. The unique environment of the eye related to anatomical and physiological barriers and constraints limits the bioavailability of existing agents. In turn, complex ethiopathogenesis of ocular disorders that used drugs generally are non-disease specific and do not act causally. Therefore, there is a need for the development of a new therapeutic and preventive approach. It seems that matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) have a significant role in the development and progression of eye diseases and could be used in the therapy of these disorders as pharmacological targets. MMPs and TIMPs play an important role in the angiogenesis, epithelial-mesenchymal transition, cell invasion, and migration, which occur in ocular diseases. In this review, we aim to describe the participation of MMPs and TIMPs in the eye diseases, such as age-related macular degeneration, cataract, diabetic retinopathy, dry eye syndrome, glaucoma, and ocular cancers, posterior capsule opacification focusing on potential mechanisms.