氨荒酸盐抑制铜在NaCl溶液中腐蚀的电化学研究

通过电化学极化曲线和失重实验,研究了氨荒酸盐对铜在氯化钠溶液中的缓蚀性能,并与相应胺的缓蚀性能进行了对比。结果表明:氨荒酸盐对铜具有较好的缓蚀性能。     

对我厂防治加热管内碳酸钙垢的思索

分析了我厂两碱法原卤净化后,加热管内壁结碳酸钙垢的原因,探讨了我厂采取加盐酸、加阻垢剂、用超声波阻垢器的方法,以及对加热管内碳酸钙垢防治的情况和存在的问题.     

Red Wine Polyphenols for Cancer Prevention

Conventional cancer therapies, the second leading cause of death worldwide, result in serious side effects and, at best, merely extend the patient''s lifespan by a few years. Searching for effective prevention is of high priority in both basic and clinical sciences. In recent decades natural products have been considered to be an important source of cancer chemopreventive agents. Red wine polyphenols, which consisted of various powerful antioxidants such as flavonoids and stilbenes, have been implicated in cancer prevention and that promote human health without recognizable side effects. Since resveratrol, a major component of red wine polyphenols, has been studied and reviewed extensively for its chemopreventive activity to interfere with the multi-stage carcinogenesis, this review focuses on recent progress in studies on cancer chemopreventive activities of red wine polyphenol extracts and fractions as well as other red wine polyphenols, like procyanidin B5 analogues and myricetin.     

防霉建筑涂料的研究与施工使用

针对国内外防霉建筑涂料存在的问题，研制开发了以合成树脂为主要成膜物质，加入环保性杀菌防霉剂及具有防腐霉的功能性颜填料，再配以树脂固化剂等成分配制而成的高性能防霉建筑涂料，并指出该涂料防霉效果良好。     

载银无机抗菌剂变色抑制剂研发现状

介绍了载银无机抗菌剂变色抑制剂如甲基苯并三唑、天然水滑石和合成水滑石等的研发现状     

Effect of different rates of N-fertilizers on nodulation, nodule activities and growth of two field grown cvs. of soybean

The effect of N fertilizers on nodulation, nitrogenase, nitrate reductase activities and growth of two cultivars of soybean, Clark and Crauford was evaluated in a field experiment. KNO₃ or NH₄Cl were applied 27 days after planting at 0,16, 32, 64 and 128 kg N/ha. Nodulation and growth of both cultivars significantly increased when N was applied at low levels whereas specific N₂-ase activity (SNA) slightly and insignificantly increased. Cv Crauford showed a greater positive response than cv. Clark. Higher rates of KNO₃ and NH₄Cl (128 kg N/ha) significantly depressed nodulation and SNA but slightly decreased the plant dry matter. Cv. Crauford was more tolerant to N fertilizers than cv. Clark. The decline in SNA was ascribed to increased nitrate reductase activity (NRA) and higher accumulation of nitrites in nodule cytosol. NRA and nitrate contents in nodules of cv. Clark were greater than that in cv. Crauford. Results showed that NH₄ ⁺ is the preferred N source with occasional increases in nodule number and weight. This study provides an evidence for the nodulation and growth variability of soybean cultivars fertilized with different levels of N. The results also suggest that diminishing NRA could contribute to increased N₂ fixation and the interaction between NO₃ ^– assimilation and N₂ fixation is strongly dependent on the plant cultivar.     

Rational Design of CYP3A4 Inhibitors: A One-Atom Linker Elongation in Ritonavir-Like Compounds Leads to a Marked Improvement in the Binding Strength

Inhibition of the major human drug-metabolizing cytochrome P450 3A4 (CYP3A4) by pharmaceuticals and other xenobiotics could lead to toxicity, drug–drug interactions and other adverse effects, as well as pharmacoenhancement. Despite serious clinical implications, the structural basis and attributes required for the potent inhibition of CYP3A4 remain to be established. We utilized a rational inhibitor design to investigate the structure–activity relationships in the analogues of ritonavir, the most potent CYP3A4 inhibitor in clinical use. This study elucidated the optimal length of the head-group spacer using eleven (series V) analogues with the R₁/R₂ side-groups as phenyls or R₁–phenyl/R₂–indole/naphthalene in various stereo configurations. Spectral, functional and structural characterization of the inhibitory complexes showed that a one-atom head-group linker elongation, from pyridyl–ethyl to pyridyl–propyl, was beneficial and markedly improved K_s, IC₅₀ and thermostability of CYP3A4. In contrast, a two-atom linker extension led to a multi-fold decrease in the binding and inhibitory strength, possibly due to spatial and/or conformational constraints. The lead compound, 3h, was among the best inhibitors designed so far and overall, the strongest binder (K_s and IC₅₀ of 0.007 and 0.090 µM, respectively). 3h was the fourth structurally simpler inhibitor superior to ritonavir, which further demonstrates the power of our approach.     

Pharmacological Evidence on Augmented Antiallodynia Following Systemic Co-Treatment with GlyT-1 and GlyT-2 Inhibitors in Rat Neuropathic Pain Model

The limited effect of current medications on neuropathic pain (NP) has initiated large efforts to develop effective treatments. Animal studies showed that glycine transporter (GlyT) inhibitors are promising analgesics in NP, though concerns regarding adverse effects were raised. We aimed to study NFPS and Org-25543, GlyT-1 and GlyT-2 inhibitors, respectively and their combination in rat mononeuropathic pain evoked by partial sciatic nerve ligation. Cerebrospinal fluid (CSF) glycine content was also determined by capillary electrophoresis. Subcutaneous (s.c.) 4 mg/kg NFPS or Org-25543 showed analgesia following acute administration (30–60 min). Small doses of each compound failed to produce antiallodynia up to 180 min after the acute administration. However, NFPS (1 mg/kg) produced antiallodynia after four days of treatment. Co-treatment with subanalgesic doses of NFPS (1 mg/kg) and Org-25543 (2 mg/kg) produced analgesia at 60 min and thereafter meanwhile increased significantly the CSF glycine content. This combination alleviated NP without affecting motor function. Test compounds failed to activate G-proteins in spinal cord. To the best of our knowledge for the first time we demonstrated augmented analgesia by combining GlyT-1 and 2 inhibitors. Increased CSF glycine content supports involvement of glycinergic system. Combining selective GlyT inhibitors or developing non-selective GlyT inhibitors might have therapeutic value in NP.     

Investigating T Cell Immunity in Cancer: Achievements and Prospects

T cells play a key role in tumour surveillance, both identifying and eliminating transformed cells. However, as tumours become established they form their own suppressive microenvironments capable of shutting down T cell function, and allowing tumours to persist and grow. To further understand the tumour microenvironment, including the interplay between different immune cells and their role in anti-tumour immune responses, a number of studies from mouse models to clinical trials have been performed. In this review, we examine mechanisms utilized by tumour cells to reduce their visibility to CD8⁺ Cytotoxic T lymphocytes (CTL), as well as therapeutic strategies trialled to overcome these tumour-evasion mechanisms. Next, we summarize recent advances in approaches to enhance CAR T cell activity and persistence over the past 10 years, including bispecific CAR T cell design and early evidence of efficacy. Lastly, we examine mechanisms of T cell infiltration and tumour regression, and discuss the strengths and weaknesses of different strategies to investigate T cell function in murine tumour models.     

If Virchow and Ehrlich Had Dreamt Together: What the Future Holds for KRAS-Mutant Lung Cancer

Non-small-cell lung cancer (NSCLC) with Kirsten rat sarcoma (KRAS) mutations has notoriously challenged oncologists and researchers for three notable reasons: (1) the historical assumption that KRAS is “undruggable”, (2) the disease heterogeneity and (3) the shaping of the tumor microenvironment by KRAS downstream effector functions. Better insights into KRAS structural biochemistry allowed researchers to develop direct KRAS(G12C) inhibitors, which have shown early signs of clinical activity in NSCLC patients and have recently led to an FDA breakthrough designation for AMG-510. Following the approval of immune checkpoint inhibitors for PDL1-positive NSCLC, this could fuel yet another major paradigm shift in the treatment of advanced lung cancer. Here, we review advances in our understanding of the biology of direct KRAS inhibition and project future opportunities and challenges of dual KRAS and immune checkpoint inhibition. This strategy is supported by preclinical models which show that KRAS(G12C) inhibitors can turn some immunologically “cold” tumors into “hot” ones and therefore could benefit patients whose tumors harbor subtype-defining STK11/LKB1 co-mutations. Forty years after the discovery of KRAS as a transforming oncogene, we are on the verge of approval of the first KRAS-targeted drug combinations, thus therapeutically unifying Paul Ehrlich’s century-old “magic bullet” vision with Rudolf Virchow’s cancer inflammation theory.