Genistein,a protein tyrosine kinase inhibitor,suppresses the fusogenicity of Moloney murine leukemia virus envelope protein in XC cells

Summary. XC cells are highly susceptible to syncytium formation by infection of ecotropic murine leukemia viruses (MLVs) and by expression of their envelope protein (Env). By this property, XC cells are widely used to determine titers of ecotropic MLVs. Number of plaques resulted from the syncytium formation in XC cells by ecotropic MLV infection is corresponding to number of the viral particles. XC cells had been established from a v-src-induced rat tumor. It has been reported that transformed cells are more sensitive to Mo-MLV-induced syncytium formation than non-transformed cells. To assess whether the transformation by v-src oncogene in XC cells is involved in the high sensitivity to ecotropic MLV-induced syncytium formation, XC cells were treated with genistein, a protein tyrosine kinase inhibitor. Genistein suppressed the syncytium formation between XC cells and ecotropic Env-expressing 293T cells. This result indicates that protein tyrosine kinase activity is associated with the high sensitivity of XC cells to ecotropic Env-induced syncytium formation.Received January 8, 2003; accepted May 26, 2003     

Reduction of trimethylamine N-oxide by Escherichia coli as anaerobic respiration

E. coli was found to grow anaerobically on lactate in the presence of trimethylamine N-oxide (TMANO), reducing it to trimethylamine. Anaerobic growth on glucose was promoted in the presence of TMANO. When a culture grown in complex medium was transferred to defined medium, growth on glucose and ammonia took place in the presence of TMANO after consumption of complex nutrients introduced with the preculture, in contrast to growth in nitrate respiration. The amounts of ethanol, succinate, and lactate among the fermentation products were decreased and that of acetate was increased in the presence of TMANO. Formate generation was much reduced at pH 7.4, whereas stoichiometric formation of formate was observed in the absence of TMANO. Cells grown anaerobically in the presence of TMANO had a higher activity of amine N-oxide reductase than cells grown under other conditions. The content of cytochrome-558 was elevated in the presence of TMANO during growth in complex medium. Cytochrome c-552 found in cells grown in diluted complex medium or defined medium in the presence of TMANO was oxidized by TMANO in cell extracts. The molar growth yield on glucose was higher in the presence of TMANO than in its absence and lower than that in the presence of nitrate.     

鼻腔、咽部非霍奇金氏淋巴瘤

目的 :探讨鼻腔、咽部非霍奇金氏淋巴瘤 ( NHL)的临床特征、诊断要点及误诊原因。方法 :对1 986年～ 1 996年住院的 2 4例鼻腔、咽部非霍奇金氏淋巴瘤的患者作一回顾性分析。结果 :2 4例临床表现差异较大 ,缺乏特征性的表现。首次诊断 NHL6例 ,其余 1 8例初诊时诊断 :慢性鼻炎 8例 ,恶性肉芽肿3例 ,鼻息肉 2例 ,鼻中隔粘膜肥厚 2例 ,扁桃体炎 2例 ,慢性咽炎 1例。 2 4例均经病理切片及免疫组化确诊。结论 :鼻腔、咽部非霍奇金氏淋巴瘤临床表现复杂 ,缺乏特征性 ,早期易误诊。提高临床医师对本病的认识 ,反复活检及免疫组化等方法有利于本病的确诊。     

Adenosine infusion during early reperfusion failed to limit myocardial infarct size in a collateral deficient species.

STUDY OBJECTIVE--Intracoronary or intravenous adenosine during reperfusion in combination with lignocaine may attenuate "reperfusion injury" and limit myocardial infarct size in the canine heart. The aim of this study was to test whether intravenous adenosine also protects myocardium in the rabbit heart, which lacks xanthine oxidase and significant coronary collaterals in contrast to the canine heart. DESIGN--Five groups of rabbits underwent a 30 min occlusion of the circumflex coronary artery, followed by reperfusion. In adenosine treated groups, either a high dose of adenosine (0.37 mg.kg-1.min-1) with lignocaine treatment (5 mg intravenously 1 min before coronary occlusion and before reperfusion) or a low dose (0.15 mg.kg-1.min-1) of adenosine with or without lignocaine was infused for 60 min starting 5 min before the onset of reperfusion. Group 1 was untreated, while group 2 received a high dose of adenosine with lignocaine. These groups were reperfused for 3 h. Group 3 was untreated, group 4 received a low dose of adenosine, and group 5 a low dose of adenosine and lignocaine. These groups were reperfused for 72 h. EXPERIMENTAL MATERIAL--60 anaesthetised open chest rabbits were used. Groups 1 and 2 were killed after 3 h coronary reperfusion. Groups 3, 4, and 5 recovered from surgery for 72 h and were then killed for further study. MEASUREMENTS AND MAIN RESULTS--The high dose of adenosine reduced mean blood pressure to 44% of baseline value and diminished reactive hyperaemia in the area at risk by "coronary steal". The low dose of adenosine did not significantly alter systemic blood pressure or heart rate. Infarct size did not differ between groups 1 and 2, at 39.7(SD 20.1)% of area at risk v 33.2(15.9)% (by tetrazolium staining), nor between groups 3, 4, and 5: 50.3(12.6)% v 52.7(15.6)% v 47.8(9.3)% (by histology). CONCLUSION--Neither a high dose nor a low dose of adenosine limited myocardial infarct size in the rabbit heart even when adenosine was combined with lignocaine treatment.     

培美曲塞与奈达铂一线治疗非小细胞肺腺癌的效果和患者不良反应观察

目的 探究非小细胞肺腺癌患者接受培美曲塞与奈达铂一线治疗的效果及对不良反应的影响.方法 选取2017年5月至2019年5月本院收治的65例非小细胞肺腺癌患者,随机分为对照组(n=30)和实验组(n=35).对照组采用吉西他滨与奈达铂联合治疗,实验组采用培美曲塞与奈达铂联合治疗,比较两组患者治疗效果.结果 实验组总有效率...     

Dietary l-Lysine Prevents Arterial Calcification in Adenine-Induced Uremic Rats

Vascular calcification (VC) is a life-threatening complication of CKD. Severe protein restriction causes a shortage of essential amino acids, and exacerbates VC in rats. Therefore, we investigated the effects of dietary l-lysine, the first-limiting amino acid of cereal grains, on VC. Male Sprague-Dawley rats at age 13 weeks were divided randomly into four groups: low-protein (LP) diet (group LP), LP diet+adenine (group Ade), LP diet+adenine+glycine (group Gly) as a control amino acid group, and LP diet+adenine+l-lysine·HCl (group Lys). At age 18 weeks, group LP had no VC, whereas groups Ade and Gly had comparable levels of severe VC. l-Lysine supplementation almost completely ameliorated VC. Physical parameters and serum creatinine, urea nitrogen, and phosphate did not differ among groups Ade, Gly, and Lys. Notably, serum calcium in group Lys was slightly but significantly higher than in groups Ade and Gly. Dietary l-lysine strongly suppressed plasma intact parathyroid hormone in adenine rats and supported a proper bone-vascular axis. The conserved orientation of the femoral apatite in group Lys also evidenced the bone-protective effects of l-lysine. Dietary l-lysine elevated plasma alanine, proline, arginine, and homoarginine but not lysine. Analyses in vitro demonstrated that alanine and proline inhibit apoptosis of cultured vascular smooth muscle cells, and that arginine and homoarginine attenuate mineral precipitations in a supersaturated calcium/phosphate solution. In conclusion, dietary supplementation of l-lysine ameliorated VC by modifying key pathways that exacerbate VC.Medial vascular calcification is common in aging, diabetes, and CKD.^1–4 Because the presence of vascular calcification is strongly associated with increased cardiovascular morbidity and mortality, several studies in both animals and humans have sought ways to reduce the extent of vascular calcification.^5–10 However, satisfactory therapies have not yet been established.¹¹Adenine-induced renal failure is one of the commonly used animal models for studying the development of vascular calcification, but the prevalence of vascular calcification in this model is not very high. Indeed, Price et al. reported that vascular calcification was detected in only 30% of rats with adenine-induced chronic renal failure (adenine rats) fed a normal-protein diet.⁵ These authors speculated that consistent vascular calcification might require a longer period of adenine feeding. On the basis of this idea, they designed a low-protein (LP) diet in an attempt to reduce the nitrogen load and thus enable the rats to thrive on the adenine diet for longer periods. As a result of this attempt, Price et al. unexpectedly found that adenine rats fed a LP diet had extensive vascular calcification without a longer feeding period.⁵ All 13 adenine rats fed the LP diet had uniform alizarin red staining of the aorta, whereas only 3 of the 11 adenine rats fed a normal-protein diet had partial calcification.⁵ These findings indicated that dietary protein deficiency correlates with the extent of vascular calcification.Proteins are usually made from 20 kinds of amino acids. On the basis of nutritional requirements, these amino acids can be divided into two groups: essential amino acids (EAAs) and non-EAAs. Because restriction of dietary protein results in a shortage of EAAs, the level of dietary EAAs may be relevant to the extent of vascular calcification. Among nine EAAs, this study focused on l-lysine (l-Lys) based on the following three reasons. First, l-Lys is the first-limiting amino acid in most cereal grains.¹² Second, the safety of l-Lys supplementation has been verified in the area of animal husbandry. l-Lys has long been added to feed grains in order to improve the utility of feed proteins.¹³ Third, several studies have demonstrated that dietary supplementation with l-Lys protects bones from osteoporosis, a pathologic condition that often coexists with vascular calcification.^14,15 These points prompted us to hypothesize that supplementation with l-Lys would ameliorate vascular calcification. Therefore, in this study, we tested this hypothesis using adenine rats.     

基于代谢组学和网络药理学探讨针灸治疗缺血性脑卒中作用机制

[目的]联合网络药理学和代谢组学分析针灸治疗缺血性脑卒中的作用机制。[方法]借助Swiss Target Prediction数据库、Gene Cards数据库查找作用靶点;Cytoscape 3.9.1软件构建药物-成分-靶点网络;STRING数据库获得PPI网络图;最后利用David平台进行KEGG信号通路富集分析。采用超高效液相色谱-四极杆-飞行时间质谱（UPLC-Q-TOF/MS）分析各组大鼠代谢轮廓变化,借助Metabo Analyst数据库查询相关代谢通路。[结果]假手术组和模型组共筛选出49个基于血清的代谢生物标志物（P<0.05）,主要代谢途径为甘油磷脂代谢、亚油酸代谢、α-亚麻酸代谢、乙醚脂质代谢、赖氨酸降解、花生四烯酸代谢,其中包含的代谢产物主要是磷脂酰胆碱、溶血磷脂酰胆碱、脂肪酸及磷脂酰乙醇胺。[结论]针灸治疗可能通过多靶点、多通路来改善脑血管微循环、促进血管生成、减少脂质沉积、减缓炎症反应等改善机体免疫。结合文献数据,认为针灸的治疗具有组分多、目标多、路径多的特点,对于缺血性脑卒中有一定疗效。