红细胞载体的渗透脆性及血红蛋白溢出率研究

目的:考察高渗法制备载体红细胞过程中渗透压对红细胞(RBC)的渗透脆性以及血红蛋白(Hb)溢出率的影响.方法:模拟高渗法制备吗啡载体红细胞的过程,制备成载体红细胞RBC1和RBC2,并测定其渗透脆性,估算50%红细胞溶血时的渗透压(H50);测定计算Hb溢出率.结果:和正常RBC一样,载体RBC1和载体RBC2的OFC也呈S型,RBC、RBC1和RBC2的H50分别为151.8,175.6,153.6 mOsm·L-1;等渗和低渗溶液中Hb溢出率分别为(36.3±5.9)%和(32.1±4.1)%,差异无显著性.结论:高渗法制备的红细胞裁体时,虽然经过高渗糖的脱水,红细胞脱水变形,经过重涨后其形状和细胞膜的弹性可以恢复,载体红细胞的渗透脆性变化不大.     

D-serine reduces memory impairment and neuronal damage induced by chronic lead exposure

Although exogenous D-serine has been applied as a neural regulatory intervention in many studies, the role played by D-serine in hippocampal injuries caused by lead exposure remains poorly understood. Rat models of chronic lead exposure were established through the administration of 0.05% lead acetate for 8 weeks. Simultaneously, rats were administered 30 or 60 mg/kg D-serine, intraperitoneally, twice a day. Our results showed that D-serine treatment shortened the escape latency from the Morris water maze, increased the number of times that mice crossed the original platform location, and alleviated the pathological damage experienced by hippocampal neurons in response to lead exposure. Although D-serine administration did not increase the expression levels of the N-methyl-D-aspartate receptor subtype 2 B(NR2 B) in the hippocampi of lead-exposed rats, 60 mg/kg D-serine treatment restored the expression levels of NR2 A, which are reduced by lead exposure. These findings suggested that D-serine can alleviate learning and memory impairments induced by lead exposure and that the underlying mechanism is associated with the increased expression of NR2 A in the hippocampus. This study was approved by the Animal Ethics Committee of North China University of Science and Technology, China(approval No. LX2018155) on December 21, 2018.     

High prevalence of neonatal presentation in Korean patients with citrullinemia type 1, and their shared mutations

Type 1 citrullinemia (CTLN1) often presents as a hyperammonemic encephalopathy in the neonatal period, but it can also develop in the late-infantile period and in adults. In addition, some patients can be identified in the presymptomatic period by neonatal or family member screening. In this study, twenty Korean patients with CTLN1 (19 families) were examined; fourteen patients with neonatal-onset, three with late-onset, and three that were identified presymptomatically. The 13 patients with hyperammonemic encephalopathy received continuous venovenous hemofiltration (CVVH) or peritoneal dialysis (PD). Although the hyperammonemia was relieved more effectively in the six patients on CVVH than the seven on PD, most of these patients suffered from severe neurologic deficits. Recurrent hyperammonemic episodes (7 pts, 35%), recurrent and reversible acute hepatic dysfunction (5 pts, 25%), and focal cerebral infarction (2 pts, 10%) were noted. The neonates with hyperammonemic encephalopathy had extensive brain injuries at the onset of hyperammonemia, followed by encephalomalacia and brain atrophy at quite an early age. Genetic testing for the ASS1 gene revealed a different mutation spectrum from those of other ethnicities; Three common mutations, c.421-2A > G (37.8%), c.1128-6_1188dup67 (18.9%), and p.Gly324Ser (16.2%), accounted for 73% of the mutations. The poor outcome was expected in patients with the peak ammonia level at onset over 600 μmol/L, whose proportion was higher in the neonatal presentation group than in the presymptomatic/late presentation group. Our findings add to the current understanding of the ethnic diversity of CTLN1 from both clinical and genetic perspectives.     

音乐疗法缓解手外伤患者疼痛的临床应用及研究进展

归纳音乐疗法缓解疼痛的原理及疼痛可能给手外伤患者带来的后果,介绍音乐疗法在缓解手外伤患者疼痛中的临床应用及研究现状,阐述音乐疗法在缓解手外伤患者疼痛应用中的注意事项,以期为音乐疗法的临床护理实践提供信息。     

Norepinephrine provides short-term neuroprotection against Aβ1–42 by reducing oxidative stress independent of Nrf2 activation

Pathophysiological evidence correlating locus ceruleus neuron loss with increased Alzheimer's disease pathology suggests that norepinephrine (NE) is neuroprotective. Here, we evaluated the effects of NE on amyloid-β (Aβ)1-42–induced neurotoxicity and determined how NE exerts its actions in human SK-N-SH neurons. NE protected SK-N-SH cells against Aβ1-42–induced neurotoxicity only after a 4-hour treatment. The ability of NE to reduce Aβ1-42–induced neurotoxicity was independent of the adrenoceptor signaling pathway. Notably, NE downregulated Aβ1-42–mediated increases in intracellular reactive oxygen species (ROS) production. However, NE did not affect Aβ1-42–induced activation of the nuclear factor erythroid 2–related factor 2 (Nrf2) redox signaling pathway, known to be involved in oxidative stress. Among the antioxidants tested, N-acetyl cysteine and glutathione, which are not only ROS scavengers but also thiol-reducing agents, mimicked the protective effects of NE. Consistently, Kelch-like ECH-associating protein 1 inhibitors, which activated the Nrf2 pathway, failed to decrease Aβ1-42–induced ROS generation and elicited no protection against Aβ1–42. Taken together, these findings suggest that NE could exert neuroprotective function against Aβ1–42 via redox cycling and reduction of intracellular oxidative stress regardless of downstream activation of the Nrf2 pathway.     

玉竹多糖干预后衰老模型鼠抗氧化系统及免疫功能的变化

目的:观察具有扶正固本,养阴润燥和滋补强壮功效的百合科黄精属植物药玉竹的提取物玉竹多糖对D-半乳糖致亚急性衰老模型小鼠血清中超氧化物歧化酶活性和丙二醛含量的抗氧化系统作用及免疫功能的影响,探讨玉竹多糖抗衰老的可能作用途径。方法:实验于2004-07/2005-05锦州医学院免疫教研室完成。①取昆明小鼠50只,随机分为5组:正常对照组、衰老模型组和低、中、高剂量玉竹多糖治疗组。除正常对照组外,其余各组每只颈背部皮下注射50g/LD-半乳糖0.5mL,连续6周。同时低、中、高剂量玉竹多糖治疗组分别腹腔注射0.5,1,2g/kg剂量的玉竹多糖(玉竹为百合科黄精属植物药,药用根茎,由锦州医学院免疫教研室采摘,经中国医科大学免疫教研室潘兴瑜教授乙醇回流脱脂、水提纯、浓缩、醇沉、除蛋白、离心、真空干燥等程序,得到玉竹多糖;玉竹产自锦州凌海市温滴楼乡岩井寺工区)溶液0.5mL,正常对照组和衰老模型组小鼠给予腹腔注射生理盐水0.5mL。②给药6周后,麻醉下将小鼠摘除眼球取血,常规分离血清,在4℃下3000r/min离心5min,取上清待测。用分光光度计检测小鼠血清中超氧化物歧化酶活性和丙二醛水平,并将小鼠称质量并剖取小鼠胸腺和脾脏,用电子天平称质量,以脏器湿质量(mg/g)表示小鼠脾指数和胸腺指数,用MTT法测定脾淋巴细胞转化指数,用免疫荧光法测定脾T淋巴细胞亚群,观察玉竹多糖对免疫功能的影响。③多组间样本均数比较采用方差分析。结果:昆明种小鼠50只均进入结果分析。①衰老模型组小鼠血清中超氧化物歧化酶活性明显低于正常对照组,丙二醛水平明显高于正常对照组(P<0.05)。高剂量玉竹多糖治疗组小鼠血清中超氧化物歧化酶活性明显高于衰老模型组,丙二醛水平明显低于衰老模型组(P<0.01,0.05);中、低剂量玉竹多糖治疗组与衰老模型组血清中超氧化物歧化酶活性和丙二醛水平比较,差异不明显(P>0.05)。②衰老模型组小鼠胸腺指数和脾指数明显低于正常对照组(P<0.01,0.05);低、中、高剂量玉竹多糖治疗组的胸腺指数和脾指数均明显高于衰老模型组(P<0.05～0.01),以中剂量玉竹多糖治疗组作用最明显(P<0.01);3个剂量玉竹多糖治疗组之间胸腺指数和脾指数差异不明显。③衰老模型组小鼠脾T和B淋巴细胞转化刺激指数均明显低于正常对照组(P<0.05,0.01);高剂量玉竹多糖治疗组小鼠脾T淋巴细胞转化刺激指数和各剂量玉竹多糖治疗组小鼠脾B淋巴细胞转化刺激指数明显高于衰老模型组(P<0.05)。④各组小鼠脾脏中CD4 细胞数差异不明显(P>0.05);正常对照组和各剂量玉竹多糖治疗组小鼠脾脏中CD8 细胞数明显多于衰老模型组(P<0.05～0.01),CD4 /CD8 比值则明显低于衰老模型组(P<0.01)。结论:①玉竹多糖可能通过提高衰老小鼠血清超氧化物歧化酶活性,增强对自由基的清除能力,抑制脂质过氧化,降低丙二醛含量,从而减轻衰老小鼠机体组织损伤程度,以延缓衰老。②玉竹多糖对亚急性衰老小鼠免疫器官的功能具有一定的调节作用,可改善机体的免疫失衡状态,从而增强机体的细胞及体液免疫功能,延缓衰老。     

Possible pathophysiology of ketamine‐related cystitis and associated treatment strategies

Ketamine‐related cystitis is characterized by ketamine‐induced urinary frequency and bladder pain. It has become a serious problem in recent years. The most typical grossly pathological bladder change with ketamine related cystitis is a contracted bladder and bladder wall thickening. Ulcerative cystitis with an easily bleeding mucosa is a common cystoscopic finding. Microscopically, the urothelium is denuded and is infiltrated by inflammatory cells, such as mast cells and eosinophils. The pathogenesis of ketamine‐related cystitis is complicated and involves many different pathways. Past evidence suggests a direct toxic effect, bladder barrier dysfunction, neurogenic inflammation, immunoglobulin‐E‐mediated inflammation, overexpression of carcinogenic genes, abnormal apoptosis and nitric oxide synthase‐mediated inflammation contribute to the pathogenesis of ketamine‐related cystitis. The first step to managing ketamine‐related cystitis is always asking patients to cease ketamine. Medical treatment might be helpful in patients with early ketamine‐related cystitis and abstinence from ketamine. Several case studies showed that the intravesical installation of hyaluronic acid and intravesical injection of botulinum toxin type A were effective for symptom relief in selected patients. For patients with irreversible pathological change, such as contracted bladder, augmentation enterocystoplasty might be the only solution to increase bladder capacity and relieve intractable bladder pain.     

Changes in Fitness Components After a Four-Week Bicycle Tour

Three men and four women, ages 19 to 60, were measured on a battery of laboratory tests before and after a four-week bicycle tour to determine the effects of long-distance bicycling on physical fitness. There was no significant body weight change, although the average total fat weight loss was 1.4 kg. Total skinfold measures showed a significant reduction, and the waist girth reduced 2%. Trunk flexion showed significant improvement, and trunk extension and ankle flexibility showed a slight reduction. Maximal oxygen intake increased significantly (11%). The greatest improvement was the mean bicycle ergometer riding time and resistance to higher work loads (17%).