Chronic green tea extract supplementation reduces hemodialysis-enhanced production of hydrogen peroxide and hypochlorous acid, atherosclerotic factors, and proinflammatory cytokines

BACKGROUND: Oxidative stress increases in patients with end-stage renal disease and exaggerates the related comorbidities. OBJECTIVE: The aim of the study was to evaluate the effects of supplementation with decaffeinated green tea extract (catechins) on hemodialysis-induced reactive oxygen species, atherosclerotic disease risk factors, and proinflammatory cytokines. DESIGN: We enrolled 6 healthy subjects and 54 hemodialysis patients for the study. First, the pharmacokinetics of one oral dose of catechins was compared between healthy subjects (n = 6) and hemodialysis patients (n = 10). Second, in the 10 hemodialysis patients, we compared the antioxidant effects of 3 different doses (0, 455, and 910 mg) of oral catechins with that of oral vitamin C (500 mg) during a hemodialysis session. Third, the other 44 hemodialysis patients participated in a 7-mo interventional study, in which 30 patients received placebo throughout and 14 patients received catechins (455 mg/d) from the third to the fifth month. RESULTS: After one oral dose, the hemodialysis patients (n = 10) had later peaks and slower decay of plasma catechins than did the healthy subjects. In the 10 hemodialysis patients, catechin supplementation reduced hemodialysis-enhanced plasma hypochlorous acid activity more effectively than did placebo or vitamin C. Between treatments with 455 or 910 mg catechins, no significant difference was found in the reduction of plasma hypochlorous acid activity. Catechins also significantly reduced proinflammatory cytokine expression enhanced by hemodialysis. In the 7-mo interventional study, the 14 patients who received daily supplementation of catechins for 3 mo had less predialysis plasma hydrogen peroxide activity, lower hypochlorous acid activity, and lower phosphatidylcholine hydroperoxide, C-reactive protein, and proinflammatory cytokine concentrations than did the 30 hemodialysis patients who received placebo. CONCLUSION: Catechins reduce hemodialysis-induced production of hydrogen peroxide and hypochlorous acid, atherosclerotic disease risk factors, and proinflammation.     

重视老年重症患者的疾病复杂性

由于老化和多病、共病的存在,使得老年患者器官的储备能力下降,疾病复杂性增加,容易发生感染、营养不良、药物不良反应及器官功能损害,导致并发症及多器官功能障碍的发生率升高,病死率增加。因此,充分认识老年患者疾病的复杂性,积极采取应对措施,对改善老年危重患者的预后非常重要。     

自发性脑出血早期血肿增大

脑出血早期血肿增大严重影响患者的预后。文章对脑出血早期血肿增大的发生率、诊断标准、影响因素和防治方法进行了综述。     

胚胎干细胞源性树突状细胞对同源性神经前体细胞脑内移植耐受诱导

目的:观察脑缺血环境下胚胎干细胞源性树突状细胞(es DCs)能否诱导同源性神经前体细胞(NPCs)的移植耐受。方法:分别自129/svj p CX-e GFP ES-D3诱生NPCs及129/svj ES-D3诱生es DCs。线栓法制作MCAo模型SD大鼠并相应分为预处理组及对照组,术后1周预处理组经尾静脉注射es DCs而对照组注射PBS,两组动物在预处理1周后侧脑室注射NPCs,2周后(MCAo术后4周)免疫组化观察纹状区CD4+、CD8+、ED1+细胞的分布差异,MTT法观察颈部淋巴细胞增殖性(PI),逆转录PCR(RT-PCR)半定量局部IL-10、IFN-γmRNA表达差异,荧光显微镜观察GFP标记NPCs海马存活率。结果:预处理组大鼠,CD4+细胞浸润显著低于对照组(134.7±36.2 vs 198.8±59.6,P0.05),NPCs存活率显著高于对照组(P0.05),但预处理组对ED1+(298.8±75.9 vs 302.2±88.5)、CD8+(145.8±45.4 vs 134.3±39.0)细胞浸润、局部细胞因子mRNA IFN-γ(1.697±0.273 vs 1.829±0.250)、IL-10(1.147±0.260 vs 1.264±0.119)及外周淋巴细胞增长率(PI,1.245±0.211 vs1.331±0.235)无明显影响。结论:es DC可能通过降低局部CD4+细胞反应诱导针对同源性NPCs免疫耐受,尚无确切证据表明细胞因子途径参与该过程,确切的机理尚需更深入研究。     

阿魏酸钠对脑缺血大鼠海马CA1区神经细胞凋亡的影响

为了探讨脑缺血迟发性神经细胞死亡与细胞凋亡的关系以及阿魏酸钠的抗凋亡作用,利用大鼠全脑缺血及再灌流模型,TUNEL法原位标记DNA片段,观察用阿魏酸钠后海马CA_1区神经细胞凋亡改变.结果发现,脑缺血10min再灌流3d后海马CA_1区存在较明显的神经细胞凋亡现象,凋亡细胞分布与光镜下神经细胞迟发性死亡的病理改变相对应,缺血前用药组神经细胞凋亡数目较对照组明显减少,神经细胞迟发性改变减轻.而缺血后用药组未见显效.结果提示,脑缺血海马CA_1区神经细胞迟发性死亡可能是通过细胞凋亡完成,阿魏酸钠对脑缺血再灌流引起的海马CA_1区神经细胞凋亡具有一定的防止作用.     

Alleviation of brain edema by L-arginine following experimental subarachnoid hemorrhage in a rat model

Decreased levels of nitric oxide play a role in the development of cerebral ischemia secondary to subarachnoid hemorrhage (SAH). The protective effect of L-arginine on brain edema following SAH was investigated in this study. Rats were divided randomly into a sham-operated, a SAH+saline group and a SAH+L-arginine group. At different time points, brain water content was determined using the wet and dry weight compared method. Brain sodium content, potassium content and calcium content were detected using an atomic absorption spectral photometer. Somatosensory evoked potentials (SEP) were also detected. It was found that rat SAH models were successfully replicated. In the SAH+saline group, brain water and sodium content were significantly higher at 6 h and 24 h than those in the sham-operated group, while brain potassium content was statistically lower than that in the sham-operated group. Brain calcium content increased from 1 h to 24 h after induction of SAH. SEP latency progressively delayed. In the SAH+L-arginine group, increases in brain water content, sodium content and calcium content, as well as decreases in brain potassium content, were not as obvious as in the SAH+saline group. L-arginine partly prevented a delay in SEP latency. In conclusion, L-arginine, a substrate of nitric oxide synthesis, may relieve brain edema in rats with experimental SAH.     

L-arginine improves cerebral blood perfusion and vasomotion of microvessels following subarachnoid hemorrhage in rats

The purpose of this study is to investigate the effect of L-arginine (L-Arg) on cerebral blood perfusion and vasomotion (perfusion motion) in microvessels following subarachnoid hemorrhage (SAH). Rat noncraniotomy SAH models were used and animals were divided into sham-operated, saline-treated, and L-Arg-treated groups. L-Arg was injected intraperitoneally 30 minutes before the operation and repeated every 6 hours, with a single dose of 0.5 g/kg bw. Dynamic changes in regional cerebral blood flow (CBF) and vasomotion within 24 hours were measured using a laser Doppler flow-meter probe. Serum nitric oxide (nitrite/nitrate) and plasma endothelin-1 levels were also measured at different time points within 24 hours. Morphologic changes in neurons in the hippocampus CA1 region were examined. SAH gave rise to an immediate and persistent decrease in CBF in saline-treated rats. Abnormal vasomotions with decreased frequency and amplitude were observed. Serum nitric oxide decreased, while plasma endothelin-1 increased significantly. Neurons in the hippocampus CA1 region were severely damaged. The above pathological alterations in the L-Arg-treated group were alleviated. It was concluded that L-Arg, which increases cerebral blood perfusion and improves vasomotions of microvessels by enhancing nitric oxide levels and decreasing endothelin-1 levels in blood, exerts a protective effect on secondary cerebral ischemic injury following experimental SAH.     

抗原处理相关转运因子在小儿急性白血病患者中的表达及其临床意义

背景与目的:抗原处理相关转运因子(transporterassociatedwithantigenprocessing,TAP)参与免疫监视,因而可能与肿瘤发生有关。本文旨在探讨急性白血病TAP分子表达及其临床意义,探讨急性白血病的治疗策略。方法:采用RT-PCR检测34例初治急性淋巴细胞白血病(acutelymphoblasticleukemia,ALL)(初治组)、15例复发ALL(复发组)及20例急性髓系白血病(acutemyeloidleukemia,AML)患者骨髓中TAP亚单位TAP1和TAP2的表达。20例无全身性疾病外科住院患儿作为对照组。使用数码成像分析仪测定并计算扩增条带的相对于阳性内对照GAPDH的吸光度(A)值。结果:ALL初治组和ALL复发组的TAP1A值(分别为0.448±0.167和0.169±0.021)及TAP2的A值(分别为0.196±0.180和0.112±0.020)均低于对照组,P均<0.01;AML组TAP2的A值低于对照组(P<0.01);ALL复发组TAP1的A值低于ALL初治组,P<0.05;ALL初治组复发者(6/34)TAP1的A值(0.215±0.159)较持续完全缓解(constantcompleteremission,CCR)者低(24/34,0.462±0.189,P<0.05)。结论:小儿ALL和AML均存在TAP分子低表达,这可能促使白血病细胞逃避免疫监视;TAP1亚单位低表达可能与ALL的复发有关。     

Immunohistochemical characterization of intrathyroid lymphocytes in Graves' disease: Interstitial and intraepithelial populations

The phenotypic cell surface markers of the lymphocytes present in thyroid tissue from four patients with Graves' disease were quantitatively analyzed using the avidin-biotin immunoperoxidase technique. As control specimens, normal perinodular tissues from three patients who had benign thyroid nodules resected were also studied. In contrast to normal thyroid tissue, which contained very few T cells and no B cells, thyroid tissue of all four patients with Graves' disease contained a lymphocytic infiltrate, and this could be divided into two populations of lymphocytes. The first population was located in the follicular epithelium and expressed a cytotoxic-suppressor T cell marker (Leu2a). On the average, these cells were 4.2 times as numerous in Graves' tissues as in normal tissues (p < 0.05). Most of these cells did not express Leu1, a pan-T cell marker. The second population was found in the interstitial tissues, often within lymphoid aggregates, and 70 to 83 percent of the cells expressed Leu1. The majority of these cells expressed a helperinducer T cell marker, Leu3a; $\text{Leu3a}\text{Leu2a}$ ratios within aggregates ranged from 1.9 to 2.1. The number of B cells present was small, ranging from 5.8 to 12.1 percent of the interstitial lymphocytes. These findings are consistent with the involvement of both helperinducer and suppressor-cytotoxic T cells in a localized autoimmune reaction directed, at least in part, against the thyroid follicular epithelial cells.