缬沙坦对豚鼠心室肌细胞离子通道电流的影响

目的 观察血管紧张素Ⅱ受体拮抗剂对缬沙坦对豚鼠心室肌细胞离子通道电流的影响.方法 采用全细胞膜片钳技术的电压钳方法记录心室肌细胞的离子通道电流,包括L-Ca2+电流(L-ICa);延迟整流钾电流(IK)及内向整流钾电流(Ik1).结果 缬沙坦100μmol/L组的心室肌细胞IK峰值电流,为7.15±0.78(pA/pF),明显低于对照组(6.42±0.85(pA/pF),(P＜0.01)呈电压依赖性.缬沙坦100 μmol/L不影响心室肌细胞Ik1及L-ICa电流.结论 高浓度缬沙坦抑制心室肌细胞延迟外向钾电流,而不影响内向整流钾电流及内向L-ICa.提示缬沙坦抑制延迟外向钾电流,适度延长动作电位时程,从而延长心室有效不应期,有助于折返引起的快速室性心律失常的防治.类似Ⅲ类抗心律失常的作用.     

低场强磁共振FLAIR序列成像参数对脑脊液内钆剂检出影响的研究

目的探讨低场磁共振液体衰减反转恢复(FLAIR)序列T2WI成像参数的变化对脑脊液（CSF）内钆浓度检出的影响,为临床应用提供依据。方法分别采用新鲜熟蛋清模拟正常脑实质、浓度在0~8 mmol/L之间的钆喷替酸葡甲胺（Gd-DTPA）人工CSF溶液模拟CSF内不同的强化水平,使用0.35T机型,对样本行不同参数的FLAIR序列T2WI扫描,以明确各成像参数变化对CSF内钆浓度检出的影响。结果TEeff固定为150 ms,当TR从5000 ms延长到20000 ms（其TI随之从1600 ms延长至2800 ms）时,但其所能检出的最低钆浓度无变化,均约为0.0078 mmol/L。当TR和TI分别固定为7079 ms、2000 ms, TEeff从20 ms延长至280 ms时,其所能识别的钆剂浓度从0.0625 mmol/L降为0.002 mmol/L（P＜0.0001）。结论在0.35T场强的FLAIR序列T2W上,当TR超过5000 ms时,采用的TEeff越长,对CSF内钆剂的检出浓度越低,而延长TR/TI对其检出几乎无影响。     

白癜风患者皮肤组织液氧化-抗氧化物水平比较分析

目的探讨体内氧化-抗氧化状态与白癜风发病的关系。方法采用化学比色法,对24例白癜风患者白斑和非白斑(正常部位皮肤)以及10例健康者组织液进行过氧化氢(H2O2)、过氧化氢酶(CAT)和谷胱甘肽过氧化物酶(GSH-PX)检测。结果白癜风患者白斑H2O2水平(53.97±19.03)mmol/L明显高于健康组(28.98±22.81)mmol/L,进展期患者白斑H2O2水平(56.64±19.91)mmol/L明显高于非白斑(34.71±22.23)mmol/L,差异均有统计学意义(P均﹤0.01);白癜风白斑CAT水平(17.34±11.05)U/mL明显低于健康组(41.29±16.57)U/mL,差异有统计学意义(P﹤0.01),进展期白斑CAT水平(13.63±8.32)U/mL低于非白斑(35.72±16.14)U/mL,差异有统计学意义(P﹤0.05);进展期患者的白斑与非白斑处GSH-PX均高于健康组,差异有统计学意义(P均﹤0.05)。结论白癜风发病可能与H2O2增高、CAT降低等氧化-抗氧化失衡有关。     

尿微量蛋白诊断系统性红斑狼疮肾脏早期损伤

目的探讨早期诊断系统性红斑狼疮(SLE)肾脏损伤的方法.方法采用速率散射比浊法测定18例尿蛋白定性阴性和42例尿蛋白定性阳性SLE患者晨尿转铁蛋白(TF)、尿微量白蛋白(UMA)和免疫球蛋白G(IgG).结果正常对照组(n=45)晨尿TF为0.48±0.46mg/L,UMA为7.1±6.4mg/L和IgG为3.3±2.2mg/L.尿蛋白定性阴性SLE组(n=18)晨尿TF为2.6±3.2mg/L,UMA为50±64mg/L和IgG为15.2±10mg/L,该组患者TF、UMA和IgG均显著高于对照组(P＜0.01),三项指标联合检测在该组SLE中阳性率达89%.尿蛋白定性阳性组三项指标均极显著高于对照组,各项检出率均达100%.结论联合检测晨尿TF、UMA和IgG是诊断SLE肾脏早期损伤灵敏、可靠的实验指标.     

碱性成纤维细胞生长因子对皮肤萎缩性瘢痕中成纤维细胞的作用

目的探讨人碱性成纤维细胞生长因子(bFGF)对豚鼠皮肤萎缩性瘢痕中成纤维细胞的作用。方法取实验用成年豚鼠20只,于脊柱旁两侧A,B,C三处皮肤分别人工造成萎缩性瘢痕后,实验组在A处真皮层注射50μg/L的bFGF0.1mL,隔日1次,共4次;在C处真皮层注射同剂量生理盐水作阴性对照,B处不作任何处理做空白对照。术后第21天切取瘢痕组织行病理切片,应用鼠抗人ki-67单克隆抗体行免疫组化,显微镜下计算增殖成纤维细胞所占百分率。结果实验组、阴性对照组和空白对照组切口瘢痕增殖成纤维细胞百分率分别为(7.63±1.42)%,(0.98±0.33)%和(1.22±0.34)%。实验组增殖成纤维细胞百分率与阴性对照组及空白对照组比较显著增高,差异有统计学意义(P<0.05)。结论 bFGF可以促进豚鼠皮肤萎缩性瘢痕中的成纤维细胞增殖。     

过敏性紫癜患者血管内皮生长因子含量测定

目的　探讨血浆血管内皮生长因子 (VEGF)在过敏性紫癜中的变化和意义。方法　采用ELISA方法对2 6例过敏性紫癜患者 (急性期 12例和静止期 14例 )血浆VEGF浓度进行检测 ,并以 2 0例健康人血浆VEGF浓度作为对照。结果　 2 0例健康人血浆VEGF含量为 (63 .8± 5 9.3 ) μg/L ,急性期和静止期过敏性紫癜患者血浆VEGF含量分别为(5 5 7.3± 3 89.4) μg/L ,(13 5 .9± 80 .4) μg/L ,两组与健康人比较 ,差异均有高度显著性 (P <0 .0 1)。 结论　VEGF在过敏性紫癜的发病中可能起一定的作用。     

抗Dectin-1单克隆抗体在白念珠菌刺激小鼠腹腔巨噬细胞释放TNF-α和NO中的作用

目的探讨抗Dectin-1单克隆抗体在白念珠菌刺激小鼠腹腔巨噬细胞释放肿瘤坏死因子-α(TNF-α)和一氧化氮(NO)中的作用。方法①体外培养小鼠腹腔巨噬细胞,设置处理组(抗Dectin-1单克隆抗体组)、阴性对照组与空白对照组,分别给予灭活或活的白念珠菌刺激。②刺激1h,3h,6h,8h后用酶联免疫吸附试验检测各组分泌的TNF-α水平,③刺激6h后Griess法检测各组产生NO的水平。结果①刺激1h后抗体浓度为20μg/mL处理组分泌的TNF-α水平(79.82±11.74pg/mL)低于阴性对照组(105.15±12.36pg/mL)(P<0.05),3h,6h,8h后各浓度处理组TNF-α水平均低于阴性对照组(P均<0.01),且呈浓度依赖性;②6h后各浓度处理组NO水平(61.24±8.85μmol/L,45.36±3.92μmol/L,36.37±2.58μmol/L)均低于阴性对照组(87.65±9.17μmol/L)(P<0.05)。结论抗Dectin-1单克隆抗体在白念珠菌刺激小鼠巨噬细胞释放TNF-α和NO中发挥抑制作用。     

慢性荨麻疹伴甲状腺疾病的诊治方法探讨

目的探讨总结慢性荨麻疹伴自身免疫性甲状腺疾病的诊治方法。方法对我院2000年~2004年收治的8例确诊为慢性荨麻疹伴甲状腺自身免疫性疾病的临床资料进行回顾性分析。结果8例中,7例的FT3(25.81±3.50)pmol/L,FT4(60.56±6.20)pmol/L,均明显高于正常值,uTSH(0.116±0.012)m IU/L明显低于正常值,给予抗甲亢、手术和抗组胺等同时治疗后,荨麻疹与甲亢症状消失。结论对于原因不明的慢性荨麻疹患者,应作甲状腺功能检查。若伴甲状腺疾病者应同时给予抗组胺并针对甲状腺疾病进行治疗。     

肽聚糖对正常人表皮角质形成细胞分泌趋化因子的影响及Toll样受体2的作用

Objective To investigate the effect ofpeptidoglycan from Staphylococcus aureus on the release of several chemokines including intedeukin 8 (IL-8), regulated upon activation, normal T cell expressed and secreted (RANTES), macrophage-derived chemokine (MDC) by normal human epidermal keratinocytes (KCs) and the role of Toll-like receptor 2 (TLR2) in this process. Methods KCs were derived from the foreskin of a healthy boy and propagated. After 2 - 4 passages, KCs were collected and treated with various concentrations (3, 10, 30 and 100 mg/L) of peptidoglycan for 24 hours or with peptidoglycan of 100 mg/L for varying durations (3, 6, 12, 36 hours). A fi'action of KCs were pretreated with functional grade purified anti-TLR2 monoclonal antibody before the treatment with peptidoglycan of 100 mg/L. After additional 12-hour culture following the treatment, enzyme linked immunosorbent assay was used to detect the level of IL-8, RANTES and MDC in culture supernatants of KCs. Results KCs spontaneously released IL-8 and RANTES. Peptidoglycan increased the production of IL-8 but decreased that of RANTES by KCs. The levels of IL-8 were 209.96 ± 10.31 ng/L, 250.28 ± 9.52 ng/L, 285.11 ± 10.28 ng/L, 359.40 ± 6.93 ng/L in KCs treated with peptidoglycan of 3, 10, 30, 100 mg/L, respectively, compared to 135.41 ± 14.37 ng/L in untreated KCs (all P < 0.05). On the contrary, a significant decrement was seen in the secretion of RANTES by KCs treated with peptidoglycan of 10, 30, 100 mg/L compared with untreated KCs (110.72 ± 8.51 ng/L, 90.50 ±2.45 ng/L, 49.89 ± 13.74 ng/L vs 149.94 ± 18.71 ng/L, all P < 0.05). The monoclonal antibody to TLR-2 could markedly suppress the promotion of IL-8 production by peptidoglycan, but had no obvious influence on the inhibition of RANTES production by peptidoglycan. MDC could not be detected in the culture super-natants of KCs with or without peptidoglycan stimulation. Conclusion Peptidoglycan could inhibit RANTES secretion but induce IL-8 production by KCs likely via TLR2.     

肽聚糖对正常人表皮角质形成细胞分泌趋化因子的影响及Toll样受体2的作用

Objective To investigate the effect ofpeptidoglycan from Staphylococcus aureus on the release of several chemokines including intedeukin 8 (IL-8), regulated upon activation, normal T cell expressed and secreted (RANTES), macrophage-derived chemokine (MDC) by normal human epidermal keratinocytes (KCs) and the role of Toll-like receptor 2 (TLR2) in this process. Methods KCs were derived from the foreskin of a healthy boy and propagated. After 2 - 4 passages, KCs were collected and treated with various concentrations (3, 10, 30 and 100 mg/L) of peptidoglycan for 24 hours or with peptidoglycan of 100 mg/L for varying durations (3, 6, 12, 36 hours). A fi'action of KCs were pretreated with functional grade purified anti-TLR2 monoclonal antibody before the treatment with peptidoglycan of 100 mg/L. After additional 12-hour culture following the treatment, enzyme linked immunosorbent assay was used to detect the level of IL-8, RANTES and MDC in culture supernatants of KCs. Results KCs spontaneously released IL-8 and RANTES. Peptidoglycan increased the production of IL-8 but decreased that of RANTES by KCs. The levels of IL-8 were 209.96 ± 10.31 ng/L, 250.28 ± 9.52 ng/L, 285.11 ± 10.28 ng/L, 359.40 ± 6.93 ng/L in KCs treated with peptidoglycan of 3, 10, 30, 100 mg/L, respectively, compared to 135.41 ± 14.37 ng/L in untreated KCs (all P < 0.05). On the contrary, a significant decrement was seen in the secretion of RANTES by KCs treated with peptidoglycan of 10, 30, 100 mg/L compared with untreated KCs (110.72 ± 8.51 ng/L, 90.50 ±2.45 ng/L, 49.89 ± 13.74 ng/L vs 149.94 ± 18.71 ng/L, all P < 0.05). The monoclonal antibody to TLR-2 could markedly suppress the promotion of IL-8 production by peptidoglycan, but had no obvious influence on the inhibition of RANTES production by peptidoglycan. MDC could not be detected in the culture super-natants of KCs with or without peptidoglycan stimulation. Conclusion Peptidoglycan could inhibit RANTES secretion but induce IL-8 production by KCs likely via TLR2.     

外阴Pinkus纤维上皮瘤

报告1例外阴Pinkus纤维上皮瘤。患者女,71岁。左大阴唇外侧斑块10余年。皮肤科检查见左大阴唇外侧一2cm&#215;2cm灰黑色浸润性斑块．质地中等,边缘清楚,表面散在红色点状糜烂面,无明显渗液。皮损组织病理检查：棘层下方大量基底样细胞增生．增生的细胞呈条索状嵌入真皮增生的纤维间质中,彼此吻合形成网状,基底细胞胞核大而深染,胞质少,呈嗜碱性,表皮基膜完整,真皮内有以淋巴细胞为主的大量炎性细胞浸润。诊断：外阴Pinkus纤维上皮瘤。