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1.
毛囊无色素性黑素细胞可以作为皮肤黑素细胞的储库,给白癜风的治疗提供黑素细胞来源。人黑素细胞(melanocyte,MC)起源于胚胎神经嵴,在胚胎发育2~5周开始向表皮和毛囊移行。向表皮移行的黑素细胞最终定居在基底膜上,形成连续产生黑素的成熟黑素细胞;而向毛囊移行的黑素细胞则分为两种类型:一种是位于生长期毛囊毛母质和漏斗部具有黑素合成活性的黑素细胞;另一种是分布于生长期毛发外毛根鞘(Outer Root Sheath,ORS)中,无黑素合成活性、未活化的无色素性黑素细胞(amelanotic melanocyte,AMMC)。 相似文献
2.
喹诺酮类药物是一类通过抑制细菌的DNA旋转酶而起杀菌作用的合成抗菌药物。按抗菌性能不同分为一、二、三代,由于抗菌活性强、不易产生耐药性、毒副反应轻、抗菌谱广、生物利用度高、吸收分布好、半衰期长等特点被人们广泛应用。另外,此类药物注射时无皮试也被人们所接受。但随着人们越来越广泛的应用。也出现了较多的不良反应: 相似文献
3.
同种异体黑素细胞移植治疗白癜风 总被引:2,自引:2,他引:0
0 引言 白癜风患者免疫紊乱 ,黑素细胞 (melanocyte,MC)异体移植有可能不被排斥 ,治疗如成功将有很大临床前景 [1 ] .探索同种异体黑素细胞移植后的效果很有意义 .1 病例报告 女 ,2 7岁 ,确诊白癜风 (稳定期 ) ,患者皮肤自幼出现色素脱失斑 ,逐渐增多扩大 . 1996年外用“敏白灵”,前2 mo有效 . 1999- 0 7外用补骨酯酊 ,日服 5 g· L- 1 硫酸铜 10m L和中药 1剂 ,转移因子 4m L ,sc,1· 2 d- 1 .皮损缩小 ,4mo后稳定 .用健康男青年环切的包皮培养 MC,第 4代大约80 %融合时 ,用 2 .5 g· L- 1 胰酶消化 5 min,加入含 2 0 0 g·L- 1小… 相似文献
4.
1 临床资料1 .1 年龄与性别 全组 82例胃癌患者中 ,男性 38例 ,占 5 8.5 % ,女性 34例 ,占 41 .5 %。1 .2 组织学分类情况 82例胃癌患者均有病理组织活检报告证实。组织学分类以腺癌发病率最高 ,其中低分化腺癌占腺癌的6 3.6 3% ,粘液细胞癌发病率居第二 ,未分化癌发病率低。各年龄组与胃癌组织学分类关系见表 2。表 1 82例胃癌患者的年龄、性别年龄 2 0~ 2 930~ 394 0~ 4 950~ 596 0~ 6 9>70合计男例数 0 7 6 10 16 94 8女例数 37 0 12 84 34表 2 82例胃癌组织学分类情况组织学类 型2 0~ 2 9例30~ 39例4 0~ 4 9例50~ 5… 相似文献
5.
目的 探究产妇宫颈液内炎症因子及菌群水平与早产的相关性.方法 选取2017年10月-2019年10月我院收治的年龄20-40岁早产孕妇100例,早产孕妇(孕周<37周+0天)和足月孕妇各50例.孕妇分娩42天后,采集宫颈分泌物,和灌洗液.通过16S rRNA测序检测样本菌群多样性,Luminex多重分析检测宫颈灌洗中炎... 相似文献
6.
7.
本组25例。男19例,女6例。年龄44—73岁。均因无诱因持续黑便或呕血而入院,无吞咽困难。其中7例伴有上腹疼痛不适,入院后经X线钡餐检查诊断为贯门癌2例,急诊内窥镜检查诊断为贲门癌11例。 相似文献
8.
BACKGROUND: Recent studies have demonstrated that phenolic alkaloids from Menispermum dauricum (PAMD) can protect the heart and brain from ischemia/reperfusion injury, and promote neuron survival by inhibiting neuronal Bax and upregulating Bcl-2 expression following ischemia/reperfusion.
OBJECTIVE: To investigate the neuroprotective effects of PAMD versus exogenous melatonin against ischemia/reperfusion injury.
DESIGN, TIME AND SETTING: Observation and comparison experiments at a cellular level were performed at the Department of Biochemistry and Molecular Biology, Tongji Medical College of Huazhong University of Science and Technology between February 2007 and February 2008.
MATERIALS: PAMD (95% purity) was provided by Kunming Institute of Botany, Chinese Academy of Sciences; melatonin was provided by Sigma, USA.
METHODS: N2a mouse neuroblastoma cells were cultured in vitro deprived of glucose, serum and oxygen for 90 minutes, then cultured in normal medium containing different concentrations of PAMD (0.1, 1.0, 10 mg/L) or melatonin (1, 10, and 100 μmol/L). Cells cultured in normal conditions served as a control.
MAIN OUTCOME MEASURES: The culture solution was collected to determine the content of ex- citatory neurotransmitters such as glutamic acid and aspartic acid; cell viability was detected by MTT methods; reactive oxygen species production was determined by fluorescence spectroscopy; mito- chondrial transmembrane potential (?Ψm) was detected by laser confocal scanning; cytochrome C was measured by western blotting; and caspase-3 activity was determined by visible spectropho- tometry.
RESULTS: Melatonin and PAMD both promoted oxygen-glucose-serum deprivation-mediated N2a cell survival (P 〈 0.01) and inhibited glutamic acid release (P 〈 0.01), but melatonin did not inhibit aspartic acid production. The protective effects were the strongest using melatonin 100 μmol/L and PAMD 10 mg/L, so subsequent experiments were the performed at those doses. Although PAMD could no longer maintain mitochondrial transmembrane potential 6 hours after reperfusion, its in- hibitory effects on cytochrome C release from mitochondria and scavengers of reactive oxygen species were stronger than those of melatonin (P 〈 0.01). However, its inhibitory effect on caspase-3 activity was weaker than that of melatonin: PAMD could inhibit caspase-3 activity 12 hours after reperfusion (P 〈 0.01), but melatonin inhibited caspase-3 activity 28 hours after reperfusion (P 〈 0.01).
CONCLUSION: The results show that melatonin and PAMD have neuroprotective effects, but that the mechanisms are varied. Melatonin can maintain mitochondrial transmembrane potential, but its inhibitory effects on cytochrome C release, caspase-3 activity, and reactive oxygen species scav-enging are different from those of PAMD. 相似文献
OBJECTIVE: To investigate the neuroprotective effects of PAMD versus exogenous melatonin against ischemia/reperfusion injury.
DESIGN, TIME AND SETTING: Observation and comparison experiments at a cellular level were performed at the Department of Biochemistry and Molecular Biology, Tongji Medical College of Huazhong University of Science and Technology between February 2007 and February 2008.
MATERIALS: PAMD (95% purity) was provided by Kunming Institute of Botany, Chinese Academy of Sciences; melatonin was provided by Sigma, USA.
METHODS: N2a mouse neuroblastoma cells were cultured in vitro deprived of glucose, serum and oxygen for 90 minutes, then cultured in normal medium containing different concentrations of PAMD (0.1, 1.0, 10 mg/L) or melatonin (1, 10, and 100 μmol/L). Cells cultured in normal conditions served as a control.
MAIN OUTCOME MEASURES: The culture solution was collected to determine the content of ex- citatory neurotransmitters such as glutamic acid and aspartic acid; cell viability was detected by MTT methods; reactive oxygen species production was determined by fluorescence spectroscopy; mito- chondrial transmembrane potential (?Ψm) was detected by laser confocal scanning; cytochrome C was measured by western blotting; and caspase-3 activity was determined by visible spectropho- tometry.
RESULTS: Melatonin and PAMD both promoted oxygen-glucose-serum deprivation-mediated N2a cell survival (P 〈 0.01) and inhibited glutamic acid release (P 〈 0.01), but melatonin did not inhibit aspartic acid production. The protective effects were the strongest using melatonin 100 μmol/L and PAMD 10 mg/L, so subsequent experiments were the performed at those doses. Although PAMD could no longer maintain mitochondrial transmembrane potential 6 hours after reperfusion, its in- hibitory effects on cytochrome C release from mitochondria and scavengers of reactive oxygen species were stronger than those of melatonin (P 〈 0.01). However, its inhibitory effect on caspase-3 activity was weaker than that of melatonin: PAMD could inhibit caspase-3 activity 12 hours after reperfusion (P 〈 0.01), but melatonin inhibited caspase-3 activity 28 hours after reperfusion (P 〈 0.01).
CONCLUSION: The results show that melatonin and PAMD have neuroprotective effects, but that the mechanisms are varied. Melatonin can maintain mitochondrial transmembrane potential, but its inhibitory effects on cytochrome C release, caspase-3 activity, and reactive oxygen species scav-enging are different from those of PAMD. 相似文献
9.
目的:探讨神经科危重症患者发生护理意外的危险因素,观察护理干预疗效。方法纳入神经科危重症患者275例,对这些患者的基本信息进行记录存档,并就意外危险因素进行调查。2013年5月前入院的患者137例作为对照组,接受常规护理,其中男86例,女51例,2013年5月起入院的患者138例作为观察组,在常规护理的基础上就危险因素进行特定护理干预,其中男92例,女46例,观察二组患者意外发生情况,判断护理干预对神经科危重症患者发生意外的效果。结果神经科危重症患者发生护理意外的危险因素有活动能力(OR =3.54,P=0.000<0.01)、意识状态(OR =6.12,P=0.000<0.01)、吞咽能力(OR =4.82,P=0.016<0.05)、颅内压(OR =2.36,P=0.024<0.05);观察组较对照组发生护理意外的几率明显降低。结论针对神经科危重症患者发生护理意外的危险因素如活动能力、意识状态、吞咽能力、颅内压开展护理干预具有明显的临床效果和重要的意义。 相似文献
10.
目的评价利拉鲁肽与二甲双胍联合用药对减重治疗失败的多囊卵巢综合征(PCOS)不孕患者临床妊娠率及累计妊娠率的影响,同时评价联合用药对卵母细胞和胚胎质量、减重以及代谢和内分泌指数的影响。方法选取2017年6月至2018年12月间在我院治疗的186例减重失败的PCOS肥胖患者。186例患者随机分为联合用药组(联合组)与二甲双胍组,每组93例。二甲双胍组服用二甲双胍片治疗,联合组在二甲双胍组治疗的基础上,加用利拉鲁肽皮下注射治疗,初始剂量为0.6 mg,1次/d,3 d后增加至1.2 mg。所有患者均治疗12周。治疗的同时对所有患者进行积极生活方式干预,干预措施包括控制食物热量及每天进行至少30 min中等强度的身体活动,在药物治疗1个月后给予患者体外受精(IVF)手术,对患者进行12个月随访,记录患者的自然妊娠情况。比较基线期与治疗后患者的人体测量参数、内分泌参数、体脂分布参数及IVF结果。结果治疗后,联合组与二甲双胍组患者体重均较基线期显著降低(t=2.65,P<0.01;t=4.05,P<0.01)。二甲双胍组和联合组患者体重分别下降(5.98±5.03)kg和(7.52±3.90)kg。与二甲双胍组比较,联合组患者体重较基线降低值显著提高(t=2.33,P=0.02)。2组患者内脏脂肪含量、体积和面积均较基线期显著降低(P<0.05)。与二甲双胍组比较,联合组的临床妊娠率(84.0%vs.28.3%,χ^2=30.42,P<0.01)和累计妊娠率(68.8%vs.37.6%,χ^2=18.16,P<0.01)显著提高。两组患者恶心与腹泻发生率比较差异无统计学意义(χ^2=1.56,P=0.21;χ^2=0.58,P=0.45)。结论低剂量利拉鲁肽联合二甲双胍对超重不孕的PCOS患者进行短期干预,可以显著提高患者的临床妊娠率和累计妊娠率,并显著降低PCOS患者的体重、内脏脂肪组织,没有显著增加患者的药物不良反应。 相似文献