白芍总苷对纤丝状Aβ42诱导脑内炎症因子及磷酸化MAPK信号分子表达的影响

目的:观察Aβ42沉积对大脑海马炎症因子和磷酸化MAPK信号分子表达的影响及白芍总苷(TGP)的干预作用.方法:选用12周龄雌性SD大鼠,随机分为6组,应用立体定位注射技术一次性大脑海马定位注射纤丝状Aβ42复制AD病理模型,并给予TGP(0.822,0.411 g·Kg-1·d-1)进行干预,以西乐葆(0.183 g·kg-1·d-1)为对照,用免疫组化方法显示炎症因子及磷酸化MAPK通路信号分子表达情况,并用分析软件进行图像分析.结果:与对照组相比,AD模型组的IL-1β,IL-6及p-p38,p-JNK,p-MEK3/6的阳性细胞染色面积均增加而染色强度值均下降(蛋白表达量与染色强度值成反比);与AD模型组相比,各给药组的IL-1β,IL-6阳性染色面积均下降;TGP高、低剂量组的IL-1β,IL-6,染色强度值均明显增加,西乐葆对照组的IL-1β染色强度值亦增加,而IL-6染色强度值仅表现为增加的趋势.另外,与AD模型组比较,除了TGP低剂量组的p-JNK表现为降低的趋势外,其余各给药组的p-p38,p-JNK,p-MEK阳性染色面积均明显下降;而除了TGP高剂量组的p-p38及西乐葆组的p-MEK3/6无明显变化外,其余各给药组的p-p38,p-JNK,p-MEK3/6染色强度值均明显增加.结论:Aβ42沉积可诱导大脑海马炎症反应和炎症细胞因子IL-1β,IL-6及磷酸化MAPK信号分子p-p38,p-JNK,p-M EK3/6等的过表达,而抑制IL-1β,IL-6及磷酸化MAPK信号分子的过表达,从而抑制AD模型脑内炎症,可能是TGP拮抗AD的主要作用机制.     

白芍总苷对Aβ42沉积诱导脑内炎症因子及CD45、磷酸化tau蛋白表达的影响

目的:观察Aβ42沉积对大脑海马CD45、炎症因子和磷酸化tau蛋白(p-tau)表达的影响及白芍总苷(TGP)的干预作用。方法:应用立体定位注射技术对12周龄雌性SD大鼠1次性大脑海马定位注射纤丝状A 42复制AD病理模型,并给予白芍总苷进行干预,用免疫组化方法显示CD45、炎症因子及p-tau表达情况,并用分析软件进行图像分析。结果:与正常对照组相比,AD模型组的CD45、IL-1β、IL-6及p-tau阳性细胞染色面积(染色面积与染色的阳性细胞数成正比)均增加而染色强度值均下降(蛋白表达量与染色强度值成反比);与AD模型组比较,各给药组的IL-1β、IL-6染色面积均下降;除西乐葆对照组的IL-6染色强度值仅表现为增加的趋势外,其余各给药组的IL-1β、IL-6染色强度值均增加。另外,与AD模型组相比,白芍总苷高剂量组和西乐葆组的p-tau、CD45染色面积均下降而染色强度值均升高,TGP低剂量组的p-tau、CD45染色面积则有下降的趋势而染色强度值则有升高的趋势。结论:Aβ42沉积可诱导大脑海马炎症反应、小胶质细胞激活和炎症细胞因子过表达以及tau蛋白的过度磷酸化,而抑制小胶质细胞的激活及炎症细胞因子的过表达,从而抑制脑内炎症及tau蛋白的过度磷酸化,可能是TGP拮抗AD的主要作用机制。     

补益脾胃元气方药对Aβ诱导的海马神经元JNK及p38MAPK信号通路相关蛋白及其磷酸化表达的影响

目的:通过研究补益脾胃元气类方药人参、大补元煎、洗心汤对β淀粉样蛋白(β-amyloid protein,Aβ)诱导的海马神经元JNK(c-Jun N-terminal kinase,JNK)及p38MAPK(p38mitogen-activated protein kinase,p38MAPK)信号通路的影响,探讨补益脾胃元气方对Aβ诱导的海马神经元损伤的保护作用及防治阿尔茨海默病(Alzheimer'sdisease,AD)的可能机制。方法:通过寡聚肽Aβ_(1～42)诱导海马神经元损伤模拟AD细胞模型;分别以蒸馏水、人参、洗心汤、大补元煎颗粒剂溶液对新西兰家兔灌胃给药,14天后抽取各组脑脊液,与终浓度为25μmol/L的寡聚肽Aβ_(1～42)单独或共同作用于原代海马神经元48小时,分别检测模型组、正常脑脊液对照组、安理申组、人参组、大补元煎组、洗心汤组海马神经元JNK和磷酸化JNK(phosphorylated JNK,p-JNK)及p-38MAPK和磷酸化p38MAPK(phosphorylated p38,p-p38MAPK)的表达水平。结果:对培养至7～8天的成熟原代海马神经元,进行神经元树突标志物微管相关蛋白-MAP2标记,结果显示原代海马神经元在所培养的总细胞中所占比例达到95%以上。免疫荧光实验显示,人参、大补元煎及洗心汤三组补益脾胃元气方药中p-JNK、p-p38MAPK的表达明显降低(P0.05),蛋白印迹实验中三组补益脾胃元气方药中p-JNK、p-p38MAPK的表达同样降低(P0.05)。结论:补益脾胃元气方药可通过抑制JNK和p38MAPK信号通路中关键信号分子p-JNK、p-p38MAPK蛋白的表达,有效拮抗Aβ_(1～42)神经毒性,抑制由Aβ_(1～42)诱导的JNK和p38MAPK信号通路激活所引发的炎症信号通路活性增强及细胞损伤凋亡发生,起到神经保护作用。     

苦参颗粒对兔耳痤疮模型P38MAPK/ERK相关信号通路的影响

目的:探讨苦参颗粒溶液对兔耳痤疮模型P38MAPK/ERK相关信号通路的影响及其治疗效果。方法:家兔除空白对照组外,其余各组用kligman法建立兔耳痤疮模型,于造模成功后,予模型组、夫西地酸乳膏组、苦参颗粒100、200、400mg/ml组分别涂敷生理盐水和相应药物,每日一次,连续14d。通过HE染色显微镜下判断其治疗效果;免疫组化检测TNF-α、IL-6、IL-8蛋白的表达;Western blot法检测p-p38MAPK、p-ERK、p38MAPK、ERK蛋白表达;ELISA测定法p-p38MAPK、p-ERK蛋白的含量。结果:与空白组比较,模型组TNF-α、IL-6、IL-8 MOD值和p-p38MAPK、p-ERK表达明显升高,p38MAPK、ERK表达明显下降;与模型组相比,给药各组TNF-α、IL-6和IL-8 MOD值和p-p38MAPK、p-ERK表达明显降低,p38MAPK、ERK表达明显增加。结论:苦参颗粒溶液能降低TNF-α、IL-6、IL-8含量,下调p-p38MAPK、p-ERK蛋白表达,上调p38MAPK、ERK蛋白表达,干预ERK、p38MAPK通路,从而干预痤疮的形成,对痤疮有疗效。     

鲜枸杞子提取物通过p38 MAPK信号通路抑制人肝癌细胞HepG2诱导小鼠恶病质的作用及机制

目的:探讨鲜枸杞子提取物(LBL)对人类肝癌细胞系HepG2诱导的小鼠恶病质模型的作用及其相关机制研究。方法:小鼠分为正常组,恶病质模型组,LBL低剂量组(LBL 5 mg·kg~(-1)),LBL高剂量组(LBL 25 mg·kg~(-1))。采用人肝癌细胞系HepG2成功建立小鼠恶病质模型,待小鼠的体质量明显下降时,连续灌喂生理盐水或不同剂量LBL 28 d后,记录各组小鼠的体质量,酶联免疫吸附测定(enzyme linked immunosorbent assay,ELISA)检测血浆肌酸激酶(creatine kinase,CK),促炎因子白细胞介素-1β(interleukin-1β,IL-1β),白细胞介素-6(interleukin-6,IL-6),肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)的水平,采用免疫组织化学检测小鼠肌肉降解水平及p38丝裂原活化蛋白激酶(p38 mitogen-activated protein kinase,p38 MAPK)的表达,蛋白免疫印迹法(Western blot)检测磷酸化p38 MAPK(phospho-p38 mitogen-activated protein kinase,p-p38 MAPK),炎症信号通路核转录因子-κB(nuclear factorκB,NF-κB)的表达。结果:与恶病质模型组比较,LBL低、高剂量组小鼠体质量明显下降(P0.05,P0.01),肌肉降解程度明显抑制(P0.05),CK水平显著下降(P0.01);LBL低、高剂量组小鼠血浆IL-1β,IL-6,TNF-α表达水平明显下调(P0.05,P0.01)。免疫组织化学结果显示,LBL低、高剂量组p38 MAPK蛋白表达降低(P0.05),Western blot结果进一步证实p-p38 MAPK,NF-κB蛋白表达降低(P0.01)。与LBL低剂量组比较,LBL高剂量组血浆肌酸激酶,p38 MAPK,p-p38 MAPK,NF-κB蛋白表达明显降低(P0.05,P0.01)。结论:鲜枸杞子提取物能够抑制人类肝癌细胞系HepG2诱导的小鼠恶病质模型的恶病质的进程,其作用机制可能与其下调促炎因子IL-1β,IL-6,TNF-α,从而抑制p38 MAPK,p-p38 MAPK,NF-κB的表达相关。     

p38丝裂原活化蛋白激酶在大鼠肾小管上皮细胞转分化中的作用及大黄素的干预研究

目的探讨p38丝裂原活化蛋白激酶(p38MAPK)在IL-1β诱导大鼠肾小管上皮细胞-肌成纤维细胞转分化中的作用及大黄素的干预效应。方法将体外培养的正常大鼠肾小管上皮细胞株(NRK52E)分为对照组、IL-1β诱导组、IL-1β+SB 203580组和IL-1β+大黄素组。培养48 h后用倒置相差显微镜观察细胞形态,细胞免疫化学染色检测α-平滑肌肌动蛋白(α-SMA)、角蛋白(CK)、p38MAPK及磷酸化-p38MAPK(p-p38MAPK)的表达情况。结果IL-1β可诱导部分NRK52E由卵圆形转变为梭形,同时CK表达减弱,α-SMA、p38MAPK及p-p38MAPK的表达增强。SB 203580阻断p38MAPK通路后可显著抑制IL-1β诱导的细胞形态改变,同时上调CK表达,下调α-SMA及p-p38MAPK的表达。大黄素对IL-1β诱导的细胞形态改变及α-SMA、p38MAPK及p-p38MAPK的表达也有明显抑制作用,其抑制作用与SB 203580的阻断作用相比无显著性差异。结论p38MAPK参与介导IL-1β诱导大鼠肾小管上皮细胞-肌成纤维细胞转分化过程,大黄素可通过干扰p38MAPK信号通路抑制大鼠肾小管上皮细胞转分化。     

养阴润目丸对干眼症大鼠结膜上皮细胞IL-1β、ICAM-1、p-p38MAPK的影响

目的:探讨养阴润目丸对干眼症大鼠结膜上皮细胞白介素-1β(IL-1β)、细胞间黏附分子-1(ICAM-1)、磷酸化-丝裂原活化蛋白激酶p38抗体(p-p38MAPK)的影响。方法:将健康雄性SD大鼠60只随机分成正常组、假手术组、养阴润目丸组、新泪然组、模型组,分别用A、B、C、D、E组表示,每组12只。A组不作处理;B组只切开阴囊,不切除睾丸;C、D、E 3组切除睾丸及附睾制备干眼症大鼠模型。造模成功7d后,各组分别给药治疗。采用Western blot方法观察给药3个月后干眼症大鼠结膜上皮细胞IL-1β、ICAM-1、p-p38MAPK的表达。结果:A、B组结膜上皮细胞中IL-1β、ICAM-1、pp38MAPK蛋白含量低,即无阳性表达,而C、D、E组结膜上皮细胞中IL-1β、ICAM-1、p-p38MAPK蛋白含量较多,呈阳性表达;C、D组结膜上皮细胞中IL-1β、ICAM-1、p-p38MAPK蛋白含量明显低于E组(P0.01);C、D组两组间差异不显著(P0.05)。结论:养阴润目丸能够下调干眼症大鼠结膜上皮细胞中IL-1β、ICAM-1、p-p38MAPK蛋白含量;干眼症的发病机制与炎症及p38MAPK信号通路相关。     

电针通过p38 MAPK和STAT3信号通路抑制糖尿病认知障碍大鼠促炎性细胞因子生成改善学习记忆

目的:观察电针对糖尿病认知障碍大鼠海马及前额叶皮层细胞因子的影响,探讨p38丝裂原活化蛋白激酶(p38 MAPK)和信号转导及转录激活子3(STAT3)在电针改善学习记忆中的作用。方法:SD大鼠随机分为正常组10只,造模组90只,造模组大鼠以高脂高糖饲料喂养1个月后,采用小剂量链脲佐菌素腹腔注射法建立糖尿病模型。通过Morris水迷宫实验筛选出糖尿病模型大鼠中出现认知障碍的大鼠20只,随机分为模型组和电针组各10只。电针组大鼠予针刺"后三里""内庭"及"胰俞",其中"后三里"和"内庭"予以电针干预,每周6次,每次20 min,连续治疗4周。针刺干预结束后,检测各组大鼠随机血糖值;应用Morris水迷宫实验测定大鼠学习与记忆能力;采用Western blot及实时荧光定量PCR法检测各组大鼠海马及前额叶皮层中白细胞介素(IL)-6、IL-1β、肿瘤坏死因子(TNF)-α、p38 MAPK、磷酸化(p)-p38 MAPK、STAT3和p-STAT3蛋白及mRNA相对表达量;采用免疫荧光法检测各组大鼠海马及前额叶皮层中p38 MAPK和STAT3表达。结果:实验结束时,模型组大鼠随机血糖值较正常组明显升高(P0.001);与模型组比较,电针组大鼠随机血糖值明显降低(P0.05)。模型组大鼠较正常组大鼠水迷宫逃避潜伏期明显延长(P0.01);与模型组比较,电针组大鼠水迷宫逃避潜伏期明显缩短(P0.05)。模型组大鼠海马及前额叶皮层IL-6、IL-1β、TNF-α、p38 MAPK、p-p38 MAPK、STAT3和p-STAT3蛋白及mRNA表达较正常组明显升高(P0.001);与模型组比较,电针组大鼠海马及前额叶皮层IL-6、IL-1β、TNF-α、p38 MAPK、p-p38 MAPK、STAT3和p-STAT3蛋白及mRNA表达明显降低(P0.001)。模型组大鼠海马及前额叶皮层中p38 MAPK和STAT3的平均荧光强度值明显高于正常组(P0.001);与模型组比较,电针组大鼠海马及前额叶皮层中p38 MAPK、STAT3的平均荧光强度值明显降低(P0.001,P0.05)。结论:电针可以抑制糖尿病认知障碍大鼠海马和前额叶皮层中促炎性细胞因子的过量产生,p38 MAPK和STAT3信号通路可能参与其中。     

电针“内关”对心肌肥厚模型大鼠p38丝裂原激活蛋白激酶信号通路的影响

目的:探讨电针“内关”穴治疗心肌肥厚的作用机制.方法:SD大鼠40只用随机数字表法分为正常组、模型组、模型+p38抑制剂组、模型十电针组,每组10只.采用皮下注射盐酸异丙肾上腺素3 mg/(kg·d)建立心肌肥厚大鼠模型,模型+p38抑制剂组在造模基础上每日皮下注射0.3 mg/kg p38丝裂原激活蛋白激酶(p38 MAPK)特异性抑制剂SB 203580;模型十电针组电针“内关”穴,采用连续波,频率2 Hz,强度1 mA,通电20 min,1次/d,共14 d.其他两组不予治疗干预.放射免疫法技术检测心肌组织肿瘤坏死因子-α(TNF-α)和白细胞介素-1β(IL-1β)含量,免疫印迹法检测p38MAPK、磷酸化p38 MAPK(p-p38 MAPK)含量.观察电针“内关”穴对TNF-α和IL-1β、p38 MAPK、p-p38 MAPK的影响.结果:与正常组大鼠比较,模型组大鼠TNF-α和IL-1β、p38 MAPK、p-p38 MAPK均显著升高(均P＜0.01);经抑制剂和电针处理后,模型+p38抑制剂组和模型十电针组大鼠TNF-α、IL-1β、p38 MAPK、p-p38 MAPK均明显降低,与模型组比较差异有统计学意义(均P＜0.05),与正常组比较差异亦有统计学意义(P＜0.05,P＜0.01);模型+p38抑制剂组和模型十电针组之间比较差异无统计学意义(P＞0.05).结论:电针“内关”可以明显抑制心肌肥厚p38 MAPK的磷酸化,这种保护作用可能通过抑制TNF-α、IL-1β等炎性因子的表达实现对p38 MAPK信号通路调节.     

山香圆总黄酮对LPS诱导的RAW264.7细胞MAPK信号通路的影响

目的观察山香圆总黄酮对脂多糖诱导的RAW264.7细胞MAPK信号通路的影响。方法采用脂多糖刺激RAW264.7细胞制备炎症模型;CCK-8法测定细胞活力;ELISA法检测TNF-α、IL-1β、IL-6的分泌量;western blot法检测ERK1/2、JNK和p38蛋白的磷酸化水平。结果低于400μg/mL的山香圆总黄酮对RAW264.7细胞生长无影响;山香圆总黄酮各剂量组均能抑制p-ERK1/2、p-JNK、p-p38蛋白的表达以及TNF-α、IL-1β、IL-6的分泌,中、高剂量组呈显著性抑制(P0.05,P0.01)。结论山香圆总黄酮能通过抑制ERK1/2、JNK、p38磷酸化水平,降低TNF-α、IL-1β、IL-6的分泌,发挥抗炎作用。     

基于ICP-MS法的加味左金丸中无机元素分析

目的 通过电感耦合等离子体质谱（inductively coupled plasma mass spectrometry,ICP-MS）法建立加味左金丸中Cd、Pb、As、Hg、Co、V、Ni、Cu、Li、Sb、Ba、Mo、Sn、Cr、Na、Mg、Al、Ca、Ti、Mn、Fe、Zn、Ga、Se、Sr、Tl共计26种无机元素的测定方法。方法 加味左金丸通过微波消解法处理后,根据相对分子质量的大小选择内标物,其中⁷Li、²³Na、²⁴Mg、²⁷Al、⁴⁰Ca、⁴⁸Ti、⁵¹V、⁵²Cr、⁵⁵Mn、⁵⁶Fe、⁵⁸Ni、⁵⁹Co、⁶³Cu、⁶⁶Zn、⁷⁰Ga、⁷⁵As、⁷⁷Se、⁸⁶Sr以⁷²Ge作为内标;⁹⁵Mo、¹¹⁴Cd、¹¹⁸Sn、¹²¹Sb、¹³⁷Ba以¹¹⁵In作为内标;²⁰²Hg、²⁰⁵Tl、²⁰⁸Pb以²⁰⁹Bi作为内标。对标准品溶液、空白溶液与供试品溶液进行分析,采用标准曲线法进行定量分析。通过ICP-MS法进行测定。结果 26种无机元素线性的相关系数r ≥ 0.999 6,检出限为0.001~1.500μg/L,定量限为0.01~5.00 μg/L,精密度与重复性试验的RSD均小于5%,平均回收率在82.64%~106.44%,RSD均小于5%。对3个厂家的12批样品进行了测定,26种元素的含量差异较大,其中Na、Mg、Ca、Fe 4种元素的含量比较高,均大于500 μg/g,Cd、Pb、As、Hg、Co、Li、Sb、Mo、Sn、Cr、Se、Tl的含量比较低,均小于1 μg/g。由结果可知,人体的常量元素,如Na、Mg、Ca的含量比较高,Cd、Pb、As、Hg等有害元素含量比较低。根据《中国药典》2020年版一部的要求,本品中Cd、Pb、As、Hg与Cu均符合规定。结论 该方法快速、准确,可以用于加味左金丸中无机元素的测定。     

Erstaunliches Ergebnis einer Schädelakupunktur nach Yamamoto bei Hemihypsarrhythmie rechts

A girl, three and a half years old at the respective date, premature in 25th week of gestation, had been presented. On day three after birth, she had had a IVH III° right and left with severe involvement of parenchyma and other multiple complications, e. a. infant respiratory distress syndrome up to the 42nd day postpartum, and epileptic attacks with apnoeic events.     

七味红花殊胜散对缺血再灌注肝损伤的保护作用

目的::研究七味红花殊胜敬对缺血再灌注肝损伤的保护作用.方法:在大鼠肝缺血再灌注模型上,观察七味红花殊胜散对缺血再灌注肝损伤引起的血清丙二醛(MDA)、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、一氧化氮(NO)含量的变化.结果:七味红花殊胜散对大鼠血清MDA、SOD、GSH与再灌组比较有明显差异(P<0.05),NO含量与再灌组比较有明显差异(P<0.05).结论:七味红花殊胜散对大鼠急性缺血再灌注肝损伤具有保护作用.     

Methodology of Canine/Feline YNSA and Tail Acupuncture

BackgroundYamamoto New Scalp Acupuncture (YNSA) is a well-known acupuncture system for human patients which was developed by Dr. Yamamoto.ObjectiveMy aim was to transpose the human YNSA map onto canines and felines.MethodI started researching a canine/feline YNSA map in 2002. I investigated approximately 3,000 canines and felines for YNSA and 2,500 for Tail Acupuncture. The ratio of canines and felines was 6 to 4. I researched and found all the equivalent points by palpating animal patients on the basis of an exact Neck Diagnosis.ResultsI nearly completed the map in 2006. The points in the occipital region are incomplete and my research is still in progress. In the process of researching canine/feline YNSA points, I accidentally found the other microsystems around the tail and named it “Tail Acupuncture”.ConclusionsYNSA and Tail Acupuncture are acupuncture systems utilizing microsystems and support each other in canines and felines. The merits of YNSA and Tail Acupuncture are 1) immediate effects, such as in cases of lameness, 2) simplicity in finding the exact points to treat and 3) the scalp and the tail can be utilized separately or together as treatment zones, according to the situation.     

Chinesische Orthopädie: Teil 1: Die Zukunft der Akupunktur in der Postmoderne

The locomotor system is one of the major fields of application for acupuncture. The results of the large acupuncture studies funded by German Health Insurances from 2000 until 2006 are impressive and repressive: they restrict acupuncture application by allocation of reimbursement and create the necessity of reorientation, since acupuncture can neither be adequately described nor prescribed solely on the basis of disease entities. Regarding these disease entities, it seems rather necessary to analyse the layers of problems and formulate a hierarchy of therapeutic goals instead. Only in this way the effects of acupuncture, related techniques and further therapeutic modalities can be matched with the set of objectives. The article presents general principles and follows their application from biological aspects to implications for the locomotor system and consequences for the application of physical therapy. The manual of acupuncture focuses on therapeutic effects and objectives first, and then goes on to sketch simple therapeutic strategies and finally complex approaches within acupuncture. These may encompass acupuncture, microsystem acupuncture and complex therapeutic modes.     

Fallbericht: Patientin mit Schlafstörung

Background

Since the onset of her menopause about ten years ago, a sixty-year old patient has been suffering from hot flashes and sleep disorders causing her to become increasingly anxious and nervous. As the patient's mother had died of breast cancer, substitution of hormones was not advisable. Relaxation methods such as Yoga and Autogenic Training could only mildly alleviate the symptoms.

Objective

To effectively treat the sleep disorder, improve quality of life, lessen frequency and severity of hot flashes

Methods

Weekly sessions with ear- and body acupuncture for ten weeks

Results

After the third acupuncture session the patient reported a decrease of nightly waking episodes but suffered from acute pain in the neck as well as shoulder region. After nine therapy sessions, the patient reported a 50% decrease of nightly waking episodes. The hot flashes, however, remained unchanged.

Discussion

In this case, acupuncture significantly improved the patient's sleeping disorder. It also reduced the symptoms of anxiety and nervousness. Other menopausal symptoms such as hot flashes and dryness of mucous tissues, could not be influenced.     

Patientin mit chronisch rezidivierenden Gelenks- und Wirbelsäulenschmerzen

Background

Acupuncture as a regulative therapy is well-suited for the treatment of functional, reversible disorders. Additionally, the WHO recommends its application for pain therapy in cases of arthritis and back pain due to various causes. This case study should clarify which paths to take in the case of a multi-morbid patient suffering from chronic pains due to polyarthrosis.

Objective

Pain reduction and improvement of quality of life as well as improvement of sleep quality.

Methods

Annual treatment series consisting of 10 sessions each, one session per week.

Results

short-term pain reduction before undergoing endoprosthetic surgery; considerable improvement of general status and sleep.

Conclusions

Acupuncture may bring temporal relief in cases of chronic pain due to osteoarthritis and should therefore be applied in combination with western medicine. Acupuncture is particularly well-suited to treat the co-emergent vegetative symptoms.     

常见证候荷瘤小鼠神经内分泌免疫组织基因转录的总体特征

目的揭示常见证候荷瘤小鼠神经-内分泌-免疫组织基因转录的总体特征。方法采用小鼠标准化四诊及辨证方法，及Gene Chip Mouse Exon1．0ST Array等技术，检测H22荷瘤小鼠早期邪毒壅盛（邪毒）和气虚、中期阳气虚、中晚期气阴阳虚等4个常见证候下丘脑、垂体、肾上腺、睾丸、脾脏、胸腺、肿瘤RNA的转录与剪接。结果正常昆明种雄性小鼠下丘脑、垂体、肾上腺RNA电泳的28S峰低于18S，而睾丸、脾脏、胸腺、肿瘤相反。肿瘤发生的早期，下丘脑、垂体、肾上腺基因表达模式发生显著改变，邪毒尤甚，出现了失代偿。下丘脑28SRNA迅速抬升并持续，气虚强于邪毒。垂体RNA总量降低，28S陡降，邪毒尤甚。肾上腺RNA电泳特征类似垂体，气虚与邪毒相近，中晚期气阴阳虚尤甚。睾丸变化不明显。随着病情发展，脾脏重量持续增加，而胸腺相反，重量持续下降，蛋白合成和糖代谢下降。肿瘤组织蛋白合成与糖代谢，邪毒大于气虚。以上7个组织与正常对照组相比，有9127个基因表达发生差异、51126个外显子剪接发生差异。结论神经-内分泌-免疫网络组织基因转录的差异是荷瘤小鼠不同证候内在重要的物质基础。