穴位敷贴对支气管哮喘豚鼠肿瘤坏死因子及白细胞介素2的影响——空白对照与标准对照

目的：观察中药穴位敷贴对实验性哮喘豚鼠血清中哮喘相关细胞因子肿瘤坏死因子及白细胞介素2的影响，并与地塞米松的作用效应相比较。方法：实验于2004—05／06在广州中医药大学动物实验中心完成。选用健康Hartly豚鼠60只，随机分为4组，每组各15只。采用卵蛋白致敏制作豚鼠支气管哮喘模型，用中药穴位敷贴治疗（穴位敷贴组）与地塞米松组（标准对照）及模型组（空白对照）和正常对照组比较。①穴位敷贴组于造模成功，哮喘发作次日开始治疗。治疗穴位选择大椎、肺俞、肾俞。用大块胶布将药物敷贴固定于穴位处。每次敷药6h，隔日治疗1次，共治疗7次。②地塞米松组采用腹腔注射地塞米松0．5mg／kg，治疗时间与次数同敷贴组。③模型组造模成功后令其自然恢复。正常对照组不造模，不给予任何治疗。④各组动物治疗结束后血清肿瘤坏死因子和白细胞介素2水平的检测采用放射免疫分析法。结果：在造模及治疗阶段模型组死亡4只、穴位敷贴组死亡3只，地塞米松组死亡2只，正常对照组死亡2只。每组取10只共40只进入结果分析。①模型组豚鼠血清肿瘤坏死因子、白细饱介素2水平均高于正常对照组[（0．707&;#177;0．113），（0．377&;#177;0．134）mg／L；（1．552&;#177;0．315），（0．790&;#177;0．311）mg／L，P〈0．05]。②穴位敷贴组和地塞米松组血清肿瘤坏死因子、白细胞介素2水平明显低于模型组[（0．445&;#177;0．195），（0．330&;#177;0．132），（0．707&;#177;0．113）mg／L；（1．033&;#177;0．541），（0．971&;#177;0．502）。（1．552&;#177;0．315）mg／L，P分别小于0．05和0．01]。③穴位敷贴组和地塞米松组肿瘤坏死因子、白细胞介素2水平差异不显著[（0．445&;#177;0．195），（0．330&;#177;0．132）mg／L；（1．033&;#177;0．541），（0．971&;#177;0．502）mg／L，P〉0．05]。结论：穴位敷贴与地塞米松均可降低血清肿瘤坏死因子、白细胞介素2水平，但差异不显著，说明穴位敷贴与地塞米松的标准作用一致。穴位敷贴治疗哮喘可能是通过降低血清肿瘤坏死因子、白细胞介素暑水平这些炎症因子而发挥起效应。     

穴位敷贴对支气管哮喘豚鼠肿瘤坏死因子及白细胞介素2的影响空白对照与标准对照

目的观察中药穴位敷贴对实验性哮喘豚鼠血清中哮喘相关细胞因子肿瘤坏死因子及白细胞介素2的影响,并与地塞米松的作用效应相比较. 方法实验于2004-05/06在广州中医药大学动物实验中心完成.选用健康Hartly豚鼠60只,随机分为4组,每组各15只.采用卵蛋白致敏制作豚鼠支气管哮喘模型,用中药穴位敷贴治疗(穴位敷贴组)与地塞米松组(标准对照)及模型组(空白对照)和正常对照组比较.①穴位敷贴组于造模成功,哮喘发作次日开始治疗.治疗穴位选择大椎、肺俞、肾俞.用大块胶布将药物敷贴固定于穴位处.每次敷药6 h,隔日治疗1次,共治疗7次.②地塞米松组采用腹腔注射地塞米松0.5 mg/kg,治疗时间与次数同敷贴组.③模型组造模成功后令其自然恢复,正常对照组不造模,不给予任何治疗.④各组动物治疗结束后血清肿瘤坏死因子和白细胞介素2水平的检测采用放射免疫分析法.结果在造模及治疗阶段模型组死亡4只、穴位敷贴组死亡3只,地塞米松组死亡2只,正常对照组死亡2只.每组取10只共40只进入结果分析.①模型组豚鼠血清肿瘤坏死因子、白细胞介素2水平均高于正常对照组[(0.707±0.113),(0.377±0.134)mg/L;(1.552±0.315),(0.790±0.311)mg/L,P＜0.05].②穴位敷贴组和地塞米松组血清肿瘤坏死因子、白细胞介素2水平明显低于模型组[(0.445±0.195),(0.330±0.132),(0.707±0.113)mg/L;(1.033±0.541),(0.971±0.502),(1.552±0.315)mg/L,P分别小于0.05和0.01].③穴位敷贴组和地塞米松组肿瘤坏死因子、白细胞介素2水平差异不显著[(0.445±0.195),(0.330±0.132)mg/L;(1.033±0.541),(0.971±0.502)mg/L,P＞0.05]. 结论穴位敷贴与地塞米松均可降低血清肿瘤坏死因子、白细胞介素2水平,但差异不显著,说明穴位敷贴与地塞米松的标准作用一致.穴位敷贴治疗哮喘可能是通过降低血清肿瘤坏死因子、白细胞介素2水平这些炎症因子而发挥起效应.     

大黄甘草汤治疗化疗呕吐的效果观察

目的:观察大黄甘草汤对化疗呕吐的应用效果。方法：将本科2018年1月—2019年6月首次诊断鼻咽癌行放化疗,使用含顺铂化疗方案的住院患者合计60例,便利抽样法分为对照组和透皮剂贴敷组。对照组患者实施肿瘤放化疗及立必复和地塞米松止吐治疗。透皮剂贴敷组患者采用大黄甘草汤透皮剂穴位贴敷和立必复与地塞米松止吐治疗,并实施肿瘤放化疗;剔除两组基线资料有差异的对象后,两组均30例,然后,对比两组患者恶心呕吐等胃肠道不良反应发生情况和患者舒适度。结果：透皮剂贴敷组患者恶心呕吐发生次数、腹痛腹胀以及便秘程度均比对照组更少更轻(P<0.05),透皮剂贴敷组患者身体舒适需求被满足度更高(P<0.05)。结论：患者化疗后胃肠道不良反应,应用大黄甘草汤透皮剂贴穴位贴敷联合西药治疗后,能够得到改善,患者满意。     

自制中药药饼穴位贴敷治疗支气管哮喘70例临床观察

目的：观察自制中药药饼穴位贴敷对支气管哮喘的治疗作用。方法：根据中医明病取阳理论，自制贴敷药饼，选择夏日三伏之每伏第1天为治疗时机，对70例支气管哮喘患者进行连续3年治疗。结果：有效率为91．4％，对各证型的治疗结果无显著性差异（P＞0．05）。结论：自制药饼特定时期在特定穴位上的贴敷应用，可有效治疗支气管哮喘。     

冬病夏治穴位贴敷治疗对慢性支气管炎患者血清炎症介质水平的影响

目的 通过检测慢性支气管炎患者冬病夏治穴位贴敷治疗前、后血清中白细胞介素-2(IL-2)、白细胞介素-4(IL-4)、白细胞介素-8(IL-8)、肿瘤坏死因子-α(TNF-α)等水平,探讨冬病夏治穴位贴敷疗法对人体血清IL-2、IL-4、IL-8、TNF-α水平的影响。方法 将确诊为慢性支气管炎非急性期且未进行其他相关治疗的患者30例随机、平均分为穴位贴敷治疗组(治疗组)和对照组。治疗组给予“三伏贴”穴位贴敷疗法,对照组给予“安慰贴”穴位贴敷疗法;对比2组治疗前及治疗后的血清IL-2、IL-4、IL-8、TNF-α水平。结果 在治疗组中,患者治疗后血清IL-2水平显著高于治疗前(P<0.05),IL-8、TNF-α水平显著低于治疗前(P<0.05);在治疗后,治疗组血清IL-2、IL-4水平显著高于对照组(P<0.05),IL-8、TNF-α显著低于对照组(P<0.05)。结论 冬病夏治穴位贴敷治疗能有效提高慢支炎患者血清IL-2水平,降低IL-8、TNF-α水平,从而提高自身免疫调节能力,降低炎症发生程度。     

ADM对哮喘豚鼠气道炎症影响及机理研究

目的：通过观察肾上腺髓质素（adrenomedullin,ADM)在豚鼠哮喘模型肺内的表达，及其对嗜酸性粒细胞（EOS），中性粒细胞（N），内皮素－1（ET－1），肿瘤坏死因子－α（TNF－α）的影响了解ADM在哮喘发病机制中的作用。方法：原位杂交方法检测ADMmRNA在豚鼠哮喘模型肺内的表达，静脉给予ADM后用放免法检测哮喘豚鼠血浆内ET－1，TNF－α的浓度。观察气道内EOS，N的浸润程度，结果：正常及哮喘豚鼠肺内均有ADM mRNA的表达，但哮喘组较正常组明显增多（P＜0．05），ADM可抑制哮喘豚鼠血浆内ET－1，TNF－α的水平及气道内EOS，N的浸润。结论：哮喘时，肺内ADM mRNA的表达明显增多，且外源性ADM抑制气道炎症细胞及部分炎症因子，提示ADM在哮喘病过程中起重要作用。     

肺炎支原体感染和哮喘患儿血清肿瘤坏死因子-α与IgE水平的表达

目的:检测哮喘患儿感染肺炎支原体与非感染者血清肿瘤坏死因子-α与总IgE的水平,分析其与病因、病程之间的关系,探讨小儿肺炎支原体感染与支气管哮喘的相关性。方法:选择哮喘患儿82例,分为感染肺炎支原体(感染组)40例和非感染肺炎支原体(非感染组)42例。采用酶联免疫方法测定肿瘤坏死因子-α,用放射免疫方法测血清总IgE水平,并与36例健康体检者(对照组)作正常对照。结果:感染组肿瘤坏死因子-α和IgE较非感染组显著升高,差异有统计学意义(P<0.05);感染组、非感染组肿瘤坏死因子-α和血清总IgE水平较对照组明显升高,差异有统计学意义(P<0.05)。不同病程患儿血清肿瘤坏死因子-αI、gE水平三组相比差异有统计学意义(P<0.05)。结论:肺炎支原体感染与支气管哮喘存在一定的相关性,肿瘤坏死因子-α可能参与了支气管哮喘的发病过程,其水平与病因无相关性;但病程长者肿瘤坏死因子-α及IgE水平较高;肿瘤坏死因子-α与总IgE水平的测定可作为哮喘患儿感染肺炎支原体的诊断与预后的参考指标之一。     

穴位贴敷联合布地奈德雾化吸入治疗支气管哮喘患儿的效果观察

目的：探讨穴位贴敷与布地奈德雾化吸入联合治疗支气管哮喘（简称哮喘）患儿的临床价值,并观察该方案对患儿炎症因子及呼吸道重塑的影响。方法：按照随机数字表法将2021年3月至2023年3月于河南省郑州市第七人民医院接受治疗的哮喘患儿126例分为对照组与观察组,各63例。对照组采用布地奈德治疗,观察组采用布地奈德+穴位贴敷治疗。对比两组中医证候积分、肺功能[用力肺活量（FVC）、第1秒用力呼吸容积（FEV1）、呼气峰流速值（PEF）]、炎症因子[白介素-8(IL-8)、C反应蛋白（CRP）、肿瘤细胞坏死因子-α(TNF-α)]、呼吸道重塑指标水平,同时记录两组治疗期间并发症发生状况。结果：治疗3个月后两组中医证候积分低于治疗前,哮喘控制测试（ACT）问卷评分高于治疗前,且观察组变化幅度更大（P<0.05）;治疗3个月后两组FVC、FEV1、PEF水平高于治疗前,IL-8、CRP、TNF-α水平低于治疗前,且观察组变化幅度更大（P<0.05）;治疗3个月后两组肌纤维母细胞计数、支气管黏膜基底膜厚度（TRBM）、呼出气一氧化氮（FENO）水平均低于治疗前,且观察组更低（P<0.0...     

支气管哮喘与细胞因子的关系

目的：探讨白细胞介素13和肿瘤坏死因子α表达与支气管哮喘的关系,并作痰液与血液检测的可行性及方便性比较.方法：[1]选择2003/01-2003/08哈尔滨医科大学附属二院呼吸科哮喘疾病急性发作期患者30例为患者组,男14例,女16例.选择同期本院健康体检者30人为对照组,男12人,女18人,年龄（32&;#177;2）岁.纳入对象对检测项目知情同意.[2]采用酶联免疫法分别检测哮喘患者和健康人痰液及血液中的白细胞介素13和肿瘤坏死因子α水平.[3]将患者组和对照组标本浓度值分别作正态性检验（矩法）,发现呈偏态分布,经对数变换方法进行数据转换,因浓度有小于1的小数值,转换公式为：log（浓度值＋1）,经再次正态性检验,对数变换数据呈正态分布,可以利用t检验作统计分析.结果：哮喘患者30例和健康者30人均进入结果分析.[1]痰及血液中白细胞介素13水平对数值：哮喘组明显高于对照组（1.190 1&;#177;0.380 4,0.735 0&;#177;0.501 9;0.821 7&;#177;0.358 6,0.491 1&;#177;0.344 3,P＜0.01,0.05）.[2]痰及血液中肿瘤坏死因子α水平对数值：哮喘组明显高于对照组（2.992 5&;#177;0.257 3,1.235 2&;#177;0.130 6;2.219 5&;#177;0.152 2,1.153 5&;#177;0.078 9,P＜0.01）.[3]哮喘急性发作期,痰液中白细胞介素13和肿瘤坏死因子α水平对数值明显高于血液（P＜0.05）.[4]哮喘急性发作期患者白细胞介素13和肿瘤坏死因子α的相关性：血液和痰液中白细胞介素13和肿瘤坏死因子α均呈显著正相关（r=0.45,0.53,P＜0.05,0.01）.结论：[1]白细胞介素13在哮喘的发作过程中起重要作用,肿瘤坏死因子α在哮喘发展中也起一定作用,且与白细胞介素13相关.[2]临床工作中检测哮喘患者痰液较血液更为有效和简便.     

穴位疗法治疗支气管哮喘100例

目的 探索治疗支气管哮喘的新途径.方法 选择符合诊断标准的支气管哮喘患者100例,伏天采用针、灸和穴位贴敷疗法治疗,半年内观察疗效,一年后随访.结果 治愈38例,好转58例,无效4例,总有效率96.0%.结论 采用针、灸和穴位贴敷综合疗法治疗支气管哮喘,效果显著.     

Diagnosis--serodiagnosis of alpha herpesviruses

Herpes simplex virus(HSV) serodiagnosis concerns type-common diagnosis and type-specific diagnosis. Primary HSV infections can be diagnosed by type-common serological assays, and in the ideal case, in combination with virus isolation. HSV type 1 and HSV type 2 are very similar except for glycoprotein G(gG). This glycoprotein can be used to determine type-specific antibodies especially during initial non-primary infections. However, antibody response to gG is late compared to the response to type-common antibodies. A rapid diagnosis of acute varicella-zoster virus(VZV) infections are often needed in clinical settings and in these situations, diagnosis is performed by methods for rapid viral detection, and not by serology. Serological tests are usually used to screen for immunity against VZV.     

The alpha 4 integrin chain is a ligand for alpha 4 beta 7 and alpha 4 beta 1

The heterodimeric alpha 4 integrins alpha 4 beta 7 lymphocyte Peyer's patch adhesion molecule ([LPAM]-1) and alpha 4 beta 1 (very late antigen-4) are cell surface adhesion molecules involved in lymphocyte trafficking and lymphocyte-cell and matrix interactions. Known cellular ligands include vascular cell adhesion molecule (VCAM)-1, which binds to alpha 4 beta 1 and alpha 4 beta 7, and the mucosal addressin cell adhesion molecule (MAdCAM)-1, which binds to alpha 4 beta 7. Here we show that the alpha 4 chain of these integrins can itself serve as a ligand. The alpha 4 chain, immunoaffinity purified and immobilized on glass slides, binds thymocytes and T lymphocytes. Binding exhibits divalent cation requirements and temperature sensitivity which are characteristic of integrin-mediated interactions, and is specifically inhibited by anti-alpha 4 integrin antibodies, which exert their effect at the cell surface. Cells expressing exclusively alpha 4 beta 7 (TK-1) or alpha 4 beta 1 (L1-2) both bound avidly, whereas alpha 4-negative cells did not. A soluble 34-kD alpha 4 chain fragment retained binding activity, and it inhibited lymphocyte adhesion to alpha 4 ligands. It has been shown that alpha 4 integrin binding to fibronectin involves an leucine-aspartic acid-valine (LDV) motif in the HepII/IIICS region of fibronectin (CS-1 peptide), and homologous sequences are important in binding to VCAM-1 and MAdCAM-1. Three conserved LDV motifs occur in the extracellular sequence of alpha 4. A synthetic LDV-containing alpha 4- derived oligopeptide supports alpha 4-integrin-dependent lymphocyte adhesion and blocks binding to the 34-kD alpha 4 chain fragment. Our results suggest that alpha 4 beta 7 and alpha 4 beta 1 integrins may be able to bind to the alpha 4 subunit on adjacent cells, providing a novel mechanism for alpha 4 integrin-mediated and activation-regulated lymphocyte interactions during immune responses.     

Differential cardiovascular regulatory activities of the alpha 1B- and alpha 1D-adrenoceptor subtypes

The regulation of cardiac and vascular function by the alpha 1B- and alpha 1D-adrenoceptors (ARs) has been assessed in two lines of transgenic mice, one over-expressing a constitutively active alpha 1B-AR mutation (alpha 1B-ARC128F) and the other an alpha 1D-AR knockout line. The advantage of using mice expressing a constitutively active alpha 1B-AR is that the receptor is tonically active, thus avoiding the use of nonselective agonists that can activate all subtypes. In hearts from animals expressing alpha 1B-ARC128F, the activities of the mitogen-activated protein kinases, extracellular signal-regulated kinase, and c-Jun N-terminal kinase were significantly elevated compared with nontransgenic control animals. Mice over-expressing the alpha 1B-ARC128F had echocardiographic evidence of contractile dysfunction and increases in chamber dimensions. In isolated-perfused hearts or left ventricular slices from alpha 1B-ARC128F-expressing animals, the ability of isoproterenol to increase contractile force or increase cAMP levels was significantly decreased. In contrast to the prominent effects on the heart, constitutive activation of the alpha 1B-AR had little effect on the ability of phenylephrine to induce vascular smooth muscle contraction in the isolated aorta. The ability of phenylephrine to stimulate coronary vasoconstriction was diminished in alpha 1D-AR knockout mice. In alpha 1D-AR knockout animals, no negative effects on cardiac contractile function were noted. These results show that the alpha1-ARs regulate distinctly different physiologic processes. The alpha 1B-AR appears to be involved in the regulation of cardiac growth and contractile function, whereas the alpha 1D-AR is coupled to smooth muscle contraction and the regulation of systemic arterial blood pressure.     

Orofacial alpha herpesvirus infection

The mouth is the most common site of primary and recurrent herpes simplex virus (HSV) infection. The clinical appearance of recurrent intraoral HSV infection is similar to that of recurrent aphthous stomatitis. Reactivation of HSV occurs in bone marrow transplantation and is more frequent in patients conditioned with total body irradiation than in patients conditioned without total body irradiation. Although the effect of oral acyclovir to prevent recurrent herpes labialis is not confirmed, recurrent HSV lesions can be treated with the ointment formulation successfully. A therapeutic approach using replication-competent HSV may be useful in the treatment of tumors of epithelial origin, such as carcinoma of the upper aerodigestive tract.     

Development of CD8alpha/alpha and CD8alpha/beta T cells in major histocompatibility complex class I-deficient mice.

Peripheral CD8(+) T cells mainly use CD8alpha/beta, and their development is mainly dependent on the major histocompatibility complex (MHC) class I proteins K(b) and D(b) in H-2(b) mice. In this report, we have shown that the development of CD8alpha/beta TCR-alpha/beta cells in lymphoid organs as well as in intestinal intraepithelial lymphocytes (iIELs) is dependent on the MHC class I K(b) and D(b) proteins. In contrast, TCR-alpha/beta CD8alpha/alpha cells are found mainly in iIELs, and their numbers are unaffected in K(b)D(b) double knockout mice. Most of the TCR-gamma/delta cells in the iIELs also bear CD8alpha/alpha, and they are also unaffected in K(b)D(b) -/- mice. In beta2-microglobulin (beta2m)-deficient mice, all of the TCR-alpha/beta CD8alpha/alpha and CD8alpha/beta T cells disappear, but TCR-gamma/delta cells are unaffected by the absence of beta2m.     

Qa-2-dependent selection of CD8alpha/alpha T cell receptor alpha/beta(+) cells in murine intestinal intraepithelial lymphocytes

Murine intestinal intraepithelial lymphocytes (iIELs) are made up of a heterogeneous mix of T cells with unique phenotypes. Whereas CD8(+) T cells in peripheral lymphoid organs use CD8alpha/beta and are selected on MHC class Ia molecules, a majority of iIELs use CD8alpha/alpha. Here, we report that the presence of CD8alpha/alpha TCR-alpha/beta cells in iIELs is independent of classical MHC class I molecules K(b) and D(b), as illustrated by their presence in K(b)/D(b) double-knockout mice and in mice lacking a nonclassical MHC class I molecule, CD1d. Most strikingly, their presence is decreased by approximately 70% in mice lacking transporter associated with antigen processing (TAP). The TAP-dependent nonclassical MHC class I molecule Qa-2 is strongly implicated in the presence of these cells, as inferred from the low numbers of CD8alpha/alpha TCR-alpha/beta T cells in mice deficient in Qa-2 genes. Second, a Qa-2-transgenic mouse made in a Qa-2(-) strain showed an increase in the numbers of CD8alpha/alpha cells among its iIELs. Thus, the presence of CD8alpha/alpha TCR-alpha/beta cells in iIELs is mainly dependent on the nonclassical MHC class I molecule Qa-2.