Guidelines for Trials of Behavioral Treatments for Recurrent Headache, First Edition: American Headache Society Behavioral Clinical Trials Workgroup

Guidelines for design of clinical trials evaluating behavioral headache treatments were developed to facilitate production of quality research evaluating behavioral therapies for management of primary headache disorders. These guidelines were produced by a Workgroup of headache researchers under auspices of the American Headache Society. The guidelines are complementary to and modeled after guidelines for pharmacological trials published by the International Headache Society, but they address methodologic considerations unique to behavioral and other nonpharmacological treatments. Explicit guidelines for evaluating behavioral headache therapies are needed as the optimal methodology for behavioral (and other nonpharmacologic) trials necessarily differs from the preferred methodology for drug trials. In addition, trials comparing and integrating drug and behavioral therapies present methodological challenges not addressed by guidelines for pharmacologic research. These guidelines address patient selection, trial design for behavioral treatments and for comparisons across multiple treatment modalities (eg, behavioral vs pharmacologic), evaluation of results, and research ethics. Although developed specifically for behavioral therapies, the guidelines may apply to the design of clinical trials evaluating many forms of nonpharmacologic therapies for headache.     

腹腔镜治疗精索静脉曲张235例

目的探讨腹腔镜治疗精索静脉曲张的疗效. 方法回顾分析1993年9月～2003年7月235例经腹腔镜精索静脉高位结扎术的临床资料. 结果 235例手术均获成功,手术时间5～20 min,平均12 min.术后住院2～5 d,平均3 d.210例随访6～18个月,9例复发,复发率4.3%(9/210),不育11例术后6～12个月后其妻受孕. 结论腹腔镜精索静脉高位结扎术微创、美观、疗效好,对双侧精索静脉曲张、开放性手术后复发和有腹股沟区手术史者尤为适用.     

高功率微波辐照对大鼠血睾屏障通透性的影响

目的 探讨高功率微波（HPM）辐照大鼠睾丸对血睾屏障的影响。方法 雄性SD大鼠35只，随机分为7组，每组5只。6组为辐照组，1组为对照组。于辐照后2、6、12、4．8、96h和8d活杀大鼠后取双侧睾丸组织各约1mm^3，镧-醛固定液固定后制备电镜标本，在透射电镜下进行观察。结果 对照组可见硝酸镧主要沉积在曲细精管基膜部和精原细胞周围，未越过紧密连接；辐照后2-6h电镜下所见与对照组大致相同；辐照后12-96h，从基底部到管腔面的各层生精细胞之间、支持细胞内都有大量的镧颗粒沉积；辐照后8d，仍可见细胞间隙增大，部分区域靠近精子表面的镧颗粒沉积甚至比前面时间点的更为严重。结论 高功率微波辐照能够改变细胞的通透性，破坏血睾屏障的保护作用。     

Regulators of Cardiac Cell Growth, Differentiation, and Apoptosis

The pathogenesis of heart hypertrophy and failure have been the focus of intense clinical and basic science investigation, yet the signal transduction pathways and molecular process that underlie the compensatory growth process that ultimately leads to heart failure remain enigmatic. Since ventricular myocytes have exited the cell cycle, growth of the myocardium in response to hemodynamic load occurs by cellular hypertrophy and not by hyperplasia. In this article, we document the potential involvement of tumor suppressor pocket proteins and cell cycle regulators that may impinge on the growth, differentiation, and apoptosis of cardiac muscle. This revised version was published online in August 2006 with corrections to the Cover Date.     

P1 blood group antigen expression and epidemic hemolytic uremic syndrome

P1 blood group positivity has been postulated as a host factor which may provide protection against the development of post-enteropathic hemolytic uremic syndrome (HUS). In this study, blood group status in 20 Inuit survivors ofEscherichia coli 0157: H7-associated HUS was compared with age-and sex-matched controls from the same community who had experienced uncomplicated diarrheal illness due to the same pathogen. Of 20 HUS survivors, 6 were P1 antigen positive compared with 8 of the 20 controls (P=0.7). We conclude that P1 antigen positivity was not protective against HUS in this population. Further studies of this condition to clarify the role of host factors in verotoxin-induced endothelial damage are indicated.     

Rh血型不合新生儿溶血病检测方法及应用

产前检测Ｒｈ，Ｄ因子及抗人球蛋白（ｃｏｏｍｂｓ）试验是必要的。测定Ｒｈ，Ｄ因子及抗Ｄ滴度使用木瓜酶方法。通过对１１２６１例孕妇常规检查Ｒｈ，Ｄ因子，发现Ｄ阴性７４例。Ｒｈ，Ｄ阴性妇女占６．５‰。２２例Ｒｈ，Ｄ阴性的孕妇所分娩的新生儿均为Ｒｈ，Ｄ阳性。其中２例孕妇血清抗Ｄ滴度为１∶３２，病情严重，宫内输血无效，胎死宫内。初产妇１３例，占５９％。活产２０例，存活率９０％。Ｒｈ因子及抗人球蛋白试验方法简便、易行，一般医院均可进行。对有流产史、输血史的孕妇检查Ｒｈ因子是十分必要的。在有条件的医院，对Ｒｈ，Ｄ阴性的产妇分娩Ｒｈ，Ｄ阳性的新生儿之后，产妇应预防性注射抗Ｄ免疫球蛋白     

Purification of antigenically intact Ro ribonucleoproteins; biochemical and immunological evidence that the 52-kD protein is not a Ro protein.

Anti-Ro sera immunoprecipitate Ro ribonucleoproteins (RNPs) from human cell extracts. Ro RNPs are biochemically heterogeneous particles whose functions are unknown and whose exact composition remains controversial. In addition to 60-kD Ro and to La proteins, a 52-kD polypeptide (p52) has been proposed to be a stable component of the Ro RNPs. To confirm the immunological studies supporting this hypothesis, we have biochemically purified Ro RNPs from HeLa cells using non-denaturing conditions. Ro RNPs segregated into three distinct populations, one of which only contained hY5 RNA (RohY5 RNPs). No p52 co-purified with Ro RNPs. Despite the absence of p52, purified Ro RNPs had biochemical and immunological properties identical to those of unfractionated Ro RNPs. Many anti-Ro sera only recognize p52 in immunoblots, and are said to be monospecific anti-p52. Preincubation with purified RohY5 RNPs (free of p52) of all human anti-Ro (including so-called monospecific anti-p52) sera abolished their capacity to immunoprecipitate Ro RNPs from unfractionated HeLa cell extracts. Conversely, preincubation of anti-Ro sera with purified p52 protein specifically inhibited recognition of p52 in immunoblots, but did not interfere with immunoprecipitation of Ro RNPs. Our data demonstrate that anti-p52 antibodies do not target intact Ro RNPs, nor do they target the native 60-kD Ro protein. Contrary to previous reports, p52 protein is not a stable component of antigenically intact Ro RNPs.     

Interaction of B and T lymphocyte subsets with high endothelial venules in the rat: binding in vitro does not reflect homing in vivo

Lymphocytes continuously migrate through the body, and their efficient extravasation from the blood via high endothelial venules (HEV) is essential for initiating an appropriate immune response. Most investigations have focused on the lymphocyte/HEV interaction in vitro. However, to what extent such systems reflect the situation in vivo is not known. It is also unclear whether lymphocyte subsets immigrate into the HEV in proportion to their presence in the blood, and whether import capacity is limited by the HEV. When rat mesenteric lymph node lymphocytes were incubated in vitro on cryostat sections, the well-known preferential binding of B lymphocytes to HEV of Peyer's patches (PP) and T cells to HEV of axillary lymph nodes (axLN) was observed (axLN vs. PP: B lymphocytes 21.2 ± 5.0% vs. 40.6 ± 11.0%, T lymphocytes 84.6 ± 6.3% vs. 56.5 ± 12.9%). However, when labeled mesenteric lymph node lymphocytes were injected and their location within the HEV was analyzed 15 min later, no preferential interaction was seen. After injection of labeled thoracic duct lymphocytes, the percentage of labeled cells among B and T lymphocytes in the blood was significantly different (4.4 ± 0.9% vs. 8.9 ± 3.6%), whereas that in HEV of axLN (19.0 ± 6.4% vs. 16.6 ± 6.0%) and PP (30.6 ± 6.1% vs. 33.9 ± 4.4%) was comparable. Although the number of injected lymphocytes was similar in magnitude to the total blood lymphocyte pool, after injection there was no increase in lymphocyte numbers in the HEV. Thus, the adhesion assay in vitro does not completely reflect immigration into HEV in vivo. In addition, our data suggest that both the availability of lymphocyte subsets in small venules and the immigration rate into HEV are actively regulated in vivo.