唾液富组蛋白5抗白念珠菌作用实验性研究

目的探讨不同浓度的富组蛋白5（histidine rich protein5，HRPs5）在体外杀灭白念珠菌孢子、芽管的作用及抑制孢子形成芽管的作用。方法将一定数量的孢子和芽管分别与不同浓度的HRPs5混合培养后，置于400倍的倒置显微下观察菌落数，得出杀孢子率、杀芽管率和抑制孢子不形成芽管率。结果当25μml或更高浓度的HRPs5和白色念珠菌孢子作用后，可使90％以上的孢子丧失活力；100μml的HRPs5和白色念珠菌芽管作用后，可使90％以上的孢子丧失活力；400μg／ml的HRPs5和白色念珠菌孢子作用后，可使100％孢子受到抑制而不形成芽管。而50μg／ml的HRPs5对白色念珠菌孢子形成芽管仅有轻微的抑制作用。结论HRPs5在体外具有较强杀灭白念珠菌孢子、芽管的作用及抑制孢子形成芽管的作用，且随着HRPs5浓度的升高其作用愈强。     

肘关节后脱位伴桡骨头和尺骨冠突骨折 (恐怖三联征)5例初步报告

[目的]介绍"肘关节恐怖三联征"的概念(肘关节后脱位同时伴有桡骨头和尺骨冠突骨折),并报告5例患者的临床治疗体会。[方法]自2004年4月～2007年3月,作者共收治肘关节三联征损伤5例。桡骨头骨折按Mason法分类:Ⅱ型4例,Ⅲ型1例;按Schatzker法分类:Ⅰ型1例,Ⅱ型3例,Ⅲ型1例。尺骨冠突骨折按Regan-Morrey法分类:Ⅰ型1例,Ⅱ型4例;按O′Driscoll法分类:5例均为Ⅰ型。4例采取了手术内固定治疗,以3 mm钛空心拉力螺钉或1 mm K针分别固定冠突和桡骨头,并缝合修复肘内外侧副韧带。术后屈肘90°前臂旋转中立位石膏外固定3周,开始屈伸和旋转康复训练。[结果]4例手术治疗的患者经3个月～3年随访,骨折愈合,肘关节稳定,无疼痛。肘关节屈伸幅度平均120°,前臂旋转幅度平均110°。3例随访1年以上,Mayo肘关节功能评分:优2例,良1例。未手术治疗的1例功能评定为差,有肘关节不稳定和疼痛。[结论]肘关节恐怖三联征的骨折片虽然很小,但伴有肘内外侧副韧带撕裂,肘关节严重不稳定。只有在重建了骨关节和软组织结构稳定的基础上,及早(3周内)进行康复锻炼,才能获得较好的功能恢复。     

Chemical Pathways of Peptide Degradation. V. Ascorbic Acid Promotes Rather than Inhibits the Oxidation of Methionine to Methionine Sulfoxide in Small Model Peptides

The effect of primary structure and external conditions on the oxidation of methionine to methionine sulfoxide by the ascorbate/Fe³⁺ system was studied in small model peptides. Degradation kinetics and yield of sulfoxide formation were dependent on the concentration of ascorbate and H⁺, with a maximum rate observed at pH 6–7. Phosphate buffer significantly accelerated the peptide degradation compared to Tris, HEPES, and MOPS buffers; however, the formation of sulfoxide was low. The oxidation could not be inhibited by the addition of EDTA. Other side products besides sulfoxide were observed, indicating the existence of various other pathways. The influence of methionine location at the C terminus, at the N terminus, and in the middle of the sequence was investigated. The presence of histidine in the sequence markedly increased the degradation rate as well as the sulfoxide production. The histidine catalysis of methionine oxidation occurred intramolecularly with a maximum enhancement of the oxidation rate and sulfoxide production when one residue was placed between the histidine and the methionine residue.     

经母腹取胎血及其脆性X检测的临床应用

本文报道在B超监护下经母腹作脐静脉穿刺取胎血33例,其中30例咨询孕妇作产前诊断,3例中孕引产。成功率为93.9％。孕龄与穿刺命中率,胎盘位置与穿刺命中率均不相关(P>0.05及P>0.05)。手术最佳时间是孕24周前后。手术并发症有胎心率变慢(或快),胎盘渗血,脐带渗血,脐血管空气栓塞等。但未发生死胎、流产、胎膜早破及感染。胎血的脆性X(fra(x))表达率较高,但脆性X并不复制。本法有可能成为fra(x)综合征的一种快速,可靠,安全,经济的产前诊断新方法。     

Neuronal histamine inhibits methamphetamine-induced locomotor hyperactivity in mice

Mianserin (5-20 mg/kg), like chlordiazepoxide (2.5-10 mg/kg), inhibits the shock-induced suppression of drinking (SSD) in rats. However, in contrast to chlordiazepoxide, the effect of mianserin is not blocked by the benzodiazepine antagonist, Ro 15-1788 (10 mg/kg). Although mianserin does not inhibit [3H]diazepam binding in vitro it has now been found to enhance [3H]flunitrazepam binding to mouse whole brain in vivo at 10-100 mg/kg p.o. These results suggest that mianserin does influence central benzodiazepine receptors, but the mechanism by which it does so differs from that of chlordiazepoxide.     

Osteopathia striata with cranial sclerosis: Highly variable expression within a family including cleft palate in two neonatal cases

Cranial sclerosis with osteopathia striata was diagnosed in four members of a family in three generations. The expression of the gene varied from mild cranial enlargement to cranial abnormality associated with severe Pierre-Robin triad. The disorder was diagnosed prenatally in the most severely affected member of the family from the finding of an increased biparietal diameter of the fetal head on ultrasound examination.     

Negative regulatory effect of histamine in DNFB-induced contact hypersensitivity

Histamine plays an important role in the regulation of various immunological functions. To evaluate the role of histamine in contact hypersensitivity, contact dermatitis was induced with dinitrofluorobenzene (DNFB) in histidine decarboxylase knockout (HDC-/-) histamine-deficient and wild-type mice. The DNFB-induced increase of the ear thickness was significantly higher in HDC-/- mice than in wild-type mice. Using flow cytometry, significantly lower percentages of CD4+ Th and CD8+ Tc cells, and significantly higher percentages of CD45R+ B cells were observed in the regional lymph nodes in HDC-/- mice than in wild-type mice. In the ear specimens of both groups, the majority of the infiltrating cells were neutrophils and macrophages at 24 and 48 h after challenge. Using immunohistochemistry, we observed significantly more CD45+ leukocytes in HDC-/- mice than in wild-type mice. The expression of Th1 (IL-2, IFN-gamma, TNF-alpha) and Th2 (IL-4) mRNAs was examined by quantitative real time RT-PCR in the ear samples. The levels of Th1 cytokine mRNAs both at 24 and 48 h after challenge and IL-4 mRNA at 48 h showed a significantly higher increase in HDC-/- mice than in wild-type mice. These results suggest that histamine plays a negative immunoregulatory role in DNFB-induced contact hypersensitivity.     

Collegiate Athletic Trainers' Confidence in Helping Female Athletes With Eating Disorders

OBJECTIVE: To examine college athletic trainers' confidence in helping female athletes who have eating disorders. DESIGN AND SETTING: We mailed a 4-page, 53-item survey to head certified athletic trainers at all National Collegiate Athletic Association Division IA and IAA institutions (N = 236). A 2- wave mailing design was used to increase response rate. SUBJECTS: A total of 171 athletic trainers returned completed surveys for a response rate of 77%. Eleven institutions either did not identify their head athletic trainer or did not have an identifiable mailing address. Two surveys were undeliverable because of incorrect mailing addresses. MEASUREMENTS: The survey consisted of 4 subscales: (1) efficacy expectation, (2) outcome expectation, (3) outcome value, and (4) experience in dealing with eating disorders. Content validity was established by review from a national panel of experts. Reliability ranged from.66 to.73 for the subscales. RESULTS: Although virtually all athletic trainers (91%) had dealt with a female athlete with an eating disorder, only 1 in 4 (27%) felt confident identifying a female athlete with an eating disorder, and only 1 in 3 (38%) felt confident asking an athlete if she had an eating disorder. One in 4 athletic trainers (25%) worked at an institution that did not have a policy on handling eating disorders. Almost all athletic trainers (93%) felt that increased attention needs to be paid to preventing eating disorders among collegiate female athletes. CONCLUSIONS: Collegiate athletic programs are encouraged to develop and implement eating-disorder policies. Continuing education on the prevention of eating disorders among athletes is also strongly recommended.     

Fibrinogen osaka IV: A congenital dysfibrinogenemia found in a patient originally reported in relation to surgery,now defined to have an Aα arginine-16 to histidine substitution

We discovered a congenital heterozygous dysfibrinogen in a patient and reported this case in relation to surgery some time ago (Jpn J Surg (1988) 18:43–46).³ Further studies on the isolated abnormal population of fibrinogen derived from this patient have revealed that fibrinopeptide A was not cleaved by ancrod, a snake venom-derived thrombin-like enzyme, but by thrombin, slowly but completely. The released fibrinopeptide A components, being the A, AY, and AP peptides, were all found to be abnormal, as evidenced by slightly earlier elution positions on high-performance liquid chromatography, compared with the normal counterparts. By analyzing their amino acid sequence, we have identified an arginine to histidine substitution at position 16 of the A chain, the thrombin cleavage site. Utilizing insolubilized abnormal fibrinogen, we confirmed that the polymerization site assigned to the central E domain, the A site, was exposed by thrombin, but not by ancrod. This dysfibrinogen, designated as fibrinogen Osaka IV, is the second abnormal molecule with an A arginine-16 to histidine substitution identified among Japanese families.