THE MANAGEMENT OF RECTAL BLEEDING

Rectal bleeding is a common symptom in the general population;¹ it may signal the presence of serious gastrointestinal disease but more frequently is caused by minor and self-limiting local ano-rectal conditions. Appropriate and accurate evaluation of rectal bleeding requires an investigative approach which balances an appreciation of the need to provide an adequate explanation for the bleeding against over-investigation, excessive referral and wasted resources. As doctors of first contact, general practitioners (GPs) are frequently faced with difficult questions concerning the optimum management of rectal bleeding. This paper was prepared as a result of a series of interactive meetings with over 1,000 GPs from throughout the UK, which revealed wide variations in the possession and use of investigative equipment in the surgery, access to secondary care facilities, estimates of the prevalence and potential seriousness of rectal bleeding and the management strategies adopted in response to a series of case histories. We highlight a number of unresolved issues about the roles of GPs and hospital specialists in the management of rectal bleeding and the need for research directed at answering outstanding questions. In addition, a management strategy is proposed which might form the basis for a protocol for care, shared between general practice and the hospital.     

尼莫地平对烫伤大鼠脑内ZO-1 mRNA及血脑屏障通透性的影响

目的:观察尼莫地平对严重烫伤大鼠脑内紧密连接相关蛋白ZO-1mRNA及血脑屏障通透性的影响。方法:实验于2005-04/10在南昌大学基础医学院应用解剖实验室完成。①取健康SD大鼠132只分为正常对照组12只、烫伤组60只,尼莫地平组60只,后两组又设烫伤后1,3,6,12,24h5个时间点,每个时间点12只,其中6只用于脑组织伊文思蓝含量的测定,剩余6只用于ZO-1mRNA的检测。②烫伤组和尼莫地平组大鼠100℃开水烫伤15s,造成背部30%体表总面积Ⅲ度烧伤。尼莫地平组大鼠于烫伤后即刻腹腔注射尼莫地平(0.5mg/kg),其他2组不给药。③各组大鼠于相应的时间点麻醉并处死动物取材,应用化学定量方法检测大鼠脑组织内伊文思蓝含量,运用RT-PCR方法检测大鼠脑内ZO-1mRNA的表达变化。结果:经补充后132只大鼠进入结果分析。①大脑伊文思蓝含量:正常对照组为(10.18±1.79)μg/g,烫伤组伤后1,3,6,12h均高于正常对照组(P<0.05),其高峰在烫伤后6h,为(20.00±0.58)μg/g;尼莫地平组伤后1,6,12h均低于烫伤组(P<0.01),烫伤后6h时为(16.74±0.78)μg/g。②小脑伊文思蓝含量:正常对照组为(12.90±1.32)μg/g,烫伤组伤后1,3,6,12h均高于正常对照组(P<0.05),其高峰在烫伤后6h,为(31.3±1.47)μg/g;尼莫地平组伤后1,3,6,12h均低于烫伤组(P<0.01),烫伤后6h时为(21.05±2.36)μg/g。③脑组织ZO-1mRNA的表达:烫伤组烫伤后3,6,12,24h分别为正常对照组的(0.1235±0.0158),(0.1890±0.0531),(0.2014±0.0412),(0.1555±0.0163)倍(P<0.01);尼莫地平组较烫伤组高,以烫伤后3,6h最为明显,分别为烫伤组的3.96及1.81倍(P<0.01).结论:①严重烫伤后血脑屏障通透性增高,脑内ZO-1mRNA表达下降。②烫伤后早期应用尼莫地平能防止脑内ZO-1mRNA表达下降,并能起到保护血脑屏障功能的作用。     

The effect of sterilization on transforming growth factor beta isolated from demineralized human bone

Growth factors have been identified as the primary cause of osteoinduction in bone healing. Transforming growth factor beta (TGF- beta) has been shown to promote bone formation and is present in bone in high quantities. The aims of the present study were to isolate TGF- beta from human bone, demonstrate its biologic activity, and analyze the effects of conventional sterilization techniques on activity. Bone, obtained from femoral heads of five patients (mean age, 70 years) was ground, demineralized, and freeze-dried, and samples from each patient were divided into three groups: no treatment, sterilization with 1.60 to 1.94 Mrad of 60Co irradiation, and sterilization with ethylene oxide (ETO). Carrier-free recombinant TGF-beta control was also treated and was totally inactivated by ETO but not by irradiation (p < 0.01). TGF- beta activity in demineralized bone was not significantly diminished (p > 0.1) by either sterilization procedure, and substantial amounts of active TGF-beta were recovered in all bone samples: 1.04 +/− 0.77 ng per mg of protein in irradiated samples, 0.67 +/− 0.26 ng per mg in ETO- treated samples, and 1.04 +/− 0.33 in untreated samples, respectively (mean +/− SD). Although a recent report demonstrated that the osteoinductive activity of bone morphogenetic protein in bone powder is diminished considerably by ETO and by 2.5 Mrad of irradiation sterilization of bone powder, these data demonstrate that TGF-beta activity, with its osteoinductive properties, was not destroyed in more coarsely ground, demineralized bone by ETO or by lower doses of irradiation. These findings support the use of human bone allografts in clinical instances involving impaired bone formation.     

Unusual association of a unique CAG interruption in 5′ of DM1 CTG repeats with intergenerational contractions and low somatic mosaicism

Myotonic dystrophy type 1 (DM1) is a dominant multisystemic disorder associated with high variability of symptoms and anticipation. DM1 is caused by an unstable CTG repeat expansion that usually increases in successive generations and tissues. DM1 family pedigrees have shown that ～90% and 10% of transmissions result in expansions and contractions of the CTG repeat, respectively. To date, the mechanisms of CTG repeat contraction remain poorly documented in DM1. In this report, we identified two new DM1 families with apparent contractions and no worsening of DM1 symptoms in two and three successive maternal transmissions. A new and unique CAG interruption was found in 5′ of the CTG expansion in one family, whereas multiple 5′ CCG interruptions were detected in the second family. We showed that these interruptions are associated with maternal intergenerational contractions and low somatic mosaicism in blood. By specific triplet‐prime PCR, we observed that CTG repeat changes (contractions/expansions) occur preferentially in 3′ of the interruptions for both families.     

The effect of prestorage irradiation on posttransfusion red cell survival

Transfusion-associated graft-versus-host disease (TA-GVHD) may occur whenever immunologically competent allogeneic lymphocytes are transfused to an immunocompromised recipient. Irradiation of blood components eliminates the risk of TA-GVHD but may damage the cellular elements in the transfused component, particularly if the cells are stored for prolonged periods in the irradiated state. To study the effect of irradiation on long-term storage of red cells, AS-1 red cells from eight normal subjects were prepared on two occasions. On one occasion, the units were stored as standard AS-1 red cells for 42 days at 4 degrees C; on the other, they were exposed to 3000 cGy radiation within 4 hours of collection and then were stored as AS-1 red cells for 42 days at 4 degrees C. The donations were at least 12 weeks apart. Irradiated units demonstrated significant elevations in poststorage plasma hemoglobin (Hb) (623 +/- 206 vs. 429 +/- 194 g/dL [6230 +/- 2060 vs. 4290 +/- 1940 g/L], p less than 0.02) and plasma potassium (78 +/- 4 vs. 43 +/- 9 mEq/L [78 +/- 4 vs. 43 +/- 9 mmol/L], p less than 0.01) and significant decreases in red cell ATP (1.9 +/- 0.2 vs. 2.1 +/- 0.3 microM/g Hb, p less than 0.04) and 24-hour posttransfusion red cell recovery (68.5 vs. 78.4%, p less than 0.02), as compared to nonirradiated units. It can be concluded that irradiation with 3000 cGy damages red cells and that long-term storage in the irradiated state may enhance this damage. Red cells should not be stored for 42 days after irradiation with 3000 cGy.