老年糖尿病患者强化糖尿病教育的效果与评价

目的:观察强化糖尿病教育对老年2型糖尿病患者血糖控制的影响,并对教育的方法模式及患者的顺应性作出评价。方法:①随机选取老年2型糖尿病患者156例,均为2004-03/07青岛大学医学院附属医院门诊就诊患者,年龄(64.7±6.6)岁,病程(10.54±7.06)年。②入选患者在原有糖尿病治疗方案的基础上进行强化糖尿病教育:入选后半年之内每月进行一次糖尿病教育,半年后每3个月一次教育,教育以糖尿病有关知识专题集体讲座为主,辅以答疑。专人负责电话通知患者教育讲座的具体的时间、地点和内容。每次讲座时监测空腹血糖、餐后2h血糖,入选时、教育后第6,12个月测定糖化血红蛋白;同时记录患者接受教育频率,计算依从率。③采用随机区组设计的方差分析(广义线性模型)分析数据完整的患者的空腹血糖、餐后2h血糖及糖化血红蛋白随时间变化情况(入选时、第6,12个月时)。结果:①依从率:入选时156例,第2次教育时为125例,依从率74.8%,随着时间的延长,接受强化教育的患者逐渐减少,至第6个月时依从率28.1%,至1年时仅有33例接受教育,依从率为21.2%。②完成全程教育的33例患者的资料:教育第6,12个月时的空腹血糖、餐后2h血糖较入选时下降[空腹血糖:(7.9±2.1),(7.8±1.4),(9.7±2.1)mmol/L,F=31.05,P<0.01;餐后2h血糖:(12.0±4.0),(12.2±3.3),(17.8±3.8)mmol/L,F=56.61,P<0.01];糖化血红蛋白在教育第6,12个月也较入选时下降,但无统计学意义[(7.0±1.1)%,(6.9±1.1)%,(7.6±1.7)%,F=2.97,P=0.06]。结论:强化糖尿病教育可使老年2型糖尿病患者血糖有效持续稳定地控制,但患者接受强化教育的依从性差。     

Factors in the liquid portion of stored blood inhibit the proliferative response in mixed lymphocyte cultures

The transfusion of blood may suppress the immune responses of patients with renal transplants and with malignant disorders. To study the in vitro suppressive effects of banked blood, 4 units of blood were stored in CPDA-1 and ADSOL at 4 degrees C for 14 days. Lymphocytes and plasma or ADSOL supernatants were harvested on Days 0, 4, 7, 10, and 14. Subpopulations of lymphocytes were enumerated by flow cytometry. Recalcified and heat-treated plasma and supernatants from the units of blood were added to mixed lymphocyte cultures (MLC) composed of cells from normal individuals. No significant changes were noted in the proportions of T or B cells from blood stored under these conditions. A 60 +/− 3 percent inhibition in the proliferative response was observed when plasma from CPDA-1 units was added to MLCs (p less than 0.02). Supernatants from ADSOL units demonstrated a 29 +/− 4 percent inhibition (p less than 0.10) of the proliferative response, and this inhibition of response was observed on all 14 days of the study. When appropriate concentrations of dextrose or adenine were added to other MLCs, adenine (at the concentration found in ADSOL) caused a significant inhibition of the proliferative response. This inhibition was not, however, as marked as that observed with recalcified, heat- treated plasma from CPDA-1 units. We conclude that adenine plus some additional factor(s) found in the liquid portion of stored blood inhibits the proliferative response of normal lymphocytes. It is possible that these factors contribute to the immune suppression observed in vivo in some patients who receive blood transfusions.     

Cannabidiolic acid prevents vomiting in Suncus murinus and nausea-induced behaviour in rats by enhancing 5-HT1A receptor activation

Background and Purpose

To evaluate the ability of cannabidiolic acid (CBDA) to reduce nausea and vomiting and enhance 5-HT_1A receptor activation in animal models.

Experimental Approach

We investigated the effect of CBDA on (i) lithium chloride (LiCl)-induced conditioned gaping to a flavour (nausea-induced behaviour) or a context (model of anticipatory nausea) in rats; (ii) saccharin palatability in rats; (iii) motion-, LiCl- or cisplatin-induced vomiting in house musk shrews (Suncus murinus); and (iv) rat brainstem 5-HT_1A receptor activation by 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) and mouse whole brain CB₁ receptor activation by CP55940, using [³⁵S]GTPγS-binding assays.

Key Results

In shrews, CBDA (0.1 and/or 0.5 mg·kg⁻¹ i.p.) reduced toxin- and motion-induced vomiting, and increased the onset latency of the first motion-induced emetic episode. In rats, CBDA (0.01 and 0.1 mg·kg⁻¹ i.p.) suppressed LiCl- and context-induced conditioned gaping, effects that were blocked by the 5-HT_1A receptor antagonist, WAY100635 (0.1 mg·kg⁻¹ i.p.), and, at 0.01 mg·kg⁻¹ i.p., enhanced saccharin palatability. CBDA-induced suppression of LiCl-induced conditioned gaping was unaffected by the CB₁ receptor antagonist, SR141716A (1 mg·kg⁻¹ i.p.). In vitro, CBDA (0.1–100 nM) increased the E_max of 8-OH-DPAT.

Conclusions and Implications

Compared with cannabidiol, CBDA displays significantly greater potency at inhibiting vomiting in shrews and nausea in rats, and at enhancing 5-HT_1A receptor activation, an action that accounts for its ability to attenuate conditioned gaping in rats. Consequently, CBDA shows promise as a treatment for nausea and vomiting, including anticipatory nausea for which no specific therapy is currently available.     

Presence of the red cell alloantibody anti-E in an 11-week-old infant

The development of red cell (RBC) alloantibodies in infants less than 4 months of age is believed to be rare. Though there are no well-documented published accounts, the formation of alloanti-E in a multiply transfused 11-week-old infant is reported here. The infant, blood group B, D +, developed necrotizing enterocolitis and renal failure requiring 31 transfusions of washed and unwashed RBCs (group B and group O), as well as fresh-frozen plasma and platelets. Six weeks after the first blood transfusion, alloanti-E was detected. The anti-E weakly agglutinated R2R2 screening RBCs at 37 degrees C and sensitized these RBCs to react with anti-IgG. The infant's RBCs were typed as E-. Passive transfer of alloanti-E was ruled out by the negative antibody screening tests of each donor unit and the absence of any RBC alloantibodies in the mother's serum. Stored samples of the infant's sera were tested, and anti-E was shown to be present approximately 11 days after exposure to a known E+ RBC unit. The appearance of alloanti-E in this time frame is consistent with a secondary immune response. Primary immunization most likely took place in the first 4 weeks of transfusion therapy.     

The double-fissure sign: a motion artifact on thin-section CT scans

A motion artifact has been observed that may affect the number of fine interstitial lines seen at thin-section (1.5-mm-collimation) computed tomography (CT) for the evaluation of interstitial lung disease. In 14 of 42 patients, one or both major fissures appeared as two parallel lines rather than as a single line. This was more common in the left lung base. Using a phantom, the authors were able to reproduce the phenomenon by simulating cardiac motion. Therefore, this motion may lead to an artifactual increase in the number of interstitial lines.     

Vesiculation of sickle erythrocytes during thermal stress

Since it is not known why sickle RBCs tend to undergo microvesiculation, we have investigated their susceptibility to thermal stress. While normal RBCs start to vesiculate at 49.0 +/- 0 degrees C (n = 14), sickle RBCs begin to vesiculate at 47.9 +/- 0.5 degrees C, with a range of 46.5 to 48.5 degrees C (n = 14). This abnormality is reproduced by treating normal RBCs with phenazine methosulfate (PMS), which stimulates the excess intracellular generation of superoxide characteristic of sickle RBCs. For PMS-treated RBCs, there is a strong correlation between membrane protein thiol oxidation and vesiculation temperature (r = .977, P less than .001). The abnormal vesiculation temperature of both unmanipulated sickle RBCs and PMS-treated RBCs is significantly improved by treatment of the RBCs with dithiothreitol. The most dense sickle RBCs are most prone to vesiculation during thermal stress, and they are the subpopulation having the greatest amount of thiol oxidation. We conclude that the tendency of sickle RBCs to vesiculate during thermal stress is further evidence for functional abnormality of the RBC cytoskeleton due to thiol oxidation.     

Regulation of streptokinase-human plasmin complex by the plasma proteinase inhibitors alpha 2-antiplasmin and alpha 2-macroglobulin is species specific and temperature dependent

Streptokinase-plasmin complex (SkPl) was prepared with human plasminogen. Regulation of SkPl and plasmin by the plasma proteinase inhibitors, alpha 2-antiplasmin (alpha 2AP) and alpha 2-macroglobulin (alpha 2M), was studied as a function of temperature in plasminogen- depleted human plasma, mouse plasma, and solutions of purified proteins. The reaction of plasmin with proteinase inhibitors in human plasma was complete. alpha 2AP was the predominant inhibitor. The fraction of alpha 2M-plasmin recovered was not affected significantly by incubation temperature. In contrast, the reaction of SkPl with human proteinase inhibitors was markedly temperature dependent. The apparent second-order rate constant for the reaction of SkPl with purified alpha 2AP at 37 degrees C (1.5 x 10(2) mol/L-1 s-1) was greater than 150-fold higher than the constant derived at 4 degrees C. In human plasma and in solutions containing mixtures of purified human proteins, alpha 2AP was the principal inhibitor of SkPl. Elevating the temperature enhanced the reaction of SkPl with alpha 2AP and alpha 2M comparably. Equivalent results were obtained when incubations were performed in platelet-rich plasma (PRP) or whole blood. In murine plasma, SkPl reacted readily with the proteinase inhibitors. The principal inhibitor of SkPl was alpha 2M. Maximum reaction between SkPl and murine alpha 2M was observed at 37 degrees C; however, significant reaction also occurred at 4 degrees C. alpha 2 AP was the predominant inhibitor of plasmin in mouse plasma. Reaction of alpha 2AP with SkPl in murine plasma was significant only after the alpha 2M was inactivated with methylamine. These results were not affected by platelets or whole blood cells. We conclude that the thrombolytic efficacy of streptokinase reflects not only the nature of the plasminogen activator complex but also the function of the proteinase inhibitors.