Medical abortion in late second trimester--a comparative study with misoprostol through vaginal versus oral followed by vaginal route

A randomised controlled trial was conducted to compare the relative efficacies of two regimens: Misoprostol given only vaginally or orally followed by vaginal administration of the same drug, for second trimester abortion. Multiparous women with a pregnancy of 16 to 20 weeks with no contra-indications to the drug were selected. They were randomly allocated into two groups. Patients in the first group, the 'only vaginal misoprostol' group (n = 30), were given misoprostol 400 microg 6 hourly only through vaginal route up to a maximum of 4 such doses. Women in the other group, the 'oral plus vaginal misoprostol' group (n = 24), received 400 microg of the drug at intervals of 12 hours for 2 doses, followed by 400 microg 6 hourly per vaginum up to a maximum of 4 such. Ten units of oxytocin was started in all cases when os was 4 cm dilated. Complete expulsion was 83.33% with an average time of 13.28 hours in the only vaginal misoprostol group. Complete expulsion occurred in 87.5% of women receiving oral followed by vaginal misoprostol with an average time of 8.93 +/- 0.01 hours from the first vaginal dose (p<0.05). More importantly, 66.67% women in second group delivered within 10 hours of the vaginal dose. Complete expulsion was defined in those cases where no check curettage was needed. Side-effects were not significant. This implies that misoprostol given by the vaginal route following oral priming doses had a higher success rate and a potential for a reduced hospital stay and higher bed turn-over rate.     

水胶体减压贴预防俯卧位手术患者面部压疮效果观察

目的 观察水胶体减压贴在俯卧位手术患者面部压疮预防中的应用效果.方法 将398例在骨科手术室行俯卧位手术患者随机分为观察组和对照组各199例.对照组前额、颧弓、下颌等受压处与头托之间垫10 cm×15 cm×2 cm棉垫;观察组采用水胶体减压贴,使用时根据各部位大小裁剪后垫于患者前额、颧弓、下颌等受压处.结果 两组患者...     

Postreperfusion myocardial technetium-99m-sestamibi defect corresponds to area at risk: experimental results from an ischemia-reperfusion porcine model

Introduction

Technetium-99m–sestamibi (MIBI) is the most frequently used myocardial perfusion tracer in patients with ischemic heart disease. In patients with acute ST-elevation myocardial infarction, we previously found that the defect in myocardial MIBI uptake was the same in patients injected with MIBI before primary angioplasty and in patients injected immediately after successful treatment. Thus, reperfusion may not be followed by increased uptake of MIBI. Instead, the MIBI defect after reperfusion may reflect the area at risk (AAR) defined by MIBI injected before treatment. We intended to investigate whether myocardial imaging with MIBI administered after reperfusion reflects myocardial perfusion or rather the ischemic AAR.

Methods

In 12 pigs, left anterior descending coronary artery was totally occluded for 45 min with an angioplasty balloon. After a 2-h reperfusion, MIBI was injected intravenously, and ¹⁵³Gd-microspheres were injected in left atrium. AAR and infarct size (IS) were determined by histochemical staining. MIBI and microsphere distribution were evaluated by counting the sliced left ventricle on a gamma camera. Defects were defined as uptake less than 45% of maximum uptake.

Results

The mean±S.D. defect size as a fraction of left ventricle was for MIBI 21%±5.5%, AAR 25%±6.3%, IS 13%±3.9% and microspheres defect size 7.3%±5.5%. MIBI defect size overestimated IS (P=.0005) and microspheres defect size (P=.0001), but it was not significantly different from AAR (P=.30).

Conclusion

In a porcine model of myocardial infarction after 45 min of ischemia, MIBI administered 120 min after reperfusion delineates AAR.     

Atheroprotective Roles of Adiponectin via CCL2 Inhibition

Aim: Adiponectin (APN) exhibits different atheroprotective effects, and we have previously reported that APN function is modulated by its binding proteins, E-selectin ligand 1, Mac-2 binding protein, and cystatin C. In the present study, we aimed to identify a novel atheroprotective mechanism of APN via C–C motif chemokine 2 (CCL2). Methods: We conducted iMAP ^® -intravascular ultrasound (IVUS) in 111 Japanese male patients with stable angina. The plaque characteristics were determined where “plaque burden” [(EEM CSA − lumen CSA)/(EEM CSA)×100 (%)] ＞50%, and their correlation with serum CCL2 and APN levels was analyzed. Using western blot analysis, the effects of APN on the biological effects of CCL2 were examined in their mutual binding by co-immunoprecipitation assay, the monocyte migration, and the phosphorylation of MAP kinases. Results: In a clinical study, we found that the percentage of plaque in the culprit lesion was correlated positively with serum CCL2 and negatively with serum APN levels, with significance. We identified CCL2 as a novel APN-binding serum protein using immunoprecipitation and western blot analysis. CCL2-induced phosphorylation of MAP kinases and monocyte migration was significantly attenuated by APN in vitro . Conclusion: The opposite association of APN and CCL2 on the percentage of coronary plaque might be caused by their direct interaction and competitive functions on monocyte migration.     

Hb Oslo [β42(CD1)Phe→Ile; HBB: c.127T>A]: A Novel Unstable Hemoglobin Variant Found in a Norwegian Patient

Unstable hemoglobin (Hb) variants are the result of sequence variants in the globin genes causing precipitation of Hb molecules in red blood cells (RBCs). Intracellular inclusions derived from the unstable Hb reduce the life-span of the red cells and may cause hemolytic anemia. Here we describe a patient with a history of hemolytic anemia and low oxygen saturation. She was found to be carrier of a novel unstable Hb variant, Hb Oslo [β42(CD1)Phe→Ile (TTT>ATT), HBB: c.127T>A] located in the heme pocket of the β-globin chain. Three-dimensional modeling suggested that isoleucine at position 42 creates weaker interactions with distal histidine and with the heme itself, which may lead to altered stability and decreased oxygen affinity. At steady state, the patient was in good clinical condition with a Hb concentration of 8.0–9.0?g/dL. During virus infections, the Hb concentration fell and on six occasions during 4 years, the patient needed a blood transfusion.     

Characterization of Two Deep Intronic Variants on the β-Globin Gene with Inconsistent Interpretations of Clinical Significance

Sequence variants located in the introns of the β-globin gene may affect the mRNA processing and cause β-thalassemia (β-thal). Sequence variants that change one of the invariant dinucleotides at the exon-intron boundaries may have fatal consequences for normal mRNA splicing. Intronic variants located far from obvious regulatory sequences can be more difficult to evaluate. There is a potential for misinterpretation of such sequence variants. Hence, thorough evaluation of patient data together with critical use of databases and in silico prediction tools are important. Here, we describe two rare sequence variants in the second intron of the β-globin gene, HBB: c.316-70C>G and HBB: c.316-125A>G (NM_000518.4), both previously reported as variants causing β-thal, and later as benign sequence variants. Due to the limited number of published cases and inconsistent interpretations, the significance of these sequence variants has been unclear. We have identified these two sequence variants in multiple individuals, alone and in a variety of combinations with other δ- and β-globin defects, and we find no influence of the sequence variants on the phenotype.