3D打印制备不同重量比例的n-HA/PLA/PVA复合膜性能比较

目的:通过3D打印的方法制备的不同重量比例的纳米羟基磷灰石/聚乳酸/聚乙烯醇(n-HA/PLA/PVA)复合膜,并对其相关性能检测。方法:采用3D打印技术制备不同重量比例的n-HA/PLA/PVA复合膜,分别为PLA/PVA复合膜、15%n-HA/PLA/PVA复合膜、50%n-HA/PLA/PVA复合膜、75%n-HA/PLA/PVA复合膜。扫描电镜下观察各组膜形态,对其力学性能、细胞毒性及动物实验相应指标进行检测。结果:扫描电镜下观察,n-HA/PLA/PVA复合膜呈现三维网状结构,各材料间相互结合,孔隙分布不均,大小不一。随着n-HA质量浓度的提高,电镜下见各材料间孔隙逐渐减小,形成结构均匀的复合膜。力学性能及吸水率检测中,随着nHA含量的增加,n-HA/PLA/PVA复合膜的拉伸强度及吸水率呈下降趋势;细胞毒性检测,不同比例复合膜的细胞增殖率无明显差别,无细胞毒性。动物实验测量牙周菌斑指数及龈沟出血指数未发现不同比例n-HA/PLA/PVA复合膜有统计学差异。结论:3D打印不同比例的n-HA/PLA/PVA复合膜具有良好的物理性能和细胞生物相容性,n-HA比例更高的复合膜可能具有更好的物理性能及良好的生物相容性。     

Arachidonic acid-stimulated platelet tests: Identification of patients less sensitive to aspirin treatment

Serum thromboxane-B2 (TxB2), together with arachidonic acid (AA)-induced platelet aggregation, are, at the moment, the most used tests to identify patients displaying high on-aspirin treatment platelet reactivity (HAPR). Both tests are specific for aspirin action on cyclooxygenase-1. While the correlation between serum TxB2 assay and clinical outcome is established, data are conflicting with regard to aspirin treatment and a possible association with AA-stimulated platelet markers and clinical outcome. To understand such discrepancy, we performed a retrospective study to compare both assays. We collected data from 132 patients receiving a daily dose of aspirin (100?mg/day) and data from 48 patients receiving aspirin on alternate days. All Patients who received a daily dose of aspirin were studied for AA-induced platelet aggregation together with serum TxB2 levels and AA-induced TxB2 formation was also studied in 71 patients out of entire population. Consistent with recommendations in the literature, we defined HAPR by setting a cut-off point at 3.1?ng/ml for serum levels of thromboxane B2 and 20% for AA-induced platelet aggregation. According to this cut-off point, we divided our overall population into two groups: (1) TxB2?<?3.1?ng/ml and (2) TxB2?>?3.1?ng/ml. We found low agreement between such tests to identify patients displaying HAPR. Our results show that AA-induced platelet aggregation >20% identify a smaller number of HAPR patients in comparison with TxB2. A good correlation between serum TxB2 and arachidonic acid-induced TxB2 production was found (r?=?0.76619).     

脑脊液降钙素原及乳酸测定在早期诊断颅脑术后颅内感染的意义

目的研究降钙素原(PCT)及乳酸水平在早期诊断颅脑术后颅内感染的意义。方法颅脑术后颅内感染患者(n=20)和非颅内感染患者(n=20)的脑脊液和血液样本,检测脑脊液和血清PCT,脑脊液和血液乳酸水平等指标并进行统计分析。结果感染组脑脊液和血清PCT、乳酸水平较非感染组显著升高,差异有统计学意义(P0.05)。脑脊液PCT和乳酸水平诊断敏感性及特异性均较血清PCT和乳酸水平高。结论脑脊液PCT、乳酸在颅脑手术术后颅内感染的诊断中均有意义,其中脑脊液PCT较乳酸敏感性更高,临床应用价值更大。     

Ensayo clínico para determinar si el momento de administración del ácido tranexámico en la cirugía de prótesis total de rodilla con torniquete influye en el sangrado perioperatorio

Background and objectivesThe ideal timing of tranexamic acid administration in total knee arthroplasty with tourniquet remains unclear. Our primary objective was to prove if administering it before surgical incision, instead of before releasing the tourniquet, reduces postoperative bleeding. A second objective was to determine whether a second dose reduces post-operative bleeding.Material and methodsA prospective, double-blind clinical trial was performed on 212 patients scheduled for total knee arthroplasty. They were randomised into 4 groups. Tranexamic acid was administered before the surgical incision in “pre-induction groups” (1 and 2), and just before the tourniquet release in “pre-release groups” (3 and 4). Groups 2 and 4 received a second dose 3 hours post-surgery. Main outcome was postoperative bleeding (visible blood loss and calculated total bleeding). Secondary outcomes were haemoglobin variations, complications and transfusion rate.ResultsThe mean calculated total bleeding was 1563 ml (95%CI: 1445 to 1681) in preinduction groups versus 1576 ml (95%CI: 1439 to 1713) in pre-release groups (P = .9); 1579 ml (95%CI: 1452 to 1706) in single-dose groups versus 1559 ml (95%CI: 1431 to 1686) in double-dose groups (P = .82). One patient was transfused. The mean haemoglobin at discharge was 10.4 g/dl (95%CI: 10.2 to 10.7) in singledose groups versus 10.8 (95%CI: 10.6 to 11.1) in double-dose groups (P = .06).ConclusionsThere were no differences in bleeding or transfusion regarding the time of tranexamic acid administration. The second dose had not impact on outcomes.Trial registration: EudraCT 2016-000071-24.     

益母草中阿魏酸对含益母草中成药质量标准影响的探讨

目的：建立HPLC/TQ-MS测定益母草中阿魏酸含量的方法并测定不同产地益母草中阿魏酸含量，评价益母草中阿魏酸对中成药调经止痛片及新生化颗粒的质量影响，为制定含有益母草并以阿魏酸为定量指标的中成药质量标准提供参考。方法：采用薄层色谱法及UPLC-Q/TOF定性鉴别及分析益母草中阿魏酸，采用HPLC/TQ-MS定量分析10批不同产地益母草中阿魏酸含量。基于定量分析结果及处方用量探讨益母草中阿魏酸含量对其中成药质量标准的影响。结果：薄层鉴别及UPLC-Q/TOF定性分析结果显示，10批不同产地益母草中均含有阿魏酸。HPLC/TQ-MS定量分析结果显示，益母草中阿魏酸含量在0.004 2%~0.006 5%之间。结论：益母草与当归、川芎等含有阿魏酸的药材配伍且其用量较大时，益母草中阿魏酸含量会对其质量评价产生一定的影响。     

Investigation of non-linear Mate1-mediated efflux of trimethoprim in the mouse kidney as the mechanism underlying drug-drug interactions between trimethoprim and organic cations in the kidney

The purpose of this study was to elucidate the involvement of Mate1 in the tubular secretion of trimethoprim and saturation of Mate1-mediated efflux to address the mechanisms underlying the pharmacokinetic drug interactions with trimethoprim. Trimethoprim is a more potent inhibitor of MATE2-K than MATE1 with K_i values (μM) of 0.030–0.28 and 2.4–5.9, respectively. Trimethoprim is a substrate of human MATE1 and MATE2-K with K_m values of 2.3 ± 0.9 and 0.018 ± 0.004 μM, and mouse Mate1, but not human OCT2, mouse Oct1 and Oct2. Pyrimethamine significantly reduced the renal clearance (CL_R) of trimethoprim (mL/min/kg) from 40.0 ± 5.1 to 20.1 ± 3.7 (p < 0.05). Trimethoprim was given to mice at three infusion rates (150, 500, and 1500 nmol/min/kg). Together with an increase in the plasma concentrations of trimethoprim, the CL_R (mL/min/kg) of trimethoprim decreased to 25.9 ± 3.2, 13.5 ± 5.7, and 8.92 ± 1.50 at the respective rates. Trimethoprim decreased the CL_R of rhodamine 123 in an infusion rate-dependent manner: 11.5 ± 1.3 (control), 5.17 ± 1.55, 1.31 ± 0.50, and 0.532 ± 0.180. These results suggest that Mate1 mediates the tubular secretion of trimethoprim, and at therapeutic doses, MATEs-mediated efflux can be saturated, and thereby, cause drug interactions with other MATE substrates.