Roles and mechanisms of the CD38/cyclic adenosine diphosphate ribose/Ca^(2+) signaling pathway

Mobilization of intracellular Ca2+ stores is involved inmany diverse cell functions, including: cell proliferation;differentiation; fertilization; muscle contraction; secre-tion of neurotransmitters, hormones and enzymes;and lymphocyte activation and proliferation. Cyclic ad-enosine diphosphate ribose(cADPR) is an endogenousCa2+ mobilizing nucleotide present in many cell typesand species, from plants to animals. cADPR is formedby ADP-ribosyl cyclases from nicotinamide adenine di-nucleotide. The main ADP-ribosyl cyclase in mammalsis CD38, a multi-functional enzyme and a type Ⅱ mem-brane protein. It has been shown that many extracel-lular stimuli can induce cADPR production that leadsto calcium release or influx, establishing cADPR as asecond messenger. cADPR has been linked to a widevariety of cellular processes, but the molecular mecha-nisms regarding cADPR signaling remain elusive. Theaim of this review is to summarize the CD38/cADPR/Ca2+ signaling pathway, focusing on the recent advanc-es involving the mechanism and physiological functionsof cADPR-mediated Ca2+ mobilization.

Electrochemical Studies of Effect of Eu^(3+) on Adenosine-5′-Diphosphate at Mercury Electrode

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Poly adenosine diphosphate-ribosylation, a promising target for colorectal cancer treatment

The development of colorectal cancer(CRC)can result from changes in a variety of cellular systems within the tumor microenvironment.Particularly,it is primarily associated with genomic instability that is the gradual accumulation of genetic and epigenetic changes consisting of a characteristic set of mutations crucial for pathways in CRC progression.Based on this background,the potential to focus on poly[adenosine diphosphate(ADP)-ribose]polymerase(PARP)-1 and poly-ADP ribosylation(PARylation)as the main causes of malignant formation of CRC may be considered.One of the important functions of PARP-1 and PARylation is its deoxyribonucleic acid(DNA)repair function,which plays a pivotal role in the DNA damage response and prevention of DNA damage maintaining the redox homeostasis involved in the regulation of oxidation and superoxide.PARP-1 and PARylation can also alter epigenetic markers and chromatin structure involved in transcriptional regulation for the oncogenes or tumor suppressor genes by remodeling histone and chromatin enzymes.Given the high importance of these processes in CRC,it can be considered that PARP-1 and PARylation are at the forefront of the pathological changes required for CRC progression.Therefore,this review addresses the current molecular biological features for understanding the multifactorial function of PARP-1 and PARylation in CRC related to the aforementioned roles;furthermore,it presents a summary of recent approaches with PARP-1 inhibition in non-clinical and clinical studies targeting CRC.This understanding could help embrace the importance of targeting PARP-1 and PARylation in the treatment of CRC,which may present the potential to identify various research topics that can be challenged both nonclinically and clinically.

Effects of procainamide on adenosine diphosphate-induced platelet aggregation and thromboxane B_2 production in rabbits in vitro

Turbidimetry and radioimmunoassay were used to study the effects of procainamide (PA ) onadenosine diphosphate (ADP)-induced rabbit platelet aggregation and thromboxane B2 (TXB2) production invitro. PA 8. 5--544. 0 μmol L-1 inhibited ADP-induced platelet aggregation and TXB2 production, and theinhibition rates were 26. 7% -- 66. 7 % and 21. 4 % -- 70. 1 %, respectively. There was positive correlation between PA concentration and its efficiency in inhibiting the platelet aggregation and TXB2 production, and alsobetween the inhibition rates of platelet aggregation and that of TXB2 production. The three linear equationsand main parameters were The results indicate that PA could significantly inhibit ADP--induced platelet aggregation and TXB2 production in rabbits.

Pretreatment with adenosine and adenosine A1 receptor agonist protects against intestinal ischemia-reperfusion injury in rat

AIM: To examine the effects of adenosine and A1 re- ceptor activation on reperfusion-induced small intestinal injury. METHODS: Rats were randomized into groups with sham operation, ischemia and reperfusion, and systemic treatments with either adenosine or 2-chloro-N6-cyclo- pentyladenosine, A1 receptor agonist or 8-cyclopentyl- 1,3-dipropylxanthine, A1 receptor antagonist, plus ade- nosine before ischemia. Following reperfusion, contra- ctions of ileum segments in response to KCl, carbachol and substance P were recorded. Tissue myeloperoxidase, malondialdehyde, and reduced glutathione levels were measured. RESULTS: Ischemia significantly decreased both contra- ction and reduced glutathione level which were ameliora- ted by adenosine and agonist administration. Treatment also decreased neutrophil infiltration and membrane lipid peroxidation. Beneficial effects of adenosine were abolis- hed by pretreatment with A1 receptor antagonist. CONCLUSION: The data suggest that adenosine and A1 receptor stimulation attenuate ischemic intestinal in- jury via decreasing oxidative stress, lowering neutrophil infiltration, and increasing reduced glutathione content.

熊果苷对心肌纤维化模型大鼠的改善作用及机制研究

目的研究熊果苷对心肌纤维化(MF)模型大鼠的改善作用及机制。方法采用网络药理学方法预测熊果苷改善MF的潜在靶点并进行分子对接验证。将50只SD大鼠皮下注射异丙肾上腺素(5 mg/kg,每天1次,连续14 d)复制MF模型。将造模成功的大鼠随机分为模型组、卡托普利组(9 mg/kg)和熊果苷低、中、高剂量组(50、100、200 mg/kg),每组10只;另取10只未造模大鼠作为正常组。各组大鼠给予相应药物干预,每天1次,连续28 d。末次给药24 h后,检测大鼠心电图、心脏相关指数[心脏质量指数(HWI)、左心室质量指数(LVWI)],检测大鼠心肌组织中肌酸激酶(CK)、乳酸脱氢酶(LDH)、N末端前脑钠肽前体(NT-proBNP)、Ⅰ型胶原蛋白(ColⅠ)、ColⅢ水平,观察大鼠心肌组织病理形态学变化,检测大鼠心肌组织中腺苷脱氨酶(ADA)、腺苷激酶(ADK)蛋白及其mRNA表达水平。结果网络药理学结果显示,熊果苷改善MF的主要靶点为ADA、ADK。分子对接结果显示,熊果苷与ADA、ADK结合稳定。验证实验结果显示,与模型组比较,各给药组大鼠心电图ST波段和T波的振幅有所恢复,心房出现扑动的症状减轻;HWI(熊果苷中剂量组除外)、LVWI和心肌组织中CK、LDH、NT-proBNP、ColⅠ、ColⅢ水平均显著降低(P<0.05);大鼠心肌纤维化程度减轻;心肌组织中ADA、ADK蛋白及其mRNA表达水平均显著升高(P<0.05)。结论熊果苷可改善MF模型大鼠心脏纤维化和心脏功能,其作用机制可能与上调ADA、ADK蛋白及其mRNA表达,影响核苷酸代谢及胶原生成有关。

AA抑制率和ADP抑制率对脑出血后再出血及预后的预测价值分析

目的 本研究的目的是评估血栓弹力图(thrombelasto graphy,TEG)测试中AA抑制率和ADP抑制率在预测脑出血(ICH)后再出血和不良功能预后方面的有效性。方法 选取苏州市立医院2019年4月至2022年6月之间114例出现症状6 h内接受CT检查的原发性脑出血患者作为研究对象,评估两组患者入院后TEG指标中花生四烯酸(AA)抑制率、二磷酸腺苷(ADP)抑制率等与脑出血后再出血及病残率、病死率等结局的关系,以及与格拉斯哥昏迷量表评分的相关性。结果 未再出血组AA抑制率和ADP抑制率均明显低于再出血组(P<0.05);再出血组中死亡患者AA抑制率和ADP抑制率均明显高于康复组及病残组(P<0.05);AA抑制率和ADP抑制率与GCS评分呈负相关(r=-0.702,P=0.008)。结论在脑出血后再出血及预后的评估中,AA抑制率和ADP抑制率具有较好的预测价值,值得临床推广。

蛋白质ADP核糖基化对秦川牛肉品质的影响

为研究蛋白质ADP核糖基化对宰后成熟初期秦川牛肉线粒体功能及肉品质的影响,以20µmol/L Rucaparib(ADP核糖聚合酶1(poly(ADP-ribose)polymerase 1,PARP1)抑制剂)处理的秦川牛背最长肌为研究对象,测定贮藏0 h、6 h、12 h、2 d、4 d、8 d对照组和抑制剂处理组样品的线粒体相关指标及肌原纤维小片化指数(myofibril fragmentation index,MFI)、剪切力、pH值等品质指标,并采用免疫印迹(Western Blot)法检测PARP1、肌间线蛋白表达水平。结果表明:0 h~8 d(12 h除外)抑制剂组活性氧含量显著低于对照组(P<0.05),宰后0~12 h抑制剂组Caspase-3活性、MFI显著低于对照组(P<0.05);在2~4 d抑制剂组线粒体膜电位较对照组高,4~8 d抑制剂处理组琥珀酸脱氢酶(succinate dehydrogenase,SDH)活性显著高于对照组(P<0.05)。说明抑制表征ADP核糖基化反应进行的PARP1后,线粒体膜电位下降变缓,SDH活性升高,这一定程度上维持了线粒体功能,使MFI下降、肌间线蛋白降解变缓,从而延缓肉品嫩化。

Sitravatinib联合Niraparib对黏膜黑色素瘤细胞系增殖、凋亡和自噬的影响及其机制

目的研究抗血管生成药物Sitravatinib联合多聚(腺苷二磷酸[ADP]-核糖)聚合酶抑制剂(PARPi)Niraparib对黏膜黑色素瘤细胞的作用及其可能的机制。方法CCK8法检测Sitravatinib和Niraparib在黏膜黑色素瘤(MM)细胞系的半数抑制浓度(IC 50);CompuSyn模型计算不同浓度联合条件下的联合指数(CI)。细胞集落形成实验测定细胞增殖;流式细胞测量术测定细胞凋亡;Western blot检测蛋白质表达;RT-qPCR检测mRNA表达。结果在人阴道黏膜来源黑色素瘤细胞系(HMVⅡ)和人外阴黏膜黑色素瘤腹股沟淋巴结转移病灶来源细胞系(GAK)中Sitravatinib(2μmol/L)联合Niraparib(20μmol/L)条件下CI值分别为0.19和0.15;与对照组及单药组相比,联合组细胞增殖能力显著下降(P<0.05或P<0.01或P<0.001);细胞凋亡率显著升高(P<0.01或P<0.001),凋亡标志物蛋白质和mRNA表达均显著升高(P<0.001);细胞自噬标志物蛋白质和mRNA表达显著升高(P<0.01或P<0.001);DNA损伤相关蛋白质表达显著升高。而与对照组相比,Sitravatinib单药组和联合组重组酶辐射敏感蛋白51(RAD51)表达显著下降。随着Sitravatinib剂量逐渐升高至2μmol/L,RAD51蛋白和mRNA表达显著下降(P<0.05或P<0.01),BRCA1与BRCA2的mRNA表达显著下降(P<0.05或P<0.01或P<0.001)。结论Sitravatinib联合Niraparib可抑制黏膜黑色素瘤细胞增殖,诱导细胞凋亡并促进细胞自噬,其机制可能与Sitravatinib抑制同源重组修复(HRR)水平相关。

疏肝健脾补髓方防治多腺苷二磷酸核糖聚合酶抑制剂维持治疗卵巢癌所致血液毒性的效果观察

目的观察疏肝健脾补髓方防治多腺苷二磷酸核糖聚合酶抑制剂(PARPi)维持治疗卵巢癌所致血液毒性的效果。方法选取2021年8月至2023年12月就诊于安徽医科大学第一附属医院中西医结合肿瘤科及医联体科室符合纳入标准的卵巢癌患者60例,按照随机数字表法分为观察组(30例)及对照组(30例)。对照组予以PARPi维持治疗,观察组在对照组基础上联合疏肝健脾补髓方同步治疗。治疗3个月后比较2组血液毒性发生率、严重程度、持续时间、中医证候积分及疗效、不良反应情况。结果治疗3个月后,观察组贫血、血小板减少及中性粒细胞减少发生率[26.7%(8/30)比53.3%(16/30)、23.3%(7/30)比50.0%(15/30)、20.0%(6/30)比46.7%(14/30)]及严重程度均低于对照组,差异均有统计学意义(均P<0.05)。观察组贫血及血小板减少的持续时间均短于对照组[(2.56±1.33)d比(4.21±2.00)d、(7.33±0.38)d比(9.26±1.22)d],差异均有统计学意义(均P<0.05)。治疗3个月后,观察组中医证候积分明显低于对照组,中医证候疗效好于对照组,差异均有统计学意义(均P<0.05)。观察组恶心呕吐、腹泻、便秘发生情况轻于对照组(均P<0.05)。结论疏肝健脾补髓方可减轻血液毒性发生率及严重程度,缩短发生时间,同时改善患者中医证候疗效,安全性尚可,维护了PARPi治疗的应答持续性。

高效液相色谱法同时测定烟酰胺单核苷酸中5种有关物质

目的构建同时检测烟酰胺单核苷酸(nicotinamide mononucleotide,NMN)中5种有关物质[烟酰胺氧化物、三磷酸腺苷(adenosine triphosphate,ATP)、二磷酸腺苷(adenosine diphosphate,ADP)、一磷酸腺苷(adenosine monophosphate,AMP)及烟酰胺]含量的高效液相色谱法。方法采用C18色谱柱(250 mm×4.6 mm,5μm),以50 mmol/L磷酸二氢钾缓冲盐溶液(用磷酸调节pH为4.5)-甲醇为流动相进行梯度洗脱,流速为1 mL/min,进样量为20μL,检测波长210 nm,柱温20℃,试样盘控温:5℃,并对方法的专属性、灵敏性、准确性、重复性、耐用性及适用性进行验证。结果烟酰胺氧化物、ATP、ADP、AMP及烟酰胺分别在质量浓度0.4060~16.2402、0.4110~16.4403、0.4150~16.6010、0.4163~16.6507、0.4028~16.1206μg/mL范围内,质量浓度与峰面积呈现良好的线性关系,线性系数r^(2)值均大于0.998;加标回收率范围分别为98.5%~102.6%、95.6%~104.1%、98.9%~104.6%、100.0%~102.8%、100.6%~101.3%;3批样品中5种杂质含量检测结果分别为0.18%、0.20%、0.16%、0.14%、0.26%;5种杂质的检出限范围为0.04028~0.04163μg/mL,定量限范围为0.4028~0.4163μg/mL,灵敏度高;专属性、重复性和耐用性均良好。结论该方法简便易行、适用性广,适用于NMN中5种有关物质的检测,为提升其质量标准奠定基础,为食品安全提供保障。

ARL14 在结直肠癌中的表达及其与肿瘤相关成纤维细胞浸润的关系

目的:探究二磷酸腺苷核糖基化因子样蛋白14(adenosine diphosphate-ribosylation factor-like protein 14,ARL14)在结直肠癌(colorectal cancer,CRC)中的表达水平及其与肿瘤微环境中浸润细胞的关系。方法:分析TCGA-CRC数据集中607例CRC组织与51例正常组织中ARL14的表达差异及其与预后之间的关系,并预测参与上游表达调控的转录因子和miRNA。应用生物信息学方法分析ARL14表达与肿瘤微环境中各细胞浸润的关系。收集2020年1月至2021年1月于天津医科大学肿瘤医院院行手术治疗的45例CRC患者的肿瘤及配对正常组织,使用免疫组织化学染色检测ARL14、平滑肌肌动蛋白-α(smooth muscle actin-α,α-SMA)和成纤维细胞活化蛋白(fibroblast activation protein,FAP)的表达情况,验证ARL14表达与成纤维细胞活化的关系。结果:差异分析显示CRC中ARL14的表达量显著低于正常组织(P<0.001)。与ARL14高表达患者相比,低表达患者的预后更差(P=0.025)。MCPcounter分析显示ARL14表达与成纤维细胞的浸润呈负相关(P<0.0001)。免疫组织化学染色结果显示ARL14在肿瘤中的表达显著低于正常组织(P<0.01),ARL14与间质中α-SMA、FAP的表达均为负相关。结论:ARL14可能在CRC中发挥肿瘤抑制基因的作用,并可能抑制成纤维细胞的活化。

Use of tailored loading-dose clopidogrel in patients undergoing selected percutaneous coronary intervention based on adenosine diphosphate-mediated platelet aggregation

Background Adenosine phosphate-mediated platelet aggregation is a prognostic factor for major adverse cardiac events in patients who have undergone selective percutaneous coronary interventions. This study aimed to assess whether an adjusted loading dose of clopidogrel could more effectively inhibit platelet aggregation in patients undergoing selected percutaneous coronary intervention.Methods A total of 205 patients undergoing selected percutaneous coronary intervention were enrolled in this multicenter, prospective, randomized study. Patients receiving domestic clopidogrel （n=104） served as the Talcom （Taijia）group; others （n=101） received Plavix, the Plavix group, Patients received up to 3 additional 300-mg loading doses of clopidogrel to decrease the adenosine phosphate-mediated platelet aggregation index by more than 50% （the primary endpoint） compared with the baseline. The secondary endpoint was major adverse cardiovascular events at 12 months.Results Compared with the rational loading dosage, the tailored loading dosage better inhibited platelet aggregation based on a ＞50% decrease in adenosine phosphate-mediated platelet aggregation （rational loading dosage vs. tailored loading dosage, 48% vs. 73%, P=0.028）. There was no significant difference in the eligible index between the Talcom and Plavix groups （47% vs. 49% at 300 mg; 62% vs. 59% at 600 mg; 74% vs. 72% at 900 mg; P ＞0.05） based on a standard adenosine diphosphate-mediated platelet aggregation decrease of ＞50%. After 12 months of follow-up, there were no significant differences in major adverse cardiac events （2.5% vs. 2.9%, P=5.43）. No acute or subacute stent thrombosis events occurred.Conclusion An adjusted loading dose of clopidogrel could have significant effects on antiplatelet aggregation compared with a rational dose, decreasing 1-year major adverse cardiac events in patients undergoing percutaneous coronary interventions based on adenosine phosphate-mediated platelet aggregation with no increase in bleeding.

Adenosine Diphosphate Ribosylation Factor-GTPase-Activating Protein Stimulates the Transport of AUX1 Endosome,Which Relies on Actin Cytoskeletal Organization in Rice Root Development

Polar auxin transport,which depends on polarized subcellular distribution of AUXIN RESISTANT 1/LIKE AUX1（AUX1/LAX） influx carriers and PIN-FORMED（PIN） efflux carriers,mediates various processes of plant growth and development.Endosomal recycling of PIN1 is mediated by an adenosine diphosphate（ADP）ribosylation factor（ARF）-GTPase exchange factor protein,GNOM.However,the mediation of auxin influx carrier recycling is poorly understood.Here,we report that overexpression of OsAGAP,an ARF-GTPase-activating protein in rice,stimulates vesicle transport from the plasma membrane to the Golgi apparatus in protoplasts and transgenic plants and induces the accumulation of early endosomes and AUX1.AUX1 endosomes could partially colocalize with FM4-64 labeled early endosome after actin disruption.Furthermore,OsAGAP is involved in actin cytoskeletal organization,and its overexpression tends to reduce the thickness and bundling of actin filaments.Fluorescence recovery after photobleaching analysis revealed exocytosis of the AUX1 recycling endosome was not affected in the OsAGAP overexpression cells,and was only slightly promoted when the actin filaments were completely disrupted by Lat B.Thus,we propose that AUX1 accumulation in the OsAGAP overexpression and actin disrupted cells may be due to the fact that endocytosis of the auxin influx carrier AUX1 early endosome was greatly promoted by actin cytoskeleton disruption.

Blocking Cyclic Adenosine Diphosphate Ribose-mediated Calcium Overload Attenuates Sepsis-induced Acute Lung Injury in Rats

Background： Acute lung injury （ALI） is a common complication of sepsis that is associated with high mortality, lntracellular Ca^2＋ overload plays an important role in the pathophysiology of sepsis-induced ALl, and cyclic adenosine diphosphate ribose （cADPR） is an important regulator of intracellular Ca^2＋ mobilization. The cluster of differentiation 38 （CD38）/cADPR pathway has been found to play roles in multiple inflammatory processes but its role in sepsis-induced ALl is still unknown. This study aimed to investigate whether the CD38/cADPR signaling pathway is activated in sepsis-induced ALl and whether blocking cADPR-mediated calcium overload attenuates ALl. Methods： Septic rat models were established by cecal ligation and puncture （CLP）. Rats were divided into the sham group, the CLP group, and the CLP＋ 8-bromo-cyclic adenosine diphosphate ribose （8-Br-cADPR） group. Nicotinamide adenine dinucleotide （NAD＋）, cADPR, CD38, and intracellular Ca^2＋ levels in the lung tissues were measured at 6, 12, 24, and 48 h after CLP surgery. Lung histologic injury, tumor necrosis factor （TNF）-a, malondialdehyde （MDA） levels, and superoxide dismutase （SOD） activities were measured. Results： NAD＋, cADPR, CD38, and intracellular Ca-＋ levels in the lungs of septic rats increased significantly at 24 h after CLP surgery. Treatment with 8-Br-cADPR, a specific inhibitor of cADPR, significantly reduced intracellular Ca^2＋ levels （P = 0.007）, attenuated lung histological injury （P = 0.023）, reduced TNF-a and MDA levels （P 〈 0.001 and P = 0.002, respectively） and recovered SOD activity （P = 0.031） in the lungs of septic rats. Conclusions： The CD38/cADPR pathway is activated in the lungs of septic rats, and blocking cADPR-mediated calcium overload with 8-Br-cADPR protects against sepsis-induced ALl.

GNOM-LIKE 2, Encoding an Adenosine Diphosphate-Ribosylation Factor-Guanine Nucleotide Exchange Factor Protein Homologous to GNOM and GNL1, is Essential for Pollen Germination in Arabidopsis

In flowering plants, male gametes are delivered to female gametophytes by pollen tubes. Although it is important for sexual plant reproduction, little is known about the genetic mechanism that controls pollen germination and pollen tube growth. Here we report the identification and characterization of two novel mutants, gnom-like 2-1 （gnl2-1） and gn12-2 in Arabidopsis thaliana, in which the pollen grains failed to germinate in vitro and in vivo. GNL2 encodes a protein homologous to the adenosine diphosphate-ribosylation factor-guanine nucleotide exchange factors, GNOM and GNL1 that are involved in endosomal recycling and endoplasmic reticulum-Golgi vesicular trafficking. It was prolifically expressed in pollen grains and pollen tubes. The results of the present study suggest that GNL2 plays an important role in pollen germination.

Ectopic Overexpression of Wheat Adenosine Diphosphate-ribosylation Factor,TaARF,Increases Growth Rate in Arabidopsis

Differential gene expression between hybrids and their parents is considered to be associated with heterosis. However, the physiological functions and possible contribution to heterosis of these differentially expressed genes are unknown. We have isolated one hybrid upregulated gene encoding putative wheat ADP-ribosylation factor, designated TaARF. In this study, real-time quantitative reverse transcription-polymerase chain reaction analysis indicated that the TaARF transcript was preferentially expressed in root, node and crown, and the accumulation of TaARF mRNA in hybrid was more than 1.5-fold higher than that in two parents. In order to understand possible roles of the putative wheat ARF gene, TaARF was overexpressed in Arabidopsis, and the transgenic plants were characterized. We show that ectopic overexpression of TaARF in Arabidopsis leads to increased leaf area, increased growth rate and earlier transition to flowering, suggesting that TaARF plays significant roles in growth and development. This study provides evidence demonstrating that TaARF plays important roles in growth and development and we speculate that the upregulated expression of this gene might contribute to the heterosis observed in wheat root and leaf growth.

预防性护理降低卵巢癌患者使用多腺苷二磷酸核糖聚合酶抑制剂后不良反应发生率

目的:探讨预防性护理对卵巢癌患者使用多腺苷二磷酸核糖聚合酶[poly(adenosine diphosphate ribose)polymerase,PARP]抑制剂后预防不良反应的效果。方法:收集2020年4月至2022年7月苏北人民医院收治的56例卵巢癌患者,随机分为对照组和观察组。对照组实施常规护理,观察组在常规护理的基础上实施预防性护理,比较2组满意度、疗效、焦虑自评量表(Self-Rating Anxiety Scale,SAS)和抑郁自评量表(Self-Rating Depression Scale,SDS)评分以及不良反应发生率。结果:观察组满意度96.43%,显著高于对照组71.42%(P<0.05),2组患者疗效差异无统计学意义(P>0.05);2组患者护理后SAS、SDS评分均显著低于护理前(均P<0.05);观察组不良反应发生率为14.29%,低于对照组的42.85%,差异有统计学意义(P<0.05)。结论:对使用PARP抑制剂的卵巢癌患者实施预防性护理干预,可有效降低患者使用PARP抑制剂后不良反应的发生率,可在临床推广。

二磷酸腺苷抑制率指导轻型脑卒中或高危短暂性脑缺血发作双联抗血小板方案

目的探讨二磷酸腺苷(ADP)抑制率指导轻型脑卒中或高危短暂性脑缺血发作(TIA)患者调整双联抗血小板方案的可行性和安全性。方法选取2020-01—2022-03在陕西省人民医院接受治疗的轻型脑卒中或高危TIA患者268例,所有患者在发病24 h内采用阿司匹林联合氯吡格雷进行抗血小板治疗,治疗3 d后检测ADP抑制率,根据ADP抑制率分为A组、B组和C组。A组患者不调整治疗方案,B组和C组患者在医师指导下选择原方案治疗或将氯吡格雷改为替格瑞洛。观察出院时间、治疗期间的血小板反应指数(PRI)和血小板-纤维蛋白凝块强度(MAADP)、出血事件和不良反应以及随访3个月的再发脑卒中率。结果A组119例患者中未调整治疗方案,B组79例患者中40例调整了治疗方案,C组70例患者中36例调整了治疗方案。A组患者的住院时间、MAADP、PRI、再发脑卒中率均低于B组和C组(P<0.05),B组和C组的住院时间、MAADP、PRI、再发脑卒中率比较差异无统计学意义(P>0.05)。B组和C组中调整治疗方案患者的住院时间、MAADP、PRI、再发脑卒中率均低于未调整治疗方案者(P<0.05)。B组和C组中调整治疗方案患者的住院时间、MAADP、PRI、再发脑卒中率与A组比较差异无统计学意义(P>0.05)。各组患者均未发生出血事件。各组患者的不良反应发生率比较差异无统计学意义(P>0.05)。结论ADP抑制率>70%的轻型脑卒中或高危TIA患者采用阿司匹林联合氯吡格雷方案治疗可取得满意的治疗效果,ADP抑制率较低的患者更换治疗方案可获益。

电阻抗法对2型糖尿病患者血小板聚集功能水平的研究

目的:通过研究2型糖尿病(T2DM)患者的血小板聚集功能水平,为2型糖尿病患者血栓(及出血)防治提供客观的依据。方法:入选231例该院住院的T2DM患者作为研究对象(研究组),以健康体检者222例作为对照组,利用PL-12型全自动血小板功能分析仪分别检测花生四烯酸(AA)和二磷酸腺苷(ADP)诱导的血小板聚集率。对研究组和对照组的血小板聚集率进行比较,收集并分析研究组血小板聚集率与糖化血红蛋白(HbA1c)、平均血小板体积(MPV)、病程之间的相关性,比较研究组不同血糖控制水平之间、有/无并发症之间的血小板聚集率差异。结果:研究组AA和ADP诱导的血小板聚集率均明显高于对照组,差异均有统计学意义(P<0.05)。研究组AA和ADP诱导的血小板聚集率与HbA1c水平和病程均无相关性(P>0.05,r>0);研究组ADP诱导的血小板聚集率与MPV呈负相关(P<0.05,r<0),AA诱导的血小板聚集率与MPV无相关性(P>0.05,r<0)。研究组AA和ADP诱导的血小板聚集率在不同血糖控制水平之间差异均无统计学意义(P>0.05)。研究组AA和ADP诱导的无并发症患者的血小板聚集率与有并发症患者差异均无统计学意义(P>0.05)。结论:T2DM患者的血小板聚集功能水平明显增强,与HbA1c、MPV、病程和并发症无明显关联。