冠心病患者颈动脉粥样硬化超声相关参数与病变严重程度的关系

目的:研究冠心病患者颈动脉粥样硬化超声相关参数与病变严重程度的关系,为冠心病的诊断提供依据。方法:选取2015年1月至2016年6月我院收治的冠心病患者100例作为研究组,根据冠状动脉造影结果分为1支病变组(24例),2支病变组(44例)和3支病变组(32例)。根据Gensini评分分为轻度病变组(Gensini评分20分,n=26),中度病变组(20分≤Gensini评分40分,n=45)和重度病变组(Gensini评分≥40分,n=29)。另选取同期医院体检的健康体检者30例作为对照组。应用颈动脉超声多普勒检查各组颈动脉超声相关参数,采用Pearson相关性分析超声相关参数与病变严重程度的关系。结果:研究组颈动脉中膜厚度(IMT)、颈总动脉硬化度(β)、颈动脉顺应性(AC)、弹性系数(EP)、脉搏波传导速度(PEVβ)均显著高于对照组,差异有统计学意义(P0.05)。随着冠状动脉病变支数增加,受试者IMT、β、EP、AC、PEVβ升高,其中3支病变组2支病变组1支病变组对照组(P0.05)。随着冠状动脉病变程度增加,受试者IMT、β、EP、AC、PEVβ升高,其中重度病变组中度病变组轻度病变组对照组(P0.05)。经Pearson相关性分析显示:冠心病患者IMT、β、EP、AC、PEVβ与病变血管支数呈正相关(r=0.607,0.428,0.532,0.507,0.556,均P0.05),与Gensini评分呈正相关(r=0.624,0.432,0.517,0.521,0.543,均P0.05)。结论:冠心病患者颈动脉粥样硬化超声相关参数与患者病变程度相关,颈动脉超声检查可以作为冠心病的诊断手段。     

颈动脉内-中膜厚度对冠状动脉病变的预测价值

目的:探讨颈动脉内-中膜厚度对冠状动脉病变的预测价值。方法:根据冠状动脉造影结果,将183例行冠状动脉造影的患者分为3组:正常组59例为冠状动脉造影阴性;A组54例冠状动脉狭窄率50%;B组70例冠状动脉狭窄率≥50%。根据冠状动脉病变数量将124例冠状动脉狭窄的患者进一步分为单支病变组40例,双支病变组38例和多支病变组46例。所有患者行颈动脉超声检查,测量颈动脉内-中膜厚度。结果:A组、B组的颈动脉内-中膜厚度和冠脉积分(Gensini评分)均明显高于正常对照组,且B组颈动脉内-中膜厚度和Gensini评分均较A组明显增加,差异均有统计学意义(P0.05)。随着冠状动脉狭窄程度的加重,颈动脉内-中膜厚度和Gensini评分逐渐增加。多支病变组、双支病变组IMT值和Gensini评分均显著高于单支病变组(P0.05),而双支病变组与多支病变组比较差异均无统计学意义(P0.05)。颈动脉IMT厚度与冠状动脉病变数量相关性不大,与Gensini评分呈显著性正相关(P0.01)。结论:颈动脉内-中膜厚度能较好地预测冠状动脉病变程度,但不能预测冠状动脉病变范围。     

急性脑出血患者颈动脉斑块与血清hs CRP 及HbAlc的相关性研究

目的:探究急性脑出血患者颈动脉斑块与血清超敏C反应蛋白(hs-CRP)及糖化血红蛋白(Hb Alc)的相关性。方法:随机选取我院2013年5月至2015年1月脑科收治的急性脑出血患者84例,根据颈动脉粥样硬化标准将所有患者分为单纯脑出血组(n=25)、轻度粥样硬化组(n=34)和重度粥样硬化组(n=25)三组,另选取同期我院健康体检者50人(对照组)。对比分析四组颈总动脉膜厚度(IMT)空腹血糖(FPG)、三酰甘油(TG)、总胆固醇(TC)、低密度脂蛋白(LDL)、高密度脂蛋白(HDL)、hs-CRP与Hb Alc水平,分析急性脑出血患者颈动脉斑块的危险因素。结果:四组的IMT、TC、TG、HDL、LDL、hs-CRP和Hb Alc水平差异均具有统计学意义(P0.05),其中hs-CRP和Hb Alc水平在单纯脑出血组轻度粥样硬化组重度粥样硬化组(P0.05);IMT与hs-CRP和Hb Alc均呈现正相关(r=0.388、0.420,P0.05);IMT、hs-CRP和Hb Alc均为颈动脉粥样硬化的危险因素(OR=3.065、1.978、1.647,P0.05)。结论:急性脑出血患者体内hs-CRP及Hb Alc水平是颈动脉斑块形成的危险因素。     

RDW和hs-CRP水平在急性心肌梗死中的表达及与冠状动脉狭窄程度的关系

目的:研究红细胞分布宽度(RDW)和高敏C反应蛋白(hs-CRP)水平在急性心肌梗死中的表达及与冠状动脉狭窄程度的关系。方法:选取2010年1月到2015年1月我院收治的急性心肌梗死患者300例(研究组),另选取单纯心绞痛患者300例(对照组),比较两组RDW、hs-CRP、Gensini评分和冠状动脉病变支数,并分析RDW、hs-CRP和Gensini评分、冠状动脉病变支数的关系。结果:研究组RDW、hs-CRP、Gensini评分和冠状动脉病变支数均显著高于对照组,两组比较差异具有统计学意义(P0.05);冠状动脉Gensini评分和病变支数与RDW、hs-CRP呈正相关关系(r=0.58,0.69,0.49,0.57,P0.05),同时RDW和hs-CRP呈正相关关系(P0.05)。结论:急性心肌梗死患者会出现RDW和hs-CRP水平增高现象,和冠状动脉狭窄程度呈正相关关系。     

急性脑梗死患者血清RBP、NLR、PTX3水平与颈动脉粥样硬化斑块稳定性的关系研究

目的:探讨急性脑梗死(ACI)患者血清视黄醇结合蛋白(RBP)、中性粒细胞与淋巴细胞比值(NLR)、内正五聚蛋白3(PTX3)水平与颈动脉粥样硬化斑块稳定性的关系。方法:收集我院2017年1月～2019年1月收治的300例ACI患者,根据颈动脉粥样硬化斑块超声结果分为稳定斑块组(n=173)和不稳定斑块组(n=127),另选同期在我院体检中心进行健康体检的志愿者100例为对照组。对ACI患者和对照组进行RBP、NLR、PTX3、血脂指标的检测,并进行组间统计学对比。采用Pearson检验对ACI患者的RBP、NLR、PTX3与血脂指标的相关性进行分析。结果:三组受试者性别、年龄、体质指数(BMI)、吸烟史、饮酒史等基础资料对比无显著性差异(P0.05)。稳定斑块组、不稳定斑块组患者的RBP、NLR、PTX3水平均高于对照组,且不稳定斑块组上述指标水平高于稳定斑块组(P0.05)。稳定斑块组、不稳定斑块组患者的总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白(LDL-C)、纤维蛋白原(FIB)水平均高于对照组,且不稳定斑块组上述指标水平高于稳定斑块组(P0.05)。经Pearson检验分析,ACI患者的RBP、NLR、PTX3水平与TC、TG、LDL-C、FIB均呈正相关性(P0.05)。结论:在ACI患者中RBP、NLR、PTX3水平较高,并与患者的颈动脉粥样硬化斑块的稳定性有紧密的关联性。初步推测RBP、NLR、PTX3可能参与颈动脉粥样硬化斑块的形成,进而影响ACI疾病的发生发展过程。     

不同性别间颈动脉粥样硬化相关危险因素差异的研究

目的:探讨中年人群中不同性别间颈动脉粥样硬化相关危险因素的差异。方法:将104例中年颈动脉粥样硬化患者作为研究对象,其中男53例,女51例,比较两组体质量指数(BMI)、收缩压(SBP)、舒张压(DBP)、甘油三酯(TG)、总胆固醇(TC)、低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C)、脂蛋白(a)[Lp(a)]、空腹血糖(FBG)、血尿酸(UA)、超敏CRP(hs-CRP)的差异。结果:男性组BMI、TG、UA较女性组高,HDL-C、Lp(a)较女性组低,差异有统计学意义(P<0.05)。结论:有些颈动脉粥样硬化相关危险因素在不同性别中年人群中具有差异。     

冠心病患者颈动脉粥样硬化与血管内皮功能的临床研究价值

目的:探讨颈动脉粥样硬化与血管内皮功能与冠心病患者的相关性。方法:选取114例冠心病患者(54例单支病变和60例多支病变)为观察组和60例健康体检者为对照组,对两组患者动脉粥样硬化及血管内皮功能进行分析。结果:观察组患者TC、TG、HDL及血糖水平均高于对照组,观察组LDL水平显著低于对照组,两组比较差异有统计学意义(P<0.05);观察组患者颈动脉IMT、斑块积分及斑块数明显高于对照组(P<0.05),观察组FMD显著降低(P<0.05),多支病变组病变程度更严重(P<0.05)。结论:颈动脉粥样硬化与血管内皮功能可作为预测冠心病的重要指标,对预防和治疗冠心病具有重要意义。     

血清CK-MB和FIB水平与急性心肌梗死患者的冠状动脉狭窄程度关联

为了研究急性心肌梗死患者血清CK-MB、FIB与冠状动脉狭窄程度的相关性。本研究选择116例行冠状动脉造影检查者分为急性心肌梗死组(n=81)、对照组(n=35;冠状动脉造影阴性者)。用Gensini积分评定冠状动脉狭窄程度,根据评分将患者分为4组:Ⅰ组(0～7分) 8例,Ⅱ组(8～25分) 15例,Ⅲ组(26～46分) 30例及Ⅳ组(46分) 28例。测定各组血清CK-MB、FIB水平,并进行比较。研究结果表明:对照组和急性心肌梗死组年龄、体重、身高、舒张压、收缩压、脉压、心律、吸烟率、血清总胆固醇(total cholesterol, TC)、甘油三酯(triglyceride, TG)、低密度脂蛋白胆固醇(low density lipoprotein cholesterol, LDL-C)、高密度脂蛋白胆固醇(high density lipoprotein cholesterol, HDL-C)、左心室射血分数(left ventricular ejection fraction, LVEF)、左心室舒张末期容积(left ventricular end-diastolic volume, LVEDV)及左心室收缩末期容积(left ventricular endsystolic volume, LVESV)比较,差异无统计学意义(p0.05)。对照组和急性心肌梗死各组间Gensini评分具有显著性差异(p0.01)。对照组和Ⅰ、Ⅱ、Ⅲ、Ⅳ组之间血清CK-MB、FIB水平具有差异性,且有统计学意义(F=8.164, p0.017; F=6.351, p0.028)。对照组血清CK-MB与FIB水平与Gensini积分无相关性(r=0.13, p=0.35; r=0.19, p=0.27)。急性心肌梗死患者血清CK-MB与FIB水平和Gensini积分均呈正相关(r=0.66, p0.001; r=0.77, p0.001)。我们初步认为急性心肌梗死患者血清CK-MB和FIB水平显著升高,且与冠状动脉狭窄程度具有相关性。     

冠心病患者血清HN、CTRP3与血脂及病情严重程度的关系研究

摘要 目的：分析血清抗凋亡多肽（HN）、补体C1q肿瘤坏死因子相关蛋白因子3（CTRP3）与冠心病（CHD）患者血脂及病情严重程度的关系。方法：选取2017年1月至2018年12月期间西安医学院第二附属医院收治的CHD患者360例（CHD组）,另选取同期健康体检者100例作为对照组（NC组）,比较两组血清HN、CTRP3、血脂水平及基线资料;根据CHD患者病变支数分为单支病变组（n=131）、双支病变组（n=119）、多支病变组（n=110）,根据冠状动脉造影结果测定Gensini积分,采用Pearson相关分析HN、CTRP3与血脂及Gensini积分的相关性。结果：CHD组患者吸烟史比例、收缩压、空腹血糖、总胆固醇（TC）、甘油三酯（TG）及低密度脂蛋白（LDL-C）水平均高于NC组（P<0.05）,血清HN、CTRP3和高密度脂蛋白（HDL-C）均低于NC组（P<0.05）;CHD双支病变组和多支病变组患者吸烟史、空腹血糖、TC水平以及Gensini积分均高于单支病变组,CTRP3和HDL-C水平均低于单支病变组,多支病变组收缩压高于单支病变组,多支病变组吸烟史、空腹血糖和Gensini积分均高于双支病变组,且多支病变组CTRP3低于双支病变组（均P<0.05）;Pearson相关分析结果显示：CHD患者血清HN水平与HDL-C水平呈正相关性,CHD患者血清CTRP3水平与Gensini积分呈负相关（P<0.05）。结论：CHD患者血清中HN、CTRP3水平均显著降低,HN与HDL-C水平呈正相关,CTRP3降低程度与CHD患者病情严重程度有关,临床可考虑将其作为评估CHD患者病情严重程度的辅助血清学指标。     

血清尿酸水平对急性脑梗死患者颈动脉粥样硬化斑块的影响

目的:探讨血清尿酸(UA)水平对急性脑梗死患者颈动脉粥样硬化斑块的影响。方法:回顾性分析2011年6月至2016年1月我院收治的251例急性脑梗死患者的临床资料,根据有无颈动脉粥样硬化斑块分为伴颈动脉粥样硬化斑块组(观察组)176例和无颈动脉粥样硬化斑块组(对照组)75例,观察组根据颈动脉粥样硬化程度分为斑块形成组(113例)、内中膜增厚组(63例),根据颈动脉斑块稳定程度分为不稳定组(106例)、稳定组(70例),比较各组血清UA水平,根据UA水平不同分为高UA组(134例)和正常UA组(117例),进行颈动脉斑块发生情况比较。结果:观察组的血清UA水平显著高于对照组,差异有统计学意义(P0.05)。(1)斑块形成组和内中膜增厚组血清UA水平显著高于对照组(P0.05),而斑块形成组和内中膜增厚组血清UA水平比较,差异无统计学意义(P0.05);(2)不稳定组血清UA水平显著高于对照组和稳定组(P0.05),而稳定组和对照组血清UA水平比较,差异无统计学意义(P0.05);(3)正常UA组和高UA组颈动脉斑块的发生情况比较,差异无统计学意义(P0.05)。结论:血清UA水平可以作为表征急性脑梗死患者伴随出现颈动脉粥样硬化斑块的生物学指标之一,此外,血清UA的水平在颈动脉粥样硬化斑块形成者和不稳定者表达更高,但血清UA水平与颈动脉斑块形成无明显联系。     

斜纹夜蛾核多角体病毒(SpltNPV)基因组EcoR I-G片段的序列分析

斜纹夜蛾核多角体病毒(SpltNPV)基因组EcoR I-G片段全长7 450bp,包括7个开放读码框vp39、lef-4、cg30、p91、vp33、tlp20、AcMNPV ORF81同源基因和一个同源区(hr).基因组排列比较分析发现,这些基因在基因组中的排列,在所有已知序列的杆状病毒中都比较保守.     

Effects of increasing the number of players and memory size in the iterated Prisoner's Dilemma: a numerical approach

The Prisoner''s Dilemma has become a paradigm for the evolution of altruistic behaviour. Here we present results of numerical simulations of the infinitely iterated stochastic simultaneous Prisoner''s Dilemma considering players with longer memory, encounters of more than two players as well as different pay-off values. This provides us with a better foundation to compare theoretical results to experimental data. We show that the success of the strategy Pavlov, regardless of its simplicity, is far more general by having an outstanding role in the iterated N-player N-memory Prisoner''s Dilemma. Besides, we study influences of increased memory sizes in the iterated two-player Prisoner''s Dilemma, and present comparisons to results of experiments with first-year students.     

两湖泊轮虫群落结构的时空动态对水体氮磷含量及“下行效应”的响应

为探讨氮和磷、"上行效应"和"下行效应"在轮虫群落结构时空变动调控中的相对重要性,于2011年7月至2012年6月每月两次采集了芜湖市九莲塘和汀棠湖中的轮虫样品,利用相关分析法和典范对应分析法(CCA)分析了轮虫群落结构的时空变动与水体理化因子及其潜在捕食者密度间的关系。卡尔森营养状态指数表明,两湖均处在富营养化初期。除了总氮和硝态氮的年均浓度、晶囊轮虫(Asplanchna)和剑水蚤(Cyclopoidea)无节幼体的年均密度存在显著差异外(P0.05),两湖泊的其他水环境因子间并未表现出明显的差异(P0.05)。实验室鉴定发现九莲塘中共有轮虫48种,隶属于15科21属;汀棠湖中共有轮虫55种,隶属于15科24属。两湖泊中,疣毛轮虫(Synchaeta)、臂尾轮虫(Brachionus)和异尾轮虫(Trichocerca)均是主要轮虫类群,而密度优势种分别有7种和4种。相关分析结果显示,P含量与九莲塘轮虫群落的均匀度和物种多样性指数间均呈现显著的负相关(P0.05),而N含量却与汀棠湖轮虫群落的物种多样性指数呈现显著的正相关(P0.05);两湖泊中的轮虫物种多样性指数均与水体中的TN∶TP(质量比)间呈现显著的正相关(P0.05)。CCA分析结果显示,九莲塘中桡足类和其无节幼体密度显著高于其他采样批次时的轮虫群落聚成Ⅰ类,汀棠湖中晶囊轮虫密度显著高于其他批次时的轮虫群落聚成Ⅱ类,而其他的轮虫潜在捕食者密度很低或未出现时的轮虫群落聚成Ⅲ类。研究结果表明,湖泊中的TN∶TP(质量比)可能是反映N和P含量对轮虫群落物种多样性影响程度的较为合适的指标。当水体中的轮虫潜在捕食者密度较高时,两湖泊轮虫群落结构的变动均主要取决于"下行效应";而当轮虫潜在捕食者密度很低时,"上行效应"可能是调控两湖泊轮虫群落结构变动的主要因素。     

Hamilton's rule meets the Hamiltonian: kin selection on dynamic characters

Many biological characters of interest are temporal sequences of decisions. The evolution of such characters is often modelled using dynamic optimization methods such as the maximum principle. A quantity central to these analyses is the ''Hamiltonian'' function, named after the mathematician William R. Hamilton. On the other hand, evolutionary models in which individuals interact with relatives are usually based on Hamilton''s rule, named after the evolutionary biologist William D. Hamilton. In this article we present a generalized maximum principle that includes the effects of interactions among relatives and we show that a time-dependent (dynamic) version of Hamilton''s rule holds involving the Hamiltonian. This result brings together the power and generality of both the maximum principle and Hamilton''s rule thereby providing a natural framework for understanding the evolution of ''dynamic'' characters under kin selection.     

丘脑底核-深部脑刺激术术后淡漠的研究进展

帕金森病(Parkinson's disease,PD)是一种由于中脑黑质以及其他核团结构的多巴胺能神经元变性所致的以进行性运动功能障碍为主要表现的疾病。近年来,双侧高频刺激的丘脑底核-深部脑刺激术(STN-DBS)治疗PD效果确切,疗效较好,但其出现了术后淡漠等类似副作用,严重影响了PD治疗效果和患者的生活质量,引起了临床医生的高度重视。本文对STN-DBS术后淡漠发病情况、表现及治疗进行综述,为临床诊治提供思路。     

Effect of amyloids on the vesicular machinery: implications for somatic neurotransmission

Certain neurodegenerative diseases are thought to be initiated by the aggregation of amyloidogenic proteins. However, the mechanism underlying toxicity remains obscure. Most of the suggested mechanisms are generic in nature and do not directly explain the neuron-type specific lesions observed in many of these diseases. Some recent reports suggest that the toxic aggregates impair the synaptic vesicular machinery. This may lead to an understanding of the neuron-type specificity observed in these diseases. A disruption of the vesicular machinery can also be deleterious for extra-synaptic, especially somatic, neurotransmission (common in serotonergic and dopaminergic systems which are specifically affected in Alzheimer''s disease (AD) and Parkinson''s disease (PD), respectively), though this relationship has remained unexplored. In this review, we discuss amyloid-induced damage to the neurotransmitter vesicular machinery, with an eye on the possible implications for somatic exocytosis. We argue that the larger size of the system, and the availability of multi-photon microscopy techniques for directly visualizing monoamines, make the somatic exocytosis machinery a more tractable model for understanding the effect of amyloids on all types of vesicular neurotransmission. Indeed, exploring this neglected connection may not just be important, it may be a more fruitful route for understanding AD and PD.     

多奈哌齐治疗阿尔兹海默症患者的临床剂量使用探讨

目的:评价多奈哌齐治疗阿尔兹海默症(AD)的疗效及疗效与用药剂量的关系,探讨检测血清中胰岛素样生长因子-I(IGF-I)来指导治疗剂量的可行性。方法:87例轻中度的AD患者,患者使用5 mg/d多奈哌齐疗效不佳。在增加剂量之前,根据血清胰岛素样生长因子-I(IGF-I)水平和简易智力状态检查表(MMSE)得分之间的一致性,将患者分为3组。A组:n=27,IGF-I≤99ng/m L,MMSE≤37;B组:n=33,IGF-I≤99 ng/m L,MMSE18;C组:n=27,IGF-I99 ng/m L,MMSE18。A、B组中,血清IGF-I水平显著低于C组。试验开始后将多奈哌齐的剂量从5 mg/d增加到10 mg/d,服用12周后,观察血清IGF-I水平同MMSE和阿尔兹海默症评定量表(ADAS)得分的相关性及三组患者的临床改善情况。结果:血清IGF-I水平同认知功能有明显相关性。IGF-I同MMSE正相关(r=0.478,P=0.036),IGF-I同ADAS得分负相关(r=-0.464,P=0.029)。增加多奈哌齐(10 mg/d)剂量治疗后,只有A组患者MMSE得到显著改善。A组患者对治疗的敏感性显著高于B、C组患者。结论:血清中IGF-I水平和MMSE分值可以做为一种标志物,判断对低剂量多奈哌齐(5 mg/d)无效的轻中度AD患者,能否采用高剂量多奈哌齐(10 mg/d)进行治疗。     

Interpretation of the dissolution of insoluble peptide sequences based on the acid-base properties of the solvent

The dissolution process of model insoluble peptide sequences was investigated in view of the electron acceptor (AN) and electron donor (DN) solvent properties. The Alzheimer's disease-inducing (1-42) Abeta-amyloid peptide and its (1-21) fragment, the (66-97) transmembrane bradykinin B2 receptor sequence, and the strongly aggregated VVLGAAIV were selected as models of insoluble peptides. Solvents presenting similar AN and DN values failed, despite their polarities, to dissociate peptide chains (free in solution or bound to a polymer). The maximum solubility of these aggregated sequences was attained in solvents presenting the highest possible (AN-DN) values (in positive or negative mode). The AN-DN values ranged from approximately -20 to +80 and, notably, the lowest dissociation power was ascribed to solvents presenting values of approximately +40. The strong hydrogen bond donor water is located in this region, indicating that, for dissociation of specific insoluble segments, the solvent should appropriately combine its acid/base strength with the potential for van der Waals interactions. We also observed a sequence-dependent pH effect on peptide solubility confirmed through circular dichroism spectroscopy. This approach also revealed a complex but, in many cases, consistent influence of peptide conformation on its solubility degree, even when structure-inducing solvents were added. In conclusion, the random method of selecting solvents to dissolve insoluble and intractable peptide sequences, still in use by some, could be partially supplanted by the strategy described herein, which may be also applicable to other solute dissociation processes.     

Discovery of catalytically active orthologues of the Parkinson's disease kinase PINK1: analysis of substrate specificity and impact of mutations

Missense mutations of the phosphatase and tensin homolog (PTEN)-induced kinase 1 (PINK1) gene cause autosomal-recessive Parkinson's disease. To date, little is known about the intrinsic catalytic properties of PINK1 since the human enzyme displays such low kinase activity in vitro. We have discovered that, in contrast to mammalian PINK1, insect orthologues of PINK1 we have investigated-namely Drosophila melanogaster (dPINK1), Tribolium castaneum (TcPINK1) and Pediculus humanus corporis (PhcPINK1)-are active as judged by their ability to phosphorylate the generic substrate myelin basic protein. We have exploited the most active orthologue, TcPINK1, to assess its substrate specificity and elaborated a peptide substrate (PINKtide, KKWIpYRRSPRRR) that can be employed to quantify PINK1 kinase activity. Analysis of PINKtide variants reveal that PINK1 phosphorylates serine or threonine, but not tyrosine, and we show that PINK1 exhibits a preference for a proline at the +1 position relative to the phosphorylation site. We have also, for the first time, been able to investigate the effect of Parkinson's disease-associated PINK1 missense mutations, and found that nearly all those located within the kinase domain, as well as the C-terminal non-catalytic region, markedly suppress kinase activity. This emphasizes the crucial importance of PINK1 kinase activity in preventing the development of Parkinson's disease. Our findings will aid future studies aimed at understanding how the activity of PINK1 is regulated and the identification of physiological substrates.