hypoperfusion

灌注不足
  • 文章类型: Journal Article
    使用可行的方法识别和验证具有高特异性的早期路易体痴呆(DLB)的生物标志物对于增强当前的次优诊断程序至关重要。先前的研究揭示了异常,包括组水平的右前岛叶皮质灌注不足,在前驱DLB中。探索右前岛叶灌注不足,在个体水平,并评估其作为早期DLB潜在成像生物标志物的相关性,has,根据我们的知识,没有被调查。我们的初步研究旨在评估该技术的可行性,并为进一步研究提供方法框架。我们评估了每动脉自旋标记磁共振成像(ASL-MRI)作为早期DLB诊断生物标志物的右前岛叶灌注不足的可行性和准确性,并提供了其敏感性和特异性的粗略估计。根据先前的研究定义感兴趣的区域,我们将生物标志物确定为右前岛叶灌注不足.与对照组的难治性抑郁症患者相比,评估了辨别和分析性能。在两种情况下,贝叶斯诊断推理用于评估早期DLB中生物标志物的诊断可用性:健康的老年人对照和轻度认知障碍。此外,我们通过整合来自Mayo-clinical认知波动量表的数据和实时振动诱导转化(RT-QuIC)α-突触核蛋白数据更新了概率.最后,我们对DLB患者进行了全脑灌注分析,以进一步确定具有辨别能力的脑区.我们在所有DLB患者的个体水平上成功复制了右前岛叶灌注不足(RAI-Hypo)。生物标志物的总体敏感性为96%,特异性为92%。贝叶斯测试揭示了生物标志物在具有认知波动的早期DLB中的最高表现,展示了与高精度和中等准确性相关的诊断潜力。在认知无障碍的人群中,RAI-Hypo显示出有限的可用性,并且缺乏作为筛选工具的选择性.探索性全脑分析显示,双侧前叶和左下顶叶小叶具有完美的判别能力。需要进一步的研究来证实我们的初步结果。如果在后续研究中保持性能,并与更合适的对照人群进行比较,所提出的生物标志物最终可能足以区分早期DLB和非DLB.
    Identifying and validating a biomarker with high specificity in early-stage dementia with Lewy bodies (DLB) using a feasible method is crucial to enhance the current suboptimal diagnostic procedure. Previous research revealed abnormalities, including hypoperfusion in the right anterior insular cortex at group level, in prodromal DLB. Exploring hypoperfusion of the right anterior insula, at an individual-level and assessing its relevance as a potential imaging biomarker in early DLB, has, to our knowledge, not been investigated. Our preliminary study aims to assess the feasibility of the technique and to provide a methodological framework for further investigation. We assessed the feasibility and accuracy of the hypoperfusion of the right anterior insula per arterial spin labelling magnetic resonance imaging (ASL-MRI) as a diagnostic biomarker in early DLB and provided rough estimates of its sensitivity and specificity. Defining the region of interest based on previous research, we established the biomarker as the hypoperfusion of the right anterior insula. Discriminative and analytical performances were assessed in comparison to a control group of treatment-resistant depression patients. Bayesian diagnostic reasoning was employed to assess the biomarker diagnostic usability in early DLB in two scenarios: healthy elderly controls and mild cognitive impairment. Additionally, we updated probabilities by integrating data from the Mayo-clinic cognitive fluctuations scale and real-time quaking-induced conversion (RT-QuIC) α-synuclein data. Lastly, a whole-brain perfusion analysis of DLB patients was conducted to identify further brain regions with discriminative abilities. We successfully replicated the right anterior insular hypoperfusion (RAI-Hypo) in all DLB patients at the individual level. The overall sensitivity of the biomarker was 96%, and the specificity was 92%. Bayesian testing revealed the biomarker\'s highest performance in early-stage DLB with cognitive fluctuations, showcasing a diagnostic potential associated with a high precision and moderate accuracy. In a cognitively non-impaired population, the RAI-Hypo showed a limited usability and lacked in selectivity to qualify as a screening tool. The exploratory whole-brain analysis revealed perfect discriminative capacities in the bilateral anterior insulae and the left inferior parietal lobule. Further studies are needed to confirm our preliminary results. If performance is maintained in subsequent studies and is compared to a more suitable control population, the proposed biomarker may be eventually sufficient to discriminate early-stage DLB from non-DLB.
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  • 文章类型: Journal Article
    低灌注,许多重大疾病的常见表现,可能导致体表热分布异常。然而,热图像的解释是困难的。我们的目的是通过红外热成像结合深度学习方法,在前瞻性队列中评估处于灌注不足风险的危重患者的死亡风险。
    这项事后研究基于高灌注风险的队列。选择患者的腿作为感兴趣的区域。收集热图像和常规灌注不足参数。尝试了六个深度学习模型来得出每位患者的死亡风险(范围:0至100%)。使用受试者工作特征曲线下面积(AUROC)来评估预测准确性。
    在由373名患者组成的队列中发生了55例住院死亡。常规灌注不足(毛细血管再充盈时间和舒张压)和热(低温面积率和标准偏差)参数对医院死亡率的预测准确性相似(AUROC0.73和0.77)。深度学习方法,尤其是ResNet(18),可以进一步提高精度。当使用36%的截止值时,ResNet(18)的AUROC为0.94,灵敏度为84%,特异性为91%。ResNet(18)在正常血压患者的死亡风险中呈现显著增加的趋势(13[7to26]),低血压(18[8至32])和休克(28[14至62])。
    用深度学习解释红外热成像可以准确且无创地评估存在灌注不足风险的患者的严重程度。
    UNASSIGNED: Hypoperfusion, a common manifestation of many critical illnesses, could lead to abnormalities in body surface thermal distribution. However, the interpretation of thermal images is difficult. Our aim was to assess the mortality risk of critically ill patients at risk of hypoperfusion in a prospective cohort by infrared thermography combined with deep learning methods.
    UNASSIGNED: This post-hoc study was based on a cohort at high-risk of hypoperfusion. Patients\' legs were selected as the region of interest. Thermal images and conventional hypoperfusion parameters were collected. Six deep learning models were attempted to derive the risk of mortality (range: 0 to 100%) for each patient. The area under the receiver operating characteristic curve (AUROC) was used to evaluate predictive accuracy.
    UNASSIGNED: Fifty-five hospital deaths occurred in a cohort consisting of 373 patients. The conventional hypoperfusion (capillary refill time and diastolic blood pressure) and thermal (low temperature area rate and standard deviation) parameters demonstrated similar predictive accuracies for hospital mortality (AUROC 0.73 and 0.77). The deep learning methods, especially the ResNet (18), could further improve the accuracy. The AUROC of ResNet (18) was 0.94 with a sensitivity of 84% and a specificity of 91% when using a cutoff of 36%. ResNet (18) presented a significantly increasing trend in the risk of mortality in patients with normotension (13 [7 to 26]), hypotension (18 [8 to 32]) and shock (28 [14 to 62]).
    UNASSIGNED: Interpreting infrared thermography with deep learning enables accurate and non-invasive assessment of the severity of patients at risk of hypoperfusion.
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  • 文章类型: Journal Article
    背景:脊髓损伤(SCI)破坏肠屏障功能,从而增加抗原渗透并导致不良结果。尽管肠道的解剖和生理异质性,SCI后的研究尚未全面解决肠道病理生理学和区域特异性。
    目的:我们使用高胸椎SCI的实验模型来研究(1)使用二氢乙啶标记的局部粘膜氧化应激;(2)通过Ussing室对小分子和大分子探针的局部细胞旁通透性;(3)局部肠紧密连接(TJ)蛋白表达;(4通过肠系膜尾动脉的后)肠灌注。
    结果:在SCI后3天,十二指肠粘膜内二氢乙啶染色显著升高。SCI后3天,[14C]-尿素的摩尔通量在十二指肠和近端结肠中显着升高,而[3H]-菊粉的摩尔通量仅在SCI后3天在十二指肠中显着升高。SCI后3天,十二指肠和近端结肠中成孔TJ蛋白claudin-2的表达显着增加反映了屏障通透性。在SCI后3周时,近端结肠中Claudin-2的表达仍然显着升高。SCI后3天,十二指肠中屏障形成TJ蛋白闭塞蛋白的表达显着降低。尽管平均动脉压显着降低,但SCI在3天或3周时肠系膜尾动脉血流没有变化。
    结论:这些数据表明T3-SCI引起粘膜氧化应激升高,TJ蛋白表达改变,和近端肠道的肠屏障通透性升高。相比之下,SCI后后肠粘膜氧化应激和肠屏障通透性无变化。这种区域异质性可能是由于对肠系膜灌注减少的敏感性不同所致。尽管需要进一步的研究来建立因果关系。了解肠道病理生理学的区域差异对于为SCI患者开发有效的治疗方法和护理标准至关重要。
    BACKGROUND: Spinal cord injury (SCI) disrupts intestinal barrier function, thereby increasing antigen permeation and leading to poor outcomes. Despite the intestinal tract\'s anatomic and physiologic heterogeneity, studies following SCI have not comprehensively addressed intestinal pathophysiology with regional specificity.
    OBJECTIVE: We used an experimental model of high thoracic SCI to investigate (1) regional mucosal oxidative stress using dihydroethidium labeling; (2) regional paracellular permeability to small- and large-molecular probes via Ussing chamber; (3) regional intestinal tight junction (TJ) protein expression; and (4) hindgut perfusion via the caudal mesenteric artery.
    RESULTS: Dihydroethidium staining was significantly elevated within duodenal mucosa at 3-day post-SCI. Molar flux of [14C]-urea was significantly elevated in duodenum and proximal colon at 3-day post-SCI, while molar flux of [3H]-inulin was significantly elevated only in duodenum at 3-day post-SCI. Barrier permeability was mirrored by a significant increase in the expression of pore-forming TJ protein claudin-2 in duodenum and proximal colon at 3-day post-SCI. Claudin-2 expression remained significantly elevated in proximal colon at 3-week post-SCI. Expression of the barrier-forming TJ protein occludin was significantly reduced in duodenum at 3-day post-SCI. Caudal mesenteric artery flow was unchanged by SCI at 3 days or 3 weeks despite significant reductions in mean arterial pressure.
    CONCLUSIONS: These data show that T3-SCI provokes elevated mucosal oxidative stress, altered expression of TJ proteins, and elevated intestinal barrier permeability in the proximal intestine. In contrast, mucosal oxidative stress and intestinal barrier permeability were unchanged in the hindgut after SCI. This regional heterogeneity may result from differential sensitivity to reduced mesenteric perfusion, though further studies are required to establish a causal link. Understanding regional differences in intestinal pathophysiology is essential for developing effective treatments and standards of care for individuals with SCI.
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  • 文章类型: Journal Article
    背景:保持向组织的充足的氧供应对于维持器官功能是基本的。然而,我们在腹部手术期间识别高危人群和及时识别组织灌注不足的能力有限.为了解决这个问题,我们的目标是开发一种新的灌注监测方法,该方法可在外科手术过程中使用,并帮助外科医生做出决策.
    方法:在本实验猪研究中,13名受试者被随机分配一个感兴趣的器官[胃(n=3),升结肠(n=3),直肠(n=3),和脾脏(n=3)]。基线灌注记录后,使用高频,低剂量推注与体重调整(0.008mg/kg)ICG,人工完全闭塞器官供血动脉,导致靶器官灌注不足.在整个实验条件下进行连续的器官灌注监测。
    结果:手动封堵预选器官供血动脉后,外周动脉供应的闭塞转化为大多数器官的振荡信号立即降低(3/3心室,3/3升结肠,3/3直肠,2/3脾)。中央动脉供应的阻塞导致心室中的振荡曲线进一步减少或完全消失(3/3),升结肠(3/3),直肠(3/3),和脾脏(1/3)。
    结论:使用高频率的连续器官灌注监测,低剂量ICG推注方案可以实时检测器官灌注不足。
    BACKGROUND: Preserving sufficient oxygen supply to the tissue is fundamental for maintaining organ function. However, our ability to identify those at risk and promptly recognize tissue hypoperfusion during abdominal surgery is limited. To address this problem, we aimed to develop a new method of perfusion monitoring that can be used during surgical procedures and aid surgeons\' decision-making.
    METHODS: In this experimental porcine study, thirteen subjects were randomly assigned one organ of interest [stomach (n = 3), ascending colon (n = 3), rectum (n = 3), and spleen (n = 3)]. After baseline perfusion recordings, using high-frequency, low-dose bolus injections with weight-adjusted (0.008 mg/kg) ICG, organ-supplying arteries were manually and completely occluded leading to hypoperfusion of the target organ. Continuous organ perfusion monitoring was performed throughout the experimental conditions.
    RESULTS: After manual occlusion of pre-selected organ-supplying arteries, occlusion of the peripheral arterial supply translated in an immediate decrease in oscillation signal in most organs (3/3 ventricle, 3/3 ascending colon, 3/3 rectum, 2/3 spleen). Occlusion of the central arterial supply resulted in a further decrease or complete disappearance of the oscillation curves in the ventricle (3/3), ascending colon (3/3), rectum (3/3), and spleen (1/3).
    CONCLUSIONS: Continuous organ-perfusion monitoring using a high-frequency, low-dose ICG bolus regimen can detect organ hypoperfusion in real-time.
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  • 文章类型: Journal Article
    腹主动脉瘤(AAA)是一种涉及主动脉壁扩张的血管疾病。吸烟是一个既定的危险因素和破裂,尼古丁可能是AAA发病的主要原因。在人类中,这种情况与血管狭窄(VV)有关,这可能是由尼古丁引起的。在这项研究中,我们评估了尼古丁对VV病理的影响。用渗透泵给大鼠服用尼古丁4周后,尼古丁给药组的VV通畅率明显低于对照组。细胞增殖标志物Ki-67的水平,在尼古丁组中含有VV的区域显着增加,缺氧诱导因子-α水平也是如此。尼古丁组VV周围的胶原蛋白水平显着低于对照组。我们的数据表明,尼古丁可以通过诱导VV中平滑肌细胞的异常增殖而导致VV狭窄。吸烟导致的AAA发展风险增加可能部分解释为尼古丁诱导的VV变性和胶原纤维降解。
    Abdominal aortic aneurysm (AAA) is a vascular disease that involves aortic wall dilation. Cigarette smoking is an established risk factor and rupture, and nicotine may be a major contributor to the onset of AAA. In humans the condition is associated with stenosis of the vasa vasorum (VV), which may be caused by nicotine. In this study, we evaluated the effects of nicotine on VV pathology. After 4 weeks of nicotine administration to rats using an osmotic pump, the VV patency rate in the nicotine administration group was significantly lower than that in the control group. The levels of Ki-67, a cell proliferation marker, were significantly increased in the regions containing VV in the nicotine group, as were hypoxia inducible factor-α levels. Collagen levels around VV were significantly lower in the nicotine group than in the controls. Our data suggest that nicotine can cause VV stenosis by inducing abnormal proliferation of smooth muscle cells in the VV. The increased risk of AAA development due to cigarette smoking may be partially explained by nicotine-induced VV denaturation and collagen fiber degradation.
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  • 文章类型: Journal Article
    背景:大脑灌注不足与身体恶化有关,多发性硬化症(MS)的认知和MRI结果。了解与灌注不足相关的蛋白质组特征可以提供对病理生理机制的见解。
    方法:包括140名MS患者(pwMS;86名临床孤立综合征(CIS)/复发缓解(RRMS)和54名进行性(PMS))。使用超声多普勒测量确定脑动脉血流(CABF),作为双侧颈总动脉和椎动脉的血流量总和。使用在Olink™平台上进行的多发性硬化疾病活性(MSDA)测试测定面板进行蛋白质组学分析。MSDA测试测量年龄和性别调整的18种蛋白质的浓度。它利用堆叠分类器逻辑回归模型来确定4种疾病途径得分(免疫调节,神经炎症,髓鞘生物学,和神经轴突完整性)以及总体疾病活动评分(1至10)。得出T2病变体积(LV)和全脑体积(WBV)的MRI测量值。
    结果:pwMS平均为54岁,平均CABF为951mL/min。CIS/RRMS与CABF之间没有差异PMS组。较低的CABF水平与总体疾病活动评分(r=-0.26,p=0.003)和神经炎症(r=-0.29,p=0.001)相关,免疫调节(r=-0.26,p=0.003)和神经轴突完整性(r=-0.23,p=0.007)途径评分。经过年龄和体重指数(BMI)调整后,较低的CABF仍然与神经炎症(r=-0.23,p=0.011)和免疫调节(r=-0.20,p=0.024)途径评分相关.校正T2-LV和WBV后,CABF与神经炎症途径评分之间的关系仍然显着(p=0.038)。个别分析确定神经丝轻链,CCL-20和TNFSF13B作为贡献者。与最高四分位数(>1133.5mL/min)相比,最低CABF四分位数(<764mL/min)的pwMS具有更大的总体疾病活动评分(p=0.003),神经炎症(p=0.001),免疫调节(p=0.004)和神经轴突完整性途径评分(p=0.007)。
    结论:MS患者大脑下动脉灌注与神经炎症/免疫调节通路及其各自的蛋白质组生物标志物的变化有关。这些发现可能表明灌注不足和促炎MS变化之间的关系,而不仅仅是能量需求降低之后的附加现象。
    BACKGROUND: Brain hypoperfusion is linked with worse physical, cognitive and MRI outcomes in multiple sclerosis (MS). Understanding the proteomic signatures related to hypoperfusion could provide insights into the pathophysiological mechanism.
    METHODS: 140 people with MS (pwMS; 86 clinically isolated syndrome (CIS)/relapsing-remitting (RRMS) and 54 progressive (PMS)) were included. Cerebral arterial blood flow (CABF) was determined using ultrasound Doppler measurement as the sum of blood flow in the bilateral common carotid arteries and vertebral arteries. Proteomic analysis was performed using the Multiple Sclerosis Disease Activity (MSDA) test assay panel performed on the Olink™ platform. The MSDA test measures the concentrations of 18 proteins that are age and sex-adjusted. It utilizes a stacked classifier logistic regression model to determine 4 disease pathway scores (immunomodulation, neuroinflammation, myelin biology, and neuroaxonal integrity) as well as an overall disease activity score (1 to 10). MRI measures of T2 lesion volume (LV) and whole brain volume (WBV) were derived.
    RESULTS: The pwMS were on average 54 years old and had an average CABF of 951 mL/min. There were no differences in CABF between CIS/RRMS vs. PMS groups. Lower CABF levels were correlated with the overall disease activity score (r = -0.26, p = 0.003) and with the neuroinflammation (r = -0.29, p = 0.001), immunomodulation (r = -0.26, p = 0.003) and neuroaxonal integrity (r = -0.23, p = 0.007) pathway scores. After age and body mass index (BMI)-adjustment, lower CABF remained associated with the neuroinflammatory (r = -0.23, p = 0.011) and immunomodulation (r = -0.20, p = 0.024) pathway scores. The relationship between CABF and the neuroinflammation pathway score remained significant after adjusting for T2-LV and WBV (p = 0.038). Individual analyses identified neurofilament light chain, CCL-20 and TNFSF13B as contributors. When compared to the highest quartile (>1133.5 mL/min), the pwMS in the lowest CABF quartile (<764 mL/min) had greater overall disease activity score (p = 0.003), neuroinflammation (p = 0.001), immunomodulation (p = 0.004) and neuroaxonal integrity pathway scores (p = 0.007).
    CONCLUSIONS: Lower cerebral arterial perfusion in MS is associated with changes in neuroinflammatory/immunomodulation pathways and their respective proteomic biomarkers. These findings may suggest a relationship between the hypoperfusion and pro-inflammatory MS changes rather than being merely an epiphenomenon subsequent to lower energy demands.
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  • 文章类型: Journal Article
    脂水肿是一种进行性结缔组织疾病,伴有脂肪组织增大,纤维化,流体收集,和真皮增厚。在这里,我们介绍了一例与皮肤灌注不足和溃疡相关的脂肪水肿,其中通过吸脂术使软组织减积改善了患者的症状。一名39岁的女性出现不对称的进行性最初的单侧下肢肿胀,并伴有严重的疼痛,随后出现皮肤溃疡。保守的管理未能改善她的状况。排除其他原因并进行详细的放射学检查后,脂水肿被诊断为相关的皮肤灌注受损。局部伤口护理和压迫疗法的试验未能改善病情。随后通过圆周吸脂术和溃疡清创术以及立即压迫进行的软组织减积显示出症状和皮肤灌注的显着改善。这种情况的独特性质揭示了作为疏松结缔组织疾病的脂水肿。炎症和微血管病变解释了与低灌注和溃疡相关的疼痛非常不典型,部分可能与基质蛋白和钠含量的大量积累有关,导致微血管脆性,伴有频繁的瘀点和血肿以及随后的组织缺血。保守措施如压迫治疗在病程中起着重要作用。手术减积与吸脂术被证明是有效的,在减少软组织负荷和改善四肢疼痛,水肿,周长,和我们病人的皮肤灌注。脂水肿是一种经常误诊的疾病,具有残疾特征。已显示皮肤受累于伴有潜在的灌注不足,需要进一步研究。
    Lipedema is a progressive connective tissue disease with enlargement of adipose tissue, fibrosis, fluid collection, and dermal thickening. Herein, we present a case of lipedema associated with skin hypoperfusion and ulceration in which soft tissue debulking with liposuction improved patients\' symptoms. A 39-year-old female presented with asymmetric progressive initially unilateral lower limb swelling with severe pain with subsequent skin ulceration. Conservative management failed to improve her condition. After excluding other causes and detailed radiologic investigation, lipedema was diagnosed with an associated impaired skin perfusion. Trial of local wound care and compression therapy failed to improve the condition. Subsequent soft tissue debulking with circumferential liposuction and ulcer debridement and immediate compression showed dramatic improvement of the symptoms and skin perfusion. The unique nature of this case sheds light on lipedema as a loose connective tissue disease. Inflammation and microangiopathies explain the associated pain with hypoperfusion and ulceration being quite atypical and in part might be related to the large buildups of matrix proteins and sodium contents leading to fragility in microvessels with frequent petechiae and hematoma and subsequent tissue ischemia. Conservative measures like compression therapy plays a significant role in disease course. Surgical debulking with liposuction was shown to be efficacious in reducing the soft tissue load with improvement in limb pain, edema, circumference, and skin perfusion that was seen in our patient. Lipedema is a frequently misdiagnosed condition with disabling features. Skin involvement in lipedema with potential hypoperfusion was shown and it requires further investigation.
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  • 文章类型: Journal Article
    探讨超早期急性脑梗死患者阻塞性睡眠呼吸暂停(OSA)与低灌注的关系。
    回顾性收集了2020年1月至2022年1月我院收治的急性脑梗死患者的数据,这些患者在发病6h内接受了全面的全脑CT灌注成像和血管造影检查。F-stroke软件自动评估并获得相关数据(Tmax)。患者接受了睡眠呼吸暂停的初步筛查。根据他们的呼吸暂停-呼吸不足指数(AHI),患者分为AHI≤15(n=22)或AHI>15(n=25)组.比较了剩余函数的最大时间(Tmax)>6s体积的成对差异,以及AHI之间的相关性,平均脉搏氧饱和度(SpO2),氧饱和度指数(ODI),氧饱和度<90%的时间百分比(T90%),并分析了Tmax>6s的体积。
    AHI>15组的Tmax>6s体积明显大于AHI≤15组[109(62-157)与59(21-106)mL,p=0.013]。Spearman相关分析显示Tmax>6s体积与AHI显著相关,平均SpO2,ODI,AHI>15组的T90%,然而,在AHI≤15组中没有观察到显著的相关性.控制闭塞部位和多相CT血管造影(mCTA)评分,AHI(β=0.919,p<0.001),平均SpO2(β=-0.460,p=0.031),ODI(β=0.467,p=0.032),在AHI>15组中,T90%(β=0.478,p=0.026)与早期低灌注相关。
    在急性脑梗死患者中,AHI>15,平均SpO2、ODI和T90%与早期灌注不足相关。然而,AHI≤15的患者之间不存在这种关系.
    UNASSIGNED: To explore the relationship between obstructive sleep apnea (OSA) and hypoperfusion during ultra-early acute cerebral infarction.
    UNASSIGNED: Data were retrospectively collected from patients admitted to our hospital with acute cerebral infarction between January 2020 and January 2022, who underwent comprehensive whole-brain computed tomography perfusion imaging and angiography examinations within 6 h of onset. The F-stroke software automatically assessed and obtained relevant data (Tmax). The patients underwent an initial screening for sleep apnea. Based on their Apnea-Hypopnea Index (AHI), patients were categorized into an AHI ≤15 (n = 22) or AHI >15 (n = 25) group. The pairwise difference of the time-to-maximum of the residue function (Tmax) > 6 s volume was compared, and the correlation between AHI, mean pulse oxygen saturation (SpO2), oxygen desaturation index (ODI), percentage of time with oxygen saturation < 90% (T90%), and the Tmax >6 s volume was analyzed.
    UNASSIGNED: The Tmax >6 s volume in the AHI > 15 group was significantly larger than that in the AHI ≤ 15 group [109 (62-157) vs. 59 (21-106) mL, p = 0.013]. Spearman\'s correlation analysis revealed Tmax >6 s volume was significantly correlated with AHI, mean SpO2, ODI, and T90% in the AHI > 15 group, however, no significant correlations were observed in the AHI ≤ 15 group. Controlling for the site of occlusion and Multiphase CT angiography (mCTA) score, AHI (β = 0.919, p < 0.001), mean SpO2 (β = -0.460, p = 0.031), ODI (β = 0.467, p = 0.032), and T90% (β =0.478, p = 0.026) remained associated with early hypoperfusion in the AHI > 15 group.
    UNASSIGNED: In patients with acute cerebral infarction and AHI > 15, AHI, mean SpO2, ODI and T90% were associated with early hypoperfusion. However, no such relationship exists among patients with AHI ≤ 15.
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  • 文章类型: Journal Article
    分水岭梗死(WIs)是一种不同类型的卒中,其临床表现变化,影响两个脑动脉区域之间的边界区域,并且通常与血流动力学损害和颈内动脉狭窄相关。然而,关于其与娱乐性物质和药物滥用历史的关联的数据很少。
    本病例报告显示了一名23岁男性的双侧内部分水岭梗塞的独特实例,该患者有多种物质滥用史,包括美沙酮和可卡因.病人的陈述包括混乱,下肢无力,和全身性并发症,如急性肝损伤和心肌坏死,潜在的临床方案的复杂性。
    调查显示没有动脉狭窄或血栓形成的证据,得出的结论是,梗死可能是由于药物滥用相关的脑灌注不足和血管收缩导致的完全意识丧失。美沙酮和可卡因,两者都与血管收缩有关,降低癫痫发作阈值并导致QTc延长,从而导致意识丧失,被确定为该事件的潜在触发因素。
    在年轻的成年人口中,重要的是将药物滥用视为分水岭梗塞的病因诱因,而多系统的参与和非典型的表现突出了全面方法的必要性。
    UNASSIGNED: Watershed infarcts (WIs) are a distinct type of stroke with a varying clinical presentation that affects the border areas between the territories of two cerebral arteries and are typically associated with hemodynamic impairment and internal carotid artery stenosis. However, there is a paucity of data concerning its association with the history of recreational substance and drug abuse.
    UNASSIGNED: This case report presents a unique instance of bilateral internal watershed infarcts in a 23-year-old male with a history of polysubstance abuse, including methadone and cocaine. The patient\'s presentation included confusion, lower limb weakness, and systemic complications such as acute liver injury and myonecrosis, underlying the complexity of the clinical scenario.
    UNASSIGNED: The investigation revealed no evidence of arterial stenosis or thrombosis, leading to the conclusion that the infarctions were likely precipitated by a total loss of consciousness due to substance abuse-related cerebral hypoperfusion and vasoconstriction. Methadone and cocaine, both implicated in vasoconstriction, lowering the seizure threshold and contributing to QTc prolongation, thus leading to loss of consciousness, were identified as potential triggers for the episode.
    UNASSIGNED: In the young adult population, it is important to consider drug abuse as an etiological trigger for watershed infarcts, whereas the multi-system involvement and atypical presentation highlight the need for a comprehensive approach.
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  • 文章类型: Journal Article
    阿尔茨海默病(AD)与血管功能障碍之间的紧密关系已成为老龄化社会日益关注的焦点。在本研究中,我们研究了扇贝衍生的缩醛磷脂(sPlas)对脑低灌注(HP)AD小鼠模型脑内血管重塑相关蛋白的长期影响.我们证明了,第一次,脑HP激活了晚期糖基化终产物受体(RAGE)/磷酸化信号转导和转录激活因子3(pSTAT3)/莫洛尼鼠白血病病毒1(PIM1)/活化T细胞核因子1(NFATc1)的前病毒整合位点,解释了这种脑血管重塑。此外,我们还发现脑HP加速了pSTAT3介导的星形胶质细胞增生和核苷酸结合域和富含亮氨酸重复蛋白3(NLRP3)炎性体的激活,可能导致认知能力下降。另一方面,sPlas治疗减弱了独立于RAGE的pSTAT3/PIM1/NFATc1轴的激活,并显着抑制了NLRP3炎性体的激活,证明对AD的有益作用。
    A strong relationship between Alzheimer\'s disease (AD) and vascular dysfunction has been the focus of increasing attention in aging societies. In the present study, we examined the long-term effect of scallop-derived plasmalogen (sPlas) on vascular remodeling-related proteins in the brain of an AD with cerebral hypoperfusion (HP) mouse model. We demonstrated, for the first time, that cerebral HP activated the axis of the receptor for advanced glycation endproducts (RAGE)/phosphorylated signal transducer and activator of transcription 3 (pSTAT3)/provirus integration site for Moloney murine leukemia virus 1 (PIM1)/nuclear factor of activated T cells 1 (NFATc1), accounting for such cerebral vascular remodeling. Moreover, we also found that cerebral HP accelerated pSTAT3-mediated astrogliosis and activation of the nucleotide-binding domain and leucine-rich repeat protein 3 (NLRP3) inflammasome, probably leading to cognitive decline. On the other hand, sPlas treatment attenuated the activation of the pSTAT3/PIM1/NFATc1 axis independent of RAGE and significantly suppressed NLRP3 inflammasome activation, demonstrating the beneficial effect on AD.
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