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1

Olson, Timothy M., David J. Driscoll, William D. Edwards, Francisco J. Puga, and Gordon K. Danielson. "Pulmonary microthrombi." Journal of Thoracic and Cardiovascular Surgery 106, no. 4 (1993): 739–44. http://dx.doi.org/10.1016/s0022-5223(19)33719-5.

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Fitzpatrick, James E., Carl Johnson, M. C. Major, Paul Simon, James Owenby, and Lieutenant Colonel. "Cutaneous Microthrombi." American Journal of Dermatopathology 9, no. 5 (1987): 419–22. http://dx.doi.org/10.1097/00000372-198710000-00008.

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Mihalko, Emily P., Megan Sandry, Nicholas Mininni, et al. "Fibrin-modulating nanogels for treatment of disseminated intravascular coagulation." Blood Advances 5, no. 3 (2021): 613–27. http://dx.doi.org/10.1182/bloodadvances.2020003046.

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Abstract Disseminated intravascular coagulation (DIC) is a pathological coagulopathy associated with infection that increases mortality. In DIC, excessive thrombin generation causes symptoms from formation of microthrombi to multiorgan failure; bleeding risks can also be a concern because of clotting factor consumption. Different clinical events lead to DIC, including sepsis, trauma, and shock. Treatments for thrombotic episodes or bleeding presentation in DIC oppose each other, thus creating therapeutic dilemmas in management. The objective of this study was to develop fibrin-specific core-sh
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Shao, Bojing, Mark G. Wahrenbrock, Longbiao Yao, et al. "Carcinoma mucins trigger reciprocal activation of platelets and neutrophils in a murine model of Trousseau syndrome." Blood 118, no. 15 (2011): 4015–23. http://dx.doi.org/10.1182/blood-2011-07-368514.

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Abstract Trousseau syndrome is classically defined as migratory, heparin-sensitive but warfarin-resistant microthrombi in patients with occult, mucinous adenocarcinomas. Injecting carcinoma mucins into mice generates platelet-rich microthrombi dependent on P- and L-selectin but not thrombin. Heparin prevents mucin binding to P- and L-selectin and mucin-induced microthrombi. This model of Trousseau syndrome explains resistance to warfarin, which inhibits fluid-phase coagulation but not selectins. Here we found that carcinoma mucins do not generate microthrombi in mice lacking P-selectin glycopr
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Jilientasia, Godrace Lilihataa, Pujo Semedia Bambang, Utariania Arie, et al. "Histopathological Examination with Cd61 Confirms D-Dimer as a Predictor of Diffuse Pulmonary Microthrombi Findings in Covid-19 Patients." International Journal of Innovative Science and Research Technology 7, no. 1 (2022): 349–55. https://doi.org/10.5281/zenodo.5910705.

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COVID-19 is a global concern that emerged and became a pandemic at March 2020. It is related to dysregulation of immune system causing excessive immune response known as cytokine storm. Other than that there is hypercoagulation that could progress to thrombosis and embolism in various vital organs. Pulmonary embolism is one of the dire consequences of hypercoagulation. CTPA and V/Q scan are the gold standards in pulmonary embolism diagnosis. However in developing countries like Indonesia these facilities are often absent. Thus a simple blood test like Ddimer could aid the detection of pulmonar
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6

Park, Sohyung, and Byung-Ha Choi. "Acute Myocardial Infarction with Microthrombi in Cardiac Small Vessels after COVID-19 Vaccination (ChAdOx1 nCov-19): A Case Report." Korean Journal of Legal Medicine 45, no. 4 (2021): 127–32. http://dx.doi.org/10.7580/kjlm.2021.45.4.127.

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We present the postmortem findings of an unexpected death due to acute myocardial infarction (AMI) with microthrombi and thrombosis in other vessels after the first dose of coronavirus disease 2019 (COVID-19) vaccination (ChAdOx1 nCov-19). The deceased was a 69-year-old woman who complained of nonspecific symptoms shortly after vaccination and was found dead on the sixth day. Postmortem examination revealed AMI and complications (left ventricular rupture, hemopericardium) with microthrombi in small cardiac vessels, which are similar to the characteristic findings of myocardial injury caused by
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7

Neil, Desley A. H. "CD31 highlights platelet-rich microthrombi." Histopathology 54, no. 3 (2009): 387–88. http://dx.doi.org/10.1111/j.1365-2559.2008.03215.x.

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Dienel, Ari, Remya Ammassam Veettil, Sung-Ha Hong, et al. "Microthrombi Correlates With Infarction and Delayed Neurological Deficits After Subarachnoid Hemorrhage in Mice." Stroke 51, no. 7 (2020): 2249–54. http://dx.doi.org/10.1161/strokeaha.120.029753.

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Background and Purpose: Delayed neurological deficits are a devastating consequence of subarachnoid hemorrhage (SAH), which affects about 30% of surviving patients. Although a very serious concern, delayed deficits are understudied in experimental SAH models; it is not known whether rodents recapitulate the delayed clinical decline seen in SAH patients. We hypothesized that mice with SAH develop delayed functional deficits and that microthrombi and infarction correlate with delayed decline. Methods: Adult C57BL/6J mice of both sexes were subjected to endovascular perforation to induce SAH. Mic
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9

Taha, Aladdin, Magdolna Nagy, Hajo M. Hund, et al. "Vascular injury and occurrence of microthrombi after endovascular therapy for acute ischaemic stroke in a thromboembolic model." BMJ Neurology Open 7, no. 1 (2025): e000989. https://doi.org/10.1136/bmjno-2024-000989.

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BackgroundEndovascular catheters and devices used for thrombectomy in patients who had a stroke can damage the vessel lumen leading to microthrombi. During stroke recanalisation, microthrombi could migrate distally and occlude cerebral microvasculature, potentially limiting the benefit of recanalisation therapy.ObjectivesTo describe vascular injury occurring after endovascular therapy (EVT), with stent retrievers (SR) and direct aspiration (DA), to open up avenues for further improvement of EVT technique.MethodsSR and DA were performed according to clinical procedures in extracranial vessels i
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10

Samal, Bibek, Ari Dienel, Sungha Hong, and Devin Mcbride. "1139 Role of Platelets in the Development of Neurological Deficits Resulting From Subarachnoid Hemorrhage in Mice." Neurosurgery 71, Supplement_1 (2025): 175. https://doi.org/10.1227/neu.0000000000003360_1139.

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INTRODUCTION: Microthrombosis (platelet aggregation) has been suggested as a major factor contributing to delayed neurological deterioration in patients after subarachnoid hemorrhage (SAH). However, experimental studies on the role of microthrombi in delayed deficits after SAH have not been investigated in depth. Similarly, the only clinically existing antiplatelet therapy is nimodipine, with other therapies being invasive. METHODS: SAH was induced in adult male and female C57BL/6 mice via endovascular perforation. Mice were randomly assigned into sham (n=6/sex) or SAH groups (n=22-24/sex). A
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11

Redfern, Andrew, Huda Mahmoud, Tom McCulloch, et al. "Renal Arcuate Vein Microthrombi-Associated AKI." Clinical Journal of the American Society of Nephrology 10, no. 2 (2014): 180–86. http://dx.doi.org/10.2215/cjn.01540214.

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Skjørten, Fredrik. "ON THE NATURE OF HYALINE MICROTHROMBI." Acta Pathologica Microbiologica Scandinavica 73, no. 4 (2009): 489–501. http://dx.doi.org/10.1111/j.1699-0463.1968.tb03208.x.

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Skjørten, Fredrik. "HYALINE MICROTHROMBI IN AN AUTOPSY MATERIAL." Acta Pathologica Microbiologica Scandinavica 76, no. 3 (2009): 361–75. http://dx.doi.org/10.1111/j.1699-0463.1969.tb03267.x.

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Huber, Alfred, Alexander Dorn, Alfred Witzmann, and Jorge Cerv�s-Navarro. "Microthrombi formation after severe head trauma." International Journal of Legal Medicine 106, no. 3 (1993): 152–55. http://dx.doi.org/10.1007/bf01225238.

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Fernández-Ruiz, Irene. "Microthrombi cause cardiac injury in COVID-19." Nature Reviews Cardiology 18, no. 5 (2021): 306. http://dx.doi.org/10.1038/s41569-021-00524-5.

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Aikawa, Tadao, Jiro Ogino, Yuichi Kita, and Naohiro Funayama. "Myocardial microthrombi after COVID-19 mRNA vaccination." European Heart Journal 42, no. 43 (2021): 4501. http://dx.doi.org/10.1093/eurheartj/ehab727.

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17

Spurlock, Ben O., and A. B. Chandler. "Microthrombi in Human Atherogenesis: A Sem Report." Proceedings, annual meeting, Electron Microscopy Society of America 43 (August 1985): 690–91. http://dx.doi.org/10.1017/s042482010012014x.

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The response to injury hypothesis for the pathogenesis of atherosclerosis as outlined by Ross and associates focuses on three major events: 1) that lesions of athero sclerosis are initiated in response to some form of injury to the arterial endothelium; 2) that focal sites of injury permit circulating blood elements; i.e., platelets, monocytes and lipoproteins to adhere to the subendothelial connective tissue; 3) that adherent platelets release platelet derived growth factor (PDGF) from their granules and lead to the proliferation of smooth muscle cells in the intima. if there is early repair
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18

Fox, S. B., C. A. Day, and K. C. Gatter. "Association between platelet microthrombi and finger clubbing." Lancet 338, no. 8762 (1991): 313–14. http://dx.doi.org/10.1016/0140-6736(91)90452-u.

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Kincaid-Smith, P. "Points: Myocardial microthrombi in systemic lupus erythematosus." BMJ 297, no. 6646 (1988): 489. http://dx.doi.org/10.1136/bmj.297.6646.489-d.

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Zhen, Zhu-Yin, Yu-Cheng Guo, Zhi-Gao Zhang, Liang-Yan, Pin-Ji Ge, and Hui-Ming Jin. "Experimental Study on Microthrombi and Myocardial Injuries." Microvascular Research 51, no. 1 (1996): 99–107. http://dx.doi.org/10.1006/mvre.1996.0010.

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Geys, Lotte, Dries Bauters, Elien Roose, et al. "ADAMTS13 deficiency promotes microthrombosis in a murine model of diet-induced liver steatosis." Thrombosis and Haemostasis 117, no. 01 (2017): 19–26. http://dx.doi.org/10.1160/th16-03-0195.

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SummaryADAMTS13 cleaves ultralarge multimeric von Willebrand Factor (VWF), thereby preventing formation of platelet-rich microthrombi. ADAMTS13 is mainly produced by hepatic stellate cells, and numerous studies have suggested a functional role of ADAMTS13 in the pathogenesis of liver diseases. The aim of our study was to investigate a potential role of ADAMTS13 in formation of hepatic microthrombi and development of non-alcoholic steatohepatitis (NASH), and furthermore to evaluate whether plasmin can compensate for the absence of ADAMTS13 in removal of thrombi. Therefore, we used a model of hi
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22

Fernando, Deepani D., Simone L. Reynolds, Gunter Hartel, et al. "A unique group of scabies mite pseudoproteases promotes cutaneous blood coagulation and delays plasmin-induced fibrinolysis." PLOS Neglected Tropical Diseases 15, no. 1 (2021): e0008997. http://dx.doi.org/10.1371/journal.pntd.0008997.

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Background Scabies, a highly contagious skin disease affecting more than 200 million people worldwide at any time, is caused by the parasitic mite Sarcoptes scabiei. In the absence of molecular markers, diagnosis requires experience making surveillance and control challenging. Superficial microthrombi in the absence of vasculitis in scabies-affected skin are a recognised, yet unexplained histopathological differential of scabies infection. This study demonstrates that a family of Scabies Mite Inactivated Cysteine Protease Paralogues (SMIPP-Cs) excreted by the mites plays a role in formation of
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23

MOHANAKRISHNAN, BALAJI PRASAD ELLAPPAN, KATHERINE G HOLDER, SARIA TASNIM, MANISH L PATEL, and NICOLE L DAVEY-RANASINGHE. "A RARE MICROTHROMBI DISEASE: CATASTROPHIC ANTIPHOSPHOLIPID ANTIBODY SYNDROME." Chest 162, no. 4 (2022): A982. http://dx.doi.org/10.1016/j.chest.2022.08.774.

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Simon, David, Laura Finn, and Allison Eddy. "Subepithelial Humps and Microthrombi: Looking for a Mechanism." American Journal of Kidney Diseases 47, no. 2 (2006): 365–70. http://dx.doi.org/10.1053/j.ajkd.2005.07.052.

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Heye, N., C. Paetzold, R. Steinberg, and J. Cervos-Navarro. "The topography of microthrombi in ischemic brain infarct." Acta Neurologica Scandinavica 86, no. 5 (1992): 450–54. http://dx.doi.org/10.1111/j.1600-0404.1992.tb05122.x.

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Sabri, M., J. Ai, K. Lakovic, J. D’abbondanza, D. Ilodigwe, and R. L. Macdonald. "Mechanisms of microthrombi formation after experimental subarachnoid hemorrhage." Neuroscience 224 (November 2012): 26–37. http://dx.doi.org/10.1016/j.neuroscience.2012.08.002.

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V. Tyravska, Yuliya. "Case of Lambl’s Excrescences And Microthrombosis Intracardially In Young Female With INOCA." Journal of Clinical Case Reports and Studies 5, no. 8 (2024): 01–06. https://doi.org/10.31579/2690-8808/221.

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Ischemia and No Obstructive Coronary Artery Disease (INOCA) causes angina pectoris in 30-50% of young females leading to higher risk of major adverse cardiovascular events (death, non-fatal myocardial infarction, stroke), increased frequency of hospitalization, decreased quality of life and functional status. Missed diagnosis and mismanagement is rather typical of patients with INOCA. It can be provoked by mental stress, vasoconstriction, infections (including viral), vaccination, Lambl’s excrescences, which may lead to local blood rheology disorders and intracardial microthrombi formation. Th
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Pellegrini, Dario, Rika Kawakami, Giulio Guagliumi, et al. "Microthrombi as a Major Cause of Cardiac Injury in COVID-19." Circulation 143, no. 10 (2021): 1031–42. http://dx.doi.org/10.1161/circulationaha.120.051828.

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Background: Cardiac injury is common in patients who are hospitalized with coronavirus disease 2019 (COVID-19) and portends poorer prognosis. However, the mechanism and the type of myocardial damage associated with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) remain uncertain. Methods: We conducted a systematic pathological analysis of 40 hearts from hospitalized patients dying of COVID-19 in Bergamo, Italy, to determine the pathological mechanisms of cardiac injury. We divided the hearts according to presence or absence of acute myocyte necrosis and then determined the underly
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Hosseinnejad, Aisa, Nadine Ludwig, Ann-Katrin Wienkamp, et al. "DNase I functional microgels for neutrophil extracellular trap disruption." Biomaterials Science 10, no. 1 (2022): 85–99. http://dx.doi.org/10.1039/d1bm01591e.

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Non-fouling DNase I conjugated microgel provide a novel biohybrid platform to disrupt Neutrophil extracellular traps (NETs) and can be used as a non-thrombogenic coating for reduction of NET-mediated inflammation and microthrombi formation.
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Kim, Hee Sung, Yoon-Sun Chun, Sung Nam Chang, and Wook-Hwa Park. "Hypereosinophilic syndrome: correlation between clinical severity and cutaneous microthrombi." International Journal of Dermatology 40, no. 5 (2001): 330–32. http://dx.doi.org/10.1046/j.1365-4362.2001.00971.x.

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Rapp, Joseph H., Kelsy Hollenbeck, and Xian Mang Pan. "An experimental model of lacunar infarction: Embolization of microthrombi." Journal of Vascular Surgery 48, no. 1 (2008): 196–200. http://dx.doi.org/10.1016/j.jvs.2008.01.038.

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Hamada, Takahiro. "Hypereosinophilic Syndrome With Peripheral Circulatory Insufficiency and Cutaneous Microthrombi." Archives of Dermatology 143, no. 6 (2007): 799. http://dx.doi.org/10.1001/archderm.143.6.812.

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Ramón y Cajal Agüeras, Santiago. "COVID-19 and pathology: What do we know?" ANALES RANM 137, no. 137(02) (2020): 133–39. http://dx.doi.org/10.32440/ar.2020.137.02.rev06.

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The experience of recent months in the study of the pathology associated with COVID-19 infection is showing histological alterations similar to other infections associated with previous pandemics, such as diffuse alveolar damage, signs of endotheliitis, inflammatory infiltrates and fibrin microthrombi. In the samples of patients with COVID-19, a greater number of cases with signs of endothelitis and a greater number of microthrombi stand out, both at the level of the lung parenchyma and in other locations, such as the colon, myocardium, liver … The study of the biopsies of patients who have ov
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Hoque, Muhammad Mazharul, Motiul Islam, Tarikul Hamid, Rabiul Halim, Rajib Hasan, and Kazi Nuruddin Ahmed. "Tissue plasminogen activator (tPA) treatment for COVID_19 associated acute respiratory distress syndrome (ARDS): A case report." Bangladesh Critical Care Journal 9, no. 1 (2021): 49–51. http://dx.doi.org/10.3329/bccj.v9i1.53059.

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Coagulopathy has proven to be a common complication of the novel coronavirus SARS-CoV-21. Some of the COVID-19 associated pneumonia patients exhibit relatively preserved lung compliance and high alveolar‐arterial oxygen gradient. Pathology reports consistently demonstrate diffuse pulmonary microthrombi on autopsy, consistent with a vascular occlusive etiology of respiratory failure rather than the more classic findings of ARDS2. Pulmonary microthrombi induced respiratory failure is very difficult to prove because the patients are so critically ill that transfer to CT suit to do CTPA often beco
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Bai, Sheng, Jintang Liao, Bo Zhang, et al. "Multimodal and multifunctional nanoparticles with platelet targeting ability and phase transition efficiency for the molecular imaging and thrombolysis of coronary microthrombi." Biomaterials Science 8, no. 18 (2020): 5047–60. http://dx.doi.org/10.1039/d0bm00818d.

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In this article, we constructed PLGA-cRGD-PFH-ICG NPs through emulsification process and then the bi-modal imaging of coronary microthrombi in ischemia/reperfusion rat model and thrombolysis of clots in vitro were both successfully completed by these NPs.
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Stein, Sherman C., Xiao-Han Chen, Grant P. Sinson, and Douglas H. Smith. "Intravascular coagulation: a major secondary insult in nonfatal traumatic brain injury." Journal of Neurosurgery 97, no. 6 (2002): 1373–77. http://dx.doi.org/10.3171/jns.2002.97.6.1373.

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Object. The goal of this study was to determine the frequency with which cerebral intravascular coagulation (IC) complicates traumatic brain injury (TBI). The authors also investigated the incidence of IC in relation to varying mechanisms, time courses, and severities of TBI and in different species. Methods. Tissue was sampled from surgical specimens of human cerebral contusions, from rats with lateral fluid-percussion injuries, and from pigs with head rotational acceleration injuries. Immunohistochemical fluorescent staining for antithrombin III was performed to detect cerebral intravascular
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Islam, Md Motiul, Muhammad Mazharul Hoque, Tarikul Hamid, Muhammad Rabiul Halim, Kazi Nuruddin Ahmed, and Rajib Hasan. "Tissue plasminogen activator (tPA) treatment for COVID 19 associated respiratory failure: A case Series." Bangladesh Critical Care Journal 10, no. 1 (2022): 62–67. http://dx.doi.org/10.3329/bccj.v10i1.59207.

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The global pandemic of COVID-19 has oversaturated the medical care facilities with a large proportion of patient associated with acute respiratory distress syndrome (ARDS). ARDS in patients with COVID-19 is associated with high incidence of pulmonary embolism, pulmonary hypertension and microthrombotic complications. Although heparin is frequently used to treat thrombotic pathology COVID-19, pulmonary embolism is still observed in severe cases. Pathology reports consistently demonstrate diffuse pulmonary microthrombi on autopsy, consistent with vascular occlusive etiology of respiratory failur
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Wang, Xue-Feng, Pei-Pei Jin, Tong Zhou, et al. "MR Molecular Imaging of Thrombus: Development and Application of a Gd-based Novel Contrast Agent Targeting to P-selectin." Clinical and Applied Thrombosis/Hemostasis 16, no. 2 (2009): 177–83. http://dx.doi.org/10.1177/1076029608330470.

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Molecular imaging of thrombus formation at initial stage requires a robust thrombus-specific contrast agent with high sensitivity. In this study, we report a novel P-selectin-targeted paramagnetic molecular imaging agent and the agent’s potential to sensitively detect occult microthrombi on the intimal surface of endothelium. Platelet clots and blood clots targeted in vitro with paramagnetic nanoparticles presented a highly detectable, homogeneous T1-weighted contrast enhancement that was improved with increasing gadolinium level. In vivo contrast enhancement under part of circulation conditio
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Krivosikova, Lucia, Michal Palkovic, Pavol Janega, Kristina Mikus Kuracinova, Andrea Janegova, and Pavel Babal. "A Comprehensive Clinicopathological Analysis of the First Wave of COVID-19 in Slovakia." COVID 5, no. 3 (2025): 29. https://doi.org/10.3390/covid5030029.

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The early introduction of strict measures during the first wave of COVID-19 in Slovakia resulted in a low number of fatal cases. Most of them (27/28) were autopsied with microscopic evaluation focusing on changes in the lungs. The average age of the patients was 79. The most common microscopic finding was diffuse alveolar damage in various stages. There were statistically significant relationships between microthrombi and neutrophil count, level of C-reactive protein, and immobility. Oxygen therapy, as a factor that might cause changes typical for diffuse alveolar damage, showed statistically
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Zuo, Yu, Yogendra Kanthi, Jason S. Knight, and Alfred H. J. Kim. "The interplay between neutrophils, complement, and microthrombi in COVID-19." Best Practice & Research Clinical Rheumatology 35, no. 1 (2021): 101661. http://dx.doi.org/10.1016/j.berh.2021.101661.

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Wehn, Antonia, Andrey Klymchenko, Nikolaus Plesnila, and Igor Khalin. "Microthrombi-Mediated Blood-Brain-Barrier Dysfunction after Traumatic Brain Injury." Brain and Spine 4 (2024): 103402. http://dx.doi.org/10.1016/j.bas.2024.103402.

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Giles, W., D. Pepperall, and N. Wilson. "Abnormal placental doppler studies not related to platelet microthrombi formation." Placenta 15, no. 7 (1994): A19. http://dx.doi.org/10.1016/0143-4004(94)90079-5.

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Shehi, Elona, Sridhar Chilimuri, Dongmin Shin, Madanmohan Patel, Nisha Ali, and Masooma Niazi. "Microthrombi in skin biopsy of a patient with COVID-19." JAAD Case Reports 6, no. 12 (2020): 1327–29. http://dx.doi.org/10.1016/j.jdcr.2020.10.009.

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Guagliumi, Giulio, Aurelio Sonzogni, Irene Pescetelli, Dario Pellegrini, and Aloke V. Finn. "Microthrombi and ST-Segment–Elevation Myocardial Infarction in COVID-19." Circulation 142, no. 8 (2020): 804–9. http://dx.doi.org/10.1161/circulationaha.120.049294.

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Chavanon, Olivier, Monsef Hlal, Abderhamane Bakkali, et al. "Multiple Microthrombi on a Papillary Fibroelastoma of the Aortic Valve." Annals of Thoracic Surgery 93, no. 1 (2012): 304–6. http://dx.doi.org/10.1016/j.athoracsur.2011.06.043.

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Thorp, K. E., James A. Thorp, Elise M. Thorp, Margery M. Thorp, and Paul R. Walker. "COVID-19: Energy, Protein Folding & Prion Disease." Gazette of Medical Sciences 3, no. 1 (2022): 179–206. http://dx.doi.org/10.46766/thegms.neuro.22083101.

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The recent recognition of intravascular amyloid formation with deposition of insoluble microthrombi throughout the circulatory system in primary COVID-19 infection or following administration of mRNA vaccines is a pivotal discovery that alters conventional notions about the nature of the underlying pathologic process at play in SARS-CoV-2 infection.
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Linneweber, J., T. Chow, T. Takano, et al. "FLOW CYTOMETRIC ASSAY TO QUANTIFY PUMP INDUCED MICROTHROMBI DURING CARDIOPULMONARY BYPASS." ASAIO Journal 46, no. 2 (2000): 182. http://dx.doi.org/10.1097/00002480-200003000-00127.

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Muto, Yuko, Kokichi Suzuki, Eriko Sato, and Hidemi Ishii. "Carboxypeptidase B inhibitors reduce tissue factor-induced renal microthrombi in rats." European Journal of Pharmacology 461, no. 2-3 (2003): 181–89. http://dx.doi.org/10.1016/s0014-2999(03)01297-4.

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Brown, J. H., C. C. Doherty, D. C. Allen, and P. Morton. "Fatal cardiac failure due to myocardial microthrombi in systemic lupus erythematosus." BMJ 296, no. 6635 (1988): 1505. http://dx.doi.org/10.1136/bmj.296.6635.1505.

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Guria, G. T., M. A. Herrero, and K. E. Zlobina. "Ultrasound detection of externally induced microthrombi cloud formation: a theoretical study." Journal of Engineering Mathematics 66, no. 1-3 (2009): 293–310. http://dx.doi.org/10.1007/s10665-009-9340-9.

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