126 results on '"microthrombosis"'
Search Results
102. Monoclonal cryoglobulin of IgG (λ) type interacting with transferrin.
- Author
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Hilgard, P., Linder, K., and Wetter, O.
- Abstract
We report on a 49 year old patient with myeloma who suffered from serious disturbance of the blood circulation in both legs and who had a fatal outcome. Histologically ubiquitous thrombosis of the small arteries and veins of the skin and muscles was found. The formation of these thrombi is probably caused by the intravascular precipitation of a fragment of a monoclonal cryoglobulin of the IgG (λ) type. The peculiarity of this cryoglobulin was its occurrence 'in vitro' in a complex with transferrin and fibrinogen. The interaction between transferrin and paraprotein was verified by chromatography of the serum of this patient on DEAE Sephadex A-50 ion exchanger. The spontaneous precipitation of the cryoglobulin in EDTA plasma was observed immediately after the venipuncture even if the sample was kept at 37°C whereas in the serum a faint precipitate formed only after a period of 48 h storage at 4°C. This precipitate would have been overlooked under routine conditions. It seems that 'in vitro' the interaction between transferrin and paraprotein fragment initiates the formation of the complex which then is completed by fibrinogen in the presence of EDTA. [ABSTRACT FROM AUTHOR]
- Published
- 1981
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103. Unique Contribution of Haptoglobin and Haptoglobin Genotype in Aneurysmal Subarachnoid Hemorrhage
- Author
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Jessica C. Cardenas, Devin W. McBride, Jaroslaw Aronowski, Pramod K. Dash, Jenna L Leclerc, Hussein A. Zeineddine, James C. Grotta, H. Alex Choi, Peeyush T. Kumar, Sylvain Doré, and Spiros Blackburn
- Subjects
0301 basic medicine ,medicine.medical_specialty ,Subarachnoid hemorrhage ,Physiology ,subarachnoid hemorrhage ,Mini Review ,Ischemia ,Gastroenterology ,lcsh:Physiology ,neuroinflammation ,03 medical and health sciences ,0302 clinical medicine ,Cerebral vasospasm ,Physiology (medical) ,Internal medicine ,Diabetes mellitus ,Medicine ,heme ,biology ,lcsh:QP1-981 ,microthrombosis ,business.industry ,Haptoglobin ,personalized medicine ,medicine.disease ,3. Good health ,Red blood cell ,030104 developmental biology ,medicine.anatomical_structure ,cerebral vasospasm ,Toxicity ,biology.protein ,genetic biomarker ,Subarachnoid space ,business ,030217 neurology & neurosurgery ,prognostic marker - Abstract
Survivors of cerebral aneurysm rupture are at risk for significant morbidity and neurological deficits. Much of this is related to the effects of blood in the subarachnoid space which induces an inflammatory cascade with numerous downstream consequences. Recent clinical trials have not been able to reduce the toxic effects of free hemoglobin or improve clinical outcome. One reason for this may be the inability to identify patients at high risk for neurologic decline. Recently, haptoglobin genotype has been identified as a pertinent factor in diabetes, sickle cell, and cardiovascular disease, with the Hp 2-2 genotype contributing to increased complications. Haptoglobin is a protein synthesized by the liver that binds free hemoglobin following red blood cell lysis, and in doing so, prevents hemoglobin induced toxicity and facilitates clearance. Clinical studies in patients with subarachnoid hemorrhage indicate that Hp 2-2 patients may be a high-risk group for hemorrhage related complications and poor outcome. We review the relevance of haptoglobin in subarachnoid hemorrhage and discuss the effects of genotype and expression levels on the known mechanisms of early brain injury (EBI) and cerebral ischemia after aneurysm rupture. A better understanding of haptoglobin and its role in preventing hemoglobin related toxicity should lead to novel therapeutic avenues.
- Published
- 2018
104. Gerinnungsanalytische und pathologisch-anatomische Untersuchungen beim traumatischen Schock.
- Author
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Loew, D., Wiedemann, R., and Remmele, W.
- Abstract
Copyright of Klinische Wochenschrift is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
- Published
- 1971
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105. The Role of Statins in the Management of Delirium: Recent Advances.
- Author
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Chen J, Wang Y, Hu X, Li M, Xiong K, Zhang Z, and Chen Q
- Subjects
- Humans, Neuroinflammatory Diseases drug therapy, Delirium drug therapy, Hydroxymethylglutaryl-CoA Reductase Inhibitors therapeutic use
- Abstract
Delirium is a clinical syndrome characterized by a temporary organic mental disorder, as well as abnormal attention and cognition. It is a very common, serious, and costly disease with high misdiagnosis and death/disability rates, especially for older patients after surgery. Several factors, such as systemic neuroinflammation, neurotransmitters, cerebral hypoperfusion and microthrombosis, contribute to the progress of delirium; however, the exact pathophysiologic mechanisms are not well known. Therefore, there are no specific therapeutic approaches that can treat delirium effectively. Statins, as inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, have been identified as potential medications for the treatment of delirium because they can significantly reduce the incidence of delirium. The major objective of the current review is to summarize recent advances in the understanding of the effects and mechanisms of statins on delirium. In basic research, statins can alleviate delirium via attenuation of neuroinflammation, neurotransmitters, cerebral hypoperfusion, and microthrombosis, which may highlight their potential clinical application for the treatment of delirium. Despite this, the clinical effects of statins still provoke debate., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)
- Published
- 2021
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106. More than Pneumonia: Distinctive Features of SARS-Cov-2 Infection. From Autopsy Findings to Clinical Implications: A Systematic Review.
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D'Errico, Stefano, Zanon, Martina, Montanaro, Martina, Radaelli, Davide, Sessa, Francesco, Di Mizio, Giulio, Montana, Angelo, Corrao, Salvatore, Salerno, Monica, and Pomara, Cristoforo
- Subjects
AUTOPSY ,ADULT respiratory distress syndrome ,SARS-CoV-2 ,MULTIPLE organ failure ,COVID-19 ,PNEUMONIA - Abstract
Despite safety recommendations for the management of corpses with COVID-19 infection and the high number of deaths worldwide, the post-mortem investigation rate is extremely low as well as the scientific contributions describing the pathological features. The first results of post-mortem investigations provided interesting findings and contributed to promoting unexplored therapeutic approaches and new frontiers of research. A systematic review is provided with the aim of summarizing all autopsy studies up to February 2020 in which a complete post-mortem investigation in patients with COVID-19 disease was performed, focusing on histopathological features. We included case reports, case series, retrospective and prospective studies, letters to the editor, and reviews. A total of 28 studies fulfilled the inclusion criteria, producing a pooled dataset of 407 full autopsies. Analyzing the medical history data, only 12 subjects had died without any comorbidities (for 15 cases the data were not available). The post-mortem investigation highlighted that acute respiratory distress syndrome (ARDS) and multiple organ failure represent the main clinical features of COVID-19 disease, often leading to pulmonary thromboembolism and superimposed bronchopneumonia. The discussed data showed a strict relationship among the inflammatory processes, diffuse alveolar, and endothelial damage. In light of these results, the full autopsy can be considered as the gold standard to investigate unknown infections or pathogens resulting in death. [ABSTRACT FROM AUTHOR]
- Published
- 2020
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107. Filament perforation model for mouse subarachnoid hemorrhage: Surgical-technical considerations
- Author
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Kazuo Okuchi, Carl Muroi, Michihiro Fujiwara, Masayuki Fujioka, Javier Fandino, Yuya Sakamoto, Kenichi Mishima, Emanuela Keller, Katsunori Iwasaki, University of Zurich, and Muroi, C
- Subjects
Male ,medicine.medical_specialty ,Subarachnoid hemorrhage ,subarachnoid hemorrhage ,mouse model ,Perforation (oil well) ,610 Medicine & health ,Neurosurgical Procedures ,Mice ,10180 Clinic for Neurosurgery ,Cerebral vasospasm ,medicine.artery ,medicine ,Surgical technical ,Animals ,cardiovascular diseases ,vasospasm ,Histological examination ,microthrombosis ,business.industry ,Vasospasm ,General Medicine ,medicine.disease ,2746 Surgery ,Surgery ,nervous system diseases ,Mice, Inbred C57BL ,Disease Models, Animal ,2728 Neurology (clinical) ,Anesthesia ,Circle of Willis ,Neurology (clinical) ,10023 Institute of Intensive Care Medicine ,Medline database ,business - Abstract
Mouse subarachnoid hemorrhage (SAH) models are becoming increasingly important. We aimed to report and discuss the detailed technical surgical approach and difficulties associated with the circle of Willis perforation (cWp) model with reference to the existing literature. METHODS: First the cWp model was reproduced using ddY mice following scarification at 0 h Days 1 2 and 3 after SAH. Second C57BL/6 mice were subjected to SAH with histological examination on Days 1 2 and 3. Sham operated mice were sacrificed on Day 2. Neurological performance amount of subarachnoid blood cerebral vasospasm (CVS) and neuronal injury were assessed. Relevant articles found in the MEDLINE database were reviewed. RESULTS: Induction of SAH was successfully reproduced. The volume of subarachnoid blood decreased with time due to resorption. Neurological performance was worse in SAH compared with sham. Signs of CVS could be confirmed on Days 2 and 3 but not Day 1. The cumulative number of microthrombi was significantly higher on Days 2 and 3 but not Day 1. Apoptotic and degenerative neurons were found in the cortex and hippocampal area. Our review of the literature revealed the cWp model to be the most frequently used. The present findings largely confirmed previously published results. However detailed technical surgical description and its discussion were sparse which we provide here. CONCLUSIONS: The current study provides additional useful information characterizing the cWp model. This model may be of first choice at present as important pathologies can be reproduced and most findings in the literature are based on it.
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- 2014
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108. Recombinant Human Milk Fat Globule-Epidermal Growth Factor 8 Attenuates Microthrombosis after Subarachnoid Hemorrhage in Rats.
- Author
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Wang, Jikai, Zuo, Yuchun, Zhuang, Kai, Luo, Kui, Yan, Xiaoxin, Li, Jianming, Zhang, John H., and Liu, Fei
- Abstract
Background: Microthrombosis after subarachnoid hemorrhage has an adverse effect on prognosis. Milk fat globule-epidermal growth factor 8 promotes phagocytosis of phagocytic cells and may reduce microthrombosis. This study investigated the effects of recombinant human milk fat globule-epidermal growth factor 8 on microthrombosis and neurological function after subarachnoid hemorrhage.Methods: Rats subarachnoid hemorrhage model was induced by intravascular puncture method. Western blot was performed to measure the expression of endogenous milk fat globule-epidermal growth factor 8 after subarachnoid hemorrhage. Microthrombosis was quantified by microthrombi count using immunohistochemistry and immunofluorescence. The neuroprotective effect of recombinant human milk fat globule-epidermal growth factor 8 administration was evaluated by modified Garcia score, beam balance, Rotarod test, and Morris water maze.Results: Endogenous milk fat globule-epidermal growth factor 8 protein level increased after subarachnoid hemorrhage. Microthrombosis was significantly increased in subarachnoid hemorrhage rats brain, while recombinant human milk fat globule-epidermal growth factor 8 dramatically reduced microthrombosis as well as improve short- and long- term neurobehavior after subarachnoid hemorrhage.Conclusions: Recombinant human milk fat globule-epidermal growth factor 8 reduces microthrombosis and improves neurological function after subarachnoid hemorrhage, which may be an effective strategy for treating subarachnoid hemorrhage. [ABSTRACT FROM AUTHOR]- Published
- 2020
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109. Diets and Cellular-Derived Microparticles: Weighing a Plausible Link With Cerebral Small Vessel Disease.
- Author
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Nassir CMNCM, Ghazali MM, Hashim S, Idris NS, Yuen LS, Hui WJ, Norman HH, Gau CH, Jayabalan N, Na Y, Feng L, Ong LK, Abdul Hamid H, Ahamed HN, and Mustapha M
- Abstract
Cerebral small vessel disease (CSVD) represents a spectrum of pathological processes of various etiologies affecting the brain microcirculation that can trigger neuroinflammation and the subsequent neurodegenerative cascade. Prevalent with aging, CSVD is a recognized risk factor for stroke, vascular dementia, Alzheimer disease, and Parkinson disease. Despite being the most common neurodegenerative condition with cerebrocardiovascular axis, understanding about it remains poor. Interestingly, modifiable risk factors such as unhealthy diet including high intake of processed food, high-fat foods, and animal by-products are known to influence the non-neural peripheral events, such as in the gastrointestinal tract and cardiovascular stress through cellular inflammation and oxidation. One key outcome from such events, among others, includes the cellular activations that lead to elevated levels of endogenous cellular-derived circulating microparticles (MPs). MPs can be produced from various cellular origins including leukocytes, platelets, endothelial cells, microbiota, and microglia. MPs could act as microthrombogenic procoagulant that served as a plausible culprit for the vulnerable end-artery microcirculation in the brain as the end-organ leading to CSVD manifestations. However, little attention has been paid on the potential role of MPs in the onset and progression of CSVD spectrum. Corroboratively, the formation of MPs is known to be influenced by diet-induced cellular stress. Thus, this review aims to appraise the body of evidence on the dietary-related impacts on circulating MPs from non-neural peripheral origins that could serve as a plausible microthrombosis in CSVD manifestation as a precursor of neurodegeneration. Here, we elaborate on the pathomechanical features of MPs in health and disease states; relevance of dietary patterns on MP release; preclinical studies pertaining to diet-based MPs contribution to disease; MP level as putative surrogates for early disease biomarkers; and lastly, the potential of MPs manipulation with diet-based approach as a novel preventive measure for CSVD in an aging society worldwide., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2021 Nassir, Ghazali, Hashim, Idris, Yuen, Hui, Norman, Gau, Jayabalan, Na, Feng, Ong, Abdul Hamid, Ahamed and Mustapha.)
- Published
- 2021
- Full Text
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110. Rescue therapy with thrombolysis in patients with severe COVID-19-associated acute respiratory distress syndrome.
- Author
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Price LC, Garfield B, Bleakley C, Keeling AGM, Mcfadyen C, McCabe C, Ridge CA, Wort SJ, Price S, and Arachchillage DJ
- Abstract
Acute respiratory distress syndrome in patients with Coronavirus disease 19 is associated with an unusually high incidence of pulmonary embolism and microthrombotic disease, with evidence for reduced fibrinolysis. We describe seven patients requiring invasive ventilation for COVID-19-associated acute respiratory distress syndrome with pulmonary thromboembolic disease, pulmonary hypertension ± severe right ventricular dysfunction on echocardiography, who were treated with alteplase as fibrinolytic therapy. All patients were non-smokers, six (86%) were male and median age was 56.7 (50-64) years. They had failed approaches including therapeutic anticoagulation, prone ventilation ( n = 4), inhaled nitric oxide ( n = 5) and nebulised epoprostenol ( n = 2). The median duration of mechanical ventilation prior to thrombolysis was seven (5-11) days. Systemic alteplase was administered to six patients (50 mg or 90 mg bolus over 120 min) at 16 (10-22) days after symptom onset. All received therapeutic heparin pre- and post-thrombolysis, without intracranial haemorrhage or other major bleeding. Alteplase improved PaO
2 /FiO2 ratio (from 97.0 (86.3-118.6) to 135.6 (100.7-171.4), p = 0.03) and ventilatory ratio (from 2.76 (2.09-3.49) to 2.36 (1.82-3.05), p = 0.011) at 24 h. Echocardiographic parameters at two (1-3) days ( n = 6) showed right ventricular systolic pressure (RVSP) was 63 (50.3-75) then 57 (49-66) mmHg post-thrombolysis ( p = 0.26), tricuspid annular planar systolic excursion (TAPSE) was unchanged (from 18.3 (11.9-24.5) to 20.5 (15.4-24.2) mm, p = 0.56) and right ventricular fractional area change (from 15.4 (11.1-35.6) to 31.2 (16.4-33.1)%, p = 0.09). At seven (1-13) days after thrombolysis, using dual energy computed tomography imaging ( n = 3), average relative peripheral lung enhancement increased from 12.6 to 21.6% ( p = 0.06). In conclusion, thrombolysis improved PaO2 /FiO2 ratio and ventilatory ratio at 24 h as rescue therapy in patients with right ventricular dysfunction due to COVID-19-associated ARDS despite maximum therapy, as part of a multimodal approach, and warrants further study., (© The Author(s) 2020.)- Published
- 2020
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111. Letter in response to: Coagulation markers are independent predictors of increased oxygen requirements and thrombosis in COVID-19.
- Author
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Bhogal P, Jensen M, Collins G, Spooner O, Makalanda L, Hart D, and Jaffer O
- Subjects
- Biomarkers, Humans, Oxygen, SARS-CoV-2, COVID-19, Thrombosis diagnosis
- Published
- 2020
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112. Fibrinogen-like protein 2 expression correlates with microthrombosis in rats with type 2 diabetic nephropathy
- Author
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Yuhua Liao, Wenzhu Li, Zhaohui Wang, Kun Liu, Guanhua Su, Jue Wang, Yan Wang, and Xiao-Wei Li
- Subjects
chemistry.chemical_classification ,medicine.medical_specialty ,Messenger RNA ,microthrombosis ,Renal ischemia ,business.industry ,diabetic nephropathy ,fibrinogen-like protein 2 ,General Medicine ,Type 2 diabetes ,medicine.disease ,General Biochemistry, Genetics and Molecular Biology ,FGL2 ,Diabetic nephropathy ,Enzyme ,Endocrinology ,chemistry ,Prothrombinase ,Internal medicine ,medicine ,Tumor necrosis factor alpha ,type 2 diabetes ,tumor necrosis factor-α ,business ,Research Paper - Abstract
Fibrinogen-like protein 2 (fgl2), a novel prothrombinase, is involved in microthrombosis. We examined fgl2 expression in the glomerular and tubulointerstitial capillaries and its correlation with microthromsis in rats with streptozocin-induced type 2 diabetic nephropathy. Our RT-PCR and immunoblotting analysis showed that fgl2 mRNA and protein levels were increased in microvascular endothelial cells of the glomeruli and renal interstitia at week 19 and became significantly elevated with the development of diabetic nephropathy (P < 0.01). Fgl2 was not or only weakly expressed in the renal tissues of normal rats. Furthermore, a direct significant correlation (r = 0.543, P < 0.01) was found between fgl2 expression and microthrombotic capillaries in the renal tissues. Enzyme linked immunosorbent assays (ELISA) additionally showed that circulating TNF-α levels in rats with type 2 diabetes were significantly elevated and closely correlated with fgl2 expression (r = 0.871, P < 0.01). Our results suggest that fgl2 may activate renal microthrombosis, thus contributing to glomerular hypertension and renal ischemia.
- Published
- 2011
113. Negative Allosteric Modulator of mGluR1 Improves Long-Term Neurologic Deficits after Experimental Subarachnoid Hemorrhage.
- Author
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Wang HB, Wang WQ, Wu QJ, Hou YJ, Li HX, Yang HJ, Yang MF, Sun BL, and Zhang ZY
- Subjects
- Animals, Disease Models, Animal, Rats, Receptors, Metabotropic Glutamate, Subarachnoid Hemorrhage complications, Subarachnoid Hemorrhage drug therapy, Vasospasm, Intracranial
- Abstract
Aneurysmal subarachnoid hemorrhage (SAH) causes permanent neurological sequelae, but the underlying mechanism needs to be further clarified. Here, we show that inhibition of metabotropic glutamate receptor 1 (mGluR1) with negative allosteric modulator JNJ16259685 improves long-term neurobehavioral outcomes in an endovascular perforation model of SAH. JNJ16259685 improves cerebrovascular dysfunction through attenuation of cerebral blood flow (CBF) reduction, cerebral vasoconstrictio, and microthrombosis formation in a rat SAH model. Moreover, JNJ16259685 reduces experimental SAH-induced long-term neuronal damage through alleviation of neuronal death and degeneration. Mechanically, JNJ16259685 maintains phosphorylation of endothelial NO synthase (eNOS) and vasodilator-stimulated phosphoprotein (VASP) and decreases apoptosis-related factors Bax, active caspase-9, and active caspase-3 following experimental SAH. Altogether, our results suggest JNJ16259685 improves long-term functional impairment through neurovascular protection.
- Published
- 2020
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114. The evolution of pulmonary pathology in fatal COVID-19 disease: an autopsy study with clinical correlation.
- Author
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Bösmüller H, Traxler S, Bitzer M, Häberle H, Raiser W, Nann D, Frauenfeld L, Vogelsberg A, Klingel K, and Fend F
- Subjects
- Aged, Autopsy, Betacoronavirus, COVID-19, Female, Humans, Male, Middle Aged, Pandemics, SARS-CoV-2, Thrombosis pathology, Thrombosis virology, Coronavirus Infections pathology, Lung Diseases pathology, Lung Diseases virology, Pneumonia, Viral pathology
- Abstract
The pandemia of coronavirus disease 2019 (COVID-19) has caused more than 355,000 confirmed deaths worldwide. However, publications on postmortem findings are scarce. We present the pulmonary findings in four cases of fatal COVID-19 with a spectrum of lung pathology reflecting disease course and duration, invasive therapies, and laboratory features. Early disease is characterized by neutrophilic, exudative capillaritis with microthrombosis and high levels of IL-1beta and IL-6. Later stages are associated with diffuse alveolar damage and ongoing intravascular thrombosis in small to medium-sized pulmonary vessels, occasionally with areas of infarction equivalents, accompanied by laboratory features of disseminated intravascular coagulation. In late stages, organizing pneumonia with extensive intra-alveolar proliferation of fibroblasts and marked metaplasia of alveolar epithelium can be observed. Viral RNA is encountered in the lung, with virus particles in endothelial cells and pneumocytes. In many patients, multi-organ failure with severe liver damage sets in finally, possibly as consequence of an early-onset pro-inflammatory cytokine storm and/or thrombotic microangiopathy.
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- 2020
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115. Are chilblains a skin expression of COVID-19 microangiopathy?
- Author
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Baeck M, Herman A, Peeters C, Marot L, and Hermans C
- Subjects
- Biopsy, Disease Outbreaks, Fluorescent Antibody Technique, Humans, Immunoglobulin A immunology, Immunoglobulin M immunology, Inflammation, Skin pathology, COVID-19 blood, COVID-19 complications, Chilblains blood, Chilblains complications, Vascular Diseases blood, Vascular Diseases complications
- Published
- 2020
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116. Hemostasis and fibrinolysis in delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage : a systematic review
- Author
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Jacoline Boluijt, Mervyn D.I. Vergouwen, Joost C. M. Meijers, and Gabriel J.E. Rinkel
- Subjects
ANTIPHOSPHOLIPID ANTIBODIES ,Subarachnoid hemorrhage ,subarachnoid hemorrhage ,medicine.medical_treatment ,VASOSPASM ,Ischemia ,Review Article ,Review ,Research Support ,CONTROLLED-TRIAL ,Brain Ischemia ,Cerebrospinal fluid ,Fibrinolytic Agents ,Von Willebrand factor ,CEREBROSPINAL-FLUID ,Fibrinolysis ,medicine ,Journal Article ,Animals ,Humans ,coagulation ,Non-U.S. Gov't ,biology ,microthrombosis ,business.industry ,Research Support, Non-U.S. Gov't ,Intracranial Aneurysm ,Vasospasm ,ANTITHROMBIN-III COMPLEX ,medicine.disease ,ADAMTS13 ,PLATELET-ACTIVATING-FACTOR ,Neurology ,TISSUE FACTOR ,Anesthesia ,Hemostasis ,biology.protein ,delayed cerebral ischemia ,hemostasis ,biomarker ,THROMBOXANE RELEASE ,fibrinolysis ,Neurology (clinical) ,Cardiology and Cardiovascular Medicine ,business ,Biomarkers - Abstract
Delayed cerebral ischemia (DCI) after aneurysmal subarachnoid hemorrhage (aSAH) has been associated with microthrombosis, which can result from activated hemostasis, inhibited fibrinolysis, or both. We systematically searched the PUBMED and EMBASE databases to identify hemostatic or fibrinolytic parameters that can be used for the prediction or diagnosis of DCI, or that inform on the pathogenesis of DCI and may serve as treatment targets. We included 24 studies that fulfilled predefined criteria and described 39 biomarkers. Only one study fulfilled predefined criteria for high quality. Since no parameter on admission was associated with DCI and in none of the included studies blood was drawn at the time of clinical deterioration, none of the studied parameters can presently be used for the prediction or diagnosis of DCI. Regarding the pathogenesis of DCI, it was shown that compared with patients without DCI those with DCI had higher levels of von Willebrand factor and platelet activating factor in plasma 5 to 9 days after aSAH, membrane tissue factor in cerebrospinal fluid 5 to 9 days after aSAH, and D-dimer in plasma 11 to 14 days after aSAH. Confirmation in high-quality studies is needed to investigate whether these parameters can serve as targets for new intervention studies.
- Published
- 2015
117. Boon's disease
- Subjects
CHLORDIMEFORM ,microthrombosis ,CARCINOMA ,cytology ,apoptosis ,VIRUS ,hemorrhagic cystitis ,anuria ,BONE-MARROW TRANSPLANTATION ,URINARY-BLADDER ,DIAGNOSIS ,long-distance air travel ,CYCLOPHOSPHAMIDE THERAPY - Abstract
Hemorrhagic cystitis is a well-defined clinical emergency, usually occurring in the course of treatment with toxic agents such as cyclophosphamide. We present a case of hemorrhagic cystitis in an otherwise completely healthy female. The three documented attacks it-ere severe and started during intercontinental flights. This type of hemorrhagic cystitis as a disease proved to be a boon, treatable by drinking large amounts of water, and was diagnosed by and in Dr. Boon; thus was the appellation Boon's disease coined. Cellular changes in the urine specimen taken after onset of the disease indicated massive exfoliation of degenerated urothelial cells with morphological features suggestive of apoptosis. It seems likely that this process can be initiated by any event which is associated with compromise of vitality of the urinary bladder lining, such as may occur in hypovolemia. This type of hemorrhagic cystitis is most probably not uncommon in susceptible individuals during intercontinental flights. (C) 2001 Wiley-Liss, Inc.
- Published
- 2001
118. Hypothermia-induced activation of the splenic platelet pool as a risk factor for thrombotic disease in a mouse model.
- Author
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Horioka K, Tanaka H, Isozaki S, Okuda K, Asari M, Shiono H, Ogawa K, and Shimizu K
- Subjects
- Animals, Cell Degranulation, Chemokines, CXC blood, Disease Models, Animal, Fibrin Fibrinogen Degradation Products metabolism, Fibrinolysis, Male, Mice, Inbred C57BL, P-Selectin blood, Platelet Factor 4 blood, Signal Transduction, Thrombosis blood, von Willebrand Factor metabolism, Blood Coagulation, Blood Platelets metabolism, Hypothermia, Induced, Platelet Activation, Spleen metabolism, Thrombosis etiology
- Abstract
Background: Hypothermia, either therapeutically induced or accidental (ie, an involuntary decrease in core body temperature to <35°C), results in hemostatic disorders. However, it remains unclear whether hypothermia enhances or inhibits coagulation, especially in severe hypothermia. The present study evaluated the thrombocytic and hemostatic changes in hypothermic mice., Methods: C57Bl/6 mice were placed at an ambient temperature of -20°C under general anesthesia. When the rectal temperature decreased to 15°C, 10 mice were immediately euthanized, while another 10 mice were rewarmed, kept in normal conditions for 24 hours, and then euthanized. These treatments were also performed in 20 splenectomized mice., Results: The hypothermic mice had adhesion of CD62P-positive platelets with high expression of von Willebrand factor (vWF) in their spleens, while the status of the peripheral platelets was unchanged. Furthermore, the plasma levels of platelet factor 4 (PF4) and pro-platelet basic protein (PPBP), which are biomarkers for platelet degranulation, were significantly higher in hypothermic mice than in control mice, indicating that hypothermia activated the platelets in the splenic pool. Thus, we analyzed these biomarkers in asplenic mice. There was no increase in either PF4 or PPBP in splenectomized hypothermic mice. Additionally, the plasma D-dimer elevation and microthrombosis were caused in rewarmed mice, but not in asplenic rewarmed mice., Conclusions: Our results indicate that hypothermia leads to platelet activation in the spleen via the upregulation of vWF, and this activation causes hypercoagulability after rewarming., (© 2019 The Authors. Journal of Thrombosis and Haemostasis published by Wiley Periodicals, Inc. on behalf of International Society on Thrombosis and Haemostasis.)
- Published
- 2019
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119. Management of Symmetrical Peripheral Gangrene.
- Author
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Foead AI, Mathialagan A, Varadarajan R, and Larvin M
- Abstract
Symmetrical peripheral gangrene (SPG) is a rare, debilitating disease that deserves more widespread concern among the medical fraternities. The objective of this review is to outline the etiology, pathology findings, and management practices of SPG. About 18%-40% mortality rate was reported, and survivors have high frequency of multiple limb amputations. SPG is the hallmark of disseminated intravascular coagulation (DIC). The main pathogenesis theory, to date, is microthrombosis associated with disturbed procoagulant-anticoagulant balance. The treatment of SPG is largely anecdotal and theoretically involves heparin-based anticoagulation and substitution of natural anticoagulants. Early recognition, prompt management of DIC, and underlying conditions may halt the progression of the disease. The multicenter randomized controlled trial should be set up to formulate the proper treatment guidelines., Competing Interests: There are no conflicts of interest.
- Published
- 2018
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120. [Disturbances of the hemostatic system in patients with aneurysmal subarachnoid hemorrhage].
- Author
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Baranich AI, Savin IA, Tabasaranskiy TF, Polupan AA, Sychev AA, Kurdyumova NV, Pilipenko YV, Mikeladze KG, and Eliava SS
- Subjects
- Anticoagulants administration & dosage, Anticoagulants adverse effects, Anticoagulants therapeutic use, Antifibrinolytic Agents administration & dosage, Antifibrinolytic Agents adverse effects, Antifibrinolytic Agents therapeutic use, Brain Ischemia blood, Brain Ischemia etiology, Brain Ischemia prevention & control, Hemostasis drug effects, Humans, Intracranial Aneurysm complications, Subarachnoid Hemorrhage etiology, Vasospasm, Intracranial blood, Vasospasm, Intracranial etiology, Vasospasm, Intracranial prevention & control, Hemostasis physiology, Intracranial Aneurysm blood, Subarachnoid Hemorrhage blood
- Abstract
Subarachnoid hemorrhages due to rupture of cerebral aneurysms are characterized by high mortality. More than 25% of patients who have survived the first hours after aneurysmal SAH (aSAH) develop delayed cerebral ischemia that is one of the main causes of disability. The mechanisms underlying delayed ischemia have not yet been fully understood. Previously, the development of vasospasm was believed to be the only cause for development of delayed ischemia. In recent years, there has been evidence that hemostatic system disorders typical of this category of patients are the cause of cerebral artery thrombosis, which is one of the main pathophysiological mechanisms for the development of delayed cerebral ischemia. This review presents an analysis of published papers on hemostasis disturbances in patients with aSAH, their pathophysiological mechanisms, and their role in the development of cerebral ischemia.
- Published
- 2018
121. Boon's disease: Hemorrhagic cystitis in conjunction with massive exfoliation of degenerated urothelial cells (apoptosis?) during intercontinental flights in an otherwise healthy person
- Author
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Lambrecht P. Kok
- Subjects
Pathology ,medicine.medical_specialty ,Histology ,Urothelial Cell ,Cyclophosphamide ,Aircraft ,CARCINOMA ,Hemorrhage ,anuria ,Disease ,DIAGNOSIS ,Pathology and Forensic Medicine ,Recurrence ,Hypovolemia ,Cystitis ,Carcinoma ,Medicine ,Humans ,Travel ,CHLORDIMEFORM ,Urinary bladder ,microthrombosis ,business.industry ,apoptosis ,General Medicine ,BONE-MARROW TRANSPLANTATION ,Middle Aged ,medicine.disease ,medicine.anatomical_structure ,cytology ,VIRUS ,Anuria ,Female ,hemorrhagic cystitis ,medicine.symptom ,Urothelium ,business ,URINARY-BLADDER ,long-distance air travel ,CYCLOPHOSPHAMIDE THERAPY ,Hemorrhagic cystitis ,medicine.drug - Abstract
Hemorrhagic cystitis is a well-defined clinical emergency, usually occurring in the course of treatment with toxic agents such as cyclophosphamide. We present a case of hemorrhagic cystitis in an otherwise completely healthy female. The three documented attacks it-ere severe and started during intercontinental flights. This type of hemorrhagic cystitis as a disease proved to be a boon, treatable by drinking large amounts of water, and was diagnosed by and in Dr. Boon; thus was the appellation Boon's disease coined. Cellular changes in the urine specimen taken after onset of the disease indicated massive exfoliation of degenerated urothelial cells with morphological features suggestive of apoptosis. It seems likely that this process can be initiated by any event which is associated with compromise of vitality of the urinary bladder lining, such as may occur in hypovolemia. This type of hemorrhagic cystitis is most probably not uncommon in susceptible individuals during intercontinental flights. (C) 2001 Wiley-Liss, Inc.
- Published
- 2001
122. Mechanism of microthrombosis in HUS.
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Rock, Gail A. and Clark, William F.
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MONOCLONAL antibodies , *BACTERIAL cell walls , *STAPHYLOCOCCUS aureus , *HOMOLOGY (Biology) , *BLOOD plasma - Abstract
The mechanism of formation of the microthrombi in hemolytic uremic syndrome (HUS) is not known. Plasma from five adult and six pediatric cases of HUS showed aggregation and release of adenosine triphosphate from normal platelets. When the plasma was absorbed with staphylococcal protein A and again exposed to normal platelets there was no aggregation or release, indicating that an antibody was responsible for the aggregation. The plasma reacted with platelet lysate in a western blot, showing reactivity with CD36. This was confirmed by probing with Mo91, a monoclonal antibody to CD36. When the patient's plasma was used to probe purified verotoxin-2, bands of 32 and 7.7 kDa were obtained. Similar results were obtained using Mo91. The reactions suggest structural homologies between CD36 and verotoxin. Although a direct cause–effect relationship is not yet established, the data support the concept of an immunological pathogenesis for HUS with the formation of cross-reacting antibodies.Kidney International (2009) 75, S15–S16; doi:10.1038/ki.2008.611 [ABSTRACT FROM AUTHOR]
- Published
- 2009
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123. ADAMTS13 deficiency promotes microthrombosis in a murine model of diet-induced liver steatosis.
- Author
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Geys L, Bauters D, Roose E, Tersteeg C, Vanhoorelbeke K, Hoylaerts MF, Lijnen RH, and Scroyen I
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- ADAMTS13 Protein genetics, Animals, Disease Models, Animal, Fibrinolysin metabolism, Fibrinolysis, Genetic Predisposition to Disease, Inflammation Mediators metabolism, Liver pathology, Male, Mice, 129 Strain, Mice, Inbred C57BL, Mice, Knockout, Non-alcoholic Fatty Liver Disease enzymology, Non-alcoholic Fatty Liver Disease genetics, Obesity etiology, Oxidative Stress, Phenotype, Thrombosis blood, Thrombosis enzymology, Thrombosis genetics, Triglycerides metabolism, alpha-2-Antiplasmin metabolism, von Willebrand Factor metabolism, ADAMTS13 Protein deficiency, Blood Coagulation, Diet, High-Fat adverse effects, Liver enzymology, Non-alcoholic Fatty Liver Disease etiology, Thrombosis etiology
- Abstract
ADAMTS13 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 high-fat diet-induced steatosis in Adamts13 deficient (Adamts13
-/- ) and wild-type (WT) control mice. Microthrombi were more abundant in the liver of obese Adamts13-/- as compared to obese WT or to lean Adamts13-/- mice. Obese Adamts13-/- mice displayed lower platelet counts and higher prevalence of ultra-large VWF multimers. Hepatic plasmin-α2-antiplasmin complex levels were comparable for obese WT and Adamts13-/- mice and were lower for lean Adamts13-/- than WT mice, not supporting marked activation of the fibrinolytic system. High fat diet feeding, as compared to normal chow, resulted in enhanced liver triglyceride levels for both genotypes (p < 0.0001) and steatosis (p < 0.0001 for WT mice, p = 0.002 for Adamts13-/- mice) without differences between the genotypes. Expression of markers of inflammation, oxidative stress, steatosis and fibrosis was affected by diet, but not by genotype. Thus, our data confirm that obesity promotes NASH, but do not support a detrimental role of ADAMTS13 in its development. However, Adamts13 deficiency in obese mice promotes hepatic microthrombosis, whereas a compensatory role of plasmin in removal of microthrombi in the absence of ADAMTS13 could not be demonstrated.- Published
- 2017
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124. Intravenous and oral administrations of DD2 [7-Amino-2-(sulfanylmethyl)heptanoic acid] produce thrombolysis through inhibition of plasma TAFIa in rats with tissue factor-induced microthrombosis
- Author
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Sasaki, Tomoyuki, Yoshimoto, Nobuko, Sugimoto, Katsuyoshi, Takada, Kimihiko, Murayama, Norie, Yamazaki, Hiroshi, Yamamoto, Keiko, and Ishii, Hidemi
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ORAL medication , *INTRAVENOUS therapy , *BLOOD plasma , *THROMBOLYTIC therapy , *THROMBOPLASTIN , *AMINO acids , *ANTIFIBRINOLYTIC agents , *LABORATORY rats - Abstract
Abstract: Thrombin-activatable fibrinolysis inhibitor (TAFI) is a plasma zymogen that is activated by thrombin in plasma. In fibrinolytic processes, carboxy-terminal lysine (Lys) residues in partially degraded fibrin are important sites for plasminogen binding and activation, and an active form of TAFI (TAFIa) inhibits fibrinolysis by eliminating these residues proteolytically. We synthesized DD2 [7-Amino-2-(sulfanylmethyl)heptanoic acid], a Lys analogue containing sulfur, as an inhibitor of TAFIa and investigated its pharmacological profile and pathophysiological role in thrombolysis via in vitro and in vivo studies. DD2 specifically inhibited plasma TAFIa activity with an apparent IC50 (50% inhibitory concentration) value of 3.4×10-8 M under the present experimental condition and enhanced tissue plasminogen activator-mediated clot lysis in a concentration-dependent manner. In order to study tissue factor (TF)-induced microthrombosis in an animal model, rats were given intravenous injection (2.5mg/kg and higher) or oral administration (10mg/kg and higher) of DD2. This attenuated TF-induced glomerular fibrin deposition and increased the plasma levels of fibrin degradation products and D-dimer in a dose-dependent manner. A DD2 dose approximately 4X higher than the dose used in intravenous injections was required to achieve an equivalent thrombolytic effect to that seen following oral administration. Moreover, the oral absorption efficiency of DD2 into the vasculature was 29.8%. These results indicate that both intravenous and oral administration of DD2 enhanced endogenous fibrinolysis and reduced thrombi in a TF-induced microthrombosis model. [Copyright &y& Elsevier]
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- 2012
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125. The role of antiphospholipid antibodies (aPls) in infertile women: the long-lasting experience.
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Ulcova-Gallova Z
- Abstract
Antiphospholipid antibodies (aPls) are generally characterized as heterogeneous and non-specific autoantibodies directed against various phospholipids such as cardiolipin, ph-serine, ph-inositol, ph-acid, ph-glycerol, ph-sphyngomyelin, ph-choline, annexins, and co-factor β2-glycoprotein I. aPls occur not only during autoimmune diseases but also during infectious diseases, essential hypertension, neurological complication, metabolic diseases, some drug abuse, and transplant loss. aPls are very often found in connection with reproductive failure such as repeated pregnancy loss and/or missed abortion, intrauterine fetal death, in preeclampsia, and repeated delivery of hypothrophic fetus. The presence of aPls, thrombosis, and fertility failure create primary or secondary antiphospholipid syndrome. This article explains some aspects and clinical and laboratory significance of the aPls in female infertility.
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- 2014
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126. Correlation of fibrinogen-like protein 2 with progression of acute pancreatitis in rats.
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Ye XH, Chen TZ, Huai JP, Lu GR, Zhuge XJ, Chen RP, Chen WJ, Wang C, and Huang ZM
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- Acute Disease, Animals, Biomarkers metabolism, Disease Models, Animal, Fibrinogen genetics, Leukocytes, Mononuclear metabolism, Male, Pancreas pathology, Pancreatitis chemically induced, Pancreatitis genetics, Pancreatitis pathology, RNA, Messenger metabolism, Rats, Rats, Sprague-Dawley, Severity of Illness Index, Taurocholic Acid, Thrombosis etiology, Time Factors, Up-Regulation, Fibrinogen metabolism, Pancreas metabolism, Pancreatitis metabolism
- Abstract
Aim: To examine fibrinogen-like protein 2 (fgl2) expression during taurocholate-induced acute pancreatitis progression in rats and its correlation with pancreatic injury severity., Methods: Forty-eight male Sprague-Dawley rats were randomly divided into the severe acute pancreatitis (SAP) group (n = 24) and the sham operation (SO) group (n = 24). Sodium taurocholate (4% at doses of 1 mL/kg body weight) was retrogradely injected into the biliopancreatic ducts of the rats to induce SAP. Pancreatic tissues were prepared immediately after sacrifice. At the time of sacrifice, blood was obtained for determination of serum amylase activity and isolation of peripheral blood mononuclear cells (PBMCs). Pancreatic tissue specimens were obtained for routine light microscopy including hematoxylin and eosin staining, and the severity of pancreatic injury was evaluated 1, 4 and 8 h after induction. Expression of fgl2 mRNA was measured in the pancreas and PBMCs using reverse transcription polymerase chain reaction. Expression of fgl2 protein was evaluated in pancreatic tissues using Western blotting and immunohistochemical staining. Masson staining was also performed to observe microthrombosis., Results: At each time point, levels of fgl2 mRNAs in pancreatic tissues and PBMCs were higher (P < 0.05) in the SAP group than in the SO group. For pancreatic tissue in SAP vs SO, the levels were: after 1 h, 3.911 ± 1.277 vs 1.000 ± 0.673; after 4 h, 9.850 ± 3.095 vs 1.136 ± 0.609; and after 8 h, 12.870 ± 3.046 vs 1.177 ± 0.458. For PBMCs in SAP vs SO, the levels were: after 1 h, 2.678 ± 1.509 vs 1.000 ± 0.965; after 4 h, 6.922 ± 1.984 vs 1.051 ± 0.781; and after 8 h, 13.533 ± 6.575 vs 1.306 ± 1.179. Levels of fgl2 protein expression as determined by Western blotting and immunohistochemical staining were markedly up-regulated (P < 0.001) in the SAP group compared with those in the SO group. For Western blotting in SAP vs SO, the results were: after 1 h, 2.183 ± 0.115 vs 1.110 ± 0.158; after 4 h, 2.697 ± 0.090 vs 0.947 ± 0.361; and after 8 h, 3.258 ± 0.094 vs 1.208 ± 0.082. For immunohistochemical staining in SAP vs SO, the results were: after 1 h, 1.793 ± 0.463 vs 0.808 ± 0.252; after 4 h, 4.535 ± 0.550 vs 0.871 ± 0.318; and after 8 h, 6.071 ± 0.941 vs 1.020 ± 0.406. Moreover, we observed a positive correlation in the pancreas (r = 0.852, P < 0.001) and PBMCs (r = 0.735, P < 0.001) between fgl2 expression and the severity of pancreatic injury. Masson staining showed that microthrombosis (%) in rats with SAP was increased (P < 0.001) compared with that in the SO group and it was closely correlated with fgl2 expression in the pancreas (r = 0.842, P < 0.001). For Masson staining in SAP vs SO, the results were: after 1 h, 26.880 ± 9.031 vs 8.630 ± 3.739; after 4 h, 53.750 ± 19.039 vs 8.500 ± 4.472; and after 8 h, 80.250 ± 12.915 vs 10.630 ± 7.003., Conclusion: Microthrombosis due to fgl2 overexpression contributes to pancreatic impairment in rats with SAP, and fgl2 level may serve as a biomarker during early stages of disease.
- Published
- 2013
- Full Text
- View/download PDF
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