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Immunobiology. 2000 Sep;202(3):239-53.
Parenteral administration of an activating monoclonal antibody to the alpha1beta1 integrin in dogs.
Bank I, Hardan I, Lokshin E, Nas D, Miron S, Ohad D, Spong S, Garrod DR.
Department of Medicine F, Chaim Sheba Medical Center, Tel Hashomer, Israel. ibanost.tau.ac.il
In mice, monoclonal antibody (mAb) to the alpha1 integrin abrogate gastro-intestinal damage during graft-versus-host-disease (GVHD), suggesting anti alpha1 mAb as candidates for treatment in humans as well. Our current data show that one such reagent, mAb 1B3.1, when immobilized to plastic wells via rabbit- anti murine (ram) immunoglobulin (Ig) induces a protein kinase-dependent spreading of activated human T cells. Furthermore, it significantly increases the proliferative response, and expression of interleukin-2 (IL-2) receptors (R) and CD69, of resting T cells, expressing minimal integrin on the cell surface, to sub-optimal stimulation by anti-CD3 mAb. We found, in addition, that mAb 1B3.1 a) immuno-precipitates alpha1beta1 integrins from cell-surface iodinated canine epithelial cells b) is highly reactive with canine T cells after their activation and c) inhibits adhesion of canine T cells to collagen IV. Despite the potential ability of the mAb to co-activate T cells in vitro, two dogs that received 4 injections of 0.5-0.3 mg/Kg of mAb 1B3.1 remained healthy, developing only marginal transient lymphopenia. Injection of 0.75mg/Kg in a third dog induced a more marked lymphopenia, and an additional dose of 1.0 mg/Kg 2 weeks later was followed by gastrointestinal hemorrhage. importantly, the lymphopenia was associated with a greater and more persistent decrease of CD8+ than of CD4+ T cells, leading to an increase in the CD4/CD8 ratio 24 hours after the injection. Thus, despite it's co-activating effects in vitro, administration of this mAb in vivo is feasible when appropriately dosed, and may have immuno-modulatory effects.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11045660&dopt=Abstract hemorrhage
Am J Physiol Heart Circ Physiol. 2000 Nov;279(5):H2405-13.
Effects of hemoglobin on heme oxygenase gene expression and viability of cultured smooth muscle cells.
Marton LS, Wang X, Kowalczuk A, Zhang ZD, Windmeyer E, Macdonald RL.
Section of Neurosurgery, Department of Surgery, Pritzker School of Medicine, University of Chicago Medical Center, Chicago, Illinois 60637, USA.
Ferrous Hb contributes to cerebral vasospasm after subarachnoid hemorrhage, although the mechanisms involved are uncertain. The hypothesis that cytotoxic effects of ferrous Hb on smooth muscle cells contribute to vasospasm was assessed. Cultured rat basilar artery smooth muscle cells were exposed to pure Hb, dog erythrocyte hemolysate, or Hb breakdown products; and heme oxygenase (HO-1 and HO-2) and ferritin mRNA and protein were measured. Cytotoxicity was assessed by lactate dehydrogenase release and fluorescence assays. Pure Hb or hemolysate caused dose- and time-dependent increases in HO-1 mRNA and protein. Hemin was the component of Hb that increased HO-1 mRNA. Cycloheximide inhibited the increase in HO-1 mRNA in response to hemin. Ferritin protein heavy chain but not mRNA increased upon exposure of cells to Hb. Hemin and ferric but not ferrous Hb were toxic to smooth muscle cells. Toxicity was increased by exposure to Hb plus tin protoporphyrin IX. In conclusion, exposure of smooth muscle cells to Hb induces HO-1 mRNA and protein through pathways that involve new protein synthesis. Hemin is the component of Hb that induces HO-1. Hemin and ferric but not ferrous Hb are toxic.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11045978&dopt=Abstract hemorrhage
Ophthal Plast Reconstr Surg. 2002 Nov;18(6):409-15.
Hemorrhagic complications of oculoplastic surgery.
Custer PL, Trinkaus KM.
Department of Ophthalmology and Visual Sciences, Washington University School of Medicine, St. Louis, Missouri, USA. custeision.wustl.edu
PURPOSE: To determine the incidence and risk factors of hemorrhagic complications associated with selected oculoplastic procedures. METHODS: A prospective study was performed to document the severity of intraoperative hemorrhage and postoperative bruising in patients undergoing oculoplastic procedures. The use of anticoagulant or platelet-inhibiting medications, systemic medical conditions, patient age, patient sex, and type of procedure were examined to identify risk factors for hemorrhagic complications. RESULTS: Troublesome intraoperative bleeding prolonged surgery in 9.2% of cases. Severe bleeding with the potential to affect surgical outcome was encountered in 0.4% of procedures. There was little correlation between severity of bleeding and degree of postoperative bruising. Male sex, a history of heart disease, or age >60 years imparted a slightly greater risk of intraoperative bleeding. Age >60 years, hypertension, or recent cessation of aspirin may increase the risk of postoperative bruising. A history of previous stroke increased the risk of postoperative bleeding. There was no statistical difference in the incidence of hemorrhagic complications among patients currently treated with antiplatelet/anticoagulant agents, those who had stopped these medications before surgery, and those who were not treated with these agents. No patient had permanent sequelae related to hemorrhage. Two patients had postoperative systemic complications possibly attributable to withholding anticoagulant/antiplatelet medications in preparation for surgery. CONCLUSIONS: Although serious hemorrhagic complications may be associated with oculoplastic procedures, the incidence of these complications is low. The decision to withhold antiplatelet or anticoagulant medications before surgery should be individualized. Selected procedures can be safely performed without stopping these agents.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12439052&dopt=Abstract hemorrhage
Radiographics. 2000 Oct;20 Spec No:S53-66.
CT of unusual iliopsoas compartment lesions.
Muttarak M, Peh WC.
Department of Radiology, Chiang Mai University, Chiang Mai, Thailand.
The authors reviewed the anatomy of the iliopsoas compartment and a spectrum of unusual lesions affecting structures in this compartment, with emphasis on the role of computed tomography (CT). Lesions in the iliopsoas compartment are caused by acute infection, tumor, or hemorrhage. The knowledge of detailed clinical data can help improve the diagnostic accuracy, particularly with regard to primary iliopsoas lesions. CT is useful for delineating the source of secondary iliopsoas lesions, guiding biopsy, and performing follow-up of treated lesions. Nonenhanced CT can help detect fresh hemorrhage, fat-containing tumor, and calcification, whereas contrast material enhanced CT optimizes imaging of infection, tumor, and aneurysm.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11046162&dopt=Abstract hemorrhage
J Radiol. 1999 Sep;80(9):913-6.
[MRI imaging in cortical laminar necrosis]
[Article in French]
el Quessar A, Meunier JC, Delmaire C, Soto Ares G, Pruvo JP.
Service de Neuroradiologie, Hopital R Salengro, CHRU de Lille.
PURPOSE: The goal of this study was to follow over time the MR imaging features of cortical laminar necrosis. PATIENTS AND METHODS: Six patients with cortical laminar necrosis were included. There were two women and four men aged 54-84 years, with a mean age of 68 years. In four patients, cortical laminar necrosis was caused by ischemic stroke, one case occurred after a cardiac arrest and the last patient had a meningoencephalitis. The time delay from insult to the first MR study varied between one week and 3 months. RESULTS: The MRI showed hyperintense lesions in the cerebral cortex on T1W and T2W images. The high intensity signal was still observed a few months after the insult. Cortical laminar necrosis lesions did not demonstrate hemorrhage on CT and MRI studies. CONCLUSION: MRI allowed detection of cortical laminar necrosis and could differentiate it from hemorrhage.
Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11048544&dopt=Abstract hemorrhage
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