biotin/edema

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Cellular accumulation of extravasated serum protein and DNA fragmentation following vasogenic edema.

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Accumulation of serum protein has been demonstrated in injured brain cells following vasogenic brain edema. The present study was conducted to test whether this phenomenon is also observed in apoptotic cells as well as in necrotic cells. Apoptotic cell death has been implicated in a variety of brain

Anthrax edema toxin impairs clearance in mice.

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The anthrax edema toxin (ET) of Bacillus anthracis is composed of the receptor-binding component protective antigen (PA) and of the adenylyl cyclase catalytic moiety, edema factor (EF). Uptake of ET into cells raises intracellular concentrations of the secondary messenger cyclic AMP, thereby

Accumulation of hyaluronan (hyaluronic acid) in myocardial interstitial tissue parallels development of transplantation edema in heart allografts in rats.

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By using biotin-labeled proteoglycan core protein, hyaluronan (hyaluronic acid; HA) was visualized in rat heart grafts at different times (2, 4, and 6 d) after transplantation. In normal, nontransplanted hearts HA was present in the adventitia of arteries and veins and in the myocardial interstitial

Hyaluronic acid accumulation and redistribution in rejecting rat kidney graft. Relationship to the transplantation edema.

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By using biotin-labeled proteoglycan core protein and an avidin-enzyme system, hyaluronic acid (HA) was visualized in rat kidney. In the normal kidney, HA was localized in the extracellular space of the inner medulla and increased markedly towards the papillary tip. No staining for HA was seen in

Hyaluronic acid accumulation; the mechanism behind graft rejection edema.

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Hyaluronic acid (HA) is an important stabilizing consistuent of the loose connective tissue and regulates water homeostasis. Thus, excessive accumulation of HA in interstitial tissue immobilizes water and may thereby contribute to interstitial tissue edema. By the use of biotin labelled core protein

Occurrence of apoptosis following cold injury-induced brain edema in mice.

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Apoptosis has been known to contribute to neuronal death following a variety of brain insults. However, the role of vasogenic brain edema in neuronal apoptosis is unknown. We studied the temporal pattern of brain edema and neuronal apoptosis following cold injury. Cold injury-induced brain edema,

Ameliorative effect of glial cell line-derived neurotrophic factor on brain edema formation after permanent middle cerebral artery occlusion in rats.

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Glial cell line-derived neurotrophic factor (GDNF) was applied topically on the brain surface immediately after permanent middle cerebral artery (MCA) occlusion in rats. In contrast to the cases treated with vehicle, a formation of brain edema was significantly reduced at one day by the treatment

Amelioration of brain edema by topical application of glial cell line-derived neurotrophic factor in reperfused rat brain.

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Glial cell line-derived neurotrophic factor (GDNF) was applied topically on the brain surface of reperfused rat brain after 90 min of transient middle cerebral artery occlusion. In contrast to the cases treated with vehicle, a formation of brain edema was greatly reduced at 2 days by the treatment

Extracorporeal immunoadsorption from whole blood based on the avidin-biotin concept. Evaluation of a new method.

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This study of 36 rats with rat colon adenocarcinoma transplants was carried out to investigate the efficacy of a new method of whole blood immunoadsorption (WBIA) in removing biotinylated monoclonal antibodies (MAbs) directly from unseparated blood, in order to increase 'the tumor/normal-tissue

Comparative study of the behavior of p53 immunoexpression in smoking associated lesions: Reinke's edema and laryngeal carcinoma.

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OBJECTIVE To assess the behavior of the immunoexpression of protein p53 in Reinke's edema and laryngeal squamous cell carcinoma. METHODS retrospective. METHODS we recovered the histological paraffin blocks of patients who were subjected to Reinke's edema and laryngeal squamous cell carcinoma surgery

Reinkes' edema: immunoexpression study of fibronectin, laminin and collagen IV in 60 cases by immunohistochemical techniques.

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Reinke's edema is chronic laryngeal disease in which the superficial layer of the lamina propria is expanded by thick mucus, giving it a gelatin aspect. The disease is directly related to smoking and more frequent in women, who end up having a lower tone of voice. Its histological characteristics

Biotin-responsive basal ganglia disease revisited: clinical, radiologic, and genetic findings.

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OBJECTIVE To investigate the clinical, genetic, and neuroradiologic data of biotin-responsive basal ganglia disease (BBGD) and clarify the disease spectrum. METHODS We first investigated all patients attending our Division of Pediatric Neurology with a genetically proven diagnosis of BBGD between

Cold injury in mice: a model to study mechanisms of brain edema and neuronal apoptosis.

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Small rodents, mice in particular, have been widely used for genetic manipulation because of the extensive knowledge in development, embryology and other molecular aspects of this species. However, the use of mice for neurobiology research in the area of brain edema and neuronal injury has not been

Hyperglycemia exacerbates brain edema and perihematomal cell death after intracerebral hemorrhage.

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OBJECTIVE Hyperglycemia has a deleterious effect on brain ischemia. However, the effect of hyperglycemia in intracerebral hemorrhage (ICH) is not well known. We investigated the effect of hyperglycemia on the development of brain edema and perihematomal cell death in ICH. METHODS Hyperglycemia was

Lutein-Loaded, Biotin-Decorated Polymeric Nanoparticles Enhance Lutein Uptake in Retinal Cells

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Age related macular degeneration (AMD) is one of the leading causes of visual loss and is responsible for approximately 9% of global blindness. It is a progressive eye disorder seen in elderly people (>65 years) mainly affecting the macula. Lutein, a carotenoid, is an antioxidant, and has shown

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