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papilledema/albumin
Länken sparas på Urklipp
Sida 1 från 16 resultat
Optic disk manifestation in diabetic eyes with low serum albumin: late fluorescein staining and high blood flow velocities in the optic disk.
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OBJECTIVE
To evaluate ocular findings and blood flow characteristics in diabetes mellitus (DM) patients with low serum albumin (ALB).
METHODS
We studied 106 eyes of 53 type II DM patients without proliferative diabetic retinopathy and panretinal photocoagulation. All underwent standard ophthalmic
Mechanisms of fluid accumulation in retinal edema.
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This paper reviews the anatomic and physiologic conditions which predispose to fluid accumulation within the retina. Retinal edema has its inception in disease that causes a breakdown of the blood-retinal barrier in retinal capillaries and/or the retinal pigment epithelium (RPE). Edema develops not
Protective effects of intraperitoneal vitamin C, aprotinin and melatonin administration on retinal edema during experimental uveitis in the guinea pig.
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A considerable amount of clinical and experimental evidence exists suggesting the involvement of reactive oxygen substances (ROS) in the aetiology of uveitis. The activated phagocytic system of polymorphonuclear leucocytes in uveitis is involved in the generation of ROS. In addition to their direct
C-type natriuretic peptide protects the retinal pigment epithelium against advanced glycation end product-induced barrier dysfunction.
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In diabetic retinopathy, vision loss is usually secondary to macular edema, which is thought to depend on the functional integrity of the blood-retina barrier. The levels of advanced glycation end products in the vitreous correlate with the progression of diabetic retinopathy. Natriuretic peptides
The eyes of transforming growth factor-sZ1 (TGF-sZ1) transgenic mice Morphology and the development of endotoxin-induced uveitis.
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Transforming growth factor-beta (TGFsZ) is a potent regulator of cellular growth and immune function. The authors studied ocular histology and endotoxin-induced uveitis in a TGF-sZ(1) transgenic (Tg) murine model. TGF-sZ(1) Tg mice were generated by micro injecting a gene constructed by fusing the
TRPV4 inhibition prevents increased water diffusion and blood-retina barrier breakdown in the retina of streptozotocin-induced diabetic mice.
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A better understanding of the molecular and cellular mechanisms involved in retinal hydro-mineral homeostasis imbalance during diabetic macular edema (DME) is needed to gain insights into retinal (patho-)physiology that will help elaborate innovative therapies with lower health care costs. Transient
Hyperactivation of retina by light in mice leads to photoreceptor cell death mediated by VEGF and retinal pigment epithelium permeability.
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Light toxicity is suspected to enhance certain retinal degenerative processes such as age-related macular degeneration. Death of photoreceptors can be induced by their exposure to the visible light, and although cellular processes within photoreceptors have been characterized extensively, the role
Induction of ischemic tolerance protects the retina from diabetic retinopathy.
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Diabetic retinopathy is a leading cause of acquired blindness. Available treatments are not very effective. We investigated the effect of a weekly application of retinal ischemia pulses (ischemic conditioning) on retinal damage induced by experimental diabetes. Diabetes was induced by an
[Cerebral venous thrombosis in minimal change nephrotic syndrome].
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A 46-year old man presented with an eight-day history of edema and was found to be nephrotic, with a plasma albumin level of 1.1 g/dl and urine protein excretion of 13.3 g/24 hrs. The level of plasma creatinine was normal at 1.0 mg/dl. A finding of renal biopsy was consistent with minimal change
[Acute quinine poisoning treated with high dose of diazepam].
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BACKGROUND
High concentrations of quinine, the drug of choice for severe malaria, are toxic to the cardiovascular system, producing hypotension and abnormal myocardial conduction.
METHODS
An 8 year-old girl was admitted for fever, headache and arthralgias. Examination of a thick film of blood showed
The inhibition of advanced glycation end-products-induced retinal vascular permeability by silver nanoparticles.
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The increased permeability of the blood-retinal barrier is known to occur in patients with diabetes, and this defect contributes to retinal edema. This study aimed to determine the effects of silver nanoparticles (Ag-NPs) on advanced glycation end-products (AGEs)-induced endothelial cell
Morphologic alterations in rat retina after hypervolemic infusion of cross-linked hemoglobin.
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Hypervolemic infusion in rats of bis (3,5-dibromosalicyl) fumarate cross-linked hemoglobin (DBBF-Hb) to 40-60% of blood volume produced histologic lesions in retina which were not observed in rats similarly infused with human serum albumin or lactated Ringer's solution. Rats treated with 40%
Vascular endothelial growth factor modulates the function of the retinal pigment epithelium in vivo.
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OBJECTIVE
Retinal edema, the accumulation of extracellular fluid in the retina is usually attributed to inner blood retina barrier (BRB) leakage. Vascular endothelial growth factor plays an important role in this process. The effects of VEGF on the outer BRB, the RPE, however, have received limited
Clinical features of patients with high-altitude pulmonary edema in Japan.
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Clinical studies were performed in 27 consecutive patients with high-altitude pulmonary edema who were transported from the mountains to Shinshu University Hospital, Matsumoto, Japan. The altitude of onset was 2,680 m to 3,190 m above sea level. Symptoms included marked dyspnea, cough, and stridor.
POEMS Syndrome: 2019 Update on diagnosis, risk-stratification, and management.
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