Fluorescein
Fluoresceins
Fluorescein Angiography
Fluorescein-5-isothiocyanate
Fluorophotometry
Fundus Oculi
Fluorescent Dyes
Choroidal Neovascularization
Choroid
Dextrans
Dry Eye Syndromes
Vitreous Body
Indocyanine Green
Laser Coagulation
Visual Acuity
Rose Bengal
Rhodamines
Capillary Permeability
Choroid Diseases
Macular Degeneration
Microscopy, Fluorescence
Macula Lutea
Fluorometry
Tomography, Optical Coherence
Cornea
Ophthalmic Solutions
Blood-Retinal Barrier
Erythrosine
Macular Edema
Permeability
Eosine I Bluish
Diabetic Retinopathy
Retina
Retinal Artery
Coloring Agents
Rabbits
Retinal Vein Occlusion
Anterior Chamber
Staining and Labeling
Photography
Microscopy, Confocal
Fluorescence
Retinal Vein
Retinal Artery Occlusion
Light Coagulation
Fluorescent Antibody Technique
Retinal Neovascularization
Fovea Centralis
Sclera
Intravitreal Injections
Aqueous Humor
Retinal Detachment
Lasers
Iris
Lissamine Green Dyes
Conjunctiva
Pigment Epithelium of Eye
Flow Cytometry
Fluorescence Polarization
Photochemotherapy
Papilledema
Epithelium, Corneal
Blood-Aqueous Barrier
Central Serous Chorioretinopathy
Hydrogen-Ion Concentration
Ophthalmoscopes
Keratoconjunctivitis Sicca
Retinal Vasculitis
Probenecid
Microscopy, Ultraviolet
Energy Transfer
Cerebrospinal Fluid Rhinorrhea
Extravasation of Diagnostic and Therapeutic Materials
Diffusion
Meibomian Glands
Cell Membrane Permeability
Telangiectasis
Drug Delivery Systems
Retinal Drusen
Phycoerythrin
Photosensitizing Agents
Retinal Pigment Epithelium
Biological Transport
Choroid Neoplasms
Chorioretinitis
Exudates and Transudates
Administration, Topical
Lacrimal Apparatus
Cells, Cultured
Haptens
Benzalkonium Compounds
Binding Sites
The bystander effect in the HSVtk/ganciclovir system and its relationship to gap junctional communication. (1/2851)
The bystander effect (BSE) is an interesting and important property of the herpes thymidine kinase/ganciclovir (hTK/GCV) system of gene therapy for cancer. With the BSE, not only are the hTK expressing cells killed upon ganciclovir (GCV) exposure but also neighboring wild-type tumor cells. On testing a large number of tumor cell lines in vitro, a wide range of sensitivity to bystander killing was found. Since transfer of toxic GCV metabolites from hTK-modified to wild-type tumor cells via gap junctions (GJ) seemed to be a likely mechanism of the BSE, we tested GJ function in these various tumors with a dye transfer technique and pharmacological agents known to affect GJ communication. We confirmed that mixtures of tumor cell resistant to the BSE did not show dye transfer from cell to cell while bystander-sensitive tumor cells did. Dieldrin, a drug known to decrease GJ communication, diminished dye transfer and also inhibited the BSE. Forskolin, an upregulator of cAMP did increase GJ, but directly inhibited hTK and therefore its effect on BSE could not be determined. We conclude that these observations further support port the concept that functional GJ play an important role in the BSE and further suggest that pharmacological manipulation of GJ may influence the outcome of cancer therapy with hTK/GCV. (+info)Overexpression of the multidrug resistance-associated protein (MRP1) in human heavy metal-selected tumor cells. (2/2851)
Cellular and molecular mechanisms involved in the resistance to cytotoxic heavy metals remain largely to be characterized in mammalian cells. To this end, we have analyzed a metal-resistant variant of the human lung cancer GLC4 cell line that we have selected by a step-wise procedure in potassium antimony tartrate. Antimony-selected cells, termed GLC4/Sb30 cells, poorly accumulated antimony through an enhanced cellular efflux of metal, thus suggesting up-regulation of a membrane export system in these cells. Indeed, GLC4/Sb30 cells were found to display a functional overexpression of the multidrug resistance-associated protein MRP1, a drug export pump, as demonstrated by Western blotting, reverse transcriptase-polymerase chain reaction and calcein accumulation assays. Moreover, MK571, a potent inhibitor of MRP1 activity, was found to markedly down-modulate resistance of GLC4/Sb30 cells to antimony and to decrease cellular export of the metal. Taken together, our data support the conclusion that overexpression of functional MRP1 likely represents one major mechanism by which human cells can escape the cytotoxic effects of heavy metals. (+info)Fluorimetric multiparameter cell assay at the single cell level fabricated by optical tweezers. (3/2851)
A fluorimetric multi-parameter cell sensor at the single cell level is presented which makes it possible to observe the physiological behavior of different cell lines, different physiological parameters, and statistical data at the same time. Different cell types were immobilized at predefined positions with high accuracy using optical tweezers and adhesion promoting surface layers. The process is applicable to both adherent and non-adherent cells. Coating of the immobilization area with mussel adhesive protein was shown to be essential for the process. Intracellular proton and calcium concentrations in different cell classes were simultaneously imaged and the specific activation of T lymphocytes was demonstrated. This method should be especially useful for drug screening due to the small sample volume and high information density. (+info)Shrinkage-induced activation of Na+/H+ exchange in rat renal mesangial cells. (4/2851)
Using the pH-sensitive dye 2', 7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein (BCECF), we examined the effect of hyperosmolar solutions, which presumably caused cell shrinkage, on intracellular pH (pHi) regulation in mesangial cells (single cells or populations) cultured from the rat kidney. The calibration of BCECF is identical in shrunken and unshrunken mesangial cells if the extracellular K+ concentration ([K+]) is adjusted to match the predicted intracellular [K+]. For pHi values between approximately 6.7 and approximately 7.4, the intrinsic buffering power in shrunken cells (600 mosmol/kgH2O) is threefold larger than in unshrunken cells (approximately 300 mosmol/kgH2O). In the nominal absence of CO2/HCO-3, exposing cell populations to a HEPES-buffered solution supplemented with approximately 300 mM mannitol (600 mosmol/kgH2O) causes steady-state pHi to increase by approximately 0.4. The pHi increase is due to activation of Na+/H+ exchange because, in single cells, it is blocked in the absence of external Na+ or in the presence of 50 microM ethylisopropylamiloride (EIPA). Preincubating cells in a Cl--free solution for at least 14 min inhibits the shrinkage-induced pHi increase by 80%. We calculated the pHi dependence of the Na+/H+ exchange rate in cell populations under normosmolar and hyperosmolar conditions by summing 1) the pHi dependence of the total acid-extrusion rate and 2) the pHi dependence of the EIPA-insensitive acid-loading rate. Shrinkage alkali shifts the pHi dependence of Na+/H+ exchange by approximately 0.7 pH units. (+info)Distribution of 5-chloromethylfluorescein diacetate staining during meiotic maturation and fertilization in vitro of mouse oocytes. (5/2851)
The aim of this confocal microscopy study was to determine whether the pattern of CellTracker Green 5-chloromethylfluorescein diacetate (CMFDA) staining changes during meiotic maturation and fertilization in vitro of mouse oocytes. At different times during meiotic maturation and fertilization, oocytes, zygotes and two-cell embryos were stained with CMFDA to demonstrate intracellular glutathione S-transferase activity. After washing in CMFDA-free medium, most oocytes, zygotes and embryos were stained with dihydroethidium (HE) to visualize DNA structures. Meiotic maturation and fertilization in vitro of mouse oocytes were associated with changes in the pattern of intracellular CMFDA staining. In particular, accumulations of CMFDA-positive membranes were observed around the nucleus of germinal vesicle (GV) oocytes, overlaying the sperm nucleus as well as overlaying the first mitotic spindle if this approached the plasma membrane. Staining of oocytes and zygotes with the probes 3,3'-dihexyloxacarbocyanine iodine [DiOC6(3)], which stains all the intracellular membranes, and rhodamine 123, which stains active mitochondria, demonstrated that the intracellular structures evidenced by CMFDA staining did not correspond to accumulations of mitochondria. Exposure of oocytes and zygotes to the microtubule-disrupting agent nocodazole or the actin-depolymerizing drug cytochalasin D revealed an autonomous microfilament-dependent transport and relocation of CMFDA-positive membranes during meiotic maturation and fertilization. Such a transport of CMFDA-positive membranes may be envisaged as a protective shield built to prevent damage to DNA from endogenous and exogenous mutagen metabolites. (+info)Partitioning of triphenylalkylphosphonium homologues in gel bead-immobilized liposomes: chromatographic measurement of their membrane partition coefficients. (6/2851)
Unilamellar liposomes of small or large size, SUVs and LUVs, respectively, were stably immobilized in the highly hydrophilic Sepharose 4B or Sephacryl S-1000 gel beads as a membrane stationary phase for immobilized liposome chromatography (ILC). Lipophilic cations of triphenylmethylphosphonium and tetraphenylphosphonium (TPP+) have been used as probes of the membrane potential of cells. Interaction of TPP+ and triphenylalkylphosphonium homologues with the immobilized liposomal membranes was shown by their elution profiles on both zonal and frontal ILC. Retardation of the lipophilic cations on the liposome gel bed was increased as the hydrophobicity of the cations increased, indicating the partitioning of lipophilic cations into the hydrocarbon region of the membranes. The cations did not retard on the Sepharose or Sephacryl gel bed without liposomes, confirming that the cations only interact with the immobilized liposomes. Effects of the solute concentration, flow rate, and gel-matrix substance on the ILC were studied. The stationary phase volume of the liposomal membranes was calculated from the volume of a phospholipid molecule and the amount of the immobilized phospholipid, which allowed us to determine the membrane partition coefficient (KLM) for the lipophilic cations distributed between the aqueous mobile and membrane stationary phases. The values of KLM were generally increased with the hydrophobicity of the solutes increased, and were higher for the SUVs than for the LUVs. The ILC method described here can be applied to measure membrane partition coefficients for other lipophilic solutes (e.g., drugs). (+info)Chemical transformations in individual ultrasmall biomimetic containers. (7/2851)
Individual phospholipid vesicles, 1 to 5 micrometers in diameter, containing a single reagent or a complete reaction system, were immobilized with an infrared laser optical trap or by adhesion to modified borosilicate glass surfaces. Chemical transformations were initiated either by electroporation or by electrofusion, in each case through application of a short (10-microsecond), intense (20 to 50 kilovolts per centimeter) electric pulse delivered across ultramicroelectrodes. Product formation was monitored by far-field laser fluorescence microscopy. The ultrasmall characteristic of this reaction volume led to rapid diffusional mixing that permits the study of fast chemical kinetics. This technique is also well suited for the study of reaction dynamics of biological molecules within lipid-enclosed nanoenvironments that mimic cell membranes. (+info)Kinetics of lactate and pyruvate transport in cultured rat myotubes. (8/2851)
Skeletal muscle transport of lactate and pyruvate was studied in primary cultures of rat myotubes, applying the pH-sensitive fluorescent indicator 2', 7'-bis(carboxyethyl)-5(6)-carboxyfluorescein. The initial rate of decrease in intracellular pH (pHi) upon lactate or pyruvate incubation was used to determine total transport (carrier mediated and diffusion). Both lactate and pyruvate transport could be inhibited by a combination of 0.5 mM 4,4'-diisothiocyanostilbene-2, 2'-disulfonic acid, 5 mM mersalyl and 10 mM alpha-cyano-4-hydroxycinnamate. The kinetic parameters, Km and Vmax, for carrier-mediated transport of lactate were 9.9+/-1.1 mM and 0. 69+/-0.02 mmol l-1 s-1, respectively. For pyruvate, Km and Vmax were 4.4+/-1.3 mM and 0.30+/-0.05 mmol l-1 s-1, respectively. The diffusion component of the total transport was 0.0040+/-0.0005[S] (n=4) and 0.0048+/-0.0003[S] (n=4) for lactate and pyruvate, respectively. Furthermore, it was observed that the two monocarboxylate transporter isoforms present in mature skeletal muscles, MCT1 and MCT4 (formerly called MCT3 (M.C. Wilson, V.N. Jackson, C. Heddle, N.T. Price, H. Pilegaard, C. Juel, A. Bonen, I. Montgomery, O.F. Hutter, A.P. Halestrap, Lactic acid efflux from white skeletal muscle is catalyzed by the monocarboxylate transporter isoform MCT3, J. Biol. Chem. 273 (1998) 15920-15926)), were also expressed in primary culture of myotubes. (+info)CNV develops when the underlying choroidal layers experience changes that lead to the growth of new blood vessels, which can leak fluid and cause damage to the retina. This can result in vision distortion, loss of central vision, and even blindness if left untreated.
The formation of CNV is a complex process that involves various cellular and molecular mechanisms. It is thought to be triggered by factors such as oxidative stress, inflammation, and the presence of certain growth factors and proteins.
There are several clinical signs and symptoms associated with CNV, including:
1. Distortion of vision, including metamorphopsia (distorted vision of geometric shapes)
2. Blind spots or scotomas
3. Decreased central vision
4. Difficulty reading or performing other daily tasks
5. Reduced color perception
6. Sensitivity to light and glare
The diagnosis of CNV is typically made based on a comprehensive eye exam, including a visual acuity test, dilated eye exam, and imaging tests such as fluorescein angiography or optical coherence tomography (OCT).
There are several treatment options for CNV, including:
1. Anti-vascular endothelial growth factor (VEGF) injections: These medications work by blocking the growth of new blood vessels and can help improve vision and reduce the risk of further damage.
2. Photodynamic therapy: This involves the use of a light-sensitive medication and low-intensity laser therapy to damage and shrink the abnormal blood vessels.
3. Focal photocoagulation: This involves the use of a high-intensity laser to destroy the abnormal blood vessels in the central retina.
4. Vitrectomy: In severe cases, a vitrectomy may be performed to remove the vitreous gel and blood vessels that are causing the CNV.
It is important to note that these treatments do not cure CNV, but they can help improve vision and slow the progression of the disease. Regular follow-up appointments with an eye care professional are necessary to monitor the condition and adjust treatment as needed.
There are several types of dry eye syndromes, including:
1. Dry eye disease (DED): This is the most common type of dry eye syndrome and is characterized by a deficiency in the tear film that covers the surface of the eye. It can be caused by a variety of factors such as aging, hormonal changes, medications, and environmental conditions.
2. Meibomian gland dysfunction (MGD): This type of dry eye syndrome is caused by problems with the meibomian glands, which are located in the eyelids and produce the fatty layer of the tear film. MGD can be caused by inflammation, blockages, or other issues that prevent the glands from functioning properly.
3. Aqueous deficient dry eye (ADDE): This type of dry eye syndrome is caused by a lack of the aqueous layer of the tear film, which is produced by the lacrimal gland. It can be caused by surgical removal of the lacrimal gland, injury to the gland, or other conditions that affect its function.
4. Evaporative dry eye (EDE): This type of dry eye syndrome is caused by a problem with the meibomian glands and the lipid layer of the tear film. It can be caused by inflammation, blockages, or other issues that prevent the glands from functioning properly.
5. Contact lens-related dry eye (CLDE): This type of dry eye syndrome is caused by wearing contact lenses, which can disrupt the natural tear film and cause dryness and irritation.
6. Sjögren's syndrome: This is an autoimmune disorder that affects the glands that produce tears and saliva, leading to dry eye syndrome and other symptoms.
7. Medications: Certain medications, such as antihistamines, decongestants, and blood pressure medications, can reduce tear production and lead to dry eye syndrome.
8. Hormonal changes: Changes in hormone levels, such as during menopause or pregnancy, can lead to dry eye syndrome.
9. Environmental factors: Dry air, smoke, wind, and dry climates can all contribute to dry eye syndrome.
10. Nutritional deficiencies: A lack of omega-3 fatty acids in the diet has been linked to an increased risk of dry eye syndrome.
It is important to note that dry eye syndrome can be a complex condition and may involve multiple factors. A comprehensive diagnosis from an eye doctor or other healthcare professional is necessary to determine the underlying cause and develop an effective treatment plan.
Examples of retinal diseases include:
1. Age-related macular degeneration (AMD): a leading cause of vision loss in people over the age of 50, AMD affects the macula, the part of the retina responsible for central vision.
2. Diabetic retinopathy (DR): a complication of diabetes that damages blood vessels in the retina and can cause blindness.
3. Retinal detachment: a condition where the retina becomes separated from the underlying tissue, causing vision loss.
4. Macular edema: swelling of the macula that can cause vision loss.
5. Retinal vein occlusion (RVO): a blockage of the small veins in the retina that can cause vision loss.
6. Retinitis pigmentosa (RP): a group of inherited disorders that affect the retina and can cause progressive vision loss.
7. Leber congenital amaurosis (LCA): an inherited disorder that causes blindness or severe visual impairment at birth or in early childhood.
8. Stargardt disease: a rare inherited disorder that affects the retina and can cause progressive vision loss, usually starting in childhood.
9. Juvenile macular degeneration: a rare inherited disorder that causes vision loss in young adults.
10. Retinal dystrophy: a group of inherited disorders that affect the retina and can cause progressive vision loss.
Retinal diseases can be diagnosed with a comprehensive eye exam, which includes a visual acuity test, dilated eye exam, and imaging tests such as optical coherence tomography (OCT) or fluorescein angiography. Treatment options vary depending on the specific disease and can include medication, laser surgery, or vitrectomy.
It's important to note that many retinal diseases can be inherited, so if you have a family history of eye problems, it's important to discuss your risk factors with your eye doctor. Early detection and treatment can help preserve vision and improve quality of life for those affected by these diseases.
Some common examples of choroid diseases include:
1. Choroidal neovascularization (CNV): This is a condition where new blood vessels grow under the retina, often as a result of age-related macular degeneration (AMD) or other eye conditions. These new vessels can cause vision loss and distortion.
2. Choroidal melanoma: This is a type of cancer that develops in the choroid layer of the eye. It is usually slow-growing, but it can spread to other parts of the body if left untreated.
3. Choroiditis: This is an inflammatory condition that affects the choroid layer of the eye, often as a result of infection or autoimmune disorders. It can cause vision loss and pain in the affected eye.
4. Choroidal rupture: This is a rare condition where the choroid layer of the eye ruptures, leading to bleeding and potentially severe vision loss.
5. Other conditions: There are several other conditions that can affect the choroid layer of the eye, such as choroidal vasculitis, choroidal effusion, and choroidal tumors. These conditions can cause a range of symptoms, including vision loss, pain, and distortion.
Overall, choroid diseases can have a significant impact on vision and eye health, and it is important to seek medical attention if any symptoms persist or worsen over time. Early detection and treatment can help to mitigate the risk of long-term vision loss and other complications.
There are two main types of MD:
1. Dry Macular Degeneration (DMD): This is the most common form of MD, accounting for about 90% of cases. It is caused by the gradual accumulation of waste material in the macula, which can lead to cell death and vision loss over time.
2. Wet Macular Degeneration (WMD): This type of MD is less common but more aggressive, accounting for about 10% of cases. It occurs when new blood vessels grow underneath the retina, leaking fluid and causing damage to the macula. This can lead to rapid vision loss if left untreated.
The symptoms of MD can vary depending on the severity and type of the condition. Common symptoms include:
* Blurred vision
* Distorted vision (e.g., straight lines appearing wavy)
* Difficulty reading or recognizing faces
* Difficulty adjusting to bright light
* Blind spots in central vision
MD can have a significant impact on daily life, making it difficult to perform everyday tasks such as driving, reading, and recognizing faces.
There is currently no cure for MD, but there are several treatment options available to slow down the progression of the disease and manage its symptoms. These include:
* Anti-vascular endothelial growth factor (VEGF) injections: These medications can help prevent the growth of new blood vessels and reduce inflammation in the macula.
* Photodynamic therapy: This involves the use of a light-sensitive drug and low-intensity laser to damage and shrink the abnormal blood vessels in the macula.
* Vitamin supplements: Certain vitamins, such as vitamin C, E, and beta-carotene, have been shown to slow down the progression of MD.
* Laser surgery: This can be used to reduce the number of abnormal blood vessels in the macula and improve vision.
It is important for individuals with MD to receive regular monitoring and treatment from an eye care professional to manage their condition and prevent complications.
Symptoms of macular edema may include blurred vision, distorted vision, blind spots, and sensitivity to light. Diagnosis is typically made through a comprehensive eye exam, including a visual acuity test and imaging tests such as optical coherence tomography (OCT).
Treatment for macular edema depends on the underlying cause of the condition. In some cases, medications such as anti-vascular endothelial growth factor (VEGF) injections or corticosteroids may be prescribed to reduce fluid buildup and swelling in the retina. In more severe cases, surgical intervention may be necessary, such as a vitrectomy to remove the vitreous gel and relieve pressure on the retina.
Prevention of macular edema includes managing underlying conditions such as diabetes and age-related macular degeneration, as well as maintaining regular eye exams to detect and treat any changes in the retina early on. Early detection and treatment can help prevent vision loss from macular edema.
There are two main types of DR:
1. Non-proliferative diabetic retinopathy (NPDR): This is the early stage of DR, where the blood vessels in the retina become damaged and start to leak fluid or bleed. The symptoms can be mild or severe and may include blurred vision, floaters, and flashes of light.
2. Proliferative diabetic retinopathy (PDR): This is the advanced stage of DR, where new blood vessels start to grow in the retina. These vessels are weak and can cause severe bleeding, leading to vision loss.
DR is a common complication of diabetes, and it is estimated that up to 80% of people with diabetes will develop some form of DR over their lifetime. The risk of developing DR increases with the duration of diabetes and the level of blood sugar control.
Early detection and treatment of DR can help to prevent vision loss, so it is important for people with diabetes to have regular eye exams to monitor their retinal health. Treatment options for DR include laser surgery, injections of anti-vascular endothelial growth factor (VEGF) medications, and vitrectomy, a surgical procedure to remove the vitreous gel and blood from the eye.
Preventing Diabetic Retinopathy
While there is no surefire way to prevent diabetic retinopathy (DR), there are several steps that people with diabetes can take to reduce their risk of developing this complication:
1. Control blood sugar levels: Keeping blood sugar levels within a healthy range can help to slow the progression of DR. This can be achieved through a combination of diet, exercise, and medication.
2. Monitor blood pressure: High blood pressure can damage the blood vessels in the retina, so it is important to monitor and control blood pressure to reduce the risk of DR.
3. Maintain healthy blood lipids: Elevated levels of low-density lipoprotein (LDL) cholesterol and lower levels of high-density lipoprotein (HDL) cholesterol can increase the risk of DR.
4. Quit smoking: Smoking can damage the blood vessels in the retina and increase the risk of DR.
5. Maintain a healthy weight: Obesity is a risk factor for DR, so maintaining a healthy weight can help to reduce the risk of this complication.
6. Get regular eye exams: Regular eye exams can help to detect DR in its early stages, when it is easier to treat and prevent vision loss.
Preventing Diabetic Retinopathy
While there is no cure for diabetic retinopathy (DR), there are several treatment options available to help manage the condition and prevent vision loss. These include:
1. Laser surgery: This is a common treatment for early-stage DR, where a laser is used to shrink abnormal blood vessels in the retina and reduce the risk of further damage.
2. Injection therapy: Medications such as anti-vascular endothelial growth factor (VEGF) injections can be used to shrink abnormal blood vessels and reduce swelling in the retina.
3. Vitrectomy: In severe cases of DR, a vitrectomy may be performed to remove scar tissue and blood from the center of the eye.
4. Blood pressure control: Maintaining healthy blood pressure can help to slow the progression of DR.
5. Blood glucose control: Keeping blood sugar levels under control can also slow the progression of DR.
6. Follow-up care: Regular follow-up appointments with an eye doctor are important to monitor the progress of DR and adjust treatment as needed.
Early detection and treatment of diabetic retinopathy can help to prevent vision loss and improve outcomes for individuals with this complication of diabetes. By managing blood sugar levels, blood pressure, and cholesterol, and by getting regular eye exams, individuals with diabetes can reduce their risk of developing DR and other diabetic complications.
The symptoms of RVO can vary depending on the severity of the blockage, but may include:
* Blurred vision
* Double vision
* Flashes of light
* Eye pain
* Reduced peripheral vision
RVO is typically diagnosed through a comprehensive eye exam, which may include imaging tests such as fluorescein angiography or optical coherence tomography (OCT).
Treatment for RVO depends on the severity of the condition and may include:
* Medications to reduce inflammation and improve blood flow
* Injections of medication into the eye
* Laser surgery to clear blockages or reduce inflammation
* Vitrectomy, a surgical procedure to remove the vitreous gel and blood from the eye
Early diagnosis and treatment of RVO can help prevent or reduce vision loss. However, in some cases, permanent vision loss may occur despite treatment.
Preventing RVO is not always possible, but controlling risk factors such as high blood pressure, diabetes, and hypertension can help reduce the likelihood of developing the condition. Maintaining a healthy lifestyle, including regular exercise, a balanced diet, and not smoking, can also help reduce the risk of RVO.
There are many different types of uveal diseases, including:
1. Uveitis: This is inflammation of the uvea, which can be caused by a variety of factors such as infection, injury, or autoimmune disorders.
2. Iridocyclitis: This is inflammation of the iris and ciliary body.
3. Choroiditis: This is inflammation of the choroid layer of the uvea.
4. Retinal vein occlusion: This is a blockage of the veins that carry blood away from the retina, which can cause vision loss.
5. Macular edema: This is swelling of the macula, the part of the retina responsible for central vision.
6. Age-related macular degeneration (AMD): This is a condition that affects the macula and can cause vision loss over time.
7. Diabetic retinopathy: This is a complication of diabetes that can cause damage to the blood vessels in the retina and lead to vision loss.
8. Retinal detachment: This is a condition where the retina becomes separated from the underlying tissue, leading to vision loss.
9. Retinal vein thrombosis: This is a blockage of the veins that carry blood away from the retina, which can cause vision loss.
10. Uveal melanoma: This is a type of cancer that affects the uvea and can be potentially life-threatening.
These are just a few examples of uveal diseases, and there are many other conditions that can affect the uvea as well. Treatment options for uveal diseases vary depending on the specific condition and its cause, but may include medications, laser surgery, or other procedures to treat inflammation, reduce swelling, or remove tumors.
There are two main types of retinal artery occlusion: central retinal artery occlusion (CRAO) and branch retinal artery occlusion (BRAO). Central retinal artery occlusion occurs when the central retinal artery, which supplies blood to the macula, becomes blocked. This can cause sudden vision loss in one eye, often with a painless, blinding effect. Branch retinal artery occlusion, on the other hand, occurs when one of the smaller retinal arteries that branch off from the central retinal artery becomes blocked. This can cause vision loss in a specific part of the visual field, often with some preserved peripheral vision.
Retinal artery occlusion is often caused by a blood clot or other debris that blocks the flow of blood through the retinal arteries. It can also be caused by other conditions such as diabetes, high blood pressure, and atherosclerosis (the buildup of plaque in the arteries).
Retinal artery occlusion is a medical emergency that requires prompt treatment. Treatment options may include intravenous injection of medications to dissolve the clot or other debris, laser surgery to repair damaged retinal tissue, and/or vitrectomy (surgical removal of the vitreous gel) to remove any blood or debris that has accumulated in the eye.
In summary, retinal artery occlusion is a serious condition that can cause sudden vision loss and potentially lead to permanent blindness. It is important to seek medical attention immediately if you experience any symptoms of retinal artery occlusion, such as sudden vision loss or blurred vision in one eye, flashes of light, floaters, or pain in the eye.
Retinal hemorrhage can cause vision loss or blindness if not treated promptly. The bleeding can lead to scarring, which can cause permanent damage to the retina and affect vision. In some cases, retinal hemorrhage can be a sign of a more serious underlying condition that requires immediate medical attention.
Retinal hemorrhage is diagnosed through a comprehensive eye exam, which includes a visual acuity test, dilated eye exam, and imaging tests such as fluorescein angiography or optical coherence tomography. Treatment options for retinal hemorrhage depend on the underlying cause and can include laser surgery, medication, or vitrectomy.
In summary, retinal hemorrhage is a serious condition that can cause vision loss or blindness if not treated promptly. It is essential to seek medical attention if symptoms such as blurred vision, flashes of light, or floaters are noticed. Early detection and treatment can help prevent or reduce vision loss in cases of retinal hemorrhage.
The growth of new blood vessels in the retina is a natural response to hypoxia (lack of oxygen) and inflammation caused by these diseases. However, these new blood vessels are fragile and can cause damage to the retina, leading to vision loss. In some cases, RNV can also lead to vitreous hemorrhage, retinal detachment, or glaucoma, which can further exacerbate vision loss.
The diagnosis of RNV is typically made through a comprehensive eye exam, including a visual acuity test, dilated eye exam, and imaging tests such as fluorescein angiography or optical coherence tomography (OCT). Treatment options for RNV depend on the underlying cause of the condition and may include medications, laser therapy, or vitrectomy.
In summary, retinal neovascularization is a common complication of various retinal diseases that can lead to vision loss if left untreated. Early detection and prompt treatment are essential to prevent further damage and preserve visual function.
The retina is a layer of cells that lines the inside of the eye and senses light to send visual signals to the brain. When the retina becomes detached, it can no longer function properly, leading to vision loss or distortion.
Retinal detachment can be caused by a variety of factors, including:
1. Age-related changes: As we age, the vitreous gel that fills the eye can become more liquid and pull away from the retina, causing a retinal detachment.
2. Injury or trauma: A blow to the head or a penetrating injury can cause a retinal detachment.
3. Medical conditions: Certain conditions, such as diabetes, high blood pressure, and sickle cell disease, can increase the risk of developing a retinal detachment.
4. Genetic factors: Some people may be more prone to developing a retinal detachment due to inherited genetic factors.
Symptoms of retinal detachment may include:
1. Flashes of light: People may see flashes of light in the peripheral vision.
2. Floaters: Specks or cobwebs may appear in the vision, particularly in the periphery.
3. Blurred vision: Blurred vision or distorted vision may occur as the retina becomes detached.
4. Loss of vision: In severe cases, a retinal detachment can cause a complete loss of vision in one eye.
If you experience any of these symptoms, it is important to seek medical attention immediately. A comprehensive eye exam can diagnose a retinal detachment and determine the appropriate treatment.
Treatment for retinal detachment typically involves surgery to reattach the retina to the underlying tissue. In some cases, laser surgery may be used to seal off any tears or holes in the retina that caused the detachment. In more severe cases, a scleral buckle or other device may be implanted to support the retina and prevent further detachment.
In addition to surgical treatment, there are some lifestyle changes you can make to help reduce your risk of developing a retinal detachment:
1. Quit smoking: Smoking has been linked to an increased risk of retinal detachment. Quitting smoking can help reduce this risk.
2. Maintain a healthy blood pressure: High blood pressure can increase the risk of retinal detachment. Monitoring and controlling your blood pressure can help reduce this risk.
3. Wear protective eyewear: If you participate in activities that could potentially cause eye injury, such as sports or working with hazardous materials, wearing protective eyewear can help reduce the risk of retinal detachment.
4. Get regular eye exams: Regular comprehensive eye exams can help detect any potential issues with the retina before they become serious problems.
Overall, a retinal detachment is a serious condition that requires prompt medical attention to prevent long-term vision loss. By understanding the causes and symptoms of retinal detachment, as well as making lifestyle changes to reduce your risk, you can help protect your vision and maintain good eye health.
The term "papilledema" comes from the Greek words "papilla," meaning "little nipple," and "dema," meaning "swelling." This refers to the appearance of the optic disc when it is swollen, as it looks like a small, round nipple on the surface of the retina.
Papilledema can be caused by a variety of conditions, including high blood pressure, brain tumors, and aneurysms. It can also be a symptom of other conditions such as meningitis or multiple sclerosis. The diagnosis of papilledema is typically made through a comprehensive eye exam, which includes visual acuity testing, refraction, and retinoscopy. Imaging tests such as MRI or CT scans may also be used to evaluate the cause of the swelling.
Treatment of papilledema depends on the underlying cause of the condition. In cases where high blood pressure is the cause, medication to lower blood pressure may be prescribed. In other cases, surgery or other interventions may be necessary to relieve pressure on the brain and reduce swelling in the optic disc.
It's important for individuals with papilledema to work closely with their healthcare provider to monitor and manage their condition, as untreated papilledema can lead to permanent vision loss.
The exact cause of CSR is not fully understood, but it is thought to be related to changes in blood flow and inflammation in the retina. It can occur in people of all ages and is more common in males than females.
Symptoms of CSR may include:
* Blurred vision or blind spots
* Distorted vision
* Sensitivity to light
* Floating objects or cobwebs in vision
* Eye pain or discomfort
Diagnosis of CSR typically involves a comprehensive eye exam, including a visual acuity test, dilated eye exam, and imaging tests such as optical coherence tomography (OCT).
Treatment for CSR depends on the underlying cause and severity of the condition. In some cases, no treatment may be necessary, as the condition may resolve on its own over time. Other treatments may include:
* Medications to reduce inflammation and improve blood flow in the retina
* Photodynamic therapy (PDT) to reduce the amount of fluid in the retina
* Vitrectomy, a surgical procedure to remove the vitreous gel and relieve pressure on the retina.
It is important for individuals with CSR to follow their treatment plan and have regular follow-up appointments with their eye care professional to monitor the progression of the condition and adjust treatment as needed. With appropriate treatment, many people with CSR experience improvement in their vision.
Symptoms of choroiditis may include blurred vision, sensitivity to light, redness and pain in the affected eye, and seeing floaters or flashes of light. In severe cases, it can lead to retinal detachment, which can cause permanent vision loss if not treated promptly.
Diagnosis of choroiditis typically involves a comprehensive eye exam, including a visual acuity test, dilated eye exam, and imaging tests such as fluorescein angiography or optical coherence tomography to evaluate the retina and choroid. Treatment options for choroiditis depend on the underlying cause, but may include antibiotics or anti-inflammatory medications, corticosteroids, and in some cases, surgery.
The disease typically affects both eyes and can cause symptoms such as redness, discharge, excessive tearing, and squinting. If left untreated, KCS can lead to complications such as ulcers on the cornea, inflammation of the iris, and vision loss.
There are several risk factors for developing KCS, including Cocker Spaniels, Poodles, West Highland White Terriers, and other breeds with shallow eye sockets. Environmental factors such as dry climates, allergies, and exposure to chemicals can also contribute to the development of the disease.
Treatment for KCS usually involves medication to reduce inflammation and manage symptoms, as well as measures to keep the eyes moist and clean. In severe cases, surgery may be necessary to repair damage to the cornea or iris. With proper care and management, however, many dogs with KCS can lead happy and comfortable lives.
The exact cause of retinal vasculitis is not known, but it is believed to be an autoimmune disorder, meaning that the body's immune system mistakenly attacks its own tissues. It can occur at any age but is more common in adults between 30 and 60 years old.
Symptoms of retinal vasculitis include:
1. Blurred vision or blind spots
2. Floaters (specks or cobwebs in vision)
3. Flashes of light
4. Redness and pain in the eye
5. Sensitivity to light
6. Blindness in one or both eyes
Retinal vasculitis is diagnosed through a comprehensive eye exam, including a visual acuity test, dilated eye exam, and imaging tests such as fluorescein angiography and optical coherence tomography (OCT).
Treatment options for retinal vasculitis include:
1. Corticosteroids to reduce inflammation
2. Immunosuppressive drugs to suppress the immune system
3. Anti-vascular endothelial growth factor (VEGF) injections to prevent the growth of new blood vessels
4. Photodynamic therapy to damage and shrink the abnormal blood vessels
5. Vitrectomy, a surgical removal of the vitreous gel and any blood or scar tissue in the eye
The prognosis for retinal vasculitis varies depending on the severity and location of the disease, but it can lead to significant vision loss if left untreated. It is important to seek medical attention if symptoms persist or worsen over time.
Angioid streaks can be detected during an eye exam using a specialized microscope called a fundus camera. If the streaks are caused by diabetic retinopathy or other underlying conditions, treatment may involve managing the underlying condition to prevent further damage to the blood vessels in the retina. In some cases, laser surgery may be recommended to seal off leaking blood vessels and prevent further bleeding.
In summary, Angioid streaks are a sign of damage to the blood vessels in the retina and can be a warning sign of more serious underlying conditions such as diabetic retinopathy or hypertensive retinopathy. It is important to seek medical attention if you notice any changes in your vision or see flashes of light, as these can be signs of a more serious condition.
Causes of cerebrospinal fluid rhinorrhea may include:
1. Skull fracture or depression: Trauma to the skull can cause a tear in the meninges, the membranes that cover the brain and spinal cord, leading to CSF leakage.
2. Spinal tap or lumbar puncture: This medical procedure can sometimes result in a small amount of CSF leaking into the nasopharynx.
3. Infection: Meningitis or encephalitis can cause CSF to leak into the nose and throat.
4. Brain tumors: Tumors in the brain can cause CSF to leak out of the sinuses or nose.
5. Cerebral aneurysm: A ruptured aneurysm in the brain can cause CSF to leak out of the nose or sinuses.
6. Vasculitic diseases: Conditions such as Wegener's granulomatosis or Takayasu arteritis can cause inflammation and damage to blood vessels, leading to CSF leakage.
7. Congenital conditions: Some individuals may have a congenital skull defect or abnormality that allows CSF to escape into the nasopharynx or sinuses.
Symptoms of cerebrospinal fluid rhinorrhea may include:
1. Clear, colorless discharge from the nose or sinuses
2. Thick, sticky discharge or pus in the nose or sinuses
3. Headache, fever, or neck stiffness
4. Nausea, vomiting, or dizziness
5. Weakness or numbness in the face, arms, or legs
6. Seizures or convulsions
7. Change in mental status or consciousness
Diagnosis of cerebrospinal fluid rhinorrhea typically involves a combination of physical examination, imaging studies such as CT or MRI scans, and laboratory tests to rule out other possible causes of nasal discharge. Treatment depends on the underlying cause of the condition and may include antibiotics, anti-inflammatory medications, or surgery to repair any defects or obstructions in the skull or sinuses.
The term extravasation is commonly used in medical contexts to describe the leakage of fluids or medications from a blood vessel or other body structure. In the context of diagnostic and therapeutic materials, extravasation can refer to the leakage of materials such as contrast agents, medications, or other substances used for diagnostic or therapeutic purposes.
Extravagation of diagnostic and therapeutic materials can have significant consequences, including tissue damage, infection, and systemic toxicity. For example, if a contrast agent used for imaging purposes leaks into the surrounding tissues, it can cause inflammation or other adverse reactions. Similarly, if a medication intended for injection into a specific location leaks into the surrounding tissues or organs, it can cause unintended side effects or toxicity.
To prevent extravasation of diagnostic and therapeutic materials, healthcare providers must follow proper techniques and protocols for administration and use of these materials. This may include using sterile equipment, following proper injection techniques, and monitoring the patient closely for any signs of complications. In cases where extravasation does occur, prompt treatment and management are essential to minimize potential harm and prevent long-term consequences.
In the medical field, telangiectasis may be diagnosed through a physical examination and/or imaging tests such as ultrasound or MRI. Treatment options for telangiectasis depend on the underlying cause of the condition but may include topical creams or ointments, laser therapy, or lifestyle changes.
Some synonyms for telangiectasis are: spider veins, telangiectatic vessels, and spider naevi.
Note: Telangiectasis is not to be confused with telengectasis which is a condition where the blood vessels in the lung become dilated and can lead to pulmonary embolism.
There are many different types of eye diseases, including:
1. Cataracts: A clouding of the lens in the eye that can cause blurry vision and blindness.
2. Glaucoma: A group of diseases that damage the optic nerve and can lead to vision loss and blindness.
3. Age-related macular degeneration (AMD): A condition that causes vision loss in older adults due to damage to the macula, the part of the retina responsible for central vision.
4. Diabetic retinopathy: A complication of diabetes that can cause damage to the blood vessels in the retina and lead to vision loss.
5. Detached retina: A condition where the retina becomes separated from the underlying tissue, leading to vision loss.
6. Macular hole: A small hole in the macula that can cause vision loss.
7. Amblyopia (lazy eye): A condition where one eye is weaker than the other and has reduced vision.
8. Strabismus (crossed eyes): A condition where the eyes are not aligned properly and point in different directions.
9. Conjunctivitis: An inflammation of the conjunctiva, the thin membrane that covers the white part of the eye and the inside of the eyelids.
10. Dry eye syndrome: A condition where the eyes do not produce enough tears, leading to dryness, itchiness, and irritation.
Eye diseases can be caused by a variety of factors, including genetics, age, environmental factors, and certain medical conditions. Some eye diseases are inherited, while others are acquired through lifestyle choices or medical conditions.
Symptoms of eye diseases can include blurry vision, double vision, eye pain, sensitivity to light, and redness or inflammation in the eye. Treatment options for eye diseases depend on the specific condition and can range from medication, surgery, or lifestyle changes.
Regular eye exams are important for detecting and managing eye diseases, as many conditions can be treated more effectively if caught early. If you experience any symptoms of eye disease or have concerns about your vision, it is important to see an eye doctor as soon as possible.
Some common types of eyelid diseases include:
1. Blepharitis: Inflammation of the eyelids, often caused by bacterial infection or allergies.
2. Chalazion: A small, usually painless lump on the eyelid, caused by a blockage of the oil gland in the eyelid.
3. Stye: A red, tender bump on the eyelid caused by a bacterial infection.
4. Entropion: A condition in which the eyelid turns inward and the eyelashes rub against the cornea.
5. Ectropion: A condition in which the eyelid turns outward and the cornea is exposed.
6. Cancer: Malignant growths on the eyelid, including basal cell carcinoma, squamous cell carcinoma, and melanoma.
7. Ptosis: A condition in which the upper eyelid droops or falls, often caused by nerve damage or muscle weakness.
8. Dacryostenosis: A blockage of the tear ducts, which can cause tears to overflow and create a crusty discharge around the eyes.
9. Meibomian gland dysfunction: A condition in which the glands in the eyelids that produce the oily substance meibum become clogged or inflamed.
Eyelid diseases can be diagnosed through a comprehensive eye exam, which may include a visual examination of the eyelids, as well as tests to assess tear production and the health of the eyelid glands. Treatment options for eyelid diseases depend on the specific condition and may include antibiotics, surgery, or other therapies.
Retinal drusen appear as small, flat spots or patches in the retina and are usually yellow or orange in color. They are made up of lipids (fatty substances) and other waste products that have accumulated in the retina over time. The exact cause of retinal drusen is not known, but they are thought to be related to the natural aging process and the decline in the function of the retina over time.
Retinal drusen can be diagnosed with a comprehensive eye exam, which includes a visual acuity test, dilated eye exam, and imaging tests such as optical coherence tomography (OCT). There is no treatment for retinal drusen, but they can be monitored with regular eye exams to ensure that they are not progressing or causing any vision problems.
In some cases, retinal drusen may be a sign of a more serious underlying condition such as macular degeneration, which can cause vision loss if left untreated. It is important for individuals over the age of 50 to have regular comprehensive eye exams to detect any changes in the retina and to prevent vision loss.
In summary, retinal drusen are small deposits that accumulate in the retina and are a common age-related change. They do not cause vision problems on their own but can be an early warning sign of more serious eye diseases such as macular degeneration. Regular comprehensive eye exams can detect any changes in the retina and prevent vision loss.
Some common types of choroid neoplasms include:
1. Choroidal melanoma: A malignant tumor that arises from the pigment-producing cells of the choroid. It is the most common type of primary intraocular cancer and can spread to other parts of the body if left untreated.
2. Choroidal hemangioma: A benign tumor that arises from the blood vessels of the choroid. It can cause changes in vision and may require treatment to prevent complications.
3. Choroidal naevus: A benign growth that occurs in the choroid and can be inherited. It is usually asymptomatic but can sometimes cause changes in vision.
4. Other rare types of choroid neoplasms include choroidal lymphoma, choroidal osteochondromatosis, and choroidal metastasis (metastasis of cancer from another part of the body to the choroid).
Choroid neoplasms can be diagnosed using a variety of tests, including imaging studies such as ultrasound, CT or MRI scans, and visual field testing. Treatment options vary depending on the type and location of the neoplasm, and may include observation, laser therapy, photodynamic therapy, or surgery.
Overall, choroid neoplasms are complex and varied conditions that require careful evaluation and treatment by an ophthalmologist or other eye care professional to prevent complications and preserve vision.
Symptoms of chorioretinitis may include blurred vision, sensitivity to light, floaters, and flashes of light. Diagnosis is typically made through a combination of physical examination, imaging tests such as fluorescein angiography or optical coherence tomography, and laboratory testing to rule out other conditions.
Treatment for chorioretinitis usually involves antibiotics or antiviral medication to clear the infection, as well as steroids to reduce inflammation. In severe cases, surgery may be necessary to remove the affected area of the retina. Prognosis is generally good if the disease is caught early and treated promptly, but vision loss may occur if the disease is left untreated for an extended period of time.
Example Sentences:
1. The patient was diagnosed with iris disease and was prescribed antibiotic eye drops to help clear up the infection.
2. The doctor suspected that the patient's blurred vision was caused by an iris disease, so he referred the patient to a specialist for further evaluation.
3. Although the symptoms of iris disease can be uncomfortable, most cases can be effectively treated with medication and proper care.
Types of Eye Injuries:
1. Corneal abrasion: A scratch on the cornea, the clear outer layer of the eye.
2. Conjunctival bleeding: Bleeding in the conjunctiva, the thin membrane that covers the white part of the eye.
3. Hyphema: Blood in the space between the iris and the cornea.
4. Hemorrhage: Bleeding in the eyelid or under the retina.
5. Retinal detachment: Separation of the retina from the underlying tissue, which can cause vision loss if not treated promptly.
6. Optic nerve damage: Damage to the nerve that carries visual information from the eye to the brain, which can cause vision loss or blindness.
7. Orbital injury: Injury to the bones and tissues surrounding the eye, which can cause double vision, swelling, or vision loss.
Symptoms of Eye Injuries:
1. Pain in the eye or around the eye
2. Redness and swelling of the eye or eyelid
3. Difficulty seeing or blurred vision
4. Sensitivity to light
5. Double vision or loss of vision
6. Discharge or crusting around the eye
7. Swelling of the eyelids or face
Treatment of Eye Injuries:
1. Depending on the severity and nature of the injury, treatment may include antibiotics, pain relief medication, or surgery.
2. In some cases, a tube may be inserted into the eye to help drain fluid or prevent pressure from building up.
3. In severe cases, vision may not return completely, but there are many options for corrective glasses and contact lenses to improve remaining vision.
4. It is essential to seek medical attention immediately if there is a foreign object in the eye, as this can cause further damage if left untreated.
5. In cases of penetrating trauma, such as a blow to the eye, it is important to seek medical attention right away, even if there are no immediate signs of injury.
6. Follow-up appointments with an ophthalmologist are essential to monitor healing and address any complications that may arise.
Fluorescein
Fluorescein amidite
Fluorescein isothiocyanate
Fluorescein angiography
Fluorescein diacetate hydrolysis
Fluorescein (medical use)
Fluorescein-labeled proaerolysin
60 Cycle
Angiography
Heinz Falk
Biological effects of high-energy visible light
Optical coherence tomography angiography
Joey Rubenstein
Uveitis
Fluorescent glucose biosensor
Pyranine
Resorcinol
Optical Confederation
Bascom Palmer Eye Institute
Oligonucleotide synthesis
Arnall Patz
Branch retinal vein occlusion
Fluorescent tag
Eosin Y
Susac's syndrome
6-Carboxyfluorescein
Ventricular septal defect
Corneal ulcer
Jeffrey W. Berger
K-casein
Fluorescein eye stain: MedlinePlus Medical Encyclopedia
DailyMed - GLOSTRIPS- fluorescein sodium strip
MedlinePlus - Search Results for: Fluorescein
C.I. Acid Yellow 73 (Fluorescein Sodium)
Fluorescein - PubMed
fluorescein - PubChem Substance - NCBI
Fluorescein - Drugs and Lactation Database (LactMed®) - NCBI Bookshelf
Fluorescein-12-dUTP Solution (1 mM)
Lectins: Aleuria Aurantia Lectin (AAL), fluorescein labeled
Long Wavelength Fluorescein Analogues - ChemistryViews
Human EGFR Fluorescein-conjugated Antibody FAB10951F: R&D Systems
Preparation and Characterization of Disodium Fluorescein Powders in Association with Lauric and Capric Acids | RTI
fluorescein dye in ophthalmology ppt
Morning glory optic nerve in Aicardi syndrome: Report of a case with fluorescein angiography - PubMed
AID 165319 - Inhibitory activity against protein tyrosine phosphatase 1B (PTP1B) was determined in fluorescein diphosphate (FDP...
Purdue e-Pubs - The Summer Undergraduate Research Fellowship (SURF) Symposium: Fluorescein Dye for Exploring Anti-Cancer Drug...
Fluorescein sodium - ICROM
Fluorescein Polysaccharide Products | Order PEG Supplies
Human PAI-1, N-Terminal Fluorescein Labeled (Latent Wild Type) | Oxford Biomedical Research
Fluorescein (FITC)-conjugated Affinipure Goat Anti-Mouse IgG(H+L) Secondary Antibody SA00003-1 | Proteintech | Proteintech
Comparison of OCT and Fluorescein Angiographic Features of Choroidal Neovascularization Due to Age-related Macular Degeneration...
Subjects: Fluorescein - Digital Collections - National Library of Medicine Search Results
Rat IgG Fluorescein (012-0202) | Rockland
DailyMed - AK-FLUOR- fluorescein sodium injection
Pregnancy Special Considerations: Overview, Physiologic Ocular Changes Occurring During Pregnancy, Pathologic Ocular Changes...
Fluorescein-Based Electrophoretic Mobility Shift Assay. | Methods Mol Biol;2316: 133-140, 2022. | MEDLINE
Choroidal melanoma: Risk factors, treatment, and outlook
Fluorescein | LGC, Biosearch Technologies
Angiography14
- Home » Our Services » Fundus Fluorescein Angiography (FFA) Fundus Fluorescein Angiography (FFA) This test involves injecting dye into the bloodstream and taking a picture of it as it runs through the eyes. (papercritters.com)
- Type I PED well-defined area of early hyperF, Type II late leak of undeyermined source not, Fluorescein Angiography, technique interpretation. (papercritters.com)
- Fundus fluorescein angiography shows leakage of fluorescein dye from neovasculazation at the disc, neovascularization elsewhere and areas of retinal periphlebitis. (papercritters.com)
- length when stimulated by a shorter Fluorescein angiography was first successfully used in the human eye in 1961* and has evolved since then as one of the fundamental imaging techniques in the eye. (papercritters.com)
- Here, we report the first published fluorescein angiography (FA) study of a morning glory optic nerve in a patient with Aicardi syndrome and contralateral persistent fetal vasculature (PFV). (nih.gov)
- Fluorescein angiography of the eye showed and late staining in the areas of ellipsoid chorioretinal lacunae emanating from the optic nerve and extensive peripapillary staining and late leakage of the optic nerve. (nih.gov)
- AK-FLUOR ® is indicated in diagnostic fluorescein angiography or angioscopy of the retina and iris vasculature. (nih.gov)
- Fluorescein angiography involves a doctor injecting a dye into a person's arm. (medicalnewstoday.com)
- Fluorescein angiography is the practice of taking photographs of blood vessels inside the eye (an angiogram) with the help of a contrast dye (fluorescein dye). (whitewatereyecenters.com)
- Fluorescein angiography is a clinical test to look at blood circulation in the retina at the back of the eye. (centerforeyecare.com)
- After your angiography, your skin and urine may appear discolored for a short time until the Fluorescein is completely out of your system. (centerforeyecare.com)
- There is little risk in having fluorescein angiography, though some people may have mild allergic reactions to the dye that can cause itching, excessive sneezing, flushing of skin and nausea. (centerforeyecare.com)
- Automated detection of vascular leakage on fluorescein angiography [Poster]. (nih.gov)
- 14. [Fluorescein angiography. (nih.gov)
FITC2
- Fluorescein Polysaccharide - Fluorescent dye labeled polysaccharide reagents with fluorescein, FITC. (creativepegworks.com)
- 1X10^6 HeLa cells were stained with 0.2 ug Lamin B1 antibody (66095-1-Ig, red) and Fluorescein (FITC)-conjugated Affinipure Goat Anti-Mouse IgG(H+L) (SA00003-1) with dilution 1:100. (ptglab.com)
Concentration3
- By 76 hours after the dose, the milk fluorescein concentration was 170 mcg/L. The half-life of fluorescein in milk was 62 hours. (nih.gov)
- The dye sodium fluorescein can be used either in concentration of 10% or 20% in the form of intravenous bolus injection.It is used to image retinal, choroidal, optic disc, or iris vasculature, or a combination of these. (papercritters.com)
- Experimental results explored the excitation and/or emission wavelength maxima value's dependence on upon the concentration of fluorescein incorporated into paclitaxel nanocrystals. (purdue.edu)
Aqueous3
- Thermo Scientific Fluorescein-12-dUTP (fluorescein-5(6)-carboxaminocaproyl-[5-{3-aminoallyl}-2'-deoxyuridine-5-triphosphate]) is supplied as 1 mM aqueous solution. (thermofisher.com)
- 1871 Baeryer combined resorcinal phthalic acid, 1882 Ehrlich introduced fluorescein into, 1940 Gifford studied aqueous dynamics after, 80 albumin bound 20 left for fluorescence, Rapid diffusion through intra extracellular, Diffuses freely through choriocapillaris, Bruchs, Stains skin mucous membranes yellow for 24, Metabolised by liver excreted via kidneys, Absorbs light in blue range (490nm) emits in. (papercritters.com)
- On examination with slit lamp using cobalt-blue filter, fluorescein will be diluted by aqueous at the site of leakage. (epomedicine.com)
Injection4
- A woman received 5 mL of 10% fluorescein (500 mg) injection shortly after delivering a set of twins. (nih.gov)
- Fluorescein flows from the injection site to the heart and then, is pushed into the systemic vascular tree. (papercritters.com)
- If the needle has extravasated, the patient's blood will be seen to bulge the skin and the injection should be stopped before any fluorescein is injected. (nih.gov)
- When assured that extravasation has not occurred, the room light may be turned off and the fluorescein injection completed. (nih.gov)
Fluorescent3
- Nanocrystal formulations of paclitaxel were created which included various concentrations of fluorescein and were then analyzed using fluorescent spectroscopy. (purdue.edu)
- RAT IgG whole molecule Fluorescein conjugated is designed for immunofluorescence microscopy, fluorescence based plate assays (FLISA) and fluorescent western blotting. (rockland.com)
- Here we demonstrate that fluorescein diacetate (FDA), a fluorescent probe used for vital staining, is a fluorescently activated by esterolytic activity of human GSTP1 (hGSTP1) selectively among various cytosolic GSTs. (inra.fr)
Ophthalmology2
- And to provide you with relevant advertising - as everyone knows that DR is very serious eye disorder fluorescein dye in ophthalmology ppt affects. (papercritters.com)
- Fluorescein sodium is a diagnostic dye used extensively in the field of ophthalmology and optometry. (icrom.com)
Epithelial defects1
- Special water-soluble fluorescein dye drops reveal smaller or larger epithelial defects which can look identical to corneal abrasions Policy. (papercritters.com)
Angioscopy1
- The right eye imaging could not be captured due to the severe microphthalmos and cataract, however, fluorescein angioscopy was performed. (nih.gov)
Excitation1
- Fluorescein is divided into four categories according to the excitation wavelength, which are mainly 375nm, 405nm, 488nm and 633nm. (adcreviews.com)
Moiety1
- CPG column used to incorporate a Fluorescein-dT dye moiety at the3'-end of an oligonucleotide. (biosearchtech.com)
Ophthalmic1
- ICROM manufactures Fluorescein Sodium for the global market* for injectable as well as ophthalmic formulations. (icrom.com)
Drops1
- Alternatively, fluorescein drops can also be used. (epomedicine.com)
Interpretation1
- Purpose : Clinician interpretation of fluorescein angiograms (FA) can be subjective. (nih.gov)
Vein2
- group of pictures is taken, a dye called fluorescein is injected into a vein. (nih.gov)
- During the test, a harmless orange-red dye called Fluorescein will be injected into a vein in your arm. (centerforeyecare.com)
Catalog1
- A431 human epithelial carcinoma cell line was stained with Rat Anti-Human EGF R/ErbB1 Fluorescein-conjugated Monoclonal Antibody (Catalog # FAB10951F, filled histogram) or isotype control antibody (Catalog # IC006F , open histogram). (rndsystems.com)
Absorption2
- Because absorption from the eye is limited, fluorescein would not be expected to cause any adverse effects in breastfed infants. (nih.gov)
- Xiaojun Peng and colleagues, State Key Laboratory of Fine Chemicals, Dalian University of Technology, China, have developed a series of photostable fluorescein analogues (pictured) with absorption and emission in the red or near-infrared region. (chemistryviews.org)
Approximately2
- Approximately 80% of fluorescein dye remains in the intravascular compartment binding to albumin, while remaining is free. (papercritters.com)
- Formation of the main metabolite prednisolone and of fluorescein ranked as: RHS approximately RHE>excised human skin and keratinocytes>fibroblasts, respectively. (inra.fr)
Characteristics2
- Fluorescein labeled Aleuria aurantia lectin has an appropriate number of fluorochromes bound to provide the optimum staining characteristics for this lectin. (vectorlabs.com)
- This research aims to utilize quenching characteristics of fluorescein in order to provide pharmacokinetic information to aid in the improvement of nanoparticulate delivery formulations. (purdue.edu)
Probe1
- Staining of presumptive injured neurons by these agents was not modified when Zn(2+) in the brain section was removed by prior chelation with EDTA or TPEN, whereas staining by a non-fluorescein containing Zn(2+) probe, N-(6-methoxy-8-quinolyl)-p-toluenesulfonamide (TSQ), was suppressed by prior chelation. (nih.gov)
Evaluate2
- Instill fluorescein in inferior fornix of both eyes, wait 5 minutes, then evaluate for asymmetric clearance of dye from tear meniscus. (epomedicine.com)
- Fluorescein allows us to evaluate the physical fit of a contact lens, or the bearing relationship that exists between a transparent contact lens and the eye. (epomedicine.com)
Test3
- This is a test that uses orange dye (fluorescein) and a blue light to detect foreign bodies in the eye. (medlineplus.gov)
- Genetic Toxicity Evaluation of C.I. Acid Yellow 73 (Fluorescein Sodium) in Salmonella/E.coli Mutagenicity Test or Ames Test. (nih.gov)
- Home » Chemical Effects in Biological Systems (CEBS) » Genetic Toxicity Evaluation of C.I. Acid Yellow 73 (Fluorescein Sodium) in Salmonella/E.coli Mutagenicity Test or Ames Test. (nih.gov)
Description1
- Description: Hyaluronic Acid is labeled with Fluorescein. (haworksusa.com)
Yellow1
- A yellow-green glow indicates the presence of fluorescein and therefore clearance between the lens and cornea. (epomedicine.com)
Strip1
- Each strip is impregnated with 1.0 mg of fluorescein sodium USP. (nih.gov)
Blood1
- Insert the needle and draw the patient's blood to the hub of the syringe so that a small air bubble separates the patient's blood in the tubing from the fluorescein. (nih.gov)
Human2
- Maguire AM, Bennett J. Fluorescein elimination in human breast milk. (nih.gov)
- We have compared the esteratic cleavage of the prednisolone diester prednicarbate and the enzyme kinetic parameters (Vmax and S0.5) of the model substrate fluorescein diacetate (FDA) in commercially available RHS and RHE with excised human skin and monolayer cultures of normal and immortalised human keratinocytes and of fibroblasts. (inra.fr)
Found1
- Among the FDA derivatives examined, FOMe-Ac, the acetyl ester of fluorescein O-methyl ether, was found to be a potential reporter for GSH-dependent GSTP1 activity as well as for carboxylesterase activity. (inra.fr)
Method1
- Here, we describe a method based on fluorescein -labeled RNA for EMSA. (bvsalud.org)
Blue light1
- It is noted after instilling a drop of fluorescein and examining in a cobalt-blue light of a slit-lamp. (epomedicine.com)
Completely1
- The fluorescein is completely cohesive it looks like it has adequate central, mid peripheral and peripheral zones. (neuroptometry.com)
Patient2
- A drop of fluorescein is instilled into the lower fornix and patient is asked to blink to spread the dye evenly. (epomedicine.com)
- After anaesthetising the cornea with a drop of 2 per cent xylocaine and staining the tear film with fluorescein patient is made to sit in front of slit-lamp. (epomedicine.com)