Bowman Membrane
Descemet Membrane
Cornea
Bowman Capsule
Membranes
Membrane Lipids
Cell Membrane
Intracellular Membranes
Basement Membrane
Membrane Potentials
Kidney Glomerulus
Membranes, Artificial
Erythrocyte Membrane
Membrane Fluidity
Olfactory Mucosa
Cell Membrane Permeability
Microscopy, Electron
Corneal Stroma
Corneal Dystrophies, Hereditary
Trypsin Inhibitor, Bowman-Birk Soybean
Kidney
Epithelium, Corneal
Glomerulonephritis
Podocytes
Orthokeratologic Procedures
Membrane Transport Proteins
Keratoplasty, Penetrating
Glomerulosclerosis, Focal Segmental
Lipid Bilayers
Keratoconus
Glomerular Basement Membrane
Fluorescent Antibody Technique
Mitochondrial Membranes
Microscopy, Confocal
Protein Transport
Epithelium
Synaptic Membranes
Immunohistochemistry
Kidney Tubules
Microscopy, Immunoelectron
Ophthalmic Nerve
Liposomes
Nasal Mucosa
Molecular Sequence Data
Protein Binding
Nephrosis
Calcium
Compositional differences between infant and adult human corneal basement membranes. (1/17)
PURPOSE: Adult human corneal epithelial basement membrane (EBM) and Descemet's membrane (DM) components exhibit heterogeneous distribution. The purpose of the study was to identify changes of these components during postnatal corneal development. METHODS: Thirty healthy adult corneas and 10 corneas from 12-day- to 3-year-old children were studied by immunofluorescence with antibodies against BM components. RESULTS: Type IV collagen composition of infant corneal central EBM over Bowman's layer changed from alpha1-alpha2 to alpha3-alpha4 chains after 3 years of life; in the adult, alpha1-alpha2 chains were retained only in the limbal BM. Laminin alpha2 and beta2 chains were present in the adult limbal BM where epithelial stem cells are located. By 3 years of age, beta2 chain appeared in the limbal BM. In all corneas, limbal BM contained laminin gamma3 chain. In the infant DM, type IV collagen alpha1-alpha6 chains, perlecan, nidogen-1, nidogen-2, and netrin-4 were found on both faces, but they remained only on the endothelial face of the adult DM. The stromal face of the infant but not the adult DM was positive for tenascin-C, fibrillin-1, SPARC, and laminin-332. Type VIII collagen shifted from the endothelial face of infant DM to its stromal face in the adult. Matrilin-4 largely disappeared after the age of 3 years. CONCLUSIONS: The distribution of laminin gamma3 chain, nidogen-2, netrin-4, matrilin-2, and matrilin-4 is described in the cornea for the first time. The observed differences between adult and infant corneal BMs may relate to changes in their mechanical strength, corneal cell adhesion and differentiation in the process of postnatal corneal maturation. (+info)A novel phenotype-genotype relationship with a TGFBI exon 14 mutation in a pedigree with a unique corneal dystrophy of Bowman's layer. (2/17)
PURPOSE: Corneal dystrophy of Bowman's layer (CDB) belongs to a group of dystrophies associated with mutations in the transforming growth factor-beta-induced (TGFBI) gene. CDB is further divided into a geographic variant (CDB1/Reis Bucklers, RBCD), and a honeycomb variant (CDB2/Thiel Behnke, TBCD). We undertook mutational analysis of TGFBI in a family with an unusual CDB variant and describe a novel phenotype-genotype association. METHODS: Individuals from a pedigree with CDB underwent extensive phenotyping, including laser scanning in vivo confocal microscopy, and histological examination of four corneal buttons obtained at penetrating keratoplasty. Transmission electron microscopy of an excised allograft cornea from one affected individual was also performed. Following informed consent, DNA samples were collected. Polymerase chain reaction (PCR) and sequencing of all coding exons of TGFBI was performed. Family members were recruited with subsequent phenotyping and genotyping, and paternity testing. RESULTS: Clinical examination and other phenotypic information confirmed a diagnosis of CDB, with various features either more suggestive of CDB1 or of CDB2. A mutation in exon 14, H626P, segregated with the disease in this pedigree. This mutation was confirmed with NlaIII restriction enzyme digest, and was not seen in 100 control chromosomes. CONCLUSIONS: Within this pedigree, CDB segregates with an H626P mutation, which is previously described occurring in lattice corneal dystrophy. The majority of mutations in TGFBI previously described segregating with CDB1 and CDB2 are R124L and R555Q, respectively. Although a Bowman's layer dystrophy, the phenotype in this pedigree does not closely conform to the classical diagnostic criteria for either CDB1 or CDB2, and therefore represents a novel phenotype-genotype correlation. (+info)The role of Bowman's layer in corneal regeneration after phototherapeutic keratectomy: a prospective study using in vivo confocal microscopy. (3/17)
(+info)In vivo observation of Langerhans cells by laser confocal microscopy in Thygeson's superficial punctate keratitis. (4/17)
PURPOSE: To characterize the cornea of individuals with Thygeson's superficial punctate keratitis (TSPK) at the cellular level by laser confocal biomicroscopy. METHODS: Both corneas of three patients with TSPK referred to Yamaguchi University Hospital were imaged with a laser confocal biomicroscope. Morphological changes were evaluated for each layer of the cornea. RESULTS: The number of Langerhans cells was greatly increased in the basal cell layer of the focal corneal epithelium and in Bowman's layer in the four eyes affected by TSPK. Aggregates of these cells were associated with the subepithelial nerve plexus. Langerhans cells were also evident in the unaffected eyes of the two patients with unilateral TSPK, although their numbers were much smaller than those in the affected eyes. Topical treatment with betamethasone phosphate resulted in the virtual disappearance of Langerhans cells from the affected eyes. CONCLUSION: The prominent association of Langerhans cells with TSPK suggests that the activation of these cells by inflammatory conditions might contribute to the pathogenesis of this disorder. (+info)Three-dimensional analysis of collagen lamellae in the anterior stroma of the human cornea visualized by second harmonic generation imaging microscopy. (5/17)
(+info)Ultrastructural changes in the developing chicken cornea following caffeine administration. (6/17)
(+info)In vivo morphologic characteristics of Salzmann nodular degeneration with ultra-high-resolution optical coherence tomography. (7/17)
(+info)Image reconstruction of the subbasal nerve plexus with in vivo confocal microscopy. (8/17)
(+info)There are several types of hereditary corneal dystrophies, each with different clinical features and modes of inheritance. Some of the most common forms include:
1. Keratoconus: This is a progressive thinning of the cornea, which can cause irregular astigmatism and visual distortion. It is the most common form of corneal dystrophy and usually affects both eyes.
2. Familial Corneal Dystrophy Type 1 (FCD1): This is an autosomal dominant disorder that affects the central cornea, causing progressive opacification and visual loss.
3. Familial Corneal Dystrophy Type 2 (FCD2): This is an autosomal recessive disorder that affects both eyes and causes progressive opacification of the peripheral cornea.
4. Granular Corneal Dystrophy (GCD): This is a rare form of corneal dystrophy characterized by the accumulation of granular material in the cornea, leading to vision loss.
5. Avellar Corneal Dystrophy: This is a rare autosomal recessive disorder that affects both eyes and causes progressive opacification of the central cornea.
The diagnosis of hereditary corneal dystrophies is based on a combination of clinical examination, imaging studies (such as optical coherence tomography), and genetic testing. Treatment options vary depending on the specific type of dystrophy and the severity of symptoms, but may include glasses or contact lenses, corneal transplantation, or phototherapeutic keratectomy.
In conclusion, hereditary corneal dystrophies are a group of genetic disorders that affect the cornea and can cause significant vision loss and blindness. Early diagnosis and treatment are crucial to prevent or slow down the progression of these diseases. Ophthalmologists play a key role in the diagnosis and management of hereditary corneal dystrophies, and genetic testing may be useful in identifying the specific type of dystrophy and guiding treatment decisions.
The symptoms of glomerulonephritis can vary depending on the underlying cause of the disease, but may include:
* Blood in the urine (hematuria)
* Proteinuria (excess protein in the urine)
* Reduced kidney function
* Swelling in the legs and ankles (edema)
* High blood pressure
Glomerulonephritis can be caused by a variety of factors, including:
* Infections such as staphylococcal or streptococcal infections
* Autoimmune disorders such as lupus or rheumatoid arthritis
* Allergic reactions to certain medications
* Genetic defects
* Certain diseases such as diabetes, high blood pressure, and sickle cell anemia
The diagnosis of glomerulonephritis typically involves a physical examination, medical history, and laboratory tests such as urinalysis, blood tests, and kidney biopsy.
Treatment for glomerulonephritis depends on the underlying cause of the disease and may include:
* Antibiotics to treat infections
* Medications to reduce inflammation and swelling
* Diuretics to reduce fluid buildup in the body
* Immunosuppressive medications to suppress the immune system in cases of autoimmune disorders
* Dialysis in severe cases
The prognosis for glomerulonephritis depends on the underlying cause of the disease and the severity of the inflammation. In some cases, the disease may progress to end-stage renal disease, which requires dialysis or a kidney transplant. With proper treatment, however, many people with glomerulonephritis can experience a good outcome and maintain their kidney function over time.
The term "segmental" refers to the fact that the scarring or hardening occurs in a specific segment of the glomerulus. Focal segmental glomerulosclerosis can be caused by a variety of factors, including diabetes, high blood pressure, and certain infections or injuries.
Symptoms of focal segmental glomerulosclerosis may include proteinuria (excess protein in the urine), hematuria (blood in the urine), and decreased kidney function. Treatment options vary depending on the underlying cause, but may include medications to control high blood pressure or diabetes, as well as immunosuppressive drugs in cases where the condition is caused by an autoimmune disorder. In severe cases, dialysis or kidney transplantation may be necessary.
While there is no cure for keratoconus, there are several treatment options available to help manage the condition. These include eyeglasses or contact lenses, specialized contact lenses called rigid gas permeable (RGP) lenses, and corneal transplantation in severe cases. Other treatments that may be recommended include phototherapeutic keratectomy (PTK), which involves removing damaged tissue from the cornea using a laser, or intacs, which are tiny plastic inserts that are placed into the cornea to flatten it and improve vision.
Keratoconus is relatively rare, affecting about 1 in every 2,000 people worldwide. However, it is more common in certain groups of people, such as those with a family history of the condition or those who have certain medical conditions, such as Down syndrome or sickle cell anemia. It typically affects both eyes, although one eye may be more severely affected than the other.
While there is no known cause for keratoconus, researchers believe that it may be linked to genetics, environmental factors, or a combination of both. The condition usually begins in adolescence or early adulthood and can progress over several years. In some cases, keratoconus can also be associated with other eye conditions, such as cataracts, glaucoma, or retinal detachment.
1. Keratoconus: This is a progressive thinning of the cornea that can cause it to bulge into a cone-like shape, leading to blurred vision and sensitivity to light.
2. Fuchs' dystrophy: This is a condition in which the cells in the innermost layer of the cornea become damaged, leading to clouding and blurred vision.
3. Bullous keratopathy: This is a condition in which there is a large, fluid-filled bubble on the surface of the cornea, which can cause blurred vision and discomfort.
4. Corneal ulcers: These are open sores on the surface of the cornea that can be caused by infection or other conditions.
5. Dry eye syndrome: This is a condition in which the eyes do not produce enough tears, leading to dryness, irritation, and blurred vision.
6. Corneal abrasions: These are scratches on the surface of the cornea that can be caused by injury or other conditions.
7. Trachoma: This is an infectious eye disease that can cause scarring and blindness if left untreated.
8. Ocular herpes: This is a viral infection that can cause blisters on the surface of the cornea and lead to scarring and vision loss if left untreated.
9. Endophthalmitis: This is an inflammation of the inner layer of the eye that can be caused by bacterial or fungal infections, and can lead to severe vision loss if left untreated.
10. Corneal neovascularization: This is the growth of new blood vessels into the cornea, which can be a complication of other conditions such as dry eye syndrome or ocular trauma.
These are just a few examples of the many different types of corneal diseases that can affect the eyes. It's important to seek medical attention if you experience any symptoms such as pain, redness, or blurred vision in one or both eyes. Early diagnosis and treatment can help prevent complications and preserve vision.
Nephrosis is a condition that affects the function of the kidneys, leading to damage and loss of their filtering ability. It can be caused by a variety of factors and can lead to a range of symptoms and complications. In this article, we will explore the definition and causes of nephrosis, as well as treatment options and outcomes for patients with this condition.
Definition of Nephrosis
Nephrosis is a medical term used to describe damage to the kidneys that leads to a loss of their function. The kidneys play a critical role in filtering waste products and excess fluids from the blood, and when they are not functioning properly, these waste products can build up in the body. Nephrosis can be caused by a variety of factors, including diabetes, high blood pressure, and certain medications.
Causes of Nephrosis
There are several factors that can cause nephrosis. Some of the most common causes include:
1. Diabetes: High blood sugar levels can damage the kidneys over time, leading to nephrosis.
2. High Blood Pressure: Uncontrolled high blood pressure can damage the blood vessels in the kidneys, leading to nephrosis.
3. Medications: Certain medications, such as nonsteroidal anti-inflammatory drugs (NSAIDs) and certain antibiotics, can be harmful to the kidneys and cause nephrosis.
4. Infections: Severe infections, such as pyelonephritis, can damage the kidneys and lead to nephrosis.
5. Glomerulonephritis: This is a type of inflammation of the glomeruli, the tiny blood vessels in the kidneys that filter waste products from the blood.
6. Interstitial Nephritis: This is a type of inflammation of the tissue between the nephrons, the tiny tubules in the kidneys that filter waste products from the blood.
7. Kidney Disease: Any type of kidney disease, such as polycystic kidney disease or membranous nephropathy, can cause nephrosis.
8. Obesity: Excess weight can increase the risk of developing high blood pressure and diabetes, both of which are leading causes of nephrosis.
9. Family History: A family history of kidney disease increases the risk of developing nephrosis.
10. Age: The risk of developing nephrosis increases with age, especially after the age of 50.
Symptoms of Nephrosis
The symptoms of nephrosis can vary depending on the underlying cause and the severity of the condition. Some common symptoms include:
1. Proteinuria: The presence of protein in the urine, which can be detected by a simple urine test.
2. Hematuria: The presence of blood in the urine, which can be seen with the naked eye or detected by a urine test.
3. Edema: Swelling in the legs, ankles, and feet caused by fluid retention.
4. High Blood Pressure: Hypertension is common in people with nephrosis and can further damage the kidneys.
5. Fatigue: Weakness and fatigue are common symptoms of nephrosis due to anemia and nutrient deficiencies.
6. Nausea and Vomiting: Some people with nephrosis may experience nausea and vomiting due to electrolyte imbalances.
7. Weight Loss: Weight loss can occur in advanced cases of nephrosis as the body is unable to retain enough fluid.
8. Decreased Urine Output: A decrease in urine output can be a sign of nephrosis, especially if it is accompanied by other symptoms such as proteinuria and hematuria.
9. Flank Pain: Some people with nephrosis may experience flank pain, which is pain in the side or back of the abdomen.
10. Pericarditis: Inflammation of the pericardium, the membrane surrounding the heart, can occur in some cases of nephrosis.
It's important to note that not everyone with nephrosis will experience all of these symptoms, and the severity of the disease can vary from person to person. If you suspect you or someone you know may have nephrosis, it is important to seek medical attention as soon as possible for proper diagnosis and treatment.
Proteinuria is usually diagnosed by a urine protein-to-creatinine ratio (P/C ratio) or a 24-hour urine protein collection. The amount and duration of proteinuria can help distinguish between different underlying causes and predict prognosis.
Proteinuria can have significant clinical implications, as it is associated with increased risk of cardiovascular disease, kidney damage, and malnutrition. Treatment of the underlying cause can help reduce or eliminate proteinuria.
Bowman's membrane
Glued intraocular lens
Meesmann corneal dystrophy
Stroma of cornea
Christmas eye
McDonough syndrome
Cornea
Reis-Bucklers corneal dystrophy
LASIK
Band keratopathy
Fryns syndrome
Recurrent corneal erosion
Membrane oxygenator
Sir William Bowman, 1st Baronet
Bowman
Photodisruption
List of MeSH codes (A09)
Eye development
List of human anatomical parts named after people
Ultrafiltration (kidney)
Bowman's capsule
Glomerulonephritis
Passive transport
Renal corpuscle
Vanadate
Glomerular basement membrane
Plasmodium falciparum erythrocyte membrane protein 1
Nasal glands
Urinary system
V-ATPase
Nephron
Squalene
Kizzmekia Corbett
Risk factors of schizophrenia
Diffuse proliferative nephritis
Praziquantel
Major histocompatibility complex, class II, DQ alpha 1
Forth Bridge
Polyethylene glycol
Johann Peter Gogarten
Cat
Transferrin
RGS1
Heparin-binding EGF-like growth factor
Index of anatomy articles
Banteng
University of La Verne
Salt and cardiovascular disease
Reduced dimensions form
Immersive virtual musical instrument
Cyclic di-AMP
Dehalogenimonas lykanthroporepellens
Hypertensive kidney disease
Theodor Kolobow
GSTM3
Lysozyme
ALPPL2
Toll-like receptor 2
Search results for: bowman's membrane | National Eye Institute (NEI) Media Library
Cornea
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Córnea/ultraestructura
Epithelial cells. Medical search
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NEW (2006) MESH HEADINGS WITH SCOPE NOTES (UNIT RECORD FORMAT; 9/3/2005
particles
Bowman's6
- Histology of Bowman's membrane in cases of glaucoma. (nih.gov)
- Bowman's membrane appears on day 23 of pregnancy and disappears on day 30. (bvsalud.org)
- The epithelium is attached to a thin layer known as the Bowman's membrane. (ocularexpert.com)
- The attachment of epithelium to Bowman's membrane may be thought of as a layer of paint on primer. (ocularexpert.com)
- The outer most layer is called the epithelium, then the Bowman's Membrane, Stroma, Descement's Membrane, and lastly the endothelium. (redroverventures.org)
- This gene encodes a glycoprotein that is restricted within the kidney to the basement membranes underlying the epithelium of Bowman's capsule and proximal and distal tubules. (nih.gov)
Descemet's Membrane4
- This study aimed to characterize the ultrastructure of the posterior stroma and interfacial zone of Descemet's membrane (DM) in canine eyes. (bvsalud.org)
- The Descemet's membrane appears at this time and continues to thicken postnatally. (bvsalud.org)
- A layer called Descemet's membrane lines the internal portion of corneal stroma. (ocularexpert.com)
- Each type removes damaged cells from an inner layer of the cornea called Descemet's membrane. (drishtieyecentre.in)
Stroma1
- Transmission electron micrographs of the epithelial flap and underlying stroma of the chick corneas immediately after creation of the flap using 20% alcohol showing the superficial epithelial cell layers (A) and the basement membrane zone (B). Bars indicate 10 µm. (jamanetwork.com)
Cornea1
- A, Untreated chick cornea showed the typical 5 to 7 epithelial cell layers with microplicae on the superficial corneal epithelial cells and the acellular Bowman layer (arrow). (jamanetwork.com)
Basement8
- Transmission electron micrographs of the basement membrane zone and the Bowman layer of white leghorn chick corneas. (jamanetwork.com)
- a unilamellar basement membrane is noted. (jamanetwork.com)
- B, After 30 seconds' exposure to 20% alcohol, minimal change in the basement membrane zone is noted. (jamanetwork.com)
- E, After 2 minutes' exposure, the basement membrane layer is discontinuous. (jamanetwork.com)
- Irregular granular extracellular matrix fragments (arrow) are evident across the corneal basement membrane zone. (jamanetwork.com)
- B, Higher magnification of the basement membrane zone shows a relatively normal chromatin appearance in the nucleus of the underlying keratocyte (arrow). (jamanetwork.com)
- Autoantibodies against this protein are found in sera of patients with tubulointerstital nephritis, membranous nephropathy and anti-glomerular basement membrane nephritis. (nih.gov)
- The histopathological findings in the IR group confirmed that there was an increase in the hyaline cast and thickening of the Bowman capsule basement membrane. (traumamon.com)
Plasma membrane3
- Orientation of intracellular structures especially with respect to the apical and basolateral domains of the plasma membrane. (lookformedical.com)
- 1. Plasma membrane structures of medulloblastoma and cerebellar sarcoma. (nih.gov)
- 11. A freeze-fracture paradigm of the mechanism for delivery and insertion of gap junction particles into the plasma membrane. (nih.gov)
Apical1
- The current model of ion transport in the Malpighian tubules of D. melanogaster proposes that a vacuolar-type H + -ATPase acts as a primary active ion pump to maintain a proton gradient across the apical membrane, thus providing a driving force for the secondary active transport of alkali cations from the cell to the lumen through apical Na + /H + or K + /H + exchangers. (silverchair.com)
Wastewater1
- Bound Liquid Ion Exchange Membranes for Recovery of Chromium from Wastewater. (cdc.gov)
Proteins1
- CRISPR-mediated isogenic cell-SELEX approach for generating highly specific aptamers against native membrane proteins. (vanderbilt.edu)
Layer1
- Acute Hydrops After Bowman Layer Transplantation for Keratoconus May Indicate that Descemet Membrane Rupture Is Secondary to Hydrops. (harvard.edu)
Surgical1
- Other therapy options remain surgical procedures such as lacrimal duct probing (Bowman probe) or surgical reconstruction procedures. (eurorad.org)
Cells1
- The retinula cells modify their adjacent membranes into numerous linear microvilli, which form an analogue of the rhabdom among adjacent retinula cells. (bvsalud.org)
Cell2
- 9. Cell membrane structure of human giant-celled glioblastoma. (nih.gov)
- The cell membrane of the basal epithelial cell shows minimal undulations and is lined by electron-dense hemidesmosomes (arrow). (jamanetwork.com)
Activation2
- Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. (lookformedical.com)
- The activation of ROCK-1 is necessary for membrane blebbing during apoptosis. (nih.gov)
Anterior1
- He also observed that injury to the Descemet membrane was greater than that induced by injury on the Bowman layer, suggesting that surgery on the posterior cornea would be more effective than surgery on the anterior cornea. (medscape.com)