Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Choroiditis”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 721 records · Page 40Linked to original sources

Taurine transport in cultured choroid plexus.

PURPOSE: Taurine, a beta-amino acid, is a neuromodulator which interacts functionally with the glycinergic, GABAergic, cholinergic and adrenergic systems. Although a continuous cell culture model is not available for the choroid plexus epithelia, we recently described a primary cell culture of rabbit choroid plexus epithelia. The goal of the current study was to determine the suitability of this primary cell culture for the study of the Na(+)-taurine transporter in the rabbit choroid plexus. METHODS: A primary cell culture of rabbit choroid plexus epithelial cells was grown on semi-permeable filters and kinetics of 3H-taurine uptake were ascertained. RESULTS: Taurine transport in the cultured choroid plexus cell was Na(+)-dependent and saturable (Km = 156 microM). The beta-amino acids, beta-alanine and taurine, significantly inhibited Na(+)-driven taurine transport whereas L-alanine partially inhibited taurine transport in the cultured cells. In addition, we observed that the activity of the Na(+)-taurine transporter is affected by exposure to taurine in the media. CONCLUSIONS: These results-demonstrate that a Na(+)-taurine transporter with characteristics similar to those in the intact tissue is expressed in cultured choroid plexus epithelial cells. The transporter may undergo adaptive regulation and play a role in taurine homeostasis in the central nervous system.

Animals↗

Transpupillary thermotherapy in the treatment of choroidal metastasis from breast carcinoma.

BACKGROUND: Most patients who develop metastatic carcinoma to the choroid are managed by local radiation or chemotherapy. Since transpupillary thermotherapy (TTT) is currently gaining attention as an optional treatment for choroidal melanomas and hemangiomas, we sought to determine whether TTT is suitable for treatment of solitary choroidal metastasis at the posterior pole. METHOD: We report on a patient with decreased vision due to a serous macular detachment in a eye with a solitary choroidal metastasis from breast carcinoma, who was managed by TTT. RESULTS: After two months of follow up, total re-absorption of the serous macular detachment was achieved and the patient recovered full visual acuity in the treated eye. The choroidal mass became atrophic and hyperpigmentation of the retinal pigment epithelium and retinal folds in the macular region were observed. After six months of TTT, the ocular picture remained unchanged. CONCLUSION: TTT can be considered an acceptable therapeutic option for solitary choroidal metastasis associated with serous retinal detachment.

Adult↗

Pars plana vitrectomy for regression of choroidal neovascularization with age-related macular degeneration.

OBJECTIVE: In age-related macular degeneration, the posterior vitreous surface often remains attached to a higher degree than expected for the patient's age, suggesting the involvement of the posterior vitreous membrane in the pathophysiology of choroidal neovascularization. Thus, we performed simple pars plana vitrectomy and artificial posterior vitreous detachment in order to induce regression of choroidal neovascularization. METHODS: Vitrectomy was performed in 12 eyes of 11 patients with age-related macular degeneration in whom the posterior vitreous surface remained attached, and in whom there was evidence of highly active choroidal neovascularization. The posterior vitreous membrane was artificially detached during surgery, but photocoagulation and/or a subretinal procedure for choroidal neovascularization was not performed. Patients underwent fluorescein and indocyanine green angiography both pre- and postoperatively to assess the status of choroidal neovascularization. RESULTS: Six months after surgery, 6 of the 12 eyes showed regression of choroidal neovascularization, and in 2 eyes it had disappeared completely. Subretinal exudative changes in 8 eyes had improved. Visual acuity testing showed improved vision in 4 eyes, unchanged vision in 4 eyes, and worsening of vision in 4 eyes. The final best corrected visual acuity was 10/20 or better in one eye, 10/ 20 to 20/200 in 7 eyes, and 20/200 or worse in 4 eyes. CONCLUSION: The results of the present study suggest the involvement of the posterior vitreous membrane in the pathophysiology of age-related macular degeneration. Furthermore, the minimally invasive pars plana vitrectomy may represent a new treatment for age-related macular degeneration.

Aged↗

Identification of an S-antigen-like molecule in human choroid plexus and cerebrospinal fluid.

Sensitisation to retinal S-antigen has been implicated in the pathogenesis of several clinical forms of posterior uveitis. S-antigen-like molecules have recently been demonstrated in the brain and choroid plexus of experimental animals. We used a panel of four monoclonal antibodies (MAbs), MAbF4-C1, MAbC10-C10, MAbA2-G5 and MAbA9-C6, which define specific epitopes in the amino, mid and carboxyl terminal portions of S-antigen in order to identify an S-antigen-like molecule in human choroid plexus and cerebrospinal fluid (CSF). Three MAbs, MAbF4-C1, MAbC10-C10 and MAbA9-C6, localised an S-antigen-like molecule to the cytoplasm of the epithelial cells of the human choroid plexus. Polymerase chain reaction of cDNA from choroid plexus verified the presence of S-antigen homologues in the choroid plexus. The presence of an S-antigen-like molecule in the CSF was demonstrated by western blots in seven CSF samples from patients with a variety of neuropathological disorders. It is proposed that immunological cross-reactivity and biochemical similarity between retinal S-antigen and an S-antigen-like molecule in human choroid plexus and CSF could form a basis for neurological manifestations observed in certain clinical forms of uveitides.

Adult↗

Autonomic nerves in the mammalian choroid plexus and their influence on the formation of cerebrospinal fluid.

The choroid plexuses of all ventricles receive a well-developed adrenergic and cholinergic innervation reaching both the secretory epithelium and the vascular smooth muscle cells. Also peptidergic nerves, containing vasoactive intestinal polypeptide, are present but primarily associated only with the vascular bed. A sympathetic inhibitory effect on the plexus epithelium has been indicated in determinations of carbonic anhydrase activity and by studies of various aspects of active transport in isolated plexus tissue. Pharmacological analysis in vitro has shown the choroidal arteries to possess both vasoconstrictory alpha-adrenergic and vasodilatory beta-adrenergic receptors. Electrical stimulation of the sympathetic nerves, which originate in the superior cervical ganglia, induces as much as 30% reduction in the net rate of cerebrospinal fluid (CSF) production, while sympathectomy results in a pronounced increase, about 30% above control, in the CSF formation. There is strong reason to believe that the choroid plexus is under the influence of a considerable sympathetic inhibitory tone under steady-state conditions. From pharmacological and biochemical experiments it is suggested that the sympathomimetic reduction in the rate of CSF formation is the result of a combined beta-receptor-mediated inhibition of the secretion from the plexus epithelium and a reduced blood flow in the choroid plexus tissue resulting from stimulation of the vascular alpha-receptors. The choroid plexus probably also represents an important inactivation site and gate mechanism for sympathomimetic amines, as evidenced by considerable local activity of catechol-O-methyl transferase and monoamine oxidase, primarily type B. The CSF production rate is also reduced by cholinomimetic agents, suggesting the presence of muscarinic-type cholinergic receptors in the choroid plexus.

Acetylcholinesterase↗

Photodynamic therapy with verteporfin for subfoveal choroidal neovascularization secondary to toxoplasmic chorioretinal scar.

BACKGROUND: To assess the effect of photodynamic therapy in the treatment of subfoveal choroidal neovascularization consecutive to a toxoplasmic chorioretinal scar. HISTORY AND SIGNS: Three patients with a previous history of toxoplasmic chorioretinal scar noticed a decrease in visual acuity and metamorphopsia. Fundus examination and fluorescein angiography revealed the presence of subfoveal choroidal neovascularization at the edge of the toxoplasmic chorioretinal scar. THERAPY AND OUTCOME: The first patient, aged 78, was treated by photodynamic therapy followed by three subsequent treatments of feeder vessel by laser photocoagulation. Visual acuity decreased during follow-up in the presence of recurrence of choroidal neovascularization and subretinal fibrosis. The second patient, a 20-year-old lady, was treated with three sessions of photodynamic therapy for a subfoveal choroidal neovascularization related to a toxoplasmic scar. Visual acuity was stabilized on the last follow-up visit at 0.3. The third patient, aged 53, received four treatments with photodynamic therapy at an interval of 3 - 4 months. choroidal neovascularization was stabilized and the last visual acuity was 0.2. CONCLUSIONS: This preliminary report suggests that photodynamic therapy with verteporfine may be an effective therapeutic modality for subfoveal choroidal neovascularization related to a toxoplasmic chorioretinal scar. Further assessment is needed in order to confirm this preliminary findings.

Adult↗

[Tumor regression and visual outcome after transpupillary thermotherapy (TTT) for malignant choroidal melanoma].

BACKGROUND: The aim of this study was to evaluate the course of tumor regression and visual impairment in choroidal melanomas treated by transpupillary thermotherapy (TTT) alone. PATIENTS AND METHODS: In a prospective, non-randomized analysis 26 patients suffering from primary choroidal melanoma (posterior to the equator with base < or = 12 and thickness < or = 4.5 mm) were treated with the TTT standard protocol and followed for 33 - 45 months. Fluorescein and ICG angiographies were performed initially and after tumor regression clinically. RESULTS: 22 tumors were significantly flattened after 1 - 3 TTT sessions. 4 tumors required additional therapy with ruthenium plaque. Visual acuity remained unchanged or improved in 11 eyes. In all eyes fluorescein and indocyanine green angiography revealed a sharp demarcation of the heat-treated area. Except for macular edema and gliosis in 6 eyes no vascular or retinal tissue damage was noticed outside the treatment zone. In the periphery of the treatment zone all eyes showed residual choriocapillaries remaining perfused. During follow-up 2 eyes revealed tumor regrowth at the posterior margin of the scar, which was successfully managed by TTT or a ruthenium plaque. 2 eyes developed late choroidal neovascularizations (CNV) in the heat-treated area. One patient died of liver metastases. CONCLUSIONS: Fluorescein and indocyanine green angiographic findings after TTT for small choroidal melanomas suggest that the tissue damage in the choroidal layer is less effective, which perhaps can lead to a higher rate of tumor regrowth. Development of choroidal neovascularization may be a sign of late heat-induced side effects of TTT.

Adult↗

[Significance of infrared angiography in the differential diagnosis of choroid tumors].

With infrared light and a dye (Indocyanin green) bound to proteins it is possible to study the choroidal circulation much better than with usual fluorescein angiography. For the differential diagnosis of choroidal tumors, this method contributes the following: (1) The diagnosis of choroidal hemangioma can be made with confidence. (2) while it is not yet possible to differentiate between a nevus and a melanoma, choroidal angiography nevertheless represents a second vascular parameter (in addition to the retina) for monitoring the growth of potentially malignant tumors. (3) The value of this method for the diagnosis of choroidal metastases and rare choroidal tumors - such as the case of an osteoma presented here - has yet to be studied.

Adult↗

Isolated choroid plexus cyst in low-risk women less than 35 years old.

OBJECTIVE: The purpose of this study was to determine the incidence of trisomy 18 in women who are <35 years old and who have sonographically detected isolated choroid plexus cyst. STUDY DESIGN: A meta-analysis of prospective trials that were published in the English language between 1990 and 2000 was performed. Each trial met the following inclusion criteria: (1) prospective trial, (2) total population screened during the study period reported, (3) maternal age (either numeric or descriptive) reported, and (4) pregnancy/neonatal outcomes reported. An isolated choroid plexus cyst for the purpose of this study was defined as absence of sonographically detected structural abnormalities and normal serum analyte screens, if reported. RESULTS: Eight trials met the criteria and were used for analysis. A total of 106,732 women were screened through articles that were published between 1990 and 2000. The total number of fetuses with choroid plexus cysts that were identified in second-trimester scans were 1,235 (incidence, 1.2%). The incidence of isolated choroid plexus cysts in women who were <35 years old was 1.0% (n = 1,017 women). There were no cases of trisomy 18 in women with isolated choroid plexus cyst who were <35 years old. Four structural abnormalities were noted on postnatal examination; all four neonates had normal karyotypes. CONCLUSION: There is no evidence that detection of isolated choroid plexus cyst in women who are <35 years of age increases the risk of trisomy 18. Therefore, amniocentesis is not warranted because of the inherent risk of pregnancy loss that is associated with the procedure. Better algorithms are needed to screen women who have a low risk for trisomy 18.

Adult↗

Visual rehabilitation in a child with diffuse choroidal hemangioma by using aggressive amblyopia therapy with low-dose external beam irradiation.

Diffuse choroidal hemangioma is a congenital vascular hamartoma often associated with hemangiomatous lesions of the brain, orbit, and periocular skin (nevus flammeus) in the Sturge-Weber syndrome. Visual loss from diffuse choroidal hemangioma may result from chronic serous retinal detachments causing retinal pigment epithelial, photoreceptor or cystoid degeneration, and glaucomatous optic atrophy. Low-dose external beam irradiation has successfully resolved exudative retinal detachment and caused shrinkage of the choroidal hemangioma.(1-3) Visual loss in Sturge-Weber syndrome with diffuse choroidal hemangioma often begins during amblyogenic years. Visual rehabilitation may thus require not only therapeutic intervention to address organic disease but also amblyopia therapy. Though many of the previously reported cases address treatment of the diffuse choroidal hemangioma with laser or radiotherapy, none advocate or emphasize treatment of nonorganic amblyopia associated with this condition. We report the case of a child with Sturge-Weber syndrome and unilateral diffuse submacular choroidal hemangioma who developed an exudative retinal detachment that responded to the combination of low-dose external beam irradiation and aggressive amblyopia therapy.

Amblyopia↗

OB protein binds specifically to the choroid plexus of mice and rats.

Binding studies were conducted to identify the anatomical location of brain target sites for OB protein, the ob gene product. 125I-labeled recombinant mouse OB protein or alkaline phosphatase-OB fusion proteins were used for in vitro and in vivo binding studies. Coronal brain sections or fresh tissue from lean, obese ob/ob, and obese db/db mice as well as lean and obese Zucker rats were probed to identify potential central OB protein-binding sites. We report here that recombinant OB protein binds specifically to the choroid plexus. The binding of OB protein (either radiolabeled or the alkaline phosphatase-OB fusion protein) and its displacement by unlabeled OB protein was similar in lean, obese ob/ob, and obese db/db mice as well as lean and obese Zucker rats. These findings suggest that OB protein binds with high affinity to a specific receptor in the choroid plexus. After binding to the choroid plexus receptor, OB protein may then be transported across the blood-brain barrier into the cerebrospinal fluid. Alternatively, binding of OB protein to a specific receptor in the choroid plexus may activate afferent neural inputs to the neural network that regulates feeding behavior and energy balance or may result in the clearance or degradation of OB protein. The identification of the choroid plexus as a brain binding site for OB protein will provide the basis for the construction of expression libraries and facilitate the rapid cloning of the choroid plexus OB receptor.

Alkaline Phosphatase↗

Role of endothelium-derived vasodilators and K(+) channels in ischemic vasodilation of guinea-pig choroidal arterioles.

PURPOSE: To assess the roles of endothelium-derived vasodilators and K(+) channels on metabolic ischemia-induced vasodilation from diameter changes in choroidal arterioles of the guinea-pig. METHODS: The choroid was isolated from the guinea-pig eye-ball, pinned flat on a silicone rubber plate, and superfused with oxygenated warmed (35 degrees C) Krebs solution. Diameters of choroidal arterioles were measured using video microscopy and a computer program for analysis. Vasodilatory effects were examined after the choroid was exposed to glucose-free/NaCN solutions for 10 minutes. The effects of Nomega-nitro-L-arginine (nitroarginine), indomethacin, and K(+)<?Pub Caret> channel inhibitors (glibenclamide [Glib] and charybdotoxin [ChTX]) on ischemic vasodilation were assessed. RESULTS: Reversible vasodilation was observed when the choroid was exposed to glucose-free/NaCN (10(-3) M) solutions. Nitroarginine (10( -4) M), Glib (2x10(-5) M) and ChTX (10(-7) M) significantly inhibited glucose-free/NaCN (10(-3) M)-induced vasodilation by 47%, 62%, and 24%, respectively. No significant inhibitory effect was observed with indomethacin (10(-5) M). Simultaneous application of Glib and ChTX reduced vasodilation by 77%. When Glib and ChTX were added together to nitroarginine, dilation was reduced by 86%. With high K(+) ([K]o = 47.2 mM) Krebs solution, ischemia caused a slight vasodilation (11%), which was significantly inhibited by nitroarginine. CONCLUSIONS: In guinea-pig choroidal arterioles, glucose-free/ NaCN-induced ischemic vasodilation was mainly mediated by NO and K(ATP) channels. A part of NO-mediated vasodilation was induced independent of the opening of K(+) channels.

Animals↗

Influence of diffuse luminance flicker on choroidal and optic nerve head blood flow.

PURPOSE: In the retina there is general agreement that blood flow adapts in response to different conditions of light and darkness including diffuse luminance flicker. By contrast, regulation of choroidal blood flow in response to different light conditions is still a matter of controversy. Thus, we investigated the effect of diffuse luminance flicker on choroidal and optic nerve head blood flow. METHODS: In a group of 14 healthy volunteers, choroidal blood flow and ocular fundus pulsation amplitude were assessed with laser Doppler flowmetry and laser interferometry, respectively. Measurements were done before, during and after stimulation with diffuse luminance flicker. Furthermore, the response of optic nerve head blood flow (ONHBF) to flicker stimulation was measured. Flicker stimuli were generated by a Grass PS2 photostimulator, stimulating at a frequency of 8 Hz. Flicker light consisted of light flashes at a wavelength below 550 nm and produced a retinal irradiance of 140 microW/cm( 2). Blood pressure and pulse rate were measured non-invasively. Paired t-test was used for statistical analysis. RESULTS: ONHBF increased immediately after onset of flicker stimulation. The maximum increase in ONHBF was 30% +/- 10% (mean +/- SEM, p < 0.008). Both choroidal perfusion parameters were only slightly increased during flicker stimulation, by 2 +/- 2% (laser Doppler flowmetry, p < 0.5) and by 4 +/- 1% (laser interferometry, p < 0.12). After the end of stimulation all values returned to baseline levels. CONCLUSION: Our study clearly demonstrates that diffuse luminance flicker increases optic nerve head blood flow. In contrast, increased neural activity in the retina has no effect on choroidal blood flow. Thus, choroidal blood flow appears to be largely independent of alterations in retinal metabolism.

Choroid↗

Effective transfection of a cis element "decoy" of the nuclear factor-kappaB binding site into the experimental choroidal neovascularization.

PURPOSE: To evaluate the efficacy of the gene transfer of a double-stranded phosphorothioate oligonucleotides (ODNs), called a "decoy", against the NF-kappaB binding site into cells of an experimentally-induced choroidal neovascularization. METHODS: FITC-labeled decoy was injected into the subretinal space of rat eyes by the HVJ-liposome delivery system, and 3 days later, choroidal neovascularization was induced by laser photocoagulation. The eyes were removed and the transfected cells were detected by fluorescence microscopy and also detected by immunohistochemistry. The degree of neovascularization was evaluated by fluorescein angiography. RESULTS: The decoy was transfected into the retinal pigment epithelial (RPE) cells, inner and outer segment of the photoreceptors at 3 days after the injection. When choroidal neovascularization was induced, highly effective transfection of the decoy was observed 3 to 14 days after photocoagulation, after which the level decreased. Decoys were transfected into the RPE cells and macrophages in the choroidal neovascularization. The eyes transfected with NF-kappaB decoy showed a weaker leakage in fluorescein angiograms than that of the control eyes transfected with scrambled decoy. CONCLUSIONS: A decoy can be transfected into retinal cells and cells within a choroidal neovascularization by the HVJ-liposome method. The transferred NF-kappaB decoy reduced the degree of choroidal neovascularization. Decoy targeted against NF-kappaB may be considered as a potential therapy for neovascularization.

Animals↗

Mechanisms for sickle red blood cell retention in choroid.

PURPOSE: Although sickle (SS) red cell-mediated vaso-occlusion in retina and resultant retinopathy is well documented, the effects of SS red cells on choroidal vasculature are poorly understood. The intent of this study was to determine, using a rat model, the conditions under which retention of sickle erythrocytes in choroid occur and if that retention can be inhibited. METHODS: Sickle red cells were density separated into high density (SS4) or normal density, reticulocyte-enriched fractions (SS2). Red cells were labeled with FITC and administered IV to anesthetized Sprague Dawley rats. Rats were made either hypoxic or were given TNF-alpha intraperitoneally 5 hours before intravenous administration of red cells. Five minutes after administration of red cells, rats were exsanguinated, the retinas removed, and choroids prepared as flatmounts. The number of red cells retained in five high power fields of choroid was then determined. In other experiments, SS red cells were preincubated with the cyclic peptide TBC772 [inhibits binding of alpha4beta1 (VLA-4) and alpha4beta7 to their ligands], a control peptide TBC1194, or a VLA-4 neutralizing antibody before administration to the rat or antibodies against VLA-4 ligands were delivered IV before administration of SS red cells. RESULTS: Hypoxic conditions before administration of SS red cells significantly stimulated retention of SS4 cells (P = 0.0003), but did not significantly increase retention of SS2 cells. Administration of TNF-alpha significantly increased retention of all types of SS red cells (P < 0.001). Preincubation of cells with anti-VLA-4 or TBC 772 inhibited retention of SS red cells in choriocapillaris of TNF-alpha-treated rats (P < 0.0001). Complete inhibition of cytokine-stimulated retention was also accomplished by IV administration of monoclonal antibodies against fibronectin or its CS-1 domain, a ligand for VLA-4. CONCLUSIONS: The mechanisms for retention of SS red cells in retina and choroid appear identical: hypoxia-mediated retention of dense red cells and adherence of red cells in reticulocyte-rich fractions after cytokine stimulation. TNF-alpha-stimulated retention of SS red cells in choroid appears to be mediated by VLA-4, presumably on the surface of some reticulocytes. This increased retention was inhibited by a VLA-4 antagonist (TBC772), a VLA-4 neutralizing antibody or by blocking one of VLA-4's ligands, the CS-1 portion of fibronectin.

Anemia, Sickle Cell↗

Choroid plexus transporters for drugs and other xenobiotics.

The transporter mediated uptake of various drugs and toxic compounds by choroid plexuses has been extensively described over the last decades. In conjunction with several other specific features of the choroidal tissue such as its drug metabolism and antioxidant capacities, these transport activities contribute to the neuroprotective functions attributed to the choroid plexus. Recently, the molecular identity and localization of the proteins responsible for the influx and efflux of drugs and metabolites at the choroid plexus has started to be deciphered, thus allowing a better understanding of the directionality and significance of the transport processes observed at the choroid plexus. Transport of drugs and metabolites involves mainly the SLC (solute carrier) and ABC (ATP-Binding Cassette) transporter super-families. In this review, we describe the identity and mechanism of transport of the SLC and ABC members so far characterized at the choroid plexus.

ATP-Binding Cassette Transporters↗

Overexpression of FasL in retinal pigment epithelial cells reduces choroidal neovascularization.

Choroidal neovascularization (CNV) is responsible for the severe visual loss in age-related macular degeneration. CNV formation is considered to be due to an imbalance between pro- and antiangiogenic factors that lead to neovascular growth from the choriocapillaris into the subretinal space. To define whether FasL overexpression in retinal pigment epithelial cells (RPE) can inhibit choroidal neovascularization through Fas-FasL-mediated apoptosis, we examined the role of this pathway in a mouse model of laser-induced choroidal neovascularization. FasL was expressed in the retinal pigment epithelium of transgenic mice. Polymerase chain reaction (PCR), immunoblot, and immunohistochemistry confirmed that the transgene FasL was specifically expressed in RPE. The established laser model was used to induce choroidal neovascularization (CNV) in wild-type (WT) and transgenic mice. CNV formation was compared with respect to fluorescein angiographic leakage (at days 0 and 14 after laser injury) and histological appearance. The lesions were assessed on RPE-choroidal flatmounts after CD31-labeling and with confocal microscopy after perfusion with rhodamine-labeled concanavalin A (Con A). Apoptosis was quantified by TUNEL positivity and caspase activation. FasL mRNA and protein were highly expressed in the RPE of the transgenic mice before and after laser photocoagulation. In contrast, FasL was only weakly expressed in the RPE layer of WT C57BL/6J mice. While ruptures of Bruch's membrane and CNV formation were observed histologically two weeks after laser photocoagulation in transgenic as well as control eyes, the shape and size of CNV lesions were reduced in the transgenic mice. The area of leakage was decreased by 70% in FasL transgenic mice compared with WT mice (P<0.005). The number of TUNEL-positive cells was greater in FasL-overexpressing mice and correlated with the expression of activated caspases. Th expression of other antiangiogenic factors such as PEDF remained unchanged. The specific overexpression of FasL in RPE layer reduced CNV formation in our laser model. Our results strongly point to the FasL-Fas pathway as a potential therapeutic target in controlling pathological choroidal neovascularization.

Animals↗

Differential expression of transthyretin in papillary tumors of the endolymphatic sac and choroid plexus.

Aggressive papillary tumors of the temporal bone, occurring sporadically or as part of von Hippel-Lindau disease, have been shown to originate within the endolymphatic sac or duct. Also implicated as a potential precursor from which some of these tumors may arise is ectopic choroid plexus epithelium. To aid in the differentiation between papillary tumors of endolymphatic sac and duct origin and those arising from choroid plexus, an immunohistochemical study using stains for transthyretin (TTR), cytokeratins, S-100 protein, epithelial membrane antigen (EMA), and glial fibrillary acidic protein (GFAP) was carried out on archival specimens of normal and neoplastic endolymphatic sac and duct and choroid plexus epithelium. Transthyretin, a marker for choroid plexus epithelium, was found to show differential expression between choroid plexus papillomas and aggressive papillary tumors of the endolymphatic sac or duct. Therefore the use of TTR in concert with other immunohistochemical stains appear to aid in the differentiation between intracranial and intratemporal papillary tumors arising from choroid plexus and endolymphatic sac or duct epithelium.

Adenoma↗