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Biomedical subjects

Morton F Goldberg

Publications and source records attributed to Morton F Goldberg.

At least 19 recordsLinked to original sources
PubMed2005

A potential role for beta- and gamma-crystallins in the vascular remodeling of the eye.

We demonstrate that expression of beta- and gamma-crystallins is associated with intraocular vessels during normal vascular development of the eye and also in the Nuc1 rat, a mutant in which the hyaloid vascular system fails to regress normally. Real-Time RT PCR, Western blot and metabolic labeling studies indicate an increased expression of beta- and gamma-crystallins in Nuc1 retina. The increased expression of crystallins was localized to the astrocytes surrounding the intraocular vessels. A similar pattern of crystallin expression was also observed in the retinal vessels during normal development. Cultured human astrocytes exposed to 3-nitropropionic acid, an established model of neuronal hypoxia, increased VEGF expression, as expected, but also increased expression of crystallins. Our data suggest that crystallins may function together with VEGF during vascular remodeling. Interestingly, in human PFV (persistent fetal vasculature) disease, where the hyaloid vasculature abnormally persists after birth, we show that astrocytes express both VEGF and crystallins.

Animals↗
PubMed2005

A spontaneous mutation affects programmed cell death during development of the rat eye.

We have discovered a spontaneous mutation in the Sprague-Dawley rat with a novel eye phenotype that we have named Nuc1. The Nuc1 mutation behaves as a single semi-dominant locus with an intermediate phenotype in the heterozygotes. Heterozygotes exhibit nuclear cataracts. Homozygous Nuc1 rats are fully viable and have microphthalmia, retinal abnormalities and disruption of lens structure shortly before birth. The homozygous mutant shows no obvious pathology outside of the eye, indicating that the mutation is highly eye specific in its effects. An unusual feature of the mutation is that it prevents the normal programmed loss of nuclei from lens fiber cells, but does not affect the loss of other organelles. TUNEL, light, and electron microscopic studies show normal intact nuclei in lens fibers, in contrast to many other models with degenerate nuclei and unlike normal lenses where no such nuclei remain. The beaded filament protein, filensin, is down-regulated in fibers of Nuc1, while heat shock cognate 70 is up-regulated. Homozygous retinas are thicker than normal, and TUNEL labeling indicates roughly half the number of apoptotic cells compared to a wild-type retina. The transient layer of Chievitz persists in adult Nuc1 retina, indicative of delayed development. Hence, Nuc1 is a novel mutation that could be an eye-specific regulator of apoptosis.

Animals↗
PubMed2005

Preface.

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Biomedical Research↗
PubMed2004

Persistence of fetal vasculature in a patient with Knobloch syndrome: potential role for endostatin in fetal vascular remodeling of the eye.

OBJECTIVE: To report a child with Knobloch syndrome (KS) with features of persistent fetal vasculature (PFV) and to discuss the possible role of endostatin in vascular remodeling of the fetal eye. DESIGN: Case report with enzyme-linked immunosorbent assay (ELISA) analysis of serum endostatin. MAIN OUTCOME MEASURES: Ocular examination, fluorescein angiography, echography, ELISA analysis of serum endostatin, and typing for pathogenic mutations in COL18A1. RESULTS: Slit-lamp examination in the left eye disclosed numerous findings of PFV, including an extensive persistent pupillary membrane, scarcity of iris crypts, and pigmented epicapsular stellate remnants on the anterior lens surface. Dilated fundus examination revealed a total posterior vitreous detachment, despite the young age of the patient, with numerous white intragel opacities that were compatible with remnants of the vasa hyaloidea propria. The fundus had a tesselated appearance with angiographically visible large choroidal vessels. There was a retinochoroidal staphyloma inferotemporal to the optic disc. There were no retinal vessels visible temporally, and there was no macular differentiation or foveal pit. Competitive ELISA analysis disclosed no detectable serum endostatin. None of the 8 reported pathogenic mutations in the COL18A1 gene was found in the patient. CONCLUSIONS: Persistent fetal vasculature may be a clinical and important manifestation in some patients with KS and can be explained by a deficiency in endostatin. Endostatin deficiency may result in reduced or delayed regression of fetal blood vessels in the eye (including the intravitreal compartment), thereby resulting in incomplete development of the normal vasculature in the retina. Our typing results for the reported COL18A1 mutations confirm the genetic heterogeneity of KS.

Cerebellum↗
PubMed2004

Retrospective case series of juxtafoveal choroidal neovascularization treated with photodynamic therapy with verteporfin.

PURPOSE: To describe visual acuity and angiographic outcomes of juxtafoveal choroidal neovascularization (CNV) treated with photodynamic therapy and verteporfin (PDT). METHODS: Four hundred eighty-four consecutive eyes of 446 patients treated with PDT from January 1, 2001, to June 30, 2002, were identified from billing records. Fluorescein angiograms were reviewed retrospectively to identify juxtafoveal CNV. Eligible patients had CNV in which the central boundary of the lesion was between 1 and 199 microm from the geometric center of the foveal avascular zone (FAZ). Patient charts were reviewed for visual acuity of the treated eye before PDT and at 6- and 12-month follow-up examinations. Presence of subfoveal CNV at 6 and 12 months of follow-up was determined by review of fluorescein angiograms. A lesion was considered subfoveal if it extended underneath the geometric center of the FAZ. RESULTS: Twenty-one eyes had juxtafoveal CNV. Median change in visual acuity both 6 and 12 months after the initial PDT was 0 lines (n = 18 at 6 months, range -14 to + 8 lines; n = 17 at 12 months, range -18 to + 7 lines). Eleven lesions progressed to a subfoveal location by 12 months. Visual acuity in eyes with progressive lesions decreased a median of 4 lines of vision. CONCLUSIONS: Despite a small sample size and limited length of follow-up, this study shows that visual acuity on average can remain stable for at least 12 months after PDT of juxtafoveal lesions. Growth through the foveal center still can occur, however, and this can be associated with substantial visual loss.

Adult↗
PubMed2003

Anecortave acetate as monotherapy for treatment of subfoveal neovascularization in age-related macular degeneration: twelve-month clinical outcomes.

PURPOSE: To evaluate safety and efficacy of the angiostatic agent anecortave acetate, compared with a placebo, for treatment of subfoveal choroidal neovascularization (CNV). DESIGN: Ongoing masked, randomized, placebo-controlled, parallel evaluation of anecortave acetate (30 mg, 15 mg, and 3 mg) versus a placebo. PARTICIPANTS: There were 128 eyes of 128 patients with subfoveal CNV secondary to age-related macular degeneration who were enrolled and treated, with 80% (102/128) of eyes presenting with predominantly classic lesions at baseline. METHODS: All eyes received a posterior juxtascleral depot application of masked study medication or a placebo, with retreatment at 6-month intervals if the masked investigator believed the patient could benefit. Patients received periodic detailed ophthalmic examinations with both fluorescein and indocyanine green angiography, general physical examinations with electrocardiograms, and hematology/serum chemistry/urinalysis. All ophthalmic and systemic safety data were periodically reviewed by the Independent Safety Committee overseeing the study. MAIN OUTCOME MEASURES: Best-corrected logarithm of the minimum angle of resolution (logMAR) vision and fluorescein angiographic lesion characteristics were compared over time and among treatment groups. RESULTS: At month 12, anecortave acetate (15 mg) administered at 6-month intervals was statistically superior to the placebo for 3 measures of clinical efficacy: mean change from baseline vision (P = 0.0131), stabilization of vision (<3 logMAR line change; P = 0.0323), and prevention of severe vision loss (decrease of > or = 6 logMAR lines from baseline; P = 0.0224). Subgroup analysis of predominantly classic lesions revealed that anecortave acetate (15 mg) was also superior to the placebo at 1 year for each of these 3 measures of visual outcome (Ps = 0.0022, 0.0100, and 0.0299, respectively). Anecortave acetate (15 mg) trended toward significance over the placebo at month 12 for inhibition of total lesion growth and for inhibition of both the total CNV component and the classic CNV component in both the overall and subgroup analyses. The Independent Safety Committee identified no clinically relevant treatment-related safety issues. CONCLUSIONS: Anecortave acetate (15 mg) is safe and clinically efficacious at 1 year for maintaining vision, preventing severe vision loss, and inhibiting subfoveal CNV lesion growth.

Aged↗
PubMed2003

A phase III, multicenter, randomized, placebo-controlled clinical trial of topical aminocaproic acid (Caprogel) in the management of traumatic hyphema.

OBJECTIVE: To determine the safety and efficacy of topical aminocaproic acid (Caprogel) in the management of traumatic hyphema. DESIGN: Multicenter, randomized, double-masked, placebo-controlled clinical trial. PARTICIPANTS: A total of 51 patients participated in this trial (power = 36%, 2-tailed test). INTERVENTION: Patients presenting with traumatic hyphema were randomly assigned to 5-day treatment with topical aminocaproic acid or a placebo gel. Patients were monitored daily with ocular examination and vital sign testing for the 5 days of treatment and at 24 and 48 hours after treatment. General physical examination and laboratory testing were performed at baseline and day 5. MAIN OUTCOME MEASURES: The main efficacy variable was the rate of rebleeding. Secondary efficacy variables included time to hyphema clearance, intraocular pressure, time to secondary hemorrhage, and visual acuity. Safety variables included adverse events, vital signs, and laboratory measurements. RESULTS: Rebleeding occurred in 30% of the placebo group (8 of 27; 95% confidence interval [CI] = 14-50%), versus 8% of the treatment group (2 of 24; 95% CI = 1-27%), for an estimated continuity-corrected difference in percentage of patients with bleeding of 17% (95% CI = -3-38%). Secondary efficacy variables were similar in the groups, except that there was a trend towards more visual improvement in the topical aminocaproic acid group (54%) than in the placebo group (30%) at the last measurement (P = 0.08). Adverse events were similar. CONCLUSIONS: This study provides evidence that topical aminocaproic acid is safe and demonstrates trends towards reducing the rebleeding rate in the management of traumatic hyphema. However, because the study was terminated before complete enrollment, more definitive recommendations will require a larger trial.

Administration, Topical↗
PubMed2003

A novel mitochondrial tRNA(Leu(UUR)) mutation in a patient with features of MERRF and Kearns-Sayre syndrome.

In a patient with clinical features of both myoclonus epilepsy ragged-red fibers (MERRF) and Kearns-Sayre syndrome (KSS), we identified a novel guanine-to-adenine mitochondrial DNA (mtDNA) mutation at nucleotide 3255 (G3255A) of the tRNA(Leu(UUR)) gene. Approximately 5% of the skeletal muscle fibers had excessive mitochondria by succinate dehydrogenase histochemistry while a smaller proportion showed cytochrome c oxidase (COX) deficiency. In skeletal muscle, activities of mitochondrial respiratory chain complexes I, I + III, II + III, and IV were reduced. The G3255A transition was heteroplasmic in all tissues tested: muscle (53%), urine sediment (67%), peripheral leukocytes (22%), and cultured skin fibroblasts (< 2%). The mutation was absent in 50 control DNA samples. Single-fiber analysis revealed a higher proportion of mutation in COX-deficient RRF (94% +/- 5, n = 25) compared to COX-positive non-RRF (18% +/- 9, n = 21). The identification of yet another tRNA(Leu(UUR)) mutation reinforces the concept that this gene is a hot-spot for pathogenic mtDNA mutations.

Adenine↗
PubMed2003

Anecortave acetate as monotherapy for the treatment of subfoveal lesions in patients with exudative age-related macular degeneration (AMD): interim (month 6) analysis of clinical safety and efficacy.

PURPOSE: To evaluate clinical safety and efficacy of the angiostatic agent anecortave acetate for treatment of subfoveal choroidal neovascularization secondary to AMD. METHODS: 128 patients were randomized to placebo treatment or one of three anecortave acetate doses. Study medication was administered as a posterior juxtascleral injection onto the posterior scleral surface. Best-corrected logMAR vision was obtained at baseline and follow-up visits. Fluorescein angiograms were evaluated for eligibility before enrollment and posttreatment. RESULTS: Six months after a single treatment, visual acuity (mean change from baseline logMAR values) was significantly better (P = 0.003) after anecortave acetate 15 mg than placebo. More patients treated with anecortave acetate 15 mg than placebo maintained vision (88% versus 70%, P = 0.080), especially those with predominantly classic lesions (92% versus 65%, P = 0.021). Anecortave acetate 15 mg inhibited lesion growth significantly better than placebo (P = 0.001). Trends favoring the other doses over placebo were observed for vision preservation and lesion inhibition, but statistical significance was not achieved. The Independent Safety Committee overseeing this study identified no clinically relevant treatment-related changes. CONCLUSION: Anecortave acetate 15 mg is safe and effective for preserving or improving vision and for inhibiting lesion growth in patients with subfoveal AMD.

Aged↗
PubMed2003

Acute posterior multifocal placoid pigment epitheliopathy associated with a systemic necrotizing vasculitis.

PURPOSE: The authors present a case of acute posterior multifocal placoid pigment epitheliopathy (APMPPE) associated with a systemic necrotizing vasculitis with mixed features of Wegener granulomatosis and polyarteritis nodosa (PAN). METHODS: Case report. RESULTS: A 29-year-old woman developed a severe nosebleed, followed by a low-grade fever, night sweats, and a productive cough. One month later, she began experiencing high fevers, headache, myalgia, neck stiffness, and abdominal pain as well as bilateral blurred vision from APMPPE. Systemic evaluation revealed nasal ulcerations, bilateral pleural effusions, and a bilateral maxillary and ethmoid sinusitis, consistent with Wegener granulomatosis. However, ANCA testing was negative, and a renal and mesenteric angiogram showed aneurysmal dilatations suggestive of PAN. Her ocular and systemic symptoms markedly improved with systemic corticosteroids. CONCLUSIONS: The cause of APMPPE is unknown. This case of APMPPE associated with systemic necrotizing vasculitis provides support for the choroid as being primarily involved by a diffuse vasculitic process that interrupts choroidal perfusion and causes the characteristic fundus findings in APMPPE.

Adult↗