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Dive into the research topics where Joel S. Mindel is active.

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Featured researches published by Joel S. Mindel.


The Lancet | 2005

Age-related cataract

Penny A. Asbell; Ivo Dualan; Joel S. Mindel; Dan Brocks; Mehdi Ahmad; Seth P. Epstein

Cataract, opacification of the lens, is one of the commonest causes of loss of useful vision, with an estimated 16 million people worldwide affected. Several risk factors have been identified in addition to increasing age--genetic composition, exposure to ultraviolet light, and diabetes. However, no method to halt the formation of a cataractous lens has been shown to be effective. Nevertheless, advances in surgical removal of cataracts, including small-incision surgery, use of viscoelastics, and the development of intraocular lenses, have made treatment very effective and visual recovery rapid in most cases. Despite these advances, cataract continues to be a leading public-health issue that will grow in importance as the population increases and life expectancy is extended worldwide.


Survey of Ophthalmology | 1995

Antimicrobial prophylaxis for ophthalmic surgery

Joel S. Mindel; Michael B. Starr; Joseph M. Lally

Preoperative, intraoperative, and postoperative antibiotic agents have been used by ophthalmic surgeons routinely as prophylaxis for postoperative endophthalmitis. The rationale for such prophylaxis and the evidence which supports its efficacy are well founded. The optimal choice of antibiotic agent--from the standpoint of efficacy, route of delivery, adverse reactions, and cost--is far less established. This review considers these issues, as well as the role of topical disinfectants, including povidone-iodine, in preoperative prophylaxis.


American Journal of Ophthalmology | 1978

Value of Hyaluronidase in Ocular Surgical Akinesia

Joel S. Mindel

In a study of 27 cases of surgery for cataract extraction, mepivacaine 2% with hyaluronidase was found to shorten the induction times of facial nerve and retrobulbar blocks when compared to injections of mepivacaine 2% alone. The mean induction time of facial nerve blocks with hyaluronidase was 1.3 +/- 0.4 minutes. This was significantly (P less than .01) shorter than the mean induction time without hyaluronidase, 2.9 +/- 1.8 minutes. The use of hyaluronidase significantly (P less than .02) shortened the induction time of retrobulbar blocks. The median induction time with hyaluronidase was three minutes, whereas that without hyaluronidase was ten minutes. However, the use of hyaluronidase did not significantly (.25 less than P less than .50) alter the success rate of retrobulbar blocks.


Experimental Eye Research | 1977

Variability of choline acetyltransferase in ocular tissues of rabbits, cats, cattle and humans

Joel S. Mindel; Thomas W. Mittag

In order, to determine if one eye could serve as control for the other, the variation of choline acetyltransferase in the two eyes of rabbits, cats, cattle and humans was investigated. The enzyme activities of the two corneas, irides, ciliary bodies, retinas and pigment epithelium-choroids of each species varied, on the average, by less than 20% with these exceptions: human corneas (35%), feline ciliary bodies (24%), bovine ciliary bodies (49%), feline retinas (44%), bovine retinas (28)% and rabbit pigment epithelium-choroids (39%). Ocular choline acetyltransferase activity has been shown to vary markedly within a given species, e.g., the corneal activity of one rabbit could be 50 times that of another rabbit. When the enzyme activities of littermates and highly inbred rabbits were compared to those from randomly bred animals, the data suggested that ocular choline acetyltransferase activity was partially under genetic control. Highly inbred rabbits (F = 82–85%) exhibited significantly less variation (P < 0·005) than randomly chosen rabbits. The location and distribution of corneal epithelium choline acetyltransferase were investigated by performing regional assays and denervation experiments in rabbits. Central cornea had the highest enzyme activity (P < 0·05) and superior and temporal cornea had the least. Denervation by retrobulbar ethanol did not lower corneal choline acetyltransferase activity although that of iris-ciliary body fell 63–91% within one week. It was concluded that corneal choline acetyltransferase resides primarily, or entirely, within the epithelial cells and not in the sensory terminals of the trigeminal nerve.


Ophthalmology | 1979

Similarity of the Intraocular Pressure Response to Different Corticosteroid Esters when Compliance is Controlled

Joel S. Mindel; Judith D. Goldberg; Henry O. Tavitian

Fifty-four subjects with initial intraocular pressures under 20 mm Hg received a different commercial corticosteroid ester of prednisolone or dexamethasone in each eye for three to six weeks. Compliance was controlled. The intraocular pressure responses of the two eyes of a subject were similar. It was concluded that the absorptions of all four corticosteroids were in excess of the minimum amounts needed to maximally elevate pressure. Subjects complained that prednisolone acetate was irritating. Corticosteroid-induced uveitis developed in 3% (3) of the eyes.


American Heart Journal | 2008

Amiodarone and optic neuropathy

Joel S. Mindel

inc the is The case report literature would suggest that amiodarone can produce a toxic optic neuropathy. Patients receiving amiodarone have lost vision. However, a quandary exists when any drug is implicated as a cause of optic neuropathy—a drug toxicity can be mimicked by idiopathic anterior ischemic neuropathy. The 2 entities can have overlapping characteristics. Key features of toxic optic neuropathies are simultaneous bilaterality, progression at dose-related rates, and occurrences at higher incidences than can be explained by idiopathic anterior ischemic optic neuropathy. Significant reversibility on discontinuation of the drug, if it occurred consistently, would also be an important feature. Ethambutal provides a good example of such a toxic agent. Idiopathic anterior ischemic optic neuropathy, in contrast, is usually unilateral at onset (with estimates of simultaneous or subsequent contralateral involvement ranging from 10%-73%), attacks an optic nerve only once (though that initial visual loss can progress stepwise for up to 3 weeks), and causes vision loss that is not completely reversible (with 6 months follow-up, 43% improved≥3 lines of vision). Awide variety of etiologies have been attributed to idiopathic anterior optic neuropathy as follows: cardiovascular (nocturnal hypotension, sleep apnea), immunologic (Chlamydia seropositivity), genetic (glycoprotein 1bα gene), metabolic (hyperhomocystinemia), and local pathologic conditions (“crowded” optic disc, optic disc traction from vitreous adhesions). The prior annual incidence estimates of amiodaronetoxic optic neuropathy have been based on the retrospective case report literature. Those range from 0.36% (a 5-year incidence of 1.79%) to 2%. The incidence estimates for idiopathic anterior ischemic optic neuropathy in patients ≥50 years are far less—0.0023% to 0.03% (10 year incidence 0.3%). Three lines of data have recently raised doubts that amiodarone is toxic to the optic nerves: (1) pharmaceutical sales of amiodarone; (2) Food and Drug Administration (FDA) records of amiodarone-associated optic neuropathy; and (3) a prospective, double-masked, randomized trial. on


American Journal of Ophthalmology | 1981

Ocular ergotamine tartrate toxicity during treatment of Vacor-induced orthostatic hypotension.

Joel S. Mindel; Allan E. Rubenstein; Bonita Franklin

A 20-year-old woman developed severe orthostatic hypotension after attempting suicide by ingesting the rodenticide, Vacor. Oral ergotamine tartrate, 6 mg a day, was useful in treating the orthostatic hypotension. However, a bilateral toxic retinal vasculopathy, consisting of a severe generalized vasoconstriction and mild macular edema, occurred within three weeks. Additional findings were an extinguished electroretinogram and a reduced dark-adaptation retinal sensitivity; because we performed these two tests after instituting ergotamine therapy we do not know whether to attribute their abnormal results to Vacor toxicity, ergotamine toxicity, or a combination of the two.


Ophthalmology | 1980

Succinyldicholine-induced Return of the Eyes to the Basic Deviation: A Motion picture Study

Joel S. Mindel; Edward L. Raab; James B. Eisenkraft; Grete Teutsch

Succinyldicholine 2 mg/kg body weight returned the eyes of 20 anesthetized subjects to the same basic horizontal position as when conscious. The distance between the two eyes, as measured from motion pictures, agreed when the patient was in the conscious state and succinyldicholine-stimulated unconscious state by 99 +/- 10%. Since succinyldicholine has been shown by others to selectively produce a sustained contraction of en grappe muscle fibers, these muscle fibers are implicated as determinants of the basic ocular position and a cause of strabismus.


Experimental Eye Research | 1979

The effects of blepharorrhaphy induced depression of corneal cholinergic activity

Joel S. Mindel; Peter I.A. Szilagyi; Jose A. Zadunaisky; Thomas W. Mittag; Juan Orellana

Abstract Unilateral lid closure for 8 or more days had previously been shown to reduce rabbit corneal epithelial choline acetyltransferase (ChAc) activity without affecting lactic dehydrogenase activity or thymidine, uridine, leucine and alanine incorporation rates. In the present study, the reduction in ChAc activity was found to be associated with a similar reduction in acetylcholine (ACh) content, to a mean value of 16 and 17%, respectively, of control eye levels. However, on reopening the lids, ACh levels recovered much more rapidly, achieving a mean value 67% of control values (P > 0·05) in 48 hr while ChAc activity was only 23% of control eye levels at 48 hr and required more than 30 days to fully recover. Unilateral lid closure of 10 days was also associated with a small increase in corneal thickness, 0·46±0·09 mm vs. 0·41±0·04 mm (P m , pilocarpine 10−4 m , eserine 10−6 m or carbachol 10−5 m to the epithelial side of corneas mounted in chambers immediately after reopening the lids failed to elevate either the standing electrical potentials or short-circuit currents; a causal relationship between cholinergic activity and corneal electrical phenomena could not be demonstrated.


Acta Ophthalmologica | 2009

DIFFUSE CHOROIDAL ATROPHY AND KLINEFELTER SYNDROME

Murray Wolkstein; Adam Atkin; Judith P. Willner; Joel S. Mindel

We report the first case of diffuse choroidal atrophy associated with Klinefelter syndrome. Retinal findings included midperipheral bone corpuscular pigmentation, large areas suggestive of choroidal atrophy, and unusual golden crystalline structures that apparently were mainly in the neurosensory retina. A sensorineural hearing deficit was also noted. Biochemical studies, including amino acid blood levels, were within normal limits. This case is of interest because of the rarity of association between Klinefilter syndrome and retinal or, in fact, any ocular abnormalities.

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Steven M. Podos

Icahn School of Medicine at Mount Sinai

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Edward L. Raab

Icahn School of Medicine at Mount Sinai

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James B. Eisenkraft

Icahn School of Medicine at Mount Sinai

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Penny A. Asbell

Icahn School of Medicine at Mount Sinai

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Alex B. Kharlamb

Icahn School of Medicine at Mount Sinai

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Grete Teutsch

Icahn School of Medicine at Mount Sinai

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Henry O. Tavitian

Icahn School of Medicine at Mount Sinai

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Aran Safir

Icahn School of Medicine at Mount Sinai

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