Dr. Arnold J Levine M.D.
Ophthalmologist
2100 Bartow Ave Suite 308 Bronx NY, 10475About
Dr. Arnold Levine is an ophthalmologist practicing in Bronx, NY. Dr. Levine specializes in eye and vision care. As an ophthalmologist, Dr. Levine can practice medicine as well as surgery. Opthalmologists can perform surgeries because they have their medical degrees along with at least eight years of additional training. Dr. Levine can diagnose and treat diseases, perform eye operations and prescribe eye glasses and contacts. Ophthalmologists can also specialize even further in a specific area of eye care.
Education and Training
Tufts Univ Sch of Med, Boston Ma 1974
Tufts University School of Medicine 1974
Board Certification
OphthalmologyAmerican Board of OphthalmologyABO
Provider Details
Expert Publications
Data provided by the National Library of Medicine- WISP-1 attenuates p53-mediated apoptosis in response to DNA damage through activation of the Akt kinase.
- p53 regulates cell survival by inhibiting PIK3CA in squamous cell carcinomas.
- Novel gain of function activity of p53 mutants: activation of the dUTPase gene expression leading to resistance to 5-fluorouracil.
- Stochastic gene expression in a single cell.
- Overexpression of WISP-1 down-regulated motility and invasion of lung cancer cells through inhibition of Rac activation.
- CIAP1 and the serine protease HTRA2 are involved in a novel p53-dependent apoptosis pathway in mammals.
- The presence of p53 mutations in human osteosarcomas correlates with high levels of genomic instability.
- Beclin 1, an autophagy gene essential for early embryonic development, is a haploinsufficient tumor suppressor.
- Dynamics of the p53-Mdm2 feedback loop in individual cells.
- P53 is a tumor suppressor gene.
- Activation of NF-kappaB and inhibition of p53-mediated apoptosis by
- Actvation of NF-kappaB by the API2/MALT1 fusions inhibits p53 dependant but not FAS induced apoptosis: a directional link between NF-kappaB and p53.
- Tissue-specific codon usage and the expression of human genes.
- Epigenetic and genetic loss of Hic1 function accentuates the role of p53 in tumorigenesis.
- A single nucleotide polymorphism in the MDM2 promoter attenuates the p53 tumor suppressor pathway and accelerates tumor formation in humans.
Treatments
- Cataracts
- Diabetes
- Pterygium
- Macular Degeneration
- Glaucoma
- Diabetic Retinopathy
- Macular Hole
- Type 2 Diabetes
- Blepharitis
- Conjunctivitis
- Dry Eye Syndrome
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