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Conjunctival melanoma is a relatively rare condition, occurring only 1/40th as often as choroidal melanoma and approximately 500 times less often than cutaneous melanoma. Its incidence is 0.2 to 0.8 per million in white populations. [1][2][3][4] Conjunctival melanoma is a potentially lethal neoplasm, with an average 10-year mortality rate of 30%. 1 It is identified most frequently in the perilimbal interpalpebral bulbar conjunctiva with tumors located in the palpebral or fornical conjunctiva or caruncle, plica semilunaris or eyelid margins having a worse prognosis for survival. 1,5 Conjunctival melanoma has no sexual predilection, and it is found predominately in middle-aged Malignant Melanoma of the Conjunctiva

Retinopathy is a serious microvascular complication of diabetes and a major cause of blindness in young adults, worldwide. Early diabetic retinopathy is characterized by a loss of pericytes from retinal capillaries, the appearance of acellular capillaries and microaneurysms, and a breakdown of the blood-retinal barrier. In later stages, this can evolve into the proliferative phase in which there is neovascularization of the retina, which greatly increases the probability of vision loss. Advanced glycation end products (AGEs) which accumulate under hyperglycemic conditions are thought to play an important role in the pathogenesis of diabetic retinopathy. AGEs arise primarily by the modification of amine groups of proteins by reactive dicarbonyls such as methylglyoxal. Intracellular proteins including anti-oxidant enzymes, transcription factors and mitochondrial proteins are targets of dicarbonyl modification and this can modify their functional properties and thus compromise cellular physiology. Likewise, modification of extracellular proteins by dicarbonyls can impair cell adhesion and can generate ligands that can potentially bind to cell surface AGE receptors that activate pro-inflammatory signaling pathways. AGE inhibitors have been shown to provide protection in animal models of diabetic retinopathy and currently are being evaluated in clinical trials.

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The porous polyethylene orbital implant represents an alternative implant for use after enucleation or evisceration or for secondary implantation. In our rabbit model, the porous polyethylene implant was well tolerated without complication. Complete fibrovascularization was first seen at 12 weeks. Porous polyethylene orbital implants appear to vascularize more slowly than Bio-Eye coralline HA, FCI(3) synthetic HA, and aluminum oxide implants.

Transgenic mice carrying the v-Ha-ras oncogene under the control of the mouse mammary tumor virus long terminal repeat were produced. These mice exhibit several phenotypes: mammary tumors, bilateral hyperplasia of the harderian lacrimal gland, primary bronchio-alveolar lung adenocarcinoma, and splenomegaly. High levels of the transgene RNA were detected in mammary, harderian, and lung tumors. Accumulation of cells of the myeloid lineages was found in enlarged spleens. This phenotype may represent an indirect effect of v-Ha-ras expression on myeloid progenitors. Our data illustrate the cell-specific effects of v-Ha-ras.The Ha-ras proto-oncogene is a member of a larger family of related proteins (Ras family) which have been frequently found activated in several animal and human tumors and are thought to play an important role in the emergence of these malignancies (34). An activated c-Ha-ras oncogene has been identified repeatedly in mammary carcinoma induced by N-nitroso-N-methylurea and by dimethylbenzanthracene in rats (37) and by dimethylbenzanthracene in mice (5). Similarly, activated c-Ha-ras or K-ras oncogenes have been detected in a number of human breast carcinoma cell lines (17,18,23), and some specific Ha-ras alleles were found at a higher frequency in patients with breast tumor than in normal patients (19). In fact, most human breast carcinoma revealed elevated levels of c-Ha-ras RNA and protein (4, 10, 33). These results suggest a role for this oncogene in the initiation or progression of this malignancy or both.Transgenic mice offer an attractive system to study the effect of an oncogene in a given tissue under normal physiological conditions. To study the role of the activated v-Ha-ras oncogene in the development of mammary tumors, we constructed transgenic mouse lines carrying the v-Ha-ras oncogene under the control of the mouse mammary tumor virus (MMTV) enhancer-promoter.A 4.2-kilobase-pair EcoRI-NcoI fragment containing the MMTV long terminal repeat (LTR) linked to the v-Ha-ras oncogene was purified from pA9 DNA (15) (Fig. 1) and microinjected into the male pronucleus of (C3H x C57BL/6)F2 zygotes (14). Five animals carrying the transgene (founders) were produced. Four transmitted the transgene to their progeny and were bred as lines (designated lines MR2 to MR5) by mating with BALB/c J mice, as this strain is known to be among the most susceptible to MMTV-induced mammary carcinoma.Predominant phenotypes of transgenic mice. Five phenotypes not seen in control mice were observed in the transgenic mice: mammary tumors, exophthalmia, splenomegaly, salivary gland tumors, and lung tumors.

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