High impact information on Ocular Physiology

• In flies lacking endogenous eye-PKC (inaCp215), normal visual physiology is restored upon expression of wild-type eye-PKC, whereas the eye-PKCI700D mutant is completely inactive [1].
• Elucidating the roles of TSP1 and TSP2 in ocular physiology and pathobiology may lead to improved therapies for neovascular, neoplastic, reparative and other ophthalmic diseases [2].
• Eventual identification of molecules that bear the HNK-1 epitope in the eye will likely shed light on many aspects of ocular physiology and pathobiology[3]
• The cacH18 mutant exhibits defects in visual physiology (including complete unresponsiveness to light in certain genetic combinations) and visually mediated behaviors; this mutant (originally nbAH18) has a stop codon in an alternative exon (within the cac ORF), which is differentially expressed in the eye [4].
• The cacS mutant, which exhibits defects in the patterning of courtship lovesong and a newly revealed but subtle abnormality in visual physiology, is mutated such that a highly conserved phenylalanine (in one of the quasi-homologous intrapolypeptide regions called IIIS6) is replaced by isoleucine [4].

Associations of Ocular Physiology with chemical compounds

• The presence of this enzyme activity in ocular fluids suggests that angiotensin II may play a role in normal ocular physiology [5].
• Relation between retinal melatonin and corneal mitotic rhythms in the Japanese quail was investigated in experiments manipulating the ocular physiology by treatments with formoguanamine hydrochloride (FG) and eye-lid suture [6].
• Changes in ocular physiology, tear film characteristics, and symptomatology with 18 months silicone hydrogel contact lens wear [7].
• In many experiments in visual physiology which employ halothane anesthesia, it is difficult to judge accurately an animal's anesthetic state, particularly so because of the necessity for paralysis and artificial respiration [8].

Gene context of Ocular Physiology

• These studies present the first characterization of alpha 2M* and RBF signaling in a primary human cell type and suggest a role for alpha 2M* in the physiology of the eye [9].
• The present findings extend prior reports in the human eye, indicating a potential role for VIP in ocular physiology [10].

References