To evaluate the efficacy and safety of olopatadine 0.1% ophthalmic solution and bepotastine 1.5% ophthalmic solution in patients with vernal keratoconjunctivitis in a tertiary care hospital.

INTRODUCTION: Vernal conjunctivitis comprises 0.5% of allergic eye diseases. The study is intended to collate the effectiveness of drugs by observing the reduction in signs and symptoms. OBJECTIVES: The objective of the study is to evaluate the effectiveness and safety of olopatadine 0.1% ophthalmic drops with bepotastine besilate 1.5% ophthalmic drops in patients with vernal keratoconjunctivitis (VKC). MATERIALS AND METHODS: A randomized, open-label, comparative study conducted in Sarojini Devi Eye Hospital, Telangana. The study included 50 patients diagnosed with VKC, of which Group A and Group B were given olopatadine 0.1% ophthalmic drops and bepotastine besilate 1.5% ophthalmic drops, respectively, twice a day for 8 weeks. The reduction in signs and symptoms in both groups was compared. The observations and results were tabulated accordingly, and data were analyzed using the SPSS. The unpaired t-test is used as the test of significance in between two groups. P value is statistically significant when it is less than 0.05. RESULTS: Overall, 50 cases were included in the study, 72% of total patients were in the age group of 5-10 years, and 28% were in the age group of 11-15 years. There were 39 males and 11 females. After 8 weeks of follow-up, the mean reduction in the scoring of symptoms and signs provided better and quicker relief of watering, ocular discomfort, and conjunctival hyperemia with bepotastine 1.5% eye drops. Olopatadine 0.1% eye drops provided faster improvement in papillary hypertrophy. Both drugs were equally effective in reducing itching. Laboratory findings of absolute eosinophil count had no statistical significance in between the two groups. CONCLUSIONS: In this study, based on the evaluation of therapeutic performance, bepotastine eye drops proved quicker relief of symptoms and signs compared to olopatadine eye drops but was not statistically significant which would prove beneficial for the patients.

Regional differences in the temporal expression of non-apoptotic caspase-3-positive bergmann glial cells in the developing rat cerebellum.

Although caspases have been intimately linked to apoptotic events, some of the pro-apoptotic caspases also may regulate differentiation. We previously demonstrated that active caspase-3 is expressed and has an apparent non-apoptotic function during the development of cerebellar Bergmann glia. The current study seeks to further correlate active/cleaved caspase-3 expression with the developmental phenotype of Bergmann glia by examining regional differences in the temporal pattern of expression of cleaved caspase-3 immunoreactivity in lobules of the cerebellar vermis. In general, we found that the expression pattern of cleaved caspase-3 corresponds to the reported developmental temporal profile of the lobes and that its levels peak at 15 days and declines thereafter. Compared to intermediate or late maturing lobules, early maturing lobules had higher levels of active caspase-3 at earlier postnatal times. This period of postnatal development is precisely the time during which Bergmann glia initiate differentiation.

AMPA-induced dark cell degeneration is associated with activation of caspases in pyramidal neurons of the rat hippocampus.

Various neurons in the central nervous system (CNS) exhibit selective vulnerability to AMPA-induced delayed neurotoxicity known as dark cell degeneration. Hippocampal pyramidal neurons in the CA1 and CA3 regions display such vulnerability that encompasses morphological changes including cytoplasmic and nuclear condensation, neuronal shrinkage, formation of cytoplasmic vacuoles, and general failure of physiology. The present study was undertaken to ascertain the potential involvement of initiator (caspase-9) and executor (caspase-3) caspases in AMPA-receptor-induced dark cell degeneration in pyramidal neurons. Immunohistochemical analyses revealed that immunoreactivity of the active form of caspase-9 and -3 was increased in pyramidal neurons in CA1 and CA3 regions of the hippocampus following AMPA (100 microM). Elevated levels of active caspase-9 immunoreactivity generally preceded elevations in active caspase-3 immunoreactivity. The pan caspase inhibitor FK011 effectively attenuated AMPA-induced dark cell degeneration in both CA1 and CA3 regions. Collectively, the data suggest a role for these caspases in mediating AMPA-induced toxicity in pyramidal neurons of the rat hippocampus.

Involvement of calpain in AMPA-induced toxicity to rat cerebellar Purkinje neurons.

AMPA receptor-elicited excitotoxicity is manifested as both a type of programmed cell death termed dark cell degeneration and edematous necrosis, both of which are linked to increased intracellular Ca2+ concentration. The appearance of marked cytoskeletal changes in response to abusive AMPA receptor activation, coupled with increased intracellular Ca2+ concentration suggests activation of various destructive enzymes such as calpains, a family of Ca2+-dependent cysteine proteases. Since calpains and AMPA have been linked to both necrotic cell death and programmed cell death, we sought to determine the role of calpains in mediating both types of AMPA-mediated toxicity in Purkinje neurons of the cerebellum. These studies employed immunohistochemistry for cytoskeletal breakdown products of calpain activity coupled with confocal microscopy and pharmacological interventions with calpain and AMPA receptor antagonists. The present study identifies an early involvement of calpains in mediating AMPA-induced dark cell degeneration, but not edematous necrosis, based upon the effectiveness of AMPA to generate calpain-derived alpha-spectrin cleavage products in cerebellar Purkinje neurons that express dark cell degeneration, and the effectiveness of calpain antagonists, PD150606 and MDL28170, to attenuate AMPA-induced dark cell degeneration. Moreover, the AMPA receptor antagonist CNQX, a proven inhibitor of AMPA-elicited dark cell degeneration, also blocked AMPA-induced increases in alpha-spectrin, further suggesting interplay between abusive AMPA receptor activation, calpain activation and dark cell degeneration. Since AMPA-induced dark cell degeneration possesses morphological changes that resemble those that occur following brain ischemia in vivo, hypoglycemia, or extended seizure episodes, the involvement of calpains as mediators of cell death is potentially far reaching and has widespread therapeutic implications in numerous CNS disorders.