Purpose To examine the relationship between oral contraceptive pill (OCP) use, contact lens wear, and dry eye signs and symptoms in healthy young females. Methods Fifty-two women using OCPs and forty-five women not using any form of hormonal contraception were enrolled. Medical, menstrual, and contact lens histories were obtained and dry eye symptoms were assessed using the Ocular Surface Disease Index (OSDI) and Symptom Assessment iN Dry Eye (SANDE) questionnaires. Tear osmolarity testing was performed using the TearLab™ Osmolarity System. Results Mean age of all subjects was 26.0 ± 3.7 years. There were no significant differences in any of the measurements between the follicular and luteal phases. While SANDE scores were significantly higher in subjects with OCP and recent contact lens use (p<0.01), there were no significant differences in OSDI and tear osmolarity amongst the same subject groups. Subjects who reported both OCP and recent contact lens use had significantly higher OSDI and SANDE scores (p=0.015 and p<0.001, respectively). Conclusions There were no differences between the phases of the menstrual cycle. Tear osmolarity was not affected by OCP or contact lens use in young females. However, the combination of OCP use and contact lens wear may increase the severity of dry eye symptoms.
Aβ in the form of soluble oligomers or amyloid deposits has been identified as an endogenous substance responsible for the induction of neuro degeneration in Alzheimer's disease. To study Aβ-related processes, we evaluated both input-output electrophysiology and gene expression in hippocampi from Tg2576 and wild-type control mice 7 months of age. In hippocampal CA1 f-EPSP recordings, the postsynaptic response was reduced in Tg2576, while there was no significant difference in fiber volley amplitude or paired-pulse facilitation. Gene expression was evaluated on RNA extracted from hippocampi contralateral to those used for electrophysiology. Robust gene expression differences were observed between Tg2576 and WT hippocampi, many of which reflected deficits in glutamatergic synaptic transmission. These results support the identification of synaptic deficits in young adult Tg2576 mice, and identify gene products that potentially could be used as biomarkers for Aβ toxicity or as mechanistic targets in further studies.
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