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The IOP during LMK was higher than previously reported, and this may increase the risk for complications in certain patient groups.

Hypothermia has been reported to be beneficial in CNS physical injury and ischemia. We previously reported that posttraumatic cooling to 17 degrees C for 2 h increased survival of mouse spinal cord (SC) neurons subjected to physical injury (dendrite transection) but that cooling below 17 degrees C caused a lethal NMDA receptor-linked stress to both lesioned and uninjured neurons. The present study tested whether cooling below 17 degrees C increases extracellular levels of excitatory amino acids (EAA). SC cultures were placed at 10 degrees C or 37 degrees C. Glutamate (Glu) and aspartate (Asp) levels were higher in the medium of the cooled cultures after 0.5 h (23 +/- 4 nM/microgram vs. 4 +/- 1 nM/microgram and 4 +/- 1 nM/microgram vs. 1 +/- 0 nM/microgram, respectively). The concentration of each EAA then declined and reached a plateau at 2-4 h that was still significantly higher than control levels (p < 0.0001, two-factor ANOVA, three cultures per group). Other amino acids (glycine, asparagine, glutamine, serine) showed an opposite pattern, with higher levels in the 37 degrees C group. Both NMDA and non-NMDA antagonists prevented the lethal cold injury. Survival of SC neurons cooled at 10 degrees C for 2 h and rewarmed for 22 h was 58% +/- 25% in the control group, 94% +/- 5% in the CNQX-treated group, 97% +/- 5% in the DAPV-treated group, and 99% +/- 2% in the group treated with both antagonists [p < 0.0006, one factor ANOVA, five cultures (> 120 neurons) per group]. These results show that death of neurons cooled to 10 degrees C is caused by elevated extracellular Glu and Asp and requires activation of both the NMDA and non-NMDA receptor subtypes.

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The importance of transparency with financial ties in biomedical research is widely recognized, and most peer-reviewed journals require declarations of Conflicts of Interest (COI). Nonetheless, variability in the consistency of declarations of COI has been sparsely assessed. To assess consistency and rates of COI declarations in the ophthalmic literature and the effectiveness of journal COI policies. We analyzed consistency and completeness of declaration of COI in the ophthalmic literature and compared the levels of completeness to specific journal requirements. Six-hundred forty-two peer reviewed articles satisfied the inclusion criteria. In 64%, COIs were unreported, in 25% declaration of COI was incomplete, and 11% of the articles reviewed had complete declaration of COI. Of the 33 journals in which the most frequently published authors' articles appeared, 10 required the authors to complete the International Committee of Medical Journal Editors (ICMJE) form or an equivalent form, but this did not affect the rates of COI declaration. In a random sampling of the most frequently published authors in the field of ophthalmology, declaration of COI was low and highly inconsistent. Requiring a standardized COI form has no significant effect on the rate of accurate COI reporting. Our findings lend support to the growing body of literature that shows that journals and editors may need to take a more active role in ensuring accurate and consistent COI reporting.

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