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Background/Purpose Full-field optical coherence tomography (FFOCT) is an emerging imaging technique for rapid histological analysis. As FFOCT is introduced into the Mohs workflow, it is important to document the effect of tissue freezing on FFOCT images and any effect FFOCT has on frozen sections. Our study aimed to evaluate the changes on FFOCT images after tissue freezing as well as FFOCT imaging effects on frozen sectioning. Methods Six normal skin specimens were imaged using FFOCT and subsequently frozen using a cryostat. The specimens were then reimaged using FFOCT and compared for any differences. To evaluate the effect of FFOCT imaging on frozen sections, five normal skin specimens were bisected and one half was imaged using FFOCT. Both halves underwent frozen sectioning and analysis. Results Significant changes in the fat, sebaceous glands, eccrine glands, and dermal collage and minimal changes in the epidermis were seen after freezing. No effect on frozen sectioning was seen after FFOCT imaging. Conclusion As FFOCT is studied for use in Mohs, clinicians should be aware that freezing prior to imaging introduces significant artifact in the FFOCT image. If possible, specimens should undergo imaging prior to being frozen. [ABSTRACT FROM AUTHOR]

The polypeptides in the leaf blades, petioles and apices from photoinduced and noninduced Xanthium strumarium L. were compared by two dimensional gel-electro-phoresis. A 15 kDa and a 16 kDa polypeptide were detected in gels of the leaf blade from noninduced, but not from induced, plants. Similarly, an acidic 9 kDa polypeptide was detected in the apices from noninduced plants, not in apices from induced plants. Both the apices and petioles from noninduced plants showed a 34 kDa polypeptide which was absent in tissues from induced plants. Thus, the disappearence of identifiable polypeptides from photoinduced tissues may be associated with the photoinductive short-day treatment that leads to flowering. [ABSTRACT FROM AUTHOR]

Abstract: Several lines of evidence indicate that a rapid loss ofneuronal protein kinase C (PKC) activity is a characteristic feature ofcerebral ischemia and is a necessary step in the NMDA-induced death ofcultured neurons. Exposing embryonic day 18 primary rat cortical neurons to 50μM NMDA or 50 μM glutamate for 10 min caused ~80% celldeath over the next 24 h, but excitotoxic death was largely averted, i.e., by70-80%, in cells pretreated with brain-derived neurotrophic factor (BDNF). An8-h preexposure to BDNF (50-100 ng/ml) maximally protected cortical cells fromthe effects of NMDA and glutamate, although the transient application of BDNFbetween 8 and 4 h before NMDA was equally protective. These effects of BDNFwere abolished at supralethal, i.e., >100 μM, NMDAconcentrations. It is significant that BDNF pretreatment prevented theinactivation of PKC in cortical cells normally seen 30 min to 2 h followinglethal NMDA or glutamate exposure. This BDNF effect did not arise from changesin NMDA channel activity because neither whole-cell NMDA current amplitudesnor increases in intracellular free Ca[sup 2+] concentration were alteredby the 8-h BDNF pretreatment. Furthermore, BDNF offered no neuroprotection tocells treated with the PKC inhibitors staurosporine (10-20 nM),calphostin C (1-2.5 μM), or GF-109203X (100 nM) at thetime of NMDA addition. These results underscore the importance of PKCinactivation in glutamate-induced neuronal death. They also suggest that BDNFneuroprotection arises, at least in part, via its ability to block themechanism by which pathophysiological Ca[sup 2+] influx through the NMDAreceptor causes membrane PKC inactivation. [ABSTRACT FROM AUTHOR]