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“PURPOSE: To calculate the exact geometry of custom intraocular lenses (IOLs) for pseudophakic eyes and theoretically predict the residual wavefront error by real ray tracing based on Snell’s law.
SETTING: Centre for Ophthalmology,
University Hospital, Tobingen, Germany.
METHODS: Individual computer models were constructed based on measurements, including corneal topography and axial length. The geometry of custom spherical, aspheric, toric, and toric aspheric IOLs was calculated in an optimization process with real ray tracing to provide the minimum root mean square wavefront error. The geometric optical properties in terms of residual wavefront error was simulated and approximated by Zernike polynomials.
RESULTS: Data from 45 pseudophakic eyes were used to construct the models. Defocus was almost completely corrected by the spherical IOL and astigmatism, by the toric IOL. The aspheric IOL strongly reduced spherical aberration but only slightly reduced total higher-order aberrations (HOAs); both theoretical predictions corresponded to clinical investigations of wavefront measurements in pseudophakic eyes with a spherical or aspheric IOL.
CONCLUSIONS: Real ray tracing calculated the exact geometry of custom IOLs to provide the minimum wavefront error, going beyond simple diopter information.
Results show spherical aberration can be significantly reduced with aspheric IOLs. However, the limited possible reduction of total HOAs, Rabusertib in vivo even perfectly positioned custom aspheric IOLs, may be a reason for the unclear results in studies assessing the potential benefit to visual performance of currently used aspheric IOLs. J Cataract Refract Surg 2009; 35:1984-1994 (C) 2009 ASCRS and ESCRS”
“Deposits of the misfolded neuronal protein tau are major hallmarks of neurodegeneration in Alzheimer’s disease (AD) and other tauopathies. The etiology of the transformation process of the intrinsically disordered soluble protein tau into the insoluble
misordered AZD6094 aggregate has attracted much attention. Tau undergoes multiple modifications in AD, most notably hyperphosphorylation and truncation. Hyperphosphorylation is widely regarded as the hottest candidate for the inducer of the neurofibrillary pathology. However, the true nature of the impetus that initiates the whole process in the human brains remains unknown. In AD, several site-specific tau cleavages were identified and became connected to the progression of the disease. In addition, western blot analyses of tau species in AD brains reveal multitudes of various truncated forms. In this review we summarize evidence showing that tau truncation alone is sufficient to induce the complete cascade of neurofibrillary pathology, including hyperphosphorylation and accumulation of misfolded insoluble forms of tau.