Background and Purpose-Varicella zoster virus-induced vasculopathy and postherpes zoster attack stroke syndromes have been reported previously; nevertheless, data regarding the exact prevalence and risk of stroke occurring postherpes zoster attack are still lacking. This study aims to investigate the frequency and risk of stroke after a herpes zoster attack using a nationwide, population-based study of a retrospective cohort design. Method-A total of 7760 patients who had received treatment for herpes zoster between 1997 and 2001 were included and matched with 23 280 randomly selected subjects. A 1-year stroke-free survival rate was then estimated using the Kaplan-Meier method. After adjusting for potential confounders, Cox proportional hazard regressions were carried out to compute the adjusted 1-year survival rate. Results-Of the sampled patients, 439 patients (1.41%) developed strokes within the 1-year follow-up period, that is, 133 individuals (1.71% of the patients with herpes zoster) from the study cohort and 306 individuals (1.31% of patients in the comparison cohort) from the comparison cohort. The log rank test indicated that patients with herpes zoster had significantly lower 1-year stroke-free survival rates than the control (PϽ0.001). The adjusted hazard ratios of stroke after herpes zoster and herpes zoster ophthalmicus during the 1-year follow-up period were 1.31 and 4.28, respectively. Conclusion-The risk for stroke increased after a zoster attack. Although varicella zoster virus vasculopathy is a well-documented complication that may induce a stroke postherpes zoster attack, it does not fully account for the unexpectedly high risk of stroke in these patients.

Herpes zoster ophthalmicus may represent a marker of increased risk of stroke development during the 1-year follow-up period.

The unconstrained green fluorescence protein (GFP)-like chromophore m-DMABDI displays a high solvatofluorochromicity in aprotic solvents, but the fluorescence is quenched in protic solvents. According to the site-specific intramolecularly hydrogen-bonded analogs 1OH and 2OH, the hydrogen bonding to the carbonyl oxygen is more important than that to the imino nitrogen of the imidazolinone group in the fluorescence quenching.

Low-resistance ohmic contacts with high transparency to p-type GaN have been developed by oxidizing Ni/Au thin films. Compared to the metallic Ni/Au contacts, the oxidized Ni/Au contacts exhibited lower specific contact resistance and much improved transparency. The transparency was from 65% to 80% in the wavelength of 450–550 nm. A specific contact resistance below 1.0×10−4 Ω cm2 was obtained by oxidizing Ni(10 nm)/Au(5 nm) on p-type GaN. The mechanism of low-resistance ohmic contact could be related to the formation of NiO.

A contact has been developed to achieve a low specific contact resistance to p-type GaN. The contact consisted of a bi-layer Ni/Au film deposited on p-type GaN followed by heat treatment in air to transform the metallic Ni into NiO along with an amorphous Ni–Ga–O phase and large Au grains. A specific contact resistance as low as 4.0×10−6 Ω cm2 was obtained at 500 °C. This low value was obtained by the optimization of Ni/Au film thickness and heat treatment temperatures. Below about 400 °C, Ni was not completely oxidized. On the other hand, at temperatures higher than about 600 °C, the specific contact resistance increased because the NiO detached from p-GaN and the amount of amorphous Ni–Ga–O phase formed was more than that of the sample annealed at 500 °C. The mechanism of obtaining low-resistance ohmic contacts for the oxidized Ni/Au films was explained with a model using energy band diagrams of the Au/p-NiO/p-GaN structure.

Using the Pentacam-derived keratometric index improved the prediction accuracies of total and posterior corneal powers.

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