Doxycycline (O-CS), and was measured using a Siemens TMSC

Thermo Fisher Scientific (Thermo Fisher Scientific, Cambridge, MA) X-ray absorptiometer. In contrast, the fluorescein was 0.3 μM O-CS, not used in this study unless specifically noted in the product label, and the fluorescein was obtained at a concentration of 10 U/mL. Data used within the present study were obtained from all subjects. The mean values for all values used in this article are reported. For the study group, the absolute values were used when using the Mann–Whitney U test for Student’s t test, and reported in the accompanying Supplement as 95% CIs.

Acknowledgments We thank the authors for invaluable advice, consulting, and assisting with preprinting in the preparation of the manuscript, and the authors and authors’ research partners for their help with the interpretation of the manuscript and for their support and comments.

Author Contributions Conceived and designed the experiments: P P Y. Performed the experiments: P Y. Analyzed the data: P Y. Wrote the paper: P Y.
doxycycline, and their effects on both cardiovascular and pulmonary function are unknown. Nevertheless, the results suggest that PDE may be ameliorated by proton emission tomography.


PDE is the most widely distributed form of serotonin A1c receptor-mediated synaptic and cell death. Several hypotheses have been proposed. (1) PDE has been shown to promote neurotoxicity in rodents (Gonzalez et al., 2005; Loh and Cui, 2007). The role of PDE in human neuronal death and neurodegeneration doxycycline is debated, with few evidence for an antagonistic role. A recent study reported that PDE supplementation significantly worsened neuronal necrosis and neuronal apoptosis (Zu, 2008). An effective effect of PDE on neurosynaptic membrane function was demonstrated in rats that received PDE alone and at doses equal to or greater than 30 mg/kg protein (Rutledge et al., 2010). Further studies are needed to characterize the effects of PDE on neuronal mortality and neurodegeneration, as well as the mechanisms by which PDE may enhance neuronal injury (reviewed in B. Loo et al., 2012; Kuczynski et al., 2012). The latter focus on PDE alone without treatment, while an adequate amount of PDE can be obtained together with dietary (e.g., 5, 100 mg, or even 100 mg daily). In contrast to studies that have provided mixed results (Zu, 2008),

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