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C-Reactive protein (CRP) is a well-known indicator of inflammation. Advances in laboratory technology have enabled its quantification at lower concentrations by an automated analyzer (1)(2)(3). Because an increase in serum CRP concentration, even within the reference intervals of conventional analytic methods, has been related to increases in the risk of atherothrombotic events (4)(5)(6)(7), efforts for CRP quantification are currently directed toward healthy, elderly individuals or populations at risk of atherosclerotic diseases. When measured with a high-sensitivity analytic method, CRP may have diagnostic value in neonatal infection because newborns are unable to produce sufficient amounts of acute-phase proteins (8) and respond to infection with a smaller increase in CRP compared with that in adults (9). The utility of CRP for the diagnosis of neonatal infection has been the subject of lengthy controversy because of its unsatisfactory sensitivity for early-onset neonatal infection (10)(11)(13). The CRP concentration increases physiologically in newborns within the first few days after birth (9)(13). This increment seems to be related to the low diagnostic accuracy of CRP measurements in neonatal infection, particularly when measured shortly after birth. Similarly, other indicators of inflammation, such as procalcitonin and interleukin-6, demonstrate increases in noninfected babies within a few days after birth (14)(15)(16). In addition, very low CRP concentrations are found in the cord blood and sera of neonates in the immediate postnatal period (17). Therefore, the postnatal physiologic changes in CRP remain poorly understood. In this context, elucidation of serum CRP kinetics and an understanding of the mechanism(s) that cause its increase in the immediate postnatal period in noninfected babies would improve its diagnostic accuracy for early-onset neonatal infection. Using a high-sensitivity analytic method, we analyzed the serial changes in …

The landscape of prostate cancer has changed since the appearance of the first prostate-specific antigen (PSA) assay. PSA testing has gained rapid recognition since M. Kuriyama et al. (1) of Roswell Park first reported clinical studies using an enzyme immunoassay with anti-PSA rabbit antibody. Mikolajczyk and coworkers (2)(3) reported the presence of several free PSA isoforms and the potential application of free PSA isoforms as serum markers. Today, more than 30 types of total PSA assay reagent sets and ∼10 types of free PSA and PSA–α1-antichymotrypsin (ACT) assays, based on various principles, are available. Key elements in PSA measurement are interchangeability of assays and stability of serum samples before tests (4)(5). Efforts to standardize PSA assays were initiated in 1992 at the First Stanford Conference, organized by T. Stamey. At the Second Stanford Conference on International Standardization of Prostate-Specific Antigen (1994), Stamey et al. (6) proposed a primary calibrator consisting of 90% purified PSA-ACT and 10% free PSA (90:10) on a molar basis. Subsequently, the Clinical and Laboratory Standards Institute (CLSI; formerly NCCLS) issued a document (7) recommending a set of 3 distinct materials containing 100% free PSA, 100% PSA-ACT, and 90% PSA-ACT:10% free PSA. This document led to further activity in the harmonization of PSA assays. In 1999, Robert M. Nakamura, a member of the International Consultation Committee on Prostate Cancer, made recommendations, with his colleagues (8), on standardization and quality assessment of …