Single tooth tells us the date of birth.

The atmospheric carbon-14 ((14)C) concentration remained relatively stable until 1955, but then rapidly increased after 1955 by nuclear bomb tests, peaked in 1963, and decreased thereafter. Recently, Spalding et al. proposed epoch-making method for determining date of birth (DOB) using the tooth enamel (14)C incorporated during enamel formation. However, because the (14)C level analyzed in one tooth gives two possible age ranges (up-slope or down-slope of the bomb curve), a variety of teeth that formed in different periods are required for estimating DOB in this method. Enamel formation in a tooth moves from the incisal (occlusal) side to the cervical side. Taking advantage of this characteristic, we have first succeeded in specifying the age range from only single tooth by measuring (14)C in the incisal (occlusal) and cervical regions of the enamel separately. To date, no method of determining DOB or age estimation from single tooth enamel has been made. Furthermore, this method of dividing tooth into smaller parts could be useful for producing a more accurate DOB. Our new method is a powerful tool for identification when we can use only extremely few specimens in forensic casework.

Brief exposure to carbon monoxide preconditions cardiomyogenic cells against apoptosis in ischemia-reperfusion.

We examined whether and how pretreatment with carbon monoxide (CO) prevents apoptosis of cardioblastic H9c2 cells in ischemia-reperfusion. Reperfusion (6 h) following brief ischemia (10 min) induced cytochrome c release, activation of caspase-9 and caspase-3, and apoptotic nuclear condensation. Brief CO pretreatment (10 min) or a caspase-9 inhibitor (Z-LEHD-FMK) attenuated these apoptotic changes. Ischemia-reperfusion increased phosphorylation of Akt at Ser472/473/474, and this was enhanced by CO pretreatment. A specific Akt inhibitor (API-2) blunted the anti-apoptotic effects of CO in reperfusion. In normoxic cells, CO enhanced O2(-) generation, which was inhibited by a mitochondrial complex III inhibitor (antimycin A) but not by a NADH oxidase inhibitor (apocynin). The CO-enhanced Akt phosphorylation was suppressed by an O2(-) scavenger (Tiron), catalase or a superoxide dismutase (SOD) inhibitor (DETC). These results suggest that CO pretreatment induces mitochondrial generation of O2(-), which is then converted by SOD to H2O2, and subsequent Akt activation by H2O2 attenuates apoptosis in ischemia-reperfusion.