5, so we model the rate of SIDS per 1000 = 2.5 (1. ? 0.9(LBO+1)) selleck kinase inhibitor and show our predictions in the lower row in Table 3. The unweighted correlation of predictions and observations is r = 0.9966. 3.6. Pa, Probability of Physiological Anemia Causing Apnea and Hypoxia that Are SIDS Risk Factors Infant anemia has not been considered directly as a risk factor for SIDS per se, because ��accurate hemoglobin [Hb] levels cannot be determined after death [18]�� due to rapid Hb breakdown resulting in the mottled and reddened areas known as livor mortis. A study in mice shows how Hb is already significantly decreased in the first postmortem hour [28]. Because the exact time of SIDS during sleep is not known it would be impossible to correct for the variable amount of Hb lost between the instant of SIDS death and autopsy.

��There is, however, indirect evidence suggesting a relationship between anemia and SIDS: the peak incidence of SIDS coincides with the nadir [of Hb] in the physiological anemia of infancy.�� [18]. Anemia does contribute to apnea and apparent life-threatening events (ALTEs) from causing longer cyanotic breath-holding spells [29�C32] that are risk factors for SIDS, leading to ��The Apnea Hypothesis.�� [3, 32]. Therefore anemia is treated by us as a risk factor for SIDS. Let Pa = exp [?loge2 ([(m + 0.31)/(�� + 0.31)]/[(41.2 ? m)/(41.2 ? ��)])/(2��2)], as found in the Johnson SB model [23] as (2), represent an anemia-cum-apnea risk factor rising from 0 at birth, reaching a peak at the median (�� = 3.1 months) and decreasing to zero at 41.2 months.

Anemia in infancy may be defined relatively as any value for the hemoglobin [Hb] less than two standard deviations (<�C2��) below the mean for age [33], or absolutely as less than a fixed value, such as 13.5g/dL which is the ?2�� level below mean cord blood Hb and mean Hb at 1 week [34]. Infant physiological anemia is a risk factor that is virtually zero at birth due to placental transfusion during labor [35] and at birth Hb concentration in the blood can reach +2�� of 23.7g/dL [36]. We propose that this high at birth Hb phenomenon accounts for the relative protection from SIDS during the first week of life. In the following weeks, total Hb decreases rapidly as fetal hemoglobin (HbF) is removed faster than it can be replaced by adult hemoglobin (HbA).

A nadir in total Hb occurs at or about 2 months of age for a term infant that corresponds to the 63rd day mode of the SIDS SB age distribution [18, 21]. Table 4 shows the ?2��Hbg/dL level (lowest 2.5% of all infants) [33]. Table 4 The ?2�� lower limit of normal term infant Hemoglobin (Hb, g/dL) [33]. By definition, approximately 25 in 1000 term infants have a Hb value below the ?2�� value shown, and preterm infants will fall under this value with a higher frequency, perhaps related to their increased risk of SIDS. Of those 25 in 1000, the one with the lowest Hb would be at the highest Anacetrapib risk of apnea and therefore SIDS.