588 in 9ICD and 0.601 in 10ICD. In the UK from 1979 to 2006 ��Other diseases of the digestive system�� (not ulcer-appendicitis-hernia-obstruction-chronic liver disease-cirrhosis) were 458 male and 329 female for a male fraction of 0.581 similar to the US data [14]. We speculate www.selleckchem.com/products/Perifosine.html that a linkage between the mechanism for the similar male fraction from digestive disease as SIDS may be from digestive causes such as malabsorption of iron and glucose in celiac disease and insufficient vascularization that would limit uptake and transport of glucose, respectively. This could lead to hypoglycemia that is a known risk factor for SIDS and sudden death [15, 16]. ��In the older infant, the resistance to hypoxia is much less than for the neonate, reflecting the diminished stores of glycogen and therefore limited substrate for anaerobic metabolism [3].

�� An enzyme, such as Glucose-6-phosphate dehydrogenase (G6PD) could play a role [15] as its X-linked gene locus is at Xq28 and it has a great multiplicity of alleles that are associated in their deficiency with nonspherocytic hemolytic anemia [17], and anemia is a likely risk factor for SIDS [18]. G6PD catalyzes initiation of glucose oxidation via the hexose-monophosphate pathway that may be a critical requirement for neuronal survival during cerebral anoxia. There could be more complicated X-linked processes such as requiring two (or more) independent X-linked alleles with probabilities q1 and q2, with probability of simultaneous presence (q = q1q2) that would equal the qvalues listed above for a single X-linked allele.

Alternatively, a gene locus such as G6PD could have many recessive alleles (q1, q2, q3,��) that are nonprotective of SIDS that could sum up to the q values listed above for the same risk of SIDS (q = q1 + q2 + q3 + ). We have chosen a single-gene X-linkage process for simplicity of discussion, and note that any genome-wide association study required to test our model can test for all possibilities. 3.3. The Age Distribution of SIDS The age distribution of SIDS is unique: ��Any viable hypothesis for the cause of SIDS must account for its characteristic age distribution.�� [19]. Raring [20] first noted that the unique and characteristic age distribution of SIDS appeared to follow a 2-parameter lognormal model. Mage [21] reviewed the SIDS age literature and in a meta-analysis of 15 global SIDS age data sets obtained the distribution of some 20 000 ages of SIDS shown in Figure 2.

In construction of Figure Drug_discovery 2, 1-month is <28 days of life. Other monthly intervals are approximate as 365 is not divisible by 12. Age data in weeks of life were divided by 4.33 to convert to months and the Althoff [22] data from Cologne reported as age within midmonth intervals (e.g., 1.5�C2.5 month) were plotted to estimate the corresponding integer month intervals (e.g., 1-2 months and 2-3 months) for pooling with the other monthly SIDS data.