I've been long 4ever and lurking for a year. Just signed up cause I wanted to see if the lawyers felt a stat person could present graphics to Judge Du to demonstrate the deficiencies in the Mori paper. Sorry if this is duplicative - Im hundreds of posts behind. <br /> <br /> Problems w Mori(2000) which negate any value in evaluating AMRN patent <br /> 1. Baseline (N=19) TG level FOR EPA GROUP reported as 2.01 ± 0.19 mmol/L [x ± SEM]. Converting SEM to sd --> 0.19 * sqrt 19 = 2.01 ± 0.8282 [x ± sd]. 1.96 sd = 1.623. So 97.5% of group have a baseline TG < 3.633 mmol/L == 321.8 mg/dl.(ie <b>expect >18.5 of 19 patients in the EPA group to have a TG < 322)</b>. Aren't the patents in question in patients with TG >500? <br /> <br /> 2. Post treatment <b>decrease in TG levels 21.6% greater for DHA than EPA</b> - so expect LDL-C to increase more in the DHA group. I don't know if it is proper to refer to the Friedewald equation, but LDL-C est as = TC- HDL-C - (TG/5) suggests that decreasing TG by 21% more could increase LDL-C by 4.2% more. <br /> <br /> 3. Post treatment LDL-C INCREASED in the EPA Group from 4.28 ± 0.19 [x ± SEM] to 4.46 ± 0.10 [x ± SEM] (+ 4.0%) while in the DHA Group from 4.27 ± 0.17 to 4.64 ± 0.10 (+ 8.7%). How do we know a 21% greater reduction in TG levels (by DHA cf EPA) shouldn't be expected to increase LDL-C by this amount over EPA? It seems to concur with the 4.2% expected above. <br /> <br /> 4. The paper compared the EPA group to the control and the DHA group to the contol - but not to each other. Converting to std dev gives a post treatment LDL-C range [x-sd to x+sd] of 4.024 - 4.896 for the EPA group and 4.248 - 5.052 in the DHA group. I think we would need to know the TG and LDL-C levels for each individual patient to know for sure, but I'd bet there would be enormous overlap between these 2 groups and some stats guru could prove.