Optimal group testing designs for estimating prevalence with uncertain testing errors.

We construct optimal designs for group testing experiments where the goal is to estimate the prevalence of a trait using a test with uncertain sensitivity and specificity. Using optimal design theory for approximate designs, we show that the most efficient design for simultaneously estimating the prevalence, sensitivity, and specificity requires three different group sizes with equal frequencies. However, if estimating prevalence as accurately as possible is the only focus, the optimal strategy is to have three group sizes with unequal frequencies. Based on a Chlamydia study in the United States, we compare performances of competing designs and provide insights into how the unknown sensitivity and specificity of the test affect the performance of the prevalence estimator. We demonstrate that the proposed locally D- and Ds -optimal designs have high efficiencies even when the prespecified values of the parameters are moderately misspecified.

Reactive thrombocytosis without endothelial damage does not affect the microvascular anastomotic patency.

There is still controversy about the correlation of thrombocytosis and thrombosis complication. Using a rodent splenectomy-induced thrombocytosis model and a thrombogenic endothelial damage model (inverted suture resulting in an intraluminal thrombogenic adventitia of divided femoral artery), the authors investigated whether reactive thrombocytosis with or without endothelial damage contributes to the patency of microvascular anastomosis. Four experimental groups were evaluated in this study: 1) sham operation without thrombogenic anastomosis after femoral artery division; 2) sham operation with thrombogenic anastomosis; 3) thrombocytosis alone without thrombogenic anastomosis; 4) thrombocytosis with thrombogenic anastomosis (each subgroup n = 10, total N = 40). Vascular patency was assessed after immediate operation and on the seventh day postoperatively. Platelet counts and platelet activation (CD62P) were studied in correlation to microvascular patency. In rats without thrombogenic anastomosis groups, there were no significant differences in CD62P expression on platelets (p = 0.09), the patency rates (p = 0.561), or perfusion units (p = 0.746) before and after arterial reanastomosis between rats with and without thrombocytosis, respectively. However, the thrombogenic anastomosis of femoral artery in thrombocytosis and control groups showed significantly increased CD62P expression (p < 0.05), decreased the perfusion unit (p < 0.05), and patency rate (p < 0.001), compared with rats without thrombogenic anastomosis of femoral artery in both groups. In summary, this study demonstrates that microvascular anastomosis can be performed safely with reactive thrombocytosis alone without thrombogenic anastomosis. Meticulous microvascular anastomosis without triggering platelet activation is the most important factor to prevent thrombosed vessels in microsurgical anastomosis.

Reactive thrombocytosis alone does not affect the patency of microvascular anastomosis in the splenectomy rat.

Vascular thrombosis is a harbinger of failure in microsurgery. However, there is still controversy regarding the correlation of the complications of thrombocytosis and thrombosis. Some evidence indicates that patients with elevated platelet counts tend to have a higher flap failure rate, and surgeons usually hesitate to operate on patients with thrombocytosis. Nevertheless, the authors have experienced successful free tissue transfer in seven patients with thrombocytosis resulting from traumatic splenectomy or multiple trauma. On the basis of clinical observation, the authors investigated whether reactive thrombocytosis contributes to the patency of a microvascular anastomosis. In a rodent splenectomy-induced thrombocytosis model (n = 40), stable reactive thrombocytosis occurred after postoperative days 5 to 10, with the peak on postoperative day 7. Femoral artery division and reanastomosis was performed in rats with or without splenectomy-induced thrombocytosis, and vascular patency was assessed. Platelet counts and platelet activation were studied in correlation to microvascular patency. Platelet activation as demonstrated by CD62P expression on platelets was not significantly different between rats with and without thrombocytosis (6.41 +/- 0.95 percent versus 4.51 +/- 0.55 percent, respectively; p = 0.089). As immature platelets were not increased (2.86 +/- 0.33 percent versus 1.99 +/- 0.32 percent, p = 0.074), it seems that the splenectomy-induced thrombocytosis is the result of redistribution of platelets instead of an increase in bone marrow production. There were no significant differences in the patency rates or perfusion units of femoral artery after arterial anastomosis between rats with and without thrombocytosis (90 percent and 95 percent, respectively; p = 0.561). In conclusion, this study demonstrates that microvascular anastomosis can be performed safely in patients with reactive thrombocytosis without platelet activation.