Microcirculatory flow was assessed using the microcirculation flow index (MFI) at 6 and 24 h in GSK2126458 the cardiac arrest patients, and within 6 h of emergency department admission in the sepsis and control patients.

Results: We evaluated 30 post-cardiac arrest patients, 16 severe sepsis/septic shock patients, and 9 healthy control patients. Sublingual microcirculatory blood flow was significantly impaired

in post-cardiac arrest patients at 6 h (MFI 2.6 [IQR: 2-2.9]) and 24 h (2.7 [IQR: 2.3-2.9]) compared to controls (3.0 [IQR: 2.9-3.0]; p<0.01 and 0.02, respectively). After adjustment for initial APACHE II score, post-cardiac arrest patients had significantly lower MFI at 6-h compared to sepsis patients (p<0.03). In the post-cardiac arrest group, patients with good neurologic outcome had better microcirculatory blood flow as compared to patients with poor neurologic outcome (2.9 [IQR: 2.4-3.0] vs. 2.6 [IQR: 1.9-2.8]; p < 0.03). There was a trend toward higher median MFI at 24h in survivors vs. non-survivors (2.8 [IQR: 2.4-3.0] vs. 2.6 [IQR: 2.1-2.8] respectively; p<0.09). We found a negative correlation between MFI-6 and vascular endothelial growth factor (VEGF) (r=-0.49, p = 0.038). However,

GW786034 after Bonferroni adjustment for multiple comparisons, this correlation was statistically CAL-101 non-significant.

Conclusion: Microcirculatory dysfunction occurs early in post-cardiac arrest

patients. Better microcirculatory function at 24h may be associated with good neurologic outcome. (C) 2013 Elsevier Ireland Ltd. All rights reserved.”
“The development of genetically engineered models (GEM) of epithelial ovarian cancer (EOC) has been very successful, with well validated models representing high grade and low grade serous adenocarcinomas and endometrioid carcinoma (EC). Most of these models were developed using technologies intended to target the ovarian surface epithelium (OSE), the cell type long believed to be the origin of EOC. More recent evidence has highlighted what is likely a more prevalent role of the secretory cell of the fallopian tube in the ontogeny of EOC, however none of the GEM of EOC have demonstrated successful targeting of this important cell type.

The precise technologies exploited to develop the existing GEM of EOC are varied and carry with them advantages and disadvantages. The use of tissue specific promoters to model disease has been very successful, but the lack of any truly specific OSE or oviductal secretory cell promoters makes the outcomes of these models quite unpredictable.