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1.  Ultrasonic scalpel causes greater depth of soft tissue necrosis compared to monopolar electrocautery at standard power level settings in a pig model 
BMC Surgery  2012;12:3.
Background
Ultrasonic scalpel (UC) and monopolar electrocautery (ME) are common tools for soft tissue dissection. However, morphological data on the related tissue alteration are discordant. We developed an automatic device for standardized sample excision and compared quality and depth of morphological changes caused by UC and ME in a pig model.
Methods
100 tissue samples (5 × 3 cm) of the abdominal wall were excised in 16 pigs. Excisions were randomly performed manually or by using the self-constructed automatic device at standard power levels (60 W cutting in ME, level 5 in UC) for abdominal surgery. Quality of tissue alteration and depth of coagulation necrosis were examined histopathologically. Device (UC vs. ME) and mode (manually vs. automatic) effects were studied by two-way analysis of variance at a significance level of 5%.
Results
At the investigated power level settings UC and ME induced qualitatively similar coagulation necroses. Mean depth of necrosis was 450.4 ± 457.8 μm for manual UC and 553.5 ± 326.9 μm for automatic UC versus 149.0 ± 74.3 μm for manual ME and 257.6 ± 119.4 μm for automatic ME. Coagulation necrosis was significantly deeper (p < 0.01) when UC was used compared to ME. The mode of excision (manual versus automatic) did not influence the depth of necrosis (p = 0.85). There was no significant interaction between dissection tool and mode of excision (p = 0.93).
Conclusions
Thermal injury caused by UC and ME results in qualitatively similar coagulation necrosis. The depth of necrosis is significantly greater in UC compared to ME at investigated standard power levels.
doi:10.1186/1471-2482-12-3
PMCID: PMC3305372  PMID: 22361346
2.  Preoperative Chemoradiotherapy in Locally Advanced Rectal Cancer: Correlation of a Gene Expression-Based Response Signature with Recurrence 
Cancer Genetics and Cytogenetics  2009;190(2):57-65.
Background
Preoperative chemoradiotherapy is recommended for locally advanced rectal cancer (UICC stage II/III). We recently demonstrated that responsive and non-responsive tumors showed differential expression levels of 54 genes. In this follow-up study, we investigated the relationship between this gene-set and disease-free (DFS) and overall survival (OS).
Methods
Pre-therapeutic biopsies from 30 participants in the CAO/ARO/AIO-94 trial of the German Rectal Cancer Study Group were analyzed using gene expression microarrays. Statistical analysis was performed to identify differentially expressed genes between recurrent and non-recurrent tumors and to correlate these changes with disease recurrence and outcome.
Results
After a median follow-up of 59 months, seven of eight patients with recurrent disease belonged to the group of non-responders, while one responsive tumor recurred. Response to chemoradiotherapy was significantly correlated with an improved DFS (log rank p=0.028), while the OS did not differ significantly (p=0.11). Applying a class comparison analysis we identified 20 genes that were differentially expressed between recurrent and non-recurrent tumors at p<0.001. Analyzing the first two principal components of the 54 genes previously identified to predict response, we observed that this response signature correlated with an increased risk of cancer recurrence.
Conclusions
These data suggest that the genetic basis of local response also affects the genetic basis of tumor recurrence, and we demonstrated that genes that are indicative of non-response to preoperative chemoradiotherapy might also be linked to an increased risk of tumor recurrence.
doi:10.1016/j.cancergencyto.2008.11.011
PMCID: PMC2766806  PMID: 19380020
Rectal cancer; gene expression profiling; 5-FU-based preoperative chemoradiotherapy; recurrence; prognosis
3.  Genetics of Hemostasis: Differential Effects of Heritability and Household Components Influencing Lipid Concentrations and Clotting Factor Levels in 282 Pediatric Stroke Families 
Environmental Health Perspectives  2008;116(6):839-843.
Background
The identification of heritable and environmental factors possibly influencing a condition at risk should be a prerequisite for the search for the proportion of variance attributable for shared environmental effects (c2) modulating the risk of disease. Such epidemiologic approaches in families with a first acute ischemic stroke during early childhood are lacking.
Objectives
Our goal was to estimate the phenotypic variation within lipid concentrations and coagulation factor levels and to estimate the proportions attributable to heritability (h2r) and c2 in pediatric stroke families.
Methods
Blood samples were collected from 1,002 individuals from 282 white stroke pedigrees. We estimated h2r and c2 for lipoprotein (a) [Lp(a)], cholesterol, high-density lipoprotein, low-density lipoprotein (LDL), fibrinogen, factor (F) II, FV, FVIIIC, von Willebrand factor (vWF), antithrombin, protein C, protein S, plasminogen, protein Z, total tissue factor pathway inhibitor (TFPI), prothrombin fragment F1.2, and D-dimer, using the variance component method in sequential oligogenetic linkage analysis routines.
Results
When incorporating h2r and c2 in one model adjusted for age, blood group, sex, smoking, and hormonal contraceptives, significant h2r estimates were found for Lp(a), LDL, fibrinogen, protein C, and protein Z. In addition to the significant h2r estimates, c2 showed a significant effect on phenotypic variation for fibrinogen, protein C, and protein Z. A significant c2 effect was found for cholesterol, and plasma levels of FII, FV, vWF, antithrombin, protein S, plasminogen, and TFPI, ranging from 9.3% to 33.2%.
Conclusions
Our research stresses the importance of research on the genetic variability and lifestyle modifications of risk factors associated with pediatric stroke.
doi:10.1289/ehp.10754
PMCID: PMC2430243  PMID: 18560491
heritability; household; lifestyle; pediatric stroke; smoking

Results 1-3 (3)