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To test the hypothesis that male harassment of females reduces adult female time spent on the water foraging (water use), and thus cannibalism by adult females on juveniles, we manipulated heterospecific prey availability, and social context in adult water striders and measured their effects on: 1) cannibalism of juveniles, 2) activity of adults and 3) habitat use of adults and juveniles. Cannibalism rarely occurred with alternative prey present, but was common without alternative prey. Without alternative prey, females cannibalized much more than males, but contrary to predictions, male presence did not reduce cannibalism rates. Male presence decreased female water use; however, this was counteracted by the fact that the lack of alternative prey increased female water use and activity while on the water. Furthermore, in groups of 4 males with 4 females, lack of alternative prey reduced male activity while on the water. Thus the predicted negative effect of sexual conflict on cannibalism was reduced by female and male responses to low food availability. Juveniles increased time off the water when more females or males were more on the water and active. Overall, cannibalism rates depended on alternative prey, male-female social dynamics, female foraging and juvenile refuge use.

Although nonneurologic organ dysfunction (NNOD) has been shown to significantly affect mortality in subarachnoid hemorrhage, the contribution of NNOD to mortality after severe traumatic brain injury (TBI) has yet to be defined. We hypothesized that NNOD has a significant impact on mortality after severe TBI. The trauma registry was queried for all patients admitted between January 2004 and December 2004 who died during their initial hospitalization after severe TBI (head Abbreviated Injury Score 3 or greater). Cause of death and contributing factors to mortality were determined by an attending trauma surgeon from the medical record. The data were analyzed using both Fisher's exact and Wilcoxon rank sum. One hundred thirty-five patients met inclusion criteria. Sixty-seven per cent were males, 83 per cent were white, and the mean age was 38.5 years. Mean length of stay was 2.9 days. Fifty-four patients (40%) had isolated TBI (chest Abbreviated Injury Score = 0, abdominal Abbreviated Injury Score = 0). Of the 81 deaths attributed to a single cause, 48 (60%) patients died from nonsurvivable TBI or brain death, whereas 33 (40%) died of a nonneurologic cause. Cardiovascular and respiratory dysfunction (excluding pneumonia) contributed to mortality in 51.1 per cent and 34.1 per cent of patients, respectively. NNOD contributes to approximately two-thirds of all deaths after severe TBI. These complications occur early and are seen even among those with isolated head injuries. These findings demonstrate the impact of the extracranial manifestations of severe TBI on overall mortality and highlight potential areas for future intervention and research.

Background & Aims The enzyme cyclooxygenase-2 is expressed in a majority of colorectal carcinomas (CRCs) and is important in prostaglandin production. We have developed an accurate method to measure the urinary metabolite of prostaglandin E2 (PGE-M) using recently developed mass spectrometric techniques. The purpose of this pre-validation study was to determine if urinary PGE-M levels can be used as a biomarker to discriminate between healthy patients and those with colorectal disease. Methods Urine PGE-M was assessed in a total of 228 patients with CRC, colonic adenomatous polyps, Crohn's disease, and in subjects with no endoscopically detectable disease. Thirteen rectal carcinoma patients were treated with celecoxib and urinary PGE-M was measured before and after treatment. Results Urine PGE-M levels were increased among healthy men compared with healthy women (median, 8.59 [interquartile range (IQR), 5.67–22.3] vs 4.25 [IQR, 2.35–6.03], P = .0027). Urine PGE-M levels among patients with Crohn's disease (median, 19.85 [IQR, 6.89–90.2]), CRC (median, 14.65 [IQR, 5.94–92.1]), or large adenomas greater than 1 cm in size (median, 18.85 [IQR, 11.9–25.6]) were significantly increased when compared with patients who had either small polyps less than 1 cm in size (median, 9.69 [IQR, 6.41–22.2]), or no polyps (median, 7.05 [IQR, 2.35–24.7]) (P = .0001). PGE-M levels decreased significantly after celecoxib treatment in patients with rectal cancer (median, 21.7 [IQR, 16.2–29.9] vs 9.14 [IQR, 7.14–13.2], P = .009). Conclusions The increase in urinary PGE-M in patients with colorectal cancers and large adenomas suggests that urinary PGE-M is a potentially useful biomarker for the detection of advanced colorectal neoplasia.

Background & aims Staging inadequately predicts metastatic risk in patients with colon cancer. We used a gene expression profile derived from invasive, murine colon cancer cells that were highly metastatic in an immunocompetent mouse model to identify patients with colon cancer at risk of recurrence. Methods This phase 1, exploratory biomarker study used 55 patients with colorectal cancer from Vanderbilt Medical Center (VMC) as the training dataset and 177 patients from the Moffitt Cancer Center as the independent dataset. The metastasis-associated gene expression profile developed from the mouse model was refined with comparative functional genomics in the VMC gene expression profiles to identify a 34-gene classifier associated with high risk of metastasis and death from colon cancer. A metastasis score derived from the biologically based classifier was tested in the Moffitt dataset. Results A high score was significantly associated with increased risk of metastasis and death from colon cancer across all pathologic stages and specifically in stage II and stage III patients. The metastasis score was shown to independently predict risk of cancer recurrence and death in univariate and multivariate models. For example, among stage III patients, a high score translated to increased relative risk of cancer recurrence (hazard ratio, 4.7; 95% confidence interval, 1.566–14.05). Furthermore, the metastasis score identified patients with stage III disease whose 5-year recurrence-free survival was >88% and for whom adjuvant chemotherapy did not increase survival time. Conclusion A gene expression profile identified from an experimental model of colon cancer metastasis predicted cancer recurrence and death, independently of conventional measures, in patients with colon cancer.

Although nonneurologic organ dysfunction (NNOD) has been shown to significantly affect mortality in subarachnoid hemorrhage, the contribution of NNOD to mortality after severe traumatic brain injury (TBI) has yet to be defined. We hypothesized that NNOD has a significant impact on mortality after severe TBI. The trauma registry was queried for all patients admitted between January 2004 and December 2004 who died during their initial hospitalization after severe TBI (head Abbreviated Injury Score 3 or greater). Cause of death and contributing factors to mortality were determined by an attending trauma surgeon from the medical record. The data were analyzed using both Fisher's exact and Wilcoxon rank sum. One hundred thirty-five patients met inclusion criteria. Sixty-seven per cent were males, 83 per cent were white, and the mean age was 38.5 years. Mean length of stay was 2.9 days. Fifty-four patients (40%) had isolated TBI (chest Abbreviated Injury Score = 0, abdominal Abbreviated Injury Score = 0). Of the 81 deaths attributed to a single cause, 48 (60%) patients died from nonsurvivable TBI or brain death, whereas 33 (40%) died of a nonneurologic cause. Cardiovascular and respiratory dysfunction (excluding pneumonia) contributed to mortality in 51.1 per cent and 34.1 per cent of patients, respectively. NNOD contributes to approximately two-thirds of all deaths after severe TBI. These complications occur early and are seen even among those with isolated head injuries. These findings demonstrate the impact of the extracranial manifestations of severe TBI on overall mortality and highlight potential areas for future intervention and research.

Background: The purpose of this study was to define donation patterns and lost donor opportunities in severe traumatic brain injury (TBI) patients. Methods: The trauma registry was queried for all deaths after severe TBI in 2004; this was cross matched with the regional organ procurement organization database and subjected to post hoc statistical analysis. Results: One hundred thirty-five patients met criteria for inclusion. Forty percent had isolated TBI. Forty-two patients (31%) were eligible for deceased donation. Seventeen eligible patients (40%) did not convert to donation, 15 from family declining. Twenty-five eligible patients (60%) donated 85 organs (yield 3.4 organs/donor). Yield was similar in both isolated TBI (3.2) and patients with head injuries (3.5). Ineligible patients had higher admission Glasgow Coma Scale scores, lower head Abbreviated Injury Scale scores, and were more likely to develop cardiovascular or pulmonary dysfunction (p < 0.05). Of the 25 donors, 48% did not donate hearts and 84% did not donate lungs, despite the absence of chest trauma in the majority of patients. Conclusion: Less than one-third of severe TBI patients were identified as eligible organ donors and only 40% actually donated. Half of all donors fail to donate hearts and over 80% fail to donate lungs. Within this population, opportunities may exist to improve both donor conversion and organ yield.

Sequencing of the human genome and the acquisition of genomic data combined with advances in genomic and proteomic technologies have fueled a revolution in understanding disease. The combination of genomics and proteomics has provided a unique opportunity to diagnose, classify, and detect malignant disease, to better understand and define the behavior of specific tumors, and to provide direct and targeted therapy. Nevertheless, challenges remain, including integration and standardization of techniques and validation against accepted clinical and pathologic parameters. This article provides a summary of technologies, potential clinical applications, and challenges.

This study investigates the ability of endoscopic ultrasound (EUS) and computed tomography (CT) to predict a margin negative (R0) resection and the need for venous resection in patients undergoing pancreaticoduodenectomy (PD).Patients with pancreatic head adenocarcinoma undergoing surgery with intent to resect during the last 5 years were identified. EUS and CT data on vascular involvement were collected. Preoperative imaging was compared to intraoperative findings and final pathology. Contingency table analysis using Fisher's exact test identified imaging features of EUS and CT associated with unresectability and positive margins.Seventy-six patients met study criteria. Forty-seven (62%) underwent potentially curative PD. The R0 resection rate was 70%. There were 16 unresectable patients because of locally advanced disease. Venous involvement180 degrees and arterial involvement90 degrees by CT had 100% positive predictive value for failure to achieve R0 resection (p.01). If patients with prestudy biliary stents were excluded, EUS venous abutment or invasion also predicted R0 failure (p=.02). Combined but not individual EUS and CT findings were predictive of need for vein resection.Pancreas protocol CT imaging appears to be a better predictor of resectability compared to EUS. EUS accuracy is affected by the presence of biliary stents.

Patients with familial adenomatous polyposis (FAP) have a cumulative lifetime risk of over 90% for developing duodenal adenomas, which are the precursor lesions for duodenal adenocarcinoma. Consequently, these patients have a 5% to 10% lifetime risk of periampullary or duodenal adenocarcinoma, making this the leading cause of cancer death in FAP patients who have had prophylactic colectomies. The increased relative risk of duodenal carcinoma in FAP patients and the poor outcomes associated with the treatment of advanced duodenal cancer have led to the development of prevention strategies for this cancer in the setting of FAP. It is generally accepted that surveillance for duodenal adenomas and adenocarcinomas should be included in the management of patients with FAP, although there are few data from clinical trials that demonstrate the effectiveness of surveillance strategies or chemoprevention for the prevention of death from duodenal cancer. Prospective case series have shown that endoscopic surveillance with endoscopic or surgical treatment of high-risk lesions in the duodenal or periampullary region can be performed with successful removal of the at-risk lesion(s). Surveillance should begin at about 21 years of age and should be performed using both an end-viewing and a side-viewing upper endoscope. An interval of 3 to 5 years between examinations appears to be adequate if no polyposis is evident. Once polyposis develops, an interval of 1 to 3 years between screenings for mild polyposis is appropriate. Patients with denser polyposis or larger adenomas are recommended to undergo examination every 6 to 12 months because of their increased risk of developing duodenal adenocarcinoma. Nonsteroidal anti-inflammatory drug therapy with sulindac, a nonselective cyclooxygenase (COX) inhibitor, or celecoxib, a COX-2 selective inhibitor, may be of benefit after the development of duodenal polyposis by inducing the regression or stabilization of the polyposis, although there is limited evidence from randomized, controlled trials to support its routine use. Almost all cases of adenocarcinoma occur in patients with advanced polyposis (Spigelman stage IV disease), and approximately 33% of this group will go on to develop adenocarcinoma if left untreated. The most definitive procedure for reducing the risk of adenocarcinoma is surgical resection of the ampulla and/or duodenum. Pancreaticoduodenectomy or pancreas-sparing duodenectomy are appropriate surgical therapies that are believed to substantially reduce the risk of developing periampullary adenocarcinoma. However, these procedures are associated with significant morbidity and mortality, including the risk of inducing desmoid tumor formation in FAP patients.

Magnetic resonance imaging (MRI) and positron emission tomography (PET) with fluorodeoxyglucose were used to study the size and shape of the corpus callosum in 20 patients with unipolar depressive disorder and 16 normal controls. An automated algorithm outlined the corpus callosum and divided it into quarters. The anterior and posterior quarters of the corpus callosum were larger in depressed patients than in controls, findings similar to most earlier MRI studies of the corpus callosum in schizophrenics. The patient-normal difference was more marked in females than in males. PET glucose metabolic values were higher in patients with thinner or smaller callosums. The presence of marked sex differences makes future larger studies controlling body size and age important.

Positron emission tomography (PET) measurements of cerebral glucose use were made in 18 patients with generalized anxiety disorder (GAD) during a passive viewing task off medication, and an active vigilance viewing task before and after medication or placebo treatment. In the passive viewing task, patients with GAD were compared with 15 normal controls. A significant difference in pattern of absolute brain metabolism was found. Patients showed lower absolute metabolic rates in basal ganglia and white matter. Relative metabolism was increased in the left inferior area 17 in the occipital lobe, right posterior temporal lobe, and the right precentral frontal gyrus. Significant left-right asymmetry of the parahippocampal gyri was not found in patients with GAD. An active vigilance task resulted in activation of relative basal ganglia metabolism in patients. Benzodiazepine therapy resulted in decreases in absolute metabolic rates for cortical surface, limbic system, and basal ganglia and was not associated with normalization of patterns of glucose metabolism. Change in anxiety scores was significantly correlated with change in limbic system and basal ganglia for the placebo group. The normal-anxious difference in the basal ganglia and the change seen in this region after benzodiazepine treatment are suggestive of a role in anxiety for this structure.