Patient-controlled sedation is an effective alternative to premedication with narcotic/benzodiazepine combinations during colonoscopy.

We conclude that placental RAGE is activated during PE and that RAGE-mediated inflammation in the trophoblast involves increased pro-inflammatory cytokine secretion.

IntroductionRecent advances in operative procedures and surgical instrumentation have enabled the application of laparoscopic techniques to more complex surgeries. However, complex procedures require extended insuffl ation times (typically greater than 3 hours) 1-6 and consequently patients undergo prolonged periods of elevated intraabdominal pressure. And while the benefi ts of using minimally invasive techniques for longer procedures are presumed to be similar to those obtained for "simple" laparoscopic surgeries, it is now recognized that carbon dioxide (CO 2 ) pneumoperitoneum and the resultant rise in intra-abdominal pressure can produce reductions in organ blood fl ow, acidosis, and alterations in cardiovascular and respiratory status, 5-10 all of which can impact postoperative organ function and patient recovery; the severity of these eff ects correlates to the duration of insuffl ation. 11To some extent, the acidosis and systemic effects of pneumoperitoneum can be controlled by altering ventilation rates and/or administration of vasoactive agents but such interventions have minimal ability to preserve end-organ blood fl ow and oxygen delivery. Th is is because local tissue blood fl ow, rather than blood oxygen content, is the primary determinant of oxygen delivery. Local tissue perfusion is regulated by a physiological response termed hypoxic vasodilation in which tissue oxygen requirements are directly coupled to blood fl ow, the domain of nitric oxide (NO) bioactivity.12 Second to second changes in microcirculatory fl ow are controlled by complex interactions between oxygen, NO, and hemoglobin (Hb) within the red blood cell with Hb serving as an oxygen sensor and as a hypoxia-responsive transducer of NO signals. 13,14 Vasodilation by S-nitrosoHb (SNO-Hb; i.e., release of NO bioactivity) is linked to Hb desaturation and provides a regulated mechanism for matching blood fl ow and oxygen delivery with local metabolic demand. 15Decreased levels and/or impaired processing of SNO-Hb have been observed in disparate diseases characterized by tissue hypoxemia; [16][17][18][19][20][21][22] where examined, red blood cells from these patients exhibited impaired vasodilatory capacity. Such data suggest that red blood cell derived NO bioactivity plays an important role in the respiratory cycle and that impairment of this activity might contribute to the pathophysiology of ischemic conditions. Based on these fi ndings, we reasoned that insuffl ationinduced reductions in splanchnic blood fl ow may be due, at least in part, to alterations (reductions) in SNO-Hb homeostasis. By extension, an intervention directed toward increasing NO bioactivity could potentially ameliorate pneumoperitoneuminduced reductions in organ blood fl ow. Th eoretical support for this hypothesis comes from the observations that reductions in blood pH, as occur during CO 2 pneumoperitoneum, accelerate SNO-Hb decay 23,24 and increased mechanical ventilation (as may be initiated to control hybercarbia) increases the concentration of exhaled NO 25 b...

The biogeography of Central America is viewed as a classic case study in understanding the impact of vicariant events on patterns of biotic dispersal. While many biogeographers have focused on community composition and geographical limits of species at broad scales across Central America, much less work has focused on post-colonization diversification patterns at finer scales. The livebearing freshwater fish Xenophallus umbratilis presents an ideal system for determining the impact of recent Earth history events on biodiversity in northern Costa Rica. Here, we test the hypotheses that marine inundation of the San Carlos and northern Limón basins during the Pliocene and Pleistocene has caused genetic fragmentation among X. umbratilis populations, despite contemporary freshwater connections. To test this idea, we collected mitochondrial (cytochrome b) sequence data in 162 individuals taken from 27 localities across northern Costa Rica. We employed a variety of analytical approaches, including: maximum parsimony and maximum likelihood, analysis of molecular variance, and demographic analysis of population size through time. We found four major clades within X. umbratilis, each geographically isolated with no shared haplotypes across drainages. Oddly, clades that occupy adjacent drainages are not always sister taxa in the phylogeny, suggesting that colonization in this species is more complex than a simple model of isolation by distance. All our results are consistent with the hypothesis that changes in sea level associated with glacial eustatic cycles have had an important effect in shaping diversification patterns in this species.

The receptor for advanced glycation end-products (RAGE) has increasingly been demonstrated to be an important modulator of inflammation in cases of pulmonary disease. Published reports involving tobacco smoke exposure have demonstrated increased expression of RAGE, its participation in proinflammatory signaling, and its role in irreversible pulmonary remodeling. The current research evaluated the in vivo effects of short-term secondhand smoke (SHS) exposure in RAGE knockout and control mice compared with identical animals exposed to room air only. Quantitative PCR, immunoblotting, and immunohistochemistry revealed elevated RAGE expression in controls after 4 wk of SHS exposure and an anticipated absence of RAGE expression in RAGE knockout mice regardless of smoke exposure. Ras activation, NF-κB activity, and cytokine elaboration were assessed to characterize the molecular basis of SHS-induced inflammation in the mouse lung. Furthermore, bronchoalveolar lavage fluid was procured from RAGE knockout and control animals for the assessment of inflammatory cells and molecules. As a general theme, inflammation coincident with leukocyte recruitment was induced by SHS exposure and significantly influenced by the availability of RAGE. These data reveal captivating information suggesting a role for RAGE signaling in lungs exposed to SHS. However, ongoing research is still warranted to fully explain roles for RAGE and other receptors in cells coping with involuntary smoke exposure for prolonged periods of time.