Scientific rationale for Uranus and Neptune <i>in situ</i> explorations

The ice giants Uranus and Neptune are the least understood class of planets in our solar system but the most frequently observed type of exoplanets. Presumed to have a small rocky core, a deep interior comprising ∼70% heavy elements surrounded by a more dilute outer envelope of H2 and He, Uranus and Neptune are fundamentally different from the better-explored gas giants Jupiter and Saturn. Because of the lack of dedicated exploration missions, our knowledge of the composition and atmospheric processes of these distant worlds is primarily derived from remote sensing from Earth-based observatories and space telescopes. As a result, Uranus's and Neptune's physical and atmospheric properties remain poorly constrained and their roles in the evolution of the Solar System not well understood. Exploration of an ice giant system is therefore a high-priority science objective as these systems (including the magnetosphere, satellites, rings, atmosphere, and interior) challenge our understanding of planetary formation and evolution. Here we describe the main scientific goals to be addressed by a future in situ exploration of an ice giant. An atmospheric entry probe targeting the 10-bar level, about 5 scale heights beneath the tropopause, would yield insight into two broad themes: i) the formation history of the ice giants and, in a broader extent, that of the Solar System, and ii) the processes at play in planetary atmospheres. The probe would descend under parachute to measure composition, structure, and dynamics, with data returned to Earth using a Carrier Relay Spacecraft as a relay station. In addition, possible mission concepts and partnerships are presented, and a strawman ice-giant probe payload is described. An ice-giant atmospheric probe could represent a significant ESA contribution to a future NASA ice-giant flagship mission

The significance of bowel permeability

PURPOSE OF REVIEW: In clinical research, increased permeability has been scrutinized as a potential indicator of the severity of gastrointestinal disease and as a potential cause of the perpetuation of severe inflammatory activity in infectious states. This review discusses old and recent epidemiological and clinical evidence to establish whether increased permeability in sepsis is a sequel or a cause of multiple organ failure. In addition, old and new evidence linking inflammation and permeability in abnormal gastrointestinal anatomy and function to liver abnormalities in susceptible patients will be reviewed. RECENT FINDINGS: Intestinal permeability has been found to be increased in several gastrointestinal diseases but not to be a very good marker of the severity of disease. Evidence is put forward supporting the claim that increased intestinal permeability is part of generalized leakiness of tight junctions in multiple organ failure and to play a less strong role as a primary event in its pathogenesis. Endemic malnutrition has been shown to be caused by interplay between malnutrition and intestinal inflammation. Recently experimental evidence has been put forward suggesting that enteral fat has anti-inflammatory effects on the intestine via the autonomic nervous system. Old clinical and new epidemiological evidence links intestinal inflammation, disruption of the enterohepatic cycle of bile acids, and liver disease. SUMMARY: The implications of the described findings are that inflammatory activity, locally induced by abnormal intestinal anatomy and disruption of the bile acid pool, or systemically by severe and uncontrolled inflammation/infection, should be the focus of treatment or research. In addition, the connection between intestinal inflammation and liver disease should be investigated

Lipid-rich enteral nutrition reduces postoperative ileus in rats via activation of cholecystokinin-receptors

OBJECTIVE: This study investigates the effect of lipid-rich nutrition on the local inflammatory response and gastrointestinal hypomotility in a rat model of postoperative ileus. BACKGROUND: Postoperative ileus is a major clinical problem, in which inflammation of the intestinal muscularis plays a key pathogenic event. Previously, administration of lipid-rich nutrition has been shown to reduce inflammation by activation of the autonomic nervous system via cholecystokinin-receptors. METHODS: Postoperative ileus was induced by manipulation of the small intestine in rats. Peritoneal lavage fluid, plasma, and jejunal segments were collected at several time points to determine inflammatory mediators in fasted rats and rats fed a lipid-rich or control nutrition. Gastrointestinal transit was measured 24 hours after surgery. RESULTS: Administration of lipid-rich nutrition markedly reduced the manipulation-induced local inflammatory response compared to rats treated with control nutrition. The intervention with lipid-rich nutrition significantly reduced plasma levels of rat mast cell protease-II (P < 0.05) and peritoneal levels of tumor necrosis factor-alpha (P < 0.01) and interleukin-6 (P < 0.05). Furthermore, the influx of neutrophils, expressed as tissue level myeloperoxidase was significantly prevented by lipid-rich nutrition (P < 0.05). Above all administration of lipid-rich enteral nutrition resulted in a significant improvement of gastrointestinal transit compared to control nutrition (P < 0.05). Blocking of cholecystokinin-receptors prevented the anti-inflammatory and motility promoting effect of lipid-rich feeding. CONCLUSION: Our data demonstrate that nutritional stimulation of the autonomic nervous system with enteral lipids reduces postoperative ileus by inhibition of inflammation. Clinically, lipid-rich enteral nutrition may be a new therapeutic option in the treatment of postoperative ileus

Pretreatment with high-fat enteral nutrition reduces ondotoxin and tumor necrosis factor-alpha and preserves gut barrier function early after hemorrhagic shock

Gram-negative sepsis is a potentially fatal clinical syndrome characterized by a proinflammatory response (tumor necrosis factor-alpha) to bacterial (endo)toxins and gut barrier function loss. Recently, we found that high-fat enteral nutrition protects against late bacterial translocation in a model of hemorrhagic shock in rats. However, the basis for this protection is unknown. We hypothesized that the observed protection is the result of an early inhibition of endotoxin and the subsequent inflammatory response resulting in a preserved gut barrier function. Sprague-Dawley rats were divided into a group that was starved overnight (HS-S), fed with a low-fat enteral diet (HS-LF) or fed wih a high-fat enteral diet (HS-HF), and subsequently subjected to a nonlethal hemorrhagic shock. Ninety minutes after hemorrhage, arterial endotoxin significantly decreased in HS-HF rats (4.0 +/- 0.6 pg/mL) compared with HS-LF rats (10.7 +/- 0.9 pg/mL, P = 0.002) and HS-S rats (15.2 +/- 2.2 pg/mL P = 0.001). Interestingly, arterial tumor necrosis factor-a was also decreased in HS-HF rats (17.9 +/- 10.4 pg/mL) compared with HS-LF (83.5 +/- 16.7 pg/mL, P <0.01) and HS-S rats (180.9 +/- 67.9 pg/mL, P <0.02). Loss of tight junction structure (ZO-1) observed in ileum and colon of control hemorrhagic shock rats was prevented in HS-HF rats. In parallel, intestinal barrier function was preserved in HS-HF rats, evidenced by a reduced permeability to horseradish peroxidase (P <0.05), less bacterial invasion, and a 10-fold reduction of bacterial translocation early after hemorrhagic shock. This report describes a new strategy to nutritionally prevent endotoxemia, the subsequent inflammatory response and gut barrier failure following hemorrhagic shock. High-fat enteral nutrition requires further evaluation as an intervention to prevent a potentially fatal systemic inflammatory response in patients at risk for sepsis

Static and dynamic postural control in low-vision and normal-vision adults

OBJECTIVE: This study aimed to evaluate the influence of reduced visual information on postural control by comparing low-vision and normal-vision adults in static and dynamic conditions. METHODS: Twenty-five low-vision subjects and twenty-five normal sighted adults were evaluated for static and dynamic balance using four protocols: 1) the Modified Clinical Test of Sensory Interaction on Balance on firm and foam surfaces with eyes opened and closed; 2) Unilateral Stance with eyes opened and closed; 3) Tandem Walk; and 4) Step Up/Over. RESULTS: The results showed that the low-vision group presented greater body sway compared with the normal vision during balance on a foam surface (p&#8804;0.001), the Unilateral Stance test for both limbs (p&#8804;0.001), and the Tandem Walk test. The low-vision group showed greater step width (p&#8804;0.001) and slower gait speed (p&#8804;0.004). In the Step Up/Over task, low-vision participants were more cautious in stepping up (right p&#8804;0.005 and left p&#8804;0.009) and in executing the movement (p&#8804;0.001). CONCLUSION: These findings suggest that visual feedback is crucial for determining balance, especially for dynamic tasks and on foam surfaces. Low-vision individuals had worse postural stability than normal-vision adults in terms of dynamic tests and balance on foam surfaces

Lipid-enriched enteral nutrition controls the inflammatory response in murine Gram-negative sepsis.

OBJECTIVES:: Controlling the inflammatory cascade during sepsis remains a major clinical challenge. Recently, it has become evident that the autonomic nervous system reduces inflammation through the vagus nerve. The current study investigates whether nutritional stimulation of the autonomic nervous system effectively attenuates the inflammatory response in murine Gram-negative sepsis. DESIGN:: Controlled in vivo and ex vivo experimental study. SETTINGS:: Research laboratory of a university hospital. SUBJECTS:: Male C57bl6 mice. INTERVENTIONS:: Mice were intraperitoneally challenged with lipopolysaccharide derived from Escherichia coli. Before lipopolysaccharide administration, mice were fasted or enterally fed either lipid-rich nutrition or low-lipid nutrition. Antagonists to cholecystokinin receptors or nicotinic receptors were administered before lipopolysaccharide administration. Blood and tissue samples were collected at 90 mins. Mesenteric afferent discharge was determined in ex vivo preparations in response to both nutritional compositions. MEASUREMENTS AND MAIN RESULTS:: Both lipid-rich and low-lipid nutrition dose-dependently reduced lipopolysaccharide-induced tumor necrosis factor-alpha release (high dose: both 1.4 +/- 0.4 ng/mL) compared with fasted mice (3.7 +/- 0.8 ng/mL; p < .01). The antiinflammatory effect of both nutritional compositions was mediated through cholecystokinin receptors (p < .01), activation of mesenteric vagal afferents (p < .05), and peripheral nicotinic receptors (p < .05). Lipid-rich nutrition attenuated the inflammatory response at lower dosages than low-lipid nutrition, indicating that enrichment of enteral nutrition with lipid augments the antiinflammatory potential. Administration of lipid-rich nutrition prevented endotoxin-induced small intestinal epithelium damage and reduced inflammation in the liver and spleen compared with fasted (all p < .01) and low-lipid nutrition controls (all p < .05). CONCLUSIONS:: The current study demonstrates that lipid-rich nutrition attenuates intestinal damage and systemic as well as organ-specific inflammation in murine Gram-negative sepsis through the nutritional vagal antiinflammatory pathway. These findings implicate enteral administration of lipid-enriched nutrition as a promising intervention to modulate the inflammatory response during septic conditions