Planetary radio astronomy observations from Voyager-2 near Saturn

Voyager-2 planetry radio astronomy measurements obtained near Saturn are discussed. They indicate that Saturnian kilometric radiation is emitted by a strong, dayside source at auroral latitudes in the northern hemisphere and by a weaker (by more than an order of magnitude) source at complementary latitudes in the southern hemisphere. These emissions are variable both due to Saturn's rotation and, on longer time scales, probably due to influences of the solar wind and the satellite Dione. The Saturn electrostatic discharge bursts first discovered by Voyager-1 and attributed to emissions from the B-ring were again observed with the same broadband spectral properties and a 10(h)11(m) + or - 5(m) episodic recurrence period but with an occurrence frequency of only of about 30 percent of that detected with Voyager-1. During the crossing of the ring plane at a distance of 2.88 R sub S, an intense noise event is interpreted to be consequence of the impact/vaporization/ionization of charged micron-size G-ring particles distributed over a total vertical thickness of about 1500 km

Weaning from Mechanical Ventilation

For most patients who require mechanical ventilation weaning and extubation is simple. In these patients a variety of strategies can be successful. In addition, sim ple criteria may predict when the patient is ready for extubation. For the small group of patients who require prolonged mechanical ventilation, however, contro versy exists about how best to remove ventilator sup port by weaning, and available data are sparse. Much of the controversy has centered on T-piece weaning ver sus intermittent mandatory ventilation. To date no con trolled study has demonstrated the superiority of either intermittent mandatory ventilation or T-piece weaning in difficult-to-wean patients. In the evolution of this con troversy, concern has developed over the potential for increased inspiratory work and expiratory resistance that may be associated with certain intermittent manda tory ventilation systems. The possibility that significant inspiratory work may occur during assist-control venti lation has also been demonstrated. Respiratory muscle weakness and fatigue is likely important in failure to wean. Other possible causes are failure of the cardiovas cular system and impaired ability of the lung to carry out gas exchange. In this article we first examine criteria and techniques for weaning short-term ventilator pa tients. We then examine criteria to begin the weaning process in prolonged ventilation patients, potential causes of failure to wean, and techniques that can be used to remove ventilator support from patients who are difficult to wean. Much literature has been devoted to techniques and criteria for weaning and extubation of patients from mechanical ventilation. For most patients who require ventilatory support, weaning and extuba tion can be easily accomplished by a variety of tech niques [1-4]. At one referral center 77.2% of all surviving patients were weaned from the ventilator within 72 hours of the onset of mechanical ventila tion, and 91% were weaned within 7 days [1]. Less than 10% of ventilated patients potentially posed problems in weaning from mechanical ventilation. Similarly, at a community hospital, few surviving patients required prolonged ventilatory support [2]. In easy-to-wean patients, Sahn and Lakshminarayan [5] described simple criteria that are predictive of successful discontinuation of ventilator support. For the small group of patients who require pro longed mechanical ventilation, however, minimal data are available. In these patients criteria to deter mine weaning ability or which measurements to follow are not clearly defined. Furthermore, no controlled trials are available to compare the differ ent weaning techniques proposed. In this article we first address routine weaning of the patient who has not required prolonged ventilator support. We then examine the difficult-to-wean patient and dis cuss criteria to begin the weaning process, poten tial causes of failure to wean, and available weaning techniques.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/68923/2/10.1177_088506668800300207.pd

A Blind Search for Magnetospheric Emissions from Planetary Companions to Nearby Solar-type Stars

This paper reports a blind search for magnetospheric emissions from planets around nearby stars. Young stars are likely to have much stronger stellar winds than the Sun, and because planetary magnetospheric emissions are powered by stellar winds, stronger stellar winds may enhance the radio luminosity of any orbiting planets. Using various stellar catalogs, we selected nearby stars (<~ 30 pc) with relatively young age estimates (< 3 Gyr). We constructed different samples from the stellar catalogs, finding between 100 and several hundred stars. We stacked images from the 74-MHz (4-m wavelength) VLA Low-frequency Sky Survey (VLSS), obtaining 3\sigma limits on planetary emission in the stacked images of between 10 and 33 mJy. These flux density limits correspond to average planetary luminosities less than 5--10 x 10^{23} erg/s. Using recent models for the scaling of stellar wind velocity, density, and magnetic field with stellar age, we estimate scaling factors for the strength of stellar winds, relative to the Sun, in our samples. The typical kinetic energy carried by the stellar winds in our samples is 15--50 times larger than that of the Sun, and the typical magnetic energy is 5--10 times larger. If we assume that every star is orbited by a Jupiter-like planet with a luminosity larger than that of the Jovian decametric radiation by the above factors, our limits on planetary luminosities from the stacking analysis are likely to be a factor of 10--100 above what would be required to detect the planets in a statistical sense. Similar statistical analyses with observations by future instruments, such as the Low Frequency Array (LOFAR) and the Long Wavelength Array (LWA), offer the promise of improvements by factors of 10--100.Comment: 11 pages; AASTeX; accepted for publication in A

Bilirubin decreases NOS2 expression via inhibition of NAD(P)H oxidase: implications for protection against endotoxic shock in rats.

We investigated a possible beneficial role for bilirubin, one of the products of heme degradation by the cytoprotective enzyme heme oxygenase-1 in counteracting Escherichia coli endotoxin-mediated toxicity. Homozygous jaundice Gunn rats, which display high plasma bilirubin levels due to deficiency of glucuronyl transferase activity, and Sprague-Dawley rats subjected to sustained exogenous bilirubin administration were more resistant to endotoxin (LPS)-induced hypotension and death compared with nonhyperbilirubinemic rats. LPS-stimulated production of nitric oxide (NO) was significantly decreased in hyperbilirubinemic rats compared with normal animals; this effect was associated with reduction of inducible NO synthase (NOS2) expression in renal, myocardial, and aortic tissues. Furthermore, NOS2 protein expression and activity were reduced in murine macrophages stimulated with LPS and preincubated with bilirubin at concentrations similar to that found in the serum of hyperbilirubinemic animals. This effect was secondary to inhibition of NAD(P)H oxidase since 1) inhibition of NAD(P)H oxidase attenuated NOS2 induction by LPS, 2) bilirubin decreased NAD(P)H oxidase activity in vivo and in vitro, and 3) down-regulation of NOS2 by bilirubin was reversed by addition of NAD(P)H. These findings indicate that bilirubin can act as an effective agent to reduce mortality and counteract hypotension elicited by endotoxin through mechanisms involving a decreased NOS2 induction secondary to inhibition of NAD(P)H oxidase

Association of circulating angiotensin converting enzyme activity with respiratory muscle function in infants

<p>Abstract</p> <p>Background</p> <p>Angiotensin converting enzyme (ACE) gene contains a polymorphism, consisting of either the presence (I) or absence (D) of a 287 base pair fragment. Deletion (D) is associated with increased circulating ACE (cACE) activity. It has been suggested that the D-allele of ACE genotype is associated with power-oriented performance and that cACE activity is correlated with muscle strength. Respiratory muscle function may be similarly influenced. Respiratory muscle strength in infants can be assessed specifically by measurement of the maximum inspiratory pressure during crying (Pi_max). Pressure-time index of the respiratory muscles (PTImus) is a non-invasive method, which assesses the load to capacity ratio of the respiratory muscles.</p> <p>The objective of this study was to determine whether increased cACE activity in infants could be related to greater respiratory muscle strength and to investigate the potential association of cACE with PTImus measurements as well as the association of ACE genotypes with cACE activity and respiratory muscle strength in this population.</p> <p>Methods</p> <p>Serum ACE activity was assayed by using a UV-kinetic method. ACE genotyping was performed by polymerase chain reaction amplification, using DNA from peripheral blood. PTImus was calculated as (Pi_mean/Pi_max) × (Ti/Ttot), where Pi_meanwas the mean inspiratory pressure estimated from airway pressure, generated 100 milliseconds after an occlusion (P_0.1), Pi_maxwas the maximum inspiratory pressure and Ti/Ttot was the ratio of the inspiratory time to the total respiratory cycle time. Pi_maxwas the largest pressure generated during brief airway occlusions performed at the end of a spontaneous crying effort.</p> <p>Results</p> <p>A hundred and ten infants were studied. Infants with D/D genotype had significantly higher serum ACE activity than infants with I/I or I/D genotypes. cACE activity was significantly related to Pi_maxand inversely related to PTImus. No association between ACE genotypes and Pdi_maxmeasurements was found.</p> <p>Conclusions</p> <p>These results suggest that a relation in cACE activity and respiratory muscle function may exist in infants. In addition, an association between ACE genotypes and cACE activity, but not respiratory muscle strength, was demonstrated.</p

Dust detection by the wave instrument on STEREO: nanoparticles picked up by the solar wind?

The STEREO/WAVES instrument has detected a very large number of intense voltage pulses. We suggest that these events are produced by impact ionisation of nanoparticles striking the spacecraft at a velocity of the order of magnitude of the solar wind speed. Nanoparticles, which are half-way between micron-sized dust and atomic ions, have such a large charge-to-mass ratio that the electric field induced by the solar wind magnetic field accelerates them very efficiently. Since the voltage produced by dust impacts increases very fast with speed, such nanoparticles produce signals as high as do much larger grains of smaller speeds. The flux of 10-nm radius grains inferred in this way is compatible with the interplanetary dust flux model. The present results may represent the first detection of fast nanoparticles in interplanetary space near Earth orbit.Comment: In press in Solar Physics, 13 pages, 5 figure

Using venous blood gas analysis in the assessment of COPD exacerbations: a prospective cohort study

Introduction: Identifying acute hypercapnic respiratory failure is crucial in the initial management of acute exacerbations of COPD. Guidelines recommend obtaining arterial blood samples but these are more difficult to obtain than venous. We assessed whether blood gas values derived from venous blood could replace arterial at initial assessment. Methods: Patients requiring hospital treatment for an exacerbation of COPD had paired arterial and venous samples taken. Bland–Altman analyses were performed to assess agreement between arterial and venous pH, CO2 and . The relationship between SpO2 and SaO2 was assessed. The number of attempts and pain scores for each sample were measured. Results: 234 patients were studied. There was good agreement between arterial and venous measures of pH and (mean difference 0.03 and −0.04, limits of agreement −0.05 to 0.11 and −2.90 to 2.82, respectively), and between SaO2 and SpO2 (in patients with an SpO2 of >80%). Arterial sampling required more attempts and was more painful than venous (mean pain score 4 (IQR 2–5) and 1 (IQR 0–2), respectively, p<0.001). Conclusions: Arterial sampling is more difficult and more painful than venous sampling. There is good agreement between pH and values derived from venous and arterial blood, and between pulse oximetry and arterial blood gas oxygen saturations. These agreements could allow the initial assessment of COPD exacerbations to be based on venous blood gas analysis and pulse oximetry, simplifying the care pathway and improving the patient experience

Biological effects of particles from the paris subway system

Particulate matter (PM) from atmospheric pollution can easily deposit in the lungs and induce recruitment of inflammatory cells, a source of inflammatory cytokines, oxidants, and matrix metalloproteases (MMPs), which are important players in lung structural homeostasis. In many large cities, the subway system is a potent source of PM emission, but little is known about the biological effects of PM from this source. We performed a comprehensive study to evaluate the biological effects of PM sampled at two sites (RER and Metro) in the Paris subway system. Murine macrophages (RAW 264.7) and C57Bl/6 mice, respectively, were exposed to 0.01-10 microg/cm2 and 5-100 microg/mouse subway PM or reference materials [carbon black (CB), titanium dioxide (TiO2), or diesel exhaust particles (DEPs)]. We analyzed cell viability, production of cellular and lung proinflammatory cytokines [tumor necrosis factor alpha (TNFalpha), macrophage inflammatory protein (MIP-2), KC (the murin analog of interleukin-8), and granulocyte macrophage-colony stimulating factor (GM-CSF)], and mRNA or protein expression of MMP-2, -9, and -12 and heme oxygenase-1 (HO-1). Deferoxamine and polymixin B were used to evaluate the roles of iron and endotoxin, respectively. Noncytotoxic concentrations of subway PM (but not CB, TiO2, or DEPs) induced a time- and dose-dependent increase in TNFalpha and MIP-2 production by RAW 264.7 cells, in a manner involving, at least in part, PM iron content (34% inhibition of TNF production 8 h after stimulation of RAW 264.7 cells with 10 microg/cm2 RER particles pretreated with deferoxamine). Similar increased cytokine production was transiently observed in vivo in mice and was accompanied by an increased neutrophil cellularity of bronchoalveolar lavage (84.83+/-0.98% of polymorphonuclear neutrophils for RER-treated mice after 24 h vs 7.33+/-0.99% for vehicle-treated animals). Subway PM induced an increased expression of MMP-12 and HO-1 both in vitro and in vivo. PM from the Paris subway system has transient biological effects. Further studies are needed to better understand the pathophysiological implications of these findings

Allergic rhinitis: evidence for impact on asthma

BACKGROUND: This paper reviews the current evidence indicating that comorbid allergic rhinitis may have clinically relevant effects on asthma. DISCUSSION: Allergic rhinitis is very common in patients with asthma, with a reported prevalence of up to 100% in those with allergic asthma. While the temporal relation of allergic rhinitis and asthma diagnoses can be variable, the diagnosis of allergic rhinitis often precedes that of asthma. Rhinitis is an independent risk factor for the subsequent development of asthma in both atopic and nonatopic individuals. Controlled studies have provided conflicting results regarding the benefits for asthma symptoms of treating comorbid allergic rhinitis with intranasal corticosteroids. Effects of other treatments for comorbid allergic rhinitis, including antihistamines, allergen immunotherapy, systemic anti-IgE therapy, and antileukotriene agents, have been examined in a limited number of studies; anti-IgE therapy and antileukotriene agents such as the leukotriene receptor antagonists have benefits for treating both allergic rhinitis and asthma. Results of observational studies indicate that treating comorbid allergic rhinitis results in a lowered risk of asthma-related hospitalizations and emergency visits. Results of several retrospective database studies in the United States and in Europe indicate that, for patients with asthma, the presence of comorbid allergic rhinitis is associated with higher total annual medical costs, greater prescribing frequency of asthma-related medications, as well as increased likelihood of asthma-related hospital admissions and emergency visits. There is therefore evidence suggesting that comorbid allergic rhinitis is a marker for more difficult to control asthma and worsened asthma outcomes. CONCLUSION: These findings highlight the potential for improving asthma outcomes by following a combined therapeutic approach to comorbid allergic rhinitis and asthma rather than targeting each condition separately