Hot super-Earths stripped by their host stars.

Simulations predict that hot super-Earth sized exoplanets can have their envelopes stripped by photoevaporation, which would present itself as a lack of these exoplanets. However, this absence in the exoplanet population has escaped a firm detection. Here we demonstrate, using asteroseismology on a sample of exoplanets and exoplanet candidates observed during the Kepler mission that, while there is an abundance of super-Earth sized exoplanets with low incident fluxes, none are found with high incident fluxes. We do not find any exoplanets with radii between 2.2 and 3.8 Earth radii with incident flux above 650 times the incident flux on Earth. This gap in the population of exoplanets is explained by evaporation of volatile elements and thus supports the predictions. The confirmation of a hot-super-Earth desert caused by evaporation will add an important constraint on simulations of planetary systems, since they must be able to reproduce the dearth of close-in super-Earths.

Kepler detected gravity-mode period spacings in a red giant star.

Stellar interiors are inaccessible through direct observations. For this reason, helioseismologists made use of the Sun's acoustic oscillation modes to tune models of its structure. The quest to detect modes that probe the solar core has been ongoing for decades. We report the detection of mixed modes penetrating all the way to the core of an evolved star from 320 days of observations with the Kepler satellite. The period spacings of these mixed modes are directly dependent on the density gradient between the core region and the convective envelope.

Th17 cytokines interleukin (IL)-17 and IL-22 modulate distinct inflammatory and keratinocyte-response pathways.

BACKGROUND: Psoriasis vulgaris is an inflammatory skin disease mediated by Th1 and Th17 cytokines, yet the relative contribution of interferon (IFN)-gamma, interleukin (IL)-17 and IL-22 on disease pathogenesis is still unknown. OBJECTIVES: In this study, we sought to identify the cytokines produced by skin-resident T cells in normal skin, localize the receptors for these cytokines, and examine how these cytokines alter gene expression profiles of the cells bearing cognate receptors. METHODS: We used intracellular cytokine staining and flow cytometry to evaluate T cell cytokine production, and immunohistochemistry and double-label immunofluorescence to localize cytokine receptors in skin. Gene array analysis of cytokine-treated keratinocytes was performed using moderated paired t-test controlling for false discovery rate using the Benjamini-Hochberg procedure. RESULTS: We demonstrate that T-helper cells producing IL-17, IL-22 and/or IFN-gamma, as well as the cells bearing cognate cytokine receptors, are present in normal human skin. Keratinocytes stimulated with IL-17 expressed chemokines that were different from those induced by IFN-gamma, probably contributing to the influx of neutrophils, dendritic cells and memory T cells into the psoriatic lesion. In contrast, IL-22 downregulated genes associated with keratinocyte differentiation and caused epidermal alterations in an organotypic skin model. CONCLUSIONS: Our results suggest that the Th17 cytokines IL-17 and IL-22 mediate distinct downstream pathways that contribute to the psoriatic phenotype: IL-17 is more proinflammatory, while IL-22 retards keratinocyte differentiation.

Correlations between serotonin level and single-cell firing in the rat's nucleus raphe magnus.

The relation between serotonin release and electrical activity was examined in the nucleus raphe magnus of rats anesthetized with pentobarbital. Serotonin levels were monitored through a carbon-fiber microelectrode by fast cyclic voltammetry (usually at 1 Hz). Single-cell firing was recorded through the same microelectrode, except during the voltammetry waveform and associated electrical artifact (totaling about 30 ms). Multi-barrel micropipettes incorporating the voltammetry electrode were used for iontophoresis of drugs. Cells were inhibited, excited or unaffected by noxious mechanical skin stimulation. These were respectively designated as off(M) cells, on(M) cells and neutral(M) cells, M denoting mechanical. During 3 min of pinching, serotonin slowly rose near seven of 14 on(M) cells and 26 of 46 off(M) cells; it fell near two off(M) cells; it was unchanged near all other cells, including six neutral(M) cells. On a finer spatiotemporal scale, near four of seven on(M) cells, 10 of 14 off(M) cells and 0 of four neutral(M) cells, average serotonin levels fell significantly within +/- 100 ms of spontaneous spikes. Lower serotonin may have caused the higher spike probability; the converse is theoretically unlikely, since delays between release and detection are estimated to exceed 100 ms. Increased serotonin and decreased firing were always seen following iontophoresis or intravenous injection (1 mg/kg) of the serotonin re-uptake inhibitor clomipramine (n = 7). Iontophoresis of +/- propranolol, whose serotonergic actions include antagonism and partial agonism at 5-HT1 receptors, also increased serotonin and decreased firing (n=4). Methiothepin (intravenous, 1 mg/kg), whose serotonergic actions include 5-HT1 and 5-HT2 antagonism, typically raised serotonin levels (four of five cells) and always blocked inhibition by clomipramine (n = 3). Iontophoresis of glutamate always lowered serotonin and increased firing (n = 4). Since serotonin levels and firing were usually inversely correlated, except near on(M) cells during pinch, we propose that serotonin is released from terminals of incoming nociceptive afferents. Prior neuroanatomical knowledge favors a midbrain origin for these afferents, while some of the drug findings suggest that their terminals possess inhibitory serotonergic autoreceptors, possibly of 5-HT1b subtype. The released serotonin could contribute to the inhibition of off(M) cells and excitation of on(M) cells by noxious stimulation, since inhibitory 5-HT1a receptors and excitatory 5-HT2 receptors, respectively, have previously been shown to dominate their serotonergic responses.

Frequency, causes, and outcome of home ventilator failure.

STUDY OBJECTIVES: The safety of home ventilators has been questioned. We collected data to study the following: frequency of home ventilator failure, apparent causes for the failure or malfunction, and adverse consequences following the failure. STUDY DESIGN: Information on all requests to correct home ventilator failures reported to a home respiratory equipment vendor was collected prospectively between November 1991, and November 1992. PATIENTS: There were 150 ventilator-assisted patients aged 2 to 77 years; 44 were < or = 18 years. They received 841,234 h of home mechanical ventilation (average, 15.4 h/d per ventilator-assisted patient). RESULTS: There were 189 reports of home ventilator failure. Defective equipment or mechanical failure was found in only 39% (73 reports), equivalent to one home ventilator failure for every 1.25 years of continuous use. Other causes of ventilator failure included the following: improper care, damage, or tampering with the ventilator by caregivers (13%), functional equipment improperly used by caregivers (30%), and equipment functional but the patient's condition changed, mimicking ventilator failure (3%). No problem could be identified in 16%. The following actions were required: ventilator replacement (44%), repair of a defective part (6%), replacement of a functioning ventilator for psychological comfort (14%), ventilator adjustments made (21%), caregiver reeducation (7%), caregiver anxiety or distress reduced (3%), and no action required (4%). Hospitalization was required only in two cases (1%). No adverse outcomes, deaths, or serious injuries were associated with home ventilator failure. CONCLUSIONS: We conclude that in 150 patients requiring home mechanical ventilation, ventilator failure occurred relatively infrequently, and there were no adverse outcomes as a result of equipment failure at home. We speculate that equipment failure is not a frequent or serious problem for ventilator-assisted patients treated at home.

Evidence for rhythmic firing being caused by feedback inhibition in pinch-inhibited raphe magnus neurons.

Raphe magnus cells that are inhibited by skin pinching fire spontaneously with strongly preferred interspike intervals (mean cycle 85 ms, n = 33). In pentobarbital-anesthetized rats, mid-cycle cathodal activation (0.3 ms) or end-cycle anodal black (30-60 ms) at approximately 1 Hz through the extracellular recording microelectrode delayed expected spikes; respective post-stimulus latencies peaked on average at 1.17 (n = 14) and 0.40 (n = 6) cycles. Feedback inhibition following random excitation, but not free-running intrinsic or afferent oscillations, may therefore cause the rhythm.

A double-blind placebo-controlled study of thymostimulin (TP-1) for the treatment of atopic eczema.

Twenty-nine patients with severe atopic eczema were entered into a randomized double-blind, placebo-controlled trial of the polypeptide thymus extract, thymostimulin (TP-1). The treatment period was 10 weeks with a subsequent follow-up period of up to 1 year. Of the 18 patients receiving TP-1 and the 11 patients on the placebo, 15 and 11 patients, respectively, were fully evaluable. There was no significant difference in either clinical or immunological status between the two treatment groups at baseline. At the 3-month follow-up clinic visit there was a statistically significant difference in the total clinical score, calculated as a percentage of baseline, in favour of the TP-1-treated patients. This difference was not maintained in the subsequent follow-up period and was not accompanied by an improvement in the patient's subjective well-being. There was no significant difference between the treatment groups with respect to the immunological parameters as measured at the 3-month clinic visit.

Effects of alcohol on pilot performance in simulated flight.

Ethyl alcohol's known ability to produce reliable decrements in pilot performance was used in a study designed to evaluate objective methods for assessing pilot performance. Four air carrier pilot volunteers were studied during eight simulated flights between San Francisco and Los Angeles in a Boeing 727-232 simulator. Two flights were conducted at each of four target blood alcohol levels, 0, 0.025, 0.050, and 0.075%. Each flight lasted about 1 h. Flights were conducted with full crews in a full simulated ATC environment. Data from direct observations and videotapes were used to examine discrete errors committed by the subjects. Total errors increased linearly and significantly with increasing blood alcohol. Planning and performance errors, procedural errors and failures of vigilance each increased significantly in one or more pilots and in the group as a whole. Failures of crew coordination were not associated with blood alcohol level. Serious errors increased significantly even at the lowest alcohol level studied, 0.025% (25 mg/dl), compared with control values.

The effect of lentinan on the resistance of mice to Mesocestoides corti.

CBA/H mice were given the immunomodulator lentinan in multiple, ascending doses before (prophylactic) or after (therapeutic) inoculation with tetrathyridia of Mesocestoides corti or as a single prophylactic dose. The latter was without effect, but increasing multiple prophylactic and therapeutic doses of lentinan resulted in a marked reduction in the numbers of parasites in the peritoneal cavity, particularly in those mice that received lentinan therapeutically. In mice that received multiple doses of lentinan, liver granulomas were larger than in controls and there was more collagen deposition and fibrosis. Encapsulated parasites were dead or dying, and such damage appeared to be mediated by increased numbers of macrophages and giant cells.

Characterization of a monoclonal antibody (SBU-1) made to the thymic rudiment of sheep.

A monoclonal antibody (SBU-1) was raised to sheep thymic rudiment by fusion of NSI myeloma cells with spleen cells from BALB/c mice immunized with thymic rudiment isolated from fetal sheep between 25-30 days of gestation. By employing the indirect immunoperoxidase technique the antigen recognized by SBU-1 was found to be present in the epithelial reticular cells of the fetal sheep thymus. The intensity of staining decreased as gestation progressed. In the adult thymus the antigen was mainly restricted to Hassall's corpuscles and occasional epithelial cells in the medulla. In addition, the antigen was also shown to be present in epithelial cells of the small intestine, the bronchiole, the keratinized epithelium of the rumen, and the epithelial cells of the kidney tubules. By use of immunofluorescence the antigen was shown to be present in most of the cells of wool follicles and the cortex of developing wool fibers. Western blotting of SBU-1 against the low-sulfur alpha-keratin proteins of wool confirmed that the antigen recognized by SBU-1 belongs to a family of keratins. It was concluded that SBU-1 was raised against alpha-keratin expressed by the epithelial cells of the thymic rudiment and that the expression of this antigen on the reticular network of the thymus declined with advancement of pregnancy.

Studies on the distribution of binucleate cells in the placenta of the sheep with a monoclonal antibody SBU-3.

The distribution of cells recognised by the monoclonal antibody SBU-3 raised against trophoblast microvilli during development of the sheep placenta was investigated using the indirect immunoperoxidase technique. At 21 days of gestation, the placental antigen recognised by the monoclonal antibody SBU-3 was observed in the binucleate cells in the trophoblast located in close apposition to the caruncular epithelium. From 30-100 days there was a dramatic increase in the number of SBU-3-positive cells in the placentomal trophoblast and the syncytial layer in the placentome. An insignificant number of SBU-3-positive cells was observed in the interplacentomal trophoblast. By 120-145 days, the syncytial layer became less intensely stained, but strongly SBU-3-positive binucleate cells were still present in the placentomal trophoblast. It is concluded that the antigen recognised by the monoclonal antibody SBU-3 is a secretory product of the binucleate cells of the trophoblast, whose function is at present unknown. The findings in this study are consistent with the theory that the syncytium is formed by fusion of migrating fetal binucleate cells.

Factors influencing the establishment of Mesocestoides corti in mice following oral inoculation of tetrathyridia.

Factors which influence the establishment of tetrathyridia of Mesocestoides corti in mice following inoculation per os were examined. Only a proportion of the tetrathyridia penetrate the gut wall and gain access to the peritoneal cavity and liver, and most of these penetrate through the wall of the small intestine. It appears that tetrathyridia must attach to the intestinal mucosa and commence penetration immediately or they pass into the large intestine and are voided. Establishment was not influenced by strain, sex or age of host. However, the temperature at which tetrathyridia were maintained before inoculation influence their ability to penetrate the intestinal wall. Additionally it appears that tetrathyridia have to undergo a morphological change before or during, this penetration phase.

The effects of selective immunosuppression on resistance to Mesocestoides corti in strains of mice showing high and low initial susceptibility.

Previous work has shown that C57BL/6 mice had the lowest initial susceptibility to Mesocestoides corti of six strains of mice examined. Parasite burdens in this strain and in CBA/H mice, a strain showing a higher initial susceptibility to M. corti, were compared following selective immunosuppressive treatments. Irradiation, splenectomy and the administration of cyclophosphamide and methyl prednisolone all resulted in higher parasite burdens in C57BL/6 mice. In contrast these treatments had a minimal effect on parasite burdens in CBA/H mice. In the light of these results the role of antibody in controlling parasite proliferation is discussed.

Pathophysiology of Mesocestoides corti infection in the mouse.

Liver histology and serum enzyme and protein changes were studies in two strains of mice showing different initial susceptibilities to infection with Mesocestoides corti. The results show an increase in ALT and AST levels during the period of invasion and proliferation in the liver and a decrease in the levels of these two enzymes following encapsulation of the parasite in the liver and liver regeneration. A progressive loss of albumin was accompanied by increases in the levels of the beta- and gamma-globulins. These changes are discussed in the light of our knowledge of the effects of this parasite upon its host.

BCG-induced inhibition and destruction of Taenia taeniaeformis in mice.

Pretreatment of mice with BCG induced a high level of protection against infection with Taenia taeniaeformis. Protection was manifested both during and after establishment by the parasite suggesting that two separate mechanisms were stimulated by BCG. The first inhibits initial establishment by the parasite and may be antibody mediated. The second is responsible for the destruction of developing strobilocerci in the liver and may require the involvement of cellular defence mechanisms.