266 research outputs found
Thoracoscopic lobectomy for lung cancer in a patient with a partial anomalous pulmonary venous connection: a case report
The dependence of protoplanet migration rates on coorbital torques
We investigate the migration rates of high-mass protoplanets embedded in
accretion discs via two and three-dimensional hydrodynamical simulations. The
simulations follow the planet's radial motion and employ a nested-grid code
that allows for high resolution close to the planet. We concentrate on the
possible role of the coorbital torques in affecting migration rates. We analyse
two cases: (a) a Jupiter-mass planet in a low-mass disc and (b) a Saturn-mass
planet in a high-mass disc. Planet migration in case (b) is much more
susceptible to coorbital torques than in case (a). We find that the coorbital
torques in both cases do not depend sensitively on whether the planet is
allowed to migrate through the disc or is held on a fixed orbit. We also
examine the dependence of the planet's migration rate on the numerical
resolution near the planet. For case (a), numerical convergence is relatively
easy to obtain, even when including torques arising from deep within the
planet's Hill sphere. The migration rate in this case is numerically on order
of the Type II migration rate and much smaller than the Type I rate, if the
disc has 0.01 solar-masses inside 26 AU. Torques from within the Hill sphere
provide a substantial opposing contribution to the migration rate. In case (b),
the gas mass within the Hill sphere is larger than the planet's mass and
convergence is more difficult to obtain. If the torques within the Hill sphere
are ignored, convergence is more easily achieved but the migration rate is
artificially large. At our highest resolution, the migration rate for case (b)
is much less than the Type I rate, but somewhat larger than the Type II rate.Comment: 20 pages, 17 figures, 3 tables. To appear in the Monthly Notices of
the Royal Astronomical Societ
Recent developments in planet migration theory
Planetary migration is the process by which a forming planet undergoes a
drift of its semi-major axis caused by the tidal interaction with its parent
protoplanetary disc. One of the key quantities to assess the migration of
embedded planets is the tidal torque between the disc and planet, which has two
components: the Lindblad torque and the corotation torque. We review the latest
results on both torque components for planets on circular orbits, with a
special emphasis on the various processes that give rise to additional, large
components of the corotation torque, and those contributing to the saturation
of this torque. These additional components of the corotation torque could help
address the shortcomings that have recently been exposed by models of planet
population syntheses. We also review recent results concerning the migration of
giant planets that carve gaps in the disc (type II migration) and the migration
of sub-giant planets that open partial gaps in massive discs (type III
migration).Comment: 52 pages, 18 figures. Review article to be published in "Tidal
effects in Astronomy and Astrophysics", Lecture Notes in Physic
Longitudinal association of C-reactive protein and Haemoglobin A1c over 13Β years: the European Prospective Investigation into Cancer - Norfolk study
Gastric outlet obstruction secondary to solid-pseudopapillary neoplasm of the pancreas in an eight year old child. Report of a case
Deciphering von Hippel-Lindau (VHL/Vhl)-Associated Pancreatic Manifestations by Inactivating Vhl in Specific Pancreatic Cell Populations
The von Hippel-Lindau (VHL) syndrome is a pleomorphic familial disease characterized by the development of highly vascularized tumors, such as hemangioblastomas of the central nervous system, pheochromocytomas, renal cell carcinomas, cysts and neuroendocrine tumors of the pancreas. Up to 75% of VHL patients are affected by VHL-associated pancreatic lesions; however, very few reports in the published literature have described the cellular origins and biological roles of VHL in the pancreas. Since homozygous loss of Vhl in mice resulted in embryonic lethality, this study aimed to characterize the functional significance of VHL in the pancreas by conditionally inactivating Vhl utilizing the Cre/LoxP system. Specifically, Vhl was inactivated in different pancreatic cell populations distinguished by their roles during embryonic organ development and their endocrine lineage commitment. With Cre recombinase expression directed by a glucagon promoter in Ξ±-cells or an insulin promoter in Ξ²-cells, we showed that deletion of Vhl is dispensable for normal functions of the endocrine pancreas. In addition, deficiency of VHL protein (pVHL) in terminally differentiated Ξ±-cells or Ξ²-cells is insufficient to induce pancreatic neuroendocrine tumorigenesis. Most significantly, we presented the first mouse model of VHL-associated pancreatic disease in mice lacking pVHL utilizing Pdx1-Cre transgenic mice to inactivate Vhl in pancreatic progenitor cells. The highly vascularized microcystic adenomas and hyperplastic islets that developed in Pdx1-Cre;Vhl f/f homozygous mice exhibited clinical features similar to VHL patients. Establishment of three different, cell-specific Vhl knockouts in the pancreas have allowed us to provide evidence suggesting that VHL is functionally important for postnatal ductal and exocrine pancreas, and that VHL-associated pancreatic lesions are likely to originate from progenitor cells, not mature endocrine cells. The novel model systems reported here will provide the basis for further functional and genetic studies to define molecular mechanisms involved in VHL-associated pancreatic diseases
Anti-inflammatory recombinant TSG-6 stabilizes the progression of focal retinal degeneration in a murine model
<p>Abstract</p> <p>Background</p> <p>Inflammatory responses are detected in the retina of patients with age-related macular degeneration and <it>Ccl2<sup>-/-</sup>/Cx3cr1<sup>-/- </sup></it>mice on rd8 background,(<it>Ccl2<sup>-/-</sup>/Cx3cr1<sup>-/- </sup></it>mice) a model that develops progressive age-related macular degeneration-like retinal lesions including focal photoreceptor degeneration, abnormal retinal pigment epithelium and A2E accumulation. Tumor necrosis factor-inducible gene 6 protein is an anti-inflammatory protein and has been shown to improve myocardial infarction outcome and chemically injured cornea in mice by suppressing inflammation. In this study, we evaluated the effect of an intravitreous injection of recombinant TSG-6 on the retinal lesions of <it>Ccl2<sup>-/-</sup>/Cx3cr1<sup>-/- </sup></it>mice.</p> <p>Methods</p> <p>Recombinant TSG-6 (400 ng) was administered by intravitreous injection into the right eye of six-week-old C<it>cl2<sup>-/-</sup>/Cx3cr1<sup>-/- </sup></it>mice. Their left eye was injected with phosphate-buffered saline as a control. Funduscopic pictures were taken before injection and sequentially once a month after injection. The mice were killed two months after injection and the ocular histology examined. Retinal A2E, a major component of lipofuscin, was measured by high performance liquid chromatography. The microarray of ocular mRNA of 92 immunological genes was performed. The genes showing differentiated expression in microarray were further compared between the injected right eye and the contralateral (control) eye by [real-time quantitative reverse transcription polymerase chain reaction] qRT-PCR.</p> <p>Results</p> <p>The continuous monitoring of the fundus for two months showed a slower progression or alleviation of retinal lesions in the treated right eyes as compared with the untreated left eyes. Among 23 pairs of eyes, the lesion levels improved in 78.3%, stayed the same in 8.7% and progressed in 13.0%. Histology confirmed the clinical observation. Even though there was no difference in the level of A2E between the treated and the untreated eyes, microarray analysis of 92 immune genes showed that <it>IL-17a </it>was substantially decreased after the treatment. Expression of <it>TNF-Ξ± </it>showed a similar pattern to <it>IL-17a</it>. The results were consistent in duplicated arrays and confirmed by qRT-PCR.</p> <p>Conclusions</p> <p>We concluded that intravitreous administration of recombinant TSG-6 might stabilize retinal lesions in <it>Ccl2<sup>-/-</sup>/Cx3cr1<sup>-/- </sup></it>mice on rd8 background. Modulation of ocular immunological gene expressions, especially IL-17a, could be one of the mechanisms.</p
Genome Sequence of the Versatile Fish Pathogen Edwardsiella tarda Provides Insights into its Adaptation to Broad Host Ranges and Intracellular Niches
BACKGROUND:Edwardsiella tarda is the etiologic agent of edwardsiellosis, a devastating fish disease prevailing in worldwide aquaculture industries. Here we describe the complete genome of E. tarda, EIB202, a highly virulent and multi-drug resistant isolate in China. METHODOLOGY/PRINCIPAL FINDINGS:E. tarda EIB202 possesses a single chromosome of 3,760,463 base pairs containing 3,486 predicted protein coding sequences, 8 ribosomal rRNA operons, and 95 tRNA genes, and a 43,703 bp conjugative plasmid harboring multi-drug resistant determinants and encoding type IV A secretion system components. We identified a full spectrum of genetic properties related to its genome plasticity such as repeated sequences, insertion sequences, phage-like proteins, integrases, recombinases and genomic islands. In addition, analysis also indicated that a substantial proportion of the E. tarda genome might be devoted to the growth and survival under diverse conditions including intracellular niches, with a large number of aerobic or anaerobic respiration-associated proteins, signal transduction proteins as well as proteins involved in various stress adaptations. A pool of genes for secretion systems, pili formation, nonfimbrial adhesions, invasions and hemagglutinins, chondroitinases, hemolysins, iron scavenging systems as well as the incomplete flagellar biogenesis might feature its surface structures and pathogenesis in a fish body. CONCLUSION/SIGNIFICANCE:Genomic analysis of the bacterium offered insights into the phylogeny, metabolism, drug-resistance, stress adaptation, and virulence characteristics of this versatile pathogen, which constitutes an important first step in understanding the pathogenesis of E. tarda to facilitate construction of a practical effective vaccine used for combating fish edwardsiellosis
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