88 research outputs found
The K giant star Arcturus: the hybrid nature of its infrared spectrum
We study infrared spectrum of Arcturus to clarify the nature of the cool
component of its atmosphere, referred to as the CO-mosphere, with the use of
the IR spectral atlas by Hinkle et al.(1995). The nature of CO lines shows an
abrupt change at logW/nu = -4.75, and the lines stronger than this limit can no
longer be analyzed by the classical line-formation theory. A more simple
manifestation of this fact is that the curves-of-growth (CG) of CO lines show
an unpredictable upturn at logW/nu = -4.75. Similar unusual behaviors of
empirical CG are confirmed in other red (super)giant stars, and it looks as if
the CG is a hybrid of at least two components of different origins. Although
strong lines of the CO fundamentals observed in Arcturus show strengthening
compared with the predicted photospheric spectrum, the weaker lines show slight
weakening, and we interpret these results as due to absorption/emission by the
molecular clouds formed in the extended atmosphere. Now do clouds exist in
stellar atmospheres? It is by no means easy to answer this question by
spectroscopic observations alone, but we find several arguments in favor of
such a possibility in Arcturus by analyzing the CO lines. In cooler
(super)giant stars in which CO lines show similar unusual behaviors as in
Arcturus, the presence of molecular clouds in the outer atmospheres was
demonstrated by direct observations with spatial interferometry. We suggest
that the formation of molecular clouds is a general feature in cool luminous
stars from early K to late M (super)giant stars.Comment: 18 pages, 15 Postscript figures, 1 Table in electronic form, Accepted
for publication in Astronomy and Astrophysic
An ultraviolet-optical flare from the tidal disruption of a helium-rich stellar core
The flare of radiation from the tidal disruption and accretion of a star can
be used as a marker for supermassive black holes that otherwise lie dormant and
undetected in the centres of distant galaxies. Previous candidate flares have
had declining light curves in good agreement with expectations, but with poor
constraints on the time of disruption and the type of star disrupted, because
the rising emission was not observed. Recently, two `relativistic' candidate
tidal disruption events were discovered, each of whose extreme X-ray luminosity
and synchrotron radio emission were interpreted as the onset of emission from a
relativistic jet. Here we report the discovery of a luminous
ultraviolet-optical flare from the nuclear region of an inactive galaxy at a
redshift of 0.1696. The observed continuum is cooler than expected for a simple
accreting debris disk, but the well-sampled rise and decline of its light curve
follows the predicted mass accretion rate, and can be modelled to determine the
time of disruption to an accuracy of two days. The black hole has a mass of
about 2 million solar masses, modulo a factor dependent on the mass and radius
of the star disrupted. On the basis of the spectroscopic signature of ionized
helium from the unbound debris, we determine that the disrupted star was a
helium-rich stellar core.Comment: To appear in Nature on May 10, 201
Regular use of aspirin and pancreatic cancer risk
BACKGROUND: Regular use of aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs) has been consistently associated with reduced risk of colorectal cancer and adenoma, and there is some evidence for a protective effect for other types of cancer. As experimental studies reveal a possible role for NSAIDs is reducing the risk of pancreatic cancer, epidemiological studies examining similar associations in human populations become more important. METHODS: In this hospital-based case-control study, 194 patients with pancreatic cancer were compared to 582 age and sex-matched patients with non-neoplastic conditions to examine the association between aspirin use and risk of pancreatic cancer. All participants received medical services at the Roswell Park Cancer Institute in Buffalo, NY and completed a comprehensive epidemiologic questionnaire that included information on demographics, lifestyle factors and medical history as well as frequency and duration of aspirin use. Patients using at least one tablet per week for at least six months were classified as regular aspirin users. Unconditional logistic regression was used to compute crude and adjusted odds ratios (ORs) with 95% confidence intervals (CIs). RESULTS: Pancreatic cancer risk in aspirin users was not changed relative to non-users (adjusted OR = 1.00; 95% CI 0.72–1.39). No significant change in risk was found in relation to greater frequency or prolonged duration of use, in the total sample or in either gender. CONCLUSIONS: These data suggest that regular aspirin use may not be associated with lower risk of pancreatic cancer
Galanin and galanin receptor expression in neuroblastic tumours: correlation with their differentiation status
Neuroblastoma and its benign differentiated counterpart, ganglioneuroma, are paediatric neuroblastic tumours arising in the sympathetic nervous system. Their broad spectrum of clinical virulence is mainly related to heterogeneous biologic background and tumour differentiation. Neuroblastic tumours synthesize various neuropeptides acting as neuromodulators. Previous studies suggested that galanin plays a role in sympathetic tissue where it could be involved in differentiation and development. We investigated the expression and distribution of galanin and its three known receptors (Gal-R1, Gal-R2, Gal-R3) in 19 samples of neuroblastic tumours tissue by immunohistochemistry, in situ hybridization and fluorescent-ligand binding. This study provides clear evidence for galanin and galanin receptor expression in human neuroblastic tumours. The messengers coding for galanin, Gal-R1 and -R3 were highly expressed in neuroblastoma and their amount dramatically decreased in ganglioneuroma. In contrast, Gal-R2 levels remained unchanged. Double labelling studies showed that galanin was mainly co-expressed with its receptors whatever the differentiation stage. In neuroblastic tumours, galanin might promote cell-survival or counteract neuronal differentiation through the different signalling pathways mediated by galanin receptors. Finally, our results suggest that galanin influences neuroblastoma growth and development as an autocrine/paracrine modulator. These findings suggest potential critical implications for galanin in neuroblastic tumours development
Activation of PPARγ in Myeloid Cells Promotes Lung Cancer Progression and Metastasis
Activation of peroxisome proliferator-activated receptor-γ (PPARγ) inhibits growth of cancer cells including non-small cell lung cancer (NSCLC). Clinically, use of thiazolidinediones, which are pharmacological activators of PPARγ is associated with a lower risk of developing lung cancer. However, the role of this pathway in lung cancer metastasis has not been examined well. The systemic effect of pioglitazone was examined in two models of lung cancer metastasis in immune-competent mice. In an orthotopic model, murine lung cancer cells implanted into the lungs of syngeneic mice metastasized to the liver and brain. As a second model, cancer cells injected subcutaneously metastasized to the lung. In both models systemic administration of pioglitazone increased the rate of metastasis. Examination of tissues from the orthotopic model demonstrated increased numbers of arginase I-positive macrophages in tumors from pioglitazone-treated animals. In co-culture experiments of cancer cells with bone marrow-derived macrophages, pioglitazone promoted arginase I expression in macrophages and this was dependent on the expression of PPARγ in the macrophages. To assess the contribution of PPARγ in macrophages to cancer progression, experiments were performed in bone marrow-transplanted animals receiving bone marrow from Lys-M-Cre+/PPARγflox/flox mice, in which PPARγ is deleted specifically in myeloid cells (PPARγ-Macneg), or control PPARγflox/flox mice. In both models, mice receiving PPARγ-Macneg bone marrow had a marked decrease in secondary tumors which was not significantly altered by treatment with pioglitazone. This was associated with decreased numbers of arginase I-positive cells in the lung. These data support a model in which activation of PPARγ may have opposing effects on tumor progression, with anti-tumorigenic effects on cancer cells, but pro-tumorigenic effects on cells of the microenvironment, specifically myeloid cells
Identification of a potent herbal molecule for the treatment of breast cancer
<p>Abstract</p> <p>Background</p> <p>Breast cancer (BCa)-related mortality still remains the second leading cause of cancer-related deaths worldwide. Patients with BCa have increasingly shown resistance and high toxicity to current chemotherapeutic drugs for which identification of novel targeted therapies are required.</p> <p>Methods</p> <p>To determine the effect of PDBD on BCa cells, estrogen-receptor positive (ER<sup>+</sup>)-MCF-7 and estrogen-receptor negative (ER<sup>-</sup>)-MDA 231 cells were treated with PDBD and the cell viability, apoptotic, cell cycle, Western blot and Promoter assays were performed.</p> <p>Results</p> <p>PDBD inhibits cell viability of ER<sup>+ </sup>and ER<sup>- </sup>BCa cells by inducing apoptosis without causing significant toxicity in normal breast epithelial cells. While dissecting the mechanism of action of PDBD on BCa, we found that PDBD inhibits Akt signaling and its downstream targets such as NF-κB activation, IAP proteins and Bcl-2 expression. On the other hand, activation of JNK/p38 MAPK-mediated pro-apoptotic signaling was observed in both ER<sup>+ </sup>and ER<sup>- </sup>BCa cells.</p> <p>Conclusion</p> <p>These findings suggest that PDBD may have wide therapeutic application in the treatment of BCa.</p
Regulator of G-Protein Signaling 14 (RGS14) Is a Selective H-Ras Effector
Background: Regulator of G-protein signaling (RGS) proteins have been well-described as accelerators of Ga-mediated GTP hydrolysis (‘‘GTPase-accelerating proteins’’ or GAPs). However, RGS proteins with complex domain architectures are now known to regulate much more than Ga GTPase activity. RGS14 contains tandem Ras-binding domains that have been reported to bind to Rap- but not Ras GTPases in vitro, leading to the suggestion that RGS14 is a Rap-specific effector. However, more recent data from mammals and Drosophila imply that, in vivo, RGS14 may instead be an effector of Ras.Methodology/Principal Findings: Full-length and truncated forms of purified RGS14 protein were found to bind indiscriminately in vitro to both Rap- and Ras-family GTPases, consistent with prior literature reports. In stark contrast, however, we found that in a cellular context RGS14 selectively binds to activated H-Ras and not to Rap isoforms. Co- transfection / co-immunoprecipitation experiments demonstrated the ability of full-length RGS14 to assemble a multiprotein complex with components of the ERK MAPK pathway in a manner dependent on activated H-Ras. Small interfering RNA-mediated knockdown of RGS14 inhibited both nerve growth factor- and basic fibrobast growth factor- mediated neuronal differentiation of PC12 cells, a process which is known to be dependent on Ras-ERK signaling.Conclusions/Significance: In cells, RGS14 facilitates the formation of a selective Ras?GTP-Raf-MEK-ERK multiprotein complex to promote sustained ERK activation and regulate H-Ras-dependent neuritogenesis. This cellular function for RGS14 is similar but distinct from that recently described for its closely-related paralogue, RGS12, which shares the tandem Ras- binding domain architecture with RGS14
A functional sgRNA-CRISPR screening method for generating murine RET and NTRK1 rearranged oncogenes
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