The triple system KR Com

Aims: We present the detailed analysis of triple system KR Com with different observational techniques - photometry, interferometry, and period variation. Methods: The use of BVR photometry of the close-contact binary KR Com, which is the primary component of a triple system, helps us to better describe the properties of the components. The interferometric data obtained during the last 30 years sufficiently determine the visual orbit, but the use of minima timings of KR Com for the study of period variation together with the visual orbit is a novel approach in this system. Results: Basic physical parameters resulting from the light curve analysis agree well with the previous results from spectroscopy. The temperatures for the primary and secondary component resulted in 5549 and 6072 K, respectively, and the amount of the third light in all filters is about 1/3 of the total luminosity. The distant third component revolves around the common barycenter on 11 yr orbit with a very high eccentricity (0.934) and this movement is also detectable via the period variation, which is clearly visible in the O-C diagram of times of minima observations. The use of minima times for the combined analysis helps us to independently determine the distance to the system (64.02 +/- 9.42 pc) and also to confirm the orientation of the orbit in space. Conclusions: New minima observations and also spectroscopy would be very profitable, especially during the next periastron passage in the year 2017.Comment: 7 pages, 7 figures, published in 2010A&A...519A..78

Collection of Minima of Eclipsing Binaries, part III.

We present CCD times of minima for selected eclipsing binaries, mainly parts of the multiple systems

The first study of 54 new eccentric eclipsing binaries in our Galaxy

We present an analysis of the apsidal motion and light curve parameters of 54 galactic Algol-type binaries never before studied. This is the first analysis of such a large sample of eccentric eclipsing binaries in our Galaxy, and has enabled us to identify several systems that are worthy of further study. Bringing together data from various databases and surveys, supplemented with new observations, we have been able to trace the long-term evolution of the eccentric orbit over durations extending back up to several decades. Our present study explores a rather different sample of stars to those presented in the previously published catalogue of eccentric eclipsing binaries by Bulut & Demircan (2007), sampling to fainter magnitudes, covering later spectral types, sensitive to different orbital periods with more than 50% of our systems having periods longer than 6 days. The typical apsidal motion in the sample is rather slow (mostly of order of centuries long), although in some cases this is less than 50 years. All of the systems, except one, have eccentricities less than 0.5, with an average value of 0.23. Several of the stars also show evidence for additional period variability. In particular we can identify three systems in the sample, HD 44093, V611 Pup, and HD 313631, which likely represent relativistic apsidal rotators

Circulating endothelial cell-derived extracellular vesicles mediate the acute phase response and sickness behaviour associated with CNS inflammation.

Brain injury elicits a systemic acute-phase response (APR), which is responsible for co-ordinating the peripheral immunological response to injury. To date, the mechanisms responsible for signalling the presence of injury or disease to selectively activate responses in distant organs were unclear. Circulating endogenous extracellular vesicles (EVs) are increased after brain injury and have the potential to carry targeted injury signals around the body. Here, we examined the potential of EVs, isolated from rats after focal inflammatory brain lesions using IL-1β, to activate a systemic APR in recipient naïve rats, as well as the behavioural consequences of EV transfer. Focal brain lesions increased EV release, and, following isolation and transfer, the EVs were sequestered by the liver where they initiated an APR. Transfer of blood-borne EVs from brain-injured animals was also enough to suppress exploratory behaviours in recipient naïve animals. EVs derived from brain endothelial cell cultures treated with IL-1β also activated an APR and altered behaviour in recipient animals. These experiments reveal that inflammation-induced circulating EVs derived from endothelial cells are able to initiate the APR to brain injury and are sufficient to generate the associated sickness behaviours, and are the first demonstration that EVs are capable of modifying behavioural responses

Expression and Differential Responsiveness of Central Nervous System Glial Cell Populations to the Acute Phase Protein Serum Amyloid A

Acute-phase response is a systemic reaction to environmental/inflammatory insults and involves hepatic production of acute-phase proteins, including serum amyloid A (SAA). Extrahepatically, SAA immunoreactivity is found in axonal myelin sheaths of cortex in Alzheimer's disease and multiple sclerosis (MS), although its cellular origin is unclear. We examined the responses of cultured rat cortical astrocytes, microglia and oligodendrocyte precursor cells (OPCs) to master pro-inflammatory cytokine tumour necrosis factor (TNF)-\u3b1 and lipopolysaccaride (LPS). TNF-\u3b1 time-dependently increased Saa1 (but not Saa3) mRNA expression in purified microglia, enriched astrocytes, and OPCs (as did LPS for microglia and astrocytes). Astrocytes depleted of microglia were markedly less responsive to TNF-\u3b1 and LPS, even after re-addition of microglia. Microglia and enriched astrocytes showed complementary Saa1 expression profiles following TNF-\u3b1 or LPS challenge, being higher in microglia with TNF-\u3b1 and higher in astrocytes with LPS. Recombinant human apo-SAA stimulated production of both inflammatory mediators and its own mRNA in microglia and enriched, but not microglia-depleted astrocytes. Co-ultramicronized palmitoylethanolamide/luteolin, an established anti-inflammatory/neuroprotective agent, reduced Saa1 expression in OPCs subjected to TNF-\u3b1 treatment. These last data, together with past findings suggest that co-ultramicronized palmitoylethanolamide/luteolin may be a novel approach in the treatment of inflammatory demyelinating disorders like MS

Serum amyloid A primes microglia for ATP-dependent interleukin-1\u3b2 release

Acute-phase response is a systemic reaction to environmental/inflammatory insults and involves production of acute-phase proteins, including serum amyloid A (SAA). Interleukin-1\u3b2 (IL-1\u3b2), a master regulator of neuroinflammation produced by activated inflammatory cells of the myeloid lineage, in particular microglia, plays a key role in the pathogenesis of acute and chronic diseases of the peripheral nervous system and CNS. IL-1\u3b2 release is promoted by ATP acting at the purinergic P2X7 receptor (P2X7R) in cells primed with toll-like receptor (TLR) ligands

Organization and Biology of the Porcine Serum Amyloid A (SAA) Gene Cluster: Isoform Specific Responses to Bacterial Infection.

Serum amyloid A (SAA) is a prominent acute phase protein. Although its biological functions are debated, the wide species distribution of highly homologous SAA proteins and their uniform behavior in response to injury or inflammation in itself suggests a significant role for this protein. The pig is increasingly being used as a model for the study of inflammatory reactions, yet only little is known about how specific SAA genes are regulated in the pig during acute phase responses and other responses induced by pro-inflammatory host mediators. We designed SAA gene specific primers and quantified the gene expression of porcine SAA1, SAA2, SAA3, and SAA4 by reverse transcriptase quantitative polymerase chain reaction (RT-qPCR) in liver, spleen, and lung tissue from pigs experimentally infected with the Gram-negative swine specific bacterium Actinobacillus pleuropneumoniae, as well as from pigs experimentally infected with the Gram-positive bacterium Staphylococcus aureus. Our results show that: 1) SAA1 may be a pseudogene in pigs; 2) we were able to detect two previously uncharacterized SAA transcripts, namely SAA2 and SAA4, of which the SAA2 transcript is primarily induced in the liver during acute infection and presumably contributes to circulating SAA in pigs; 3) Porcine SAA3 transcription is induced both hepatically and extrahepatically during acute infection, and may be correlated to local organ affection; 4) Hepatic transcription of SAA4 is markedly induced in pigs infected with A. pleuropneumoniae, but only weakly in pigs infected with S. aureus. These results for the first time establish the infection response patterns of the four porcine SAA genes which will be of importance for the use of the pig as a model for human inflammatory responses, e.g. within sepsis, cancer, and obesity research