COSMOSOMAS Observations of the CMB and Galactic Foregrounds at 11 GHz: Evidence for anomalous microwave emission at high Galactic Latitude

We present observations with the new 11 GHz radiometer of the COSMOSOMAS experiment at the Teide Observatory (Tenerife). The sky region between 0 deg <= RA <= 360 deg and 26 deg <= DEC 49 deg (ca. 6500 square degrees) was observed with an angular resolution of 0.9 deg. Two orthogonal independent channels in the receiving system measured total power signals from linear polarizations with a 2 GHz bandwidth. Maps with an average sensitivity of 50 microK per beam have been obtained for each channel. At high Galactic latitude (|b|>30deg) the 11 GHz data are found to contain the expected cosmic microwave background as well as extragalactic radiosources, galactic synchrotron and free-free emission, and a dust-correlated component which is very likely of galactic origin. At the angular scales allowed by the window function of the experiment, the dust-correlated component presents an amplitude \Delta T aprox. 9-13 microK while the CMB signal is of order 27 microK. The spectral behaviour of the dust-correlated signal is examined in the light of previous COSMOSOMAS data at 13-17 GHz and WMAP data at 22-94 GHz in the same sky region. We detect a flattening in the spectral index of this signal below 20 GHz which rules out synchrotron radiation as being responsible for the emission. This anomalous dust emission can be described by a combination of free-free emission and spinning dust models with a flux density peaking around 20 GHz.Comment: 17 pages, 10 tables, 20 figures. Details on the COSMOSOMAS experiment can be found at http://www.iac.es/project/cmb/cosmosomas

CMB observations with the Jodrell Bank - IAC interferometer at 33 GHz

The paper presents the first results obtained with the Jodrell Bank - IAC two-element 33 GHz interferometer. The instrument was designed to measure the level of the Cosmic Microwave Background (CMB) fluctuations at angular scales of 1 - 2 degrees. The observations analyzed here were taken in a strip of the sky at Dec = +41 deg with an element separation of 16.7 lambda, which gives a maximum sensitivity to ~1.6 deg structures on the sky. The data processing and calibration of the instrument are described. The sensitivity achieved in each of the two channels is 7 micro K per resolution element. A reconstruction of the sky at Dec = +41 deg using a maximum entropy method shows the presence of structure at a high level of significance. A likelihood analysis, assuming a flat CMB spatial power spectrum, gives a best estimate of the level of CMB fluctuations of Delta Tl = 43 (+13,-12) micro K for the range l = 109 +/- 19; the main uncertainty in this result arises from sample variance. We consider that the contamination from the Galaxy is small. These results represent a new determination of the CMB power spectrum on angular scales where previous results show a large scatter; our new results are in agreement with the theoretical predictions of the standard inflationary cold dark matter models.Comment: 11 pages, 11 figures. Web site at http://www.jb.man.ac.uk/research/cmb/ Accepted for publication in MNRA

Catabolic cytokine expression in degenerate and herniated human intervertebral discs: IL-1β and TNFα expression profile

Low back pain is a common and debilitating disorder. Current evidence implicates intervertebral disc (IVD) degeneration and herniation as major causes, although the pathogenesis is poorly understood. While several cytokines have been implicated in the process of IVD degeneration and herniation, investigations have predominately focused on Interleukin 1 (IL-1) and tumor necrosis factor alpha (TNFα). However, to date no studies have investigated the expression of these cytokines simultaneously in IVD degeneration or herniation, or determined which may be the predominant cytokine associated with these disease states. Using quantitative real time PCR and immunohistochemistry we investigated gene and protein expression for IL-1β, TNFα and their receptors in non-degenerate, degenerate and herniated human IVDs. IL-1β gene expression was observed in a greater proportion of IVDs than TNFα (79% versus 59%). Degenerate and herniated IVDs displayed higher levels of both cytokines than non-degenerate IVDs, although in degenerate IVDs higher levels of IL-1β gene expression (1,300 copies/100 ng cDNA) were observed compared to those of TNFα (250 copies of TNFα/100 ng cDNA). Degenerate IVDs showed ten-fold higher IL-1 receptor gene expression compared to non-degenerate IVDs. In addition, 80% of degenerate IVD cells displayed IL-1 receptor immunopositivity compared to only 30% of cells in non-degenerate IVDs. However, no increase in TNF receptor I gene or protein expression was observed in degenerate or herniated IVDs compared to non-degenerate IVDs. We have demonstrated that although both cytokines are produced by human IVD cells, IL-1β is expressed at higher levels and in more IVDs, particularly in more degenerate IVDs (grades 4 to 12). Importantly, this study has highlighted an increase in gene and protein production for the IL-1 receptor type I but not the TNF receptor type I in degenerate IVDs. The data thus suggest that although both cytokines may be involved in the pathogenesis of IVD degeneration, IL-1 may have a more significant role than TNFα, and thus may be a better target for therapeutic intervention

The role of interleukin-1 in the pathogenesis of human Intervertebral disc degeneration

In this study, we investigated the hypotheses that in human intervertebral disc (IVD) degeneration there is local production of the cytokine IL-1, and that this locally produced cytokine can induce the cellular and matrix changes of IVD degeneration. Immunohistochemistry was used to localize five members of the IL-1 family (IL-1α, IL-1β, IL-1Ra (IL-1 receptor antagonist), IL-1RI (IL-1 receptor, type I), and ICE (IL-1β-converting enzyme)) in non-degenerate and degenerate human IVDs. In addition, cells derived from non-degenerate and degenerate human IVDs were challenged with IL-1 agonists and the response was investigated using real-time PCR for a number of matrix-degrading enzymes, matrix proteins, and members of the IL-1 family. This study has shown that native disc cells from non-degenerate and degenerate discs produced the IL-1 agonists, antagonist, the active receptor, and IL-1β-converting enzyme. In addition, immunopositivity for these proteins, with the exception of IL-1Ra, increased with severity of degeneration. We have also shown that IL-1 treatment of human IVD cells resulted in increased gene expression for the matrix-degrading enzymes (MMP 3 (matrix metalloproteinase 3), MMP 13 (matrix metalloproteinase 13), and ADAMTS-4 (a disintegrin and metalloproteinase with thrombospondin motifs)) and a decrease in the gene expression for matrix genes (aggrecan, collagen II, collagen I, and SOX6). In conclusion we have shown that IL-1 is produced in the degenerate IVD. It is synthesized by native disc cells, and treatment of human disc cells with IL-1 induces an imbalance between catabolic and anabolic events, responses that represent the changes seen during disc degeneration. Therefore, inhibiting IL-1 could be an important therapeutic target for preventing and reversing disc degeneration

Interleukin-1 receptor antagonist delivered directly and by gene therapy inhibits matrix degradation in the intact degenerate human intervertebral disc: an in situ zymographic and gene therapy study

Data implicate IL-1 in the altered matrix biology that characterizes human intervertebral disc (IVD) degeneration. In the current study we investigated the enzymic mechanism by which IL-1 induces matrix degradation in degeneration of the human IVD, and whether the IL-1 inhibitor IL-1 receptor antagonist (IL-1Ra) will inhibit degradation. A combination of in situ zymography (ISZ) and immunohistochemistry was used to examine the effects of IL-1 and IL-1Ra on matrix degradation and metal-dependent protease (MDP) expression in explants of non-degenerate and degenerate human IVDs. ISZ employed three substrates (gelatin, collagen, casein) and different challenges (IL-1β, IL-1Ra and enzyme inhibitors). Immunohistochemistry was undertaken for MDPs. In addition, IL-1Ra was introduced into degenerate IVD explants using genetically engineered constructs. The novel findings from this study are: IL-1Ra delivered directly onto explants of degenerate IVDs eliminates matrix degradation as assessed by multi-substrate ISZ; there is a direct relationship between matrix degradation assessed by ISZ and MDP expression defined by immunohistochemistry; single injections of IVD cells engineered to over-express IL-1Ra significantly inhibit MDP expression for two weeks. Our findings show that IL-1 is a key cytokine driving matrix degradation in the degenerate IVD. Furthermore, IL-1Ra delivered directly or by gene therapy inhibits IVD matrix degradation. IL-1Ra could be used therapeutically to inhibit degeneration of the IVD