The Likelihood Ratio as a tool for Radio Continuum Surveys with SKA precursor telescopes

In this paper we investigate the performance of the likelihood ratio method as a tool for identifying optical and infrared counterparts to proposed radio continuum surveys with SKA precursor and pathfinder telescopes. We present a comparison of the infrared counterparts identified by the likelihood ratio in the VISTA Deep Extragalactic Observations (VIDEO) survey to radio observations with 6, 10 and 15 arcsec resolution. We cross-match a deep radio catalogue consisting of radio sources with peak flux density $>$ 60 $\mu$Jy with deep near-infrared data limited to $K_{\mathrm{s}}\lesssim$ 22.6. Comparing the infrared counterparts from this procedure to those obtained when cross-matching a set of simulated lower resolution radio catalogues indicates that degrading the resolution from 6 arcsec to 10 and 15 arcsec decreases the completeness of the cross-matched catalogue by approximately 3 and 7 percent respectively. When matching against shallower infrared data, comparable to that achieved by the VISTA Hemisphere Survey, the fraction of radio sources with reliably identified counterparts drops from $\sim$89%, at $K_{\mathrm{s}}\lesssim$22.6, to 47% with $K_{\mathrm{s}}\lesssim$20.0. Decreasing the resolution at this shallower infrared limit does not result in any further decrease in the completeness produced by the likelihood ratio matching procedure. However, we note that radio continuum surveys with the MeerKAT and eventually the SKA, will require long baselines in order to ensure that the resulting maps are not limited by instrumental confusion noise.Comment: 10 pages, 7 figures, accepted for publication in mnra

Loss of heterozygosity for defined regions on chromosomes 3, 11 and 17 in carcinomas of the uterine cervix.

Loss of heterozygosity (LOH) frequently occurs in squamous cell carcinomas of the uterine cervix and indicates the probable sites of tumour-suppressor genes that play a role in the development of this tumour. To define the localization of these tumour-suppressor genes, we studied loss of heterozygosity in 64 invasive cervical carcinomas (stage IB and IIA) using the polymerase chain reaction with 24 primers for polymorphic repeats of known chromosomal localization. Chromosomes 3, 11, 13, 16 and 17, in particular, were studied. LOH was frequently found on chromosome 11, in particular at 11q22 (46%) and 11q23.3 (43%). LOH on chromosome 11p was not frequent. On chromosome 17p13.3, a marker (D17S513) distal to p53 showed 38% LOH, whereas p53 itself showed only 20% LOH. On the short arm of chromosome 3, LOH was frequently found (41%) at 3p21.1. The beta-catenin gene is located in this chromosomal region. Therefore, expression of beta-catenin protein was studied in 39 cases using immunohistochemistry. Staining of beta-catenin at the plasma membrane of tumour cells was present in 38 cases and completely absent in only one case. The tumour-suppressor gene on chromosome 3p21.1 may be beta-catenin in this one case, but (an)other tumour-suppressor gene(s) must also be present in this region. For the other chromosomes studied, 13q (BRCA-2) and 16q (E-cadherin), only sporadic losses (< 15% of cases) were found. Expression of E-cadherin was found in all of 37 cases but in six cases the staining was very weak. No correlation was found between clinical and histological parameters and losses on chromosome 3p, 11q and 17p. In addition to LOH, microsatellite instability was found in one tumour for almost all loci and in eight tumours for one to three loci. In conclusion, we have identified three loci with frequent LOH, which may harbour new tumour-suppressor genes, and found microsatellite instability in 14% of cervical carcinomas

Rat interleukin-2-activated natural killer (A-NK) cell-mediated lysis is determined by the presence of CD18 on A-NK cells and the absence of major histocompatibility complex class I on target cells

The precise mechanism by which target cells are recognized and subsequently lysed by interleukin-2-activated natural killer (A-NK) cells is poorly understood. In this study the role of major histocompatibility complex (MHC) class I and adhesion molecules in the recognition and lysis of tumor cells was investigated in a syngeneic Wag rat model. Preincubation of tumor cells with F(ab′)2 fragments of anti-MHC class I monoclonal antibody (mAb) OX18 strongly enhanced the A-NK cell-mediated lysis. Also normal syngeneic cells such as T cells and A-NK cells became highly sensitive for lysis by A-NK cells after preincubation with mAb OX18. Two other mAb against MHC class I had no effect on lysis of target cells. These data indicate that masking of MHC class I on syngeneic tumor and normal cells by mAb OX18 is sufficient for A-NK cells to recognize target cells as non-self, resulting in lysis. In addition, we found that the presence of mAb against the β2 (CD18)-integrins blocked the lysis of all tumor cell lines by A-NK cells in 51Cr-release assays, also when target cells were preincubated with mAb OX18. Because of the absence of CD18 on most tumor cells we concluded that a CD18-associated integrin on A-NK cells is essential for lysis of target cells. These results show that in this syngeneic rat model CD18 on A-NK cells together with MHC class I on tumor cells determine A-NK cell-mediated lysis. Furthermore, we hypothesize that the anti-MHC class I OX18 recognizes an epitope on rat MHC class I which is, or is very close to, the restriction element determining A-NK cell-mediated lysis