RNA editing in human cancer: reviewŠKARDA, JOZEF; AMARIGLIO, NINETTE; RECHAVI, GIDEON
doi: 10.1111/j.1600-0463.2009.02505.xpmid: 19664125
Notice of Retraction: ‘RNA editing in human cancer: review’ (APMIS 2009;117:551–7) The following article from APMIS, ‘RNA editing in human cancer: review’ by Jozef Skarda, Ninette Amariglio and Gideon Rechavi, published online (2 July 2009) in Wiley InterScience (http://www.interscience.wiley.com) and in Volume 117, Issue 8 (August 2009), has been retracted by agreement between the authors, the journal Editors‐in‐Chief E. Ralfkiær and B. Norrild and John Wiley & Sons A/S. The retraction has been agreed as a result of textual overlap with a paper published in the journal RNA Biology, ‘A‐to‐I RNA editing and cancer: from pathology to basic science’ by Angela Gallo and Silvia Galardi, published in Volume 5, Issue 3 (September 2008). Jozef Skarda takes full responsibility for the textual overlap.
IL‐6, but not IL‐4, stimulates chemokinesis and TNF stimulates chemotaxis of tissue mast cells: involvement of both mitogen‐activated protein kinases and phosphatidylinositol 3‐kinase signalling pathwaysMISIAK‐TŁOCZEK, ANNA; BRZEZIŃSKA‐BŁASZCZYK, EWA
doi: 10.1111/j.1600-0463.2009.02518.xpmid: 19664126
Misiak‐Tłoczek A, Brzezińska‐Błaszczyk E. IL‐6, but not IL‐4, stimulates chemokinesis and TNF stimulates chemotaxis of tissue mast cells: Involvement of both mitogen‐activated protein kinases and phosphatidylinositol 3‐kinase signalling pathways. APMIS 2009; 117: 558–67. An increase in the number of mast cells within tissues is observed in many pathophysiological conditions. Current data indicate that migration of mature mast cells might be one of the key mechanisms responsible for rapid local accumulation of these cells. Considering that interleukin (IL)‐6 and IL‐4, as well as tumour necrosis factor (TNF), influence mast cell activity in various ways, the purpose of the current study was to examine whether these cytokines function as rat peritoneal mast cell chemoattractants. We showed that IL‐4, in the concentration range from 10−6 to 10−3 ng/ml, did not induce a mast cell migratory response, even in the presence of laminin and fibronectin. Under the same experimental conditions, mast cells were shown to migrate in response to IL‐6 stimulation in the presence of laminin. The optimal concentration of IL‐6 for maximal migration of mast cells was 10−4 ng/ml (i.e. ∼5 nM). In comparison, the optimal concentration of TNF for maximal migration of mast cells was 5 × 10−5 ng/ml (i.e. ∼3 fM). IL‐6‐stimulated mast cell migration was the result of chemokinesis, whereas TNF‐induced migration was the result of chemotaxis. Mast cell migratory responses to IL‐6 and TNF were entirely blocked by specific anti‐IL‐6R and anti‐TNFR1 antibodies. We also documented that the migration response of mast cells to stimulation with IL‐6 and TNF was mediated through signal transduction pathways involving mitogen‐activated protein kinases and phosphatidylinositol 3‐kinase. Taken together, our results indicate that IL‐6, as well as TNF, induces tissue mast cell migration. Thus, these proinflammatory cytokines can be responsible for mast cell accumulation at the site of diverse conditions accompanied by inflammation.
Renal tubular expression of Toll‐like receptor 4 in cyclosporine nephrotoxicityLIM, BEOM JIN; HONG, SOON WON; JEONG, HYEON JOO
doi: 10.1111/j.1600-0463.2009.02514.xpmid: 19664129
Lim BJ, Hong SW, Jeong HJ. Renal tubular expression of Toll‐like receptor 4 in cyclosporine nephrotoxicity. APMIS 2009; 117: 583–91. Exploring the expression of Toll‐like receptor (TLR) in cyclosporine (CsA)‐induced renal injury in humans, we evaluated the expression of TLR4 in both biopsied renal tissue and cultured tubular cells. Immunohistochemical stains for TLR4, heat shock protein (HSP) 47, and HSP70 were performed in both pre‐ and post‐treatment biopsies obtained from 18 patients of minimal change nephrotic syndrome or IgA nephropathy treated with CsA, and the percentage of positive tubules was compared in each case. For in vitro experiments, HK‐2 cells were treated with CsA (2, 5, and 10 μg/ml) for 24, 48, and 72 h. TLR4 mRNA and protein were measured using real‐time RT‐PCR and Western blot. In addition, hypoxic effect was added by GasPak System. The tubular expressions of TLR4 (2.2 ± 1.2% vs 4.4 ± 2.0%, p < 0.001) and HSP70 (2.6 ± 2.8% vs 6.1 ± 4.2%, p = 0.002) were increased after CsA treatment. TLR4 mRNA and protein expression were also increased in a dose‐dependent manner. Hypoxia enormously increased TLR4 expression. In summary, CsA increased tubular expression of TLR4 and its ligand HSP70. As hypoxia was shown to be a strong stimulus for TLR4 expression, it can be said that TLR4 is influenced by both direct toxicity and impediment of renal microcirculation in human CsA nephrotoxicity.
Real‐time PCR with internal amplification control for detecting tuberculosis: method design and validationFLORES, E.; RODRÍGUEZ, J. C.; GARCIA‐PACHÓN, E.; SOTO, J. L.; RUIZ, M.; ESCRIBANO, I.; ROYO, G.
doi: 10.1111/j.1600-0463.2009.02508.xpmid: 19664130
Flores E, Rodríguez JC, Garcia‐Pachón E, Soto JL, Ruiz M, Escribano I, Royo G. Real‐time PCR with internal amplification control for detecting tuberculosis: method design and validation. APMIS 2009; 117: 592–7. Real‐time PCR has been a major development in the diagnosis of tuberculosis. However, most tests do not include an internal amplification control (IAC), which therefore limits it clinical application. In this study a new, easy to perform real‐time PCR test with IAC was designed and validated in clinical samples. The primers amplified a 163‐bp fragment of IS6110 of Mycobacterium tuberculosis and the IAC was designed with a fragment of a different microorganism (Chlamydia trachomatis). The interassay and intraassay variation of this test were very low (0.45–1.65% and 0.18–1.80%, respectively). The detection accuracy was validated in 50 samples (25 urine, 25 sputum) with different concentrations of M. tuberculosis, 18 clinical isolates of non‐tuberculous mycobacteria and 148 samples with clinical suspicion of pulmonary tuberculosis. The specificity was 100%. The detection limit of this PCR test without IAC was approximately 15 bacteria and with IAC approximately 32 bacteria. This real‐time PCR with IAC assay can improve the detection of M. tuberculosis and contribute to standardization of this diagnostic technique.
Predicting the incidence of human campylobacteriosis in Finland with time series analysisSUMI, AYAKO; HEMILÄ, HARRI; MISE, KEIJI; KOBAYASHI, NOBUMICHI
doi: 10.1111/j.1600-0463.2009.02507.xpmid: 19664133
Sumi A, Hemilä H, Mise K, Kobayashi N. Predicting the incidence of human campylobacteriosis in Finland with time series analysis. APMIS 2009; 117: 614–22. Human campylobacteriosis is a common bacterial cause of gastrointestinal infections. In this study, we tested whether spectral analysis based on the maximum entropy method (MEM) is useful in predicting the incidence of campylobacteriosis in five provinces in Finland, which has been accumulating good quality incidence data under the surveillance program for water‐ and food‐borne infections. On the basis of the spectral analysis, we identified the periodic modes explaining the underlying variations of the incidence data in the years 2000–2005. The optimum least squares fitting (LSF) curve calculated by using the periodic modes reproduced the underlying variation of the incidence data. We extrapolated the LSF curve to the years 2006 and 2007 and predicted the incidence of campylobacteriosis. Our study suggests that MEM spectral analysis allows us to model temporal variations of the disease incidence with multiple periodic modes much more effectively than using the Fourier model, which has been previously used for modeling seasonally varying incidence data.
Immunohistochemical analysis of NF‐κB signaling proteins IKKε, p50/p105, p52/p100 and RelA in prostate cancersSEO, SEONG IL; SONG, SANG YONG; KANG, MI RAN; KIM, MIN SUNG; OH, JI EUN; KIM, YOO RI; LEE, JI YOUL; YOO, NAM JIN; LEE, SUG HYUNG
doi: 10.1111/j.1600-0463.2009.02506.xpmid: 19664134
Seo SI, Song SY, Kang MR, Kim MS, Oh JE, Kim YR, Lee JY, Yoo NJ, Lee SH. Immunohistochemical analysis of NF‐κB signaling proteins IKKε, p50/p105, p52/p100 and RelA in prostate cancers. APMIS 2009; 117:623–8. Activation of nuclear factor‐kappa B (NF‐κB) signaling is considered an important mechanism in the development of prostate cancers. A recent study revealed that IκB kinase epsilon (IKKε), an activator of NF‐κB, was overexpressed in breast cancers and acted as an oncogene. Expression of NF‐κB members has been reported in prostate cancer tissues, but expression of IKKε has not yet been studied in prostate cancers. In this study, we attempted to explore as to whether expressions of IKKε and NF‐κB members p50/105, p52/p100 and RelA are altered in prostate cancers. We analyzed the expression of IKKε, p50/105, p52/p100 and RelA in 107 prostate adenocarcinoma tissues by immunohistochemistry using a tissue microarray (TMA) method. In the TMA, IKKε is expressed in basal cells, but not in alveolar cells in normal prostate glands. IKKε is expressed in 60.0% of prostate intraepithelial neoplasm (PIN) and 70.1% of the prostate cancers in the cytoplasm. Nuclear immunostainings of NF‐κB members p50/105, p52/p100 and RelA, which are considered activation of NF‐κB signaling, were observed respectively in 28.0%, 18.7% and 37.4% of the cancers. Nuclear staining was detected neither in normal alveolar cells nor in PIN. However, none of the expression of p50/105 nor p52/p100 nor RelA nor IKKε was associated with pathologic characteristics, including size of the cancers, age, Gleason score and stage. The increased cytoplasmic expression of IKKε as well as the increased nuclear expressions of p50/105, p52/p100 and RelA in the prostate cancers compared to normal alveolar cells suggested that overexpression of these proteins may be related to activation of the NF‐κB pathway and might play a role in tumorigenesis of prostate cancers.