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Background A previous study revealed that matrin-3 is an essential component in maintaining fibroblast growth factor 2 (FGF2)-mediated undifferentiation of neural stem cells (NSCs) using a proteomics approach. Malignant melanoma (MM) arises from melanocytes that originate from neural crest stem cells during development. Additionally, it has been reported that the expression of FGF2 is positively correlated with the progression of MM. Objective We expected that matrin-3, as a downstream component of FGF2, might be associated with the aggressiveness or differentiation of MM. Methods Matrin-3 expression was measured in human melanoma patient tissues and human MM cell lines. We analyzed the effect of matrin-3 siRNA on the proliferation of human MM cell lines and focused on cell cycle progression and apoptosis. We carried out in vivo xenograft tumor experiments by implanting A375 cells transfected with matrin-3 shRNA. Results Matrin-3 was highly expressed in MM, and matrin-3 knockdown inhibited the proliferation of melanoma cellsin vivo and in vitro. Furthermore, we found that matrin-3 knockdown led to an accumulation of cells in the G1 phase and an increase in apoptotic cell number. Conclusion Our results suggest that matrin-3 could be a new therapeutic target for the treatment of MM.

Background Recent studies have suggested that there is a close association between the administration of gadolinium (Gd)-based contrast agents and the development of nephrogenic systemic fibrosis (NSF), an acquired disorder characterized by systemic fibrosis and abnormal calcification in patients with severe renal dysfunction. However, the causative roles of Gd remain unknown. Objective The aim of this in vitro study was to investigate the effect of Gd on the development of fibrosis and calcification in cultured cells. Methods MC3T3-E1 cells (pre-osteoblastic cells), human adipose tissue-derived mesenchymal stem cells (HAMSCs), human subcutaneous preadipocytes, and human dermal fibroblasts (HDFs) were each cultured in differentiation medium with or without gadolinium chloride. Calcium deposition of MC3T3-E1 cells, HAMSCs, and HDFs was determined by alzarin red S staining. Adipogenic differentiation of human subcutaneous preadipocytes and HAMSCs was determined by oil red O staining. Fibrogenesis of HDFs was determined by real-time PCR to measure the mRNA expression of type I collagen. Cell proliferation was determined by MTS assay. Results Gd induced calcium deposition in MC3T3-E1 cells, HAMSCs and HDFs in osteogenic differentiation media. Gd did not induce adipogenic differentiation in human subcutaneous preadipocytes and HAMSCs. Gd did not increase the mRNA expression of type I collagen in HDFs, but did promote cell proliferation. Conclusions We have demonstrated a direct effect of Gd on calcium deposition in cultured cells. The result will help us to understand the mechanism of abnormal calcification in NSF.

During the course of anaphylaxis, occurrence of myocardial ischaemia has been known, which have recently been named as Kounis syndrome [1]. Regarding treatment for this syndrome, early intravenous administration of adrenaline is the key points for managing anaphylaxis [2–4] but adrenaline can aggravate myocardial ischaemia. Moreover, whether adrenaline is effective or not is controversial [5,6]. We report a case of Kounis syndrome during general anaesthesia in which administration of adrenaline was effective in both anaphylactic shock and myocardial ischaemia, and discuss perioperative problems about diagnosis and therapy. A 61-yr-old man was scheduled for varicose vein stripping. He had in good health, had no past history suggestive of allergy, and took no medications. The operation began uneventfully under spinal anaesthesia. Ten minutes after the start of surgery, the patient became confusional, severely hypotensive and tachycardic. Ephedrine, phenylephrine and noradrenaline were administered in addition to rapid infusion of normal saline but the patient remained hypotensive and tachycardic. Fifteen minutes after occurrence of hypotension, the ECG revealed ST segment elevation in a MCL5 lead. We suspected that hypotension was caused by left ventricular dysfunction as a result of myocardial ischaemia, and started nitroglycerin and noradrenaline continuously. But the patient's condition remained unchanged. A few minutes later, the anaesthetist noticed a mildly or moderately erythematous rash at the patient's face for the first time and

The detection of fusion transcripts of the collagen type 1α1 (COL1A1) and platelet-derived growth factor-BB (PDGFB) genes by genetic analysis has recognized as a reliable and valuable molecular tool for the diagnosis of dermatofibrosarcoma protuberans (DFSP). To detect the COL1A1-PDGFB fusion, almost previous reports performed reverse transcription polymerase chain reaction (RT-PCR) using multiplex forward primers from COL1A1. However, it has possible technical difficulties with respect to the handling of multiple primers and reagents in the procedure. The objective of this study is to establish a rapid, easy, and efficient one-step method of PCR using only a single primer pair to detect the fusion transcripts of the COL1A1 and PDGFB in DFSP. To validate new method, we compared the results of RT-PCR in five patients of DFSP between the previous method using multiplex primers and our established one-step RT-PCR using a single primer pair. In all cases of DFSP, the COL1A1-PDGFB fusion was detected by both previous method and newly established one-step PCR. Importantly, we detected a novel COL1A1 breakpoint in exon 5. The newly developed method is valuable to rapidly identify COL1A1-PDGFB fusion transcripts in DFSP.