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Background Coronary Aneurysms are a focal dilatation of an artery segment >1.5-fold the normal size of adjacent segments. Although some series have suggested a prevalence of 0.3–12%, data are lacking. In addition, they are not mentioned in practice guidelines. Our aim was investigate its prevalence, management and long-term outcomes. Methods and results The coronary artery aneurysm registry (CAAR) involved 32 hospitals across 9 countries in America and Europe. We reviewed 436,467 consecutive angiograms performed over the period 2004–2016. Finally, 1565 patients were recruited. Aneurysm global prevalence was 0.35%. Most patients were male (78.5%) with a mean age of 65 years and frequent cardiovascular risk factors. The main indication for angiogram was an acute coronary syndrome, 966 cases. The number of aneurisms was ≤2 per patient in 95.8% of the cases, mostly saccular, most frequently found in the left anterior descending and with numbers proportional with coronary stenosis. Aortopathies were related with more aneurysms too. Most patients received any revascularization procedure (69%), commonly percutaneous (53%). After a median follow-up of 37.2 months, 485 suffered a combined event (MACE) and 240 died. Without major differences comparing CABG vs PCI, MACE and death were more frequent in patients who received bare metal stents. Conclusions Coronary artery aneurysms are not uncommon. Usually, they are associated with coronary stenosis and high cardiovascular risk. Antiplatelet therapy seems reasonable and a percutaneous approach is safe and effective.

Mutant-enriched PCR and reverse dot blot hybridization in microplates were applied for examining K-ras status in stools and tissue samples from patients with pancreatic tumors and chronic pancreatitis. In tissue samples, K-ras mutations were found in 32 of 35 cases of ductal adenocarcinoma, in 5 of 7 periampullary cancers, in 1 cystadenocarcinoma, and in 3 of 5 patients with chronic pancreatitis. In stools, mutated K-ras was seen in 10 of 25 cases of ductal adenocarcinoma, in 1 case of cystadenocarcinoma, and in 2 of 6 cases of chronic pancreatitis. These data indicate that the K-ras status of stool samples may help identify pancreatic carcinoma and persons at risk for cancer development; however, it does not allow discrimination of malignant from nonmalignant diseases.

The diagnostic specificity of the detection of disseminated prostatic cells by reverse-transcriptase polymerase chain reaction (RT-PCR) of PSA mRNA was investigated. A sensitive nested PCR was developed. In blood samples from 10 healthy female and 10 healthy male persons examined by RT-PCR, mRNA of PSA was detected 3 times in each group. In the groups of patients suffering from benign prostate hyperplasia and prostate cancer, 6 of 11 and 5 of 12, respectively, gave positive RT-PCR results. With increasing analytical sensitivity of the RT-PCR of PSA mRNA, the diagnostic specificity of the assay is decreased. Further development of this diagnostic method requires the introduction of the quantitative PCR which may make possible discrimination between prostatic and non-prostatic source of PSA mRNA by quantification.

The isopeptide bonds formed by ubiquitin or its relatives are cleaved by hydrolases with active site cysteines. Recent studies have revealed that similar metalloprotease motifs – JAMMs – in the Rpn11 subunit of the 26S proteasome lid and in the Csn5 subunit of the COP9 signalosome are involved in deubiquitination and deneddylation, respectively.

We report the case of a 44-year-old man who underwent a partial medial meniscectomy for a meniscal tear whose postoperative course was complicated by the development of heterotopic ossification (HO) within the medial arthroscopic portal. Following a routine initial procedure, the patient presented with ongoing pain and a palpable, painful lump around the previous medial arthroscopy portal. Plain radiographs and MRI were suggestive of a bony structure within the soft tissues. Histopathological examination at repeat arthropscopy confirmed osseous tissue consistent with HO. Recovery after the second procedure was rapid and resulted in normal knee function and complete pain relief. HO within an arthroscopy portal is a rare complication following arthroscopic partial meniscectomy in the knee and has not previously been described in the literature.

Background The COP9 signalosome (CSN) is a conserved protein complex in eukaryotic cells consisting of eight subunits (CSN1 to CSN8). Recent data demonstrate that the CSN is a regulator of the ubiquitin (Ub) proteasome system (UPS). It controls substrate ubiquitination by cullin-RING Ub ligases (CRLs), a process that determines substrate specificity of the UPS. The intrinsic deneddylating activity localized to CSN5 as well as the associated kinases and deubiquitinating activity are involved in the regulatory function of CSN. The exact mechanisms are unclear. In this study we knocked down CSN1 (siCSN1), CSN3 (siCSN3) and CSN5 (siCSN5) by specific siRNA oligos permanently expressed in HeLa cells. The analysis and comparison of siRNA cells revealed differential impact of individual subunits on CSN structure and function. Results Permanent knockdowns of CSN1 and CSN3 led to a reduction of the subunits to approximately 40%, which is accompanied by a proportional decrease of the CSN holocomplex. In contrast, downregulation of CSN5 in HeLa cells reduced the CSN5 protein below 20% without significant effects on the remaining complex. The CRL component Rbx1 was characterized by accelerated proteolysis in siCSN1 and siCSN3 and also in siCSN5 cells, however, with lesser extent. Immunoprecipitated CSN complex from siCSN5 cells was less effective in phosphorylating c-Jun and p27. Accelerated degradation of c-Jun in siCSN5 cells was rescued by overexpression of CSN5 as well as of the deneddylation mutant CSN5D151N. Overexpression of CSN5 cannot rescue c-Jun destabilization in siCSN1. Conclusion There exists a coordinated downregulation of CSN subunits in the CSN1 and CSN3 knockdowns. The underlying regulatory mechanisms are obscure. CSN5 seems to possess a specific status in HeLa cells. Its reduction is not connected with coordinated downregulation of other subunits. CSN knockdowns confirm that the stabilization of the CRL component Rbx1 is a major CSN function. In addition, downregulation of CSN subunits influences the stability of important cellular regulators such as c-Jun and p27.