One year outcomes after glucose-insulin-potassium in ST elevation myocardial infarction. The Glucose-insulin-potassium study II

BackgroundThere are conflicting data concerning the effect of treatment with glucose–insulin–potassium (GIK) in ST segment elevation myocardial infarction (STEMI). Early studies showed beneficial effects of GIK, however, recent large sample size trials did not confirm this, or suggested only benefits in patients without heart failure. We aimed to evaluate long-term effects of GIK in patients with STEMI without signs of heart failure, all treated with reperfusion therapy.MethodsFrom August 2003 to December 2004, 889 STEMI patients without signs of heart failure were randomized to standard care (N = 445) or additional GIK infusion (N = 444). Glucose–potassium (20% glucose with 80 mmol potassium/l) was infused at 2 ml/kg body weight per hour for 12 h through a peripheral line. Short-acting insulin was started according to admission glucose and adjusted based on hourly measured glucose. Clinical end points were of number of death, reinfarction and revascularization at 1 year.ResultsOne year follow-up was available in 864 patients (97.2%), 432 in the GIK group and 432 in the control group. Mortality rate was 5.3% in GIK and 3.9% in control patients, p = 0.33. Rates of reinfarction and revascularization 4.6% vs. 4.6% and 15.5% and 15.0%, in GIK vs. control patients.ConclusionIn patients with STEMI without signs of heart failure treated with reperfusion therapy, GIK therapy offers no clinical benefit at 1 year.     

Gluten sensitivity enteropathy in patients with recurrent aphthous stomatitis

Background  

Gluten sensitive enteropathy (GSE) is an autoimmune enteropathy triggered by the ingestion of gluten-containing grains in susceptible individuals. Recurrent aphthous stomatitis (RAS) may be the sole manifestation of GSE. The aim of this study was to determine the prevalence of gluten sensitivity enteropathy (GSE) in a large group of patients with RAS and assess the efficacy of gluten free diet (GFD) on the improvement of aphthous lesions in those who were diagnosed with GSE.     

Identification of 3{alpha}-hydroxy-cyproterone acetate as a metabolite of cyproterone acetate in the bile of female rats and the potential of this and other already known or putative metabolites to form DNA adducts in vitro

Cyproterone acetate (CPA) is a synthetic steroid hormone usedin the therapy of prostate cancer in men and different formsof acne and hirsutism in women. CPA has been shown by ³²P-postlabelinganalysis to bind covalently to hepatic DNA of rats in vivo andin vitro. A prerequisite for DNA adduct formation of CPA ismetabolic activation of the drug to a reactive intermediate.In the present study bile was collected from [³H]CPA-treatedfemale rats and, following chromatographic separation of bileextracts, fractions of the eluate were examined for the presenceof reactive metabolites which were able to form adducts withcalf thymus DNA in vitro. The formation of adducts was detectedby ³²P-postlabeling analysis. One major metabolite of CPA presentin the bile extracts was isolated and, following a thoroughstructural elucidation by mass spec-trometry and ¹H-NMR, thismetabolite was identified as 3     

Clear Cell Odontogenic Carcinoma: First Report of Novel EWSR1–CREM Fusion Gene in Case of Long-Term Misdiagnosis

Clear Cell odontogenic Carcinomas (CCOC) are rare, aggressive malignant odontogenic tumours which are often misdiagnosed as benign odontogenic tumours due to the non-specific histologic appearance, and benign early clinical presentation. However, due to their propensity to metastasize, the best outcomes are experienced with they are diagnosed early and treated aggressively. In this paper, we present a case of a CCOC misdiagnosed as a clear cell calcifying epithelial odontogenic tumour which was only found to be a CCOC after cervical node metastasis. The original diagnosis was questioned and confirmed to be a CCOC by identification of the chromosomal translocation EWSR1 on fluorescence in situ hybridization. This has recently been described in CCOC and a wide variety of other mesenchymal and epithelial neoplasms. Previous reports have demonstrated EWSR1–ATF1 and EWSR1–CREB1 fusions in CCOC. Next generation sequencing of this case demonstrated the EWSR1–CREM fusion gene which has not been previously reported for CCOC. CREM fusion proteins have only recently been found in several tumour types including the closely associated hyalinizing clear cell carcinoma of salivary glands. This is discussed in this paper, and the role of the discovery of the CREM fusion protein in CCOC adds to your understating of the role of CREM in oncogenesis, and the possible link between CCOCs and hyalinizing clear cell carcinomas.     

Phytochemicals and antioxidant activity of alcoholic/hydroalcoholic extract of Trifolium pratense

Objective: Trifolium pratense has many healing properties, including fewer complications of menopause, cancer cell suppression, reducing blood glucose and lipids, as well as cardiovascular beneficial effects. The purpose of this study was to identify the phytochemical and mineral composition of T. pratense. Methods: Plant aerial parts were harvested and dried, and then hydroalcoholic and alcoholic extracts were prepared. Gas chromatography–mass spectrometry (GC-MS) analytical method was used to identify volatile compounds then liquid chromatography-electrospray ionization mass spectrometry (LC-ESI-MS) was used to identify polyphenols and the mineral elements were identify by inductively coupled plasma atomic emission spectrometer/ICP-AES and scanning electron microscope-energy-dispersive X-ray spectroscopy (SEM-EDS) methods. Total phenolic content (TPC) was determined based on colorimetric method, and total flavonoid content (TFC) was established based on the folin-chiocalteau reagent. Furthermore, two assays (DPPH and FRAP) were used to measure the antioxidant capacity of T. pratense ethanolic extract. Results: A total of 37 polyphenol and 107 peaks were identified by LC-ESI-MS analysis, and the GC/MS method also detected 21 volatile compounds, the most important of which were methylcyclopentane, dimethylpentanal and hexadecanol. A total of 18 mineral elements, including K, Mg, Al, Si, Zn, Ni, Cu, Se, Co, Fe, Mn, and Ca in the plant, were identified ICP-AES and SEM-EDS analysis. Conclusion: T. pratense has many therapeutic compounds such as polyphenol (isoflavone and flavonoids), volatile compounds, and essential mineral elements, which can be formulated purely and used in the pharmaceutical and traditional medicine industries.     

Antifibrotic effect of Ac-SDKP and angiotensin-converting enzyme inhibition in hypertension

OBJECTIVE: N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) is a potent natural inhibitor of hematopoietic stem cell proliferation which is degraded mainly by angiotensin-converting enzyme (ACE). In vitro, Ac-SDKP inhibits collagen production by cardiac fibroblasts; while in vivo it blocks collagen deposition in the left ventricle (LV) of rats with hypertension or myocardial infarction (MI). In addition, it reportedly prevents and reverses macrophage infiltration in the LV of rats with MI. We tested the hypothesis that when Ac-SDKP is infused at doses that cause plasma concentrations similar to those observed after ACE inhibition, it mimics the anti-inflammatory and antifibrotic effects of ACE inhibitors (ACEi) in the heart, and, further, that these effects are independent of changes in blood pressure. DESIGN AND METHODS: Rats were divided into five groups: (1) controls, (2) Ang II (750 microg/kg per day, s.c.), (3) Ang II + captopril (100 mg/kg per day in drinking water), (4) Ang II + Ac-SDKP (400 microg/kg per day, s.c.), and (5) Ang II + Ac-SDKP (800 microg/kg per day, s.c.). We measured LV cell proliferation, inflammatory cell infiltration, cytokine expression, hypertrophy and fibrosis. RESULTS: Plasma Ac-SDKP was five-fold higher in rats given ACEi and four- and ten-fold higher in rats given 400 and 800 microg/kg per day Ac-SDKP, respectively. ACEi significantly decreased Ang II-induced cell proliferation (Ki-67), LV macrophage/mast cell infiltration, transforming growth factor-beta, connective tissue growth factor and collagen deposition without affecting hypertension, LV hypertrophy or myocyte cross-sectional area, and these effects were mimicked by exogenous Ac-SDKP (400 microg/kg per day) which raised plasma Ac-SDKP to levels similar to ACEi. BP was not decreased by either ACEi or Ac-SDKP. CONCLUSIONS: We concluded that Ac-SDKP may be an important mediator of the anti-inflammatory and antifibrotic effects of ACEi in hypertension independent of its hemodynamic effects.