Acute Cholecystitis and Acute Pancreatitis related to Hemobilia after Percutaneous Liver Biopsy

Percutaneous liver biopsy is a reliable method used for the diagnosis and follow-up of many liver diseases. Although it is safe, major complications, such as free intraperitoneal bleeding, hemothorax, pneumothorax, hemobilia, and Pseudoaneurysm, have rarely been reported to be related to the procedure. The reported rate of hemobilia after performing percutaneous liver biopsy is approximately 0.06%. This event usually results from a hepatic artery pseudoaneurysm and can potentially cause fatal bleeding. In addition, acute cholecystitis and pancreatitis are rare complications of hemobilia. To the best of our knowledge, we report the third case of a patient who developed hemobilia, acute cholecystitis, and acute pancreatitis from a pseudoaneurysm after performing percutaneous liver biopsy. The bleeding was successfully controlled by angiographic embolization with glue and lipidiol

Apoptotic and necrotic effects of carboxylated quercetin/polyethylenimine complex on HeLa cells

WOS: 000295799500013The effects of quercetin (Q), carboxylated quercetin (CQ) and carboxylated quercetin/polyethylenimine (CQ/PEI) complex on HeLa cell cultures were investigated. Firstly, carboxylated quercetin was acquired through hydroxyl groups of quercetin, using chloroacetic acid. The complex of CQ/PEI was acquired by electron cooperation path over polietilenimine amine groups and quercetin carboxyl groups. CQ and CQ/PEI obtained were characterised by FTIR and H-1-NMR methods. Cytotoxicity was determined by MTT assay. Apoptotic and necrotic indexes were obtained by immunocytochemical staining with the M30 antibodies and double staining and double staining, respectively. It was determined that quercetin caused lower rates of necrosis and apoptosis on HeLa cells by itself, but CQ/PEI complex resulted in high levels. As a result, it was observed that transition of quercetin to HeLa via binding it to polyethylenimine increased its anticarcinogenic effects.Kirikkale University Science Research FoundationKirikkale University [2007/70]; Kirikkale University of TurkeyKirikkale UniversityThis work was supported by Kirikkale University Science Research Foundation Project (number; 2007/70) of Kirikkale University of Turkey

BIOENGINEERING FUNCTIONAL COPOLYMERS. XV. SYNTHESIS OF ORGANOBORON AMIDE-ESTER BRANCHED DERIVATIVES OF OLIGO(MALEIC ANHYDRIDE) AND THEIR INTERACTION WITH HeLa AND L929 FIBROBLAST CELLS

WOS: 000298002900006Novel bioengineering functional organoboron oligomers were synthesized by (i) amidolysis of oligo(maleic anhydride) (OMA) with 2-aminoethyldiphenylborinate (2-AEPB), (ii) esterification of organoboron oligomer (OMA-B) with alpha-hydroxy-omega-methoxypoly(ethylene oxide) (PEO) as a compatibilizer and (iii) conjugation of organoboron PEO branches (OMA-B-PEO) with folic acid as a taggering agent. Structure and composition of the synthesized oligomers were characterized by FTIR-ART and (1)H ((13)C) NMR spectroscopy, chemical and physical analysis methods. Interaction of functional oligomers and oligomer center dot center dot center dot FA complex (OMA-B-PEO-F) with HeLa and L929 fibroblast cells were investigated by using different biochemical methods such as cytotoxicity, statistical, apoptotic and necrotic cell indexes, double staining and caspase-3 immunostaining, light and fluorescence inverted microscope analyses. It was found that citotoxisity and apoptotic/necrotic effects of oligomers significantly depend on the structure and composition of studied oligomers, and increase the following raw: OMA << OMA-B < OMA-B-PEO < OMA-B-PEO-F. A folic acid complex (MA-PEG-B-F) at 400 mu g ml(-1) (2.36 mu mol ml(-1)) concentration as a therapeutic drug exhibits minimal toxcisity toward the fibroblast cells, but influential for HeLa cells.TAEKMinistry of Energy & Natural Resources - Turkey; TUBITAK (Turkish National Scientific and Technology Research Council)Turkiye Bilimsel ve Teknolojik Arastirma Kurumu (TUBITAK) [TBAG-2386]Supports: TAEK and TUBITAK (Turkish National Scientific and Technology Research Council) - TBAG-2386 project

Oxovanadium(IV) complexes based on S-alkyl-thiosemicarbazidato ligands. Synthesis, characterization, electrochemical, and antioxidant studies

Reaction of VOSO4 with 2-hydroxy-napthaldeyde-S-R-thiosemicarbazones (R: methyl, ethyl, propyl or allyl) and salicyl aldehyde yielded five-coordinate oxovanadium(IV) complexes having a N-1,N-4-diarylidene-S-R-thiosemicarbazidato structures. The compounds were characterized by elemental analysis, magnetic measurements, electronic, infrared, H-1-NMR, and electron paramagnetic resonance (EPR) spectra. The X-band EPR signals were recorded from powder forms and also in solution. All the complexes have a single asymmetric line shape and theoretical fit studies prove the presence of axial symmetry around the paramagnetic vanadium ions. A computer simulation of the EPR spectrum of each complex was carried out to derive the related EPR parameters. Cyclic voltammograms of the complexes exhibited two metal-based reversible redox peaks around 500 and -800 mV corresponding to one electron oxidation/reduction of (VO)-O-IV/(VO)-O-V and (VO)-O-IV/(VO)-O-III, respectively. The reductive response in the 50-350 mV region was assigned to ligand reduction. Antioxidant activities of the compounds were determined with CUPric Reducing Antioxidant Capacity, 2,2-azino-bis-3-ethylbenzothiazoline-6-sulfonic acid, and 1,1-diphenyl-2-picrylhydrazyl assays. The test results indicated that the antioxidant capacity of the compounds increases with the carbon number of saturated hydrocarbon chain on sulfur atom

Clinical and molecular evaluation of MEFV gene variants in the Turkish population: a study by the National Genetics Consortium

Familial Mediterranean fever (FMF) is a monogenic autoinflammatory disorder with recurrent fever, abdominal pain, serositis, articular manifestations, erysipelas-like erythema, and renal complications as its main features. Caused by the mutations in the MEditerranean FeVer (MEFV) gene, it mainly affects people of Mediterranean descent with a higher incidence in the Turkish, Jewish, Arabic, and Armenian populations. As our understanding of FMF improves, it becomes clearer that we are facing with a more complex picture of FMF with respect to its pathogenesis, penetrance, variant type (gain-of-function vs. loss-of-function), and inheritance. In this study, MEFV gene analysis results and clinical findings of 27,504 patients from 35 universities and institutions in Turkey and Northern Cyprus are combined in an effort to provide a better insight into the genotype-phenotype correlation and how a specific variant contributes to certain clinical findings in FMF patients. Our results may help better understand this complex disease and how the genotype may sometimes contribute to phenotype. Unlike many studies in the literature, our study investigated a broader symptomatic spectrum and the relationship between the genotype and phenotype data. In this sense, we aimed to guide all clinicians and academicians who work in this field to better establish a comprehensive data set for the patients. One of the biggest messages of our study is that lack of uniformity in some clinical and demographic data of participants may become an obstacle in approaching FMF patients and understanding this complex disease