605 research outputs found
Outcomes of bipolar radial head prosthesis to treat complex radial head fractures in 22 patients with a mean follow-up of 50 months
AbstractBackgroundRadial head replacement is indicated to treat complex proximal radial fractures that are not amenable to internal fixation.HypothesisImplantation of a bipolar radial head prosthesis after radial head excision ensures stability of the elbow and forearm, thereby promoting ligament healing and restoring elbow function.Material and methodsTwenty-two patients managed with implantation of a bipolar radial head prosthesis (Guepar®) were evaluated after a mean follow-up of 50 months. The procedure was performed in the acute setting in 16 patients, including 13 with associated injuries; and at the stage of sequelae in 6 patients.ResultsProsthesis removal was required in 4 patients. Of the remaining 18 patients, 14 (77%) had satisfactory Mayo Elbow Performance Score values, 14 (77%) little or no functional impairment, and 11 (61%) little or no pain. Mean motion arcs were 100° in flexion-extension and 143° in pronation-supination. Mean elbow strength in flexion and mean wrist strength were 67% and 86%, respectively, of those on the contralateral normal side. Radio-lucent lines were visible around the prosthesis in 5 patients, radial neck osteolysis in 10 patients, and capitellar erosion in 7 patients. Seven patients each experienced a complication. Early revision surgery to treat elbow instability was required in 6 patients.DiscussionOutcomes after Guepar® bipolar radial head prosthesis implantation were disappointing in patients with complex radial head fractures seen in the acute or chronic setting. The associated injuries to bones and ligaments and the measures taken to repair them influence the prognosis. The complication rate is non-negligible and seems to increase over time.Level of evidenceIV, retrospective study
P18-01. Exquisite specificity of CTL response to the M184V mutation
International audiencen.
Equine lamellar energy metabolism studied using tissue microdialysis
Failure of lamellar energy metabolism may contribute to the pathophysiology of equine laminitis. Tissue microdialysis has the potential to dynamically monitor lamellar energy balance over time. The objectives of this study were to develop a minimally invasive lamellar microdialysis technique and use it to measure normal lamellar energy metabolite concentrations over 24h. Microdialysis probes were placed (through the white line) into either the lamellar dermis (LAM) (n=6) or the sublamellar dermis (SUBLAM) (n=6) and perfused continuously over a 24h study period. Probes were placed in the skin dermis (SKIN) for simultaneous comparison to LAM (n=6). Samples were collected every 2h and analysed for glucose, lactate, pyruvate, urea and glycerol concentrations. LAM was further compared with SUBLAM by simultaneous placement and sampling in four feet from two horses over 4h. Horses were monitored for lameness, and either clinically evaluated for 1month after probe removal (n=4) or subjected to histological evaluation of the probe site (n=10).There were no deleterious clinical effects of probe placement and the histological response was mild. Sample fluid recovery and metabolite concentrations were stable for 24h. Glucose was lower (and lactate:glucose ratio higher) in LAM compared with SUBLAM and SKIN (
An Optimized Protocol for Molecular Screening of Avian Pathogenic Escherichia Coli From Broiler Chickens in South East Queensland, Australia
Avian pathogenic Escherichia coli (APEC) is the causative agent of avian colibacillosis and causes localized and/or systemic infections in poultry. The presence of various virulence genes (VGs) may be a useful marker for the detection of APEC directly from fecal samples. The objectives of this study were to evaluate and compare 3 different DNA extraction methods from cloacal swabs and fecal samples of broiler chickens and determine if APEC can be detected directly from feces. The DNA extraction methods were assessed by measuring DNA yield and purity, absence of DNA shearing, 16S ribosomal DNA amplification, and reproducibility. Repeated bead beating plus column (RBB+C) was the preferred extraction method, as it yielded an adequate amount of quality DNA for PCR directly from feces. The DNA extracted from feces, with RBB+C method and DNA extracted from E. coli isolates of organs and feces, taken from 23 broiler chickens (10 healthy, 9 with colibacillosis, and 4 unhealthy with other infections), were screened with a pentaplex-PCR for the prevalence of APEC-associated VGs: iroN, ompT, iutA, iss, and hlyF. There was a statistically significant correlation between the presence of the 5 VGs in E. coli cultured from the cloaca, fecal, and organs samples from chicken affected with colibacillosis. However, screening extracted DNA from the feces for the selected VGs was not an effective diagnostic tool to detect APEC as all of the VGs were detected in the extracted fecal DNA from all chickens
Production of the soluble pattern recognition receptor PTX3 by myeloid, but not plasmacytoid, dendritic cells
PTX3 is a prototypic of long pentraxin consisting of an N-terminal portion coupled to a C-terminal pentraxin domain, the latter related to short pentraxins (C-reactive protein and serum amyloid P component). PTX3 is a soluble pattern recognition receptor, which plays a non-redundant role in resistance against selected pathogens and in female fertility. The present study was designed to analyze the production of PTX3 by human dendritic cells (DC) and to define the role of different innate immunity receptors in its induction. Human monocyte-derived DC produced copious amounts of PTX3 in response to microbial ligands engaging different members of the Toll-like receptor (TLR) family (TLR1 through TLR6), whereas engagement of the mannose receptor had no substantial effect. DC were better producers of PTX3 than monocytes and macrophages. Freshly isolated peripheral blood myeloid DC produced PTX3 in response to diverse microbial stimuli. In contrast, plasmacytoid DC exposed to influenza virus or to CpG oligodeoxynucleotides engaging TLR9, did not produce PTX3. PTX3-expressing DC were present in inflammatory lymph nodes from HIV-infected patients. These results suggest that DC of myelomonocytic origin are a major source of PTX3, a molecule which facilitates pathogen recognition and subsequent activation of innate and adaptive immunity
AUTOCOUNTER, an ImageJ JavaScript to analyze LC3B-GFP expression dynamics in autophagy-induced astrocytoma cells
An ImageJ JavaScript, AUTOCOUNTER, was specifically developed to monitor and measure LC3B-GFP expression in living human astrocytoma cells, namely T98G and U373-MG. Discrete intracellular GFP fluorescent spots derived from transduction of a Baculovirus replication-defective vector (BacMam LC3B-GFP), followed by microscope examinations at different times. After viral transgene expression, autophagy was induced by Rapamycin administration and assayed in ph-p70S6K/p70S6K and LC3B immunoblotting expression as well as by electron microscopy examinations. A mutated transgene, defective in LC3B lipidation, was employed as a negative control to further exclude fluorescent dots derived from protein intracellular aggregation. The ImageJ JavaScript was then employed to evaluate and score the dynamics changes of the number and area of LC3B-GFP puncta per cell in time course assays and in complex microscope examinations. In conclusion, AUTOCOUNTER enabled to quantify LC3B-GFP expression and to monitor dynamics changes in number and shapes of autophagosomal-like vesicles: it might therefore represent a suitable algorithmic tool for in vitro autophagy modulation studies
A unique MSH2 exon 8 deletion accounts for a major portion of all mismatch repair gene mutations in Lynch syndrome families of Sardinian origin
Lynch syndrome is an autosomal-dominant hereditary condition predisposing to the development of specific cancers, because of germline mutations in the DNA-mismatch repair (MMR) genes. Large genomic deletions represent a significant fraction of germline mutations, particularly among the MSH2 gene, in which they account for 20% of the mutational spectrum. In this study we analyzed 13 Italian families carrying MSH2 exon 8 deletions, 10 of which of ascertained Sardinian origin. The overrepresentation of Sardinians was unexpected, as families from Sardinia account for a small quota of MMR genes mutation tests performed in our laboratory. The hypothesis that such a result is owing to founder effects in Sardinia was tested by breakpoint junctions sequencing and haplotype analyses. Overall, five different exon eight deletions were identified, two of which recurrent in families, all apparently unrelated, of Sardinian origin (one in eight families, one in two families). The c.1277–1180_1386+2226del3516insCATTCTCTTTGAAAA deletion shares the same haplotype between all families and appears so far restricted to the population of South-West Sardinia, showing the typical features of a founder effect. The three non-Sardinian families showed three different breakpoint junctions and haplotypes, suggesting independent mutational events. This work has useful implications in genetic testing for Lynch syndrome. We developed a quick test for each of the identified deletions: this can be particularly useful in families of Sardinian origin, in which MSH2 exon 8 deletions may represent 50% of the overall mutational spectrum of the four MMR genes causing Lynch syndrome
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