71 research outputs found

    Risk factors associated with intraoperative complications in primary shoulder arthroplasty

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    Background and purpose - Increasing numbers of shoulder arthroplasty are performed internationally. The predictors of intraoperative complications when implanting primary shoulder replacements are unknown. We determined the incidence of intraoperative complications during primary shoulder arthroplasty using the National Joint Registry of England, Wales, Northern Ireland and the Isle of Man (NJR), and analyzed the associated risk factors for complications. Patients and methods - NJR data on primary shoulder arthroplasty were scrutinized for intraoperative complications. 2 analyses were performed: the first examined the incidence and predictors of any recorded complication; the second examined the incidence and predictors for intraoperative fractures specifically. Analysis of risk factors was performed using multivariable binary logistic regression modeling. Results - 12,559 primary shoulder arthroplasties were recorded, with an intraoperative complication rate of 2.5%, the majority being fractures (1.6% overall). The incidence of all complications was lower in men (RR vs. women =0.63 (95% CI 0.47-0.84)). Patients undergoing surgery for avascular necrosis (RR =2.3 (1.3-4.2)) or trauma sequelae (RR =1.6 (1.2-2.7)) had a higher risk of complications compared with OA. Patients undergoing a stemmed hemiarthroplasty (RR =1.8 (1.2-2.5)) and reverse shoulder arthroplasty (RR 1.6 (1.1-2.5)) had a higher risk of complications compared with total shoulder arthroplasty. The incidence of all complications was less in patients undergoing resurfacing arthroplasty (vs. total shoulder arthroplasty (RR 0.42 (0.24-0.73)) and when performing the superior approach (vs. deltopectoral (RR 0.56 (0.39-0.80)). Interpretation - This is the first study to use a national data set to examine risk factors for intraoperative complications during all types of primary shoulder arthroplasty, and identifies several previously unrecognized risk factors, such as surgical approach

    The non-pathogenic mycobacteria M. smegmatis and M. fortuitum induce rapid host cell apoptosis via a caspase-3 and TNF dependent pathway

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    <p>Abstract</p> <p>Background</p> <p>The HIV pandemic raised the potential for facultative-pathogenic mycobacterial species like, <it>Mycobacterium kansasii</it>, to cause disseminating disease in humans with immune deficiencies. In contrast, non-pathogenic mycobacterial species, like <it>M. smegmatis</it>, are not known to cause disseminating disease even in immunocompromised individuals. We hypothesized that this difference in phenotype could be explained by the strong induction of an innate immune response by the non-pathogenic mycobacterial species.</p> <p>Results</p> <p>A comparison of two rapid-growing, non-pathogenic species (<it>M. smegmatis </it>and <it>M. fortuitum</it>) with two facultative-pathogenic species (<it>M. kansasii </it>and <it>M. bovis </it>BCG) demonstrated that only the non-pathogenic bacteria induced strong apoptosis in human THP-1 cells and murine bone marrow-derived macrophages (BMDM) and dendritic cells (BMDD). The phospho-<it>myo</it>-inositol modification of lipoarabinomannan (PI-LAM) isolated from non-pathogenic species may be one of the cell wall components responsible for the pro-inflammatory activity of the whole bacteria. Indeed, PI-LAM induces high levels of apoptosis and IL-12 expression compared to the mannosyl modification of LAM isolated from facultative-pathogenic mycobacteria. The apoptosis induced by non-pathogenic <it>M. smegmatis </it>was dependent upon caspase-3 activation and TNF secretion. Consistently, BALB/c BMDM responded by secreting large amounts of TNF upon infection with non-pathogenic but not facultative-pathogenic mycobacteria. Interestingly, C57Bl/6 BMDM do not undergo apoptosis upon infection with non-pathogenic mycobacteria despite the fact that they still induce an increase in TNF secretion. This suggests that the host cell signaling pathways are different between these two mouse genotypes and that TNF is necessary but not sufficient to induce host cell apoptosis.</p> <p>Conclusion</p> <p>These results demonstrate a much stronger induction of the innate immune response by non-pathogenic versus facultative-pathogenic mycobacteria as measured by host cell apoptosis, IL-12 and TNF cytokine induction. These observations lend support to the hypothesis that the strong induction of the innate immune response is a major reason for the lack of pathogenicity in fast-growing mycobacteria.</p

    Risk factors for revision after shoulder arthroplasty: 1,825 shoulder arthroplasties from the Norwegian Arthroplasty Register

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    Background and purpose Previous studies on shoulder arthroplasty have usually described small patient populations, and few articles have addressed the survival of shoulder implants. We describe the results of shoulder replacement in the Norwegian population (of 4.7 million) during a 12-year period. Trends in the use of shoulder arthroplasty during the study period were also investigated

    Biomarkers for Detecting Resilience against Mycobacterial Disease in Animals

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    Transcortical motor aphasia

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    The defining symptoms of transcortical motor aphasia (TCMA) are nonfluent verbal output with relatively preserved repetition. Other symptoms, such as naming difficulties, agrammatic output, or even some paraphasias, may occur, but these are not cardinal symptoms defining TCMA and are not necessary for the diagnosis. The core anatomy involved in TCMA is a lesion of the medial frontal cortex, especially the left presupplementary motor area (pre-SMA) and adjacent Brodmann’s area 32; a lesion of the left posterior inferior frontal cortex, especially pars opercularis and ventral lateral premotor cortex; or a lesion of the pathways between these frontal structures. TCMA occasionally has been reported with a lesion of the left basal ganglia, the left thalamus, or the ascending dopaminergic pathways. From a cognitive standpoint, TCMA can be conceptualized as a disorder of intention, in other words, as a disorder of initiation and continuation of spoken language that is internally motivated. The medial frontal cortex provides the impetus to speak; this impetus to speak is conveyed to lateral frontal structures through frontal-subcortical pathways where it activates various language production mechanisms. The influence of the ascending dopaminergic pathways may occur either through their heavy connections with the pre- SMA region or through their influence on the basal ganglia. The influence of the basal ganglia and thalamus probably occurs through their connections with the medial frontal cortex. Assessments for TCMA should involve a thorough evaluation of conversational or narrative language output and repetition. New treatments are available that attemto engage right- hemisphere intention mechanisms with left- hand movements and may be effective in TCMA. Although dopamine agonists have also shown some positive effects in increasing verbal output in TCMA, trials have been small, and some caution must be exercised in interpreting these findings

    Treatment of Glenohumeral Arthrosis

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    Sampling phase lock loop (PLL) with low power clock buffer

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    A sampling phase locked loop (PLL) circuit includes a pull-up/down buffer configured to convert an oscillator reference clock into a square wave sampling control signal input to a sampling phase detector. The buffer circuit is configured to reduce power by controlling the switching of the pull-up and pull-down transistors (and thereby the transitions of the sampling control signal) so that the transistors are not on at the same time

    Low power and low spur sampling PLL

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    Abstract Control circuitry and method of controlling a sampling phase locked loop (PLL). By controlling the duty cycle of one or more sampling control signals, power consumption by the reference signal buffer and spurious output signals from the sampling PLL being controlled can be reduced

    Phase-locked loop including sampling phase detector and charge pump with pulse width control

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    Phase-locked loop (PLL) circuitry in which a sampling phase detector samples the output signal in accordance with the reference signal and a frequency detector detects the output signal frequency in accordance with the reference signal
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