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- 저자 : Merriman, Tony R. (검색결과 6 건)
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Acute Compartment Syndrome after Non-Contact Peroneus Longus Muscle Rupture
Jarrad Merriman,Diego Villacis,Curtis Kephart,Anthony Yi,Russ Romano,George F. Rick Hatch 대한정형외과학회 2015 Clinics in Orthopedic Surgery Vol.7 No.4
This case demonstrates a rare variation in the pattern of injury and the presentation of acute lateral compartment syndrome of the leg. Although uncommon, lateral compartment syndrome of the leg after an ankle inversion leading to peroneus longus muscle rupture has been previously documented. This case was unusual because there was no overt ankle injury and the patient was able to continue physical activity, in spite of a significant rupture of the peroneus longus muscle that was determined later. This case highlights the necessary vigilance clinicians must maintain when assessing non-contact injuries in patients with possible compartment syndrome.
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Mobility/Fixity: Rethinking Binaries in Mobility Studies
Peter Merriman Academy of Mobility Humanities 2023 Mobility Humanities Vol.2 No.1
In this paper, I outline some of the different conceptual approaches to mobility and immobility/fixity that have emerged in mobility studies over the past few decades, connecting this work to broader philosophical and methodological debates in the humanities and social sciences. I discuss writings which have distinguished between mobility and moorings, mobility and motility, and nomadic and sedentary metaphysics, before focussing upon studies which either approach mobility-fixity as a continuum, or highlight the many qualities, events and experiences which traverse or cut across this binary. In the final section I outline Gilles Deleuze and Félix Guattari’s theoretical approach to movement, affect and becoming, in which they distinguish between molar and molecular becomings and movements. By adopting a processual and non-representational approach to mobility and stasis I argue that the problem is not one of understanding when and why things move or are still, but of tracing when and how movements become perceptible and imperceptible.
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Impact of skeletal divergence on oral health-related quality of life and self-reported jaw function
Joseph Safwat Antoun,William Murray Thomson,Tony Raymond Merriman,Roberto Rongo,Mauro Farella 대한치과교정학회 2017 대한치과교정학회지 Vol.47 No.3
Objective: To investigate the differences in oral health-related quality of life (OHRQoL) and self-reported jaw function between patients with hyperdivergent and normodivergent facial types. Methods: Eighty patients with a distinctively hyperdivergent facial type (mandibular plane angle greater than 2 standard deviations, or 42°) and 80 controls were individually matched according to age, sex, ethnicity, and treatment stage. Data were collected using self-report questionnaires such as the Oral Health Impact Profile (OHIP-14) and Jaw Functional Limitation Scale (JFLS-8). Results: The mean age of the patients was 17.2 ± 4.6 years (range, 12–49 years), with most (65.0%) being female and of New Zealand European origin (91.3%). Individuals with hyperdivergent facial types had higher overall and social domain scores on the OHIP-14 (p < 0.05) than did the ones with normodivergent facial types. However, the intergroup differences in JFLS-8 scores were not significant (p > 0.05). Conclusions: Jaw function appears to be similar in individuals with hyperdivergent and normodivergent facial morphologies. However, those with hyperdivergent facial types are more likely to self-report poorer OHRQoL than are those with normal faces, especially in relation to social aspects.
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Jordan, Daniel M.,Choi, Hyon K.,Verbanck, Marie,Topless, Ruth,Won, Hong-Hee,Nadkarni, Girish,Merriman, Tony R.,Do, Ron Public Library of Science 2019 PLoS medicine Vol.16 No.1
<▼1><P><B>Background</B></P><P>Studies have shown strong positive associations between serum urate (SU) levels and chronic kidney disease (CKD) risk; however, whether the relation is causal remains uncertain. We evaluate whether genetic data are consistent with a causal impact of SU level on the risk of CKD and estimated glomerular filtration rate (eGFR).</P><P><B>Methods and findings</B></P><P>We used Mendelian randomization (MR) methods to evaluate the presence of a causal effect. We used aggregated genome-wide association data (<I>N</I> = 110,347 for SU, <I>N</I> = 69,374 for gout, <I>N</I> = 133,413 for eGFR, <I>N</I> = 117,165 for CKD), electronic-medical-record-linked UK Biobank data (<I>N</I> = 335,212), and population-based cohorts (<I>N</I> = 13,425), all in individuals of European ancestry, for SU levels and CKD. Our MR analysis showed that SU has a causal effect on neither eGFR level nor CKD risk across all MR analyses (all <I>P</I> > 0.05). These null associations contrasted with our epidemiological association findings from the 4 population-based cohorts (change in eGFR level per 1-mg/dl [59.48 μmol/l] increase in SU: −1.99 ml/min/1.73 m<SUP>2</SUP>; 95% CI −2.86 to −1.11; <I>P</I> = 8.08 × 10<SUP>−6</SUP>; odds ratio [OR] for CKD: 1.48; 95% CI 1.32 to 1.65; <I>P</I> = 1.52 × 10<SUP>−11</SUP>). In contrast, the same MR approaches showed that SU has a causal effect on the risk of gout (OR estimates ranging from 3.41 to 6.04 per 1-mg/dl increase in SU, all <I>P</I> < 10<SUP>−3</SUP>), which served as a positive control of our approach. Overall, our MR analysis had >99% power to detect a causal effect of SU level on the risk of CKD of the same magnitude as the observed epidemiological association between SU and CKD. Limitations of this study include the lifelong effect of a genetic perturbation not being the same as an acute perturbation, the inability to study non-European populations, and some sample overlap between the datasets used in the study.</P><P><B>Conclusions</B></P><P>Evidence from our series of causal inference approaches using genetics does not support a causal effect of SU level on eGFR level or CKD risk. Reducing SU levels is unlikely to reduce the risk of CKD development.</P></▼1><▼2><P><B>Author summary</B></P><P><B>Why was this study done?</B></P><P>Epidemiological studies have shown strong correlations between serum urate (SU) levels and chronic kidney disease (CKD) risk.</P><P>Elevated SU levels are often found in patients with CKD, but it is not clear whether high serum urate is a cause of kidney disease or just a common co-occurrence.</P><P>Previous studies examining whether SU levels had a causal effect on CKD were limited due to not having large enough samples to detect a true causal relationship if it existed and/or had limitations related to the methodology.</P><P>Several clinical trials have been started that aim to use urate-lowering medication to prevent CKD.</P><P><B>What did the authors do and find?</B></P><P>To determine whether SU level has a causal effect on CKD, we used a methodology known as Mendelian randomization to test whether genetic variants known to increase SU level also increased the risk of CKD.</P><P>We used multiple datasets to perform Mendelian randomization analyses, which included meta-analyses performed across multiple population-based cohorts, 4 individual population-based cohorts, and the large electronic-medical-record-linked UK Biobank.</P><P>Across all datasets, we found no significant causal connection between SU level and risk of CKD.</P><P><B>What do these findings mean?</B></P><P>Our findings do not support a causal role of SU level in CKD.</P><P>Lower SU levels would be unlikely to translate into reduced risk of CKD.</P></▼2>
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