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Saskia PJ Verkleij Pim AJ Luijsterburg Sten P Willemsen Bart W Koes Arthur M Bohnen Sita MA Bierma-Zeinstra 《The British journal of general practice》2015,65(637):e530-e537
Background
The effectiveness of diclofenac versus paracetamol in primary care patients with pain caused by knee osteoarthritis is unclear.Aim
To assess the effectiveness of diclofenac compared with paracetamol over a period of 2, 4, and 12 weeks in patients with knee osteoarthritis.Design and setting
Randomised controlled trial in general practice.Method
There were 104 patients included in the study, they were aged ≥45 years consulting their GP with knee pain caused by knee osteoarthritis. Patients were randomly allocated to diclofenac (n = 52) or paracetamol (n = 52) for at least 2 weeks. Primary outcomes were daily knee pain severity, and knee pain and function measured with the Knee Injury and Osteoarthritis Outcome Score (KOOS).Results
Over a period of 2- and 4-weeks follow-up, no significant difference in daily knee pain was found between the patient groups: estimated differences of 0.5 (95% CI = −0.2 to 1.3) and −0.2 (95% CI = −1.0 to 0.7), respectively. Over the 12-weeks follow-up, no significant differences were found between both groups for KOOS pain: estimated difference of −2.8 (95% CI = −10.7 to 5.1) and KOOS function of −2.7 (−10.6 to 5.0).Conclusion
Over a period of 2- and 4-weeks follow-up no significant difference in daily measured knee pain severity was found between primary care patients with knee osteoarthritis taking paracetamol or diclofenac. Also, over a period of 12-weeks follow-up no significant differences were found regarding KOOS pain and KOOS function between both groups. Patients more frequently reported minor adverse events after taking diclofenac (64%) than paracetamol (46%). 相似文献87.
Robert L. Kline PhD Johannes van der Mark MSc David F. Cechetto PhD 《The American journal of cardiology》1994,74(13):A20-A24
Rilmenidine binds to 2-adrenoceptors and imidazoline receptors in the central nervous system and the kidney. To test the hypothesis that rilmenidine would increase sodium excretion, renal function was studied in rats with innervated and denervated kidneys to distinguish between indirect (via renal sympathetic nerves) and direct effects of rilmenidine on the kidney. Standard clearance techniques were used in Wistar rats anesthetized with thiobutabarbital to measure renal function during 80 minutes of infusion of 0.9% NaCl or rilmenidine (20 or 50 μg · kg−1 · min−1 intravenously). Snares on abdominal arteries were used to offset hypotension induced by rilmenidine. Heart rate decreased by 80–120 beats/min with either dose of rilmenidine. At 20 μg · kg−1 · min−1, rilmenidine increased total and fractional excretion of sodium and clearance of osmoles while decreasing free water clearance from innervated kidneys. There were no changes in these variables in chronically denervated kidneys. Direct recording of renal sympathetic nerve activity showed a progressive, marked decrease in nerve activity during the low-dose infusion of rilmenidine. At 50 μg · kg−1 · min−1, rilmenidine produced a differential effect on the clearance of osmoles by innervated and denervated kidneys but both kidneys had an increase in free water clearance. The data indicate that rilmenidine increases sodium excretion indirectly in anesthetized rats by decreasing renal sympathetic nerve activity. At doses and infusion periods used in these studies, there was no evidence for a direct effect of rilmenidine on sodium excretion. The increase in free water clearance seen with the high dose of rilmenidine suggests that the inhibitory effect of 2-adrenoceptor activation on vasopressin is involved at this dose. On the other hand, the effect of rilmenidine on sodium excretion may involve central imidazoline receptors. 相似文献
88.
Styles LA; Schalkwijk CG; Aarsman AJ; Vichinsky EP; Lubin BH; Kuypers FA 《Blood》1996,87(6):2573-2578
Acute chest syndrome (ACS) is associated with significant morbidity and is the leading cause of death in patients with sickle cell disease (SCD). Recent reports suggest that bone marrow fat embolism can be detected in many cases of severe ACS. Secretory phospholipase A2 (sPLA2) is an important inflammatory mediator and liberates free fatty acids, which are felt to be responsible for the acute lung injury of the fat embolism syndrome. We measured SPLA2 levels in 35 SCD patients during 20 admissions for ACS, 10 admissions for vaso-occlusive crisis, and during 12 clinic visits when patients were at the steady state. Eleven non-SCD patients with pneumonia were also evaluated. To determine if there was a relationship between sPLA2 and the severity of ACS we correlated SPLA2 levels with the clinical course of the patient. In comparison with normal controls (mean = 3.1 +/- 1.1 ng/mL), the non- SCD patients with pneumonia (mean = 68.6 +/- 82.9 ng/mL) and all three SCD patient groups had an elevation of SPLA2 (steady state mean = 10.0 +/- 8.4 ng/mL; vaso-occlusive crisis mean = 23.7 +/- 40.5 ng/mL; ACS mean = 336 +/- 209 ng/mL). In patients with ACS sPLA2 levels were 100- fold greater than normal control values, 35 times greater than values in SCD patients at baseline, and five times greater than non-SCD patients with pneumonia. The degree of SPLA2 elevation in ACS correlated with three different measures of clinical severity and, in patients followed sequentially, the rise in SPLA2 coincided with the onset of ACS. The dramatic elevation of SPLA2 in patients with ACS but not in patients with vaso-occlusive crisis or non-SCD patients with pneumonia and the correlation between levels of SPLA2 and clinical severity suggest a role for SPLA2 in the diagnosis and, perhaps, in the pathophysiology of patients with ACS. 相似文献
89.
Samuel O. Ewalefo Malcolm Dombrowski Takashi Hirase Jorge L. Rocha Mitchell Weaver Alex Kline Dwayne Carney MaCalus V. Hogan 《Current reviews in musculoskeletal medicine》2018,11(4):546-557
Purpose of Review
Trauma is the principle cause of osteoarthritis in the ankle, which is associated with significant morbidity. This review highlights the current literature for the purpose of bringing the reader up-to-date on the management of posttraumatic ankle arthritis, describing treatment efficacy, indications, contraindications, and complications.Recent Findings
Recent studies on osteoarthritis have demonstrated variability among anatomic locations regarding the mechanisms and rates of development for posttraumatic osteoarthritis, which are attributed to newly discovered biological differences intrinsic to each joint. Regarding surgical management of posttraumatic ankle arthritis, osteochondral allograft transplantation of the talus, and supramalleolar osteotomies have demonstrated promising results. Additionally, the outpatient setting was found to be appropriate for managing pain following total ankle arthroplasty, associated with low complication rates and no readmission.Summary
Management for posttraumatic ankle arthritis is generally progressive. Initial treatment entails nonpharmacologic options with surgery reserved for posttraumatic ankle arthritis refractory to conservative treatment. Patient demographics and lifestyles should be carefully considered when formulating a management strategy, as outcomes are dependent upon the satisfaction of each set of respective criteria. Ultimately, the management of posttraumatic ankle arthritis should be individualized to satisfy the needs and desires, which are specific to each patient.90.
Gayatri Shankar Chilambi Iris H. Gao Bo Kyeong Yoon Soohyun Park Lisa M. Kawakami Vikashini Ravikumar Mary B. Chan-Park Nam-Joon Cho Guillermo C. Bazan Kimberly A. Kline Scott A. Rice Jamie Hinks 《RSC advances》2018,8(19):10284
The growing problem of antibiotic resistant bacteria, along with a dearth of new antibiotics, has redirected attention to the search for alternative antimicrobial agents. Conjugated oligoelectrolytes (COEs) are an emerging class of antimicrobial agents which insert into bacterial cell membranes and are inhibitory against a range of Gram-positive and Gram-negative bacteria. In this study, the extent of COE resistance that Enterococcus faecalis could achieve was studied. Enterococci are able to grow in hostile environments and develop resistance to membrane targeting antibiotics such as daptomycin in clinical settings. Herein we expand our knowledge of the antimicrobial mechanism of action of COEs by developing COE-resistant strains of E. faecalis OG1RF. Evolution studies yielded strains with a moderate 4–16 fold increase in antimicrobial resistance relative to the wild type. The resistant isolates accumulated agent-specific mutations associated with the liaFSR operon, which is a cell envelope-associated stress-response sensing and regulating system. The COE resistant isolates displayed significantly altered membrane fatty acid composition. Subsequent, exogenous supplementation with single fatty acids, which were chosen based on those dominating the fatty acid profiles of the mutants, increased resistance of the wild-type E. faecalis to COEs. In combination, genetic, fatty acid, and uptake studies support the hypothesis that COEs function through insertion into and disruption of membranes and that the mechanism by which this occurs is specific to the disrupting agent. These results were validated by a series of biophysical experiments showing the tendency of COEs to accumulate in and perturb adapted membrane extracts. Collectively, the data support that COEs are promising antimicrobial agents for targeting E. faecalis, and that there is a high barrier to the emergence of severely resistant strains constrained by biological limits of membrane remodeling that can occur in E. faecalis.COEs are emerging antimicrobials to combat drug resistant infections and to which bacteria develop only limited resistance. 相似文献