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41.
Marcus Dill-Macky Christopher Frazer W Bastiaan de Boer 《Journal of Medical Imaging and Radiation Oncology》1999,43(3):315-320
The magnetic resonance imaging (MRI) features of 11 biopsy-proven lesions of focal nodular hyperplasia (FNH) of the liver were reviewed retrospectively. Only three lesions showed atypical features. It is believed MRI can reliably differentiate FNH from other liver tumours when strict criteria are fulfilled. 相似文献
42.
Helena M. de Wit Gerald M. M. Vervoort Henry J. Jansen Wim J. C. de Grauw Bastiaan E. de Galan Cees J. Tack 《Diabetologia》2014,57(9):1812-1819
Aims/hypothesis
The best treatment strategy for a patient with type 2 diabetes who shows pronounced weight gain after the introduction of insulin treatment is unclear. We determined whether addition of a glucagon-like peptide-1 (GLP-1) analogue could reverse pronounced insulin-associated weight gain while maintaining glycaemic control, and compared this with the most practised strategy, continuation and intensification of standard insulin therapy.Methods
In a 26-week, randomised controlled trial (ELEGANT), conducted in the outpatient departments of one academic and one large non-academic teaching hospital in the Netherlands, adult patients with type 2 diabetes with ≥4% weight gain during short-term (≤16 months) insulin therapy received either open-label addition of liraglutide 1.8 mg/day (n?=?26) or continued standard therapy (n?=?24). A computer-generated random number list was used to allocate treatments. Participants were evaluated every 4–6 weeks for weight, glycaemic control and adverse events. The primary endpoint was between-group weight difference after 26 weeks of treatment (intention to treat).Results
Of 50 randomised patients (mean age 58 years, BMI 33 kg/m2, HbA1c 7.4% [57 mmol/mol]), 47 (94%) completed the study; all patients were analysed. Body weight decreased by 4.5 kg with liraglutide and increased by 0.9 kg with standard therapy (mean difference ?5.2 kg [95% CI ?6.7, ?3.6 kg]; p?0.001). The respective changes in HbA1c were ?0.77% (?8.4 mmol/mol) and +0.01% (+0.1 mmol/mol) (difference ?0.74% [?8.1 mmol/mol]) ([95% CI ?1.08%, ?0.41%] [?11.8, ?4.5 mmol/mol]; p?0.001); respective changes in insulin dose were ?29 U/day and +5 U/day (difference ?33 U/day [95% CI ?41, ?25 U/day]; p?0.001). In five patients (19%), insulin could be completely discontinued. Liraglutide was well tolerated; no severe adverse events or severe hypoglycaemia occurred.Conclusions/interpretation
In patients with pronounced insulin-associated weight gain, addition of liraglutide to their treatment regimen reverses weight, decreases insulin dose and improves glycaemic control, and hence seems a valuable therapeutic option compared with continuation of standard insulin treatment. Trial registration ClinicalTrials.gov NCT01392898 Funding The study was funded by Novo Nordisk. 相似文献43.
44.
Jame C. McCrae Noel Sharkey David J. Webb A. D. Bastiaan Vliegenthart James W. Dear 《Clinical toxicology (Philadelphia, Pa.)》2016,54(1):53-55
Introduction: MicroRNA 122 (miR-122) is a new circulating biomarker for liver injury, which increases earlier than conventional markers in patients with acetaminophen hepatotoxicity. However, as co-ingestion of ethanol is common with drug overdose, a confounding effect of acute ethanol consumption on serum miR-122 must be examined. Methods: Blood was collected from healthy volunteers before and after recreational consumption of ethanol. Routine biochemistry and haematology measurements were performed, and serum miR-122 was measured by qPCR. The primary outcome was the difference in serum miR-122 with ethanol consumption. Results: We recruited 18 participants (72% male). Their mean serum ethanol concentration was 113?mg/dl (95% confidence interval [CI] 91–135?mg/dl) after consuming ethanol. Serum miR-122 increased from a mean of 71.3 million (95% CI 29.3–113.2 million) to 139.1 million (95% CI 62.6–215.7 million) copies/ml (2.2-fold increase). There was no significant difference in serum alanine aminotransferase activity before and after ethanol consumption. Conclusion: miR-122 increased with moderate ethanol consumption, but the fold change was modest. As increases with acetaminophen toxicity are 100- to 10 000-fold, moderate ethanol intoxication is unlikely to confound the use of this biomarker of hepatotoxicity. 相似文献
45.
Floating stones were noted in the nonopacified gallbladder at ultrasound examination. Gas-containing fissures in these stones could be demonstrated pre- and postoperatively (Mercedes Benz sign). 相似文献
46.
47.
Arjan P. Schouten van der Velden M.D. Ph.D. Margrethe S. Schlooz-Vries M.D. Carla Boetes M.D. Ph.D. Theo Wobbes M.D. Ph.D. 《American journal of surgery》2009,198(2):262-269
Background
After breast-conserving surgery of ductal carcinoma in situ (DCIS) of the breast or invasive breast carcinoma with an extensive intraductal component, tumor-positive surgical margins are frequently found. Therefore, the extent of the intraductal disease needs to be accurately determined preoperatively.Methods
Data for this review were identified by search of PubMed. Reference lists of selected articles were cross-searched for additional literature.Results
DCIS is accurately detected with magnetic resonance imaging (MRI), but the typical malignant features are inconsistently seen and most often in high-grade DCIS or in DCIS with a small invasive component. The histopathologic extent of DCIS is more accurately demonstrated with MRI. However, overestimation due to benign proliferative lesions does frequently occur. An improved depiction of DCIS could lead to improved preoperative staging. Conversely, the identification of more extensive disease on MRI could give rise to unnecessary interventions. Therefore, MRI should be used carefully and preferable in specialized and experienced centers.Conclussion
To date, there is no evidence that the use of MRI improves outcomes (ie, decreases recurrence rates) in patients with DCIS. 相似文献48.
Samyra H.J. Keus PT MSc Marten Munneke PT PhD Maarten J. Nijkrake PT MSc Gert Kwakkel PT PhD Bastiaan R. Bloem MD PhD 《Movement disorders》2009,24(1):1-14
Even with optimal medical management using drugs or neurosurgery, patients with Parkinson's disease (PD) are faced with progressively increasing mobility problems. For this reason, many patients require additional physical therapy. Here, we review the professional evolution and scientific validation of physical therapy in PD, and highlight several future challenges. To gain insight in ongoing, recently completed or published trials and systematic reviews, we performed a structured literature review and contacted experts in the field of physical therapy in PD. Following publication of the first controlled clinical trial in 1981, the quantity and quality of clinical trials evaluating the efficacy of physical therapy in PD has evolved rapidly. In 2004 the first guideline on physical therapy in PD was published, providing recommendations for evidence‐based interventions. Current research is aiming to gather additional evidence to support specific intervention strategies such as the prevention of falls, and to evaluate the implementation of evidence into clinical practice. Although research focused on physical therapy for PD is a relatively young field, high‐quality supportive evidence is emerging for specific therapeutic strategies. We provide some recommendations for future research, and discuss innovative strategies to improve the organization of allied health care in PD, making evidence‐based care available to all PD patients. © 2008 Movement Disorder Society 相似文献
49.
50.
Bart F.L. van Nuenen MD Thilo van Eimeren MD Joyce P.M. van der Vegt MD Carsten Buhmann MD Christine Klein MD PhD Bastiaan R. Bloem MD PhD Hartwig R. Siebner MD 《Movement disorders》2009,24(Z2):S703-S710
Mutations in the Parkin (PARK2) and PINK1 gene (PARK 6) can cause recessively inherited Parkinson's disease (PD). The presence of a single Parkin or PINK1 mutation is associated with a dopaminergic nigrostriatal dysfunction and conveys an increased risk to develop PD throughout lifetime. Therefore neuroimaging of non‐manifesting individuals with a mutant Parkin or PINK1 allele opens up a window for the investigation of preclinical and very early phases of PD in vivo. Here we review how functional magnetic resonance imaging (fMRI) can be used to identify compensatory mechanisms that help to prevent development of overt disease. In two separate experiments, Parkin mutation carriers displayed stronger activation of rostral supplementary motor area (SMA) and right dorsal premotor cortex (PMd) during a simple motor sequence task and anterior cingulate motor area and left rostral PMd during internal movement selection as opposed to externally cued movements. The additional recruitment of the rostral SMA and right rostral PMd during the finger sequence task was also observed in a separate group of nonmanifesting mutation carriers with a single heterozygous PINK1 mutation. Because mutation carriers were not impaired at performing the task, the additional recruitment of motor cortical areas indicates a compensatory mechanism that effectively counteracts the nigrostriatal dysfunction. These first results warrant further studies that use these imaging genomics approach to tap into preclinical compensation of PD. Extensions of this line of research involve fMRI paradigms probing nonmotor brain functions. Additionally, the same fMRI paradigms should be applied to nonmanifesting mutation carriers in genes linked to autosomal dominant PD. This will help to determine how “generically” the human brain compensates for a preclinical dopaminergic dysfunction. © 2009 Movement Disorder Society 相似文献