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Objective: To investigate the effect of individualized contrast administration in improving the enhancement homogeneity in vessels and image quality in coronary CT angiography (CCTA). Methods: Sixty CCTA patients were randomly divided into two groups with different contrast injection protocols: treatment group (n=30) was treated with weight-dependent injection protocol at 22 mg/(g•s) of idion, injection velocity=body mass×22/contrast agent concentration. Control group (n=30) was treated with a different injection protocol. The iodine flow rate in this group was determined by patient body mass index (BMI), iodine flow rate=1.2 g/s, 1.4 g/s and 1.6 g/s. Injection flow rate= iodine flow rate/contrast agent concentration. Theiohexol (350 mg/mL) was used in both groups, and the injection time was fixed at 10 s and contrast agent dose=injection velocity×injection time. The other scanning parameters were the same. The enhancement change rate in AS and the three major arteries was calculated for the patient population. The subjective image quality scores were also compared. Results: The change rates of vascular enhancement at interested blood vessels in treatment group (12.9%, 11.8%, 11.0% and 11.1%, respectively) were significantly lower than those in in control group (23.3%, 18.7%, 16.7% and 20.5%, respectively) (P=0.001). There was no significant difference between the two groups in subjective image quality score (P=0.095). Conclusion: Individualized contrast injection protocol in CCTA can provide us with a more uniform enhancement in coronary arteries, and improve the overall image quality.
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Objective To explore the value of intravoxel incoherent motion diffusion weighted imaging (IVIM-DWI ) in patients with progressive muscular dystrophy .Methods We enrolled 7 patients with known progressive muscular dystrophy (4 Becker muscle dystrophy ,BMD;3 limb-girdle muscle dystrophy ,LGMD) in this study .Both IVIM ,T1 WI and T2 STIR sequences were performed on both thighs of all the subjects .Slow ADC ,fast ADC and fraction of fast ADC (Ff ) were measured .Tl weighted images were used to assess the fat infiltration of their thigh muscles using a 0-5 modified version of Mercuri's scale .Slow ADC ,fast ADC and fraction of fast ADC (Ff) were compared among the fatty infiltration ,edematous muscle and unaffected muscle (neither edematous nor fatty infiltration muscles in patients ) .One-way analysis of variance was used for statistical analyses with a significance of P < 0 .05 . Results The mean slow ADC value of fatty infiltration . edematous muscle . and unaffected muscle was 0 .75+0.39,1 .14±0 .19,and 1.00±0 .11 (10 -3 mm2/s ) , respectively ( P < 0 .05 ) .The mean fast ADC value in the three groups was 7 .14±6 .51,13 .56±9 .67,and 4 .02±1.89 (10-3 mm2 /s ) , respectively (P< 0 .05 ) . There was no significant difference in the Ff values among the three groups ( P > 0 .05 ) .The mean slow ADC value in different grades of steatosis was 1 .00±0 .11, 0.98±0 .17, and 0 .50±0 .29 (10-3 mm2/s) , respectively ; the slow ADC value in heavy fat infiltration group differed significantly from that in the other two groups( P<0.05 ).Conclusion IVIM-DWI can be used to quantitatively evaluate the thigh diffusion and microcirculation characteristics of muscles in patients with PMD , make a quantitative analysis of edema and steatosis of the muscle .and reflect the degree of muscle steatosis .
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A sensitive and selective liquid chromatography-tandem mass spectrometric (LC-MS/MS) method was developed and validated for the determination of betamethasone in human plasma. The analyte was isocratically eluted on a Venusil XBP C8 column (200 mm x 3.9 mm ID, 5 microm) with methanol-water mol x L(-1) ammonium formate) (80:20) at a flow rate of 0.4 mL x min(-1), and detected (containing 5 mmol x L(-1) ammonium formate) (80:20) at a flow rate of 0.4 mL x min(-1), and detected with a triple quad LC-MS/MS using ESI with positive ionization. Ions monitored in the multiple reaction monitoring (MRM) mode were m/z 393.3-->355.2 for betamethasone and m/z 361.3-->343.2 for prednisolone (IS). Betamethasone was extracted from 0.5 mL human plasma with ethyl acetate. The average recovery is 88.24% and the low limit of quantitation (LLOQ) was 0.5 ng x mL(-1). The 3-day validation study demonstrated excellent precision and accuracy across the calibration range of 0.5-80.0 ng x mL(-1). The method was successfully applied to the pharmacokinetic study of compound betamethason injection in healthy Chinese volunteers.
Subject(s)
Humans , Male , Young Adult , Anti-Inflammatory Agents , Blood , Pharmacokinetics , Area Under Curve , Betamethasone , Blood , Pharmacokinetics , Chromatography, Liquid , Methods , Injections, Intramuscular , Spectrometry, Mass, Electrospray Ionization , Methods , Tandem Mass Spectrometry , MethodsABSTRACT
<p><b>OBJECTIVE</b>To determine the antibiotics resistance, aminoglycoside-modifying enzymes and homology of high-level gentamycin resistant enterococcus in clinical specimens.</p><p><b>METHODS</b>The high-level gentamicin resistant (HLGR) isolates were screened by the agar method and the resistance of 14 antimicrobial agents was determined by K-B method. The aminoglycoside-modifying enzyme genes were detected by polymerase chain reaction (PCR). Pulsed-field gel electrophoresis (PFGE) was used to analyze the homology of HLGR isolates.</p><p><b>RESULTS</b>The ratio of HLGR was 64.2% (68/106). Among the HLGR,there were no isolates resistant to linezolid, vancomycin and tecoplanin, and Enterococcus faecium was more resistant to beta-lactam antibiotics and quinolone than Enterococcus faecalis. The positive rate of aac(6')-Ie-aph(2')-Ia was 92.6% and 3 isolates had the resistance gene mostly similar to aph(2')-Id. And among 51 HLGR isolates from the hospitalized patients, PFGE grouped 17 E. faecalis isolates into 4 clusters (A-D), and 33 E. faecium isolates into 8 clusters (A-H) with A cluster as predominant.</p><p><b>CONCLUSION</b>HLGR has become the important antibiotic resistance bacteria which results in nosocomial infection; and aac(6')-Ie-aph(2')-Ia is the main aminoglycoside-modifying enzyme gene which causes HLGR.</p>