ABSTRACT
Objective To investigate the technical requirements for the 3.0T multi-modal quantitative MR imaging of the rabbit liver.Methods A total of 8 rabbits were scanned and T1 mapping,T2 mapping,MT and Gd EOB-DTPA dynamic enhancement images were acquired.For the dynamic enhanced scanning,injecting contrast medium was followed by saline flush with different combinations of injection flow rate (1.5 mL/s and 2 mL/s) and injection volume(6 mL and 8 mL).The quality of the images was assessed and analyzed statistically.Results The total scanning time was about 20-25 min.High-quality images were acquired by T1 mapping,T2 mapping and MT sequences.There was no significant difference in image quality among different groups in Gd-EOB-DTPA dynamic enhanced scanning(P＞0.05).Two rabbits died when the combination of injection flow rate of 2 mL/s and injection volume of 8 mL was used.Conclusion 3.0 T multi-modal quantitative MR scanning of rabbit liver can be achieved successfully if scanning parameters are properly chosen.
ABSTRACT
Spikes in Lamotrigine concentrations levels and associated clinical toxicity may occur unpredictably. This study describes the development and validation of a simple, more rapid, highly sensitive and economical method for measuring Lamotrigine [LTG] concentration levels in human plasma using HPLC-UV and its clinical applications. Analyte from plasma was extracted with methanol [protein precipitation] and separated on the analytical column Diamonsil C[18] [150mmx4.6mm, 5 micro m] Waters-Milford, MA, United States. Mixture of 0.1% Trifluoroacetate and Methanol used as mobile phase in a 59:41 volume/volume mixture with an isocratic flow rate of 1.5 ml/min and wavelength was adjusted to 260nm. Standard curve of lamotrigine showed good linearity over the range of 1.0-50 micro g/mL [r[2]=0.9961] and LLOQ was 1.0 micro g/ml. The Specificity, Recovery, Accuracy, Stability, Robustness and RSDs for both intraday and interday precision were within acceptable limits. The highly sensitive HPLC assay for determination of LTG in human plasma was demonstrated, validated and applied in Therapeutic Drug Monitoring [TDM] of sixty seven epilepsy patients who were using LTG. The proposed method can be easily applied in routine Therapeutic monitoring of LTG, Besides TDM, stated method can be also very useful for Bioequivalence studies, Pharmacovigilance and Pharmacokinetics studies
ABSTRACT
Objective To study the sodium channel α1-subunit (SCN1A) gene in a pair of monozygotic twins with borderland severe myoclonic epilepsy in infancy (SMEB) and its characteristic of clinical manifestations. Methods The clinical features of 2 monozygotic twins were summarized. All 26 exons of SCNIA genes were screened with denaturing high performance liquid chromatography (DHPLC), and direct sequence analysis was performed on those with abnormal elution peak. Results The proband and her sister showed typical clinical features of SMEB. The same heterozygous mutations on exon 26 which caused the related amino acid change were found among them (c. 5348C > T, A1783E). Conclusion Monozygotic twins with similar clinical phenotype of SMEB have same SCN1A gene mutation.
ABSTRACT
Objective To study the SCN1A gene in a family with partial epilepsy with febrile seizures plus ( PEFS+ ) and its characteristics of inheritance. Methods The clinical features of the 2 patients and their father were summarized. All 26 exons of SCN1A gene were screened with denaturing high performance liquid chromatography (DHPLC), and direct sequence analysis was pedormed on those with abnormal elution peak. Pyrosequencing was subsequently performed in those without abnormality in direct sequence analysis. Results The proband and his sister had the phenotype of PEFS+ . The same heterozygous mutations (AS768G) on exon 26 which caused the related amino acid change (Q1923R) were found among them. Their father had frequent febrile seizures (FS) in childhood, and seizures stopped spontaneously. No abnormality was found in direct sequence but mosaic mutation in the same site was discovered with pyrosequencing (mutation quantity was 25% ). Conclusions The mutatin of SCN1A could cause partial epilepsy. PEFS+ could be inherited, the relatives carrying the affected gene may have mild clinical symptoms, possibly resulting from the low concentration of the mutated gene due to mosaic mutation.