A bibliometric review of research trends in neuroimaging

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At the Leading Front of Neuroscience: A Bibliometric Study of the 100 Most-Cited Articles

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Basic taste processing recruits bilateral anteroventral and middle dorsal insulae: An activation likelihood estimation meta-analysis of fMRI studies

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The Changing Landscape of Neuroscience Research, 2006–2015: A Bibliometric Study

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Double balloon catheter for induction of labour in Chinese women with previous caesarean section: one-year experience and literature review

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Alterations of CD8+CD28- T cells in systemic lupus erythematosus and rheumatoid arthritis

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A Review of Superior Vena Cava Obstruction in Hong Kong Chinese Patients

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Effects of triptolide, an active ingredient of trypterygium Wilfordii Hook F (Thunder God Vine, a traditional Chinese herb), on rheumatoid synovial fibroblast function

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Breast Conservation Treatment in Hong Kong – Early Results of 203 Patients: Retrospective Study

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BCR-ABL mutational studies for predicting the response of patients with chronic myeloid leukaemia to second-generation tyrosine kinase inhibitors after imatinib fail

Imatinib is the standard treatment for chronic myeloid leukaemia. BCR-ABL kinase domain mutation is the commonest mechanism implicated in imatinib resistance. In in-vitro studies, kinase domain mutations are variably resistant to second-line agents. We performed BCR-ABL kinase domain mutational studies in 25 patients in five institutions who failed imatinib and were treated with either nilotinib or dasatinib, to see if their mutational status would predict their clinical responses. Kinase domain mutations involving 11 amino acid substitutions were found in 12 (48%) patients. Most patients showed single kinase domain mutations. There was some concordance between reported drug sensitivity patterns and patient responses. Discordant responses could be related to drug dosage variations and unknown BCR-ABL independent mechanisms. The response prediction for patients with multiple kinase domain mutations was challenging and their mutational patterns could change after tyrosine kinase inhibitor therapy. Although BCR-ABL kinase domain mutational analysis has limitations as a means of predicting the clinical response to second-line tyrosine kinase inhibitors, it helps inform therapy decisions in the management of chronic myeloid leukaemia after imatinib failure.published_or_final_versio