Objective To observe the lumbosacral plexus nerves by diffusion tensor tractography (DTT) and quantitatively evaluate them by using diffusion tensor imaging (DTI) in healthy volunteers.Methods A total of 60 healthy volunteers (30 males and 30 females) underwent DTI scanning.Mean FA values of the lumbosacral plexus nerves (both sides of lumbar roots L3 to S1,proximal and distal to the lumbar foraminal zone) were quantified.Differences among various segments of lumbar nerve roots were compared with ANOVA test and SNK test.Differences between two sides of the lumbar nerve roots at the same lumbar segment were compared with paired-samples t test.Differences between the proximal and the distal nerve to the the lumbar foraminal zone at the same lumbar segment were compared with paired-samples t test.The lumbosacral plexus nerve was visualized with tractography.Results (1) The lumbosacral plexus nerve was clearly visualized with tractography.(2) Mean FA values of the lumbar nerve roots L3 to S1 were as followings:proximal to the left lumbar foraminal zone 0.202 ± 0.021,0.201 ± 0.026,0.201 ± 0.027,0.191 ±0.016,distal to the left lumbar foraminal zone 0.222 ± 0.034,0.250 ± 0.028,0.203 ± 0.026,0.183 ± 0.020,proximal to the right lumbar foraminal zone 0.200 ± 0.023,0.202 ± 0.023,0.205 ± 0.027,0.191 ±0.017,distal to the right lumbar foraminal zone 0.225 ±0.032,0.247 ±0.027,0.205 ± 0.033,0.183 ±0.021.Mean FA values were significantly different between the proximal nerve to the distal nerve in lumbar nerve roots L3,L4,S1 (t =-9.114-2.366,P ＜ 0.05),but not significantly different in L5 (P ＞ 0.05).Differences were not found between the right and left side nerves at the same lumbar segment (P ＞ 0.05).(3) The whole length of the lumbar roots nerve L3 to S1 can be visualized clearly by using DTT.Conclusions Diffusion tensor imaging and tractography can show and provide quantitative information of human lumbosacral plexus nerves.DTI is a potential tool for the diagnosis of lumbosacral plexus nerve disease.

OBJECTIVE: To explore the effect of hnRNPK/Beclin1 signaling on the drug resistance of imatinib in Ph⁺ leukemia. METHODS: Expression level of hnRNPK was verified in the imatinib resistant and sensitive Ph⁺ leukemia cell lines by using Western blot. hnRNPK expression was down-regulated by using RNAi. Expression level of LC3I/II and Beclin1 were detected by Western blot and the sensitivity of imatinib was analyzed by CCK-8 assay before and after modulation of hnRNPK expression. RESULTS: hnRNPK showed overexpressed in imatinib resistant leukemia cell line. After the expression level of hnRNPK was down-regulated by RNAi, the sensitivity of drug resistance lines to imatinib restored, while the expression level of LC3I/II and Beclin1 were consistant with the modulation of hnRNPK expression. CONCLUSION hnRNP K/Beclin1 signaling may be involved in the development of imatinib resistance in Ph⁺ leukemia through the regulation of autophagy.
Antineoplastic Agents/pharmacology* ; Beclin-1 ; Cell Line, Tumor ; Drug Resistance ; Drug Resistance, Neoplasm ; Heterogeneous-Nuclear Ribonucleoprotein K ; Humans ; Imatinib Mesylate/pharmacology* ; Leukemia

OBJECTIVETo explore the role of heterogeneous nuclear ribonucleoprotein(hnRNP) K regulating autophagy in the drug resistance of acute myeloid leukemia, so as to provide a new molecular marker for treatment of leukemia.

METHODSThe relationship between the expression level of hnRNP K and the drug resistance of myeloid leukemia was verified by fluorescence quantitative PCR; the expression of autophagy related protein LC3I/ II was detected by Western blot after the hnRNP K was modulated by RNA interference technology; the sensitivity of leukemia cells to doxorubicin was analyzed before and after the expression of hnRNP K were modulatd.

RESULTSThe expression of hnRNP K and LC3I/II significantly increased in bone marrow nonremission patients and in drug resistant cell line, however, the expression of LC3I/ II decreased when the expression of hnRNP K were reduced, while the sensitivity of cells to adriamycin could be recovered.

CONCLUSIONhnRNP K may be involved in the formation of adriamycin resistance in acute myeloid leukemia by regulating autophagy.