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1.
Journal of Experimental Hematology ; (6): 1297-1304, 2019.
Article in Chinese | WPRIM | ID: wpr-775725

ABSTRACT

OBJECTIVE@#To explore the clinical feature of liver injury in patients with hemophagocytic syndrome (HPS).@*METHODS@#The clinical data of 92 patients with HPS in our hospital were analyzed retrospectively, and the characteristics of hepatic lesion and its relationship with prognosis in HPS patients were explored.@*RESULT@#92 cases of HPS showed different degrees of liver dysfunction from mild to moderate. The clinical parameters of liver dysfunction included the increased level of LDH (89.13%), AST (64.13%), TBIL (59.78%) and decreased level of ALB (90.22%). Moreover, 76.09% and 67.39% of the patients had the prolonging of APTT and PT respectively. The ALB level of patients in rheumatoid immune group were higher than that in infection, maglinancy and unexplained groups, all with statistically and significant difference (P<0.05, P<0.05 and P<0.01), the ALB level of patients in infection group were statistically and significantly higher than that in unexplained group (P<0.01). The Fbg level of patients in infection group were lower than that in maglinancy group, unexplained group and rheumatoid immune group, all the differences were statistically significant (P<0.05, P<0.01 and P<0.05). Child-Pugh grading was further carried out in HPS patients with liver disfunction. Survival time of the patients grade A was significantly higher than that of grade B and C of patients. Univariate analysis showed that the patients with LDH≥2000 U/L, ALB<30 g/L and PT≥15.1 s had a survival time inferior to control patients (P<0.05, P<0.01 and P<0.01, respectively). Multivariate analysis showed that ALB<30 g/L was an independent adverse prognostic factor for these patients (P<0.01).@*CONCLUSION@#Patients with HPS generally have impaired liver function mainly manifested with elevated LDH and AST levels, and declined ALB level, which may correlate with the disease cause and prognosis. Patients with LDH≥2000 U/L, ALB<30 g/L and PT≥15.1 s have a poorer prognosis and should be treated as soon as possible.


Subject(s)
Humans , Liver Diseases , Lymphohistiocytosis, Hemophagocytic , Prognosis , Retrospective Studies
2.
Journal of Experimental Hematology ; (6): 1696-1701, 2017.
Article in Chinese | WPRIM | ID: wpr-278759

ABSTRACT

<p><b>OBJECTIVE</b>To explore the amplification rate, clinical correlation and prognostic significance of 1q21 amplification in newly diagnosed patients with multiple myeloma (MM).</p><p><b>METHODS</b>I-FISH was performed on purified 138plasma cells from 72 newly diagnosed MM patients from February 2013 to February 2016 receiving bortezomib-based chemotherapy by using probe covered 1q21 region. Cut off value is 20%. Amplification rate, clinical relevance and prognostic significance were analysed in MM patients.</p><p><b>RESULTS</b>Among 72 patients, male 52, femail 20, the median age was 58(33-80).The amplification rate of 1q21 was 45.8%, the 1q21 amplification was positivly correlated with 13q14 deletion(P=0.041)and ISS III stage (P=0.002). With a median follow-up time of 17.0(3.0-40.0)months, the estimated median progression-free survival(PFS) time and overall survival(OS) time for patients with 1q21 amplification were 17.0 and 22.0 months, however, they did not reach in patients without 1q21 amplification(P=0.000, P=0.001). The multivariate analysis showed that del(17p13), 1q21 amplification and LDH≥220 U/L remained as independent risk factors for PFS and OS.</p><p><b>CONCLUSION</b>1q21 amplification is an important genetics prognosis indicator in newly diagnosed multiple myeloma patients receiving bortezomib-based first-line treatment. Bortezomib-based treatment can not improve the poor survival in patients with 1q21 amplification.</p>

3.
Journal of Zhejiang University. Medical sciences ; (6): 387-391, 2009.
Article in Chinese | WPRIM | ID: wpr-259294

ABSTRACT

<p><b>OBJECTIVE</b>To investigate the mechanism related to the inhibition of leukemia K562 cells by berbamine.</p><p><b>METHODS</b>After K562 cells were treated with 8 microg/ml berbamine, the expression levels of NF-kappaB, IkappaBalpha, pIkappaBalpha, IKKalpha, A20 were determined by Western blot.</p><p><b>RESULTS</b>With the exposure time extending, the total NF-kappaB showed no significant changes,but NF-kappaB expression in nucleus was decreased dramatically after treated with berbamine for 24 h. The ratio of nucleus NF-kappaB/histone H1 was decreased from 59.2%,gradually to 31.4%,19.7%,4.1%,and 0%. At the same time,the expression of A20 was increased,while the expression of pIkappaBalpha, IKKalpha was down-regulated.</p><p><b>CONCLUSION</b>Berbamine may induce K562 cell apoptosis through NF-kappaB pathway. Down-regulation of NF-kappaB and bcr-abl gene expression might be involved in cell apoptosis.</p>


Subject(s)
Humans , Antineoplastic Agents, Phytogenic , Pharmacology , Apoptosis , Benzylisoquinolines , Pharmacology , Cell Nucleus , Metabolism , Down-Regulation , Fusion Proteins, bcr-abl , Genetics , Metabolism , K562 Cells , NF-kappa B , Genetics , Metabolism
4.
Journal of Zhejiang University. Medical sciences ; (6): 439-444, 2009.
Article in Chinese | WPRIM | ID: wpr-259285

ABSTRACT

<p><b>OBJECTIVE</b>To investigate the effect of berbamine (BBM) on multiple myeloma (MM) cell line RPMI 8226 and its mechanism.</p><p><b>METHODS</b>MTT bioassay was used to examine the effect of berbamine on cell growth and IC(50) was calculated. Apoptosis was observed by flow cytometry (FCM) and DNA gelose electrophoresis. p53, p21, GADD45 mRNA were measured by RT-PCR. The alterations in p53, J NK, p-JNK and c-Jun proteins were detected by Western blot method.</p><p><b>RESULT</b>The growth of RPMI 8226 cells was suppressed in a dose-dependent manner after treatment with BBM(P<0.05), and its IC(50) value was 3.83 microg/ml at 48 h. Both DNA ladder and FCM results showed that BBM induced apoptosis of RPMI 8226 cells with concomitant increase of activated p53, p21 and GADD45gamma mRNA. After treatment with BBM at 8 microg/ml for 24 h, the percentage of apoptotic cells increased from 1.07% to 24.84%. p-JNK and c-Jun proteins were activated.</p><p><b>CONCLUSION</b>BBM can inhibit the growth of RPMI 8226 cells, which is associated with activation of GADD45/JNK signaling pathway and induction of cell apoptosis.</p>


Subject(s)
Humans , Apoptosis , Benzylisoquinolines , Pharmacology , Cell Cycle Proteins , Metabolism , Cell Line, Tumor , Dose-Response Relationship, Drug , JNK Mitogen-Activated Protein Kinases , Metabolism , Multiple Myeloma , Pathology , Nuclear Proteins , Metabolism , Signal Transduction
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