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  • 1
    Online Resource
    Online Resource
    The Phenotypic and Genetic Spectrum of Paroxysmal Kinesigenic Dyskinesia in China
    Wiley ; 2020
    In:  Movement Disorders Vol. 35, No. 8 ( 2020-08), p. 1428-1437
    Details
    In: Movement Disorders, Wiley, Vol. 35, No. 8 ( 2020-08), p. 1428-1437
    Abstract: Paroxysmal kinesigenic dyskinesia is a spectrum of involuntary dyskinetic disorders with high clinical and genetic heterogeneity. Mutations in proline‐rich transmembrane protein 2 have been identified as the major pathogenic factor. Objectives We analyzed 600 paroxysmal kinesigenic dyskinesia patients nationwide who were identified by the China Paroxysmal Dyskinesia Collaborative Group to summarize the clinical phenotypes and genetic features of paroxysmal kinesigenic dyskinesia in China and to provide new thoughts on diagnosis and therapy. Methods The China Paroxysmal Dyskinesia Collaborative Group was composed of departments of neurology from 22 hospitals. Clinical manifestations and proline‐rich transmembrane protein 2 screening results were recorded using unified paroxysmal kinesigenic dyskinesia registration forms. Genotype‐phenotype correlation analyses were conducted in patients with and without proline‐rich transmembrane protein 2 mutations. High‐knee exercises were applied in partial patients as a new diagnostic test to induce attacks. Results Kinesigenic triggers, male predilection, dystonic attacks, aura, complicated forms of paroxysmal kinesigenic dyskinesia, clustering in patients with family history, and dramatic responses to antiepileptic treatment were the prominent features in this multicenter study. Clinical analysis showed that proline‐rich transmembrane protein 2 mutation carriers were prone to present at a younger age and have longer attack duration, bilateral limb involvement, choreic attacks, a complicated form of paroxysmal kinesigenic dyskinesia, family history, and more forms of dyskinesia. The new high‐knee‐exercise test efficiently induced attacks and could assist in diagnosis. Conclusions We propose recommendations regarding diagnostic criteria for paroxysmal kinesigenic dyskinesia based on this large clinical study of paroxysmal kinesigenic dyskinesia. The findings offered some new insights into the diagnosis and treatment of paroxysmal kinesigenic dyskinesia and might help in building standardized paroxysmal kinesigenic dyskinesia clinical evaluations and therapies. © 2020 International Parkinson and Movement Disorder Society
    Type of Medium: Online Resource
    ISSN: 0885-3185 , 1531-8257
    URL: Issue
    URL: Article
    DOI: 10.1002/mds.v35.8
    DOI: 10.1002/mds.28061
    RVK:
    XA 10000
    Language: English
    Publisher: Wiley
    Publication Date: 2020
    detail.hit.zdb_id: 2041249-6
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  • 2
    Online Resource
    Online Resource
    TMEM151A Variants Cause Paroxysmal Kinesigenic Dyskinesia: A Large‐Sample Study
    Wiley ; 2022
    In:  Movement Disorders Vol. 37, No. 3 ( 2022-03), p. 545-552
    Details
    In: Movement Disorders, Wiley, Vol. 37, No. 3 ( 2022-03), p. 545-552
    Abstract: Paroxysmal kinesigenic dyskinesia (PKD) is the most common type of paroxysmal dyskinesias. Only one‐third of PKD patients are attributed to proline‐rich transmembrane protein 2 ( PRRT2 ) mutations. Objective We aimed to explore the potential causative gene for PKD. Methods A cohort of 196 PRRT2 ‐negative PKD probands were enrolled for whole‐exome sequencing (WES). Gene Ranking, Identification and Prediction Tool, a method of case–control analysis, was applied to identify the candidate genes. Another 325 PRRT2 ‐negative PKD probands were subsequently screened with Sanger sequencing. Results Transmembrane Protein 151 ( TMEM151A) variants were mainly clustered in PKD patients compared with the control groups. 24 heterozygous variants were detected in 25 of 521 probands (frequency = 4.80%), including 18 missense and 6 nonsense mutations. In 29 patients with TMEM151A variants, the ratio of male to female was 2.63:1 and the mean age of onset was 12.93 ± 3.15 years. Compared with PRRT2 mutation carriers, TMEM151A ‐related PKD were more common in sporadic PKD patients with pure phenotype. There was no significant difference in types of attack and treatment outcome between TMEM151A ‐positive and PRRT2 ‐positive groups. Conclusions We consolidated mutations in TMEM151A causing PKD with the aid of case–control analysis of a large‐scale WES data, which broadens the genotypic spectrum of PKD. TMEM151A ‐related PKD were more common in sporadic cases and tended to present as pure phenotype with a late onset. Extensive functional studies are needed to enhance our understanding of the pathogenesis of TMEM151A ‐related PKD. © 2021 International Parkinson and Movement Disorder Society
    Type of Medium: Online Resource
    ISSN: 0885-3185 , 1531-8257
    URL: Issue
    URL: Article
    DOI: 10.1002/mds.v37.3
    DOI: 10.1002/mds.28865
    RVK:
    XA 10000
    Language: English
    Publisher: Wiley
    Publication Date: 2022
    detail.hit.zdb_id: 2041249-6
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  • 3
    Online Resource
    Online Resource
    Daunorubicin Loaded Magnetic Nanoparticles of Fe3O4 Greatly Enhance the Responses to Chemotherapy and Induce Apoptosis of Multidrug-Resistant K562 Cells in a Human-Nude Mice Xenograft Leukemia Model
    American Society of Hematology ; 2008
    In:  Blood Vol. 112, No. 11 ( 2008-11-16), p. 5038-5038
    Details
    In: Blood, American Society of Hematology, Vol. 112, No. 11 ( 2008-11-16), p. 5038-5038
    Abstract: Object: To the effect of Fe3O4-magnetic nanoparticle loaded with DNR on multidrugresistant K562 cells in vivo. Methods: K562-n and its MDR counterpart K562-n/VCR cell were inoculated subcutaneously into both sides of the back of nude mice (5×106 cells/each) to establish a human leukemia xenograft model. The mice were randomly divided into group A receiving normal saline every other day for 20days, group B receiving DNR every other day for 20days, group C receiving Fe3O4-magnetic nanoparticle every other day for 20days, group D receiving Fe3O4-magnetic nanoparticle loaded with DNR every other day for 20days, and group E receiving Fe3O4-magnetic nanoparticle containing DNR every other day for 20days with a magnetic field built on the surface of the tumor tissue. The tumor volume was measured on the day 1, 5, 9, 13, 17 and 21d after the first treatment. Tumor tissues were isolated for examination of the expression of mdr-1, bcl-2, bax and caspase-3 by reverse transcription polymerase chain reaction and Western blotting. Results: For K562-n/VCR tumor, the tumor volume was markedly lower in groups D and E than in groups A, B and C (group D or E vs group A, B or C, P & lt; 0.05). The transcription of mdr-1 and Bcl-2 gene was significantly lower in groups D and E than in groups A, B and C (group D or E vs group A, B or C, P & lt; 0.05). So did the protein expression of Bcl-2. However, there were no differences among these groups about the protein expression of P-gp. The protein and mRNA expressions of Bax and Caspase-3 in groups D and E were increased significantly compared with groups A, B and C (group D or E vs group A, B or C, P & lt; 0.05). The tumor volume of K562-n was markedly lower in groups C, D and E than in groups A and B (group C, D or E vs group A or B, P & lt; 0.05). Conclusion: In conclusion, DNR loaded Fe3O4-magnetic nanoparticles can suppress the growth and induce apoptosis further on the MDR K562-n/VCR tumor in vivo compared to DNR alone but not on the K562-n tumor. The external magnetic field failed to improve the antitumor effect.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V112.11.5038.5038
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2008
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
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  • 4
    Online Resource
    Online Resource
    Magnetic Nanoparticle of Fe3O4 Loaded with Daunorubicin Reverse Leukemia Multidrug Resistance in Vivo
    American Society of Hematology ; 2008
    In:  Blood Vol. 112, No. 11 ( 2008-11-16), p. 5062-5062
    Details
    In: Blood, American Society of Hematology, Vol. 112, No. 11 ( 2008-11-16), p. 5062-5062
    Abstract: Object: To the effect of Fe3O4-magnetic nanoparticle loaded with DNR on In order to study the multidrug-resistant reversal effect of Fe3O4-magnetic nanoparticle loaded with DNR in vivo. Methods: K562-n,a leukemia cell line with high tumorigenicity in nude mice and its multidrug-resistant counterpart K562-n/VCR cells were inoculated subcutaneously into each groins of nude mice (5×106 cells/each) to establish a human leukemia xenograft model. The mice were randomly divided into group A receiving normal saline, group B receiving anti-tumor drugs daunorubicin (DNR), group C receiving Fe3O4-magnetic nanoparticle, group D receiving Fe3O4-magnetic nanoparticle loaded with DNR, and group E receiving Fe3O4-magnetic nanoparticle containing DNR with a magnetic field built on the surface of tumor tissues. After 20 days treatments, mice were killed and tumor tissues were isolated for pathological observation. The volume and weight of tumors were measured, then tumor suppression rate was calculated. The side effects of DNR loaded Fe3O4-magnetic nanoparticle were also evaluated. Results: The results showed that DNR loaded Fe3O4-magnetic nanoparticle can significantly suppress the growth of K562-n/VCR tumor in vivo, DNR alone can greatly suppress the growth of K562-n, Fe3O4-magnetic nanoparticle loaded with DNR can not further inhibit the K562-n tumor. Conclusion: In conclusion, Fe3O4-magnetic nanoparticle loaded with DNR can reverse the leukemia multidrug resistance in vivo.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V112.11.5062.5062
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2008
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
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  • 5
    Online Resource
    Online Resource
    Mechanisms of 2-Methoxyestradiol-Induced Apoptosis on Myelodysplastic Syndrome MUTZ-1 Cell Lines.
    American Society of Hematology ; 2007
    In:  Blood Vol. 110, No. 11 ( 2007-11-16), p. 4590-4590
    Details
    In: Blood, American Society of Hematology, Vol. 110, No. 11 ( 2007-11-16), p. 4590-4590
    Abstract: Objective: To study the mechanism of proliferation inhibition and apoptosis of MDS-RAEB MUTZ-1 cells by 2-methoxyestradiol(2-ME). Methods: MUTZ-1 cells were treated with different concentrations of 2-ME;cellular proliferation was determined by MTT assay;apoptosis rate was determined with annexinV-FITC/PI double staining and cell cycle was analyzed by flow cytometry (FCM);the changes of morphologic features of MUTZ-1 cells were investigated by cytomorphology with Wright-Giemsa’s staining; lactate dehydrogenises (LD) was determined by Beckman Counter and agarose gel electrophoresis was used to verify whether 2-ME could induce apoptosis in MUTZ-1 cells. Moreover, the activity of telomerase in MUTZ-1 cells was examined by TRAP-ELISA. Results: The results showed that 1∼4μmol/L 2-ME inhibited the proliferation of MUTZ-1 cells in a dose-and time-dependent manner; the typical apoptotic morphological features appeared in MUTZ-1 cells after being treated with 4μmol/L 2-ME for 12hours; the marked DNA ladder pattern of internucleosomal fragmentation was observed after being treated with 4μmol/L 2-ME for 24hours and the up-regulated production of LD was assayed after treatment of 2-ME for 36hours. The number of MUTZ-1 cells of G0/G1 phase and S phase decreased, while the number of G2/M phase increased after MUTZ-1 cells were incubated with 1,2 and 4μmol/L2-ME for 12 hours, respectively(P 〈 0.05). The inhibition effect of telomerase activity was enhanced in a dose- and time- dependent manner. Moreover, telomerase activity was significant negatively correlated with increased apoptosis (r =−0.954, p=0.046) and the number of sustained G2/M phase(r=−0.979, p=0.021) at the corresponding time point, respectively. Conclusions :It is concluded that the mechanism of proliferation inhibition and apoptosis of MUTZ-1 cells induced by 2-ME is probably related with inhibition of telomerase activity and G2/M cell cycle arrest; 2-ME may be a potentially useful, adjunctive anticancer drug in treating myelodysplastic syndrome.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V110.11.4590.4590
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2007
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
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  • 6
    Online Resource
    Online Resource
    Activation of δ-opioid Receptors in Anterior Cingulate Cortex Alleviates Affective Pain in Rats
    Elsevier BV ; 2022
    In:  Neuroscience Vol. 494 ( 2022-07), p. 152-166
    Details
    In: Neuroscience, Elsevier BV, Vol. 494 ( 2022-07), p. 152-166
    Type of Medium: Online Resource
    ISSN: 0306-4522
    URL: Article
    DOI: 10.1016/j.neuroscience.2022.05.008
    RVK:
    XA 10000
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2022
    detail.hit.zdb_id: 1498423-4
    SSG: 12
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  • 7
    Online Resource
    Online Resource
    Single‐Cell Profiling of Bone Marrow B Cells and Early B Cell Developmental Disorders Associated With Systemic Lupus Erythematosus
    Wiley ; 2024
    In:  Arthritis & Rheumatology Vol. 76, No. 4 ( 2024-04), p. 599-613
    Details
    In: Arthritis & Rheumatology, Wiley, Vol. 76, No. 4 ( 2024-04), p. 599-613
    Abstract: The peripheral B cell compartment is heavily disturbed in systemic lupus erythematosus (SLE), but whether B cells develop aberrantly in the bone marrow (BM) is largely unknown. Methods We performed single‐cell RNA/B cell receptor (BCR) sequencing and immune profiling of BM B cells and classified patients with SLE into two groups: early B cell (Pro‐B and Pre‐B) normal (EB nor ) and EB defective/low (EB lo ) groups. Results The SLE‐EB lo group exhibited more severe disease activity and proinflammatory status, overaction of type I interferon signaling and metabolic pathways within the B cell compartment, and aberrant BCR repertoires compared with the SLE‐EB nor group. Moreover, in one patient with SLE who was initially classified in the SLE‐EB lo group, early B cell deficiency and associated abnormalities were largely rectified in a second BM sample at the remission phase. Conclusion In summary, this study suggests that early B cell loss in BM defines a unique pathological state in a subset of patients with SLE that may play an active role in the dysregulated autoimmune responses.
    Type of Medium: Online Resource
    ISSN: 2326-5191 , 2326-5205
    URL: Issue
    URL: Article
    DOI: 10.1002/art.v76.4
    DOI: 10.1002/art.42750
    RVK:
    XA 10000
    RVK:
    XA 30325
    Language: English
    Publisher: Wiley
    Publication Date: 2024
    detail.hit.zdb_id: 2754614-7
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  • 8
    Online Resource
    Online Resource
    Corticosterone impairs gap junctions in the prefrontal cortical and hippocampal astrocytes via different mechanisms
    Elsevier BV ; 2018
    In:  Neuropharmacology Vol. 131 ( 2018-03), p. 20-30
    Details
    In: Neuropharmacology, Elsevier BV, Vol. 131 ( 2018-03), p. 20-30
    Type of Medium: Online Resource
    ISSN: 0028-3908
    URL: Article
    DOI: 10.1016/j.neuropharm.2017.12.003
    RVK:
    XA 10000
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2018
    detail.hit.zdb_id: 1500655-4
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  • 9
    Online Resource
    Online Resource
    Polymorphisms In Signal Transducer and Activator of Transcription 5 (STAT5) and Response to Cytarabine-Based Chemotherapy In Acute Myeloid Leukemia Patients
    American Society of Hematology ; 2010
    In:  Blood Vol. 116, No. 21 ( 2010-11-19), p. 4859-4859
    Details
    In: Blood, American Society of Hematology, Vol. 116, No. 21 ( 2010-11-19), p. 4859-4859
    Abstract: Abstract 4859 Objectives: Signal transducer and activator of transcription 5 (STAT5) protein is one of the concernful part of STATs families. The constitutive STATs activation has been especially showed in transformation by fusion genes in leukemias. Methods: In this study, we aimed to investigate whether the genetic polymorphisms in the STAT5 gene are associated with the treatment outcomes of Ara-C-based chemotherapy regimens in Acute Myeloid Leukemia (AML) patients. 152 AML patients in a Chinese sample were enrolled in our study. Peripheral blood samples were analyzed by matrix assisted laser desorption ionisation-time of flight mass spectrometry (MALDI-TOF-MS). Results: The results showed that the frequencies of the T/T genotype in rs2293157 and rs1135669 were higher in unfavorable and intermediate group respectively (P=0.023 and P=0.033). The frequency of patients with T/T genotype of rs1135669 was significantly higher in complete remission (CR) group. Conclusions: We concluded that the T/T genotype of rs1135669 might be an important marker for therapeutic efficiency of Ara-C-based chemotherapy in AML patients, especially in Chinese population. Disclosures: No relevant conflicts of interest to declare.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V116.21.4859.4859
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2010
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
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  • 10
    Online Resource
    Online Resource
    The Effect of Phenylhexyl Isothiocyanate on Drug Resistance of K562/A02 Cell Line
    American Society of Hematology ; 2008
    In:  Blood Vol. 112, No. 11 ( 2008-11-16), p. 5061-5061
    Details
    In: Blood, American Society of Hematology, Vol. 112, No. 11 ( 2008-11-16), p. 5061-5061
    Abstract: Objective: To investigate the effect of 6-phenylhexyl isothiocyanate (PHI) on drug resistance and sensitivity on K562/A02 cell line to ADM and elucidate the probable mechanisms. Methods: We measured growth inhibition of ADM on K562/A02 cell line by MTT assay. Apoptosis rate of K562/A02 cell line, the change of intracellular ADM and MRP1 protein level were detected by Flow Cytometry. Intracellular deoxidized GSH by spectrometric enzyme assay and MRP1 mRNA by RT-PCR semiquantitative assay were observed anteroposterior using PHI. Results: PHI can enhance the sensitivity of K562/A02 cell line to ADM, survival rate of K562/A02 cell line decreased with the increasing concentration of PHI and ADM. Apoptosis rate increased with treating by combination of two above drugs, and multiple of drug resistance had statistical significance (P & lt;0.05) when the concentration of PHI was more than 20μmol/l. Intracellular GSH of K562/A02 cell line reduced 5% when 1μg/ml ADM was single used, and when more than 10μmol/l PHI was used it increased slightly at first then decreased. When more than 20μmol/l PHI and 1μg/ml ADM were used combination, intracellular GSH of K562/A02 cell line decreased progressively with increasing the concentration of PHI. Protein and gene level of MRP1 have no statistical significance (P & gt;0.05) no matter after or before PHI was used on different concentration. Conlusion: The depletion effect of PHI on the intracellular GSH can not only partly enhance the reverse effect of ADM, but also enhance the sensitivity of K562/A02 cell line to ADM. Such depletion may diminish side effect and treatment dosage of ADM. It provides a new view to the therapy of leukaemia.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V112.11.5061.5061
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2008
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
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