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Diffuse large B-cell lymphoma (DLBCL) is the most common subtype of aggressive lymphoma. The relapsed/refractory DLBCL patients have poor outcomes and DLBCL is still lack of effective treatment standard regimens. How to effectively treat relapsed/refractory DLBCL patients has become a research hotspot, and the current treatment methods include bispecific antibody therapy, chimeric antigen receptor T-cell (CAR-T) therapy, antibody-drug conjugates (ADC) therapy. This paper reviews the progress of targeted drugs/cell treatment for DLBCL at the 64th American Society of Hematology annual meeting.
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Objective:To explore the correlation between post-transplant non-HLA antibodies and humoral rejection(HR)after kidney transplantation(KT).Methods:A retrospective study was conducted for KT recipients with non-HLA antibody level detected from September 2019 to January 2021.The recipients with biopsy confirmed HR and donor-specific HLA antibodies negative or feeble positive at the time of HR were designated as HR group while recipients with stable renal allograft function from 2 weeks post-KT to the time of detecting non-HLA antibody as stable group.The levels of HLA antibody, MHC classⅠchain-related gene A(MICA)antibody and 32 non-HLA antibodies were tested by Luminex single antigen bead and the levels of angiotensin Ⅱ type 1 receptor(AT1R)antibody quantified by enzyme-linked immunosorbent assay (ELISA). Inter-group differences in positive rate of non-HLA antibodies and number of positive non-HLA antibodies were analyzed.Results:Twenty-four recipients had positive non-HLA antibodies while the remainders had no positive non-HLA antibodies.Three HR recipients were positive for actin antibody, collagen Ⅲ antibody, glutathione S-transferase theta-1 antibody or IFN-γ antibody respectively.However, all four non-HLA antibodies of stable recipients were negative.There was significant inter-group difference( P=0.017). Four HR recipients were positive for collagenⅡantibody while only 1 stable recipient was positive for collagenⅡantibody.The positive rate of collagenⅡ antibody was significantly higher in HR recipients than that in stable recipients( P=0.023). HR recipients had an average of 2.36 positive non-HLA antibodies while stable recipients had an average of 0.90.There was significant inter-group difference ( P=0.008). Conclusions:A high level of non-HLA antibodies may elevate the risk of HR after KT.
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Objective:To explore the protective effects of exosomes derived from bone marrow mesenchymal stem cells(BMSC)on ischemia-reperfusion injury(IRI)in mice.Methods:A total of 30 C57BL/6 mice were randomly grouped into 6 groups of control, Norm-BMSC-exo, Hypo-BMSC-exo, IRI, Norm-BMSC-exo+ IRI and Hypo-BMSC-exo+ IRI.The model for IRI(25 min)was constructed.The serum levels of creatinine(Cr)and blood urea nitrogen(BUN)and histomorphology were examined at 24 h post-reperfusion.The levels of tumor necrosis factor-alpha (TNF-α), interleukin-1β(IL-1β)monocyte chemoattractant protein-1(MCP-1)and interleukin-10 (IL-10)were measured.The survival rate was observed for 7 days post-IRI.We also detected macrophage polarization glycolysis and oxidative phosphorylation(OXPHOS).Results:Compared with IRI group, Norm-BMSC-exo+ IRI group showed low levels of creatinine(Cr)and blood urea nitrogen(BUN)and mild pathological injury.The protective effects were enhanced in Hypo-BMSC-exo+ IRI group.BMSC-exo pretreatment could significantly improve the survival rate of mice post-IRI.Reverse transcription-polymerase chain reaction(RT-PCR)revealed that BMSC-exo significantly lowered the levels of TNF-α, IL-1β, MCP-1 and elevated the level of IL-10.BMSC exosomes polarized macrophage toward an M2 phenotype.And Hypo-exo could reprogramme macrophages to undergo a metabolic switch toward OXPHOS and away from glycolysis.Conclusions:Hypo-BMSC-exo could improve kidney injury via inducing M2 polarization in macrophages through promoting OXPHOS and suppressing glycolysis.
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Objective:To explorer the optimal method of detecting donor kidney carrier carbapenem-resistant Klebsiella pneumoniae (CRKP).Methods:Clinical data were retrospectively analyzed for 1120 donation-after-circulatory-death (DCD) kidneys and bacterial detection of kidney perfusion fluid was performed from January 2015 to January 2019. A total of 1120 kidney perfusion fluid samples were collected with sterile tubes and submitted for culturing. And 451 specimens were delivered in sterile tubes and blood culture bottles simultaneously And 729 specimens assayed for carbapenemase genes with GeneXpert.Results:Among 1120 kidneys, CRKP was confirmed in 21 grafts with an infection rate of 1.87 %. The detection of carbapenemase genes with Genexpert showed that KPC was positive for 9/16 CRKP positive grafts. Sensitivity, specificity, false-positive rate, false-negative rate and ROC-AUC were calculated at 56.3 %, 100 %, 0, 43.7 % and 0.781 respectively. And 11 specimens delivered with sterile tube were culture positive for CRKP. Sensitivity, specificity, false-positive rate, false-negative rate and ROC-AUC were calculated at 52.3 %, 100 %, 0, 47.6 % and 0.762 respectively. Among 451 perfusion fluid samples collected with anaerobic blood culture bottle, 15 samples had a positive culture for CRKP. Sensitivity, specificity, false-positive rate, false-negative rate and ROC-AUC were calculated at 100 %, 100 %, 0, 0 and 1 respectively. In terms to anaerobic blood culture bottle, sensitivity, specificity, false-positive rate, false-negative rate and ROC-AUC were calculated at 60 %, 100 %, 0 , 40 % and 0.80 respectively.Conclusions:Genexpert assay is suitable for rapid and convenient detection of carbapenemase genes using kidney perfusion fluid. Culturing perfusion fluid samples collected with anaerobic blood culture bottle is clinically valuable diagnostic tool of CRKP. A combination of both methods is worthy of clinical promotion and application diagnosis of donor kidney derived CRKP in terms of greater accuracy and timeliness.
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Objective To explore the rapid diagnosis and clinic treatment of donor-derived carbapenem-resistant Klebsiella pneumoniae (CRKP) infection in renal transplant recipients .Methods Retrospective analysis was performed for clinical data and the diagnosis and treatment of 9 renal transplant recipients with donor-derived CRKP infection from March 2017 to May 2019 .Results Among 526 renal transplant recipients ,nine were diagnosed with donor-derived CRKP infection by bacterial culture or KPC enzyme gene test .The infection rate was 1 .71％ .One recipient receiving carbapenem and tigecycline died while the remainders survived after a treatment of ceftazidime-avibactam and carbapenem . One recipient underwent graft resection . Among 8 recipients on ceftazidime-avibactam ,5 cases received a standard dose of 3 .75 g/d while another 3 cases had a high dose of 7 .5 g/d .One patient in standard-dose group underwent graft resection due to an arteriorrhexis of artery anastomosis .After graft resection ,the patient received a high dose of ceftazidime-avibactam and survived to date .The grafts of three patients in high-dose treatment group survived .Conclusions KPC enzyme gene detection plus injecting lavage fluid into blood culture bottle for bacterial culture is rapid and accurate for diagnosing donor-derived CRKP infection . A combination of ceftazidime-avibactam plus carbapenem is effective for donor-derived CRKP infection .A high dose of ceftazidime-avibactam may improve the efficacy without obvious side effects .
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To investigate the relationship between transcription factor and the change of protein expression levels in heart failure. Methods Bioinformatic method was used to analyze the data of binding-sites on the 5 ' flaking regions of four genes whose mRNA level changed in failing heart from three databases about nucleic acid-EMBL, transcriptional regulation factor-TRANSFAC and protein-SWISS-PORT.The expression level of selected transcription factor was determined by immunohischemical method.Results Nine transcription factors were inferred to influence the proteins' levels in occurrence and development of heart failure.Serum response factor (SRF) was selected from the nine factors and assayed. The results showed that there was a higher level of SRF in healthy group than in chronic heart failure (CHF), and the level was associated with the degree of CHF. It was also found that there was a relative higher level of SRF in the acute myocardial infarction (AMI) than that in CHF, but which was lower than the healthy. Conclusion It showed that SRF had a quantitative change in the development of heart failure, and suggested SRF might play an important regulative role in heart failure. The expression changes of proteins related to myocardial function might be regulated by the quantitative change of transcription factor(s).