Objective To discuss the quality of life in the postoperative patients with aortic valve replacement (AVR) and related influencing factors .Methods The changes of preoperative and postoperative survival quality in 102 cases of AVR surgery were assessed by using the SF‐36 scale ,and the Logistic regression was used to analyze the impact of age ,effective valve orifice area and prosthetic valve on the quality of life .Results Five patients died during follow‐up .The relative baseline survey after postopera‐tive 1 year showed that the quality of life of patients was significantly improved ,the Logistic regression analysis revealed that a lar‐ger effective orifice area(EOA) and biological valve replacement could have higher health scale scores ,and showed a positive corre‐lation .Conclusion The quality of life in the postoperative patients with AVR is affected by the valve type and EOA of prosthetic valve .

Acute myeloid leukemia (AML),the most common disease in acute leukemia,is a highly heterogeneous invasive hematological disease.The t(8;21)(q22;q22) translocation is the most common chromosomal translocation in AML,generating AML1-ETO fusion gene and encoding AML1-ETO fusion protein.This article summarizes the two-hit hypothesis in AML occurrence,the pathogenesis of t(8;21)AML,all features involved in t(8;21)AML,and the function of the components in AML1-ETO fusion protein,providing important basic information for the treatment and prognosis of t(8;21)AML.Meanwhile,this article also summarizes the progress of next generation sequencing technique in leukemia,providing a new technique for the accurate therapy of (8;21)AML.

Objective To investigate the clinical characteristics,treatment and prognosis of single-system Langerhans cell histiocytosis (LCH) in children.Methods A retrospective analysis was performed in single-system LCH patients registered between January 2006 and December 2012 in Beijing Children＇s Hospital Affiliated to Capital Medical University.The patients were divided into 2 groups:the bone involvement group and the other organ involvement group.The patients were assessed at 5 weeks,11 weeks,25 weeks,3 months,6 months,1 year and 3 years.The data were analyzed by using SPSS 17.0 software.Results A total of 112 patients (66 boys and 4,6 girls) with a median age of 5 years at diagnosis of LCH were analyzed.The most frequently affected organ was the bones(91 cases,81.3％),followed by skin(15 cases,13.4％).Few patients (27.6％) had acentral nervous system risk lesion,who were younger than those with other bone lesion(2.5 years vs 6.6 years).Patients with bone lesions were diagnosed at a significantly older age than other patients(5.6 years vs 1.5 years) (P ＜ 0.01).All patients received chemotherapy that included Prednisone and Vinblastine for 25 weeks.Twenty-five patients (22.3 ％) showed reactivation.Of these,4 patients exhibited reactivation in the pituitary.Three-year overall survival rate was expected to reach 100％,and no-event survival was expected at (73.22 ± 4.47) ％.Age of less than 2 years old was the factor of reactivation (P =0.033);sex,organ involvement and member of bone involved were not related with reactivation (P =0.679,0.142,0.639).Conclusions The bones were the frequent involvement organ in single-system LCH patients.These patients have a good prognosis.The rate of reactivation of single system-LCH can be decreased by chemotherapy.

Glycyrrhiza uralensis Fisch. ex DC is widely used in traditional Chinese medicine (TCM). Among its various active components, glycyrrhizic acid is believed to be the marker component. Squalene synthase (SQS) and beta-amyrin synthase (beta-AS) are key enzymes in the biosynthetic pathway of glycyrrhizic acid in G uralensis. To reveal the effects of co-expression of SQS1 and beta-AS genes on this pathway, 7 yeast expression vectors harboring different SQS1 variants and beta-AS were constructed and expressed in Saccharomyces cerevisiae as fusion proteins. TLC and GC-MS results showed that co-expression of SQS1 and beta-AS enhanced the accumulation of beta-amyrin. The effects of SQS12 were more obvious than the other two SQS1 variants. This study is significant for further investigations concerned with exploring the biosynthesis of glycyrrhizic acid in vitro and strengthening the efficacy of G. uralensis by means of increasing the content of glycyrrhizic acid.

Objective To investigate the clinical characteristics,treatment,and prognostic factors for Langerhans cell histiocytosis (LCH) in children.Methods A retrospective review of patients diagnosed as LCH was carried out between January 2007 and December 2012 in Beijing Children's Hospital,Capital Medical University.Target patients were divided into multi-organ high-risk groups (Group Ⅰ),multi-organ low-risk groups (Group Ⅱ),single-organ groups (GroupⅢ),and the corresponding intensity of chemotherapy was given.SPSS 17.0 statistical software was used to analyze the findings.The correlations among the affected organ,the early treatment response and the prognosis were analyzed.Results A total of 217 patients were analyzed including 127 boys and 90 girls with ratio of 1.4 ∶ 1.0 and a median age of 36 months (ranged from 2 months to 14 years) on the diagnosis of LCH,and there were 132 cases (60.8％) in group Ⅰ,33 cases (15.3％) in group Ⅱ and 52 cases (23.9％) in group Ⅲ.The median age on diagnosis was 20 months in group Ⅰ,42 months in group Ⅱ and 72 months in group Ⅲ.The most frequently affected organ was the bone (176 cases,81.2％).Among 217 patients,55 cases (25.3％) had recurrence and 12 cases died.The rate of 3-year overall survival was expected to be 90.78％.The rate of 3-year event free survival was expected to be 76.5％.Myelosuppression,liver function damage and infection were the most common side effects due to chemotherapy with the percentages of 48.4％ (105 cases),24.0％ (52 cases) and 12.4％ (27 cases).Risk organs involvement and no-response to initial therapy (after 6 weeks) indicated a worse prognosis (x2 =10.60,12.84,P =0.017,0.001).Conclusions Incidence of LCH in boys is slightly higher than girls in children.Peak age at onset of LCH in children is 1-3 years old.Bone is the most frequent involved organ.Involvement of risk organs and no-response to initial therapy are key factors in determining worse prognosis.A rescue therapy should be introduced earlier in these patients.

Objective To analyze the role of preoperative peripheral blood inflammatory parameters and postoperative lymph-node ratio (LNR) in the prognosis of gastric cancer patients treated with chemotherapy. Methods The neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), systemic immune inflammatory response index (SII), lymphocyte-to-monocyte ratio (LMR), Onodera prognostic nutritional index (OPNI), and LNR of 108 patients with gastric cancer were classified into high and low groups to analyze their prognostic value on the overall survival (OS) of gastric cancer patients treated with chemotherapy. The independent prognostic indicators were plotted in columns to predict the survival rate of gastric cancer patients. Results NLR was statistically significant in the prognostic assessment of gastric cancer patients treated with chemotherapy (P < 0.001). Moreover, the high PLR group, high SII group, high LNR group, N3 stage, TNM (Ⅲ-Ⅳ) stage, nerve invasion, and carcinoembryonic antigen (CEA) were independent risk factors for the prognosis of gastric cancer (all P < 0.05). These findings indicated that in predicting the prognosis of gastric cancer, the combination of LNR, PLR, and SII (AUC=0.875) was better than that of LNR, PLR, and SII alone or in pairwise combination. Conclusion Elevated NLR, LNR, PLR, and SII are associated with significantly reduced survival of patients. LNR, PLR, and SII could be used as independent risk factors for the prognosis of gastric cancer patients treated with chemotherapy, and their combination can predict the survival of gastric cancer patients.

Tyrosine kinase inhibitors (TKIs) have revolutionized the treatment landscape for chronic myeloid leukemia (CML). However, TKI resistance poses a significant challenge, leading to treatment failure and disease progression. Resistance mechanisms include both BCR::ABL1-dependent and BCR::ABL1-independent pathways. The mechanisms underlying BCR::ABL1 independence remain incompletely understood, with CML cells potentially activating alternative signaling pathways, including the AKT/mTOR and JAK2/STAT5 pathways, to compensate for the loss of BCR::ABL1 kinase activity. This study explored tumoral VISTA (encoded by VSIR) as a contributing factor to TKI resistance in CML patients and identified elevated tumoral VISTA levels as a marker of resistance and poor survival. Through in vitro and in vivo analyses, we demonstrated that VSIR knockdown and the application of NSC-622608, a novel VISTA inhibitor, significantly impeded CML cell proliferation and induced apoptosis by attenuating the AKT/ mTOR and JAK2/STAT5 pathways, which are crucial for CML cell survival independent of BCR::ABL1 kinase activity. Moreover, VSIR overexpression promoted TKI resistance in CML cells. Importantly, the synergistic effect of NSC-622608 with TKIs offers a potent therapeutic avenue against both imatinib-sensitive and imatinib-resistant CML cells, including those harboring the challenging T315I mutation. Our findings highlight the role of tumoral VISTA in mediating TKI resistance in CML, suggesting that inhibition of VISTA, particularly in combination with TKIs, is an innovative approach to enhancing treatment outcomes in CML patients, irrespective of BCR::ABL1 mutation status. This study not only identified a new pathway contributing to TKI resistance but also revealed the possibility of targeting tumoral VISTA as a means of overcoming this significant clinical challenge.

Tyrosine kinase inhibitors (TKIs) have revolutionized the treatment landscape for chronic myeloid leukemia (CML). However, TKI resistance poses a significant challenge, leading to treatment failure and disease progression. Resistance mechanisms include both BCR::ABL1-dependent and BCR::ABL1-independent pathways. The mechanisms underlying BCR::ABL1 independence remain incompletely understood, with CML cells potentially activating alternative signaling pathways, including the AKT/mTOR and JAK2/STAT5 pathways, to compensate for the loss of BCR::ABL1 kinase activity. This study explored tumoral VISTA (encoded by VSIR) as a contributing factor to TKI resistance in CML patients and identified elevated tumoral VISTA levels as a marker of resistance and poor survival. Through in vitro and in vivo analyses, we demonstrated that VSIR knockdown and the application of NSC-622608, a novel VISTA inhibitor, significantly impeded CML cell proliferation and induced apoptosis by attenuating the AKT/ mTOR and JAK2/STAT5 pathways, which are crucial for CML cell survival independent of BCR::ABL1 kinase activity. Moreover, VSIR overexpression promoted TKI resistance in CML cells. Importantly, the synergistic effect of NSC-622608 with TKIs offers a potent therapeutic avenue against both imatinib-sensitive and imatinib-resistant CML cells, including those harboring the challenging T315I mutation. Our findings highlight the role of tumoral VISTA in mediating TKI resistance in CML, suggesting that inhibition of VISTA, particularly in combination with TKIs, is an innovative approach to enhancing treatment outcomes in CML patients, irrespective of BCR::ABL1 mutation status. This study not only identified a new pathway contributing to TKI resistance but also revealed the possibility of targeting tumoral VISTA as a means of overcoming this significant clinical challenge.

Tyrosine kinase inhibitors (TKIs) have revolutionized the treatment landscape for chronic myeloid leukemia (CML). However, TKI resistance poses a significant challenge, leading to treatment failure and disease progression. Resistance mechanisms include both BCR::ABL1-dependent and BCR::ABL1-independent pathways. The mechanisms underlying BCR::ABL1 independence remain incompletely understood, with CML cells potentially activating alternative signaling pathways, including the AKT/mTOR and JAK2/STAT5 pathways, to compensate for the loss of BCR::ABL1 kinase activity. This study explored tumoral VISTA (encoded by VSIR) as a contributing factor to TKI resistance in CML patients and identified elevated tumoral VISTA levels as a marker of resistance and poor survival. Through in vitro and in vivo analyses, we demonstrated that VSIR knockdown and the application of NSC-622608, a novel VISTA inhibitor, significantly impeded CML cell proliferation and induced apoptosis by attenuating the AKT/ mTOR and JAK2/STAT5 pathways, which are crucial for CML cell survival independent of BCR::ABL1 kinase activity. Moreover, VSIR overexpression promoted TKI resistance in CML cells. Importantly, the synergistic effect of NSC-622608 with TKIs offers a potent therapeutic avenue against both imatinib-sensitive and imatinib-resistant CML cells, including those harboring the challenging T315I mutation. Our findings highlight the role of tumoral VISTA in mediating TKI resistance in CML, suggesting that inhibition of VISTA, particularly in combination with TKIs, is an innovative approach to enhancing treatment outcomes in CML patients, irrespective of BCR::ABL1 mutation status. This study not only identified a new pathway contributing to TKI resistance but also revealed the possibility of targeting tumoral VISTA as a means of overcoming this significant clinical challenge.

Tyrosine kinase inhibitors (TKIs) have revolutionized the treatment landscape for chronic myeloid leukemia (CML). However, TKI resistance poses a significant challenge, leading to treatment failure and disease progression. Resistance mechanisms include both BCR::ABL1-dependent and BCR::ABL1-independent pathways. The mechanisms underlying BCR::ABL1 independence remain incompletely understood, with CML cells potentially activating alternative signaling pathways, including the AKT/mTOR and JAK2/STAT5 pathways, to compensate for the loss of BCR::ABL1 kinase activity. This study explored tumoral VISTA (encoded by VSIR) as a contributing factor to TKI resistance in CML patients and identified elevated tumoral VISTA levels as a marker of resistance and poor survival. Through in vitro and in vivo analyses, we demonstrated that VSIR knockdown and the application of NSC-622608, a novel VISTA inhibitor, significantly impeded CML cell proliferation and induced apoptosis by attenuating the AKT/ mTOR and JAK2/STAT5 pathways, which are crucial for CML cell survival independent of BCR::ABL1 kinase activity. Moreover, VSIR overexpression promoted TKI resistance in CML cells. Importantly, the synergistic effect of NSC-622608 with TKIs offers a potent therapeutic avenue against both imatinib-sensitive and imatinib-resistant CML cells, including those harboring the challenging T315I mutation. Our findings highlight the role of tumoral VISTA in mediating TKI resistance in CML, suggesting that inhibition of VISTA, particularly in combination with TKIs, is an innovative approach to enhancing treatment outcomes in CML patients, irrespective of BCR::ABL1 mutation status. This study not only identified a new pathway contributing to TKI resistance but also revealed the possibility of targeting tumoral VISTA as a means of overcoming this significant clinical challenge.