ObjectiveTo observe the effect of recombinant human interleukin-11 combined with ciclosporin in treatment of giucocorticoid invalid idiopathic thrombocytopenic purpura.MethodsFrom August 2009 to August 2011,35 cases with glucocorticoid invalid idiopathic thrombocytopenic purpura patients were divided into two groups according to the treatment method:13 cases in control group were treated with ciclosporin and 22 cases in observation group were treated with recombinant human interleukin-11 at basis of above method.The clinical effect and platelet counts between two groups were compared.Results The total effective rate in observation group was 90.9％ (20/22),which was significantly higher than that in control group [53.8％ (7/13)] (P ＜0.05).After treatment,the platelet counts in both two groups were significantly increased [control group:( 112.5 ± 15.4) × 109/t vs.(13.2 ± 1.8 ) × 109/L; observation group:( 132.7 ± 22.3 ) × 109/L vs.(12.9 ± 1.6) × 109/L] (P ＜ 0.05 ).Moreover,the platelet counts after treatment in observation group was significantly more than that in control group (P ＜ 0.05).ConclusionRecombinant human interleukin-11combined with ciclosporin in treatment of glucocorticoid invalid idiopathic thrombocytopenic purpura is a good treatment scheme,which can be applied in clinic.

Hematopoietic Stem Cell Transplantation ; Humans ; Tissue Donors ; Transplantation Chimera

BACKGROUND: A polygenic risk score (PRS) derived from 112 single-nucleotide polymorphisms (SNPs) for gastric cancer has been reported in Chinese populations (PRS-112). However, its performance in other populations is unknown. A functional PRS (fPRS) using functional SNPs (fSNPs) may improve the generalizability of the PRS across populations with distinct ethnicities. METHODS: We performed functional annotations on SNPs in strong linkage disequilibrium (LD) with the 112 previously reported SNPs to identify fSNPs that affect protein-coding or transcriptional regulation. Subsequently, we constructed an fPRS based on the fSNPs by using the LDpred2-infinitesimal model and then analyzed the performance of the PRS-112 and fPRS in the risk prediction of gastric cancer in 457,521 European participants of the UK Biobank cohort. Finally, the performance of the fPRS in combination with lifestyle factors were evaluated in predicting the risk of gastric cancer. RESULTS: During 4,582,045 person-years of follow-up with a total of 623 incident gastric cancer cases, we found no significant association between the PRS-112 and gastric cancer risk in the European population (hazard ratio [HR] = 1.00 [95% confidence interval (CI) 0.93-1.09], P = 0.846). We identified 125 fSNPs, including seven deleterious protein-coding SNPs and 118 regulatory non-coding SNPs, and used them to construct the fPRS-125. Our result showed that the fPRS-125 was significantly associated with gastric cancer risk (HR = 1.11 [95% CI, 1.03-1.20], P = 0.009). Compared to participants with a low fPRS-125 (bottom quintile), those with a high fPRS-125 (top quintile) had a higher risk of incident gastric cancer (HR = 1.43 [95% CI, 1.12-1.84], P = 0.005). Moreover, we observed that participants with both an unfavorable lifestyle and a high genetic risk had the highest risk of incident gastric cancer (HR = 4.99 [95% CI, 1.55-16.10], P = 0.007) compared to those with both a favorable lifestyle and a low genetic risk. CONCLUSION These results indicate that the fPRS-125 derived from fSNPs may act as an indicator to measure the genetic risk of gastric cancer in the European population.
Humans ; Prospective Studies ; Stomach Neoplasms/genetics* ; Genetic Predisposition to Disease/genetics* ; Risk Factors ; Multifactorial Inheritance/genetics* ; Polymorphism, Single Nucleotide/genetics* ; Genome-Wide Association Study