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C8H11NO7, triclinic, P1̄ (no. 2), a = 5.5944(13) Å, b = 10.402(3) Å, c = 10.666(3) Å, α = 110.297(2)o, β = 101.342(3)o, γ = 104.701(2)o, V = 534.6(2) Å3, Z = 2, Rgt(F) = 0.0318, wRref(F2) = 0.0833, T = 293(2) K.

Blockade of the immunosuppressive checkpoint receptors cytotoxic T-lymphocyte-associated protein 4 (CTLA4) or programmed death 1 (PD-1) and its cognate ligand, programmed death 1 ligand (PD-L1), has altered the landscape of anti-tumor immunotherapy. B7 family and tumor necrosis factor receptor (TNFR) superfamily play a crucial role in T cell activation, tolerance, and anergy through co-stimulatory and inhibitory signal transduction. Investigating the immune molecular landscapes of the B7 and TNFR families is critical in defining the promising responsive candidates. Herein, we performed comprehensive alteration analysis of the B7 and TNFR family genes across six hepatocellular carcinoma (HCC) datasets with over 1000 patients using cBioPortal TCGA data. About 16% of patients had both B7 and TNFR gene alterations. TNFR gene amplifications were relatively more common (1.73–8.82%) than B7 gene amplifications (1.61–2.94%). Analysis of 371 sequenced samples revealed that all genes were upregulated: B7 and TNFR mRNA were upregulated in 23% of cases (86/371) and 28% of cases (105/371), respectively. Promoter methylation analysis indicated an epigenetic basis for B7 and TNFR gene regulation. The mRNA levels of B7 and TNFR genes were inversely correlated with promoter methylation status. B7-H6 expression was significantly associated with worse overall survival, and B7-H6 mRNA was increased gradually in cases with gene copy number alterations. B7-H6 overexpression was associated with aggressive clinicopathologic features and poor prognosis in HCC. Downregulation of B7-H6 in HCC cells significantly inhibited cell adhesion, proliferation, migration, and invasion. Knockdown of B7-H6 in HCC cells inhibited tumor growth and metastasis in vivo. B7-H6 promoted HCC metastasis via induction of MMP-9 expression and STAT3 activation. B7-H6 and STAT3 performed functional overlapping roles on enhancing the MMP-9 promoter activity in HCC cells. These results suggest that alterations of the immunologic co-stimulator B7 and TNFR families correlate with HCC metastasis and prognosis, and especially B7-H6 plays a critical role in promoting metastasis of HCC.

Objective: To investigate the effect of Treg-cells on the primary immune thrombocytopenia by detecting the level changes of peripheral blood regulatory T cells of the patients with ITP before and after the treatments. Methods: 276 patients with ITP who were treated in the department of hematology in our hospital from June 2010 to July 2013 were enrolled in the study. According to the different therapeutic methods, the selected patients were divided into three groups. DXM group (90 cases): dexamethasone 40 mg/d taken by mouth in 4 days; Prednisolone group(98 cases): prednisolone 1.5 mg-kg-1.d-1 taken by mouth; DXM+low dose Rituximab group (88 cases): dexamethasone 40 mg/d taken by mouth form the 1st day to the 4th, and then the Rituximab 100 mg was given by intravenous drip on the 7th, 14th, 21th and 28th. Another 60 healthy people who were inspected in our hospital were chosen to be the control group. The peripheral vein blood of patients in each group at the 14th and 28th day before and after the treatments was taken separately in order to detect the levels of CD4+, CD25+, CD127- in Tr cells were examined by flow cytometry. Results: On the 28th day, the total effective rate of Prednisolone group, Dexamethasone (DXM) group and DXM+low dose Rituximab group was 69.4%, 66.7% and 79.5%, respectively, with no significant difference. In the 12-months' follow-up, the continuous effective rate of DXM+low dose Rituximab group (66.7%) was higher than Prednisolone group(37.8%) and Dexamethasone (DXM) group (22.7%) with a significant difference(P<0.05). There was no significant difference between Prednisolone group and Dexamethasone (DXM) group. The expression levels on peripheral blood CD4+, CD25+ and CD127-T cells of the all ITP patients were lower than those of the patients in the health control group before the treatments[(1.66± 0.69)%VS(4.01± 0.38)%, P<0.05]. On the 14th day, the levels of CD4+, CD25+ and CD127-Tr cells of patients in Prednisolone group and Dexamethasone (DXM) group were higher than before with an average rate of [(3.46± 0.76)% VS (1.68± 0.72)%, (3.22± 0.77)% VS (1.69± 0.74)%, respectively, P<0.05]; On the 14th and 28th day of the treatments, the levels of CD4+, CD25+ and CD127- of the DXM+low dose Rituximab group were higher than before with significant differences (P<0.05). On the 28th day, the levels of CD4+, CD25+ and CD127-Tr cells of patients in Prednisolone group and Dexamethasone (DXM) group were (2.68± 0.63)% and (2.58± 0.66)% which showed no significant difference when comparing with before. Conclusion: The regimen of DXM+low dose Rituximab is superior to single medication of prednisolone and dexamethasone in promoting the number of T cells and long-term treatments. [ABSTRACT FROM AUTHOR]

In order to improve the dissolution and absorption of the water insoluble drug repaglinide, a solid dispersion was developed by solvent method using polyvinylpyrrolidone K30 (PVP K30) as the hydrophilic carrier for the first time. Studies indicated that both solubility and the dissolution rate of repaglinide were significantly increased in the solid dispersion system compared with that of repaglinide raw material or physical mixtures. The repaglinide solid dispersions with PVP K30 solid state was characterized by polarizing microscopy, differential scanning calorimetry (DSC), X-ray diffraction (XRD), and Fourier transform infrared spectroscopy (FT-IR). DSC and XRD studies indicated that repaglinide existed in an amorphous form in the solid dispersion. FT-IR analysis demonstrated the presence of intermolecular hydrogen bonding between repaglinide and PVP K30 in the solid dispersion. In the in situ gastrointestinal perfusion experiment, solid dispersion was shown to remarkably enhance the absorption of repaglinide in stomach and all segments of intestine. In vivo pharmacokinetic study in rats showed that immediate and complete release of repaglinide from the solid dispersion resulted in rapid absorption that significantly increased the bioavailability and the maximum plasma concentration over repaglinide raw material. These results demonstrated PVP K30 was an appropriate carrier for solid dispersion of repaglinide, with increased dissolution and oral absorption. [ABSTRACT FROM AUTHOR]

C8H11NO7, triclinic, P1̄ (no. 2), a = 5.5944(13) Å, b = 10.402(3) Å, c = 10.666(3) Å, α = 110.297(2)o, β = 101.342(3)o, γ = 104.701(2)o, V = 534.6(2) Å3, Z = 2, Rgt(F) = 0.0318, wRref(F2) = 0.0833, T = 293(2) K. [ABSTRACT FROM AUTHOR]

C8H11NO7, triclinic, P1̄ (no. 2), a = 5.5944(13) Å, b = 10.402(3) Å, c = 10.666(3) Å, α = 110.297(2)o, β = 101.342(3)o, γ = 104.701(2)o, V = 534.6(2) Å3, Z = 2, Rgt(F) = 0.0318, wRref(F2) = 0.0833, T = 293(2) K. [ABSTRACT FROM AUTHOR]

Objective: To investigate a family with congenital dysfibrinogenemia, and analyze the risk of hemorrhage and thrombosis and blood transfusion strategies., Methods: Prothrombin time (PT), activated partial thromboplastin time (APTT) and thrombin time (TT) of the proband and her family members were detected by automatic coagulometer, fibrinogen (Fg) activity and antigen were detected by Clauss method and PT algorithm respectively. Meanwhile, thromboelastometry was analyzed for proband and her family members. Then, peripheral blood samples of the proband and her family members were collected, and all exons of FGA, FGB and FGG and their flanks were amplified by PCR and sequenced to search for gene mutations., Results: The proband had normal APTT and PT, slightly prolonged TT, reduced level of Fg activity (Clauss method). The Fg of the proband's aunt, son and daughter all decreased to varying degrees. The results of thromboelastogram indicated that Fg function of the proband and her family members (except her son) was basically normal. Gene analysis showed that there were 6233 G/A (p.AαArg35His) heterozygous mutations in exon 2 of FGA gene in the proband, her children and aunt. In addition, 2 polymorphic loci were found in the family, they were FGA gene g.9308A/G (p.AαThr331Ala) and FGB gene g.12628G/A (p.BβArg478Iys) polymorphism, respectively. The proband was injected with 10 units of cryoprecipitate 2 hours before delivery to prevent bleeding, and no obvious bleeding occurred during and after delivery., Conclusion: Heterozygous mutation of 6233G/A (p.AαArg35His) of FGA gene is the biogenetic basis of the disease in this family with congenital dysfibrinogenemia.

Objective: Through analysis of ABO blood group gene typing technology, to assist in the identification of difficult clinical serological specimens., Methods: A total of 10 forwardreverse typing ambiguous samples were collected from January 2021 to August 2021 in our hospital.ABO genotypes were analysed by gene sequencing., Results: The genotypes of 10 ABO ambiguous blood group samples were A102/BW11, A102/BW12, O02/O02, A102/B303, A102/B101, BW11/O02, B101/O04, BW11/O01, BW11/O01, A101/O02, respectively. The genotype results of 6 cases was consistent with the serological phenotype, and the serological phenotype of 4 cases were different from the geno sequencing., Conclusion: ABO blood groups genotyping technology combined with serological typing can be used for accurate typing of ambiguous blood group, and better ensure the safety of blood transfusion.