Objective:To investigate the effect of calcium ionorphore on B7 costimulatory molecules of chronic myeloid leukemia cells line K562.Methods:Well growing K562 cells were cultured in the medium containing calcium ionorphore(375 ng/ml),with K562 cells without CI treatment as control.The cells′ viability and number were calculated by Trypan Blue exclusion at 0,48 and 96 h.Before and after 96 h of cultured,B7-1 and B7-2 expression was assayed by flow cytometry.The proliferation of allogeneic human T cells was measured by MTT colorimetry.Results:B7 costimulatory molecules were abcent or lowly expressed on K562 cells.After 96 h of CI treatment,B7 costimulatory molecules of K562 cells were markedly upregulated and marked activation of allogeneic T cells occurred.No notable morphological change was found during the culture.K562 cells cultured in medium with CI grow slowly than that without CI.Conclusion:B7 costimulatory molecules expression on chronic myeloid leukemia cells line K562 surface was defective.These costimulatory molecules on K562 cells can be upregulated by calcium ionorphore.Calcium ionorphore may inhibit the growth of K562 cells.

Objective To evaluate cystatin C(CysC)in early impairment of renal function in patients of gestational hypertension(GH).Methods Forty patients of GH,70 normotensive pregnant women(35 of early pregnany and 35 of late pregnancy)and 30 normotensive healthy women were enrolled.CysC and ?2-M were measured by particle enhanced nephelometric assay,SCr,BUN and UA were measured by biochemistry analysis.Results The level of CysC in normotensive late pregnancy subjects(1.22?0.19 mg/L)and GH patients(1.93?0.48 mg/L)were higher than that in normal healthy women(0.78?0.22 mg/L,P

In four patients with chronic pancreatitis from two hereditary pancreatitis (HP) families and 63 normal controls, five exons of cationic trypsinogen gene (PRSS1) were amplified by PCR and it's products were analyzed by sequencing, related clinical data were also collected. All the four patients were found mutations in the PRSS1 gene but their clinical feature is absolutely different. Six patients with diabetes mellitus were found in pedigree No. 1, it's members show pancreatitis symptom later, at about 29, the tumor markers (CA19-9, CA72-4) is obviously higher than the patients in pedigree No. 2, two patients with chronic pancreatitis in pedigree No. 2, show symptom earlier without diabetes mellitus, their clinical characterization are different too. The number of CD4+T cell/CD8+T is very low in Ⅲ 8, but Ⅲ 7 is normal, and the level of anti-HBs of Ⅲ 8 is variable in the course of pancreatitis, but the phenomenon was not found in Ⅲ 7. In their PRSS1 gene two guanosine (G) to adenosine (A) mutations were found in PRSS1 exon 3 of pedigree No. 1, one was detected at 336 basyl, the other mutation occurs at 361 basyl. The results of the mutations were Lys →Lys and Ala →Thr. While thymine (T) to adenosine (A) and (guanosine) G→(adenosine) A mutation in PRSS1 exon 3 was detected in the other patient of pedigree No. 2 (Ⅲ 8). One was 361 basyl, the other at 415 basyl. While c.415 T→A was not found in the proband of pedigree No. 2 PRSS1 gene (Ⅲ 7). All of the mutations were heterozygous mutation, that is to say all of the trypsinogen were wild type and mutant type concomitance, the normal and abnormal pathway of active trypsinogen exist partially. At the same time, the mutations of SPINK1 were not observed. Compared with the documents and registration of NCBI, it can be concluded that PRSS1 gene had many kinds of mutations in hereditary pancreatitis, the heterozygous mutations (c.336 G→A, c.415 T→A) were the novel mutations and related with clinical phenotype. What's more, it's the first time that the multisite heterozygous mutations of PRSS1 gene were reported. The presence of the mutations in four patients with chronic pancreatitis, it's absence in their relatives and the strong evolutionary conservation of the mutation, all indicate that the trypsinogen mutation is associated with hereditary pancreatitis and for the first time raises the question whether a gain or a loss of trypsin function participates in the onset of Chinese pancreatitis.