The body fat measurements in old persons were carried out using two indirect methods; hydrostatic weighing and skinfold measurement.In comparison it was discovered that the skinfold measurement was significantly different from hydrostatic weighing method. Based on data of the circumference measurements which included forearm circumference (xl), arm circumference (x2), leg circumference(x3) thigh circumference(x4), abdomen circumference (x5) and buttock circumference(x6), two regression equations for the percentage of the body fat measurements were established as follows: male: F(%)=- 15.88 + 1.37BMI + 0.0102Y, female. F(%)= -34.9684 + 0.51BMI + 0.1469Y. Where Y = x1 + x2 + x3 + x4 + x5 + x6; BM1 (Body mass index) = weight(kg)/height(m)2Because the systematic error of skinfold measurements was bigger than those of circumference measurements, it was suggested that the above regression models could be used to estimate body fat in a simpler and easier way. At the same time the method of using percentage of body fat to classify obesity was compared with other two methods, excess body weight and BMI. The results showed that the rate of obesity based on BMI method was higher, and that based on excess body weight was lower than that of percentage of body fat measured by the water displacement method.

Objective To explore the effect of interleukin-6 (IL-6) and Interleukin-12(IL-12) on immune response to hepatitis B vaccination in infants of HBsAg-positive mothers.Methods A total of 91 neonates whose mothers were HBsAg-positive were included and followed up for 12 months.HBV DNA and HBV serological markers in the peripheral blood of the neonates and infants were detected with fluorescence quantitative polymerase chain reaction (FQ-PCR) and chemiluminescence immunoassay (CLIA),and the levels of IL-6 and IL-12 in the peripheral blood of the neonates and infants were detected with enzyme-linked immunosorbent assay (ELISA).Results The non-/hypo-response rate to hepatitis B vaccination was 35.16％ (32/91) in the 91 infants.In the neonatal period and infantile period,the level of IL-6 in non-/hypo-response group was lower than that in high-response group,while the level of IL-12 was higher than that in high-response group,and there was significant difference (P＜0.01).From the neonatal period to the infantile period,the level of IL-6 increased,while the level of IL-12 descended in both groups,and there was significant difference (P＜0.01).Furthermore,the level of anti-HBs of infants was positively correlated with the level of IL-6 (rs =0.70,0.79,P＜ 0.01),and was negatively correlated with the level of IL-12 (rs=-0.71,-0.72,P＜0.01) in the neonatal period and the infantile period.From the neonatal period to the infantile period,the increased level of IL-6 was positively associated with the level of anti-HBs (rs =-0.74,P＜0.01),while the decreased level of IL-12 was negatively associated with the level of anti-HBs (rs=-0.42,P＜0.01).The level of IL-6 was negatively correlated with the level of IL-12 in the neonatal period and the infantile period (rs=-0.68,-0.70,P＜0.01).Conclusions IL-6 might promote the immune response to hepatitis B vaccination in infants whose mothers were HBsAg-positive,while IL-12 might inhibit the immune response.IL-6 and IL-12 would affect the immune response to hepatitis B vaccination in infants of HBsAg-positive mothers at the same time.

Objective To investigate the influencing factors for non/low-response to hepatitis B vaccine in infants of HBsAg-positive mothers.Methods A total of 286 HBsAg-positive pregnant women and their infants were recruited from the Third People's Hospital of Taiyuan during July 2011 to January 2013.The infants were immunized with hepatitis B vaccine according to the 0-1-6 month vaccination schedule and followed up for 12 months.The serum HBV DNA level of mothers,neonates and infants were detected by electro chemilum inescence immunoassay kits and fluorescene quantiative polymerase chain rection.Results Among 286 infants,the rate of non/low-response to hepatitis B vaccine was 18.53％ (53/286).Non-conditional logistic regression analysis indicated that the mother's HBV DNA level ≥ 1 × 107 copies/ml (0R=2.592,95％CI:1.121-5.996) and natural birth (OR=1.932,95％CI:1.021-3.654) were the risk factors for non/low-response to hepatitis B vaccine,the risks were 2.592 times and 1.932 times higher compared with the infants whose mothers were HBV DNA negative and the infants whose mothers had cesarean delivery.There was no multiplicative or additive interaction between high HBV DNA load and natural birth (OR=1.055,95％CI:0.209-5.321),(RERI=1.617,95％CI:-4.038-7.272;AP=0.364,95％CI:-).527-1.225;SI=1.195,95％CI:0.270-13.135).After stratified analysis of mother's HBV DNA level,delivery mode of mothers was not associated with non/low-response of their infants.Conclusion The mother's load of HBV DNA ≥ 1 × 107 copies/ml might be the factor for non/low-response to hepatitis B vaccine in infants of HBsAg positive mothers.

OBJECTIVETo identify the MPL L391-V392ins12 spliceosome and analyze its frequencies in patients with myeloproliferative neoplasms (MPN).

METHODSMPL aberrant spliceosome was identified through reverse transcription polymerase chain reaction (RT-PCR)combined with cloning sequencing. The mutation of this spliceosome in 248 MPN patients and 200 normal people was determined by allele-specific polymerase chain reaction (AS-PCR).

RESULTSA novel aberrant spliceosome of MPL gene (MPL L391-V392ins12)was identified, i.e. 36 bp intron was retained between exon7 and exon8, and there were 12 amino acids (EGLKLLPADIPV)inserted. MPL L391-V392ins12 mutation was detected in 19 (7.66%)of the 248 patients with MPN, including 1 (1.92%) of 52 patients with PV, 14 (9.66%) of 145 with ET, and 4 (7.84%) of 51 with PMF. And the mutation was not detected in the group of 200 normal people.

CONCLUSIONMPL L391-V392ins12 spliceosome is an aberrant spliceosome present in the MPN. It can be detected in PV, ET and PMF, and more frequently in ET and PMF. This mutation may play an important role in the process of MPN.

Humans ; Mutation ; Myeloproliferative Disorders ; genetics ; Neoplasms ; genetics ; Polymerase Chain Reaction ; Receptors, Thrombopoietin ; genetics ; Spliceosomes