This article discussed the applications of body language in rehabilitation teaching from 3 aspects including the concept, thetype and the application methods of body language.

Objective To explore the relationship of depth of trophoblastic invasion with trophoblast cell activity and serum β-hCG according to the expression of proliferation antigen Ki-67 which viewed as an indicator of cell proliferation activity.Methods Fallopian tube specimens collected from 108 patients who underwent operation treatment for fallopian tubal pregnancy in our hospital were investigated by light microscopic examination.They were divided into three groups according to the depth of trophoblastic infiltration: Ⅰ group (stage): trophoblastic invasion of tubal mucosa,Ⅱ group(stage): trophoblastic invasion of the muscularis,Ⅲ group(stage): trophoblast invasion of serosa layer(muscularis penetration).The expression of Ki-67 was detected by SP method and blood β-hCG was detected within 2 hours of preoperative.The level of β-hCG,the expression of Ki-67 and the depth of trophoblast invasion were analyzed.Results Mean level of serumβ-hCG in Group Ⅰ,Ⅱ and Ⅲ were(1416.64 ± 859.94)U/L,(3380.33 ± 2392.36)U/L and(6999.33 ± 4949.90)U/L respectively.Positive expression rate of cell proliferation antigen Ki-67 in Group Ⅰ,Ⅱ and Ⅲ were 21.95％,53.66％ and 6.40％ respectively.There were significant difference on the expression of Ki-67 between group Ⅰ and group Ⅱ,group Ⅱ and Ⅲ group,group Ⅰ and group Ⅲ(x2 =3.94,4.07,4.35,respectively,P ＜ 0.05).The serumβ-hCG level also displayed statistics difference in the three groups(F =9.914,P ＜ 0.01).The positive expression of Ki-67 and serum β-hCG level were positively correlated with each other(r =0.678,P ＜ 0.05)Conclusion The high level of the serum β-hCG indicates high expression of Ki-67 and deeper trophoblast invasion of tubal wall.

Objective To evaluate the correlation between microvascular invasion(MVI) and prognosis in patients with hepatocellular carcinoma (HCC),and to analyse the influencing factors of MVI in patients with HCC.Methods Total of 81 patients with hepatocellular carcinoma treated in Beijing Hospital from January 2014 to December 2016 were retrospectively studied.There were 65 males and 16 females.The mean age was 59.6± 12.7 years,and the age ranged from 21 to 87 years old.Pathological examination showed presence of MVI in 35 patients.Results Total of seventy-six patients with hepatocellular carcinoma were followed-up.The 1-,2-,3-and 4-year overall survival rates in the 35 patients with microvascular invasion of hepatocellular carcinoma were 78.6％,55.4％,38.3％,and 32.2％,respectively.The 1-,2-,3-,and 4-year overall survival rates of the 41 patients without microvascular invasion were 93.4％,76.5％,68.2％ and 68.2％,respectively.The difference was significant (P＜0.05).Cox multivariate regression analysis showed that microvascular invasion was an independent risk factor of overall survival after surgery (HR=3.071,95％ CI:1.239～7.610,P＜0.05).Sub-group analysis was done on patients with microvascular invasion based on pathological results which included the number of MVI lesions,the call number in the MVI lesion,the distance of the MVI to the primary liver cancer,and the gradings of MVI.There were no significant differences in the overall survival outcomes (P＞0.05).Multivariate logistic regression analysis showed the maximum diameter of tumor ＞ 5 cm (OR =6.340,95％ CI:2.000 ～ 20.096),preoperative total bilirubin (TBil) ＞ 17 μmol/L (OR =5.067,95％CI:1.386 ～ 18.525),and preoperative alpha-fetoprotein (AFP) ＞400 μg/L (OR =6.042,95％ CI:1.435 ～ 25.444) were independent risk factors of microvascular invasion (P＜ 0.05).Conclusion Hepatocellular carcinoma patients with microvascular invasion had poor prognosis.Preoperative AFP,preoperative TBil,and diameter of tumor were independent risk factors of microvascular invasion in patients with hepatocellular carcinoma.

OBJECTIVE: To screen for LDLR gene mutations in 9 patients with familial hypercholesterolemia (FH). METHODS: All exons of the LDLR gene and flanking intronic sequences were amplified by PCR and subjected to automatic DNA sequencing. For patients with homozygous or compound heterozygous mutations, parental DNA sequencing or T cloning sequencing was carried out to determine the parental origin of the mutant alleles. RESULTS: Direct sequencing of PCR products revealed 8 LDLR variants in 7 patients, which included c.259T>G, c.513delC, c.530C>T, c.682G>T, c.763C>T, c.1187-10G>A, c.1948delG, and c.1730G>A, among which c.1948delG was novel. Four patients have carried heterozygous mutations, two carried homozygous mutations, and one carried compound heterozygous mutations. The patients with biallelic mutations presented with a more severe phenotype compared those carrying heterozygous mutations. CONCLUSION LDLR mutations were identified in 7 out of 9 patients with FH. Among the 8 identified LDLR mutations, c.1948delG was firstly reported. Above findings have expanded the mutation spectrum of LDLR gene.
DNA Mutational Analysis ; Genetic Testing ; Humans ; Hyperlipoproteinemia Type II ; genetics ; Mutation ; Phenotype ; Receptors, LDL ; genetics