Objective To explore the effect of quality control circle (QCC) on health education in stroke rehabilitation nursing. Methods Such activities were conducted in the VIP ward of neurological rehabilitation in our hospital as: theme selecting, activity planning, status mastering, cause analyzing, countermeasures formulating and implementing, etc., in accordance with QCC theory from January to April, 2014. Results The satisfaction of stroke patients to health education rose from 80.1% to 91.1% (P<0.001), and the dissatisfaction to guidance of activities of daily living and prevention of complications decreased significantly (P<0.05) after the implementation of QCC program. All the circle members benefited from the improvement of QCC technique, team work, professional knowledge, communication and coordination, activity confidence, duty and honor. Conclusion Carrying out the QCC activities can play a positive role on health education in stroke rehabilitation nursing.

OBJECTIVETo analyze genetic mutation and molecular pathogenesis in a family affected with inherited coagulation factor XII(FXII) deficiency.

METHODSActivated partial thromboplastin time (APTT), FXII procoagulant activity (FXII:C), FXII antigen (FXII:Ag) and other coagulants were measured. For affected members of the family, exons 1-14 and flanking intronic regions of the FXII gene were amplified with polymerase chain reaction (PCR) and sequenced thereafter. Expression plasmids containing mutant FXII cDNA was constructed and transfected into COS7 cells transiently. Expressions of FXII:Ag and FXII:C were analyzed.

RESULTSThe proband has manifested a prolonged APTT of 108.1 s (reference range: 27.0-41.0 s). Her husband has a normal APTT. Other members of the family had slightly increased APTT. The FXII:C and FXII:Ag of the proband have both dropped to about 0.01 (reference range: 0.72-1.13). The FXII:C levels of her husband, son, daughter and grandchild were 0.57, 0.24, 0.14, 0.16, respectively. And the FXII:Ag levels in her husband, son, daughter and grandchild were 0.55, 0.27, 0.15, 0.21, respectively. The proband and her daughter have both carried a heterozygous deletional mutation 6800-6808delAGCTGGGAG (6800-6808del9bp) in exon 9. For the promoter region of the FXII gene, the genotypes of the proband, her son, daughter and grandchild was TT, whilst that of her husband was CT. Expression study has shown that, whilst the mutant FXII protein has accumulated in the cells similar to wild-type protein, its secretion has reduced approximately by half.

CONCLUSIONA novel deletional mutation 6800-6808del9bp has been identified in the FXII gene. Although mutant FXII protein can still accumulate in cells, its secretion has become insufficient. The 6800-6808del9bp mutation and 46T/T have both contributed to the pathogenesis of FXII deficiency in the family, but may have not been the sole cause.

Adult ; Aged ; Animals ; Base Sequence ; COS Cells ; Cell Line ; Cercopithecus aethiops ; Factor XII ; genetics ; metabolism ; Factor XII Deficiency ; diagnosis ; genetics ; Female ; Gene Expression ; Genotype ; Humans ; Male ; Middle Aged ; Molecular Sequence Data ; Mutation ; Pedigree ; Phenotype ; Young Adult