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Objective:To investigate the current situation of paternal self-efficacy of support breastfeeding of late prematurity and analyze the factors affectingpaternal self-efficacy of support breastfeeding.Methods:This study was a cross-sectional survey. From July to October 2021, the fathers of 210 late prematurity in Neonatology and NICU wards of Shanxi Children′s Hospital, were selected by convenience sampling method for the research object. The survey was carried out using the General Information Questionnaire, Iowa Infant Feeding Attitude Scale and Father Support Breastfeeding Self-Efficacy Scale-Short Form, multiple linear regression was used to analyze the influencing factors of paternal self-efficacy of support breastfeeding of late prematurity.Results:The total score of Father Support Breastfeeding Self-Efficacy Scale-Short Form was 46.22 ± 10.03, and the total score of Iowa Infant Feeding Attitude Scale was 59.31 ± 5.65, which were positively correlated ( r = 0.224, P<0.01). In the multiple linear regression analysis, whether or not to receive breastfeeding education, feeding methods, family opinions, and fathers′ attitudes towards breastfeeding were the main factors affecting fathers′ self-efficacy in supporting breastfeeding ( t values were - 3.07 to 2.35, all P<0.05). Conclusions:The paternal support breastfeeding of late prematurity level was at a lower level. It is suggested that medical staff should not only pay attention to puerpera and baby, but also pay attentionto father and family, and construct personalized health education based on co-parenting theory.
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<p><b>OBJECTIVE</b>To detect potential mutation of immunoglobulin μ -binding protein 2 (IGHMBP2) gene in a two-year-old patient with spinal muscular atrophy with respiratory distress type 1 (SMARD1).</p><p><b>METHODS</b>Genomic DNA was extracted from peripheral blood sample from the patient and her parents, as well as cord blood sample from the fetus. Potential mutations of the coding region of the IGHMBP2 gene was detected with PCR and Sanger sequencing.</p><p><b>RESULTS</b>A heterozygous missense mutation c.1060G>A and a frameshift mutation c.2356delG was detected in the patient. The mutations were respectively inherited from her father and mother. Neither mutation was found in DNA derived from the cord blood sample.</p><p><b>CONCLUSION</b>The missense mutation c.1060G>A and frameshift mutation c.2356delG were probably causative for the disease. Analysis of the IGHMBP2 gene has provided an important clue for the etiology and prenatal diagnosis of SMARD1.</p>