ABSTRACT
Background: Parents may consider interrupting breastfeeding to manage neonatal jaundice (NJ). Our aims were to determine correlations of breastfeeding with NJ by examining infants' manifestations in the first week after birth and to understand parents' perceptions toward NJ in relation to breastfeeding. Materials and Methods: This prospective cross-sectional study was conducted in a tertiary medical center by examining infants and administering a questionnaire survey to their parents. All healthy infants admitted to the well-baby nursery were eligible for enrollment. A 16-item questionnaire was distributed to parents of enrolled infants from October 2017 to February 2019. Items of the questionnaire included perceptions and knowledge of NJ. In addition, clinical information of enrolled infants was obtained from medical records. Hyperbilirubinemia was defined as a peak transcutaneous bilirubinometer value ≥15 mg/dL. Results: In total, 449 parents completed the consent form and participated in the study. Results showed that exclusive breastfeeding was more common in infants with a vaginal delivery (p < 0.001), who were nonprimiparous (p = 0.004) and who had weight loss of >7% (p < 0.001). There was no significant correlation of exclusive breastfeeding with hyperbilirubinemia (p = 0.414). Approximately two-thirds of parents were worried about NJ occurring in their child. Most parents were aware of phototherapy as management of NJ. However, their knowledge of risk factors, complications, and assessments of NJ was relatively deficient. Overall, 29.6% of parents rated breastfeeding as a risk factor for NJ, and 24% of parents indicated that cessation of breastfeeding was a management option for NJ. Conclusions: The results indicated that NJ in the first few days after birth poses a significant barrier to breastfeeding. Our findings provide critical information for plotting strategies to enhance parents' willingness to continue breastfeeding.
Subject(s)
Breast Feeding , Jaundice, Neonatal , Child , Cross-Sectional Studies , Female , Humans , Infant , Infant, Newborn , Parents , Perception , Pregnancy , Prospective StudiesABSTRACT
Prolonged jaundice is a commonly evaluated condition. The aim of this study was to assess the risk factors of jaundice in healthy infants at one month of age. This prospective cohort study enrolled 509 healthy infants from 2013 to 2018. Those with gestational age (GA) less than 35 weeks, birth weight less than 2000 grams, and illness were not enrolled. Jaundice was defined as a transcutaneous bilirubin value ≥5 mg/dL at 25-45 days of age. Umbilical cord blood samples were obtained to examine seven common gene variants. The incidence of prolonged jaundice was 32.2%. Prolonged jaundice was more common in infants with exclusive breastfeeding (p < 0.001), GA 35~37 w (p = 0.001), stool passage >4 times/d (p < 0.001), previous phototherapy (p < 0.001), and gene variant of G to A at nt 211 of UGT1A1 (p = 0.004). A multivariate logistic regression analysis demonstrated the greatest risk for prolonged jaundice was exclusive breastfeeding (OR = 2.818, 95% CI = 1.851-4.292), followed by previous phototherapy (OR = 2.593, 95% CI = 1.716-3.919), GA 35~37 w (OR = 2.468, 95% CI = 1.350-4.512), and G to A at nt 211 of UGT1A1 (OR = 1.645, 95% CI = 1.070-2.528). In conclusion, infants with exclusive breastfeeding, GA 35~37 w, previous phototherapy, or G to A at nt 211 of UGT1A1 are at greater risk of prolonged jaundice. Healthcare professionals should consider these risk factors in their assessment of prolonged jaundice.
Subject(s)
Jaundice, Neonatal/epidemiology , Jaundice, Neonatal/pathology , Bilirubin/blood , Breast Feeding , Female , Humans , Incidence , Infant , Infant, Newborn , Jaundice, Neonatal/therapy , Male , Phototherapy , Prospective Studies , Risk Assessment , Risk FactorsABSTRACT
A range of biological and molecular effects caused by nicotine are considered to effect bone metabolism. Vitamin C functions as a biological antioxidant. This study was to evaluate the in vitro effects of nicotine on human bone marrow stromal cells and whether Vitamin C supplementation show the antagonism action to high concentration nicotine. We used CCK-8, alkaline phosphatase (ALP) activity assay, Von Kossa staining, real-time polymerase chain reaction and Western Blot to evaluate the proliferation and osteogenic differentiation. The results indicated that the proliferation of BMSCs increased at the concentration of 50, 100 ng/ml, got inhibited at 1,000 ng/ml. When Vitamin C was added, the OD for proliferation increased. For ALP staining, we found that BMSCs treated with 50 and 100 ng/ml nicotine showed a higher activity compared with the control, and decreased at the 1,000 ng/ml. Bone morphogenetic protein-2 (BMP-2) expression and the calcium depositions decreased at 100 and 1,000 ng/ml nicotine, while the addition of Vitamin C reversed the down regulation. By real-time PCR, we detected that the mRNA expression of collagen type I (COL-I) and ALP were also increased in 50 and 100 ng/ml nicotine groups (P < 0.05), while reduced at 1,000 ng/ml (P < 0.05). When it came to osteocalcin (OCN), the changes were similar. Taken all together, it is found that nicotine has a two-phase effect on human BMSCs, showing that low level of nicotine could promote the proliferation and osteogenic differentiation while the high level display the opposite effect. Vitamin C could antagonize the inhibitory effect of higher concentration of nicotine partly.
Subject(s)
Antioxidants/pharmacology , Ascorbic Acid/pharmacology , Bone Marrow Cells/metabolism , Cell Differentiation/drug effects , Cell Proliferation/drug effects , Ganglionic Stimulants/pharmacology , Nicotine/pharmacology , Osteogenesis/drug effects , Adult , Aged , Ascorbic Acid/antagonists & inhibitors , Bone Marrow Cells/cytology , Bone Morphogenetic Protein 2/biosynthesis , Cells, Cultured , Dose-Response Relationship, Drug , Drug Antagonism , Female , Ganglionic Stimulants/antagonists & inhibitors , Gene Expression Regulation/drug effects , Humans , Male , Middle Aged , Nicotine/antagonists & inhibitors , Stromal Cells/cytology , Stromal Cells/metabolismABSTRACT
Thymoquinone (TQ), the predominant bioactive constituent derived from the medicinal spice Nigella sativa (also known as black cumin), has been applied for medical purposes for more than 2,000 years. Recent studies reported that thymoquinone exhibited inhibitory effects on the cell proliferation of several cancer cell lines. This study was performed to investigate the antitumor and anti-angiogenic effects of thymoquinone on osteosarcoma in vitro and in vivo. Our results showed that thymoquinone induced a higher percentage of growth inhibition and apoptosis in the human osteosarcoma cell line SaOS-2 compared to that of control, and thymoquinone significantly blocked human umbilical vein endothelial cell (HUVEC) tube formation in a dose-dependent manner. To investigate the possible mechanisms involved in these events, we performed electrophoretic mobility shift assay (EMSA) and western blot analysis, and found that thymoquinone significantly downregulated NF-κB DNA-binding activity, XIAP, survivin and VEGF in SaOS-2 cells. Moreover, the expression of cleaved caspase-3 and Smac were upregulated in SaOS-2 cells after treatment with thymoquinone. In addition to these in vitro results, we also found that thymoquinone inhibits tumor angiogenesis and tumor growth through suppressing NF-κB and its regulated molecules. Collectively, our results demonstrate that thymoquinone effectively inhibits tumor growth and angiogenesis both in vitro and in vivo. Moreover, inhibition of NF-κB and downstream effector molecules is a possible underlying mechanism of the antitumor and anti-angiogenic activity of thymoquinone in osteosarcoma.
Subject(s)
Antineoplastic Agents/therapeutic use , Benzoquinones/therapeutic use , Bone Neoplasms/blood supply , Bone Neoplasms/drug therapy , NF-kappa B/metabolism , Osteosarcoma/blood supply , Osteosarcoma/drug therapy , Animals , Antigens, CD34/metabolism , Antineoplastic Agents/pharmacology , Apoptosis/drug effects , Benzoquinones/pharmacology , Bone Neoplasms/pathology , Caspase 3/metabolism , Cell Line, Tumor , Cell Proliferation/drug effects , Cell Survival/drug effects , Human Umbilical Vein Endothelial Cells/drug effects , Humans , Inhibitor of Apoptosis Proteins/metabolism , Ki-67 Antigen/metabolism , Male , Mice , Mice, Inbred BALB C , Neovascularization, Pathologic/drug therapy , Oligopeptides/metabolism , Osteosarcoma/pathology , Signal Transduction/drug effects , Survivin , X-Linked Inhibitor of Apoptosis Protein/metabolismABSTRACT
Our objective was to identify the association between maternal diet with Chinese herbal medicines and prolonged jaundice of breast-fed infants. Healthy infants at 25 to 45 days of age were eligible for enrollment into this prospective study. Jaundice was defined as a transcutaneous bilirubin (TcB) value ≥ 5 mg/dL. A questionnaire survey asking feeding type, stool pattern, and maternal diet was conducted at the time of TcB measurement. A total of 1148 infants were enrolled, including 151 formula-fed, 436 combination-fed, and 561 breast-fed infants. The incidences of jaundice were 4.0% in formula-fed infants, 15.1% in combination-fed infants, and 39.8% in breast-fed infants (P < 0.001). In addition, jaundice was noted in 37.1% of preterm infants and 25.0% of term infants (P < 0.001). Furthermore, jaundice was more common in breast-fed infants whose mothers did not consume the traditional Chinese herbal medicines than in breast-fed infants whose mothers did consume such medicines (P < 0.001). In conclusion, this cohort study has identified late-preterm birth and breast feeding as the contributory factors for prolonged jaundice of apparently well infants. The data indicate that postpartum diet with Chinese herbal medicines is associated with breast milk jaundice.