Association between Intrapartum Interventions and Breastfeeding Duration

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Factors associated with breastfeeding duration and exclusivity in mothers returning to paid employment postpartum

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Practices, predictors and consequences of expressed breast-milk feeding in healthy full-term infants

To investigate the prevalence and predictors of expressed breast-milk feeding in healthy full-term infants and its association with total duration of breast-milk feeding. Prospective cohort study. In-patient postnatal units of four public hospitals in Hong Kong. A total of 2450 mother–infant pairs were recruited in 2006–2007 and 2011–2012 and followed up prospectively for 12 months or until breast-milk feeding had stopped. Across the first 6 months postpartum, the rate of exclusive expressed breast-milk feeding ranged from 5·1 to 8·0 % in 2006–2007 and from 18·0 to 19·8 % in 2011–2012. Factors associated with higher rate of exclusive expressed breast-milk feeding included supplementation with infant formula, lack of previous breast-milk feeding experience, having a planned caesarean section delivery and returning to work postpartum. Exclusive expressed breast-milk feeding was associated with an increased risk of early breast-milk feeding cessation when compared with direct feeding at the breast. The hazard ratio (95 % CI) ranged from 1·25 (1·04, 1·51) to 1·91 (1·34, 2·73) across the first 6 months. Mothers of healthy term infants should be encouraged and supported to feed directly at the breast. Exclusive expressed breast-milk feeding should be recommended only when medically necessary and not as a substitute for feeding directly at the breast. Further research is required to explore mothers’ reasons for exclusive expressed breast-milk feeding and to identify the health outcomes associated with this practice.postprin

Effect on Baby-Friendly Hospital Steps When Hospitals Implement a Policy to Pay for Infant Formula

Background: The Baby-Friendly Hospital Initiative requires hospitals to pay market price for infant formula. No studies have specifically examined the effect of hospitals paying for infant formula on breastfeeding mothers' exposure to Baby-Friendly steps. Objectives: To investigate the effect of hospitals implementing a policy of paying for infant formula on new mothers' exposure to Baby-Friendly steps and examine the effect of exposure to Baby-Friendly steps on breastfeeding rates. Methods: We used a repeated prospective cohort study design. We recruited 2 cohorts of breastfeeding mother-infant pairs (n = 2470) in the immediate postnatal period from 4 Hong Kong public hospitals and followed them by telephone up to 12 months postpartum. We assessed participants' exposure to 6 Baby-Friendly steps by extracting data from the medical record and by maternal self-report. Results: After hospitals began paying for infant formula, new mothers were more likely to experience 4 out of 6 Baby-Friendly steps. Breastfeeding initiation within the first hour increased from 28.7% to 45%, and in-hospital exclusive breastfeeding rates increased from 17.9% to 41.4%. The proportion of mothers who experienced all 6 Baby-Friendly steps increased from 4.8% to 20.5%. The risk of weaning was progressively higher among participants experiencing fewer Baby-Friendly steps. Each additional step experienced by new mothers decreased the risk of breastfeeding cessation by 8% (hazard ratio = 0.92; 95% CI, 0.89-0.95). Conclusion: After implementing a policy of paying for infant formula, breastfeeding mothers were exposed to more Baby-Friendly steps, and exposure to more steps was significantly associated with a lower risk of breastfeeding cessation.postprin

Effect of a hospital policy of not accepting free infant formula on in-hospital formula supplementation rates and breast-feeding duration

OBJECTIVE: To investigate the effect of public hospitals in Hong Kong not accepting free infant formula from manufacturers on in-hospital formula supplementation rates and breast-feeding duration. DESIGN: Prospective cohort study. SETTING: In-patient postnatal units of four public hospitals in Hong Kong. SUBJECTS: Two cohorts of breast-feeding mother-infant pairs (n 2560). Cohort 1 (n 1320) was recruited before implementation of the policy to stop accepting free infant formula and cohort 2 (n 1240) was recruited after policy implementation. Participants were followed prospectively for 12 months or until they stopped breast-feeding. RESULTS: The mean number of formula supplements given to infants in the first 24 h was 2·70 (sd 3·11) in cohort 1 and 1·17 (sd 1·94) in cohort 2 (P<0·001). The proportion of infants who were exclusively breast-fed during the hospital stay increased from 17·7 % in cohort 1 to 41·3 % in cohort 2 (P<0·001) and the risk of breast-feeding cessation was significantly lower in cohort 2 (hazard ratio=0·81; 95 % CI 0·73, 0·90). Participants who non-exclusively breast-fed during the hospital stay had a significantly higher risk of stopping any or exclusive breast-feeding. Higher levels of formula supplementation also increased the risk of breast-feeding cessation in a dose-response pattern. CONCLUSIONS: After implementation of a hospital policy to pay market price for infant formula, rates of in-hospital formula supplementation were reduced and the rates of in-hospital exclusive breast-feeding and breast-feeding duration increased.postprin

An Inhibitory Antibody Blocks Interactions between Components of the Malarial Invasion Machinery

Host cell invasion by apicomplexan pathogens such as the malaria parasite Plasmodium spp. and Toxoplasma gondii involves discharge of proteins from secretory organelles called micronemes and rhoptries. In Toxoplasma a protein complex comprising the microneme apical membrane antigen 1 (AMA1), two rhoptry neck proteins, and a protein called Ts4705, localises to the moving junction, a region of close apposition between parasite and host cell during invasion. Antibodies against AMA1 prevent invasion and are protective in vivo, and so AMA1 is of widespread interest as a malaria vaccine candidate. Here we report that the AMA1 complex identified in Toxoplasma is conserved in Plasmodium falciparum. We demonstrate that the invasion-inhibitory monoclonal antibody (mAb) 4G2, which recognises P. falciparum AMA1 (PfAMA1), cannot bind when PfAMA1 is in a complex with its partner proteins. We further show that a single completely conserved PfAMA1 residue, Tyr251, lying within a conserved hydrophobic groove adjacent to the mAb 4G2 epitope, is required for complex formation. We propose that mAb 4G2 inhibits invasion by preventing PfAMA1 from interacting with other components of the invasion complex. Our findings should aid the rational design of subunit malaria vaccines based on PfAMA1

Protein Kinase A Dependent Phosphorylation of Apical Membrane Antigen 1 Plays an Important Role in Erythrocyte Invasion by the Malaria Parasite

Apicomplexan parasites are obligate intracellular parasites that infect a variety of hosts, causing significant diseases in livestock and humans. The invasive forms of the parasites invade their host cells by gliding motility, an active process driven by parasite adhesion proteins and molecular motors. A crucial point during host cell invasion is the formation of a ring-shaped area of intimate contact between the parasite and the host known as a tight junction. As the invasive zoite propels itself into the host-cell, the junction moves down the length of the parasite. This process must be tightly regulated and signalling is likely to play a role in this event. One crucial protein for tight-junction formation is the apical membrane antigen 1 (AMA1). Here we have investigated the phosphorylation status of this key player in the invasion process in the human malaria parasite Plasmodium falciparum. We show that the cytoplasmic tail of P. falciparum AMA1 is phosphorylated at serine 610. We provide evidence that the enzyme responsible for serine 610 phosphorylation is the cAMP regulated protein kinase A (PfPKA). Importantly, mutation of AMA1 serine 610 to alanine abrogates phosphorylation of AMA1 in vivo and dramatically impedes invasion. In addition to shedding unexpected new light on AMA1 function, this work represents the first time PKA has been implicated in merozoite invasion

Dark Matter from Minimal Flavor Violation

We consider theories of flavored dark matter, in which the dark matter particle is part of a multiplet transforming nontrivially under the flavor group of the Standard Model in a manner consistent with the principle of Minimal Flavor Violation (MFV). MFV automatically leads to the stability of the lightest state for a large number of flavor multiplets. If neutral, this particle is an excellent dark matter candidate. Furthermore, MFV implies specific patterns of mass splittings among the flavors of dark matter and governs the structure of the couplings between dark matter and ordinary particles, leading to a rich and predictive cosmology and phenomenology. We present an illustrative phenomenological study of an effective theory of a flavor SU(3)_Q triplet, gauge singlet scalar.Comment: 10 pages, 2 figures; v2: references added, minor changes to collider analysis, conclusions unchange

Distinct Mechanisms for Induction and Tolerance Regulate the Immediate Early Genes Encoding Interleukin 1β and Tumor Necrosis Factor α

Interleukin-1β and Tumor Necrosis Factor α play related, but distinct, roles in immunity and disease. Our study revealed major mechanistic distinctions in the Toll-like receptor (TLR) signaling-dependent induction for the rapidly expressed genes (IL1B and TNF) coding for these two cytokines. Prior to induction, TNF exhibited pre-bound TATA Binding Protein (TBP) and paused RNA Polymerase II (Pol II), hallmarks of poised immediate-early (IE) genes. In contrast, unstimulated IL1B displayed very low levels of both TBP and paused Pol II, requiring the lineage-specific Spi-1/PU.1 (Spi1) transcription factor as an anchor for induction-dependent interaction with two TLR-activated transcription factors, C/EBPβ and NF-κB. Activation and DNA binding of these two pre-expressed factors resulted in de novo recruitment of TBP and Pol II to IL1B in concert with a permissive state for elongation mediated by the recruitment of elongation factor P-TEFb. This Spi1-dependent mechanism for IL1B transcription, which is unique for a rapidly-induced/poised IE gene, was more dependent upon P-TEFb than was the case for the TNF gene. Furthermore, the dependence on phosphoinositide 3-kinase for P-TEFb recruitment to IL1B paralleled a greater sensitivity to the metabolic state of the cell and a lower sensitivity to the phenomenon of endotoxin tolerance than was evident for TNF. Such differences in induction mechanisms argue against the prevailing paradigm that all IE genes possess paused Pol II and may further delineate the specific roles played by each of these rapidly expressed immune modulators. © 2013 Adamik et al

Projected WIMP sensitivity of the LUX-ZEPLIN dark matter experiment

LUX-ZEPLIN (LZ) is a next-generation dark matter direct detection experiment that will operate 4850 feet underground at the Sanford Underground Research Facility (SURF) in Lead, South Dakota, USA. Using a two-phase xenon detector with an active mass of 7 tonnes, LZ will search primarily for low-energy interactions with weakly interacting massive particles (WIMPs), which are hypothesized to make up the dark matter in our galactic halo. In this paper, the projected WIMP sensitivity of LZ is presented based on the latest background estimates and simulations of the detector. For a 1000 live day run using a 5.6-tonne fiducial mass, LZ is projected to exclude at 90% confidence level spin-independent WIMP-nucleon cross sections above 1.4×10-48 cm2 for a 40 GeV/c2 mass WIMP. Additionally, a 5σ discovery potential is projected, reaching cross sections below the exclusion limits of recent experiments. For spin-dependent WIMP-neutron(-proton) scattering, a sensitivity of 2.3×10-43 cm2 (7.1×10-42 cm2) for a 40 GeV/c2 mass WIMP is expected. With underground installation well underway, LZ is on track for commissioning at SURF in 2020