bluuebunny/crossref_metadata_2025_split huggingface dataset:
Maternal Weight Over Successive Pregnancies and Breastfeeding Initiation, Duration and Exclusivity
Authors: Metallinos‐Katsaras Elizabeth , Siu Elizabeth Colavito , Colchamiro Rachel 
Published: November 2023

Maternal overweight and obesity have been shown to adversely affect breastfeeding success. This study aims to examine the relationship between maternal weight status over the course of 2 successive pregnancies and breastfeeding initiation, duration and exclusivity among a low income diverse sample. Mothers enrolled in Massachusetts WIC (2001–2009) with two consecutive (linked) pregnancies were included. Only those with singleton, full term, live, adequate‐birth‐weight infants and with complete breastfeeding (2nd birth) and covariate (n=10,157)) data were included. Maternal weight status was examined using the following variables: change in weight classification between pregnancies 1–2 using pre‐pregnancy weight (none, decrease, increase), 2nd pre‐pregnancy weight status (underweight, normal weight, overweight, obese) and gestational weight gain (IOM 2009 recommendations) during the second pregnancy. Breastfeeding outcomes were initiation, duration and whether or not infants were exclusively breastfed for at least 4 weeks. Covariates included the following: race/Hispanic ethnicity, maternal age and education, first pregnancy breastfeeding initiation/duration, timing of WIC entry, smoking post‐partum. Multivariate Logistic Regression was used to examine associations with breastfeeding initiation, and exclusivity, while General Linear Model Regression was used to examine breastfeeding duration. The sample was diverse (52.4% nonwhite) with a mean age of 24.5 years (SD=5.0). At the start of their second pregnancy, 50.7% of women were overweight or obese; 28.1% of women shifted to a higher weight status classification between their 1st and 2nd pregnancies, while 5.0% shifted to a lower weight class. After the second pregnancy, 58.6% initiated breastfeeding; mean breastfeeding duration was 9.0 weeks among initiators (SD=15.9). Weight gain during pregnancy was not associated with any of the breastfeeding outcomes, however, 2nd pregnancy's pre‐pregnancy weight status, and change in weight class category were. Women who were obese prior to their second pregnancy were 24% less likely to initiate breastfeeding (AOR(95%CI))=0.76 (0.67–0.87) than those normal weight. Those whose weight class declined between pregnancies were 30% more likely to initiate breastfeeding (AOR=1.30 95% CI=1.03–1.64) than those whose weight status stayed the same. Mothers who were obese, breastfed for a shorter duration (p<.05) than those who were overweight (12.2 vs. 13.9 weeks), or normal weight (13.2 weeks). Obese mothers were less likely to exclusively breastfeed for at least four weeks compared to normal weight mothers (AOR=0.57, p < .05). No associations were found with other weight status categories. Both weight status prior to pregnancy and changes over subsequent pregnancies appear to be associated with breastfeeding success in a low income diverse population.Support or Funding InformationNo support.
Milk Production in Mothers with and without Signs of Insulin Resistance
Authors: Nommsen‐Rivers Laurie Ann , Riddle Sarah Ann , Thompson Amy , Ward Laura , Wagner Erin 
Published: November 2023

Maternal obesity is associated with shortened breastfeeding duration. Insulin resistance is a physiologic hallmark of obesity and may underlie lactation difficulties in obese and other insulin resistant mothers. Our objective is to compare 24‐hour milk production in mothers with signs of insulin resistance (IR) versus those without. We examined baseline data from the MALMS study, a randomized placebo‐controlled trial of metformin to augment low milk supply. Baseline eligibility includes: mother 1–8 weeks postpartum, healthy term infant that is currently requiring formula supplement to achieve sufficient growth, but mother has strong desire to improve breast milk production. Mothers fitting this description were referred to the study by area health care providers. At baseline, all women complete a weighed record of milk production over 24 hours and undergo evaluation for trial eligibility, including the following signs of IR: fasting plasma glucose ≥ 95 mg/dL, abdominal obesity, recent gestational diabetes, or polycystic ovary syndrome. We compared relative ranking of baseline 24‐hour milk production in IR versus no IR groups, and then in obese versus non‐obese groups, with the Wilcoxon test. Of 48 women who completed baseline measurements, 33 (69%) exhibited signs of IR. Mean age (±SD) of mother (31±5 years) and infant (4±2 weeks) did not differ between groups, but BMI was significantly higher in the IR group (36.9z±7.9 versus 25.4±3.6 kg/m2, P<0.001). Relative ranking of milk production was significantly lower in IR versus no‐IR: Median [interquartile range], 216[158–332] versus 377[294–598], P=0.004. Differences were less pronounced when milk output rankings were compared for obese versus non‐obese, P=0.05. While suboptimal lactation management may have contributed to low production at Baseline in some participants, our results point to an additional deficit associated with IR.Support or Funding InformationNIH 5 K12 HD051953 (PI, Tsevat, University of Cincinnati), Bridging Interdisciplinary Research Careers in Women's Health (BIRCWH award to LN‐R)
Mitigating climate change with a carbon tax on foods: What are the ethical implications?
Authors: Downs Shauna , Fox Elizabeth L , Fanzo Jessica 
Published: November 2023

The global production of food is responsible for approximately 30% of all greenhouse gas emissions, a significant portion of which can be attributed to red meat. As the global population and growth in per capita income increases, the demand for red meat will continue to rise putting further pressure on the planet. Numerous recent studies have explored the environmental and health impacts of different diets and have identified red meat (and beef in particular) as one of the key contributors to greenhouse gas emissions and adverse health outcomes. Shifting dietary patterns to reduce red meat intakes could help reduce greenhouse gas emission and improve health outcomes. In exploring strategies to mitigate such environmental and health impacts for current and future generations, a number of policy recommendations have been proposed. One popular proposal is carbon taxation of foods that capture the actual environmental cost of producing and consuming such foods. In Denmark, a carbon tax on red meat was recently proposed to help curb emissions and reduce population intakes. However, such recommendations are wrought with ethical dilemmas. Using an ethics framework for public health developed by Kass (2001), we critically analyzed the proposal of carbon taxation for its public health and environmental goals, potential burdens and minimization of burdens, fairness of distribution, and implications for individuals' autonomy. We determine that the distribution of burden resulting from such policies is inequitable and regressive, having negative tradeoffs for low‐income stakeholders and individuals from low‐income countries. We also determine that the potential burden and autonomy of future generations is not evenly distributed. Current policy proposals aimed at enhancing the sustainability of our diets often result in unethical tradeoffs. Policymakers and key stakeholders should consider the ethical dimensions of interventions and policies promoting sustainable diets, and should consider who bears the weight of such policy decisions before enacting them.Support or Funding InformationThis project does not have funding.
Whole Body Net Protein Balance Plateaus in Response to Varying Protein Intakes During Post‐Exercise Recovery: Identification of a Maximal Anabolic Intake
Authors: Mazzulla Michael , Kato Hiroyuki , Packer Jeff , Wooding Denise , Moore Daniel 
Published: November 2023

Dietary protein is important for the repair and/or rebuilding of skeletal muscle and body proteins and is required to induce a net anabolic environment during recovery from exercise. While the majority of studies assess the effect of protein intake on protein synthesis (S), maximizing net balance [NB; the algebraic difference between S and breakdown (B)] would presumably optimize post‐exercise recovery for athletes. Given the suggestion by some that there is no practical limit to the anabolic response to mixed meal ingestion at rest, the present analysis sought to determine whether net protein balance plateaued in response to varying protein intakes within a mixed macronutrient meal during post‐exercise recovery. After a 2‐d controlled diet, 6 healthy, active males (23 ± 1 y; 82.3 ± 5.7 kg; 71.1 ± 5.1 kg fat‐free mass; mean ± 95% CI) and 7 females (21.4 ± 0.8 y; 68.5 ± 9.3 kg; 53.3 ± 8.6 kg fat‐free mass) consumed a liquid meal (1 g·kg−1 carbohydrate) prior to performing a variable intensity exercise protocol (Loughborough Intermittent Shuttle Test). During the 8‐h post‐exercise recovery period, participants consumed isoenergetic mixed meals providing 0.42 g·kg−1·h−1 of carbohydrate and a variable amount of fat (0.08–0.18 g·kg−1·h−1) and protein (0.02–0.22 g·kg−1·h−1). Protein was provided as crystalline amino acids modeled on the basis of egg protein with the exception of tyrosine (3.33 mg·kg−1·h−1) and phenylalanine (2.5 mg·kg−1·h−1), the latter of which contained 0.46 mg·kg−1·h−1 of l‐[13C]phenylalanine to model steady state phenylalanine kinetics. Breath and urine samples were taken at isotopic steady state to determine phenylalanine oxidation (O) and phenylalanine turnover (Q; corrected for phenylalanine intake), respectively, as an estimate of B. NB was determined from the difference between S (Q – O) and B. Mixed modeling bi‐phase linear regression (R2 = 0.62; P < 0.05) explained a greater proportion of NB variance than linear regression (R2 = 0.49; P < 0.05), indicating NB reached a plateau. NB was not different between males and females (P > 0.05) and increased up to a plateau at 0.13 ± 0.03 g·kg−1·h−1 (0.16 ± 0.02 g·kg−1 fat‐free mass·h−1) or the equivalent of 1.6 ± 0.32 g·kg−1·12h−1 when collapsed across sexes. The breakpoint in NB corresponded to a dietary protein:carbohydrate ratio of 1:3.2. Linear modeling revealed no discernible effect of protein intake on S (P = 0.79) or B (P = 0.17) suggesting the increase in NB was a combination of subtle changes in these kinetics. These data suggest there is a practical limit to the anabolic response to mixed meal ingestion during recovery from variable intensity exercise in active males and females. Athletes should consume ~1.6 g protein·kg−1·d−1 with adequate carbohydrate to maximize whole body NB and thus optimize post‐exercise recovery.Support or Funding InformationSupported by the Ajinomoto Innovation Alliance Program
Analyzing Short Term Protein Oxidation Provides Evidence about Its Role in Whole Body Protein Metabolism
Authors: Reckman Gerlof , Priebe Marion , Koehorst Martijn , Boer Theo , Vonk Roel J 
Published: November 2023

INTRODUCTIONProtein intake has been suggested to play an important role in development of obesity; on one hand in newborn, where excess protein intake might stimulate development of obesity in later life (Kirchberg et al. 2014). On the other hand, protein consumption is promoted for weight management (Martens et al. 2014). At present, no formal recommendations for the upper limit of protein intake have been presented. Information about rate‐limiting steps in protein catabolism is scarce. We therefore studied the role of protein oxidation in this process.OBJECTIVESTo monitor protein oxidation we have developed a non‐invasive natural enriched 13C‐protein breath test using naturally enriched 13C‐milk protein (fractions). We used this technique to analyze the kinetics of protein oxidation and its interfering factors.METHOD/DESIGNThe breath test was preceded by an overnight fast. After consuming the substrate, dissolved in 500 ml water, breath samples were collected up to 330 minutes and analyzed by Isotope Ratio Mass Spectrometry for the 13CO2:12CO2 ratio.RESULTSWhey was oxidized for 28.6% ± 6.8% (mean ± SD) after 240 minutes, compared to 22.9% ± 6.2% for glucose in the same period. Postprandial oxidation kinetics of glucose and whey started to diverge after 70 min after which whey was being oxidized faster than glucose.Different doses of milk protein (10, 30, 50, 60, 70 g) were oxidized for 15.3, 24.2, 22.3, 21.5 and 14.5% respectively. Maximal milk protein oxidation was measured during the 60 g dose at a rate of 0.062 g/min, leading to a maximal oxidation capacity of 1.3 g/kg bodyweight/day.Combining protein (30 g 13C‐whey) with carbohydrates (30 g non‐labeled glucose) resulted in two‐fold increase in oxidation of 13C‐whey compared to oxidation of 13C‐whey alone. A three‐fold increase in oxidation of 13C‐glucose was measured when non‐labeled whey was added compared to oxidation of 13C‐glucose alone.CONCLUSIONSWhey is oxidized faster than glucose from 70 min onwards, which seem to suggest that stomach emptying was not the cause of the difference in oxidation. The interaction of whey and glucose suggest that the oxidation of whey is not driven by energy demand. The stimulating effect of glucose might hint to the involvement of insulin. Oxidation of whey protein is quantitatively of high importance and not down regulated by concomitant administration of other substrates. Analyzing biological variations in acute protein oxidation in defining the upper limit of intake, seem to be relevant.Support or Funding InformationThe 13C‐milk substrates were provided by Hanze Nutrition BV.
Lack of Arginase II Spares Arginine and Restores Growth in Mice
Authors: Marini Juan C. , Mohammad Mahmoud A. , Didelija Inka C. 
Published: November 2023

Arginine (Arg) is an essential amino acid for growth in C57BL/6 (BL6) mice, but not for Swiss mice. BL6 mice fed an Arg free diet after weaning fail to achieve maximal growth rate due to limited endogenous de novo Arg synthesis. In contrast, Swiss mice have a greater synthesis of citrulline and Arg and thus do not require dietary Arg. Alternatively, reducing Arg disposal has the potential to increase Arg availability and increase growth rate. To test this hypothesis, mice lacking arginase II were studied during the post‐weaning period. Arginase II ko (ARGII, n= 20) and wild type (WT, n= 20) male littermates were weaned at 21 d of age. After a 3 d adaptation period to a powder standard diet, mice were fed either an Arg‐free or Arg sufficient diet (8 g Arg/kg diet) for 3 weeks. Mice were weighed twice a week to monitor growth. The data generated was analyzed using a logistic model for growth (A‐B*exp(‐k*time), where A is the mature weight, (A‐B) is the initial weight and k is the growth constant). At the end of the feeding trial, [13CD4] citrulline and [15N2] arginine were infused in fasted mice to determine the flux of Arg and de novo Arg synthesis rate. ARGII mice were slightly heavier than their WT littermates (A‐B= 15.5 vs 14.2 g, respectively) at the beginning of the feeding trial on d 24, but without reaching significance (P = 0.15). No genotype or dietary Arg intake effect was detected for the asymptotic mature weight of these mice (A= 25.9±1 g). Both ARGII mice and mice fed the Arg sufficient diet grew faster (k; P < 0.001) than WT mice and mice fed the Arg free diet, respectively. At the end of the trial ARGII mice fed the Arg free diet achieved a similar body weight than WT mice fed the Arg sufficient diet (21.3 vs 21.8 g, respectively; P = 0.94). ARGII mice had greater plasma Arg concentration (100 vs 79 μmol/L; P < 0.001) and fluxes (460 vs 390 μmol•kg−1•h−1; P < 0.001) than WT mice; there was no dietary treatment effect for these parameters (P > 0.6). Citrulline production was greater in WT mice (95 vs 86 μmol•kg−1•h−1; P < 0.01) and in mice fed the Arg‐free diet (98 vs 84 μmol•kg−1•h−1; P < 0.001). However, this did not translate in a higher de novo Arg synthesis rate (78 μmol•kg−1•h−1; P >0.05). In conclusion, ARGII mice have greater Arg availability (Arg flux and plasma concentration) than their WT counterparts. This higher Arg availability allows ARGII mice to grow in an Arg‐free diet and achieve a growth rate similar to WT mice fed an Arg sufficient diet. This work shows that reducing the disposal rate of Arg through limiting arginase activity abolishes the dietary requirement for Arg for growth in BL mice.Support or Funding InformationNIH R01 GM108940
Lipidomic profiling of erythocytes in septic patients revels novel biomarkers
Authors: Mecatti Giovana Colozza , Messias Marcia Cristina Fernandes , Angolini Célio Fernando Figueiredo , de Oliveira Carvalho Patricia 
Published: November 2023

Sepsis is common and often deadly. It remains the primary cause of death from infection, despite modern medicine. The identification of reliable diagnostic biomarkers for the early detection of this disease is critical and may reduce the mortality rate as it could allow early treatments. The present study deals with the plasma and red cells blood lipidome profiling of patients diagnosed with sepsis and septic shock and aimed to find possible sepsis biomarkers using GC and ESI‐MS (q‐ToF). The data was treated with multivariate data analysis, including principal component analysis (PCA) and (orthogonal) partial least squared discriminant analysis ((O)PLS‐DA). Potential biomarkers including lysophosphatidylcholines (lyso‐PCs) and sphingomyelin (SMs) with specific fatty acid chains were identified. Lyso‐PCs and SMs were down‐regulated whereas saturated and unsaturated phosphatidylcholine (PCs) were up‐regulated in the plasma and erythrocytes of septic patients, which is evidence for deregulated activity of phospholipases. An increase of oleic acid (C18:1 n‐9) accompanied by a decrease in the unsaturation index as well as in the abundances of n‐3 polyunsaturated fatty acids (n‐3 PUFA) was observed in erythrocytes phospholipids patients as compared with healthy controls. This study thus provides new insights into underlying sepsis lipids pathophysiology which may serve clinical diagnosisSupport or Funding InformationFAPESP (Fundação de Amparo à Pesquisa do Estado de São Paulo)
Heparanase contributes to idiopathic pulmonary fibrosis via regulation of A20/TNFAIP3 expression
Authors: Yang Yimu , Lara Abigail , Rutebemberwa Alleluiah , Schmidt Eric 
Published: November 2023

We have previously demonstrated that heparanase, a mammalian endoglycosidase that cleaves the extracellular glycosaminoglycan heparan sulfate (HS), is activated during acute lung inflammation, contributing to the acute respiratory distress syndrome. The impact of heparanase on chronic lung injury (such as idiopathic pulmonary fibrosis, IPF) is uncertain. We found increased heparanase expression within the lungs of patients with severe IPF, co‐localized with clusters of pathologically‐activated myofibroblasts. Similar heparanase induction was noted in a bleomycin mouse model of pulmonary fibrosis. Proliferation of myofibroblasts during Idiopathic Pulmonary Fibrosis (IPF) has been attributed to increased resistance to apoptosis. To determine effect of heparanase on apoptosis, normal human lung fibroblasts (HLF) were treated with heparanase, TGFβ1 (a pro‐fibrotic mediator), CXCL10 (anti‐fibrotic chemokine) or combinations thereof for 48 hours. We measured gene expression of A20/TNFAIP3, an anti‐apoptotic protein which protects cells from TNF‐induced cell death. A20/TNFAIP3 expression was increased in heparanase‐treated human lung fibroblasts. Heparanase‐induced A20/TNFAIP3 expression was augmented by CXCL10, and abolished by TGFb1. Pharmacological inhibition of heparanase activity did not change A20/TNFAIP3 expression, suggesting that heparanase may regulate A20/TNFAIP3 expression via non‐enzymatic effects. Taken together, these findings suggest that heparanase induction may promote fibroblast survival and pathological collagen deposition in IPF.Support or Funding InformationR01 HL125371
Effect of Losartan on 2 Types of Macrophages in a Chronic Rat Model of Fat Embolism
Authors: Arif D. , Khalafi F. , Siddiqi A. , Philips S. , Said A. , Ponnapureddy R. , Tappeta K. , Poisner A. , Hamidpour S. , Molteni A. 
Published: November 2023

IntroductionIn a rat model of pulmonary fat embolism (FE) using triolein (T), we showed that the long term histopathological effects of T‐induced FE extend to 10 weeks, are inhibited by losartan (LOS), an angiotensin II type one receptor blocker, and augmented by a second hit with LPS (1,2). We also observed that mast cell (MC) numbers increased in T‐treated rats vs. saline controls and even more when LPS was added to T. This MC increase was blocked by losartan treatment. LOS or LPS alone did not increase the MC number (3). In view of mast cells' interaction with macrophages in the inflammatory process leading to fibrosis, we extended our study to the identification of macrophages in the same organ.MethodsThirty‐six Sprague Dawley rats were treated with T (0.2 ml i.v.) or saline. After 6 weeks, half of the groups were given saline or LPS 0.1 mL (3 mg/kg) i.p. followed one hour later with saline or LOS (10 mg/kg i.p.), and then by LOS in the drinking water (50 mg/L). 4 weeks later (10 weeks after T), the rats were necropsied after isoflurane anesthesia. Lungs were fixed in 10% formalin and stained with H&E for morphometric scoring, Masson Trichrome for fibrosis and CD68 for macrophage counts. Two pathologists unaware of the slides' identity took 10 photographs at random in each slide at 400× and counted the macrophage number.ResultsAs reported previously, T injection induced severe fibrosis, even more marked by LPS addition. LOS reduced the damage (4). Two types of macrophages were observed: one with compact cytoplasm and with similar size of mast cells, the second one with a larger vacuolated cytoplasm. Contrarily to what was observed for mast cells (3) no increase was seen for the small macrophages nor LOS reduced their number. Large vacuolated macrophages however were markedly increased vs controls in T + saline and LPS + saline groups (p<0.05 and p<0.01). LOS reduced the number in all groups with exception of the LPS + LOS. Contrarily to the increase seen both with T + saline and LPS + saline and the losartan effect, the group receiving both T + LPS in saline treatment did not show any increase. The findings suggest the existence of different cellular responses to the inflammatory and fibrotic stimuli given to the animals.Support or Funding InformationCatherine T. Geldmacher Foundation St. Louis, MO