The Importance of Intra-Islet Communication in the Function and Plasticity of the Islets of Langerhans during Health and Diabetes.

Islets of Langerhans are anatomically dispersed within the pancreas and exhibit regulatory coordination between islets in response to nutritional and inflammatory stimuli. However, within individual islets, there is also multi-faceted coordination of function between individual beta-cells, and between beta-cells and other endocrine and vascular cell types. This is mediated partly through circulatory feedback of the major secreted hormones, insulin and glucagon, but also by autocrine and paracrine actions within the islet by a range of other secreted products, including somatostatin, urocortin 3, serotonin, glucagon-like peptide-1, acetylcholine, and ghrelin. Their availability can be modulated within the islet by pericyte-mediated regulation of microvascular blood flow. Within the islet, both endocrine progenitor cells and the ability of endocrine cells to trans-differentiate between phenotypes can alter endocrine cell mass to adapt to changed metabolic circumstances, regulated by the within-islet trophic environment. Optimal islet function is precariously balanced due to the high metabolic rate required by beta-cells to synthesize and secrete insulin, and they are susceptible to oxidative and endoplasmic reticular stress in the face of high metabolic demand. Resulting changes in paracrine dynamics within the islets can contribute to the emergence of Types 1, 2 and gestational diabetes.

In vivo models of gestational and type 2 diabetes mellitus characterized by endocrine pancreas cell impairments.

Insulin resistance contributes to the development of various diseases, including type 2 diabetes and gestational diabetes. Even though gestational diabetes is specific to pregnancy, it can result in long-term glucose intolerance and type 2 diabetes after delivery. Given the substantial health and economic burdens associated with diabetes, it is imperative to better understand the mechanisms leading to insulin resistance and type 2 diabetes so that treatments targeted at reversing symptoms can be developed. Considering that the endocrine cells of the pancreas (islets of Langerhans) largely contribute to the pathogenesis of diabetes (beta-cell insufficiency and dysfunction), the elucidation of the various mechanisms of endocrine cell plasticity is important to understand. By better defining these mechanisms, targeted therapeutics can be developed to reverse symptoms of beta-cell deficiency and insulin resistance in diabetes. Animal models play an important role in better understanding these mechanisms, as techniques for in vivo imaging of endocrine cells in the pancreas are limited. Therefore, this review article will discuss the available rodent models of gestational and type 2 diabetes that are characterized by endocrine cell impairments in the pancreas, discuss the models with a comparison to human diabetes, and explore the potential mechanisms of endocrine cell plasticity that contribute to these phenotypes, as these mechanisms could ultimately be used to reverse blood glucose dysregulation in diabetes.

Water splitting with silicon p-i-n superlattices suspended in solution.

Photoelectrochemical (PEC) water splitting to produce hydrogen fuel was first reported 50 years ago1, yet artificial photosynthesis has not become a widespread technology. Although planar Si solar cells have become a ubiquitous electrical energy source economically competitive with fossil fuels, analogous PEC devices have not been realized, and standard Si p-type/n-type (p-n) junctions cannot be used for water splitting because the bandgap precludes the generation of the needed photovoltage. An alternative paradigm, the particle suspension reactor (PSR), forgoes the rigid design in favour of individual PEC particles suspended in solution, a potentially low-cost option compared with planar systems2,3. Here we report Si-based PSRs by synthesizing high-photovoltage multijunction Si nanowires (SiNWs) that are co-functionalized to catalytically split water. By encoding a p-type-intrinsic-n-type (p-i-n) superlattice within single SiNWs, tunable photovoltages exceeding 10 V were observed under 1 sun illumination. Spatioselective photoelectrodeposition of oxygen and hydrogen evolution co-catalysts enabled water splitting at infrared wavelengths up to approximately 1,050 nm, with the efficiency and spectral dependence of hydrogen generation dictated by the photonic characteristics of the sub-wavelength-diameter SiNWs. Although initial energy conversion efficiencies are low, multijunction SiNWs bring the photonic advantages of a tunable, mesoscale geometry and the material advantages of Si-including the small bandgap and economies of scale-to the PSR design, providing a new approach for water-splitting reactors.

Anti-Fouling Surfaces for Extracorporeal Membrane Oxygenation by Surface Grafting of Hydrophilic Sulfoxide Polymers.

Non-thrombogenic surfaces for extracorporeal membrane oxygenation (ECMO) devices are important to increase their duration of usage and to enable long-term life support. However, the contact of blood with the hydrophobic synthetic ECMO membrane materials such as poly(4-methyl-1-pentene) (PMP) can activate the coagulation cascade, causing thrombosis and a series of consequent complications during ECMO operation. Targeting this problem, we proposed to graft highly hydrophilic sulfoxide polymer brushes onto the PMP surfaces via gamma ray irradiation-initiated polymerization to improve the hemocompatibility of the membrane. Through this chemical modification, the surface of the PMP film is altered from hydrophobic to hydrophilic. The extent of plasma protein adsorption and platelet adhesion, the prerequisite mediators of the coagulation cascade and thrombus formation, are drastically reduced compared with those of the unmodified PMP film. Therefore, the method provides a facile approach to modify PMP materials with excellent antifouling properties and improved hemocompatibility demanded by the applications in ECMO and other blood-contacting medical devices.

Observations by health care professionals about wound healing in Ghanaian patients who skin-bleach.

Skin-bleaching is a common practice globally and is associated with many cutaneous and systemic health risks. Anecdotally, skin-bleaching is linked to impairments in wound healing, but there are little data to support the claim. This cross-sectional survey of health care professionals serving the Greater Accra Region, Ghana region investigates their observations of wound healing in patients who skin-bleach and their methods for screening skin-bleach use in patients. A 25-item self-administered questionnaire using 5-point Likert scale was distributed with convenient sampling to physicians and nurses employed at Ghanaian hospitals. Fifty-seven electronic and 78 paper responses were collected (total = 135). Most respondents agreed that wounds in skin-bleaching patients heal more slowly (4.22), are more prone to infection (4.11), haemorrhage (3.89), wound dehiscence (3.9), and are more difficult to manage (4.13). No respondent reported universal screening of all patients for skin-bleaching, but most ask about skin-bleaching if there is suspicion of it (42.2%). Our findings support the anecdotes about observable wound healing impairments in patients who skin-bleach. There is also wide variation in skin-bleaching screening practices, suggesting a need for guidelines to properly identify these patients and facilitate early risk prevention.

Pleiotrophin Expression and Actions in Pancreatic ß-Cells.

Pleiotrophin (PTN) is a heparin-binding cytokine that is widely expressed during early development and increases in maternal circulation during pregnancy.Aged PTN-deficient mice exhibit insulin resistance, suggesting a role in metabolic control. The objectives of this study were to determine if PTN is expressed in mouse pancreatic ß-cells in young vs. adult animals, and its effects on DNA synthesis, ß-cell gene expression and glucose-stimulated insulin secretion (GSIS). The Ptn gene was expressed in isolated fractions of young mouse ß-cells, especially within immature ß-cells with low glucose transporter 2 expression. Expression was retained in the adult pancreas but did not significantly change during pregnancy. PTN and its receptor, phosphotyrosine phosphatase-ß/ζ, were also expressed in the proliferative INS1E ß-cell line. Fluorescence immunohistochemistry showed that PTN peptide was present in islets of Langerhans in adult mice, associated predominantly with ß-cells. The percentage of ß-cells staining for PTN did not alter during mouse pregnancy, but intense staining was seen during ß-cell regeneration in young mice following depletion of ß-cells with streptozotocin. Incubation of INS1E cells with PTN resulted in an increased DNA synthesis as measured by Ki67 localization and increased expression of Pdx1 and insulin. However, both DNA synthesis and GSIS were not altered by PTN in isolated adult mouse islets. The findings show that Ptn is expressed in mouse ß-cells in young and adult life and could potentially contribute to adaptive increases in ß-cell mass during early life or pregnancy.

Impact of the exposome on the development and function of pancreatic ß-cells.

The development and plasticity of the endocrine pancreas responds to both the intrauterine and postnatal exposome in a constant attempt to predict and respond to alterations in nutritional availability and metabolic requirements. Both under- and over-nutrition in utero, or exposure to adverse environmental pollutants or maternal behaviors, can each lead to altered ß-cell or function at birth, and a subsequent mismatch in pancreatic hormonal demands and secretory capacity postnatally. This can be further exacerbated by metabolic stress postnatally such as from obesity or pregnancy, resulting in an increased risk of gestational diabetes, type 2 diabetes, and even type 1 diabetes. This review will discuss evidence identifying the cellular pathways in early life whereby the plasticity of the endocrine pancreatic can become pathologically limited. By necessity, much of this evidence has been gained from animal models, although extrapolation to human fetal development is possible from the fetal growth trajectory and study of the newborn. Cellular limitations to plasticity include the balance between ß-cell proliferation and apoptosis, the appearance of ß-cell oxidative stress, impaired glucose-stimulated insulin secretion, and sensitivity to circulating cytokines and responsiveness to programmed death receptor-1. Evidence suggests that many of the cellular pathways responsible for limiting ß-cell plasticity are related to paracrine interactions within the islets of Langerhans.

Acetone Ingestion Mimics a Fasting State to Improve Glucose Tolerance in a Mouse Model of Gestational Hyperglycemia.

Gestational diabetes mellitus results, in part, from a sub-optimal ß-cell mass (BCM) during pregnancy. Artemisinins were reported to increase BCM in models of diabetes by α- to ß-cell conversion leading to enhanced glucose tolerance. We used a mouse model of gestational glucose intolerance to compare the effects of an artemisinin (artesunate) on glycemia of pregnant mice with vehicle treatment (acetone) or no treatment. Animals were treated daily from gestational days (GD) 0.5 to 6.5. An intraperitoneal glucose tolerance test was performed prior to euthanasia at GD18.5 or post-partum. Glucose tolerance was significantly improved in both pregnant and non-pregnant mice with both artesunate and vehicle-alone treatment, suggesting the outcome was primarily due to the acetone vehicle. In non-pregnant, acetone-treated animals, improved glucose tolerance was associated with a higher BCM and a significant increase in bihormonal insulin and glucagon-containing pancreatic islet cells, suggesting α- to ß-cell conversion. BCM did not differ with treatment during pregnancy or post-partum. However, placental weight was higher in acetone-treated animals and was associated with an upregulation of apelinergic genes. Acetone-treated animals had reduced weight gain during treatment despite comparable food consumption to non-treated mice, suggesting transient effects on nutrient uptake. The mean duodenal and ileum villus height was reduced following exposure to acetone. We conclude that acetone treatment may mimic transient fasting, resulting in a subsequent improvement in glucose tolerance during pregnancy.

A Study of the Antimicrobial Activity of Combined Black Pepper and Cinnamon Essential Oils against Escherichia fergusonii in Traditional African Yoghurt.

The antimicrobial activity of the essential oils of black pepper (BPE) and cinnamon bark (CE) extracts against E. fergusonii was assessed in pasteurized full cream milk during and post-fermentation. The milk was fermented with 1% (v/v) of Lactobacillus delbrueckii subspecies bulgaricus (NCIMB 11778) and Streptococcus thermophilus (NCIMB 10387) (approx. 106 cfu/mL each) and incubated and stored at 25 °C for 5 days (144 h) or at 43 °C for 24 h and then stored at 25 °C for 120 h. The milk was spiked with E. fergusonii at the start of fermentation by the lactic acid bacteria (pre-fermentation contamination) for after fermentation (post fermentation contamination). BPE and CE were applied at concentrations based on their minimum inhibitory concentration of 0.5% and 0.25% respectively as follows: 0.5% BPE alone; 0.125% BPE with 0.1875% CE; 0.25% BPE with 0.125% CE; 0.375% BPE with 0.0625% CE; 0.25% CE alone. Results showed that during fermentation at 25 °C, E. fergusonii grew to a similar level (approx. 109 CFU/mL) in control samples and 108 CFU/mL when BPE or CE were added alone. Whereas, in the samples with the combined essential oils, the bacterium grew to 106-107 CFU/mL only. During the milk fermentation at 43 °C, E. fergusonii grew to approx. 109 CFU/mL in samples without treatment. However, it was not detected in samples containing mixed BPE with CE after 8, 10 and 12 h of fermentation. Subsequent storage at 25 °C resulted in undetectable levels of the bacterium in all the samples treated with BPE or CE after 24 h of storage. These results indicated that BPE in combination with CE reduced growth during fermentation and was bactericidal during storage.

Ontology of the apelinergic system in mouse pancreas during pregnancy and relationship with ß-cell mass.

The apelin receptor (Aplnr) and its ligands, Apelin and Apela, contribute to metabolic control. The insulin resistance associated with pregnancy is accommodated by an expansion of pancreatic ß-cell mass (BCM) and increased insulin secretion, involving the proliferation of insulin-expressing, glucose transporter 2-low (Ins+Glut2LO) progenitor cells. We examined changes in the apelinergic system during normal mouse pregnancy and in pregnancies complicated by glucose intolerance with reduced BCM. Expression of Aplnr, Apelin and Apela was quantified in Ins+Glut2LO cells isolated from mouse pancreata and found to be significantly higher than in mature ß-cells by DNA microarray and qPCR. Apelin was localized to most ß-cells by immunohistochemistry although Aplnr was predominantly associated with Ins+Glut2LO cells. Aplnr-staining cells increased three- to four-fold during pregnancy being maximal at gestational days (GD) 9-12 but were significantly reduced in glucose intolerant mice. Apelin-13 increased ß-cell proliferation in isolated mouse islets and INS1E cells, but not glucose-stimulated insulin secretion. Glucose intolerant pregnant mice had significantly elevated serum Apelin levels at GD 9 associated with an increased presence of placental IL-6. Placental expression of the apelinergic axis remained unaltered, however. Results show that the apelinergic system is highly expressed in pancreatic ß-cell progenitors and may contribute to ß-cell proliferation in pregnancy.

Zero-Error Consensus Tracking With Preassignable Convergence for Nonaffine Multiagent Systems.

In this paper, we investigate the consensus tracking control problem for networked multiagent systems (MASs) with unknown nonaffine dynamics. Our goal is to achieve asymptotic (rather than ultimately uniformly bounded) consensus tracking, which is quite challenging especially if nonvanishing/nonparametric uncertainties are involved and at the same time the control protocol is required to be fully distributed and continuous everywhere. Here, we present a conceptually new and structurally simple solution with distributed and continuous control action. The developed method is capable of ensuring zero-error tracking with a unique converging feature in that the consensus tracking error first converges to a small adjustable residual set around zero within a prescribed finite time, and then further shrinks to zero exponentially. The key technique lies in the utilization of a state transformation based on certain scaling function. Our method also prevents the restrictive requirement that all subsystems have access to the linearly parameterized information as imposed in most existing consensus tracking results for nonlinear MAS.

Fault Detection for a Class of Uncertain Sampled-Data Systems Using Deterministic Learning.

In this article, we propose a learning-based fault diagnosis approach for a class of nonlinear sampled-data systems. First, the unmodeled sampled dynamics is acquired by the using deterministic learning method. The knowledge of the sampled dynamics of the normal and fault patterns is stored in the form of constant neural networks. Second, a fault detection scheme is designed in which memories of the learned knowledge can be recalled to give a rapid response to a fault. Third, analytical results concerning the fault detection condition and detection time are derived. It is shown that the mismatch function plays an important role in the performance properties of the diagnosis scheme. To analyze the effect of mismatch function on the residual, the concept of duty ratio is developed. Moreover, by comparing the constant neural networks of the normal and fault patterns, an extraction operator is designed to capture the feature of the mismatch function. By using this method, the performance of the diagnosis scheme can be improved. A simulation study is included to demonstrate the effectiveness of the approach.

Less sedentary time is associated with a more favourable glucose-insulin axis in obese pregnant women-a secondary analysis of the DALI study.

BACKGROUND/OBJECTIVES: Obese pregnant women are at high risk of developing gestational diabetes mellitus (GDM), which might be reduced by sufficient physical activity (PA) and reduced sedentary time (ST). We assessed whether PA and ST are longitudinally associated with the glucose-insulin axis in obese pregnant women. SUBJECTS/METHODS: In this secondary analysis of the DALI (vitamin D And Lifestyle Intervention for gestational diabetes mellitus prevention) study, pregnant women, <20 weeks gestation, with a pre-pregnancy body mass index (BMI) ≥ 29 kg/m2, without GDM on entry were included. Time spent in moderate-to-vigorous PA (MVPA) and ST were measured objectively with accelerometers at <20 weeks, 24-28 weeks and 35-37 weeks of gestation. Fasting glucose (mmol/l) and insulin (mU/l), insulin resistance (HOMA-IR) and first-phase and second-phase insulin release (Stumvoll first and second phase) were assessed at the same time. Linear mixed regression models were used to calculate between-participant differences and within-participant changes over time. Analyses were adjusted for gestational age, randomisation, pre-pregnancy BMI, education and age. MVPA, Insulin, HOMA-IR and Stumvoll first and second phase were log-transformed for analyses due to skewness. RESULTS: 232 women were included in the analysis. Concerning differences between participants, more ST was associated with higher fasting glucose (Estimate: 0.008; 95% CI: 0.002, 0.014), fasting insulin (0.011; 0.002, 0.019), HOMA-IR (0.012; 0.004, 0.021) and Stumvoll first and second phase (0.008; 0.001, 0.014 and 0.007; 0.001, 0.014). Participants with more MVPA had lower Stumvoll first and second phase (-0.137; -0.210, -0.064 and -0.133; -0.202, -0.063). Concerning changes over time, an increase in ST during gestation was associated with elevated Stumvoll first and second phase (0.006; 0.000, 0.011). CONCLUSIONS: As the glucose-insulin axis is more strongly associated with ST than MVPA in our obese population, pregnant women could be advised to reduce ST in addition to increasing MVPA. Moreover, our findings suggest that behaviour change interventions aiming at GDM risk reduction should start in early or pre-pregnancy.

The importance of maternal insulin resistance throughout pregnancy on neonatal adiposity.

BACKGROUND: Although previous studies evaluated the association of maternal health parameters with neonatal adiposity, little is known regarding the complexity of the relationships among different maternal health parameters throughout pregnancy and its impact on neonatal adiposity. OBJECTIVES: To evaluate the direct and indirect associations between maternal insulin resistance during pregnancy, in women with obesity, and neonatal adiposity. In addition, associations between maternal fasting glucose, triglycerides (TG), non-esterified fatty acids (NEFA), and neonatal adiposity were also assessed. METHODS: This is a longitudinal, secondary analysis of the DALI study, an international project conducted in nine European countries with pregnant women with obesity. Maternal insulin resistance (HOMA-IR), fasting glucose, TG, and NEFA were measured three times during pregnancy (<20, 24-28, and 35-37 weeks of gestation). Offspring neonatal adiposity was estimated by the sum of four skinfolds. Structural equation modelling was conducted to evaluate the direct and indirect relationships among the variables of interest. RESULTS: Data on 657 mother-infant pairs (50.7% boys) were analysed. Neonatal boys exhibited lower mean sum of skinfolds compared to girls (20.3 mm, 95% CI 19.7, 21.0 vs 21.5 mm, 95% CI 20.8, 22.2). In boys, maternal HOMA-IR at <20 weeks was directly associated with neonatal adiposity (ß = 0.35 mm, 95% CI 0.01, 0.70). In girls, maternal HOMA-IR at 24-28 weeks was only indirectly associated with neonatal adiposity, which implies that this association was mediated via maternal HOMA-IR, glucose, triglycerides, and NEFA during pregnancy (ß = 0.26 mm, 95% CI 0.08, 0.44). CONCLUSIONS: The timing of the role of maternal insulin resistance on neonatal adiposity depends on fetal sex. Although the association was time-dependent, maternal insulin resistance was associated with neonatal adiposity in both sexes.

Differential temporal and spatial post-injury alterations in cerebral cell morphology and viability.

Combination of ischemia and ß-amyloid (Aß) toxicity has been shown to simultaneously increase neuro-inflammation, endogenous Aß deposition, and neurodegeneration. However, studies on the evolution of infarct and panorama of cellular degeneration as a synergistic or overlapping mechanism between ischemia and Aß toxicity are lacking. Here, we compared fluorojade B (FJB) and hematoxylin and eosin (H&E) stains primarily to examine the chronology of infarct, and the viability and morphological changes in neuroglia and neurons located in different brain regions on d1, d7, and d28 post Aß toxicity and endothelin-1 induced ischemia (ET1) in rats. We demonstrated a regional difference in cellular degeneration between cortex, corpus callosum, striatum, globus pallidus, and thalamus after cerebral injury. Glial cells in the cortex and corpus callosum underwent delayed FJB staining from d7 to d28, but neurons in cortex disappeared within the first week of cerebral injury. Striatal lesion core and globus pallidus of Aß + ET1 rats showed extensive degeneration of neuronal cells compared with ET1 rats alone starting from d1. Differential and exacerbated expressions of cyclooxygenase-2 might be the cause of excessive neuronal demise in the striatum of Aß + ET1 rats. Such an investigation may improve our understanding to identify and manipulate a critical therapeutic window post comorbid injury.

Metabolic Adaptations to Pregnancy in Healthy and Gestational Diabetic Pregnancies: The Pancreas - Placenta Axis.

Normal pregnancy is associated with increased insulin resistance as a metabolic adaptation to the nutritional demands of the placenta and fetus, and this is amplified in obese mothers. Insulin resistance is normally compensated for by an adaptive increase in pancreatic ß-cell mass together with enhanced glucose-stimulated insulin release. Placentally-derived hormones and growth factors are central to the altered pancreatic morphology and function. A failure of ß-cells to undergo adaptive change after the first trimester has been linked with gestational diabetes. In the pregnant mouse, an increase in ß-cell replication contributes to a 2-3-fold increase in mass peaking in late gestation, depending on the proliferation of existing ß-cells, the differentiation of resident progenitor ß-cells, or islet cell transdifferentiation. Using mouse models and human studies placenta- and islet of Langerhans-derived molecules have been identified that are likely to contribute to the metabolic adaptations to pregnancy and whose physiology is altered in the obese, glucose-intolerant mother. Maternal obesity during pregnancy can create a pro-inflammatory environment that can disrupt the response of the ß-cells to the endocrine signals of pregnancy and limit the adaptive changes in ß-cell mass and function, resulting in an increased risk of gestational diabetes.

Increased alpha and beta cell mass during mouse pregnancy is not dependent on transdifferentiation.

Maternal pancreatic beta-cell mass (BCM) increases during pregnancy to compensate for relative insulin resistance. If BCM expansion is suboptimal, gestational diabetes mellitus can develop. Alpha-cell mass (ACM) also changes during pregnancy, but there is a lack of information about α-cell plasticity in pregnancy and whether α- to ß-cell transdifferentiation can occur. To investigate this, we used a mouse model of gestational glucose intolerance induced by feeding low-protein (LP) diet from conception until weaning and compared pregnant female offspring to control diet-fed animals. Control and LP pancreata were collected for immunohistochemical analysis and serum glucagon levels were measured. In order to lineage trace α- to ß-cell conversion, we utilized transgenic mice expressing yellow fluorescent protein behind the proglucagon gene promoter (Gcg-Cre/YFP) and collected pancreata for histology at various gestational timepoints. Alpha-cell proliferation increased significantly at gestational day (GD) 9.5 in control pregnancies resulting in an increased ACM at GD18.5, and this was significantly reduced in LP animals. Despite these changes, serum glucagon was higher in LP mice at GD18.5. Pregnant Gcg-Cre/YFP mice showed no increase in the abundance of insulin+YFP+glucagon- cells (phenotypic ß-cells). A second population of insulin+YFP+glucagon+ cells was identified which also did not alter during pregnancy. However, there was an altered anatomical distribution within islets with fewer insulin+YFP+glucagon- cells but more insulin+YFP+glucagon+ cells being present in the islet mantle at GD18.5. These findings demonstrate that dynamic changes in ACM occur during normal pregnancy and were altered in glucose-intolerant pregnancies.

Performance of early pregnancy HbA1c for predicting gestational diabetes mellitus and adverse pregnancy outcomes in obese European women.

AIMS: To investigate the performance of early pregnancy HbA1c for predicting gestational diabetes mellitus (GDM) and adverse pregnancy outcomes in obese women. METHODS: Post hoc analysis using data from the Vitamin D And Lifestyle Intervention for GDM prevention trials conducted across 9 European countries (2012-2014). Pregnant women (BMI ≥ 29 kg/m2) underwent a baseline HbA1c and oral glucose tolerance tests at < 20 weeks, 24-28 weeks, and 35-37 weeks. Women with GDM were referred for treatment. RESULTS: Among the 869 women tested, the prevalence of GDM was 25.9% before 20 weeks, with a further 8.6% at 24-28 weeks. The areas under the curves for HbA1c at the two time points were 0.55 (0.50-0.59) and 0.54 (0.47-0.61), respectively. An early HbA1c ≥ 5.7% (39 mmol/mol) (N = 111) showed low sensitivity (18.2%) with 89.1% specificity for GDM before 20 weeks, at 24-28 weeks (sensitivity of 8.0% and specificity of 88.6% after excluding early GDM), and throughout gestation (sensitivity of 15.9% and specificity of 89.4%). The ≥ 5.7% (39 mmol/mol) threshold was significantly associated with concurrent GDM before 20 weeks (adjusted OR (aOR) 2.77(1.39-5.51)) and throughout gestation (aOR 1.72 (1.02-2.89)), but not adverse pregnancy outcomes. CONCLUSIONS: Early pregnancy HbA1c is of limited use for predicting either GDM or adverse outcomes in overweight/obese European women.

Protein adsorption to poly(tetrafluoroethylene) membranes modified with grafted poly(acrylic acid) chains.

Protein adsorption to biomaterial surfaces is important for the function of such materials with anchorage-dependent cell adhesion requiring the presence of adsorbed proteins. The current study evaluated five solid surfaces with poly(acrylic acid) (PAA) grafted from the surface of a poly(tetrafluoroethylene) membrane with respect to the adsorption of serum albumin (SA), lactoferrin (Lf), and lysozyme (Lys) from a phosphate buffer and NaCl solution or water for specific combinations. With the use of x-ray photoelectron spectroscopy, the relative amounts and protein layer thickness were evaluated. SA adsorption was governed by ionic repulsive forces and hydrophobic interactions as evidenced from an increase in the protein adsorption at lower pH (6.5 compared to 7.4) and a correlation with surface coverage when water (pH 6.5) was used as the medium. The adsorption of Lf and Lys followed similar trends for all samples. In general, ionic attractive forces dominated and a strong correlation of increasing protein adsorption with the PAA chain length was evident. This study concluded that all surfaces appear suitable for use in biomaterial applications where tissue ingrowth is desired and that the enhanced protein adsorption in a medium with high ionic strength (e.g., biological fluid) correlates with the PAA chain length rather than the surface coverage.