Quality Improvement to Increase Breastfeeding in Preterm Infants: Systematic Review and Meta-Analysis

Background and Objective: Due to its numerous health benefits, breast milk (BM) is recommended for preterm infants. Despite such recommendations, the rates of breastfeeding in preterm infants are lower than that in term infants. Quality improvement (QI) bundles increase breastfeeding in preterm infants, but their replication in neonatal intensive care units has had inconsistent outcomes.Methods: We used the Population or Problem, Intervention, Comparison, and Outcomes (PICO) framework to develop our search strategy, and searched MEDLINE, Embase, and the Cochrane Library from inception through January 15, 2021. Studies describing any active QI intervention to increase BM use in preterm infants were included. The primary outcome measure was the rate of any breastfeeding or exclusive mother's own milk (MOM) at discharge or during hospitalization.Results: Sixteen studies were eligible for inclusion and showed an acceptable risk of bias, and included 1 interrupted time series, study 3 controlled before-and-after studies, and 12 uncontrolled before-and-after studies; of these, 3 studies were excluded due to insufficient dichotomous data, 13 were included in the meta-analysis. In the meta-analysis, the rate of any breastfeeding was significantly improved at discharge and during hospitalization after QI [risk ratio (RR) = 1.23, 95% confidence interval (CI): 1.14–1.32, P < 0.00001 and RR = 1.89, 95% CI: 1.09–3.29, P = 0.02, respectively]. The rate of exclusive MOM after QI was also significantly increased at discharge (RR = 1.51, 95% CI: 1.04–2.18, P = 0.03), but not during hospitalization (RR = 1.53, 95% CI: 0.78–2.98, P = 0.22). However, after sensitivity analysis, the comprehensive results still suggested that QI could significantly improve the rate of exclusive MOM during hospitalization (RR = 1.21, 95% CI: 1.08–1.35, P = 0.001). Funnel plots and Egger's test indicated publication bias in the rate of any BF at discharge. We corrected publication bias by trim and fill analysis, and corrected RR to 1.272, 95% CI: (1.175, 1.369), which was consistent with the results of the initial model.Conclusions: A QI bundle appears to be effective for promoting BM use in preterm infants at discharge or during hospitalization

Computing Offloading for RIS-Aided Internet of Everything:A Cybertwin Version

Cybertwin technology introduces a novel paradigm employing digital twins to model complex physical systems within a cyber environment, thus enhancing communication, collaboration, and decision-making capabilities. By harnessing advanced technologies, such as reconfigurable intelligent surfaces (RISs) and multi-access edge computing (MEC), seamless interaction between physical and virtual entities is facilitated. In this paper, we propose a cybertwin-driven edge computing framework that leverages RIS technology, complemented by an efficient computing offloading strategy to support largescale Internet of Everything (IoE) applications. Specifically, the proposed strategy focuses on a multi-cell system where numerous randomly distributed end users have the option to offload delay-sensitive and computing-intensive tasks to edge computing nodes. The offloading channels are enhanced by RISs through passive beamforming, while cybertwin technology directs resource cooperation among multi-cells and allocates computing and communication resources. Our main objective is to optimize the system’s utility with respect to task completion latency and energy consumption reduction. To achieve this goal, we conduct the joint optimization of task offloading and resource allocation. Furthermore, we develop a joint task offloading and resource allocation (JTORA) algorithm to derive optimal solutions for passive beamforming design, computing offloading decisions, communication resource scheduling, and computing capacity allocation. The simulation results demonstrate the superiority of the proposed algorithm over benchmark schemes in terms of edge computing efficiency. Furthermore, the system utility can be further enhanced by increasing the number of embedded RIS elements

4-(4-Cyano-2-fluoro­phen­oxy)phenyl 4-methyl­benzene­sulfonate

The title compound, C20H14FNO4S, was synthesized from hydro­quinone, p-toluene­sulfonyl chloride and 3,4-difluoro­benzonitrile. A folded conformation is adopted by the crystal structure. Inter­molecular C—H⋯N hydrogen bonds form dimers arranged around inversion centers

External α-carbonic anhydrase and solute carrier 4 are required for bicarbonate uptake in a freshwater angiosperm

The freshwater monocot Ottelia alismoides is the only known species to operate three CO2-concentrating mechanisms (CCMs): constitutive bicarbonate (HCO3–) use, C4 photosynthesis, and facultative Crassulacean acid metabolism, but the mechanism of HCO3– use is unknown. We found that the inhibitor of an anion exchange protein, 4,4'-diisothio-cyanatostilbene-2,2'-disulfonate (DIDS), prevented HCO3– use but also had a small effect on CO2 uptake. An inhibitor of external carbonic anhydrase (CA), acetazolamide (AZ), reduced the affinity for CO2 uptake but also prevented HCO3– use via an effect on the anion exchange protein. Analysis of mRNA transcripts identified a homologue of solute carrier 4 (SLC4) responsible for HCO3– transport, likely to be the target of DIDS, and a periplasmic α-carbonic anhydrase 1 (α-CA1). A model to quantify the contribution of the three different pathways involved in inorganic carbon uptake showed that passive CO2 diffusion dominates inorganic carbon uptake at high CO2 concentrations. However, as CO2 concentrations fall, two other pathways become predominant: conversion of HCO3– to CO2 at the plasmalemma by α-CA1 and transport of HCO3– across the plasmalemma by SLC4. These mechanisms allow access to a much larger proportion of the inorganic carbon pool and continued photosynthesis during periods of strong carbon depletion in productive ecosystems

Identification and Characterization of Two Novel Compounds: Heterozygous Variants of Lipoprotein Lipase in Two Pedigrees With Type I Hyperlipoproteinemia

BackgroundType I hyperlipoproteinemia, characterized by severe hypertriglyceridemia, is caused mainly by loss-of-function mutation of the lipoprotein lipase (LPL) gene. To date, more than 200 mutations in the LPL gene have been reported, while only a limited number of mutations have been evaluated for pathogenesis.ObjectiveThis study aims to explore the molecular mechanisms underlying lipoprotein lipase deficiency in two pedigrees with type 1 hyperlipoproteinemia.MethodsWe conducted a systematic clinical and genetic analysis of two pedigrees with type 1 hyperlipoproteinemia. Postheparin plasma of all the members was used for the LPL activity analysis. In vitro studies were performed in HEK-293T cells that were transiently transfected with wild-type or variant LPL plasmids. Furthermore, the production and activity of LPL were analyzed in cell lysates or culture medium.ResultsProband 1 developed acute pancreatitis in youth, and her serum triglycerides (TGs) continued to be at an ultrahigh level, despite the application of various lipid-lowering drugs. Proband 2 was diagnosed with type 1 hyperlipoproteinemia at 9 months of age, and his serum TG levels were mildly elevated with treatment. Two novel compound heterozygous variants of LPL (c.3G>C, p. M1? and c.835_836delCT, p. L279Vfs*3, c.188C>T, p. Ser63Phe and c.662T>C, p. Ile221Thr) were identified in the two probands. The postheparin LPL activity of probands 1 and 2 showed decreases of 72.22 ± 9.46% (p<0.01) and 54.60 ± 9.03% (p<0.01), respectively, compared with the control. In vitro studies showed a substantial reduction in the expression or enzyme activity of LPL in the LPL variants.ConclusionsTwo novel compound heterozygous variants of LPL induced defects in the expression and function of LPL and caused type I hyperlipoproteinemia. The functional characterization of these variants was in keeping with the postulated LPL mutant activity

Novel Zinc Finger Transcription Factor ZFP580 Facilitates All-Trans Retinoic Acid -Induced Vascular Smooth Muscle Cells Differentiation by Rarα-Mediated PI3K/Akt and ERK Signaling

Background/Aims: Phenotypic switching of vascular smooth muscle cells (VSMC) plays a vital role in the development of vascular diseases. All-trans retinoic acid (ATRA) is known to regulate VSMC phenotypes. However, the underlying mechanisms remain completely unknown. Here, we have investigated the probable roles and underlying mechanisms of the novel C2H2 zinc finger transcription factor ZFP580 on ATRA-induced VSMC differentiation. Methods: VSMCs were isolated, cultured, and identified. VSMCs were infected with an adenovirus encoding ZFP580 or Ad-siRNA to silence ZFP580. The expression levels of ZFP580, SMα-actin, SM22α, SMemb, RARα, RARβ, and RARγ were assayed by Q-PCR and western blot. A rat carotid artery injury model and morphometric analysis of intimal thickening were also used in this study. Results: ATRA caused a significant reduction of VSMC proliferation and migration in a doseand time-dependent manner. Moreover, it promoted VSMC differentiation by enhancing expression of differentiation markers and reducing expression of dedifferentiation markers. This ATRA activity was accompanied by up-regulation of ZFP580, with concomitant increases in RARα expression. In contrast, silencing of the RARα gene or inhibiting RARα with its antagonist Ro41-5253 abrogated the ATRA-induced ZFP580 expression. Furthermore, ATRA binding to RARα induced ZFP580 expression via the PI3K/Akt and ERK pathways. Adenovirusmediated overexpression of ZFP580 promoted VSMC differentiation by enhancing expression of SM22α and SMα-actin and reducing expression of SMemb. In contrast, silencing ZFP580 dramatically reduced the expression of differentiation markers and increased expression of dedifferentiation markers. The classic rat carotid artery balloon injury model demonstrated that ZFP580 inhibited proliferation and intimal hyperplasia in vivo. Conclusion: The novel zinc finger transcription factor ZFP580 facilitates ATRA-induced VSMC differentiation by the RARα-mediated PI3K/Akt and ERK signaling pathways. This might represent a novel mechanism of regulation of ZFP580 by ATRA and RARα, which is critical for understanding the biological functions of retinoids during VSMC phenotypic modulation

Potential applications of nanotechnology in thermochemical conversion of microalgal biomass

The rapid decrease in fossil reserves has significantly increased the demand of renewable and sustainable energy fuel resources. Fluctuating fuel prices and significant greenhouse gas (GHG) emission levels have been key impediments associated with the production and utilization of nonrenewable fossil fuels. This has resulted in escalating interests to develop new and improve inexpensive carbon neutral energy technologies to meet future demands. Various process options to produce a variety of biofuels including biodiesel, bioethanol, biohydrogen, bio-oil, and biogas have been explored as an alternative to fossil fuels. The renewable, biodegradable, and nontoxic nature of biofuels make them appealing as alternative fuels. Biofuels can be produced from various renewable resources. Among these renewable resources, algae appear to be promising in delivering sustainable energy options. Algae have a high carbon dioxide (CO2) capturing efficiency, rapid growth rate, high biomass productivity, and the ability to grow in non-potable water. For algal biomass, the two main conversion pathways used to produce biofuel include biochemical and thermochemical conversions. Algal biofuel production is, however, challenged with process scalability for high conversion rates and high energy demands for biomass harvesting. This affects the viable achievement of industrial-scale bioprocess conversion under optimum economy. Although algal biofuels have the potential to provide a sustainable fuel for future, active research aimed at improving upstream and downstream technologies is critical. New technologies and improved systems focused on photobioreactor design, cultivation optimization, culture dewatering, and biofuel production are required to minimize the drawbacks associated with existing methods. Nanotechnology has the potential to address some of the upstream and downstream challenges associated with the development of algal biofuels. It can be applied to improve system design, cultivation, dewatering, biomass characterization, and biofuel conversion. This chapter discusses thermochemical conversion of microalgal biomass with recent advances in the application of nanotechnology to enhance the development of biofuels from algae. Nanotechnology has proven to improve the performance of existing technologies used in thermochemical treatment and conversion of biomass. The different bioprocess aspects, such as reactor design and operation, analytical techniques, and experimental validation of kinetic studies, to provide insights into the application of nanotechnology for enhanced algal biofuel production are addressed

Finishing the euchromatic sequence of the human genome

The sequence of the human genome encodes the genetic instructions for human physiology, as well as rich information about human evolution. In 2001, the International Human Genome Sequencing Consortium reported a draft sequence of the euchromatic portion of the human genome. Since then, the international collaboration has worked to convert this draft into a genome sequence with high accuracy and nearly complete coverage. Here, we report the result of this finishing process. The current genome sequence (Build 35) contains 2.85 billion nucleotides interrupted by only 341 gaps. It covers ∼99% of the euchromatic genome and is accurate to an error rate of ∼1 event per 100,000 bases. Many of the remaining euchromatic gaps are associated with segmental duplications and will require focused work with new methods. The near-complete sequence, the first for a vertebrate, greatly improves the precision of biological analyses of the human genome including studies of gene number, birth and death. Notably, the human enome seems to encode only 20,000-25,000 protein-coding genes. The genome sequence reported here should serve as a firm foundation for biomedical research in the decades ahead