Continuous carbon capture in an electrochemical solid-electrolyte reactor.

Electrochemical carbon-capture technologies, with renewable electricity as the energy input, are promising for carbon management but still suffer from low capture rates, oxygen sensitivity or system complexity1-6. Here we demonstrate a continuous electrochemical carbon-capture design by coupling oxygen/water (O2/H2O) redox couple with a modular solid-electrolyte reactor7. By performing oxygen reduction reaction (ORR) and oxygen evolution reaction (OER) redox electrolysis, our device can efficiently absorb dilute carbon dioxide (CO2) molecules at the high-alkaline cathode-membrane interface to form carbonate ions, followed by a neutralization process through the proton flux from the anode to continuously output a high-purity (>99%) CO2 stream from the middle solid-electrolyte layer. No chemical inputs were needed nor side products generated during the whole carbon absorption/release process. High carbon-capture rates (440 mA cm-2, 0.137 mmolCO2 min-1 cm-2 or 86.7 kgCO2 day-1 m-2), high Faradaic efficiencies (>90% based on carbonate), high carbon-removal efficiency (>98%) in simulated flue gas and low energy consumption (starting from about 150 kJ per molCO2) were demonstrated in our carbon-capture solid-electrolyte reactor, suggesting promising practical applications.

Changes in above- versus belowground biomass distribution in permafrost regions in response to climate warming.

Permafrost regions contain approximately half of the carbon stored in land ecosystems and have warmed at least twice as much as any other biome. This warming has influenced vegetation activity, leading to changes in plant composition, physiology, and biomass storage in aboveground and belowground components, ultimately impacting ecosystem carbon balance. Yet, little is known about the causes and magnitude of long-term changes in the above- to belowground biomass ratio of plants (η). Here, we analyzed η values using 3,013 plots and 26,337 species-specific measurements across eight sites on the Tibetan Plateau from 1995 to 2021. Our analysis revealed distinct temporal trends in η for three vegetation types: a 17% increase in alpine wetlands, and a decrease of 26% and 48% in alpine meadows and alpine steppes, respectively. These trends were primarily driven by temperature-induced growth preferences rather than shifts in plant species composition. Our findings indicate that in wetter ecosystems, climate warming promotes aboveground plant growth, while in drier ecosystems, such as alpine meadows and alpine steppes, plants allocate more biomass belowground. Furthermore, we observed a threefold strengthening of the warming effect on η over the past 27 y. Soil moisture was found to modulate the sensitivity of η to soil temperature in alpine meadows and alpine steppes, but not in alpine wetlands. Our results contribute to a better understanding of the processes driving the response of biomass distribution to climate warming, which is crucial for predicting the future carbon trajectory of permafrost ecosystems and climate feedback.

Virus classification for viral genomic fragments using PhaGCN2.

Viruses are the most ubiquitous and diverse entities in the biome. Due to the rapid growth of newly identified viruses, there is an urgent need for accurate and comprehensive virus classification, particularly for novel viruses. Here, we present PhaGCN2, which can rapidly classify the taxonomy of viral sequences at the family level and supports the visualization of the associations of all families. We evaluate the performance of PhaGCN2 and compare it with the state-of-the-art virus classification tools, such as vConTACT2, CAT and VPF-Class, using the widely accepted metrics. The results show that PhaGCN2 largely improves the precision and recall of virus classification, increases the number of classifiable virus sequences in the Global Ocean Virome dataset (v2.0) by four times and classifies more than 90% of the Gut Phage Database. PhaGCN2 makes it possible to conduct high-throughput and automatic expansion of the database of the International Committee on Taxonomy of Viruses. The source code is freely available at https://github.com/KennthShang/PhaGCN2.0.

Advances in new target molecules against schistosomiasis: A comprehensive discussion of physiological structure and nutrient intake.

Schistosomiasis, a severe parasitic disease, is primarily caused by Schistosoma mansoni, Schistosoma japonicum, or Schistosoma haematobium. Currently, praziquantel is the only recommended drug for human schistosome infection. However, the lack of efficacy of praziquantel against juvenile worms and concerns about the emergence of drug resistance are driving forces behind the research for an alternative medication. Schistosomes are obligatory parasites that survive on nutrients obtained from their host. The ability of nutrient uptake depends on their physiological structure. In short, the formation and maintenance of the structure and nutrient supply are mutually reinforcing and interdependent. In this review, we focus on the structural features of the tegument, esophagus, and intestine of schistosomes and their roles in nutrient acquisition. Moreover, we introduce the significance and modes of glucose, lipids, proteins, and amino acids intake in schistosomes. We linked the schistosome structure and nutrient supply, introduced the currently emerging targets, and analyzed the current bottlenecks in the research and development of drugs and vaccines, in the hope of providing new strategies for the prevention and control of schistosomiasis.

Evaluation of maize varieties via multivariate analysis: Roles of ionome, antioxidants, and autophagy in salt tolerance.

Salt stress presents a major obstacle to maize (Zea mays L.) production globally, impeding its growth and development. In this study, we aimed to identify salt-tolerant maize varieties through evaluation using multivariate analysis and shed light on the role of ionome, antioxidant capacity, and autophagy in salt tolerance. We investigated multiple growth indices, including shoot fresh weight, shoot dry weight, plant height, chlorophyll content, electrolyte leakage, potassium and sodium contents, and potassium-to-sodium ratio in 20 maize varieties at the V3 stage under salt stress (200 mM NaCl). The results showed significant differences in the growth indices, accompanied by a wide range in their coefficient of variation, suggesting their suitability for screening salt tolerance. Based on D values, clustering analysis categorized the 20 varieties into four distinct groups. TG88, KN20, and LR888 (group I) emerged as the most salt-tolerant varieties, while YD9, XD903, and LH151 (group IV) were identified as the most sensitive. TG88 showcased nutrient preservation and redistribution under salt stress, surpassing YD9. It maintained nitrogen and iron levels in roots while YD9 experienced decreases. TG88 redistributed more nitrogen, zinc, and potassium to its leaves, outperforming YD9. TG88 preserved sulfur levels in both roots and leaves, unlike YD9. Additionally, TG88 demonstrated higher enzymatic antioxidant capacity (SOD, POD, APX, and GR) both at the enzyme and gene expression levels, upregulation of autophagy-related (ATG) genes (ZmATG6, ZmATG8a, and ZmATG10), and increased autophagic activity. Overall, this study offers insights into accurate maize varieties evaluation methods and the physiological mechanisms underlying salt tolerance and identifies promising materials for further research.

Whole genome sequencing of Crassostrea ariakensis (Mollusca: Ostreidae) and C. hongkongensis expands understandings of stress resistance in sessile oysters.

To understand the environmental adaptations among sessile bivalves lacking adaptive immunity, a series of analyses were conducted, with special emphasis on the widely distributed C. ariakensis. Employing Pacbio sequencing and Hi-C technologies, whole genome for each of a C. ariakensis (southern China) and C. hongkongensis individual was generated, with the contig N50 reaching 6.2 and 13.0 Mb, respectively. Each genome harbored over 30,000 protein-coding genes, with approximately half of each genome consisting of repeats. Genome alignment suggested possible introgression between C. gigas and C. ariakensis (northern China), and re-sequencing data corroborated this result and indicated significant gene flow between C. gigas and C. ariakensis. These introgressed candidates, well-represented by genes related to immunity and osmotic pressure, may be associated with environmental stresses. Gene family dynamics modeling suggested immune-related genes were well represented among the expanded genes in C. ariakensis. These outcomes could be attributed to the spread of C. ariakensis.

Macrophage KLF15 prevents foam cell formation and atherosclerosis via transcriptional suppression of OLR-1.

BACKGROUND: Macrophage-derived foam cells are a hallmark of atherosclerosis. Scavenger receptors, including lectin-like oxidized low-density lipoprotein (LDL) receptor-1 (OLR-1), are the principal receptors responsible for the uptake and modification of LDL, facilitating macrophage lipid load and the uptake of oxidized LDL by arterial wall cells. Krüppel-like factor 15 (KLF15) is a transcription factor that regulates the expression of genes by binding to the promoter during transcription. Therefore, this study aimed to investigate the precise role of macrophage KLF15 in atherogenesis. METHODS: We used two murine models of atherosclerosis: mice injected with an adeno-associated virus (AAV) encoding the Asp374-to-Tyr mutant version of human PCSK9, followed by 12 weeks on a high-fat diet (HFD), and ApoE-/-- mice on a HFD. We subsequently injected mice with AAV-KLF15 and AAV-LacZ to assess the role of KLF15 in the development of atherosclerosis in vivo. Oil Red O, H&E, and Masson's trichome staining were used to evaluate atherosclerotic lesions. Western blots and RT-qPCR were used to assess protein and mRNA levels, respectively. RESULTS: We determined that KLF15 expression was downregulated during atherosclerosis formation, and KLF15 overexpression prevented atherosclerosis progression. KLF15 expression levels did not affect body weight or serum lipid levels in mice. However, KLF15 overexpression in macrophages prevented foam cell formation by reducing OLR-1-meditated lipid uptake. KLF15 directly targeted and transcriptionally downregulated OLR-1 levels. Restoration of OLR-1 reversed the beneficial effects of KLF15 in atherosclerosis. CONCLUSION: Macrophage KLF15 transcriptionally downregulated OLR-1 expression to reduce lipid uptake, thereby preventing foam cell formation and atherosclerosis. Thus, our results suggest that KLF15 is a potential therapeutic target for atherosclerosis.

Pd-Mn/NC Dual Single-Atomic Sites with Hollow Mesopores for the Highly Efficient Semihydrogenation of Phenylacetylene.

The direct pyrolysis of metal-zeolite imidazolate frameworks (M-ZIFs) has been widely recognized as the predominant approach for synthesizing atomically dispersed metal-nitrogen-carbon single-atom catalysts (M/NC-SACs), which have exhibited exceptional activity and selectivity in the semihydrogenation of acetylene. However, due to weak adsorption of reactants on the single site and restricted molecular diffusion, the semihydrogenation of large organic molecules (e.g., phenylacetylene) was greatly limited for M/NC-SACs. In this work, a dual single-atom catalyst (h-Pd-Mn/NC) with hollow mesopores was designed and prepared using a general host-guest strategy. Taking the semihydrogenation of phenylacetylene as an example, this catalyst exhibited ultrahigh activity and selectivity, which achieved a turnover frequency of 218 molC═CmolPd-1 min-1, 16-fold higher than that of the commercial Lindlar catalyst. The catalyst maintained high activity and selectivity even after 5 cycles of usage. The superior activity of h-Pd-Mn/NC was attributed to the 4.0 nm mesopore interface of the catalyst, which enhanced the diffusion of macromolecular reactants and products. Particularly, the introduction of atomically dispersed Mn with weak electronegativity in h-Pd-Mn/NC could drive the electron transfer from Mn to adjacent Pd sites and regulate the electronic structure of Pd sites. Meanwhile, the strong electronic coupling in Pd-Mn pairs enhanced the d-electron domination near the Fermi level and promoted the adsorption of phenylacetylene and H2 on Pd active sites, thereby reducing the energy barrier for the semihydrogenation of phenylacetylene.

Variability in Leaf Color Induced by Chlorophyll Deficiency: Transcriptional Changes in Bamboo Leaves.

The diversity of leaf characteristics, particularly leaf color, underscores a pivotal area of inquiry within plant science. The synthesis and functionality of chlorophyll, crucial for photosynthesis, largely dictate leaf coloration, with varying concentrations imparting different shades of green. Complex gene interactions regulate the synthesis and degradation of chlorophyll, and disruptions in these pathways can result in abnormal chlorophyll production, thereby affecting leaf pigmentation. This study focuses on Bambusa multiplex f. silverstripe, a natural variant distinguished by a spectrum of leaf colors, such as green, white, and green-white, attributed to genetic variations influencing gene expression. By examining the physiological and molecular mechanisms underlying chlorophyll anomalies and genetic factors in Silverstripe, this research sheds light on the intricate gene interactions and regulatory networks that contribute to leaf color diversity. The investigation includes the measurement of photosynthetic pigments and nutrient concentrations across different leaf color types, alongside transcriptomic analyses for identifying differentially expressed genes. The role of key genes in pathways such as ALA biosynthesis, chlorophyll synthesis, photosynthesis, and sugar metabolism is explored, offering critical insights for advancing research and plant breeding practices.

Transverse endoplasmic reticulum expansion in hereditary spastic paraplegia corticospinal axons.

Hereditary spastic paraplegias (HSPs) comprise a large group of inherited neurologic disorders affecting the longest corticospinal axons (SPG1-86 plus others), with shared manifestations of lower extremity spasticity and gait impairment. Common autosomal dominant HSPs are caused by mutations in genes encoding the microtubule-severing ATPase spastin (SPAST; SPG4), the membrane-bound GTPase atlastin-1 (ATL1; SPG3A) and the reticulon-like, microtubule-binding protein REEP1 (REEP1; SPG31). These proteins bind one another and function in shaping the tubular endoplasmic reticulum (ER) network. Typically, mouse models of HSPs have mild, later onset phenotypes, possibly reflecting far shorter lengths of their corticospinal axons relative to humans. Here, we have generated a robust, double mutant mouse model of HSP in which atlastin-1 is genetically modified with a K80A knock-in (KI) missense change that abolishes its GTPase activity, whereas its binding partner Reep1 is knocked out. Atl1KI/KI/Reep1-/- mice exhibit early onset and rapidly progressive declines in several motor function tests. Also, ER in mutant corticospinal axons dramatically expands transversely and periodically in a mutation dosage-dependent manner to create a ladder-like appearance, on the basis of reconstructions of focused ion beam-scanning electron microscopy datasets using machine learning-based auto-segmentation. In lockstep with changes in ER morphology, axonal mitochondria are fragmented and proportions of hypophosphorylated neurofilament H and M subunits are dramatically increased in Atl1KI/KI/Reep1-/- spinal cord. Co-occurrence of these findings links ER morphology changes to alterations in mitochondrial morphology and cytoskeletal organization. Atl1KI/KI/Reep1-/- mice represent an early onset rodent HSP model with robust behavioral and cellular readouts for testing novel therapies.

Advanced glycation end product-modified low-density lipoprotein promotes pro-osteogenic reprogramming via RAGE/NF-κB pathway and exaggerates aortic valve calcification in hamsters.

BACKGROUND: Advanced glycation end product-modified low-density lipoprotein (AGE-LDL) is related to inflammation and the development of atherosclerosis. Additionally, it has been demonstrated that receptor for advanced glycation end products (RAGE) has a role in the condition known as calcific aortic valve disease (CAVD). Here, we hypothesized that the AGE-LDL/RAGE axis could also be involved in the pathophysiological mechanism of CAVD. METHODS: Human aortic valve interstitial cells (HAVICs) were stimulated with AGE-LDL following pre-treatment with or without interleukin 37 (IL-37). Low-density lipoprotein receptor deletion (Ldlr-/-) hamsters were randomly allocated to chow diet (CD) group and high carbohydrate and high fat diet (HCHFD) group. RESULTS: AGE-LDL levels were significantly elevated in patients with CAVD and in a hamster model of aortic valve calcification. Our in vitro data further demonstrated that AGE-LDL augmented the expression of intercellular cell adhesion molecule-1 (ICAM-1), interleukin-6 (IL-6) and alkaline phosphatase (ALP) in a dose-dependent manner through NF-κB activation, which was attenuated by nuclear factor kappa-B (NF-κB) inhibitor Bay11-7082. The expression of RAGE was augmented in calcified aortic valves, and knockdown of RAGE in HAVICs attenuated the AGE-LDL-induced inflammatory and osteogenic responses as well as NF-κB activation. IL-37 suppressed inflammatory and osteogenic responses and NF-κB activation in HAVICs. The vivo experiment also demonstrate that supplementation with IL-37 inhibited valvular inflammatory response and thereby suppressed valvular osteogenic activities. CONCLUSIONS: AGE-LDL promoted inflammatory responses and osteogenic differentiation through RAGE/NF-κB pathway in vitro and aortic valve lesions in vivo. IL-37 suppressed the AGE-LDL-induced inflammatory and osteogenic responses in vitro and attenuated aortic valve lesions in a hamster model of CAVD.

Interpregnancy interval and early infant neurodevelopment: the role of maternal-fetal glucose metabolism.

BACKGROUND: Interpregnancy interval (IPI) is associated with a variety of adverse maternal and infant outcomes. However, reports of its associations with early infant neurodevelopment are limited and the mechanisms of this association have not been elucidated. Maternal-fetal glucose metabolism has been shown to be associated with infant neurodevelopmental. The objective of this study was to determine whether this metabolism plays a role in the relationship between IPI and neurodevelopment. METHODS: This prospective birth cohort study included 2599 mother-infant pairs. The IPI was calculated by subtracting the gestational age of the current pregnancy from the interval at the end of the previous pregnancy. Neurodevelopmental outcomes at 12 months in infants were assessed by the Ages and Stages Questionnaire Edition 3 (ASQ-3). Maternal fasting venous blood was collected at 24-28 weeks and cord blood was collected at delivery. The association between IPI and neurodevelopment was determined by logistic regression. Mediation and sensitivity analyses were also conducted. RESULTS: In our cohort, 14.0% had an IPI < 12 months. IPI < 12 months increased the failure of the communication domain, fine motor domain, and personal social domain of the ASQ (relative risks (RRs) with 95% confidence interval (CI): 1.73 [1.11,2.70]; 1.73 [1.10,2.72]; 1.51 [1.00,2.29]). Maternal homeostasis model assessment of insulin resistance (HOMA-IR) and cord blood C-peptide was significantly associated with failure in the communication domain [RRs with 95% CI: 1.15 (1.02, 1.31); 2.15 (1.26, 3.67)]. The proportion of the association between IPI and failure of the communication domain risk mediated by maternal HOMA-IR and cord blood C-peptide was 14.4%. CONCLUSIONS: IPI < 12 months was associated with failing the communication domain in infants. Maternal-fetal glucose metabolism abnormality may partially explain the risk of neurodevelopmental delay caused by short IPI.

Gap State-Modulated Van Der Waals Short-Term Memory with Broad Band Negative Photoconductance.

Floating gate memory (FGM), composed of van der Waals (vdW) junctions with an atomically thin floating layer for charge storage, is widely employed to develop logic-in memories and in-sensor computing devices. Most research efforts of FGM are spent on achieving long-term charge storage and fast reading/writing for flash and random-access memory. However, dynamic modulation of memory time via a tunneling barrier and vdW interfaces, which is critical for synaptic computing and machine vision, is still lacking. Here, a van der Waals short-term memory with tunable memory windows and retention times from milliseconds to thousands of seconds is reported, which is approximately exponentially proportional to the thickness h-BN (hexagonal boron nitride) barrier. The specific h-BN barrier with fruitful gap states provides charge release channels for trapped charges, making the vdW device switchable between positive photoconductance and negative photoconductance with a broadband light from IR to UV range. The dynamic short-term memory with tunable photo response highlights the design strategy of novel vdW memory vis interface engineering for further intelligent information storage and optoelectronic detection.

Reversible Switching Between Microwave Absorption and EMI Shielding of VO2 Composite Foam.

Developing lightweight composite with reversible switching between microwave (MW) absorption and electromagnetic interference (EMI) shielding is promising yet remains highly challenging due to the completely inconsistent attenuation mechanism for electromagnetic (EM) radiation. Here, a lightweight vanadium dioxide/expanded polymer microsphere composites foam (VO2/EPM) is designed and fabricated with porous structures and 3D VO2 interconnection, which possesses reversible switching function between MW absorption and EMI shielding under thermal stimulation. The VO2/EPM exhibits MW absorption with a broad effective absorption bandwidth of 3.25 GHz at room temperature (25 °C), while provides EMI shielding of 23.1 dB at moderately high temperature (100 °C). This reversible switching performance relies on the porous structure and tunability of electrical conductivity, complex permittivity, and impedance matching, which are substantially induced by the convertible crystal structure and electronic structure of VO2. Finite element simulation is employed to qualitatively investigate the change in interaction between EM waves and VO2/EPM before and after the phase transition. Moreover, the application of VO2/EPM is demonstrated with a reversible switching function in controlling wireless transmission on/off, showcasing its excellent cycling stability. This kind of smart material with a reversible switching function shows great potential in next-generation electronic devices.

Non-iridium-based electrocatalyst for durable acidic oxygen evolution reaction in proton exchange membrane water electrolysis.

Iridium-based electrocatalysts remain the only practical anode catalysts for proton exchange membrane (PEM) water electrolysis, due to their excellent stability under acidic oxygen evolution reaction (OER), but are greatly limited by their high cost and low reserves. Here, we report a nickel-stabilized, ruthenium dioxide (Ni-RuO2) catalyst, a promising alternative to iridium, with high activity and durability in acidic OER for PEM water electrolysis. While pristine RuO2 showed poor acidic OER stability and degraded within a short period of continuous operation, the incorporation of Ni greatly stabilized the RuO2 lattice and extended its durability by more than one order of magnitude. When applied to the anode of a PEM water electrolyser, our Ni-RuO2 catalyst demonstrated >1,000 h stability under a water-splitting current of 200 mA cm-2, suggesting potential for practical applications. Density functional theory studies, coupled with operando differential electrochemical mass spectroscopy analysis, confirmed the adsorbate-evolving mechanism on Ni-RuO2, as well as the critical role of Ni dopants in stabilization of surface Ru and subsurface oxygen for improved OER durability.

Integrinß-1 in disorders and cancers: molecular mechanisms and therapeutic targets.

Integrinß-1 (ITGB1) is a crucial member of the transmembrane glycoprotein signaling receptor family and is also central to the integrin family. It forms heterodimers with other ligands, participates in intracellular signaling and controls a variety of cellular processes, such as angiogenesis and the growth of neurons; because of its role in bidirectional signaling regulation both inside and outside the membrane, ITGB1 must interact with a multitude of substances, so a variety of interfering factors can affect ITGB1 and lead to changes in its function. Over the past 20 years, many studies have confirmed a clear causal relationship between ITGB1 dysregulation and cancer development and progression in a wide range of benign diseases and solid tumor types, which may imply that ITGB1 is a prognostic biomarker and a therapeutic target for cancer treatment that warrants further investigation. This review summarizes the biological roles of ITGB1 in benign diseases and cancers, and compiles the current status of ITGB1 function and therapy in various aspects of tumorigenesis and progression. Finally, future research directions and application prospects of ITGB1 are suggested. Video Abstract.

Photocatalytic Generation of H2O2 Via a Hydrogen-Abstraction Pathway by Bi2.15WO6 under Visible Light.

Photocatalytic technology is a popular research area for converting solar energy into environmentally friendly chemicals and is considered the greenest approach for producing H2O2. However, the corresponding reactive oxygen species (ROS) and pathway involved in the photocatalytic generation of H2O2 by the Bi2.15WO6-glucose system are still not clear. Quenching experiments have established that neither •OH nor h+ contribute to the formation of H2O2, and show that the formed surface superoxo (≡Bi-OO•) and peroxo (≡Bi-OOH) species are the predominant ROS in H2O2 generation. In addition, various characterizations indicate the enhanced electron-transfer on the surface of Bi2.15WO6 with increasing contents of glucose via the ligand-to-metal charge transfer pathway, confirming H-transfer from glucose to ≡Bi-OO• or ≡Bi-OOH. The increased production of H2O2 with decreasing bond dissociation energy (BDEO-H) values of various phenolic compounds again supports the H-transfer mechanism from phenolic compounds to ≡Bi-OO• and then to ≡Bi-OOH. DFT calculations further reveal that on the Bi2.15WO6 surface, oxygen is sequentially reduced to ≡Bi-OO• and ≡Bi-OOH, while H-transfer from H2O or glucose to ≡Bi-OO• and ≡Bi-OOH, resulting in the production of H2O2. The lower energy barrier of H-transfer from adsorbed glucose (0.636 eV) than that from H2O (1.157 eV) indicates that H-transfer is more favorable from adsorbed glucose. This work gives new insight into the photocatalytic generation of H2O2 by Bi2.15WO6 in the presence of glucose/phenolic compounds via the H-abstraction pathway.

Association Between Preeclampsia and Blood Pressure in Offspring: A Systematic Review and Meta-Analysis.

PURPOSE OF REVIEW: Pregnancy-induced preeclampsia is a severe pregnancy complication and preeclampsia has been associated with an increased risk of chronic hypertension for offspring. However, the magnitude of the overall effect of exposure to preeclampsia in pregnancy on blood pressure (BP) in offspring is unknown. This systematic review and meta-analysis was sought to systematically assess the effects of preeclampsia on the BP of the offspring. RECENT FINDINGS: Of 2550 publications identified, 23 studies were included. The meta-analysis indicated that preeclampsia increases the potential risk of hypertension in offspring. Systolic blood pressure (SBP) was 2.0 mm Hg (95% CI: 1.2, 2.8) and diastolic blood pressure (DBP) was 1.4 mm Hg (95% CI: 0.9, 1.9) higher in offspring exposed to pre-eclampsia in utero, compared to those born to normotensive mothers. The correlations were similar in stratified analyses of children and adolescents by sex, geographic area, ages, and gestational age. During childhood and young adulthood, the offspring of pregnant women with preeclampsia are at an increased risk of high BP. It is crucial to monitor their BP.

Development and validation of genome-wide SSR molecular markers of Tapes dorsatus.

BACKGROUND: Tapes dorsatus is an economically important benthic animal in the Beibu Gulf of China. However, the deficiency of microsatellite markers has hindered the study of its genetics. The development of microsatellite markers will provide useful tools for genetic improvement, variety identification, phylogenetic analysis and resource conservation. METHODS AND RESULTS: Within the genome sequence, 145,008 simple sequence repeats (SSRs) were identified, and 29,691 primer pairs were designed successfully. A total of 100 primer pairs were randomly synthesized for testing, and 93 primers yielded products. Sixty highly polymorphic primers were used to reveal the genetic diversity of 50 T. dorsatus individuals. The average number of alleles (Na) of the population was 10.40; the average number of effective alleles was 6.16, the average expected heterozygosity (He) was 0.82, and the average polymorphic information content was 0.80. The genetic structure of the population was detected, by which the population could be divided into three subpopulations. CONCLUSION: We identified 145,008 SSRs in the genome of T. dorsatus and designed 29,691 primer pairs in this study. Of 100 synthesized primers, 60 were highly polymorphic and used to reveal the genetic diversity and structure of the population. The SSR markers identified here will provide useful tools and a foundation for genetic diversity, linkage mapping and molecular marker-aided breeding in T. dorsatus.

A class of dynamin-like GTPases involved in the generation of the tubular ER network.

The endoplasmic reticulum (ER) consists of tubules that are shaped by the reticulons and DP1/Yop1p, but how the tubules form an interconnected network is unknown. Here, we show that mammalian atlastins, which are dynamin-like, integral membrane GTPases, interact with the tubule-shaping proteins. The atlastins localize to the tubular ER and are required for proper network formation in vivo and in vitro. Depletion of the atlastins or overexpression of dominant-negative forms inhibits tubule interconnections. The Sey1p GTPase in S. cerevisiae is likely a functional ortholog of the atlastins; it shares the same signature motifs and membrane topology and interacts genetically and physically with the tubule-shaping proteins. Cells simultaneously lacking Sey1p and a tubule-shaping protein have ER morphology defects. These results indicate that formation of the tubular ER network depends on conserved dynamin-like GTPases. Since atlastin-1 mutations cause a common form of hereditary spastic paraplegia, we suggest ER-shaping defects as a neuropathogenic mechanism.