Dehydration-induced corrugated folding in Rhapis excelsa plant leaves.

Plant leaves, whose remarkable ability for morphogenesis results in a wide range of petal and leaf shapes in response to environmental cues, have inspired scientific studies as well as the development of engineering structures and devices. Although some typical shape changes in plants and the driving force for such shape evolution have been extensively studied, there remain many poorly understood mechanisms, characteristics, and principles associated with the vast array of shape formation of plant leaves in nature. Here, we present a comprehensive study that combines experiment, theory, and numerical simulations of one such topic-the mechanics and mechanisms of corrugated leaf folding induced by differential shrinking in Rhapis excelsa. Through systematic measurements of the dehydration process in sectioned leaves, we identify a linear correlation between change in the leaf-folding angle and water loss. Building on experimental findings, we develop a generalized model that provides a scaling relationship for water loss in sectioned leaves. Furthermore, our study reveals that corrugated folding induced by dehydration in R. excelsa leaves is achieved by the deformation of a structural architecture-the "hinge" cells. Utilizing such connections among structure, morphology, environmental stimuli, and mechanics, we fabricate several biomimetic machines, including a humidity sensor and morphing devices capable of folding in response to dehydration. The mechanisms of corrugated folding in R. excelsa identified in this work provide a general understanding of the interactions between plant leaves and water. The actuation mechanisms identified in this study also provide insights into the rational design of soft machines.

Insect-scale jumping robots enabled by a dynamic buckling cascade.

Millions of years of evolution have allowed animals to develop unusual locomotion capabilities. A striking example is the legless-jumping of click beetles and trap-jaw ants, which jump more than 10 times their body length. Their delicate musculoskeletal system amplifies their muscles' power. It is challenging to engineer insect-scale jumpers that use onboard actuators for both elastic energy storage and power amplification. Typical jumpers require a combination of at least two actuator mechanisms for elastic energy storage and jump triggering, leading to complex designs having many parts. Here, we report the new concept of dynamic buckling cascading, in which a single unidirectional actuation stroke drives an elastic beam through a sequence of energy-storing buckling modes automatically followed by spontaneous impulsive snapping at a critical triggering threshold. Integrating this cascade in a robot enables jumping with unidirectional muscles and power amplification (JUMPA). These JUMPA systems use a single lightweight mechanism for energy storage and release with a mass of 1.6 g and 2 cm length and jump up to 0.9 m, 40 times their body length. They jump repeatedly by reengaging the latch and using coiled artificial muscles to restore elastic energy. The robots reach their performance limits guided by theoretical analysis of snap-through and momentum exchange during ground collision. These jumpers reach the energy densities typical of the best macroscale jumping robots, while also matching the rapid escape times of jumping insects, thus demonstrating the path toward future applications including proximity sensing, inspection, and search and rescue.

Transient Amplification of Broken Symmetry in Elastic Snap-Through.

A snap-through bifurcation occurs when a bistable structure loses one of its stable states and moves rapidly to the remaining state. For example, a buckled arch with symmetrically clamped ends can snap between an inverted and a natural state as the ends are released. A standard linear stability analysis suggests that the arch becomes unstable to asymmetric perturbations. Surprisingly, our experiments show that this is not always the case: symmetric transitions are also observed. Using experiments, numerics, and a toy model, we show that the symmetry of the transition depends on the rate at which the ends are released, with sufficiently fast loading leading to symmetric snap-through. Our toy model reveals that this behavior is caused by a region of the system's state space in which any initial asymmetry is amplified. The system may not enter this region when loaded fast (hence remaining symmetric), but will traverse it for some interval of time when loaded slowly, causing a transient amplification of asymmetry. Our toy model suggests that this behavior is not unique to snapping arches, but rather can be observed in dynamical systems where both a saddle-node and a pitchfork bifurcation occur in close proximity.

Expression of hepatic genes involved in bile acid metabolism in dairy cows with fatty liver.

Bile acids are cholesterol-derived molecules that are primarily produced in the liver. In nonruminants with fatty liver, overproduction of bile acids is associated with liver injury. During the transition period, fatty liver is a metabolic disorder that can affect up to 50% of high-producing dairy cows. The purpose of this study was to provide a comprehensive evaluation on hepatic bile acid metabolism in dairy cows with fatty liver by assessing expression changes of genes involved in bile acid synthesis, export and uptake. The serum activities of aspartate aminotransferase, alanine aminotransferase and glutamate dehydrogenase and concentration of total bile acids were all greater, whereas serum concentration of total cholesterol was lower in cows with fatty liver than in healthy cows. Content of total bile acids was higher but total cholesterol was slightly lower in liver tissues from fatty liver cows than from healthy cows. The hepatic mRNA abundance of cholesterol 7a-hydroxylase (CYP7A1), hydroxy-delta-5-steroid dehydrogenase, 3 ß- and steroid delta-isomerase 7 (HSD3B7) and sterol 12α-hydroxylase (CYP8B1), enzymes involved in the classic pathway of bile acid synthesis, was higher in fatty liver cows than in healthy cows. Compared with healthy cows, the hepatic mRNA abundance of alternative bile acid synthesis pathway-related genes sterol 27-hydroxylase (CYP27A1) and oxysterol 7α-hydroxylase (CYP7B1) did not differ in cows with fatty liver. The protein and mRNA abundance of bile acid transporter bile salt efflux pump (BSEP) were lower in the liver of dairy cow with fatty liver. Compared with healthy cows, the hepatic mRNA abundance of bile acid transporters solute carrier family 51 subunit α (SLC51A), ATP binding cassette subfamily C member 1 (ABCC1) and 3 (ABCC3) was greater in cows with fatty liver, whereas the solute carrier family 51 subunit ß (SLC51B) did not differ. The expression of genes involved in bile acid uptake, including solute carrier family 10 member 1 (NTCP), solute carrier organic anion transporter family member 1A2 (SLCO1A2) and 2B1 (SLCO2B1) was upregulated in dairy cows with fatty liver. Furthermore, the hepatic protein and mRNA abundance of bile acid metabolism regulators farnesoid X receptor (FXR) and small heterodimer partner (SHP) were lower in cows with fatty liver than in healthy cows. Overall, these data suggest that inhibition of FXR signaling pathway may lead to the increased bile acid synthesis and uptake and decreased secretion of bile acids from hepatocytes to the bile, which elevates hepatic bile acids content in dairy cows with fatty liver. As the hepatotoxicity of bile acids has been demonstrated on nonruminant hepatocytes, it is likely that the liver injury is induced by increased hepatic bile acids content in dairy cows with fatty liver.

Thioredoxin-2 suppresses hydrogen peroxide-activated nuclear factor kappa B signaling via alleviating oxidative stress in bovine adipocytes.

During the periparturient period, both oxidative stress, and inflammation of adipose tissue are considered high risk factors for metabolic disorder of dairy cows. Oxidative stress can activate transcription factor nuclear factor kappa B (NF-κB), which lead to the upregulation of genes involved in inflammatory pathways. Thioredoxin-2 (TXN2) is a mitochondrial protein that regulates cellular redox by suppressing mitochondrial reactive oxygen species (ROS) generation in nonruminant, whereas the function of TXN2 in bovine adipocytes was unclear. Thus, the objective of this study was to evaluate how or by which mechanisms TXN2 regulates oxidative stress and NF-κB signaling pathway in bovine adipocytes. Bovine pre-adipocytes isolated from 5 healthy Holstein cows were differentiated and used for (1) treatment with different concentrations of hydrogen peroxide (H2O2; 0, 25, 50, 100, 200, or 400 µM) for 2 h; (2) transfection with or without TXN2 small interfering RNA (si-TXN2) for 48 h and then treated with or without 200 µM H2O2 for 2 h; (3) transfection with scrambled negative control siRNA (si-control) or si-TXN2 for 48 h, and then treatment with or without 10 mM N-acetylcysteine (NAC) for 2 h; (4) transfection with or without TXN2-overexpressing plasmid for 48 h and then treatment with or without 200 µM H2O2 for 2 h. High concentrations of H2O2 (200 and 400 µM) decreased protein and mRNA abundance of TXN2, reduced total antioxidant capacity (T-AOC) and ATP content in adipocytes. Moreover, 200 and 400 µM H2O2 reduced protein abundance of inhibitor of kappa B α (IκBα), increased phosphorylation of NF-κB and upregulated mRNA abundance of tumor necrosis factor-α (TNFA) and interleukin-1B (IL-1B), suggesting that H2O2-induced oxidative stress and activated NF-κB signaling pathway. Silencing of TXN2 increased intracellular ROS content, phosphorylation of NF-κB and mRNA abundance of TNFA and IL-1B, decreased ATP content and protein abundance of IκBα in bovine adipocytes. Knockdown of TXN2 aggravated H2O2-induced oxidative stress and inflammation. In addition, treatment with antioxidant NAC ameliorated oxidative stress and inhibited NF-κB signaling pathway in adipocytes transfected with si-TXN2. In bovine adipocytes treated with H2O2, overexpression of TXN2 reduced the content of ROS and elevated the content of ATP and T-AOC. Overexpression of TXN2 alleviated H2O2-induced inflammatory response in adipocytes, as demonstrated by decreased expression of phosphorylated NF-κB, TNFA, IL-1B, as well as increased expression of IκBα. Furthermore, the protein and mRNA abundance of TXN2 was lower in adipose tissue of dairy cows with clinical ketosis. Overall, our studies contribute to the understanding of the role of TXN2 in adipocyte oxidative stress and inflammatory response.

Liver fibrosis is a common pathological change in the liver of dairy cows with fatty liver.

Fatty liver (i.e., hepatic lipidosis) is a prevalent metabolic disorder in dairy cows during the transition period, characterized by excess hepatic accumulation of triglyceride (TG), tissue dysfunction, and cell death. Detailed pathological changes, particularly hepatic fibrosis, during fatty liver remain to be determined. Liver fibrosis occurs as a consequence of liver damage, resulting from the excessive accumulation of extracellular matrix, which distorts the architecture of the normal liver, compromising its normal synthetic and metabolic functions. Thus, we aimed to investigate liver fibrosis status and its potential causal factors including oxidative stress, hepatocyte apoptosis, and production of inflammatory cytokines in the liver of cows with fatty liver. Forty-five dairy cows (parity, 3-5) were selected, and liver biopsy and blood were collected on the second week postpartum (days in milk, 10-14 d). On the basis of the degree of lipid accumulation in liver, selected cows were categorized into normal (n = 25; TG <1% wet wt), mild fatty liver (n = 15; 1% ≤ TG <5% wet wt), and moderate fatty liver (n = 5; 5% ≤ TG <10% wet wt). Compared with normal cows, blood concentrations of nonesterified fatty acids and ß-hydroxybutyrate, along with alanine aminotransferase and aspartate aminotransferase activities, were greater in the cows with fatty liver (mild and moderate). Hepatic extracellular matrix deposition, as indicated by Picrosirius red staining, was greater in cows with fatty liver than those with normal ones. In addition, we observed an increased proportion of collagen type I fiber in extracellular matrix with increased lipid accumulation in the liver. Compared with normal cows, the area of α-smooth muscle actin (α-SMA)-positive staining along with the mRNA abundance of collagen type I α 1 (COL1A1), ACTA2 (gene encoding α-SMA), and transforming growth factor-ß (TGFB) were greater in cows with fatty liver. Compared with normal cows, hepatic contents of malondialdehyde, glutathione disulfide, and 8-isoprostane were greater, whereas total antioxidant capacity, the hepatic content of glutathione, and activities of antioxidant indicators, including superoxide dismutase, glutathione peroxidase, and catalase, were lower in cows with fatty liver. The number of terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling-positive cells and abundance of apoptosis-related molecules BAX, CASP3, CASP8, and CASP9 were greater in cows with fatty liver. However, mRNA abundance of the anti-apoptotic gene BCL2 did not differ. The mRNA abundance of pro-inflammatory cytokines including tumor necrosis factor-α (TNFA), interleukin-1ß (IL1B), and interleukin-6 (IL6) was greater in the liver of cows with fatty liver. Overall, the present study indicated that fibrosis is a common pathological response to liver damage and is associated with oxidative stress, hepatocyte death, and inflammation.

Protective effects of agrimonolide on hypoxia-induced H9c2 cell injury by maintaining mitochondrial homeostasis.

Cardiomyocyte death caused by hypoxia is one of the main causes of myocardial infarction or heart failure, and mitochondria play an important role in this process. Agrimonolide (AM) is a monomeric component extracted from Agrimonia pilosa L. and has antioxidant, antitumor, and anti-inflammatory effects. This study aimed to investigate the role and mechanism of AM in improving hypoxia-induced H9c2 cell damage. The results showed that low AM concentrations promote H9c2 cell proliferation and increase cellular ATP content. Transcriptome sequencing showed that AM induces differential expression of genes in H9c2 cells. Gene ontology (GO) function and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses revealed that these genes were concentrated in mitochondrial function. Subsequent experiments confirmed that AM regulates hypoxia-induced cell cycle arrest. AM inhibited the rate of apoptosis by regulating the expression of apoptosis-related proteins, reducing the level of cleaved Caspase 3 and Bax, and increasing the level of Bcl2, thereby protecting H9c2 cells from hypoxia-induced apoptosis. AM restored the mitochondrial membrane potential, inhibited the generation of ROS, maintained the normal shape of the mitochondria, improved the level of the mitochondrial functional proteins OPA1, MFN1, MFN2, Tom20, and increased the level of ATP. In conclusion, AM protects H9c2 cells from hypoxia-induced cell damage.

Staphylococcus aureus mediates pyroptosis in bovine mammary epithelial cell via activation of NLRP3 inflammasome.

Cell death and inflammation are intimately linked during mastitis due to Staphylococcus aureus (S. aureus). Pyroptosis, a programmed necrosis triggered by gasdermin protein family, often occurs after inflammatory caspase activation. Many pathogens invade host cells and activate cell-intrinsic death mechanisms, including pyroptosis, apoptosis, and necroptosis. We reported that bovine mammary epithelial cells (MAC-T) respond to S. aureus by NOD-like receptor protein 3 (NLRP3) inflammasome activation through K+ efflux, leading to the recruitment of apoptosis-associated speck-like protein (ASC) and the activation of caspase-1. The activated caspase-1 cleaves gasdermin D (GSDMD) and forms a N-terminal pore forming domain that drives swelling and membrane rupture. Membrane rupture results in the release of the pro-inflammatory cytokines IL-18 and IL-1ß, which are activated by caspase-1. Can modulate GSDMD activation by NLRP3-dependent caspase-1 activation and then cause pyroptosis of bovine mammary epithelial cells.

Phenotypic plasticity and exotic plant invasions: Effects of soil nutrients, species nutrient requirements, and types of traits.

High-phenotypic plasticity has long been considered as a characteristic promoting exotic plant invasions. However, the results of the studies testing this hypothesis are still inconsistent. Overlooking the effects of species resource requirements and environmental resource availability may be the main reasons for the ambiguous conclusions. Here, we compared phenotypic plasticity between five noxious invasive species with different nutrient requirements (evaluated using the soil nutrient status of their natural distribution ranges) and their phylogenetically related natives under five nutrient levels. We found that species with high-nutrient requirements showed greater plasticity of total biomass than species with low-nutrient requirements, regardless of their status (invasive or native). Invasives with high-nutrient requirements had greater growth plasticity than their related natives, which may contribute to their invasiveness under high-nutrient environments. However, compared with the related natives, a higher growth plasticity may not help exotic species with low-nutrient requirements to invade nutrient-rich habitats, and exotic species with high-nutrient requirements to invade nutrient-limited habitats. In contrast, invasives with low-nutrient requirements exhibited lower growth plasticity than their related natives, contributing to their invasiveness under nutrient-limited habitats. Functional traits showed growth-related plasticity in only 10 cases (3.8%), and there was no functional trait whose plastic response to soil nutrients was beneficial to exotic plant invasions. Our study indicates that low-growth plasticity could also promote exotic plant invasions, high plasticity may not necessarily lead to invasiveness. We must test the adaptive significance of plasticity of functional traits when studying its biological roles.

Snap-through of graphene nanowrinkles under out-of-plane compression.

Nanowrinkles (i.e. the buckled nanoribbons) are widely observed in nano-devices assembled by two-dimensional (2D) materials. The existence of nanowrinkles significantly affects the physical (such as mechanical, electrical and thermal) properties of 2D materials, and thus further, impedes the applications of those devices. In this paper, we take the nanowrinkle formed in a monolayer graphene as a model system to study its deformation behaviours, especially the configuration evolution and the snap-through buckling instabilities, when subjected to the out-of-plane compression. By performing molecular dynamics simulation, the graphene nanowrinkles with or without self-adhesion (which are notated as 'clipped' state or 'bump' state, respectively) are obtained depending on the geometric size and the applied axial compressive pre-strain. The elastica theory is employed to quantify the shape of 'bump' nanowrinkles, as well as the critical condition of the transition between 'clipped' and 'bump' states. By applying out-of-plane compression to the generated graphene nanowrinkle, it flips to an opposite configuration via snap-through buckling. We identify four different buckling modes according to the configuration evolution. An unified phase diagram is constructed to describe those buckling modes. For the cases with negligible van der Waals interaction getting involved in the snap-buckling process, i.e. without self-adhesion, the force-displacement curves for nanowrinkles with same axial pre-strain but different sizes can be scaled to collapse. Moreover, the critical buckling loads can also be scaled and predicted by the extended elastica theory. Otherwise, for the cases with self-adhesion, which corresponds to the greater axial pre-strain, the van der Waals interaction makes the scaling collapse break down. It is expected that the analysis about the snap-through buckling of graphene nanowrinkles reported in this work will advance the understanding of the mechanical behaviours of wrinkled 2D materials and promote the design of functional nanodevices, such as nanomechanical resonators and capacitors.

A genetically novel avian Hepatitis E virus in China.

Hepatitis E virus (HEV) infection has a global distribution with diverse hosts, including mammals and avians. In this study, an avian Hepatitis E virus (aHEV) strain with a high mortality rate of about 30%, designated as SDXT20, was obtained from the liver of 30-week-old Hubbard chickens with severe hepatosplenomegaly in 2020 in Eastern China and HEV was proved to be the only pathogen by next-generation sequencing. Its complete genome, which encodes three open reading frames (ORFs), is 6649 nt in length. ORF1-3 encodes three proteins with lengths of 1532 aa, 606 aa, and 82 aa, respectively, and ORF2 and ORF3 overlap with each other. BLAST-based similarity analysis of the complete viral genome demonstrated that SDXT20 had merely 80.5-92.2% similarity with avian Avihepevirus magniiecur strains and 50.4%-54.8% lower similarity with Paslahepevirus balayani, Rocahepevirus ratti, and Chirohepevirus eptesici species. Further genetic evolution analysis of the complete genome and ORF2 revealed that the isolate was genetically distinct from known aHEVs, and it belonged to a novel genetically distinct aHEV. This study provides data for further analysis of the multi-host and cross-host genetic evolution of HEVs.

Inherent conflicts between reaction norm slope and plasticity indices when comparing plasticity: a conceptual framework and empirical test.

Phenotypic plasticity index (PI), the slope of reaction norm (K) and relative distances plasticity index (RDPI), the most commonly used estimators, have occasionally been found to generate different plasticity rankings between groups (species, populations, cultivars or genotypes). However, no effort has been made to determine how frequent this incongruence is, and the factors that influence the occurrence of the incongruence. To address these problems, we first proposed a conceptual framework and then tested the framework (its predictions) by reanalyzing 1248 sets of published data. Our framework reveals inherent conflicts between K and PI or RDPI when comparing plasticity between two groups, and the frequency of these conflicts increases with increasing inter-group initial trait difference and/or K values of the groups compared. More importantly, the estimators also affect the magnitude of the inter-group plasticity differences even when they do not change groups' plasticity rankings. The above-mentioned effects of plasticity estimators were confirmed by our empirical test using data from the literature, and the conflicts occur in 203 (16%) of the 1248 comparisons between K and indices, indicating that a considerable proportion of the comparative conclusions on plasticity in literature are estimator-dependent. The frequency of the conflicts is influenced by phylogenetic relatedness of the groups compared, being lower when comparing within relative to between species, but not by specific types of environments, traits and species. Our study indicates that care is needed to select estimator when comparing groups' plasticity, and that the conclusions in relevant literature should be treated with great caution.

Histamine promotes adhesion of neutrophils by inhibition of autophagy in dairy cows with subacute ruminal acidosis.

Subacute ruminal acidosis (SARA), a common digestive disease in dairy cows, is accompanied by systemic inflammation and high concentrations of histamine in blood. Histamine-induced neutrophil adhesion may play an important role in the systemic inflammation experienced by cows during SARA. Autophagy, an intracellular degradation system, regulates recycling of membrane-associated integrin and may be involved in histamine-induced adhesion of bovine neutrophils. In the present study, 20 multiparous mid-lactation cows (average body weight 486 ± 24 kg) fitted with ruminal fistula were assigned to a control group (n = 10) or a SARA group (n = 10). We induced SARA by feeding different combinations of wheat-barley pellets and chopped alfalfa hay for 8 wk; SARA was defined as a ruminal pH <5.6 for at least 3 h/d. Blood samples were collected in wk 8. Compared with controls, SARA cows had greater serum concentrations of tumor necrosis factor-α, IL-6, IL-1ß, lipopolysaccharide (LPS)-binding protein, haptoglobin, and serum amyloid A. Serum concentrations of these proinflammatory factors had strong positive correlations with the concentration of serum histamine and LPS. In ex vivo adhesion experiments, the number of adherent neutrophils was greater in the SARA group. Additionally, membrane protein abundance of adhesion molecules such as integrin α-L precursor (CD11a) and integrin α-M precursor (CD11b) was greater in neutrophils of the SARA group, confirming enhanced adhesion ability. Neutrophils of SARA cows had greater number of autophagosomes, greater protein abundance of autophagy substrate sequestosome-1 (p62), and higher ratio of microtubule associated proteins 1A/1B light chain 3 (LC3)-II to LC3-I, indicating congestion during the late phase of autophagy flux. For in vitro experiments, neutrophils isolated from control cows were incubated with 0.4 endotoxin units (EU)/mL LPS or 7 µM histamine for 0, 1, 2, and 4 h, respectively. We detected linear and quadratic effects for the number of adherent neutrophils after histamine treatment with a peak response at 2 h, whereas no significant effect was detected after LPS treatment. Membrane protein abundance of CD11a and CD11b was greater after histamine treatment, suggesting that it may have an inhibitory effect on the degradation of adhesion molecules. The greater abundance of p62, higher ratio of LC3-II to LC3-I, and increased co-localization between CD11b and LC3 after histamine treatment indicated that recycling of adhesion molecules and autophagy flux were blocked. These effects were not aggravated further in the presence of chloroquine, a specific inhibitor of the late phase of autophagy flux. Overall, our results revealed that histamine increases adhesion of neutrophils by inhibiting autophagy in dairy cows with SARA.

Tumor necrosis factor-α promotes lipolysis and reduces insulin sensitivity by activating nuclear factor kappa B and c-Jun N-terminal kinase in primary bovine adipocytes.

Sustained lipolysis and insulin resistance increase the risk of metabolic dysfunction in dairy cows during the transition period. Proinflammatory cytokines are key regulators of adipose tissue metabolism in nonruminants, but biological functions of these molecules in ruminants are not well known. Thus, the objective of this study was to investigate whether tumor necrosis factor-α (TNF-α) could affect insulin sensitivity and lipolysis in bovine adipocytes as well as the underlying mechanisms. Bovine adipocytes (obtained from the omental and mesenteric adipose depots) isolated from 5 Holstein female calves (1 d old) with similar body weight (median: 36.9 kg, range: 35.5-41.2 kg) were differentiated and used for (1) treatment with different concentrations of TNF-α (0, 0.1, 1, or 10 ng/mL) for 12 h; (2) pretreatment with 10 µM lipolytic agonist isoproterenol (ISO) for 3 h, followed by treatment with or without 10 ng/mL TNF-α for 12 h; and (3) pretreatment with the c-Jun N-terminal kinase (JNK) inhibitor SP600125 (20 µM for 2 h) and nuclear factor kappa B (NF-κB) inhibitor BAY 11-7082 (10 µM for 1 h) followed by treatment with or without 10 ng/mL TNF-α for 12 h. The TNF-α increased glycerol content in supernatant, decreased triglyceride content and insulin-stimulated phosphorylation of protein kinase B suggesting activation of lipolysis and impairment of insulin sensitivity. The TNF-α reduced cell viability, upregulated mRNA abundance of Caspase 3 (CASP3), an apoptosis marker, and increased activity of Caspase 3. In addition, increased phosphorylation of NF-κB and JNK, upregulation of mRNA abundance of interleukin-6 (IL-6), TNFA, and suppressor of cytokine signaling 3 (SOCS3) suggested that TNF-α activated NF-κB and JNK signaling pathways. Furthermore, ISO plus TNF-α-activated NF-κB and JNK signaling pathway to a greater extent than TNF-α alone. Combining TNF-α and ISO aggravated TNF-α-induced apoptosis, insulin insensitivity and lipolysis. In the absence of TNF-α, inhibition of NF-κB and JNK did not alter glycerol content in supernatant, triglyceride content or insulin-stimulated phosphorylation of protein kinase B. In the presence of TNF-α, inhibition of NF-κB and JNK alleviated TNF-α-induced apoptosis, insulin insensitivity and lipolysis. Overall, TNF-α impairs insulin sensitivity and induces lipolysis and apoptosis in bovine adipocytes, which may be partly mediated by activation of NF-κB and JNK. Thus, the data suggested that NF-κB and JNK are potential therapeutic targets for alleviating lipolysis dysregulation and insulin resistance in adipocytes.

Effects of co-exposure to lead and manganese on learning and memory deficits.

Lead (Pb) and manganese (Mn) are common neurotoxins. However, individuals are subject to co-exposures in real life, and it is therefore important to study these metals in combination. Weaning Sprague-Dawley rats were given ad libitum access to drinking water solutions containing Pb (100 mg/L), Mn (2.5 mg/mL) or a mixture, and each treatment had its own minocycline (50 mg/(kg•day)) supplement group. The results showed a significant difference in spatial memory and induction levels of hippocampal long-term potentiation (LTP) in all exposure groups when compared with controls. The combined-exposure group exhibited the most pronounced effect when compared with each of the single-metal exposure groups. Microglia displayed activation at day 3 after exposure alone or in combination, while astrocytes showed activation at day 5, accompanied by decreased expression levels of GLAST, GLT-1, and GS. Furthermore, the levels of glutamate in the synaptic cleft increased significantly. When microglial activation was inhibited by minocycline, the activation of astrocytes and the expression of GLAST, GLT-1, and GS were both reversed. In addition, upon minocycline treatment, hippocampal LTP impairment and cognitive injury were significantly alleviated in each of the exposure groups. These results suggest that combined exposure to Pb and Mn can cause greater effects on cognition and synaptic plasticity when compared to single-metal exposure groups. The reason may involve abnormal activation of microglia leading to excessive regulation of astrocytes, resulting in glutamate reuptake dysfunction in astrocytes and leading to perturbed cognition and synaptic plasticity.

The influence of hypoglycemia on the specific quality of life in type 2 diabetes mellitus: a comparative cross-sectional study of diabetics with and without hypoglycemia in Xi'an, China.

PURPOSE: This study aims to explore the incidence of hypoglycemia in patients with type 2 diabetes mellitus (T2DM) and the influence of hypoglycemia on the specific quality of life in T2DM patients. METHODS: It was a comparative cross-sectional study consisting of 519 T2DM patients in Xi'an, China and patients were investigated by self-reported hypoglycemia and specific quality of life questionnaires from September 2019 to January 2020. Descriptive analysis, t-test, Chi-square test, hierarchical regression analysis and stepwise multiple regression analysis were applied to assess the influence of hypoglycemia on the specific quality of life. RESULTS: The incidence of hypoglycemia in T2DM patients was 32.18%. The mean score of specific quality of life in diabetes without hypoglycemia was 57.33 ± 15.36 and was 61.56 ± 17.50 in those with hypoglycemia, which indicated that hypoglycemia had a serious impact on the quality of life of diabetics (t = - 5.172, p = 0.000). In the Univariate analysis of specific quality of life, age, education background, marital status, living status, duration of diabetes, monthly income per capita were independent and significant factors associated with specific quality of life of two groups of T2DM patients (p < 0.05). In the hierarchical regression analysis, the duration of the diabetes more than 11 years and the frequency of hypoglycemia more than 6 times in half a year entered the equation of specific quality of life of 519 diabetics respectively (p < 0.001). In multiple linear regression analysis, age, marital status and income all entered the regression equation of quality of life of the two groups (p < 0.05). CONCLUSION: Hypoglycemia will have a serious impact on the quality of life of T2DM patients. In order to improve the living quality in diabetics, effective measurements should be taken to strengthen the management of blood glucose and to avoid hypoglycemia.

Riverside underwater noise pollution threaten porpoises and fish along the middle and lower reaches of the Yangtze River, China.

The Yangtze River exhibits a high biodiversity and plays an important role in global biodiversity conservation. As the world's busiest inland river in regard to shipping, little attention has been paid to underwater noise pollution. In 2017, the underwater noise level in 25 riverside locations along the middle and lower reaches of the Yangtze River mainly at night time were investigated by using passive acoustic monitoring method. Approximately 88% and 40% of the sampled sites exhibit noise levels exceeding the underwater acoustic thresholds of causing responsiveness and temporary threshold shift, respectively, in cetacean. Noise pollution may impose a high impact on fish with physostomous swim bladders and Weberian ossicles, such as silver carp, bighead carp, goldfish and common carp, whereas it may affect fish with physoclistous swim bladders and without Weberian ossicles, such as lake sturgeon and paddlefish, to a lesser extent. Noise levels reductions of approximately 10 and 20 dB were observed in the middle and lower reaches, respectively, of the Yangtze River over the 2012 level. The green development mode of the ongoing construction of green shipping in the Yangtze River Economic Belt, including the development of green shipping lanes, ports, ships and transportation organizations, may account for the alleviated underwater noise pollution. Follow-up noise mitigation endeavors, such as the extension of ship speed restrictions and the study and implementation of the optimal navigation speed in ecologically important areas, are required to further reduce the noise level in the Yangtze River to protect local porpoises and fish.

Tapered elasticæ as a route for axisymmetric morphing structures.

Transforming flat two-dimensional (2D) sheets into three-dimensional (3D) structures by combining carefully made cuts with applied edge-loads has emerged as an exciting manufacturing paradigm in a range of applications from mechanical metamaterials to flexible electronics. In Kirigami, patterns of cuts are introduced that allow solid faces to rotate about each other, deforming in three dimensions whilst remaining planar. In other scenarios, however, the solid elements bend in one direction. In this paper, we model such bending deformations using the formulation of an elastic strip whose thickness and width are tapered (the 'tapered elastica'). We show how this framework can be exploited to design the tapering patterns required to create planar sheets that morph into desired axisymmetric 3D shapes under a combination of horizontal and vertical edge-loads. We exhibit this technique by recreating miniature structures with positive, negative, and variable apparent Gaussian curvatures. With sheets of constant thickness, the resulting morphed shapes may leave gaps between the deformed elements. However, by tapering the thickness of the sheet too, these gaps can be closed, creating tessellated three-dimensional structures. Our theoretical approaches are verified by both numerical simulations and physical experiments.

Cracking to curling transition in drying colloidal films.

Drying-induced cracking is widely encountered in nature and is of fundamental interest in industrial applications. During desiccation, the evolution of water content is nonlinear. Considering the inhomogeneous procedure of desiccation, it is worth considering whether water content will affect the crack pattern formation. To address this concern, in this paper, we report an experimental investigation on the effect of water content on the failure mode in drying colloidal films. A distinct failure transition from random cracking to curling is found when the initial water content increases gradually. When the water content is below a critical value for given film thickness, random desiccation cracking driven by shrinkage is observed. Beyond this critical water content, the film curls with the advent of several main cracks. It is also found that the critical water content corresponding to the transition point depends on the film thickness. In order to qualitatively interpret the experimental observation, a theoretical model is established by adopting the fracture mechanics based on the energy method. The model is found to agree well with the experimental results, elucidating the effects of initial water content on the crack patterns and the transition of failure modes.

Higher photosynthesis, nutrient- and energy-use efficiencies contribute to invasiveness of exotic plants in a nutrient poor habitat in northeast China.

The roles of photosynthesis-related traits in invasiveness of introduced plant species are still not well elucidated, especially in nutrient-poor habitats. In addition, little effort has been made to determine the physiological causes and consequences of the difference in these traits between invasive and native plants. To address these problems, we compared the differences in 16 leaf functional traits related to light-saturated photosynthetic rate (Pmax ) between 22 invasive and native plants in a nutrient-poor habitat in northeast China. The invasive plants had significantly higher Pmax , photosynthetic nitrogen- (PNUE), phosphorus- (PPUE), potassium- (PKUE) and energy-use efficiencies (PEUE) than the co-occurring natives, while leaf nutrient concentrations, construction cost (CC) and specific leaf area were not significantly different between the invasive and native plants. The higher PNUE contributed to higher Pmax for the invasive plants, which in turn contributed to higher PPUE, PKUE and PEUE. CC changed independently with other traits such as Pmax , PNUE, PPUE, PKUE and PEUE, showing two trait dimensions, which may facilitate acclimation to multifarious niche dimensions. Our results indicate that the invasive plants have a superior resource-use strategy, i.e. higher photosynthesis under similar resource investments, contributing to invasion success in the barren habitat.