Fabrication of Self-Wrinkling Polymer Films with Tunable Patterns through an Interfacial-Fuming-Induced Surface Instability Process.

Inspired by the superglue fuming method for fingerprint collection, this study developed a novel interfacial-fuming-induced surface instability process to generate wrinkled patterns on polymeric substrates. High-electronegativity groups are introduced on the substrate surface to initiate the polymerization of monomer vapors, such as ethyl cyanoacrylate, which results in the formation of a stiff poly(ethyl cyanoacrylate) capping layer. Moreover, interfacial polymerization resulted in the covalent bonding of the substrate, which led to the volumetric shrinkage of the composite and the accumulation of compressive strain. This process ultimately resulted in the development and stabilization of wrinkled surface morphologies. The authors systematically examined parameters such as the modulus of the epoxy substrate, prestrain, the flow rate of fuming, and operating temperature. The aforementioned technique can be easily applied to architectures with complex outer morphologies and inner surfaces, thereby enabling the construction of surface patterns under ambient conditions without vacuum limitations or precise process control. This study is the first to combine fuming-induced interfacial polymerization with surface instability to create robust wrinkles. The proposed method enables the fabrication of intricate microwrinkled patterns and has considerable potential for use in various practical applications, including microfluidics, optical components, bioinspired adhesive devices, and interfacial engineering.

The kinase GLK controls autoimmunity and NF-κB signaling by activating the kinase PKC-θ in T cells.

Protein kinase C-θ (PKC-θ) is required for activation of the transcription factor NF-κB induced by signaling via the T cell antigen receptor (TCR); however, the direct activator of PKC-θ is unknown. We report that the kinase GLK (MAP4K3) directly activated PKC-θ during TCR signaling. TCR signaling activated GLK by inducing its direct interaction with the upstream adaptor SLP-76. GLK-deficient mice had impaired immune responses and were resistant to experimental autoimmune encephalomyelitis. Consistent with that, people with systemic lupus erythematosus had considerable enhanced GLK expression and activation of PKC-θ and the kinase IKK in T cells, and the frequency of GLK-overexpressing T cells was directly correlated with disease severity. Thus, GLK is a direct activator of PKC-θ, and activation of GLK-PKC-θ-IKK could be used as new diagnostic biomarkers and therapeutic targets for systemic lupus erythematosus.

A distinct sensitivity to the priming effect between labile and stable soil organic carbon.

Soil organic carbon (SOC) is a mixture of various carbon (C) compounds with different stability, which can be distinctly affected by the priming effect (PE). However, little is known about how the PE changes with SOC stability. We address this issue by combining results from two experiments and a metaanalysis. We found that the PE increased with the prolongation of soil preincubation, suggesting that higher PE occurred for more stable SOC than for labile SOC. This was further supported by the metaanalysis of 42 observations. There were significant negative relationships between the difference in PE (ΔPE) between labile and more stable SOC and their differences in SOC, microbial biomass C and soil C : N ratio, indicating that soil C availability exerts a vital control on ΔPE. We conclude that, compared with labile SOC, stable SOC can be more vulnerable to priming once microbes are provided with exogenous C substrates. This high vulnerability of stable SOC to priming warrants more attention in future studies on SOC cycling and global change.

Peer Victimization Trajectory and Psychosocial Maladjustment in Early Taiwanese Adolescents: A Longitudinal Study.

This study examined the peer victimization trajectory and maladjustment outcomes among early Taiwanese adolescents. Data were extracted from a large-scale longitudinal study with a national representative sample. A total of 1691 school students in 4th, 6th, and 8th grade were analyzed. Using latent profile analysis, students were classified into four trajectories, chronic victims, late onset victims, desisters, and non-victims, based on their self-reported physical and verbal victimization at three time points. Maladjustment, including psychological distress, reduced school attachment, internet addiction, and suicidal ideation in 8th grade, were assessed. The results showed significant differences in adjustment among students in the four trajectories. Chronic victims had the poorest outcomes on most variables, followed by late onset victims and desisters, while non-victims had the least maladjustment. The findings highlight the need for future interventions that would consider students' victim status over time and pay particular attention to those who suffer constant bullying and abuse.

Genetic variation in catechol-O-methyltransferase is associated with individual differences in conditioned pain modulation in healthy subjects.

BACKGROUND: Genetic variation in the catechol-O-methyltransferase (COMT) gene is associated with sensitivity to both acute experimental pain and chronic pain conditions. Four single nucleotide polymorphisms (SNPs) have traditionally been used to infer three common haplotypes designated as low, average and high pain sensitivity and are reported to affect both COMT enzymatic activity and pain sensitivity. One mechanism that may partly explain individual differences in sensitivity to pain is conditioned pain modulation (CPM). We hypothesized that variation in CPM may have a genetic basis. METHODS: We evaluated CPM in 77 healthy pain-free Caucasian subjects by applying repeated mechanical stimuli to the dominant forearm using 26-g von Frey filament as the test stimulus with immersion of the non-dominant hand in hot water as the conditioning stimulus. We assayed COMT SNP genotypes by the TaqMan method using DNA extracted from saliva. RESULTS: SNP rs4680 (val158 met) was not associated with individual differences in CPM. However, CPM was associated with COMT low pain sensitivity haplotypes under an additive model (p = 0.004) and the effect was independent of gender. CONCLUSIONS: We show that, although four SNPs are used to infer COMT haplotypes, the low pain sensitivity haplotype is determined by SNP rs6269 (located in the 5' regulatory region of COMT), suggesting that inherited variation in gene expression may underlie individual differences in pain modulation. Analysis of 13 global populations revealed that the COMT low pain sensitivity haplotype varies in frequency from 13% to 44% and showed that two SNPs are sufficient to distinguish all COMT haplotypes in most populations.

Applying Hierarchy of Expert Performance (HEP) to investigative interview evaluation: strengths, challenges and future directions.

The purpose of this paper is to systematically examine the research literature on the decision of expert interviewers within the theoretical framework of the Hierarchy of Expert Performance (HEP). After providing an overview of the HEP framework, existing research in the investigative interviewing at each of the eight levels of the HEP framework is reviewed. The results identify areas of strength in reliability between experts' observations (Level 2) and of weakness in reliability between experts' conclusions (Level 6). Biases in investigative interview experts' decision making is also revealed at biasability between expert conclusions (Level 8). Moreover, no published data are available in reliability within experts at the level of observations (Level 1) or conclusions (Level 5), biasability within or between expert observations (Level 3 and 4) and biasability within expert conclusions (Level 7). The findings highlight areas where future research and practical endeavour are much needed for the investigative interview.

A Single Session of Heart Rate Variability Biofeedback Produced Greater Increases in Heart Rate Variability Than Autogenic Training.

Heart rate variability biofeedback (HRV-BF) has been confirmed to increase heart rate variability (HRV) and cardiac outflows by baroreflex in healthy populations and clinical patients. Autogenic training (AT) is common used in the psychological intervention. This study integrates a single-session of HRV-BF and AT into a high-technology mobile application (app), and examines the effects on HRV indices, breathing rates, and subjective relaxation scores. Healthy college students were recruited and assigned to the single-session HRV-BF group or AT group. Participants in the HRV-BF group received HRV-BF combined with paced breathing training, which gradually stepped down their breathing rates from 12, to 8, to 6 breaths/per min; and received feedback of HRV indices from the app. Participants in the AT group received autogenic training and feedback of heart rate from the app. A chest belt Zephyr BioHarness was connected through Bluetooth to a Zenfone5 mobile phone, it collected the signals of interbeat intervals and breathing rates at pre-training, mid-training, and post-training stages. The Kubios HRV software was used to analyze HRV indices. The results reveal higher HRV indices and lower breathing rates during mid-training and post-training in the HRV-BF group compared to the AT group. There were higher high-frequency of HRV at post-training than pre-training in the AT group. Participants of both groups increased their subjective relaxation scores after training. The HRV-BF protocol increased cardiac outflows by baroreflex and decreased breathing rates, and the AT protocol increased high-frequency of HRV. These high-technology wearable devices combined with psychological interventions will apply to various populations in the future.

Associations Between Parenting Styles and Perceived Child Effortful Control Within Chinese Families in the United States, the United Kingdom, and Taiwan.

The current study examined the associations between parentally perceived child effortful control (EC) and the parenting styles of 122 Chinese mothers (36 first-generation Chinese immigrants in the United Kingdom, 40 first-generation Chinese immigrants in the United States, and 46 Taiwanese mothers) of 5- to 7-year-old (M age = 5.82 years, SD = .805; 68 boys and 54 girls) children. The findings showed significant cultural group differences in mothers' reported authoritarian parenting style. Significant associations also emerged between mothers' reports of their children's EC and some parenting dimensions, although there were no cultural group differences in perceived child EC. Different patterns of associations between perceived child EC and parenting styles in these three groups also demonstrated heterogeneity within the Chinese population, and highlighted the need to consider differences between original and receiving societies when seeking to understand parenting and child development in different immigrant groups.

Dual-specificity phosphatase 14 (DUSP14/MKP6) negatively regulates TCR signaling by inhibiting TAB1 activation.

T cell activation is dependent upon phosphorylation of MAPKs, which play a critical role in the regulation of immune responses. Dual-specificity phosphatase 14 (DUSP14; also known as MKP6) is classified as a MAPK phosphatase. The in vivo functions of DUSP14 remain unclear. Thus, we generated DUSP14-deficient mice and characterized the roles of DUSP14 in T cell activation and immune responses. DUSP14 deficiency in T cells resulted in enhanced T cell proliferation and increased cytokine production upon T cell activation. DUSP14 directly interacted with TGF-ß-activated kinase 1 (TAK1)-binding protein 1 (TAB1) and dephosphorylated TAB1 at Ser(438), leading to TAB1-TAK1 complex inactivation in T cells. The phosphorylation levels of the TAB1-TAK1 complex and its downstream molecules, including JNK and IκB kinase, were enhanced in DUSP14-deficient T cells upon stimulation. The enhanced JNK and IκB kinase activation in DUSP14-deficient T cells was attenuated by TAB1 short hairpin RNA knockdown. Consistent with that, DUSP14-deficient mice exhibited enhanced immune responses and were more susceptible to experimental autoimmune encephalomyelitis induction. Thus, DUSP14 negatively regulates TCR signaling and immune responses by inhibiting TAB1 activation.

Endoluminal release of ureteral ligature after hysterectomy.

Iatrogenic ureteral injury is a well-recognized complication of abdominal total hysterectomy. We report a case of a 57-year-old female who underwent abdominal total hysterectomy for a uterine myoma and experienced severe right flank pain postoperatively. The imaging study displayed an obstruction of the right distal ureter. Under ureteroscopy, an extraluminal ligature was released with a holmium:yttrium-aluminum-garnet laser. The stenotic segment was immediately relieved. Two months later, the intravenous urogram illustrated patency of the distal ureter with regression of right hydronephrosis. There was no recurrent hydronephrosis during 1 year of follow-up.

53BP1 facilitates long-range DNA end-joining during V(D)J recombination.

Variable, diversity and joining (V(D)J) recombination and class-switch recombination use overlapping but distinct non-homologous end joining pathways to repair DNA double-strand-break intermediates. 53BP1 is a DNA-damage-response protein that is rapidly recruited to sites of chromosomal double-strand breaks, where it seems to function in a subset of ataxia telangiectasia mutated (ATM) kinase-, H2A histone family member X (H2AX, also known as H2AFX)- and mediator of DNA damage checkpoint 1 (MDC1)-dependent events. A 53BP1-dependent end-joining pathway has been described that is dispensable for V(D)J recombination but essential for class-switch recombination. Here we report a previously unrecognized defect in the joining phase of V(D)J recombination in 53BP1-deficient lymphocytes that is distinct from that found in classical non-homologous-end-joining-, H2ax-, Mdc1- and Atm-deficient mice. Absence of 53BP1 leads to impairment of distal V-DJ joining with extensive degradation of unrepaired coding ends and episomal signal joint reintegration at V(D)J junctions. This results in apoptosis, loss of T-cell receptor alpha locus integrity and lymphopenia. Further impairment of the apoptotic checkpoint causes propagation of lymphocytes that have antigen receptor breaks. These data suggest a more general role for 53BP1 in maintaining genomic stability during long-range joining of DNA breaks.

Taurine Rescues Cancer-induced Atrophy in Human Skeletal Muscle Cells via Ameliorating the Inflammatory Tumor Microenvironment.

BACKGROUND/AIM: Cancer cachexia is a wasting syndrome that has a devastating impact on the prognosis of patients with cancer. It is well-documented that pro-inflammatory cytokines are involved in the progression of this disorder. Therefore, this study was conducted to investigate the protective effect of taurine, an essential nonprotein amino acid with great anti-inflammatory properties, in attenuating muscle atrophy induced by cancer. MATERIALS AND METHODS: Conditioned media (CM) derived from T24 human bladder carcinoma cells with or without 5 mM taurine were incubated with human skeletal muscle cells (HSkMCs) and their differentiation was examined. The intracellular reactive oxygen species (ROS), morphology, and the catabolic pathway were monitored. RESULTS: T24-derived CM with high levels of TNF-α and IL-6 caused aberrant ROS accumulation and formation of atrophic myotubes by HSkMCs. In T24 cancer cells, taurine significantly inhibited the production of TNF-α and IL-6. In HSkMCs, taurine increased ROS clearance during differentiation and preserved the myotube differentiation ability impaired by the inflammatory tumor microenvironment. In addition, taurine ameliorated myotube atrophy by regulating the Akt/FoxO1/MuRF1 and MAFbx signaling pathways. CONCLUSION: Taurine rescues cancer-induced atrophy in human skeletal muscle cells by ameliorating the inflammatory tumor microenvironment. Taurine supplementation may be a promising approach for intervening with the progression of cancer cachexia.

Fabrication of Stable Liquid-like Wetting Buckled Surfaces as Bioinspired Antibiofouling Coatings by Using Silicon-Containing Block Copolymers.

Inspired by animals with a slippery epidermis, durable slippery antibiofouling coatings with liquid-like wetting buckled surfaces are successfully constructed in this study by combining dynamic-interfacial-release-induced buckling with self-assembled silicon-containing diblock copolymer (diBCP). The core diBCP material is polystyrene-block-poly(dimethylsiloxane) (PS-b-PDMS). Because silicon-containing polymers with intrinsic characters of low surface energy, they easily flow over and cover a surface after it has undergone controlled thermal treatment, generating a slippery wetting layer on which can eliminate polar interactions with biomolecules. Additionally, microbuckled patterns result in curved surfaces, which offer fewer points at which organisms can attach to the surface. Different from traditional slippery liquid-infused porous surfaces, the proposed liquid-like PDMS wetting layer, chemically bonded with PS, is stable and slippery but does not flow away. PS-b-PDMS diBCPs with various PDMS volume fractions are studied to compare the influence of PDMS segment length on antibiofouling performance. The surface characteristics of the diBCPs─ease of processing, transparency, and antibiofouling, anti-icing, and self-cleaning abilities─are examined under various conditions. Being able to fabricate ecofriendly silicon-based lubricant layers without needing to use fluorinated compounds and costly material precursors is an advantage in industrial practice.

TBK1-associated protein in endolysosomes (TAPE)/CC2D1A is a key regulator linking RIG-I-like receptors to antiviral immunity.

Retinoic acid-inducible gene I (RIG-I)-like receptors (RLRs) are key RNA viral sensors for triggering antiviral immunity. The underlying mechanisms for RLRs to trigger antiviral immunity have yet to be explored. Here we report the identification of TAPE (TBK1-associated protein in endolysosomes) as a novel regulator of the RLR pathways. TAPE functionally and physically interacts with RIG-I, MDA5, and IPS-1 to activate the IFN-ß promoter. TAPE knockdown impairs IFN-ß activation induced by RLRs but not IPS-1. TAPE-deficient cells are defective in cytokine production upon RLR ligand stimulation. During RNA virus infection, TAPE knockdown or deficiency diminishes cytokine production and antiviral responses. Our data demonstrate a critical role for TAPE in linking RLRs to antiviral immunity.

Defects in coding joint formation in vivo in developing ATM-deficient B and T lymphocytes.

Ataxia-telangiectasia mutated (ATM)-deficient lymphocytes exhibit defects in coding joint formation during V(D)J recombination in vitro. Similar defects in vivo should affect both T and B cell development, yet the lymphoid phenotypes of ATM deficiency are more pronounced in the T cell compartment. In this regard, ATM-deficient mice exhibit a preferential T lymphopenia and have an increased incidence of nontransformed and transformed T cells with T cell receptor alpha/delta locus translocations. We demonstrate that there is an increase in the accumulation of unrepaired coding ends during different steps of antigen receptor gene assembly at both the immunoglobulin and T cell receptor loci in developing ATM-deficient B and T lymphocytes. Furthermore, we show that the frequency of ATM-deficient alphabeta T cells with translocations involving the T cell receptor alpha/delta locus is directly related to the number of T cell receptor alpha rearrangements that these cells can make during development. Collectively, these findings demonstrate that ATM deficiency leads to broad defects in coding joint formation in developing B and T lymphocytes in vivo, and they provide a potential molecular explanation as to why the developmental impact of these defects could be more pronounced in the T cell compartment.

DUSP4 deficiency enhances CD25 expression and CD4+ T-cell proliferation without impeding T-cell development.

The differentiation and activation of T cells are critically modulated by MAP kinases, which are in turn feed-back regulated by dual-specificity phosphatases (DUSPs) to determine the duration and magnitude of MAP kinase activation. DUSP4 (also known as MKP2) is a MAP kinase-induced DUSP member that is dynamically expressed during thymocyte differentiation. We generated DUSP4-deficient mice to study the function of DUSP4 in T-cell development and activation. Our results show that thymocyte differentiation and activation-induced MAP kinase phosphorylation were comparable between DUSP4-deficient and WT mice. Interestingly, activated DUSP4(-/-) CD4(+) T cells were hyperproliferative while DUSP4(-/-) CD8(+) T cells proliferated normally. Further mechanistic studies suggested that the hyperproliferation of DUSP4(-/-) CD4(+) T cells resulted from enhanced CD25 expression and IL-2 signaling through increased STAT5 phosphorylation. Immunization of DUSP4(-/-) mice recapitulated the T-cell hyperproliferation phenotype in antigen recall responses, while the profile of Th1/Th2-polarized antibody production was not altered. Overall, these results suggest that other DUSPs may compensate for DUSP4 deficiency in T-cell development, MAP kinase regulation, and Th1/Th2-mediated antibody responses. More importantly, our data indicate that DUSP4 suppresses CD4(+) T-cell proliferation through novel regulations in STAT5 phosphorylation and IL-2 signaling.

Berezinskii-Kosterlitz-Thouless transition from neural network flows.

We adopt the neural network (NN) flow method to study the Berezinskii-Kosterlitz-Thouless (BKT) phase transitions of the two-dimensional q-state clock model with q≥4. The NN flow consists of a sequence of the same units that proceed with the flow. This unit is a variational autoencoder trained by the data of Monte Carlo configurations in unsupervised learning. To gauge the difference among the ensembles of Monte Carlo configurations at different temperatures and the uniqueness of the ensemble of NN-flow states, we adopt the Jensen-Shannon divergence (JSD) as the information-distance measure "thermometer." This JSD thermometer compares the probability distribution functions of the mean spin value of two ensembles of states. Our results show that the NN flow will flow an arbitrary spin state to some state in a fixed-point ensemble of states. The corresponding JSD of the fixed-point ensemble takes a unique profile with peculiar features, which can help to identify the critical temperatures of BKT phase transitions of the underlying Monte Carlo configurations.

Patterns and trajectories of children's maltreatment experiences in Taiwan: Latent transition analysis of a nationally representative longitudinal study.

BACKGROUND: Little is known about the patterns of child maltreatment change over time and vary according to gender and child protective services (CPS) experience in Taiwan. OBJECTIVE: To examine the latent status and the trajectories of child maltreatment and to identify effects that gender and CPS have on these statuses and trajectories in Taiwan. PARTICIPANTS AND SETTING: A national proportionately stratified sample of 6233 4th-grade students were recruited from 314 elementary schools in Taiwan, and followed up at 6th and 8th graders. A total of 1908 students completed valid data at all three time points was analyzed. METHODS: Latent class analysis and latent transition analysis were used to identify the number of latent variables and the patterns of child maltreatment. Multiple-group model was used to test with gender difference. RESULTS: Four latent maltreatment statuses were identified: high all maltreatment, high psychological maltreatment, high neglect, and no/low maltreatment. A reduction in maltreatment severity occurred over time was found. The percentage of students in the "high all maltreatment" and "high neglect" groups decreased whereas those in the "high psychological maltreatment" and "no/low maltreatment" groups increased. Differences in the transition probabilities of latent maltreatment status by gender was revealed. The percentage of CPS recipients in the "high all maltreatment" decreased over time. CONCLUSIONS: This study highlighted the dynamic nature of child maltreatment and described the timing, continuity, and change that characterizes children's exposure to maltreatment in Taiwan. Policies and interventions geared toward early detection, mitigation, and prevention of child maltreatment are needed.

ATM stabilizes DNA double-strand-break complexes during V(D)J recombination.

The ATM (ataxia-telangiectasia mutated) protein kinase mediates early cellular responses to DNA double-strand breaks (DSBs) generated during metabolic processes or by DNA-damaging agents. ATM deficiency leads to ataxia-telangiectasia, a disease marked by lymphopenia, genomic instability and an increased predisposition to lymphoid malignancies with chromosomal translocations involving lymphocyte antigen receptor loci. ATM activates cell-cycle checkpoints and can induce apoptosis in response to DNA DSBs. However, defects in these pathways of the DNA damage response cannot fully account for the phenotypes of ATM deficiency. Here, we show that ATM also functions directly in the repair of chromosomal DNA DSBs by maintaining DNA ends in repair complexes generated during lymphocyte antigen receptor gene assembly. When coupled with the cell-cycle checkpoint and pro-apoptotic activities of ATM, these findings provide a molecular explanation for the increase in lymphoid tumours with translocations involving antigen receptor loci associated with ataxia-telangiectasia.