Coronin 1B regulates the TNFα-induced apoptosis of HUVECs by mediating the interaction between TRADD and FADD.

Coronin 1B is an actin-binding protein that plays important roles in actin-dependent cellular processes. We previously reported that coronin 1B is involved in vascular endothelial cell growth factor-induced migration of human umbilical vein endothelial cells (HUVECs). However, the role of coronin 1B in tumor necrosis factor alpha (TNFα)-induced endothelial cell apoptosis remained unknown. In this study, we investigated whether coronin 1B affects TNFα-induced HUVEC apoptosis and sought to elucidate the mechanism by which coronin 1B regulates this cellular process. Depletion of coronin 1B by siRNA transfection decreased TNFα-induced apoptosis of HUVECs, as determined by MTT, terminal deoxynucleotidyl transferase dUTP nick end labeling and caspase-3 activity assays. Coronin 1B depletion also decreased caspase-8 cleavage via a JNK-independent pathway. Coronin 1B interacted with Fas-associated death domain protein (FADD) in both a plasmid overexpression system in HEK293T cells and at the endogenous protein level in TNFα-stimulated HUVECs. Immunoprecipitation and in situ proximity ligation assays showed that coronin 1B depletion diminished the interaction between TNFα-induced TNF receptor-1-associated death domain protein (TRADD) and FADD, suggesting that coronin 1B is required for the TNFα-induced TRADD and FADD interaction and subsequent caspase-8/caspase-3 cascade activation, ultimately leading to apoptosis.

Binding of coronin 1B to TßRI negatively regulates the TGFß1 signaling pathway.

Coronin 1B is an actin-binding protein that regulates several actin-dependent cellular processes including migration and endocytosis. However, the role of coronin 1B in the tumor growth factor (TGF)ß signaling pathway is largely unknown. Here, we investigated whether coronin 1B affects the TGFß signaling cascade and found that coronin 1B negatively regulates the TGFß signaling pathway. Immunoprecipitation and glutathione-S-transferase-pulldown assays revealed that coronin 1B directly associated with TGFß receptor I (TßRI). Overexpression of coronin 1B inhibited the TGFß1-induced interaction between TßRI and Smad2/3 in plasmid-transfected HEK293T cells. Coronin 1B was basally bound to TßRI in vascular smooth muscle cells (VSMCs), but TGFß1 stimulation did not affect their association, suggesting constitutive binding between coronin 1B and TßRI. Overexpression of coronin 1B suppressed TGFß1-induced activation of a Smad-binding element-luciferase reporter construct and a plasminogen activator inhibitor (PAI)-1 promoter-luciferase reporter construct in HEK293T cells. By contrast, depletion of coronin 1B by siRNA transfection increased TGFß1-induced Smad2/3 phosphorylation and PAI-1 expression in VSMCs. These results suggest that coronin 1B regulates the TGFß1 signaling cascade by constitutively interacting with TßRI and inhibiting the binding of Smad2/3 to TßRI in response to TGFß1 stimulation.

CHOP deficiency prevents methylglyoxal-induced myocyte apoptosis and cardiac dysfunction.

Epidemiological studies indicate that methylglyoxal (MGO) plasma levels are closely linked to diabetes and the exacerbation of diabetic cardiovascular complications. Recently, it was established that endoplasmic reticulum (ER) stress importantly contributes to the pathogenesis of diabetes and its cardiovascular complications. The objective of this study was to explore the mechanism by which diabetes instigates cardiomyocyte apoptosis and cardiac dysfunction via MGO-mediated myocyte apoptosis. Intriguingly, the MGO activated unfolded protein response pathway accompanying apoptotic events, such as cleavages of PARP-1 and caspase-3. In addition, Western blot analysis revealed that MGO-induced myocyte apoptosis was inhibited by depletion of CHOP with siRNA against Ddit3, the gene name for rat CHOP. To investigate the physiologic roles of CHOP in vivo, glucose tolerance and cardiac dysfunction were assessed in CHOP-deficient mice. No significant difference was observed between CHOP KO and littermate naïve controls in terms of the MGO-induced impairment of glucose tolerance. In contrast, myocyte apoptosis, inflammation, and cardiac dysfunction were significantly diminished in CHOP KO compared with littermate naïve controls. These results showed that CHOP is the key signal for myocyte apoptosis and cardiac dysfunction induced by MGO. These findings suggest a therapeutic potential of CHOP inhibition in the management of diabetic cardiovascular complications including diabetic cardiomyopathy.

Memristive Monte Carlo DropConnect crossbar array enabled by device and algorithm co-design.

Device and algorithm co-design aims to develop energy-efficient hardware that directly implements complex algorithms and optimizes algorithms to match the hardware's characteristics. Specifically, neuromorphic computing algorithms are constantly growing in complexity, necessitating an ongoing search for hardware implementations capable of handling these intricate algorithms. Here, we present a memristive Monte Carlo DropConnect (MC-DC) crossbar array developed through a hardware algorithm co-design approach. To implement the MC-DC neural network, stochastic switching and analog memory characteristics are required, and we achieved them using Ag-based diffusive selectors and Ru-based electrochemical metalization (ECM) memristors, respectively. The devices were integrated with a one-selector one-memristor (1S1M) structure, and their well-matched operating voltages and currents enabled stochastic readout and deterministic analog programming. With the integrated hardware, we successfully demonstrated the MC-DC operation. Additionally, the selector allowed for the control of switching polarity, and by understanding this hardware characteristic, we were able to modify the algorithm to fit it and further improve the network performance.

Stochastic switching and analog-state programmable memristor and its utilization for homomorphic encryption hardware.

Homomorphic encryption performs computations on encrypted data without decrypting, thereby eliminating security issues during the data communication between clouds and edges. As a result, there is a growing need for homomorphic encryption hardware (HE-HW) for the edges, where low power consumption and a compact form factor are desired. Here, a Pt/Ta2O5/Mo metallic cluster-type memristors (Mo-MCM) characterized by the Mo as a mobile species, and its utilization for the HE-HW via a 1-trasistor-1-memristor (1T1M) array as a prototype HE-HW is proposed. The Mo-MCM exhibits inherent stochastic set-switching behavior, which can be utilized for generating the random numbers required for encryption key generation. Furthermore, the device can accurately store analog conductance states after set-switching, which can be used as an analog non-volatile memristor. By simultaneously leveraging these two characteristics, encryption key generation, data encryption, and decryption are possible within a single device through an in-memory computing manner.

Fully Memristive Elementary Motion Detectors for a Maneuver Prediction.

Insects can efficiently perform object motion detection via a specialized neural circuit, called an elementary motion detector (EMD). In contrast, conventional machine vision systems require significant computational resources for dynamic motion processing. Here, a fully memristive EMD (M-EMD) is presented that implements the Hassenstein-Reichardt (HR) correlator, a biological model of the EMD. The M-EMD consists of a simple Wye (Y) configuration, including a static resistor, a dynamic memristor, and a Mott memristor. The resistor and dynamic memristor introduce different signal delays, enabling spatio-temporal signal integration in the subsequent Mott memristor, resulting in a direction-selective response. In addition, a neuromorphic system is developed employing the M-EMDs to predict a lane-changing maneuver by vehicles on the road. The system achieved a high accuracy (> 87%) in predicting future lane-changing maneuvers on the Next Generation Simulation (NGSIM) dataset while reducing the computational cost by 92.9% compared to the conventional neuromorphic system without the M-EMD, suggesting its strong potential for edge-level computing.

Methionine sulfoxide reductase B2 protects against cardiac complications in diabetes mellitus.

Diabetes mellitus (DM) is a progressive, chronic metabolic disorder characterized by high oxidative stress, which can lead to cardiac damage. Methionine sulfoxylation (MetO) of proteins by excessive reactive oxygen species (ROS) can impair the basic functionality of essential cellular proteins, contributing to heart failure. Methionine sulfoxide reductase B2 (MsrB2) can reverse oxidation induced MetO in mitochondrial proteins, so we investigated its role in diabetic cardiomyopathy. We observed that DM-induced heart damage in diabetic mice model is characterized by increased ROS, increased protein MetO with mitochondria structural pathology, and cardiac fibrosis. In addition, MsrB2 was significantly increased in mouse DM cardiomyocytes, supporting the induction of a protective process. Further, MsrB2 directly induces Parkin and LC3 activation (mitophagy markers) in cardiomyocytes. In MsrB2, knockout mice displayed abnormal electrophysiological function, as determined by ECG analysis. Histological analysis confirmed increased cardiac fibrosis and disrupted cardiac tissue in MsrB2 knockout DM mice. We then corroborated our findings in human DM heart samples. Our study demonstrates that increased MsrB2 expression in the heart protects against diabetic cardiomyopathy.

p62 binding to protein kinase C ζ regulates tumor necrosis factor α-induced apoptotic pathway in endothelial cells.

OBJECTIVE: Protein kinase C (PKC) ζ is a key pathological mediator of endothelial cell apoptosis. p62 is a scaffold protein that regulates several cell signaling pathways by binding to target proteins. Because PKCζ and p62 contain Phox/Bem1p (PB1) modules that mediate protein-protein interactions, we hypothesized that an interaction between p62 and PKCζ is required for tumor necrosis factor α-induced PKCζ signaling in endothelial cells. METHODS AND RESULTS: In human umbilical vein endothelial cell, tumor necrosis factor α (10 ng/mL) enhanced the interaction between p62 and PKCζ. Transfection with p62 small interfering RNA reduced the activation of both PKCζ and its downstream targets JNK and caspase 3, suggesting that p62 is necessary for PKCζ signaling. Overexpression of only the PB1 domain of p62 inhibited p62-PKCζ interaction, showing that binding of these 2 proteins is mediated by their PB1 domains. Furthermore, overexpression of the p62 PB1 domain suppressed tumor necrosis factor α-induced PKCζ activation and subsequent activation of JNK and caspase 3. Finally, transfection of either p62 small interfering RNA or the PB1 domain of p62 inhibited human umbilical vein endothelial cell apoptosis. CONCLUSIONS: Our results suggest a novel function of p62 that regulates the activity of PKCζ by binding to PKCζ, thereby activating the PKCζ-JNK-caspase 3 apoptotic pathway in endothelial cells.

Psychological essentialism among Korean children and adults: a modified replication study.

Developmental psychologists have shown interest in the development of psychological essentialism among children; that is, a belief that certain psychological characteristics (such as personality) are relatively stable and unchanging. Although previous studies have shown that children are essentialistic about human traits, and the coherence among various essentialism dimensions increases with age, moderating cultural factors in the development of essentialism, especially among Asian children, have received little attention. Using the methodologies of Gelman, Heyman, and Legare (2007), levels of psychological essentialism among Korean children and adults were measured, and compared with the original US data. Results demonstrated cross-cultural similarity in the development of coherence in essentialistic thought, and difference in the level of essentialism among adult participants. The present findings imply that different cultural values between Asians and Westerners can play a role in the developmental trajectory of psychological essentialism.

Threshold Modulative Artificial GABAergic Nociceptor.

Gamma-aminobutyric acid (GABA) is a crucial inhibitory neurotransmitter of the central nervous system. It modifies the signal threshold of the nociceptor, allowing it to react to external stimuli in various circumstances. Thus, GABAergic behaviors are critical characteristics of adaptive behavior in life. Here, a threshold-modulative artificial GABAergic nociceptor is reported for the first time at a Pt/Ti/Nb2 O5- x /Al2 O3- y /Pt/Ti (top to bottom) of the double charge trapping structure. The Al2 O3- y layer contains deep defect states that function similarly to the GABA neurotransmitter in modulating the signal threshold. Meanwhile, the Nb2 O5- x layer traps volatile charges and produces nociceptive behaviors. The combined dynamics of the two layers readily offer threshold-modulative GABAergic nociceptive behaviors. Based on these GABAergic behaviors, a method of implementing hot- and cold-sensitive thermoreceptors is demonstrated and shows its potential applications in advanced sensory devices.

Retention Secured Nonlinear and Self-Rectifying Analog Charge Trap Memristor for Energy-Efficient Neuromorphic Hardware.

A memristive crossbar array (MCA) is an ideal platform for emerging memory and neuromorphic hardware due to its high bitwise density capability. A charge trap memristor (CTM) is an attractive candidate for the memristor cell of the MCA, because the embodied rectifying characteristic frees it from the sneak current issue. Although the potential of the CTM devices has been suggested, their practical viability needs to be further proved. Here, a Pt/Ta2 O5 /Nb2 O5- x /Al2 O3- y /Ti CTM stack exhibiting high retention and array-level uniformity is proposed, allowing a highly reliable selector-less MCA. It shows high self-rectifying and nonlinear current-voltage characteristics below 1 µA of programming current with a continuous analog switching behavior. Also, its retention is longer than 105 s at 150 °C, suggesting the device is highly stable for non-volatile analog applications. A plausible band diagram model is proposed based on the electronic spectroscopy results and conduction mechanism analysis. The self-rectifying and nonlinear characteristics allow reducing the on-chip training energy consumption by 71% for the MNIST dataset training task with an optimized programming scheme.

Proteomic analysis reveals activation of platelet- and fibrosis-related pathways in hearts of ApoE-/- mice exposed to diesel exhaust particles.

Air pollution is an environmental risk factor linked to multiple human diseases including cardiovascular diseases (CVDs). While particulate matter (PM) emitted by diesel exhaust damages multiple organ systems, heart disease is one of the most severe pathologies affected by PM. However, the in vivo effects of diesel exhaust particles (DEP) on the heart and the molecular mechanisms of DEP-induced heart dysfunction have not been investigated. In the current study, we attempted to identify the proteomic signatures of heart fibrosis caused by diesel exhaust particles (DEP) in CVDs-prone apolipoprotein E knockout (ApoE-/-) mice model using tandem mass tag (TMT)-based quantitative proteomic analysis. DEP exposure induced mild heart fibrosis in ApoE-/- mice compared with severe heart fibrosis in ApoE-/- mice that were treated with CVDs-inducing peptide, angiotensin II. TMT-based quantitative proteomic analysis of heart tissues between PBS- and DEP-treated ApoE-/- mice revealed significant upregulation of proteins associated with platelet activation and TGFß-dependent pathways. Our data suggest that DEP exposure could induce heart fibrosis, potentially via platelet-related pathways and TGFß induction, causing cardiac fibrosis and dysfunction.

Androgen receptor is up-regulated by a BLT2-linked pathway to contribute to prostate cancer progression.

The androgen receptor (AR) plays a central role in the development and progression of prostate cancer. AR expression is maintained throughout the progression of prostate cancer and is also associated with an aggressive, castration-resistant (CR) phenotype. Despite the critical roles of AR expression in prostate cancer progression, the exact signaling mechanism regulating AR expression remains unclear. In this study, we demonstrated that AR expression was increased by a low-affinity leukotriene B(4) receptor (BLT2)-linked pathway. We found that BLT2 was overexpressed in AR-positive prostate cancer cells, such as LNCaP cells, and BLT2 inhibition, using an inhibitor or siRNA knockdown, clearly attenuated AR expression and triggered apoptosis in these cells. These results suggest a role for BLT2 in AR expression and the survival of AR-positive prostate cancer cells. Moreover, we found that the NADPH oxidase family protein, Nox4, lay downstream of BLT2 and mediated the production of reactive oxygen species (ROS) and subsequent NF-κB stimulation, thereby inducing AR expression. Taken together, our results demonstrate that BLT2 plays a critical role in AR expression via a Nox4-ROS-NF-κB-linked pathway, thereby mediating the survival of AR-positive prostate cancer cells. Our findings point to BLT2 as a key regulator of AR expression and will contribute to the development of novel therapies for AR-positive prostate cancers, including androgen-responsive and CR prostate cancers.

Proinflammatory cytokine IL-1beta stimulates IL-8 synthesis in mast cells via a leukotriene B4 receptor 2-linked pathway, contributing to angiogenesis.

Recent studies have suggested that mast cells have critical roles in angiogenesis. However, the detailed mechanism by which mast cells contribute to angiogenesis is not yet clearly understood, especially in response to proinflammatory cytokines. In this study, we showed that the proinflammatory cytokine IL-1beta induces the synthesis of IL-8, a potent angiogenic factor, in human mast cells via the leukotriene B(4) receptor (BLT)2. We also characterized the BLT2 downstream signaling pathway and determined that BLT2-mediated IL-8 synthesis involves the upregulation of Nox1, a member of the NADPH oxidase family, Nox1-dependent reactive oxygen species generation and the subsequent activation of the redox-sensitive transcription factor NF-kappaB. For instance, knockdown of BLT2 and Nox1 with specific small interfering RNA, treatment with a specific BLT2 antagonist, LY255283, or treatment with a potential Nox inhibitor, diphenylene iodonium, suppressed IL-1beta-induced IL-8 synthesis. We found that the conditioned media collected from IL-1beta-treated human mast cell line HMC-1 had significantly enhanced angiogenic activity that could be dramatically attenuated by either small interfering RNA knockdown of BLT2 or treatment with neutralizing Ab to IL-8. Finally, the experiments were repeated using human primary cord blood-derived mast cells, and the results were clearly reproduced. Taken together, our results suggest that BLT2-Nox1-reactive oxygen species-dependent pathway plays a role in promoting the secretion of IL-8 from human mast cells in response to the proinflammatory cytokine IL-1beta, thus contributing to angiogenesis.

Diesel exhaust particles induce human umbilical vein endothelial cells apoptosis by accumulation of autophagosomes and caspase-8 activation.

Diesel exhaust particles (DEP) are risk factors for endothelial cells (ECs) dysfunction. However, the mechanism by which DEP induce ECs apoptosis remains unclear. Here, we investigated how DEP induce death of human umbilical vein ECs (HUVECs), with a focus on the autophagy-mediated apoptotic pathway. DEP induced dose-dependent HUVECs death and exposure to the IC50 concentration of DEP (70 µg/ml) led to apoptosis. DEP phosphorylated Beclin-1 (Ser93) and increased protein levels of p62 and LC3BII and the number of LC3B puncta, indicating autophagy initiation. DEP increased expression of pro- and mature forms of cathepsin D, which increases lysosomal activity. However, DEP suppressed expression of the soluble N-ethylmaleimide-sensitive factor attachment protein receptor proteins (STX17, VAMP8, SNAP29, YKT6, and STX7) to inhibit autolysosome formation, resulting in accumulation of autophagosomes. LC3B, p62, and caspase-8 form a tertiary complex in accumulated autophagosomes, which is known to serve as a platform for caspase-8 activation. Indeed, DEP activates caspase-8 and pretreatment with a caspase-8 inhibitor suppressed DEP-induced apoptosis. Furthermore, depletion of p62 decreased caspase-8 and caspase-3 activation and inhibited the DEP-induced apoptosis. Taken together, these findings demonstrated that DEP induced HUVECs apoptosis by inhibiting autophagosome maturation and identified caspase-8 as a novel mediator of DEP-induced ECs apoptosis.

Ovarian tumor diagnosis using deep convolutional neural networks and a denoising convolutional autoencoder.

Discrimination of ovarian tumors is necessary for proper treatment. In this study, we developed a convolutional neural network model with a convolutional autoencoder (CNN-CAE) to classify ovarian tumors. A total of 1613 ultrasound images of ovaries with known pathological diagnoses were pre-processed and augmented for deep learning analysis. We designed a CNN-CAE model that removes the unnecessary information (e.g., calipers and annotations) from ultrasound images and classifies ovaries into five classes. We used fivefold cross-validation to evaluate the performance of the CNN-CAE model in terms of accuracy, sensitivity, specificity, and the area under the receiver operating characteristic curve (AUC). Gradient-weighted class activation mapping (Grad-CAM) was applied to visualize and verify the CNN-CAE model results qualitatively. In classifying normal versus ovarian tumors, the CNN-CAE model showed 97.2% accuracy, 97.2% sensitivity, and 0.9936 AUC with DenseNet121 CNN architecture. In distinguishing malignant ovarian tumors, the CNN-CAE model showed 90.12% accuracy, 86.67% sensitivity, and 0.9406 AUC with DenseNet161 CNN architecture. Grad-CAM showed that the CNN-CAE model recognizes valid texture and morphology features from the ultrasound images and classifies ovarian tumors from these features. CNN-CAE is a feasible diagnostic tool that is capable of robustly classifying ovarian tumors by eliminating marks on ultrasound images. CNN-CAE demonstrates an important application value in clinical conditions.

Transcriptional analysis of gasoline engine exhaust particulate matter 2.5-exposed human umbilical vein endothelial cells reveals the different gene expression patterns related to the cardiovascular diseases.

Particulate matter (PM) causes several diseases, including cardiovascular diseases (CVDs). Previous studies compared the gene expression patterns in airway epithelial cells and keratinocytes exposed to PM. However, analysis of differentially expressed gene (DEGs) in endothelial cells exposed to PM2.5 (diameter less than 2.5 µm) from fossil fuel combustion has been limited. Here, we exposed human umbilical vein endothelial cells (HUVECs) to PM2.5 from combustion of gasoline, performed RNA-seq analysis, and identified DEGs. Exposure to the IC50 concentrations of gasoline engine exhaust PM2.5 (GPM) for 24 h yielded 1081 (up-regulation: 446, down-regulation: 635) DEGs. The most highly up-regulated gene is NGFR followed by ADM2 and NUPR1. The most highly down-regulated gene is TNFSF10 followed by GDF3 and EDN1. Gene Ontology enrichment analysis revealed that GPM regulated genes involved in cardiovascular system development, tube development and circulatory system development. Kyoto Encyclopedia of Genes and Genomes and Reactome pathway analyses showed that genes related to cytokine-cytokine receptor interactions and cytokine signaling in the immune system were significantly affected by GPM. We confirmed the RNA-seq data of some highly altered genes by qRT-PCR and showed the induction of NGFR, ADM2 and IL-11 at a protein level, indicating that the observed gene expression patterns were reliable. Given the adverse effects of PM2.5 on CVDs, our findings provide new insight into the importance of several DEGs and pathways in GPM-induced CVDs.

Modified Dynamic Physical Model of Valence Change Mechanism Memristors.

Valence change-type resistance switching behaviors in oxides can be understood by well-established physical models describing the field-driven oxygen vacancy distribution change. In those models, electroformed residual oxygen vacancy filaments are crucial as they work as an electric field concentrator and limit the oxygen vacancy movement along the vertical direction. Therefore, their movement outward by diffusion is negligible. However, this situation may not be applicable in the electroforming-free system, where the field-driven movement is less prominent, and the isotropic oxygen vacancy diffusion by concentration gradient is more significant, which has not been given much consideration in the conventional model. Here, we propose a modified physical model that considers the change in the oxygen vacancies' charged state depending on their concentrations and the resulting change in diffusivity during switching to interpret the electroforming-free device behaviors. The model suggests formation of an hourglass-shaped filament constituting a lower concentration of oxygen vacancies due to the fluid oxygen diffusion in the thin oxide. Consequently, the proposed model can explain the electroforming-free device behaviors, including the retention failure mechanism, and suggest an optimized filament configuration for improved retention characteristics. The proposed model can plausibly explain both the electroformed and the electroforming-free devices. Therefore, it can be a standard model for valence change memristors.

Role of the low-affinity leukotriene B4 receptor BLT2 in VEGF-induced angiogenesis.

OBJECTIVE: The leukotriene B(4) (LTB(4)) receptor BLT2 is expressed in endothelium, but no clear physiological function for it has yet been identified, especially in vascular angiogenesis. The purpose of this study is to characterize the potential function of BLT2 in vascular endothelial growth factor (VEGF)-induced angiogenesis. METHODS AND RESULTS: VEGF significantly upregulates BLT2 expression in human umbilical vein endothelial cells (HUVECs), and BLT2 knockdown by siRNA or inhibition of BLT2 by a specific BLT2 antagonist LY255283 attenuates VEGF-induced angiogenesis, which was determined by its effect on the formation of tube-like structures and on transmigration. The role of BLT2 in VEGF-induced angiogenesis was more evident in vivo, where BLT2 inhibition by LY255283 almost completely blocked VEGF-induced vessel formation in Matrigel-plug assays. In addition, we found that VEGF upregulates synthesis of the BLT2 ligand, 12(S)-hydroxyeicosatetraenoic acid (HETE). siRNA knockdown of 12-lipoxygenase (12-LO) expression attenuates VEGF-induced angiogenesis in HUVECs, and the addition of 12(S)-HETE to the 12-LO knockdown-HUVECs restores VEGF-induced angiogenesis. The activation of BLT2 itself by either 12(S)-HETE or LTB(4) evoked significant angiogenic phenotypes, both in vitro and in vivo. CONCLUSIONS: Our findings indicate that BLT2 plays an essential role in mediating VEGF-induced angiogenesis.

Effect of using powdered biochar and surfactant on desorption and biodegradability of phenanthrene sorbed to biochar.

The present study aimed to investigate the relationship between the desorption and biodegradability of phenanthrene sorbed to biochars by employing two approaches that may change the desorption and biodegradability: the use of powdered biochars and nonionic surfactants. Biochars derived from two feedstocks (rice husk and sewage sludge; pyrolyzed at 500 °C but showing different aromaticity) were used. When the biochars were powdered to obtain particles <250 µm the mass fractions of the desorbed phenanthrene at ∼80 days (fdes) increased from 0.303 to 0.431 for sewage sludge biochars. On the other hand, fdes for rice husk biochars remained virtually unchanged (from 0.264 to 0.255). The mass fractions of the biodegraded phenanthrene (fbio) increased from 0.191 to 0.306 for rice husk biochars and from 0.077 to 0.168 for sewage sludge biochars. When a nonionic surfactant was added at the sub-critical micelle concentration (CMC), fbio increased by 4.7 times and 8.3 times for rice husk and sewage sludge biochars. For both types of biochars, fbio was larger than fdes when the surfactant was added. This study suggests that the addition of nonionic surfactants can be considered if the inhibition of microbial activity is of concern in soils and sediments treated by biochar.