Plasmonic Bound States in the Continuum Metasurface-Semiconductor-Metal Architecture Enables Efficient Hot-Electron-Based Photodetector.

Plasmonic hot-electron-based photodetectors (HEB-PDs) have received widespread attention for their ability to realize effective carrier collection under sub-bandgap illumination. However, due to the low hot electron emission probability, most of the existing HEB-PDs exhibit poor responsivity, which significantly restricts their practical applications. Here, by employing the binary-pore anodic alumina oxide template technique, we proposed a compact plasmonic bound state in continuum metasurface-semiconductor-metal-based (BIC M-S-M) HEB-PD. The symmetry-protected BIC can manipulate a strong gap surface plasmon in the stacked M-S-M structure, which effectively enhances light-matter interactions and improves the photoresponse of the integrated device. Notably, the optimal M-S-M HEB-PD with near-unit absorption (∼90%) around 800 nm delivers a responsivity of 5.18 A/W and an IPCE of 824.23% under 780 nm normal incidence (1 V external bias). Moreover, the ultrathin feature of BIC M-S-M (∼150 nm) on the flexible substrate demonstrates excellent stability under a wide range of illumination angles from -40° to 40° and at the curvature surface from 0.05 to 0.13 mm-1. The proposed plasmonic BIC strategy is very promising for many other hot-electron-related fields, such as photocatalysis, biosensing, imaging, and so on.

6-Gingerol attenuates hepatic ischemia/reperfusion injury through regulating MKP5-mediated P38/JNK pathway.

6-Gingerol, the main bioactive compound of ginger, has antioxidant, anti-inflammatory, anti-cancer and neuroprotective effects. However, it is unclear whether 6-Gingerol has protective effects against hepatic ischemia/reperfusion (I/R) injury. In this study, the mouse liver I/R injury model and the mouse AML12 cell hypoxia/reoxygenation (H/R) model were established by pretreatment with 6-Gingerol at different concentrations to explore the potential effects of 6-Gingerol. Serum transaminase levels, liver necrotic area, cell viability, inflammatory response, and cell apoptosis were used to assess the effect of 6-Gingerol on hepatic I/R or cell H/R injury. Quantitative polymerase chain reaction (qPCR) and Western blotting were used to detect the mRNA and protein expression. The results show that 6-Gingerol decreased serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) levels, liver necrosis, inflammatory cytokines IL-1ß, IL-6, MCP-1, TNF-α expression, Ly6g+ inflammatory cell infiltration, protein phosphorylation of NF-κB signaling pathway, Terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) positive cells, cell apoptosis rate, the protein expression of pro-apoptotic protein BAX and C-Caspase3, increased cell viability, and expression of anti-apoptotic protein BCL-2. Moreover, 6-Gingerol could increase the mRNA and protein expression of mitogen activated protein kinase phosphatase 5 (MKP5) and inhibit the activation of P38/JNK signaling pathway. In MKP5 knockout (KO) mice, the protective effect of 6-gingerol and the inhibition of P38/JNK pathway were significantly weakened. Therefore, our results suggest that 6-Gingerol exerts anti-inflammatory and anti-apoptotic effects to attenuate hepatic I/R injury by regulating the MKP5-mediated P38/JNK signaling pathway.

Alternative Oxidase: From Molecule and Function to Future Inhibitors.

In the respiratory chain of the majority of aerobic organisms, the enzyme alternative oxidase (AOX) functions as the terminal oxidase and has important roles in maintaining metabolic and signaling homeostasis in mitochondria. AOX endows the respiratory system with flexibility in the coupling among the carbon metabolism pathway, electron transport chain (ETC) activity, and ATP turnover. AOX allows electrons to bypass the main cytochrome pathway to restrict the generation of reactive oxygen species (ROS). The inhibition of AOX leads to oxidative damage and contributes to the loss of adaptability and viability in some pathogenic organisms. Although AOXs have recently been identified in several organisms, crystal structures and major functions still need to be explored. Recent work on the trypanosome alternative oxidase has provided a crystal structure of an AOX protein, which contributes to the structure-activity relationship of the inhibitors of AOX. Here, we review the current knowledge on the development, structure, and properties of AOXs, as well as their roles and mechanisms in plants, animals, algae, protists, fungi, and bacteria, with a special emphasis on the development of AOX inhibitors, which will improve the understanding of respiratory regulation in many organisms and provide references for subsequent studies of AOX-targeted inhibitors.

Enhanced CO2 Electroreduction to Multi-Carbon Products on Copper via Plasma Fluorination.

The electroreduction of carbon dioxide (CO2) to multi-carbon (C2+) compounds offers a viable approach for the up-conversion of greenhouse gases into valuable fuels and feedstocks. Nevertheless, current industrial applications face limitations due to unsatisfactory conversion efficiency and high overpotential. Herein, a facile and scalable plasma fluorination method is reported. Concurrently, self-evolution during CO2 electroreduction is employed to control the active sites of Cu catalysts. The copper catalyst modified with fluorine exhibits an impressive C2+ Faradaic efficiency (FE) of 81.8% at a low potential of -0.56 V (vs a reversible hydrogen electrode) in an alkaline flow cell. The presence of modified fluorine leads to the exposure and stabilization of high-activity Cu+ species, enhancing the adsorption of *CO intermediates and the generation of *CHO, facilitating the subsequent dimerization. This results in a notably improved conversion efficiency of 13.1% and a significant reduction in the overpotential (≈100 mV) for the C2+ products. Furthermore, a superior C2+ FE of 81.6% at 250 mA cm-2, coupled with an energy efficiency of 31.0%, can be achieved in a two-electrode membrane electrode assembly electrolyzer utilizing the fluorine-modified copper catalyst. The strategy provides novel insights into the controllable electronic modification and surface reconstruction of electrocatalysts with practical potential.

[Predictive value of PASS score combined with NLR and CRP for infected pancreatic necrosis in patients with severe acute pancreatitis].

OBJECTIVE: To investigate the predictive value of pancreatitis activity scoring system (PASS) combined with Neutrophil to lymphocyte ratio (NLR) and C-reactive protein (CRP) for infected pancreatic necrosis (IPN) in patients with severe acute pancreatitis (SAP). METHODS: Clinical data of SAP patients admitted to the First Affiliated Hospital of Zhengzhou University from January 2020 to January 2023 were retrospectively collected, including basic information, vital signs at admission, first laboratory indexes within 48 hours of admission. The PASS scores at admission and 24, 48 and 72 hours after admission were calculated. According to the diagnostic criteria of IPN, the patients were divided into the non-IPN group and the IPN group, and the independent risk factors of SAP complicating IPN were determined by using univariate analysis and multifactorial Logistic regression. The receiver operator characteristic curve (ROC curve) was drawn to evaluate the predictive value of NLR, CRP, and PASS score, alone and in combination for IPN in patients with SAP. RESULTS: A total of 149 SAP patients were enrolled, including 102 in the non-IPN group and 47 in the IPN group. The differences in PASS score at each time point, NLR, CRP, procalcitonin (PCT), blood urea nitrogen, blood chloride, and days of hospitalization between the two groups were statistically significant. Multifactorial Logistic regression analysis showed that 72 hours admission PASS score [odds ratio (OR) = 1.034, 95% confidence interval (95%CI) was 1.005-1.065, P = 0.022], NLR (OR = 1.284, 95%CI was 1.139-1.447, P = 0.000), and CRP (OR = 1.015, 95%CI was 1.006-1.023, P = 0.001) were independent risk factors for IPN in patients with SAP. ROC curve analysis showed that the area under the ROC curve (AUC) of the PASS score at 72 hours of admission, NLR, and CRP alone in predicting IPN in SAP patients were 0.828, 0.771, and 0.701, respectively. The AUC of NLR combined with CRP, PASS combined with NLR, and PASS combined with CRP were 0.818, 0.895, and 0.874, respectively. The combination of PASS score at 72 hours after admission, NLR, and CRP had a better predictive ability for IPN in patients with SAP (AUC = 0.922, 95%CI was 0.877-0.967), and the sensitivity was 72.3% when the cut-off value was 0.539. CONCLUSIONS: The predictive value of the PASS score at 72 hours after admission, NLR and CRP in combination for IPN in SAP patients is better than that of the combination of each two and individual detection and has better test efficacy.

Sirtuin4 alleviates severe acute pancreatitis by regulating HIF-1α/HO-1 mediated ferroptosis.

Acute pancreatitis (AP) is a common emergency of the digestive system and serious cases can develop into severe acute pancreatitis (SAP), which ortality rates up to 30%. Sirtuin4 (SIRT4) is a member of the sirtuin family, and plays a key role in inflammation and oxidative stress. However, the potential role of SIRT4 in SAP has yet to be elucidated. In the present study, we found that the expression level of SIRT4 in human AP was downregulated by screening a public database, suggesting that SIRT4 may play a role in AP. Subsequently, we used L-arginine (L-Arg) to induce SAP in SIRT4 knockout (SIRT4_KO) and SIRT4 overexpression (AAV_SIRT4) mice. The results showed that the pancreatic tissue injury and related lung and kidney injury were serious in SIRT4_KO mice after SAP induction, but were significantly reduced in AAV_SIRT4 mice. More importantly, we found that the levels of antioxidant factors GSH and SOD were decreased in SIRT4_KO mice, and the production of oxidative products and lipid peroxidation markers was increased, suggesting that SIRT4 was involved in inflammation and oxidative stress during SAP. Further studies showed that the absence or overexpression of SIRT4 affected the expression level of Hypoxia-inducible factor-1α (HIF-1α) after SAP induction, and regulated the expression of ferroptosis related proteins by mediating HIF-1α/HO-1 pathway. Collectively, our study revealed that SIRT4 plays a protective role in SAP by regulating the HIF-1α/HO-1 pathway to inhibit ferroptosis.

Oridonin ameliorates doxorubicin induced-cardiotoxicity via the E2F1/Sirt6/PGC1α pathway in mice.

Doxorubicin induced cardiotoxicity (DIC) arises from mitochondrial dysfunction and oxidative stress. Oridonin (Ori), a natural tetracycline diterpenoid, has shown cardiac protective effect; however, its role in DIC remains unclear. This study investigates the protective effect of Ori against DIC and elucidates its underlying molecular mechanisms. The results demonstrate that Ori significantly alleviated DIC by improving myocardial structure, reducing the proportion of apoptotic cells, and alleviating the myocardial oxidative damage and mitochondrial dysfunction both in vivo and in vitro. Doxorubicin significantly decreased Sirt6 and PGC1α levels in cardiac tissues, which was reversed by Ori. Furthermore, Sirt6 overexpression significantly improved myocardial structure and reduced the proportion of apoptotic cells by reducing oxidative stress and improving mitochondrial function. The protective effect of Ori is neutralized by the Sirt6 inhibitor OSS_128167, evidenced by downregulated mRNA and protein expression of PGC1α. The transcription factor E2F1 was upregulated by doxorubicin, leading to decreased Sirt6 expression-an effect mitigated by Ori. Molecular docking simulations indicate direct binding between Ori and specific amino acid residues on E2F1 through hydroxyl bonds. These findings uncover a novel mechanism whereby Ori attenuates DIC by modulating the E2F1/Sirt6/PGC1α pathway.

Mitogen activated protein kinase phosphatase 5 alleviates liver ischemia-reperfusion injury by inhibiting TAK1/JNK/p38 pathway.

Mitogen activated protein kinase phosphatase 5 (MKP5) is a member of the MKP family and has been implicated in diverse biological and pathological conditions. However, it is unknown what role MKP5 plays in liver ischemia/reperfusion (I/R) injury. In the present study, we used MKP5 global knockout (KO) and MKP5 overexpressing mice to establish a liver I/R injury model in vivo, and MKP5 knockdown or MKP5 overexpressing HepG2 cells to establish a hypoxia-reoxygenation (H/R) model in vitro. In this study we demonstrated that protein expression of MKP5 was significantly downregulated in liver tissue of mice after I/R injury, and HepG2 cells subjected to H/R injury. MKP5 KO or knockdown significantly increased liver injury, as demonstrated by elevated serum transaminases, hepatocyte necrosis, infiltrating inflammatory cells, secretion of pro-inflammatory cytokines, apoptosis, oxidative stress. Conversely, MKP5 overexpression significantly attenuated liver and cell injury. Furthermore, we showed that MKP5 exerted its protective effect by inhibiting c-Jun N-terminal kinase (JNK)/p38 activity, and its action was dependent on Transforming growth factor-ß-activated kinase 1 (TAK1) activity. According to our results, MKP5 inhibited the TAK1/JNK/p38 pathway to protect liver from I/R injury. Our study identifies a novel target for the diagnosis and treatment of liver I/R injury.

Endoscopy-assisted purely total outer wall excision for pediatric Sylvian arachnoid cysts.

BACKGROUND: To present a novel endoscopy-assisted surgical strategy of Sylvian arachnoid cysts (ACs). CASE PRESENTATION: Endoscopy-assisted surgery was performed on 9 children (May 2019-December 2021). All patients were evaluated with CT and/or MRI and had regular follow-up examinations. The procedure consisted of performing a small temporal craniotomy (2 cm) behind the hairline. After dural opening, the surgery was performed with the assistance of a rigid 30-degree transcranial endoscope, self-irrigating bipolar forceps, and other standard endoscopic instruments. Steps included total excision of the AC outer wall and dissection of arachnoid adhesion around the cystic edge to communicate the residual cyst cavity with subdural space. Compared with the microscopical procedure, a 30-degree transcranial endoscope provides a wider view, especially for the lateral part exposure of the outer wall. The average age of the patients was 27.7 months (range 13-44 months). The Sylvian AC was in the right hemisphere in three patients and six in the left, respectively. 1 patient suffered transient postoperative epilepsy. There was no mortality or additional postoperative neurological deficit in this series. All of the patients achieved significant clinical improvement after surgery. Radiological examination after the operation showed a significant reduction in all cases (100%, 9/9) and disappearance in one case (11.1%, 1/9). Postoperative subdural fluid collection occurred in six cases and completely resolved spontaneously in 9 months. CONCLUSION: The study demonstrated the minimally invasive, safety, and effectivity of the endoscopy-assisted purely total outer wall excision.

KLF6 alleviates hepatic ischemia-reperfusion injury by inhibiting autophagy.

Hepatic ischemia-reperfusion (I/R) injury, a common clinical complication of liver transplantation, gravely affects patient prognosis. Krüppel-like factors (KLFs) constitute a family of C2/H2 zinc finger DNA-binding proteins. KLF6, a member of the KLF protein family, plays crucial roles in proliferation, metabolism, inflammation, and injury responses; however, its role in HIR is largely remains unknown. After I/R injury, we found that KLF6 expression in mice and hepatocytes was significantly upregulated. Mice were then subjected to I/R following injection of shKLF6- and KLF6-overexpressing adenovirus through the tail vein. KLF6 deficiency markedly exacerbated liver damage, cell apoptosis, and activation of hepatic inflammatory responses, whereas hepatic overexpression of KLF6 in mice produced the opposite results. In addition, we knocked out or overexpressed KLF6 in AML12 cells before exposing them to a hypoxia-reoxygenation challenge. KLF6 knockout decreased cell viability and increased hepatocyte inflammation, apoptosis, and ROS, whereas KLF6 overexpression had the opposite effects. Mechanistically, KLF6 inhibited the overactivation of autophagy at the initial stage, and the regulatory effect of KLF6 on I/R injury was autophagy-dependent. CHIP-qPCR and luciferase reporter gene assays confirmed that KLF6 bound to the promoter region of Beclin1 and inhibited its transcription. Additionally, KLF6 activated the mTOR/ULK1 pathway. Finally, we performed a retrospective analysis of the clinical data of liver transplantation patients and identified significant associations between KLF6 expression and liver function following liver transplantation. In conclusion, KLF6 inhibited the overactivation of autophagy via transcriptional regulation of Beclin1 and activation of the mTOR/ULK1 pathway, thereby protecting the liver from I/R injury. KLF6 is expected to serve as a biomarker for estimating the severity of I/R injury following liver transplantation.

Bidirectional Synaptic Phototransistor Based on Two-Dimensional Ferroelectric Semiconductor for Mixed Color Pattern Recognition.

Optoelectronic synaptic devices capable of processing multiwavelength inputs are critical for neuromorphic vision hardware, which remains an important challenge. Here, we develop a bidirectional synaptic phototransistor based on a two-dimensional ferroelectric semiconductor of α-In2Se3, which exhibits bidirectional potentiated and depressed synaptic weight update under optical pulse stimulation. Importantly, the bidirectional optoelectronic synaptic behavior can be extended to multiwavelengths (blue, green, and red light), which could be used for color recognition. The mechanism underlying the bidirectional synaptic characteristics is attributed to the gate-configurable barrier heights as revealed by the Kelvin probe force microscopy measurement. The α-In2Se3 device exhibits versatile synaptic plasticity such as paired-pulse facilitation, short- and long-term potentiation, and long-term depression. The bidirectional optoelectronic synaptic weight updates under multiwavelength inputs enable a high accuracy of 97% for mixed color pattern recognition.

Natural Flavonoids and Ferroptosis: Potential Therapeutic Opportunities for Human Diseases.

Flavonoids are a class of bioactive phytochemicals containing a core 2-phenylchromone skeleton and are widely found in fruits, vegetables, and herbs. Such natural compounds have gained significant attention due to their various health benefits. Ferroptosis is a recently discovered unique iron-dependent mode of cell death. Unlike traditional regulated cell death (RCD), ferroptosis is associated with excessive lipid peroxidation on cellular membranes. Accumulating evidence suggests that this form of RCD is involved in a variety of physiological and pathological processes. Notably, multiple flavonoids have been shown to be effective in preventing and treating diverse human diseases by regulating ferroptosis. In this review, we introduce the key molecular mechanisms of ferroptosis, including iron metabolism, lipid metabolism, and several major antioxidant systems. Additionally, we summarize the promising flavonoids targeting ferroptosis, which provides novel ideas for the management of diseases such as cancer, acute liver injury, neurodegenerative diseases, and ischemia/reperfusion (I/R) injury.

Ultra-thin gate insulator of atomic-layer-deposited AlOxand HfOxfor amorphous InGaZnO thin-film transistors.

To strengthen the downscaling potential of top-gate amorphous oxide semiconductor (AOS) thin-film transistors (TFTs), the ultra-thin gate insulator (GI) was comparatively implemented using the atomic-layer-deposited (ALD) AlOxand HfOx. Both kinds of high-kGIs exhibit good insulating properties even with the physical thickness thinning to 4 nm. Compared to the amorphous indium-gallium-zinc oxide (a-IGZO) TFTs with 4 nm AlOxGI, the 4 nm HfOxenables a larger GI capacitance, while the HfOx-gated TFT suffers higher gate leakage current and poorer subthreshold slope, respectively originating from the inherently small band offset and the highly defective interface between a-IGZO and HfOx. Such imperfect a-IGZO/HfOxinterface further causes noticeable positive bias stress instability. Both ALD AlOxand HfOxwere found to react with the underneath a-IGZO channel to generate the interface defects, such as metal interstitials and oxygen vacancies, while the ALD process of HfOxgives rise to a more severe reduction of a-IGZO. Moreover, when such a defective interface is covered by the top gate, it cannot be readily restored using the conventional oxidizing post-treatments and thus desires the reduction-resistant pre-treatments of AOSs.

Customizing 2.5D Out-of-Plane Architectures for Robust Plasmonic Bound-States-in-the-Continuum Metasurfaces.

Bound states in the continuum (BICs) have a superior ability to confine electromagnetic waves and enhance light-matter interactions. However, the quality-factor of quasi-BIC is extremely sensitive to structural perturbations, thus the BIC metasurfaces usually require a very-high precision nanofabrication technique that greatly restricts their practical applications. Here, distinctive 2.5D out-of-plane architectures based plasmonic symmetry protected (SP)-BIC metasurfaces are proposed, which could deliver robust quality factors even with large structural perturbations. The high-throughput fabrication of such SP-BIC metasurfaces is realized by using the binary-pore anodic aluminum oxide template technique. Moreover, the deep neural network (DNN) is adapted to conduct multiparameter fittings, where the 2.5D hetero-out-of-plane architectures with robust high quality-factors and figures of merit are rapidly predicted and fabricated. Finally, owning to its large second-order surface sensitivity, the desired 2.5D hetero-out-of-plane architecture demonstrates a detection limit of endotoxin as low as 0.01 EU mL-1 , showing a good perspective of biosensors and others.

Near-Ideal Top-Gate Controllability of InGaZnO Thin-Film Transistors by Suppressing Interface Defects with an Ultrathin Atomic Layer Deposited Gate Insulator.

An ultrathin atomic-layer-deposited (ALD) AlOx gate insulator (GI) was implemented for self-aligned top-gate (SATG) amorphous InGaZnO (a-IGZO) thin-film transistors (TFTs). Although the 4.0-nm thick AlOx exhibited ideal insulating properties, the interaction between ALD AlOx and predeposited a-IGZO caused a relatively defective interface, thus giving rise to hysteresis and bias stress instabilities. As analyzed using high-resolution transmission electron microscopy, X-ray photoelectron spectroscopy, and the Hall measurement, the chemical reaction between the ALD precursor and a-IGZO is revealed. This was effectively prevented by preoxidizing a-IGZO with nitrous oxide (N2O) plasma. With 4 nm-AlOx GI and low-defect interfaces, high performance and stability were simultaneously achieved on SATG a-IGZO TFTs, including a near-ideal record-low subthreshold swing of 60.8 mV/dec, a low operation voltage below 0.4 V, a moderate mobility of 13.3 cm2/V·s, a low off-current below 10-13 A, a large on/off ratio over 109, and negligible threshold-voltage shifts less than 0.04 V against various bias-temperature stresses. This work clarifies the vital interfacial reaction between top-gate high-k dielectrics and amorphous oxide semiconductors (AOSs) and further provides a feasible way to remove this obstacle to downscaling SATG AOS TFTs.

Oridonin ameliorates acetaminophen-induced acute liver injury through ATF4/PGC-1α pathway.

Acetaminophen (APAP) overdose-induced acute liver injury (ALI) causes hepatocyte cell death, oxidative stress, and inflammation. Oridonin (Ori), a covalent NLRP3-inflammasome inhibitor, ameliorates APAP-induced ALI through an unclear molecular mechanism. This study found that Ori decreased hepatic cytochrome P450 2E1 level and increased glutathione content to prevent APAP metabolism, and then reduced the necrotic area, improved liver function, and inhibited APAP-induced proinflammatory cytokines and oxidative stress. Ori also decreased activating transcription factor 4 (ATF4) protein levels and increased peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) to reduce APAP-induced endoplasmic reticulum stress activation and mitochondrial dysfunction. Furthermore, western blot and luciferase assay found that ATF4 inhibited transcription in the PGC-1α promoter -507 to -495 region to reduce PGC-1α levels, while ATF4 knockdown neutralized the hepatoprotective effect of Ori. Molecular docking showed that Ori bound to ATF4's amino acid residue glutamate 302 through 6, 7, and 18 hydroxyl bands. Our findings demonstrated that Ori prevented metabolic activation of APAP and further inhibited the ATF4/PGC-1α pathway to alleviate APAP overdose-induced hepatic toxicity, which illuminated its potential therapeutic effects on ALI.

Integrated genetic analysis of leaf blast resistance in upland rice: QTL mapping, bulked segregant analysis and transcriptome sequencing.

Elite upland rice cultivars have the advantages of less water requirement along with high yield but are usually susceptible to various diseases. Rice blast caused by Magnaporthe oryzae is the most devastating disease in rice. Identification of new sources of resistance and the introgression of major resistance genes into elite cultivars are required for sustainable rice production. In this study, an upland rice genotype UR0803 was considered an emerging source of blast resistance. An F2 mapping population was developed from a cross between UR0803 and a local susceptible cultivar Lijiang Xintuan Heigu. The individuals from the F2 population were evaluated for leaf blast resistance in three trials 7 days after inoculation. Bulked segregant analysis (BSA) by high-throughput sequencing and SNP-index algorithm was performed to map the candidate region related to disease resistance trait. A major quantitative trait locus (QTL) for leaf blast resistance was identified on chromosome 11 in an interval of 1.61-Mb genomic region. The candidate region was further shortened to a 108.9-kb genomic region by genotyping the 955 individuals with 14 SNP markers. Transcriptome analysis was further performed between the resistant and susceptible parents, yielding a total of 5044 differentially expressed genes (DEGs). There were four DEGs in the candidate QTL region, of which, two (Os11g0700900 and Os11g0704000) were upregulated and the remaining (Os11g0702400 and Os11g0703600) were downregulated in the susceptible parent after inoculation. These novel candidate genes were functionally annotated to catalytic response against disease stimulus in cellular membranes. The results were further validated by a quantitative real-time PCR analysis. The fine-mapping of a novel QTL for blast resistance by integrative BSA mapping and transcriptome sequencing enhanced the genetic understanding of the mechanism of blast resistance in upland rice. The most suitable genotypes with resistance alleles would be useful genetic resources in rice blast resistance breeding.

Differential proteomics of placentas reveals metabolic disturbance and oxidative damage participate yak spontaneous miscarriage during late pregnancy.

BACKGROUND: High spontaneous miscarriage rate in yak, especially during late pregnancy, have caused a great economic loss to herdsmen living in the Qinghai-Tibet plateau. However, the mechanism underlying spontaneous miscarriage is still poorly understood. In the present study, placenta protein markers were identified to elucidate the pathological reasons for yak spontaneous miscarriage through isobaric tags for relative and absolute quantification (iTRAQ) proteomic technology and bioinformatic approaches. RESULTS: Subsequently, a total of 415 differentially expressed proteins (DEPs) were identified between aborted and normal placentas. The up-regulated DEPs in the aborted placentas were significantly associated with "spinocerebellar ataxia", "sphingolipid signalling", "relaxin signalling", "protein export", "protein digestion and absorption" and "aldosterone synthesis and secretion" pathway. While the down-regulated DEPs in the aborted placentas mainly participated in "valine, leucine and isoleucine degradation", "PPAR signalling", "peroxisome", "oxidative phosphorylation", "galactose metabolism", "fatty acid degradation", "cysteine and methionine metabolism" and "citrate cycle" pathway. CONCLUSIONS: The results implied that the identified DEPs could be considered as placental protein markers for yak miscarriage during late pregnancy, and biomacromolecule metabolic abnormality and oxidative damage might be responsible for the high spontaneous miscarriage rate in yak. These findings provide an important theoretical basis for deciphering the pathologic mechanism of late spontaneous miscarriage in yak.

Surface Engineering of Laser-Induced Graphene Enables Long-Term Monitoring of On-Body Uric Acid and pH Simultaneously.

Laser-induced graphene (LIG) suffers from serious decay in long-term biosensing, which greatly restricts its practical applications. Herein, we report a new strategy to engineer the LIG surface with Au clusters and chitosan sequentially to form a C-Au-LIG electrode with a superhydrophilic and highly conductive 3D graphene surface, which demonstrates superior performance and negligible decay in both long-term storage and practical usage in vitro and in vivo environments. Moreover, the C-Au-LIG electrode can be used for detecting uric acid (UA) and pH simultaneously from a single differential pulse voltammetry curve with low-detection limitation, high accuracy, and negligible interference with other sweat biomarkers. The integrated C-Au-LIG wearable biosensor was employed to continuously monitor the UA content in human sweat, which can well reflect the daily intake of purines for at least 10 days. Therefore, the C-Au-LIG electrode demonstrates significant application potential and provides inspiration for surface engineering of other biosensor materials and electrodes.

Self-assembled peptides-modified flexible field-effect transistors for tyrosinase detection.

Flexible biosensors have received intensive attention for real-time, non-invasive monitoring of cancer biomarkers. Highly sensitive tyrosinase biosensors, which are important for melanoma screening, remained a hurdle. Herein, high-performance tyrosinase-sensing field-effect transistor-based biosensors (bio-FETs) have been successfully achieved by self-assembling nanostructured tetrapeptide tryptophan-valine-phenylalanine-tyrosine (WVFY) on n-type metal oxide transistors. In the presence of target tyrosinase, the phenolic hydroxyl groups in WVFY are rapidly converted to benzoquinone with the consumption of protons, which could be detected potentiometrically by bio-FETs. As a result, the WVFY-modified bio-FETs exhibited an ultra-low detection limit of 1.9 fM and an optimal detection range of 10 fM to 1 nM toward tyrosinase sensing. Furthermore, flexible devices fabricated on ∼2.9-µm-thick polyimide (PI) substrates illustrated robust mechanical flexibility, which could be attached to human skin conformally. These achievements hold promise for wearable melanoma screening and provide designing guidelines for detecting other important cancer biomarkers with bio-FETs.