Cretaceous fossil reveals a new pattern in mammalian middle ear evolution.

The evolution of the mammalian middle ear is thought to provide an example of 'recapitulation'-the theory that the present embryological development of a species reflects its evolutionary history. Accumulating data from both developmental biology and palaeontology have suggested that the transformation of post-dentary jaw elements into cranial ear bones occurred several times in mammals1,2. In addition, well-preserved fossils have revealed transitional stages in the evolution of the mammalian middle ear1,3,4. But questions remain concerning middle-ear evolution, such as how and why the post-dentary unit became completely detached from the dentary bone in different clades of mammaliaforms. Here we report a definitive mammalian middle ear preserved in an eobaatarid multituberculate mammal, with complete post-dentary elements that are well-preserved and detached from the dentary bones. The specimen reveals the transformation of the surangular jaw bone from an independent element into part of the malleus of the middle ear, and the presence of a restricted contact between the columelliform stapes and the flat incus. We propose that the malleus-incus joint is dichotomic in mammaliaforms, with the two bones connecting in either an abutting or an interlocking arrangement, reflecting the evolutionary divergence of the dentary-squamosal joint4. In our phylogenetic analysis, acquisition of the definitive mammalian middle ear in allotherians such as this specimen was independent of that in monotremes and therians. Our findings suggest that the co-evolution of the primary and secondary jaw joints in allotherians was an evolutionary adaptation allowing feeding with unique palinal (longitudinal and backwards) chewing. Thus, the evolution of the allotherian auditory apparatus was probably triggered by the functional requirements of the feeding apparatus.

Heteroatoms-Doped Mesoporous Carbon Nanosheets with Dual Diffusion Pathways for Highly Efficient Potassium Ion Storage.

The high potassization/depotassization energy barriers and lack of efficient ion diffusion pathways are two serious obstacles for carbon-based materials to achieve satisfactory potassium ion storage performance. Herein, a facile and controllable one-step exfoliation-doping-etching strategy is proposed to construct heteroatoms (N, O, and S)-doped mesoporous few-layer carbon nanosheets (NOS-C). The mixed molten salts of KCl/K2SO4 are innovatively used as the exfoliators, dopants, and etching agents, which enable NOS-C with expanded interlayer spacing and uniformly distributed mesopores with the adjusted electronic structure of surrounding carbon atoms, contributing efficient dual (vertical and horizontal) K-ion diffusion pathways, low potassization/depotassization energy barriers and abundant active sites. Thus, the NOS anodes achieve a high reversible capacity of 516.8 mAh g-1 at 0.05 A g-1, superior rate capability of 202.8 mAh g-1 at 5 A g-1 and excellent long-term cyclic stability, and their practical application potential is demonstrated by the assembled potassium-ion full batteries. Moreover, a surface-interlayer synergetic K+ storage mechanism is revealed by a combined theoretical and experimental approach including in situ EIS, in situ Raman, ex situ XPS, and SEM analysis. The proposed K+ storage mechanism and unique structural engineering provide a new pathway for potassium-ion storage devices and even beyond.

Proteomic analysis of exosomal proteins associated with bone healing speed in a rat tibial fracture model.

This study investigates the impact of exosomes on bone fracture healing in a rat tibial model, distinguishing between fast and slow healing processes. Bone healing and protein expression were assessed through X-ray examinations, hematoxylin and eosin staining, and immunohistochemical staining. Exosomes were isolated, characterized and subjected to liquid chromatography-mass spectrometry for protein analysis. Molecular differences were explored using differentially expressed protein analysis, Kyoto Encyclopedia of Genes and Genomes pathway enrichment and protein-protein interaction networks. Differential bone healing patterns and protein expressions were observed between the control and model groups. Exosomes were successfully isolated and characterized, revealing 2004 identified proteins, including distinct expression profiles. Notably, ribosomal proteins, ferritin and beta-actin emerged as pivotal players in bone fracture healing. This study unveils dynamic changes in bone healing and underscores the role of exosomes in the process. Identified proteins and pathways offer valuable insights for developing innovative therapeutic strategies for bone healing.

Calcineurin inhibitors ameliorate PAN-induced podocyte injury through the NFAT-Angptl4 pathway.

Podocyte injury plays a vital role in proteinuria and nephrotic syndrome. Calcineurin (CaN) inhibitors are effective in reducing proteinuria. However, their molecular mechanism is still not fully understood. Angiopoietin-like-4 (ANGPTL4) is a secreted protein that mediates proteinuria in podocyte-related nephropathy. In this study, we established a puromycin aminonucleoside (PAN)-induced minimal-change disease (MCD) rat model and a cultured podocyte injury model. We found that CaN inhibitors protected against PAN-induced podocyte injury, accompanied by an inhibition of Nfatc1 and Angptl4 both in vivo and in vitro. Nfatc1 overexpression and knockdown experiments indicated that Angptl4 was regulated by Nfatc1 in podocytes. ChIP assays further demonstrated that Nfatc1 increased Angptl4 expression by binding to the Angptl4 promoter. In addition, overexpression and knockdown of Angptl4 revealed that Angptl4 directly induced rearrangement of the cytoskeleton of podocytes, reduced the expression of synaptopodin, and enhanced PAN-induced podocyte apoptosis. Furthermore, in a cohort of 83 MCD and 94 membranous nephropathy (MN) patients, we found increased expression of serum ANGPTL4 compared to 120 healthy controls, and there were close correlations between serum ANGPTL4 and Alb, urinary protein, urinary Alb, eGFR, Scr, and BUN in MCD patients. No obvious correlation was found in MN patients. Immunofluorescence studies indicated that increased ANGPTL4 in MCD and MN patients was located mostly in podocytes. In conclusion, our results demonstrate that CaN inhibitors ameliorate PAN-induced podocyte injury by targeting Angptl4 through the NFAT pathway, and Angptl4 plays a vital role in podocyte injury and is involved in human podocyte-related nephropathy. © 2020 The Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.

Enhancing performance of perovskite solar cells with efficiency exceeding 21% via a graded-index mesoporous aluminum oxide antireflection coating.

Antireflection (AR) film is a widely used technology to enhance the performance of photovoltaic devices that require transparent electrodes in the photovoltaic industry. At present, several AR films including monolayer MgF2 or multilayered composite films, textured polydimethylsiloxane (PDMS) and porous SiO2 have been successfully applied due to their excellent properties. Nevertheless, all of the above-mentioned AR films have some minor drawbacks to overcome, for instance, the cost or thermal durability. Herein, we report a cost-effective and low-temperature method to fabricate a mesoporous aluminum oxide (meso-Al2O3) layer as the AR coating with high thermal durability, which will meet the fabrication condition of various photovoltaic devices. Briefly, the process begins at magnetron sputtering a compact Al2O3 film, which shows no AR effect, followed by a hot water treatment at 80 °C to turn the compact film into a mesoporous film with graded-index and AR effect. The application of meso-Al2O3 AR film enhances the maximum transmittance of our laboratory-used fluorine-doped tin oxide (FTO) from 84% to 89%, which is in good agreement with our theoretical simulation named graded-index approximation. Taking perovskite solar cells (PSCs) as an example, planar PSCs with meso-Al2O3 AR film deliver excellent photon conversion efficiency of 21.5%, which is higher than that of cells without meso-Al2O3 AR film (20.9%).

TGF-ß1 mediated Smad signaling pathway and EMT in hepatic fibrosis induced by Nano NiO in vivo and in vitro.

Nickel oxide nanoparticles (Nano NiO) bears hepatotoxicity, while whether it leads to liver fibrosis remains unclear. The aim of this study was to establish the Nano NiO-induced hepatic fibrosis model in vivo and investigate the roles of transforming growth factor ß1 (TGF-ß1) in Smad pathway activation, epithelial-mesenchymal transition (EMT) occurrence, and extracellular matrix (ECM) deposition in vitro. Male Wistar rats were exposed to 0.015, 0.06, and 0.24 mg/kg Nano NiO by intratracheal instilling twice a week for 9 weeks. HepG2 cells were treated with 100 µg/mL Nano NiO and TGF-ß1 inhibitor (SB431542) to explore the mechanism of collagen formation. Results of Masson staining as well as the elevated levels of type I collagen (Col-I) and Col-III suggested that Nano NiO resulted in hepatic fibrosis in rats. Furthermore, Nano NiO increased the protein expression of TGF-ß1, p-Smad2, p-Smad3, alpha-smooth muscle actin (α-SMA), matrix metalloproteinase9 (MMP9), and tissue inhibitors of metalloproteinase1 (TIMP1), while decreased the protein content of E-cadherin and Smad7 in rat liver and HepG2 cells. Most importantly, Nano NiO-triggered the abnormal expression of the abovementioned proteins were all alleviated by co-treatment with SB431542, implying that TGF-ß1-mediated Smad pathway, EMT and MMP9/TIMP1 imbalance were involved in overproduction of collagen in HepG2 cells. In conclusion, these findings indicated that Nano NiO induced hepatic fibrosis via TGF-ß1-mediated Smad pathway activation, EMT occurrence, and ECM deposition.

Activation of CaMKKß-AMPK-mTOR pathway is required for autophagy induction by ß,ß-dimethylacrylshikonin against lung adenocarcinoma cells.

ß,ß-Dimethylacrylshikonin (DMAS), an active ingredient of Lithospermum erythrorhizon and Arnebia euchroma, possess anti-neoplasm properties. Recently, DMAS was reported to stimulate autophagy in lung adenocarcinoma cells. However, the mechanisms by which DMAS modulates autophagy. have not yet been clearly elucidated. In this study, we found that DMAS significantly elevated intracellular free calcium accumulation. This activated the CaMKKß-AMPK-mTOR pathway, subsequently inhibited mTOR and its substrate p70s6k and 4E-BP1, eventually leading to autophagy. In addition, we demonstrated that inhibition of autophagy by BAPTA-AM or STO-609 or compound C potently enhanced DMAS-induced lung adenocarcinoma cells apoptosis and growth inhibition. Overall, our results suggested that cytoprotective autophagy was triggered by DMAS via CaMKKß-AMPK-mTOR signaling cascade in human lung adenocarcinoma cells, meaning that combining use of DMAS and autophagy inhibitors as a novel therapeutic option for lung adenocarcinoma will be very promising.

Endoplasmic reticulum stress-mediated autophagy protects against ß,ß-dimethylacrylshikonin-induced apoptosis in lung adenocarcinoma cells.

ß,ß-Dimethylacrylshikonin (DMAS) is an anti-cancer compound extracted from the roots of Lithospermum erythrorhizon. The present study aims to investigate the effects of DMAS on human lung adenocarcinoma cells in vitro and explore the mechanisms of its anti-cancer action. We showed that DMAS markedly inhibited cell viability in a dose- and time-dependent way, and induced apoptosis as well as autophagy in human lung adenocarcinoma cells. Furthermore, we found that DMAS stimulated endoplasmic reticulum stress and mediated autophagy through the PERK-eIF2α-ATF4-CHOP and IRE1-TRAF2-JNK axes of the unfolded protein response in human lung adenocarcinoma cells. We also showed that the autophagy induced by DMAS played a prosurvival role in human lung adenocarcinoma cells and attenuated the apoptotic cascade. Collectively, combined treatment of DMAS and pharmacological autophagy inhibitors could offer an effective therapeutic strategy for lung adenocarcinoma treatment.

PARP-1 inhibition attenuates cardiac fibrosis induced by myocardial infarction through regulating autophagy.

Post-MI heart failure is characterized by structural remodeling, in which intramyocardial fibrosis takes a important part. Poly(ADP-ribose) polymerase 1 (PARP-1) is a extensive nuclear enzyme and plays a critical role in various diseases. It was shown that PARP-1 inhibition could alleviate heart failure and dowregulate autophagy, but whether PARP-1 regulates autophagy and thus impacts the activities of CFs remain unknown. We transfected cultured cardiac fibroblasts (CFs) with small interfere RNA-PARP-1 (siPARP-1) to downregulate PARP-1 and analyzed the ability of proliferation, migration, differentiation, and autophagy levels of CFs under different treatments using CCK8 assays, transwell migration assays, immunofluorescence assays detecting expression of α-SMA, western blot assays detecting autophagy-related proteins respectively. Furthermore, rat models of myocardial infarction (MI) were induced by ligation of left anterior descending coronary artery and PARP-1 inhibitor, 4-aminobenzamide (4-AB), was injected intraperitoneally after MI, followed by echocardiography detection, masson assays, immunohistochemistry assays detecting expression of α-SMA and western blot assays detecting autophagy-related proteins to investigate whether PARP-1 inhibition could regulate autophagy, alleviate cardiac fibrosis and improve cardiac function in vivo. In cultured CFs, siPARP-1 repressed TGF-ß1-induced proliferation, migration, and differentiation through regulating autophagic levels. The in vitro results was verified by the in vivo study, indicating that PARP-1 inhibition partially decreased autophagy, abrogated cardiac fibrosis and significantly improved cardiac function post-MI. In conclusion, this work demonstrated the vital connection of PARP-1 and autophagy in the activation of CFs, and provided solid evidence supporting PARP-1 inhibition as a feasible strategy for the treatment of post-MI heart failure.

Cryptotanshinone inhibits VEGF-induced angiogenesis by targeting the VEGFR2 signaling pathway.

OBJECTIVE: Anti-angiogenesis has been proposed as an important strategy for angiogenesis-related diseases. Cryptotanshinone (CPT), an active component of Salvia miltiorrhiza, may be a potential inhibitor of angiogenesis. However, the molecular mechanisms underlying its anti-angiogenic activities remain poorly understood. This study is to investigate the effects of CPT on VEGF-induced angiogenesis and VEGFR2 signaling pathway in human umbilical vein endothelial cells (HUVECs). METHODS: HUVECs were treated with different concentration of CPT (5-20µmol/L) and the viability, endothelial cell migration, invasion, and tubular-like structure formation of HUVECs were detected by MTT, wound-healing migration, Transwell invasion and Matrigel tube formation assays, respectively. To assess the effect of CPT on VEGFR2 signaling pathway, VEGF-induced phosphorylation of VEGFR2 and its downstream molecules, including ERK1/2, p90RSK, Src and FAK were analyzed by Western blot. RESULTS: CPT significantly suppressed VEGF-induced cells proliferation, migration, invasion, and tubular-like structure formation in HUVECs in a dose- and time-dependent manner. Western blot results revealed that CPT significantly suppressed VEGF-induced phosphorylation of VEGFR2 and its key downstream protein kinases, including p-ERK1/2, p-p90RSK, pY416-Src and pY576/577-FAK, which are responsible for endothelial cell migration, proliferation, and survival. CONCLUSION: Our study suggested that CPT potently inhibits VEGF-induced angiogenesis by suppressing VEGFR2 activation and its downstream Src/FAK and ERK1/2 signaling pathways in HUVECs, highlighting the therapeutic potential for the treatment of angiogenesis-related diseases.

ß, ß-Dimethylacrylshikonin induces mitochondria-dependent apoptosis of human lung adenocarcinoma cells in vitro via p38 pathway activation.

AIM: ß, ß-Dimethylacrylshikonin (DMAS) is an anticancer compound extracted from the roots of Lithospermum erythrorhizon. In the present study, we investigated the effects of DMAS on human lung adenocarcinoma cells in vitro and explored the mechanisms of its anti-cancer action. METHODS: Human lung adenocarcinoma A549 cells were tested. Cell viability was assessed using an MTT assay, and cell apoptosis was evaluated with flow cytometry and DAPI staining. The expression of the related proteins was detected using Western blotting. The mitochondrial membrane potential was measured using a JC-1 kit, and subcellular distribution of cytochrome c was analyzed using immunofluorescence staining. RESULTS: Treatment of A549 cells with DMAS suppressed the cell viability in dose- and time-dependent manners (the IC50 value was 14.22 and 10.61 µmol/L, respectively, at 24 and 48 h). DMAS (7.5, 10, and 15 µmol/L) dose-dependently induced apoptosis, down-regulated cIAP-2 and XIAP expression, and up-regulated Bax and Bak expression in the cells. Furthermore, DMAS resulted in loss of mitochondrial membrane potential and release of cytochrome c in the cells, and activated caspase-9, caspase-8, and caspase-3, and subsequently cleaved PARP, which was abolished by pretreatment with Z-VAD-FMK, a pan-caspase inhibitor. DMAS induced sustained p38 phosphorylation in the cells, while pretreatment with SB203580, a specific p38 inhibitor, blocked DMAS-induced p38 activation and apoptosis. CONCLUSION: DMAS inhibits the growth of human lung adenocarcinoma A549 cells in vitro via activation of p38 signaling pathway.

Element geochemical analysis of the contribution of aeolian sand to suspended sediment in desert stream flash floods.

The interaction of wind and water in semiarid and arid areas usually leads to low-frequency flash flood events in desert rivers, which have adverse effects on river systems and ecology. In arid zones, many aeolian dune-fields terminate in stream channels and deliver aeolian sand to the channels. Although aeolian processes are common to many desert rivers, whether the aeolian processes contribute to fluvial sediment loss is still unknown. Here, we identified the aeolian-fluvial cycling process responsible for the high rate of suspended sediment transport in the Sudalaer desert stream in the Ordos plateau of China. On the basis of element geochemistry data analysis, we found that aeolian sand was similar to suspended sediment in element composition, which suggests that aeolian sand contributes to suspended sediment in flash floods. Scatter plots of some elements further confirm that aeolian sand is the major source of the suspended sediment. Factor analysis and the relation between some elements and suspended sediment concentration prove that the greater the aeolian process, the higher the suspended sediment concentration and the greater the contribution of aeolian sand to suspended sediment yield. We conclude that aeolian sand is the greatest contributor to flash floods in the Sudalaer desert stream.

Taxus chinensis var. mairei (Lemée et Lévl) Cheng et L.K. Fu overcomes the resistance to osimertinib in EGFR-mutant non-small-cell lung cancer via suppression of ERK1/2-related cholesterol biosynthesis.

ETHNOPHARMACOLOGICAL RELEVANCE: Acquired resistance to osimertinib limits its clinical efficacy in non-small cell lung cancer (NSCLC) with EGFR mutations. The widespread recognition of Taxus chinensis var. Mairei (Lemée et Lévl) Cheng et L.K. Fu (Chinese yew) as a natural anti-cancer medication is well-established. However, the specific contribution of Taxus chinensis var. Mairei (Lemée et Lévl) Cheng et L.K. Fu in addressing resistance to osimertinib is still uncertain. AIM OF THE STUDY: Based on the biological behaviors and lipid metabolism, we investigated whether aqueous extract of Taxus chinensis var. Mairei (Lemée et Lévl) Cheng et L.K. Fu (AETC) could enhance the antitumor effect of osimertinib in NSCLC with an investigation on the precise mechanisms. MATERIALS AND METHODS: The effect of AETC on enhancing osimertinib sensitivity was assessed via cell viability measurements, levels of reactive oxygen species (ROS), apoptosis, and lipid levels. Western blotting was used to verify the mechanisms of AETC responsible for overcoming the resistance to osimertinib via ERK1/2 overexpression and knockdown models. In vivo validation was conducted using subcutaneous xenografts from osimertinib-resistant cells in nude mice. RESULTS: Osimertinib-resistant cells exhibited altered cholesterol biosynthesis, which was induced by ERK1/2 activation. The combination of AETC and osimertinib can synergistically decrease the levels of ROS in cells, enhance apoptosis, and inhibit the growth of osimertinib-resistant cells. Mechanistic experiments demonstrated that AETC can downregulate the key regulators of cholesterol biosynthesis by regulating ERK1/2, inhibiting the endogenous synthesis rate of cholesterol, and suppressing the level of lipids in osimertinib-resistant cells and xenograft tumors when combined with osimertinib, ultimately reversing resistance to osimertinib. CONCLUSIONS: The resistance to osimertinib is significantly influenced by cholesterol biosynthesis, highlighting its pivotal role in this context. AETC can enhance osimertinib sensitivity via ERK/SREBP-2/HMGCR-mediated cholesterol biosynthesis. These results provide a promising therapeutic target and potential treatment option for resistance to osimertinib.

Correlation of chronic atrophic gastritis with gastric-specific circulating biomarkers.

BACKGROUND AND STUDY AIMS: It has been suggested that the combined detection of multiple serum biomarkers can effectively screen out the high-risk population of chronic atrophic gastritis in the general population. Therefore, it is necessary to establish an effective predictive model of chronic atrophic gastritis. PATIENTS AND METHODS: Serum biopsies were assessed using five stomach-specific circulating biomarkers pepsinogen I (PGI), PGII, PGI/II ratio, anti- H. pylori antibody, and gastrin-17 (G-17) to identify high-risk individuals and evaluate the risk of developing chronic atrophic gastritis. RESULTS: In the cross-sectional analysis, PGII, the PG ratio, G17, anti- H. pylori IgG were positively associated with the presence of chronic atrophic gastritis, and combined prediction of the five biomarkers was more accurate than single-factor prediction ((0.692 vs 0.54(PG1), 0.604 (PGⅡ), 0.616(PGI/II ratio), 0.629(G-17)). CONCLUSION: The combination of PGI, PGII, the PGI/II ratio, G17, and anti-H. pylori antibodies for serological analysis are helpful to screen chronic atrophic gastritis high-risk subjects from the general population and recommend that these people carry out further endoscopy and biopsy.

Change pattern and stability of oasisization land in Mu Us Sandy Land.

Understanding land structure change and stability in the process of oasisization is particularly important for the desertification control in sandy land. Based on land use data of eight periods from 1980 to 2020, we extracted the spatial distribution information of oasis land in Mu Us Sandy Land, and analyzed the spatio-temporal variations of land transformation patterns and stability of oasis land with overlay analysis and grid analysis. The results showed that desertification in the Mu Us Sandy Land had reversed, with a significant process of oasis. The area of forest and grassland increased from 10.2% in 1980 to 73.7% in 2020, while the area of oasisization land increased from 32500 km2 in 1980 to 33900 km2 in 2020. The area of extremely severe, severe, and moderate desertification significantly decreased, while the area of non-desertification and mild desertification obviously increased. The four patterns of oasisization land transformation, including stability, fluctuation, expansion, and retreat, which accounted for 78.7%, 12.2%, 6.2%, and 2.9% of the oasisization land area in 2020, respectively. The oasisization land with low change intensity (the cumulative change intensity less than 0.12) in the Mu Us Sandy Land accounted for 82.7% of the total oasisization area, and the oasisization land in the sandy land was generally stable. Zoning management strategies should be applied according to the stability of sand belt and transformation pattern of oasisization land to achieve the goal of efficient system management and improvement, including eliminating sand hazards at desertification expansion areas with strong wind and sand activities, consolidating sand resources at oasisization areas where ecologically fragile desertification was frequent, and sustainably managing and utilizing sand resources at stable expansion of oases in forest- and grass-rich oasisization areas.

Tailoring Perovskite Surface Potential and Chelation Advances Efficient Solar Cells.

Modifying perovskite surface using various organic ammonium halide cations has proven to be an effective approach for enhancing the overall performance of perovskite solar cells. Nevertheless, the impact of the structural symmetry of these ammonium halide cations on perovskite interface termination has remained uncertain. Here, this work investigates the influence of symmetry on the performance of the devices, using molecules based on symmetrical bis(2-chloroethyl)ammonium cation (B(CE)A+) and asymmetrical 2-chloroethylammonium cation (CEA+) as interface layers between the perovskite and hole transport layer. These results reveal that the symmetrical B(CE)A+ cations lead to a more homogeneous surface potential and more comprehensive chelation with uncoordinated Pb2+ compared to the asymmetrical cations, resulting in a more favorable energy band alignment and strengthened defect healing. This strategy, leveraging the spatial geometrical symmetry of the interface cations, promotes hole carrier extraction between functional layers and reduces nonradiative recombination on the perovskite surface. Consequently, perovskite solar cells processed with the symmetrical B(CE)A+ cations achieve a power conversion efficiency (PCE) of 25.60% and retain ≈91% of their initial PCE after 500 h of maximum power point operation. This work highlights the significant benefits of utilizing structurally symmetrical cations in promoting the performance and stability of perovskite solar cells.

MorphBungee: A 65-nm 7.2-mm2 27-µJ/image Digital Edge Neuromorphic Chip with On-Chip 802-frame/s Multi-Layer Spiking Neural Network Learning.

This paper presents a digital edge neuromorphic spiking neural network (SNN) processor chip for a variety of edge intelligent cognitive applications. This processor allows high-speed, high-accuracy and fully on-chip spike-timing-based multi-layer SNN learning. It is characteristic of hierarchical multi-core architecture, event-driven processing paradigm, meta-crossbar for efficient spike communication, and hybrid and reconfigurable parallelism. A prototype chip occupying an active silicon area of 7.2 mm2 was fabricated using a 65-nm 1P9M CMOS process. when running a 256-256-256-256-200 4-layer fully-connected SNN on downscaled 16 × 16 MNIST images. it typically achieved a high-speed throughput of 802 and 2270 frames/s for on-chip learning and inference, respectively, with a relatively low power dissipation of around 61 mW at a 100 MHz clock rate under a 1.0V core power supply, Our on-chip learning results in comparably high visual recognition accuracies of 96.06%, 83.38%, 84.53%, 99.22% and 100% on the MNIST, Fashion-MNIST, ETH-80, Yale-10 and ORL-10 datasets, respectively. In addition, we have successfully applied our neuromorphic chip to demonstrate high-resolution satellite cloud image segmentation and non-visual tasks including olfactory classification and textural news categorization. These results indicate that our neuromorphic chip is suitable for various intelligent edge systems under restricted cost, energy and latency budgets while requiring in-situ self-adaptative learning capability.

Application of a novel nested ensemble algorithm in predicting motor function recovery in patients with traumatic cervical spinal cord injury.

Traumatic cervical spinal cord injury (TCSCI) often causes varying degrees of motor dysfunction, common assessed by the International Standards for Neurological Classification of Spinal Cord Injury (ISNCSCI), in association with the American Spinal Injury Association (ASIA) Impairment Scale. Accurate prediction of motor function recovery is extremely important for formulating effective diagnosis, therapeutic and rehabilitation programs. The aim of this study is to investigate the validity of a novel nested ensemble algorithm that uses the very early ASIA motor score (AMS) of ISNCSCI examination to predict motor function recovery 6 months after injury in TCSCI patients. This retrospective study included complete data of 315 TCSCI patients. The dataset consisting of the first AMS at ≤ 24 h post-injury and follow-up AMS at 6 months post-injury was divided into a training set (80%) and a test set (20%). The nested ensemble algorithm was established in a two-stage manner. Support Vector Classification (SVC), Adaboost, Weak-learner and Dummy were used in the first stage, and Adaboost was selected as second-stage model. The prediction results of the first stage models were uploaded into second-stage model to obtain the final prediction results. The model performance was evaluated using precision, recall, accuracy, F1 score, and confusion matrix. The nested ensemble algorithm was applied to predict motor function recovery of TCSCI, achieving an accuracy of 80.6%, a F1 score of 80.6%, and balancing sensitivity and specificity. The confusion matrix showed few false-negative rate, which has crucial practical implications for prognostic prediction of TCSCI. This novel nested ensemble algorithm, simply based on very early AMS, provides a useful tool for predicting motor function recovery 6 months after TCSCI, which is graded in gradients that progressively improve the accuracy and reliability of the prediction, demonstrating a strong potential of ensemble learning to personalize and optimize the rehabilitation and care of TCSCI patients.

Middle ear innovation in Early Cretaceous eutherian mammals.

The middle ear ossicles in modern mammals are repurposed from postdentary bones in non-mammalian cynodonts. Recent discoveries by palaeontological and embryonic studies have developed different models for the middle ear evolution in mammaliaforms. However, little is known about the evolutionary scenario of the middle ear in early therians. Here we report a detached middle ear preserved in a new eutherian mammal from the Early Cretaceous Jehol Biota. The well-preserved articulation of the malleus and incus suggest that the saddle-shaped incudomallear joint is a major apomorphy of Early Cretaceous eutherians. By contrast to the distinct saddle-like incudomallear articulation in therians, differences between the overlapping versus the half-overlapping incudomallear joints in monotremes and stem mammals would be relatively minor. The middle ear belongs to the microtype by definition, indicating its adaptation to high-frequency hearing. Current evidence indicates that significant evolutionary innovations of the middle ear in modern therians evolved in Early Cretaceous.

A new soft tissue constructed with chitosan for wound dressings-incorporating nanoparticles for medical and nursing therapeutic efficacy.

The skin, being the largest organ in the human body, plays a vital role in shielding internal organs from external physical and chemical factors. However, skin damage caused by various factors such as injuries, surgeries, diabetes, or burns can lead to wounds that diminish the skin's protective function. Monitoring essential physiological parameters like temperature, moisture, and pH is crucial to facilitate antibiotic treatment, remote physician monitoring, patient comfort, cost reduction, and prevention of hospital-acquired infections. To this end, innovative wound coverings made of biological materials like gelatin, carboxymethyl chitosan, and titanium nanoparticles have been developed, mainly for hospital and pediatric applications. These wound coverings come equipped with sensors to monitor temperature, pH, and moisture and are suitable for pediatric hospitals where children experience difficulty in wound healing due to their sensitive skin. The temperature monitoring feature allows physicians to accurately assess the wound's temperature, detect potential infections, and take prompt actions. These wound coverings can significantly enhance wound treatment for patients, as real-time monitoring of physiological parameters enables informed decision-making by physicians, leading to better therapeutic outcomes. Furthermore, the use of these wound coverings can minimize the risk of hospital-acquired infections. Their adaptability and flexibility make them ideal for various wound types and sizes, ensuring patient comfort and compliance with the treatment plan. In conclusion, the development of innovative and flexible wound coverings using biological materials and equipped with sensors represents a significant breakthrough in wound management. The use of these wound coverings has the potential to revolutionize wound care and improve patient outcomes, particularly in pediatric hospitals where wound healing is often challenging.