Explore the vast range of titles available.

We report epidemiologic, laboratory, and clinical findings for 7 patients with 2019 novel coronavirus disease in a 2-family cluster. Our study confirms asymptomatic and human-to-human transmission through close contacts in familial and hospital settings. These findings might also serve as a practical reference for clinical diagnosis and medical treatment.

Osteomyelitis is a devastating disease caused by microbial infection in deep bone tissue. Its high recurrence rate and impaired restoration of bone deficiencies are major challenges in treatment. Microbes have evolved numerous mechanisms to effectively evade host intrinsic and adaptive immune attacks to persistently localize in the host, such as drug-resistant bacteria, biofilms, persister cells, intracellular bacteria, and small colony variants (SCVs). Moreover, microbial-mediated dysregulation of the bone immune microenvironment impedes the bone regeneration process, leading to impaired bone defect repair. Despite advances in surgical strategies and drug applications for the treatment of bone infections within the last decade, challenges remain in clinical management. The development and application of tissue engineering materials have provided new strategies for the treatment of bone infections, but a comprehensive review of their research progress is lacking. This review discusses the critical pathogenic mechanisms of microbes in the skeletal system and their immunomodulatory effects on bone regeneration, and highlights the prospects and challenges for the application of tissue engineering technologies in the treatment of bone infections. It will inform the development and translation of antimicrobial and bone repair tissue engineering materials for the management of bone infections.

Background Predicting individual patient responses to anticancer drugs is a central challenge in precision oncology, hindered by the scarcity of clinical pharmacogenomic data and substantial biological dissimilarity between preclinical models and patient tumors. Patient-derived xenograft (PDX) models offer significantly enhanced tumor biological fidelity compared to in vitro cancer cell line models, yet computational methods to translate PDX-based drug response predictions (DRP) into clinical settings remain limited. Methods We developed TRANSPIRE-DRP, a deep learning framework that bridges the translational gap between PDX models and patient tumors through unsupervised domain adaptation. The framework employs a two-stage architecture: first, an autoencoder-based pretraining phase learns domain-invariant genomic representations from large-scale unlabeled data; second, an adversarial adaptation phase aligns these representations while preserving drug response signals from PDX models. We evaluated TRANSPIRE-DRP across three therapeutic agents—Cetuximab, Paclitaxel, and Gemcitabine—in real-life clinical prediction scenarios. Results TRANSPIRE-DRP consistently outperformed both cell line-based state-of-the-art models and PDX-based baselines, demonstrating superior translational capacity. Notably, the learned representations preserved tumor-specific molecular features and spontaneously recapitulated established drug-cancer type associations without requiring explicit histological annotations. Interpretability analyses revealed biologically coherent pathway enrichments consistent with known drug mechanisms of action, including EGFR-Wnt signaling crosstalk for Cetuximab, mitotic arrest mechanism for Paclitaxel, and NF-κB-mediated immunomodulation for Gemcitabine. Conclusions TRANSPIRE-DRP establishes a scalable, interpretable, and clinically relevant framework for translating preclinical PDX data into personalized therapeutic predictions, providing a robust computational foundation for advancing precision oncology beyond the inherent limitations of traditional in vitro systems.

Regulating macrophage activation precisely is crucial in treating chronic inflammation in osteoarthritis (OA). However, the stable pro-inflammatory state and deep distribution of macrophages in vivo pose a great challenge to treatment. In this study, inspired by the innate immune, immune cell mobilized hydrogel microspheres were constructed by microfluidic methods and load chemokines, macrophage antibodies and engineered cell membrane vesicles (sEVs) via covalent and non-covalent junctions. The immune cell mobilized hydrogel microspheres, based on a mixture of streptavidin grafted hyaluronic acid methacrylate (HAMA-SA) and Chondroitin sulfate methacrylate (ChSMA) microspheres (HCM), can recruit, capture and reprogram proinflammatory macrophages in the joint cavity to improve the joint inflammatory microenvironment. In vitro experiments demonstrated that immune cell mobilized hydrogel microspheres had excellent macrophage recruitment, capture, and reprogramming abilities. Pro-inflammatory macrophages can be transformed into anti-inflammatory macrophages with an efficiency of 88.5 %. Animal experiments also revealed significant reduction in synovial inflammation and cartilage matrix degradation of OA. Therefore, the immune cell mobilized hydrogel microspheres may be an effective treatment of OA inflammation for the future.

The mechanical deformation of coals occurring extensively during the geological period (tectonically deformed coals) can directly alter their pore structures and then the storage of coalbed methane. This study in-situ investigated the effects of different mechanical deformations on the ultramicropore structure and the methane adsorption of coal molecules using molecular simulations. The results show that the shear deformation (< 0.23 GPa) of coals was much easier than the compression (~ 20 GPa). Further, the shear deformation can increase the void fraction (200%) and the surface area (30%) of coal molecules, comparing to the reduction of them by the compressive deformation. Accordingly, compression is not benefited to the methane storage (only remaining 14-22% adsorption amount). While, the shear deformation of coals can increase the methane adsorption amount (reaching 42–50 mmol/g). The ~ 7.5 Å is a key pore size to evaluate the effect of the shear deformation on the methane adsorption amount. Also, the adsorption sites for methane depends on the deformation mode of coals (compression: heteroatoms; shear: C atoms). Overall, the strained Wiser (bituminous, medium-rank) coal shows relatively superiority in the methane storage, while the methane adsorption of Wender (lignite, low-rank) coal is much more sensitive to the mechanical strain.

Background G protein‐coupled receptors (GPCRs), the largest family of cell‐surface molecules involve in various signal transduction, have recently been recognized as important drivers of cancer. However, few studies have reported on the potential of GPCRs as therapeutic targets or biomarkers in lung adenocarcinoma (LUAD). Methods The expression profiles and clinical data of LUAD in the GSE30219 and GSE18842 datasets of the Cancer Genome Atlas were analyzed. LUAD‐associated module genes were screened utilizing weighted gene co‐expression network analysis (WGCNA). Prognostic signature genes were identified by univariate Cox survival analysis, LASSO regression, and multivariate Cox regression analyses. The immune status was evaluated and drug sensitivity was determined, conducting in vitro experiments for validation. Results Patients with LUAD exhibited lower GPCR score than the controls, and 38 dysregulated GPCRs were identified by screening with differential analysis and WGCNA module genes. An optimal prognostic signature was identified, including OR51E1, LGR4, ADRB1, ADGRD1, and ADGRE3. The model established based on these five genes harbored moderate predictive performance for the survival of patients with LUAD. The risk score was negatively correlated with the infiltrating levels of multiple immune cells, including M2 macrophages, myeloid dendritic cells, and neutrophils, but positively correlated with fewer immune cells, such as Th1/Th2 CD4 + T cell. ADGRE3 and OR51E1 expression was positively correlated with drug sensitivity, including to cisplatin, ribociclib, and pevonedistat. Silencing OR51E1 inhibited the malignant cytological behaviors of LUAD cells. Conclusion GPCRs demonstrated prognostic potential in LUAD, with five genes identified as potential therapeutic targets and prognostic biomarkers for LUAD. This integrated analysis demonstrates the involvements of G protein‐coupled receptors (GPCRs) in lung adenocarcinoma developments and proves the potential of five key GPCRs as prognostic biomarkers and targets in lung adenocarcinoma.

Subcellular mitochondria serve as sensors for energy metabolism and redox balance, and the dynamic regulation of functional and dysfunctional mitochondria plays a crucial role in determining cells' fate. Selective removal of dysfunctional mitochondria at the subcellular level can provide chondrocytes with energy to prevent degeneration, thereby treating osteoarthritis. Herein, to achieve an ideal subcellular therapy, cartilage affinity peptide (WYRGRL)-decorated liposomes loaded with mitophagy activator (urolithin A) were integrated into hyaluronic acid methacrylate hydrogel microspheres through microfluidic technology, named HM@WY-Lip/UA, that could efficiently target chondrocytes and selectively remove subcellular dysfunctional mitochondria. As a result, this system demonstrated an advantage in mitochondria function restoration, reactive oxygen species scavenging, cell survival rescue, and chondrocyte homeostasis maintenance through increasing mitophagy. In a rat post-traumatic osteoarthritis model, the intra-articular injection of HM@WY-Lip/UA ameliorated cartilage matrix degradation, osteophyte formation, and subchondral bone sclerosis at 8 weeks. Overall, this study indicated that HM@WY-Lip/UA provided a protective effect on cartilage degeneration in an efficacious and clinically relevant manner, and a mitochondrial-oriented strategy has great potential in the subcellular therapy of osteoarthritis.

The \"geochemical effect of lanthanides\" is a new concept proposed by the authors during the past decade. This concept reflects lanthanide shrinkage in elemental geochemistry, and it is statistically quantifiable. However, the geological significance of the various parameters of the equations obtained following quantization is not entirely clear. Cooperation and discussions from scholars in related research fields of rare earth elements in geology are required. In the present paper, from the perspective of coal geochemistry, the metamorphic coal seam of C2 series in Fengfeng Mine of Handan Coalfield in Hebei Province, China was used as an example. The geochemical significance of parameters in geochemical effect regression equation for lanthanides was evaluated, and two new formulas (regression equations) that characterized the geochemical behaviors of lanthanides were proposed. On this basis, concepts related to the geochemical effect of lanthanides, such as “individual parameters”, “parameters in common”, “two-sided parameters”, and the “deviation value” of lanthanides, were proposed. In this study, it was proved that the goodness of fit for all types of function regression equations for lanthanides and the radii of their trivalent ions, and the “deviation value” of lanthanides, were all “individual parameters” that could indicate the post-modified geological environment of C2 coal seam, such as the influence from magmatic-hydrothermal fluids. A covariant figure was constructed according to these individual parameters and other indexes, and the C2 coal seam in Handan was effectively divided into two different metamorphic series of A (C2 coal seam uninfluenced or slightly influenced by magmatic-hydrothermal fluids) and B (C2 coal seam strongly influenced and evidently changed by magmatic-hydrothermal fluids). Consequently, the scientific significance of all the parameters for lanthanides in an identifying series of metamorphic coals within the geochemical effect regression equation was further clarified.

Background The immune evasion and prolonged survival of Staphylococcus aureus ( S. aureus ) within macrophages are key factors contributing to the difficulty in curing osteomyelitis. Although macrophages play a vital role as innate immune cells, the mechanisms by which S. aureus survives within them and suppresses host immune functions remain incompletely understood. Methods This study employed confocal microscopy, flow cytometry, ELISA, and siRNA technology to assess the survival capacity of S. aureus within macrophages and the impact of inflammatory cytokines on its persistence. Proteomics was used to investigate the potential mechanisms and differential proteins involved in S. aureus intracellular survival. Additionally, confocal microscopy, flow cytometry, Mdivi-1 intervention, and Western blot were utilized to validate the role of mitophagy in supporting S. aureus survival. The study further explored how the HDAC11/IL10 axis enhances mitophagy to promote intracellular S. aureus survival by using HDAC11 overexpression, siRNA, and rapamycin intervention combined with confocal microscopy and flow cytometry. Results The findings demonstrated that IL10 promotes mitophagy to clear mitochondrial reactive oxygen species (mtROS), thereby enhancing the intracellular survival of S. aureus within macrophages. Additionally, we discovered that the transcriptional repressor of IL10, HDAC11, was significantly downregulated during S. aureus infection. Overexpression of HDAC11 and the use of the autophagy activator rapamycin further validated that the HDAC11/IL10 axis regulates mitophagy via the mTOR pathway, which is essential for supporting S. aureus intracellular survival. Conclusion This study reveals that S. aureus enhances IL10 production by inhibiting HDAC11, thereby promoting mitophagy and mtROS clearance, which supports its survival within macrophages. These findings offer new insights into the intracellular survival mechanisms of S. aureus and provide potential therapeutic approaches for the clinical management of osteomyelitis.

In SRAM cells, as the size of transistors and the distance between transistors decrease rapidly, the critical charge of the sensitive node decreases, making SRAM cells more susceptible to soft errors. If radiation particles hit the sensitive nodes of a standard 6T SRAM cell, the data stored in the cell are flipped, resulting in a single event upset. Therefore, this paper proposes a low-power SRAM cell, called PP10T, for soft error recovery. To verify the performance of PP10T, the proposed cell is simulated by the 22 nm FDSOI process, and compared with the standard 6T cell and several 10T SRAM cells, such as Quatro-10T, PS10T, NS10T, and RHBD10T. The simulation results show that all of the sensitive nodes of PP10T can recover their data, even when S0 and S1 nodes flip at the same time. PP10T is also immune to read interference, because the change of the ‘0’ storage node, directly accessed by the bit line during the read operation, does not affect other nodes. In addition, PP10T consumes very low-holding power due to the smaller leakage current of the circuit.