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Conventional wireless communication architecture, a backbone of our modern society, relies on actively generated carrier signals to transfer information, leading to important challenges including limited spectral resources and energy consumption. Backscatter communication systems, on the other hand, modulate an antenna’s impedance to encode information into already existing waves but suffer from low data rates and a lack of information security. Here, we introduce the concept of massive backscatter communication which modulates the propagation environment of stray ambient waves with a programmable metasurface. The metasurface’s large aperture and huge number of degrees of freedom enable unprecedented wave control and thereby secure and high-speed information transfer. Our prototype leveraging existing commodity 2.4 GHz Wi-Fi signals achieves data rates on the order of hundreds of Kbps. Our technique is applicable to all types of wave phenomena and provides a fundamentally new perspective on the role of metasurfaces in future wireless communication. Leveraging the large aperture and huge number of degrees of freedom offered by a programmable metasurface, the authors modulate the propagation environment of existing background commodity Wi-Fi signals to implement a secure and high-speed massive-backscatter communication link.

Conventional microwave imagers usually require either time-consuming data acquisition, or complicated reconstruction algorithms for data post-processing, making them largely ineffective for complex in-situ sensing and monitoring. Here, we experimentally report a real-time digital-metasurface imager that can be trained in-situ to generate the radiation patterns required by machine-learning optimized measurement modes. This imager is electronically reprogrammed in real time to access the optimized solution for an entire data set, realizing storage and transfer of full-resolution raw data in dynamically varying scenes. High-accuracy image coding and recognition are demonstrated in situ for various image sets, including hand-written digits and through-wall body gestures, using a single physical hardware imager, reprogrammed in real time. Our electronically controlled metasurface imager opens new venues for intelligent surveillance, fast data acquisition and processing, imaging at various frequencies, and beyond. Conventional imagers require time-consuming data acquisition, or complicated reconstruction algorithms for data post-processing. Here, the authors demonstrate a real-time digital-metasurface imager that can be trained in-situ to show high accuracy image coding and recognition for various image sets.

A microarray analysis of an animal model with experimental sepsis induced by caecal ligation and puncture revealed that the level of microRNA-195 (miR-195) was upregulated. However, to the best of our knowledge, the role of miR-195 in sepsis remains unknown. The present study investigated the effect of miR-195 on apoptosis in sepsis and investigated the underlying mechanism. The level of miR-195 was measured in human intestinal epithelial cells following exposure to lipopolysaccharide (LPS). Cell viability and apoptosis were detected using Cell Counting kit-8 and flow cytometry assays. The expression levels of apoptosis-associated proteins were determined using western blot analysis. In addition, a dual-luciferase reporter assay was employed to verify the association between miR-195 and sirtuin 1 (SIRT1). Furthermore, the SIRT1 inhibitor EX527 was applied to further confirm the regulatory network of miR-195/SIRT1 in LPS-induced apoptosis. It was demonstrated that LPS significantly inhibited cell viability and promoted cell apoptosis in NCM460 cells in a dose-dependent manner. In addition, miR-195 was significantly upregulated following LPS treatment. The present results revealed that silencing miR-195 prevented apoptosis and alleviated cell injury in LPS-induced NCM460 cells. Further investigation demonstrated that miR-195 bound directly to and negatively regulated SIRT1. Inhibition of SIRT1 reversed the protective effects of miR-195-silencing on the apoptosis and viability of NCM460 cells. Furthermore, silencing miR-195 prevented endoplasmic reticulum (ER) stress-induced apoptosis via a downregulation of SIRT1 and its downstream effectors, including activating transcription factor 4, C/EBP homologous protein, glucose-regulated protein 78 and growth arrest and DNA-damage protein 34, as well as the phosphorylation of eukaryotic translation initiation factor 2A. In conclusion, the present study revealed a novel mechanism by which miR-195 regulates SIRT1-mediated downstream effectors in ER stress-induced apoptosis in sepsis.

Osteoporosis is a metabolic bone disease that seriously jeopardizes the health of middle‐aged and elderly people. Mesenchymal stem cell‐based transplantation for osteoporosis is a promising new therapeutic strategy. Induced mesenchymal stem cells (iMSCs) are a new option for stem cell transplantation therapy. Acquired mouse skin fibroblasts were transduced and reprogrammed into induced pluripotent cells and further induced to differentiate into iMSCs. The iMSCs were tested for pluripotency markers, trilineage differentiation ability, cell surface molecular marker tests, and gene expression patterns. The iMSCs were injected into the tail vein of mice by tail vein injection, and the distribution of cells in various organs was observed. The effect of iMSCs on the bone mass of mice was detected after injection into the mouse osteoporosis model. The effects of iMSCs infusion on metabolites in femoral tissue and peripheral blood plasma were detected based on LC–MS untargeted metabolomics. iMSCs have similar morphology, immunophenotype, in vitro differentiation potential, and gene expression patterns as mesenchymal stem cells. The iMSCs were heavily distributed in the lungs after infusion and gradually decreased over time. The iMSCs in the femoral bone marrow cavity gradually increased with time. iMSCs infusion significantly avoided bone loss due to oophorectomy. The results of untargeted metabolomics suggest that amino acid and lipid metabolic pathways are key factors involved in iMSCs bone protection and prevention of osteoporosis formation. iMSCs obtained by reprogramming‐induced differentiation had cellular properties similar to those of bone marrow mesenchymal stem cells. The iMSCs could promote the remodelling of bone structure in ovariectomy‐induced osteoporotic mice and affect the changes of several key metabolites in bone and peripheral blood. Some of these metabolites can serve as potential biomarkers and therapeutic targets for iMSCs intervention in osteoporosis. Investigating the effects of iMSCs on osteoporosis and the influence of metabolic pathways will provide new ideas and methods for the clinical treatment of osteoporosis.

Background Human immunodeficiency virus (HIV) and enteric parasite co-infection not only aggravates the clinical symptoms of parasites but also accelerates acquired immunodeficiency syndrome (AIDS) progression. However, co-infection research on men who have sex with men (MSM), the predominant high-risk population of HIV/AIDS in China, is still limited. In this study, we investigated the epidemiology of enteric parasites, risk factors, and associations with clinical significance in an MSM HIV/AIDS population in Heilongjiang Province, northeast China. Methods We recruited 308 MSMs HIV/AIDS patients and 199 HIV-negative individuals in two designated AIDS hospitals in Heilongjiang between April 2016 and July 2017. Fresh stool samples were collected. DNA extraction, molecular identification, and genotyping of Cryptosporidium species, Entamoeba histolytica, Cyclospora cayetanensis, Enterocytozoon bieneusi, and Blastocystis hominis were performed. Fourteen diarrhea-related pathogens were examined to exclude the influence of other bacterial pathogens on diarrhea incidence. Results 31.5% of MSM HIV/AIDS participants were infected with at least one parasite species, a significantly higher proportion than that found in the HIV-negative individuals (2.5%). E. bieneusi presented the highest prevalence, followed by B. hominis, E. histolytica, Cryptosporidium spp., and C. cayetanensis. Warm seasons were the risk factor for parasitic infections in this population [odds ratio (OR) = 2.6, 95% CI: 1.47-4.57]. In addition, these individuals showed a higher proportion (35.8%) of present diarrhea (PD) compared with men who have sex with women (MSW) with HIV/AIDS (16.7%). The infection proportions of both Cryptosporidium spp. and E. histolytica were significantly higher in the PD. E. bieneusi infection was more prevalent in the historic diarrhea (HD) group. CD4.sup.+ T cell counts in the MSM patients with the above three parasites were significantly lower. New species and genotypes were found, and MSM patients had a wider range of species or genotypes. Conclusions Enteric parasitic infection was prevalent in the MSM HIV/AIDS population, especially in patients with present diarrhea during warm seasons. E. histolytica and B. hominis should also be considered high-risk parasites for opportunistic infections in AIDS patients in addition to Cryptosporidium spp.

OP, a systemic bone disorder marked by reduced bone mass and heightened fracture risk, poses a significant global health burden, particularly among aging populations. Current treatments, including bisphosphonates and calcium supplementation, are limited by adverse effects and incomplete efficacy. Emerging research highlights ferroptosis—an iron-dependent cell death driven by lipid peroxidation—as a critical contributor to OP pathogenesis, characterized by dysregulated iron metabolism, oxidative stress, and lipid peroxide accumulation, which disrupt bone remodeling by impairing osteoblast function and enhancing osteoclast activity. This review elucidates the mechanistic interplay between ferroptosis and OP subtypes (diabetic osteoporosis (DOP), glucocorticoid-induced (GIOP), and postmenopausal osteoporosis (PMOP)) and evaluates the efficacy of Chinese herbal interventions in mitigating ferroptosis-driven bone loss. Key findings reveal that excess iron exacerbates lipid peroxidation via the Fenton reaction, while glutathione peroxidase 4 (GPX4) inactivation and system Xc- inhibition amplify oxidative damage. In DIOP, hyperglycemia-induced ROS and advanced glycation end products suppress osteogenesis, countered by melatonin and naringenin via nuclear factor -related factor 2 (Nrf2)/GPX4 activation. GIOP involves dexamethasone-mediated GPX4 downregulation, mitigated by exosomes and melatonin through phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling. PMOP driven by estrogen deficiency-induced iron overload is alleviated by aconitine and icariin (ICA) via nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and signal transducer and activator of transcription 3 (STAT3) pathways. Chinese herbs, including active compounds (quercetin, gastrodin, ICA, etc.) and formulations (Bugu Shengsui Capsule, Erxian Decoction (EXD), etc.), regulate iron metabolism, enhance antioxidant defenses (Nrf2/heme oxygenase 1(HO-1)), and inhibit lipid peroxidation, effectively restoring bone homeostasis. These findings underscore ferroptosis as a pivotal mechanism in OP progression and highlight the therapeutic promise of Chinese herbs in bridging traditional medicine with modern mechanistic insights. Future research should prioritize elucidating precise molecular targets, optimizing formulations, and validating clinical efficacy to address current therapeutic gaps.

Background: An accurate and objective criterion is needed to determine candidates who are suitable for hip arthroscopy in patients with femoroacetabular impingement (FAI). Purpose: To determine whether improvement in pain after ultrasound (US)-guided intra-articular hip injection during standardized examinations can be used to predict the outcomes of hip arthroscopy in patients with FAI. Study Design: Cohort study; Level of evidence, 3. Methods: We enrolled 119 patients with FAI who underwent US-guided intra-articular hip injection of local anesthesia during standardized examinations, carried out from May 2018 to February 2020 (within 2 weeks before hip arthroscopy). All patients had undergone a minimum of 6 months of nonoperative treatment without remission and had 2-year follow-up data. Pain visual analog scale (VAS) scores (0-10) were recorded for 7 different physical examination tests, and a total score (0 [best] to 70 [worst]) was obtained. In addition, International Hip Outcome Tool–12 (iHOT-12) and modified Harris Hip Score (mHHS) scores were recorded before hip arthroscopy and at final follow-up. According to whether patients achieved the substantial clinical benefit (SCB) on the iHOT-12, they were divided into SCB and non-SCB groups, and the improvement in VAS pain scores from preinjection to postinjection (ΔVAS pain) was compared between the 2 groups. Logistic regression analysis was used to predict the achievement of SCB, and the area under the receiver operating characteristic curve (AUC) was used to estimate the accuracy of the prediction. Results: There was a significant pre- to postoperative increase in iHOT-12 (31.6 points; P < .001) and mHHS (20.0 points; P < .001) scores, and 84 (70.6%) patients achieved the SCB. The ΔVAS pain score was significantly greater in the SCB versus the non-SCB group (16.0 vs 7.0 points; respectively; P < .001). Logistic regression analysis demonstrated an optimal cutoff value of 8.5 points for ΔVAS pain (AUC, 0.772; 95% CI, 0.687-0.858). For patients with more severe symptoms (total preinjection VAS pain score of >10 out of 70), the accuracy of the prediction for ΔVAS pain had a better evaluation value (AUC, 0.834; 95% CI, 0.676-0.992). Conclusion: Improvement in pain after US-guided intra-articular hip injection predicted the outcomes of hip arthroscopy in patients with FAI in this study, especially for patients with more severe pain.

Diagnostic markers for both colorectal cancer (CRC) and its precursor lesions are lacking. Although aberrant methylation of the secretin receptor (SCTR) gene was observed in CRC, the diagnostic performance has not been evaluated. Therefore, this study aimed to assess and verify the diagnostic value of SCTR methylation of CRC and its precursor lesions through integrating the largest methylation data. The diagnostic performance of SCTR methylation was analyzed in the discovery set from The Cancer Genome Atlas (TCGA) CRC methylation data (N = 440), and verified in a large‐scale test set (N = 938) from the Gene Expression Omnibus (GEO). Targeted bisulfite sequencing analysis was developed and applied to detect the methylation status of SCTR in our independent validation set (N = 374). Our findings revealed that the SCTR gene was frequently hypermethylated at its CpG islands in CRC. In the TCGA discovery set, the diagnostic score was constructed using 4 CpG sites (cg01013590, cg20505223, cg07176264, and cg26009192) and achieved high diagnostic performance (area under the ROC curve [AUC] = 0.964). In the GEO test set, the diagnostic score had robust diagnostic ability to distinguish CRC (AUC = 0.948) and its precursor lesions (AUC = 0.954) from normal samples. Moreover, hypermethylation of the SCTR gene was also found in cell‐free DNA samples collected from CRC patients, but not in those from healthy controls. In the validation set, consistent results were observed using the targeted bisulfite sequencing array. Our study highlights that hypermethylation at CpG islands of the SCTR gene is a potential diagnostic biomarker in CRCs and its precursor lesions. Hypermethylation at CpG island of the SCTR gene holds great promise as a diagnostic biomarker of CRC and its precursor lesions.

Background and aims Recent studies have demonstrated the relationship between Helicobacter pylori infection and the risk of colorectal carcinoma. However, the results of these studies remain controversial as the studies were relatively small in size and partially differed in designs, and so we reviewed the published studies and carried out a meta-analysis to further explore this relationship. Materials and methods We performed an extensive systematic review to find all the published case–control studies up to Jan. 2007 using electronic searching, hand searching, and reference lists of retrieved articles. Odds ratio (OR) was employed to evaluate the relationship of H. pylori infection and risk of colorectal cancer. Summary estimates were obtained using random effect models according to the result of a statistical test for heterogeneity across the studies. The presence of possible publication bias was assessed using different statistical approaches. Results Thirteen studies were included, and summary OR 1.49 (95% confidence interval [CI] 1.17–1.91) was estimated for the association between H. pylori infection and colorectal cancer. Summary OR 1.56 (95% CI 1.14–2.14) was estimated for the association between immunoglobulin G antibody and colorectal cancer risk. By trimming and filling, the number of inputted studies was zero, and summary OR was still 1.49 (95% CI 1.17–1.91). The graphical funnel plot appeared asymmetrical, but there was no statistical evidence of publication bias. The method of fail-safe suggested that the effect of publication bias was small. Conclusion Current evidence, though limited, suggests that there is a possible increase in risk of colorectal cancer because of H. pylori infection.

The association between non-steroidal anti-inflammatory drugs (NSAIDs) use and breast cancer has remained controversial. Therefore, an overall quantitative estimate of the association needs to be studied. A systematic review and meta-analysis was executed to explore the pooled estimate for relative risk (RR) and 95% confidence interval (CI) using random or fixed effects models based on heterogeneity analysis. Overall 26 studies with 528,705 participants were included. The RR of NSAIDs use and the incidence of breast cancer was 0.94 (95% CI: 0.88-1.00) with random effects model. A slight reduction of breast cancer by taking aspirin and ibuprofen was both observed with pooled RR of 0.91 (95% CI: 0.83-0.98) and 0.81 (95% CI: 0.67-0.97), respectively. Our results indicate that NSAIDs use is associated with a slight decrease for the development of breast cancer with a marginally statistical significant difference. The associations are slightly more obvious in aspirin and ibuprofen use.