Revealing the effect of sea buckthorn oil, fish oil and structured lipid on intestinal microbiota, colonic short chain fatty acid composition and serum lipid profiles in vivo.

In this study, the effects of sea buckthorn oil (SBO), fish oil (FO) and an enzymatically synthesized structured lipid (SL) on serum, short-chain fatty acids (SCFAs) and intestinal microbiota in Sprague-Dawley (SD) rats were investigated. The results demonstrated that FO, SBO, and SL effectively reduced the levels of high-density lipoprotein cholesterol and low-density lipoprotein cholesterol in the serum of SD rats. SBO increased serum triglyceride levels, while FO elevated total cholesterol levels. Furthermore, all three dietary lipids decreased short-chain fatty acid production and enhanced intestinal microbiota diversity. FO increased the abundance of intestinal microbiota including Romboutsia, Lactobacillus, Escherichia-Shigella, and Lachnospiraceae_NK4A136_group. Conversely, all three dietary lipids reduced the abundance of Klebsiella and Blautia. These findings provide a foundation for understanding the functionality of SBO and FO as well as their potential application in synthesizing novel SLs to regulate intestinal microbiota.

A lever hypothesis for Synaptotagmin-1 action in neurotransmitter release.

Neurotransmitter release is triggered in microseconds by Ca2+-binding to the Synaptotagmin-1 C2 domains and by SNARE complexes that form four-helix bundles between synaptic vesicles and plasma membranes, but the coupling mechanism between Ca2+-sensing and membrane fusion is unknown. Release requires extension of SNARE helices into juxtamembrane linkers that precede transmembrane regions (linker zippering) and binding of the Synaptotagmin-1 C2B domain to SNARE complexes through a 'primary interface' comprising two regions (I and II). The Synaptotagmin-1 Ca2+-binding loops were believed to accelerate membrane fusion by inducing membrane curvature, perturbing lipid bilayers or helping bridge the membranes, but SNARE complex binding orients the Ca2+-binding loops away from the fusion site, hindering these putative activities. Molecular dynamics simulations now suggest that Synaptotagmin-1 C2 domains near the site of fusion hinder SNARE action, providing an explanation for this paradox and arguing against previous models of Sytnaptotagmin-1 action. NMR experiments reveal that binding of C2B domain arginines to SNARE acidic residues at region II remains after disruption of region I. These results and fluorescence resonance energy transfer assays, together with previous data, suggest that Ca2+ causes reorientation of the C2B domain on the membrane and dissociation from the SNAREs at region I but not region II. Based on these results and molecular modeling, we propose that Synaptotagmin-1 acts as a lever that pulls the SNARE complex when Ca2+ causes reorientation of the C2B domain, facilitating linker zippering and fast membrane fusion. This hypothesis is supported by the electrophysiological data described in the accompanying paper.

Combining GC-MS/MS with a LLE-SPE sample pretreatment step to simultaneously analyse enrofloxacin and ofloxacin residues in chicken tissues and pork.

A widely applicable original gas chromatography-tandem mass spectrometry (GC-MS/MS) method was explored to qualitatively and quantitatively measure enrofloxacin and ofloxacin residues in chicken tissues and pork. The experimental samples were processed based on liquid-liquid extraction (LLE) and solid-phase extraction (SPE). Trimethylsilyl diazomethane (TMSD) was chosen to react derivatively with enrofloxacin and ofloxacin. In total, 78.25% âˆ¼ 90.56% enrofloxacin and 78.43% âˆ¼ 91.86% ofloxacin was recovered from the blank fortified samples. The limits of detection (LODs) were 0.7-1.0 µg/kg and 0.1-0.2 µg/kg, respectively. The limits of quantitation (LOQs) were 1.6-1.9 µg/kg and 0.3-0.4 µg/kg, respectively. It was verified that various experimental data met the requirements of the FAO & WHO (2014) for the detection of veterinary drug residues. Real samples obtained from local markets were analysed using the established method, and no residues of enrofloxacin or ofloxacin were detected in the samples.

Dynamic patterns of carbohydrate metabolism genes in bacterioplankton during marine algal blooms.

Carbohydrates play a pivotal role in nutrient recycling and regulation of algal-bacterial interactions. Despite their ecological significance, the intricate molecular mechanisms governing regulation of phycosphere carbohydrates by bacterial taxa linked with natural algal bloom have yet to be fully elucidated. Here, a comprehensive temporal metagenomic analysis was conducted to explore the carbohydrate-active enzyme (CAZyme) genes in two discrete algal bloom microorganisms (Gymnodinium catenatum and Phaeocystis globosa) across three distinct bloom stages: pre-bloom, peak bloom, and post-bloom. Elevated levels of extracellular carbohydrates, primarily rhamnose, galactose, glucose, and arabinose, were observed during the initial and post-peak stages. The prominent CAZyme families identified-glycoside hydrolases (GH) and carbohydrate-binding modules (CBMs)-were present in both algal bloom occurrences. In the G. catenatum bloom, GH23/24 and CBM13/14 were prevalent during the pre-bloom and peak bloom stages, whereas GH2/3/30 and CBM12/24 exhibited increased prevalence during the post-bloom phase. In contrast, the P. globosa bloom had a dominance of GH13/23 and CBM19 in the initial phase, and this was succeeded by GH3/19/24/30 and CBM54 in the later stages. This gene pool variation-observed distinctly in specific genera-highlighted the dynamic structural shifts in functional resources driven by temporal alterations in available substrates. Additionally, ecological linkage analysis underscored a correlation between carbohydrates (or their related genes) and phycospheric bacteria, hinting at a pattern of bottom-up control. These findings contribute to understanding of the dynamic nature of CAZymes, emphasizing the substantial influence of substrate availability on the metabolic capabilities of algal symbiotic bacteria, especially in terms of carbohydrates.

Optimal tibial tunnel angulation for anatomical anterior cruciate ligament reconstruction using transtibial technique.

Numerous studies have suggested that the primary cause of failure in transtibial anterior cruciate ligament reconstruction (ACLR) is often attributed to non-anatomical placement of the bone tunnels, typically resulting from improper tibial guidance. We aimed to establish the optimal tibial tunnel angle for anatomical ACLR by adapting the transtibial (TT) technique. Additionally, we aimed to assess graft bending angle (GBA) and length changes during in vivo dynamic flexion of the knee. Twenty knee joints underwent a CT scan and dual fluoroscopic imaging system (DFIS) to reproduce relative knee position during dynamic flexion. For the single-legged lunge, subjects began in a natural standing position and flexed the right knee beyond 90° When performing the lunge task, the subject supported the body weight on the right leg, while the left leg was used to keep the balance. The tibial and femoral tunnels were established on each knee using a modified TT technique for single-bundle ACLR. The tibial tunnel angulation to the tibial axis and the sagittal plane were measured. Considering that ACL injuries tend to occur at low knee flexion angles, GBA and graft length were measured between 0° and 90° of flexion in this study. The tibial tunnel angulated the sagittal plane at 42.8° ± 3.4°, and angulated the tibial axis at 45.3° ± 5.1° The GBA was 0° at 90° flexion of the knee and increased substantially to 76.4 ± 5.5° at 0° flexion. The GBA significantly increased with the knee extending from 90° to 0° (p < 0.001). The ACL length was 30.2mm±3.0 mm at 0° flexion and decreased to 27.5mm ± 2.8 mm at 90° flexion (p = 0.072). To achieve anatomic single-bundle ACLR, the optimal tibial tunnel should be angulated at approximately 43° to the sagittal plane and approximately 45° to the tibial axis using the modified TT technique. What's more, anatomical TT ACLR resulted in comparable GBA and a relatively constant ACL length from 0° to 90° of flexion. These findings provide theoretical support for the clinical application and the promotion of the current modified TT technique with the assistance of a robot to achieve anatomical ACLR.

A Volcano Correlation between Catalytic Activity for Sulfur Reduction Reaction and Fe Atom Count in Metal Center.

Sulfur reduction reaction (SRR) facilitates up to 16 electrons, which endows lithium-sulfur (Li-S) batteries with a high energy density that is twice that of typical Li-ion batteries. However, its sluggish reaction kinetics render batteries with only a low capacity and cycling life, thus remaining the main challenge to practical Li-S batteries, which require efficient electrocatalysts of balanced atom utilization and site-specific requirements toward highly efficient SRR, calling for an in-depth understanding of the atomic structural sensitivity for the catalytic active sites. Herein, we manipulated the number of Fe atoms in iron assemblies, ranging from single Fe atom to diatomic and triatomic Fe atom groupings, all embedded within a carbon matrix. This led to the revelation of a "volcano peak" correlation between SRR catalytic activity and the count of Fe atoms at the active sites. Utilizing operando X-ray absorption and X-ray diffraction spectroscopies, we observed that polysulfide adsorption-desorption and electrochemical conversion kinetics varied up and down with the incremental addition of even a single iron atom to the catalyst's metal center. Our results demonstrate that the metal center with exactly two iron atoms represents the optimal configuration, maximizing atom utility and adeptly handling the conversion of varied intermediate sulfur species, rendering the Li-S battery with a high areal capacity of 23.8 mAh cm-2 at a high sulfur loading of 21.8 mg cm-2. Our results illuminate the pivotal balance between atom utilization and site-specific requirements for optimal electrocatalytic performance in SRR and diverse electrocatalytic reactions.

Intra-Articular Platelet-Rich Plasma Injection After Anterior Cruciate Ligament Reconstruction: A Randomized Clinical Trial.

Importance: Platelet-rich plasma (PRP) has been considered a promising treatment for musculoskeletal disorders. The effects of PRP on clinical outcomes of anterior cruciate ligament reconstruction (ACLR) are controversial. Objective: To compare subjective outcomes and graft maturity in patients undergoing ACLR with and without postoperative intra-articular PRP injection. Design, Setting, and Participants: This surgeon- and investigator-masked randomized clinical trial included patients treated at a national medical center in China who were aged 16 to 45 years and scheduled to undergo ACLR. Participants were enrolled between March 21, 2021, and August 18, 2022, and followed up for 12 months, with the last participant completing follow-up on August 28, 2023. Interventions: Participants were randomized 1:1 to the PRP group (n = 60), which received 3 doses of postoperative intra-articular PRP injection at monthly intervals, or to the control group (n = 60), which did not receive postoperative PRP injection. Both groups had the same follow-up schedule. Main Outcomes and Measures: The primary outcome was the mean score for 4 subscales of the Knee Injury and Osteoarthritis Outcome Score (KOOS4) (range, 0-100, with higher scores indicating better knee function and fewer symptoms) at 12 months postoperatively. Secondary outcomes were patient-reported outcomes, graft maturity (on magnetic resonance imaging), and physical examinations at 3, 6, and 12 months. Results: Among the 120 randomized participants (mean [SD] age, 29.0 [8.0] years; 84 males [70%]), 114 (95%) were available for the primary outcome analysis. The mean KOOS4 scores at 12 months were 78.3 (SD, 12.0; 95% CI, 75.2-81.4) in the PRP group and 76.8 (SD, 11.9; 95% CI, 73.7-79.9) in the control group (adjusted mean between-group difference, 2.0; 95% CI, -2.3 to 6.3; P = .36). Secondary outcomes were not statistically significantly different between the 2 groups except for sports and recreation level and graft maturity at 6 months. Intervention-related adverse events included pain at the injection site and knee swelling after injection. Conclusions and Relevance: In this randomized clinical trial among patients undergoing ACLR, the addition of postoperative intra-articular PRP injection did not result in superior improvement of knee symptoms and function at 12 months compared with no postoperative injection. Further studies are required to determine appropriate indications for PRP in musculoskeletal disorders. Trial Registration: Chinese Clinical Trial Registry Identifier: ChiCTR2000040262.

Electron-deficient Co7Fe3 induced by interfacial effect of molybdenum carbide boosting oxygen evolution reaction.

Developing a high-activity and low-cost catalyst to reduce the anodic overpotential is essential for hydrogen production from water splitting. In this work, a hetero-structured Co7Fe3/Mo2C@C catalyst has been developed to efficiently catalyze oxygen evolution reaction (OER), the overpotential (ƞ10) of Co7Fe3/Mo2C@C-catalyzed OER with current density of 10 mA/cm2 is about 254 mV, substantially lower than the counterparts of Co7Fe3@C-catalyzed OER (ƞ10, 308 mV) and Mo2C@C-catalyzed OER (ƞ10, 439 mV), close to that of OER catalyzed by commercial RuO2. The mechanistic studies reveal that the distinct electron transfer across the Co7Fe3/Mo2C interface results in electron-deficient Co7Fe3, which has been identified as the highly active catalytic sites. Density functional theory (DFT) calculations manifest that Mo2C induces a distinct decrease in electron density on Co7Fe3 and upgrades the d-band centers of Co and Fe in Co7Fe3 towards Fermi energy level, thus substantially lowering the energy barrier of the rate-determining reaction step and conferring significantly improved OER activity on the Co7Fe3/Mo2C@C catalyst.

Signaling pathways in liver cancer: pathogenesis and targeted therapy.

Liver cancer remains one of the most prevalent malignancies worldwide with high incidence and mortality rates. Due to its subtle onset, liver cancer is commonly diagnosed at a late stage when surgical interventions are no longer feasible. This situation highlights the critical role of systemic treatments, including targeted therapies, in bettering patient outcomes. Despite numerous studies on the mechanisms underlying liver cancer, tyrosine kinase inhibitors (TKIs) are the only widely used clinical inhibitors, represented by sorafenib, whose clinical application is greatly limited by the phenomenon of drug resistance. Here we show an in-depth discussion of the signaling pathways frequently implicated in liver cancer pathogenesis and the inhibitors targeting these pathways under investigation or already in use in the management of advanced liver cancer. We elucidate the oncogenic roles of these pathways in liver cancer especially hepatocellular carcinoma (HCC), as well as the current state of research on inhibitors respectively. Given that TKIs represent the sole class of targeted therapeutics for liver cancer employed in clinical practice, we have particularly focused on TKIs and the mechanisms of the commonly encountered phenomena of its resistance during HCC treatment. This necessitates the imperative development of innovative targeted strategies and the urgency of overcoming the existing limitations. This review endeavors to shed light on the utilization of targeted therapy in advanced liver cancer, with a vision to improve the unsatisfactory prognostic outlook for those patients.

Melatonin ameliorates 10-hydroxycamptothecin-induced oxidative stress and apoptosis via autophagy-regulated p62/Keap1/Nrf2 pathway in mouse testicular cells.

10-Hydroxycamptothecin (HCPT) is a widely used clinical anticancer drug but has a significant side effect profile. Melatonin has a beneficial impact on the chemotherapy of different cancer cells and reproductive processes, but the effect and underlying molecular mechanism of melatonin's involvement in the HCPT-induced side effects in cells, especially in the testicular cells, are poorly understood. In this study, we found that melatonin therapy significantly restored HCPT-induced testicular cell damage and did not affect the antitumor effect of HCPT. Further analysis found that melatonin therapy suppressed HCPT-induced DNA damage associated with ataxia-telangiectasia mutated- and Rad3-related and CHK1 phosphorylation levels in the testis. Changes in apoptosis-associated protein levels (Bax, Bcl-2, p53, and Cleaved caspase-3) and in reactive oxygen species-associated proteins (Nrf2 and Keap1) and index (malondialdehyde and glutathione) suggested that melatonin treatment relieved HCPT-induced cell apoptosis and oxidative damage, respectively. Mechanistically, melatonin-activated autophagy proteins (ATG7, Beclin1, and LC3bII/I) may induce p62-dependent autophagy to degrade Keap1, eliciting Nrf2 from Keap1-Nrf2 interaction to promote antioxidant enzyme expression such as HO-1, which would salvage HCPT-induced ROS production and mitochondrial dysfunction. Collectively, this study reveals that melatonin therapy may protect testicular cells from HCPT-induced damage via the activation of autophagy, which alleviates oxidative stress, mitochondrial dysfunction, and cell apoptosis.

Sweet regulation - The emerging immunoregulatory roles of hexoses.

BACKGROUND: It is widely acknowledged that dietary habits have profound impacts on human health and diseases. As the most important sweeteners and energy sources in human diets, hexoses take part in a broad range of physiopathological processes. In recent years, emerging evidence has uncovered the crucial roles of hexoses, such as glucose, fructose, mannose, and galactose, in controlling the differentiation or function of immune cells. AIM OF REVIEW: Herein, we reviewed the latest research progresses in the hexose-mediated modulation of immune responses, provided in-depth analyses of the underlying mechanisms, and discussed the unresolved issues in this field. KEY SCIENTIFIC CONCEPTS OF REVIEW: Owing to their immunoregulatory effects, hexoses affect the onset and progression of various types of immune disorders, including inflammatory diseases, autoimmune diseases, and tumor immune evasion. Thus, targeting hexose metabolism is becoming a promising strategy for reversing immune abnormalities in diseases.

Global research trends and hotspots of artificial intelligence research in spinal cord neural injury and restoration-a bibliometrics and visualization analysis.

Background: Artificial intelligence (AI) technology has made breakthroughs in spinal cord neural injury and restoration in recent years. It has a positive impact on clinical treatment. This study explores AI research's progress and hotspots in spinal cord neural injury and restoration. It also analyzes research shortcomings related to this area and proposes potential solutions. Methods: We used CiteSpace 6.1.R6 and VOSviewer 1.6.19 to research WOS articles on AI research in spinal cord neural injury and restoration. Results: A total of 1,502 articles were screened, in which the United States dominated; Kadone, Hideki (13 articles, University of Tsukuba, JAPAN) was the author with the highest number of publications; ARCH PHYS MED REHAB (IF = 4.3) was the most cited journal, and topics included molecular biology, immunology, neurology, sports, among other related areas. Conclusion: We pinpointed three research hotspots for AI research in spinal cord neural injury and restoration: (1) intelligent robots and limb exoskeletons to assist rehabilitation training; (2) brain-computer interfaces; and (3) neuromodulation and noninvasive electrical stimulation. In addition, many new hotspots were discussed: (1) starting with image segmentation models based on convolutional neural networks; (2) the use of AI to fabricate polymeric biomaterials to provide the microenvironment required for neural stem cell-derived neural network tissues; (3) AI survival prediction tools, and transcription factor regulatory networks in the field of genetics were discussed. Although AI research in spinal cord neural injury and restoration has many benefits, the technology has several limitations (data and ethical issues). The data-gathering problem should be addressed in future research, which requires a significant sample of quality clinical data to build valid AI models. At the same time, research on genomics and other mechanisms in this field is fragile. In the future, machine learning techniques, such as AI survival prediction tools and transcription factor regulatory networks, can be utilized for studies related to the up-regulation of regeneration-related genes and the production of structural proteins for axonal growth.

Dendritic copper oxide catalyst engineering weak-polarity Cu-O bond for high-efficiency nitrate electroreduction.

Nitrate reduction reaction (NO3RR) is deemed a promising pathway for both ammonia synthesis and water purification. Developing a high-efficiency catalyst with excellent NH3 selectivity and catalytic stability is desirable but remains challenging. In this work, a dendritic copper oxide catalyst (Cu-B2) has been developed to efficiently catalyze NO3RR for ammonia production, the Cu-B2 exhibits excellent catalytic performance, achieving an NH3 Faradaic efficiency as high as 94 % and an NH3 yield of 16.9 mg h-1 cm-2 with a current density of 192.3 mA cm-2 at - 0.6 V (vs. RHE, reversible hydrogen electrode). During NO3RR testing, the Cu-B2 catalysts are reduced in situ to form highly active Cu0/Cu+ sites, while retaining its dendritic morphology. Compared with other catalysts, the Cu-O bond in Cu-B2 catalyst has weaker polarity, resulting in Cu0/Cu+ sites in lower oxidation states. In situ attenuated total reflection surface enhanced infrared absorption spectroscopy (ATR-SEIRAS) studies reveal the Cu-B2 catalyst exhibits a potential-independent capability for *NO3- adsorption and high conversion efficiency of NO2- intermediate into ammonia, DFT calculations reveal that Cu-B2 exhibts higher NO3- adsorption energy and lower NO3- adsorption energy barrier than Cu-B1, thus endowing it with a remarkably improved catalytic activity and durability.

Spatio-temporal spread and evolution of Lassa virus in West Africa.

BACKGROUND: Lassa fever is a hemorrhagic disease caused by Lassa virus (LASV), which has been classified by the World Health Organization as one of the top infectious diseases requiring prioritized research. Previous studies have provided insights into the classification and geographic characteristics of LASV lineages. However, the factor of the distribution and evolution characteristics and phylodynamics of the virus was still limited. METHODS: To enhance comprehensive understanding of LASV, we employed phylogenetic analysis, reassortment and recombination detection, and variation evaluation utilizing publicly available viral genome sequences. RESULTS: The results showed the estimated the root of time of the most recent common ancestor (TMRCA) for large (L) segment was approximately 634 (95% HPD: [385879]), whereas the TMRCA for small (S) segment was around 1224 (95% HPD: [10301401]). LASV primarily spread from east to west in West Africa through two routes, and in route 2, the virus independently spread to surrounding countries through Liberia, resulting in a wider spread of LASV. From 1969 to 2018, the effective population size experienced two significant increased, indicating the enhanced genetic diversity of LASV. We also found the evolution rate of L segment was faster than S segment, further results showed zinc-binding protein had the fastest evolution rate. Reassortment events were detected in multiple lineages including sub-lineage IIg, while recombination events were observed within lineage V. Significant amino acid changes in the glycoprotein precursor of LASV were identified, demonstrating sequence diversity among lineages in LASV. CONCLUSION: This study comprehensively elucidated the transmission and evolution of LASV in West Africa, providing detailed insights into reassortment events, recombination events, and amino acid variations.

Willingness to receive the second booster of COVID-19 vaccine among older adults with cancer: a stratified analysis in four provinces of China.

Background: Despite the elevated COVID-19 risk for older adults with cancer, vaccine hesitancy poses a significant barrier to their immunization. Intriguingly, there is limited research on the prevalence of willingness to receive the second booster dose and associated determinants in older adults with cancer. Objective: Our objective was to ascertain the level of awareness about COVID-19 vaccines and to uncover the factors influencing the willingness to receive the second booster among Chinese cancer patients aged 65 years and over. Methods: To achieve our objective, we conducted a multicenter cross-sectional study in four tertiary hospitals from four provinces of China. This involved using a Health Belief Model (HBM) based self-administered questionnaire and medical records. Subsequently, we employed multivariable logistic regression to identify factors influencing the second COVID-19 booster vaccine willingness. Results: Our results showed that among 893 eligible participants, 279 (31.24%) were aged 65 years and over, and 614 (68.76%) were younger. Interestingly, the willingness to receive the second COVID-19 booster vaccine was 34.1% (95/279) (OR: 1.043, 95% CI: 0.858, 1.267) in participants aged 65 years and over, which was similar to participants aged under 65 years (34.1% vs. 35.5%, p = 0.673). Furthermore, our findings revealed that a positive attitude toward the booster and recommendations from healthcare providers and family members were positively associated with vaccine willingness. Conversely, perceptions of negative impacts on cancer control and vaccine accessibility regarding the second COVID-19 booster were inversely related to the outcome event (all p < 0.05). Conclusion: Our study concludes with the finding of a low willingness toward the second COVID-19 booster in Chinese cancer patients, particularly in the older adults, a fact which warrants attention. This reluctance raises their risk of infection and potential for severe outcomes. Consequently, we recommend using media and community outreach to dispel misconceptions, promote the booster's benefits, and encourage vaccine discussions with healthcare providers and family members.

Detection of Single Nucleotide Polymorphisms of Circulating Tumor DNA by Strand Displacement Amplification Coupled with Liquid Chromatography.

The detection of multiple single nucleotide polymorphisms (SNPs) of circulating tumor DNA (ctDNA) is still a great challenge. In this study, we designed enzyme-assisted nucleic acid strand displacement amplification combined with high-performance liquid chromatography (HPLC) for the simultaneous detection of three ctDNA SNPs. First, the trace ctDNA could be hybridized to the specially designed template strand, which initiated the strand displacement nucleic acid amplification process under the synergistic action of DNA polymerase and restriction endonuclease. Then, the targets would be replaced with G-quadruplex fluorescent probes with different tail lengths. Finally, the HPLC-fluorescence assay enabled the separation and quantification of multiple signals. Notably, this method can simultaneously detect both the wild type (WT) and mutant type (MT) of multiple ctDNA SNPs. Within a linear range of 0.1 fM-0.1 nM, the detection limits of BRAF V600E-WT, EGFR T790M-WT, and KRAS 134A-WT and BRAF V600E-MT, EGFR T790M-MT, and KRAS 134A-MT were 29, 31, and 11 aM and 22, 29, and 33 aM, respectively. By using this method, the mutation rates of multiple ctDNA SNPs in blood samples from patients with lung or breast cancer can be obtained in a simple way, providing a convenient and highly sensitive analytical assay for the early screening and monitoring of lung cancer.

Janus Membranes Patch Achieves High-Quality Tendon Repair: Inhibiting Exogenous Healing and Promoting Endogenous Healing.

The imbalance between endogenous and exogenous healing is the fundamental reason for the poor tendon healing. In this study, a Janus patch was developed to promote endogenous healing and inhibit exogenous healing, leading to improved tendon repair. The upper layer of the patch is a poly(dl-lactide-co-glycolide)/polycaprolactone (PLGA/PCL) nanomembrane (PMCP-NM) modified with poly(2-methylacryloxyethyl phosphocholine) (PMPC), which created a lubricated and antifouling surface, preventing cell invasion and mechanical activation. The lower layer is a PLGA/PCL fiber membrane loaded with fibrin (Fb) (Fb-NM), serving as a temporary chemotactic scaffold to regulate the regenerative microenvironment. In vitro, the Janus patch effectively reduced 92.41% cell adhesion and 79.89% motion friction. In vivo, the patch inhibited tendon adhesion through the TGF-ß/Smad signaling pathway and promoted tendon maturation. This Janus patch is expected to provide a practical basis and theoretical guidance for high-quality soft tissue repair.

[Endoscopic ultrasonography features of benign esophageal stenosis in children]. / å„¿ç«¥é£Ÿç®¡è‰¯æ€§ç‹­çª„çš„è¶ å£°å† é•œç‰¹å¾åˆ†æž.

OBJECTIVES: To investigate the endoscopic ultrasonography (EUS) features of benign esophageal stenosis in children. METHODS: A retrospective analysis was conducted on the medical data of the children who were diagnosed with benign esophageal stenosis from February 2019 to February 2022. The clinical manifestations, EUS findings, and treatment outcome were analyzed to summarize the EUS features of benign esophageal stenosis in children. RESULTS: A total of 42 children with benign esophageal stenosis were included. Among these children, 19 (45%) had anastomotic stenosis after surgery for esophageal atresia, with unclear echogenic boundary of the esophageal walls and uneven thicknesses of the surrounding wall on EUS, and had 0-12 sessions of endoscopic treatment (average 2.1 sessions); 5 children (12%) had corrosive esophageal stenosis and 1 child (2%) had physical esophageal stenosis, with unclear stratification of the esophageal walls on EUS, and they had 2-9 sessions of endoscopic treatment (average 5.3 sessions); 1 child (2%) had patchy irregular hypoechoic areas of the esophageal walls on EUS and was diagnosed with tracheobronchial remnants with reference to pathology; 16 children (38%) had unexplained esophageal stenosis and unclear stratification of the esophageal walls on EUS, among whom 6 received endoscopic treatment. During follow-up, 95% (40/42) of the children had significant alleviation of the symptoms such as vomiting and dysphagia. CONCLUSIONS: For benign esophageal stenosis in children, EUS can help to evaluate the degree of esophageal wall involvement in esophageal stenosis lesions, possible etiologies, and the relationship between the esophagus and the lesion and provide an important basis for selecting treatment modality and avoiding complications, thereby helping to optimize the treatment regimen.