Failure Of Regeneration Research Articles

Coordinated Control of the Onboard and Wayside Energy Storage System of an Urban Rail Train Based on Rule Mining

There are three major challenges to the broad implementation of energy storage systems (ESSs) in urban rail transit: maximizing the absorption of regenerative braking power, enabling online global optimal control, and ensuring algorithm portability. To address these problems, a coordinated control framework between onboard and wayside ESSs is proposed in this study, and the related control strategy is obtained by transforming the global optimization problem into a combination of rule-based and local optimization problems. The design process of the strategy is divided into three parts: offline optimization, rule extraction, and local optimization. First, a genetic algorithm is used to optimize the charge/discharge threshold curves under typical operational conditions. Then, the rules of offline optimization results are obtained from an expert system, and the nonlinear rules are mined with local optimization methods. Finally, a coordinated strategy is presented based on the outcomes of the three parts. A power hardware-in-the-loop (PHIL) experimental platform based on RTLAB is built, and the above coordination strategy is verified based on data for the Beijing Metro Batong Line. The experimental results show that the strategy can effectively improve the energy-saving rate and reduce the regeneration failure rate substantially, with the effect being close to the offline global optimal solution. The algorithm proposed in this paper achieves near global optimal energy-saving optimization results with lower computational costs, and has strong portability, providing a good solution for the large-scale application of onboard and wayside energy storage coordination control.

The Association Between Low Preoperative Phosphate Levels and Postliver Surgery Outcomes–A Single Center Experience

IntroductionPrevious research has demonstrated the impact of postoperative phosphate levels on liver regeneration and outcomes after liver resection surgeries, a potential predictor for regenerative success and liver failure. However, little is known about the association between low preoperative serum phosphate levels and outcomes in liver resections. MethodsWe performed a retrospective analysis of liver resections performed at our institution. Patients were categorized based on preoperative phosphate levels (low versus normal). Our primary outcome measure was posthepatectomy liver failure. ResultsA total of 265 cases met the study criteria. 71 patients (26.7%) had low preoperative phosphate levels. The incidence of posthepatectomy liver failure was higher in the low preoperative phosphate group (19.2% versus 12.4%). However, after propensity score matching, rates of posthepatectomy liver failure were similar between low and normal preoperative phosphate cohorts (13% versus 14%, P = 0.83). ConclusionsLow preoperative phosphate levels were not associated with worse postoperative outcomes in this study. Further studies are warranted to investigate this association and its relevance as a clinical prognostic factor for postoperative liver failure.

Senolytics ameliorate the failure of bone regeneration through the cell senescence-related inflammatory signalling pathway

Stress-induced premature senescent (SIPS) cells induced by various stresses deteriorate cell functions. Dasatinib and quercetin senolytics (DQ) can alleviate several diseases by eliminating senescent cells. α-tricalcium phosphate (α-TCP) is a widely used therapeutic approach for bone restoration but induces bone formation for a comparatively long time. Furthermore, bone infection exacerbates the detrimental prognosis of bone formation during material implant surgery due to oral cavity bacteria and unintentional contamination. It is essential to mitigate the inhibitory effects on bone formation during surgical procedures. Little is known that DQ improves bone formation in Lipopolysaccharide (LPS)-contaminated implants and its intrinsic mechanisms in the study of maxillofacial bone defects. This study aims to investigate whether the administration of DQ ameliorates the impairments on bone repair inflammation and contamination by eliminating SIPS cells. α-TCP and LPS-contaminated α-TCP were implanted into Sprague-Dawley rat calvaria bone defects. Simultaneously, bone formation in the bone defects was investigated with or without the oral administration of DQ. Micro-computed tomography and hematoxylin-eosin staining showed that senolytics significantly enhanced bone formation at the defect site. Histology and immunofluorescence staining revealed that the levels of p21- and p16-positive senescent cells, inflammation, macrophages, reactive oxygen species, and tartrate-resistant acid phosphatase-positive cells declined after administering DQ. DQ could partially alleviate the production of senescent markers and senescence-associated secretory phenotypes in vitro. This study indicates that LPS-contaminated α-TCP-based biomaterials can induce cellular senescence and hamper bone regeneration. Senolytics have significant therapeutic potential in reducing the adverse osteogenic effects of biomaterial-related infections and improving bone formation capacity.

Metabolic reprogramming: a new option for the treatment of spinal cord injury.

Spinal cord injuries impose a notably economic burden on society, mainly because of the severe after-effects they cause. Despite the ongoing development of various therapies for spinal cord injuries, their effectiveness remains unsatisfactory. However, a deeper understanding of metabolism has opened up a new therapeutic opportunity in the form of metabolic reprogramming. In this review, we explore the metabolic changes that occur during spinal cord injuries, their consequences, and the therapeutic tools available for metabolic reprogramming. Normal spinal cord metabolism is characterized by independent cellular metabolism and intercellular metabolic coupling. However, spinal cord injury results in metabolic disorders that include disturbances in glucose metabolism, lipid metabolism, and mitochondrial dysfunction. These metabolic disturbances lead to corresponding pathological changes, including the failure of axonal regeneration, the accumulation of scarring, and the activation of microglia. To rescue spinal cord injury at the metabolic level, potential metabolic reprogramming approaches have emerged, including replenishing metabolic substrates, reconstituting metabolic couplings, and targeting mitochondrial therapies to alter cell fate. The available evidence suggests that metabolic reprogramming holds great promise as a next-generation approach for the treatment of spinal cord injury. To further advance the metabolic treatment of the spinal cord injury, future efforts should focus on a deeper understanding of neurometabolism, the development of more advanced metabolomics technologies, and the design of highly effective metabolic interventions.

Age-dependent loss of Crls1 causes myopathy and skeletal muscle regeneration failure

Skeletal muscle aging results in the gradual suppression of myogenesis, leading to muscle mass loss. However, the specific role of cardiolipin in myogenesis has not been determined. This study investigated the crucial role of mitochondrial cardiolipin and cardiolipin synthase 1 (Crls1) in age-related muscle deterioration and myogenesis. Our findings demonstrated that cardiolipin and Crls1 are downregulated in aged skeletal muscle. Moreover, the knockdown of Crls1 in myoblasts reduced mitochondrial mass, activity, and OXPHOS complex IV expression and disrupted the structure of the mitochondrial cristae. AAV9-shCrls1-mediated downregulation of Crls1 impaired muscle regeneration in a mouse model of cardiotoxin (CTX)-induced muscle damage, whereas AAV9-mCrls1-mediated Crls1 overexpression improved regeneration. Overall, our results highlight that the age-dependent decrease in CRLS1 expression contributes to muscle loss by diminishing mitochondrial quality in skeletal muscle myoblasts. Hence, modulating CRLS1 expression is a promising therapeutic strategy for mitigating muscle deterioration associated with aging, suggesting potential avenues for developing interventions to improve overall muscle health and quality of life in elderly individuals.

Assessing giant sequoia mortality and regeneration following high‐severity wildfire

AbstractFire is a critical driver of giant sequoia (Sequoiadendron giganteum [Lindl.] Buchholz) regeneration. However, fire suppression combined with the effects of increased temperature and severe drought has resulted in fires of an intensity and size outside of the historical norm. As a result, recent mega‐fires have killed a significant portion of the world's sequoia population (13%–19%), and uncertainty surrounds whether severely affected groves will be able to recover naturally, potentially leading to a loss of grove area. To assess the likelihood of natural recovery, we collected spatially explicit data assessing mortality, crown condition, and regeneration within four giant sequoia groves that were severely impacted by the SQF‐ (2020) and KNP‐Complex (2021) wildfires within Sequoia and Kings Canyon National Parks. In total, we surveyed 5.9 ha for seedlings and assessed the crown condition of 1104 giant sequoias. To inform management, we used a statistical methodology that robustly quantifies the uncertainty in inherently “noisy” seedling data and takes advantage of readily available remote sensing metrics that would make our findings applicable to other recently burned groves. A loss of giant sequoia grove area would be a consequence of giant sequoia tree mortality followed by a failure of natural regeneration. We found that areas that experienced very high‐severity fire (above ~800 RdNBR) are at substantial risk for the loss of grove area, with tree mortality rapidly increasing and giant sequoia seedling density simultaneously decreasing with fire severity. Such high‐severity areas comprised 17.8, 142.0, 14.6, 1.6 ha and ~90%, ~14%, ~53%, and ~27% of Board Camp, Redwood Mountain, Suwanee, and New Oriole Lake groves, respectively. In all sampling areas, we found that seedling densities fell far below the average density measured after prescribed fires, where seedling numbers were almost certainly adequate to maintain giant sequoia populations and postfire conditions were more in keeping with historical norms. Importantly, spatial pattern is also important in assessing the risk of grove loss, and in two groves, Suwanee and New Oriole Lake, the high‐severity patches were not always contiguous, potentially making some areas more resilient to regeneration failure due to the proximity of surviving trees.

Bornean tropical forests recovering from logging at risk of regeneration failure.

Active restoration through silvicultural treatments (enrichment planting, cutting climbers and liberation thinning) is considered an important intervention in logged forests. However, its ability to enhance regeneration is key for long-term recovery of logged forests, which remains poorly understood, particularly for the production and survival of seedlings in subsequent generations. To understand the long-term impacts of logging and restoration we tracked the diversity, survival and traits of seedlings that germinated immediately after a mast fruiting in North Borneo in unlogged and logged forests 30-35 years after logging. We monitored 5119 seedlings from germination for ~1.5 years across a mixed landscape of unlogged forests (ULs), naturally regenerating logged forests (NR) and actively restored logged forests via rehabilitative silvicultural treatments (AR), 15-27 years after restoration. We measured 14 leaf, root and biomass allocation traits on 399 seedlings from 15 species. Soon after fruiting, UL and AR forests had higher seedling densities than NR forest, but survival was the lowest in AR forests in the first 6 months. Community composition differed among forest types; AR and NR forests had lower species richness and lower evenness than UL forests by 5-6 months post-mast but did not differ between them. Differences in community composition altered community-weighted mean trait values across forest types, with higher root biomass allocation in NR relative to UL forest. Traits influenced mortality ~3 months post-mast, with more acquisitive traits and relative aboveground investment favoured in AR forests relative to UL forests. Our findings of reduced seedling survival and diversity suggest long time lags in post-logging recruitment, particularly for some taxa. Active restoration of logged forests recovers initial seedling production, but elevated mortality in AR forests lowers the efficacy of active restoration to enhance recruitment or diversity of seedling communities. This suggests current active restoration practices may fail to overcome barriers to regeneration in logged forests, which may drive long-term changes in future forest plant communities.

Trajectories and tipping points of piñon-juniper woodlands after fire and thinning.

Piñon-juniper (PJ) woodlands are a dominant community type across the Intermountain West, comprising over a million acres and experiencing critical effects from increasing wildfire. Large PJ mortality and regeneration failure after catastrophic wildfire have elevated concerns about the long-term viability of PJ woodlands. Thinning is increasingly used to safeguard forests from fire and in an attempt to increase climate resilience. We have only a limited understanding of how fire and thinning will affect the structure and function of PJ ecosystems. Here, we examined vegetation structure, microclimate conditions, and PJ regeneration dynamics following ~20 years post-fire and thinning treatments. We found that burned areas had undergone a state shift that did not show signs of returning to their previous state. This shift was characterized by (1) distinct plant community composition dominated by grasses; (2) a lack of PJ recruitment; (3) a decrease in the sizes of interspaces in between plants; (4) lower abundance of late successional biological soil crusts; (5) lower mean and minimum daily soil moisture values; (6) lower minimum daily vapor pressure deficit; and (7) higher photosynthetically active radiation. Thinning created distinct plant communities and served as an intermediate between intact and burned communities. More intensive thinning decreased PJ recruitment and late successional biocrust cover. Our results indicate that fire has the potential to create drier and more stressful microsite conditions, and that, in the absence of active management following fire, there may be shifts to persistent ecological states dominated by grasses. Additionally, more intensive thinning had a larger impact on community structure and recruitment than less intensive thinning, suggesting that careful consideration of goals could help avoid unintended consequences. While our results indicate the vulnerability of PJ ecosystems to fire, they also highlight management actions that could be adapted to create conditions that promote PJ re-establishment.

Study on 3D printed MXene-berberine-integrated scaffold for photo-activated antibacterial activity and bone regeneration.

The repair of mandibular defects is a challenging clinical problem, and associated infections often hinder the treatment, leading to failure in bone regeneration. Herein, a multifunctional platform is designed against the shortages of existing therapies for infected bone deficiency. 2D Ti3C2 MXene and berberine (BBR) are effectively loaded into 3D printing biphasic calcium phosphate (BCP) scaffolds. The prepared composite scaffolds take the feature of the excellent photothermal capacity of Ti3C2 as an antibacterial, mediating NIR-responsive BBR release under laser stimuli. Meanwhile, the sustained release of BBR enhances its antibacterial effect and further accelerates the bone healing process. Importantly, the integration of Ti3C2 improves the mechanical properties of the 3D scaffolds, which are beneficial for new bone formation. Their remarkable biomedical performances in vitro and in vivo present the outstanding antibacterial and osteogenic properties of the Ti3C2-BBR functionalized BCP scaffolds. The synergistic therapy makes it highly promising for repairing infected bone defects and provides insights into a wide range of applications of 2D nanosheets in biomedicine.

Impact of transient steatosis on liver regeneration and post-hepatectomy liver failure in rats

Impact of transient steatosis on liver regeneration and post-hepatectomy liver failure in rats

Alginate and Collagen Composite for Hard Tissue Generation: A Mini Review

The bone regeneration process involves the formation of the regenerative cells, the cell proliferation to produce new tissue and subsequently will repair the fractured area. During regeneration process, the osteoblast cells will secrete several proteins, organic and inorganic components as the base components to form the bone tissues or known as matrix. However, some conditions such as bone tumor removal, massive bone loss injury, extensive infections at the bone, minerals deficiency resulting the failure of bone regeneration and lead to prolonged bone fracture. To overcome this, bone scaffold is implanted or encapsulated bioactive cells are applied at the damaged area to support the bone regeneration. The materials should be osteogenic, osteoconductive and have osteoinductive properties. Natural polymer such as alginate and collagen are often used as biomaterials due to their high biocompatibility, degradability, low toxicity and easy to form a crosslinker with other materials through various method process. Therefore, this review will highlight the properties of alginate and collagen, the fabrication method to form composite and its application in biomedical area.

Transformation of non-neuritic into neuritic plaques during AD progression drives cortical spread of tau pathology via regenerative failure

Extracellular amyloid-β (Aβ) plaques and intracellular aggregates of tau protein in form of neurofibrillary tangles (NFT) are pathological hallmarks of Alzheimer’s disease (AD). The exact mechanism how these two protein aggregates interact in AD is still a matter of debate. Neuritic plaques (NP), a subset of Aβ plaques containing dystrophic neurites (DN), are suggested to be unique to AD and might play a role in the interaction of Aβ and tau. Quantifying NP and non-NP in postmortem brain specimens from patients with increasing severity of AD neuropathological changes (ADNC), we demonstrate that the total number of Aβ plaques and NP increase, while the number of non-NP stagnates. Furthermore, investigating the correlation between NP and NFT, we identified unexpected brain region-specific differences when comparing cases with increasingly more severe ADNC. In neocortical regions NFT counts increase in parallel with NP counts during the progression of ADNC, while this correlation is not observed in hippocampus. These data support the notion that non-NP are transformed into NP during the progression of ADNC and indicate that NP might drive cortical NFT formation. Next, using spatial transcriptomics, we analyzed the gene expression profile of the microenvironment around non-NP and NP. We identified an upregulation of neuronal systems and Ca-dependent event pathways around NP compared to non-NP. We speculate that the upregulation of these transcripts may hint at a compensatory mechanism underlying NP formation. Our studies suggest that the transformation of non-NP to NP is a key event in ADNC progression and points to regenerative failure as a potential driving force of this process.

Defaunated and invaded insular tropical rainforests will not recover alone: Recruitment limitation factors disentangled by hierarchical models of spontaneous and assisted regeneration

Abstract Most tropical forests are now severely degraded and their ability to recover is highly dependent on frugivores which ensure seed dispersal for most woody plants. The global collapse of large vertebrates therefore raises major concerns about tropical forest succession, but few field studies have been conducted to disentangle recruitment limitations during disrupted succession. This study took place on Réunion (Mascarenes) where all large native frugivores have been extinct since human colonisation in 1665 and where multiple invasions threaten native ecosystems. We set up 20 experimental blocks on a lava flow dated back to 1800, in plant‐impoverished post‐defaunation vegetation bordered by old‐growth forests. We assessed fecundity, seed dispersal and seedling recruitment of the complete fleshy‐fruited plant community and used Bayesian analyses to disentangle the impact of multiple factors on these key processes. In the same blocks, we sowed four native trees assumed to be disperserless to test their capacity to establish, controlling for two additional post‐dispersal limitations (seed predation and competition with invasive plants). On the flow, small‐seeded native plants were fairly dispersed but did not recruit, probably due to strong competition with invasive plants; the few native species that recruited somehow were mostly medium‐seeded plants that were still dispersed; large‐seeded plants were absent from seed rain (which shows that invasive frugivores did not replace extinct ones) and subsequently from spontaneous recruitment. Instead, some alien plants, notably the tiny‐seeded highly dispersed Clidemia hirta and the medium‐seeded Psidium cattleianum largely dominated seedling recruitment. Native plants recruited better at the forest margin, including some large‐seeded species nearby mother trees. Sown large‐seeded species were able to emerge and survive in all plots whatever the treatment, which demonstrates that dispersal loss was the primary cause of regeneration failure on the flow. Synthesis. The strong modulation of the establishment capacity of native plants by seed mass shows that invasive plants win by forfeit of large‐seeded plants after native frugivores loss. Our study emphasises the fundamental role of dispersal loss and competition with invasive plants in the disruption of ecological succession, as well as the urgency of restoring seed dispersal and strengthening biosecurity regulations.

Porous Three-Dimensional Polyurethane Scaffolds Promote Scar-Free Endogenous Regeneration After Acute Brain Hemorrhage.

Intracerebral hemorrhage (ICH) is the most lethal subtype of stroke and is associated with significant morbidity and mortality. Despite advances in the clinical treatment of ICH, limited progress has been made regarding endogenous brain regeneration after ICH. Failure of brain regeneration is mainly attributed to the inhibitive regenerative microenvironment caused by secondary injury after ICH. In this study, we investigated a three-dimensional biodegradable waterborne polyurethane (BWPU) scaffold as a tool to promote brain regeneration after ICH. After implantation into the cavity following hematoma evacuation, these implanted scaffolds could act as a reservoir; store a series of necrotic debris, cytokines, and chemokines; and attract microglia/macrophages to their pores. Subsequently, these microglia/macrophages were polarized into the M1-like subtype to eliminate these substances. This process disperses M1-like immune cells and prevents the formation of dense glial scar-free structures after ICH. Inflammatory cells in scaffolds include scar-free secreted growth factors and extracellular matrix (ECM) proteins, and further induce a M2-like immune cells enriched regeneration-predominant microenvironment to promote endogenous brain regeneration with functional recovery. In summary, in this work, we have revealed the potential and mechanism of the BWPU scaffold as a tool to promote endogenous brain tissue regeneration after ICH.

Population Structure and Regeneration Dynamics of Tree Species in Banj Oak Forests of Tehri Garhwal, Western Himalaya

Forest regeneration is a natural process of forest resource reclamation through production of young ones (saplings and seedlings). Tree species show variable regeneration potential in different associations and response to natural and man-made factors. Banj oak (Quercus leucotrichophora A. Camus), one of the important forest forming tree species in western montane Himalaya, is facing regeneration failure in different locations. The present study attempted to assess the population structure and regeneration of Q. leucotrichophora and associated tree species in five different stands (sites) of a less explored region (Tehri Garhwal, Uttarakhand, Western Himalaya). To investigate the phytosociological attributes, ten sampling quadrats (400 m2) were laid in random sampling manner in each forest stand for surveying tree layer, 2 sub-quadrats (25 m2) for saplings, and 5 sub-quadrats (1 m2) for seedlings in each sampling quadrat. Among the studied forest stands, tree species richness ranged 8 to 11 (8.8±1.3), total stem density (ind/ha) 750 to 950 (846±85.6), and total basal area (m2/ha) 18.68 to 29.18 (24.1±3.9). Based on abundance data the banj oak showed ‘good’ regeneration statuses (density of seedling > saplings > adult trees) in all forests. The distribution of adult tree individuals into different size classes (DBH classes) also indicate ‘good’ regeneration pattern (higher density in lower size classes and gradual decrease in density towards higher classes or forming a reverse J-shaped pattern). However, majority of the banj oak associated species (e.g. Prunus cerasoides, Pyrus pashia, Rhododendron arboreum, etc.) represented ‘fair’ regeneration statuses (seedlings > or ≤ saplings ≤ adult trees). Overall, the results of this study shed light on the positive prospects for Q. leucotrichophora regeneration and the importance of sustainable coexistence between human communities and these vital forest ecosystems.

Skeletal muscle regeneration failure in ischemic-damaged limbs is associated with pro-inflammatory macrophages and premature differentiation of satellite cells

BackgroundChronic limb-threatening ischemia (CLTI), a severe manifestation of peripheral arterial disease (PAD), is associated with a 1-year limb amputation rate of approximately 15–20% and substantial mortality. A key feature of CLTI is the compromised regenerative ability of skeletal muscle; however, the mechanisms responsible for this impairment are not yet fully understood. In this study, we aim to delineate pathological changes at both the cellular and transcriptomic levels, as well as in cell–cell signaling pathways, associated with compromised muscle regeneration in limb ischemia in both human tissue samples and murine models of CLTI.MethodsWe performed single-cell transcriptome analysis of ischemic and non-ischemic muscle from the same CLTI patients and from a murine model of CLTI. In both datasets, we analyzed gene expression changes in macrophage and muscle satellite cell (MuSC) populations as well as differential cell–cell signaling interactions and differentiation trajectories.ResultsSingle-cell transcriptomic profiling and immunofluorescence analysis of CLTI patient skeletal muscle demonstrated that ischemic-damaged tissue displays a pro-inflammatory macrophage signature. Comparable results were observed in a murine CLTI model. Moreover, integrated analyses of both human and murine datasets revealed premature differentiation of MuSCs to be a key feature of failed muscle regeneration in the ischemic limb. Furthermore, in silico inferences of intercellular communication and in vitro assays highlight the importance of macrophage-MuSC signaling in ischemia induced muscle injuries.ConclusionsCollectively, our research provides the first single-cell transcriptome atlases of skeletal muscle from CLTI patients and a murine CLTI model, emphasizing the crucial role of macrophages and inflammation in regulating muscle regeneration in CLTI through interactions with MuSCs.

Genetic, virological, infectious, and pharmacological risk factors for CD4<sup>+</sup> T-cell regeneration failure in HIV-infected subjects receiving ART

In 10 to 40% of HIV-infected patients being adherent to highly active antiretroviral therapy (HAART), viral load suppression is not accompanied by a significant increase in the number of CD4+ T-lymphocytes. This phenomenon, known as immunological non-response to treatment, is associated with a high risk of developing AIDS-associated and non-AIDS-associated diseases, as well as premature death. The bases of immunological non-response to HAART are poorly understood, while information on the risk factors for its development is scattered.The aim of the present review is to organize data on non-immune-system risk factors for the development of immunological nonresponse to HAART.Materials and methods. Electronic searching using PubMed, Science Direct, and Scopus were conducted.Results and discussion. The database search delivered information on genetic, virological, infectious, and pharmacological risk factors for the development of immunological non-response to HAART. Each factor contribution might be substantially different. Still, none of them can be considered a trigger mechanism for this phenomenon.Conclusion. Immunological non-response to HAART is a polyetiological condition. Apparently, this phenomenon is based on normally imperceptible immune system features or defects, which manifest during the CD4+ T-cell regeneration.

Senescent Schwann cells induced by aging and chronic denervation impair axonal regeneration following peripheral nerve injury

Following peripheral nerve injury, successful axonal growth and functional recovery require Schwann cell (SC) reprogramming into a reparative phenotype, a process dependent upon c‐Jun transcription factor activation. Unfortunately, axonal regeneration is greatly impaired in aged organisms and following chronic denervation, which can lead to poor clinical outcomes. While diminished c‐Jun expression in SCs has been associated with regenerative failure, it is unclear whether the inability to maintain a repair state is associated with the transition into an axonal growth inhibition phenotype. We here find that reparative SCs transition into a senescent phenotype, characterized by diminished c‐Jun expression and secretion of inhibitory factors for axonal regeneration in aging and chronic denervation. In both conditions, the elimination of senescent SCs by systemic senolytic drug treatment or genetic targeting improved nerve regeneration and functional recovery, increased c‐Jun expression and decreased nerve inflammation. This work provides the first characterization of senescent SCs and their influence on axonal regeneration in aging and chronic denervation, opening new avenues for enhancing regeneration and functional recovery after peripheral nerve injuries.

Mechanisms of Regeneration and Fibrosis in the Endometrium.

The uterine lining (endometrium) regenerates repeatedly over the life span as part of its normal physiology. Substantial portions of the endometrium are shed during childbirth (parturition) and, in some species, menstruation, but the tissue is rapidly rebuilt without scarring, rendering it a powerful model of regeneration in mammals. Nonetheless, following some assaults, including medical procedures and infections, the endometrium fails to regenerate and instead forms scars that may interfere with normal endometrial function and contribute to infertility. Thus, the endometrium provides an exceptional platform to answer a central question of regenerative medicine: Why do some systems regenerate while others scar? Here, we review our current understanding of diverse endometrial disruption events in humans, nonhuman primates, and rodents, and the associated mechanisms of regenerative success and failure. Elucidating the determinants of these disparate repair processes promises insights into fundamental mechanisms of mammalian regeneration with substantial implications for reproductive health.

Antibacterial efficacy of epigallocatechin-3-gallate cross-linked small intestinal submucosa guided bone regeneration membrane.

The leading cause of guided bone regeneration (GBR) failure is infection. Herein, we developed a new GBR membrane with good mechanical and osteogenic properties by crosslinking the small intestinal submucosa (SIS) with epigallocatechin-3-gallate (EGCG). Meanwhile, EGCG is also a natural antibacterial agent. This study aimed to investigate the antibacterial efficacy of EGCG-crosslinked SIS (E-SIS) against Staphylococcus aureus and Escherichia coli through EGCG release, bacterial count, live/dead staining, scanning electron microscopy, growth curve, and biofilm formation tests. The results showed that E-SIS effectively inhibited bacteria's growth and adhesion, and its antibacterial activity against Staphylococcus aureus was stronger than that against Escherichia coli. 0.5% E-SIS had the most potent antibacterial activity. The antibacterial mechanism of E-SIS might be related to the release of EGCG and the surface properties of E-SIS. In conclusion, 0.5% E-SIS is a promising GBR membrane with good osteogenic and antibacterial properties.