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Stem cell therapy may replace lost photoreceptors and preserve residual photoreceptors during retinal degeneration (RD). Unfortunately, the degenerative microenvironment compromises the fate of grafted cells, demanding supplementary strategies for microenvironment regulation. Donor cells with both proper regeneration capability and intrinsic ability to improve microenvironment are highly desired. Here, we use cell surface markers (C-Kit + /SSEA4 − ) to effectively eliminate tumorigenic embryonic cells and enrich retinal progenitor cells (RPCs) from human embryonic stem cell (hESC)-derived retinal organoids, which, following subretinal transplantation into RD models of rats and mice, significantly improve vision and preserve the retinal structure. We characterize the pattern of integration and materials transfer following transplantation, which likely contribute to the rescued photoreceptors. Moreover, C-Kit + /SSEA4 − cells suppress microglial activation, gliosis and the production of inflammatory mediators, thereby providing a healthier host microenvironment for the grafted cells and delaying RD. Therefore, C-Kit + /SSEA4 − cells from hESC-derived retinal organoids are a promising therapeutic cell source. Stem cell transplantation to treat retinal degeneration could be limited by the degenerative microenvironment. Here, the authors show that C-Kit + /SSEA4 –  progenitor cells enriched from human embryonic stem cell derived retinal organoids protect retinal structure, suppress microglial activation, gliosis and inflammation.

Cable-suspended photovoltaic (PV) systems have gained traction due to their lightweight structure and adaptability to complex terrains. However, the wind-induced vibration behavior of these systems, particularly the contribution of glass–glass PV modules to structural stiffness, remains inadequately addressed in current design codes. This study presents a comprehensive finite element analysis to investigate the mechanical role of glass–glass PV modules in cable-suspended PV systems. A high-fidelity model (HFM) capturing detailed structural features of the PV module is established and used as a reference to develop an equivalent stiffness model (ESM). Through modal decomposition under wind excitation, it is shown that module deformation primarily manifests as torsion, which significantly contributes to the overall stiffness of the support structure. Comparative simulations reveal that conventional modeling approaches, including the inaccurate simplified model (ISM), overestimate stiffness, potentially compromising structural safety. The ESM, by accurately replicating the HFM’s torsional response, enables efficient and reliable wind-induced vibration analysis. The results also indicate that modules at the cable span edges experience greater torsional deformation, especially under suction forces, highlighting a critical zone for structural reinforcement.

Müller glia originate from neuroepithelium and are the principal glial cells in the retina. During retinal development, Müller glia are one of the last cell types to be born. In lower vertebrates, such as zebrafish, Müller glia possess a remarkable capacity for retinal regeneration following various forms of injury through a reprogramming process in which endogenous Müller glia proliferate and differentiate into all types of retinal cells. In mammals, Müller glia become reactive in response to damage to protect or to further impair retinal function. Although mammalian Müller glia have regenerative potential, it is limited as far as repairing damaged retina. Lessons learned from zebrafish will help reveal the critical mechanisms involved in Müller glia reprogramming. Progress has been made in triggering Müller glia to reprogram and generate functional neurons to restore vision in mammals indicating that Müller glia reprogramming may be a promising therapeutic strategy for human retinal diseases. This review comprehensively summarizes the mechanisms related to retinal regeneration in model animals and the critical advanced progress made in Müller glia reprogramming in mammals.

Retinal regeneration and self-repair, whether in response to injury or degenerative disease, are severely impeded by glial scar formation by Müller cells (specialized retinal macroglia). We have previously demonstrated that the activation of Müller cells and gliosis in the degenerative retina are significantly suppressed by the subretinal transplantation of a mixture of olfactory ensheathing cells (OECs) and olfactory nerve fibroblasts. However, the underlying molecular mechanism has remained elusive. Here we transplanted purified rat OECs into the subretinal space of pigmented Royal College of Surgeons (RCS) rats, a classic rodent model of retinal degeneration. Using behavioral testing and electroretinography, we confirmed that the grafted OECs preserved the visual function of rats for 8 weeks, relative to vehicle controls (phosphate-buffered saline). Histological evaluation of outer nuclear layer thickness and composition demonstrated that more photoreceptors and ON-bipolar cells were preserved in the retinas of OEC-treated RCS rats than in controls. The grafted OECs migrated into the outer plexiform layer, inner nuclear layer, and inner plexiform layer. They interacted directly with Müller cells in the retina of RCS rats, in three distinct patterns, and secreted matrix metalloproteinases 2 and 3. Previous studies have demonstrated that rat OECs express delta-like ligand (DLL), while Müller cells express Notch3, the receptor for DLL. Here we found that the grafted OECs significantly decreased the expression, by retinal cells, of Notch signaling pathway components (including Notch3, Notch4, DLL1, DLL4, Jagged1, Hes1, and Hes5) 2 weeks after the cell transplantation and that this effect persisted for a further 2 weeks. Based on these findings, we suggest that transplanted OECs inhibit the activation of Müller cells and the associated gliosis, at least partly through suppression of the Notch pathway.

Diabetic retinopathy (DR), one of the leading causes of vision loss worldwide, is characterized by neurovascular disorders. Emerging evidence has demonstrated retinal neurodegeneration in the early pathogenesis of DR, and no treatment has been developed to prevent the early neurodegenerative changes that precede detectable microvascular disorders. Bone marrow CD133+ stem cells with revascularization properties exhibit neuroregenerative potential. However, whether CD133+ cells can ameliorate the neurodegeneration at the early stage of DR remains unclear. In this study, mouse bone marrow CD133+ stem cells were immunomagnetically isolated and analyzed for the phenotypic characteristics, capacity for neural differentiation, and gene expression of neurotrophic factors. After being labeled with enhanced green fluorescent protein, CD133+ cells were intravitreally transplanted into streptozotocin (STZ)-induced diabetic mice to assess the outcomes of visual function and retina structure and the mechanism underlying the therapeutic effect. We found that CD133+ cells co-expressed typical hematopoietic/endothelial stem/progenitor phenotypes, could differentiate to neural lineage cells, and expressed genes of robust neurotrophic factors in vitro. Functional analysis demonstrated that the transplantation of CD133+ cells prevented visual dysfunction for 56 days. Histological analysis confirmed such a functional improvement and showed that transplanted CD133+ cells survived, migrated into the inner retina (IR) over time and preserved IR degeneration, including retina ganglion cells (RGCs) and rod-on bipolar cells. In addition, a subset of transplanted CD133+ cells in the ganglion cell layer differentiated to express RGC markers in STZ-induced diabetic retina. Moreover, transplanted CD133+ cells expressed brain-derived neurotrophic factors (BDNFs) in vivo and increased the BDNF level in STZ-induced diabetic retina to support the survival of retinal cells. Based on these findings, we suggest that transplantation of bone marrow CD133+ stem cells represents a novel approach to ameliorate visual dysfunction and the underlying IR neurodegeneration at the early stage of DR.

Tissue-specific extracellular matrix plays an important role in promoting tissue regeneration and repair. We hypothesized that decellularized annular fibrosus matrix may be an appropriate scaffold for annular fibrosus tissue engineering. We aimed to determine the optimal decellularization method suitable for annular fibrosus. Annular fibrosus tissue was treated with 3 different protocols with Triton X-100, sodium dodecyl sulfate (SDS) and trypsin. After the decellularization process, we examined cell removal and preservation of the matrix components, microstructure and mechanical function with the treatments to determine which method is more efficient. All 3 protocols achieved decellularization; however, SDS or trypsin disturbed the structure of the annular fibrosus. All protocols maintained collagen content, but glycosaminoglycan content was lost to different degrees, with the highest content with TritonX-100 treatment. Furthermore, SDS decreased the tensile mechanical property of annular fibrosus as compared with the other 2 protocols. MTT assay revealed that the decellularized annular fibrosus was not cytotoxic. Annular fibrosus cells seeded into the scaffold showed good viability. The Triton X-100-treated annular fibrosus retained major extracellular matrix components after thorough cell removal and preserved the concentric lamellar structure and tensile mechanical properties. As well, it possessed favorable biocompatibility, so it may be a suitable candidate as a scaffold for annular fibrosus tissue engineering.

Regeneration/repair after injury can be endowed by adult stem cells (ASCs) or lineage restricted and even terminally differentiated cells. In corneal epithelium, regeneration after a large wound depends on ASCs (limbal epithelial stem cells, LESCs), whereas repair after a small wound is LESCs-independent. Here, using rat corneal epithelial wounds with different sizes, we show that YAP activation promotes the activation and expansion of LESCs after a large wound, as well as the reprogramming of local epithelial cells (repairing epithelial cells) after a small wound, which contributes to LESCs-dependent and -independent wound healing, respectively. Mechanically, we highlight that the reciprocal regulation of YAP activity and the assembly of cell junction and cortical F-actin cytoskeleton accelerates corneal epithelial healing with different-sized wounds. Together, the common YAP activation and the underlying regulatory mechanism are harnessed by LESCs and lineage-restricted epithelial cells to cope with corneal epithelial wounds with different sizes.

The cable-suspended PV system has gained increasing popularity due to its large span and good site adaptability. However, this structure is quite sensitive to wind actions, and wind-induced module damage and structure failure have been frequently reported. Therefore, in this study, we carried out wind tunnel tests to study wind load effects on PV arrays with different lengths and widths. Considering the wind sheltering effects of upstream modules, reduction factors for the wind load were proposed in different array zones. Numerical simulations of wind-induced vibration and equivalent static analysis were conducted to yield gust loading factors for the PV array. This study showed that the maximum wind suction and pressure for the middle zone occurred at 0° and 180°, respectively, while those for the outermost zone appeared under oblique flows (e.g., 30° and 150°). For the PV modules beyond the windward fourth row, the reduction factors of the wind loads were 0.4 (maximum suction) and 0.2 (maximum pressure) for the middle zone and 0.5 (maximum suction) and 0.75 (maximum pressure) for the outermost zone. The gust loading factors for the typical wind directions of 0° and 180° varied from 2.2 to 2.7 for the middle zone and from 1.3 to 1.5 for the outermost zone.

The production and application of nanomaterials have grown tremendously during last few decades. The widespread exposure of nanoparticles to the public is provoking great concerns regarding their toxicity to the human body. However, in comparison with the extensive studies carried out to examine nanoparticle toxicity to the human body/organs, one especially vulnerable organ, the eye, is always neglected. Although it is a small part of the body, 90% of outside information is obtained via the ocular system. In addition, eyes usually directly interact with the surrounding environment, which may get severer damage from toxic nanoparticles compared to inner organs. Therefore, the study of assessing the potential nanoparticle toxicity to the eyes is of great importance. Here, the recent advance of some representative manufactured nanomaterials on ocular toxicity is summarized. First, a brief introduction of ocular anatomy and disorders related to particulate matter exposure is presented. Following, the factors that may influence toxicity of nanoparticles to the eye are emphasized. Next, the studies of representative manufactured nanoparticles on eye toxicity are summarized and classified. Finally, the limitations that are associated with current nanoparticle‐eye toxicity research are proposed. This work covers the recent advances of toxicity of nanomaterials to eyes. It starts with an introduction of eye anatomy and disorders related to particulate matter exposure. Next, the factors that may influence toxicity of nanoparticles to the eyes and studies of representative manufactured nanomaterials on eye toxicity are summarized. Finally, the limitations that are associated with this field are proposed.

The stack effect in high-rise buildings, stemming from an inside/outside temperature difference, may produce a significant pressure difference on the elevator doors, potentially causing elevator malfunctions. This effect can also be influenced by wind action and human behaviors, e.g., opening/closing of building entrances. In this study, a wind tunnel test was conducted to determine the real wind pressure distribution on a high-rise building in northern China. A numerical simulation utilizing the Conjunction of Multizone Infiltration Specialists software (COMIS) was carried out to investigate the pressure difference of elevator doors under the effects of thermal buoyancy, wind action, and opening/closing of the first-floor lobby entrance. An alternative solution of a locally strengthened envelope is proposed and validated for the studied building zone. The study reveals that the opening of the first-floor lobby entrance increases the pressure difference regardless of the environmental conditions, and the increase of wind speed tends to increase the pressure difference in winter but decrease it in summer. The proposed countermeasure combination, involving using revolving doors instead of swing doors, increasing additional partitions, and strengthening the local building envelope, was found to be synergistic and effective in reducing the pressure difference inside the building. The research findings offer practical engineering solutions for mitigating elevator door pressure challenges in high-rise buildings.