Diabetic foot ulcers (DFU), which may lead to lower extremity amputation, is one of the severe and chronic complications of diabetic mellitus. This study aims to develop, and use dressings based on Silk fibroin (SF) as the scaffold material, gelatin microspheres (GMs) as the carrier for the neurotensin (NT), a neuropeptide that acts as an inflammatory modulator in wound healing and NT as accelerate wound healing drug to treat DFU. We evaluated the wound healing processes and neo-tissue formation in rat diabetic model by macroscopic observation, histological observation (H&E staining and Masson's trichrome staining) and immunofluorescence analysis at 3, 7, 14, 21 and 28 post-operation days. Our results show that the NT/GMs/SF group performance the best not only in macroscopic healing and less scars in 28 post-operation days, but also in fibroblast accumulation in tissue granulation, collagen expression and deposition at the wound site. From release profiles, we can know the GMs are a good carrier for control release drugs. The SEM results shows that the NT/GMs/SF dressings have an average pore size are 40-80 μm and a porosity of ∼85%, this pore size is suit for wound healing regeneration. These results suggest that the NT/GMs/SF dressings may work as an effective support for control release NT to promote DFU wound healing.

Growing human organs in animals sounds like something from the realm of science fiction, but it may one day become a reality through a technique known as interspecies blastocyst complementation. This technique, which was originally developed to study gene function in development, involves injecting donor pluripotent stem cells into an organogenesis-disabled host embryo, allowing the donor cells to compensate for missing organs or tissues. Although interspecies blastocyst complementation has been achieved between closely related species, such as mice and rats, the situation becomes much more difficult for species that are far apart on the evolutionary tree. This is presumably because of layers of xenogeneic barriers that are a result of divergent evolution. In this Review, we discuss the current status of blastocyst complementation approaches and, in light of recent progress, elaborate on the keys to success for interspecies blastocyst complementation and organ generation.

The reconstruction of extensive three-dimensional defects in the extremities is a difficult challenge. Many attempts have been made to reconstruct such defects using the chimeric flap concept, enabling flaps with larger surface areas to be used while maintaining economical tissue use. The anterolateral thigh (ALT) chimeric flap is one of the most useful tools for the reconstruction of complex three-dimensional defects in the extremities. From January 2010 to March 2012, Twenty-two patients underwent extremity reconstruction using chimeric ALT perforator flaps, which consists of a skin component on its isolated perforator and a portion of the fascia and muscle flaps on the same pedicle from the descending branch of the lateral circumflex femoral artery (LCFA). The defects were in either a lower (n = 10) or an upper extremity (n = 12). The area of the soft tissue defects ranged from 43 × 35 cm to 19 × 9 cm (mean, 25 × 18 cm), containing extensive, irregular, ring-like soft tissue defects or degloving injuries. The mean dimension of skin flap was 19.8 × 11.2 cm. The mean dimension of fascia flap was 8.9 × 7.1 cm. The mean dimension of muscle flap was 11.1 × 7.5 cm. No total flap loss occurred. One patient presented with venous thrombosis, and re-anastomosis and vein grafting were performed. Two cases exhibiting partial skin graft loss at the site at which the fascia flap was inset were treated via secondary skin grafts. During a follow-up period of 18 months-30 months, patients were satisfied with the functional and aesthetic outcome. No serious donor-site complications occurred. Chimeric anterolateral thigh perforator flap can be one of the best choice for reconstruction of complex soft-tissue defects in the extremities. The various tissue components and maximal freedom offered by chimeric tissue flaps associated with the same descending branch of the LCFA provide versatile coverage of large, complex, and irregular soft-tissue defects in the extremities.

Objective: We have demonstrated that angiogenesis in acellular nerve allografts (ANAs) can promote neuroregeneration. The present study aimed to investigate the microvascular regeneration pattern of ANAs in Sprague-Dawley (SD) rats. Methods: Sixty male SD rats were randomly divided into an autologous group and a rat acellular nerve allograft group (rANA), and 10-mm sciatic nerve defects were induced in these rats. On the 7th, 14th and 21st days after surgery, systemic perfusion with Evans Blue (EB) or lead oxide was performed on the rats through carotid intubation. Samples were then collected for gross observation, and the microvessels in the nerves were reconstructed through microscopic CT scans using MIMICS software. The vascular volume fraction (VF, %) and microvessel growth rate (V, mm/d) in both groups were then measured, and 1 month after surgery, NF-200 staining was performed to observe and compare the growth condition of the axons. Results: Early post-operative perfusion with gelatin/EB showed EB permeation around the acellular nerve. Perfusion with gelatin/lead oxide showed that the blood vessels had grown into the allograft from both ends 7 days after the operation. Fourteen days after the operation, the microvessel growth rate of the autologous group was faster than that of the rANA group (0.39 ± 0.17 mm/d vs. 0.26 ± 0.14 mm/d, p < 0.05), and the vascular VF was also higher than that of the rANA group (8.92% ± 1.54% vs. 6.31% ± 1.21%, p < 0.05). Twenty-one days after the operation, the blood vessels at both ends of the allograft had connected to form a microvessel network. The growth rate was not significantly different between the two groups; however, the vascular VF of the autologous group was higher than that of the rANA group (12.18% ± 2.27% vs. 9.92% ± 0.84%, p < 0.05). One month after the operation, the NF-200 fluorescence (IOD) in the autologous group significantly increased compared with that of the rANA group (540,278 ± 17,424 vs. 473,310 ± 14,636, respectively, p < 0.05), suggesting that the results of the repair after nerve injury were significantly better in the autologous group than in the rANA group. Conclusion: Both the autologous nerve and ANAs rely on the permeation of tissue fluids to supply nutrients during the early stage, and microvessel growth mainly starts at both ends of the graft and enters the graft along the long axis. Compared to ANAs, the growth speed of revascularization in autologous nerve grafts was faster, leading to a better outcome in the autologous nerve group.

JOURNAL/nrgr/04.03/01300535-202303000-00046/figure1/v/2026-05-25T154646Z/r/image-tiff Traumatic painful neuroma is an intractable clinical disease characterized by improper extracellular matrix (ECM) deposition around the injury site. Studies have shown that the microstructure of natural nerves provides a suitable microenvironment for the nerve end to avoid abnormal hyperplasia and neuroma formation. In this study, we used a decellularized nerve matrix scaffold (DNM-S) to prevent against the formation of painful neuroma after sciatic nerve transection in rats. Our results showed that the DNM-S effectively reduced abnormal deposition of ECM, guided the regeneration and orderly arrangement of axon, and decreased the density of regenerated axons. The epineurium-perilemma barrier prevented the invasion of vascular muscular scar tissue, greatly reduced the invasion of α-smooth muscle actin-positive myofibroblasts into nerve stumps, effectively inhibited scar formation, which guided nerve stumps to gradually transform into a benign tissue and reduced pain and autotomy behaviors in animals. These findings suggest that DNM-S-optimized neuroma microenvironment by ECM remodeling may be a promising strategy to prevent painful traumatic neuromas.

Contusion concomitant with ischemia injury to skeletal muscles is common in civilian and battlefield trauma. Despite their clinical importance, few experimental studies on these injuries are reported. The present study established a rat skeletal muscle contusion concomitant with ischemia injury model to identify skeletal muscle alterations compared with contusion injury or ischemia injury. Macroscopic and microscopic morphological evaluation showed that contusion concomitant with ischemia injury aggravated muscle edema and hematoxylin–eosin (HE) injury score at 24 h postinjury. Serum creatine kinase (CK) and lactate dehydrogenase (LDH) levels, together with gastrocnemius muscle (GM) tumor necrosis factor-alpha (TNF-α) content elevated at 24 h postinjury too. During the 28-day follow-up, electrophysiological and contractile impairment was more severe in the contusion concomitant with ischemia injury group. In addition, contusion concomitant with ischemia injury decreased the percentage of larger (600–3000 μm²) fibers and increased the fibrotic area and collagen I proportion in the GM. Smaller proportions of Pax7⁺ and MyoD⁺ satellite cells (SCs) were observed in the contusion concomitant with ischemia injury group at 7 days postinjury. In conclusion, contusion concomitant with ischemia injury to skeletal muscle not only aggravates early muscle fiber necrosis but also hinders muscle functional recovery by impairing SC differentiation and exacerbating fibrosis during skeletal muscle repair.