Ruihua Affiliated Hospital of Soochow University

Bioengineered artificial blood vessels have been a major area of interest over the last decade. Of particular interest are small diameter vessels, as surgical options are currently limited. This study aimed to fabricate a small diameter, heterogeneous bilayer blood vessel-like construct in a single step with gelatin methacryloyl (GelMA) bioink using a 3D micro-extrusion bioprinter on a solid platform. GelMA was supplemented with Hyaluronic acid (HA), glycerol and gelatin to form a GelMA bioink with good printability, mechanical strength, and biocompatibility. Two separate concentrations of GelMA bioink with unique pore sizes were selected to fabricate a heterogeneous bilayer. A higher concentration of GelMA bioink (6% w/v GelMA, 2% gelatin, 0.3% w/v HA, 10% v/v glycerol) was used to load human umbilical vein endothelial cells (HUVECs) and form an inner, endothelial tissue layer. A lower concentration of GelMA bioink (4% w/v GelMA, 4% gelatin, 0.3% w/v HA, 10% v/v glycerol) was used to load smooth muscle cells (SMCs) and form an outer, muscular tissue layer. Bioprinted blood vessel-like grafts were then assessed for mechanical properties with Instron mechanical testing, and suture-ability, and for biological properties including viability, proliferation, and histological analysis. The resulting 20 mm long, 4.0 mm diameter lumen heterogeneous bilayer blood vessel-like construct closely mimics a native blood vessel and maintains high cell viability and proliferation. Our results represent a novel strategy for small diameter blood vessel biofabrication.

Clinical settings often face significant obstacles in treating large acute wounds. The alternative of therapeutic approach is needed urgently. Hydrogels derived from natural or synthetic materials may be designed to perform a variety of functions for promoting wound healing. Herein, a 3D bioprinted hydrogel patch is designed for accelerating acute wound healing, which is fabricated with methacryloyl-substituted gelatin (GelMA) and silk fibroin (SilMA) dual-cross-linked by ultraviolet (UV) light. The GelMA with added silk fibroin (GelSilMA) shows improved biodegradation and mechanical properties. Furthermore, SilMA hydrogel can maintain a moisturized healing environment in wound area persistently with adequate degradation capacity. In vivo, GelSilMA (G-S) hydrogel can help to speed wound closure by the improved microenvironment for epidermal tissue regeneration and endogenous collagen generation accordingly. In summary, the G-S hydrogel patch can accelerate acute wound healing efficiently in a relatively simple and inexpensive manner.

Tissue engineering is a growing research area of great interest because it can produce bionic grafts to replace autologous tissue. Although many molding strategies have been tried, precellularization of small-diameter vascular grafts remains a research challenge. Here, a novel approach for fabricating bionic small-diameter vascular vessels is developed through combining nanofiber electrospinning and a specially-designed rotary bioprinter. Electrospun poly(ε-caprolactone) (PCL) provides good elasticity, and the electrospinning modification is beneficial for adhesion and functionalization of endothelial cells. A flat monolayer on the surface of PCL is formed after 7 days cultivation. Modification of the traditional three-dimensional (3D) bioprinter to increase rotation of the central axis used dual motors increase stability during the printing process. This allowed a uniform dense methacrylated gelatin (GelMA) structure containing smooth muscle cells to be bioprinted with the cells are arranged linearly along the horizontal axis of rotation. The two type cells maintain viability and proliferation in the structure during the process of cultivation. In addition, the bionic structure is superior to the natural blood vessel in anti-burst pressure and suture retention strength. This study may provide a new strategy for the development of bionic blood vascular tissue or other tubular structure.

Summary Aims Lower androgen level in elderly men is a risk factor of Alzheimer's disease ( AD ). It has been reported that androgen reduces amyloid peptides (Aβ) production and increases Aβ degradation by neurons. Activated microglia are involved in AD by either clearing Aβ deposits through uptake of Aβ or releasing cytotoxic substances and pro‐inflammatory cytokines. Here, we investigated the effect of androgen on Aβ uptake and clearance and Aβ‐induced inflammatory response in microglia, on neuronal death induced by Aβ‐activated microglia, and explored underlying mechanisms. Methods Intracellular and extracellular Aβ were examined by immunofluorescence staining and Western blot. Amyloid peptides (Aβ) receptors, Aβ degrading enzymes, and pro‐inflammatory cytokines were detected by RT ‐ PCR , real‐time PCR , and ELISA . Phosphorylation of MAP kinases and NF ‐κB was examined by Western blot. Results We found that physiological concentrations of androgen enhanced Aβ 42 uptake and clearance, suppressed Aβ 42 ‐induced IL ‐1β and TNF α expression by murine microglia cell line N9 and primary microglia, and alleviated neuronal death induced by Aβ 42 ‐activated microglia. Androgen administration also reduced Aβ 42 ‐induced IL ‐1β expression and neuronal death in murine hippocampus. Mechanistic studies revealed that androgen promoted microglia to phagocytose and degrade Aβ 42 through upregulating formyl peptide receptor 2 and endothelin‐converting enzyme 1c expression, and inhibited Aβ 42 ‐induced pro‐inflammatory cytokines expression via suppressing MAPK p38 and NF ‐κB activation by Aβ 42 , in an androgen receptor independent manner. Conclusion Our study demonstrates that androgen promotes microglia to phagocytose and clear Aβ 42 and inhibits Aβ 42 ‐induced inflammatory response, which may play an important role in reducing the neurotoxicity of Aβ.

In addition to a well-documented role in regulating T cell-mediated immune responses, B7-H3, a newly discovered member of the B7 superfamily, has been recently identified as a costimulator in the innate immunity-mediated inflammatory response. In this study, we further report that B7-H3 participates in the development of pneumococcal meningitis in a murine model. Exogenous administration of B7-H3 strongly amplified the inflammatory response, exacerbated blood-brain barrier disruption, and aggravated the clinical disease status in Streptococcus pneumoniae-infected C3H/HeN wild-type mice. Consistent with the in vivo findings, B7-H3 substantially augmented proinflammatory cytokine and chemokine production, upregulated NF-κB p65 and MAPK p38 phosphorylation, and enhanced the nuclear transactivation of NF-κB p65 at both TNF-α and IL-6 promoters in S. pneumoniae-stimulated primary murine microglia cells. These B7-H3-associated in vitro and in vivo effects appeared to be dependent on TLR2 signaling, as B7-H3 almost completely lost its amplifying actions in both TLR2-deficient microglial cells and TLR2-deficient mice. Furthermore, administration of the anti-B7-H3 mAb (MIH35) attenuated the inflammatory response and ameliorated blood-brain barrier disruption in S. pneumoniae-infected wild-type mice. Collectively, our results indicate that B7-H3 plays a contributory role in the development of S. pneumoniae infection-induced bacterial meningitis.

MicroRNAs (MiRNAs), which regulate the gene expression leading to translational inhibition or mRNA degradation, are involved in carcinogenesis and tumor progression. Previous studies have demonstrated that miR-221 was one of the most consistent overexpressed miRNAs in several types of cancer. However, the role of miR-221 in human liver cancer progression is not yet fully elucidated. Levels of miR-221 and plant homeodomain finger 2 (PHF2) expressions in human hepatocellular carcinoma (HCC) tissues and cell lines were detected using western blotting and quantitative real-time PCR (qRT-PCR). Cell migration was studied using the transwell assays. A dual-luciferase reporter system was used to validate the target gene of miR-221. The results indicated that miR-221 promoted HCC cell migration. By performing subsequent systematic bioinformatic analyses, we found PHF2 was the target gene of miR-221 and the direct binding relationship was further validated by dual-luciferase reporter assay. In addition, lower expression of PHF2 promoted HCC cell migration and linked to worse overall survival in HCC patients. Finally, the negative correlation between miR-221 and PHF2 expression levels in HCC specimens was further confirmed. Taken together, our findings implied that miR-221 could be a potential candidate for the therapeutics of HCC metastasis.

Tissue vascularization is critical to enable oxygen and nutrient supply. Therefore, establishing expedient vasculature is necessary for the survival of tissue after transplantation. The use of biomechanical forces, such as cell-induced traction forces, may be a promising method to encourage growth of the vascular network. Three-dimensional (3D) bioprinting, which offers unprecedented versatility through precise control over spatial distribution and structure of tissue constructs, can be used to generate capillary-like structures in vitro that would mimic microvessels. This study aimed to develop an in vitro, 3D bioprinted tissue model to study the effect of cellular forces on the spatial organization of vascular structures and tissue maturation. The developed in vitro model consists of a 3D bioprinted polycaprolactone (PCL) frame with a gelatin spacer hydrogel layer and a gelatin-fibrin-hyaluronic acid hydrogel layer containing normal human dermal fibroblasts and human umbilical vein endothelial cells printed as vessel lines on top. The formation of vessel-like networks and vessel lumens in the 3D bioprinted in vitro model was assessed at different fibrinogen concentrations with and without inhibitors of cell-mediated traction forces. Constructs containing 5 mg/ml fibrinogen had longer vessels compared to the other concentrations of fibrinogen used. Also, for all concentrations of fibrinogen used, most of the vessel-like structures grew parallel to the direction the PCL frame-mediated tensile forces, with very few branching structures observed. Treatment of the 3D bioprinted constructs with traction inhibitors resulted in a significant reduction in length of vessel-like networks. The 3D bioprinted constructs also had better lumen formation, increased collagen deposition, more elaborate actin networks, and well-aligned matrix fibers due to the increased cell-mediated traction forces present compared to the non-anchored, floating control constructs. This study showed that cell traction forces from the actomyosin complex are critical for vascular network assembly in 3D bioprinted tissue. Strategies involving the use of cell-mediated traction forces may be promising for the development of bioprinting approaches for fabrication of vascularized tissue constructs.

Oxidative stress and iron accumulation-induced ferroptosis occurs in injured vascular cells and can promote thrombogenesis. Transferrin receptor 1 (encoded by the TFRC gene) is an initial element involved in iron transport and ferroptosis and is highly expressed in injured vascular tissues, but its role in thrombosis has not been determined. To explore the potential mechanism and therapeutic effect of TFRC on thrombogenesis, a DVT model of femoral veins (FVs) was established in rats, and weighted correlation network analysis (WGCNA) was used to identify TFRC as a hub protein that is associated with thrombus formation. TFRC was knocked down by adeno-associated virus (AAV) or lentivirus transduction in FVs or human umbilical vein endothelial cells (HUVECs), respectively. Thrombus characteristics and ferroptosis biomarkers were evaluated. Colocalization analysis, molecular docking and coimmunoprecipitation (co-IP) were used to evaluate protein interactions. Tissue-specific TFRC knockdown alleviated iron overload and redox stress, thereby preventing ferroptosis in injured FVs. Loss of TFRC in injured veins could alleviate thrombogenesis, reduce thrombus size and attenuate hypercoagulability. The protein level of thrombospondin-1 (THBS1) was increased in DVT tissues, and silencing TFRC decreased the protein level of THBS1. In vitro experiments further showed that TFRC and THBS1 were sensitive to erastin-induced ferroptosis and that TFRC knockdown reversed this effect. TFRC can interact with THBS1 in the domain spanning from TSR1-2 to TSR1-3 of THBS1. Amino acid sites, including GLN320 of TFRC and ASP502 of THBS1, could be potential pharmacological targets. Erastin induced ferroptosis affected extracellular THBS1 levels and weakened the interaction between TFRC and THBS1 both in vivo and in vitro, and promoted the interaction between THBS1 and CD47. This study revealed a linked relationship between venous ferroptosis and coagulation cascades. Controlling TFRC and ferroptosis in endothelial cells can be an efficient approach for preventing and treating thrombogenesis.

BACKGROUND: Traumatic brain injury (TBI) is a leading cause of death and disability worldwide as well as a risk factor for neurodegenerative diseases later in life. Evodiamine (Evo), a compound derived from Evodia rutaecarpa, is known to possess pharmacological activities. However, whether Evo confers protection after TBI remains unknown. OBJECTIVE: To study whether Evo protects against TBI through inhibiting oxidative stress via the phosphoglycerate kinase 1 (PGK1)/nuclear factor erythroid 2-related factor 2 (NRF2) pathway. MATERIALS AND METHODS: stimulation for another 24 h to induce oxidative stress. Furthermore, transfection of PGK1 overexpressing vectors or PGK1 siRNAs was performed to decipher the role of PGK1 in Evo-produced effect in TBI. RESULTS: -stimulated PC12 cells. DISCUSSION AND CONCLUSIONS: Taken together, we demonstrated that Evo improved the outcomes after TBI by targeting the PGK1/NRF2 signaling-regulated oxidative stress. Evo may represent a potential therapy to promote recovery from TBI.

Advancements in 3D bioprinting, particularly the use of gelatin methacrylate (GelMA) hydrogels, are ushering in a transformative era in regenerative medicine and tissue engineering. This review highlights the pivotal role of GelMA hydrogels in wound healing and skin regeneration. Its biocompatibility, tunable mechanical properties and support for cellular proliferation make it a promising candidate for bioactive dressings and scaffolds. Challenges remain in optimizing GelMA hydrogels for clinical use, including scalability of 3D bioprinting techniques, durability under physiological conditions and the development of advanced bioinks. The review covers GelMA's applications from enhancing wound dressings, promoting angiogenesis and facilitating tissue regeneration to addressing microbial infections and diabetic wound healing. Preclinical studies underscore GelMA's potential in tissue healing and the need for further research for real-world applications. The future of GelMA hydrogels lies in overcoming these challenges through multidisciplinary collaboration, advancing manufacturing techniques and embracing personalized medicine paradigms.

Impairment of the immune system is a developing concern in evaluating the toxicity of cadmium (Cd). In the present study, we investigated if Cd could impair cutaneous wound healing through interfering with inflammation after injury. We found that exposure of mice to CdCl2 through drinking water at doses of 10, 30, and 50 mg/l for 8 weeks significantly impaired cutaneous wound healing. Chronic 30 mg/l CdCl2 treatment elevated murine blood Cd level comparable to that of low dose Cd-exposed humans, had no effect on blood total and differential leukocyte counts, but reduced neutrophil infiltration, chemokines (CXCL1 and CXCL2), and proinflammatory cytokines (TNFα, IL-1β, and IL-6) expression in wounded tissue at early stage after injury. Wounded tissue homogenates from CdCl2-treated mice had lower chemotactic activity for neutrophils than those from untreated mice. Mechanistic studies showed that chronic Cd treatment suppressed ERK1/2 and NF-κB p65 phosphorylation in wounded tissue at early stage after injury. Compared with neutrophils isolated from untreated mice, neutrophils from CdCl2 treated mice and normal neutrophils treated with CdCl2 invitro both had lower chemotactic response, calcium mobilization and ERK1/2 phosphorylation upon chemoattractant stimulation. Collectively, our study indicate that chronic low-dose Cd exposure impaired cutaneous wound healing by reducing neutrophil infiltration through inhibiting chemokine expression and neutrophil chemotactic response, and suppressing proinflammatory cytokine expression. Cd may suppress chemokine and proinflammatory expression through inactivating ERK1/2 and NF-κB, and inhibit neutrophil chemotaxis by attenuating calcium mobilization and ERK1/2 phosphorylation in response to chemoattractants.

BACKGROUND: D-allose was promising in the protection of ischemia/reperfusion (I/R) injury. We intended to investigate the function of D-allose in skin flap of rat followed by the injury of I/R and whether ERK signal pathway was involved in. METHODS: The back flap of Wistar rats was picked up with a vascular bundle of the lateral chest wall. I/R model was made by the venous clamp for 6 h. Rats received D-allose and PD-98059, the inhibitor of ERK1/2, 30 min before modeling. Morphology of tissue was observed by HE staining. Nitric oxide (NO), myeloperoxidase (MPO), malondialdehyde (MDA) and superoxide dismutase (SOD) levels in skin flap were determined by ELISA kits. mRNA and protein levels were determined by qPCR and Western blot respectively. RESULTS: D-allose alleviated the condition of pathological changes and raised the survival rate of skin flap injured by I/R. Moreover, D-allose suppressed NO, MPO and MDA while elevated SOD levels during I/R status. Furthermore, D-allose decreased MCP-1, TNF-α, IL-1β and IL-6 levels in skin flap injured by I/R. In addition, D-allose inhibited MKP-1 expression and activated ERK1/2 pathway in skin flap injured by I/R. PD-98059 partially counteracted D-allose effects on I/R injury. CONCLUSIONS: D-allose exerted its protective function via inhibiting MKP-1expression and further activated ERK1/2 pathway to suppress the progress of oxidative stress, inflammation and necrosis, contributing to the survival of skin flap injured by I/R. Thus, D-allose was promising in the transplantation of skin flap.

Skin epidermal stem cells (EpSCs) play an important role in wound healing. Quercetin is a phytoestrogen reported to accelerate skin wound healing, but its effect on EpSCs is unknown. In this study, we investigated the effect of quercetin on human EpSC proliferation and explored the underlying mechanisms. We found that quercetin at 0.1~1 μM significantly promoted EpSC proliferation and increased the number of cells in S phase. The pro-proliferative effect of quercetin on EpSCs was confirmed in cultured human skin tissue. Mechanistic studies showed that quercetin significantly upregulated the expressions of β-catenin, c-Myc, and cyclins A2 and E1. Inhibitor for β-catenin or c-Myc significantly inhibited quercetin-induced EpSC proliferation. The β-catenin inhibitor XAV-939 suppressed quercetin-induced expressions of β-catenin, c-Myc, and cyclins A2 and E1. The c-Myc inhibitor 10058-F4 inhibited the upregulation of c-Myc and cyclin A2 by quercetin. Pretreatment of EpSCs with estrogen receptor (ER) antagonist ICI182780, but not the G protein-coupled ER1 antagonist G15, reversed quercetin-induced cell proliferation and upregulation of β-catenin, c-Myc, and cyclin A2. Collectively, these results indicate that quercetin promotes EpSC proliferation through ER-mediated activation of β-catenin/c-Myc/cyclinA2 signaling pathway and ER-independent upregulation of cyclin E1 and that quercetin may accelerate skin wound healing through promoting EpSC proliferation. As EpSCs are used not only in clinic to treat skin wounds but also as seed cells in skin tissue engineering, quercetin is a useful reagent to expand EpSCs for basic research, skin wound treatment, and skin tissue engineering.

Skin epidermal stem cells (EpSCs) play critical roles in skin homeostasis and the repair of skin injury. Luteolin-7-glucoside (L7G) has been reported to accelerate skin wound healing through its anti-inflammatory and antioxidative activity. But its effect on EpSCs is not clear. In the present study, we examined the effect of L7G on the proliferation of human EpSCs and explored the mechanisms involved. MTT assay showed that L7G promoted EpSC proliferation in a dose- and time-dependent manner. BrdU incorporation assay and Ki67 immunofluorescence staining confirmed the proproliferative effect of L7G on EpSCs. Cell cycle analysis showed that treatment of EpSCs with L7G decreased the cell number in the G1 phase and increased the cell number in the S phase. In addition, L7G significantly enhanced EpSC migration. Mechanistic studies showed that L7G significantly induced the expression of β -catenin and c-Myc, as well as cyclins D 1 , A 2 , and E 1 which are critical for G1/S phase transition. L7G stimulated EpSC proliferation through β -catenin and c-Myc. We further examined the effect of L7G on EpSC proliferation in skin tissues by treatment of human skin explants with L7G and examined the number of EpSCs by immunohistochemical stain of EpSC markers α 6 integrin and β 1 integrin. We found that treatment of human skin tissue explants with L7G significantly increased the thickness of the epidermis and increased the numbers of α 6 integrin-positive and β 1 integrin-positive cells at the basal layer of the epidermis. Taken together, these results indicate that L7G promotes EpSC proliferation through upregulating β -catenin, c-Myc, and cyclin expression. L7G can be used to expand EpSCs for generating epidermal autografts and engineered skin equivalents.

Objectives To evaluate the long‐term efficacy of cannulated internal fixation in patients who sustain femoral neck fracture (FNF) and risk factors influencing the outcomes. Methods This retrospective study analyzed data from 73 elderly patients aged ≥60 years old, hospitalized for FNF and treated with cannulated internal fixation between August 2008 and July 2016. The inclusion criteria were: (i) patients aged ≥60 years; (ii) patients with recent femoral neck fracture, with times of injury ranging from 12–72 h; and (iii) patients who underwent Garden II–IV closed reduction and internal fixation. Patients were classified based on the Garden fracture type and Pauwels angle. Clinical data and radiographs before and after the surgery were collected. Subsequently, surgery was performed with the patient in supine position, under general or lumbar epidural anesthesia. Closed reduction was performed until satisfactory fracture reduction quality was achieved. The weight of all included patients were <75 kg, and thus, minimal internal fixation was performed. The ischemic necrosis of the femoral head was diagnosed by considering the symptoms, signs, and radiological findings. Harris hip scores were used to evaluate postoperative recovery of hip function. Furthermore, relationships between Garden fracture type and necrosis rate of the femoral head, Pauwels angle and necrosis rate of the femoral head, Garden fracture type and Harris hip score, and age and Harris hip score were analyzed. Results The mean duration of surgery was 1 ± 0.17 h and blood loss for all the patients was approximately 15 mL. The included patients were followed up for 13–128 months, with an average follow‐up of 61 months. Among the included 73 patients, 65 (89.0%) exhibited satisfactory union, seven (9.6%) had femoral head necrosis, and one (1.4%) had nonunion. For seven patients with femoral head necrosis, there were two, two, and three patients classified as Garden IV, Garden III, and Garden II, respectively, and two and five patients classified as Pauwels II and Pauwels III, respectively. Among the seven cases, four underwent hip replacement. Garden fracture type was not significantly associated with femoral head necrosis (χ 2 = 0.44, P > 0.05) or Harris score (χ 2 = 1.43, P > 0.05). Patients with Pauwels I (0%) and II (4.3%) fractures exhibited a significantly lower necrosis rate than those with Pauwels III fractures (41.7%) ( P < 0.05). Conclusions Cannulated internal fixation was more suitable for older Chinese patients with Pauwels I/II fractures than those with Pauwels III fractures.

BACKGROUND: To evaluate the efficacy and safety of the introduction of moxifloxacin into the recommended regimen for tuberculosis (TB) treatment. METHODS: A meta-analysis was performed of nine eligible studies regarding the effect of moxifloxacin plus the recommended regimen compared to the recommended regimen alone for the treatment of TB. RESULTS: In the efficacy analysis, the overall odds ratio (OR) for sputum culture conversion was 1.895 (95% confidence interval (CI) 1.355-2.651, p=0.000), indicating that when moxifloxacin is combined with the recommended regimen, the rate of sputum culture conversion is elevated compared to the recommended regimen alone. The overall OR for recurrence was 0.516 (95% CI 0.342-0.920, p=0.022), suggesting that the introduction of moxifloxacin into the recommended regimen reduces TB relapse after treatment. In the safety analysis, the overall OR was estimated to be 1.001 (95% CI 0.855-1.172, p=0.989), demonstrating that adding moxifloxacin to the recommended regimen does not cause more adverse events during TB treatment. CONCLUSIONS: This meta-analysis suggests that the introduction of moxifloxacin into the recommended regimen for the treatment of non-drug resistant TB improves the clinical outcome by elevating the culture conversion rate and reducing the recurrence rate.

Restoration of a wound is a common surgical procedure in clinic. Currently, the skin required for clinical use is taken from the patient's own body. However, it can be difficult to obtain enough skin sources for large-sized wounds and thus surgeons have started using commercial skin substitutes. The current commercial skin, which includes epidermis substitute, dermis substitute, and bilateral skin substitute, has been popularized in clinic. However, the application is limited by the occurrence of ischemia necrosis after transplantation. Recent studies suggest the use of pre-vascularized skin substitutes for wound healing is a promising area in the research field of skin tissue engineering. Pre-vascularization can be induced by changes in cultivation periods, exertion of mechanical stimuli, or coculture with endothelial cells and various factors. However, few methods could control the formation of vascular branches in engineering tissue in a self-assembly way. In this study, we use three-dimensional (3D) printing technology to confirm that a mechanical force can control the growth of blood vessels in the direction of mechanical stimulation with no branches, and that Yes-associated protein activity is involved in the regulatory progress. In vivo experiments verified that the blood vessels successfully function for blood circulation, and maintain the same direction. Results provide a theoretical basis for products of pre-vascularized skin tissues and other organs created by 3D bioprinting.

Three-dimensional bioprinting shows great potential for autologous vascular grafts due to its simplicity, accuracy, and flexibility. The 6-mm-diameter vascular grafts are used in clinic. However, producing small-diameter vascular grafts are still an enormous challenge. Normally, sacrificial hydrogels are used as temporary lumen support to mold tubular structure which will affect the stability of the fabricated structure. In this study, we have developed a new bioprinting approach to fabricating small-diameter vessel using two-step crosslinking process. The ¼ lumen wall of bioprinted gelatin mechacrylate (GelMA) flat structure was exposed to ultraviolet (UV) light briefly for gaining certain strength, while ¾ lumen wall showed as concave structure which remained uncrosslinked. Precrosslinked flat structure was merged towards the uncrosslinked concave structure. Two individual structures were combined tightly into an intact tubular structure after receiving more UV exposure time. Complicated tubular structures were constructed by these method. Notably, the GelMA-based bioink loaded with smooth muscle cells are bioprinted to form the outer layer of the tubular structure and human umbilical vein endothelial cells were seeded onto the inner surface of the tubular structure. A bionic vascular vessel with dual layers was fabricated successfully, and kept good viability and functionality. This study may provide a novel idea for fabricating biomimetic vascular network or other more complicated organs.

UNLABELLED: The purpose of this report was to retrospectively review the results of reconstruction of the thumb by use of combined two foot flaps with an iliac bone graft. From 2009 to 2014, nine patients with traumatic amputation of the thumb had their thumbs reconstructed. The two flaps were based on one pedicle. All flaps survived completely. Patients were followed for a mean of 15.6 months (range, 6-35 months). The appearance of the reconstructed thumb was comparable to a normal one, except for one thumb which required debulking. The appearance of the nail was satisfactory without deformity. The range of joint motion was satisfactory. The two point discrimination of the pulp ranged from 6 mm to >15 mm. The Michigan Hand Questionnaire outcome score was a mean of 76.2 ± 11.3 points and the Maryland foot rating score a mean of 94.8 ± 3.4 points. The combined two foot flaps with iliac bone graft might provide an option for the reconstruction of the thumb. LEVEL OF EVIDENCE: III.

Constipation is a common health problem that adversely affects quality of life and the prognosis of hospitalized patients with acute coronary syndromes (ACS). The purpose of this study was to develop and test the sweet potato/footbath/acupressure massage (SFA) intervention as a safe treatment for prevention of constipation and to increase satisfaction with bowel emptying in hospitalized patients with ACS. The study was a prospective, randomized controlled trial with a sample of 93 patients (SFA group, n = 44; usual care group, n = 49). Patients in the SFA group received SFA intervention combined with usual care. The results showed that there were statistical differences between the two groups in terms of (1) the incidence of constipation; (2) the use of laxatives and enemas; (3) patients' subjective satisfaction with their bowel emptying during hospitalization; and (4) sensation of incomplete evacuation and anorectal obstruction/blockade. The SFA intervention was more effective, economical, and practical than usual care alone in managing constipation and satisfaction with defecation in patients hospitalized with ACS.