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Background: Full‐thickness skin grafts are widely used in plastic and reconstructive surgery. The main limitation of skin grafting is the poor textural durability and associated contracture, which often needs further corrective surgery. Excessive inflammation is the main reason for skin graft contractions, which involve overactivation of myofibroblasts. These problems have prompted the development of new therapeutic approaches, including macrophage polarization modulation and stem cell–based therapies. Currently, adipose‐derived stem cells (ASCs) have shown promise in promoting skin grafts survival and regulating macrophage phenotypes. However, the roles of ASCs on macrophages in decreasing skin grafts contraction remain unknown. Materials and Methods: Rat adipose‐derived stem cells (rASCs) were isolated from rat inguinal adipose tissues. Full‐thickness skin graft model was constructed on male rats divided into control group and rASCs treatment group. Skin graft was assessed for concentration, elasticity modulus and stiffness. Rat bone marrow‐derived macrophages (rBMDMs) were isolated from rat femurs, and subsequent RT‐qPCR and coculture assays were carried out to explore the cellular mechanisms. Immunohistochemical and immunofluorescence staining were used to verify mechanisms in vivo. Results: In vivo results showed that after injection of ASCs, improved texture, increased survival and inhibited contraction of skin grafts were seen. Vascularization was also improved as illustrated by laser perfusion image and vascular endothelial growth factor (VEGF) concentration. Histological analysis revealed that ASCs injection significantly reduced expression of pro‐inflammatory cytokines (TNF‐a, IL‐1β) and increased expression of anti‐inflammatory (IL‐10) and pro‐healing cytokines (IGF‐1). At cellular level, after co‐culturing with rASCs, rat bone marrow derived macrophages (rBMDMs) favored M2 polarization even under inflammatory stimulus. Conclusion: ASCs treatment enhanced vascularization via angiogenic cytokines secretion and alleviated inflammatory environment in skin grafts by driving M2 macrophages polarization, which improved survival and decreased skin grafts contraction. Our work showed that ASCs transplantation can be harnessed to enhance therapeutic efficacy of skin grafting in cutaneous defects treatment. [ABSTRACT FROM AUTHOR]

Background: With widespread utilization of instant social media, people desire a minimally invasive treatment to improve alar dynamic aesthetic, but few practical procedures on reducing alar mobility have been conducted.Objectives: This study aimed to verify the effects of botulinum toxin on reducing nasal alar mobility and provide a supplemental treatment of rhinoplasty.Methods: This single-blind prospective study included a cohort of 20 participants with the desire to improve their alar dynamic aesthetic. The experimental group was injected with 3U botulinum toxin type A at dilator naris anterior, dilator naris vestibularis, levator labii superioris alaeque nasi, and dilator naris, and the control group received the equivalent of saline. Standardized facial movement (from rest to maximum smile without revealing teeth) was recorded with a 3-dimensional imaging system. The changes between rest and maximum smile statuses represented alar mobility and were generated by MOBILITY=WIDTHsmile-WIDTHrestWIDTHrest×100 % . Alar mobility and root mean square analysis were employed for postoperative evaluations.Results: In the experimental group, alar flaring mobility decreased from 10.05% ± 6.40% to 4.91% ± 3.48%(P < 0.05), and alar base mobility decreased from 16.83% ± 5.69% to 12.50% ± 4.89% (P < 0.05), whereas no significant changes in alar mobility were found in the control group. In root mean square analysis, changes in the experimental group were significantly higher than in the control group (P < 0.05).Conclusions: Botulinum toxin type A can effectively restrain alar mobility without any significant adverse events and improve alar dynamic esthetic, which can serve as a minimally invasive method or supplemental treatment for rhinoplasty.Level Of Evidence:2: [ABSTRACT FROM AUTHOR]

A novel sequential permeable reactive barrier (multibarrier), composed of oxygen-releasing compound (ORC)/clinoptilolite/spongy iron zones in series, was proposed for ammonium-nitrogen-contaminated groundwater remediation. Column experiments were performed to: (1) evaluate the overall NH-N removal performance of the proposed multibarrier, (2) investigate nitrogen transformation in the three zones, (3) determine the reaction front progress, and (4) explore cleanup mechanisms for inorganic nitrogens. The results showed that NH-N percent removal by the multibarrier increased up to 90.43 % after 21 pore volumes (PVs) at the influent dissolved oxygen of 0.68∼2.45 mg/L and pH of 6.76∼7.42. NH-N of 4.06∼10.49 mg/L was depleted and NO-N (i.e., NO-N + NO-N) of 4.26∼9.63 mg/L was formed before 98 PVs in the ORC zone. NH-N of ≤4.76 mg/L was eliminated in the clinoptilolite zone. NO-N of 10.44∼12.80 mg/L was lost before 21 PVs in the spongy iron zone. The clinoptilolite zone length should be reduced to 30 cm. Microbial nitrification played a dominant role in NH-N removal in the ORC zone. Ion exchange was majorly responsible for NH-N elimination in the clinoptilolite zone. Chemical reduction and hydrogenotrophic denitrification both contributed to NO-N transformation, but the chemical reduction capacity decreased after 21 PVs in the spongy iron. [ABSTRACT FROM AUTHOR]

Ischemic heart diseases have emerged as great threats to human health. Nowadays, restoration of cardiac blood flow supply is widely regarded as a feasible treatment choice for ischemic heart diseases; however, this intervention would contradictorily elicit reperfusion injury. Recently, myocardial ischemia/reperfusion injury (MI/RI) has aroused widespread public concerns. Remifentanil, an ultra-short acting opioid analgesic, is frequently used for surgical anesthesia. Previous studies have demonstrated the cardioprotective effects of remifentanil preconditioning in clinical practice and in vitro experimental models; however, its exact mechanisms remain largely unclear. This study aimed to further evaluate the protective effects of remifentanil preconditioning against MI/RI and elucidate the potential molecular mechanisms. Rat models of MI/RI were successfully established via ligation of left anterior descending coronary artery for 30 minutes and restoration of blood flow for 2 hours. Herein, animal experiments displayed that remifentanil preconditioning could alleviate myocardial damage in rat models of MI/RI. Consistently, cell model experiments implied that remifentanil preconditioning attenuated hypoxia/reoxygenation exposure-induced injury in rat cardiomyocytes. Moreover, our findings verified the involvement of Notch signaling pathway in the protective effects of remifentanil preconditioning. In addition, mechanistic studies revealed that remifentanil preconditioning could up-regulate Jagged-1 expression and that Jagged-1 mediated the cardioprotective effects of remifentanil preconditioning through activating Notch signaling pathway. Taken together, our data indicate that remifentanil preconditioning ameliorates myocardial damage in rat MI/RI models via Jagged-1-mediated Notch signaling pathway activation. Thus, this study may offer some novel clues for understanding the cardioprotective mechanisms of remifentanil preconditioning against MI/RI., (Copyright 2021 The Author(s).)

Tuberculosis (TB) is an important infectious disease of humans and other animals. Conventional diagnostic methods, including the tuberculin skin test, chest X‑rays and bacterial culture, have certain innate disadvantages for the early, rapid and specific diagnosis of tuberculosis. The present study aimed to identify a novel diagnostic biomarker to overcome these disadvantages. The potential target identified in the present study was tissue inhibitor of metalloproteinases 1 (TIMP‑1), which has previously been demonstrated to be critical in the immune response to TB. The concentration of TIMP‑1 in the blood was determined using a commercial ELISA kit, and the relative mRNA expression levels following bacterial infection were detected by reverse transcription‑quantitative polymerase chain reaction. Based on a clinical and microbiological diagnosis, the ELISA for plasma TIMP‑1 had a sensitivity of 91.80% [95% confidence interval (CI): 85.44, 96.00] and a specificity of 91.41% (95% CI: 85.14, 95.63). In a THP‑1 cell model, Bacillus Calmette‑Guérin and Mycobacterium bovis significantly upregulated the mRNA expression levels of TIMP‑1 post infection in a time‑dependent manner (P=0.006 for BCG 24 h PI, P=3.2x10‑7 for M. bovis 24 PI). The results of the present study indicate that plasma TIMP‑1 may be a potential biomarker for the diagnosis of TB.

Background: Understanding the pathophysiological process of calvarial bones development is important for the treatments on relative diseases such as craniosynostosis. While, the role of fibroblast growth factor (FGF) and bone morphogenetic protein (BMP) and how they interacted in osteoblast differentiation remain unclear., Methods: we digested bone fragments around the coronal and sagittal sutures from newborn rats to harvest suture cells. Markers expression at different osteoblast differentiation stage was analyzed by increasing FGF2 concentration and BMP2 blocking in these cells., Results: BMP2 expression could be stimulated by FGF2 in a dose and time dependent manner. FGF2 stimulation may decrease early marker of osteoblast differentiation (collagen type-1, COL-1) and increase the expression of continuously-expressed or late markers (alkaline phosphatase, ALP; osteocalcin, OC and bone sialoprotein, BSP) to accelerate mineralization. Inhibition of BMP2 signaling by Noggin weakens the effect of FGF2 on induction of later-stage osteoblastic differentiation of cranial suture cells., Conclusion: Our data suggest that BMP2 signaling is required for FGF2-dependent induction of later-stage of cranial suture cell osteoblastic differentiation.