Impact Force Localization and Reconstruction via ADMM-based Sparse Regularization Method

In practice,simultaneous impact localization and time history reconstruction can hardly be achieved,due to the illposed and under-determined problems induced by the constrained and harsh measuring conditions.Although l_(1) regularization can be used to obtain sparse solutions,it tends to underestimate solution amplitudes as a biased estimator.To address this issue,a novel impact force identification method with l_(p) regularization is proposed in this paper,using the alternating direction method of multipliers(ADMM).By decomposing the complex primal problem into sub-problems solvable in parallel via proximal operators,ADMM can address the challenge effectively.To mitigate the sensitivity to regularization parameters,an adaptive regularization parameter is derived based on the K-sparsity strategy.Then,an ADMM-based sparse regularization method is developed,which is capable of handling l_(p) regularization with arbitrary p values using adaptively-updated parameters.The effectiveness and performance of the proposed method are validated on an aircraft skin-like composite structure.Additionally,an investigation into the optimal p value for achieving high-accuracy solutions via l_(p) regularization is conducted.It turns out that l_(0.6)regularization consistently yields sparser and more accurate solutions for impact force identification compared to the classic l_(1) regularization method.The impact force identification method proposed in this paper can simultaneously reconstruct impact time history with high accuracy and accurately localize the impact using an under-determined sensor configuration.

Epigenetic regulation of macrophage polarization in wound healing

The immune microenvironment plays a critical role in regulating skin wound healing.Macrophages,the main component of infiltrating inflammatory cells,play a pivotal role in shaping the immune microenvironment in the process of skin wound healing.Macrophages comprise the classic proinflammatory M1 subtype and anti-inflammatory M2 population.In the early inflammatory phase of skin wound closure,M1-like macrophages initiate and amplify the local inflammatory response to disinfect the injured tissue.In the late tissue-repairing phase,M2 macrophages are predominant in wound tissue and limit local inflammation to promote tissue repair.The biological function of macrophages is tightly linked with epigenomic organization.Transcription factors are essential for macrophage polarization.Epigenetic modification of transcription factors determines the heterogeneity of macrophages.In contrast,transcription factors also regulate the expression of epigenetic enzymes.Both transcription factors and epigenetic enzymes form a complex network that regulates the plasticity of macrophages.Here,we describe the latest knowledge concerning the potential epigenetic mechanisms that precisely regulate the biological function of macrophages and their effects on skin wound healing.

Mitochondrial dysfunction and mitophagy:crucial players in burn trauma and wound healing

Burn injuries are a significant cause of death worldwide,leading to systemic inflammation,multiple organ failure and sepsis.The progression of burn injury is explicitly correlated with mitochondrial homeostasis,which is disrupted by the hyperinflammation induced by burn injury,leading to mitochondrial dysfunction and cell death.Mitophagy plays a crucial role in maintaining cellular homeostasis by selectively removing damaged mitochondria.A growing body of evidence from various disease models suggest that pharmacological interventions targeting mitophagy could be a promising therapeutic strategy.Recent studies have shown that mitophagy plays a crucial role in wound healing and burn injury.Furthermore,chemicals targeting mitophagy have also been shown to improve wound recovery,highlighting the potential for novel therapeutic strategies based on an in-depth exploration of the molecular mechanisms regulating mitophagy and its association with skin wound healing.

Platelet-rich plasma accelerates skin wound healing by promoting re-epithelialization

Background:Autologous platelet-rich plasma(PRP)has been suggested to be effective for wound healing.However,evidence for its use in patients with acute and chronic wounds remains insufficient.The aims of this study were to comprehensively examine the effectiveness,synergy and possible mechanism of PRP-mediated improvement of acute skin wound repair.Methods:Full-thickness wounds were made on the back of C57/BL6 mice.PRP or saline solution as a control was administered to the wound area.Wound healing rate,local inflammation,angiogenesis,re-epithelialization and collagen deposition were measured at days 3,5,7 and 14 after skin injury.The biological character of epidermal stem cells(ESCs),which reflect the potential for re-epithelialization,was further evaluated in vitro and in vivo.Results:PRP strongly improved skin wound healing,which was associated with regulation of local inflammation,enhancement of angiogenesis and re-epithelialization.PRP treatment significantly reduced the production of inflammatory cytokines interleukin-17A and interleukin-1β.An increase in the local vessel intensity and enhancement of re-epithelialization were also observed in animals with PRP administration and were associated with enhanced secretion of growth factors such as vascular endothelial growth factor and insulin-like growth factor-1.Moreover,PRP treatment ameliorated the survival and activated the migration and proliferation of primary cultured ESCs,and these effects were accompanied by the differentiation of ESCs into adult cells following the changes of CD49f and keratin 10 and keratin 14.Conclusion:PRP improved skin wound healing by modulating inflammation and increasing angiogenesis and re-epithelialization.However,the underlying regulatory mechanism needs to be investigated in the future.Our data provide a preliminary theoretical foundation for the clinical administration of PRP in wound healing and skin regeneration.

The molecular mechanisms supporting the homeostasis and activation of dendritic epidermal T cell and its role in promoting wound healing

The epidermis is the outermost layer of skin and the first barrier against invasion.Dendritic epidermal T cells(DETCs)are a subset ofT cells and an important component of the epidermal immune microenvironment.DETCs are involved in skin wound healing,malignancy and autoim-mune diseases.DETCs secrete insulin-like growth factor-1 and keratinocyte growth factor for skin homeostasis and re-epithelization and release inflammatory factors to adjust the inflammatory microenvironment of wound healing.Therefore,an understanding of their development,activation and correlative signalling pathways is indispensable for the regulation of DETCs to accelerate wound healing.Our review focuses on the above-mentioned molecular mechanisms to provide a general research framework to regulate and control the function of DETCs.

Emerging role of tumor cell plasticity in modifying therapeutic response

Resistance to cancer therapy is a major barrier to cancer management.Conventional views have proposed that acquisition of resistance may result from genetic mutations.However,accumulating evidence implicates a key role of non-mutational resistance mechanisms underlying drug tolerance,the latter of which is the focus that will be discussed here.Such non-mutational processes are largely driven by tumor cell plasticity,which renders tumor cells insusceptible to the drug-targeted pathway,thereby facilitating the tumor cell survival and growth.The concept of tumor cell plasticity highlights the significance of re-activation of developmental programs that are closely correlated with epithelial–mesenchymal transition,acquisition properties of cancer stem cells,and transdifferentiation potential during drug exposure.From observations in various cancers,this concept provides an opportunity for investigating the nature of anticancer drug resistance.Over the years,our understanding of the emerging role of phenotype switching in modifying therapeutic response has considerably increased.This expanded knowledge of tumor cell plasticity contributes to developing novel therapeutic strategies or combination therapy regimens using available anticancer drugs,which are likely to improve patient outcomes in clinical practice.

Photodynamic therapy accelerates skin wound healing through promoting re-epithelialization

Background:Epidermal stem cells(EpSCs)that reside in cutaneous hair follicles and the basal layer of the epidermis are indispensable for wound healing and skin homeostasis.Little is known about the effects of photochemical activation on EpSC differentiation,proliferation and migration during wound healing.The present study aimed to determine the effects of photodynamic therapy(PDT)on wound healing in vivo and in vitro.Methods:We created mouse full-thickness skin resection models and applied 5-aminolevulinic acid(ALA)for PDT to the wound beds.Wound healing was analysed by gross evaluation and haematoxylin–eosin staining in vivo.In cultured EpSCs,protein expression was measured using flow cytometry and immunohistochemistry.Cell migration was examined using a scratch model;apoptosis and differentiation were measured using flow cytometry.Results:PDT accelerated wound closure by enhancing EpSC differentiation,proliferation and migration,thereby promoting re-epithelialization and angiogenesis.PDT inhibited inflammatory infiltration and expression of proinflammatory cytokines,whereas the secretion of growth factors was greater than in other groups.The proportion of transient amplifying cells was significantly greater in vivo and in vitro in the PDT groups.EpSC migration was markedly enhanced after ALAinduced PDT.Conclusions:Topical ALA-induced PDT stimulates wound healing by enhancing re-epithelialization,promoting angiogenesis as well as modulating skin homeostasis.This work provides a preliminary theoretical foundation for the clinical administration of topical ALA-induced PDT in skin wound healing.

Epidemiological and clinical characteristics of burns in the older person:a seven-year retrospective analysis of 693 cases at a burn center in south-west China

Background:Burns are one of the major traumas that may affect older individuals.The purpose of this study was to investigate the epidemiological and clinical characteristics of geriatric burns at a major center in south-west China.Methods:This retrospective study was conducted at the Institute of Burn Research,Southwest Hospital of Army Medical University between 2010 and 2016,and the data collected from medical records included admission date,age,gender,premorbid disease,burn etiology,injured anatomical location,burn area and depth,inhalation injury,number of surgeries,length of stay(LOS),clinical outcome,and medical cost.Results:Of the 693 older burn patients included,60.75%were male and 56.85%were aged 60–69 years.Burns peaked in December–March and June.Flamewas the most common cause of burns,making up 51.95%of all cases,and also dominated in the burn patients aged 60–69 years.Limbs were the most common anatomical sites of burns(69.41%),and the median total body surface area(TBSA)was 5%(interquartile range[IQR]:2%–15%).The percentage of the patients who underwent surgeries and number of surgeries significantly increased in the cases of contact burns,younger age and full-thickness burns.Six deaths resulted in a mortality of 0.9%.The median LOSwas 16 days(IQR:8–29 days),and the main risk factors were more surgeries,better outcomes,and full-thickness burns.The median costwas 20,228 CNY(IQR:10,457–46,581.5 CNY),and major risk factors included longer LOS,larger TBSA,and more surgeries.Furthermore,compared to the earlier data from our center,the proportion of older adults among all burns(7.50%vs.4.15%),proportion of flame burns(51.95%vs.33.90%),and mean age(69.05 years vs.65.10 years)were significantly higher,while the proportion of premorbidities(16.9%vs.83.9%),mortality(0.9%vs.7.5%)and median TBSA(5%vs.21%)were significantly lower.Conclusions:This study suggested that closer attention should be paid to prevent burn injuries in older people aged 60–69 years,especially males,regarding incidents in the summer and winter,and flame burns.Moreover,tailored intervention strategies based on related risk factors should be under special consideration.

Mixed lymphocyte reaction induced by multiple alloantigens and the role for IL-10 in proliferation inhibition

The frequency of T cells that can respond to alloantigens is unusually high.It remains unclear how T cells would respond when stimulated by multiple major histocompatibility complex(MHC)disparate alloantigens in the same cultures.In this report,we examined potential interactions of T cell clones that were stimulated simultaneously by two sets of complete MHC disparate alloantigens using mixed lymphocyte reaction(MLR).In this assay,we observed that proliferation of B6 lymphocytes(H-2b)stimulated by both BALB/c(H-2d)and C_(3)H(H-2k)allogeneic cells was not increased but rather reduced as compared to B6 cells stimulated with either BALB/c or C_(3)H allogeneic cells.Interestingly,interleukin(IL)-10 expressions at both protein level and mRNA level was signifi cantly increased in cultures stimulated with the two MHC alloantigens,while IL-2,tumor necrosis factor(TNF)-α,transforming growth factor(TGF)-β1 production did not show any differences.In addition,Foxp_(3) mRNA expression was comparable amongst all groups.In conclusion,we observed an inhibitory effect in T cell proliferation in response to multiple MHC mismatched alloantigens in MLR,and this effect might be associated with the upregulation of IL-10 expression.

Mitsugumin 53 protects the kidney from severe burn injury in mice

Mitsugumin 53 (MG53), a newly identified muscle-specific protein, is an essential component of the cell membrane repair machinery in skeletal and cardiac muscle. However, the role of MG53 after burns in other tissues remains unclear. This study aims to investigate the possible roles of MG53 in the protection of the kidney after severe burn injury, and an animal scalding model of 30% of total body surface area (TBSA) was used. Recombinant human MG53 (rhMG53) or bovine serum albumin (BSA) was injected intravenously via the tail vein. Data showed that the mortality in the MG53-treated group was lower than that in control group. Administration of rhMG53 may alleviate histological alterations in renal tubular epithelial cells after burn injury. Renal tubular injury scores and the average optical density score of kidney injury molecule-1 (KIM-1) immunohistochemical staining in the MG53-treated group were significantly lower than those in control group (P < 0.001). Exogenous rhMG53 was found to be located in renal tubular epithelial cells. Numerous polymerase I and transcript release factor (PTRF) were expressed in the mouse kidney after severe scalding. In conclusion, our data indicate that MG53 protein protects the kidney by involving local PTRF after severe burn injury.

P311 promotes typeⅡtransforming growth factor-βreceptor mediated fibroblast activation and granulation tissue formation in wound healing

Background:P311,a highly conserved 8 kDa intracellular protein,has recently been reported to play an important role in aggravating hypertrophic scaring by promoting the differentiation and secretion of fibroblasts.Nevertheless,how P311 regulates the differentiation and function of fibroblasts to affect granulation tissue formation remains unclear.In this work,we studied the underlying mechanisms via which P311 affects fibroblasts and promotes acute skin wound repair.Methods:To explore the role of P311,both in vitro and in vivo wound-healing models were used.Full-thickness skin excisional wounds were made in wild-type and P311−/−C57 adult mice.Wound healing rate,re-epithelialization,granulation tissue formation and collagen deposition were measured at days 3,6 and 9 after skin injury.The biological phenotypes of fibroblasts,the expression of target proteins and relevant signaling pathways were examined both in vitro and in vivo.Results:P311 could promote the proliferation and differentiation of fibroblasts,enhance the ability of myofibroblasts to secrete extracellular matrix and promote cell contraction,and then facilitate the formation of granulation tissue and eventually accelerate skin wound closure.Importantly,we discovered that P311 acts via up-regulating the expression of type II transforming growth factor-βreceptor(TGF-βRII)in fibroblasts and promoting the activation of the TGF-βRII-Smad signaling pathway.Mechanistically,the mammalian target of rapamycin signaling pathway is closely implicated in the regulation of the TGF-βRII-Smad pathway in fibroblasts mediated by P311.Conclusions:P311 plays a critical role in activation of the TGF-βRII-Smad pathway to promote fibroblast proliferation and differentiation as well as granulation tissue formation in the process of skin wound repair.

Obstruction of the formation of granulation tissue leads to delayed wound healing after scald burn injury in mice

Background:Delayed wound healing remains a common but challenging problem in patients with acute or chronic wound following accidental scald burn injury.However,the systematic and detailed evaluation of the scald burn injury,including second-degree deep scald(SDDS)and thirddegree scald(TDS),is still unclear.The present study aims to analyze the wound-healing speed,the formation of granulation tissue,and the healing quality after cutaneous damage.Methods:In order to assess SDDS and TDS,the models of SDDS and TDS were established using a scald instrument in C57BL/6 mice.Furthermore,an excisional wound was administered on the dorsal surface in mice(Cut group).The wound-healing rate was first analyzed at days 0,3,5,7,15 and 27,with the Cut group as a control.Then,on the full-thickness wounds,hematoxylin and eosin(H&E)staining,Masson staining,Sirius red staining,Victoria blue staining and immunohistochemistry were performed to examine re-epithelialization,the formation of granulation tissue,vascularization,inflammatory infiltration and the healing quality at different time points in the Cut,SDDS and TDS groups.Results:The presented data revealed that the wound-healing rate was higher in the Cut group,when compared with the SDDS and TDS groups.H&E staining showed that re-epithelialization,formation of granulation tissue and inflammatory infiltration were greater in the Cut group,when compared with the SDDS and TDS groups.Immunohistochemistry revealed that the number of CD31,vascular endothelial growth factor A,transforming growth factor-βandα-smooth muscle actin reached preferential peak in the Cut group,when compared with other groups.In addition,Masson staining,Sirius red staining,Victoria blue staining,Gordon-Sweets staining and stress analysis indicated that the ratio of collagen I to III,reticular fibers,failure stress,Young’s modulus and failure length in the SDDS group were similar to those in the normal group,suggesting that healing quality was better in the SDDS group,when compared with the Cut and TDS groups.Conclusion:Overall,the investigators first administered a comprehensive analysis in the Cut,SDDS and TDS groups through in vivo experiments,which further proved that the obstacle of the formation of granulation tissue leads to delayed wound healing after scald burn injury in mice.

Synthesis of graphene oxide-quaternary ammonium nanocomposite with synergistic antibacterial activity to promote infected wound healing

Background: Bacterial infection is one of the most common complications in burn, trauma, and chronic refractory wounds and is an impediment to healing. The frequent occurrence of antimicrobial-resistant bacteria due to irrational application of antibiotics increases treatment cost and mortality. Graphene oxide (GO) has been generally reported to possess high antimicrobial activity against a wide range of bacteria in vitro. In this study, a graphene oxide-quaternary ammonium salt (GO-QAS) nanocomposite was synthesized and thoroughly investigated for synergistic antibacterial activity, underlying antibacterial mechanisms and biocompatibility in vitro and in vivo. Methods: The GO-QAS nanocomposite was synthesized through amidation reactions of carboxylic group end-capped QAS polymers with primary amine-decorated GO to achieve high QAS loading ratios on nanosheets. Next, we investigated the antibacterial activity and biocompatibility of GO-QAS in vitro and in vivo. Results: GO-QAS exhibited synergistic antibacterial activity against bacteria through not only mechanical membrane perturbation, including wrapping, bacterial membrane insertion, and bacterial membrane perforation, but also oxidative stress induction. In addition, it was found that GO-QAS could eradicate multidrug-resistant bacteria more effectively than conventional antibiotics. The in vitro and in vivo toxicity tests indicated that GO-QAS did not exhibit obvious toxicity towards mammalian cel s or organs at low concentrations. Notably, GO-QAS topically applied on infected wounds maintained highly efficient antibacterial activity and promoted infected wound healing in vivo. Conclusions: The GO-QAS nanocomposite exhibits excellent synergistic antibacterial activity and good biocompatibility both in vitro and in vivo. The antibacterial mechanisms involve both mechanical membrane perturbation and oxidative stress induction. In addition, GO-QAS accelerated the healing process of infected wounds by promoting re-epithelialization and granulation tissue formation. Overall, the results indicated that the GO-QAS nanocomposite could be applied as a promising antimicrobial agent for infected wound management and antibacterial wound dressing synthesis.

The progress of Chinese burn medicine from the Third Military Medical University—in memory of its pioneer,Professor Li Ao

Professor Li Ao was one of the founders of Chinese burn medicine and one of the most renowned doctors and researchers of burns in China. He established one of the Chinese earliest special departments for burns at Third Military Medical University (TMMU) in 1958. To memorialize Professor Li Ao on his 100th birthday in 2017 and introduce our extensive experience, it is our honor to briefly review the development and achievement of the Chinese burn medicine from TMMU. The epidemiology and outcomes of admitted burn patients since 1958 were reviewed. Furthermore, main achievements of basic and clinical research for the past roughly 60 years were presented. These achievements mainly included the Chinese Rule of Nine, fluid resuscitation protocol, experience in inhalation injury, wound treatment strategies, prevention and treatment of burn infections, nutrition therapy, organ support therapies, and rehabilitation. The progress shaped and enriched modern Chinese burn medicine and promoted the development of world burn medicine.

A Review of Skin Banking Guidelines and Standards Worldwide:Towards the Harmonization of Guidelines for Skin Banking in Therapeutic Applications for the Regions under the Asia Pacific Burn Association(APBA)

Currently,there are no harmonized guidelines which govern skin banking in the Asia Pacific region.Therefore,skin banks are either unregulated or rely on their nation’s legislation or international accreditation to uphold their quality standards.A new set of skin banking guidelines was devel-oped through a comprehensive review and collation of best international practices for the Asia Pacific Burn Association(APBA)members,from donor screening and testing,to skin recovery,processing,storage and distribution,and quality assurance.National regulatory requirements reviewed include the European directives,Australia’s Therapeutic Goods Administration and Sin-gapore’s tissue banking standards.Further technical and quality management recommendations are referenced from the American Association of Tissue Banks(AATB),the United States Food and Drug Administration standards and guidance documents,various relevant European guides,Japanese Society of Tissue Transplantation guidelines and the Asia Pacific Association of Surgical Tissue Banking.Adapted mainly from the AATB standards,the new Asia Pacific Burn Association Guidelines for Skin Banking in Therapeutic Applications offer a comprehensive manual,address-ing:governance and contracts;staff responsibilities;quality management;facilities,equipment and supplies management;donor consent and testing;and recommendations of good practices pertaining to skin recovery,processing,storage and distribution.Besides complementing current generic regulations,they provide technical specifications of major aspects unaddressed in most legislations.This inaugural set of new regional skin banking guidelines would be a start for regional members of the APBA to adopt,and will hopefully culminate in a set of standards so that,in the long run,skin allografts from this region can be of similar quality,which can simplify import process and facilitate the exchange of allografts between members.

巨噬细胞在创面愈合中的调节作用及其相关机制

创面愈合是一个被精准调控的复杂过程,包含了炎症、抗炎、再生等多个阶段。由于巨噬细胞具有明显的可塑性,可以在具有差异化的创面愈合过程中发挥重要的调节作用。巨噬细胞若未能适时表达特定功能,将会影响组织的愈合功能并导致组织病理性愈合。因此,了解巨噬细胞在创面愈合的不同阶段发挥的不同功能并进行针对性调控,对促进创伤组织的愈合再生有重要意义。该文根据创面愈合的基本过程,阐述了创面内不同类型巨噬细胞发挥的不同功能及其基本机制,并强调了未来可能应用于临床治疗的巨噬细胞调控策略。

纳秒激光诱导表面微纳结构对锆基金属玻璃生物兼容性的影响

针对医用植入体材料锆基金属玻璃在应用中存在的生物兼容性问题,采用纳秒激光在金属玻璃试样表面诱导产生点阵和沟槽两种微纳结构,然后采用细胞活性测试、细胞分布和形态观察评价两种微纳结构对锆基金属玻璃生物兼容性的改善效果,并从表面形貌方面讨论激光表面改性对生物兼容性的改善机理。结果表明:相对于原始试样,激光诱导产生的沟槽结构能够显著增强成骨细胞在试样表面的黏附性和细胞活性,这主要归功于显著增加的表面粗糙度;点阵结构对细胞活性的改善效果不理想。除此之外,在沟槽试样表面,激光诱导产生的沟槽以及在沟槽内附着的微纳结构是成骨细胞在沟槽内部或附近沿着沟槽方向分布的主要原因。

Neutralization of interleukin-17A alleviates burn-induced intestinal barrier disruption via reducing pro-inflammatory cytokines in a mouse model

Background:The intestinal barrier integrity can be disrupted due to burn injury,which is responsible for local and systemic inflammatory responses.Anti-inflammation strategy is one of the proposed therapeutic approaches to control inflammatory cascade at an early stage.Interleukin-17A(IL-17A)plays a critical role in inflammatory diseases.However,the role of IL-17A in the progression of burn-induced intestinal inflammation is poorly understood.In this study,we aimed to investigate the effect of IL-17A and associated pro-inflammatory cytokines that were deeply involved in the pathogenesis of burn-induced intestinal inflammatory injury,and furthermore,we sought to determine the early source of IL-17A in the intestine.Methods:Mouse burn model was successfully established with infliction of 30%total body surface area scald burn.The histopathological manifestation,intestinal permeability,zonula occludens-1 expression,pro-inflammatory cytokines were determined with or without IL-17A-neutralization.Flow cytometry was used to detect the major source of IL-17A^(+)cells in the intestine.Results:Burn caused intestinal barrier damage,increase of intestinal permeability,alteration of zonula occludens-1 expressions,elevation of IL-17A,IL-6,IL-1βand tumor necrosis factor-α(TNF-α),whereas IL-17A neutralization dramatically alleviated burn-induced intestinal barrier disruption,maintained zonula occludens-1 expression,and noticeably,inhibited pro-inflammatory cytokines elevation.In addition,we observed that the proportion of intestinal IL-17A^(+)Vγ4^(+)T subtype cells(but not IL-17A^(+)Vγ1^(+)T subtype cells)were increased in burn group,and neutralization of IL-17A suppressed this increase.Conclusions:The main original findings of this study are intestinal mucosa barrier is disrupted after burn through affecting the expression of pro-inflammatory cytokines,and a protective role of IL-17A neutralization for intestinal mucosa barrier is determined.Furthermore,Vγ4^(+)T cells are identified as the major early producers of IL-17A that orchestrate an inflammatory response in the burn model.These data suggest that IL-17A blockage may provide a unique target for therapeutic intervention to treat intestinal insult after burn.

Investigations on femtosecond laser-induced surface modification and periodic micropatterning with anti-friction properties on Ti6Al4V titanium alloy

Titanium alloys have a wide application in aerospace industries as it has greater strength and low density, but it has poor tribological properties. To improve its friction and wear performance, in present work, a femtosecond laser is used to directly irradiate the Ti6Al4V titanium alloy surface in air conditioning, which results in localized ablation and the formation of periodic microstructures but also a strong pressure wave, propagating the material inside. Through the optimization of processing parameters, surface modification and periodic micropatterning with effective anti-friction properties were successfully induced on the surface. After a treatment of femtosecond laser-induced surface modification(FsLSM), the surface microhardness was improved by 16.6% and compressive residual stress reached-746 MPa. Besides, laser-induced periodic surface structures(LIPSS) with a titanium oxide outer coating were fabricated uniformly on the titanium alloy surface. Rotary ball-on-disk wear experiments revealed that the average coefficient of friction(COF) and wear mass loss of the specimen with Fs LSM treatment were largely reduced by 68.9% and 90% as compared to that of untreated specimens, respectively. It was analyzed that the reason for the remarkable wear resistance was attributed to the comprehensive action of the generation of LIPSS, the titanium oxide outer coating, high amplitude compressive residual stress and gradient grain size distribution on the subsurface during the laser surface treatment. Since the findings here are broadly applicable to a wide spectrum of engineering metals and alloys, the present results offer unique pathways to enhancing the tribological performance of materials.

iTRAQ-based proteomic profiling reveals different protein expression between normal skin and hypertrophic scar tissue

Background:A hypertrophic scar is a unique fibrotic disease that only exists in humans.Despite advances in burn care and rehabilitation,as well as progress in the management during these decades,the hypertrophic scar remains hard to cure following surgical methods and drugs for treatment.In this study,we are looking forward to finding the multitude of possible traumatic mechanisms and the underlying molecular signal ways in the formation of the hypertrophic scar.Methods:We used isobaric tags for relative and absolute quantitation(iTRAQ)labeling technology,followed by high-throughput 2D LC-MS/MS,to determine relative quantitative differential proteins between the hypertrophic scar and normal skin tissue.Results:A total of 3166 proteins were identified with a high confidence(≥95%confidence).And,a total of 89 proteins were identified as the differential proteins between the hypertrophic scar and normal skin,among which 41 proteins were up-regulated and 48 proteins were down-regulated in the hypertrophic scar.GO-Analysis indicated the up-regulated proteins were involved in extracellular matrix,whereas the down-regulated proteins were involved in dynamic junction and structural molecule activity.Conclusions:In our study,we demonstrate 89 proteins present differently in the hypertrophic scar compared to normal skin by iTRAQ technology,which might indicate the pathologic process of hypertrophic scar formation and guide us to propose new strategies against the hypertrophic scar.