RESUMO
OBJECTIVE: Numerous studies have proposed the utilization of stromal vascular fraction (SVF), adipose-derived stem cells (ADSCs), and platelet products as auxiliary grafting techniques to improve the survival rate of fat grafts. This study aimed to evaluate the efficacy and safety of various fat grafting methods since 2010 through a network meta-analysis, aiming to identify the most effective technique for fat grafting. METHODS: Clinic trials on assisted fat grafting were searched from Pubmed, Embase, Web of Science, and the Cochrane Library, spanning the period from January 1, 2010 to March 2024. The risk of bias in the included trials was meticulously assessed using the Cochrane risk of bias tool. The survival rate of fat grafts served as the primary evaluation metric for effectiveness, while complications were employed as the indicator for safety. RESULTS: The study incorporated 31 clinic trials, involving a total of 1656 patients. The findings indicated that the survival rate with assisted fat grafting significantly surpassed that of simple fat grafting (SUCRA, 10.43%). Notably, ADSC-assisted fat grafting exhibited the highest survival rate (SUCRA, 82.17%), followed by Salvia miltiorrhiza (SM)-assisted fat grafting (SUCRA, 69.76%). In terms of safety, the most prevalent complications associated with fat grafting were fat sclerosis and fat necrosis. Adc-assisted fat grafting was correlated with the lowest incidence of complications (SUCRA, 41.00%), followed by simple fat grafting (SUCRA, 40.99%). However, PRP-assisted (SUCRA, 52.86%) and SVF-assisted fat grafting (SUCRA, 65.14%) showed higher complication rates. CONCLUSION: Various methods of assisted fat grafting can significantly enhance the survival rate, but they often fail to effectively mitigate the incidence of complications. Compared to other methods, adipose mesenchymal stem cells-assisted fat grafting consistently yielded a higher survival rate of grafts and fewer complications. Consequently, this approach represents a relatively effective method for assisting in fat grafting at present. LEVEL OF EVIDENCE III: This journal requires that authors assign a level of evidence to each article. For a full description of these Evidence-Based Medicine ratings, please refer to the Table of Contents or the online Instructions to Authors www.springer.com/00266 .
Assuntos
Tecido Adiposo , Sobrevivência de Enxerto , Metanálise em Rede , Feminino , Humanos , Masculino , Tecido Adiposo/transplante , Transplante Autólogo/métodos , Resultado do TratamentoRESUMO
To evaluate the effect of glutamine supplement on patients with burns, we conducted a systematic review and meta-analysis via synthesizing up-to-date studies. Databases including PubMed, Cochrane Central Register, EMBASE, Google scholar, Wanfang data, and ClinicalTrials.gov were searched up to October 2023 to find randomized trials evaluating glutamine supplement on patients with burns. The main outcomes included hospital stay, in-hospital mortality, infection, and wound healing. Twenty-two trials that randomized a total of 2170 patients were included in this meta-analysis. Pooled the length of hospital stay was shortened by glutamine supplement (weighted mean differences [WMD] = -7.95, 95% confidence interval [CI] -10.53 to -5.36, I2 = 67.9%, 16 trials). Both pooled wound healing rates (WMD = 9.15, 95% CI 6.30 to 12.01, I2 = 82.7%, 6 studies) and wound healing times (WMD = -5.84, 95% CI -7.42 to -4.27, I2 = 45.7%, 7 studies) were improved by glutamine supplement. Moreover, glutamine supplement reduced wound infection (risk ratios [RR] = 0.38, 95% CI 0.21 to 0.69, I2 = 0%, 3 trials), but not nonwound infection (RR = 0.88, 95% CI 0.73 to 1.05, I2 = 39.6%, 9 trials). Neither in-hospital mortality (RR = 0.95, 95% CI 0.74 to 1.22, I2 = 36.0%, 8 trials) nor the length of intensive care unit stay (WMD = 1.85, 95% CI -7.24 to 10.93, I2 = 78.2%, 5 studies) was improved by glutamine supplement. Subgroup analysis showed positive effects were either influenced by or based on small-scale, single-center studies. Based on the current available data, we do not recommend the routine use of glutamine supplement for burn patients in hospital. Future large-scale randomized trials are still needed to give a conclusion about the effect of glutamine supplement on burn patients.
Assuntos
Queimaduras , Suplementos Nutricionais , Glutamina , Tempo de Internação , Cicatrização , Humanos , Queimaduras/terapia , Queimaduras/mortalidade , Glutamina/uso terapêutico , Tempo de Internação/estatística & dados numéricos , Cicatrização/efeitos dos fármacos , Mortalidade Hospitalar , Infecção dos Ferimentos/prevenção & controleRESUMO
Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that the western blotting data shown in Fig. 5A and the cell migration and invasion assay data shown in Fig. 5C were strikingly similar to data appearing in different form in other articles by different authors at different research institutes, several of which have been retracted. Owing to the fact that the contentious data in the above article were already under consideration for publication, or had already been published, prior to its submission to Molecular Medicine Reports, the Editor has decided that this paper should be retracted from the Journal. After having been in contact with the authors, they agreed with the decision to retract the paper. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 17: 33723379, 2018; DOI: 10.3892/mmr.2017.8264].
RESUMO
Background: Early detection, timely diagnosis and rapid response are essential for case management and precautions of burn-associated sepsis. However, studies on indicators for early warning and intervention have rarely been conducted. This study was performed to better understand the pathophysiological changes and targets for prevention of severe burn injuries. Methods: We conducted a multi-center, prospective multi-omics study, including genomics, microRNAomics, proteomics and single-cell transcriptomics, in 60 patients with severe burn injuries. A mouse model of severe burn injuries was also constructed to verify the early warning ability and therapeutic effects of potential markers. Results: Through genomic analysis, we identified seven important susceptibility genes (DNAH11, LAMA2, ABCA2, ZFAND4, CEP290, MUC20 and ENTPD1) in patients with severe burn injuries complicated with sepsis. Through plasma miRNAomics studies, we identified four miRNAs (hsa-miR-16-5p, hsa-miR-185-5p, hsa-miR-451a and hsa-miR-423-5p) that may serve as early warning markers of burn-associated sepsis. A proteomic study indicated the changes in abundance of major proteins at different time points after severe burn injury and revealed the candidate early warning markers S100A8 and SERPINA10. In addition, the proteomic analysis indicated that neutrophils play an important role in the pathogenesis of severe burn injuries, as also supported by findings from single-cell transcriptome sequencing of neutrophils. Through further studies on severely burned mice, we determined that S100A8 is also a potential early therapeutic target for severe burn injuries, beyond being an early warning indicator. Conclusions: Our multi-omics study identified seven susceptibility genes, four miRNAs and two proteins as early warning markers for severe burn-associated sepsis. In severe burn-associated sepsis, the protein S100A8 has both warning and therapeutic effects.
RESUMO
INTRODUCTION: This study investigated the effects of soluble epoxide hydrolase (sEH) inhibitors on acute lung injury (ALI) using the measure of meta-analysis. METHODS: Relative publications were systematic reviewed and retrieved by searching electronic databases including the Cochrane Library, PubMed, China National Knowledge Infrastructure, Wanfang Data, and Google Scholar. RESULTS: Seven animal studies were included in this meta-analysis. Our result showed that the lung injury scores (SMD = - 2.31, 95% CI - 3.50 to - 1.12) and lung wet to dry weight ratios (WMD-1.44, 95% CI - 1.69 to - 1.18) were reduced in sEH inhibitors-treated animals compared with control. The mortality was improved by sEH inhibitors at 48 h (RR = 0.62, 95% CI 0.42 to 0.92), 72 h, and 120 h, but not at 24 h (RR = 0.59, 95% CI 0.35 to 1.01) and 96 h, after induction of ALI model. CONCLUSIONS: The sEH inhibitor is a potent candidate of pharmacological agents for ALI/acute respiratory distress syndrome, as its effects on improvement of lung injury and mortality in preclinical researches.
Assuntos
Lesão Pulmonar Aguda , Síndrome do Desconforto Respiratório , Animais , Epóxido Hidrolases , Lesão Pulmonar Aguda/tratamento farmacológico , Síndrome do Desconforto Respiratório/tratamento farmacológico , Pulmão , Inibidores EnzimáticosRESUMO
Hair follicle regeneration has been successful in mice but failed in human being for years. Dermal papilla cells, a specialized mesenchymal stem cell derived from dermal papilla within hair follicles, is considered the key cells for hair follicle regeneration function as both regeneration initiator and regulator. Injectable platelet rich fibrin (i-PRF), a novel biomaterial rich in a variety of growth factors and three-dimensional scaffolds, has shown promising effects on tissue regeneration. In this study, we aimed to evaluate the application of i-PRF in human hair follicle regeneration by examining the biological effects of i-PRF on human dermal papilla cells (hDPCs). Biomaterial compatibility, cell viability, proliferation, migration, alkaline phosphatase activity and trichogenic inductivity were assessed after exposing hDPCs to different concentrations of i-PRF extracts. In addition, we investigated the ultrastructure of i-PRF with all cell components filtered. The results revealed that i-PRF possessing excellent biocompatibility and could significantly promote hDPCs proliferation, migration, and trichogenic inductivity. Furthermore, the concentration of i-PRF is able to remarkably influence hDPCs behavior in a dose-dependent pattern. Different concentrations exhibited differential effects on hDPCs behavior. In general, lower concentration promotes cell proliferation better than higher concentration, while higher concentration promotes cell function better reversely. Best concentration for hDPCs in vitro expending is 1% concentration. 20% concentration is optimal for hair follicle regeneration. In summary, our findings concluded that i-PRF facilitates hair follicle regeneration by promoting human dermal papilla cell proliferation, migration, and trichogenic inductivity.
Assuntos
Movimento Celular/efeitos dos fármacos , Proliferação de Células/efeitos dos fármacos , Derme/efeitos dos fármacos , Folículo Piloso/efeitos dos fármacos , Peptídeos e Proteínas de Sinalização Intercelular/administração & dosagem , Fibrina Rica em Plaquetas/metabolismo , Adulto , Idoso , Idoso de 80 Anos ou mais , Diferenciação Celular/efeitos dos fármacos , Células Cultivadas , Derme/metabolismo , Feminino , Folículo Piloso/metabolismo , Humanos , Peptídeos e Proteínas de Sinalização Intercelular/metabolismo , Masculino , Pessoa de Meia-Idade , Adulto JovemRESUMO
Hyperoxic acute lung injury is a serious complication of oxygen therapy that causes high mortality. Inhibition of soluble epoxide hydrolase (sEH) has been reported to have protective effect on lipopolysaccharide-induced acute lung injury (ALI). This study investigates whether sEH plays any role in the pathogenesis of hyperoxic ALI. Wild-type and sEH gene knockout (sEH-/-) mice were exposed to 100% O2 for 72 h to induce hyperoxic ALI. Hyperoxia caused infiltration of inflammatory cells, elevation of interleukin-1ß and interleukin-6 levels, and deterioration of alveolar capillary protein leak as well as wet/dry weight ratio in the lung. The hyperoxia-induced pulmonary inflammation and edema were markedly improved in sEH-/- mice. Survival rate was significantly improved in sEH-/- mice compared with that in wild-type mice. Moreover, the levels of epoxyeicosatrienoic acids and heme oxygenase-1 activity were notably elevated in sEH-/- mice compared with those in wild-type mice after exposure to 100% O2 for 72 h. The nucleotide-binding domains and leucine-rich repeat pyrin domains containing 3 (NLRP3) inflammasome activation and caspase-1 activity induced by hyperoxia were inhibited in sEH-/- mice compared with those in wild-type mice. Inhibition of sEH by an inhibitor, AUDA, dampened hyperoxia-induced ALI. sEH plays a vital role in hyperoxic ALI and is a potential therapeutic target for ALI.
Assuntos
Lesão Pulmonar Aguda/patologia , Epóxido Hidrolases/metabolismo , Hiperóxia/complicações , Animais , Epóxido Hidrolases/deficiência , Camundongos , Camundongos Knockout , Oxigênio/farmacologia , Pneumonia/etiologia , SolubilidadeRESUMO
BACKGROUND: Angiotensin II plays a vital role in the pathogenesis of acute respiratory distress syndrome (ARDS). However, its mechanism is not well defined. Angiotensin II upregulates the expression of soluble epoxide hydrolase (sEH; Ephx2). sEH is suggested as a potential pharmacologic target for ARDS. The present study investigates whether the sEH is involved in the angiotensin II-triggered pulmonary inflammation and edema using an angiotensin II-induced lung injury animal model. METHODS: Lung injury was induced by angiotensin II intratracheally instillation in wild-type or Ephx2 deficient mice. RESULTS: sEH activities were markedly increased in wild-type mice treated with angiotensin II. Angiotensin II markedly increased the levels of tumor necrosis factor-α and interleukin-1ß in bronchoalveolar lavage fluid, worsened alveolar capillary protein leak and lung histological alterations, and elevated activity of activator protein-1 and nuclear factor-κB. However, these changes were significantly improved in Ephx2 deficient mice. Moreover, Losartan, an angiotensin II receptor 1 antagonist, abolished the sEH induction and improved mortality. CONCLUSIONS: Angiotensin II-induced lung injury was improved in sEH gene deleted mice. The angiotensin II-triggered pulmonary inflammation is mediated, at least in part, through the sEH.
Assuntos
Lesão Pulmonar Aguda/induzido quimicamente , Lesão Pulmonar Aguda/enzimologia , Angiotensina II/toxicidade , Epóxido Hidrolases/metabolismo , Pneumonia/enzimologia , Animais , Líquido da Lavagem Broncoalveolar/citologia , Epóxido Hidrolases/genética , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Knockout , Neutrófilos/citologia , Pneumonia/induzido quimicamenteRESUMO
Melanoma is derived from melanocytes and accounts for ~80% of skin cancer-associated fatalities worldwide. The dysregulation of microRNAs (miRNAs/miRs) is involved in the development and progression of melanoma. Therefore, miRNAs may be novel diagnostic or prognostic biomarkers and promising therapeutic targets in the treatment of patients with melanoma. miR675 is differentially expressed in several types of human cancer and has important roles in the pathogenesis of several diseases. However, the expression levels and the biological roles of miR675 in melanoma remain unclear. Therefore, the present study aimed to assess the expression of miR675 in melanoma, explore the effects of miR675 on melanoma cells and investigate the underlying molecular mechanisms that may be involved in the actions of miR675. The present study indicated that miR675 expression was downregulated in melanoma tissues and cell lines. Functional assays demonstrated that the upregulation of miR675 impaired cell proliferation and invasion in melanoma. Bioinformatics analysis, luciferase reporter assay, reverse transcriptionquantitative polymerase chain reaction and western blot analysis demonstrated that metadherin (MTDH) was a direct target of miR675 in melanoma. The MTDH levels were upregulated in melanoma tissues and inversely correlated with the miR675 expression. Furthermore, restored MTDH expression rescued the inhibition effects in melanoma cells caused by miR675 overexpression. Thus, miR675 may be a potential therapeutic target for melanoma.
Assuntos
Moléculas de Adesão Celular/genética , Regulação Neoplásica da Expressão Gênica , Melanoma/genética , MicroRNAs/genética , Neoplasias Cutâneas/genética , Linhagem Celular Tumoral , Movimento Celular , Proliferação de Células , Regulação para Baixo , Humanos , Melanoma/patologia , Proteínas de Membrana , Proteínas de Ligação a RNA , Neoplasias Cutâneas/patologia , Regulação para CimaRESUMO
OBJECTIVES: Inflammation plays a key role in the pathogenesis of acute lung injury (ALI). Soluble epoxide hydrolase (sEH) is suggested as a vital pharmacologic target for inflammation. In this study, we determined whether a sEH inhibitor, AUDA, exerts lung protection in lipopolysaccharide (LPS)-induced ALI in mice. METHODS: Male BALB/c mice were randomized to receive AUDA or vehicle intraperitoneal injection 4 h after LPS or phosphate buffered saline (PBS) intratracheal instillation. Samples were harvested 24 h post LPS or PBS administration. RESULTS: AUDA administration decreased the pulmonary levels of monocyte chemoattractant protein (MCP)-1 and tumor necrosis factor (TNF)-α. Improvement of oxygenation and lung edema were observed in AUDA treated group. AUDA significantly inhibited sEH activity, and elevated epoxyeicosatrienoic acids (EETs) levels in lung tissues. Moreover, LPS induced the activation of nuclear factor (NF)-κB was markedly dampened in AUDA treated group. CONCLUSION: Administration of AUDA after the onset of LPS-induced ALI increased pulmonary levels of EETs, and ameliorated lung injury. sEH is a potential pharmacologic target for ALI.
Assuntos
Lesão Pulmonar Aguda , Inibidores Enzimáticos/farmacologia , Epóxido Hidrolases/antagonistas & inibidores , Lipopolissacarídeos/toxicidade , Lesão Pulmonar Aguda/induzido quimicamente , Lesão Pulmonar Aguda/tratamento farmacológico , Lesão Pulmonar Aguda/enzimologia , Animais , Quimiocina CCL2/metabolismo , Epóxido Hidrolases/metabolismo , Masculino , Camundongos , Camundongos Endogâmicos BALB C , Fator de Necrose Tumoral alfa/metabolismoRESUMO
BACKGROUND: A previous systematic review and meta-analysis reported that omega-3 fatty acids nutrition may reduce mortality in septic patients. As new randomized controlled trials began to accumulate, we conducted an update. METHODS: A PubMed database was searched through Feb 2016, and randomized controlled trials comparing omega-3 fatty acids with control were selected by two reviewers independently. RESULTS: Eleven trials randomly assigning 808 patients were included in the present study. Using a fixed effects model, we found no significant effect of omega-3 fatty acids on overall mortality (risk ratio 0.84; 95 % confidence interval (CI): 0.67 to 1.05, P = 0.12), or infectious complications (risk ratio 0.95; 95 % CI: 0.72 to 1.25, P = 0.70). However, the duration of mechanical ventilation was markedly reduced by omega-3 fatty acids (weighted mean differences (WMD) = -3.82; 95 % CI: -4.61 to -3.04; P < 0.00001). A significant heterogeneity was found when the duration of hospital (I (2) = 93 %; WMD = -2.82; 95 % CI: -9.88 to 4.23, P = 0.43), or intensive care stay (I (2) = 87 %; WMD = -2.70; 95 % CI: -6.40 to 1.00, P = 0.15) were investigated. CONCLUSIONS: Omega-3 fatty acids confer no mortality benefit but are associated with a reduction in mechanical ventilation duration in septic patients. However, low sample size and heterogeneity of the cohorts included in this analysis limits the generalizability of our findings.
Assuntos
Ácidos Graxos Ômega-3/uso terapêutico , Ensaios Clínicos Controlados Aleatórios como Assunto , Sepse/dietoterapia , Sepse/mortalidade , Humanos , Tempo de Internação/estatística & dados numéricos , Respiração Artificial/estatística & dados numéricosRESUMO
Although hyperbaric oxygen (HBO) therapy has been reported to help heal chronic foot ulcers in patients with diabetes mellitus (DM), production of HBO-related oxidative stress is a concern. To assess the therapeutic effect and oxidative stress of HBO, a 2-week, prospective, randomized, controlled clinical study was conducted from January 1, 2010 to January1, 2012 among 36 consecutively admitted patients with diabetic foot ulcers (DFU). Average patient age was 60.08 ± 5.97 years and average DM duration was 16.4 ± 11.3 years; 86.1% had type 2 DM, and 47.2% had Wagner grade-III foot ulcers. Patients randomized to the control group (n = 18) received standard care including offloading, wound debridement, and glucose control. HBO treatment group patients (n = 18) received standard care and twice-daily HBO sessions for 90 minutes at 2.5 atmospheres absolute (ATA) 5 days a week for 2 weeks. Transcutaneous oxygen pressure (TcPo2) at the edge of the ulcer and wound size were measured at baseline and after 7 and 14 days of treatment. Ulcer tissues were harvested on days 7 and 14 to determine oxidative stress by measuring malondialdehyde (MDA) and antioxidant enzyme (superoxide dismutase [SOD], catalase [CAT], and glutathione peroxidase [GPx]) levels. Compared to baseline, TcPo2 in the HBO group increased on day 7 (477.8 ± 118.2 mm Hg versus 37.06 ± 5.23 mm Hg, P <0.01) and day 14 (501.1 ± 137.7 mm Hg versus 35.61 ± 4.85 mm Hg, P <0.01). Ulcer size reduction in the HBO group was greater than that of the control group (42.4% ± 20.0% versus 18.1% ± 6.5%, P <0.05). MDA levels, SOD, and CAT were all significantly higher in the HBO than in the control group on day 14 (P<0.05). The results of this study suggest HBO treatment for 2 weeks initiates a healing response in chronic DFUs, but the observed oxidative stress in local ulcer tissue may offset this effect long-term. Until needed additional research has been conducted, prolonged and/or inappropriate HBO treatment should be avoided.
Assuntos
Pé Diabético/terapia , Oxigenoterapia Hiperbárica , Cicatrização , Catalase/metabolismo , Pé Diabético/enzimologia , Pé Diabético/metabolismo , Glutationa Peroxidase/metabolismo , Humanos , Malondialdeído/metabolismo , Estresse Oxidativo , Estudos Prospectivos , Superóxido Dismutase/metabolismoRESUMO
OBJECTIVE: To investigate the feasibility of clinical application of the thoracodorsal artery musculocutaneous perforator flap (TAMPF). METHODS: (1) The morphosis and blood supply of TAP flap on 15 formalized adult cadavers(30 sides) were examined by microsurgery anatomy. (2) An imitative operation of the TAMP flap and latissimus dorsi flap on 1 formalized adult cadavers (2 sides) was conducted. RESULTS: (1) A total of 102 musculocutaneous perforators larger than 0.5 mm were found in 16 specimens(32 sides). 56 perforators (55%) were originated from the medial branch and 46 (45%) originated from the lateral branch. The biggest perforator is (0.82 +/- 0.11) mm (0.68 - 1.08 mm). There was an average of 1.9 perforators (range, 1 - 3 perforators) of the medial branch and an average of 1.8 perforators (range, 1 - 3 perforators) of the lateral branch. Additionally, there were 24 perforators samller than 0.5 mm, and 76 perforators originated from intercostal artery and lumbar artery. (2) Musculocutaneous perforators over 0.5 mm were found only in proximity of the medial and lateral branches within a distance of 8.5 cm (6.4 cm - 9.2 cm) distal to the neurovascular hilus. CONCLUSIONS: With the characteristics of constant position, large caliber, long pedicle, the thoracodorsal artery musculocutaneous perforator was suitable to be musclocutaneous perforator flaps and "fan-shaped" flaps.