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BACKGROUND: Axillary cicatricial contracture is a debilitating condition that can greatly impair shoulder joint function. Therefore, timely correction of this condition is imperative. In light of Ogawa's prior classification of axillary cicatricial contracture deformities, we have proposed a novel classification system and reconstruction principles based on a decade of treatment experience. Our proposed system offers a more comprehensive approach to correcting axillary cicatricial contracture deformities and aims to improve patient outcomes. METHODS: Our study included 196 patients with a total of 223 axillary cicatricial contracture deformities. The range of shoulder abduction varied between 10 and 120 degrees. Our treatment approach included various methods such as the lateral thoracic flap, transverse scapular artery flap, cervical superficial artery flap, medial upper arm flap, latissimus dorsi flap, Z-shape modification, and the use of local flaps combined with skin grafting. After 2 weeks, the sutures were removed, and patients were instructed to start functional exercises. To categorize the deformities, we divided them into 2 types: axillary-adjacent region cicatricial contracture (type I) and extended area contracture (type II). RESULTS: For each subtype, a specific treatment method was chosen based on a designed algorithm decision tree. Out of the total cases, 133 patients underwent treatment with various types of local flaps, including Z-plasty, whereas 63 patients received treatment involving skin grafting and different types of local flaps. At the time of discharge, the abduction angle of the shoulder joint ranged from 80 to 120 degrees. Among the 131 patients who were followed up, 108 of them adhered to a regimen of horizontal bar exercises. After a 1-year follow-up period, the abduction angle of the shoulder joint had significantly improved to a range of 110-180 degrees. CONCLUSIONS: We have proposed a novel classification method for the correction of axillary cicatricial contracture deformity. This approach involves utilizing distinct correction strategies, in conjunction with postoperative functional exercise, to ensure the effectiveness of axillary reconstruction.
Assuntos
Axila , Cicatriz , Contratura , Retalhos Cirúrgicos , Humanos , Contratura/cirurgia , Contratura/classificação , Contratura/etiologia , Cicatriz/classificação , Cicatriz/cirurgia , Feminino , Adulto , Masculino , Pessoa de Meia-Idade , Adolescente , Adulto Jovem , Procedimentos de Cirurgia Plástica/métodos , Amplitude de Movimento Articular/fisiologia , Articulação do Ombro/cirurgia , Articulação do Ombro/fisiopatologia , Criança , Resultado do Tratamento , IdosoRESUMO
INTRODUCTION: Non-healing wounds resulting from trauma, surgery, and chronic diseases annually affect millions of individuals globally, with limited therapeutic strategies available due to the incomplete understanding of the molecular processes governing tissue repair and regeneration. Salvianolic acid B (Sal B) has shown promising bioactivities in promoting angiogenesis and inhibiting inflammation. However, its regulatory mechanisms in tissue regeneration remain unclear. PURPOSE: This study aims to investigate the effects of Sal B on wound healing and regeneration processes, along with its underlying molecular mechanisms, by employing zebrafish as a model organism. METHODS: In this study, we employed a multifaceted approach to evaluate the impact of Sal B on zebrafish tail fin regeneration. We utilized whole-fish immunofluorescence, TUNEL staining, mitochondrial membrane potential (MMP), and Acridine Orange (AO) probes to analyze the tissue repair and regenerative under Sal B treatment. Additionally, we utilized transgenic zebrafish strains to investigate the migration of inflammatory cells during different phases of fin regeneration. To validate the importance of Caveolin-1 (Cav1) in tissue regeneration, we delved into its functional role using molecular docking and Morpholino-based gene knockdown techniques. Additionally, we quantified Cav1 expression levels through the application of in situ hybridization. RESULTS: Our findings demonstrated that Sal B expedites zebrafish tail fin regeneration through a multifaceted mechanism involving the promotion of cell proliferation, suppression of apoptosis, and enhancement of MMP. Furthermore, Sal B was found to exert regulatory control over the dynamic aggregation and subsequent regression of immune cells during tissue regenerative processes. Importantly, we observed that the knockdown of Cav1 significantly compromised tissue regeneration, leading to an excessive infiltration of immune cells and increased levels of apoptosis. Moreover, the knockdown of Cav1 also affects blastema formation, a critical process influenced by Cav1 in tissue regeneration. CONCLUSION: The results of this study showed that Sal B facilitated tissue repair and regeneration through regulating of immune cell migration and Cav1-mediated fibroblast activation, promoting blastema formation and development. This study highlighted the potential pharmacological effects of Sal B in promoting tissue regeneration. These findings contributed to the advancement of regenerative medicine research and the development of novel therapeutic approaches for trauma.
Assuntos
Benzofuranos , Caveolina 1 , Cicatrização , Peixe-Zebra , Animais , Nadadeiras de Animais/efeitos dos fármacos , Nadadeiras de Animais/fisiologia , Animais Geneticamente Modificados , Apoptose/efeitos dos fármacos , Benzofuranos/farmacologia , Caveolina 1/metabolismo , Movimento Celular/efeitos dos fármacos , Depsídeos , Potencial da Membrana Mitocondrial/efeitos dos fármacos , Simulação de Acoplamento Molecular , Regeneração/efeitos dos fármacos , Cicatrização/efeitos dos fármacos , Proteínas de Peixe-Zebra/metabolismoRESUMO
Physical unclonable function (PUF) is attractive in modern encryption technologies. Addressing the disadvantage of slow data storage/authentication in optical PUF is paramount for practical applications but remains an on-going challenge. Here, a highly efficient PUF strategy based on random structural color domains (SCDs) of cellulose nanocrystal (CNC) is proposed for the first time, combing with hyperspectral imaging system (HIS) for ultrafast storage and authentication. By controlling the growth and fusion behavior of the tactoids of CNC, the SCDs display an irregular and random distribution of colors, shapes, sizes, and reflectance spectra, which grant unique and inherent fingerprint-like characteristics that are non-duplicated. Based on images and spectra, these fingerprint features are used to develop two sets of PUF key generation methods, which can be respectively authenticated at the user-end and the manufacturer-front-end that achieving a high coding capacity of at least 22304. Notably, the use of HIS greatly shortens the time of key reading and generation (≈5 s for recording, 0.5-0.7 s for authentication). This new optical PUF labels can not only solve slow data storage and complicated authentication in optical PUF, but also impulse the development of CNC in industrial applications by reducing color uniformity requirement.
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Congenital heart disease (CHD) affects up to 1% of live births. Although a genetic etiology is indicated by an increased recurrence risk, sporadic occurrence suggests that CHD genetics is complex. Here, we show that hypoplastic left heart syndrome (HLHS), a severe CHD, is multigenic and genetically heterogeneous. Using mouse forward genetics, we report what is, to our knowledge, the first isolation of HLHS mutant mice and identification of genes causing HLHS. Mutations from seven HLHS mouse lines showed multigenic enrichment in ten human chromosome regions linked to HLHS. Mutations in Sap130 and Pcdha9, genes not previously associated with CHD, were validated by CRISPR-Cas9 genome editing in mice as being digenic causes of HLHS. We also identified one subject with HLHS with SAP130 and PCDHA13 mutations. Mouse and zebrafish modeling showed that Sap130 mediates left ventricular hypoplasia, whereas Pcdha9 increases penetrance of aortic valve abnormalities, both signature HLHS defects. These findings show that HLHS can arise genetically in a combinatorial fashion, thus providing a new paradigm for the complex genetics of CHD.