Actin Research Articles

Organometallic-Polypeptide Block Copolymers: Synthesis and Crystallization-Driven Self-Assembly in Aqueous Solutions to Rod-like and Plate-like Micelles with Polypeptide Coronas.

The synthesis of polyferrocenyldimethylsilane-b-poly(L-glutamic acid) block copolymers was systematically explored. Rod-like and plate-like micelles were prepared from self-assembly of the block copolymers in aqueous solution with two different approaches. In a dissolution-dialysis approach, micelles were prepared by dissolving a block copolymer sample in excess aqueous base followed by the dialysis of the solution against water. The morphology of the resultant micelles showed composition dependence. The block copolymer sample with the lowest soluble block content formed rod-like micelles, while the other samples with higher soluble block content formed spherical micelles. In a THF-mediated approach, THF was added into a block copolymer solution, which was first prepared by the dissolution-dialysis approach, and then the THF was evaporated slowly. Plate-like micelles were obtained from all the block copolymer samples examined, and these had a broad range of soluble block content. The formation of these plate-like micelles was attributed to the crystallization of the PFDMS blocks in the presence of THF. A tendency of large platelet micelles evolving to thin filaments over time was observed. This change may have been driven by the increase in the corona-chain stretching energy as THF evaporated.

The role of fluid friction in streamer formation and biofilm growth

Biofilms constitute one of the most common forms of living matter, playing an increasingly important role in technology, health, and ecology. While it is well established that biofilm growth and morphology are highly dependent on the external flow environment, the precise role of fluid friction has remained elusive. We grew Bacillus subtilis biofilms on flat surfaces of a channel in a laminar flow at wall shear stresses spanning one order of magnitude (τw = 0.068 Pa to τw = 0.67 Pa). By monitoring the three-dimensional distribution of biofilm over seven days, we found that the biofilms consist of smaller microcolonies, shaped like leaning pillars, many of which feature a streamer in the form of a thin filament that originates near the tip of the pillar. While the shape, size, and distribution of these microcolonies depend on the imposed shear stress, the same structural features appear consistently for all shear stress values. The formation of streamers occurs after the development of a base structure, suggesting that the latter induces a secondary flow that triggers streamer formation. Moreover, we observed that the biofilm volume grows approximately linearly over seven days for all shear stress values, with a growth rate inversely proportional to the wall shear stress. We develop a scaling model, providing insight into the mechanisms by which friction limits biofilm growth.

Freely suspended nematic and smectic films and free-standing smectic filaments in the ferroelectric nematic realm.

We show that stable, freely suspended liquid crystal films can be made from the ferroelectric nematic (NF) phase and from the recently discovered polar, lamellar SmZA and SmAF phases. The NF films display two-dimensional, smectic-like parabolic focal conic textures comprising director/polarization bend that are a manifestation of the electrostatic suppression of director splay in the film plane. In the SmZA and SmAF phases, the smectic layers orient preferentially normal to the film surfaces, a condition never found in typical thermotropic or lyotropic lamellar LC phases, with the SmZA films exhibiting focal-conic fan textures mimicking the appearance of typical smectics in glass cells when the layers are oriented normal to the plates, and the SmAF films showing a texture of plaquettes of uniform in-plane orientation where both bend and splay are suppressed, separated by grain boundaries. The SmAF phase can also be drawn into thin filaments, in which X-ray scattering reveals that the smectic layer planes are normal to the filament axis. Remarkably, the filaments are mechanically stable even if they break, forming free-standing, fluid filaments supported only at one end. The unique architectures of these films and filaments are stabilized by the electrostatic self-interaction of the liquid crystal polarization field, which enables the formation of confined, fluid structures that are fundamentally different from those of their counterparts made using previously known liquid crystal phases.

The calcium-binding protein S100A1 binds to titin's N2A insertion sequence in a pH-dependent manner.

Titin is the third contractile filament in the sarcomere, and it plays a critical role in sarcomere integrity and both passive and active tension. Unlike the thick and thin filaments, which are polymers of myosin and actin, respectively, titin is a single protein that spans from Z-disk to M-line. The N2A region within titin has been identified as a signaling hub for the muscle and is shown to be involved in multiple interactions. The insertion sequence (UN2A) within the N2A region was predicted as a potential binding site for the Ca2+-binding protein, S100A1. We demonstrate using a combination of size exclusion chromatography, surface plasmon resonance, and fluorescence resonance energy transfer that S100A1 can bind to the UN2A region. We further demonstrate that this interaction occurs under conditions where calcium is bound to S100A1, suggesting that the conformational shift in S100A1 when calcium binds is important. We also observed a conformational change in UN2A induced by shifts in pH, suggesting that conformational flexibility in UN2A plays a critical role in the interaction with S100A1. These results lead us to propose that the interaction of S100A1 and UN2A might act as a sensor to regulate titin's function in response to physiological changes in the muscle.

Tłumaczenie tekstów aktów prawnych w kontekście ich wielopoziomowości

TRANSLATION OF LEGAL ACTS IN THE CONTEXT OF THEIR MULTI-LEVEL NATUREThe main aim of the article is to discuss the problem of translating legal texts from the perspective of their multi-level nature. The need to distinguish the descriptive, normative, and presuppositional layers of legal acts, emphasized in legal doctrine, seems to strongly impact the translation strategy adopted by the translator. Starting from this assumption, the author finally formulates the thesis that the shape of the strategy mentioned earlier also affects the practice of interpretation and application of legal acts, which leads to formulating a postulate regarding the marking of the translation layer of a legal act.

Electrical stimulation of injured nerves promotes recovery in animals and humans.

The frequent poor functional outcomes after delayed surgical repair of injured human peripheral nerves results in progressive downregulation of growth-associated genes in parallel with reduced neuronal regenerative capacity under each of the experimental conditions of chronic axotomy of neurones that remain without target contact, chronic distal nerve stump denervation, and chronic muscle denervation. Brief (1h) low-frequency (20Hz) electrical stimulation (ES) accelerates the outgrowth of regenerating axons across the surgical site of microsurgical repair of a transected nerve. Exercise programmes also promote nerve regeneration with the combination of ES and exercise being the most effective. An ES conditioning lesion of intact nerve (CES) accelerates both axonal outgrowth and regeneration rate after the surgical repair of a more distal injury to the nerve, in contrast to ES of a repaired injury nerve that accelerates only the axon outgrowth. A CES accelerates both axonal outgrowth and regeneration rate after the surgical repair of a more distal injury to the nerve, in contrast to ES of a repaired injury nerve that accelerates only the axon outgrowth. The loss of contractility of permanently denervated muscles in cauda equinae-injured patients with accompanying severe loss of muscle mass, disarray of thick and thin contractile filaments, and disorganization of the sarcoplasmic reticulum that controls calcium delivery to the filaments, is alleviated by a 2-year programme of daily ES of the quadriceps muscle. These findings hold promise for recovery and rehabilitation in patients who suffer injury to the neuromuscular system. KEY POINTS: Poor functional outcomes after delayed surgical repair of injured human peripheral nerves are replicated by chronic neuronal axotomy, Schwann cell denervation in a nerve autograft, and muscle denervation. Exponential decline in expression of growth-associated genes accompanies the same decline in regenerative capacity. Brief (1h) low-frequency (20Hz) electrical stimulation (ES) that generates action potential conduction to the neuronal soma accelerates the outgrowth of regenerating axons across the surgical repair site of the transected nerve, even after delayed surgery. The same ES regimen accelerates muscle reinnervation in patients with chronic nerve injury who undergo carpal tunnel syndrome release surgery. A 2-year programme of daily ES of permanently denervated quadriceps muscles in cauda equinae-injured patients reinstated their contractility and organization.

The sole essential low molecular weight tropomyosin isoform of Caenorhabditis elegans is essential for pharyngeal muscle function.

Tropomyosin is an actin-binding protein that plays roles ranging from regulating muscle contraction to controlling cytokinesis and cell migration. The simple nematode Caenorhabditis elegans provides a useful model for studying the core functions of tropomyosin in an animal, having a relatively simple anatomy, and a single tropomyosin gene, lev-11 , that produces seven isoforms. Three higher molecular weight isoforms (LEV-11A, D, O) regulate contraction of body wall and other muscles, but comparatively less is known of the functions of four lower molecular weight isoforms (LEV-11C, E, T, U). We demonstrate here C. elegans can survive with a single low molecular weight isoform, LEV-11E. Mutants disrupted for LEV-11E die as young larvae, whereas mutants disrupted for all other short isoforms are viable with no overt phenotype. Vertebrate low molecular weight tropomyosins are often considered "nonmuscle" isoforms, but we find LEV-11E localizes to sarcomeric thin filaments in pharyngeal muscle, and co-precipitates from worm extracts with the formin FHOD-1, which is also associated with thin filaments in pharyngeal muscle. Pharyngeal sarcomere organization is grossly normal in larvae lacking LEV-11E, indicating the tropomyosin is not required to stabilize thin filaments, but pharyngeal pumping is absent, suggesting LEV-11E regulates actomyosin activity similar to higher molecular weight sarcomeric tropomyosin isoforms.

Distinct mechanisms drive divergent phenotypes in hypertrophic and dilated cardiomyopathy associated TPM1 variants.

Hypertrophic and dilated cardiomyopathies (HCM and DCM, respectively) are inherited disorders that may be caused by mutations to the same sarcomeric protein but have completely different clinical phenotypes. The precise mechanisms by which point mutations within the same gene bring about phenotypic diversity remain unclear. Our objective has been to develop a mechanistic explanation of diverging phenotypes in two TPM1 mutations, E62Q (HCM) and E54K (DCM). Drawing on data from the literature and experiments with stem cell-derived cardiomyocytes expressing the TPM1 mutations of interest, we constructed computational simulations that provide plausible explanations of the distinct muscle contractility caused by each variant. In E62Q, increased calcium sensitivity and hypercontractility was explained most accurately by a reduction in effective molecular stiffness of tropomyosin and alterations in its interactions with the actin thin filament that favor the 'closed' regulatory state. By contrast, the E54K mutation appeared to act via long-range allosteric interactions to increase the association rate of the C-terminal troponin I mobile domain to tropomyosin/actin. These mutation-linked molecular events produced diverging alterations in gene expression that can be observed in human engineered heart tissues. Modulators of myosin activity confirmed our proposed mechanisms by rescuing normal contractile behavior in accordance with predictions.

RETRACTION: Theaflavins retard human breast cancer cell migration by inhibiting NF-κB via p53-ROS cross-talk.

A. Adhikary, S. Mohanty, L. Lahiry, D. S. Hossain, S. Chakraborty and T. Das, "Theaflavins Retard Human Breast Cancer Cell Migration by Inhibiting NF-κB via p53-ROS Cross-talk," FEBS Letters 584, no. 1 (2010): 7-14, https://doi.org/10.1016/j.febslet.2009.10.081. The above article, published online on 31 October 2009 in Wiley Online Library (wileyonlinelibrary.com), has been published by agreement between the journal Editor-in-Chief, Michael Brunner; FEBS Press; and John Wiley and Sons Ltd. The retraction has been agreed due to partial duplication of micrographs observed in Figure 2C and the unexpected similarity of curves presented in 3C. Additionally, the blot against histone H1 in figure 4D (bottom-left panel) is a stretched duplication of the blot against alpha-actin in figure 3F (right-hand panel). Further, duplications have been observed between the MCF-7 p53 bands presented in Figures 1D and the p53 bands in Figure 3F; the alpha actin bands shown in Figure 3F and the Histone H1 bands in Figure 4D; and the alpha actin bands presented in Figures 3E and 4D. The authors provided some supporting data and an explanation, but the editors found them unsatisfactory. Due to the extent and nature of these concerns, the editors consider the results and conclusions of this article to be invalid. The authors disagree with the retraction.

Osteocyte Dendrites: How Do They Grow, Mature, and Degenerate in Mineralized Bone?

Osteocytes, the most abundant bone cells, form an extensive cellular network via interconnecting dendrites. Like neurons in the brain, the long-lived osteocytes perceive mechanical and biological inputs and signal to other effector cells, leading to the homeostasis and turnover of bone tissues. Despite the appreciation of osteocytes' vital roles in bone biology, the initiation, growth, maintenance, and eventual degradation of osteocyte dendrites are poorly understood due to their full encasement by mineralized matrix. With the advancement of imaging modalities and genetic models, the architectural organization and molecular composition of the osteocyte dendrites, as well as their morphological changes with aging and diseases, have begun to be revealed. However, several long-standing mysteries remain unsolved, including (1) how the dendrites are initiated and elongated when a surface osteoblast becomes embedded as an osteocyte; (2) how the dendrites maintain a relatively stable morphology during their decades-long life span; (3) what biological processes control the dendrite morphology, connectivity, and stability; and (4) if these processes are influenced by age, sex, hormones, and mechanical loading. Our review of long, thin actin filament (F-actin)-containing processes extending from other cells leads to a working model that serves as a starting point to investigate the formation and maintenance of osteocyte dendrites and their degradation with aging and diseases.

Genome-wide association and transcriptomic analysis and the identification of growth-related genes in Macrobrachium nipponense

Macrobrachium nipponense is a commercially important freshwater species of prawn that is widely distributed across Asian countries. In order to investigate the molecular mechanisms of growth in M. nipponense, and to provide a foundation for molecular breeding, we used genome-wide association analysis (GWAS) and transcriptomic analysis to screen polymorphisms and genes related to growth traits. We recorded the growth traits of 100 adult M. nipponense at the same growth stage, and each individual genotype was evaluated by whole genome resequencing. GWAS of growth traits detected 12 growth-related single-nucleotide polymorphisms (SNPs) and eight growth-related genes from 49 chromosomes. Of the 100 individuals, we sampled muscle tissue from a total of 18 female and male M. nipponense exhibiting large differences in growth rate for RNA-seq. Transcriptome analysis revealed a total of 27,996 unigenes; of these, 33 and 60 differentially expressed genes were identified from males and females, respectively. Of these, 12 genes associated with energy metabolism and cytoskeletal pathways were identified as growth-related genes. Notably, genes from the actin family and the ubiquitin C-terminal hydrolase 2 (UCH2) gene were identified by both GWAS and transcriptomic analysis. Two growth-related SNPs, S40_12327385 and S40_12327391, were found to be mapped to the ACTB gene. The ACTA1 gene, also from the actin family, was up-regulated in fast-growing males and females, while the ACT57B was down-regulated. In addition, the growth associated SNP S7_35313774 was located in the UCH2 gene; transcriptomics analysis revealed that the UCH2 gene was up-regulated in female individuals exhibiting high growth rates. Overall, our results provided a set of markers and candidate genes related to the growth of M. nipponense. These findings could facilitate the breeding management of this species and help us to further understand the genetic mechanisms of growth in crustaceans.

Novel Mutation Lys30Glu in the TPM1 Gene Leads to Pediatric Left Ventricular Non-Compaction and Dilated Cardiomyopathy via Impairment of Structural and Functional Properties of Cardiac Tropomyosin.

Pediatric dilated cardiomyopathy (DCM) is a rare heart muscle disorder leading to the enlargement of all chambers and systolic dysfunction. We identified a novel de novo variant, c.88A>G (p.Lys30Glu, K30E), in the TPM1 gene encoding the major cardiac muscle tropomyosin (Tpm) isoform, Tpm1.1. The variant was found in a proband with DCM and left ventricular non-compaction who progressed to terminal heart failure at the age of 3 years and 8 months. To study the properties of the mutant protein, we produced recombinant K30E Tpm and used various biochemical and biophysical methods to compare its properties with those of WT Tpm. The K30E substitution decreased the thermal stability of Tpm and its complex with actin and significantly reduced the sliding velocity of the regulated thin filaments over a surface covered by ovine cardiac myosin in an in vitro motility assay across the entire physiological range of Ca2+ concentration. Our molecular dynamics simulations suggest that the charge reversal of the 30th residue of Tpm alters the actin monomer to which it is bound. We hypothesize that this rearrangement of the actin-Tpm interaction may hinder the transition of a myosin head attached to a nearby actin from a weakly to a strongly bound, force-generating state, thereby reducing myocardial contractility. The impaired myosin interaction with regulated actin filaments and the decreased thermal stability of the actin-Tpm complex at a near physiological temperature likely contribute to the pathogenicity of the variant and its causative role in progressive DCM.

An integrated picture of the structural pathways controlling the heart performance

The regulation of heart function is attributed to a dual filament mechanism: i) the Ca2+-dependent structural changes in the regulatory proteins of the thin, actin-containing filament making actin available for myosin motor attachment, and ii) the release of motors from their folded (OFF) state on the surface of the thick filament allowing them to attach and pull the actin filament. Thick filament mechanosensing is thought to control the number of motors switching ON in relation to the systolic performance, but its molecular basis is still controversial. Here, we use high spatial resolution X-ray diffraction data from electrically paced rat trabeculae and papillary muscles to provide a molecular explanation of the modulation of heart performance that calls for a revision of the mechanosensing hypothesis. We find that upon stimulation, titin-mediated structural changes in the thick filament switch motors ON throughout the filament within ~½ the maximum systolic force. These structural changes also drive Myosin Binding Protein-C (MyBP-C) to promote first motor attachments to actin from the central 1/3 of the half-thick filament. Progression of attachments toward the periphery of half-thick filament with increase in systolic force is carried on by near-neighbor cooperative thin filament activation by attached motors. The identification of the roles of MyBP-C, titin, thin and thick filaments in heart regulation enables their targeting for potential therapeutic interventions.

Mavacamten facilitates myosin head ON-to-OFF transitions and shortens thin filament length in relaxed skeletal muscle.

The first-in-its-class cardiac drug mavacamten reduces the proportion of so-called ON-state myosin heads in relaxed sarcomeres, altering contraction performance. However, mavacamten is not completely specific to cardiac myosin and can also affect skeletal muscle myosin, an important consideration since mavacamten is administered orally and so will also be present in skeletal tissue. Here, we studied the effect of mavacamten on skeletal muscle structure using small-angle X-ray diffraction. Mavacamten treatment reduced the proportion of ON myosin heads but did not eliminate the molecular underpinnings of length-dependent activation, demonstrating similar effects to those observed in cardiac muscle. These findings provide valuable insights for the potential use of mavacamten as a tool to study muscle contraction across striated muscle.

A new Trunk Rot species in the genus Kretzschmaria (Xylariaceae) from Guangxi, China

Kretzschmaria shiwandashanensis sp. nov. is described and illustrated from the tropical forests of Shiwandashan National Nature Reserve in Guangxi, China. The new taxon is characterized by stromata with narrow connective tissues, crenate sloped margins, distinctive cracks on the surface, and relatively small ascospores. According to phylogenetic analysis of combined internal transcribed spacers (ITS), alpha actin (ACT), beta-tubulin (TUB2) and RNA polymerase II second largest subunit sequences (rpb2), the new species is closely related to K. sandvicensis, from which it is distinguished by its smaller perithecia and ascospores that are shorter and broader. Descriptions, illustrations, and phylogeny of the new species are provided.

Biotic and abiotic stress affects the stability of housekeeping genes in Catla Labeo catla.

The choice of a stable reference gene plays a crucial role in gene expression analysis. In most cases, the choice of housekeeping gene (HKG) is quite random. However, the expression of HKGs varies under different experimental conditions and in different tissues. The study focused on three reference genes in Catla Labeo catla-beta actin (β-actin), glyceraldehyde-3-phosphate dehydrogenase (GAPDH), and elongation factor-1 alpha (EF-1α)-under four experimental conditions: bacterial challenge, hypoxia, a combination of bacterial challenge and hypoxia, and control. The fish were subjected to the above-mentioned experimental circumstances, and five tissues (blood, gill, liver, kidney, and spleen) were collected at regular intervals. The investigation of gene expression in the five tissues was performed using real-time (RT) quantitative polymerase chain reaction (qPCR), and the resultant cycle threshold values were subjected to several statistical techniques via the RefFinder tool to determine the most stable HKG. The results were ordered in accordance with the stability of the reference genes. In this study, GAPDH was found to be the least stable gene, while β-actin and EF-1α remained stable in the kidney and liver under various circumstances. Other tissues demonstrated tissue- and treatment-specific stability for the various HKGs. The findings indicate that GAPDH should be avoided in Catla for gene expression studies and that different algorithms should be employed to validate the stability of HKGs in RT-qPCR analysis.

O-GlcNAcylation-related genes mediate tumor microenvironment characteristics and prediction of immunotherapy response in gastric cancer.

We aim to identify molecular clusters related to O-GlcNAcylation and establish a novel scoring system for predicting prognosis and immunotherapy efficacy in patients with gastric cancer (GC). The transcriptomic and clinical data are obtained from XENA-UCSC and GEO databases. The O-GlcNAcylation-related genes are obtained from the GSEA database. Consensus clustering analysis is employed to identify O-GlcNAcylation-related molecular clusters, and principal component analysis (PCA) is utilized to develop a novel prognostic scoring system for predicting GC outcomes and immunotherapy efficacy. The prognostic accuracy of the scoring system is assessed across five real-world cohorts. The biological function of actin alpha 2, smooth muscle (ACTA2) in GC is determined through experimental verification. Using 34 O-GlcNAcylation-related genes associated with prognosis in GC patients, these individuals are divided into two distinct subgroups characterized by different outcomes, tumor microenvironment profiles, and clinical case characteristics. The DEGs between the two subgroups are subsequently used to further divide the GC patients into two subgroups by consensus cluster analysis. PCA is used to construct a prognostic scoring system, which reveal that patients in the low-score subgroup have a better prognosis and greater benefit from immunotherapy. The accuracy of the scoring system is confirmed through validation in a cohort of patients receiving immunotherapy in the real world. ACTA2 promotes proliferation and inhibits apoptosis in GC cells. These findings suggest that we successfully establish molecular clusters associated with O-GlcNAcylation and develop a scoring system that demonstrates strong performance in predicting the prognosis of patients with GC and the effect of immunotherapy interventions.

Three Novel Pathogenic Variants in Unrelated Vietnamese Patients with Cardiomyopathy.

Background: Cardiomyopathy, including dilated cardiomyopathy (DCM) and hypertrophic cardiomyopathy (HCM), is a major cause of heart failure (HF) and a leading indication for heart transplantation. Of these patients, 20-50% have a genetic cause, so understanding the genetic basis of cardiomyopathy will provide knowledge about the pathogenesis of the disease for diagnosis, treatment, prevention, and genetic counseling for families. Methods: This study collected nine patients from different Vietnamese families for genetic analysis at The Cardiovascular Center, E Hospital, Hanoi, Vietnam. The patients were diagnosed with cardiomyopathy based on clinical symptoms. Whole-exome sequencing (WES) was performed in the Vietnamese patients to identify variants associated with cardiomyopathy, and the Sanger sequencing method was used to validate the variants in the patients' families. The influence of the variants was predicted using in silico analysis tools. Results: Nine heterozygous variants were detected as a cause of disease in the patients, three of which were novel variants, including c.284C>G, p.Pro95Arg in the MYL2 gene, c.2356A>G, p.Thr786Ala in the MYH7 gene, and c.1223T>A, p.Leu408Gln in the DES gene. Two other variants were pathogenic variants (c.602T>C, p.Ile201Thr in the MYH7 gene and c.1391G>C, p.Gly464Ala in the PTPN11 gene), and four were variants of uncertain significance in the ACTA2, ANK2, MYOZ2, and PRKAG2 genes. The results of the in silico prediction software showed that the identified variants were pathogenic and responsible for the patients' DCM. Conclusions: Our results contribute to the understanding of cardiomyopathy pathogenesis and provide a basis for diagnosis, treatment, prevention, and genetic counseling.

A Dual Challenge: Coxiella burnetii Endocarditis in a Patient with Familial Thoracic Aortic Aneurysm-Case Report and Literature Review.

Background/Objectives: Thoracic aortic aneurysms (TAAs) are potentially life-threatening medical conditions, and their etiology involves both genetic and multiple risk factors. Coxiella burnetii endocarditis is one of the most frequent causes of blood culture-negative infective endocarditis (BCNIE) in patients with previous cardiac surgery. Our review aims to emphasize the importance of genetic testing in patients with thoracic aortic aneurysms but also the importance of additional testing in patients with suspected endocarditis whose blood cultures remain negative. The reported case has a history of acute DeBakey type I aortic dissection that developed during her second pregnancy, for which the Bentall procedure was performed at that time. Ten years after the surgery, the patient started developing prolonged febrile syndrome with repeatedly negative blood cultures, the serological tests revealing the presence of an infection with Coxiella burnetii. Considering her family history and the onset of her aortic pathology at a young age, genetic tests were performed, disclosing a missense variant in the actin alpha-2 (ACTA2) gene in heterozygous status. Methods: For a better understanding of both conditions, our research was conducted in two directions: one reviewing the literature on patients with Coxiella burnetii BCNIE and the other focusing on patients who had a familial thoracic aortic aneurysm (FTAA) due to the ACTA2 variant. This review incorporates studies found on PubMed and ResearchGate up to August 2024. Conclusions: BCNIE represents a condition with several diagnostic challenges and may lead to severe complications if timely treatment is not initiated. Also, diagnosing an FTAA requires genetic testing, enabling better follow-up and management.

A novel green mechanical recycling strategy for carbon fiber-reinforced polymer laminates based on the glass transition principle

A novel glass transition-assisted mechanical delamination process was developed for the environmentally friendly and high-value recovery of carbon fiber reinforced polymer (CFRP) laminates. When heated to 250–350 °C for 5–15 min in an air atmosphere, the resin matrix quickly transitioned from a rigid glassy state to a flexible rubbery state, making the CFRP laminates soft and bendable. Simultaneously, the shear strength of the resin in the rubbery state decreased significantly to 0.35%–4.58 % of its original value. The softened CFRP laminates could be easily bent by a bending machine. Excessive bending deformation caused the resin between adjacent carbon fiber (CF) sheets to tear and debond, resulting in delamination of the laminates into individual CF sheets. Upon cooling to the glassy state, the shear strength of the resin was restored to 87.59%–98.55 % of its original value. This mild glass transition treatment did not significantly affect the mechanical properties of the CF. The resulting monolayer CF sheets could be easily cut into thin slices or filaments of uniform size and hot-pressed into new CFRP plates. The flexural and tensile strengths of the refabricated CFRP plates were approximately 58.98%–82.71 % and 54.55%–87.79 % of those of the original laminates, respectively.