Topological Defects in Twisted Bundles of Two-Dimensionally Ordered Filaments

Twisted assemblies of filaments in ropes, cables and bundles are essential structural elements in wide use in macroscopic materials as well as within the cells and tissues of living organisms. We develop the unique, non-linear elastic properties of twisted filament bundles that derive from generic properties of two-dimensional line-ordered materials. Continuum elasticity reveals a formal equivalence between the elastic stresses induced by bundle twist and those induced by the positive curvature in thin, elastic sheets. These geometrically-induced stresses can be screened by 5-fold disclination defects in lattice packing, and we predict a discrete spectrum elastic energy groundstates associated with integer numbers of disclinations in cylindrical bundles. Finally, we show that elastic-energy groundstates are extremely sensitive to defect position in the cross-section, with off-center disclinations driving the entire bundle to buckle, adopting globally writhing configurations.Comment: 4.1 pages; 3 figure

A model for the break-up of a tuft of fibers

A simple model for the forces acting on a single fiber as it is withdrawn from a tangled fiber assembly is proposed. Particular emphasis is placed on understanding the dynamics of the reptating fiber with respect to the entanglement of fibers within the tuft. The resulting two-parameter model captures the qualitative features of experimental simulation. The model is extended to describe the break-up of a tuft. The results show good agreement with experiment and indicate where a fiber is most likely to fracture based on the density of fiber end-points

Enhancement of Friction between Carbon Nanotubes: An Efficient Strategy to Strengthen Fibers

Interfacial friction plays a crucial role in the mechanical properties of carbon nanotube based fibers, composites, and devices. Here we use molecular dynamics simulation to investigate the pressure effect on the friction within carbon nanotube bundles. It reveals that the intertube frictional force can be increased by a factor of 1.5 ~ 4, depending on tube chirality and radius, when all tubes collapse above a critical pressure and when the bundle remains collapsed with unloading down to atmospheric pressure. Furthermore, the overall cross-sectional area also decreases significantly for the collapsed structure, making the bundle stronger. Our study suggests a new and efficient way to reinforce nanotube fibers, possibly stronger than carbon fibers, for usage at ambient conditions.Comment: revtex, 5 pages, accepted by ACS Nano 10 Dec 200

Changes on content, structure and surface distribution of lignin in jute fibers after laccase treatment

Effect of laccase treatment on the content, structure, and surface distribution of lignin in jute fibers were fundamentally investigated. Four percent lignin was removed from jute fibers via the laccase treatment. The residual lignin in the laccase-treated jute fibers showed increased molecular weights, which indicated polymerization between lignins on jute fibers. Meanwhile, the phenolic hydroxyl content in lignin decreased during the laccase oxidation accompanied by demethylation of methoxyl groups and generation of carbonyl groups. Due to the degradation and subsequent polymerization of lignin by laccase, the bulgy lignins on jute fiber surfaces were redistributed, which made the surface neat and glossy.This work was financially supported by the National Natural Science Foundations of China (51603087, 51673087), Program for Changjiang Scholars and Innovative Research Team in University (IRT_15R26), Fundamental Research Funds for the Central Universities (JUSRP51717A), Key R&D Program of Jiangsu Province (BE2016208), Portuguese Foundation for Science and Technology (UID/BIO/04469/2013 unit), and COMPETE 2020 (POCI-01-0145-FEDER006684).info:eu-repo/semantics/publishedVersio

Mutations in STK11 gene in Czech Peutz-Jeghers patients

<p>Abstract</p> <p>Background</p> <p>Peutz-Jeghers syndrome (PJS) is an autosomal dominant hereditary disease characterized by mucocutaneous pigmentation and gastrointestinal hamartomatous polyposis. The germline mutations in the serine/threonine kinase 11 (<it>STK11</it>) gene have been shown to be associated with the disease. Individuals with PJS are at increased risk for development of various neoplasms. The aim of the present study was to characterize the genotype and phenotype of Czech patients with PJS.</p> <p>Methods</p> <p>We examined genomic DNA of 8 individuals from five Czech families by sequencing analysis of <it>STK11 </it>gene, covering its promotor region, the entire coding region and the splice-site boundaries, and by multiplex ligation-dependent probe amplification (MLPA) assay designed for the identification of large exonic deletions or duplications of <it>STK11 </it>gene.</p> <p>Results</p> <p>We found pathogenic mutations in <it>STK11 </it>gene in two families fulfilling the diagnostic criteria of PJS and in one of three sporadic cases not complying with the criteria. The patient with the frameshift mutation in <it>STK11 </it>gene developed aggressive gastric cancer. No other studied proband has developed a carcinoma so far.</p> <p>Conclusion</p> <p>Our results showed that a germline mutation of <it>STK11 </it>gene can be found not only in probands fulfilling the PJS diagnostic criteria, but also in some sporadic cases not complying with the criteria. Moreover, we observed a new case of aggressive gastric cancer in a young patient with a frameshift mutation of <it>STK11 </it>gene.</p

Mutation analysis of three genes encoding novel LKB1-interacting proteins, BRG1, STRADα, and MO25α, in Peutz–Jeghers syndrome

Mutations in LKB1 lead to Peutz–Jeghers syndrome (PJS). However, only a subset of PJS patients harbours LKB1 mutations. We performed a mutation analysis of three genes encoding novel LKB1-interacting proteins, BRG1, STRADα, and MO25α, in 28 LKB1-negative PJS patients. No disease-causing mutations were detected in the studied genes in PJS patients from different European populations

Chromosome 19p13.3 deletion in a child with Peutz-Jeghers syndrome, congenital heart defect, high myopia, learning difficulties and dysmorphic features: Clinical and molecular characterization of a new contiguous gene syndrome

The Peutz-Jeghers syndrome (PJS) is an autosomal-dominant hamartomatous polyposis syndrome characterized by mucocutaneous pigmentation, gastrointestinal polyps and the increased risk of multiple cancers. The causative point mutation in the STK11 gene of most patients accounts for about 30% of the cases of partial and complete gene deletion. This is a report on a girl with PJS features, learning difficulties, dysmorphic features and cardiac malformation, bearing a de novo 1.1 Mb deletion at 19p13.3. This deletion encompasses at least 47 genes, including STK11. This is the first report on 19p13.3 deletion associated with a PJS phenotype, as well as other atypical manifestations, thereby implying a new contiguous gene syndrome

Role of LKB1 in lung cancer development

Three phenotypically related genetic syndromes and their lesions (LKB1, PTEN, and TSC1/2) are identified as frequently altered in lung cancer. LKB1, a kinase inactivated in 30% of lung cancers, is discussed in this review. Loss of LKB1 regulation often coincident with KRAS activation allows for unchecked growth and the metabolic capacity to accommodate the proliferation

Mutations in the LKB1 tumour suppressor are frequently detected in tumours from Caucasian but not Asian lung cancer patients

Somatic mutations of LKB1 tumour suppressor gene have been detected in human cancers including non-small cell lung cancer (NSCLC). The relationship between LKB1 mutations and clinicopathological characteristics and other common oncogene mutations in NSCLC is inadequately described. In this study we evaluated tumour specimens from 310 patients with NSCLC including those with adenocarcinoma, adenosquamous carcinoma, and squamous cell carcinoma histologies. Tumours were obtained from patients of US (n=143) and Korean (n=167) origin and screened for LKB1, KRAS, BRAF, and EGFR mutations using RT—PCR-based SURVEYOR-WAVE method followed by Sanger sequencing. We detected mutations in the LKB1 gene in 34 tumours (11%). LKB1 mutation frequency was higher in NSCLC tumours of US origin (17%) compared with 5% in NSCLCs of Korean origin (P=0.001). They tended to occur more commonly in adenocarcinomas (13%) than in squamous cell carcinomas (5%) (P=0.066). LKB1 mutations associated with smoking history (P=0.007) and KRAS mutations (P=0.042) were almost mutually exclusive with EGFR mutations (P=0.002). The outcome of stages I and II NSCLC patients treated with surgery alone did not significantly differ based on LKB1 mutation status. Our study provides clinical and molecular characteristics of NSCLC, which harbour LKB1 mutations

Human Nail Plate Modifications Induced by Onychomycosis : Implications for Topical Therapy

Open Access - This article is distributed under the terms of the Creative Commons Attribution License which permits any use, distribution, and reproduction in any medium, provided the original author(s) and the source are creditedConclusions: Onchomycotic nails presented a thicker but more porous barrier, and its eroded intracellular matrix rendered the tissue more permeable to topically applied chemicals when an aqueous vehicle was used.Purpose: Through the characterisation of the human onchomycotic nail plate this study aimed to inform the design of new topical ungual formulations.Methods: The mechanical properties of the human nail were characterised using a Lloyd tensile strength tester. The nail’s density was determined via pycnometry and the nail’s ultrastructure by electron microscopy. Raman spectroscopy analysed the keratin disulphide bonds within the nail and its permeability properties were assessed by quantifying water and rhodamine uptake.Results: Chronic in vivo nail plate infection increased human nailplate thickness (healthy 0.49 ± 0.15 mm; diseased 1.20 ± 0.67 mm), but reduced its tensile strength (healthy 63.7 ± 13.4 MPa; diseased 41.7 ± 5.0 MPa) and density (healthy 1.34 ± 0.01 g/cm3; diseased 1.29 ± 0.00 g/cm3). Onchomycosis caused cell-cell separation, without disrupting the nail disulfide bonds or desmosomes. The diseased and healthy nails showed equivalent water uptake profiles, but the rhodamine penetration was 4-fold higher in the diseased nails using a PBS vehicle and 3 -fold higher in an ethanol/PBS vehicle.Peer reviewe