On the Ablation Behavior of Carbon Fiber-Reinforced Plastics during Laser Surface Treatment Using Pulsed Lasers

This contribution discusses the ablation phenomena observed during laser treatment of carbon fiber-reinforced plastics (CFRPs) with pulsed lasers observed employing laser sources with wavelengths of 355 nm, 1064 nm and 10.6 µm and pulse durations from picoseconds (11 ps) to microseconds (14 µs) are analyzed and discussed. In particular, the threshold fluence of the matrix material epoxy (EP) and the damage threshold of CFRP were calculated. Moreover, two general surface pretreatment strategies are investigated, including selective matrix removal and structure generation through indentation (ablation of both, matrix material and fibers) with a cross-like morphology. The surfaces obtained after the laser treatment are characterized by means of optical and scanning electron microscopy (SEM) and Fourier transform infrared spectroscopy is employed for the analysis of composite and constituent materials epoxy and carbon fibers. As a result, different ablation mechanisms, including evaporation and delamination are observed, depending on the employed laser wavelength and pulse duration. For both 355 nm and 1064 nm wavelength, the laser radiation produces only partial ablation of the carbon fibers due to their higher absorption coefficient compared to the epoxy matrix. Although a selective matrix removal without residues is achieved using the pulsed CO₂ laser. Differently, both constituent materials are ablated with the nanosecond pulsed UV laser, producing indentations. The sum of the investigations has shown that existing theories of laser technology, such as the ablation threshold according to Liu et al., can be applied to composite materials only to a limited extent. Furthermore, it has been found that the pronounced heterogeneity of CFRP mostly leads to an inhomogeneous ablation result, both when creating grooves and during selective matrix removal, where the carbon fibers influence the ablation result by their thermal conductivity, depending on fiber direction. Finally, despite the material inhomogeneity, a scanning strategy has been developed to compensate the heterogeneous ablation results regarding structure depth, width and heat affected zone.     

Neutrophil Dependence of Vascular Remodeling after Mycoplasma Infection of Mouse Airways

Vascular remodeling is a feature of sustained inflammation in which capillaries enlarge and acquire the phenotype of venules specialized for plasma leakage and leukocyte recruitment. We sought to determine whether neutrophils are required for vascular remodeling in the respiratory tract by using Mycoplasma pulmonis infection as a model of sustained inflammation in mice. The time course of vascular remodeling coincided with the influx of neutrophils during the first few days after infection and peaked at day 5. Depletion of neutrophils with antibody RB6-8C5 or 1A8 reduced neutrophil influx and vascular remodeling after infection by about 90%. Similarly, vascular remodeling after infection was suppressed in Cxcr2^−/− mice, in which neutrophils adhered to the endothelium of venules but did not extravasate into the tissue. Expression of the venular adhesion molecule P-selectin increased in endothelial cells from day 1 to day 3 after infection, as did expression of the Cxcr2-receptor ligands Cxcl1 and Cxcl2. Tumor necrosis factor α (TNFα) expression increased more than sixfold in the trachea of wild-type and Cxcr2^−/− mice, but intratracheal administration of TNFα did not induce vascular remodeling similar to that seen in infection. We conclude that neutrophil influx is required for remodeling of capillaries into venules in the airways of mice with Mycoplasma infection and that TNFα signaling is necessary but not sufficient for vascular remodeling.Neutrophils are key effector cells of innate immunity that rapidly arrive at sites of tissue injury to kill bacteria and interact with macrophages and other cells to orchestrate a coordinated immune cell and cytokine response to injury.^1–4 Neutrophils are involved in many inflammatory diseases of the airways and lung, including pneumonia, acute lung injury, sepsis, asthma, cystic fibrosis, bronchitis, and chronic obstructive lung disease,⁵ also contribute to tissue damage in inflammatory conditions of other organs, and play a role in arterial remodeling in atherosclerosis.⁴The signals and events that bring neutrophils to sites of inflammation are well characterized.^6–8 These include expression of endothelial cell adhesion molecules to induce rolling and firm attachment, followed by extravasation into tissues where they release cytokines and other products that can kill bacteria and promote tissue remodeling. The dominant mechanism driving neutrophil influx may be organ-specific.^9,10 Blood vessels of the microcirculation undergo numerous changes in sustained inflammation, and these include structural and functional remodeling of endothelial cells and pericytes.^11–14 Among these changes, capillaries transform into venules that support plasma leakage and leukocyte influx. The contribution of neutrophils to this remodeling is not well understood. Circumferential vessel enlargement is a prominent feature of vascular remodeling–sustained airway inflammation^15–23 and is distinct from more familiar and better-documented types of sprouting angiogenesis.²⁴We asked whether incoming neutrophils contribute to the vascular remodeling, with the thought that the initial wave of leukocyte influx could render blood vessels more efficient for leukocyte adhesion and transmigration. Although leukocyte influx is known to accompany blood vessel remodeling,^15,18,22 it is unknown whether there is a causal relationship and, if so, what is the underlying mechanism? Neutrophils are attractive candidates for contributing to vascular remodeling because they are among the first leukocytes to enter inflamed tissues^4,6,25 and can produce cytokines, growth factors, proteases, and reactive oxygen species that have profound vascular effects.^2–4,26With this background, we sought to determine whether neutrophils are essential for the vascular remodeling that occurs soon after Mycoplasma pulmonis infection, when capillaries transform into venules. In particular, we asked whether neutrophil influx coincides spatially and temporally with vascular remodeling, can vascular remodeling be prevented by neutrophil depletion, and if Cxcr2 signaling is required for the neutrophil influx that accompanies vascular remodeling?To address these questions we examined the relationship between neutrophil influx and vascular remodeling during the first week after M. pulmonis infection of the respiratory tract of mice. The approach was to compare the time course of neutrophil influx and vascular remodeling in the trachea and then determine whether the remodeling was blocked by neutrophil depletion by either of two different antineutrophil antibodies: RB6-8C5 or 1A8. We also tested whether vascular remodeling was prevented by genetic deletion of Cxcr2, which mediates the actions of the chemotactic chemokines Cxcl1 and Cxcl2, which bring neutrophils into inflamed tissues. Because previous studies have shown that vascular remodeling was inhibited by blocking tumor necrosis factor α (TNFα) signaling,¹⁹ we asked whether TNFα expression was increased in wild-type and Cxcr2^−/− mice and whether intratracheal administration of TNFα was sufficient to induce vascular remodeling similar to that seen after infection. Other studies examined the expression of the Cxcr2 ligands, Cxcl1 and Cxcl2. Together, the experiments showed that neutrophil influx was required for vascular remodeling after M. pulmonis infection, and that TNF signaling was necessary but not sufficient for vascular remodeling.     

Preparation of unnatural N-to-N and C-to-C protein fusions

Standard genetic approaches allow the production of protein composites by fusion of polypeptides in head-to-tail fashion. Some applications would benefit from constructions that are genetically impossible, such as the site-specific linkage of proteins via their N or C termini, when a remaining free terminus is required for biological activity. We developed a method for the production of N-to-N and C-to-C dimers, with full retention of the biological activity of both fusion partners and without inflicting chemical damage on the proteins to be joined. We use sortase A to install on the N or C terminus of proteins of interest the requisite modifications to execute a strain-promoted copper-free cycloaddition and show that the ensuing ligation proceeds efficiently. Applied here to protein-protein fusions, the method reported can be extended to connecting proteins with any entity of interest.     

Spin electron paramagnetic resonance of albumin for diagnosis of oral squamous cell carcinoma (OSCC)

Objectives

Albumin has a known capability to modulate free serum concentrations of proteins produced by tumour cells. The technique of spin probe labelling of albumin followed by electron paramagnetic resonance (EPR) spectroscopy may allow identification of these structural and functional changes, which regularly occur as consequence of binding tumour metabolites as ligands. The aim of the present study was a proof of principle evaluation of EPR-analysis of peripheral blood samples as possible predictor for oral squamous cell carcinoma (OSCC).

Material and methods

The present study is designed as gender-matched cohort. EPR was tested after retrieval of peripheral blood samples. The study group is represented by 32 patients with OSCC, and the control group consisted of 30 healthy patients.

Results

Overall analysis exhibited a diagnostic sensitivity of 72% (23/32 OSCC group) and a specificity of 80% (24/30 control group). Subgroup analysis revealed ten patients with elevated leukocytes (>10,000/μl; n?=?9 [OSCC group] and n?=?1 [control group]). After exclusion of patients with elevated white blood cell count, sensitivity considerably increased to 87% and specificity to 83%.

Conclusion

EPR analysis of peripheral blood samples might be appropriate to support the clinician in primary and follow-up diagnosis of potential tumours such as OSCC. Unfortunately, subgroup analysis characterises the method vulnerable to inflammation.

Clinical relevance

Nevertheless, our preliminary results are intriguing, as diagnosis of OSCC appears possible by simple peripheral blood examination. Thus, further appraisal of this novel method with inclusion of different tumour entities, systemic conditions and inflammation in a larger study population appears highly valuable.     

Normative data and psychometric properties for qualitative and quantitative scoring criteria of the Five-point Test

The Five-point Test (Regard, Strauss, & Knapp, 1982) was introduced for the measurement of figural fluency as part of the examination of executive functions. Until now, no differentiated norms exist. We present normative data for adults aged 18–80 (n = 280) for the number of unique designs (productivity), the percent of perseverations (flexibility), the percent of rotated (strategic) designs, and the number of rule breakings. As age and education were correlated with test performance, norms were stratified by these two variables. Test–retest reliability and inter-rater reliability were calculated. Moreover, convergent and divergent validity as well as factorial validity were assessed through intercorrelations and correlations with other neuropsychological tests. All together, the Five-point Test proved to be reliable and valid.     

Multiaxial mechanical properties and constitutive modeling of human adipose tissue: A basis for preoperative simulations in plastic and reconstructive surgery

A preoperative simulation of soft tissue deformations during plastic and reconstructive surgery is desirable to support the surgeon’s planning and to improve surgical outcomes. The current development of constitutive adipose tissue models, for the implementation in multilayer computational frameworks for the simulation of human soft tissue deformations, has proved difficult because knowledge of the required mechanical parameters of fat tissue is limited. Therefore, for the first time, human abdominal adipose tissues were mechanically investigated by biaxial tensile and triaxial shear tests. The results of this study suggest that human abdominal adipose tissues under quasi-static and dynamic multiaxial loadings can be characterized as a nonlinear, anisotropic and viscoelastic soft biological material. The nonlinear and anisotropic features are consequences of the material’s collagenous microstructure. The aligned collagenous septa observed in histological investigations causes the anisotropy of the tissue. A hyperelastic model used in this study was appropriate to represent the quasi-static multiaxial mechanical behavior of fat tissue. The constitutive parameters are intended to serve as a basis for soft tissue simulations using the finite element method, which is an apparent method for obtaining promising results in the field of plastic and reconstructive surgery.