Extreme Tribological Characteristics of Copolymers Induced by Dynamic Rheological Instability

Nonlinear tribological behavior of polymeric microparticles under extreme collision conditions is required for an in-depth understanding of advanced applications in the fields of defense, biomedicine, and manufacturing. Laser-induced projectile impact tests with an incidence angle of 45° are conducted to investigate the tribological response at the contact interface of block copolymers with glassy–rubbery phases and a stationary substrate to induce deformations with an ultrahigh strain rate. Morphological-phase-dependent tribological and rheological responses are quantified from the mechanical interactions involving adiabatic heating, plastic flow, and interfacial shear instability. An effective coefficient of friction mechanism that depends on the rheological transition activated by impact velocity is proposed to specify the rheological response of the copolymers

Extreme Plasticity, Adhesion, and Nanostructural Changes of Diblock Copolymer Microparticles in Cold Spray Additive Manufacturing

Using the laser-induced projectile impact testing (LIPIT), the extreme plastic and adhesive responses of polystyrene-polydimethylsiloxane block copolymer (BCP) microparticles are investigated to provide the ultra-high-strain-rate behavior of individual BCP feedstock powders during their collisions with a stationary substrate in the cold spray additive manufacturing process. The onset of BCP microparticle adhesion to the substrate is precisely predicted by the maximum coefficient of dynamic friction, quantified from the angled collisions, and by the spectra of the coefficients of restitution. This finding confirms the direct correlation between friction and adhesion mechanisms in the ultra-high-strain rate regime and its significance in the consolidation process of BCP feedstock powders. Furthermore, the impact-induced adiabatic shear flows create structural ordering of initially disordered nanostructures of the block copolymers consisting of glassy and rubbery domains while generating a temperature rise beyond their glass transition temperatures. In addition to the conventional strain-hardening effect in homopolymers, nanoscale morphological ordering can provide another strain-hardening mechanism of BCP feedstock microparticles in the cold spray of additive manufacturing

Characteristics of cancer cell lines used.

<p>Characteristics of cancer cell lines used.</p

Oxygen concentration surrounding the cells and oxygen consumption rates in various cell lines.

<p>Correlation between oxygen consumption rate and oxygen concentration surrounding the cells after 3 = −23.045x +250.07 with a R² value of 0.8161. Error bars represent standard error.</p

Glucose concentration regulated intracellular hypoxia in a parabolic fashion.

<p>(A) BTP phosphorescence of the cells treated with varying concentrations of glucose. (B) Quantification of results in panel A (<i>n</i> = 10, **P<0.01, ***P<0.001 when compared to 4.5 mg/ml glucose). Error bars represent standard error.</p

Intracellular oxygen status of various cell lines.

<p>(A) Detection of intracellular hypoxia by BTP in prostate cancer cell lines LNCaP, C4-2 and PC-3 (upper panels). DIC images show the positions of imaged cells (lower panels). (B) Quantification of BTP phosphorescence in panel A (<i>n = </i>10, ***P<0.001 when compared to LNCaP). (C) Detection of intracellular hypoxia by BTP in MCF-7 and MDAMB231 (upper panels). DIC images show the positions of imaged cells (lower panels). (D) Quantification of BTP phosphorescence in panel C (<i>n</i> = 10, **P<0.01 when compared to MCF-7). Error bars represent standard error.</p

Exogenous hypoxia- and hyperoxia-induced changes in intracellular oxygen concentration.

<p>(A) BTP phosphorescence of LNCaP cells cultured at normoxia (20% O₂), hypoxia (0.2% O₂), or hyperoxia (40% O₂) for 1 hour. (B) Quantification of results in panel A (<i>n = </i>10, ***P<0.001 when compared to 20% O₂ control). Error bars represent standard error.</p

Mitochondrial Respiratory Function Induces Endogenous Hypoxia

<div><p>Hypoxia influences many key biological functions. In cancer, it is generally believed that hypoxic condition is generated deep inside the tumor because of the lack of oxygen supply. However, consumption of oxygen by cancer should be one of the key means of regulating oxygen concentration to induce hypoxia but has not been well studied. Here, we provide direct evidence of the mitochondrial role in the induction of intracellular hypoxia. We used Acetylacetonatobis [2-(2′-benzothienyl) pyridinato-k<i>N</i>, kC3’] iridium (III) (BTP), a novel oxygen sensor, to detect intracellular hypoxia in living cells via microscopy. The well-differentiated cancer cell lines, LNCaP and MCF-7, showed intracellular hypoxia without exogenous hypoxia in an open environment. This may be caused by high oxygen consumption, low oxygen diffusion in water, and low oxygen incorporation to the cells. In contrast, the poorly-differentiated cancer cell lines: PC-3 and MDAMB231 exhibited intracellular normoxia by low oxygen consumption. The specific complex I inhibitor, rotenone, and the reduction of mitochondrial DNA (mtDNA) content reduced intracellular hypoxia, indicating that intracellular oxygen concentration is regulated by the consumption of oxygen by mitochondria. HIF-1α was activated in endogenously hypoxic LNCaP and the activation was dependent on mitochondrial respiratory function. Intracellular hypoxic status is regulated by glucose by parabolic dose response. The low concentration of glucose (0.045 mg/ml) induced strongest intracellular hypoxia possibly because of the Crabtree effect. Addition of FCS to the media induced intracellular hypoxia in LNCaP, and this effect was partially mimicked by an androgen analog, R1881, and inhibited by the anti-androgen, flutamide. These results indicate that mitochondrial respiratory function determines intracellular hypoxic status and may regulate oxygen-dependent biological functions.</p></div

Androgen played a major role in the modulation of intracellular hypoxia in LNCaP.

<p>(A) LNCaP cells were incubated with indicated conditions and BTP phosphorescence was detected. (B) Quantification of results in panel A (<i>n</i> = 10, *P<0.05, **P<0.01, ***P<0.001 when compared to control, ***P<0.001 when+serum is compared to+R1881– serum, ***P<0.001 when+serum is compared to+flutamide+serum). Error bars represent standard error.</p

Oxygen concentrations surrounding the cells with different cell densities.

<p>(A) Time dependent changes in oxygen concentrations surrounding cells at an indicated cell density of LNCaP. (B) Oxygen concentration at 180 minutes from panel A (<i>n</i> = 3, ***P<0.001 when compared to 1×10⁶ cells/ml). Error bars represent standard error.</p