Temperature Dependence of Kinetic Friction: A Handle for Plastics Sortation?

Sortation is a crucial step in mechanical recycling of post-consumer plastics (PCR) whereby properties such as density or spectral signature are used to separate plastics. However it is difficult to sort polyolefin flakes at high throughput by these properties. We ask whether the frictional properties of plastics as a function of temperature may be used as an alternate sorting property. However, fundamental studies of friction at temperatures near their melting points are limited. Here we measure the temperature dependence of kinetic friction for three common polyolefins (high and low den- sity polyethylene and polypropylene) as well as polyethylene terephthalate (PET), focusing on the softening/melting regime. The results are augmented by differential scanning calorimetry and temperature dependence measurements of both dynamic modulus and and probe tack. For the polyolefins, we find strong increases in the coefficients of kinetic friction during temperature ramps in the melting/softening regime. For the PET, we report a notable peak in the kinetic friction which we associate with the glass transition and cold-crystallization. We discuss the enhanced friction in the context of rub- ber friction, which exhibits comparable coefficients of kinetic frictions.

Crystallization Kinetics in an Immiscible Polyolefin Blend.

Motivated by the problem of brittle mechanical behavior in recycled blends of high density polyethylene (HDPE) and isotactic polypropylene (iPP), we employ optical microscopy, rheo-Raman, and differential scanning calorimetry (DSC) to measure the composition dependence of their crystallization kinetics. Raman spectra are analyzed via multivariate curve resolution with alternating least-squares (MCR-ALS) to provide component crystallization values. We find that iPP crystallization behavior varies strongly with blend composition. Optical microscopy shows that three crystallization kinetic regimes correspond to three underlying two-phase morphologies: HDPE droplets in iPP, the inverse, and cocontinuous structures. In the HDPE droplet regime, iPP crystallization temperature decreases sharply with increasing HDPE composition. For cocontinuous morphologies, iPP crystallization is delayed, but the onset temperature changes little with the exact blend composition. In the iPP droplet regime, the two components crystallize nearly concurrently. Rheological measurements are consistent with these observations. DSC indicates that the enthalpy of crystallization of the blends is less than the weighted values of the individual components, providing a possible clue for the decreased iPP crystallization temperatures.

Rheology of crystallizing polymers: The role of spherulitic superstructures, gap height, and nucleation densities.

A longstanding goal in polymer rheology is to develop a physical picture that relates the growth of mechanical moduli during polymer crystallization to that of a structure. Here, we utilize simultaneous mechanical rheology and optical microscopy, with augmentation by deterministic reconstruction and stochastic simulations, to study isothermal crystallization in isotactic polypropylene. We observe the nucleation and growth of the surface and bulk spherulites, which are initially isolated and then impinge to form clusters and superstructures that eventually span the gap. We find that spherulitic superstructures play a critical role in the rheology, especially in the characteristic sharp upturn in moduli. Both the rheology and the spherulitic superstructures show pronounced gap dependencies, which we explain via finite-size effects in percolation phenomena and via surface-induced nucleation. The modulus-crystallinity relationship can be described through a general effective medium theory. It indicates that for thicker gaps, the viscoelastic liquid to solid transition can be described via percolation, whereas for our thinnest gap, it is best described by the linear mixing rule. We describe our results in terms of dimensionless nucleation rates and spherulite size, which enable the estimation of when gap-dependent superstructure effects can be anticipated.

Epidermal growth factor receptor as a therapeutic target in glioblastoma.

Glioblastoma represents one of the most challenging problems in neurooncology. Among key elements driving its behavior is the transmembrane epidermal growth factor receptor family, with the first member epidermal growth factor receptor (EGFR) centered in most studies. Engagement of the extracellular domain with a ligand activates the intracellular tyrosine kinase (TK) domain of EGFR, leading to autophosphorylation and signal transduction that controls proliferation, gene transcription, and apoptosis. Oncogenic missense mutations, deletions, and insertions in the EGFR gene are preferentially located in the extracellular domain in glioblastoma and cause constitutive activation of the receptor. The mutant EGFR may also transactivate other cell surface molecules, such as additional members of the EGFR family and the platelet-derived growth factor receptor, which ignite signaling cascades that synergize with the EGFR-initiated cascade. Because of the cell surface location and increased expression of the receptor along with its important biological function, EGFR has triggered much effort for designing targeted therapy. These approaches include TK inhibition, monoclonal antibody, vaccine, and RNA-based downregulation of the receptor. Treatment success requires that the drug penetrates the blood-brain barrier and has low systemic toxicity but high selectivity for the tumor. While the blockade of EGFR-dependent processes resulted in experimental and clinical treatment success, cells capable of using alternative signaling ultimately escape this strategy. A combination of interventions targeting tumor-specific cell surface regulators along with convergent downstream signaling pathways will likely enhance efficacy. Studies on EGFR in glioblastoma have revealed much information about the complexity of gliomagenesis and also facilitated the development of strategies for targeting drivers of tumor growth and combination therapies with increasing complexity.

Quantitative image analysis of broadband CARS hyperspectral images of polymer blends.

We demonstrate that broadband coherent anti-Stokes Raman scattering (CARS) microscopy can be very useful for fast acquisition of quantitative chemical images of multilayer polymer blends. This is challenging because the raw CARS signal results from the coherent interference of resonant Raman and nonresonant background and its intensity is not linearly proportional to the concentration of molecules of interest. Here we have developed a sequence of data-processing steps to retrieve background-free and noise-reduced Raman spectra over the whole frequency range including both the fingerprint and C-H regions. Using a classical least-squares approach, we are able to decompose a Raman hyperspectral image of a tertiary polymer blend into quantitative chemical images of individual components. We use this method to acquire 3-D sectioned quantitative chemical images of a multilayer polymer blend of polystyrene, styrene-ethylene/propylene copolymer, and polypropylene that have overlapping spectral peaks.

Flow-induced properties of nanotube-filled polymer materials.

Carbon nanotubes (CNTs) are under intense investigation in materials science owing to their potential for modifying the electrical conductivity sigma, shear viscosity eta, and other transport properties of polymeric materials. These particles are hybrids of filler and nanoscale additives because their lengths are macroscopic whereas their cross-sectional dimensions are closer to molecular scales. The combination of extended shape, rigidity and deformability allows CNTs to be mechanically dispersed in polymer matrices in the form of disordered 'jammed' network structures. Our measurements on representative network-forming multiwall nanotube (MWNT) dispersions in polypropylene indicate that these materials exhibit extraordinary flow-induced property changes. Specifically, sigma and eta both decrease strongly with increasing shear rate, and these nanocomposites exhibit impressively large and negative normal stress differences, a rarely reported phenomenon in soft condensed matter. We illustrate the practical implications of these nonlinear transport properties by showing that MWNTs eliminate die swell in our nanocomposites, an effect crucial for their processing.

The genetics of multiple sclerosis. A review.

Multiple sclerosis (MS) is characterized by chronic inflammation and demyelination in the central nervous system (CNS). Although the etiology of MS is unknown, both genetic and environmental contributions to the pathogenesis are inferred from epidemiologic studies. Geographic distributions and epidemics of MS and data from migration studies provide evidence for some, thus far unidentified, environmental effects. The co-occurrence of MS with high and low frequencies in ethnic groups often sharing an environment, the increased recurrence rate in families, and the high concordance rate among identical twins point to inheritable determinants of susceptibility. Based on the autoimmune hypothesis of demyelination, genetic studies sought associations between MS and polymorphic alleles of candidate genes which regulate either the immune response or myelin production. The most consistent finding in case-control studies was the association with the major histocompatibility complex (MHC) (also called human leukocyte antigen--HLA) class II, DR15, DQ6, Dw2 haplotype. Studies on other gene products encoded within or close to the MHC complex on chromosome 6p21.3 (e.g., HLA DP, complement components, transporter proteins, tumor necrosis factor, and myelin-oligodendrocyte glycoprotein) resulted in conflicting observations in different patient populations. The potential contribution of polymorphic alleles within the genes of the T-cell receptor alpha beta chains, immunoglobulins, cytokines, and oligodendrocyte growth factors or their receptors to MS susceptibility either remains equivocal or is rejected. Studies on families with multiple affected members have revealed that MS is a complex trait, that the contribution of individual genes to susceptibility is probably small, and that differences are possible between familial and sporadic forms. The development of molecular and computer technologies have facilitated the performance of comprehensive genomic scans in multiplex families, which have confirmed the possible linkage of multiple loci to susceptibility, each with a minor contribution. Several provisional sites were reported, but only 6p21 (MHC complex), 5p14, and 17q22 were positive in more than one study. The British update demonstrated segregation among regions of interest depending on DR15 sharing, and excluded a gene of major effect from 95%, and one with a moderate effect from 65% of the genome. The extended study by the US collaboration group revealed that the MHC linkage was limited to families segregating HLA DR2 alleles, which suggested that linkage to the MHC is related to the HLA DR2 association, and that sporadic and familial MS share at least one common susceptibility marker. Further identification of MS susceptibility loci may involve additional family sets, more polymorphic markers, and the exploration of telomeric chromosomal regions. Data from these studies may further elucidate pathogenic mechanisms of MS.

Autoreactive IgG to intracellular proteins in sera of MS patients.

IgG binding to multiple protein constituents in lysates of Jurkat cells was detected by Western blot in sera of patients with multiple sclerosis (MS) and systemic lupus erythematosus (SLE). The distribution patterns of bands with sera tested against protein lysates from normal Jurkat cells or from Jurkat cells exposed to apoptosis or oxidative stress inducing conditions were similar in most patients, but with inter-individual differences. The number of bands with sera of both patient populations far exceeded those (0 or 2 bands) detected with sera of healthy controls. Proteinase K, RNase and DNase pre-treatment of cell lysates suggested a protein nature for all of the antigens and a ribonucleoprotein (RNP) nature for some of the antigens recognized by serum IgG of MS and SLE patients. Only two MS patients had positive anti-nuclear antibody (ANA) titers, while all of them had positive Western blots. In addition to similarities, dissimilarities were also recognized between the humoral immune responses in MS and SLE. No IgG molecules were detected against phosphorylated proteins in the sera of MS patients, while multiple phosphoproteins were recognized by IgG molecules of SLE patients in immunoprecipitation experiments. These data suggest that in addition to ANA, the sera of MS patients contain autoantibodies directed against multiple intracellular proteins. The protein recognition patterns of immunoglobulins in MS share similarities, but also have distinct features when compared to those in SLE. The biological significance of these autoantibodies in MS remains to be understood.

The activation of protein kinase C induces higher production of reactive oxygen species by mononuclear cells in patients with multiple sclerosis than in controls.

OBJECTIVE: Recent findings have increasingly shown the importance of reactive oxygen species (ROS) in causing oxidative damage to macromolecules and in contributing to tissue degeneration in target organs of autoimmune diseases. This study was aimed at comparing the base line and induced production of ROS by peripheral blood mononuclear cells (PB MNCs) of patients with multiple sclerosis (MS) in remission and relapse, of patients with other neurological diseases (OND) and of healthy controls. In addition, we analyzed the underlying mechanism of ROS production. METHODS: PB MNCs were separated from 28 MS patients in remission and 13 in relapse, and from 29 healthy controls and 10 OND. ROS was measured by spectrofluorometry. Expression of proinflammatory cytokines was assessed by semi-quantitative reverse transcription polymerase chain reaction (RT-PCR). Mitochondrial (mt) DNA haplotypes were determined by using restriction site polymorphism analysis. RESULTS: The base line and tumor necrosis factor (TNF)-alpha or interferon (IFN)-gamma induced ROS values were similar in the four groups, and the individual measures did not show a correlation with MS associated mtDNA haplotypes. Phorbol ester activation of protein kinase C (PKC) induced higher ROS production in all groups, however, with significantly greater values in the MS remission group. Calphostine C, a PKC inhibitor decreased or eliminated ROS production in a dose-dependent manner, suggesting further that it was predominantly or exclusively generated by PKC activated NADPH oxidase. A trend of increased TNF-alpha and IFN-gamma expression was noted in the MS relapse group, in contrast to the high ROS release in the MS remission group. CONCLUSION: The detected phase difference between the highest ROS production vs TNF-alpha expression is compatible with the hypothesis that different subpopulations of monocytes/macrophages are involved. We suggest that the ROS producing subpopulation preferentially migrates into the central nervous system (CNS) during a relapse. The present study together with our previous observation on oxidative damage to DNA in active plaques delineates a molecular pathway likely involved in the histologic evolution of inflammatory demyelination.

Large scale screening of the mitochondrial DNA reveals no pathogenic mutations but a haplotype associated with multiple sclerosis in Caucasians.

We report the first large-scale screening of mitochondrial (mt) DNA in 77 Caucasian patients with relapsing-remitting or secondary progressive form of multiple sclerosis (MS) and in 84 Caucasian controls by using the method of restriction site polymorphism and haplotype analysis. No pathogenic mtDNA mutation was found in association with MS. However, mtDNA haplotypes K* and J* defined by the simultaneous presence of Ddel restriction sites at nucleotides 10,394 and 14,798 of the mtDNA in haplogroups K and J showed association with MS at a P-value of 0.001. A relative increase of MS patients compared to controls either with the J* or with the K* haplotype (+10,394Ddel/+14,798Ddel in haplogroup J or K) also was detected (each with a P<0.05). No distinct phenotypic characteristics of MS were observed when clinical data of patients with haplotypes K* or J* were analyzed. In addition to previous complete sequencing in several MS patients, the population screening of mtDNA presented here suggests that mtDNA point mutations are not likely to be involved in the pathogenesis of typical forms of MS. However, the mitochondrial genetic background (haplotype K* and J*) may moderately contribute to MS susceptibility. The reported association between MS and Leber's hereditary optic nerve atrophy, a disease caused by mtDNA point mutations preferentially occurring in haplogroup J, may be at least in part related to the overlapping mitochondrial genetic background of the two diseases.

Prescreening entire mammograms for masses with artificial neural networks: preliminary results.

RATIONALE AND OBJECTIVES: The authors evaluated the feasibility of combining wavelet transform and artificial neural network (ANN) technologies to prescreen mammograms for masses. METHODS AND MATERIALS: Fifty-five mammograms (29 with masses and 26 without) were digitized to 100-mm resolution and processed by using wavelet transformation. These wavelets were subjected to a linear output sequential recursive auto-associative memory ANN and cluster analysis with feature vector formation. These vectors were used in two separate experiments-one with 13 cases and another with seven cases held out in a test set-to train feed-forward ANNs to detect the mammograms with a mass. The experiments were repeated with rerandomization of the data, four and six times, respectively. RESULTS: There was a statistically significant correlation (P < .01) between the network's prediction of a mass and the presence of a mass. With majority voting, the feed-forward ANNs detected masses with 79% sensitivity and 50% specificity. CONCLUSION: Although preliminary, the combination of wavelet transform and ANN is promising and may provide a viable method to prescreen mammograms for masses with high sensitivity and reasonable specificity.

Pyrene excimer fluorescence as a proximity probe for investigation of residual structure in the unfolded state of human carbonic anhydrase II.

The excimer fluorescence from two pyrenyl moieties attached to cysteines in human carbonic anhydrase II has been monitored to characterize residual structure retained under strong denaturing conditions. A position in beta-strand 3, N67C, together with the single naturally occurring cysteine 206 in beta-strand 7, were used as attachment sites. The eximer formation by the pyrenyls, requiring proximity of the probes, revealed an unfolding transition at a GuHCl concentration significantly higher than that required to induce unfolding of the molten globule state as monitored by CD. These results indicate that the excimer transition monitors the unfolding of a residual compact structure that spans beta-strands 3-7. This region constitutes the central and the most hydrophobic part of the molecule, emphasizing the importance of hydrophobic interaction in maintaining residual structure under strong unfolding conditions.

Diagnosis of focal bone lesions using neural networks.

RATIONALE AND OBJECTIVES: Use of a neural network to diagnose focal lesions of bone was evaluated. METHODS: Imaging features of 709 lesions were encoded into a predetermined database. Data were divided into four groups and were analyzed using cross-validation by a two-layer feed-forward neural network. RESULTS: The lesions comprised 43 different pathologic diagnoses. Overall, the network was 85% accurate in distinguishing benign from malignant lesions. With a differential list of five diagnoses, the list was internally consistent regarding benign and malignant lesions 81.9% of the time. The network correctly diagnosed 56% of the lesions by pathologic diagnosis as its first choice. It included the correct diagnosis 71.8% of the time in a differential list of three diagnoses and 87.3% of the time in a differential list of nine diagnoses. CONCLUSION: Although not yet adequate for clinical use, neural network diagnosis of bone lesions is in its infancy and has important implications for the future analysis of focal bone lesions.

Preferential but not exclusive T cell receptor V beta chain utilization of myelin basic protein and peptide-specific T cell clones in mice.

The repertoire of T cell receptor (TCR) V beta chain utilization was investigated in PL/J, CXJ-1, SJL/J and B10.S-->SJL/J chimeric mice in response to either myelin basic protein (MBP) or the strain-specific encephalitogenic peptide. Our analysis showed that there was an overlapping predominance in the TCR V beta gene utilization in the MBP-specific responses, which were independent of the major histocompatibility complex (MHC) class II haplotype present, and the immunodominant peptide region recognized in these different strains. In those mice having the TCR V beta b haplotype (PL/J, CXJ-1, and the B10.S-->SJL chimera) either the TCR V beta 4, 8, and 13 or the TCR V beta 4, 6, and 13 predominated. In contrast, in mice with TCR V beta a haplotype (SJL/J) V beta 4, 6, and 17a were found. However, the quantitative distribution of these preferentially utilized TCR V beta chains in each strain was defined by the MHC class II haplotype and the immunodominant peptide recognized. The expression of the V beta 8 gene product in the peripheral TCR repertoire did not always correlate with predominant V beta 8 utilization in the MBP-specific response.

Immunopathogenic mechanisms in experimental allergic encephalomyelitis.

Experimental allergic encephalomyelitis, a cell-mediated autoimmune disease, continues to provide interesting data on the mechanisms subserving organ-specific autoimmunity. The elements of the trimolecular complex have been further defined and the conserved molecular basis of the interaction between the T-cell receptor and the major histocompatibility complex class II-peptide antigen complex is better understood. This model also provides new insights into the cellular interactions within the brain during the course of the autoimmune inflammatory response.

Monoclonal anti-gamma interferon antibodies enhance experimental allergic encephalomyelitis.

Interferon-gamma (IFN-gamma) is a cytokine with multiple activities on a variety of cells. Under various circumstances, IFN-gamma can exhibit either pro-inflammatory or inhibitory actions. Treatment of SJL/J mice with a monoclonal antibody (Mab) to IFN-gamma during the afferent limb of the immune response to myelin protein produced an enhancement of acute experimental allergic encephalomyelitis (EAE), with increased morbidity, mortality and earlier onset of disease. Systemic administration of IFN-gamma did not improve or worsen clinical outcome, but delayed disease onset. Passive transfer of immune lymph node cells co-activated with MBP and anti-IFN-gamma Mab resulted in more sever disease than that induced by MBP stimulated cells or MBP and IFN-gamma co-stimulated cells. However, in vitro proliferation of an MBP specific T cell line was not influenced by IFN-gamma nor anti-IFN-gamma treatment. Mab to IFN-gamma inhibited suppressor function, in a non-specific assay. These in vivo and in vitro results suggest that systemic IFN-gamma serves as a physiological regulator of a suppressor mechanism in EAE. The abrogation of this regulatory mechanism by anti-IFN-gamma administration contributes to a more severe form of experimental allergic encephalomyelitis.

Estradiol potentiates poke-weed mitogen-induced B cell stimulation in multiple sclerosis and healthy subjects.

Female preponderance in many diseases suggested with autoimmune pathogenesis, multiple sclerosis (MS) being classified as one of them, indicates a role for hormonal factors such as estrogen in disease development. To bypass monthly hormonal fluctuations in females, we evaluated in male patients with MS and male blood donors the effect of 17-beta-estradiol on numbers of IgG, IgA and IgM producing cells in cultures of peripheral blood lymphocytes. While estradiol alone had no effect, estradiol in combination with poke-weed mitogen (PWM) yielded in both groups higher numbers of IgG and IgA producing cells when compared with numbers obtained by PWM stimulation alone, indicating an additory effect of estradiol to that of PWM on B cell maturation. This effect was less pronounced in MS than in blood donors, especially for IgG producing cells, probably reflecting higher B cell activation in vivo taking place in MS. On the contrary, cells producing IgG, IgA and IgM antibodies against myelin, myelin basic protein and measles virus were not detectable after stimulation with PWM, nor with PWM and estradiol. Estradiol can in many patients with MS and in blood donors be considered a potent co-activator of B cells in presence of B cell stimulating factor in the form of PWM.