Hybrid denture acrylic composites with nanozirconia and electrospun polystyrene fibers.

The processing and characterization of hybrid PMMA resin composites with nano-zirconia (ZrO2) and electrospun polystyrene (PS) polymer fibers were presented in this study. Reinforcement was selected with the intention to tune the physical and mechanical properties of the hybrid composite. Surface modification of inorganic particles was performed in order to improve the adhesion of reinforcement to the matrix. Fourier transform infrared spectroscopy (FTIR) provided successful modification of zirconia nanoparticles with 3-Methacryloxypropyltrimethoxysilane (MEMO) and bonding improvement between incompatible inorganic nanoparticles and PMMA matrix. Considerable deagglomeration of nanoparticles in the matrix occurred after the modification has been revealed by scanning electron microscopy (SEM). Microhardness increased with the concentration of modified nanoparticles, while the fibers were the modifier that lowers hardness and promotes toughness of hybrid composites. Impact test displayed increased absorbed energy after the PS electrospun fibers had been embedded. The optimized composition of the hybrid was determined and a good balance of thermal and mechanical properties was achieved.

Matrix metalloproteinases 2 and 9 in the cochlea: expression and activity after aminoglycoside exposition.

The matrix metalloproteinases (MMPs) are a family of proteins involved in the remodelling and homeostasis of the extracellular matrix. These proteases have been well studied in the retina and the brain, marking their importance in neuronal cell survival and death [Chintala (2006) Exp Eye Res 82:5-12; Candelario-Jalil et al. (2009) Neuroscience 158:983-994]. The neuroepithelia of the eye and the inner ear share common characteristics. Therefore, we hypothesized that MMPs could play a similar role in the cochlea as described in the retina. We focused on the localization and function of MMP-2 and MMP-9 in the cochlea, by determining their expression and activity under normal conditions and after cochlear damage via aminoglycoside exposition. We examined their expression in 5-day-old Wistar rat cochleas by RT-PCR, real-time PCR, and Western blot. We used immunohistochemistry to investigate their location in the cochleas of adult C57BL/6 mice. We also determined whether or not the exposure of the organs of Corti to aminoglycosides would change MMP-2 and MMP-9 expression patterns. Western blotting identified MMP-2 and MMP-9 in neonatal spiral ganglion, stria vascularis, and to a lesser extent the organ of Corti. Neonatal mRNA expression of MMP-2 was approximately equivalent in all three tissues, while MMP-9 mRNA was highest in spiral ganglion. Immunohistochemistry showed MMP-2 primarily in adult spiral ganglion neurons and inner hair cells, while MMP-9 was found mainly in spiral ganglion neurons, inner hair cells and supporting cells. Organs of Corti treated with gentamicin for 24 h showed an upregulation of MMP-2 and MMP-9 proteins, but did not show a significant upregulation of mRNA expression 3, 6, 12, 24, and 36 h after gentamicin exposure. Inhibition of MMP activity in organs of Corti incubated with an MMP inhibitor in organotypic cultures resulted in hair cell death-suggesting that a basal level of MMP activity is required for hair cell survival.

Abnormal trafficking of sarcolemmal proteins in alpha-glucosidase deficiency.

The dystrophin-associated protein complex (DAP) plays an important role in the integrity and stability of the muscle membrane. Whereas much is known about the interaction between DAP members at the sarcolemmal location, intracellular DAP assembly and trafficking is still largely unknown. In alpha-glucosidase (acid maltase) deficiency (alphaGDD), accumulation of glycogen is accompanied by cytoarchitectural abnormalities impairing normal protein metabolism. In the present study, we took advantage of this fact to examine the consequences of impaired protein handling on the formation of DAP, with the aim of gaining indirect knowledge about its sarcoplasmic trafficking and a better understanding of mechanisms leading to myopathic changes found in alphaGDD. Histological examination of alphaGDD muscle confirmed a vacuolar myopathy with glycogen accumulation both in vacuoles and within the sarcoplasm. Sarcoplasmic accumulation of sarcolemmal proteins, including dystrophin and sarcoglycans, occurred around some vacuoles and within non-vacuolated fibres. Utrophin was up-regulated and found at extra-junctional sarcolemmal locations of many fibres. AlphaGDD muscle cells developed in a fashion similar to that of controls in culture. However, vacuoles were found in 2-week-old alphaGDD myotubes, and these subsequently increased in size and number. Substantial alterations in DAP handling were found, with accumulation close to the Golgi apparatus. Utrophin was not enriched in the sarcoplasm but was up-regulated along the whole sarcolemma. Our results demonstrate a close association of dystrophin and sarcoglycans during sarcoplasmic processing. Furthermore, they suggest that the myopathy found in alphaGDD is a secondary form of DAP deficiency.

Restoration of dystrophin expression in cultured hybrid myotubes.

Absence of dystrophin, as found in Duchenne boys, mdx mice and HFMD cats, leads to destabilization of the sarcolemmal-associated protein complex. Gene and cell therapy strategies aim to restore the dystrophin-associated protein complex. In order to better understand the cellular events involved in such therapy in feline and human muscular dystrophy, we asked whether dystrophin-deficient myoblasts would fuse with myoblasts expressing normal dystrophin, and whether the complex would be restored after such a fusion. Cat and human myoblasts were isolated from skeletal muscle of normal subjects and of patients with dystrophin deficiency and proliferated well. After co-culture with normal myoblasts, they fused to form hybrid myotubes. These hybrid myotubes expressed dystrophin, utrophin and dystrophin- associated proteins. Expression of these proteins were restored also in the vicinity of nuclei from dystrophin-deficient donors. These results demonstrate that dystrophin can be expressed and handled normally by hybrid myotubes. They show that myoblasts with a normal dystrophin gene can restore dystrophin expression in dystrophin-deficient myoblasts.

Strong electron correlation in photoionization of spin-orbit doublets.

A new and explicitly many-body aspect of the "leveraging" of the spin-orbit interaction is demonstrated, spin-orbit activated interchannel coupling, which can significantly alter the photoionization cross section of a spin-orbit doublet. As an example, it is demonstrated via a modified version of the spin-polarized random phase approximation with exchange, that a recently observed unexplained structure in the Xe 3d(5/2) photoionization cross section [A. Kivimäki et al., Phys. Rev. A 63, 012716 (2000)] is entirely due to this effect. Similar features are predicted for Cs 3d(5/2) and Ba 3d(5/2).

Differential expression of dystrophin, utrophin, and dystrophin-associated proteins in human muscle culture.

The dystrophin-associated protein complex (DAP) plays an important role in sarcolemmal function. Mutations of DAP elements lead to diverse forms of muscular dystrophies, among them Duchenne muscular dystrophy, one of the most severe neuromuscular diseases. Strategies in gene therapy are being assessed to restore DAP stability. However, the relationship between DAP elements and time-course of the DAP formation are still not known in detail. In order to better understand the relationship among DAP proteins, we therefore studied their expression during development in human muscle culture in comparison with developmentally regulated muscle proteins. Desmin immunoreactivity (IR) was detected by 3 days in vitro (DIV3), IR for developmental heavy-chain myosin, vimentin, utrophin, and beta-dystroglycan, as well as alpha-, beta-, and gamma-sarcoglycan, a day later. delta-Sarcoglycan was found by DIV7; dystrophin could be detected only by DIV11. In general, DAP proteins were first located in the perinuclear region, later diffusely in the cytoplasm, and finally exclusively at the membrane. This sequence of events during muscle development gives further support to our suggestion that utrophin could be a precursor of dystrophin during development and regeneration. These data also suggest that utrophin alone is sufficient to anchor the complex, which is important when utrophin replacement strategies are being investigated for the treatment of dystrophinopathies. In this study we demonstrated the establishment of a culture technique that should allow the close study of DAP expression in diseased muscle, including its use after gene modulatory strategies.

A comparison of behavioral and educational interventions for fibromyalgia.

OBJECTIVE: To compare a comprehensive behavioral intervention with an education/control condition in the treatment of patients with fibromyalgia (FM), and to explore the role of mediators of clinical improvement in both groups. METHODS: The effects of the behavioral and education/control interventions were evaluated across a 10 week treatment period and at 6 month followup on measures of pain, depression, disability, pain behaviors, and intervening variables. The behavioral intervention focused on the development of diverse pain coping skills, while the education/control condition presented information on a range of health related topic without emphasizing skill acquisition. RESULTS: Although improvement across time was found in depression, self-reported pain behaviors, observed pain behaviors, and myalgia scores, no differences in these criteria were found between the behavioral and education/control conditions. Multiple regression analyses revealed that changes in helplessness and passive coping were associated with improvement in a number of clinical outcomes. CONCLUSION: The findings illustrate the value of psychoeducational interventions in decreasing the psychological and behavioral effect of FM, and the value of reducing dysfunctional coping and helplessness in future intervention research.

A controlled study of the effects of EEG biofeedback on cognition and behavior of children with attention deficit disorder and learning disabilities.

Eighteen children with ADD/ADHD, some of whom were also LD, ranging in ages from 5 through 15 were randomly assigned to one of two conditions. The experimental condition consisted of 40 45-minute sessions of training in enhancing beta activity and suppressing theta activity, spaced over 6 months. The control condition, waiting list group, received no EEG biofeedback. No other psychological treatment or medication was administered to any subjects. All subjects were measured at pretreatment and at posttreatment on an IQ test and parent behavior rating scales for inattention, hyperactivity, and aggressive/defiant (oppositional) behaviors. At posttreatment the experimental group demonstrated a significant increase (mean of 9 points) on the K-Bit IQ Composite as compared to the control group (p <.05). The experimental group also significantly reduced inattentive behaviors as rated by parents (p < .05). The significant improvements in intellectual functioning and attentive behaviors might be explained as a result of the attentional enhancement affected by EEG biofeedback training. Further research utilizing improved data collection and analysis, more stringent control groups, and larger sample sizes are needed to support and replicate these findings.

Pain coping mechanisms in fibromyalgia: relationship to pain and functional outcomes.

OBJECTIVE: To evaluate the factor structure of the Coping Strategies Questionnaire (CSQ) in patients with fibromyalgia (FM) and to compare the factors derived from this measure, along with the active and passive pain coping scales of the Pain Management Inventory (PMI) in predicting pain, depression, quality of well being (QWB), and pain behavior concurrently and over time. METHODS: One hundred twenty-two patients with FM were recruited from medical clinics, the community, and support groups. Eligible patients completed a battery of self-report measures of pain and psychosocial functioning at baseline assessment before random assignment to a clinical trial. A subset of 69 patients who completed the clinical trial were readministered the same battery 3 mo later. Data were analyzed within the baseline period, and from the baseline period to posttreatment to evaluate the predictive effects of coping strategies on clinical outcomes. RESULTS: Principal components analysis of the CSQ revealed Coping Attempts (CA) and Pain Control and Rational Thinking (PCRT) factors, which have been found in other patient populations with chronic pain. Hierarchical multiple regression analyses revealed that high active coping and low PCRT contributed to higher concurrent pain, while low active coping and high passive coping were related to greater concurrent depression and pain behavior, respectively. Controlling for baseline scores on criterion measures, longitudinal multiple regression analyses demonstrated that high active coping and low PCRT scores contributed to greater pain, greater depression, and lower QWB at posttreatment, while low PCRT alone predicted greater pain behavior. CONCLUSION: The results show the import of the pain coping construct in FM and highlight the negative contribution of low perceived control over pain and high active coping to a range of pain outcomes. The findings on low perceived control converge with data on other chronic pain populations, while the role of active coping appears to be detrimental in FM, in contrast to its positive effects in patients with rheumatoid arthritis.

The contribution of family cohesion and the pain-coping process to depressive symptoms in fibromyalgia.

This research evaluated a model for examining the role of family cohesion and the pain-coping process in predicting depressive symptoms in fibromyalgia, a chronic pain disorder of unknown etiology. Depressive symptoms were highly prevalent in this patient group. Fifty-nine percent of the sample met or exceeded the cutoff score of 16 for depression on the Center for Epidemiological Studies Depression Scale (CES-D), while slightly greater than 50% exceeded the cutoff score of 19, a figure that is suggested for evaluating depression in chronic pain populations. Multiple regression analyses, controlling for demographic factors and medication use, revealed that low family cohesion (either reported by the patient or the patient's spouse), high pain, high helplessness, and high passive coping contributed independently to greater CES-D scores. Pain also was related to higher depression scores indirectly through its association with greater helplessness and passive coping. In contrast, no indirect effects of family cohesion were found on depressive symptoms through pain, helplessness, and passive coping. Structural equation modeling procedures provided confirmatory evidence of the significance of these relationships, indicating a high degree of goodness-of-fit with the model examined. The data illustrate the import of a multidimensionalframeworkfor conceptualizing physical, psychological, and social determinants of depressive disturbance in fibromyalgia.

Multiaxial taxonomy of fibromyalgia syndrome patients.

Pain, disability, and depression are present in various degrees in patients with fibromyalgia syndrome. Cluster analysis was used in this research to ascertain the existence of subgroups of patients in a fibromyalgia sample based on these variables. Two clusters were defined: one characterized by high levels of pain, disability, and depression (n=51) and another characterized by low levels of pain, disability, and depression (n=67). Multivariate analysis of variance (MANOVA) confirmed differences between clusters on these health status factors and a second MANOVA revealed that the subgroup with a poorer health status reported greater passive coping, helplessness, and stress, and less satisfaction with social support, than the subgroup with better health status. Logistic regression indicated that the best discriminator of subgroup membership was helplessness. These results suggest that different approaches to patient management, particularly intervention strategies aimed at reducing helplessness, may be beneficial for patients with high levels of pain, disability, and depression.

The role of helplessness in the response to disease modifying drugs in rheumatoid arthritis.

Fifty patients with rheumatoid arthritis participated in an assessment of their helplessness before and after a 3-month disease modifying drug trial. A multidimensional approach measuring helplessness was used, assessing cognitive, affective, and behavioral components. Both before and after the drug trial, helplessness indices accounted for a highly significant amount of variation in self-reported pain and functional disability. Moreover, Time 1 helplessness predicted greater flare activity after the drug trial. Helplessness indices, however, did not correlate with joint examination measures within time periods, nor did they predict change in these measures over the drug trial. The importance of the role of helplessness in subjective and objective measures of clinical status in persons undergoing drug therapy is discussed.