Anorexia nervosa and body dysmorphic disorder: A comparison of body image concerns and explicit and implicit attractiveness beliefs.

Although body image is central to the etiological models of anorexia nervosa and body dysmorphic disorder, studies comparing body image and beliefs about attractiveness between the disorders are rare. Sixty-nine individuals (anorexia nervosa: n=24, body dysmorphic disorder: n=23, healthy controls: n=22) completed self-report measures (body image and general psychopathology), diagnostic interviews, and Go/No-Go Association tasks measuring implicit associations. Compared to controls, both clinical groups exhibited greater negative body image, a more negative attitude toward their physical selves, and more dysfunctional coping strategies (ps<.001). Also, both clinical groups shared greater explicit beliefs about the importance of attractiveness (ps<.001). In addition to supporting previous research with regard to comparable body image disturbance, this study also showed that beliefs regarding the importance of appearance (e.g., "one must be attractive to be successful") might be a fruitful target for therapy across both disorders.

Burn-injured adults with long term functional impairments demonstrate the same response to resistance training as uninjured controls.

OBJECTIVE: The catabolic response associated with major burn injuries results in loss of lean body mass (LBM) and prolonged muscle weakness. Exercise training improves LBM and muscle strength in burn-injured children in the acute post injury phase, yet it is unknown whether adults will experience the same benefits when exercise training is implemented at least two years post injury. PROCEDURES: Nine burn-injured participants (%TBSA=42±18.38; time since injury=6.56±3.68 years) and 9 matched controls participated in a 12-week interval training and resistance exercise programme. Muscle strength was assessed via isokinetic dynamometry and LBM was determined via dual energy X-ray absorptiometry. Both measures were administered prior to and following the exercise programme. RESULTS: There was no significant difference in LBM or strength between the two groups at baseline. Following the exercise programme, both groups displayed significant improvements in LBM and in hip, shoulder and elbow muscle strength. There was no significant difference in muscle strength or LBM, between the groups, following the exercise training. CONCLUSION: A combined exercise training programme was able to improve muscle strength and lean body mass in adults with burn injury. There was no difference between the two groups in their response to the exercise programme, therefore general exercise prescription principles may be applied directly to the burns population.

Exercise training to improve health related quality of life in long term survivors of major burn injury: a matched controlled study.

OBJECTIVE: Patients often experience reduced health-related quality of life (HRQOL) following burn injury. Exercise training has been demonstrated to improve HRQOL in a number of clinical populations, yet it is unknown whether exercise can improve HRQOL in burns patients. PROCEDURES: Nine burn-injured participants (42±18.38%TBSA: 6.56±3.68 years after injury) and 9 matched controls participated in a 12-week exercise programme. HRQOL was assessed via the Burn Specific Health Scale-Brief (BSHS-B) and the Medical Outcomes Study 36-Item Short Form (SF-36). Activity limitation was measured using the quick Disabilities of the Arm, Shoulder and Hand (QuickDASH). RESULTS: The burns group had decreased HRQOL compared to the controls at baseline, as reported by the BSHS-B (t (16)=3.51, p=0.003) and some domains of the SF-36 including role physical (t (16)=3.79, p=0.002). Burned participants reported decreased activity levels compared to the controls as measured by the QuickDASH (t (16)=2.19, p=0.044). Exercise training improved SF-36 scores in both burn (t (8)=3.77, p=0.005) and control groups (t (8)=2.71, p=0.027). Following training there was no difference between the groups on the SF-36 or QuickDASH. CONCLUSION: Exercise training improves HRQOL and activity limitations in burn-injured patients to a level that is equivalent to that of their uninjured counterparts.

The effect of exercise training on pulmonary function and aerobic capacity in adults with burn.

PURPOSE: Pulmonary function (PF) is compromised in some individuals following burn, which may result in impaired aerobic capacity. Exercise training improves PF and exercise capacity in children recovering from burns, yet it is unknown if adults will demonstrate the same response. PROCEDURES: 9 burn injured participants (%TBSA 42 ±18.38, 6.56 years ±3.68 post injury) and 9 matched controls participated in a 12-week goal directed interval training and resistance exercise programme. PF was measured using spirometry, and a graded exercise test quantified peak oxygen consumption (Vo(2peak)), both prior to and following the exercise training. The Canadian Occupational Performance Measure assessed the participant's goal attainment. RESULTS: Burn injured participants had significantly lower PF (FEV(1)/FVC ratio) than the healthy controls both prior to and following the exercise intervention (F(1,16)=8.93, p=0.009). Exercise training did not improve PF in either group, however both groups had a significant improvement in their Vo(2peak), maximal minute ventilation, and work achieved on a graded exercise test (F(1,16)=19.325, p<0.001), (F(1,16)=51.417, p<0.001) and (F(1,16)=36.938, p<0.001), respectively, following the exercise training. All participants achieved their occupational performance goals. CONCLUSION: Although the exercise training did not alter PF, both aerobic capacity and occupational performance were improved.

Demonstration of the use of the ICF framework in detailing complex functional deficits after major burn.

Burns can result in long term impairments, activity limitations and participation restrictions in a patients' life. The focus of current surgeries and therapy is to improve body functions and structures. However, often this does not translate to an improvement in activity and participation for the patient. Improvement in activity and participation is the ultimate goal of all therapy to enhance patient's quality of life. The incorporation of assessment measures at all levels of the International Classification of Functioning, Disability and Health (ICF) can assist in a holistic, patient centred approach to identify the complex impairments that impact on activity and participation, with a view to appropriately targeting future therapeutic interventions. This paper presents an example case of how implementing measures at all levels of the ICF can improve our understanding of a patient's body functions and structures, activity and participation. A number of the outcome measures utilised in this study are novel in the burns population, such that video footage supplements the methodology where relevant.

Pulmonary function, exercise capacity and physical activity participation in adults following burn.

PURPOSE: To determine the relationship between pulmonary function, aerobic exercise capacity and physical activity participation in adults following burn. METHODS: Eight burn injured males aged 20-55 years (%TBSA 33.3±18.7, 5.1 years±1.8 post injury), and 30 healthy adult controls participated. Pulmonary function was assessed during rest via spirometry. A graded exercise test measuring peak oxygen consumption (VO(2peak)) and oxygen saturation (S(p)O(2)) was conducted, and physical activity was assessed via the Older Adult Exercise Status Inventory (OA-EI). RESULTS: No significant correlation was observed between resting pulmonary function, aerobic capacity and physical activity participation for burn injured patients or controls. Two burn injured patients presented with obstructive ventilatory defects, and one displayed a restrictive ventilatory defect. Burn injured patients had a significantly lower VO(2peak) (p<0.001) and time to fatigue (p=0.026), and a greater degree of oxygen desaturation (p=0.063, Effect Size=1.02) during a graded exercise test. Burn injured patients reported significantly less participation in leisure-related activity>9 METs (p=0.01), and significantly greater participation in work-related activity (p=0.038), than healthy controls. CONCLUSION: Compromised lung function, decreased aerobic capacity and reduced participation in leisure-related physical activity may still exist in some adults, even up to 5 years post injury. Limitations and long term outcomes of cardiopulmonary function and physical fitness need to be considered in the prescription of exercise rehabilitation programmes following burn.

The surface finite element method for pattern formation on evolving biological surfaces.

In this article we propose models and a numerical method for pattern formation on evolving curved surfaces. We formulate reaction-diffusion equations on evolving surfaces using the material transport formula, surface gradients and diffusive conservation laws. The evolution of the surface is defined by a material surface velocity. The numerical method is based on the evolving surface finite element method. The key idea is based on the approximation of Γ by a triangulated surface Γ(h) consisting of a union of triangles with vertices on Γ. A finite element space of functions is then defined by taking the continuous functions on Γ(h) which are linear affine on each simplex of the polygonal surface. To demonstrate the capability, flexibility, versatility and generality of our methodology we present results for uniform isotropic growth as well as anisotropic growth of the evolution surfaces and growth coupled to the solution of the reaction-diffusion system. The surface finite element method provides a robust numerical method for solving partial differential systems on continuously evolving domains and surfaces with numerous applications in developmental biology, tumour growth and cell movement and deformation.

Organic homojunction diodes with a high built-in potential: interpretation of the current-voltage characteristics by a generalized Einstein relation.

We realize p- and n-type doping of the organic semiconductor zinc-phthalocyanine using a novel strong organic donor. This allows us to demonstrate the first stable and reproducible organic p-n homojunctions. The diodes show very high built-in potentials, attractive, e.g., for organic solar cells. However, the diode characteristics cannot be described by the standard Shockley theory of the p-n junction since the ideality factor strongly increases with decreasing temperature. We show that this behavior can be explained by deviations from the Einstein relation for disordered materials.

Interaction of I(-) and I(3)(-) with a redox-stable Cr(III)-based structural surrogate for photo-oxidized "N3 Dye".

A series of [Cr (L)(2)(NCS)(2)]X complexes, where L = 2,2'-bipyridine (bpy) or 4,4'-dimethyl-2,2'-bipyridine (dmb) and X(-) is I(-), I(3)(-), or NO(3)(-), have been prepared for study as redox-inactive surrogates for diisothiocyanatobis(2,2'-bipyridine-4,4'-dicarboxylic acid)ruthenium(III) ("N3(+)"). Dilute solution spectra in dichloromethane or acetonitrile of the I(-) and NO(3)(-) salts are the same, but the I(-) salts show clear evidence of a charge-transfer interaction between the cation and anion in the solid state and in concentrated I(-) solutions in acetonitrile. X-ray structural determination of the dmb complex shows that this interaction is between the I(-) and one of the dmb ligands. X-ray structural determination of the bpy complex as the I(3)(-) salt indicates a similar interaction between one of the bpy ligands and one of the terminal iodine atoms of the anion. These results have potential implications in the reduction mechanism of photo-oxidized N3 dye used as a sensitizer in nanocrystalline TiO(2)-based photogalvanic cells.

Tervalent conducting polymers with tailor-made work functions: preparation, characterization, and applications as cathodes in electroluminescent devices.

A series of conducting polymers have been prepared through thermal polymerization of transition-metal diimine complexes. The as-polymerized material is electrochemically converted into its formally zerovalent form. Due to the proximity of the half-wave potentials of the formal 1+/0 and 0/1- couples, there is substantial disproportionation of the redox sites at room temperature, resulting in a conductive tervalent mixed-valent material. The redox processes that give rise to this mixed-valent material are predominantly ligand-based, and therefore are highly sensitive to substitution on the ligand periphery. Solution redox chemistry of the monomer can be used to accurately predict the work function of the corresponding zerovalent conducting polymer, which has been verified by ultraviolet photoelectron spectroscopy. Many of these materials have especially low work functions (<3.6 eV) making them appropriate materials to use as cathode materials in organic light-emitting devices (OLEDs). Working examples of tris(8-hydroxyquinoline)aluminum(III)-based OLEDs have been fabricated using one of these polymers as a cathode.

Ca2+/calmodulin-dependent protein kinase II regulates Tiam1 by reversible protein phosphorylation.

A number of guanine nucleotide exchange factors have been identified that activate Rho family GTPases, by promoting the binding of GTP to these proteins. We have recently demonstrated that lysophosphatidic acid and several other agonists stimulate phosphorylation of the Rac1-specific exchange factor Tiam1 in Swiss 3T3 fibroblasts, and that protein kinase C is involved in Tiam1 phosphorylation (Fleming, I. N., Elliott, C. M., Collard, J. G., and Exton, J. H. (1997) J. Biol. Chem. 272, 33105-33110). We now show, through manipulation of intracellular [Ca2+] and the use of protein kinase inhibitors, that both protein kinase Calpha and Ca2+/calmodulin-dependent protein kinase II are involved in the phosphorylation of Tiam1 in vivo. Furthermore, we show that Ca2+/calmodulin-dependent protein kinase II phosphorylates Tiam1 in vitro, producing an electrophoretic retardation on SDS-polyacrylamide gel electrophoresis. Significantly, phosphorylation of Tiam1 by Ca2+/calmodulin-dependent protein kinase II, but not by protein kinase C, enhanced its nucleotide exchange activity toward Rac1, by approximately 2-fold. Furthermore, Tiam1 was preferentially dephosphorylated by protein phosphatase 1 in vitro, and treatment with this phosphatase abolished the Ca2+/calmodulin-dependent protein kinase II activation of Tiam1. These data demonstrate that protein kinase Calpha and Ca2+/calmodulin-dependent protein kinase II phosphorylate Tiam1 in vivo, and that the latter kinase plays a key role in regulating the activity of this exchange factor in vitro.

Quantitative in Situ Measurement of Ion Transport in Polypyrrole/Poly(styrenesulfonate) Films Using Rotating Ring-Disk Voltammetry.

An approach based on rotating ring-disk electrode (RRDE) voltammetry is described for the quantitative, in situ measurement of ion transport between solution and conducting polymer films. The specific composite film studied in this report is polypyrrole/poly(styrenesulfonate) (pPy(+)/pSS(-)). Cation flux in and out of the polymer was obtained from the mass-transport-limited reduction current for the dopant cation(s) measured at the ring during redox cycling of the polymer. Crucial to this method is the use of a supporting electrolyte that is sterically inhibited from passing into the film and the use of dopant ions that adhere to specific electrochemical constraints. With this method it was possible to quantitatively account for all changes in charge compensation in the film by the specific cation(s) involved. Three different cations were explored alone and in paired combinations. Solutions containing mixtures of dopant cations were studied to determine whether the pPy(+)/pSS(-) films exhibit preferential doping. Kinetic factors, likely due to steric differences in the dopant cations, were found to lead to significant preferential doping of the polymer.

Introduction.

PIP: Insights on many important issues related to women's status in India are provided in the narratives written for a workshop on women's lives. Writers were asked to reflect on the lives of their mothers and their grandmothers in relation to their own life. The stories were varied in many ways. It may be a tale of how the author established her own personhood, or a tale of the role of renegade predecessors in the family who set out a pattern of independence, or are stories of strength, of personal growth, of obstacles overcome. Ultimately, almost all these stories tell of women being diminished because of their gender. In reading the eight narratives the collection contains, it can be learned that women's vulnerability to the purposes, tempers and fates of their husbands and families, both natal and affinal, stands out. Without social and economic capacities, to support themselves, even the most determined could only seek to influence the opinion of others. Finally, perhaps stories like these could inspire women to survive, to defend themselves, and to create lives for themselves, their families, and women who follow them.^ieng

Phospholipase C-gamma, protein kinase C and Ca2+/calmodulin-dependent protein kinase II are involved in platelet-derived growth factor-induced phosphorylation of Tiam1.

In Swiss 3T3 fibroblasts, the Rac1-specific guanine nucleotide exchange factor Tiam1 is phosphorylated by several different agonists. We show here that PDGF induces threonine phosphorylation of Tiam1 in a time- and dose-dependent manner. Tiam1 phosphorylation was significantly reduced by the selective protein kinase C inhibitor Ro-31-8220 and by KN93, an inhibitor of Ca2+/calmodulin-dependent protein kinase II. The Ca2+ chelator BAPTA/AM totally abrogated Tiam1 phosphorylation, indicating that Ca2+ is essential for this phosphorylation. Moreover, PDGF-stimulated Tiam1 phosphorylation was markedly reduced by 72 +/- 10% in PLC-gamma1 deficient mouse fibroblasts, compared to wild-type cells, indicating that phosphoinositide phospholipase C is involved.

Lysophosphatidic acid induces threonine phosphorylation of Tiam1 in Swiss 3T3 fibroblasts via activation of protein kinase C.

The Rho family of GTPases plays an important role in the control of cell shape, adhesion, movement, and growth. Several guanine nucleotide exchange factors have been identified that activate Rho family GTPases by promoting the binding of GTP to these proteins. However, little is known concerning the regulation of these GDP/GTP exchange factors. In this study, we demonstrate that lysophosphatidic acid (LPA) induces a rapid, sustainable phosphorylation of the Rac1-specific nucleotide exchange factor Tiam1 in Swiss 3T3 fibroblasts. LPA stimulated Tiam1 phosphorylation in a dose-dependent manner, and the protein was phosphorylated on threonine, but not tyrosine or serine. Tiam1 phosphorylation was also induced by platelet-derived growth factor, endothelin-1, bombesin, and bradykinin but not by epidermal growth factor. Significantly, pretreatment of Swiss 3T3 fibroblasts with 1 microM phorbol 12-myristate 13-acetate for 24 h, or with the selective protein kinase C inhibitor Ro-31-8220, reduced LPA-stimulated phosphorylation of Tiam1 by approximately 75%. Moreover, acute stimulation with 100 nM phorbol 12-myristate 13-acetate was sufficient to induce Tiam1 phosphorylation in vivo, and protein kinase C could phosphorylate purified Tiam1 on threonine residues in vitro. These data indicate that agonist-induced phosphorylation of Tiam1 is a general mechanism and suggest that it is likely to be important in its regulation. Protein kinase C appears to play a key role in phosphorylation of Tiam1.

Differential translocation of rho family GTPases by lysophosphatidic acid, endothelin-1, and platelet-derived growth factor.

The small GTPases of the Rho family play a key role in a number of signaling pathways activated by lysophosphatidic acid (LPA). However, little is known concerning the mechanism of regulation of these proteins. In this study we demonstrate that in Swiss 3T3 fibroblasts, LPA induces a sustained, time-dependent relocalization of RhoA to the Triton X-100-soluble low speed membrane fraction, which can be reversed by removal of LPA from the medium. Translocation was only observed with micromolar concentrations of LPA and was inhibited by pretreating the cells with pertussis toxin but not with tyrosine kinase inhibitors. LPA also induced translocation of CDC42Hs to the membranes but had no effect on the distribution of Rac1, RhoB, or Rho-GDI. Translocation of RhoA was also induced by endothelin-1. Conversely, platelet-derived growth factor did not cause the translocation of RhoA to any membrane fraction but stimulated relocalization of Rac1 to the high speed membrane fraction. Significantly, incubation of cell lysates with guanosine 5'-O-(thiotriphosphate) was sufficient to translocate RhoA, Rac1, and CDC42Hs from the cytosol to the membranes, whereas incubation with GDP had the opposite effect. These data suggest that the translocation of the Rho family proteins to the membrane fraction is controlled by their activation state and that agonists show selectivity in inducing the activation/translocation of these proteins.

Enhanced phospholipase D activity and altered morphology in RhoA-overexpressing RAT1 fibroblasts.

Small GTP-binding proteins of the Rho family are implicated in the regulation of phospholipase D (PLD). However, few studies have addressed their role in agonist-stimulated PLD activity in vivo. Stable lines of Rat1 fibroblasts overexpressing RhoA were shown to have altered morphology. Moreover, they demonstrated increased PLD activity when stimulated with lysophosphatidic acid, platelet-derived growth factor, and phorbol ester, compared with vector-transfected cells. However, phosphoinositide phospholipase C activity was unaltered by overexpression of RhoA. These data indicate a critical downstream role for RhoA in agonist-stimulated PLD activity in intact cells.

Evidence for Rho-mediated agonist stimulation of phospholipase D in rat1 fibroblasts. Effects of Clostridium botulinum C3 exoenzyme.

Small GTP-binding proteins of the Rho family are implicated in the in vitro regulation of phosphatidylcholine hydrolysis by phospholipase D (PLD). However, their role in agonist-stimulated PLD activity in whole cells is not clear. The ribosyltransferase C3 from Clostridium botulinum modifies Rho proteins and inhibits their function. When introduced into rat1 fibroblasts by scrape-loading, C3 inhibited PLD activity stimulated by lysophosphatidic acid (LPA), endothelin-1, or phorbol ester. Neither the time course nor agonist dose response for LPA-stimulated PLD activity was altered in C3-treated cells. In contrast to the effects of C3 on PLD activity, agonist-stimulated phosphatidylinositol-phospholipase C activity was not altered in C3-treated cells. Surprisingly, C3 treatment led to a decrease in the amount of RhoA protein, indicating that the loss of PLD activity in response to agonist was partly due to the loss of Rho proteins. As described previously, C3 treatment led to the inhibition of LPA-stimulated actin filament formation. However, disruption of actin filaments with cytochalasin D caused only a minor inhibition of LPA-stimulated PLD activity. Interestingly, stimulation of cells with LPA caused a rapid enrichment of RhoA in the particulate fraction of cell lysates. These data support an in vivo role for RhoA in agonist-stimulated PLD activity that is separate from its role in actin fiber formation.

Redox dependent interactions of the metal sites in carbon monoxide-bound cytochrome c oxidase monitored by infrared and UV/visible spectroelectrochemical methods.

Spectroelectrochemical titration studies involving the binding of the infrared-active probe ligand carbon monoxide (CO) to the heme alpha 3/CuB site of bovine heart cytochrome c oxidase (CcO) have been reexamined. The spectroelectrochemical cell employed was constructed to monitor both the infrared (IR) and visible/Soret spectra of the CcO-CO complex as a function of the overall oxidation state of the enzyme. A number of commonly used electron transfer mediators were employed to shuttle electrons between the redox active sites within the enzyme and the electrode surface. The well-documented shift in the CO infrared stretch band maximum from 1963.3 cm-1 (CcO fully reduced) to 1965.5 cm-1 (CcO partially oxidized) was carefully titrated electrochemically. Deconvolution of the asymmetric CO stretches indicates the existence of two different states of CO vibrators within the enzyme, presumably due to two conformers which are present in a ratio of approximately 5:1. Upon incrementally stepping the potential from the fully reduced state to the partially oxidized state, we found it possible to follow the decrease in the intensity of the original pair of these conformers and the concomitant increase of a resultant pair while maintaining this 5:1 ratio between the conformers. By plotting the change in the deconvoluted CO peak intensities vs the redox potential, as well as the absorbance changes in the visible/Soret spectra vs the redox potential, we found not only that both fit an n = 1 electron process but also that the spectral changes tracked each other identically with experimental error. Furthermore, analysis of the second derivative of the Soret spectra allowed for the qualitative monitoring of the oxidation state of the Fe alpha site which again tracked identically to that of the CO shift in the IR region. These results would seem to confirm earlier suggestions that perturbing the oxidation state of Fe alpha causes a conformational change in the enzyme which affects the binding site for CO, namely heme alpha 3. As a consequence of the CO IR stretching frequencies changing by only 2 cm-1 during this redox titration, with no accompanying changes in half band width, we suggest that it is impossible that this small but significant change seen in the CO stretching frequencies could be due to an oxidation state change in CuB, given the known sensitivity of the CO stretching frequency to perturbations and the close proximity of Cu(B) to the CO binding site at heme alpha 3 (4.5 A). Therefore, it would appear that Cu(B) must remain reduced as long as CO is bound to the heme alpha 3 site. This is consistent with earlier proposals that Fe alpha 3 and Cu(B) are acting together as a two-electron donor to dioxygen.