Inpatient rehabilitation diabetes consult service: A rehabilitation psychology approach to assessment and intervention.

Problem: Diabetes clinical practice recommendations call for assessment and intervention on diabetes self-management during inpatient hospitalization. Although diabetes is prevalent in inpatient rehabilitation settings, diabetes self-management has not traditionally been a focus of inpatient rehabilitation psychology care. This is because diabetes is often a secondary diagnosis when an individual is admitted to rehabilitation for an acute event. Objectives: The authors provide a rationale for a role for rehabilitation psychologists in assessing and intervening on the psychosocial, behavioral, and functional self-management needs of individuals with diabetes within the rehabilitation setting. The development of a rehabilitation psychology Inpatient Rehabilitation Diabetes Consultation Service is described. Theoretical and empirical bases for compilation of the assessment and intervention materials are provided. Format and implementation of the service on a university-affiliated inpatient rehabilitation unit is described, with special consideration given to professional issues faced by rehabilitation psychologists and teams. Results: A flexible consultation model was implemented using a guided diabetes psychosocial assessment with brief educational handouts addressing selected key topics (i.e., hyperglycemia, hypoglycemia, blood sugar monitoring, nutrition, physical activity, medication, and, A1C and average blood sugar). The consultation service was feasible and well-accepted by treated individuals and the rehabilitation team. Conclusions: Rehabilitation psychologists are uniquely positioned to address the functional, psychosocial, and behavioral needs of individuals with diabetes. With further research to assess clinical outcomes, this approach may further address practice recommendations for inpatient diabetes care. Moreover, such a diabetes consultation model may be useful on an outpatient rehabilitation basis as well. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Structure and surface morphology of Mn-implanted TiO2

A study of structure and surface morphology together with magnetic properties of Mn-implanted rutile-type TiO₂ single crystals is performed. Homogenous thin films of about 100 nm with different Mn_xTi_1 − xO₂ (x = 0.03; 0.05 and 0.07) chemical formula were obtained. The Mn ion implanted surface exhibited a dense microstructure with a nano grain size. The dependence of c/a axial ratio on manganese content suggests that Mn³⁺ species substituted tetragonal Ti⁴⁺. The annealing at 873 K caused changes in surface structure, morphology and roughness. A migration of manganese ions into the rutile single crystal takes place and in certain conditions Ti₂O phase occurs. Mn-implanted samples exhibit room temperature ferromagnetism and a Curie temperature of 680 K. Electron spin resonance analysis evidenced that manganese is incorporated by substitution as magnetically isolated Mn⁴⁺, Mn³⁺ and Mn²⁺ species. At 0.07% contents the Mn³⁺ species may enter in interstitial sites contributing to extinction of substitutional magnetic moment.     

Characterization of viscoelastic properties of molybdenum disulphide filled polyamide by indentation

In this paper, the creep behavior of molybdenum disulphide (MoS₂) filled polyamide 66 composite was investigated through sharp indentation at room temperature. Two types of indentation creep test, the 3-step indentation test, and the 5-step indentation test were considered in order to explore whether the measured creep response is mainly viscoelastic or includes a significant contribution from the plastic deformation developed during the loading phase. The experimental indentation creep data were analyzed within an analytical framework based on the hereditary integral operator for the ramp creep and a viscoelastic–plastic (VEP) model in order to determine the indentation creep compliance function including the short- and long-time modulus. The equivalent shear modulus calculated from the creep compliance function was compared to the indentation plane strain modulus derived from the initial slope of the unloading curve in order to investigate the validity of the Oliver and Pharr method.     

The Footprint of Kynurenine Pathway in Neurodegeneration: Janus-Faced Role in Parkinson’s Disorder and Therapeutic Implications

Progressive degeneration of neurons and aggravation of dopaminergic neurons in the substantia nigra pars compacta results in the loss of dopamine in the brain of Parkinson’s disease (PD) patients. Numerous therapies, exhibiting transient efficacy have been developed; however, they are mostly accompanied by side effects and limited reliability, therefore instigating the need to develop novel optimistic treatment targets. Significant therapeutic targets have been identified, namely: chaperones, protein Abelson, glucocerebrosidase-1, calcium, neuromelanin, ubiquitin-proteasome system, neuroinflammation, mitochondrial dysfunction, and the kynurenine pathway (KP). The role of KP and its metabolites and enzymes in PD, namely quinolinic acid (QUIN), kynurenic acid (KYNA), 3-hydroxykynurenine (3-HK), 3-hydroxyanthranillic acid (3-HAA), kunurenine-3-monooxygenase (KMO), etc. has been reported. The neurotoxic QUIN, N-methyl-D-aspartate (NMDA) receptor agonist, and neuroprotective KYNA—which antagonizes QUIN actions—primarily justify the Janus-faced role of KP in PD. Moreover, KP has been reported to play a biomarker role in PD detection. Therefore, the authors detail the neurotoxic, neuroprotective, and immunomodulatory neuroactive components, alongside the upstream and downstream metabolic pathways of KP, forming a basis for a therapeutic paradigm of the disease while recognizing KP as a potential biomarker in PD, thus facilitating the development of a suitable target in PD management.     

Generation of an Immortalized Human Adipose-Derived Mesenchymal Stromal Cell Line Suitable for Wound Healing Therapy

Adipose-derived mesenchymal stromal cells (ADSC) are a promising source for cellular therapy of chronic wounds. However, the limited life span during in vitro expansion impedes their extensive use in clinical applications and basic research. We hypothesize that by introduction of an ectopic expression of telomerase into ADSC, the cells’ lifespans could be significantly extended. To test this hypothesis, we aimed at engineering an immortalized human ADSC line using a lentiviral transduction with human telomerase (hTERT). ADSC were transduced with a third-generation lentiviral system and a hTERT codifying plasmid (pLV-hTERT-IRES-hygro). A population characterized by increased hTERT expression, extensive proliferative potential and remarkable (potent) multilineage differentiation capacity was selected. The properties for wound healing of this immortalized ADSC line were assessed after 17 passages. Their secretome induced the proliferation and migration of keratinocytes, dermal fibroblasts, and endothelial cells similarly to untransduced ADSC. Moreover, they sustained the complete re-epithelialization of a full thickness wound performed on a skin organotypic model. In summary, the engineered immortalized ADSC maintain the beneficial properties of parent cells and could represent a valuable and suitable tool for wound healing in particular, and for skin regenerative therapy in general.     

Chronic Trazodone and Citalopram Treatments Increase Trophic Factor and Circadian Rhythm Gene Expression in Rat Brain Regions Relevant for Antidepressant Efficacy

Trazodone is an efficacious atypical antidepressant acting both as an SSRI and a 5HT2A and 5HT2C antagonist. Antagonism to H1-histaminergic and alpha1-adrenergic receptors is responsible for a sleep-promoting action. We studied long-term gene expression modulations induced by chronic trazodone to investigate the molecular underpinning of trazodone efficacy. Rats received acute or chronic treatment with trazodone or citalopram. mRNA expression of growth factor and circadian rhythm genes was evaluated by qPCR in the prefrontal cortex (PFCx), hippocampus, Nucleus Accumbens (NAc), amygdala, and hypothalamus. CREB levels and phosphorylation state were evaluated using Western blotting. BDNF levels were significantly increased in PFCx and hippocampus by trazodone and in the NAc and hypothalamus by citalopram. Likewise, TrkB receptor levels augmented in the PFCx after trazodone and in the amygdala after citalopram. FGF-2 and FGFR2 levels were higher after trazodone in the PFCx. The CREB phosphorylation state was increased by chronic trazodone in the PFCx, hippocampus, and hypothalamus. Bmal1 and Per1 were increased by both antidepressants after acute and chronic treatments, while Per2 levels were specifically augmented by chronic trazodone in the PFCx and NAc, and by citalopram in the PFCx, amygdala, and NAc. These findings show that trazodone affects the expression of neurotrophic factors involved in antidepressant responses and alters circadian rhythm genes implicated in the pathophysiology of depression, thus shedding light on trazodone’s molecular mechanism of action.