Development of a short version of the Apathy Evaluation Scale specifically adapted for demented nursing home residents.

OBJECTIVE: Apathy is among the most frequent neuropsychiatric symptoms in dementia, particularly Alzheimer disease. The Apathy Evaluation Scale (AES) has been widely employed for assessing apathy in different patient groups. To further facilitate the usage of the AES, an abbreviated version was constructed. METHOD: On basis of a sample of 356 nursing home residents, a cross-validation procedure was carried out to develop a brief version of the AES. According to a thorough clinical examination, 85% of the residents were demented, 8% presented with mild cognitive impairment, whereas 7% did not present any cognitive deficits. After subdividing the patient group into two matched samples, the first subsample was used to identify problematic items due to defined psychometric and content-related criteria. The original 18-item scale was thus reduced to 10 items. Psychometric properties of the shortened version were subsequently reassessed in the second subsample. RESULTS: The short version demonstrated favorable psychometric properties that could be confirmed by cross-validation with the second sample. Correlations with the original full-length version were high (r = 0.97 for both subsamples); the shortened scale yielded no substantial losses regarding internal consistency or construct validity (correlations with the respective subscales of the Neuropsychiatric Inventory). CONCLUSION: The frequency of apathetic symptoms in the nursing home residents included confirms the clinical importance of apathy for understanding dementia. Given this specific patient population, setting, and mode of data collection, the short-version AES seems to be a valuable and time-efficient instrument for assessing apathy.     

The finite element model for the propagation of light in scattering media: a direct method for domains with nonscattering regions

We present a method for handling nonscattering regions within diffusing domains. The method develops from an iterative radiosity-diffusion approach using Green's functions that was computationally slow. Here we present an improved implementation using a finite element method (FEM) that is direct. The fundamental idea is to introduce extra equations into the standard diffusion FEM to represent nondiffusive light propagation across a nonscattering region. By appropriate mesh node ordering the computational time is not much greater than for diffusion alone. We compare results from this method with those from a discrete ordinate transport code, and with Monte Carlo calculations. The agreement is very good, and, in addition, our scheme allows us to easily model time-dependent and frequency domain problems.     

Delayed-type hypersensitivity reaction to paraphenylenediamine is mediated by 2 different pathways of antigen recognition by specific alphabeta human T-cell clones

BACKGROUND: Allergic contact dermatitis to paraphenylenediamine (PPD) is a frequent cause of morbidity and occupational disability. OBJECTIVE: The aim of the study was to characterize T-cell responses to PPD and Bandrowski's base (BB), an autoxidation product of PPD, by using polyclonal and monoclonal T-lymphocyte cultures. METHODS: PPD- and BB-driven proliferation of PBMCs and T-cell clones (TCCs) was assessed by means of tritiated thymidine incorporation. Surface markers were studied by means of flow cytometry, and cytokine generation was assessed with an ELISA. RESULTS: TCCs, with one exception, were CD4+/CD45RO+, and T-cell receptors were alphabeta+. Three of 6 TCCs expressed Vbeta 16. TCC stimulation was HLA-DP restricted, and TCCs secreted IL-4, IL-5, and marginal levels of IFN-gamma. TCCs reacted to both PPD and BB. Presentation of BB to TCCs was dependent on viable antigen-presenting cells (APCs) pulsed for 4 hours, and fixed APCs failed to stimulate TCCs. Moreover, polyclonal responses to BB were enhanced by metabolically active enzymes, such as cytochrome P450 enzymes. BB has to be metabolized and processed. In contrast, fixation of APCs did not impair their ability to present PPD to TCC, whereas pulsing of APCs with PPD failed to stimulate TCCs. Thus PPD had to be present during the process, and polyclonal stimulation was not enhanced by cytochromes. CONCLUSION: These results suggest that PPD itself can be recognized by T cells through a processing-independent pathway, whereas its autoxidation product, BB, required processing and possibly metabolism to stimulate the same TCC. Our data demonstrate that 2 distinct pathways of antigen presentation to activate specific TCCs are involved in the immune response to PPD.     

Cytogenetic studies in a canine mammary tumor

In a 9-year-old female dog (Basset Artesian Normand) with a mammary adenocarcinoma, cytogenetic evaluation of tumor cells showed a chromosome number of 76 in most metaphases (95%). The following abnormalities were found: symmetric metacentric chromosomes 1 and 6, centric fusion 3/38, a marker X-chromosome (Xmar) and a biarmed small marker chromosome (mar). In the remaining metaphases (5%) there were additional biarmed marker chromosomes present.     

Plasma leptin and adiposity during antipsychotic treatment of schizophrenia.

Alterations in plasma leptin have been reported in schizophrenia patients treated with antipsychotics, suggesting the hypothesis that impairments in leptin secretion or signaling might play a role in antipsychotic-induced weight gain. Plasma leptin was measured in 72 schizophrenia patients chronically treated with olanzapine (n=27), risperidone (n=24) or typical antipsychotics (n=21) and 124 healthy adult control subjects. ANCOVA was used to test effects of adiposity (body mass index kg/m2; BMI), subject group (treated patients vs untreated controls), and treatment group (specific medication groups and untreated controls) on plasma leptin concentrations. Additional analyses were performed in a subset of patients and controls individually matched for BMI to further assess group differences in plasma leptin independent of adiposity. BMI strongly predicted plasma leptin concentrations in the overall sample. In addition, a significant three-way interaction between BMI, subject group, and gender was observed. In the individually BMI-matched sample, modestly reduced plasma leptin levels (effect size 0.4 SD) were observed in treated patients in comparison to the BMI-matched healthy controls, with both groups including males and females. However, no differences in plasma leptin levels were observed in the matched sample when separately comparing male patients vs untreated male controls and female patients vs untreated female controls. Plasma leptin in chronically treated patients with schizophrenia is strongly predicted by adiposity, similar to untreated healthy individuals despite adequate power to detect a difference. The results argue against a role for defective leptin secretion or sensitivity in the weight gain induced by antipsychotic medications.