The effects of interior design on wellness – eye tracking analysis in determining emotional experience of architectural space. A survey on a group of volunteers from the Lublin region, Eastern Poland

Introduction and objective. Using the concepts of Ulrich’s theory of supportive design and Malkin’s healing environment, an eye tracking experiment was designed in order to measure respondents’ reactions while looking at visualisations of various interiors, with the aim of verifying whether certain parameters of an interior are related to emotional reactions in terms of positive stimulation, and the sense of security and comfort. Materials and method. 12 boards were designed, incorporating standard features of an interior, i.e. (1) proportions, (2) lighting, (3) colour scheme of a room, as well as (4) the colours and spatial arrangement of furnishings. Respondents’ reactions were recorded with an eye tracker Tobii TX300 and supplemented by self-descriptions of emotional reactions. Results. The results showed that the varying spatial and colour arrangements presented in the interior visualisations provoked different emotional responses, confirmed by pupil reaction parameters, as measured by the eye tracking device. Conclusions. Architectural space can have a diverse emotional significance and impact on an individual’s emotional state. This is an important conclusion from the point of view of optimising and creating the so-called supportive and healing environment. The results have implications for the interpretation of the pupil diameter as an index of emotional reactions to different architectural space visualisations. Testing the eye tracker as a method helpful in diagnosing the emotional reactions to features of the interior is justified, and can provide an effective tool for early diagnosis of the impact of architectural space on the well-being of individuals. It can also be a good form of testing the emotional significance of architectural designs before they are implemented

Different expression of CD180, CD284 and CD14 receptors on the CD19+ subpopulation of normal and B-CLL lymphocytes.

Numerous experimental data indicate that B-CLL development and progression are influenced by antigenic pressure. It can not be excluded that these antigens may originate from bacteria and viruses. Toll like receptors (TLRs) interact with pathogen associated molecular patterns as part of innate immunity. TLRs are currently used to target different subclasses of B-cell leukemia, and TLR agonists are being evaluated in clinical trials. It is little known regarding the repertoire and function of TLR in B-CLL. The aim of the study was to assess the CD180, CD284 and mCD14 levels in CD19+ subpopulation of B-CLL peripheral blood lymphocytes and compare them with respective levels in the normal B-cells of adult volunteers, before and after LPS stimulation. We investigated the percentage of the CD19+CD180+, CD19+CD284+, CD19+CD14+ cells and the mean fluorescence intensity (MFI) of CD180, CD284 and CD14 antigens among CD19+ B-CLL as well as in the normal B cells for comparison. MFI analysis revealed that CD180, CD284 and CD14 expression was higher on normal B cells then on CD19+ B-CLL (MFI CD180: 99.16 vs. 25.3, MFI CD284: 7.37 vs. 5.79 and MFI CD14 25.07 vs. 8.32). After 24-hour LPS activation of B-cells, CD180 MFI appeared to decrease, in both healthy and B-CLL patients. CD284 MFI in healthy controls decreased after LPS stimulation while slight increase of MFI was observed in leukemic cells. CD14 MFI in leukemic cells was moderately higher after LPS in comparison to CD14 MFI without LPS stimulation, whereas CD14 MFI in normal CD19+ cells after LPS stimulation decreased over three times. Variations observed in expression of both normal and leukemic receptors may be due to their different sensitivity to antigenic stimulation

The KMO allele encoding Arg452 is associated with psychotic features in bipolar disorder type 1, and with increased CSF KYNA level and reduced KMO expression

The kynurenine pathway metabolite kynurenic acid (KYNA), modulating glutamatergic and cholinergic neurotransmission, is increased in cerebrospinal fluid (CSF) of patients with schizophrenia or bipolar disorder type 1 with psychotic features. KYNA production is critically dependent on kynurenine 3-monooxygenase (KMO). KMO mRNA levels and activity in prefrontal cortex (PFC) are reduced in schizophrenia. We hypothesized that KMO expression in PFC would be reduced in bipolar disorder with psychotic features and that a functional genetic variant of KMO would associate with this disease, CSF KYNA level and KMO expression. KMO mRNA levels were reduced in PFC of bipolar disorder patients with lifetime psychotic features (P=0.005, n=19) or schizophrenia (P=0.02, n=36) compared with nonpsychotic patients and controls. KMO genetic association to psychotic features in bipolar disorder type 1 was studied in 493 patients and 1044 controls from Sweden. The KMO Arg(452) allele was associated with psychotic features during manic episodes (P=0.003). KMO Arg(452) was studied for association to CSF KYNA levels in an independent sample of 55 Swedish patients, and to KMO expression in 717 lymphoblastoid cell lines and 138 hippocampal biopsies. KMO Arg(452) associated with increased levels of CSF KYNA (P=0.03) and reduced lymphoblastoid and hippocampal KMO expression (P0.05). Thus, findings from five independent cohorts suggest that genetic variation in KMO influences the risk for psychotic features in mania of bipolar disorder patients. This provides a possible mechanism for the previous findings of elevated CSF KYNA levels in those bipolar patients with lifetime psychotic features and positive association between KYNA levels and number of manic episodes.Molecular Psychiatry advance online publication, 5 March 2013; doi:10.1038/mp.2013.11

Quinolinate and related excitotoxins: mechanisms of neurotoxicity and disease relevance

There are many ways in which neuronal damage can be produced in the brain, including the overactivation of depolarizing receptors, exposure to high levels of pro-inflammatory proteins such as cytokines, or miscellaneous toxins, but the kynurenine pathway has emerged as a novel but potentially major factor in regulating neuronal viability or death. It is the major route for the metabolism of the essential amino acid tryptophan, which is oxidized by indoleamine-2,3-dioxygenase (IDO) to a series of compounds which can activate, block, or modulate conventional neurotransmitter receptors. Quinolinic acid is an agonist at N-methyl-d-aspartate receptors, kynurenic acid is an antagonist at these and other glutamate receptors, and other kynurenine metabolites are highly redox-active. Superimposed on the discovery of this neuromodulatory pathway have been observations that activity in the pathway is linked to neurological and psychiatric disorders, correlating with disease state (as in Huntington’s disease) or cognitive function (as following bypass surgery). Together, the data accumulated to date make a strong case for this hitherto obscure pathway being a major factor in determining cell damage, death, or recovery in health and disease