Collaborative Filtering via Implicit Culture Support

Implicit Culture is the relation existing between a set and a group of agents such that the elements of the set behave according to the culture of the group. Earlier work claimed that supporting Implicit Culture phenomena can be useful for both articial and human agents. In particula

Implicit Culture for Multi-agent Interaction Support

Implicit Culture is the relation between a set and a group of agents such that the elements of the set behave accordingly..

The relationship between demoralization and depressive symptoms among patients from the general hospital: network and exploratory graph analysis

Introduction: Depression and demoralization are highly prevalent among individuals with physical illnesses but their relationship is still unclear. Objective: To examine the relationship between clinical features of depression and demoralization with the network approach to psychopathology. Methods: Participants were recruited from the medical wards of a University Hospital in Italy. The Demoralization Scale (DS) was used to assess demoralization, while the Patient Health Questionnaire-9 (PHQ-9) to assess depressive symptoms. The structure of the depression-demoralization symptom network was examined and complemented by the analysis of topological overlap and Exploratory Graph Analysis (EGA) to identify the most relevant groupings (communities) of symptoms and their connections. The stability of network models was estimated with bootstrap procedures and results were compared with factor analysis. Results: Life feeling pointless, low mood/discouragement, hopelessness and feeling trapped were among the most central features of the network. EGA identified four communities: (1) Neurovegetative Depression, (2) Loss of purpose, (3) Frustrated Isolation and (4) Low mood and morale. Loss of purpose and low mood/morale were largely connected with other communities through anhedonia, hopelessness and items related to isolation and lack of emotional control. Results from EGA displayed good stability and were comparable to those from factor analysis. Limitations: Cross-sectional design; sample heterogeneity Conclusions: Among general hospital inpatients, features of depression and demoralization are independent, with the exception of low mood and self-reproach. The identification of symptom groupings around entrapment and helplessness may provide a basis for a dimensional characterization of depressed/demoralized patients, with possible implications for treatment

Genetic mapping in Diversity Outbred mice identifies a Trpa1 variant influencing late-phase formalin response.

Identification of genetic variants that influence susceptibility to pain is key to identifying molecular mechanisms and targets for effective and safe therapeutic alternatives to opioids. To identify genes and variants associated with persistent pain, we measured late-phase response to formalin injection in 275 male and female Diversity Outbred mice genotyped for over 70,000 single nucleotide polymorphisms. One quantitative trait locus reached genome-wide significance on chromosome 1 with a support interval of 3.1 Mb. This locus, Nociq4 (nociceptive sensitivity quantitative trait locus 4; MGI: 5661503), harbors the well-known pain gene Trpa1 (transient receptor potential cation channel, subfamily A, member 1). Trpa1 is a cation channel known to play an important role in acute and chronic pain in both humans and mice. Analysis of Diversity Outbred founder strain allele effects revealed a significant effect of the CAST/EiJ allele at Trpa1, with CAST/EiJ carrier mice showing an early, but not late, response to formalin relative to carriers of the 7 other inbred founder alleles (A/J, C57BL/6J, 129S1/SvImJ, NOD/ShiLtJ, NZO/HlLtJ, PWK/PhJ, and WSB/EiJ). We characterized possible functional consequences of sequence variants in Trpa1 by assessing channel conductance, TRPA1-TRPV1 interactions, and isoform expression. The phenotypic differences observed in CAST/EiJ relative to C57BL/6J carriers were best explained by Trpa1 isoform expression differences, implicating a splice junction variant as the causal functional variant. This study demonstrates the utility of advanced, high-precision genetic mapping populations in resolving specific molecular mechanisms of variation in pain sensitivity

Milnacipran for neuropathic pain and fibromyalgia in adults.

BACKGROUND: Milnacipran is a serotonin-norepinephrine reuptake inhibitor (SNRI) that is sometimes used to treat chronic neuropathic pain and fibromyalgia. OBJECTIVES: To evaluate the analgesic efficacy and adverse effects of milnacipran in the management of chronic neuropathic pain or fibromyalgia. SEARCH METHODS: We searched CENTRAL, MEDLINE, and EMBASE to 4th of January 2012, together with reference lists of retrieved papers and reviews. SELECTION CRITERIA: We included randomised, double-blind studies of eight weeks duration or longer, comparing milnacipran with placebo or another active treatment in chronic neuropathic pain or fibromyalgia. DATA COLLECTION AND ANALYSIS: We extracted efficacy and adverse event data, and two study authors examined issues of study quality independently. MAIN RESULTS: Five studies (4138 participants) were included, all of which were placebo-controlled, involved participants with fibromyalgia, and used titration to a target dose of 100 mg or 200 mg milnacipran. There were no other active comparators or studies in other neuropathic pain conditions. Study quality was generally good, although the imputation method used in analyses of the primary outcomes could overestimate treatment effect.Both doses of milnacipran provided moderate levels of pain relief to about 40% of those treated, compared to 30% with placebo, giving a number needed to treat of 8 to 10. Adverse events were common in both milnacipran (87%) and placebo (78%) groups, but serious adverse events (< 2%) did not differ between groups. Nausea and constipation were the most common events showing the greatest difference between groups (number needed to treat for an additional harmful outcome of 7 and 13 respectively, compared with placebo).Withdrawals for any reason were more common with milnacipran than placebo, and more common with 200 mg than 100 mg (NNH of 23 and 8.8 respectively, compared with placebo). This was largely driven by adverse event withdrawals, where the NNH compared with placebo was 14 for 100 mg, and 7.0 for 200 mg). Withdrawals due to lack of efficacy were more common with milnacipran than placebo but did not differ between doses (number needed to treat to prevent an additional unwanted outcome of 45 and 41 respectively). AUTHORS' CONCLUSIONS: The evidence available indicates that milnacipran 100 mg or 200 mg is effective for a minority in the treatment of pain due to fibromyalgia, providing moderate levels of pain relief (at least 30%) to about 40% of participants, compared with about 30% with placebo. There were insufficient data to assess substantial levels of pain relief (at least 50%), and the use of last observation carried forward imputation may overestimate drug efficacy. Milnacipran is associated with increased adverse events and adverse event withdrawals, which were significantly greater for the higher dose. There were no data for the use of milnacipran for other chronic neuropathic pain conditions