EPRESSION IS COMMON, WITHthe 1-year prevalence rate of major depressive disorder estimated at between 6.6% and 10.3% in the general population 1,2 and roughly 25% of all primary care visits involving patients with clinically significant levels of depression. 3 Psychotherapy is effective at treating depression, 4 and most primary care patients prefer psychotherapy to antidepressant medication. 5 When referred for psychotherapy, however, only a small percentage of patients follow through. 6 Attrition from psychotherapy in randomized controlled trials is often 30% or greater 7 and can exceed 50% in clinical practice. 8 The discrepancy between patients' preference for psychotherapy and the low rates of initiation and adherence is likely due to access barriers. Approximately 75% of depressed primary care patients report barriers that make it extremely difficult or impossible to attend regular psychotherapy sessions. 9,10 These barriers are largely structural and include time constraints, lack of available and accessible services, transportation problems, and cost.

In spite of repeated calls for research and interventions to overcome individual and systemic barriers to psychological treatments, little is known about the nature of these barriers. To develop a measure of perceived barriers to psychological treatment (PBPT), items derived from 260 participants were administered to 658 primary care patients. Exploratory factor analysis on half the sample resulted in 8 factors, which were supported by confirmatory factor analysis conducted on the other half. Associations generally supported the criterion validity of PBPT scales, with self-reported concurrent use of psychotherapy and psychotherapy attendance in the year after PBPT administration. Depression was associated with greater endorsement of barriers. These findings suggest that the PBPT may be useful in assessing perceived barriers.

We recently isolated the AtBI-1 (Arabidopsis Bax Inhibitor-1) gene, the expression of which suppressed Bax-induced cell death in yeast. To determine whether the same is true in the plant system, transgenic Arabidopsis plants overexpressing Bax protein under a dexamethasone (DEX)-inducible promoter were generated. On DEX treatment, such transgenic plants exhibited marked cell death at the whole-plant level, cell shrinkage, membranous destruction, and other apoptotic phenotypes. Transgenic Bax plants were retransformed with a vector containing the AtBI-1 gene (tagged with green fluorescent protein) under the control of the cauliflower mosaic virus 35S promoter. Plants expressing both Bax and AtBI-1 were able to maintain growth on DEX-treatment by sustaining intracellular integrity. Thus, we present here direct genetic evidence that the plant antiapoptotic protein AtBI-1 is biologically active in suppressing the mammalian Bax action in planta.A lthough relatively little is known about the mechanistic details of cell death in plants, some aspects of the molecular machinery are conserved between plants and animals (1). It has been demonstrated that overexpression of Bax, which encodes a mammalian proapoptotic protein, is lethal in the budding yeast Saccharomyces cerevisiae (2-5), even though yeasts have neither Bcl-2-related proteins nor caspases. Lacomme and Santa Cruz (6) demonstrated that expression of Bax by using a tobacco mosaic virus (TMV) vector triggered cell death in tobacco leaf cells, which closely resembled the hypersensitive response (HR) induced by TMV in tobacco plants carrying the N gene. Conversely, overexpression of human Bcl-X L in transgenic tobacco suppressed HR and conferred stress tolerance (7). It was also reported that caspase-specific peptide inhibitors could abolish bacteria-induced plant programmed cell death (8). These observations clearly suggest some common features of animal and plant cell death processes.Xu and Reed (9) transformed yeast cells containing a galactose-inducible Bax plasmid by using a human cDNA library (in which cDNAs were fused to a constitutively active yeast promoter) and isolated cDNAs that prevented Bax-induced lethality in response to galactose. This resulted in the identification of a gene, termed BI-1 (Bax Inhibitor-1), which is identical to a previously isolated human gene of unknown function called TEGT (testis enhanced gene transcript; refs. 10 and 11). We have previously cloned plant BI-1 cDNAs (Arabidopsis AtBI-1, and rice OsBI-1) (12). Interestingly, Sanchez et al. (13) reported that AtBI-1, the same gene isolated by our group, was obtained by differential screening of genes from plants challenged with the phytopathogen Pseudomonas syringae. Expression of AtBI-1 was rapidly up-regulated in plants during wounding or pathogen challenge. Furthermore, accumulation of the AtBI-1 transcript is significantly delayed in coi1 plants, indicating that reduced AtBI-1 mRNA levels may contribute to the enhanced susceptibility exhibited by coi1 plants to infection by v...

The human genome sequence defines our inherent biological potential; the realization of the biology encoded therein requires knowledge of the function of each gene. Currently, our knowledge in this area is still limited. Several lines of investigation have been used to elucidate the structure and function of the genes in the human genome. Even so, gene prediction remains a difficult task, as the varieties of transcripts of a gene may vary to a great extent. We thus performed an exhaustive integrative characterization of 41,118 full-length cDNAs that capture the gene transcripts as complete functional cassettes, providing an unequivocal report of structural and functional diversity at the gene level. Our international collaboration has validated 21,037 human gene candidates by analysis of high-quality full-length cDNA clones through curation using unified criteria. This led to the identification of 5,155 new gene candidates. It also manifested the most reliable way to control the quality of the cDNA clones. We have developed a human gene database, called the H-Invitational Database (H-InvDB; http://www.h-invitational.jp/). It provides the following: integrative annotation of human genes, description of gene structures, details of novel alternative splicing isoforms, non-protein-coding RNAs, functional domains, subcellular localizations, metabolic pathways, predictions of protein three-dimensional structure, mapping of known single nucleotide polymorphisms (SNPs), identification of polymorphic microsatellite repeats within human genes, and comparative results with mouse full-length cDNAs. The H-InvDB analysis has shown that up to 4% of the human genome sequence (National Center for Biotechnology Information build 34 assembly) may contain misassembled or missing regions. We found that 6.5% of the human gene candidates (1,377 loci) did not have a good protein-coding open reading frame, of which 296 loci are strong candidates for non-protein-coding RNA genes. In addition, among 72,027 uniquely mapped SNPs and insertions/deletions localized within human genes, 13,215 nonsynonymous SNPs, 315 nonsense SNPs, and 452 indels occurred in coding regions. Together with 25 polymorphic microsatellite repeats present in coding regions, they may alter protein structure, causing phenotypic effects or resulting in disease. The H-InvDB platform represents a substantial contribution to resources needed for the exploration of human biology and pathology.