A test of the functional avoidance hypothesis in the development of overgeneral autobiographical memory.

Overgeneral memory (OGM) refers to the failure to recall memories of specific personally experienced events, which occurs in various psychiatric disorders. One pathway through which OGM is theorized to develop is the avoidance of thinking of negative experiences, whereby cumulative avoidance may maladaptively generalize to autobiographical memory (AM) more broadly. We tested this, predicting that negative experiences would interact with avoidance to predict AM specificity. In Study 1 (N = 281), negative life events (over six months) and daily hassles (over one month) were not related to AM specificity, nor was avoidance, and no interaction was found. In Study 2 (N = 318), we revised our measurements and used an increased timeframe of 12 months for both negative life events and daily hassles. The results showed no interaction effect for negative life events, but they did show an interaction for daily hassles, whereby increased hassles and higher avoidance of thinking about them were associated with reduced AM specificity, independent of general cognitive avoidance and depressive symptoms. No evidence was found that cognitive avoidance or AM specificity moderated the effect of negative experiences on depressive symptoms. Our findings suggest that life events over 6-12 months are not associated with AM specificity, but chronic daily hassles over 12 months predict reduced AM specificity when individuals avoid thinking about them. The findings provide evidence for the functional-avoidance hypothesis of OGM development and future directions for longitudinal studies.

Hemoadsorption of high-mobility group box chromosomal protein 1 using a column for large animals.

BACKGROUND: High-mobility group box chromosomal protein 1 (HMGB1) has recently been identified as an important mediator of various kinds of acute and chronic inflammation. A method for efficiently removing HMGB1 from the systemic circulation could be a promising therapy for HMGB1-mediated inflammatory diseases. MATERIALS AND METHODS: In this study, we produced a new adsorbent material by chemically treating polystyrene fiber. We first determined whether the adsorbent material efficiently adsorbed HMGB1 in vitro using a bovine HMGB1 solution and a plasma sample from a swine model of acute liver failure. We then constructed a column by embedding fabric sheets of the newly developed fibers into a cartridge and tested the ability of the column to reduce plasma HMGB1 levels during a 4-hour extracorporeal hemoperfusion in a swine model of acute liver failure. RESULTS: The in vitro adsorption test of the new fiber showed high performance for HMGB1 adsorption (96% adsorption in the bovine HMGB1 solution and 94% in the acute liver failure swine plasma, 2 h incubation at 37°C; p < 0.05 vs. incubation with no adsorbent). In the in vivo study, the ratio of the HMGB1 concentration at the outlet versus the inlet of the column was significantly lower in swine hemoperfused with the newly developed column (53 and 61% at the beginning and end of perfusion, respectively) than in those animals hemoperfused with the control column (94 and 93% at the beginning and end of perfusion, respectively; p < 0.05). Moreover, the normalized plasma level of HMGB1 was significantly lower during perfusion with the new column than with the control column (p < 0.05 at 1, 2, and 3 h after initiation of perfusion). CONCLUSION: These data suggest that the newly developed column has the potential to effectively adsorb HMGB1 during hemoperfusion in swine.

Social operant conditioning of autobiographical memory sharing.

The memories for past autobiographical experiences that we share can influence relationship formation and consolidation with important implications for our mental health. However, little is known about how people's responses to our memories can influence subsequent memory sharing. Previous research examined how operant processes (i.e., punishment with aversive sounds) influence the sharing of memories for specific events from our past. Understanding the (social) mechanisms associated with difficulty sharing specific autobiographical memories is important given the association between these difficulties and a range of psychiatric diagnoses. We investigate the effects of verbal and non-verbal social operants on the willingness to share specific autobiographical memories. Participants shared memories with a confederate who coded their memories as specific or non-specific and responded in either an engaged/attentive, dismissive manner or gave no feedback depending on participants' assigned condition. Participants who were reinforced for sharing specific memories and punished for sharing non-specific memories, were more likely to share specific than non-specific memories compared to those who received no feedback. Reinforcement alone was not sufficient for modifying specificity. The ways that we respond to people when they share memories with us can influence their subsequent willingness to share specific events from their past.

MFM and PEEM observation of micrometre-sized magnetic dot arrays fabricated by ion-microbeam irradiation in FeRh thin films.

FeRh thin films were irradiated with a 10 MeV iodine ion microbeam to produce micrometre-scale ferromagnetic microstructures by modifying the local magnetic character from antiferromagnetism to ferromagnetism using ion-microbeam irradiation. Two-dimensional magnetic dot arrays of dimensions ∼2 µm × 4 µm as well as 10 µm × 10 µm were successfully produced on the FeRh surface, which was confirmed by magnetic force microscopy (MFM). The results of photoemission electron microscopy (PEEM) combined with X-ray magnetic circular dichroism reveal that the easy axis of the magnetization of the ion-beam-irradiated ferromagnetism in the FeRh thin films lies in the film planes along the <001> direction of the MgO substrates.

The role of IL-33 and its receptor ST2 in human nasal epithelium with allergic rhinitis.

BACKGROUND: Interleukin (IL)-33 is a novel member of the IL-1 cytokine family and a ligand for the orphan IL-1 family receptor ST2. The IL-33 induces T helper 2-type inflammatory responses and is considered to play a crucial rule in allergic inflammations, such as asthma and atopic dermatitis. However, the role of IL-33 and its receptor ST2 in allergic rhinitis remains unknown. OBJECTIVE: We investigated expression of IL-33 and ST2 in the nasal epithelium of patients with allergic rhinitis and the mechanisms of the production of cytokines/chemokines induced by treatment with IL-33 using normal human nasal epithelial cells (HNECs) in vitro. METHODS: Expression of IL-33 and ST2 in normal and allergic rhinitis nasal mucosa was evaluated by reverse transcription- and real-time polymerase chain reactions and immunohistochemical methods. The IL-33 in serum, and IL-8 and GM-CSF were measured by ELISA. For in vitro experiments, HNECs in primary culture were used. RESULTS: The IL-33 levels in the sera of patients with allergic rhinitis were significantly higher than that in normal controls. Expression of IL-33 and ST2 was significantly elevated in the epithelium from patients with allergic rhinitis. The IL-33 mRNA in HNECs in vitro was significantly induced by treatment with IFN-γ and the toll-like receptor 9 ligand ODN2006. The IL-33-induced production of IL-8 and GM-CSF from HNECs in vitro was significantly suppressed by corticosteroid treatment and distinct signal transduction inhibitors of ERK, p38 MAPK, JNK, NF-κB and epidermal growth factor receptor. CONCLUSIONS AND CLINICAL RELEVANCE: The IL-33 and its receptor ST2 play important roles in allergic rhinitis. The IL-33-mediated inflammatory responses via ST2 are regulated by distinct signalling pathways in HNECs and the IL-33/ST2 pathway may provide new therapeutic targets for allergic rhinitis.

Increased plasma levels of high mobility group box 1 in patients with acute liver failure.

BACKGROUND: High-mobility group box 1 (HMGB1) is a monocyte-derived late-acting inflammatory mediator, which is released in conditions such as shock, tissue injury and endotoxin-induced lethality. In this study, we determined the plasma and hepatic tissue levels of HMGB1 in patients with acute liver failure (ALF). PATIENTS AND METHODS: We determined the plasma levels of HMGB1 and aspartate aminotransferase (AST) in 7 healthy volunteers (HVs), 40 patients with liver cirrhosis (LC), 37 patients with chronic hepatitis (CH), 18 patients with severe acute hepatitis (AH), and 14 patients with fulminant hepatitis (FH). The 14 patients with FH were divided into two subgroups depending upon the history of plasma exchange (PE) before their plasma sample collection. The hepatic levels of HMGB1 were measured in tissue samples from 3 patients with FH who underwent living-donor liver transplantation and from 3 healthy living donors. Hepatic tissue samples were also subjected to immunohistochemical examination for HMGB1. RESULTS: The plasma levels of HMGB1 (ng/ml) were higher in patients with liver diseases, especially in FH patients with no history of PE, than in HVs (0.3 ± 0.3 in HVs, 4.0 ± 2.0 in LC, 5.2 ± 2.6 in CH, 8.6 ± 4.8 in severe AH, 7.8 ± 2.7 in FH with a history of PE, and 12.5 ± 2.6 in FH with no history of PE, p < 0.05 in each comparison). There was a strong and statistically significant relationship between the mean plasma HMGB1 level and the logarithm of the mean AST level (R = 0.900, p < 0.05). The hepatic tissue levels of HMGB1 (ng/mg tissue protein) were lower in patients with FH than in healthy donors (539 ± 116 in FH vs. 874 ± 81 in healthy donors, p < 0.05). Immunohistochemical staining for HMGB1 was strong and clear in the nuclei of hepatocytes in liver sections from healthy donors, but little staining in either nuclei or cytoplasm was evident in specimens from patients with FH. CONCLUSION: We confirmed that plasma HMGB1 levels were increased in patients with ALF. Based on a comparison between HMGB1 contents in normal and ALF livers, it is very likely that HMGB1 is released from injured liver tissue.

Computerized Memory Specificity Training (c-MeST) for major depression: A randomised controlled trial.

Given modest response and high relapse after treatment for Major Depressive Episodes (MDE), the development and refinement of treatments to target cognitive vulnerabilities is indicated. Memory Specificity Training (MeST) remediates deficits in recalling detailed memories of past experiences through repeated practice of autobiographical memory retrieval. This randomised controlled trial aimed to assess the efficacy of an online, computerized version of MeST (c-MeST) for MDE. Adults (N = 245, 88.4% female; M age = 46.4) with a current MDE were randomised to the c-MeST program or wait-list control group. Significantly fewer participants in the c-MeST group, relative to control, met criteria for an MDE at one-month follow-up (35.7% c-MeST vs. 60.6% control), but not at other time-points. The c-MeST group, relative to the control group, scored significantly higher on memory specificity at all time-points following baseline (d = 0.53-0.93), and lower on depressive symptoms at one (d = 0.57) and three-month follow-up (d = 0.67). Changes in memory specificity mediated the effect of c-MeST on depressive symptoms at follow-up. c-MeST can improve memory specificity and depressive symptoms in people with an MDE, and may speed the rate of recovery. Future studies can further examine the mechanisms through which this occurs.

Emotion Regulation as a Mediator in the Relationship Between Cognitive Biases and Depressive Symptoms in Depressed, At-risk and Healthy Children and Adolescents.

Contemporary cognitive models of depression propose that cognitive biases for negative information at the level of attention (attention biases; AB) and interpretation (interpretation biases; IB) increase depression risk by promoting maladaptive emotion regulation (ER). So far, empirical support testing interactions between these variables is restricted to non-clinical and clinical adult samples. The aim of the current study was to extend these findings to a sample of children and adolescents. This cross-sectional study included 109 children aged 9-14 years who completed behavioural measures of AB (passive-viewing task) and IB (scrambled sentences task) as well as self-report measures of ER and depressive symptoms. In order to maximize the variance in these outcomes we included participants with a clinical diagnosis of depression as well as non-depressed youth with an elevated familial risk of depression and non-depressed youth with a low familial risk of depression. Path model analysis indicated that all variables (AB, IB, adaptive and maladaptive ER) had a direct effect on depressive symptoms. IB and AB also had significant indirect effects on depressive symptoms via maladaptive and adaptive ER. These findings provide initial support for the role of ER as a mediator between cognitive biases and depressive symptoms and provide the foundations for future experimental and longitudinal studies. In contrast to studies in adult samples, both adaptive as well as maladaptive ER mediated the effect of cognitive biases on depressive symptoms. This suggests potentially developmental differences in the role of ER across the lifespan.

Two percent of patients suspected of having Angelman syndrome have TCF4 mutations.

The TCF4 gene encodes a basic helix-loop-helix (bHLH) transcription factor which belongs to the family of E-proteins. E-proteins form homo- and heterodimers with other members of the HLH family and bind to the common DNA sequence called E-box. Haploinsufficiency of the TCF4 gene has been found to be associated with the Pitt-Hopkins syndrome (PTHS). PTHS is characterized by severe mental retardation, a wide mouth plus other distinctive facial features (fleshy lips, beaked nose, broad nasal bridge) and breathing abnormalities. Because of some phenotypical overlap with Angelman syndrome (AS), it has been suggested that PTHS be considered in its differential diagnosis. To explore this possibility, we screened 86 patients who were suspected of having AS. All the patients were negative for UBE3A testing, and 53 were known to be negative for methylation analysis. We identified two TCF4 mutations in this cohort. The p.S384Tfsx7 mutation lacks the bHLH domain. The p.R582P mutation lies within the bHLH domain in which seven other missense mutations have been reported. Both mutations most likely affect the critical function of the bHLH domain of the TCF4 protein. In summary, we found two TCF4 mutations in 86 patients (2%) suspected to have AS. Screening for mutations in this gene should be considered in patients who present with findings of AS but who have been negative for methylation and UBE3A testing.

Cloning of the RNase H genes from a metagenomic DNA library: identification of a new type 1 RNase H without a typical active-site motif.

AIMS: The study aimed to combine a metagenomics approach with complementary genetics to identify novel bacterial genes with orthologous functions, with the identification of novel RNase H genes as a test case. METHODS AND RESULTS: A metagenomic DNA library was prepared from leaf-and-branch compost and used to screen for the RNase H genes by their abilities to complement the temperature-sensitive growth phenotype of the rnhA mutant Escherichia coli strain MIC3001. Determination of the nucleotide sequences of the cloned DNA fragments allowed us to identify 12 different genes encoding type 1 RNases H. Eleven of them encode novel RNases H, which show 40-72% amino acid sequence identities to those available from database. One of them lacks a typical DEDD/E active-site motif, which is almost fully conserved in various RNases H. CONCLUSIONS: Functional screening of environmental DNA without cultivation of microbes is a useful procedure to isolate novel RNase H genes. SIGNIFICANCE AND IMPACT OF THE STUDY: One of the identified RNase H genes had no sequence similarity to a previously assumed conserved motif, suggesting multiple catalytic mechanisms exist. This test case illustrates that metagenomics combined with complementary genetics can identify novel genes that are orthologous without sequence similarity to those from cultivated bacteria.

An 8-month-old boy with congenital fibromuscular dysplasia presenting with shock caused by sudden renal hemorrhage.

Fibromuscular dysplasia (FMD) is a non-atheromatous, non-inflammatory, multifocal segmental angiopathy. FMD is the most common cause of pediatric renovascular hypertension. Aneurysmal formation of the main renal artery and distal branches is a rare complication of FMD in infancy. We report an 8-month-old boy with FMD presenting with shock caused by sudden renal hemorrhage that necessitated removal of one kidney. A diagnosis of renovascular hypertension resulting from intimal type FMD with aneurysmal formation was made on the basis of the presence of hypertension, elevation of PRA and aldosterone activity, pathological findings and the results of renal angiography. Our findings suggest that it is therefore necessary to consider FMD with aneurysmal formation as a possible cause of hypertension and renal hemorrhage in infants.

A study protocol for a randomised trial of adjunct computerised memory specificity training (c-MeST) for major depression in youth: targeting cognitive mechanisms to enhance usual care outcomes in mental health settings.

BACKGROUND: Youth depression is highly prevalent and is related to impairments in academic, social and behavioural functioning. Evidence-based treatments are available, but many young people do not respond or sufficiently recover with first-line options, and a significant proportion experience relapse. Consequently, there is clear scope to enhance intervention in this critical period of early-onset depression. Memory specificity training (MeST) is a low-intensity intervention for depression that targets reduced specificity when recalling memories of the past, a common cognitive vulnerability in depression. This randomised controlled trial will assess the efficacy of adding a computerised version of MeST (c-MeST) to usual care for youth depression. METHODS/DESIGN: Young people aged 15-25 years with a major depressive episode (MDE) will be recruited and randomised to have immediate access to the seven session online c-MeST program in addition to usual care, or to usual care and wait-list for c-MeST. The primary outcomes will be diagnostic status of an MDE and self-reported depressive symptoms assessed at baseline, 1-, 3- and 6-month intervals. Autobiographical memory specificity and other variables thought to contribute to the maintenance of reduced memory specificity and depression will be assessed as mediators of change. DISCUSSION: Online provision of c-MeST provides a simple, low-intensity option for targeting a cognitive vulnerability that predicts the persistence of depressive symptoms. If found to be efficacious as an adjunct to usual care for depressed youth, it could be suitable for broader roll-out, as c-MeST is highly accessible and implementation requires only minimal resources due to the online and automated nature of intervention. TRIAL REGISTRATION: Australian New Zealand Clinical Trials Registry, ACTRN12619000234112p. Registered on the 18 February 2019. All items from the WHO Trial Registration Data Set can be found within the protocol. PROTOCOL VERSION: 1.0.

Impairments in episodic future thinking for positive events and anticipatory pleasure in major depression.

BACKGROUND: Characteristic of the cardinal symptom of anhedonia, people with clinical depression report lower levels of anticipatory pleasure. However, the psychological mechanisms underlying these deficits are poorly understood. This is the first study to assess whether, and to what extent, phenomenological characteristics of episodic future thinking for positive future events are associated with anticipatory pleasure among depressed individuals. METHODS: Individuals with a Major Depressive Episode (MDE; N = 117) and without (N = 47) completed ratings scales for depressive symptoms and trait anticipatory and consummatory pleasure. They then provided descriptions of personally-relevant positive future events and rated them for phenomenological characteristics and state anticipatory pleasure. RESULTS: Between-groups analysis showed that those with MDE reported lower trait anticipatory and consummatory pleasure. They also simulated future events with less specificity, less detail/vividness, less use of mental imagery, less use of first-person perspective, less plausibility/perceived likelihood of occurring, and reported less associated state anticipatory pleasure. In regression analyses in the depressed group, lower scores for detail/vividness, mental imagery, and personal significance all uniquely predicted lower state anticipatory pleasure. LIMITATIONS: Cognitive functioning was not assessed, which may help clarify deficits that underpin these findings. History of previous depressive episodes in the comparison group were not assessed, which may mean the observed between-group effects are underestimated. CONCLUSIONS: This study provides further evidence of deficits in episodic future thinking and anticipatory pleasure in depressed individuals. It also establishes links between particular characteristics of episodic future thinking and state anticipatory pleasure, and indicates cognitive targets that may be amenable to intervention in order to reduce anhedonia.

Low-frequency eddy kinetic energy spectrum in the deep Western north pacific.

The frequency spectrum for the low-frequency eddy kinetic energy is estimated from a long-term current meter record obtained in a deep layer in the western North Pacific. The eddy field is characterized by three time scales: an "annual scale" with zonal dominance of eddy motions, a "temporal mesoscale" with meridional dominance, and a "monthly scale" with horizontal isotropy. About two-thirds of the eddy kinetic energy is contained in the temporal mesoscale.

Protein kinase C-mediated inhibition of an inward rectifier potassium channel by substance P in nucleus basalis neurons.

In nucleus basalis neurons, substance P (SP) causes a slow excitation, mediated through a pertussis toxin-insensitive G protein, by suppressing an inward rectifier K+ channel. Here we report that SP applied outside the patch pipette inhibited the single-channel activity, recorded on-cell, of the inward rectifier. The PKC inhibitors staurosporine and PKC(19-36) suppressed this effect in whole-cell mode and in on-cell single-channel mode. A diacylglycerol analog mimicked the SP effect, and PKC(19-36) suppressed this analog effect. SP irreversibly suppressed the inward rectifier in neurons treated with okadaic acid. These results indicate that a diffusible messenger mediates the SP effect, that its signal transduction involves phosphorylation by PKC, and that dephosphorylation by a serine/threonine protein phosphatase mediates its recovery.

Amyloid beta conformation in aqueous environment.

Amyloid beta peptide (Abeta), 42-residue peptide and its variations, is known to form amyloid fibrils in Alzheimer's disease. Solid-state NMR study reveals a parallel beta-sheet structure in the Abeta fibrils. The atomic level structure of Abeta in aqueous environment, however, has not been determined, because of its tendency to aggregate. There are several reports that soluble forms of Abeta possess intrinsic neurotoxicity. It has recently become possible to determine the crystal structure of Abeta fragments in an aqueous solution without organic solvents and detergents using a fusion technique with a hyperthermophile protein. Abeta28-42 forms a beta-conformation. This fusion technique enables us to obtain structural information at atomic resolution for amyloidogenic peptides in aqueous environments. This review describes our current knowledge on the Abeta conformation in aqueous environments and some viewpoints based on the knowledge.

Safety and efficacy of growth hormone (GH) during extended treatment of adult Japanese patients with GH deficiency (GHD).

OBJECTIVES: To assess the effects of a growth hormone (GH) replacement therapy using a GH dose regimen based on serum insulin-like growth factor (IGF-I) concentrations in Japanese adults with GH deficiency (GHD). DESIGN: In this multicentre, uncontrolled, open-label study, Japanese adults with GHD who had received either GH replacement therapy (GH-GH group, n=35) or placebo (Placebo-GH group, n=36) in a previous randomised, double-blind, placebo-controlled trial were treated with GH replacement therapy for 48 weeks. GH treatment was started at a dose of 0.003 mg/kg/day administered by subcutaneous injection for the first 8 weeks, after which the dose was adjusted to maintain patients' serum IGF-I levels within the reference range adjusted for age and gender. Body composition, serum lipids, serum IGF-I and IGF binding protein-3 (IGFBP-3) levels were measured throughout study. Symptom and quality of life scores were also determined. RESULTS: Lean body mass (LBM) was increased compared with baseline (the end of the preceding double-blind trial) at 24 and 48 weeks, with a mean (+/-SD) increase of 1.3% (+/-4.2%) at week 48 in the GH-GH group (an increase of 6.6% [+/-6.0%] from the start of the preceding double-blind trial) and a larger increase of 4.7% (+/-5.9%) in the Placebo-GH group. Body fat mass (BFM) increased slightly from baseline in the GH-GH group with a mean increase of 2.9+/-10.6% at week 48 (a decrease from the start of the preceding double-blind trial at 48 weeks of 7.8% [+/-15.0%]) but decreased by 6.5% (+/-11.7%) at week 48 in the Placebo-GH group. Serum lipids were unchanged or slightly increased from baseline in the GH-GH group but patients' lipid profiles improved in the Placebo-GH group. In patients who received placebo during the double-blind study, individualised GH therapy in this open-label study increased mean LBM at 48 weeks by 6.2+/-6.8% in patients with CO GHD and by 3.0+/-4.4% in patients with AO GHD. Changes in mean LBM and mean BFM at week 48 were +4.1+/-4.5% and -2.4+/-10.5%, respectively, in females and +5.0+/-6.7% and -8.9+/-11.8%, respectively, in males. In patients who received GH treatment during the double-blind study, overall changes in LBM, BFM and IGF-I SD score after 24 weeks and 48 weeks were small, with no significant differences between subgroups. While the overall incidence of adverse events was broadly similar in the GH-GH and Placebo-GH groups (97% and 89%, respectively), the incidence of treatment-related events was higher in the GH-GH group (83% vs 42% in the Placebo-GH group). Most adverse events in both treatment groups were of mild or moderate severity and not clinically significant. The incidences of oedema and cases of high IGF-I during the IGF-I level-adjusted treatment regimen were lower than those during the preceding fixed dose titration. CONCLUSION: Long-term GH replacement therapy was well tolerated in Japanese adults with GHD. GH treatment maintained the improvements in body composition and lipid profiles in the patients previously treated in the double-blind study (GH-GH group) and improved these parameters in previously untreated patients (Placebo-GH group). Individualised GH administration based on IGF-I levels was well-tolerated and effective.

Actinobacillus actinomycetemcomitans lipopolysaccharide stimulates collagen phagocytosis by human gingival fibroblasts.

INTRODUCTION: Collagen phagocytosis by fibroblasts is involved in the intracellular pathway related to collagen breakdown in soft connective tissues. The possible role of lipopolysaccharide (LPS) in regulating this fibroblast function has not been elucidated so we investigated the effect of LPS from Actinobacillus actinomycetemcomitans, a periodontopathic bacterium, on collagen phagocytic activity in human gingival fibroblasts and associated regulatory mechanisms. METHODS: LPS pretreatment stimulated binding of collagen-coated beads to cells and, subsequently, their internalization. RESULTS: The LPS-activated collagen phagocytic process was enhanced in the presence of the soluble form of CD14 (sCD14) or LPS-binding protein (LBP), while the LPS/LBP treatment activated Akt and induced actin reorganization. Furthermore, these LPS/LBP-induced effects were partially suppressed by adding phosphatidyl-inositol-3 kinase (PI3K) inhibitors. CONCLUSION: These results suggest that A. actinomycetemcomitans LPS disturbs the homeostasis of collagen metabolism within gingival tissue by facilitating collagen phagocytosis by gingival fibroblasts, and serum sCD14 and LBP positively regulate the action of LPS. In addition, the PI3K/Akt signaling is thought to partially mediate the LPS/LBP-stimulated collagen phagocytic pathway, which may be dependent on actin cytoskeletal rearrangement.

Two routes for pollen entering indoors: ventilation and clothes.

BACKGROUND: The route by which pollen enters dwellings has not been clarified. OBJECTIVE: To evaluate the amount of pollen entering dwellings by ventilation and adhesion to textile products. METHODS: The amount of pollen clinging to fabrics (clothes, laundry, and futon bedding) out of doors was measured by quantification of Japanese cedar pollen antigen Cry j 1. The effect of air ventilation on the amount of pollen indoors was also investigated using several neighboring unoccupied apartments with an identical layout while controlling the ventilation conditions. RESULTS: The amount of pollen adhering to futons was especially high. More than half of the pollen on futons or laundry remained on the surface, even after being brushed off by hand or shaken off. Vacuuming laundry and futons after airing out would be an effective way to decrease the amount of indoor pollen. A large amount of pollen entered dwellings through air ducts when the windows were closed and the ventilation fans working. Since most pollen that entered by ventilation remained near the windows, cleaning carefully and frequently near windows could reduce the amount of pollen indoors. CONCLUSIONS: To decrease the amount of pollen indoors, special attention must be paid to textile products and ventilation systems during the pollen season.

Psychopathology and episodic future thinking: A systematic review and meta-analysis of specificity and episodic detail.

Episodic future thinking (EFT) refers to the mental simulation of future events that might be personally-experienced; a crucial mental process in adaptation. Psychiatric disorders are associated with deficits in recalling episodic memory, however, no study has reviewed the empirical literature to assess for similar deficits in EFT. A systematic review comparing psychiatric groups with control groups on the specificity and episodic detail of EFT returned 19 eligible studies. An overall effect of g = -0.84 (95%CI = -1.06, - 0.62, p < .001) indicated individuals with a psychiatric diagnosis have significantly less specific and detailed EFT. Publication bias was not detected, but heterogeneity was. No methodological characteristics were significant moderators. Subgroup analyses showed significant effects for depression (g = -0.79, p < .001, k = 7), bipolar disorder (g = -1.00, p < .001, k = 2), and schizophrenia (g = -1.06, p < .001, k = 6), but not posttraumatic stress disorder (g = -1.04, p = .260, k = 2) or complicated grief (g = -0.41, p = .08, k = 2). Deficits in EFT are apparent in some psychiatric disorders. However, many clinical groups are understudied, and the causal mechanisms and remediation of these deficits require further research attention.