Association of Sleep Reactivity and Anxiety Sensitivity with Insomnia-Related Depression and Anxiety among City Government Employees in Japan

It has recently been noted that a reduction in sleep reactivity, characterized as the trait-like degree to which exposure to stress interferes with sleep, and anxiety sensitivity are associated with reduced insomnia severity. This study aimed to examine whether sleep reactivity and anxiety sensitivity are associated with insomnia-related depression and anxiety among city government employees in Japan. This cross-sectional study included 1810 city government employees of Koka City, Japan (mean age (standard deviation): 45.33 (12.20) years) who completely answered the scales for sleep reactivity, anxiety sensitivity, anxiety, and depression. Stepwise multiple regression analysis adjusted for demographic data showed that anxiety sensitivity (β = 0.39) was significantly linked to anxiety, and sleep reactivity (β = 0.36) was significantly linked to depression in individuals with insomnia. Additionally, the results of a logistic regression analysis adjusted for demographic data showed that anxiety sensitivity and sleep reactivity were relevant factors for anxious insomnia (OR = 12.69) and depressive insomnia (OR = 8.73), respectively. Whereas both sleep reactivity (OR = 14.67) and anxiety sensitivity (OR = 6.14) were associated with combined insomnia. These findings indicate that sleep reactivity is strongly associated with depressive symptoms, and anxiety sensitivity is strongly associated with anxiety symptoms in individuals with insomnia.journal articl

Analysis of Water Surface Osccilation at Open-Channel Side Cavity by Image Analysys and Large Eddy Simulation

Source: ICHE Conference Archive - https://mdi-de.baw.de/icheArchiv

Arthrogenicity of type II collagen monoclonal antibodies associated with complement activation and antigen affinity

<p>Abstract</p> <p>Background</p> <p>The collagen antibody-induced arthritis (CAIA) model, which employs a cocktail of monoclonal antibodies (mAbs) to type II collagen (CII), has been widely used for studying the pathogenesis of autoimmune arthritis. In this model, not all mAbs to CII are capable of inducing arthritis because one of the initial events is the formation of collagen-antibody immune complexes on the cartilage surface or in the synovium, and subsequent activation of the complement by the complexes induces arthritis, suggesting that a combination of mAbs showing strong ability to bind mouse CII and activate the complement may effectively induce arthritis in mice. In the present study, we examined the relationship between the induction of arthritis by the combination of IgG2a (CII-6 and C2A-12), IgG2b (CII-3, C2B-14 and C2B-16) and IgM (CM-5) subclones of monoclonal antibodies (mAb) of anti-bovine or chicken CII and the ability of mAbs to activate complement and bind mouse CII.</p> <p>Methods</p> <p>DBA/1J mice were injected with several combinations of mAbs followed by lipopolysaccharide. Furthermore, the ability of mAbs to activate the complement and bind mouse CII was examined by ELISA.</p> <p>Results</p> <p>First, DBA/1J mice were injected with the combined 4 mAbs (CII-3, CII-6, C2B-14, and CM-5) followed by lipopolysaccharide, resulting in moderate arthritis. Excluding one of the mAbs, i.e., using only CII-3, CII-6, and C2B-14, induced greater inflammation of the joints. Next, adding C2A-12 but not C2B-16 to these 3 mAbs produced more severe arthritis. A combination of five clones, consisting of all 5 mAbs, was less effective. Histologically, mice given the newly developed 4-clone cocktail had marked proliferation of synovial tissues, massive infiltration by inflammatory cells, and severe destruction of cartilage and bone. Furthermore, 4 of the 6 clones (CII-3, CII-6, C2B-14, and C2A-12) showed not only a strong cross-reaction with mouse CII but also marked activation of the complement <it>in vitro</it>.</p> <p>Conclusion</p> <p>The combination of 4 mAbs showing strong abilities to activate the complement and bind mouse CII effectively induced arthritis in DBA/1J mice. This <it>in vitro </it>system may be useful for the selection of mAbs associated with the development of arthritis.</p

Cholinergic cells in the nucleus basalis of mice express the N-methyl-D-aspartate-receptor subunit NR2C and its replacement by the NR2B subunit enhances frontal and amygdaloid acetylcholine levels

It is known that glutamatergic and cholinergic systems interact functionally at the level of the cholinergic basal forebrain. The N-methyl-D-aspartate receptor (NMDA-R) is a multiprotein complex composed of NR1, NR2 and/or NR3 subunits. The subunit composition of NMDA-R of cholinergic cells in the nucleus basalis has not yet been investigated. Here, by means of choline acetyl transferase and NR2B or NR2C double staining, we demonstrate that mice express both the NR2C and NR2B subunits in nucleus basalis cholinergic cells.We generated NR2C-2B mutant mice in which an insertion of NR2B cDNA into the gene locus of the NR2C gene replaced NR2C by NR2B expression throughout the brain. This NR2C-2B mutant was used to examine whether a subunit exchange in cholinergic neurons would affect acetylcholine (ACh) content in several brain structures. We found increased ACh levels in the frontal cortex and amygdala in the brains of NR2C-2B mutant mice. Brain ACh has been implicated in neuroplasticity, novelty-induced arousal and encoding of novel stimuli. We therefore assessed behavioral habituation to novel environments and objects as well as object recognition in NR2C-2B subunit exchange mice. The behavioral analysis did not indicate any gross behavioral alteration in the mutant mice compared with the wildtype mice. Our results show that the NR2C by NR2B subunit exchange in mice affects ACh content in two target areas of the nucleus basalis.

【高齢患者の精神科コンサルテーション・リエゾン(CLP)】身体疾患に伴う不眠

高齢者では不眠の訴えが多いが、その主要な原因には、年齢に伴う睡眠の変化、高齢者の過剰に長い床上時間、抑うつなどの精神的問題がある。これらが除外された場合に、初めて身体疾患に伴う不眠を疑う必要がある。不眠をきたす身体疾患は多岐にわたるので、不眠をきたす身体疾患について概説する

Screening of sleep apnea based on heart rate variability and long short-term memory

Purpose: Sleep apnea syndrome (SAS) is a prevalent sleep disorder in which apnea and hypopnea occur frequently during sleep and result in increase of the risk of lifestyle-related disease development as well as daytime sleepiness. Although SAS is a common sleep disorder, most patients remain undiagnosed because the gold standard test polysomnography (PSG), is high-cost and unavailable in many hospitals. Thus, an SAS screening system that can be used easily at home is needed. Methods: Apnea during sleep affects changes in the autonomic nervous function, which causes fluctuation of the heart rate. In this study, we propose a new SAS screening method that combines heart rate measurement and long short-term memory (LSTM) which is a type of recurrent neural network (RNN). We analyzed the data of intervals between adjacent R waves (R-R interval; RRI) on the electrocardiogram (ECG) records, and used an LSTM model whose inputs are the RRI data is trained to discriminate the respiratory condition during sleep. Results: The application of the proposed method to clinical data showed that it distinguished between patients with moderate-to-severe SAS with a sensitivity of 100% and specificity of 100%, results which are superior to any other existing SAS screening methods. Conclusion: Since the RRI data can be easily measured by means of wearable heart rate sensors, our method may prove to be useful as an SAS screening system at home

siRNA-dependent and -independent post-transcriptional cosuppression of the LTR-retrotransposon MAGGY in the phytopathogenic fungus Magnaporthe oryzae

The LTR-retrotransposon MAGGY was introduced into naive genomes of Magnaporthe oryzae with different genetic backgrounds (wild-type, and MoDcl1 [mdl1] and MoDcl2 [mdl2] dicer mutants). The MoDcl2 mutants deficient in MAGGY siRNA biogenesis generally showed greater MAGGY mRNA accumulation and more rapid increase in MAGGY copy number than did the wild-type and MoDcl1 mutants exhibiting normal MAGGY siRNA accumulation, indicating that RNA silencing functioned as an effective defense against the invading element. Interestingly, however, regardless of genetic background, the rate of MAGGY transposition drastically decreased as its copy number in the genome increased. Notably, in the MoDcl2 mutant, copy-number-dependent MAGGY suppression occurred without a reduction in its mRNA accumulation, and therefore by a silencing mechanism distinct from both transcriptional gene silencing and siRNA-mediated RNA silencing. This might imply that some mechanism possibly similar to post-transcriptional cosuppression of Ty1 retrotransposition in Saccharomyces cerevisiae, which operates regardless of the abundance of target transcript and independent of RNA silencing, would also function in M. oryzae that possesses the RNA silencing machinery