Are there effects of light exposure on daytime sleep for rotating shift nurses after night shift?: an EEG power analysis

IntroductionNight-shift workers often face various health issues stemming from circadian rhythm shift and the consequent poor sleep quality. We aimed to study nurses working night shifts, evaluate the electroencephalogram (EEG) pattern of daytime sleep, and explore possible pattern changes due to ambient light exposure (30 lux) compared to dim conditions (<5 lux) during daytime sleep.MoethodsThe study involved 31 participants who worked night shifts and 24 healthy adults who had never worked night shifts. The sleep macro and microstructures were analyzed, and electrophysiological activity was compared (1) between nighttime sleep and daytime sleep with dim light and (2) between daytime sleep with dim and 30 lux light conditions.ResultsThe daytime sleep group showed lower slow or delta wave power during non-rapid eye movement (NREM) sleep than the nighttime sleep group. During daytime sleep, lower sigma wave power in N2 sleep was observed under light exposure compared to no light exposure. Moreover, during daytime sleep, lower slow wave power in N3 sleep in the last cycle was observed under light exposure compared to no light exposure.DiscussionOur study demonstrated that night shift work and subsequent circadian misalignment strongly affect sleep quality and decrease slow and delta wave activities in NREM sleep. We also observed that light exposure during daytime sleep could additionally decrease N2 sleep spindle activity and N3 waves in the last sleep cycle

Hypocomplementemic Urticarial Vasculitis in Systemic Lupus Erythematosus

Urticarial vasculitis is characterized clinically by urticarial skin lesions and histologically by leukocytoclastic vasculitis. Hypocomplementemic urticarial vasculitis is associated with connective tissue diseases such as systemic lupus erythematosus (SLE). We report a case of urticarial vasculitis that preceded manifestations of SLE

A study of the relationship between clinical phenotypes and plasma iduronate-2-sulfatase enzyme activities in Hunter syndrome patients

PurposeMucopolysaccharidosis type II (MPS II or Hunter syndrome) is a rare lysosomal storage disorder caused by iduronate-2-sulfatase (IDS) deficiency. MPS II causes a wide phenotypic spectrum of symptoms ranging from mild to severe. IDS activity, which is measured in leukocyte pellets or fibroblasts, was reported to be related to clinical phenotype by Sukegawa-Hayasaka et al. Measurement of residual plasma IDS activity using a fluorometric assay is simpler than conventional measurements using skin fibroblasts or peripheral blood mononuclear cells. This is the first study to describe the relationship between plasma IDS activity and clinical phenotype of MPS II.MethodsWe hypothesized that residual plasma IDS activity is related to clinical phenotype. We classified 43 Hunter syndrome patients as having attenuated or severe disease types based on clinical characteristics, especially intellectual and cognitive status. There were 27 patients with the severe type and 16 with the attenuated type. Plasma IDS activity was measured by a fluorometric enzyme assay using 4-methylumbelliferyl-α-iduronate 2-sulphate.ResultsPlasma IDS activity in patients with the severe type was significantly lower than that in patients with the attenuated type (P=0.006). The optimal cut-off value of plasma IDS activity for distinguishing the severe type from the attenuated type was 0.63 nmol·4 hr-1·mL-1. This value had 88.2% sensitivity, 65.4% specificity, and an area under receiver-operator characteristics (ROC) curve of 0.768 (ROC curve analysis; P=0.003).ConclusionThese results show that the mild phenotype may be related to residual lysosomal enzyme activity

Novel neuroelectrophysiological age index associated with imaging features of brain aging and sleep disorders

•We proposed a sleep EEG-based brain age prediction model using convolutional neural networks.•A higher BAI is associated with cortical thinning in various functional areas.•A higher BAI for sleep disorder groups compared to healthy sleepers, as well as significant differences in the spectral pattern of EEG among different sleep disorders (lower power in slow and θ waves for sleep apnea vs. higher power in β and σ for insomnia).•This result suggested that sleep EEG-BAI may reflect not only neural electroactivity responding to the same night sleep quality/depth but also neuroelectrophysiological changes in relation to chronic neural loss and altered brain connectivity.•Suggested EEG-based BAI can be used to phenotype sleep disorders as well as screen for sleep abnormalities that potentially harm brain health. Sleep architecture and microstructures alter with aging and sleep disorder-led accelerated aging. We proposed a sleep EEG based brain age prediction model using convolutional neural networks. We then associated the estimated brain age index with brain structural aging features, sleep disorders and various sleep parameters. Our model also showed a higher BAI (predicted brain age minus chronological age) is associated with cortical thinning in various functional areas. We found a higher BAI for sleep disorder groups compared to healthy sleepers, as well as significant differences in the spectral pattern of EEG among different sleep disorders (lower power in slow and ϑ waves for sleep apnea vs. higher power in β and σ for insomnia), suggesting sleep disorder-dependent pathomechanisms of aging. Our results demonstrate that the new EEG-BAI can be a biomarker reflecting brain health in normal and various sleep disorder subjects, and may be used to assess treatment efficacy

Predicting brain age based on sleep EEG and DenseNet

We proposed a sleep EEG-based brain age prediction model which showed higher accuracy than previous models. Six-channel EEG data were acquired for 6 hours sleep. We then converted the EEG data into 2D scalograms, which were subsequently inputted to DenseNet used to predict brain age. We then evaluated the association between brain aging acceleration and sleep disorders such as insomnia and OSA.The correlation between chronological age and expected brain age through the proposed brain age prediction model was 80% and the mean absolute error was 5.4 years. The proposed model revealed brain age increases in relation to the severity of sleep disorders.In this study, we demonstrate that the brain age estimated using the proposed model can be a biomarker that reflects changes in sleep and brain health due to various sleep disorders.Clinical Relevance-Proposed brain age index can be a single index that reflects the association of various sleep disorders and serve as a tool to diagnose individuals with sleep disorders

Differential Expression of -Associated Genes in Autosomal Dominant Polycystic Kidney Disease

Autosomal dominant polycystic kidney disease (ADPKD) is characterized by formation of multiple fluid-filled cysts that expand over time and destroy renal architecture. The proteins encoded by the PKD1 and PKD2 genes, mutations in which account for nearly all cases of ADPKD, may help guard against cystogenesis. Previously developed mouse models of PKD1 and PKD2 demonstrated an embryonic lethal phenotype and massive cyst formation in the kidney, indicating that PKD1 and PKD2 probably play important roles during normal renal tubular development. However, their precise role in development and the cellular mechanisms of cyst formation induced by PKD1 and PKD2 mutations are not fully understood. To address this question, we presently created Pkd2 knockout and PKD2 transgenic mouse embryo fibroblasts. We used a mouse oligonucleotide microarray to identify messenger RNAs whose expression was altered by the overexpression of the PKD2 or knockout of the Pkd2. The majority of identified mutations was involved in critical biological processes, such as metabolism, transcription, cell adhesion, cell cycle, and signal transduction. Herein, we confirmed differential expressions of several genes including aquaporin-1, according to different PKD2 expression levels in ADPKD mouse models, through microarray analysis. These data may be helpful in PKD2-related mechanisms of ADPKD pathogenesis

Mxi1 influences cyst formation in three-dimensional cell culture

Cyst formation is a major characteristic of ADPKD and iscaused by the abnormal proliferation of epithelial cells. Renalcyst formation disrupts renal function and induces diversecomplications. The mechanism of cyst formation is unclear.mIMCD-3 cells were established to develop simple epithelialcell cysts in 3-D culture. We confirmed previously that Mxi1plays a role in cyst formation in Mxi1-deficient mice. Cysts inMxi1 transfectanted cells were showed by collagen or mebiolgels in 3-D cell culture system. Causative genes of ADPKDwere measured by q RT-PCR. Herein, Mxi1 transfectants rarelyformed a simple epithelial cyst and induced cell death.Overexpression of Mxi1 resulted in a decrease in the PKD1,PKD2 and c-myc mRNA relating to the pathway of cystformation. These data indicate that Mxi1 influences cystformation of mIMCD-3 cells in 3-D culture and that Mxi1 maycontrol the mechanism of renal cyst formation. [BMB reports2012; 45(3): 189-193

Induction of apoptosis and caspase-3 activation by chemopreventive [6]-paradol and structurally related compounds in KB cells

[6]-paradol, a pungent phenolic substance found in ginger and other Zingiberaceae plants, has been demonstrated to be an effective inhibitor of tumor promotion in mouse skin carcinogenesis. In the present study, we found that [6]-paradol and other structurally related derivatives, [10]-paradol, [3]-dehydroparadol, [6]-dehydroparadol, and [10]-dehydroparadol, with the exception of [3]-paradol induce apoptosis in an oral squamous carcinoma cell line, KB, in a dose-dependent manner. [10]paradol and [10]-dehydroparadol exhibited a similar extent of cytotoxicity to that of [6]-paradol. [6]-Dehydroparadol and [3]dehydroparadol appeared to be more potent, with an IC50 less than 40 muM. Treatment of KB cells with an apoptosis-inducing concentration of [6]-dehydroparadol caused induction of proteolytic cleavage of pro-caspase-3. These results suggest that [6]paradol and structurally related derivatives induce apoptosis through a caspase-3-dependent mechanism. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved

Single-Dose Toxicity Study on ML171, a Selective NOX1 Inhibitor, in Mice

Background. ML171 is a potent nicotinamide adenine dinucleotide phosphate oxidase (NOX) inhibitor with isoform selectivity only for NOX1. This study is aimed at investigating the safety of ML171 after a single intraperitoneal (IP) injection in mice. Methods. The toxicity of a single dose of ML171 was evaluated in 6-week-old Institute of Cancer Research (ICR) mice in a good laboratory practice (GLP) laboratory. Twenty-five mice of each sex were assigned to five groups: negative control, vehicle control, and 125, 250, and 500 mg/kg of ML171. All mice were acclimatized for one week before beginning the study. Mice received an IP injection of ML171 or vehicle. The general condition and mortality of the animals were observed. The mice were sacrificed to evaluate histopathology 14 days after the administration of ML171 or vehicle. Results. Bodyweights were not significantly different in any group. Three males and one female died due to ML171 administration in the 500 mg/kg dose group. Autopsies of the surviving mice did not reveal any significant abnormalities after the injection of 125 mg/kg of ML171. However, the anterior lobe edge of the liver was thickened and adhesions between the liver and adjacent organs were observed in mice treated with 250 or 500 mg/kg of ML171. In addition, hypertrophy of centrilobular hepatocytes and inflammatory cell infiltration were observed after injection of 250 and 500 mg/kg of ML171. Conclusion. Our results indicate that the lethal IP injection dose of ML171 is 500 mg/kg for both males and females. Mortality were not observed for lower doses of ML171. The safe dose of single IP ML171 in ICR mice was 250 mg/kg or less. Further studies are needed to confirm the safety of ML171 in the human body

Alpha1-Antitrypsin Attenuates Renal Fibrosis by Inhibiting TGF-β1-Induced Epithelial Mesenchymal Transition - Fig 8

<p><b>Immunofluorescence microscopy of α-SMA (A to D) and E-cadherin (E to H) in MDCK cells after TGF-β1 and AAT treatment.</b> AAT did not cause significant change in MDCK cells cultured in medium alone (B and F). The increased immunolabeling intensity of α-SMA (C, red) seen in response to TGF-β1 treatment was attenuated by AAT treatment (D). The decreased immunolabeling intensity of E-cadherin (G, green) in response to TGF-β1 treatment was augmented by AAT treatment (H). The blue staining (A to H) is nuclear counterstaining with DAPI.</p