Low-Quality Video Target Detection Based on EEG Signal Using Eye Movement Alignment.

The target detection based on electroencephalogram (EEG) signals is a new target detection method. This method recognizes the target by decoding the specific neural response when an operator observes the target, which has important theoretical and application values. This paper focuses on the EEG detection of low-quality video targets, which breaks through the limitation of previous target detection based on EEG signals only for high-quality video targets. We first design an experimental paradigm for EEG-based low-quality video target detection and propose an epoch extraction method based on eye movement signals to solve the asynchronous problem faced by low-quality video target detection. Then, the neural representation in the process of operator recognition is analyzed based on the time domain, frequency domain, and source space domain, respectively. We design the time-frequency features based on continuous wavelet transform according to the neural representation and obtain an average decoding test accuracy of 84.56%. The research results of this paper lay the foundation for the development of a video target detection system based on EEG signals in the future.

Copper-Bearing Metal-Organic Framework with Mucus-Penetrating Function for the Multi-Effective Clearance of Mucosal Colonized Helicobacter pylori.

Helicobacter pylori colonizes over 50% of people worldwide. Biofilm formation through penetrating gastric mucus and resistance acquired by H. pylori markedly reduces the efficacy of traditional antibiotics. The present triple therapy and bismuth-based quadruple therapy inevitably causes intestinal flora disturbance and fails to address the excessive H. pylori-triggered inflammatory response. Herein, a mucus-permeable therapeutic platform (Cu-MOF@NF) that consists of copper-bearing metal-organic framework (Cu-MOF) loaded with nitrogen-doped carbon dots and naturally active polysaccharide fucoidan is developed. The experimental results demonstrate that Cu-MOF@NF can penetrate the mucus layer and hinder H. pylori from adhering on gastric epithelial cells of the stomach. Notably, released Cu2+ can degrade the polysaccharides in the biofilm and interfere with the cyclic growing mode of "bacterioplankton ↔ biofilm", thereby preventing recurrent and persistent infection. Compared with traditional triple therapy, the Cu-MOF@NF not only possesses impressive antibacterial effect (even include multidrug-resistant strains), but also improves the inflammatory microenvironment without disrupting the balance of intestinal flora, providing a more efficient, safe, and antibiotic-free new approach to eradicating H. pylori.

Metal-Organic Framework Based Mucoadhesive Nanodrugs for Multifunction Helicobacter Pylori Targeted Eradication, Inflammation Regulation and Gut Flora Protection.

The prevalence of drug-resistant bacteria presents a significant challenge to the antibiotic treatment of Helicobacter pylori (H. pylori), while traditional antimicrobial agents often suffer from shortcomings such as poor gastric retention, inadequate alleviation of inflammation, and significant adverse effects on the gut microbiota. Here, a selenized chitosan (CS-Se) modified bismuth-based metal-organic framework (Bi-MOF@CS-Se) nanodrug is reported that can target mucin through the charge interaction of the outer CS-Se layer to achieve mucosal adhesion and gastric retention. Additionally, the Bi-MOF@CS-Se can respond to gastric acid and pepsin degradation, and the exposed Bi-MOF exhibits excellent antibacterial properties against standard H. pylori as well as clinical antibiotic-resistant strains. Remarkably, the Bi-MOF@CS-Se effectively alleviates inflammation and excessive oxidative stress by regulating the expression of inflammatory factors and the production of reactive oxygen species (ROS), thereby exerting therapeutic effects against H. pylori infection. Importantly, this Bi-MOF@CS-Se nanodrug does not affect the homeostasis of gut microbiota, providing a promising strategy for efficient and safe treatment of H. pylori infection.

Associations between one-carbon metabolism and valproic acid-induced liver dysfunction in epileptic patients.

Valproic acid (VPA) has been widely used as an antiepileptic drug for decades. Although VPA is effective and well-tolerated, long-term VPA treatment is usually associated with hepatotoxicity. However, the underlying mechanisms of VPA-caused hepatotoxicity remain unclear. In this study, a total of 157 pediatric patients with epilepsy were recruited and divided into normal liver function (NLF, 112 subjects) group and abnormal liver function (ABLF, 45 subjects) group. We observed that MTHFR A1298C and MTHFR C677T variants may be linked to VPA-induced liver dysfunction (p = 0.001; p = 0.023, respectively). We also found that the MTHFR A1298C polymorphism was associated with a higher serum Hcy level (p = 0.001) and a lower FA level (p = 0.001). Moreover, the serum Hcy levels was strongly correlated with the GSH and TBARS concentrations (r = -0.6065, P < 0.001; r = 0.6564, P < 0.001, respectively). Furthermore, logistic analysis indicated that MTHFR A1298C/C677T polymorphisms and increased Hcy concentrations may be risk factors for VPA-induced liver dysfunction. These results suggested that individual susceptibility to VPA-induced liver dysfunction may result from MTHFR A1298C/C677T polymorphisms and increased Hcy levels. This study may be helpful for the prevention and guidance of VPA-induced liver dysfunction.

Four kinds of body temperatures and their relationships with thermal perception.

Body temperature serves as the principal factor in thermal perception determination. Current thermal comfort researches mainly focused on skin temperature, while other kinds of body temperatures were often ignored. In laboratory with strictly controlled environment, 26 subjects (13 males and 13 females) remained seated for a duration of 130 min in two thermal environments (19 °C and 35 °C), arranged in a particular order; four kinds of body temperatures (skin temperature, oral temperature, auditory canal temperature and breath temperature) and three kinds of thermal perception votes (thermal sensation, thermal comfort and thermal acceptable) were regularly collected. The analysis results showed that, skin temperature and breath temperature significantly changed with ambient temperature (p < 0.001); the difference between average value of core temperature in two conditions was small (≤0.3 °C), but a significant difference was almost observed in auditory canal temperature of males (p = 0.07). Both skin temperature and breath temperature were significantly related with three subjective votes (p < 0.001), meanwhile, the prediction accuracy of breath temperature for thermal perception was in no way inferior to skin temperature. Although oral temperature and auditory canal temperature had partial significant correlations with thermal perception, they were difficult to be carried out in practical application due to their weak explanatory powers (correlation coefficient <0.3). In summary, this research tried to establish correlation laws between body temperatures and thermal perception votes during a temperature step-change experiment, while finding the potential of utilizing breath temperature for thermal perception prediction, which is expected to be further promoted in the future.

Application of biomaterials in the eradication of Helicobacter pylori: A bibliometric analysis and overview.

Helicobacter pylori is a prominent cause of gastritis, peptic ulcer, and gastric cancer. It is naturally colonized on the surface of the mucus layer and mucosal epithelial cells of the gastric sinus, surrounded not only by mucus layer with high viscosity that prevents the contact of drug molecules with bacteria but also by multitudinous gastric acid and pepsin, inactivating the antibacterial drug. With high-performance biocompatibility and biological specificity, biomaterials emerge as promising prospects closely associated with H. pylori eradication recently. Aiming to thoroughly summarize the progressing research in this field, we have screened 101 publications from the web of science database and then a bibliometric investigation was performed on the research trends of the application of biomaterials in eradicating H. pylori over the last decade utilizing VOSviewer and CiteSpace to establish the relationship between the publications, countries, institutions, authors, and most relevant topics. Keyword analysis illustrates biomaterials including nanoparticles (NPs), metallic materials, liposomes, and polymers are employed most frequently. Depending on their constituent materials and characterized structures, biomaterials exhibit diverse prospects in eradicating H. pylori regarding extending drug delivery time, avoiding drug inactivation, target response, and addressing drug resistance. Furthermore, we overviewed the challenges and forthcoming research perspective of high-performance biomaterials in H. pylori eradication based on recent studies.

YAP and ß-catenin cooperate to drive H. pylori-induced gastric tumorigenesis.

H. pylori infection is the strongest known risk factor for gastric carcinoma. The activation of the yes-associated protein 1 (YAP) and ß-catenin pathways has been associated with multiple tumor types. In this study, we investigated the crosstalk between the YAP and ß-catenin pathways in H. pylori-associated gastric tumorigenesis. Immunohistochemical analysis of YAP and ß-catenin expression was performed in human gastric cancer tissues. The small molecules Super-TDU and KYA1797K, pharmacological inhibitors of YAP and ß-catenin, respectively, were used to investigate the role of these signaling pathways in H. pylori-induced gastric carcinogenesis in murine models of infection. The common downstream targets of YAP and ß-catenin signaling were evaluated by RNA sequencing (RNA-seq). Western blot, immunofluorescence, luciferase, RT-PCR, immunoprecipitation, cell counting kit-8 (CCK8), EdU and spheroid assays were used. H. pylori infection promoted YAP and ß-catenin nuclear accumulation and transcriptional activity in gastric epithelial cells and transgenic insulin-gastrin (INS-GAS) mice, whereas silencing of both YAP and ß-catenin synergistically inhibited H. pylori-induced cell proliferation and expansion. In addition, YAP was found to directly interact with ß-catenin and knockdown of YAP suppressed H. pylori-induced nuclear translocation of ß-catenin. Moreover, downstream genes caudal-type homeobox 2 (CDX2), leucine-rich repeat containing G protein-coupled receptor 5 (LGR5) and RuvB like AAA ATPase 1 (RUVBL1) were shared by both YAP and ß-catenin signaling. Furthermore, treatment with the YAP inhibitor Super-TDU or ß-catenin inhibitor KYA1797A significantly alleviated gastric inflammation and epithelial DNA damage in H. pylori-infected mice. Finally, the elevation of gastric YAP was positively correlated with ß-catenin expression in human gastric cancer tissues. These findings indicate that YAP and ß-catenin synergistically promote H. pylori-induced gastric carcinogenesis via their physical interaction and reveal that CDX2, LGR5 and RUVBL1 are the downstream genes shared by both the YAP and ß-catenin signaling pathways, and potentially contribute to H. pylori pathogenesis.

Treatment of refractory Helicobacter pylori infection: A new challenge for clinicians.

Patients who have failed two or more attempts to eradicate Helicobacter pylori are commonly referred to as refractory. Although the incidence of refractory Helicobacter pylori infection is only 10-20%, with the increasing rate of antibiotic resistance in various regions, the treatment of refractory Helicobacter pylori infection has gradually become a difficult problem faced by clinicians. When choosing a rescue therapy, the physician must consider numerous factors. A longer treatment duration, higher doses of proton pump inhibitors (PPIs), or the use of potassium-competitive acid blocker (P-CAB) may increase the efficacy of triple therapy or bismuth quadruple therapy. Rescue treatment based on bismuth quadruple therapy usually achieves better results. At the same time, treatment based on drug susceptibility tests or genotypic resistance is recommended where available. Of course, appropriate empiric treatment can also be selected according to local drug resistance, a patient's previous medication history and compliance. It is the best choice if it can improve the success rate of the first treatment and reduce the occurrence of refractory Helicobacter pylori infection. This review aims to summarize the articles related to refractory Helicobacter pylori in recent years and to explore a better remedial treatment plan for clinicians.

Discussion on regression analysis with small determination coefficient in human-environment researches.

As the main indicator for assessing the explanatory strength of regression model, there is no denying that a bigger value of determination coefficient (R-squared, R2 ) is the consistent pursuit of researchers in human-environment field, but whether to abandon or apply the model with a small value of R2 is an ongoing argument. This paper summarizes three characteristics of human-environment researches (large number of various variables, large mathematical sample size, and polynomial regression model). Based on the mathematical mechanism of regression analysis, theoretical analysis and case study are combined to point out the misconceptions that are easy to step into and the corresponding suggested methods from three perspectives: selection of determination coefficients, consideration of independent variables, and application of regression models. An extraordinary important point is, if the regression model passes the significance test, even with a small coefficient of determination, it can still quantitatively explain the impact extent of independent variables on dependent variables, but cannot comprehensively and accurately predict the specific value of dependent variable based on existing independent variables; moreover, the larger the sample size, the closer the interpretation of dependent variables in local model to ideal model. It is expected that these cases and lessons could help researchers to better apply regression analysis in human-environment researches, and that the small value of R2 would not be an excessive restriction affecting the development of scientific research in this field.

Probiotics mitigate Helicobacter pylori-induced gastric inflammation and premalignant lesions in INS-GAS mice with the modulation of gastrointestinal microbiota.

BACKGROUND: Dysbiosis of gastric microbiota including Helicobacter pylori (H. pylori) infection is associated with the development of stomach cancer. Probiotics have been shown to attenuate H. pylori-induced gastritis, although their role in cancer prevention remains unclear. Thus, we aimed to explore the effects of probiotics on H. pylori-induced carcinogenesis and the alterations of gastrointestinal microbiota. METHODS: Male INS-GAS mice were randomly allocated to H. pylori-infected and non-infected groups. After 4 weeks, probiotic combination (containing Lactobacillus salivarius and Lactobacillus rhamnosus) was administered in drinking water for 12 weeks. Stomachs were collected for RNA-Sequencing and the differentially expressed genes were validated using RT profiler PCR array. 16S rRNA gene sequencing was performed to assess the alterations of gastrointestinal microbiota. RESULTS: Probiotics significantly alleviate H. pylori-induced gastric pathology, including reduced infiltration of inflammation and lower incidence of precancerous lesions. RNA-Sequencing results showed that probiotics treatment decreased expressions of genes involved in pro-inflammatory pathways, such as NF-κB, IL-17, and TNF signaling pathway. Of note, probiotics did not suppress the growth of H. pylori, but dramatically reshaped the structure of both gastric and gut microbiota. The microbial diversity was increased in H. pylori-infected group after probiotics treatment. While gastric cancer-associated genera Lactobacillus and Staphylococcus were enriched in the stomach of H. pylori-infected group, the beneficial short-chain fatty acids-producing bacteria, including Bacteroides, Alloprevotella, and Oscellibacter, were more abundant in mice treated with probiotics. Additionally, probiotics restored the H. pylori-induced reduction of anti-inflammatory bacterium Faecalibaculum in the gut. CONCLUSIONS: Probiotics therapy can protect against H. pylori-associated carcinogenesis probably through remodeling gastrointestinal microbiota, which in turn prevent host cells from malignant transformation.

Helicobacter pylori infection activates Wnt/ß-catenin pathway to promote the occurrence of gastritis by upregulating ASCL1 and AQP5.

Helicobacter pylori (H. pylori) infection is a well-recognized contributing factor to gastritis, but the underlying mechanisms remain to be established. It is interesting to note that AQP5 was predicted to be highly expressed in intestinal metaplasia (IM) based on H. pylori infection-related microarray data, and the transcription factor ASCL1 was bioinformatically predicted to associate with AQP5. Therefore, the purpose of this study is to evaluate the mechanistic significance of ASCL1 and AQP5 in H. pylori infection of gastritis. Gastritis mouse models were established by H. pylori infection, followed by determination of AQP5 and ASCL1 in gastric mucosa. Besides, the effects of AQP5 on H. pylori-induced gastritis were explored using AQP5-/- mice. It was observed that H. pylori infection elevated expression of AQP5 and ASCL1 in gastric mucosa and gastric epithelial cells (GECs). H. pylori induced AQP5 expression by regulating ASCL1 and activated WNT/ß-catenin signaling pathway in GECs. It was also found that AQP5 knockdown suppressed inflammatory response and apoptosis in H. pylori-infected mice. Moreover, H. pylori infection-elevated ASCL1 and AQP5 expression promoted apoptosis and inflammation in GECs. Taken together, the key findings of the present study demonstrate that H. pylori infection activated WNT/ß-catenin signaling pathway by upregulating ASCL1/AQP5 to induce gastritis.

Objective sleep assessments for healthy people in environmental research: A literature review.

To date, although many studies had focused on the impact of environmental factors on sleep, how to choose the proper assessment method for objective sleep quality was often ignored, especially for healthy subjects in bedroom environment. In order to provide methodological guidance for future research, this paper reviewed the assessments of objective sleep quality applied in environmental researches, compared them from the perspective of accuracy and interference, and statistically analyzed the impact of experimental type and subjects' information on method selection. The review results showed that, in contrast to polysomnography (PSG), the accuracy of actigraphy (ACT), respiratory monitoring-oxygen saturation monitoring (RM-OSM), and electrocardiograph (ECG) could reach up to 97%, 80.38%, and 79.95%, respectively. In terms of sleep staging, PSG and ECG performed the best, ACT the second, and RM-OSM the worst; as compared to single methods, mix methods were more accurate and better at sleep staging. PSG interfered with sleep a great deal, while ECG and ACT could be non-contact, and thus, the least interference with sleep was present. The type of experiment significantly influenced the choice of assessment method (p < 0.001), 85.3% of researchers chose PSG in laboratory study while 82.5% ACT in field study; moreover, PSG was often used in a relatively small number of young subjects, while ACT had a wide applicable population. In general, researchers need to pay more attention at selection of assessments in future studies, and this review can be used as a reliable reference for experimental design.

A positive feedback loop of the TAZ/ß-catenin axis promotes Helicobacter pylori-associated gastric carcinogenesis.

Background: Helicobacter pylori infection is the strongest known risk factor for gastric cancer. The Hippo signaling pathway controls organ size and maintains tissue homeostasis by coordinately regulating cell growth and proliferation. Here, we demonstrate the interactive role of TAZ, the transcriptional coactivator of the Hippo pathway, and beta-catenin in promoting the pathogenesis of H. pylori infection. Methods: TAZ expression was evaluated in human gastric tissues and H. pylori-infected insulin-gastrin (INS-GAS) mice. Western blot, immunofluorescence, immunohistochemistry, and RT-PCR assays were performed. Coimmunoprecipitation was performed to examine the interaction between TAZ and ß-catenin. TAZ and ß-catenin were silenced using small interfering RNAs. HA-ß-catenin and Flag-TAZ were constructed. Results: Increased TAZ was noted in human gastric cancer tissues compared to chronic gastritis tissues and in H. pylori-positive gastritis tissues compared to H. pylori-negative gastritis tissues. In addition, H. pylori infection induced TAZ expression and nuclear accumulation in the gastric tissue of INS-GAS mice and cultured gastric epithelial cells, which was dependent on the virulence factor CagA. Moreover, TAZ or ß-catenin knockdown significantly suppressed H. pylori infection-induced cell growth, survival, and invasion. Furthermore, the interactive regulation of TAZ and ß-catenin activation was revealed. Finally, ß-catenin was required for H. pylori-induced TAZ activation. Conclusion: These findings suggest the existence of a positive feedback loop of activation between TAZ and ß-catenin that could play an important role in CagA+ H. pylori infection-induced gastric carcinogenesis. TAZ inhibition represents a potential target for the prevention of H. pylori infection-associated gastric cancer.

Research trends on the relationship between gut microbiota and colorectal cancer: A bibliometric analysis.

Background: Colorectal cancer (CRC)is the third most common cancer in the world and the second leading cause of cancer-related deaths, and over the past two decades, many of these researchers have provided a substantial amount of important information on the role of gut microbes in the development and progression of CRC. A causal relationship between the presence of specific microorganisms and CRC development has also been validated. Although a large number of papers related to this area have been published, no bibliometric study has been conducted to review the current state of research in this area and to highlight the research trends and hotspots in this area. This study aims to analyze the current status and future research trends of gut microbiota and CRC through bibliometric analysis. Methods: Publications from 2001 to 2022 were retrieved from the Web of Science Core Collection database and screened according to inclusion criteria. VOSviewer and CiteSpace software were used to visualize the research trends in this field, including the analysis of title, country, institution, author, number of publications, year of publication, number of citations, journal, and H-index. Results: A total of 863 studies were eventually identified, and the articles retrieved were cited an average of 44.85 times each. The number of publications on this topic has been increased steadily since 2011. China and the USA have made the largest contribution in the field. FRONTIERS IN MICROBIOLOGY is the top productive journal with 26 papers, and Gut journal has the highest average citation (167.23). Shanghai Jiao Tong University is the most contributive institution. Professor Yu J, Sung, Joseph J. Y and Fang JY are the most productive authors in this field. Keyword co-occurrence analysis showed that the terms of "Gut Microbiota", "Colorectal Cancer", "Inflammation", "Probiotic" and "Fusobacterium Nucleatum" were the most frequent, which revealed the research hotpots and trends in this field. Conclusions: There has been a growing number of publications over the past two decades according to the global trends. China and the USA still maintained the leading position in this field. However, collaboration between institutions needs to be strengthened. It's commended to pay attention to the latest hotspots, such as "F. nucleatum" and "probiotics". This bibliometric analysis evaluates the scope and trends of gut microbiota and CRC, providing a useful perspective on current research and future directions for studying the link between the gut microbiota and CRC.

Graph Convolutional Network: Traffic Speed Prediction Fused with Traffic Flow Data.

Traffic speed prediction plays an important role in intelligent transportation systems, and many approaches have been proposed over recent decades. In recent years, methods using graph convolutional networks (GCNs) have been more promising, which can extract the spatiality of traffic networks and achieve a better prediction performance than others. However, these methods only use inaccurate historical data of traffic speed to forecast, which decreases the prediction accuracy to a certain degree. Moreover, they ignore the influence of dynamic traffic on spatial relationships and merely consider the static spatial dependency. In this paper, we present a novel graph convolutional network model called FSTGCN to solve these problems, where the model adopts the full convolutional structure and avoids repeated iterations. Specifically, because traffic flow has a mapping relationship with traffic speed and its values are more exact, we fused historical traffic flow data into the forecasting model in order to reduce the prediction error. Meanwhile, we analyzed the covariance relationship of the traffic flow between road segments and designed the dynamic adjacency matrix, which can capture the dynamic spatial correlation of the traffic network. Lastly, we conducted experiments on two real-world datasets and prove that our model can outperform state-of-the-art traffic speed prediction.

Expression and prognostic significance of the DNA damage response pathway and autophagy markers in gastric cancer.

Gastric cancer (GC) is a leading cause of mortality and morbidity worldwide. We assessed the expression patterns of DNA damage response (DDR)-related markers, including ATM, CHK2, p-p53 (S15), Rad51, and BRCA2 and autophagy-related proteins including p62 and Beclin-1 in 153 GC specimens using immunohistochemistry staining. GC tissues showed lower levels of ATM, CHK2, p-p53, BRCA2, and higher levels of Rad51 compared to adjacent normal tissues. The autophagy-related protein p62 was upregulated, whereas Beclin-1 was downregulated in human GC groups. Additionally, different statuses of DDR pathways and autophagy characterized by protein expression were associated with overall survival. Our results indicated that the impairment of DNA damage and autophagy may be implicated in gastric cancer progression and its clinical prognosis.

Upregulation of oncogene Activin A receptor type I by Helicobacter pylori infection promotes gastric intestinal metaplasia via regulating CDX2.

BACKGROUND: Activin A receptor type I (ACVR1) is involved in tumorigenesis. However, the underlying molecular mechanisms of ACVR1 in gastric cancer (GC) and its association with Helicobacter pylori remained unclear. MATERIALS AND METHODS: The Cancer Genome Atlas (TCGA) and Gene Expression Profiling Interactive Analysis (GEPIA) database were utilized to explore the ACVR1 expression in GC and normal control and its association with survival. The ACVR1 was knocked out using CRISPR/Cas-9; RNA sequencing analysis was performed in AGS cells with ACVR1 knockout and normal control. Functional experiments (CCK-8, colony-forming, and transwell assays) were conducted to demonstrate the role of ACVR1 in cell proliferation, invasion, and metastasis. H. pylori-infected C57/BL6 models were established. ACVR1, p-Smad1/5, and CDX2 were detected in AGS cells cocultured with H. pylori strains. The CDX2 and key elements of BMP signaling pathway were detected in AGS cells with ACVR1 knockout and normal control. In addition, Immunohistochemistry was performed to detect the ACVR1 and CDX2 expression in gastric samples. RESULTS: ACVR1 expression was higher in GC than normal control from TCGA, GEPIA, and samples collected from our hospital (p < 0.05). ACVR1 promoted cell proliferation, migration, and invasion in vitro. Both cagA+ and cagA- H. pylori could upregulate the expression ACVR1 (p < 0.05). Downregulation of ACVR1 inhibited the H. pylori-induced cell proliferation, migration, and invasion (p < 0.05). H. pylori increased the expression of p-Smad 1/5 and CDX2. The CDX2 and key elements of BMP signaling pathway were downregulated in AGS cells with ACVR1 knockout. ACVR1 and CDX2 were upregulated in the stage of intestinal metaplasia (IM). Moreover, ACVR1 and CDX2 expressions were higher in H. pylori-positive group than H. pylori-negative group (p < 0.05). CONCLUSION: Our data indicate that H. pylori infection increases ACVR1 expression, promoting gastric IM via regulating CDX2, which is an essential step in H. pylori carcinogenesis.

Environmental factors affecting sleep quality in summer: a field study in Shanghai, China.

Although the environment can greatly influence an individual's sleep quality, China is yet to conduct comprehensive research on the topic. This study investigated the bedroom environment and sleep quality of 41 households during summer in Shanghai. Bedroom environments were comprehensively evaluated through environmental perception questionnaires filled by participants after waking up every morning. Parameters, such as air temperature, relative humidity, CO2 concentration, and noise level were continuously monitored. Furthermore, participants' sleep quality was observed using both subjective questionnaires and physiological measures. Environmental measurements showed that the most comfortable air temperature and relative humidity was 24.8 °C and 64%, respectively. Physiological measurements showed that the average duration of slow wave sleep (SWS) and sleep efficiency (SE) was 73.8 min and 86.7%, respectively. Additionally, SWS was negatively correlated with air temperature (r = -0.377, p = 0.015) and CO2 concentration (r = -0.362, p = 0.02), and SE was negatively correlated with noise level (r = -0.32, p = 0.042). The subjective and objective results consistently indicated that higher air temperature, CO2 concentration, and noise level leads to poor sleep quality in summer. In addition, air temperature and CO2 concentration had a greater impact on the sleep quality of males, while noise level had a greater impact on the sleep quality of females.

Activation of Aquaporin 5 by carcinogenic Helicobacter pylori infection promotes epithelial-mesenchymal transition via the MEK/ERK pathway.

BACKGROUND: Helicobacter pylori (H. pylori) is a major risk factor for gastric cancer. The water channel protein Aquaporin 5 (AQP5) is involved in the tumorigenesis and progression of various cancers. In this study, we aimed to explore the role of AQP5 in H. pylori-induced gastric carcinogenesis. MATERIALS AND METHODS: We collected 160 samples which inculded CNAG, IM, Dys and gastric cancer from patients who underwent endoscopy and detected the expression of AQP5. In vivo and vitro H. pylori infection models, we explored the relationship between AQP5 and H. pylori. Plasmid, siRNA and inhibitors were used to investigated the relationship between AQP5 and EMT and the role of AQP5 in H. pylori-induced gastric carcinogenesis. RESULT: AQP5 expression was gradually increased in human gastric tissues with the progression of chronic nonatrophic gastritis to gastric cancer and associated with the H. pylori infection status. In vivo and in vitro studies showed that H. pylori infection induced AQP5 expression in gastric epithelial cells in a CagA-dependent manner. Knockdown of AQP5 reversed H. pylori-induced cell proliferation and invasion, and -suppressed cell apoptosis. Additionally, knockdown of AQP5 suppressed H. pylori-induced Epithelial-mesenchymal transition (EMT) phenotypes by regulating transcriptional factors, mesenchymal markers, and epithelial markers. CONCLUSIONS: We explored the underlying mechanism and our results indicated that knockdown of AQP5 significantly suppressed H. pylori infection-induced phosphorylation of ERK1/2, MEK and the expression levels of downstream genes. Treatment with an ERK inhibitor suppressed the EMT induced by H. pylori infection. Taken together, this study suggest that pathogenic H. pylori infection promotes AQP5 expression to induce the EMT via the MEK/ERK signaling pathway.