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.

Macrophage biology in the pathogenesis of Helicobacter pylori infection.

Infection with H. pylori induces chronic gastric inflammation, progressing to peptic ulcer and stomach adenocarcinoma. Macrophages function as innate immune cells and play a vital role in host immune defense against bacterial infection. However, the distinctive mechanism by which H. pylori evades phagocytosis allows it to colonize the stomach and further aggravate gastric preneoplastic pathology. H. pylori exacerbates gastric inflammation by promoting oxidative stress, resisting macrophage phagocytosis, and inducing M1 macrophage polarization. M2 macrophages facilitate the proliferation, invasion, and migration of gastric cancer cells. Various molecular mechanisms governing macrophage function in the pathogenesis of H. pylori infection have been identified. In this review, we summarize recent findings of macrophage interactions with H. pylori infection, with an emphasis on the regulatory mechanisms that determine the clinical outcome of bacterial infection.

Spatial Variation of the Gastrointestinal Microbiota in Response to Long-Term Administration of Vonoprazan in Mice With High Risk of Gastric Cancer.

BACKGROUND: Vonoprazan, a potassium-competitive acid blocker, is superior to traditional proton pump inhibitor (PPI) in acid suppression and has been approved in the treatment of acid-related disorders. Accumulating evidence suggest associations between PPI use and gut microbiota, yet the effect of vonoprazan on GI microbiota is obscure. METHODS: Transgenic FVB/N insulin-gastrin (INS-GAS) mice as a model of gastric cancer (GC) were administered vonoprazan by gavage every other day for 12 weeks. Stomachs were evaluated by histopathology, Ki-67 proliferation index, and inflammatory cytokines. The mucosal and lumen microbiota from stomach, jejunum, ileum, cecum, and feces were detected using 16S rRNA gene sequencing. RESULTS: Higher incidence of intestinal metaplasia and epithelial proliferation were observed in the vonoprazan group than that in the control mice. Vonoprazan also elevated the gastric expression of proinflammatory cytokines, including TNF-α, IL-1ß, and IL-6. Each mice comprised a unique microbiota composition that was consistent across different niches. The structure of GI microbiota changed dramatically after vonoprazan treatment with the stomach being the most disturbed segment. Vonoprazan administration shifted the gut microbiota toward the enrichment of pathogenic Streptococcus, Staphylococcus, Bilophila, and the loss of commensal Prevotella, Bifidobacterium, and Faecalibacterium. Interestingly, compared to the controls, microbial interactions were weaker in the stomach while stronger in the jejunum of the vonoprazan group. CONCLUSIONS: Long-term vonoprazan treatment promoted gastric lesions in male INS-GAS mice, with the disequilibrium of GI microbiome. The clinical application of vonoprazan needs to be judicious particularly among those with high risk of GC.

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.

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.

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.

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.

MiR-155 promotes colitis-associated intestinal fibrosis by targeting HBP1/Wnt/ß-catenin signalling pathway.

Intestinal fibrosis is the most common complication of Crohn's disease (CD) that is one major disorder of inflammatory bowel disease (IBD), but the precise mechanism remains unclear. MiR-155 has been involved in fibrotic diseases. Here, we determined the role of miR-155 in regulating intestinal fibrosis. MiR-155 levels were significantly up-regulated in CD patients with intestinal stricture CD. The overexpression of miR-155 significantly aggravated TNBS-induced CD-associated intestinal fibrosis. Mechanistically, we identified that HBP1, a negative regulator of the Wnt/ß-catenin signalling pathway, is a direct target of miR-155. Moreover, in vitro and in vivo experiments suggested that the miR-155/HBP1 axis activates Wnt/ß-catenin signalling pathway to induce intestinal fibrosis. Taken together, we demonstrated that miR-155 directly targets HBP1 to induce CD-associated intestinal fibrosis via Wnt/ß-catenin signalling pathway.

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.

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.

Helicobacter pylori infection worsens impaired glucose regulation in high-fat diet mice in association with an altered gut microbiome and metabolome.

Emerging evidence suggests that Helicobacter pylori infection is associated with metabolic disorders, although the underlying mechanisms are poorly defined. This study aimed to investigate the interaction among H. pylori, a high-fat diet (HFD), and the gut microbiota with glucose regulation and alterations in microbial metabolites. Mice were randomly allocated to H. pylori-infected and noninfected groups fed a chow diet or an HFD. After 4 weeks, two of the HFD groups were given antibiotic cocktails for 8 weeks to eliminate the gut microbiota. The results showed that an HFD significantly promoted increases in body weight, insulin resistance, and glucose intolerance, which were alleviated to normal after antibiotic treatment. H. pylori infection aggravated HFD-induced hyperglycemia, which could not be restored by antibiotics. The perturbation of the gut microbiota was greater in the mice cotreated with H. pylori and an HFD (HFDHp) compared to those administered either H. pylori or an HFD alone, with a loss of diversity, higher abundance of Helicobacter, and lower abundance of Lactobacillus. Furthermore, compared to that of the HFD alone group, the gut microbiota of the HFDHp group was much more susceptible to antibiotic destruction, with extremely lower diversity and dominance of Klebsiella. Fecal metabolome analyses demonstrated that the combination of H. pylori infection and an HFD altered metabolic composition and function, which were linked to glucose dysregulation. H. pylori infection may exacerbate the dysbiosis of the gut microenvironment induced by an HFD, including alterations in the microbiota and metabolites, which weakens the restorative effect of antibiotics and results in the persistence of glucose disorders. KEY POINTS: • The interplay of Hp, HFD, and antibiotics on glucose metabolism was firstly explored. • Hp infection impaired the effect of antibiotics on HFD-induced glucose dysregulation. • Hp infection altered gut microbiota and metabolites which aggravated by HFD.

Experimental study on sleep quality affected by carbon dioxide concentration.

This study comprehensively investigated the impact of indoor carbon dioxide (CO2 ) concentration on sleep quality. Three experimental conditions (800, 1900, 3000 ppm) were created in chambers decorated as bedroom and other environmental parameters that may influence the sleep quality were under strict control. Sleep quality of 12 subjects (6 men and 6 women) was monitored for 54 consecutive days through sleep quality questionnaire and physiological measures. Both subjective and physiological results showed that sleep quality decreased significantly with the increase of CO2 concentration, and the comprehensive questionnaire score at 3000 ppm was only 80.8% of that at 800 ppm. A linear positive correlation was found between sleep onset latency (SOL) and CO2 concentration, while a linear negative correlation occurred between slow-wave sleep (SWS) and CO2 concentration. In addition, in the same sleep environment, men had higher subjective questionnaire scores after wake-up, longer SWS and shorter SOL, which lead to a better sleep quality compared with women, and there was a significant gender difference in sleep quality at 800 ppm (P < .05).

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.

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.

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.

A 3-miRNA signature predicts survival of patients with hypopharyngeal squamous cell carcinoma after post-operative radiotherapy.

Since the prognosis of hypopharyngeal squamous cell carcinoma (HSCC) remains poor, identification of miRNA as a potential prognostic biomarker for HSCC may help improve personalized therapy. In the 2 cohorts with a total of 511 patients with HSCC (discovery: N = 372 and validation: N = 139) after post-operative radiotherapy, we used miRNA microarray and qRT-PCR to screen out the significant miRNAs which might predict survival. Associations of miRNAs and the signature score of these miRNAs with survival were performed by Kaplan-Meier survival analysis and multivariate Cox hazard model. Among 9 candidate, miRNAs, miR-200a-3p, miR-30b-5p, miR-3161, miR-3605-5p, miR-378b and miR-4451 were up-regulated, while miR-200c-3p, miR-429 and miR-4701 were down-regulated after validation. Moreover, the patients with high expression of miR-200a-3p, miR-30b-5p and miR-4451 had significantly worse overall survival (OS) and disease-specific survival (DSS) than did those with low expression (log-rank P < .05). Patients with a high-risk score had significant worse OS and DSS than those with low-risk score. Finally, after adjusting for other important prognostic confounders, patients with high expression of miR-200a-3p, miR-30b-5p and miR-4451 had significantly high risk of overall death and death owing to HSCC and patients with a high-risk score has approximately 2-fold increased risk in overall death and death owing to HSCC compared with those with a low-risk score. These findings indicated that the 3-miRNA-based signature may be a novel independent prognostic biomarker for patients given surgery and post-operative radiotherapy, supporting that these miRNAs may jointly predict survival of HSCC.

Cochlear implantation in patients with ossified cochleas.

PURPOSE: The timing of CI for postmeningitic deafness is controversial and differential outcomes have been reported. To review and share our surgical and auditory outcomes. MATERIALS AND METHODS: 17 patients with ossified cochleas who received CI were enrolled. Clinical data including the cause of cochlear ossification, preoperative examination, onset of deafness, age at implantation, surgical findings, and relevant auditory outcomes was analysed. RESULTS: Cochlear ossification was observed in 53% of patients with HRCT, whereas the corresponding value for MRI was 59%. Patients in both stage I and II received complete insertion of the electrode array, however, stage III patients only received partial insertion. 1 patient in stage II received bilateral CI. Hearing tests showed increased average hearing threshold for stage III patients than those in stage I and II (P < 0.05). CAP scores were much lower for stage III patients than those in stage I and II (P < 0.05). Postlingual deafness patients showed higher SIR scores than prelingual deafness children (P < 0.05). CONCLUSIONS: HRCT and MRI have comparable value in predicting the occurrence of ossification in cochleas. We recommend fast surgical intervention in the patients with bilateral profound postmeningitic deafness. If possible, bilateral cochlear implantation is recommended.

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.

Sex differences in body temperature and thermal perception under stable and transient thermal environments: A comparative study.

Sex difference stands as a crucial factor necessitating consideration in personalized thermal environment control, with the mechanisms of its emergence potentially differing across different thermal environments. However, a comparative analysis of sex differences regarding body temperature (skin and core body temperature) and thermal perception across different environments is lacking. A stable environmental experiment (comprising three conditions: 16 °C, 20 °C, and 24 °C) and a transient environmental experiment (involving a whole-body step-change from 19 °C to 35 °C and back to 19 °C) were conducted, with participation from 20 young males and 20 young females. Skin temperature and core body temperature were continuously recorded during the experiments, and three types of thermal perceptions were regularly collected. The results showed that: (1) The impact of thermal environment on females' skin temperature surpassed that on males, in stable environment, with every 1 °C rise in ambient temperature, the mean skin temperature increased by 0.28 °C for males and 0.35 °C for females respectively; in transient environment, females' mean skin temperature raise and fell at a faster rate. (2) Males exhibited stronger thermal regulation abilities than females, particularly evident during sudden increase in ambient temperature (from 19 °C to 35 °C), where the reduction magnitude of males' core body temperature was notably larger. (3) Whether in stable or transient environments, significant sex differences often occurred in skin temperature and thermal sensation at distal parts, particularly at the hand. (4) Males typically fed back higher levels of thermal comfort and thermal acceptability than females, suggesting that in addition to physiological sex differences, psychological sex distinctions also play a role. In summary, personalized design for stable thermal environment can focus on sex differences in skin temperature, while transient thermal environment requires consideration of both skin temperature and core body temperature. A comprehensive consideration of physiological and psychological sex differences aids in creating personalized thermal environments with greater precision.