Transition metals-based electrocatalysts on super-flat substrate for perovskite photovoltaic hydrogen production with 13.75% solar to hydrogen efficiency.

Harnessing the inexhaustible solar energy for water splitting is regarded one of the most promising strategies for hydrogen production. However, sluggish kinetics of oxygen evolution reaction (OER) and expensive photovoltaics have hindered commercial viability. Here, an adhesive-free electrodeposition process is developed for in-situ preparation of earth-abundant electrocatalysts on super-flat indium tin oxide (ITO) substrate. NiFe hydroxide exhibited prominent OER performance, achieving an ultra-low overpotential of 236 mV at 10 mA/cm2 in alkaline solution. With the superior OER activity, we achieved an unassisted solar water splitting by series connected perovskite solar cells (PSCs) of 2 cm2 aperture area with NiFe/ITO//Pt electrodes, yielding overall solar to hydrogen (STH) efficiency of 13.75 %. Furthermore, we upscaled the monolithic facility to utilize perovskite solar module for large-scale hydrogen production and maintained an approximate operating current of 20 mA. This creative strategy contributes to the decrease of industrial manufacturing expenses for perovskite-based photovoltaic-electrochemical (PV-EC) hydrogen production, further accelerating the conversion and utilization of carbon-free energy.

Genetically engineered CD276-anchoring biomimetic nanovesicles target senescent escaped tumor cells to overcome chemoresistant and immunosuppressive breast cancer.

Chemotherapy-induced cellular senescence leads to an increased proportion of cancer stem cells (CSCs) in breast cancer (BC), contributing to recurrence and metastasis, while effective means to clear them are currently lacking. Herein, we aim to develop new approaches for selectively killing senescent-escape CSCs. High CD276 (95.60%) expression in multidrug-resistant BC cells, facilitates immune evasion by low-immunogenic senescent escape CSCs. CALD1, upregulated in ADR-resistant BC, promoting senescent-escape of CSCs with an anti-apoptosis state and upregulating CD276, PD-L1 to promote chemoresistance and immune escape. We have developed a controlled-released thermosensitive hydrogel containing pH- responsive anti-CD276 scFV engineered biomimetic nanovesicles to overcome BC in primary, recurrent, metastatic and abscopal humanized mice models. Nanovesicles coated anti-CD276 scFV selectively fuses with cell membrane of senescent-escape CSCs, then sequentially delivers siCALD1 and ADR due to pH-responsive MnP shell. siCALD1 together with ADR effectively induce apoptosis of CSCs, decrease expression of CD276 and PD-L1, and upregulate MHC I combined with Mn2+ to overcome chemoresistance and promote CD8+T cells infiltration. This combined therapeutic approach reveals insights into immune surveillance evasion by senescent-escape CSCs, offering a promising strategy to immunotherapy effectiveness in cancer therapy.

Metabotropic Glutamate Receptor 5: A Potential Target for Neuropathic Pain Treatment.

Neuropathic pain, a multifaceted and incapacitating disorder, impacts a significant number of individuals globally. Despite thorough investigation, the development of efficacious remedies for neuropathic pain continues to be a formidable task. Recent research has revealed the potential of metabotropic glutamate receptor 5 (mGlu5) as a target for managing neuropathic pain. mGlu5 is a receptor present in the central nervous system that has a vital function in regulating synaptic transmission and the excitability of neurons. This article seeks to investigate the importance of mGlu5 in neuropathic pain pathways, analyze the pharmacological approach of targeting mGlu5 for neuropathic pain treatment, and review the negative allosteric mGlu5 modulators used to target mGlu5. By comprehending the role of mGlu5 in neuropathic pain, we can discover innovative treatment approaches to ease the distress endured by persons afflicted with this incapacitating ailment.

Integrating network pharmacology and experimental validation to investigate the effects and mechanism of Renshen Shouwu decoction for ameliorating Alzheimer's disease.

CONTEXT: The mechanism of Renshen Shouwu Decoction (RSSW) in treating Alzheimer's disease (AD) remains unknown. OBJECTIVE: This study investigates the effects and mechanism of RSSW for ameliorating AD. MATERIALS AND METHODS: Ten SAMR1 mice and 40 SAMP8 mice were divided into five groups: control (SAMR1), model (SAMP8), positive drug (Donepezil, 1.3 mg/kg/d), and RSSW (Low-dose, 117 mg/kg/d; High-dose, 234 mg/kg/d). Starting from 6 months of age, the medications were administered intragastrically for a total of 60 days. Subsequently, memory improvement in rapidly aging mice was assessed using the novel object recognition test and Morris water maze test. Through the identification of absorbed blood components and analysis of network pharmacology, active ingredients and potential targets involved in the treatment of AD were identified. Finally, AD-related biological indicators were detected using western blotting and ELISA. RESULT: Our results demonstrated that RSSW effectively ameliorated memory impairments, inhibited tau hyperphosphorylation, and reduced ß-amyloid plaque deposition in SAMP8 mice. Thirty absorbed blood components in RSSW were identified, revealing identified 96 major targets that play a key role in alleviating AD. Notably, the obtained main targets were highly enriched in SIRT1-mediated signaling pathways. Subsequent experimental validation confirmed that RSSW activated the SIRT1/NF-κB, SIRT1/AMPK, and SIRT1/p53 signaling cascades. Nine potential active ingredients were predicted through molecular docking. DISCUSSION AND CONCLUSIONS: Our research findings suggest the mechanism of RSSW treatment for AD, which ameliorates memory impairments by reducing cortical tissue inflammation and apoptosis.

The association between oral frailty and HbA1c among older adults with T2DM: the chain mediating effect of nutritional status and physical frailty.

OBJECTIVES: The present study aimed to explore the association between oral frailty and glycated hemoglobin (HbA1c), and the chain mediating role of nutritional status and physical frailty among older adults with type 2 diabetes mellitus (T2DM). METHODS: Patients with T2DM aged > 60 years were recruited from the endocrinology department of a national metabolic center from October 2023 to March 2024. Oral frailty, nutritional status, and physical frailty were assessed with Oral Frailty Index-8 (OFI-8), the Nutrition Risk Screening 2002 (NRS2002), Fatigue, Resistance, Ambulation, Illness and Loss of Weight Index (FRAIL), respectively. Their HbA1c were collected at the same time. In order to reveal the interaction and influence between multiple variables, chain mediation analyses were conducted using the "Process" macro in SPSS 26.0 to estimate the direct and indirect effects of oral frailty on nutritional status, physical frailty and HbA1c. RESULTS: A total of 292 participants (50.7% male) were enrolled in this study at a median age of 70.0 (65.2, 76.0) years and a T2DM disease duration of (16.5 ± 9.4) years. After adjustment for age, oral frailty of older people with T2DM significantly positively predicted their HbA1c (ß = 0.198, P < 0.001). In addition, oral frailty affect HbA1c through two indirect pathways, including an independent mediating effect of physical frailty (effect = 0.046) and a chain-mediating effect of nutritional status and physical frailty (effect = 0.004). CONCLUSIONS: Our findings suggest that less oral frailty of older adults with T2DM could optimize their nutritional status and physical frailty and, thus, their HbA1c. Consequently, improving oral health is expected to be a promising intervention target for reaching optimal glycaemic control in older adults with T2DM.

Error Model and Concise Temporal Network for Indirect Illumination in 3D Reconstruction.

3D reconstruction is a fundamental task in robotics and AI, providing a prerequisite for many related applications. Fringe projection profilometry is an efficient and non-contact method for generating 3D point clouds out of 2D images. However, during the actual measurement, it is inevitable to experiment with translucent objects, such as skin, marble, and fruit. Indirect illumination from these objects has substantially compromised the precision of 3D reconstruction via the contamination of 2D images. This paper presents a fast and accurate approach to correct for indirect illumination. The essential idea is to design a highly suitable network architecture founded on a precise error model that facilitates accurate error rectification. Initially, our method transforms the error generated by indirect illumination into a sine series. Based on this error model, the multilayer perceptron is more effective in error correction than traditional methods and convolutional neural networks. Our network was trained solely on simulated data but was tested on authentic images. Three sets of experiments, including two sets of comparison experiments, indicate that the designed network can efficiently rectify the error induced by indirect illumination.

Quantifying energy transition vulnerability helps more just and inclusive decarbonization.

The COP28 agreement signals "beginning of the end" of the fossil fuel era, calling on countries to contribute to global efforts to transition away from fossil fuels in energy systems in a just, orderly and equitable manner. While a quantitative assessment of country's vulnerability in energy transition is a prerequisite for national and international policy makers to ensure a just and inclusive transition, it is notably absent in the existing research. Here, we develop a conceptual framework based on the vulnerability scoping diagram (VSD) method to assess differences in energy transition vulnerability across countries, with a specific focus on the challenges associated with transitioning away from fossil fuels. The resulting energy transition vulnerability index (ETVI) scores reveal that countries in the Global South generally exhibit higher vulnerability in their energy transition compared to those in the Global North, and this gap has widened over the past decade. Moreover, the COVID-19 pandemic has disrupted the decade-long trend of continuous decline in global energy transition vulnerability. This study also provides two important applications of ETVI scores, aligning them with major global sustainable development agenda. Firstly, we identify substantial differences in the dynamics of transition vulnerability across seven major party groups in the international climate change negotiations and distinguish four energy transition statuses in relation to achieving global climate goals: Stressful, Leapfrog, Potential Challenges, and Less Painful. Secondly, we demonstrate crucial synergies between energy transition resilience and the 2030 United Nations Sustainable Development Goals (SDGs).

MEK inhibition prevents CAR-T cell exhaustion and differentiation via downregulation of c-Fos and JunB.

Clinical evidence supports the notion that T cell exhaustion and terminal differentiation pose challenges to the persistence and effectiveness of chimeric antigen receptor-T (CAR-T) cells. MEK1/2 inhibitors (MEKIs), widely used in cancer treatment due to their ability to inhibit aberrant MAPK signaling, have shown potential synergistic effects when combined with immunotherapy. However, the impact and mechanisms of MEKIs on CAR-T cells remain uncertain and controversial. To address this, we conducted a comprehensive investigation to determine whether MEKIs enhance or impair the efficacy of CAR-T cells. Our findings revealed that MEKIs attenuated CAR-T cell exhaustion and terminal differentiation induced by tonic signaling and antigen stimulation, thereby improving CAR-T cell efficacy against hematological and solid tumors. Remarkably, these effects were independent of the specific scFvs and costimulatory domains utilized in CARs. Mechanistically, analysis of bulk and single-cell transcriptional profiles demonstrates that the effect of MEK inhibition was related to diminish anabolic metabolism and downregulation of c-Fos and JunB. Additionally, the overexpression of c-Fos or JunB in CAR-T cells counteracted the effects of MEK inhibition. Furthermore, our Cut-and-Tag assay revealed that MEK inhibition downregulated the JunB-driven gene profiles associated with exhaustion, differentiation, anergy, glycolysis, and apoptosis. In summary, our research unveil the critical role of the MAPK-c-Fos-JunB axis in driving CAR-T cell exhaustion and terminal differentiation. These mechanistic insights significantly broaden the potential application of MEKIs to enhance the effectiveness of CAR-T therapy.

Periampullary duodenal neuroendocrine tumor in a patient with neurofibromatosis-1: A case report.

BACKGROUND: Patients with neurofibromatosis type 1 (NF1) are exposed to a higher risk of developing neuroendocrine tumors (NETs). Periampullary neuroendocrine neoplasms (NENs) in NF1 patients primarily affect the duodenum and periampullary region. CASE SUMMARY: A 50-year-old male patient was admitted to our hospital due to progressive skin and scleral yellowing for over 6 months. An abdominal contrast-enhanced computed tomography scan revealed a tumor in the periampullary region, which measured 1.2 cm × 1.4 cm in size and showed a progressive enhancement. Magnetic resonance cholangiopancreatography indicated the dilation of intrahepatic and extrahepatic bile ducts. The patient was diagnosed with an ampullary tumor with the possibility of malignancy. A Whipple procedure was performed. Microscopically, the duodenum tumor was found to invade the mucosa, sphincter, and muscular layer of the duodenal papilla. Histologic hematoxylin and eosin staining confirmed the presence of duodenal G1 NET. Subsequently, a bibliometric analysis was performed to evaluate the state of NEN research. Publications about periampullary NENs showed an annual increase, with most of them focusing on the treatment and diagnosis of NENs. CONCLUSION: This article reported a case of periampullary duodenal NET in a patient with NF1, and a bibliometric analysis was conducted.

PRMT1-mediated arginine methylation promotes YAP activation and hepatocellular carcinoma proliferation.

The activity of Hippo signaling is commonly dysregulated in various human malignancies, including hepatocellular carcinoma (HCC). YAP, the key effector of Hippo pathway, is regulated through several posttranslational modifications. However, the mechanism by which YAP is regulated by arginine methylation remains unknown. In this study, immunoprecipitation and mass spectrometry were used to identify the arginine methylation site of YAP in HCC cells. The transcriptional activity of YAP and TEAD were further characterized by real-time qPCR and immunofluorescence assay, and a subcutaneous and orthotopic tumor mouse model was used to assess the effect of PRMT1-knockdown on HCC tumor growth. The result of mass spectrometry analysis identified that YAP was methylated at arginine 124. Moreover, we found that arginine methyltransferase PRMT1 interacted with YAP to mediate its arginine methylation, thus inhibited YAP phosphorylation and promoted YAP activity in the nucleus. PRMT1 was up-regulated in HCC tissues and positively associated with the expressions of YAP target genes. Silencing PRMT1 in HCC cells inhibited cell proliferation and tumor growth, while PRMT1-overexpression promoted HCC growth through YAP methylation. Our study reveals that PRMT1-mediated arginine methylation at R124 is mutually exclusive with YAP S127 phosphorylation, thereby facilitating YAP activity in the nucleus and promoting tumorigenesis in HCC.

On-Chip Droplet Splitting with High Volume Ratios Using a 3D Conical Microstructure-Based Microfluidic Device.

This work reports a simple microfluidic method for splitting a mother droplet into two daughter droplets with high and precise volume ratios. To achieve this, a droplet-splitting microfluidic device embedded with a three-dimensional (3D) conical microstructure is fabricated, in which the high splitting ratios of monodisperse mother droplets are achieved. The volume ratio of the split daughter droplets can reach up to 265. In addition, we examined factors that affect the splitting ratio of the daughter droplets and found that the ratio is affected by the flow rates of the two individual outlet channels, the injection length of the conical microstructure, and the diameter of the original mother droplets. Numerical simulations of these parameters were conducted to gain a clearer understanding of the splitting behavior. The proposed droplet splitting device with a conical microstructure enables on-chip sample extraction and droplet volume control, which can be a powerful tool for various droplet-based applications in microfluidic devices such as viral infectivity assays and sequencing heterogeneous populations.

Surgical Face Mask as an Air Sampling Device for Assessing Personal Exposure to Airborne Antimicrobial Resistance Gene-Bearing Bacteria.

In this study, we assessed the feasibility of using a surgical face mask as a sampling device to collect airborne antimicrobial resistance genes (ARGs). The method entails collection of ARG-bearing microbes on face masks, followed by their DNA extraction and quantification by qPCR analysis. Analysis of masks worn by volunteers showed an apparent mask wearing time-dependent accumulation of 16S rRNA gene and select ARGs trapped on masks, highlighting the applicability of the method in monitoring personal ARG exposure through inhalation. The sampling method was then validated for reproducibility and compared with a filter-based sampling method before application in different environmental settings to further assess personal exposure to ARGs. In comparison with the filter-based method, our new sampling method does not require a sampling pump and is more user-friendly. More importantly, it records ARG exposure down to the personalized level; thus, it may be used in routine monitoring of occupational exposure and surveillance of ARG concentrations in indoor environments.

The Degradation and Migration of Cyclanilide in Soil and Sediment in China.

The environmental fate of a plant growth regulator cyclanilide was studied in this paper. The degradation, adsorption, and migration behaviors of cyclanilide were detailly measured in the laboratory. The results showed that the DT50 of cyclanilide degradation in the Jiangxi red, Taihu paddy, Changshu wushan, Shaanxi tide, and Dongbei black soils was 42.3 d, 31.9 d, 14.4 d, 30.4 d as well as 27.4 d under aerobic conditions and 32.3 d, 37.4 d, 29.3 d, 48.9 d as well as 27.0 d under water anaerobic conditions, respectively, with the main metabolite being 2,4-dichloroaniline (2,4-D). The DT50 of 2,4-D ranged from 5.26 to 27.1 days under aerobic conditions, and from 10.6 to 54.1 days under anaerobic conditions. The adsorption of cyclanilide by the soils was well fitted by the empirical linear adsorption isotherm, and the adsorption constant (Kd, H) values in the Jiangxi red, Taihu paddy, Changshu wushan, Shaanxi tide, and Dongbei black soils were 7.08, 4.49, 4.05, 3.20, and 1.41, respectively. The results of a mobility test showed that cyclanilide had strong mobility in the most test soils. Furthermore, soil pH is the dominant element affecting the adsorption of cyclanilide in the soils. Under aerobic environment, the DT50 of total cyclanilide in river and lake water-sediment systems were 30.7 d and 34.0 d, respectively; under anaerobic environment, their DT50 were 30.8 d and 31.4 d, respectively. In water-sediment systems, 2,4-D mainly exists in aqueous phase and the DT50 ranged from 5.23 to 8.76 days. This work demonstrated that cyclanilide has the potential risk to contaminate environment and attention should be paid to its application.

IL-4-Induced Gene 1: A Potential Player in Myocardial Infarction.

Myocardial infarction (MI), a severe outcome of cardiovascular disease, poses a serious threat to human health. Uncontrolled inflammation and excessive cardiomyocyte death, following an infarction event, significantly contribute to both the mortality rate and complications associated with MI. The protein IL-4-induced gene 1 (IL4I1 or FIG1) serves as a natural inhibitor of innate and adaptive immunity, playing a crucial role in CD4+ T cell differentiation, macrophage polarization, and ferroptosis inhibition. Previous studies have linked IL4I1 to acute MI. This review summarizes evidence from both basic and clinical research, highlighting IL4I1 as a critical immunoregulatory enzyme that not only regulates inflammatory responses, but also potentially mitigates MI-induced damage.

Serum metabolite biomarkers for the early diagnosis and monitoring of age-related macular degeneration.

INTRODUCTION: Age-related macular degeneration (AMD) is a leading cause of irreversible blindness worldwide, with significant challenges for early diagnosis and treatment. OBJECTIVES: To identify new biomarkers that are important for the early diagnosis and monitoring of the severity/progression of AMD. METHODS: We investigated the diagnostic and monitoring potential of blood metabolites in a cohort of 547 individuals (167 healthy controls, 240 individuals with other eye diseases as eye disease controls, and 140 individuals with AMD) from 2 centers over three phases: discovery phase 1, discovery phase 2, and an external validation phase. The samples were analyzed via a mass spectrometry-based, widely targeted metabolomic workflow. In discovery phases 1 and 2, we built a machine learning algorithm to predict the probability of AMD. In the external validation phase, we further confirmed the performance of the biomarker panel identified by the algorithm. We subsequently evaluated the performance of the identified biomarker panel in monitoring the progression and severity of AMD. RESULTS: We developed a clinically specific three-metabolite panel (hypoxanthine, 2-furoylglycine, and 1-hexadecyl-2-azelaoyl-sn-glycero-3-phosphocholine) via five machine learning models. The random forest model effectively discriminated patients with AMD from patents in the other two groups and showed acceptable calibration (area under the curve (AUC) = 1.0; accuracy = 1.0) in both discovery phases 1 and 2. An independent validation phase confirmed the diagnostic model's efficacy (AUC = 0.962; accuracy = 0.88). The three-biomarker panel model demonstrated an AUC of 1.0 in differentiating the severity of AMD via RF machine learning, which was consistent across both the discovery and external validation phases. Additionally, the biomarker concentrations remained stable under repeated freeze-thaw cycles (P > 0.05). CONCLUSIONS: This study reveals distinct metabolite variations in the serum of AMD patients, paving the way for the development of the first routine laboratory test for AMD.

Cardiovascular events in crush syndrome: on-site therapeutic strategies and pharmacological investigations.

Crush syndrome often occurs after severe crush injury caused by disasters or accidents, and is associated with high mortality and poor prognosis. Cardiovascular complications, such as cardiac arrest, hypovolemic shock, and hyperkalemia-related cardiac dysfunction, are the primary causes of on-site death in crush syndrome. Prehospital evaluation, together with timely and correct treatment, is of great benefit to crush syndrome patients, which is difficult in most cases due to limited conditions. Based on current data and studies, early fluid resuscitation remains the most important on-site treatment for crush syndrome. Novel solutions and drugs used in fluid resuscitation have been investigated for their effectiveness and benefits. Several drugs have proven effective for the prevention or treatment of cardiovascular complications in crush syndrome, such as hypovolemic shock, hyperkalemia-induced cardiac complications, myocardial ischemia/reperfusion injury, ventricular dysfunction, and coagulation disorder experimentally. Moreover, these drugs are beneficial for other complications of crush syndrome, such as renal dysfunction. In this review, we will summarize the existing on-site treatments for crush syndrome and discuss the potential pharmacological interventions for cardiovascular complications to provide clues for clinical therapy of crush syndrome.

Primary Aldosteronism Influences Cardiac Structure, Function, and Disease Risk: Evidence From Mendelian Randomization Analysis.

Although observational studies have linked primary aldosteronism (PA) with cardiovascular diseases (CVDs), the causality remains uncertain. In this study, we aimed to investigate whether PA is causally associated with CVD risk and cardiac magnetic resonance (CMR) parameters using the Mendelian randomization (MR) method. Independent and genome-wide significant single nucleotide polymorphisms for PA were extracted from genome-wide association study (GWAS) summary statistics. Genetic associations with the CVDs and CMR parameters were obtained from recent large-scale GWASs or genetic consortia. Inverse-variance weighted (IVW) method was utilized for the preliminary estimates, and multiple sensitivity analyses (including weighted median, Cochran's Q test, MR-Egger, MR-PRESSO, and leave-one-out analysis) were conducted to verify the robustness of the results. The MR analyses using the IVW method showed that genetically predicated PA was significantly associated with atrial fibrillation (OR = 1.046, 95% CI: 1.029-1.062, padj < 0.001), myocardial infarction (OR = 1.029, 95% CI: 1.005-1.053, padj = 0.027), heart failure (OR = 1.023, 95% CI: 1.004-1.042, padj = 0.027), any stroke (OR = 1.062, 95% CI: 1.031-1.095, padj < 0.001), any ischemic stroke (OR = 1.058, 95% CI: 1.022-1.095, padj = 0.004), and small vessel stroke (OR = 1.116, 95% CI: 1.041-1.196, padj = 0.004). Notably, PA also had a causal effect on adverse cardiac remodeling, including larger ventricular and atrial volumes, higher ventricular stroke volume, and reduced left atrial emptying fraction. Our findings support a causal role of PA in higher cardiovascular disease risk and adverse cardiac remodeling. Given the diagnostic delay and disease burden in PA, more attention should be paid to the screening and treatment of PA to reduce the incidence of cardiovascular outcomes.

The prevalence of alexithymia in schizophrenia: A systematic review and meta-analysis.

OBJECTIVES: This study aims to systematically evaluate the prevalence of alexithymia in patients with schizophrenia. METHODS: Computer searches were conducted in PubMed, PsycInfo, Web of Science, The Cochrane Library, EMBASE, China National Knowledge Infrastructure (CNKI), Wanfang Database, VIP Database, and China Biology Medicine (CBM) electronic databases to collect studies that utilized the TAS-20 scale as a measurement tool with clearly defined diagnostic criteria to determine the prevalence of alexithymia in patients with schizophrenia, from the inception of the databases to December 29, 2023. Two researchers independently screened the literature, extracted data, and evaluated the risk of bias in the included studies, followed by meta-analysis using Stata 16.0 software. RESULTS: A total of 17 studies with 5628 participants were included. The results of the meta-analysis showed that the prevalence of alexithymia in patients with schizophrenia was 35 % (95 % CI: 32-38 %). Subgroup analysis indicated that male gender, smoking, Asian ethnicity, case-control design and divorce were associated with higher rates of alexithymia (all P<0.05). CONCLUSION: The prevalence of alexithymia in patients with schizophrenia is relatively high (35 %). However, due to limitations in the quality and quantity of included studies, further high-quality literature is needed to confirm the above conclusion.

High-altitude cerebral oxygen saturation detection using wireless wearable cerebral oximeter.

Background: Hypobaric hypoxic conditions encountered at high altitudes can significantly impact the physiological functions of human body. Therefore, accurate and real-time monitoring of physiological characteristics is crucial for the prevention of brain injuries in individuals with acute and chronic high-altitude exposure. Methods: In this study, a wireless wearable cerebral oximeter (WORTH band) was used for the continuous, real-time monitoring of physiological parameters, including regional cerebral oxygen saturation (rSO2) and heart rate (HR), among subjects with high-altitude exposure. Results: During the high-altitude (from 46 m to 4300 m) expedition task, there was a significant decrease in rSO2 accompanied by a corresponding increase in heart rate as the altitude increased. Additionally, during the long-term (52 days) high-altitude (from 356 m to 4658 m) cycling task, the altitudes were significantly correlated with the rSO2 and SpO2 in the elderly subjects. Conclusion: The current findings indicate that the WORTH band oximeter can serve as a promising instrument for measuring rSO2 at high altitudes. We hope that the insights derived from this study could contribute to the management of cerebral oxygenation for individuals with high-altitude exposure and further expand the existing understanding of brain functional detection at high altitudes.