Expert consensus on perioperative integrated skincare for noninvasive energy-based device aesthetic procedures in clinical practice in China.

BACKGROUND: Noninvasive energy-based device (NI-EBD) aesthetic procedures has recently gained widespread usage for treating various skin conditions, enhancing skin texture and performing rejuvenation-related procedures. However, practically all NI-EBD procedures result in variable degrees of damage to the skin barrier, inducing pathological and physiological processes such as oxidative stress and inflammation, and only a small percentage of individuals possess the innate ability to restore it. OBJECTIVE: To introduce the concept of integrated skincare and establish standardized operational procedures for perioperative integrated skincare, and furnish a theoretical basis for clinical diagnosis and treatment performed by professional medical aestheticians. METHODS: The author leveraged domestic and international guidelines, clinical practice expertise and evidence-based research, adapting them to suit the specific circumstances in China. RESULTS: The consensus were provided four parts, including concept and essence of integrated skincare, integrated skincare significance during the perioperative phase of NI-EBD procedures, active ingredients and functions of effective skincare products, standardized perioperative skincare procedure for NI-EBD procedures and precautions. For the standardized perioperative skincare procedure, four recommendations were listed according to different stages during NI-EBD procedures. CONCLUSION: These recommendations create the 'Expert Consensus on Perioperative Integrated Skincare for Noninvasive Energy-Based Device Aesthetic Procedures in Clinical Practice in China'.

INDIVIDUAL ARTICLE: Real-World Patient Cases Using Botanical Serum-Containing Corrective Gel as an Adjunct to Aesthetic Facial Laser or Microneedling Radiofrequency (MRF) Treatment.

Integrated skin care is defined as the complementary use of topical treatments to nonsurgical facial rejuvenation procedures, such as lasers and radiofrequency microneedling devices, to produce pleasing aesthetic results. Real-world experience from expert dermatologists is invaluable in guiding patient treatment plans, as there are limited clinical trials on the efficacy of integrated skincare regimens. The SkinCeuticals (New York, NY) Phyto Corrective gel (botanical serum-containing corrective gel) contains a lightweight botanical serum that hydrates, calms, and soothes skin. It contains antioxidant and anti-inflammatory ingredients derived from plant and fruit extracts, making it an appealing option for adjunctive treatment of post-procedure erythema and swelling.  J Drugs Dermatol. 2024;23:3(Suppl 2):s3-s14.

Ambient precipitation determines the sensitivity of soil respiration to precipitation treatments in a marsh.

The effects in field manipulation experiments are strongly influenced by amplified interannual variation in ambient climate as the experimental duration increases. Soil respiration (SR), as an important part of the carbon cycle in terrestrial ecosystems, is sensitive to climate changes such as temperature and precipitation changes. A growing body of evidence has indicated that ambient climate affects the temperature sensitivity of SR, which benchmarks the strength of terrestrial soil carbon-climate feedbacks. However, whether SR sensitivity to precipitation changes is influenced by ambient climate is still not clear. In addition, the mechanism driving the above phenomenon is still poorly understood. Here, a long-term field manipulation experiment with five precipitation treatments (-60%, -40%, +0%, +40%, and +60% of annual precipitation) was conducted in a marsh in the Yellow River Delta, China, which is sensitive to soil drying-wetting cycle caused by precipitation changes. Results showed that SR increased exponentially along the experimental precipitation gradient each year and the sensitivity of SR (standardized by per 100 mm change in precipitation under precipitation treatments) exhibited significant interannual variation from 2016 to 2021. In addition, temperature, net radiation, and ambient precipitation all exhibited dramatic interannual variability; however, only ambient precipitation had a significant negative correlation with SR sensitivity. Moreover, the sensitivity of SR was significantly positively related to the sensitivity of belowground biomass (BGB) across 6 years. Structural equation modeling and regression analysis also showed that precipitation treatments significantly affected SR and its autotrophic and heterotrophic components by altering BGB. Our study demonstrated that ambient precipitation determines the sensitivity of SR to precipitation treatments in marshes. The findings underscore the importance of ambient climate in regulating ecosystem responses in long-term field manipulation experiments.

Time- and Dose-Resolved Proteome of PM2.5-Exposure-Induced Lung Injury and Repair in Rats.

In recent years, airborne fine particulate matter (PM2.5) is drawing more public attention due to its various physicochemical features and causing pathological harm, as proven by epidemiological and clinical studies. However, the mechanism of PM2.5-exposure-induced lung injury has not been fully characterized. Here, we established a PM2.5-induced rat injury model for both short-term and long-term exposures at different concentrations. We employed the Fast-seq technique to profile 6316 proteins and the catTFRE approach to profile 387 transcription factors (TFs) in the lung tissue. In short-term exposure, we elucidated gradually upregulated proteins enriched in response to oxidative stress, phagosome, and the extracellular matrix (ECM)-receptor interaction pathway. Long-term exposure mainly showed the immune response pathway to be consisting of increased lymphocytes and cytokines. Intriguingly, we found that immune-related proteins were recoverable during short-term exposure. During the process of PM2.5 exposure, upregulated proteins presented dose-dependence in the lung, including stress response at low dose, minor immune response at middle dose, and severe inflammatory response at high dose. This data set provides a rich resource to facilitate the understanding of PM2.5-induced lung damage and repair mechanism.

Toxicity assessment of electronic cigarettes.

Sale of electronic cigarette (e-cigarette) products has exponentially increased in the past decade, which raise concerns about its safety. This updated review provides the available toxicology profile of e-cigarettes, summarizing evidence from in vitro and in vivo studies. Data regarding which components in e-liquids exhibit potential toxicities are inconsistent. Some studies have reported that nicotine plays a significant role in inducing adverse outcomes and that solvents alone do not induce any adverse effects. However, other studies have suggested that nicotine is not associated with any adverse outcomes, whereas solvents and flavorings are the key components to elicit considerable deleterious effects on cells or animals. In addition, most of the studies that have compared the toxicity of e-cigarettes with tobacco cigarettes have suggested that e-cigarettes are less toxic than tobacco cigarettes. Nevertheless, scientific evidence regarding the toxicity profile of e-cigarette is insufficient owing to the lack of a standardized research approach. In the future, scientific toxicology data derived from standardized testing protocols including nicotine, ingredients analysis, the various e-cigarette devices made from different materials are urgently needed for thorough toxicology assessment. This review aims to update the toxicity profiles, identify knowledge gaps, and outline future directions for e-cigarettes research, which would greatly benefit public health professionals.

Effects of Personal Short-Term Exposure to Ambient Ozone on Blood Pressure and Vascular Endothelial Function: A Mechanistic Study Based on DNA Methylation and Metabolomics.

Short-term exposure to ambient ozone is associated with adverse cardiovascular effects, with inconsistent evidence on the molecular mechanisms. We conducted a longitudinal panel study among 43 college students in Shanghai to explore the effects of personal ozone exposure on blood pressure (BP), vascular endothelial function, and the potential molecular mechanisms. We measured real-time personal ozone exposure levels, serum angiotensin-converting enzyme (ACE) and endothelin-1 (ET-1), and locus-specific DNA methylation of ACE and EDN1 (coding ET-1). We used an untargeted metabolomic approach to explore potentially important metabolites. We applied linear mixed-effect models to examine the effects of ozone on the above biomarkers. An increase in 2 h-average ozone exposure was significantly associated with elevated levels of BP, ACE, and ET-1. ACE and EDN1 methylation decreased with ozone exposure, but the magnitude differed by genomic loci. Metabolomics analysis showed significant changes in serum lipid metabolites following ozone exposure that are involved in maintaining vascular endothelial function. Our findings suggested that acute exposure to ambient ozone can elevate serum levels of ACE and ET-1, decrease their DNA methylation, and alter the lipid metabolism, which may be partly responsible for the effects of ozone on BP and vascular endothelial function.

A Novel Zebrafish (Danio rerio) Assay for Assessing Musk Ambrette-Induced Toxicity.

Musk ambrette (4-tert-butyl-3-methoxy-2,6-dinitrotoluene) is a nitro musk, a cheap substitute for natural musk and a potential environmental pollutant based on its persistence, accumulation in human organisms. We investigated the acute toxicity of musk ambrette using wild-type AB and transgenic Tg(fli1a:EGFP)y1 zebrafish. Different concentrations were delivered to zebrafish by direct soaking from 6 to 72 h post-fertilization (hpf). The LC50 of musk ambrette was 76.4 µg mL-1. As musk ambrette concentration increased, zebrafish embryos showed developmental delays (50 µg mL-1, 22 hpf), pericardial edema (5 µg mL-1, 48 hpf), circulatory disturbances, curved body axis (1 µg mL-1, 72 hpf) and death (100 µg mL-1, 22 hpf). Target organ toxicity was evaluated by a zebrafish angiogenesis model. Musk ambrette induced cardiovascular morphological changes, vessel permeability variation, angiogenic changes and cardiotoxicity (10 µg mL-1, 48 hpf). The disappearance of caudal vein plexus confirmed the vascular development toxicity. Musk ambrette negatively affects early life-stage survival and demonstrates various toxicities in zebrafish.

Increased nitrogen input enhances Kandelia obovata seedling growth in the presence of invasive Spartina alterniflora in subtropical regions of China.

Mangroves in China are severely affected by the rapid invasion of the non-native species Spartina alterniflora Although many studies have addressed the possible impacts of S. alterniflora on the performance of mangrove seedlings, how excessive nitrogen (N) input due to eutrophication affects the interactions between mangrove species and S. alterniflora remains unknown. Here, we report the results from a mesocosm experiment using seedlings of the native mangrove species Kandelia obovata and the exotic S. alterniflora grown in monoculture and mixed culture under no nitrogen addition and nitrogen (N) addition treatments for 18 months. Without N addition, the presence of S. alterniflora inhibited the growth of K. obovata seedlings. Excessive N addition significantly increased the growth rate of K. obovata in both cultures. However, the positive and significantly increasing relative interaction intensity index under excessive N input suggested that the invasion of S. alterniflora could favour the growth of K. obovata under eutrophication conditions. Our results imply that excessive N input in southeastern China can increase the competitive ability of mangrove seedlings against invasive S. alterniflora.

[Intervention effects of selenium yeast on fine particulate matters-induced lung injury in rats].

OBJECTIVE: To evaluate if selenium yeast could inhibit the rat lung injury induced by ambient fine particulate matter( PM_(2. 5) ). METHODS: Fifty-six male SpragueDawley rats were randomly allocated in seven groups( n = 8 each). Saline control group, the rats were exposed to 0. 9% saline by instillation. PM_(2. 5) exposure group, rats were exposed to PM_(2. 5) by intra-tracheal instillation every other day for three times with the accumulated dose of 40 mg/kg. Selenium yeast treatment groups, three groups of rat were exposed to PM_(2. 5) . Then the rats were given low, middle and high dose of selenium yeast, and the doses were 8. 75, 17. 5 and 35 mg/kg, respectively. High dose selenium yeast control group, rats were given high dose of selenium yeast only. Solvent control group, therats were given 1% carboxymethyl cellulose. Saline and PM_(2. 5) were given in the first week. In the second week, selenium yeast and solvent were given by gavage. The rats were sacrificed 24 hours after the last gavage. The bronchoalveolar lavage fluid( BALF)was collected to count the neutrophils numbers and analyze the markers related to inflammation, oxidative stress and cell damage. The lung lobe that was not been lavaged was processed for light microscopic examination. RESULTS: The proportions of neutrophils in BALF and the pathologic scores of lung in PM_(2. 5) - exposed groups were significantly higher than control( P < 0. 05). Selenium yeast treatment caused decrease in tumor necrosis factor-α( TNF-α), interleukin-1ß( IL-1ß), lactate dehydrogenase( LDH), total protein( TP), alkaline phosphatase( AKP) and malondialdehyde( MDA) compared with the only PM_(2. 5) exposure group. Meanwhile, the dose-dependent increase in totalsuperoxide dismutase( T-SOD) and glutathione peroxidase( GSH-Px) activities were observed. There were no significant differences among the groups of saline control group, high dose selenium yeast control group and solvent control group. CONCLUSION: Selenium yeast treatment may protect against acute injury induced by PM_(2. 5) in rat lung.

[Effects of vitamin E and ω-3 fatty acids on protecting ambient PM_(2. 5)-induced cardiovascular injury].

OBJECTIVE: To observe whether vitamin E( Ve) and ω-3 polyunsaturated fatty acids( ω-3 FA) could prevent the fine particulate matter( PM_(2. 5))-induced cardiovascular injury and explore the potential mechanism. METHODS: The SD rats were assigned randomly to 8 groups, those were control group, PM_(2. 5)group, Ve treatment groups( 3, 10, 30 mg/( kg·d)) and ω-3 FA treatment groups( 10, 30 and 90 mg/( kg·d)). The rats were pretreated with different concentration of Ve and ω-3 FA separately for 14 days, then were exposed to ambient PM_(2. 5) by intratracheal instillation( 10 mg/kg BW). All the rats were sacrificed after the last PM_(2. 5) exposure, then the arterial blood, lungs and cardiac tissues were collected. The expressions of tumor necrosis factor-α( TNF-α), interleukin-1ß( IL-1ß), interleukin-6( IL-6) in serum, bronchoalveolar lavage fluid and supernatant of cardiac tissue were detected by ELISA kits. The levels of malondialdehyde( MDA), superoxide dismutase( SOD) and glutathione-peroxidase( GSH-Px) in serum and myocardium were also measured. RESULTS: Compared with the severe injury of rats in PM_(2. 5) exposure group, the rats in Ve or ω-3 FA groups had a slighter injury in lung and cardiac tissue with the increase of Ve and ω-3 FA. Similarly, the levels of IL-1ß, IL-6 in bronchoalveolar lavage fluid had a decreasing trend with the increase of Ve and ω-3 FA compared with the PM_(2. 5) exposure groups. Meanwhile, the expressions of TNF-α in Ve and ω-3 FA high dose groups were significantly reduced when compared with the PM_(2. 5) exposure group( P <0. 05). In addition, the MDA levels in serum were markedly decreased and the activities of SOD were significantly increased compared with the PM_(2. 5)exposure group( P < 0. 05 or P < 0. 01) whereas the SOD activities were elevated only in the ω-3 FA high dose groups( P < 0. 05). Meanwhile, the levels of IL-6 and TNF-α in serum had an obvious decrease compared with the PM_(2. 5) exposure group( P < 0. 01). Similarly, compared with the PM_(2. 5)exposure group, the expressions of MDA were markedly decreased and the activities of SOD and GSH-Px in myocardium were significantly increased( P < 0. 05 or P < 0. 01) in the Ve treatment group. In addition, the activities of GSH-Px was found higher only in the ω-3 FA high treatment group compared with the PM_(2. 5)exposure group( P < 0. 05). Meanwhile, the levels of IL-1ß and TNF-α in cardiac tissue had an obvious decrease trend with the increase of Ve and ω-3 FA. CONCLUSION: PM_(2. 5) exposure may increase inflammatory response and oxidative stress, supplementation with Ve and ω-3 FA could prevent the PM_(2. 5)-induced inflammatory reaction and oxidative stress damage by increasing the activities of SOD and GSH-Px.

Traffic-related air pollution is associated with cardio-metabolic biomarkers in general residents.

PURPOSE: The study was conducted to explore the mechanisms linking traffic-related air pollution and cardio-metabolic risk. METHODS: The participants included 371 men and women aged from 45 to 75 in an urban residential area in Shanghai, China. The participants were divided into four categories (≤50, 51-100, 101-200 and >200 m) according to the residential distance to major road. Additionally, the personal fine particulate matter (PM2.5) was measured from 8:00 am to 6:00 pm to assess the PM2.5 exposure in general residents. Then, the continuous subclinical measurements and biological effects related to cardio-metabolic disorders were detected. The generalized linear regression analysis was applied for estimating the adjusted hazards ratio for cardio-metabolic disorders relative to traffic-related air pollution. RESULTS: The average personal PM2.5 is 111.1 µg/m(3) in the participants living within 50 m to major road, which is significantly higher than the personal PM2.5 (68.2 µg/m(3)) in the participants living more than 200 m away from the major road. The participants living within 50 m to major road compared with those living more than 200 m away have 1.15 times higher of heart rate (HR), 1.95 times higher of fasting insulin, 1.30 times higher of homeostasis model assessment of insulin resistance (HOMA-IR), 1.56 times higher of low-density lipoprotein cholesterol (LDL-C), 8.39 times higher of interleukin 6 (IL-6), 4.30 times higher of augmentation index (AI), 1.60 times higher of systolic blood pressure (SBP) and 1.91 times higher of diastolic blood pressure (DBP). Contrary to the increase in above biological effects, there were 1.06 times lower of low frequency (LF), 1.05 times lower of high frequency (HF), 2.54 times lower of IL-10, 4.61 times lower of nitric oxide (NO), 1.19 times lower of superoxide dismutase (SOD) and 1.85 times lower of total antioxidant capacity (T-AOC). There was no clear exposure-response relationship can be observed in the fasting glucose, LF/HF, cholesterol and high-density lipoprotein (HDL). CONCLUSION: Long-term exposure to traffic-related air pollution may contribute to the development or exacerbation of cardio-metabolic disorders. The mechanisms linking air pollution and cardio-metabolic disorders may be associated with the increased systemic inflammation and oxidative stress, reduced insulin sensitivity and elevated arterial stiffness and blood pressure.

The effects of ambient temperature on outpatient visits for varicella and herpes zoster in Shanghai, China: a time-series study.

BACKGROUND: The seasonality of varicella and herpes zoster has been widely observed, but there is limited evidence on their associations with ambient temperature. OBJECTIVE: The associations between ambient temperature and outpatient visits for varicella and herpes zoster were examined. METHODS: We collected daily outpatient visit data for varicella (N = 3520) and herpes zoster (N = 6614) from a major hospital in Shanghai, China, from 2008 to 2010. We adopted the generalized additive model in time-series analysis to investigate the short-term associations between temperature and outpatient visits for varicella and herpes zoster after controlling for seasonal trends, day of the week, and humidity. RESULTS: A 1°C increase in daily mean temperature was associated with a 1.33% (95% confidence interval 0.93%-1.74%) decrease in outpatient visits for varicella whereas it was associated with a 2.18% (95% confidence interval 1.90%-2.46%) increase in outpatient visits for herpes zoster. LIMITATIONS: Only 1 hospital was included and we did not control for individual-level risk factors. CONCLUSION: Our results demonstrated that temperature variation might be an important risk factor for varicella and herpes zoster in China.

Treg responses are associated with PM2.5-induced exacerbation of viral myocarditis.

The adverse cardiovascular events induced by ambient fine particles (PM2.5) are paid more attention in the world. The current study was conducted to explore the mechanisms of T regulatory cells (Treg) responses in PM2.5-induced exacerbation of viral myocarditis. The male BALB/c mice were administered an intratracheal (i.t.) instillation of 10 mg/kg b.w. PM2.5 suspension. Twenty-four hours later, the mice were injected intraperitoneally (i.p.) with 100 µl of coxsackievirus B3 (CVB3) diluted in Eagle's minimal essential medium (EMEM). Seven days after the treatment, serum, splenetic, and cardiac tissues were examined. The results showed that pre-exposure to PM2.5 aggravated the cardiac inflammation in the CVB3-infected mice along with an increase of Treg cells in the spleen. The mRNA expressions of interleukin-6 (IL-6), TNF-α, transforming growth factor-ß (TGF-ß), and Foxp3 were up-regulated in the PM2.5-pretreated mice than that in the CVB3-treated mice. Similar results were found in the sera. In addition, compared with the CVB3-treated mice, the cardiac protein expression of TGF-ß increased in the PM2.5-pretreated mice. These results demonstrated that preexposure to PM2.5 exacerbated virus-induced myocarditis possibly through the depression of the immune response and increase of inflammation in myocardium through the Treg responses.

Rat lung response to ozone and fine particulate matter (PM2.5) exposures.

Exposure to different ambient pollutants maybe more toxic to lung than exposure to a single pollutant. In this study, we discussed the inflammation and oxidative stress responses of rat lung caused by ozone and PM2.5 versus that of rats exposed to saline, ozone, or single PM2.5 . Wistar rats inhaled 0.8 ppm ozone or air for 4 h and then placed in air for 3 h following intratracheal instillation with 0, 0.2 (low dose), 0.8 (medium dose), 3.2 (high dose) mg/rat PM2.5 dissolved in sterile saline (0.25 mL/rat), repeated twice per week for 3 weeks, the cumulative doses of PM2.5 in animals were 1.2, 4.8, and 19.2 mg. Rats were sacrificed 24 h after the last (sixth) exposure. The collected bronchoalveolar lavage fluid (BALF) was analyzed for inflammatory cells and cytokines. Lung tissues were processed for light microscopic and transmission electron microscopic (TEM) examinations. Results showed that total cell number in BALF of PM2.5 -exposed groups were higher than control (p < 0.05). PM2.5 instillation caused dose-trend increase in tumor necrosis factor alpha (TNF-α), interleukin-6, lactate dehydrogenase, and total protein of BALF. Exposure to ozone alone only caused TNF-α significant change in above-mentioned indicators of lung injury. On the other hand, ozone could enhance PM2.5-induced inflammatory changes and pathological characters in rat lungs. SOD and GSH-Px activities in lung were reduced in PM2.5-exposed rats with and without prior ozone exposure compared to control. To determine whether the PM2.5 and ozone affect endothelium system, iNOS, eNOS, and ICAM-1 mRNA levels in lung were analyzed by real-time PCR. These data demonstrated that inflammation and oxidative stress were involved in toxicology mechanisms of PM2.5 in rat lung and ozone potentiated these effects induced by PM2.5. These results have implications for understanding the pulmonary effects induced by ozone and PM2.5.

[Modification effects of ozone on the relationship between PM10 and daily mortality in three cities, China].

OBJECTIVE: To estimate the modification effects of ozone on the relationship between PM10 and daily mortality. METHODS: Daily total non-accidental, cardiovascular and respiratory motality data in Beijing, Shanghai and Suzhou from 2001 to 2008 were collected from the Center for Disease Control and Prevention of each city. The concentration of PM10 and ozone and other Meteorology data during the study period were abtained from the national air quality monitoring network. A generalized additive model (GAM) were used to estimate the acute effects of air pollution on daily mortality in the three cities. The time-series method were applied to analyze the association between air pollution and daily mortality. In order to analyze the interaction effect between PM10 and ozone, ozone were stratified into three levels (≤5% . as low from 5% - 95% . as moderate, >95%, as high) and then analyzed the effect of PM10. A Meta analysis was used to describe the effect of PM10 in all the cities. RESULTS: With the increment of ozone, PM10 corresponded to an increase of total, cardiovascular and respiratory mortality in Beijing, Shanghai and Suzhou. The result of the Meta analyses showed that on the days of "low" ozone, a 10 µg/m3 increment in PM10 corresponded to a 0.47% (95% CI - 0. 74%, 1. 67%) decrease in total mortality, 0. 36% (95% CI - 0. 59%, 1. 31%) decrease in cardiovascular mortality, and 0. 69% (95% CI - 0. 52%, 1. 90%) decrease in respiratory mortality. When it was moderate, the increment was 0.45% (95% CI 0. 26%, 0. 63%), 0. 16% (95% CI - 2. 26%, 1. 95%) and 0. 57% (95% CI 0. 13%, 1. 02%). The increment was 0. 82% (95% CI 0. 24% , 1. 39%), 0. 37% (95% CI 0. 07%, 0. 66% ) and 1. 13% (95% CI - 0. 67% , 2. 92%) while the.zone was high. CONCLUSION: Ozone could modify the effect of PM10 on the daily mortality.

[Effects of airborne fine particulate matters on pulmonary inflammation injury and Th17/Treg balance of sub-chronic exposure mice].

OBJECTIVE: To explore effects of fine particulate matters (PM 2.5) onpulmonary inflammation, and the changes of Th17/Treg balance as well as related cytokines. METHOD: Thirty-two C57BL/6 male mice were randomly divided into 4 groups including 1 saline control group and 3 PM2.5 exposure groups (1.5, 7.5 and 15 mg/kg BW, respectively). Each group received intratracheal instillation twice per week for 3 consecutive months. 24 hours after the last exposure, anaesthetize the mice with chloral hydrate, bronchoalveolar lavage fluid (BALF) was collected for inflammatory cells and cytokines analysis. The Th17- and Treg-related cytokines in BALF was measured by enzyme linked immunosorbent assay (ELISA). The level of the specific transcription factors of Th17 and Treg in lung tissue was determined by real-time PCR. Unlavaged left lung were fixed with 4% paraformaldehyde for histopathological detection. RESULTS: Th17-related cytokine IL-17 increased, but Treg-related cytokine IL-10 decreased significantly in BALF at 7.5 and 15 mg/kg BW PM2.5 exposure groups compared with control group (P < 0.05). Consistently, the relative mRNA expression of ROR-gammat (specific transcription factors of Th17) increased in a dose-response way, the relative mRNA expression of Foxp3 + (specific transcription factors of Treg) decreased in a dose-response way. CONCLUSION: Sub-chronic PM2.5 exposure caused persistent inflammation, immune injury and disordered the Th17/Treg imbalance as well as related cytokines.

Effects of a combination of Poria Cocos, Ziziphus spinose, and gamma-aminobutyric acid (GABA) on sleep quality and skin health: A randomized double-blind placebo-controlled clinical trial.

Sleep is crucial for preserving both physical and mental health, including skin health. Presently, there is a burgeoning interest in the use of herbal and natural ingredients to mitigate the adverse effects of sleep disorders. In this 4-week, randomized, double-blind, controlled trial, 70 subjects with sleep disorders were randomly assigned to receive either a placebo or a Poria cocos, Ziziphus spinose, and GABA (PZG) supplement (10 mL per day). Total sleep duration was detected by wrist actigraphy, and sleep quality was assessed by the Pittsburgh Sleep Quality Index (PSQI). Skin conditions were evaluated based on assessments of skin hydration, glossiness elasticity, color, severity of wrinkles, and skin roughness. After 4 weeks, the total sleep duration significantly increased by 12.96% (p = .006) and the PSQI score notably decreased by 59.94% (p = .000) compared to the baseline. Notably, compared to the baseline conditions, skin hydration, radiance, elasticity, firmness, wrinkle severity, and roughness were significantly improved in the PZG group. In addition, the PZG group demonstrated significantly greater improvements than the placebo group in terms of changes from baseline in total sleep duration, PSQI score, skin hydration, wrinkle severity, and skin roughness. The present results demonstrated that the combined intake of herbs and GABA can improve sleep quality and enhance skin health without adverse effects.

IRSEI-based monitoring of ecological quality and analysis of drivers in the Daling River Basin.

The Daling River Basin is an important ecological functional area in the western region of Liaoning with outstanding environmental problems. The monitoring of ecological and environmental quality in the basin and the analysis of driving factors are of great importance for the protection of the ecological environment and the improvement of economic quality. In this paper, the three periods of Landsat remote sensing images in 1995, 2010 and 2020 are used as the basic data, and platforms and technical means such as RS and GIS are used to decipher and extract the three periods of land use information, and to construct the land use type transfer matrix. The remote sensing ecological index (RSEI) was improved, and the principal component analysis method was applied to construct the improved remote sensing ecological index (IRSEI) model based on the greenness (NDVI), moisture (WET), heat (LST) and new dryness (N-NDBSI), so as to realize the dynamic monitoring of ecological and environmental quality in the study area. Based on the land use change, combined with the trend of improved remote sensing ecological index (IRSEI) of Daling River Basin, thus achieving the purpose of rapid and efficient dynamic monitoring of ecological quality of Daling River Basin from 1995 to 2020. A geoprobe model was then used to systematically assess the drivers of ecological quality in the catchment. The results show that the improved remote sensing ecological index (IRSEI) can efficiently and accurately obtain the spatial distribution pattern and temporal variation trend of IRSEI in the study area, which is more in line with the characteristics of indicators in this study area. The IRSEI in the study area showed an increasing trend from 1995 to 2020, from 0.4794 to 0.5615, and the proportion of benign ecological classes increased year by year during the period. Among the evaluation indicators, NDVI and N-NDBSI are the main factors affecting the environmental and ecological quality of the Daling River Basin, and the increase of vegetation cover, climate regulation and human activities have obvious promoting effects on the improvement of the ecological environment of the Daling River Basin. This study provides a scientific theoretical basis for the implementation of further ecological environmental protection measures.

Short-term association of particulate matter and cardiovascular disease mortality in Shanghai, China between 2003 and 2020.

Objective: Evidence regarding the effects of particulate matter (PM) pollutants on cardiovascular disease (CVD) mortality remains limited in Shanghai, China. Our objective was to thoroughly evaluate associations between PM pollutants and CVD mortality. Methods: Daily data on CVD mortality, PM (PM10 and PM2.5) pollutants, and meteorological variables in Shanghai, China were gathered from 2003 to 2020. We utilized a time-series design with the generalized additive model to assess associations between PM pollutants and CVD mortality. Additionally, we conducted stratified analyses based on sex, age, education, and seasons using the same model. Results: We found that PM pollutants had a significant association with CVD mortality during the study period. Specifically, there was a 0.29% (95%CI: 0.14, 0.44) increase in CVD mortality for every 10 µg/m3 rise in a 2-day average (lag01) concentration of PM10. A 0.28% (95% CI: 0.07, 0.49) increase in CVD mortality was associated with every 10 µg/m3 rise in PM2.5 concentration at lag01. Overall, the estimated effects of PM10 and PM2.5 were larger in the warm period compared with the cold period. Furthermore, males and the older adult exhibited greater susceptibility to PM10 and PM2.5 exposure, and individuals with lower education levels experienced more significant effects from PM10 and PM2.5 than those with higher education levels. Conclusion: Our findings suggested that PM pollutants have a substantial impact on increasing CVD mortality in Shanghai, China. Moreover, the impacts of air pollution on health may be altered by factors such as season, sex, age, and educational levels.

Tight regulation of a nuclear HAPSTR1-HUWE1 pathway essential for mammalian life.

The recently discovered HAPSTR1 protein broadly oversees cellular stress responses. This function requires HUWE1, a ubiquitin ligase that paradoxically marks HAPSTR1 for degradation, but much about this pathway remains unclear. Here, leveraging multiplexed proteomics, we find that HAPSTR1 enables nuclear localization of HUWE1 with implications for nuclear protein quality control. We show that HAPSTR1 is tightly regulated and identify ubiquitin ligase TRIP12 and deubiquitinase USP7 as upstream regulators titrating HAPSTR1 stability. Finally, we generate conditional Hapstr1 knockout mice, finding that Hapstr1-null mice are perinatal lethal, adult mice depleted of Hapstr1 have reduced fitness, and primary cells explanted from Hapstr1-null animals falter in culture coincident with HUWE1 mislocalization and broadly remodeled signaling. Notably, although HAPSTR1 potently suppresses p53, we find that Hapstr1 is essential for life even in mice lacking p53. Altogether, we identify novel components and functional insights into the conserved HAPSTR1-HUWE1 pathway and demonstrate its requirement for mammalian life.