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When the coal-seams are multi-layered, the stress and permeability of the caving zone are disturbed again during the following coal seam mining. Repeated unloading and compaction cause caved coal and rock to break further in the caving zone, which in turn affects the migration of gas in goaf. This paper briefly summarizes prior research on caving zone internal stress, porosity, permeability and other parameters of the process of longwall face advancing. The forecast methods for calculating the stress and permeability of the caved zone during its compaction are listed. On the basis, this paper describes a laboratory experiment of the broken coal and rock in the caving zone of the gob in Huainan coal mine. The laboratory test results imply that the re-crushing, re-arrangement, and compressional deformation of particles in the loading process lead to a drastic drop in the caving zone porosity, which causes the permeability reduction. The permeability sensitivity to stress of broken rock (broken coal) samples was determined by their strength. The greater the proportion of coal samples in the combined coal and rock samples, the higher the permeability stress sensitivity and the smaller the permeability.With the increase of the cyclic times, the stress sensitivity gradually weakened. Based on laboratory experiments, the stress-permeability fitting model of the broken coal and rock in the caving zone during the group coal seam mining is proposed in this paper.

With the continuous progress of information acquisition technology, the volume of LiDAR point cloud data is also expanding rapidly, which greatly hinders the subsequent point cloud processing and engineering applications. In this study, we propose a point cloud simplification strategy utilizing probabilistic membership to address this challenge. The methodology initially develops a feature extraction scheme based on curvature to identify the set of feature points. Subsequently, a combination of k-means clustering and Possibilistic C-Means is employed to partition the point cloud into subsets, and to simultaneously acquire the probabilistic membership information of the point cloud. This information is then utilized to establish a rational and efficient simplification scheme. Finally, the simplification results of the feature point set and the remaining point set are merged to obtain the ultimate simplification outcome. This simplification method not only effectively preserves the features of the point cloud while maintaining uniformity in the simplified results but also offers flexibility in balancing feature retention and the degree of simplification. Through comprehensive comparative analysis across multiple point cloud models and benchmarking against various simplification methods, the proposed approach demonstrates superior performance. Finally, the proposed algorithm was critically discussed in light of the experimental results. [ABSTRACT FROM AUTHOR]

Sarcoidosis, an enigmatic disease with unknown etiology, is characterized by inflammation and the potential involvement of various organs, predominantly the lungs and intrathoracic lymph nodes. Non-caseating granulomas can resolve spontaneously in approximately 60% of cases within 2-3 years. However, sarcoidosis-related mortality has increased. Lung fibrosis, affecting up to 20% of sarcoidosis patients, stands out as a primary cause of mortality. Traditionally, fibrosis is viewed because of prolonged inflammation, necessitating antiinflammatory treatment with systemic steroids, immunosuppressants, and anti-TNF agents to manage the disease. The recent introduction of antifibrotic drugs such as nintedanib and pirfenidone offers new avenues for treating fibrotic sarcoidosis. Nintedanib, effective in idiopathic pulmonary fibrosis (IPF) and systemic sclerosis-related interstitial lung disease (SSc-ILD), has shown promise in patients with various progressive fibrosing interstitial lung diseases (PF-ILD), including those with sarcoidosis. Pirfenidone, also effective in IPF, has demonstrated potential in managing fibrotic sarcoidosis, though results have been inconclusive due to limited participant numbers in studies. This review explores the theoretical and empirical evidence supporting the use of antifibrotics in sarcoidosis, weighing the benefits and drawbacks. While antifibrotics offer a potential therapeutic approach, further randomized controlled trials are essential to determine their efficacy in fibrotic sarcoidosis. Addressing fibrosis as a continuum of chronic inflammation, the role of antifibrotics in managing sarcoidosis remains an area requiring more in-depth research to improve patient outcomes and advance treatment paradigms. [ABSTRACT FROM AUTHOR]

Background: Intervertebral disc degeneration (IDD) can lead to disc herniation and spinal instability, sometimes requiring surgical intervention. Currently, estrogen has a potential protective effect on IDD, and estrogen is associated with an increased risk of some cancers, such as breast and endometrial cancer. Therefore, it is important to identify natural compounds that estrogen analogues treat IDD while reducing the risk of tumor development. Objective: This study aims to explore a natural metabolic treatment strategy by targeting CRISP2 with the natural compound Hesperidin to mimic the protective effects of estrogen on IDD and reduce the risk of tumor development. Methods: Microarray data from healthy volunteers and IDD patients were extracted from the Gene Expression Omnibus (GEO) database, and RNA sequencing and clinical data from various cancer types were analyzed. Differentially expressed genes (DEGs) were identified using the Bioconductor Limma package, followed by principal component analysis, volcano plot, and heatmap visualization. Additionally, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses, CIBERSORT and ssGSEA immune cell infiltration assessments, survival analysis, metabolite enrichment analysis, and molecular docking were performed. Hesperidin's interaction with CRISP2 was further validated through molecular docking and experimental studies. Results: Hesperidin significantly reduced the expression of CRISP2, iNOS, and COX2 in IDD models, decreased reactive oxygen species (ROS) and apoptosis, and diminished inflammatory markers. CIBERSORT and ssGSEA analyses revealed a correlation between CRISP2 and immune cell infiltration. Survival analysis demonstrated that CRISP2 expression levels were associated with patient survival across various cancer types. Hesperidin was found to mimic estrogen's effects on IDD and reduce tumor progression. Cell culture and experimental validation confirmed Hesperidin's protective effects on nucleus pulposus cells (NPCs). Conclusion: Hesperidin, as a potential natural metabolic regulator, not only has therapeutic effects on IDD but may also synergize with estrogen therapy to promote spinal health without increasing cancer risk. This study presents a new clinical approach for IDD treatment and lays the foundation for further drug development and experimental research. [ABSTRACT FROM AUTHOR]

Quinoa (Chenopodium quinoa Willd) sprouts are rich in bioactive compounds that offer numerous health benefits. However, limited research exists on their cultivation, nutritional value, and processing potential. This study compared the nutritional composition and antioxidant activity of quinoa sprouts from different varieties at various time points. Results showed a general increase in most nutrients over time. At the 24 h mark, JQ-W3 exhibited a 17.77% increase in leucine, 1.68 times higher than in eggs, along with a 6.11-fold elevation in GABA content. JQ-B1 exhibited the preeminent antioxidant potency composite (APC) score. Saponins, known for their bitter taste, decreased at 12 h but returned to original levels by 24 h. Based on nutritional components and saponin content, 24 h sprouted black quinoa JQ-B1 and white quinoa JQ-W3 were selected, providing a basis for quinoa sprout development in the food industry. These findings contribute to the understanding and utilization of quinoa sprouts. [ABSTRACT FROM AUTHOR]

As a promising sensing material, Molybdenum disulfide (MoS2) nanosheets is being increasingly studied for Nitrogen dioxide (NO2) gas sensing. However, the MoS2 nanosheets is prone to the stacking effect that compromises the sensing performances. Here, the stacking effect is mitigated by engineering MoS2 nanosheets into a three dimensional (3D) network microstructure, which was fabricated by method of electrostatically self-assembling of MoS2/SiO2 microspheres. The fabricated sensor based on 3D MoS2 network observed a significantly improved response of 15% to 12.3 ppm NO2, which is a 75-fold increase compared to the control sensor with pure MoS2 nanosheets. In addition, the sensitivity of the sensor with 3D MoS2 network was 6.15 times larger than that of the control sensor with pure MoS2 nanosheets. The detection limit of our sensor was 0.297 ppm, lower than most of reported MoS2-based NO2 sensors. The enhanced sensitivity and dynamic response stem from the improved interaction between NO2 molecules and MoS2 network, thanks to its increased surface area per footprint of MoS2 nanosheets compared to pure 2D MoS[sub 2] film (single- or few-layer). This work presents a new approach to enhancing the performance of gas sensors based on 2D materials. [ABSTRACT FROM AUTHOR]

Copyright of Coal Geology & Exploration is the property of Xian Research Institute of China Coal Research Institute and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Lung cancer (LC) produces some of the most malignant tumors in the world, with high morbidity and mortality. Tumor immune microenvironment (TIME), a component of the tumor microenvironment (TME), are critical in tumor development, immune escape, and drug resistance. The TIME is composed of various immune cells, immune cytokines, etc, which are important biological characteristics and determinants of tumor progression and outcomes. In this paper, we reviewed the recently published literature and discussed the potential uses of natural products in regulating TIME. We observed that a total of 37 natural compounds have been reported to exert anti-cancer effects by targeting the TIME. In different classes of natural products, terpenoids are the most frequently mentioned compounds. TAMs are one of the most investigated immune cells about therapies with natural products in TIME, with 9 natural products acting through it. 17 natural products exhibit anti-cancer properties in LC by modulating PD-1 and PD-L1 protein activity. These natural products have been extensively evaluated in animal and cellular LC models, but their clinical trials in LC patients are lacking. Based on the current review, we have revealed that the mechanisms of LC can be treated with natural products through TIME intervention, resulting in a new perspective and potential therapeutic drugs. [ABSTRACT FROM AUTHOR]

Copyright of Environmental Science & Technology (10036504) is the property of Editorial Board of Environmental Science & Technology and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Premature ovarian insufficiency (POI) induced by chemotherapy is an intractable disorder with a considerable incidence that commonly results in insufficient fertility and concomitant complications in female patients. Due to limitations in the current progress in POI diagnosis and treatment, there is an urgent need to develop novel remedies to improve ovarian function and protect fertility. The ameliorative effect of human umbilical cord mesenchymal stem cells (hUCMSCs) and exosomes derived from them in POI treatment could be a new hope for patients. Herein, we identified exosomes from hUCMSCs (hUCMSC-Exos). Then, systematic infusion of hUCMSC-Exos was accomplished via tail intravenous injection to investigate the feasibility of the treatment of rats with chemotherapy-induced POI by intraperitoneal injection of cyclophosphamide (CTX) and busulfan (BUS). Ovarian functions in the indicated group were evaluated, including oestrous cycle, serum sex hormone levels, follicle counts, ovarian pathological changes, proliferation and apoptosis of granulosa cells (GCs), and reproductive ability testing. Furthermore, the potential influence ofhUCMSC-Exos on ovarian tissues was illuminated by conducting RNA-seq and multifaceted bioinformatics analyses. POI rats with hUCMSC-Exos transplantation exhibited a decrease in follicle-stimulating hormone (FSH) and apoptosis of GCs but an increase in oestradiol (E2), anti-Müllerian hormone (AMH), and the number of ovarian follicles and foetuses in the uterus. And the immunomodulation- and cellular vitality-associated gene sets in rats had also undergone moderate changes. Our data indicated the feasibility of hUCMSC-Exos in improving ovarian function and protecting fertility in chemotherapy-induced POI rats. HUCMSC-Exos can improve the local microenvironment of ovarian tissue in POI rats by participating in immune regulation, cellular viability, inflammation regulation, fibrosis and metabolism, and other related signal pathways. [ABSTRACT FROM AUTHOR]

Copyright of Coal Geology & Exploration is the property of Xian Research Institute of China Coal Research Institute and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Recent studies have shown that physical activities can prevent aging-related neurodegeneration. Exercise improves the metabolic landscape of the body. However, the role of these differential metabolites in preventing neurovascular unit degeneration (NVU) is still unclear. Here, we performed single-cell analysis of brain tissue from young and old mice. Normalized mutual information (NMI) was used to measure heterogeneity between each pair of cells using the nonnegative Matrix Factorization (NMF) method. Astrocytes and choroid plexus epithelial cells (CPC), two types of CNS glial cells, differed significantly in heterogeneity depending on their aging status and intercellular interactions. The MetaboAnalyst 5.0 database and the scMetabolism package were used to analyze and calculate the differential metabolic pathways associated with aging in the CPC. These mRNAs and corresponding proteins were involved in the metabolites (R)-3-Hydroxybutyric acid, 2-Hydroxyglutarate, 2-Ketobutyric acid, 3-Hydroxyanthranilic acid, Fumaric acid, L-Leucine, and Oxidized glutathione pathways in CPC. Our results showed that CPC age heterogeneity-associated proteins (ECHS1, GSTT1, HSD17B10, LDHA, and LDHB) might be directly targeted by the metabolite of oxidized glutathione (GSSG). Further molecular dynamics and free-energy simulations confirmed the insight into GSSG's targeting function and free-energy barrier on these CPC age heterogeneity-associated proteins. By inhibiting these proteins in CPC, GSSG inhibits brain energy metabolism, whereas exercise improves the metabolic pathway activity of CPC in NVU by regulating GSSG homeostasis. In order to develop drugs targeting neurodegenerative diseases, further studies are needed to understand how physical exercise enhances NVU function and metabolism by modulating CPC-glial cell interactions. [ABSTRACT FROM AUTHOR]

Background: Currently, only a few studies have examined the link between dental health, cognitive impairment, and physical activity. The current study examined the relationship between denture use and physical activity in elderly patients with different cognitive abilities. Methods: The study data was sourced from the 2018 China Health and Retirement Longitudinal Study (CHARLS) database, which included information on denture use and amount of daily physical activity undertaken by older persons. Physical activity was categorized into three levels using the International Physical Activity General Questionnaire and the International Physical Activity Scale (IPAQ) rubric. The relationship between denture use and physical activity in middle-aged and older persons with varying degrees of cognitive functioning was studied using logistic regression models. Results: A total of 5,892 older people with varying cognitive abilities were included. Denture use was linked to physical activity in the cognitively healthy 60 C age group (p = 0.004). Denture use was positively related with moderate physical activity in the population (odds ratio, OR: 1.336, 95% confidence interval: 1.173–1.520, p < 0.001), according to a multivariate logistic regression analysis, a finding that was supported by the calibration curve. Furthermore, the moderate physical activity group was more likely to wear dentures than the mild physical activity group among age-adjusted cognitively unimpaired middle-aged and older persons (OR: 1.213, 95% CI: 1.053–1.397, p < 0.01). In a fully adjusted logistic regression model, moderate physical activity population had increased ORs of 1.163 (95% CI: 1.008–1.341, p < 0.05) of dentures and vigorous physical activity population had not increased ORs of 1.016 (95% CI: 0.853–1.210, p > 0.05), compared with mild physical activity population. Conclusion: This findings revealed that wearing dentures affects physical activity differently in older persons with different cognitive conditions. In cognitively unimpaired older adults, wearing dentures was associated with an active and appropriate physical activity status. [ABSTRACT FROM AUTHOR]

Fiber productivity and quality of cotton are severely affected by abiotic stresses. In this study, we identified the role of GhADF1, an actin depolymerizing factor, in cotton response to drought stress. GhADF1 expression in cotton could be induced by PEG6000. GhADF1-RNAi transgenic cotton showed increased tolerance to drought stress during seed germination and seedling development as well as at the reproductive stage. In contrast, overexpression of GhADF1 led to a drought-sensitive phenotype in transgenic plants. GhADF1-RNAi plants produced an enlarged root system with longer primary roots, more lateral roots, increased root dry biomass, and increased cell size. In leaves of GhADF1-RNAi cotton, proline content and activities of reactive oxygen species-scavenging enzymes were increased following drought stress compared with those in wild type. GhADF1-RNAi lines showed higher water-use efficiency than the wild type, accompanied by reduced leaf stomatal density and conductance. GhADF1-RNAi cotton produced higher fiber yield in the field under both normal and drought conditions. Transcriptomic analyses identified 124 differentially expressed genes in leaves of GhADF1-RNAi lines compared with the wild type following drought treatment. Upregulated genes included those encoding transcription factors, protein kinases, heat shock proteins, and other proteins known to be involved in stress responses. We conclude that GhADF1 reduces the expression of abiotic stress-associated genes in cotton response to drought stress and may be a promising candidate gene for crop improvement by genetic manipulation. [ABSTRACT FROM AUTHOR]

Pyruvate kinase (PK) is a key enzyme that catalyzes the dephosphorylation of phosphoenolpyruvate (PEP) into pyruvate, and is responsible for the production of ATP during glycolysis. As another important isozyme of PK, pyruvate kinase M2 (PKM2) exists in cells with high levels of nucleic acid synthesis, such as normal proliferating cells (e.g., lymphocytes and intestinal epithelial cells), embryonic cells, adult stem cells, and tumor cells. With further research, PKM2, as an important regulator of cellular pathophysiological activity, has attracted increasing attention in the process of autoimmune response and inflammatory. In this re]view, we examine the contribution of PKM2 to the human immune response. Further studies on the immune mechanisms of PKM2 are expected to provide more new ideas and drug targets for immunotherapy of inflammatory and autoimmune diseases, guiding drug development and disease treatment. [ABSTRACT FROM AUTHOR]

Background: Plants suffer from various abiotic stresses during their lifetime, of which drought and salt stresses are two main factors limiting crop yield and quality. Previous studies have shown that abscisic acid (ABA) responsive element binding protein (AREB)/ ABRE binding factors (ABFs) in bZIP transcription factors are involved in plant stress response in an ABA-dependent manner. However, little is known about the properties and functions of AREB/ABFs, especially ABF3, in cotton. Results: Here, we reported the cloning and characterization of GhABF3. Expression of GhABF3 was induced by drought,salt and ABA treatments. Silencing of GhABF3 sensitized cotton to drought and salt stress, which was manifested in decreased cellular antioxidant capacity and chlorophyll content. Overexpression of GhABF3 significantly improved the drought and salinity tolerance of Arabidopsis and cotton. Exogenous expression of GhABF3 resulted in longer root length and less leaf wilting under stress conditions in Arabidopsis thaliana. Overexpressing GhABF3 significantly improved salt tolerance of upland cotton by reducing the degree of cellular oxidation, and enhanced drought tolerance by decreasing leaf water loss rate. The increased expression of GhABF3 up-regulated the transcriptional abundance of downstream ABA-inducible genes under salt stress in Arabidopsis. Conclusion: In conclusion, our results demonstrated that GhABF3 plays an important role in plant drought and salt tolerance. Manipulation of GhABF3 by biotechnology might be an important strategy to alter the stress resistance of cotton. [ABSTRACT FROM AUTHOR]

Aim: To investigate the treating effect of Yiqi-Bushen-Tiaozhi (YBT) recipe on nonalcoholic steatohepatitis (NASH) mice, determine whether the outcome was associated with gut microbiota, and clarify the regulating mechanism. Methods: NASH mice were induced by high-fat and high-fructose diets (HFFD). In the fifth week, mice in the YBT group were orally administrated YBT (22.12g·kg-1·d-1) daily for 12 weeks. Fresh stool of mice was collected at the 16th week for fecal 16S rDNA analysis. Hepatic pathology and biochemical indicators were used to reflect the improvement of YBT on hepatic inflammation and lipid metabolism in NASH mice. Quantitative real-time PCR (qRT-PCR) was used to verify the results of PICRUSt analysis. Results: Results of the pathological and biochemical index showed that YBT could improve NASH mice. Compared with improving inflammation and hepatocyte damage, YBT may be more focused on enhancing metabolic disorders in mice, such as increasing HDL-c level. The diversity and richness of the gut microbiota of NASH mice induced by HFFD are significantly different from the normal control (NC) group. After YBT treatment, the diversity and richness of the mice microbiota will be increased to similar NC mice. Intestinimonas, Acetatifactor, Alistipes, Intestinimonas, Acetatifactor , and Alistipes have the most significant changes in the class level. PICRUSt analysis was performed to predict genomic functions based on the 16S rDNA results and reference sequencing. The efficacy of YBT in the treatment of NASH can be achieved by regulating the diversity and richness of gut microbiota. PICRUSt analysis results showed that the most relevant function of the microbiota construction variations is α- Linolenic acid (ALA) metabolism. Results of qRT-PCR showed significant differences between groups in the expression of Fatty acid desaturase 1 (FADS1), Fatty acid desaturase 2 (FADS2), Acyl-CoA Oxidase 1 (ACOX1), and Acyl-CoA Oxidase 2 (ACOX2) related to ALA metabolism. The expression of the above genes will be inhibited in the liver and small intestine of the HFFD group mice, and the expression can be restored after YBT treatment. Conclusion: YBT could treat NASH mice by improving the diversity and richness of gut microbiota and further the improvement of ALA metabolism. [ABSTRACT FROM AUTHOR]

Mitochondria are intracellular organelles that are instrumental in the creation of energy, metabolism, apoptosis, and intrinsic immunity. Mitochondria exhibit an extraordinarily high degree of flexibility, and are constantly undergoing dynamic fusion and fission changes. Chlamydia is an intracellular bacterium that causes serious health problems in both humans and animals. Due to a deficiency of multiple metabolic enzymes, these pathogenic bacteria are highly dependent on their eukaryotic host cells, resulting in a close link between Chlamydia infection and host cell mitochondria. Indeed, Chlamydia increase mitochondrial fusion by inhibiting the activation of dynein-related protein 1 (DRP1), which can regulate host cell metabolism for extra energy. Additionally, Chlamydia can inhibit mitochondrial fission by blocking DRP1 oligomerization, preventing host cell apoptosis. These mechanisms are critical for maintaining a favorable environment for reproduction and growth of Chlamydia. This review discusses the molecular mechanisms of mitochondrial fusion and fission, as well as the mechanisms by which Chlamydia infection alters the mitochondrial dynamics and the prospects of limiting chlamydial development by altering mitochondrial dynamics. [ABSTRACT FROM AUTHOR]

Background: Previous cluster-randomized controlled trials evaluating the impact of implementing evidence-based guidelines for nutrition therapy in critical illness do not consistently demonstrate patient benefits. A large-scale, sufficiently powered study is therefore warranted to ascertain the effects of guideline implementation on patient-centered outcomes.Methods: We conducted a multicenter, cluster-randomized, parallel-controlled trial in intensive care units (ICUs) across China. We developed an evidence-based feeding guideline. ICUs randomly allocated to the guideline group formed a local "intervention team", which actively implemented the guideline using standardized educational materials, a graphical feeding protocol, and live online education outreach meetings conducted by members of the study management committee. ICUs assigned to the control group remained unaware of the guideline content. All ICUs enrolled patients who were expected to stay in the ICU longer than seven days. The primary outcome was all-cause mortality within 28 days of enrollment.Results: Forty-eight ICUs were randomized to the guideline group and 49 to the control group. From March 2018 to July 2019, the guideline ICUs enrolled 1399 patients, and the control ICUs enrolled 1373 patients. Implementation of the guideline resulted in significantly earlier EN initiation (1.20 vs. 1.55 mean days to initiation of EN; difference - 0.40 [95% CI - 0.71 to - 0.09]; P = 0.01) and delayed PN initiation (1.29 vs. 0.80 mean days to start of PN; difference 1.06 [95% CI 0.44 to 1.67]; P = 0.001). There was no significant difference in 28-day mortality (14.2% vs. 15.2%; difference - 1.6% [95% CI - 4.3% to 1.2%]; P = 0.42) between groups.Conclusions: In this large-scale, multicenter trial, active implementation of an evidence-based feeding guideline reduced the time to commencement of EN and overall PN use but did not translate to a reduction in mortality from critical illness.Trial Registration: ISRCTN, ISRCTN12233792 . Registered November 20th, 2017. [ABSTRACT FROM AUTHOR]

Rationale: It remains unknown whether long-term ozone exposure can impair lung function. Objectives: To investigate the associations between long-term ozone exposure and adult lung function in China. Methods: Lung function results and diagnosis of small airway dysfunction (SAD) were collected from a cross-sectional study, the China Pulmonary Health Study (N = 50,991). We used multivariable linear and logistic regression models to examine the associations of long-term ozone exposure with lung function parameters and SAD, respectively, adjusting for demographic characteristics, individual risk factors, and longitudinal trends. We then performed a stratification analysis by chronic obstructive pulmonary disease (COPD). Measurements and Main Results: We observed that each 1 SD (4.9 ppb) increase in warm-season ozone concentrations was associated with a 14.2 ml/s (95% confidence interval [CI], 8.8-19.6 ml/s] decrease in forced expiratory flow at the 75th percentile of vital capacity and a 29.5 ml/s (95% CI, 19.6-39.5 ml/s) decrease in mean forced expiratory flow between the 25th and 75th percentile of vital capacity. The odds ratio of SAD was 1.09 (95% CI, 1.06-1.11) for a 1 SD increase in warm-season ozone concentrations. Meanwhile, we observed a significant association with decreased FEV1/FVC but not with FEV1 or FVC. The association estimates were greater in the COPD group than in the non-COPD group. Conclusions: We found independent associations of long-term ozone exposure with impaired small airway function and higher SAD risks, while the associations with airflow obstruction were weak. Patients with COPD appear to be more vulnerable. [ABSTRACT FROM AUTHOR]

As a life-threatening disease, stroke is the leading cause of death and also induces adult disability worldwide. To investigate the efficacy of the integrated traditional Chinese medicine (ITCM) on the therapeutic effects of acute ischemic stroke (AIS) patients, we enrolled 26 patients in the ITCM [Tanhuo decoction (THD) + Western medicine (WM)] group and 23 in the WM group. Thirty healthy people were also included in the healthy control (HC) group. ITCM achieved better functional outcomes than WM, including significant reduction of the phlegm-heat syndrome and neurological impairment, and improvement of ability. These facts were observed in different pretreatment gut enterotypes. In this paper, we collected the stool samples of all participants and analyzed the 16S rRNA sequence data of the gut microbiota. We identified two enterotypes (Type-A and Type-B) of the gut microbial community in AIS samples before treatment. Compared to Type-B, Type-A was characterized by a high proportion of Bacteroides , relatively high diversity, and severe functional damage. In the ITCM treatment group, we observed better clinical efficacy and positive alterations in microbial diversity and beneficial bacterial abundance, and the effect of approaching healthy people's gut microbiota, regardless of gut enterotypes identified in pretreatment. Furthermore, we detected several gut microbiota as potential therapeutic targets of ITCM treatment by analyzing the correlations between bacterial abundance alterations and functional outcomes, where Dorea with the strongest correlation was known to produce anti-inflammatory metabolite and negatively linked to trimethylamine-N-oxide (TMAO), a biomarker of AIS. This study analyzed clinical and gut microbial data and revealed the possibility of a broad application independent of the enterotypes, as well as the therapeutic targets of the ITCM in treating AIS patients with phlegm-heat syndrome. [ABSTRACT FROM AUTHOR]

Background: Fever of unknown origin (FUO) is still a challenge for clinicians. Next-generation sequencing technologies, such as whole exome sequencing (WES), can be used to identify genetic defects in patients and assist in diagnosis. In this study, we investigated the application of WES in individuals with FUO. Methods: We performed whole-exome sequencing on 15 FUO patients. Clinical information was extracted from the hospital information system. Results: In 7/15 samples, we found positive results, including potentially causative mutations across eight different genes: CFTR , CD209 , IRF2BP2, ADGRV 1 , TYK2 , MEFV , THBD and GATA2. Conclusions: Our results show that whole-exome sequencing can promote the genetic diagnosis and treatment of patients with FUO. [ABSTRACT FROM AUTHOR]

In some plants, sucrose: sucrose 1-fructosyltransferase (1-SST) is the first irreversible key enzyme in fructan biosynthesis. Studies have shown that fructan accumulation enhances abiotic stress tolerance of plants. To investigate the role of 1-SST in drought stress responses, a total of 37 cotton plants expressing a 1-SST gene from Allium cepa were developed by Agrobacterium -mediated transformation. Under drought stress in the field, compared with wild-type, ectopic expression of Ac1-SST in cotton resulted in significantly higher soluble sugars (especially 1-kestose), proline and relative water contents, as well as decreased malondialdehyde content, which contributed to maintaining intracellular osmoregulation and reducing membrane damage. In addition, ectopic expression of Ac1-SST in cotton significantly improved the photosynthesis rate, performance of PSII (including Pn, Fv/Fm, WUE, ΦPSII, and PItotal) and plant growth under drought stress. Furthermore, compared with the wild-type, under the droughted field, the yield loss per square meter of transgenic cotton was reduced by an average of 20.9% over two consecutive years. Our results indicate that the Ac1-SST gene can be used to improve drought tolerance and yield of cotton varieties, and might also be a promising drought-resistant gene for improving other crop varieties. [ABSTRACT FROM AUTHOR]

Background: Accumulating evidence indicates that high-fat diet (HFD) is a controllable risk factor for osteoporosis, but the underlying mechanism remains to be elucidated. As a primary biological barrier for nutrient entry into the human body, the composition and function of gut microbiota (GM) can be altered rapidly by HFD, which may trigger abnormal bone metabolism. In the current study, we analyzed the signatures of GM and serum metabolomics in HFD-induced bone loss and explored the potential correlations of GM and serum metabolites on HFD-related bone loss. Methods: We conducted a mouse model with HFD-induced bone loss through a 12-week diet intervention. Micro-CT, Osmium-μCT, and histological analyses were used to observe bone microstructure and bone marrow adipose tissue. Quantitative Real-Time PCR was applied to analyze gene expression related to osteogenesis, adipogenesis, and osteoclastogenesis. Enzyme-linked immunosorbent assay was used to measure the biochemical markers of bone turnover. 16s rDNA sequencing was employed to analyze the abundance of GM, and UHPLC-MS/MS was used to identify serum metabolites. Correlation analysis was performed to explore the relationships among bone phenotypes, GM, and the metabolome. Results: HFD induced bone loss accompanied by bone marrow adipose tissue expansion and bone formation inhibition. In the HFD group, the relative abundance of Firmicutes was increased significantly, while Bacteroidetes , Actinobacteria , Epsilonbacteraeota , and Patescibacteria were decreased compared with the ND group. Association analysis showed that thirty-two bacterial genera were significantly related to bone volume per tissue volume (BV/TV). One hundred and forty-five serum metabolites were identified as differential metabolites associated with HFD intervention, which were significantly enriched in five pathways, such as purine metabolism, regulation of lipolysis in adipocyte and cGMP-PKG signaling pathway. Sixty-four diffiential metabolites were matched to the MS2 spectra; and ten of them were positively correlated with BV/TV and five were negatively correlated with BV/TV. Conclusions: These findings indicated that the alternations of GM and serum metabolites were related to HFD-induced bone loss, which might provide new insights into explain the occurrence and development of HFD-related osteoporosis. The regulatory effects of GM and metabolites associated with HFD on bone homeostasis required further exploration. [ABSTRACT FROM AUTHOR]

Deoxyshikonin was reported to exhibit an anti-tumor effect in colorectal cancer. However, no studies are available to illustrate the effect of deoxyshikonin on acute myeloid leukemia (AML). The effects of deoxyshikonin on viability, apoptosis, caspase-3/7 activity, and cytochrome (Cyt) C expression were evaluated by Cell Counting Kit-8 assay, flow cytometry analysis, caspase-3/7 activity assay, and western blot analysis, respectively. Glucose consumption and lactate production were measured to determine the glycolysis level. The expression of pyruvate kinase M2 (PKM2) was detected by quantitative real-time polymerase chain reaction and western blot analysis. The results showed that deoxyshikonin inhibited cell viability and increased the apoptotic rate, the caspase-3/7 activity, and the Cyt C protein level in AML cells in a dose-dependent manner. Additionally, deoxyshikonin concentration-dependently decreased glucose consumption, lactate production, and PKM2 expression in AML cells. Deoxyshikonin inactivated the protein kinase B (Akt)/mammalian target of the rapamycin (mTOR) pathway. The activation of the Akt/mTOR pathway reversed the effects of deoxyshikonin on viability, apoptosis, and glycolysis in AML cells. In conclusion, deoxyshikonin dampened the viability and the glycolysis of AML cells by suppressing PKM2 via inactivation of the Akt/mTOR signaling. [ABSTRACT FROM AUTHOR]

Objective: To conduct a survey of diagnostic facility and therapeutic capability of Pulmonary thromboembolism (PE) in 90 hospitals throughout China. Method: It was a cross‐sectional study among the participating hospitals of the National Key Research & Development Program of China—the Precision Research of Standardized Management and Application of Pulmonary Thromboembolism to obtain the equipment and application of radiological facility to diagnose PE, laboratory tests for thrombophilia, coagulation function and the availability of anticoagulants and thrombolysis agents. Results: CT pulmonary arteriography is capable in all 90 hospitals, 71.11% of the hospitals could perform ventilation/perfusion scintigraphy, 24.44% of the hospitals do not routinely perform right heart evaluation by echocardiography. Protein C and protein S activity can be detected in half of the hospitals and warfarin pharmacogenomics tests can be conducted in 40 hospitals. Immune turbidimetry was used as the detection method of D‐dimer in 72.37% hospitals. About 81.11% of participating hospitals were equipped with new novel oral anticoagulants, all of which were equipped with Rivaroxaban. Conclusion: The hospitals are capable for standardized diagnosis and management PE, while the capability of precise stratification, coagulation function tests, thrombophilia screening and pharmacogenomics requires further improvement. [ABSTRACT FROM AUTHOR]

Background: Hematoma is the chief culprit in brain injury following intracranial cerebral hemorrhage (ICH). Noninvasive hematoma clearance could be an option to prevent and alleviate early brain injury after ICH. Peroxisome proliferator-activated receptor γ (PPAR-γ) and nuclear factor-erythroid 2 related factor-2 (Nrf2) facilitate removal of hematoma in ICH. Monascin acts as the natural Nrf2 activator with PPAR-γ agonist, and the long-term effects of monascin following ICH have not been elucidated. Methods: ICH in rats was induced by stereotactic, intrastriatal injection of type IV collagenase. Monascin was administered twice daily by gastric perfusion for 14 days after ICH induction. Long-term neurological scores (T maze, Garcia scales, rotor rod test, and Morris water maze), hematoma volume, as well as iron overload around hematoma and brain atrophy were evaluated at 7, 14, and 28 days after ICH. Results: The results showed that monascin improved long-term neurological deficits, spatial memory performance, learning ability, and brain shrinkage after ICH. Monascin also reduced hematoma volume at 7 days and iron content at 7 and 14 days after ICH. Conclusion: PPAR γ and Nrf2 play a crucial role in hematoma clearance after ICH in rat. As a dual agonist of PPAR γ and Nrf2, monascin improved long-term outcomes by facilitating hematoma clearance, and by attenuating iron overload and brain atrophy after experimental ICH. [ABSTRACT FROM AUTHOR]