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Equivalence ratio (Φ) is one of the most important parameters in combustion diagnostics. In previous studies, flame color characteristics have been widely applied to model the Φ of premixed hydrocarbon flames. The flame spatial characteristics also change with the varying Φ. In this paper, a high-speed color camera was employed to capture the premixed propane flame images under different Φ conditions (Φ = 0.93 to 1.53). Then, the relationship between the spatial characteristics and the Φ variation was investigated. The area and height of propane premixed flames perform a strong sensitive response to the Φ variation. Based on the research above, the Φ measurement models were constructed using color and spatial characteristics. A comparison was made between the color characteristics (Color-Φ) model and the color-spatial characteristics (Multi-dimensional-Φ) model. Both models were applied to a set of color images of a premixed propane flame, and the result indicates that the Multi-dimensional-Φ model performs with higher accuracy.

The occurrence and mechanisms of developmental adult diseases have gradually attracted attention in recent years. Exposure of gametes and embryos to adverse environments, especially during plastic development, can alter the expression of certain tissue-specific genes, leading to increased susceptibility to certain diseases in adulthood, such as diabetes, cardiovascular disease, neuropsychiatric, and reproductive system diseases, etc. The occurrence of chronic disease in adulthood is partly due to genetic factors, and the remaining risk is partly due to environmental-dependent epigenetic information alteration, including DNA methylation, histone modifications, and noncoding RNAs. Changes in this epigenetic information potentially damage our health, which has also been supported by numerous epidemiological and animal studies in recent years. Environmental factors functionally affect embryo development through epimutation, transmitting diseases to offspring and even later generations. This review mainly elaborated on the concept of developmental origins of adult diseases, and revealed the epigenetic mechanisms underlying these events, discussed the theoretical basis for the prevention and treatment of related diseases.

The spatiotemporal heterogeneity of neurons, circuits and regulators is being uncovered at a single‐cell level, from the single‐cell gene expression to functional regulations. The classifications, architectonics and functional communications amongst neural cells and circuits within the brain can be clearly delineated using single‐cell multiomics and transomics. This Editorial highlights the spatiotemporal heterogeneity of neurons and circuits as well as regulators, initiates the translation of neuronal diversity and spatial organisation at single‐cell levels into clinical considerations, and enables the discovery and development of new therapies for neurological diseases. It is predicted that single‐cell and spatial multiomics will be integrated with metabolomic profiles and corresponding gene epigenetic modifications. The interactions amongst DNAs, RNAs and proteins in a cell provide details of intracellular functional regulations and new opportunities for the translation of temporospatial diversity of neural cell subtypes/states into clinical practice. The application of single‐cell multiomics with four‐dimensional genome to the human pathological brain will lead us to a new milestone of the diagnosis and treatment. [ABSTRACT FROM AUTHOR]

Metabolic abnormalities represent one of the pathological features of chronic obstructive pulmonary disease (COPD). Glutamic pyruvate transaminase 2 (GPT2) is involved in glutamate metabolism and lipid synthesis pathways, whilst the exact roles of GPT2 in the occurrence and development of COPD remains uncertain. This study aims at investigating how GPT2 and the associated genes modulate smoking‐induced airway epithelial metabolism and damage by reprogramming lipid synthesis. The circulating or human airway epithelial metabolomic and lipidomic profiles of COPD patients or cell‐lines explored with smoking were assessed to elucidate the pivotal roles of GPT2 in reprogramming processes. We found that GPT2 regulate the reprogramming of lipid metabolisms caused by smoking, especially phosphatidylcholine (PC) and triacylglycerol (TAG), along with changes in the expression of lipid metabolism‐associated genes. GPT2 modulated cell sensitivities and survival in response to smoking by enhancing mitochondrial functions and maintaining lipid and energy homeostasis. Our findings provide evidence for the involvement of GPT2 in the reprogramming of airway epithelial lipids following smoking, as well as the molecular mechanisms underlying GPT2‐mediated regulation, which may offer an alternative of therapeutic strategies for chronic lung diseases. [ABSTRACT FROM AUTHOR]

Semiconductor photocatalysis is a potential solution to meet energy needs with green and inexhaustible solar energy. However, designing efficient and stable photocatalysts is a challenging task due to the limited ability to effectively separate electrons and holes. In this paper, by using a straightforward ethanol dispersion technique, we were able to combine ultrathin layered Cu-TCPP MOFs with g-C3N4 nanosheets, resulting in the creation of an extremely effective nano-composite photocatalyst with exceptional UV-vis activity. CT/CN heterojunctions displayed remarkable photocatalytic efficacy for the production of H2, with 3CT/CN showcasing a five-fold enhancement in photoactivity as compared to the unadorned g-C3N4. Based on the results of photoluminescence spectroscopy, electrochemical impedance spectroscopy, and electrochemical reduction, the considerably improved charge transfer and separation, together with the possible catalytic capability of uniformly distributed metal nodes in Cu-TCPP, are believed to be the underlying reason for the observed exceptional photoactivity. After thorough analysis, a potential process for charge transfer and segregation between g-C3N4 and Cu-TCPP has been suggested. [ABSTRACT FROM AUTHOR]

Peripheral immune cells play important roles in the maintenance of systemic and microenvironmental hemostasis. Measurements of circulating blood cells by single‐cell RNA sequencing (scRNA‐seq) were proposed as one of the routine measures in clinical biochemistry of hematology. Out of translational challenges, defining precise identities of cell subsets and states is more difficult, due to the complexity of immune cell development, location, regulation, function, and metabolism. It is also a challenge to precisely interpret clinical significance and impact of each cell identity marker gene panel (ciMGPs). ciMGPs have potential to advance the understanding of systemic responses of the disease, identify disease‐specific biomarkers, and to define cell heterogeneity. Recently, a large number of peripheral cell subsets and expending/activating states have been identified and validated for use in the fast developments in clinical single cell biomedicine. Defining specificity, measurability, and repeatability of cell subsets/states is important for translation of peripheral scRNA‐seq in clinical hematology and biochemistry. The development of standard operating procedure and performance of clinical trials in large populations at various ages, diseases, and therapies will promote the clinical translation of ciMGPs to measures. Thus, defining cell subset/state identities will provide the multi‐dimensional and comprehensive readouts of systemic immune cells, the precision monitoring of immune dynamics, and deeper‐understanding of the disease and response to therapy. [ABSTRACT FROM AUTHOR]

Background: Lung epithelial cells play important roles in lung inflammation and injury, although mechanisms remain unclear. Osteopontin (OPN) has essential roles in epithelial damage and repair and in lung cancer biological behaviours. Telocyte (TC) is a type of interstitial cell that interacts with epithelial cells to alleviate acute inflammation and lung injury. The present studies aim at exploring potential mechanisms by which OPN regulates the epithelial origin lung inflammation and the interaction of epithelial cells with TCs in acute and chronic lung injury. Methods: The lung disease specificity of OPN and epithelial inflammation were defined by bioinformatics. We evaluated the regulatory roles of OPN in OPN‐knockdown or over‐expressed bronchial epithelia (HBEs) challenged with cigarette smoke extracts (CSE) or in animals with genome OPN knockout (gKO) or lung conditional OPN knockout (cKO). Acute lung injury and chronic obstructive pulmonary disease (COPD) were induced by smoking or lipopolysaccharide (LPS). Effects of OPN on PI3K subunits and ERK were assessed using the inhibitors. Spatialization and distribution of OPN, OPN‐positive epithelial subtypes, and TCs were defined by spatial transcriptomics. The interaction between HBEs and TCs was assayed by the co‐culture system. Results: Levels of OPN expression increased in smokers, smokers with COPD, and smokers with COPD and lung cancer, as compared with healthy nonsmokers. LPS and/or CSE induced over‐production of cytokines from HBEs, dependent upon the dysfunction of OPN. The severity of lung inflammation and injury was significantly lower in OPN‐gKO or OPN‐cKO mice. HBEs transferred with OPN enhanced the expression of phosphoinositide 3‐kinase (PI3K)CA/p110α, PIK3CB/p110β, PIK3CD/p110δ, PIK3CG/p110γ, PIK3R1, PIK3R2 or PIK3R3. Spatial locations of OPN and OPN‐positive epithelial subtypes showed the tight contact of airway epithelia and TCs. Epithelial OPN regulated the epithelial communication with TCs, and the down‐regulation of OPN induced more alterations in transcriptomic profiles than the up‐regulation. Conclusion: Our data evidenced that OPN regulated lung epithelial inflammation, injury, and cell communication between epithelium and TCs in acute and chronic lung injury. The conditional control of lung epithelial OPN may be an alternative for preventing and treating epithelial‐origin lung inflammation and injury. [ABSTRACT FROM AUTHOR]

The burning behaviour of a wooden rod under various forced flow conditions was investigated by employing a synchronised multi-imaging system integrating visible wavelength, short-wavelength infrared (SWIR), and Schlieren techniques. The wood samples were fixed horizontally and at an inclined angle to study the effect of the surface orientation under forced flow. A small-scale wind tunnel was developed to supply three types of forced flow: concurrent, opposed and cross flow. Each imaging technique helps to gain different physical insights of different aspects of the phenomenon. The combined data provides a comprehensive understanding of the flow effect on fire propagation. It was found that the forced flow strongly influences the often-invisible hot gas flow surrounding the burning rod. The heat feedback from the attached hot flow layer helped to maintain the surface temperature, which further influenced the burning behaviour. The mechanisms that the various flow orientation caused, affected the heated gas differently. Additionally, a method was proposed to monitor the burning process, which used thermal imaging to quantitatively calculate the area of pyrolysis zone on the surface. With the visualisation of the Schlieren images at the critical timings, it was found the thick hot gas flow underneath the wooden rod was a crucial factor that determined the intensity of burning, which may provide important guidance on effective wooden beam fire suppression and control. [ABSTRACT FROM AUTHOR]

Background: The fundamental initial step in the metabolic process of fatty acids (FA) is facilitated by Acyl‐coenzyme A synthetase (ACS). ACS enables FAs to engage in both anabolic and catabolic pathways by creating thioester bonds with CoA, thus triggering their activation. This paper demonstrated the effect of in vitro cells on the ACS family of key enzymes in FA metabolism in response to inflammatory or lipid stimulating factors and provided insight into the relevant metabolic mechanisms. Methods: The expression levels of 27 ACS family members were assessed across various lung epithelial cell lines, such as HBE, SPC‐1A, or NCI‐H460, in response to external challenges including lipopolysaccharide (LPS), lysophosphatidylcholine (lysoPC), cigarette smoking extract (CSE), cholesterol, and interference with the ACSL5 gene in response to FASN, CPT1A inhibitors. Results: Our data showed that ACSF2 was highly expressed in SPC‐A1 and NCI‐H460 cells compared with HBE cell, while ACSL4 and ACSVL4 were lower expressed. The 27 ACS family genes associated with FA metabolism varied under several different exogenous stimuli. [ABSTRACT FROM AUTHOR]

T cells, with numerous classifications, are vital components of the adaptive immune system, which function to maintain homeostasis to protect against pathogens. With the rapid development of single‐cell RNA sequencing (scRNA‐seq), the specificity and functions of high‐resolution characterizations and identities of T cells are continuously explored and discovered. The exact T cell identities provide new insights for deeply understanding the heterogeneity of T cells and for the identification of previously unrecognized cell subsets. The accuracy and specificity of T cell cluster and annotation are critical and important in scRNA‐seq analyses, even though the characters and numbers of T cell marker gene panels (MGPs) are to be furthermore improved and uncovered. In order to initiate the discussion on identities of T cell subsets/clusters and impacts of identity specificity in the understanding of immune function, the present review systematically summarized the T cell identities of MGPs and functional characteristics of distinct T cell identities in the scRNA‐seq analysis. We also discussed the critical gene differences among panels across T cell subsets, cell functional states, tissue types, and diseases, with a special focus on the significance and potential values of T cell MGP accuracy and specificity in clinical applications. We hope that the precise knowledge of T cell subsets/clusters benefit decision designs and makings of biomarker discoveries and therapeutic strategies to improve the outcomes of patients. [ABSTRACT FROM AUTHOR]

Lung cancer is a widespread malignancy with a high death rate and disorder of lipid metabolism. Lysophosphatidylcholine (lysoPC) has anti‐tumour effects, although the underlying mechanism is not entirely known. The purpose of this study aims at defining changes in lysoPC in lung cancer patients, the effects of lysoPC on lung cancer cells and molecular mechanisms. Lung cancer cell sensitivity to lysoPC was evaluated and decisive roles of long‐chain acyl‐coenzyme A synthase 5 (ACSL5) in lysoPC regulation were defined by comprehensively evaluating transcriptomic changes of ACSL5‐downregulated epithelia. ACSL5 over‐expressed in ciliated, club and Goblet cells in lung cancer patients, different from other lung diseases. LysoPC inhibited lung cancer cell proliferation, by inducing mitochondrial dysfunction, altering lipid metabolisms, increasing fatty acid oxidation and reprograming ACSL5/phosphoinositide 3‐kinase/extracellular signal‐regulated kinase‐regulated triacylglycerol‐lysoPC balance. Thus, this study provides a general new basis for the discovery of reprogramming metabolisms and metabolites as a new strategy of lung cancer precision medicine. [ABSTRACT FROM AUTHOR]

With rapid developments of single‐cell sequencing and multi/trans‐omics, clinical single‐cell biomedicine is a new and emergent discipline to integrate single‐cell molecular and clinical phenomes and uncover new disease‐specific diagnoses and therapy. The journal of Clinical and Translational Medicine (CTM) launches the first CTM initiative of clinical single‐cell biomedicine (cscBioMed) to promote the discovery and development of single‐cell‐based biology and medicine, speed the translation from single‐cell biology into clinical application, and improve early diagnosis and therapy for human diseases. The cscBioMed initiative is speeding translational processes from circulating single‐cell RNA sequencing into routine measures in clinical biochemistry of haematology, from spatial transcriptomics into single‐cell pathology, and from single‐cell‐based biomarkers and targets into clinical diagnostics and target drugs. With a clear goal, we expect that cscBioMed will benefit human health by establishing a clinical single‐cell dynamic monitoring and early predicting system and by improving diagnosis and treatment. [ABSTRACT FROM AUTHOR]

In conclusion, for the first time, we developed the criteria to evaluate the ciMGPs specificity of lung cell types/subtypes from various lung diseases and characterized three categories of cell-specific, cell-associated, and cell-reference ciMGPs on basis of scRNA-seq. Intricated cell types and subtypes are defined by the provided cell annotations and further validated using cell identity marker gene panels (ciMGPs),[6] so the specificity of ciMGPs is critical to construct the single-cell profile. Of those cells, immune cells resident in the lung tissue included nine subtypes of lymphoid cells and 15 subtypes of myeloid cells,[8] and lung parenchymal cells had 15 subtypes of epithelia, nine of endothelia and nine of stromal cells, as presented in Figures S1-S48 and details in Tables S6-S11. [Extracted from the article]

General control non-repressible 5-related I N i -acetyltransferases (GNAT) family members ( I n i = 24) are primarily involved in the histone acetylation and translation process, to promote gene expression. Transcriptomic atlas of GNAT family members in pulmonary epithelia under pathological conditions using single-cell and bulk cell sequencing In order to elucidate the potential mechanism of GNAT family genes in lung diseases, we summarized and exampled critical pathways of GNAT family genes-associated regulations in gene expression of potential targets responsible for the development of lung diseases (Figure S1). [Extracted from the article]

Background: Hypercholesterolemia is found in patients with chronic lung inflammation, during which airway epithelial cells play important roles in maintenance of inflammatory responses to pathogens. The present study aims at molecular mechanisms by which cholesterol changes airway epithelial sensitivity in response to smoking. Methods: Human bronchial epithelial cells (HBEs) were stimulated with cigarette smoke extract (CSE) and mice were exposed to CS/lipopolysaccharide (LPS) as models in vitro and in vivo. Severe COPD patients and healthy volunteers were also enrolled and the level of cholesterol in plasma was detected by metabolomics. Filipin III and elisa kits were used to stain free cholesterol. Mitochondrial function was detected by mitotracker green, mitotracker green, and Seahorse. Mitochondrial morphology was detected by high content screening and electron microscopy. The mRNA and protein levels of mitochondrial dynamics‐related proteins were detected by RT‐qPCR and Western blot,respectively. BODIPY 493/503 was used to stain lipid droplets. Lipidomics was used to detect intracellular lipid components. The mRNA level of interleukin (IL)‐6 and IL‐8 were detected by RT‐qPCR. Results: We found that the cholesterol overload was associated with chronic obstructive pulmonary disease (COPD) and airway epithelia‐driven inflammation, evidenced by hypercholesterolemia in patients with COPD and preclinical models, alteration of lipid metabolism‐associated genes in CSE‐induced airway epithelia and production of ILs. External cholesterol altered airway epithelial sensitivity of inflammation in response to CSE, through the regulation of STARD3‐MFN2 pathway, cholesterol re‐distribution, altered transport and accumulation of cholesterol, activities of lipid transport regulators and disorder of mitochondrial function and dynamics. MFN2 down‐regulation increased airway epithelial sensitivity and production of ILs after smoking, at least partially by injuring fatty acid oxidation and activating mTOR phosphorylation. Conclusions: Our data provide new insights for understanding molecular mechanisms of cholesterol‐altered airway epithelial inflammation and for developing diagnostic biomarkers and therapeutic targets to improve patient outcomes. [ABSTRACT FROM AUTHOR]

The roles of type2 inflammatory markers in chronic airway diseases have been assessed in previous studies. However, the relationship between the combined value of these biomarkers and chronic obstructive pulmonary disease (COPD) has not been fully elucidated. We aimed to investigate the roles of the combined value of the fraction of exhaled nitric oxide (FeNO) level and blood eosinophil count in COPD and the predictive capability of these biomarkers. In total, 266 patients were included in our analysis. When the two type2 biomarkers were assessed separately, there were limited correlations between either increased FeNO level or blood eosinophil count and decreased incidence of total exacerbation or frequency of mild exacerbation. Combining these two biomarkers strengthened their association with both incidence and frequency of acute exacerbation. In addition, during further assessment, simultaneously increased FeNO level and blood eosinophil count were associated with both mild and moderate acute exacerbation. Among the subjects included in this analysis, although the predictive capability was improved when these two biomarkers were combined, the improvement was not statistically significant, indicating the need to increase the sample size. The combination of FeNO level and blood eosinophil count exhibited strong and independent additive value in the assessment of acute exacerbation in COPD; simultaneously increased FeNO level and blood eosinophil count played a protective role in progression of COPD. [ABSTRACT FROM AUTHOR]

Single‐cell RNA sequencing (scRNA‐seq) is considered an important approach to understand the molecular mechanisms of cancer microenvironmental functions and has the potential for clinical and translational discovery and development. The recent concerns on the impact of scRNA‐seq for clinical practice are whether scRNA can be applied as a routine measurement of clinical biochemistry to assist in clinical decision‐making for diagnosis and therapy. Pushing single‐cell sequencing into clinical application is one of the important missions for clinical and translational medicine (CTM), although there still are a large number of challenges to be overcome. The present Editorial as one of serials aims at overviewing the history of scRNA‐seq publications in CTM, sharing the understanding and consideration of the cancer microenvironment at the single‐cell solution and emphasising the objective of translating scRNA‐seq into clinical application. The dynamic characteristics and patterns of single‐cell identity, regulatory networks, and intercellular communication play decisive roles in the properties of the microenvironment, malignancy and migrative capacity of cancer cells, and defensive capacity of immune cells. The microenvironmental single‐cell transcriptomic profiles and cell clusters defined by scRNA‐seq have great value for exploring the molecular mechanisms of diseases and predicting cell sensitivities to therapy and patient prognosis. [ABSTRACT FROM AUTHOR]

Background: Serum uric acid (SUA) is suspected to be associated with atherosclerosis and calcium deposition in atherosclerosis is known to related poor prognosis, yet there is no cohort study on the aged in China. We aimed to investigate the relationships between SUA levels and coronary calcium deposition in the middle-aged and elderly populations in China. Methods: A total of 326 participants between the ages of 50 and 85 who had undergone a coronary CT scan in 2015 at the Huadong Hospital Affiliated to Fudan University (Shanghai, China) were included in this study. Univariate and multivariate binary logistic regression was performed to analyze the correlation between SUA levels and coronary artery calcium score (CACS). The changes in CACS during a five-year follow-up were analyzed through Kaplan–Meier survival and binary cox regression analysis. An observational study was done on another 104 asymptomatic middle-aged and elderly patients to compare relative mRNA expressions of proinflammatory factors in peripheral blood mononuclear cells (PBMCs) from 104 subjects. Results: Based on the first year of follow-up data analysis, the elevation of SUA levels (P< 0.001) is an independent risk factor for the increase of CACS after coordinating the confounding factors. According to five-year follow-up data, cox regression analysis proved that SUA was a risk factor for CACS (HR =5.86, P< 0.001). The mRNA expression of IL-6 and CXCL8 in the HUA and HUA patients with CAC (HUA-CAC) groups was significantly higher than that in the normal control (NC) and coronary calcium deposition (CAC) groups. Conclusion: Taken together, the findings in this study indicate that high SUA levels (P< 0.001) are an independent risk factor for CACS and elevated SUA levels increase the risk of developing coronary calcium deposition among middle-aged and old people in the Chinese population, which may be related to an increase of pro-inflammatory cytokines in the PBMCs. [ABSTRACT FROM AUTHOR]

Background: Chronic obstructive pulmonary disease (COPD) often coexists with multiple comorbidities which may have a significant impact on acute exacerbations of patients. At present, what kind of comorbidities affects acute exacerbations and how comorbidities lead to poor prognosis are still controversial. The purpose of our study is to determine the impact of comorbidities on COPD exacerbation and establish an acute exacerbation risk assessment system related to comorbidities. Methods: A total of 742 COPD patients participated in the Shanghai COPD Investigation on Comorbidity Program (SCICP, ChiCTR2000030911). Finally, the baseline information of 415 participants and one-year follow-up data were involved in the analysis. We collected hemogram indices, pulmonary function tests and acute exacerbation of COPD with regular medical follow-up. Q-type cluster analysis was used to determine the clusters of participants. Receiver operating characteristic (ROC) analysis was constructed to assess the ability of indicators in predicting acute exacerbations. Results: Almost 65% of the population we investigated had at least one comorbidity. The distribution and incidence of comorbidities differed between exacerbation group and non-exacerbation group. Three comorbidity clusters were identified: (1) respiratory, metabolic, immune and psychologic disease (non-severe cases); (2) cardiovascular and neoplastic disease (severe cases); (3) less comorbidity. Different sub-phenotypes of COPD patients showed significant distinction in health status. Anxiety (OR=5.936, P=0.001), angina (OR=10.155, P=0.025) and hypertension (OR=3.142, P=0.001) were found to be independent risk factors of exacerbation in a year. The novel risk score containing BODEx and four diseases showed great prognostic value of COPD exacerbation in developing sample. Conclusion: Our study detailed the major interaction between comorbidities and exacerbation in COPD. Noteworthily, a novel risk score using comprehensive index – BODEx – and comorbidity parameters can identify patients at high risk of acute exacerbation. [ABSTRACT FROM AUTHOR]