Bazi Bushen ameliorates age-related energy metabolism dysregulation by targeting the IL-17/TNF inflammatory pathway associated with SASP.

BACKGROUND: Chronic inflammation and metabolic dysfunction are key features of systemic aging, closely associated with the development and progression of age-related metabolic diseases. Bazi Bushen (BZBS), a traditional Chinese medicine used to alleviate frailty, delays biological aging by modulating DNA methylation levels. However, the precise mechanism of its anti-aging effect remains unclear. In this study, we developed the Energy Expenditure Aging Index (EEAI) to estimate biological age. By integrating the EEAI with transcriptome analysis, we aimed to explore the impact of BZBS on age-related metabolic dysregulation and inflammation in naturally aging mice. METHODS: We conducted indirect calorimetry analysis on five groups of mice with different ages and utilized the data to construct EEAI. 12 -month-old C57BL/6 J mice were treated with BZBS or ß-Nicotinamide Mononucleotide (NMN) for 8 months. Micro-CT, Oil Red O staining, indirect calorimetry, RNA sequencing, bioinformatics analysis, and qRT-PCR were performed to investigate the regulatory effects of BZBS on energy metabolism, glycolipid metabolism, and inflammaging. RESULTS: The results revealed that BZBS treatment effectively reversed the age-related decline in energy expenditure and enhanced overall metabolism, as indicated by the aging index of energy expenditure derived from energy metabolism parameters across various ages. Subsequent investigations showed that BZBS reduced age-induced visceral fat accumulation and hepatic lipid droplet aggregation. Transcriptomic analysis of perirenal fat and liver indicated that BZBS effectively enhanced lipid metabolism pathways, such as the PPAR signaling pathway, fatty acid oxidation, and cholesterol metabolism, and improved glycolysis and mitochondrial respiration. Additionally, there was a significant improvement in inhibiting the inflammation-related arachidonic acid-linoleic acid metabolism pathway and restraining the IL-17 and TNF inflammatory pathways activated via senescence associated secretory phenotype (SASP). CONCLUSIONS: BZBS has the potential to alleviate inflammation in metabolic organs of naturally aged mice and maintain metabolic homeostasis. This study presents novel clinical therapeutic approaches for the prevention and treatment of age-related metabolic diseases.

Hyperbaric oxygen therapy for poststroke insomnia: a systematic review and meta-analysis protocol.

INTRODUCTION: Insomnia stands as a frequent consequence of a cerebrovascular event, afflicting a substantial fraction of those who endure the aftermath of stroke. The ramifications of insomnia following a stroke can further exacerbate cognitive and behavioural anomalies while hindering the process of neurological convalescence. While several randomised controlled trials (RCTs) have scrutinised the effects of hyperbaric oxygen therapy (HBOT) on poststroke insomnia, the advantages and drawbacks persist in a state of ambiguity. We advocate for a systematic review and meta-analysis of randomised clinical trials to comprehensively evaluate the effectiveness and safety of HBOT in the context of poststroke insomnia. METHODS AND ANALYSIS: A systematic search will be conducted from nine major databases (PubMed, Web of Science, EMBASE, VIP Information Database, Cochrane Central Register of Controlled Trials, China National Knowledge Infrastructure, China Biomedical Literature Database and Wanfang Database, Physiotherapy Evidence Database (PEDro)) for HBOT for poststroke insomnia of RCTs. The search procedures will adhere to a rigorous approach, commencing from the inception date of each database and continuing until 1 November 2023, with inquiries conducted exclusively in English and Chinese. The primary outcome will focus on the alteration in the quality of sleep while secondary outcomes will encompass the evaluation of adverse events and the rate of reoccurrence. The process of selecting studies, extracting data and evaluating the quality of research will be carried out independently by two reviewers. The quality of the included literature will be assessed using the tools of the Cochrane Collaboration. Meta-analysis will be performed by using RevMan V.5.4 and STATA V.16.0.b software. Finally, the quality of evidence will be assessed using the Grading of Recommendations, Assessment, Development and Evaluation method. ETHICS AND DISSEMINATION: As all data are derived from published investigations via databases without direct patient contact, ethical approval is obviated in this study. The scientific studies will be published in professional academic publications. PROSPERO REGISTRATION NUMBER: CRD42023468442.

Leptin and risk factors for atherosclerosis: A review.

Leptin is a hormone secreted primarily by adipose tissue. It regulates an organism's metabolism, energy balance, and body weight through a negative feedback mechanism. When a person or animal has low body fat and little energy, the leptin level in the body decreases, and conversely, when there is an excess of nutrients, the leptin level increases, giving a feeling of satiety. However, when leptin levels are abnormal (too high or too low) for a number of reasons, it can negatively affect your health, inducing inflammatory responses, obesity, and other problems. Many studies have shown that abnormal leptin levels, such as hyperleptinemia, are closely associated with common risk factors for atherosclerosis (AS). This review systematically states the relationship between leptin and common risk factors for AS (inflammation, obesity, diabetes mellitus, hypertension, and sleep disorders) and provides some new thoughts on the future direction of research on both. Because the abnormal level of leptin will have adverse effects on multiple atherosclerotic risk factors, how to regulate the leptin level of patients with AS, and whether we can treat and prevent AS by intervening the leptin level, these may be our new research directions in the future.

Estrogen-Like Effect of Bazi Bushen Capsule in Ovariectomized Rats.

This study aims to show the estrogen-like effect of Bazi Bushen capsule (BZBS), a Chinese herbal compound, in ovariectomized mice. Female Sprague-Dawley (SD) rats were randomly divided into six groups: a sham-operated group, a model group (OVX), a progynova group, and BZBS groups (1, 2, and 4 d/kg/d). An ovariectomy was performed on all rats except those in the sham-operated group. Micro-computed tomography (micro-CT) scanning, hematoxylin and eosin (H&E) staining, immunohistochemistry, and enzyme-linked immunosorbent assay (ELISA) detection were performed after 4 months of BZBS treatment. As a result, compared with the OVX group, rats treated with BZBS showed an increased number and area of trabecular bone and bone marrow cells, and a decreased number of adipose cells. The bone volume, trabecular number, and trabecular thickness of the right tibia in the medication groups increased and the trabecular space decreased. The 17ß-estradiol and serum calcium levels in the medication groups were elevated, but the levels of serum phosphorus, sclerostin, ß-CTX, and TRACP-5b were decreased. In the medication groups, the RANKL and sclerostin levels were decreased, while the osteoprotegerin (OPG) level was increased. In conclusion, this protocol systematically evaluated the therapeutic effects and potential molecular mechanisms of Chinese herbal compounds in ovariectomized rats with a variety of techniques.

Bazi Bushen mitigates epigenetic aging and extends healthspan in naturally aging mice.

Bazi Bushen (BZBS), a traditional Chinese medicine, has been proven effective in the treatment of age-related disease in mouse models. However, whether its therapeutic effects are due to antiaging mechanism has not yet been explored. In the present study, we investigated the antiaging effects of BZBS in naturally aging mice by using behavioral tests, liver DNA methylome sequencing, methylation age estimation, and frailty index assessment. The methylome analysis revealed a decrease of mCpG levels in the aged mouse liver. BZBS treatment tended to restore age-associated methylation decline and prune the methylation pattern toward that of young mice. More importantly, BZBS significantly rejuvenated methylation age of the aged mice, which was computed by an upgraded DNA methylation clock. These results were consistent with enhanced memory and muscular endurance, as well as decreased frailty score and liver pathological changes. KEGG analysis together with aging-related database screening identified methylation-targeted pathways upon BZBS treatment, including oxidative stress, DNA repair, MAPK signaling, and inflammation. Upregulation of key effectors and their downstream effects on elevating Sod2 expression and diminishing DNA damage were further investigated. Finally, in vitro experiments with senescent HUVECs proved a direct effect of BZBS extracts on the regulation of methylation enzymes during cellular aging. In summary, our work has revealed for the first time the antiaging effects of BZBS by slowing the methylation aging. These results suggest that BZBS might have great potential to extend healthspan and also explored the mechanism of BZBS action in the treatment of age-related diseases.

Tongxinluo enhances the effect of atorvastatin on the treatment of atherosclerosis with chronic obstructive pulmonary disease by maintaining the pulmonary microvascular barrier.

Atherosclerosis (AS) is a common comorbidity of chronic obstructive pulmonary disease (COPD), and systemic inflammation is an important mechanism of COPD with AS. Tongxinluo (TXL) improves the function of vascular endothelial cells. We aimed to prove that impairment of pulmonary microvascular barrier function is involved in COPD-mediated aggravation of AS and investigate whether TXL enhances the effect of Ato (atorvastatin) on COPD with AS by protecting pulmonary microvascular endothelial barrier function. In vivo, a COPD with atherosclerotic apolipoprotein E knockout (AS ApoE-/-) mouse model was established by cigarette smoke combined with a high-fat diet. The animals were administered TXL, Ato, and TXL + Ato once a day for 20 weeks. Lung function, lung microvascular permeability, lung inflammation, systemic inflammation, serum lipid levels, atheromatous plaque formation, and endothelial damage biomarkers were measured. In vitro, human pulmonary microvascular endothelial cells (HPMECs) were pretreated with TXL and incubated with cigarette smoke extract to establish the model. The permeability of the endothelial monolayer, inflammatory cytokines, endothelial damage biomarkers, and tight junction (Tj) proteins were determined. Cigarette smoking significantly exacerbated the high-fat diet-induced pulmonary function decline, pulmonary microvascular endothelial barrier dysfunction, inflammation, and atherosclerotic plaques. These changes were reversed by TXL-Ato; the combination was more effective than Ato alone. Furthermore, TXL protected the HPMEC barrier and inhibited inflammation in HPMECs. COPD aggravates AS, possibly through the destruction of pulmonary microvascular barrier function; thus, lung inflammation triggers systemic inflammation. In treating COPD with AS, TXL enhances the antiatherosclerotic effect of Ato, protecting the pulmonary microvascular barrier.

Periplocin Alleviates Cardiac Remodeling in DOCA-Salt-Induced Heart Failure Rats.

Heart failure with preserved ejection fraction (HFpEF) is a common public health problem associated with increased morbidity and long-term mortality. However, effective treatment for HFpEF was not discovered yet. In the present study, we aimed to decipher the effects of Periplocin on DOCA-induced heart failure rats and explore the possible underlying mechanisms. We demonstrated that Periplocin could significantly attenuate cardiac structural remodeling and improve cardiac diastolic function. Of note, Periplocin significantly inhibited the recruitment of inflammatory and immune cells and decreased the expression of serum inflammatory cytokines. Meanwhile, Periplocin had the effect of cardiac glycosides to improve cardiomyocyte contractility and calcium transient amplitude. These findings indicate that Periplocin might be a potential medicine to treat HFpEF in patients.

Synthesis Strategies and Applications for Pitch-Based Anode: From Industrial By-Products to Power Sources.

It is significant for saving energy to manufacture superb-property batteries. Carbon is one of the most competitive anode materials in batteries, but it is hard for commercial graphite anodes to meet the increasingly higher energy-storage requirements. Moreover, the price of other better-performing carbon materials (such as graphene) is much higher than graphite, which is not conducive to massive production. Pitch, the cheap by-product in the petroleum and coal industries, has high carbon content and yield, making it possible for commercialization. Developing pitch-based anodes can not only lower raw material costs but also realize the pitch's high value-added utilization. We comprehensively reviewed the latest synthesis strategies of pitch-derived materials and then introduced their application and research progress in lithium, sodium, and potassium ion batteries (LIBs, SIBs, and PIBs). Finally, we summarize and suggest the pitch's development trend for anodes and in other fields.

Bazi Bushen capsule improves the deterioration of the intestinal barrier function by inhibiting NLRP3 inflammasome-mediated pyroptosis through microbiota-gut-brain axis.

Purpose: The senescence-accelerated prone mouse 8 (SAMP8) is a widely used model for accelerating aging, especially in central aging. Mounting evidence indicates that the microbiota-gut-brain axis may be involved in the pathogenesis and progression of central aging-related diseases. This study aims to investigate whether Bazi Bushen capsule (BZBS) attenuates the deterioration of the intestinal function in the central aging animal model. Methods: In our study, the SAMP8 mice were randomly divided into the model group, the BZ-low group (0.5 g/kg/d BZBS), the BZ-high group (1 g/kg/d BZBS) and the RAPA group (2 mg/kg/d rapamycin). Age-matched SAMR1 mice were used as the control group. Next, cognitive function was detected through Nissl staining and two-photon microscopy. The gut microbiota composition of fecal samples was analyzed by 16S rRNA gene sequencing. The Ileum tissue morphology was observed by hematoxylin and eosin staining, and the intestinal barrier function was observed by immunofluorescence. The expression of senescence-associated secretory phenotype (SASP) factors, including P53, TNF-α, NF-κB, IL-4, IL-6, and IL-10 was measured by real-time quantitative PCR. Macrophage infiltration and the proliferation and differentiation of intestinal cells were assessed by immunohistochemistry. We also detected the inflammasome and pyroptosis levels in ileum tissue by western blotting. Results: BZBS improved the cognitive function and neuronal density of SAMP8 mice. BZBS also restored the intestinal villus structure and barrier function, which were damaged in SAMP8 mice. BZBS reduced the expression of SASP factors and the infiltration of macrophages in the ileum tissues, indicating a lower level of inflammation. BZBS enhanced the proliferation and differentiation of intestinal cells, which are essential for maintaining intestinal homeostasis. BZBS modulated the gut microbiota composition, by which BZBS inhibited the activation of inflammasomes and pyroptosis in the intestine. Conclusion: BZBS could restore the dysbiosis of the gut microbiota and prevent the deterioration of intestinal barrier function by inhibiting NLRP3 inflammasome-mediated pyroptosis. These results suggested that BZBS attenuated the cognitive aging of SAMP8 mice, at least partially, by targeting the microbiota-gut-brain axis.

Promoting effect of Fe/La loading on γ-Al2O3 catalyst for hydrolysis of carbonyl sulfur.

Catalytic hydrolysis of carbonyl sulfur (COS) from blast furnace gas is one of the keys to achieving ultra-low emission in the iron-steel industry. To improve the COS hydrolysis activity on γ-Al2O3 catalyst at low temperature, catalysts with Fe or La as the active component were prepared by the impregnation method, the physical and chemical properties of the catalyst were characterized by ICP, XRF, XRD, BET, and TPD. The hydrolysis activity of COS and sulfur resistance ability on various catalysts were investigated in a fixed bed reactor combined with gas chromatography. The results show that the addition of Fe or La improves the COS hydrolysis activity due to the increase in alkaline sites on the catalyst surface. The roles of various alkaline sites on catalysts have been recognized. The weak alkaline center is the reaction site of COS hydrolysis, the middle and strong alkaline centers are the adsorption and oxidation sites of H2S. The Fe/Al2O3 catalyst has higher hydrolytic activity and oxidative capacity for H2S removal due to forming more sulfate species on Fe. The La/Al2O3 catalyst has higher hydrolysis efficiency in that H2S rapidly desorbs from the catalyst surface to the gas phase, and then, the activity of reaction sites is recovered. This provides an idea for the preparation of sulfur-resistant catalysts.

Zwitterionic ionic liquids modulating two-dimensional hierarchically porous zeolitic imidazolate framework composites.

HYPOTHESIS: Two-dimensional hierarchically porous zeolitic imidazolate frameworks (H-ZIFs) show great promising applications in catalysis, gas separation, energy storage and sensing. Herein, a facile ionic-liquid-modulation approach is proposed for constructing H-ZIFs nanosheets with tunable thickness. EXPERIMENTS: Sulfo-functionalized zwitterionic ionic liquids (SFIL) have been designed as monodentate ligands to direct the formation of microporous nanosheets (ZIF-SFIL) in aqueous solution. Anions of SFIL have been tuned to modulate the coordination environment, enabling the control of the structure, thickness and pores of the nanosheets. FINDINGS: SFIL is demonstrated to pre-coordinate with Zn(II) to induce micropores with high specific surface areas (up to 1176 m2·g-1) and accelerate the nucleation of crystals. The BF4- anion serves as a competitive ligand to partially replace SFIL to cause structural defects, thus yielding hierarchically porous ZIF-SFIL nanosheets with high specific surface areas (270-466 m2·g-1) and variable thicknesses (from ca. 58 nm to ca. 455 nm). Benefiting from the versatile designability and multifunctionality of ionic liquids, the strategy in this work offers a facile approach for designing and constructing multifunctional materials with hierarchical pores.

Biomass Carbon Magnetic Adsorbent Constructed by One-Step Activation Method for the Removal of Hg0 in Flue Gas.

Elemental mercury (Hg0) emission from industrial boilers equipped in factories such as coal-fired power plants poses serious hazards to the environment and human health. Herein, an iron-modified biomass carbon (Fe/BC) magnetic adsorbent was prepared by a one-step method using pepper straw waste as raw material and potassium oxalate and ferric nitrate as activator and catalyst precursor, respectively. A fixed-bed reactor was used to evaluate the Hg0 removal performance of the Fe/BC adsorbent. The synthesized adsorbent showed a wide temperature window for Hg0 removal. In a N2 + O2 atmosphere, the removal efficiency toward Hg0 was 97.6% at 150 °C. Further, O2 or SO2 could promote the removal of Hg0, while NO could inhibit the conversion of Hg0 over the Fe/BC adsorbent. The consequence of XPS and Hg-TPD showed that lattice oxygen in Fe2O3 and chemisorbed oxygen were the main active sites for Hg0 removal, and HgO was the main mercury species on used Fe/BC. Moreover, Fe/BC adsorbent showed a good regeneration and magnetization performance, which was conducive to the cost reduction of actual industrial application. This study provides a facile approach for efficient removal of Hg0 using biomass-derived carbon material.

Tongxinluo prevents chronic obstructive pulmonary disease complicated with atherosclerosis by inhibiting ferroptosis and protecting against pulmonary microvascular barrier dysfunction.

Cardiovascular comorbidities are pervasive in chronic obstructive pulmonary disease (COPD) and often result in serious adverse cardiovascular events. Tongxinluo (TXL) has been clinically verified to treat atherosclerosis (AS), improve lung function and alleviate dyspnoea. The present study aimed to explore the effect of lung microvascular barrier dysfunction on AS in COPD and the potential pulmonary protective mechanisms of TXL in COPD complicated with AS. COPD complicated with AS was induced in mice by cigarette smoke (CS) exposure and high-fat diet (HFD) feeding. The mice were treated with atorvastatin (ATO), TXL or combination therapy (ATO+TXL) for 20 weeks. Pulmonary function, lung pathology, serum lipid levels, atherosclerotic plaque area and indicators of barrier function, oxidative stress and ferroptosis in lung tissue were evaluated. In vitro, human pulmonary microvascular endothelial cells (HPMECs) were pretreated with TXL for 4 h and then incubated with cigarette smoke extract (CSE) and homocysteine (Hcy) for 36 h to induce barrier dysfunction. Then the indicators of barrier function, oxidative stress and ferroptosis were measured. The results demonstrate that CS aggravated dyslipidaemia, atherosclerotic plaque formation, pulmonary function decline, pathological injury, barrier dysfunction, oxidative stress and ferroptosis in the HFD-fed mice. However, these abnormalities were partially reversed by ATO and TXL. Similar results were observed in vitro. In conclusion, pulmonary microvascular barrier dysfunction plays an important role by which COPD affects the progression of AS, and ferroptosis may be involved. Moreover, TXL delays the progression of AS and reduces cardiovascular events by protecting the pulmonary microvascular barrier and inhibiting ferroptosis.

Effects of Additives on Coke Reactivity and Sulfur Transformation during Co-pyrolysis of Long Flame Coal and High-Sulfur Coking Coal.

A silica-aluminum-based mineral (GL) was selected for inspecting the effects of interactions of minerals in coal blends on the coke reactivity index (CRI) and sulfur transformation during co-pyrolysis of long flame coal and high-sulfur coking coal. Results indicate a good compatibility for the supply of active hydrogen, decomposition of sulfur, and regulation of reactivity. The experimental values of sulfur content in different coal blend cokes are lower than the calculated values, which can be determined as a result of the directional regulation effect of long flame coal on sulfur transformation. The addition of GL in coal blends significantly reduces the CRI of the corresponding coke, and the effect of GL on coke reactivity is also verified by a 10 kg coke oven experiment. When increasing the ratio of long flame coal, the sulfur fixation in the solid phase has a tendency to be enhanced by alkaline minerals. Also, GL plays a role in reducing the capture of sulfur free radicals by alkaline minerals, which improves the sulfur removal during pyrolysis of coal blends and then reduces the sulfur content in coke. This work provides a reference for using silica-aluminum-based minerals to reduce the capture of sulfur and catalytic effect on coke reactivity.

Huotan Jiedu Tongluo Decoction Inhibits Balloon-Injury-Induced Carotid Artery Intimal Hyperplasia in the Rat through the PERK-eIF2α-ATF4 Pathway and Autophagy Mediation.

In-stent restenosis (ISR) is the main factor affecting the outcome of percutaneous coronary intervention (PCI), and its main pathological feature is neointimal hyperplasia. Huotan Jiedu Tongluo decoction (HTJDTLD) is an effective traditional Chinese medicine (TCM) prescription for the treatment of vascular stenosis diseases. However, the precise anti-ISR mechanism of HTJDTLD remains unclear. Here, we investigated whether HTJDTLD can inhibit the excessive activation of endoplasmic reticulum stress (ERS) and reduce the level of autophagy factors through regulating the PERK-eIF2α-ATF4 pathway, thereby inhibiting the proliferation of the intima of blood vessels damaged by balloon injury (BI) and preventing the occurrence of ISR. In this study, a 2F Fogarty balloon was used to establish a common carotid artery (CCA) BI model in male Sprague-Dawley rats. Then, HTJDTLD (16.33 g/kg/d) or atorvastatin (1.19 mg/kg/d) was administered by gavage. Four weeks later, hematoxylin-eosin (HE) and Masson staining of the injured CCA were performed to observe the histological changes in the CCA. Immunohistochemistry (IHC) was used to assess the proliferation and dedifferentiation of vascular smooth muscle cells (VSMCs) in the CCA. Western blotting and RT-PCR were used to measure the expression of ERS- and autophagy-related proteins and mRNAs in the CCA. The results indicated that HTJDTLD significantly alleviated BI-induced carotid artery intimal hyperplasia and fibrosis and reduced the neointimal area (NIA) and NIA/medial area (MA) ratio. In addition, HTJDTLD inhibited the proliferation and dedifferentiation of VSMCs, reduced the expression of proliferating cell nuclear antigen (PCNA), and increased the smooth-muscle-α-actin- (SMα-actin-) positive area. HTJDTLD also significantly reduced the expression of the ERS-related factors: GRP78, p-PERK/PERK, p-eIF2α/eIF2α, ATF4, and CHOP. In addition, the expression of the autophagy-related factors, Beclin1, LC3B, and ATG12, was significantly decreased. In addition, in vitro experiments showed that HTJDTLD inhibited the above-mentioned ERS signal molecules in human umbilical vein endothelial cells (HUVEC) and rat aortic smooth muscle cells (A7R5) induced by tunicamycin (TM) and played a crucial role in protecting cells from damage. HTJDTLD may be a very promising drug for the treatment of ISR.

Carbon precursors in coal tar: Extraction and preparation of carbon materials.

Coke resources are abundantly available worldwide and are a large by-product of tar production. Moreover, their utilization presents a series of environmental pollution problems. Common technologies for coal tar production applications urgently need to be upgraded because coal tar is listed as a national hazardous waste. This review associates coal tar development with deep processing technology for extracting environmentally beneficial compounds from coal tar, which have never been reported. Recent studies on the innovative approaches for extracting phenols and nitrogen-containing compounds from coal tar have been addressed, as well as a preparation method of carbon materials with high catalytic activity and a well-ordered structure by confined polymerization. Tremendous demand for further research and exploration of selectively extracted compounds from coal tar implies a new opportunity for polymerizing the resin and a great challenge for the current technology implemented for valorizing coal tar into ordered carbon materials. Consequently, more concerted efforts should be implemented to achieve a wide range of polymer resin applications and improve the quality of carbon precursors extracted from the coal tar, thus increasing the economic benefit and scientific value of coal tar.

Catalytic Upgrading of Coal Pyrolysis Volatiles by Porous Carbon Materials Derived from the Blend of Biochar and Coal.

A suite of carbon materials is prepared from biochar and coal at three different blending ratios with 10, 20, and 30% biochar by mass. These carbon materials are activated by steam to obtain porous structures. The effect of the inactivated and activated carbon materials on the cracking of coal pyrolysis volatiles is evaluated. The results indicate that the inactivated carbon materials are beneficial to improve the yield of light oil with a boiling point below 170 °C. The steam-activated carbon materials are more conducive to cracking tar pitch than the inactivated carbon materials due to the increased defects in carbon structure. However, it is also easy to form more coke deposits. More components rich in hydrogen are cracked to generate radicals that could combine with the phenols' precursor over carbon materials, and the content of phenols in tar is increased. The carbon materials prepared from biochar and coal using this method show distinct advantages as filter media in the granular bed duster. It can improve the quality of tar along with reducing the dust content in tar.

Effect of hydrogen-rich gas from char gasification on rapid pyrolysis products of low rank coal in a downer pyrolyzer.

For guiding a novel integrated process of low-rank coal pyrolysis and gasification with char gasification gas as a heat carrier, this study investigated the effect of simulated coal gas from char gasification (SCGG) on rapid pyrolysis products of low rank coal from 550 to 700 °C in a downer pyrolyzer. Results indicated that the component of SCGG directly affected the distribution and composition of pyrolysis products. Compared with N2, SCGG facilitated the formation of tar below 600 °C. H2 in SCGG and that from water gas shift reaction (WGS: CO + H2O → CO2 + H2) increased the tar yield by reacting with solid-phase free radicals in coal and inhibiting the secondary reaction of gas-phase volatile radicals. Also, CO2 in SCGG raised the tar yield due to its promotion to coal cracking. When the pyrolysis temperature exceeded 600 °C, the reforming reactions of nascent tar with steam occurred, resulting in a reduced tar yield. SCGG could distinctly reduce the coke yield (coke-S) and pitch content in tar due to the inhibiting effect of H2 from SCGG and WGS on the polycondensation reactions of volatile radicals and reforming reactions of nascent tar. The chemical composition analysis of tar by GC × GC-MS demonstrated that compared with under N2, the contents of phenols, oxygenated compounds, and heterocyclic compounds in tar under SCGG were decreased while the content of aromatics was the opposite mainly due to hydrogenation and reforming reactions of nascent tar. Also, the H/C and O/C ratios of char under the action of SCGG were higher than those under N2 at the same temperature.

Outcomes and prognostic factors in 70 non-survivors and 595 survivors with COVID-19 in Wuhan, China.

Since the first outbreak of coronavirus disease 2019 (COVID-19) occurred in December 2019, more than 51 million cases had been reported globally. We aimed to identify the risk factors for in-hospital fatal outcome and severe pneumonia of this disease. This is a retrospective, multicentre study, which included all confirmed cases of COVID-19 with definite outcomes (died or discharged) hospitalized between 1 January and 4 March 2020 in Wuhan. Of all 665 patients included, 70 died and 595 discharged (including 333 mild and 262 severe cases). Underlying comorbidity was more commonly observed among deaths (72.9%) than mild (26.4%) and severe (61.5%) survivors, with hypertension, diabetes and cardiovascular as dominant diseases. Fever and cough were the primary clinical magnifications. Older age (≥65 years) (OR = 3.174, 95% CI = 1.356-7.755), diabetes (OR = 2.540, 95% CI = 0.995-6.377), dyspnoea (OR = 7.478, 95% CI = 3.031-19.528), respiratory failure (OR = 10.528, 95% CI = 4.484-25.829), acute cardiac injury (OR = 25.103, 95% CI = 9.057-76.590) and acute respiratory distress syndrome (OR = 7.308, 95% CI = 1.501-46.348) were associated with in-hospital fatal outcome. In addition, older age (OR = 2.149, 95% CI = 1.424-3.248), diabetes (OR = 3.951, 95% CI = 2.077-7.788), cardiovascular disease (OR = 3.414, 95% CI = 1.432-8.799), nervous system disease (OR = 4.125, 95% CI = 1.252-18.681), dyspnoea (OR = 31.944, 95% CI = 18.877-92.741), achieving highest in-hospital temperature of >39.0°C (OR = 37.450, 95% CI = 7.402-683.403) and longer onset of illness to diagnosis (≥9 days) were statistically associated with higher risk of developing severe COVID-19. In conclusion, the potential risk factors forolder age, diabetes, dyspnoea, respiratory failure, acute cardiac injury and acute respiratory distress syndrome could help clinicians to identify patients with poor prognosis at an early stage.

Cardiomyocyte-derived small extracellular vesicles can signal eNOS activation in cardiac microvascular endothelial cells to protect against Ischemia/Reperfusion injury.

Rationale: The crosstalk between cardiac microvascular endothelial cells (CMECs) and cardiomyocytes (CMs) has emerged as a key component in the development of, and protection against, cardiac diseases. For example, activation of endothelial nitric oxide synthase (eNOS) in CMECs, by therapeutic strategies such as ischemic preconditioning, plays a critical role in the protection against myocardial ischemia/reperfusion (I/R) injury. However, much less is known about the signals produced by CMs that are able to regulate CMEC biology. Here we uncovered one such mechanism using Tongxinluo (TXL), a traditional Chinese medicine, that alleviates myocardial ischemia/reperfusion (I/R) injury by activating CMEC eNOS. The aim of our study is to identify the signals produced by CMs that can regulate CMEC biology during I/R. Methods:Ex vivo, in vivo, and in vitro settings of ischemia-reperfusion were used in our study, with the protective signaling pathways activated in CMECs identified using genetic inhibition (p70s6k1 siRNA, miR-145-5p mimics, etc.), chemical inhibitors (the eNOS inhibitor, L-NNA, and the small extracellular vesicles (sEVs) inhibitor, GW4869) and Western blot analyses. TritonX-100 at a dose of 0.125% was utilized to inactivate the eNOS activity in endothelium to investigate the role of CMEC-derived eNOS in TXL-induced cardioprotection. Results: We found that while CMEC-derived eNOS activity was required for the cardioprotection of TXL, activation of eNOS in CMECs by TXL did not occur directly. Instead, eNOS activation in CMECs required a crosstalk between CMs and CMECs through the uptake of CM-derived sEVs. We further demonstrate that TXL induced CM-sEVs contain increased levels of Long Intergenic Non-Protein Coding RNA, Regulator Of Reprogramming (Linc-ROR). Upon uptake into CMECs, linc-ROR downregulates its target miR-145-5p leading to activation of the eNOS pathway by facilitating the expression of p70s6k1 in these cells. The activation of CMEC-derived eNOS works to increase survival in both the CMECs and the CMs themselves. Conclusions: These data uncover a mechanism by which the crosstalk between CMs and CMECs leads to the increased survival of the heart after I/R injury and point to a new therapeutic target for the blunting of myocardial I/R injury.