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China presently comprises several tectonic blocks and regions assembled over geological time and having independent histories. During the Ordovician, these blocks included South China, North China, Tarim, Qaidam, Junggar, Qiangtang-Qamdo, Lhasa and partially Himalaya, Sibumasu and Indochina, as well as the Altay-Xing’an and Songpan-Garze fold belts, which were discrete but adjacent. Twelve stratigraphic megaregions bounded by tectonic sutures or major fault zones are recognised for the Ordovician System. Some of them are further subdivided into regions according to specific lithological and biotic facies or distinct stratigraphic successions. The palaeontological features and biostratigraphic framework of these stratigraphic megaregions and regions are summarised. The unified biostratigraphic framework presented herein includes 33 graptolite and 27 conodont biozones through the Ordovician, together with supplementary biozones, communities or associations of brachiopods, trilobites, cephalopods, chitinozoans, acritarchs and radiolarians. With the constraints of integrative chronostratigraphy, biostratigraphy, chemostratigraphy, cyclostratigraphy and magnetostratigraphy, along with some geochronological data, our understanding of the temporal and spatial distribution of the Ordovician lithostratigraphic units on these major blocks has been significantly advanced. The refined integrative stratigraphic framework of the Ordovician provides a precise constraint on the major tectonic orogenies and biotic events evident in China.

In this chapter, starting with a brief review of the research history and current status in the studies of the Ordovician chronostratigraphy in China, the subdivision of the Ordovician System, definition and recognition of its series and stage boundaries, and possible stratigraphic gaps are discussed in details in order to establish a multidisciplinary stratigraphic correlation through an integrated approach including lithostratigraphy, biostratigraphy, radiometric dating, chemostratigraphy and magnetostratigraphy. Being internationally accepted, the Ordovician System is now subdivided into three series and seven stages, in ascending order, Lower (Tremadocian, Floian), Middle (Dapingian, Darriwilian) and Upper series (Sandbian, Katian, Hirnantian). Three of the seven “Golden Spikes” defining the bases of the Ordovician stages, which were established in 1997–2007, are located in China. As a regionally applied chronostratigraphy, the Ordovician System was subdivided in China into Lower (Xinchangian, Yiyangian), Middle (Dapingian, Darriwilian) and Upper series (Neichiashanian, Chientangkiangian, Hirnantian). This scheme agrees largely with the standard international classification, which can actually be directly applied to China, except for some special circumstances where the Neichiashanian and Chientangkiangian stages of the Upper Ordovician are used. Based on the new studies in recent years and distinctions and differences recognized in the development of the Ordovician System in the constituent terranes of China, a new framework for correlation among the major Chinese palaeoplates or terranes, e.g. South China, North China (including Tarim and Qaidam) and Xizang (Tibet)-western Yunnan, has been established. However, it has been recognized herein that uncertainties still remain on defining the base of the Tremadocian, Dapingian and Katian, and on the correlation between different mega-facies. More specifically, for the Tremadocian, the precise correlation of its base will depend on the better-defined conodont taxonomy, while for the Dapingian and Katian, on the correlation between different mega-facies. It is worthwhile to note that the chemostratigraphic studies of the Ordovician System in China produced the carbonate δ 13 C curves for the Darriwilian (Middle Ordovician) and Katian (Upper Ordovician), which show significant differences from the composite global curve. Record of the Ordovician isotopic dating is relatively rare in China, with only three reliable ages from zircons that are all from the upper Katian to Hirnantian of the Upper Ordovician. Abundant bentonite beds in the Upper Ordovician of South China will also provide unique opportunities to advance the isotopic dating and related researches. Studies on the Ordovician magnetostratigraphy need to be significantly enhanced in China, as currently all the available results are restricted to the Lower Ordovician of North China, although they can be correlated with those known from other parts of the world. The analysis of the durational unevenness of the seven stages in the Ordovician supports the possibility to further subdivide the long-durational Tremadocian, Darriwilian and Katian stages, each into two substages.

Stratigraphic hiatuses of variable time intervals within the Rhuddanian to early Aeronian (Llandovery, Silurian) are identified in the area bordering East Chongqing, West Hubei and Northwest Hunan in central China. Their distribution suggested the existence of a local uplift, traditionally named the Yichang Uplift. The diachronous nature of the basal black shale of the Lungmachi Formation crossing different belts of this Uplift signifies the various developing stages during the uplifting process. The present paper defines the temporal and spatial distribution pattern of the Yichang Uplift, which might be one of the important controlling factors for the preservation and distribution of the shale gas in this region, as it has been demonstrated that the shale gas exploration is generally less promising in the areas where more of the basal part of the Lungmachi Formation is missing. Therefore, better understanding of the circumjacent distribution pattern developed throughout the uplifting process may provide the important guidance for the shale gas exploration. The present work is a sister study to the published paper, “Stage-progressive distribution pattern of the Lungmachian black graplolitic shales from Guizhou to Chongqing, Central China”. These two studies thus provide a complete Ordovician-Silurian black shale distribution pattern in the Middle and Upper Yangtze, a region with the major shale gas fields in China.

The excessive release of reactive oxygen species (ROS) after myocardial infarction (MI) disrupts the natural healing process, leading to cardiac fibrosis and compromising patient prognosis. However, the clinical application of many antioxidant drugs for MI treatment is hindered by their poor antioxidant efficacy and inability to specifically target the heart. Here we developed a tannic acid-modified MnO 2 nanozyme (named MnO 2 @TA), which can achieve cardiac targeting to inhibit post-MI fibrosis and enhance cardiac function. Specifically, the MnO 2 @TA nanozyme, endowed with superoxide dismutase (SOD) and catalase (CAT) activities, effectively scavenges ROS, suppressing fibroblast activation and mitigating cardiac fibrosis without affecting cardiac repair. Notably, the incorporation of TA improves the nanozyme’s affinity for the elastin and collagen-rich extracellular matrix in cardiac tissues, significantly increasing its retention and uptake within the heart and thereby enhancing its anti-fibrotic efficacy. In a murine myocardial infarction model, MnO 2 @TA demonstrates remarkable cardiac protection and safety, significantly improving cardiac function while attenuating cardiac fibrosis. This study presents a valuable reference for clinical research aimed at inhibiting cardiac fibrosis and advancing myocardial infarction treatments. Graphical Abstract

Septic cardiomyopathy is a common complication of severe sepsis, which is one of the leading causes of death in intensive care units. Therefore, finding an effective therapy target is urgent. Neferine is an alkaloid extracted from the green embryos of mature seeds of Nelumbo nucifera Gaertn., which has been reported to exhibit various biological activities and pharmacological properties. This study aims to explore the protective effects of neferine against lipopolysaccharide (LPS)-induced myocardial dysfunction and its mechanisms. The LPS-induced cardiac dysfunction mouse model was employed to investigate the protective effects of neferine. In this study, we demonstrated that neferine remarkably improved cardiac function and survival rate and ameliorated morphological damage to heart tissue in LPS-induced mice. Neferine also improved cell viability and mitochondrial function and reduced cell apoptosis and the production of reactive oxygen species in LPS-treated H9c2 cells. In addition, neferine significantly upregulated Bcl-2 expression and suppressed cleaved caspase 3 activity in LPS-induced mouse heart tissue and H9c2 cells. Furthermore, neferine also upregulated the phosphatidylinositol 3-kinase/protein kinase B/mechanistic target of rapamycin (PI3K/AKT/mTOR) signaling pathway in vivo and in vitro . Conversely, LY294002 (a PI3K inhibitor) reversed the protective effect of neferine in LPS-induced H9c2 cells. Our findings thus demonstrate that neferine ameliorates LPS-induced cardiac dysfunction by activating the PI3K/AKT/mTOR signaling pathway and presents a promising therapeutic agent for the treatment of LPS-induced cardiac dysfunction.

Ferroptosis is a newly identified type of programmed cell death that has been shown to contribute to the progression of septic cardiomyopathy. Although the role of miR-130b-3p as an oncogene that accelerates cancer progression by suppressing ferroptosis has been demonstrated, its role in the regulation of ferroptosis and cardiac injury in Lipopolysaccharide (LPS)-induced cardiomyopathy has not been fully clarified. In this study, we demonstrated that miR-130b-3p remarkably improved cardiac function and ameliorated morphological damage to heart tissue in LPS-induced mice. miR-130b-3p also improved cell viability and mitochondrial function and reduced the production of lipid ROS and ferroptosis in LPS-treated H9c2 cells. In addition, miR-130b-3p significantly upregulated GPX4 expression and suppressed ACSL4 activity in LPS-induced mouse heart tissue and H9c2 cells. Mechanistically, we used database analysis to locate miR-130b-3p and confirmed its inhibitory effects on the ferroptosis-related gene ACSL4 and autophagy-related gene PRKAA1 using a dual-luciferase reporter assay. In addition, we found that miR-130b-3p inhibited the activation of autophagy by downregulating the expression of the AMPK/mTOR signaling pathway. Meanwhile, our results show that RAPA (an autophagy activator) reverses the protective effect of miR-130b-3p mimic against LPS-induced ferroptosis, while CQ (an autophagy inhibitor) plays a facilitative role, suggesting that miR-130b-3p plays an important role in the development of ferroptosis by regulating autophagy in vitro. The findings reveal a novel function of miR-130b-3p in attenuating ferroptosis in cardiomyocytes, providing a new therapeutic target for ameliorating septic cardiomyopathy injury.Ferroptosis is a newly identified type of programmed cell death that has been shown to contribute to the progression of septic cardiomyopathy. Although the role of miR-130b-3p as an oncogene that accelerates cancer progression by suppressing ferroptosis has been demonstrated, its role in the regulation of ferroptosis and cardiac injury in Lipopolysaccharide (LPS)-induced cardiomyopathy has not been fully clarified. In this study, we demonstrated that miR-130b-3p remarkably improved cardiac function and ameliorated morphological damage to heart tissue in LPS-induced mice. miR-130b-3p also improved cell viability and mitochondrial function and reduced the production of lipid ROS and ferroptosis in LPS-treated H9c2 cells. In addition, miR-130b-3p significantly upregulated GPX4 expression and suppressed ACSL4 activity in LPS-induced mouse heart tissue and H9c2 cells. Mechanistically, we used database analysis to locate miR-130b-3p and confirmed its inhibitory effects on the ferroptosis-related gene ACSL4 and autophagy-related gene PRKAA1 using a dual-luciferase reporter assay. In addition, we found that miR-130b-3p inhibited the activation of autophagy by downregulating the expression of the AMPK/mTOR signaling pathway. Meanwhile, our results show that RAPA (an autophagy activator) reverses the protective effect of miR-130b-3p mimic against LPS-induced ferroptosis, while CQ (an autophagy inhibitor) plays a facilitative role, suggesting that miR-130b-3p plays an important role in the development of ferroptosis by regulating autophagy in vitro. The findings reveal a novel function of miR-130b-3p in attenuating ferroptosis in cardiomyocytes, providing a new therapeutic target for ameliorating septic cardiomyopathy injury.

Background: Myocardial fibrosis is a key pathological process after myocardial infarction, which leads to poor outcomes in patients at the end stage. Effective treatments for improving prognosis of myocardial fibrosis are needed to be further developed. Methyl ferulic acid (MFA), a biologically active monomer extracted and purified from the Chinese herbal medicine, is reported as an attenuator in many diseases. In this study, we aim to reveal the role it plays in myocardial fibrosis after myocardial infarction and its possible mechanism. Results: Firstly, we found that MFA attenuated the expression of fibrosis-related proteins and the ability of migration and proliferation in TGF-β1–induced human cardiac fibroblasts (HCFs). Then, myocardial fibrosis after myocardial infarction models on mouse was built to reveal the in vivo affection of MFA. After 28 days of treatments, fibrosis areas, cardiac function, and expression of fibrosis-related proteins were all improved in the MFA-treated group than the myocardial infarction group. Finally, to elucidate the mechanism of phenomenon we observed, we found that MFA attenuated HCF differentiation after myocardial infarction by suppressing the migration and proliferation in HCFs, which was by suppressing the pRB-E2F1/CCNE2 and the RhoA/ROCK2 pathway. Conclusion: Our findings showed that MFA attenuated the expression of fibrosis-related proteins, and the ability of migration and proliferation in HCFs improved the cardiac function of myocardial infarction mice; meanwhile, the mechanism of that was by suppressing the pRB-E2F1/CCNE2 and the RhoA/ROCK2 pathway.

The prevalence of childhood leukemia is increasing rapidly all over the world. However, studies on maternal benzene exposure during pregnancy and childhood acute lymphoblastic leukemia (ALL) have not been systematically assessed. Therefore, we performed a meta-analysis to investigate the association between maternal solvent, paint, petroleum exposure, and smoking during pregnancy and risk of childhood ALL. Relevant studies up to September 1st, 2013 were identified by searching the PubMed, EMBASE, Cochrane library and the Web of Science databases. The effects were pooled using either fixed or random effect models based on the heterogeneity of the studies. Twenty-eight case-control studies and one cohort study were included for analysis, with a total of 16,695 cases and 1,472,786 controls involved. Pooled odds ratio (OR) with 95% confidence interval (CI) for ALL was 1.25 (1.09, 1.45) for solvent, 1.23 (1.02, 1.47) for paint, 1.42 (1.10, 1.84) for petroleum exposure, and 0.99 (0.93, 1.06) for maternal smoking during pregnancy. No publication bias was found in this meta-analysis and consistent results were observed for subgroup and sensitivity analyses. Childhood ALL was associated with maternal solvent, paint, and petroleum exposure during pregnancy. No association was found between ALL and maternal smoking during pregnancy. Avoidance of maternal occupational and environmental benzene exposure during pregnancy could contribute to a decrease in the risk of childhood ALL.

Diazotrophic microorganisms regulate marine productivity by alleviating nitrogen limitation. So far chemolithoautotrophic bacteria are widely recognized as the principal diazotrophs in oligotrophic marine and terrestrial ecosystems. However, the contribution of chemolithoautotrophs to nitrogen fixation in organic-rich habitats remains unclear. Here, we utilized metagenomic and metatranscriptomic approaches integrated with cultivation assays to investigate the diversity, distribution, and activity of diazotrophs residing in Zhangzhou mangrove sediments. Physicochemical assays show that the studied mangrove sediments are typical carbon-rich, sulfur-rich, nitrogen-limited, and low-redox marine ecosystems. These sediments host a wide phylogenetic variety of nitrogenase genes, including groups I–III and VII–VIII. Unexpectedly diverse chemolithoautotrophic taxa including Campylobacteria, Gammaproteobacteria, Zetaproteobacteria, and Thermodesulfovibrionia are the predominant and active nitrogen fixers in the 0–18 cm sediment layer. In contrast, the 18–20 cm layer is dominated by active diazotrophs from the chemolithoautotrophic taxa Desulfobacterota and Halobacteriota. Further analysis of MAGs shows that the main chemolithoautotrophs can fix nitrogen by coupling the oxidation of hydrogen, reduced sulfur, and iron, with the reduction of oxygen, nitrate, and sulfur. Culture experiments further demonstrate that members of chemolithoautotrophic Campylobacteria have the nitrogen-fixing capacity driven by hydrogen and sulfur oxidation. Activity measurements confirm that the diazotrophs inhabiting mangrove sediments preferentially drain energy from diverse reduced inorganic compounds other than from organics. Overall, our results suggest that chemolithoautotrophs rather than heterotrophs are dominant nitrogen fixers in mangrove sediments. This study underscores the significance of chemolithoautotrophs in carbon-dominant ecosystems.