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The biogeographical history of many lineages within the Lauraceae remains poorly known because of the difficulty of assigning macrofossils to living genera, poor pollen preservation, and the absence of sufficiently resolved or well‐supported phylogenies. Here, we utilize plastid genome sequencing to reinvestigate the phylogenetic and biogeographic history of trees in the tribe Cryptocaryeae, an important component of broad‐leaved forests worldwide, with around 800 species that rely on vertebrate frugivores to disperse their seeds. A new time‐calibrated phylogeny with high support for 176 species was used to infer the biogeographic history and speciation rates based on inferences of BAMM analyses. A monophyletic Cryptocaryeae with Aspidostemon, Beilschmiedia, Cryptocarya, Dahlgrenodendron, and Eusideroxylon clades was confirmed. The five clades of Cryptocaryeae were estimated to share a common ancestor in tropical Africa or Asia in the Early Cretaceous around 123 Ma. The Beilschmiedia and Cryptocarya clades were estimated to have originated in South America around 66 Ma. Extant subclades of the Beilschmiedia clade could colonize Australia by 35 Ma and extant subclades of the Cryptocarya clade could colonize Australia by 42 Ma. Diversification rates of the Beilschmiedia clade accelerated 14 and 12 Ma after its origin and diversification rates of the Cryptocarya clade accelerated 18 Ma after its origin. Over 45% extant Cryptocaryeae species originated in the three periods of accelerated differentiation in the Miocene of Asia and Australia. Long‐distance dispersal has had a major influence on biogeography, with dispersal to Asia likely occurring seven times, Zealandia six times, America three times, Australia three times, Africa twice, and Oceania at least once. Over 70% extant Cryptocaryeae species which diverged before the Quaternary grow in the Southern Hemisphere, while 90% extant Cryptocaryeae species which diverged in the Quaternary grow in the Northern Hemisphere. The Cryptocaryeae originated in and diversified with the first angiosperm‐dominated broad‐leaved evergreen forests, from the Cretaceous to the Paleogene. Long‐distance seed dispersal, probably by birds, although possibly also by flotation, has allowed the tribe to track these forests in space and time, despite a failure to adapt to cold, dry, or highly seasonal environments. [ABSTRACT FROM AUTHOR]

A method for determining the mode I stress intensity factor based on the symplectic geometry method is proposed. A fan-shaped region is constructed at the crack tip, and the full state vector of the crack tip is determined with the symplectic geometry method. By combining the full state vector with the displacement field at the crack tip, the stress intensity factor is calculated. Based on the theoretical solution of the displacement field around the mode I crack tip, the effects of the number of data points, the size of the central angle, and the radius on the accuracy of the stress intensity factor are studied. The results show that the number of data points has a great influence on the accuracy of mode I stress intensity factor determined with this method. As the number of data points exceeds 37, the relative error tends to zero stably; the sector central angle has little effect on the accuracy of the stress intensity factor, but under the same accuracy requirements, different sector central angles need different numbers of data points. If the sector radius is too small, the solution of stress intensity factor will be unstable, and the relative error will be large because of the influence of the plastic region at crack tip during the fracture process. By comparing the relative errors under different conditions, it is found that the mode I stress intensity factor calculated by the proposed method is highly accurate and that the stress intensity factor can be accurately obtained by obtaining just the displacement field around the crack tip, which is verified by a digital image correlation experiment. The proposed method solves the problem that the previous solution system has complex steps in the case of complex stress, resulting in the inability to accurately obtain mode I stress intensity factor. [ABSTRACT FROM AUTHOR]

• Early, tension syrinx patients benefit from SSS. • SSS should be used selectively. Syringo-subarachnoid shunt (SSS) is often considered a rescue procedure or a second-line treatment option for syringomyelia. However, the clinical efficacy of SSS in treating this condition remains controversial. To evaluate the long-term outcome of the SSS and its relationship with the syrinx area, as well as to investigate the factors that influence the prognosis. This retrospective study included twenty-seven consecutive patients who underwent SSS between 2014 and 2020. The study evaluated several independent variables such as age, sex, duration of progressive symptoms, morphological characteristics of the syrinx, changes in the syrinx area, and Chiari malformation. The long-term follow-up (>2 years) Japanese Orthopaedic Association (JOA) score was used to assess neurological function and outcome. Statistical analysis was performed using a stepwise logistic regression test. All patients were followed up for an average of 48.6 ± 14.8(26.8 to 78.0) months. Follow-up magnetic resonance imaging showed syrinx collapse to different degrees occurred in 96.3% (26 of 27) patients. The JOA score was improvedinonly6patients (22.2%), remained stable in 5 patients (18.5%),and deteriorated in 16 patients(59.3%).A logistic regression test showed that the tension syrinx (odds ratio 0.111) and early shunting intervention (odds ratio 0.138) were favorable independent prognostic factors. It is important to note that the shrinkage of the syrinx does not necessarily translate to an improvement in clinical outcomes. Therefore, the decision to perform SSS should be made with caution and considered as a last resort. [ABSTRACT FROM AUTHOR]

The study aimed to estimate the benchmark dose (BMD) of coke oven emissions (COEs) exposure based on mitochondrial damage with the mitochondrial DNA copy number (mtDNAcn) as a biomarker. A total of 782 subjects were recruited, including 238 controls and 544 exposed workers. The mtDNAcn of peripheral leukocytes was detected through the real-time fluorescence-based quantitative polymerase chain reaction. Three BMD approaches were used to calculate the BMD of COEs exposure based on the mitochondrial damage and its 95% confidence lower limit (BMDL). The mtDNAcn of the exposure group was lower than that of the control group (0.60 ± 0.29 vs. 1.03 ± 0.31; P < 0.001). A dose–response relationship was shown between the mtDNAcn damage and COEs. Using the Benchmark Dose Software, the occupational exposure limits (OELs) for COEs exposure in males was 0.00190 mg/m3. The OELs for COEs exposure using the BBMD were 0.00170 mg/m3 for the total population, 0.00158 mg/m3 for males, and 0.00174 mg/m3 for females. In possible risk obtained from animal studies (PROAST), the OELs of the total population, males, and females were 0.00184, 0.00178, and 0.00192 mg/m3 respectively. Based on our conservative estimate, the BMDL of mitochondrial damage caused by COEs is 0.002 mg/m3. This value will provide a benchmark for determining possible OELs. [ABSTRACT FROM AUTHOR]

Prolonged exposure to free silica leads to the development of silicosis, wherein activated fibroblasts play a pivotal role in its pathogenesis and progression. Fibroblast Activation Protein (FAP), as a biomarker for activated fibroblasts, its expression pattern and role in key aspects of silicosis pathogenesis remain unclear. This study elucidated the expression pattern and function of FAP through population-based epidemiological investigations, establishment of mouse models of silicosis, and in vitro cellular models. Results indicated a significant elevation of FAP in plasma from silicosis patients and lung tissues from mouse models of silicosis. In the cellular model, we observed a sharp increase in FAP expression early in the differentiation process, which remained high expression. Inhibition of FAP suppressed fibroblast differentiation, while overexpression of FAP produced the opposite effect. Moreover, fibroblast-derived FAP can alter the phenotype and function of neighboring macrophages. In summary, we revealed a high expression pattern of FAP in silicosis and its potential mechanistic role in fibrosis, suggesting FAP as a potential therapeutic target for silicosis. [Display omitted] • The expression of FAP is increased in silicosis. • FAP increases earlier than transdifferentiation markers, regulating the process. • Fibroblast-derived FAP can alter the phenotype and function of macrophages. [ABSTRACT FROM AUTHOR]

Pneumoconiosis is one of the most serious occupational diseases worldwide. Silicosis due to prolonged inhalation of free silica dust during occupational activities is one of the main types. Cuproptosis is a newly discovered mode of programmed cell death characterized by the accumulation of free copper in the cell, which ultimately leads to cell death. Increased copper in the serum of silicosis patients, suggests that the development of silicosis is accompanied by changes in copper metabolism, but whether cuproptosis is involved in the progression of silicosis is actually to be determined. To test this hypothesis, we screened the genetic changes in patients with idiopathic fibrosis by bioinformatics methods and predicted and functionally annotated the cuproptosis-related genes among them. Subsequently, we established a mouse silicosis model and detected the concentration of copper ions and the activity of ceruloplasmin (CP) in serum, as well as changes of the concentration of copper and cuproptosis related genes in mouse lung tissues. We identified 9 cuproptosis-related genes among the differential genes in patients with IPF at different times and the tissue-specific expression levels of ferredoxin 1 (FDX1) and Lipoyl synthase (LIAS) proteins. Furthermore, serum CP activity and copper ion levels in silicosis mice were elevated on days 7th and 56th after silica exposure. The expression of CP in mouse lung tissue elevated at all stages after silica exposure. The mRNA level of FDX1 decreased on days 7th and 56th, and the protein level remained in accordance with the mRNA level on day 56th. LIAS and Dihydrolipoamide dehydrogenase (DLD) levels were downregulated at all times after silica exposure. In addition, Heatshockprotein70 (HSP70) expression was increased on day 56. In brief, our results demonstrate that there may be cellular cuproptosis during the development of experimental silicosis in mice and show synchronization with enhanced copper loading in mice. • Elevated level of copper loading during the development of experimental silicosis. • The level of cuproptosis indicators changes synchronously with serum copper. • Cellular cuproptosis may exist in each phase of silicosis. [ABSTRACT FROM AUTHOR]

Manganese is essential trace elements, to participate in the body a variety of biochemical reactions, has important physiological functions, such as stimulate the immune cell proliferation, strengthen the cellular immunity, etc. However, excessive manganese exposure can cause damage to multiple systems of the body.The immune system is extremely vulnerable to external toxicants, however manganese research on the immune system are inadequate and biomarkers are lacking. Therefore, here we applied a manganese-exposed rat model to make preliminary observations on the immunotoxic effects of manganese. We found that manganese exposure inhibited humoral immune function in rats by decreasing peripheral blood IgG (ImmunoglobulinG, IgG), IgM (ImmunoglobulinM, IgM) and complement C3 levels; It also regulates rat cellular immune activity by influencing peripheral blood, spleen, and thymus T cell numbers and immune organ ICs (Immune Checkpoints, ICs) and cytokine expression. Furthermore, it was revealed that the impact of manganese exposure on the immune function of rats exhibited a correlation with both the dosage and duration of exposure. Notably, prolonged exposure to high doses of manganese had the most pronounced influence on rat immune function, primarily manifesting as immunosuppression.The above findings suggest that manganese exposure leads to impaired immune function and related changes in immune indicators, or may provide clues for the discovery of its biomarkers. • Manganese exposure may suppress humoral immune function. • Manganese exposure may suppress cellular immune function. • Laying the groundwork for research to discover biomarkers of manganese exposure. [ABSTRACT FROM AUTHOR]

Carassotrema schistorchis is a digenea parasite whose juvenile and adult stages parasitize the intestinal tract of definitive host fish. There is no available ecological information about this parasitic infection in wild host fish. The present work aimed to investigate the infection rate and distribution of C. schistorchis in wild silver carp, Hypophthalmichthys molitrix , and to assess the influence of environmental factors on infection by the parasite. From October 2016 to May 2019, a total of 554 wild silver carp were collected from two reservoirs. These collected fish were weighed, measured, and dissected to observe the presence of C. schistorchis following standard methodology. Ecological analysis results showed that the frequency distribution of C. schistorchis in the host population was aggregated distribution. The abundance of C. schistorchis exhibited a positive correlation with the host age and condition factor of silver carp, but it showed no relationship with water temperature, pH or DO. The condition factor value of infected fish was significantly higher than that of uninfected fish. These results indicated that food intake, not environmental factors, directly determined infection by the parasite in the host, indicating that an increased food intake would increase the risk of infection. Thus, the number of parasites could be used as an indirect biological marker for assessing the effectiveness of silver carp in filter-feeding on plankton. The following analysis indicated that silver carp with a body length of 50–55 cm showed the highest efficiency in controlling phytoplankton biomass. This study provides important information for understanding the ecology of C. schistorchis in wild silver carp. Image 1 • First report on the ecological information of Carassotrema schistorchis in wild silver carp. • Food intake, not environmental factors, determined the abundance of C. schistorchis in the host. • Silver carp with a body length of 50–55 cm showed the highest efficiency in controlling plankton. [ABSTRACT FROM AUTHOR]

Until now, the specific pathogenesis of silicosis is not clear. Exosomal miRNAs, as a newly discovered intercellular communication medium, play an important role in many diseases. Our previous research found that serum exosomal miR125a-5p was increased in silicosis patients by miRNAs high-throughput sequencing. TRAF6, is a target gene of miR125a-5p, which is involved in T-cell differentiation. Furthermore, results from animal study indicate that knockdown of miR-125a-5p can regulate T lymphocyte subsets and significantly reduce pulmonary fibrosis by targeting TRAF6. However, the level of serum exosomal miR125a-5p in silicosis patients has not been reported, the role of macrophages-secreted exosomal miR-125a-5p in regulating T cell differentiation to promote fibroblast transdifferentiation (FMT) remains unknown. In this study, the levels of serum exosomal miR125a-5p and serum TGF-β1, IL-17A, IL-4 cytokines in silicosis patients were elevated, with the progression of silicosis, the level of serum exosomal miR125a-5p and serum IL-4 were increased; thus, the serum level of IFN-γ was negatively correlated with the progression of silicosis. In vitro , the levels of miR125a-5p in macrophages, exosomes, and T cells stimulated by silica were significantly increased. When the mimic was transfected into T cells, which directly suppressed TRAF6 and caused the imbalance of T cells differentiation, induced FMT. To sum up, these results indicate that exosomal miR-125a-5p may by targeting TRAF6 of T cells, induces the activation and apoptosis of T cells and the remodeling of Th1/Th2 and Th17/Tregs distribution, ultimately promotes FMT. Suggesting that exosomal miR-125a-5p may be a potential therapeutic target for silicosis. [Display omitted] • Exosomal miR125a-5p, serum TGF-β1, IL-17A, IL-4 in silicosis patients were elevated. • Exosomal miR125a-5p was positively correlated with the progression of silicosis. • Exosomal miR-125a-5p can reshape CD4+ T cell subtypes distribution, promotes FMT. • Exosomal miR-125a-5p may be a biomarker and therapeutic target for silicosis. [ABSTRACT FROM AUTHOR]

Abstract Omethoate, an organophosphorous pesticide, causes a variety of health effects, especially the damage of chromosome DNA. The aim of the study was to assess the correlation between polymorphisms of encoding miRNA genes and telomere length in omethoate–exposure workers. 180 workers with more than 8 years omethoate–exposure and 115 healthy controls were recruited in the study. Genotyping for the selected single nucleotide polymorphisms loci were performed using the flight mass spectrometry. Real-time fluorescent quantitative polymerase chain reaction(PCR) method was applied to determine the relative telomere length(RTL) in human peripheral blood leukocytes DNA. After adjusting the covariate of affecting RTL, covariance analysis showed that the female was significantly longer than that of the male in control group(P < 0.046). For the miR-145 rs353291 locus, this study showed that RTL of mutation homozygous AG+GG individuals was longer than that of wild homozygous AA in the exposure group (P = 0.039). In the control group, RTL with wild homozygous TT genotype in miR-30a rs2222722 polymorphism locus was longer than that of the mutation homozygous CC genotype (P = 0.038). After multiple linear regression analysis, the independent variables of entering into the model were omethoate–exposure (b = 0.562, P < 0.001), miR-145 rs353291 (AG+GG) (b = 0.205, P = 0.010). The prolongation of relative telomere length in omethoate exposed workers was associated with AG+GG genotypes in rs353291 polymorphism of encoding miR-145 gene. Graphical abstract fx1 Highlights • The encoding miRNA genes and telomere length under omethoate exposure. • Omethoate-exposure and miR-145 genetic polymorphism affect telomere length. • Prolongation of RTL in workers exposed to omethoate with rs353291 AG+GG genotypes. [ABSTRACT FROM AUTHOR]

Omethoate, an organophosphorous pesticide, can cause a variety of health effects, especially the decrease of cholinesterase activity. The aim of this study is to explore the association of genetic polymorphisms of telomere binding proteins with cholinesterase activity in omethoate-exposed population. Cholinesterase activities in whole blood, red blood cell and plasma were detected using acetylthiocholine and dithio-bis-(nitrobenzoic acid) method; Genetic Genotyping of POT 1 rs1034794, POT 1 rs10250202, TERF 1 rs3863242 and TERT rs2736098 were performed with PCR-RFLP. The cholinesterase activities of whole blood, red blood cells and plasma in exposure group are significantly lower than that of the control group ( P  < 0.001). Multivariate analysis indicates that exposure group ( b  = − 1.016, P  < 0.001), agender ( b  = 0.365, P  < 0.001), drinking ( b  = 0.271, P  = 0.004) and TERF1 rs3863242 ( b  = − 0.368, P  = 0.016) had an impact on cholinesterase activities. The results suggest that individual carrying AG+GG genotypes in TERF 1 gene rs3863242 polymorphism were susceptible to damage in cholinesterase induced by omethoate. [ABSTRACT FROM AUTHOR]

Coke oven emissions (COEs) exposure leads to oxidative stress, an imbalance between oxidant production and antioxidant defence in the body, which then leads to shortened relative telomere length (RTL) and reduced mitochondrial DNA copy number (mtDNAcn), ultimately leading to ageing and disease. By analysing the relationship among COEs, oxidative stress, RTL and mtDNAcn, we investigated the chain-mediating effects of oxidative stress and telomeres on mitochondrial damage and mitochondria on telomere damage in coke oven workers. A total of 779 subjects were included in the study. Cumulative COEs exposure concentrations were estimated, and the RTL and mtDNAcn of peripheral blood leukocytes were measured using real-time fluorescence quantitative PCR. Total antioxidant capacity (T-AOC) was measured to reflect the level of oxidative stress. The data were statistically analysed using SPSS 21.0 software and discussed using mediation effect analysis. After adjusting for age, sex, smoking, drinking and BMI, generalised linear model revealed dose–response associations between COEs and T-AOC, RTL and mtDNAcn, respectively. (P trend < 0.05). The results of chain-mediating effect showed that the proportion of the chain-mediating effect of "CED-COEs→T-AOC→ RTL→mtDNAcn" was 0.82% (β = −0.0005, 95% CI = [-0.0012, −0.0001]), and the proportion of the chain-mediating effect of "CED-COEs→T-AOC→ mtDNAcn → RTL ″ was 2.64% (β = −0.0013, 95% CI = [-0.0025, −0.0004]). After oxidative stress is induced by COEs, mitochondria and telomeres may interact with each other while leading further to potential bodily damage. This study provides clues to explore the association between mitochondria and telomeres. [Display omitted] • Interaction between mtDNAcn and RTL occurs after oxidative stress induced by COEs. • The first study of chain mediation between COEs, oxidative stress, RTL, and mtDNAcn. • A mediating effect model for COEs, oxidative stress, RTL, and mtDNAcn is proposed. [ABSTRACT FROM AUTHOR]

Long-term inhalation of silica particles in the workplace causes silicosis, which is incurable and seriously endangers the health of workers. It is believed that silicosis is caused by an imbalance of the pulmonary immune microenvironment, in which pulmonary phagocytes play a crucial role. As an emerging immunomodulatory factor, it is unclear whether T cell immunoglobulin and mucin domain-containing protein 3 (TIM3) participate in silicosis by modulating pulmonary phagocytes function. The purpose of this study was to investigate the dynamic changes of the TIM-3 in pulmonary macrophages, dendritic cells (DCs), and monocytes during the development of silicosis in mice. The plasma levels of soluble TIM-3 in silicosis patients were also examined. Flow cytometry was used to identify alveolar macrophages (AMs), interstitial macrophages (IMs), CD11b+ DC, CD103+ DC, Ly6C+, and Ly6C- monocytes in mouse lung tissues, and further analyses were conducted on the expression of TIM-3. Results showed that soluble TIM-3 was significantly elevated in plasma of silicosis patients, and the level of which was higher in stage II and III patients than that in stage I. In silicosis mice, the protein and mRNA levels of TIM-3 and Galectin9 were significantly upregulated in lung tissues. Specific to pulmonary phagocytes, silica exposure affected TIM-3 expression in a cell-specific and dynamic manner. In macrophages, TIM-3 expression upregulated in AM after 28 days and 56 days of silica instillation, while the expression of TIM-3 in IM decreased at all observation time points. In DCs, silica exposure only caused a decrease of TIM-3 expression in CD11b+ DCs. In monocytes, TIM-3 dynamics in Ly6C+ and Ly6C- monocytes were generally consistent during silicosis development, which significant decrease after 7 and 28 days of silica exposure. In conclusion, TIM-3 may mediate the development of silicosis by regulating pulmonary phagocytes. [Display omitted] • Silicosis patients had a higher plasma sTIM-3 level than healthy individuals. • TIM-3 expression was significantly increased in lung tissue of silicosis mice. • TIM-3 may mediate the immune homeostasis of pulmonary phagocytes in silicosis. [ABSTRACT FROM AUTHOR]

Exposure to free silica induces silicosis and myofibroblasts are regarded as primary effector cells. Fibrocytes can differentiate into myofibroblast. Therefore, the present study was designed to investigate whether fibrocytes participate in silicosis. The rat model of silicosis was established. Hematoxylin-eosin stainings and Masson stainings were used to evaluate the histopathology and collagen deposition. Flow cytometry and immunofluorescence were performed to detect the number of fibrocytes and their contribution to myofibroblasts. Results showed that fibrocytes participate in silicosis. Trend analysis of different sources of myofibroblasts during silicosis indicated that fibrocytes and lung type II epithelial cell-derived myofibroblasts play an important role in the early stage of silicosis, while resident lung fibroblast-derived myofibroblasts play a predominant role during the fibrosis formative period. [ABSTRACT FROM AUTHOR]

Objective The aim of this study was to investigate the effects of SiO 2 on fibrocytes and whether fibrocytes participate in silicosis in vivo . Methods A macrophagocyte (AM)/fibrocyte coculture system was established, and AMs were treated with 100 µg/mL SiO 2 . Flow cytometry was used to detect the number of fibrocytes. Real-time PCR was performed to measure the expression of collagen I, collagen III, and α-SMA mRNA. The levels of collagen I, collagen III, and TGF-β1 protein were determined by ELISA. Immunohistochemical staining was performed to measure α-SMA protein expression. A rat silicosis model was induced by intratracheal instillation of SiO 2 . Lung histopathological evaluation was conducted using HE and Masson's trichrome staining after 1 and 9 weeks. The number of fibrocytes in peripheral blood or lung tissue of rat was detected by flow cytometry. Double-color immunofluorescence was applied to identify fibrocytes in the lung tissue. Results Peripheral blood monocytes were found to differentiate into fibrocytes in vitro in a time-dependent manner, and exposure to crystalline silica might potentiate fibrocyte differentiation. In addition, fibrocytes were able to migrate from peripheral blood to the lung tissue, and the number of fibrocytes was increased after SiO 2 exposure. Conclusion Silica exposure potentiates fibrocyte differentiation, and fibrocytes may participate in silicosis in vivo . [ABSTRACT FROM AUTHOR]