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Juniperus L. is the second largest conifer genus, having the widest distribution of all conifer genera. However, its evolution in East Asia is unclear due to the scarce fossil records. We described a set of Juniperus fossils from the Early Miocene of Tiejianggou, Chifeng, Inner Mongolia. Although only two seed cones and five branch segments were preserved, the fossils were assigned to Juniperus chifengensis Liang Xiao et Liyan Guo sp. nov. (Cupressaceae). The diagnostic characteristics include leaves in a decussate or ternate arrangement, both scalelike and needle-like leaves on mature branchlets, scalelike leaves on juvenile branchlets, leaves with two stomatal bands adaxially and abaxially, terminal seed cones, and two or four seeds, which is the most similar extant species J. chinensis morphologically. However, the cuticle of the abaxial epidermis shows longer and more disordered cells. With a close affinity to the extant Juniperus chinensis, J. chifengensis, the macrofossil record of sect. Sabina (Juniperus) in East Asia, had existed in East Asia in the early Early Miocene. The longer abaxial epidermal cells confirm its adaptation to the dry and cold climate that occurred from the Early Miocene to the present. [ABSTRACT FROM AUTHOR]

Pulmonary fibrosis is known as an incurable lung disorder with irreversible progression of chronic injury, myofibroblast proliferation, extracellular matrix (ECM) accumulation, and tissue scarring. Atmospheric particulate matter 2.5 (PM2.5) is implicated as a risk factor of several diseases, especially lung diseases such as pulmonary fibrosis. The molecular mechanism which participates PM2.5‐induced pulmonary fibrosis in type II alveolar cells (AEII) has yet to be determined. Our results proved that short‐ and long‐term exposure to PM2.5 significantly stimulated epithelial‐mesenchymal transition (EMT) activity in AEII cells, according to, changes in gene signature analyzed by RNA‐seq and cell morphology. Furthermore, Gene Ontology (GO) enrichment analysis also suggested that mitochondrial dysfunction was related to progression of pulmonary fibrosis in AEII after PM2.5 exposure. We observed a marked decline in mitochondria membrane potential (MMP), as well as fragmented mitochondria, in AEII cells exposed to PM2.5, which suggests that energy metabolism is suppressed after PM2.5 exposure. We also confirmed that PM2.5 exposure could influence the expression levels of Mfn1, Mfn2, and Drp1 in AEII. Pretreatment of mitochondrial fusion promoter M1 was able to reverse mitochondrial dysfunction as well as EMT in AEII. These data suggested the key role of mitochondrial fragmentation in AEII, which was induced by PM2.5 exposure, and participated pathogenesis of pulmonary fibrosis. Finally, we investigated the response of lung tissue exposed to PM2.5 in vivo. The data indicated that the lung tissue exposed to PM2.5 obviously induced collagen accumulation. Moreover, IHC results revealed that PM2.5 enhanced Drp1 expression but suppressed Mfn1 and Mfn2 expression in lung tissue. The current study provides novel insight of pulmonary fibrosis caused by PM2.5 exposure. [ABSTRACT FROM AUTHOR]

Objective: To evaluate Alarelin on human endometrial carcinoma HEC-1-B cells in nude mice and its mechanism. Methods: Establishment of endometrial carcinoma xenografts in nude mice, according to the nude volume, 32 nude mice were randomly divided into 4 groups (n=8) :control group, Alarelin groups (20,40,80 µg/kg,respectively). The growth curves of xenografts in nude mice were drawn and inhibition rates were measured. The morphological features were detected by hematoxylin and eosinstaining. The protein expression levels of DEDD were measured by immunohisto chemistry. Results: The growth curve showed that tumor volume in nude mice treated with Alarelin was smaller than that of control group. The rate of tumor inhibition in low, medium and high-dose Alarelin group were 12.65%,27.38% and 35.43%, all with a statistically significant difference (P<0.05). HE staining showed that tumor cells arranged in dense, with clear atypia, large nuclei, stained emitotic more,less interstitial in control group. Compared with control group, tumor cell morphology, cell arrangement sparse, showing large unstructured necrosis, tumor cell nuclei stained pyknotic more mitotic less in different dose group. Results of immunohistochemical showed that in the gray values of DEDD protein expression in low, medium and high dose groups were 156.20±5.10,142.85±7.27 and 113.65±4.38 respectively, they were significantly lower than the control group (171.75±8.21, all P<0.001). Conclusions: Alarelin can effectively inhibit the growth of tumor, the mechanism may be correlated with increasing expressions of DEDD. [ABSTRACT FROM AUTHOR]

Pulmonary fibrosis is known as an incurable lung disorder with irreversible progression of chronic injury, myofibroblast proliferation, extracellular matrix (ECM) accumulation, and tissue scarring. Atmospheric particulate matter 2.5 (PM 2.5 ) is implicated as a risk factor of several diseases, especially lung diseases such as pulmonary fibrosis. The molecular mechanism which participates PM 2.5 -induced pulmonary fibrosis in type II alveolar cells (AEII) has yet to be determined. Our results proved that short- and long-term exposure to PM 2.5 significantly stimulated epithelial-mesenchymal transition (EMT) activity in AEII cells, according to, changes in gene signature analyzed by RNA-seq and cell morphology. Furthermore, Gene Ontology (GO) enrichment analysis also suggested that mitochondrial dysfunction was related to progression of pulmonary fibrosis in AEII after PM 2.5 exposure. We observed a marked decline in mitochondria membrane potential (MMP), as well as fragmented mitochondria, in AEII cells exposed to PM 2.5 , which suggests that energy metabolism is suppressed after PM 2.5 exposure. We also confirmed that PM 2.5 exposure could influence the expression levels of Mfn1, Mfn2, and Drp1 in AEII. Pretreatment of mitochondrial fusion promoter M1 was able to reverse mitochondrial dysfunction as well as EMT in AEII. These data suggested the key role of mitochondrial fragmentation in AEII, which was induced by PM 2.5 exposure, and participated pathogenesis of pulmonary fibrosis. Finally, we investigated the response of lung tissue exposed to PM 2.5 in vivo. The data indicated that the lung tissue exposed to PM 2.5 obviously induced collagen accumulation. Moreover, IHC results revealed that PM 2.5 enhanced Drp1 expression but suppressed Mfn1 and Mfn2 expression in lung tissue. The current study provides novel insight of pulmonary fibrosis caused by PM 2.5 exposure., (© 2023 Wiley Periodicals LLC.)