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The genus Soriculus is currently recognized as monotypic, containing only one species, Soriculus nigrescens , which is distributed mainly in the Himalayas and the southern Hengduan Mountains. The taxonomy of Soriculus is ambiguous due to insufficient taxonomic sampling. We conducted extensive surveys of Soriculus across the Himalayas and Hengduan Mountains. We sequenced two mitochondrial and three nuclear genes, and the complete mitochondrial genomes of several selected specimens to infer the phylogenetic relationships of Soriculus and also analysed their morphological and morphometric variations. Our results indicate monophyly of Soriculus , and the diversity of the genus is greatly underestimated. We described two new species, Soriculus nivatus sp. nov. and Soriculus medogensis sp. nov. , and elevated S. minor as a distinct species. Additionally, we found another putative new species of Soriculus in Medog County; however, we did not formally describe it because only one specimen was collected. Divergence time estimates suggest that the global cooling and desiccating events around the Miocene/Pliocene and Pliocene/Pleistocene boundaries and the Pleistocene climatic oscillations may have played major roles in the diversification of Soriculus. Our results highlight the overlooked diversity of small mammals in the eastern Himalayas, which warrants further surveys and taxonomic studies. [ABSTRACT FROM AUTHOR]

Himalayan shrews of the genus Soriculus (Soricidae, Eulipotyphla), currently represented by four nominal species, are endemic to the Himalayas and the Gaoligong Mountains. In April 2022 and April 2023, a total of 10 specimens of Soriculus were collected from Beibeng and Damu, Medog County, Tibet, China. The morphology of the specimens was compared with the four recognised species of the genus Soriculus . Additionally, two mitochondrial ( Cyt b and 12S ) and three nuclear ( APOB , BRCAI and RAG2 ) genes were sequenced to test the phylogenetic relationships of these specimens with the other species. Our results indicate that these specimens represent a distinct species, Soriculusbeibengensis sp. nov. , which is formally described here. The new species is distinguished from the other Soriculus species by the combination of darker pelages, smaller size, the relatively stubby nasal and the widened posterior processes of incisors. Phylogenetic analyses revealed the new species is sister to S.minor . The p-distance of Cyt b gene between S.beibengensis sp. nov. and other nominal Soriculus species ranges from 9.1-16.3%. This new species has a known distribution at an elevation of 1,500-2,125 m in Medog County, Tibet, China. The discovery of this new species from Medog County has important implications for interpreting small mammal biogeographic patterns in the eastern Himalaya and the mountain chains of south-west China., Competing Interests: The authors have declared that no competing interests exist., (Xiaoxin Pei, Zhongzheng Chen, Quan Li, Xueyou Li, Changzhe Pu, Kang Luo, Jing Luo, Mingjin Pu, Hongjiao Wang, Laxman Khanal, Xuelong Jiang.)

Objective: To study the effect of down-regulating miR-488 targeting Jag1 on the injury of hypoxia-reoxygenation myocardial H9c2 cells., Methods: A hypoxic-reoxygenated myocardial H9c2 cell injury model was constructed. miR-488 inhibitor was used to transfect the cells. CCK-8 method and flow cytometry were used to detect cell proliferation and apoptosis in each group. Lactate dehydrogenase (LDH), superoxide dismutase (SOD), malonaldehyde (MDA), catalase (CAT) levels were detected. Western blotting was used to detect the expression of Bcl-2 associated X Protein (Bax) and B cell lymphoma/lewkmia-2 (Bcl-2). Target genes of miR-488 were predicted, and a luciferase reporter system was used to verify the targeting relationship between the two. Myocardial H9c2 cells were co-transfected with miR-488 inhibitor and Jag1 siRNA, and treated with hypoxia and reoxygenation, cell proliferation, apoptosis, LDH, SOD, MDA, CAT levels, and Bax, Bcl-2 protein expression were detected., Results: The expression of miR-488 in the hypoxia-reoxygenated myocardial H9c2 cells was increased, along with reduced cell proliferation, increased apoptosis, increased Bax protein expression, decreased Bcl-2 protein expression, increased MDA, decreased CAT and SOD, and increased LDH level in the supernatant of cell culture. When myocardial H9c2 cells were transfected with miR-488 inhibitor and treated with hypoxia and reoxygenation, the expression of miR-488 was decreased, along with increased cell proliferation, decreased apoptosis, decreased Bax protein expression, increased Bcl-2 protein expression, decreased MDA, increased CAT and SOD, and decreased LDH level in the supernatant of cell culture. Down-regulation of miR-488 could target and down-regulate Jag1 expression. And Jag1 siRNA could reverse the effect of miR-488 inhibitor on the proliferation, apoptosis, LDH, SOD, MDA, CAT levels and the expression of Bax and Bcl-2 of hypoxic-reoxygenated myocardial H9c2 cells., Conclusion: Down-regulating miR-488 targeted Jag1 can attenuate hypoxia-reoxygenation induced myocardial H9c2 cell injury.

Introduction: Leucine-rich repetitive kinase-2 (LRRK2) is a Parkinson's disease-related gene that also participates in many inflammatory diseases. However, the functional role of LRRK2 in cardiovascular disease is not clear., Objective: In this study, we aimed to elucidate the role of LRRK2 in cardiac remodelling under pressure overload., Methods: Aortic banding surgery was performed to induce cardiac remodelling in a LRRK2 knockout mouse model. A cardiomyocyte remodelling model was established by phenylephrine (PE) stimulation in neonatal rat cardiomyocytes., Results: LRRK2 was upregulated in remodelled mouse hearts and cardiomyocytes. Cardiac hypertrophy, fibrosis and dysfunction were ameliorated in LRRK2 knockout mice. LRRK2 silencing protected against the PE-induced cardiomyocyte hypertrophic response, while LRRK2 over-expression worsened the PE-induced hypertrophic response in cardiomyocytes. Decreased autophagy was observed in remodelled cardiomyocytes, whereas LRRK2 silencing increased autophagy levels and LRRK2 overexpression reduced autophagy levels. The autophagy inhibitors 3-MA, bafilomycin and chloroquine reversed the protective effects of LRRK2 deficiency. The autophagy activator rapamycin reversed the deleterious effects of LRRK2 overexpression. We found that LRRK2 inhibited Bcl-2 phosphorylation, thus decreasing the phosphorylation of Beclin1. The protective effects of LRRK2 knockout were partly counteracted by Beclin1(+/-) in vivo and Beclin1 silencing in vitro . We also observed an interaction between LRRK2 and Rab7, an autolysosome degradation-associated protein, which caused Rab7 downregulation. Rab7 knockdown almost completely reversed LRRK2 silencing-induced protection of cardiomyocytes., Conclusion: LRRK2 deficiency protected against cardiac remodelling under pressure overload by increasing Bcl-2/Beclin1 and Rab7-regulated autophagy levels in the heart., Competing Interests: The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (© 2022 The Authors. Published by Elsevier B.V. on behalf of Cairo University..)