Publications by authors named "Hong Tao Shao"

Sugar beet (Beta vulgaris L.) is an important crop that has significant economic value in northern regions of China, especially in Heilongjiang Province. In October 2019, root rot was discovered on the sugar beet cultivar HDW09 in Hulan (126°64' E, 46°00' N), Heilongjiang Province, China.

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Article Synopsis
  • A study on invasive pulmonary aspergillosis (IPA) highlights the role of microRNAs (miRNAs) in its regulation, particularly in immunocompromised patients with high mortality rates.
  • Researchers created a mouse model for IPA and used next-generation sequencing to analyze small RNA transcriptomes in lung tissues, discovering a total of 3759 known miRNAs, with 23 specifically linked to IPA infection.
  • Eight of these miRNAs were validated, showing consistent expression changes that may regulate important components of the NF-kappa B signaling pathway, enhancing understanding of IPA pathogenesis and the complexity of small RNAs in immune responses.
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We investigated the features of Dectin-2 expression both at transcriptional and translational levels during Aspergillus fumigatus infection in human lung. Simultaneously, the expression of CD206 was assayed as an activated marker of alveolar macrophages. The characteristic of Dectin-2 expression were then confirmed in Monocyte-derived macrophages (MDM) after A.

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Dectin-2, a C-type lectin receptor (CLR), plays an essential role in mediating nuclear factor-kappa B (NF-κB) activation and anti-fungal immunity in response to Candida albicans infection. However, the molecular mechanisms and function of Dectin-2 signaling in response to infection by the pathogenic fungus Aspergillus fumigatus have not been characterized. In order to characterize Dectin-2 signaling in response to A.

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Objective: To observe the expressions of nerve growth factor (NGF) and its tyrosine kinase A (TrkA) receptor on alveolar macrophage in a rat model of chronic obstructive pulmonary disease (COPD).

Methods: Forty healthy male SD rats were randomly divided into a control group and a COPD group. The COPD model was established by exposing the rats to cigarette smoke for 6 months, and lung function changes were measured.

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