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Sun, Y. B.

Publications and source records attributed to Sun, Y. B..

2 recordsLinked to original sources

Micro-circulating hyperdynamic blood flow as a key pathogenic factor in early sepsis

ObjectiveThe pathogenesis of sepsis is still unknown. Sepsis 3.0 points out that "how to define sepsis and septic shock itself is still a challenge". This study confirmed the inevitability and universality of Hyperdynamic microcirculation in sepsis, and put forward the detoxification mechanism of Hyperdynamic blood flow and the "Xinghuai Feng-Bernoulli warm shock" mechanism, that is, the pathogenic mechanism of sepsis. MethodsSepsis models of pigs, rabbits, Mice, rats and sheep were established by intravenous injection of lipopolysaccharide (LPS) and cecal ligation and perforation (CLP), and the changes of sublingual microcirculation velocity in the same branch before and after modeling were detected. SD rat model of mild sepsis was established to verify that the acceleration of blood flow is the manifestation of immune detoxification mechanism. ResultsThe blood flow in the same branch was accelerated after the animal sepsis model was established, which was more than doubled on average. The microcirculation blood flow accelerated before the change of cardiac output CO. Rats entered a toxic state after the rapid blood flow occurred, but they could heal themselves. ConclusionThe acceleration of microcirculation blood flow in sepsis is inevitable and universal, which is the cause of high output and low resistance of sepsis, and has the functions of accelerating detoxification and immunity. However, due to Bernoulli effect, it will cause oxygen exchange disorder, which is named "Xinghuai Feng-Bernoulli warm shock", ultimately leading to hypoxia. This is the primary pathogenic mechanism of early sepsis. Since the completion of this article in 2023, its principles have undergone multicenter, randomized, and double-blind clinical verification, achieving satisfactory results. The specifics will have to wait for the publication by the three Class A tertiary hospitals.

pathology↗

An iTSC-derived placental model of SARS-CoV-2 infection unveils ACE2-dependent susceptibility in syncytiotrophoblasts

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection causing coronavirus disease 2019 (COVID-19) has caused a global health crisis. The primary site of infection is in the respiratory tract but the virus has been associated with a variety of complications involving the gastrointestinal and cardiovascular systems. Since the virus affects a variety of tissue types, there has been interest in understanding SARS-CoV-2 infection in early development and the placenta. ACE2 and TMPRSS2, two genes that are critical for SARS-CoV-2 virus entry are expressed in placenta-specific cell types including extravillous trophoblasts (EVTs) and especially, syncytiotrophoblasts (STs). The potential of SARS-CoV-2 to infect these placental cells and its effect on placental development and function is still unclear. Furthermore, it is crucial to understand the possible mechanism of vertical transmission of SARS-CoV-2 through the placenta. Here, we developed an in vitro model of SARS-CoV-2 infection of placental cell types using induced trophoblast stem cells (iTSCs). This model allowed us to show that STs but not EVTs are infected. Importantly, infected STs lack the expression of key differentiation genes, lack typically observed differentiated morphology and produce significantly lower human chorionic gonadotropin (HCG) compared to non-infected controls. We also show that an anti-ACE2 antibody prevents SARS-CoV-2 infection and restores normal ST differentiation and function. We highlight the establishment of a platform to study SARS-CoV-2 infection in early placental cell types, which will facilitate investigation of antiviral therapy to protect the placenta during early pregnancy and development.

cell biology↗