Publications by authors named "Xun-Zhi Liu"

Article Synopsis
  • The study examines how the autophagy-lysosomal pathway (ALP) is affected in neurons after subarachnoid hemorrhage (SAH), revealing that it becomes impaired.
  • TET3, a gene regulator important for autophagy, shows decreased expression following SAH, contributing to this impairment.
  • The research suggests that elevating TET3 levels could improve ALP function and that targeting miR-93-5p, which increases after SAH and suppresses TET3, may offer new therapeutic strategies for neuroprotection.
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Article Synopsis
  • The study investigates how microglia, a type of immune cell in the brain, clear blood and maintain homeostasis after a subarachnoid hemorrhage (SAH), focusing on LC3-associated phagocytosis (LAP) and its regulation through specific gene pathways.
  • Researchers utilized an in vitro model simulating SAH to explore key signaling pathways, particularly emphasizing the P38 MAPK and DAPK1 pathways, which were linked to inhibited LAP and increased inflammation in microglia.
  • Findings revealed that the P38-DAPK1 signaling axis influences the expression of the gene BECN1, thereby affecting both the phagocytic ability and overall health of microglia in the context of SAH.
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The presence of aneurysmal subarachnoid hemorrhage (aSAH) is usually accompanied by excessive inflammatory response leading to damage of the central nervous system, and the sialic acid-binding Ig-like lectin 10 (Siglec-10) is a recognized factor being able to modify the inflammatory reaction. To investigate the potential role of Siglec-10 in aSAH, we collected the cerebrospinal fluid (CSF) of control ( = 11) and aSAH ( = 14) patients at separate times and measured the Siglec-10 concentration utilizing the enzyme-linked immunosorbent assay (ELISA) and evaluated the alterations of GOS and GCS during the disease process. In accordance with the STROBE statement, results showed that Siglec-10 in CSF rose quickly in response aSAH attack and then fell back to a slightly higher range above baseline, while it remained at relative high concentration and last longer in several severely injured patients.

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To evaluate the efficacy of liquid embolization agents for treating various hemorrhagic peripheral intracranial aneurysms. We retrospectively analyzed 38 patients who suffered from hemorrhagic peripheral intracranial aneurysms and were treated with liquid embolization agents. We used the modified Rankin scale for follow-up at 6 months postoperatively, and digital subtraction angiography follow-up was performed 6 months postoperatively.

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Endogenous host-derived molecules named damage-associated molecular patterns (DAMPs) can induce excessive non-sterile inflammatory responses on recognition of specific membrane-tethered receptors. Here in this study, we aimed to explore the role of DAMP molecule HMGB1 in astrocyte-mediated sterile neuroinflammation and the resultant influences on neurons. In vitro cultured astrocytes were challenged with rHMGB1 and then harvested at 6 h, 12 h, 24 h, 36 h, and 48 h, respectively.

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Pyruvate dehydrogenase (PDH), a key enzyme on the mitochondrial outer membrane, has been found to decrease activity notably in early brain injury (EBI) after subarachnoid hemorrhage (SAH). It has been demonstrated that PDH is associated with the production of reactive oxygen species (ROS) and apoptosis. Hence, in this study, we aimed to determine the cause of the decreased PDH activity and explore the potential role of PDH in EBI.

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Oxidative stress is a key component of the pathological cascade in subarachnoid hemorrhage (SAH). Fucoxanthin (Fx) possesses a strong antioxidant property and has shown neuroprotective effects in acute brain injuries such as ischemic stroke and traumatic brain injury. Here, we investigated the beneficial effects of Fx against SAH-induced oxidative insults and the possible molecular mechanisms.

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