Publications by authors named "Qiubo Jiang"

Mechanical circulatory support devices (MCSDs) are often associated with hemocompatible complications such as hemolysis and gastrointestinal bleeding when treating patients with end-stage heart failure. Shear stress and exposure time have been identified as the two most important mechanical factors causing blood damage. However, the materials of MCSDs may also induce blood damage when contacting with blood.

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Blood damage has been associated with patients under temporary continuous-flow mechanical circulatory support. To evaluate the side effects caused by transit blood pumping, hemocompatibility testing for blood damage in pumps is considered a necessary reference before clinical trials. The hemocompatibility of five extracorporeal centrifugal blood pumps was investigated comprehensively, including four commercial pumps (the Abbott CentriMag, the Terumo Capiox, the Medos DP3, and the Medtronic BPX-80) and a pump in development (the magAssist MoyoAssist).

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The incidence of clinical complication gastrointestinal bleeding has been proved as consequence of von Willebrand factor (VWF) damage after mechanical circulatory support in clinic. Many studies have been conducted to evaluate VWF damage, of which the most studied influencing factors are mechanical factors such as shear stress. However, in addition to mechanical factors, VWF damage may also be affected by interface factors.

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We recently discovered that the expression of PRKN, a young-onset Parkinson disease-linked gene, confers redox homeostasis. To further examine the protective effects of parkin in an oxidative stress model, we first combined the loss of prkn with Sod2 haploinsufficiency in mice. Although adult prkn//Sod2 animals did not develop dopamine cell loss in the S.

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Article Synopsis
  • The study investigates how parkin, a protein, protects the brain from Parkinson's disease, particularly focusing on its cysteine residues that undergo redox reactions and posttranslational modifications.* -
  • Research findings reveal that aging leads to parkin becoming largely insoluble due to oxidation, particularly at specific cysteine residues, and this results in increased levels of harmful hydrogen peroxide (HO) in both mice and parkin-deficient human brains.* -
  • The protective effects of wild-type parkin against dopamine toxicity are emphasized, as it reduces HO levels and neutralizes reactive dopamine metabolites, while disease-linked parkin mutants do not exhibit these protective characteristics.*
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Braak and Del Tredici have proposed that typical Parkinson disease (PD) has its origins in the olfactory bulb and gastrointestinal tract. However, the role of the olfactory system has insufficiently been explored in the pathogeneses of PD and Alzheimer disease (AD) in laboratory models. Here, we demonstrate applications of a new method to process mouse heads for microscopy by sectioning, mounting, and staining whole skulls ('holocranohistochemistry').

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Hypoxic/ischemic and traumatic injury to central nervous system myelinated axons is heavily dependent on accumulation of Ca ions in the axoplasm, itself promoted by Na influx from the extracellular space. Given the high density of nodal Na channels, we hypothesized that nodes of Ranvier might be particularly vulnerable to Ca overload and subsequent damage, as this is the expected locus of maximal Na influx. Adult rat optic nerves were exposed to in vitro anoxia and analyzed immunohistochemically for the presence of spectrin breakdown.

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Neurofilaments are key structural components of white matter axons. The effect of in vitro anoxia or oxygen-glucose deprivation (OGD) on the integrity of the 160 and 200 kDa neurofilament isoforms was studied by immunoblot, and correlated with physiological function. Adult rat optic nerves were exposed to 60 min of either anoxia or OGD.

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