Combining antioxidant astaxantin and cholinesterase inhibitor huperzine A boosts neuroprotection.

Oxidative stress is a pathophysiological condition resulting in neurotoxicity, which is possibly associated with neurodegenerative disorders. In this study, the antioxidative effects of the antioxidant astaxanthin (AXT) in combination with huperzine A (HupA), which is used as a cholinesterase inhibitor for the treatment of Alzheimer's disease, were investigated. PC12 cells were treated with either tert‑butyl hydroperoxide (TBHP), or with the toxic version of β‑amyloid, Aβ25‑35, to induce oxidative stress and neurotoxicity.

Alterations of CSF cystatin C levels and their correlations with CSF Αβ40 and Αβ42 levels in patients with Alzheimer's disease, dementia with lewy bodies and the atrophic form of general paresis.

Immunohistochemical studies have revealed that cystatin C (CysC) co-localizes with amyloid-β (Αβ) in amyloid-laden vascular walls and in the senile plaque cores of amyloid. In vitro and in vivo animal studies suggest that CysC protects against neurodegeneration by inhibition of cysteine proteases, inhibition of Αβ aggregation, induction of autophagy and induction of cell division. CysC levels may be altered and may have a potential link with cerebrospinal fluid (CSF) Aβ levels in various types of dementia with characteristic amyloid deposits, such as Alzheimer's disease (AD), dementia with Lewy bodies (DLB) and the atrophic form of general paresis (AF-GP).

[Clinical significance of determination of serum B7-H4 in patients with malignant hematologic diseases].

Aim: To study the clinical significance of determination of serum B7-H4 in patients with malignant hematologic diseases.

Methods: Serum B7-H4 levels were determined in 65 patients with leucemia, 34 patients with lymphoma, 12 patients with multiple myeloma as well as in 50 healthy controls.

Results: The serum B7-H4 levels in patients with lymphoma [(38.

Ectopic B7-H4-Ig expression attenuates concanavalin A-induced hepatic injury.

Previous studies demonstrate that both membrane B7-H4 and B7-H4-Ig fusion protein could inhibit T-cell responses. In the present study, we explored the potential effect of B7-H4-Ig on liver injury in a hepatitis mouse model induced by concanavalin A (ConA). A B7-H4-Ig construct was introduced into animals by the hydrodynamic gene delivery approach.