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The article highlights the role of cell therapy for Ischemic Stroke. It mentions cell therapies as promising paradigm for ischemic stroke and different types of cells like mesenchymal stem and stromal cells (MSCs), neural stem cells (NSCs), and mononuclear cells (MNCs); and also mentions the inadequate quality of preclinical tests considered as a major reason for unsuccessful translation of experimental stroke therapies.

Aims: To investigate the relationship between peripheral leukocyte dynamics and the outcome of large hemispheric infarction (LHI) patients. Methods: Patients with acute LHI admitted to the neuro‐intensive care unit of Xuanwu Hospital from 2013 to 2017 were prospectively enrolled and followed up for 6 months after LHI. Results: A total of 84 LHI patients were included, 38 patients suffered brain herniation and 20 patients died from stroke. Compared to patients with benign course, LHI patients with fatal outcome showed larger infarcts and more severe brain edema (P <.01), as well as increased WBC and neutrophil counts throughout the first week after stroke (P <.05). Correlation analysis revealed that neutrophil counts on D2 after LHI positively correlated with infarct and edema volumes measured from CT/MRI (R2 = 0.22 and R2 = 0.15, P <.01) and negatively correlated with Glasgow Coma Scale (ρ = −0.234, P <.05). Patients with D2 neutrophils > 7.14 × 109/L had higher risk of brain herniation [odds ratio (OR) = 7.5, 95% CI: 2.0‐28.1, P =.001], and patients with D2 neutrophils > 7.79 × 109/L had a higher risk of death (OR = 5.8, 95% CI: 1.2‐27.0, P =.015). Conclusion: Early peripheral neutrophil count after stroke relates to infarct size and the fatal outcome of LHI patients, which might help guiding acute LHI management such as reduction of intracranial pressure and potential antiinflammatory therapy in the future. [ABSTRACT FROM AUTHOR]

Sirtuin 2 (SIRT2) is an NAD+ dependent deacetylase that is the most abundant sirtuin protein in the brain. Accumulating evidence revealed the role of SIRT2 in a wide range of biological processes and age‐related diseases. However, the pivotal mechanism of SIRT2 played in Alzheimer's disease (AD) remains unknown. Here, we report that pharmacological inactivation of SIRT2 has a beneficial effect in AD. The deacetylase inhibitor of SIRT2 rescued the cognitive impairment in amyloid precursor protein/presenilin 1 transgenic mouse (APP/PS1 mouse), and the BACE1 cleavage was weakened to reduce the β‐amyloid (Aβ) production in the hippocampus. Moreover, we firstly identified that Reticulon 4B (RTN4B) played a crucial role between SIRT2/BACE1 regulation in AD. RTN4B, as a deacetylation substrate for SIRT2, the deacetylation by SIRT2 drived the ubiquitination and degradation of RTN4B and then the disturbed RTN4B interacted with and influenced the expression of BACE1. When we overexpressed RTN4B in neurons of the hippocampus in the AD mouse model, the abnormal Aβ accumulation and cognitive impairment were ameliorated, consistent with the results of SIRT2 inhibition in vivo. Moreover, we showed that the regulatory effect of SIRT2 on BACE1 is dependent on RTN4B. When RTN4B was knocked down, the effects of SIRT2 inhibition on the BACE1 level, Aβ pathology, and AD‐liked behaviors were also blocked. Collectively, we provide evidence that SIRT2 may be a potential target for AD; the new found SIRT2/RTN4B/BACE1 pathological pathway is one of the critical mechanisms for the improvement of SIRT2 on AD. [ABSTRACT FROM AUTHOR]

Aim Dysregulation of the activity of the disintegrin/metalloproteinase ADAM10 could contribute to the development of atherosclerosis. Although a number of genetic studies have focused on the association of ADAM10 gene polymorphisms with susceptibility to diseases, no genetic association studies of ADAM10 gene variability with atherosclerotic cerebral infarction ( ACI) have been conducted. The aim of this study was to analyze the potential association between ADAM10 promoter polymorphisms and ACI. Methods The associations between rs653765 and rs514049 polymorphisms of the ADAM10 promoter and the possible risk of ACI were assessed among 347 patients with ACI and 299 matched healthy individuals in a case-control study. Results Overall, there was a significant difference in the genotypes frequencies of rs653765 ( P = 0.04) between the ACI and control subjects. In addition, the rs653765 mutated allele of ADAM10 was significantly associated with increased ADAM10 expression in patients with ACI ( P = 0.032). In contrast, the allele frequency of rs514049 was not statistically associated with ACI, and the rs514049 variant A > C did not affect the expression of ADAM10 either. Conclusion Our findings indicate a positive association between the rs653765 polymorphism of ADAM10 and ACI, as well as a negative result for rs514049. In addition, a significant increase in ADAM10 expression was observed in patients with ACI carrying the rs653765 C > T mutation. This new knowledge about ADAM10 might be clinically important and confirm a role for ADAM10 in the pathophysiology of ACI, with potentially important therapeutic implications. [ABSTRACT FROM AUTHOR]

In the title complex, [Ni(C(4)N(3))(2)(C(15)H(11)N(3))](n), each of the two different Ni(II) atoms is coordinated by one 2,2':6'2''-terpyridine (terpy) and three tricyano-methanide ligands in a distorted octa-hedral geometry. The Ni(II) atoms are linked to each other, forming an infinite chain parallel to (10). π-π Stacking inter-actions of terpy mol-ecules between adjacent chains (centroid-centroid distance = 3.785 Å), along with weak inter-molecular C-H⋯N hydrogen bonds involving the uncoordinated terminal N atoms of the tricyanomethanide ions and the terpyridine H atoms, result in the formation of a three-dimensional network structure.

The two new title complexes, [Mn(C5H3N6)2(H2O)2] and [Zn(C5H3N6)2(H2O)2], are isomorphous. In both compounds, the metal atom is located on an inversion center and is coordinated by four N atoms from two 5-(pyrazin-2-yl)-1H-tetrazolate anions in the basal plane and by two O atoms of water ligands in the apical positions to form a distorted octahedral geometry. Intermolecular hydrogen-bond interactions between the uncoordinated N atoms of the tetrazolate anions and the H atoms of the water molecules lead to the formation of a three-dimensional network.