Optimal treatment determination on the basis of haematoma volume and intra-cerebral haemorrhage score in patients with hypertensive putaminal haemorrhages: a retrospective analysis of 310 patients

BACKGROUND: Hypertensive putaminal haemorrhage comprises major part of intra-cerebral haemorrhages, with particularly high morbidity and mortality. However, the optimal treatments for these individuals remain controversial. METHODS: From June 2010 to August 2013, patients with hypertensive putaminal haemorrhages were treated in the Department of Neurosurgery, West China Hospital. Information regarding the age, signs of cerebral herniation, haematoma volume, intra-ventricular haemorrhage, intra-cerebral haemorrhage score and the treatments of each patient were analyzed retrospectively. The outcome was evaluated by the 30-day mortality rate. RESULTS: The 30-day mortality rate of the patients with haematomas volume greater than or equal to 30 ml and intra-cerebral haemorrhage scores of 1 or 2 was decreased in the surgical group compared with those in the conservative group (1.92% VS. 21.40%, OR = 0.072, p = 0.028; 15.40% VS. 33.3%, OR = 0.365, p = 0.248, respectively). The mortality rate of the patients with signs of cerebral herniation was not significantly different between the surgical and conservative groups (83.30% VS. 100%; p = 0.529). The intra-cerebral haemorrhage score was significantly associated with the 30-day mortality rate of patients with intra-cerebral haemorrhages (r = -0.798, p < 0.001). CONCLUSION: Patients with basal ganglia haematomas volume greater than or equal to 30 ml and intra-cerebral haemorrhage scores of 1 or 2 could benefit from the surgical removal of haematomas. The intra-cerebral haemorrhage score can accurately predict the 30-day mortality rate of patients with hypertensive putaminal haemorrhages

Urchin-like core-shell heterostructure of In2O3 nanowires-coated ZnO microspheres with enhanced triethylamine gas-sensing properties

The urchin-like core-shell In2O3/ZnO nanocomposites were prepared via a facile solvothermal method which In2O3 nanowires were grown on the ZnO microspheres. The nanocomposite microspheres had mesoporous structure, whose large specific surface area was 58.5 m(2)/g and pore size was 14.0 nm. The influence of initial reactant In3+ content on the morphology, component and structure of composites was systemically investigated. The sensor based on In2O3-ZnO-0.1 (the addition amount of indium nitrate was 0.1 g) displayed more excellent gas-sensing performance to triethylamine (TEA) than other samples, such as higher response (221), lower working temperature (100 degrees C). The outstanding gas-sensing performance of urchin-like In2O3/ZnO nanocomposites could be attributed to the special urchin-like structure with mesoporous and high specific surface area, plentiful oxygen vacancies and the formation of n-n heterojunction

CD8 T Cell‐Derived Exosomal miR‐186‐5p Elicits Renal Inflammation via Activating Tubular TLR7/8 Signal Axis

Abstract T cells play an important role in the development of focal segmental glomerulosclerosis (FSGS). The mechanism underlying such T cell‐based kidney disease, however, remains elusive. Here the authors report that activated CD8 T cells elicit renal inflammation and tissue injury via releasing miR‐186‐5p‐enriched exosomes. Continuing the cohort study identifying the correlation of plasma level of miR‐186‐5p with proteinuria in FSGS patients, it is demonstrated that circulating miR‐186‐5p is mainly derived from activated CD8 T cell exosomes. Renal miR‐186‐5p, which is markedly increased in FSGS patients and mice with adriamycin‐induced renal injury, is mainly delivered by CD8 T cell exosomes. Depleting miR‐186‐5p strongly attenuates adriamycin‐induced mouse renal injury. Supporting the function of exosomal miR‐186‐5p as a key circulating pathogenic factor, intravenous injection of miR‐186‐5p or miR‐186‐5p‐containing T cell exosomes results in mouse renal inflammation and tissue injury. Tracing the injected T cell exosomes shows their preferential distribution in mouse renal tubules, not glomerulus. Mechanistically, miR‐186‐5p directly activates renal tubular TLR7/8 signal and initiates tubular cell apoptosis. Mutating the TLR7‐binding sequence on miR‐186‐5p or deleting mouse TLR7 largely abolishes renal tubular injuries induced by miR‐186‐5p or adriamycin. These findings reveal a causative role of exosomal miR‐186‐5p in T cell‐mediated renal dysfunction

Ambient Stable Trigonal Bipyramidal Copper(III) Complexes Equipped with an Exchangeable Axial Ligand

A stable trigonal bipyramidal copper­(III) complex, [PPN]­[Cu­(^TMSPS3)­Cl] (<b>1</b>, wherein PPN represents bis­(triphenylphosphine)­iminium), was synthesized from CuCl₂/PPNCl via intramolecular copper­(II) disproportionation. Under ambient conditions, the axial chloride of <b>1</b> is exchangeable in solution thus making <b>1</b> serve as an intermediate to prepare trigonal bipyramidal copper­(III) derivatives, e.g., [PPN]­[Cu­(^TMSPS3)­(N₃)] (<b>2</b>) and [Cu­(^TMSPS3)­(DABCO)] (<b>3</b>). Diamagnetic complexes <b>1</b>–<b>3</b> were fully characterized by X-ray crystallography, NMR, UV–vis, and Cu K-edge absorption spectroscopy. A series of UV–vis titrations were performed to investigate the relative ligand affinity toward the [Cu­(^TMSPS3)] moiety, verifying the 1:1 binding equilibrium between various ligands. Compared to known copper­(III) compounds, Cu K-edge absorptions of <b>1</b>–<b>3</b> possess lower pre-edge energy and higher shakedown transition energy, which, respectively, attribute to the electron donation from ^TMSPS3^3– ligand and their trigonal ligand field