Fine Characterization and Analysis of Drying Strain of the ELM Board via DIC Technology

In this paper,the occurrence and development mechanism of strain on the cross-section during the wood drying is explored.Therefore,strain regularity on the cross-section of 50 mm thickness elm(Ulmus rubra)board at the temperature of 40℃and 80℃is detected via digital image correlation technology.Hence,the difference between tangential and radial strain at surface and core layers was denoted.The results showed that strain distribution in the width direction of the board is uneven.Moreover,a large drying shrinkage strain occurs at the near-core layer,while the maximum strain difference reaches 4.08%.Hence,the surface of the board is cracked along the thickness direction.The radial strain of the board is higher than the tangential strain in the early stage of drying,while these strains are reversed in the later stage of drying.The temperature is related to the difference between the tangential and radial strains of the elm board.These differences at the core layer are larger than those of the surface layer.The conducted research results provide a theoretical basis for process optimization.

Fingolimod alters inflammatory mediators and vascular permeability in intracerebral hemorrhage

Intracerebral hemorrhage （ICH） leads to high rates of death and disability. The pronounced inflammatory reactions that rapidly follow ICH contribute to disease progression. Our recent clinical trial demonstrated that oral administration of an immune modulator fingolimod restrained secondary injury derived from initial hematoma, but the mechanisms remain unknown. In this study, we aim to investigate the effects of fingolimod on inflammatory mediators and vascular permeability in the clinical trial of oral fingolimod for intracerebral hemorrhage （ICH）. The results showed that fingolimod decreased the numbers of circulating CD4~ T, CD8~ T, CD19~ B, NK, and NKT cells and they recovered quickly after the drug＇ was stopped. The plasma ICAM level was decreased and IL-10 was increased by fingolimod. Interestingly, fingolimod protected vascular permeability as indicated by a decreased plasma level of MMP9 and the reduced rT1%. In conclusion, modulation of systemic inflammation by fingolimod demonstrates that it is an effective therapeutic agent for ICH. Fingolimod may prevent perihematomal edema enlargement by protecting vascular permeability.

Neural Stem Cells Transfected with Leukemia Inhibitory Factor Promote Neuroprotection in a Rat Model of Cerebral Ischemia

Leukemia inhibitory factor(LIF) contributes to the neuroprotection by neural stem cells(NSCs) after ischemic stroke. Our aim was to explore whether LIFtransfected NSCs(LIF-NSCs) can ameliorate brain injury and promote neuroprotection in a rat model of cerebral ischemia. To accomplish this goal, we transfected NSCs with a lentivirus carrying the LIF gene to stably overexpress LIF. The LIF-NSCs reduced caspase 3 activation under conditions of oxygen-glucose deprivation in vitro.Transient cerebral ischemia was induced in rats by 2 h of middle cerebral artery occlusion(MCAo), and LIF-NSCs were intravenously injected at 6 h post-ischemia. LIF-NSC treatment reduced the infarction volume and improved neurological recovery. Moreover, LIF-NSCs improved glial cell regeneration and ameliorated white matter injuryin the MCAo rats. The NSCs acted as carriers and increased the expression of LIF in the lesions to protect against cerebral infarction, suggesting that LIF-NSCs could be a potential treatment for cerebral infarction.