Key words: autophagy, Beclin 1, 3-methyladenine, amyloid β, c-secretase inhibitor, cerebral infarction, thalamus, secondary degeneration-S-phenylglycine t-butyl ester; LC3, microtubule-associated protein 1 light chain 3A; MCA, middle cerebral artery; MCAO, middle cerebral artery occlusion; RHRSP, stroke-prone renovascular hypertensive rats; shRNA, short-hairpin RNA Cerebral infarction can cause secondary degeneration of thalamus and delay functional recovery. However, the mechanisms underlying secondary degeneration are unclear. The present study aimed to determine the occurrence and contribution of autophagy to thalamic degeneration after cerebral infarction. Focal cerebral infarction was induced by distal middle cerebral artery occlusion (MCAO). Autophagic activation, Beclin 1 expression and amyloid b (Ab) deposits were determined by immunofluorescence, immunoblot and electron microscopy. Secondary damage to thalamus was assessed with Nissl staining and immunofluorescence analysis. Apoptosis was determined using TUNEL staining. The contribution of autophagy to the secondary damage was evaluated by shRNA-mediated downregulation of Beclin 1 and the autophagic inhibitor, 3-methyladenine (3-MA). The potential role of Ab in autophagic activation was determined with N-[N-(3, 5-difluorophenacetyl)-L-alanyl]-S-phenylglycine t-butyl ester (DAPT). The results showed that the conversion of LC3-II, the formation of autophagosomes, and the levels of activated cathepsin B and Beclin 1 were significantly increased in the ipsilateral thalamus at 7 and 14 d after MCAO (p , 0.05 or 0.01). Both Beclin 1 knockdown and 3-MA treatment significantly reduced LC3-II conversion and autophagosome formation, which were accompanied by obvious decreases in neuronal loss, gliosis and apoptosis in the ipsilateral thalamus (p , 0.05 or 0.01). Additionally, DAPT treatment markedly reduced Ab deposits, which coincided with decreases in LC3-II conversion and autophagosome formation (p , 0.01). These results suggest that inhibition of autophagy by Beclin 1 knockdown can attenuate the secondary thalamic damage after focal cerebral infarction. Furthermore, Ab deposits may be involved in the activation of autophagy.

T he evolution of motor function after stroke typically follows 2 strictly different patterns. Patients either recover ≈70% of maximal potential recovery (proportional recovery [PROP]) or show limited or no recovery (poor recovery [POOR]). 1-3 However, reliable predictors of motor improvement in the acute stage of stroke are scarce. Acute performance of the upper extremity on the Fugl-Meyer assessment (FMA-UE) seems to have predictive value. 1,4,5 Typically, for acute stroke patients with mild-to-moderate motor impairment of the upper extremity, motor function improves within 6 months by a relative proportion that is ≈70% of patients' maximal potential recovery. 6,7 However, initial Fugl-Meyer score alone may not reliably predict recovery of motor function in patients with acute-stage severe motor impairment of the limbs. 1,4 In addition, diffusion tensor imaging (DTI) studies have reported that the use of fractional anisotropy (FA) of corticospinal tract (CST) alone to predict future motor function of the upper extremity in patients with stroke in the acute period is also unreliable. 8-11 Researchers have proposed that more accurate prognoses may be made by combining behavioral tests with magnetic resonance imaging (MRI) determinations of the functional or structural integrity of the ipsilesional corticomotor tract. 12,13 However, it has been reported that on the base of initial impairment , adding functional MRI task-related brain activation patterns (during hand closure task) to their prediction model did Background and Purpose-Initial clinical assessment or conventional diffusion tensor imaging parameters alone do not reliably predict poststroke recovery of motor function. Recently, local diffusion homogeneity (LDH) has been proposed to represent the local coherence of water molecule diffusion and can serve as a complementary marker for investigating white matter alterations of the brain. We aimed to determine whether a combination of initial clinical assessment and LDH could predict motor recovery after acute subcortical infarction. Methods-Standard upper extremity Fugl-Meyer assessment and diffusion tensor imaging were performed 1, 4, and 12 weeks after onset in 50 patients with subcortical infarction. Proportional recovery model residuals were used to assign patients to proportional recovery and poor recovery groups. Tract-based spatial statistics analysis was used to compare diffusion differences between proportional and poor recovery outcomes. Multivariate logistic regression model was used to identify the predictors of motor improvement within 12 weeks after stroke. Results-The poor recovery group had lower LDH than the proportional recovery group, mainly in the ipsilesional corticospinal tract in the superior corona radiate and posterior limb of internal capsule 1 week after stroke (P<0.005; family-wise error corrected). Multivariate logistic regression analysis indicated that both initial Fugl-Meyer assessment and LDH in the ipsilesional corticospinal tract in the superior corona radiate and posterio...

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These results suggest that increased spontaneous neuronal activity of the PMC, a region structurally damaged secondarily to ischaemic lesion, may contribute to early motor recovery in patients with subcortical infarction.

Coalescence-induced droplet jumping has the potential to enhance the performance of a variety of applications including condensation heat transfer, surface self-cleaning, anti-icing, and defrosting to name a few. Here, we study droplet jumping on hierarchical microgrooved and nanostructured smooth superhydrophobic surfaces. We show that the confined microgroove structures play a key role in tailoring droplet coalescence hydrodynamics, which in turn affects the droplet jumping velocity and energy conversion efficiency. We observed self-jumping of individual deformed droplets within microgrooves having maximum surface-to-kinetic energy conversion efficiency of 8%. Furthermore, various coalescence-induced jumping modes were observed on the hierarchical microgrooved superhydrophobic surface. The microgroove structure enabled high droplet jumping velocity (≈0.74U) and energy conversion efficiency (≈46%) by enabling the coalescence of deformed droplets in microgrooves with undeformed droplets on adjacent plateaus. The jumping velocity and energy conversion efficiency enhancements are 1.93× and 6.67× higher than traditional coalescence-induced droplet jumping on smooth superhydrophobic surfaces. This work not only demonstrates high droplet jumping velocity and energy conversion efficiency but also demonstrates the key role played by macroscale structures on coalescence hydrodynamics and elucidates a method to further control droplet jumping physics for a plethora of applications.