Peakon, Cuspon, Compacton, and Loop Solutions of a Three-Dimensional 3DKP(3, 2) Equation with Nonlinear Dispersion

We study peakon, cuspon, compacton, and loop solutions for the three-dimensional Kadomtsev-Petviashvili equation (3DKP(3,2) equation) with nonlinear dispersion. Based on the method of dynamical systems, the 3DKP(3,2) equation is shown to have the parametric representations of the solitary wave solutions such as peakon, cuspon, compacton, and loop solutions. As a result, the conditions under which peakon, cuspon, compacton, and loop solutions appear are also given

Transfusion of Resting Platelets Reduces Brain Hemorrhage After Intracerebral Hemorrhage and tPA-Induced Hemorrhage After Cerebral Ischemia

BackgroundExacerbated blood-brain barrier (BBB) damage is related with tissue plasminogen activator (tPA)-induced brain hemorrhage after stroke. Platelets have long been recognized as the cellular orchestrators of primary haemostasis. Recent studies have demonstrated further that platelets are required for supporting intact mature blood vessels and play a crucial role in maintaining vascular integrity during inflammation. Therefore, we sought to investigate whether platelets could reduce tPA-induced deterioration of cerebrovascular integrity and lead to less hemorrhagic transformation.MethodsMice were subjected to models of collagenase-induced intracerebral hemorrhage (ICH) and transient middle cerebral artery (MCA) occlusion. After 2 h of MCA occlusion, tPA (10 mg/kg) was administered as an intravenous bolus injection of 1 mg/kg followed by a 9 mg/kg infusion for 30 min. Immediately after tPA treatment, mice were transfused with platelets. Hemorrhagic volume, infarct size, neurological deficit, tight junction and basal membrane damages, endothelial cell apoptosis, and extravascular accumulation of circulating dextran and IgG, and Evans blue were quantified at 24 h.ResultsPlatelet transfusion resulted in a significant decrease in hematoma volume after ICH. In mice after ischemia, tPA administration increased brain hemorrhage transformation and this was reversed by resting but not activated platelets. Consistent with this, we observed that tPA-induced brain hemorrhage was dramatically exacerbated in thrombocytopenic mice. Transfusion of resting platelets ameliorated tPA-induced loss of cerebrovascular integrity and reduced extravascular accumulation of circulating serum proteins and Evans blue, associated with improved neurological functions after ischemia. No changes were found for infarct volume. Inhibition of platelet receptor glycoprotein VI (GPVI) blunted the ability of platelets to attenuate tPA-induced BBB disruption and hemorrhage after ischemia.ConclusionOur findings demonstrate the importance of platelets in safeguarding BBB integrity and suggest that transfusion of resting platelets may be useful to improve the safety of tPA thrombolysis in ischemic stroke

Growth Differentiation Factor 11 Promotes Neurovascular Recovery After Stroke in Mice

Background: Growth differentiation factor 11 (GDF11), a member of transforming growth factor-β (TGF-β) superfamily, was shown to rejuvenate cardiac and skeletal muscle function and to improve cerebral vasculature and neurogenesis in old mice. However, recent experimental data reported that raising GDF11 levels inhibited skeletal muscle regeneration and had no effect on cardiac hypertrophy. Our aim was to investigate the effects of GDF11 on brain repair during the recovery phase after stroke.Methods: Mice were subjected to distal middle cerebral artery occlusion, and recombinant GDF11 (rGDF11) was injected intraperitoneally once a day during days 7–13 after stroke. Neuronal precursor cells (NPCs) proliferation and angiogenesis were assayed at 14 days. Neuronal regeneration was assayed at 42 days. The beam-walking test and CatWalk were used to evaluate behavioral functions. Downstream pathways of GDF11 were also investigated.Results: GDF11 was upregulated in the ipsilateral peri-infarct cortex and subventricular zone (SVZ) at 14 days after stroke. Treatment with rGDF11 enhanced the number of newborn NPCs and endothelial cells, microvascular length and area, and brain capillary perfusion. Western blots showed that rGDF11 upregulated brain-derived neurotrophic factor (BDNF) and increased the levels of proangiogenic factor angiopoietin-2 (Ang-2) and phosphorylation of vascular endothelial growth factor receptor-2 (VEGFR-2). We also found that rGDF11 upregulated the transcription factors Smad2 and Smad3 phosphorylation, but these activations were blocked by a TGF-β receptor inhibitor SB431542. Moreover, rGDF11-induced angiogenic remodeling and NPCs proliferation were reversed by injection of SB431542, suggesting that GDF11 may exert its effect via the TGF-β/Smad2/3 signaling pathway. Finally, treating mice with rGDF11 resulted in a significant increase in neuronal regeneration and functional recovery.Conclusion: GDF11 promoted neurogenesis and angiogenesis and contributed to functional recovery after stroke in mice

Condition Numbers for the Scaled Total Least Squares Problems ∗

The standard approaches to solving an overdetermined linear system Bx ≈ c construct minimal corrections to the vector c and/or the matrix B such that the corrected system is consistent, such as the least squares (LS), the data least squares (DLS) and the total least squares (TLS). The scaled total least squares (STLS) method unifies the LS, DLS and TLS methods. So far, the classical normwise condition numbers for the LS problem have been widely studied. However, there are no such similar results for the TLS and the STLS problems. In this paper we first present a normwise condition number for the STLS problem. Different from normwise condition numbers which measure the sizes of both input perturbations and output errors using some norms, componentwise condition numbers take into account the relation of each data component, and a possible data sparsity. Then in this paper we give explicit expressions for mixed and componentwise condition numbers for the STLS problem. Moreover, as a byproduct, we also derive normwise and componentwise condition numbers for the difference between the STLS solution and the LS solution. Since the TLS problem is a special case of the STLS problem, the condition numbers for the TLS problem follow immediately from our STLS results

Ultrasmall PEGylated MnxFe3-xO4 (x = 0-0.34) nanoparticles: Effects of Mn(ii) doping on T1- and T 2-weighted magnetic resonance imaging

We report a facile synthesis of water-soluble, ultrasmall, PEGylated MnFeO nanoparticles (MFNPs) (x = 0-0.34) and the Mn(ii) doping effects on T- and T-weighted magnetic resonance imaging (MRI). By adjusting the reaction conditions, the 'x' value can be continuously tuned from 0 to 0.34. The produced MFNPs are of high crystallinity and size uniformity with an average diameter of ∼6 nm, which show excellent colloidal stability in HO, PBS, and tolerate a high salt concentration (1 M NaCl) and a wide pH range from 7 to 11. The results of FTIR demonstrate that both HOOC-PEG-COOH and TEG were modified on the nanocrystal surfaces. The saturation magnetization of the MFNPs gradually increases with increasing Mn concentration and reaches 75.5 emu g for x = 0.34. Careful investigation of the Mn(ii) doping effects on T- and T-weighted MRI reveals that T contrast effects are enhanced while T contrast effects are weakened with the increase of the 'x' value of the MFNPs. Furthermore, the T contrast effects of the MFNPs are concentration dependant. A concentration which is lower than 0.500 mM is needed for the MFNPs to act as T and T dual contrast agents at 3 T

ADAMTS13 maintains cerebrovascular integrity to ameliorate Alzheimer-like pathology.

Blood-brain barrier (BBB) defects and cerebrovascular dysfunction contribute to amyloid-β (Aβ) brain accumulation and drive Alzheimer disease (AD) pathology. By regulating vascular functions and inflammation in the microvasculature, a disintegrin and metalloprotease with thrombospondin type I motif, member 13 (ADAMTS13) plays a significant protective effect in atherosclerosis and stroke. However, whether ADAMTS13 influences AD pathogenesis remains unclear. Using in vivo multiphoton microscopy, histological, behavioral, and biological methods, we determined BBB integrity, cerebrovascular dysfunction, amyloid accumulation, and cognitive impairment in APPPS1 mice lacking ADAMTS13. We also tested the impact of viral-mediated expression of ADAMTS13 on cerebrovascular function and AD-like pathology in APPPS1 mice. We show that ADAMTS13 deficiency led to an early and progressive BBB breakdown as well as reductions in vessel density, capillary perfusion, and cerebral blood flow in APPPS1 mice. We found that deficiency of ADAMTS13 increased brain plaque load and Aβ levels and accelerated cerebral amyloid angiopathy (CAA) by impeding BBB-mediated clearance of brain Aβ, resulting in worse cognitive decline in APPPS1 mice. Virus-mediated expression of ADAMTS13 attenuated BBB disruption and increased microvessels, capillary perfusion, and cerebral blood flow in APPPS1 mice already showing BBB damage and plaque deposition. These beneficial vascular effects were reflected by increase in clearance of cerebral Aβ, reductions in Aβ brain accumulation, and improvements in cognitive performance. Our results show that ADAMTS13 deficiency contributes to AD cerebrovascular dysfunction and the resulting pathogenesis and cognitive deficits and suggest that ADAMTS13 may offer novel therapeutic opportunities for AD

Immediate and long-term outcomes after treat-all among people living with HIV in China: an interrupted time series analysis

Abstract Background In 2003, China implemented free antiretroviral therapy (ART) for people living with HIV (PLHIV), establishing an eligibility threshold of CD4  50 (+ 7.8%, IRR = 1.078, 95% CI: 1.000–1.161; P = 0.046), heterosexual transmission (+ 12.4%, IRR = 1.124, 95% CI: 1.042–1.213; P = 0.002) and Southwestern China (+ 12.9%, IRR = 1.129, 95% CI: 1.055–1.208; P < 0.001) in the first month of treat-all. Conclusions The implementation of treat-all policy in China was associated with a positive effect on HIV care and treatment outcomes. To advance the work of rapid ART, efforts should be made to streamline the testing and ART initiation process, provide comprehensive support services, and address the issue of uneven distribution of medical resources