Recent progress in carbon-based electrochemical catalysts: From structure design to potential applications

Advances in research and development of carbon-based metal-free electrocatalysts (C-MFECs) have provided potential alternatives to precious metal catalysts for various reactions important to renewable energy and environmental remediation. This timely but critical review provides an overview of recent breakthroughs (within the past 5 years or so) on C-MFECs in all aspects, including the design and regulation of intrinsic catalytic active sites, design and synthesis of carbon composite and hybrid carbon catalysts, mechanism understanding, and potential applications in clean energy storage and energy/chemical conversion. Current challenges and future opportunities in the field of metal-free carbon electrocatalysis are also discussed to provide forward-looking opportunities for their potential applications in various catalytic processes of practical significance

CD47 blocking antibody accelerates hematoma clearance and alleviates hydrocephalus after experimental intraventricular hemorrhage

BackgroundCD47, a glycoprotein on red blood cell membranes, inhibits phagocytosis via interaction with signal regulatory protein α on phagocytes. Our previous research has demonstrated that blocking CD47 accelerates hematoma clearance and reduces brain injury after intracerebral hemorrhage. The current study investigated whether phagocytosis or erythrocyte CD47 impacts hematoma resolution and hydrocephalus development after intraventricular hemorrhage (IVH).MethodsAdult (3-month-old) male Fischer 344 rats were intraventricularly injected with 200 μl autologous blood, mixed with either CD47 blocking antibody or isotype IgG, or 200 μl saline as control. In subgroups of CD47 blocking antibody treated rats, clodronate liposomes (to deplete microglia/monocyte-derived macrophages) or control liposomes were co-injected. Magnetic resonance imaging (MRI) was used to evaluate ventricular volume and intraventricular T2* lesion volume (estimating hematoma volume). The brains were harvested after 4 or 72 h for histology to evaluate phagocytosis.ResultsIn adult male rats, CD47 blocking antibody alleviated hydrocephalus development by day 3. In addition, the CD47 blocking antibody reduced intraventricular T2* lesion and T2* non-hypointense lesion size after IVH through day 1 to day 3. Erythrophagocytosis was observed as soon as 4 h after IVH and was enhanced on day 3. Furthermore, intra-hematoma infiltration of CD68, heme oxygenase-1 and ferritin positive phagocytes were upregulated by CD47 blockade by day 3. Clodronate liposomes co-injection caused more severe hydrocephalus and weight loss.ConclusionBlocking CD47 in the hematoma accelerated hematoma clearance and alleviated hemolysis and hydrocephalus development after IVH, suggesting CD47 might be valuable in the future treatment for IVH

Mechanisms of neuroinflammation in hydrocephalus after intraventricular hemorrhage: a review

Abstract Intraventricular hemorrhage (IVH) is a significant cause of morbidity and mortality in both neonatal and adult populations. IVH not only causes immediate damage to surrounding structures by way of mass effect and elevated intracranial pressure; the subsequent inflammation causes additional brain injury and edema. Of those neonates who experience severe IVH, 25–30% will go on to develop post-hemorrhagic hydrocephalus (PHH). PHH places neonates and adults at risk for white matter injury, seizures, and death. Unfortunately, the molecular determinants of PHH are not well understood. Within the past decade an emphasis has been placed on neuroinflammation in IVH and PHH. More information has come to light regarding inflammation-induced fibrosis and cerebrospinal fluid hypersecretion in response to IVH. The aim of this review is to discuss the role of neuroinflammation involving clot-derived neuroinflammatory factors including hemoglobin/iron, peroxiredoxin-2 and thrombin, as well as macrophages/microglia, cytokines and complement in the development of PHH. Understanding the mechanisms of neuroinflammation after IVH may highlight potential novel therapeutic targets for PHH.http://deepblue.lib.umich.edu/bitstream/2027.42/173755/1/12987_2022_Article_324.pd

Lignin Pyrolysis and in Situ Hydrodeoxygenation over MoO₃: Interaction between MoO₃ and Lignin

Lignin pyrolyses and in situ hydrodeoxygenation over MoO₃ with varying lignin/MoO₃ mass ratios (L/M) at different temperatures were studied in a free-falling reactor. The presence of MoO₃ not only facilitated the depolymerization of lignin to liquid and gas products but also catalyzed the in situ hydrodeoxygenation of the resulting liquid product to phenol, both of which were further intensified with the increases of temperature and the MoO₃ amount. Negative apparent solid yield and over 100% apparent gas yield were obtained in some cases because of the reaction of MoO₃ during lignin pyrolysis. To clarify this phenomenon, detailed TG/MS, XRD, and XPS investigations on spent MoO₃ were carried out. The results indicate that Mo⁶⁺ was partly reduced to Mo⁴⁺ and Mo⁵⁺ during the lignin pyrolysis, mainly caused by the reaction with carbon from lignin rather than hydrogen from carrier gas

A timeline of oligodendrocyte death and proliferation following experimental subarachnoid hemorrhage

AimsWhite matter (WM) injury is a critical factor associated with worse outcomes following subarachnoid hemorrhage (SAH). However, the detailed pathological changes are not completely understood. This study investigates temporal changes in the corpus callosum (CC), including WM edema and oligodendrocyte death after SAH, and the role of lipocalin-2 (LCN2) in those changes.MethodsSubarachnoid hemorrhage was induced in adult wild-type or LCN2 knockout mice via endovascular perforation. Magnetic resonance imaging was performed 4 hours, 1 day, and 8 days after SAH, and T2 hyperintensity changes within the CC were quantified to represent WM edema. Immunofluorescence staining was performed to evaluate oligodendrocyte death and proliferation.ResultsSubarachnoid hemorrhage induced significant CC T2 hyperintensity at 4 hours and 1 day that diminished significantly by 8 days post-procedure. Comparing changes between the 4 hours and 1 day, each individual mouse had an increase in CC T2 hyperintensity volume. Oligodendrocyte death was observed at 4 hours, 1 day, and 8 days after SAH induction, and there was progressive loss of mature oligodendrocytes, while immature oligodendrocytes/oligodendrocyte precursor cells (OPCs) proliferated back to baseline by Day 8 after SAH. Moreover, LCN2 knockout attenuated WM edema and oligodendrocyte death at 24 hours after SAH.ConclusionsSubarachnoid hemorrhage leads to T2 hyperintensity change within the CC, which indicates WM edema. Oligodendrocyte death was observed in the CC within 1 day of SAH, with a partial recovery by Day 8. SAH-induced WM injury was alleviated in an LCN2 knockout mouse model.Lipocalin-2 deficiency attenuates corpus callosum T2 hyperintensity and oligodendrocyte death after SAH induction.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/172271/1/cns13812.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/172271/2/cns13812_am.pd

A stand-alone Co mineral deposit in northeastern Hunan Province, South China: Its timing, origin of ore fluids and metal Co, and geodynamic setting

The Hengdong cobalt (Co) deposit, located in northeastern Hunan Province of South China, is hosted by the low-grade metamorphic volcaniclastic sedimentary rocks of the early Neoproterozoic Lengjiaxi Group. The Co orebodies strictly controlled by the NE- to ENE-trending Changsha-Pingjiang deep fault zone (CPDFZ) and its secondary structures. Occurring in altered breccias and cataclasites with similar mineral assemblages, Co mineralization is characterized by zoned alteration with predominant silicification and chloritization proximal to the orebodies, and sericitization and carbonatization distal from the mineralization. The integrated field and microscope observations reveal three hydrothermal stages marked by quartz + pyrite + muscovite chalcopyrite of the early-stage mineralization (E-stage), quartz + polymetallic sulfides + chlorite of the middle stage mineralization (M - stage), and quartz + chlorite + carbonate of the late-stage mineralization (L-stage). Muscovite from both the E-stage Co-bearing altered breccia and the CPDFZ mylonite yield Ar-40-Ar-39 plateau ages of 124.7 +/- 0.6 Ma (1 sigma) and 130.3 +/- 1.4 Ma (1 sigma), respectively, indicating an early Cretaceous mineralization likely associated with the last movement of CPDFZ strike-slip shearing. The 8345 values of pyrite and chalcopyrite ranging from -1.5 to -15.9% with a majority between -7.5 and -15.9%, and the lead isotope compositions of the pyrite (Pb-206/Pb-204 = 18.156-18.761, Pb-207/Pb-204 = 15.645-15.662 and Pb-208/Pb-204 = 38.469-39.172) overlapping with those of upper crust, indicate a main crust-derived source. The chemical compositions of pyrite further indicate the ore fluids and metal Co of the Hengdong deposit are most likely linked to the meta-mafic and volcanic rocks of the Neoarchean to Paleoproterozoic Lianyunshan Group, but with a contamination by the wall rocks of Lengjiaxi Group and Lianyunshan granitoids. Fluid inclusion investigations from Hengdong deposit reveal the decreasing homogenization temperatures from similar to 250 to 320 degrees C (peak of 280-300 degrees C) at the E stage, through similar to 220-320 degrees C (peak of 270-300 degrees C) at the M stage, and to similar to 150-230 degrees C at the L stage without obviously salinity (7.0-15 wt% NaCI equiv.) changed. In the M - stage, the presence of coexisting LV inclusions and V-rich inclusions with the similar homogenization temperature, consistent with the chlorite geothermometry data, is interpreted to be the result of fluid immiscibility, which was caused by cyclic pressure release during fault-zone movement. Combined with the Late Mesozoic tectonism of South China, the present data support the Hengdong deposit formed under an extension-associated tectonic regime most likely induced by slab roll-back of the subducted Paleo-Pacific Plate during the early Cretaceous. This extensional event not only caused the reactivation of the pre-existing structures as manifested by the CPDFZ characteristic of stress transformation from compression to extension but also likely resulted in the release of large amounts of Co-bearing ore fluids from the Proterozoic or older volcanogenic rocks. When the ore fluids migrated along the CPDFZ and its secondary faults, the decompression (adiabatic cooling) of the hydrothermal fluids shifted the ore fluid to the immiscibility field, significantly reduced the degree of cobalt undersaturation, and caused cobalt to precipitate, which finally formed the Hengdong Co mineral deposit

Effects of aging on hydrocephalus after intraventricular hemorrhage

Abstract Background Hydrocephalus is a common and major complication that affects outcome after intraventricular hemorrhage (IVH). While aging impacts the occurrence of hydrocephalus in patients with IVH this and the underlying mechanisms have received little attention. The present investigation, therefore, studied the impact of aging on hydrocephalus after IVH in a rat model. Methods Young and aged (3 and 18 months old, respectively) male Fischer 344 rats had an intraventricular injection of 200 μl autologous blood or saline. Ventricular volume was estimated using magnetic resonance imaging (MRI), while ventricular wall damage, heme oxygenase-1 (HO-1) and epiplexus cell activation were quantified by histological staining and Western blot. Additionally, the impact of intraventricular iron injection was examined in young and aged rats. Results Intraventricular injection of autologous blood induced hydrocephalus in both young and aged rats but ventricular volumes were larger in aged rats compared to young rats from day 3 to day 14 followed IVH. In addition, ventricular wall damage and periventricular HO-1 upregulation were greater in aged versus young rats on day 1 after IVH. Aged rats also had more choroid plexus epiplexus cells on day 14 after IVH. Additionally, organized hematomas were observed in 23% (3/13) of aged rats but not in young rats after IVH. Organized hematomas in aged rats showed larger T2* lesions on MRI compared to rats with non-organized hematomas. Similar to the effects of IVH, intraventricular injection of iron resulted in more epiplexus cells activation and more severe hydrocephalus in aged compared to young rats. Conclusions IVH causes more severe hydrocephalus in aged compared to young rats. Enhanced ventricular wall damage, epiplexus cell activation and iron overload may contribute to this aggravated hydrocephalus development in aged animals.http://deepblue.lib.umich.edu/bitstream/2027.42/173748/1/12987_2020_Article_169.pd

Delayed Minocycline Treatment Ameliorates Hydrocephalus Development and Choroid Plexus Inflammation in Spontaneously Hypertensive Rats

Hydrocephalus is a complicated disorder that affects both adult and pediatric populations. The mechanism of hydrocephalus development, especially when there is no mass lesion present causing an obstructive, is poorly understood. Prior studies have demonstrated that spontaneously hypertensive rats (SHRs) develop hydrocephalus by week 7, which was attenuated with minocycline. The aim of this study was to determine sex differences in hydrocephalus development and to examine the effect of minocycline administration after hydrocephalus onset. Male and female Wistar–Kyoto rats (WKYs) and SHRs underwent magnetic resonance imaging at weeks 7 and 9 to determine ventricular volume. Choroid plexus epiplexus cell activation, cognitive deficits, white matter atrophy, and hippocampal neuronal loss were examined at week 9. In the second phase of the experiment, male SHRs (7 weeks old) were treated with either saline or minocycline (20 mg/kg) for 14 days, and similar radiologic, histologic, and behavior tests were performed. Hydrocephalus was present at week 7 and increased at week 9 in both male and female SHRs, which was associated with greater epiplexus cell activation than WKYs. Male SHRs had greater ventricular volume and epiplexus cell activation compared to female SHRs. Minocycline administration improved cognitive function, white matter atrophy, and hippocampal neuronal cell loss. In conclusion, while both male and female SHRs developed hydrocephalus and epiplexus cell activation by week 9, it was more severe in males. Delayed minocycline treatment alleviated hydrocephalus, epiplexus macrophage activation, brain pathology, and cognitive impairment in male SHRs