Metal-organic framework based mixed matrix membranes: a solution for highly efficient CO2 capture?

The field of metal-organic framework based mixed matrix membranes (M(4)s) is critically reviewed, with special emphasis on their application in CO2 capture during energy generation. After introducing the most relevant parameters affecting membrane performance, we define targets in terms of selectivity and productivity based on existing literature on process design for pre- and post-combustion CO2 capture. Subsequently, the state of the art in M(4)s is reviewed against these targets. Because final application of these membranes will only be possible if thin separation layers can be produced, the latest advances in the manufacture of M-4 hollow fibers are discussed. Finally, the recent efforts in understanding the separation performance of these complex composite materials and future research directions are outlined.European Commission FP7 608490 ERC 33574

Gapped itinerant spin excitations account for missing entropy in the hidden-order state of URu2Si2

Many correlated electron materials, such as high-temperature superconductors1, geometrically frustrated oxides2 and low-dimensional magnets3, 4, are still objects of fruitful study because of the unique properties that arise owing to poorly understood many-body effects. Heavy-fermion metals5\u2014materials that have high effective electron masses due to those effects\u2014represent a class of materials with exotic properties, ranging from unusual magnetism, unconventional superconductivity and 'hidden' order parameters6. The heavy-fermion superconductor URu2Si2 has held the attention of physicists for the past two decades owing to the presence of a 'hidden-order' phase below 17.5 K. Neutron scattering measurements indicate that the ordered moment is 0.03muB, much too small to account for the large heat-capacity anomaly at 17.5 K. We present recent neutron scattering experiments that unveil a new piece of this puzzle\u2014the spin-excitation spectrum above 17.5 K exhibits well-correlated, itinerant-like spin excitations up to at least 10 meV, emanating from incommensurate wavevectors. The large entropy change associated with the presence of an energy gap in the excitations explains the reduction in the electronic specific heat through the transition.NRC publication: Ye

Exogenous Bcl-XLFusion Protein SparesNeurons After Spinal Cord Injury

Spinal cord injury (SCI) induces neuronal death, includingapoptosis, which is completed within 24 hr at and aroundthe impact site. We identified early proapoptotic tran-scriptional changes, including upregulation of proapop-totic Bax and downregulation of antiapoptotic Bcl-xL,Bcl-2, and Bcl-w, using Affymetrix DNA microarrays. Be-cause Bcl-xLis the most robustly expressed antiapop-totic Bcl-2 molecule in adult central nervous system, wedecided to characterize better the effect of SCI on Bcl-xLexpression. We found Bcl-xLexpressed robustlythroughout uninjured spinal cord in both neurons and gliacells. We also found Bcl-xLlocalized in different cellularcompartments: cytoplasmic, mitochondrial, and nuclear.Bcl-xLprotein levels decreased in the cytoplasm andmitochondria 2 hr after SCI and persisted for 24 hr. Totest the contribution of proapoptotic decreases in Bcl-xLto neuronal death, we augmented endogenous Bcl-xLlevels by administering Bcl-xLfusion protein (Bcl-xLFP)into injured spinal cords. Bcl-xLFP significantly in-creased neuronal survival, suggesting that SCI-inducedchanges in Bcl-xLcontribute considerably to neuronaldeath. Because Bcl-xLFP increases survival of dorsalhorn neurons and ventral horn motoneurons, it couldbecome clinically relevant in preserving sensory and mo-tor functions after SCI.©2005 Wiley-Liss, In

Nuclear factor-κB decoy amelioration of spinal cord injury-induced inflammation and behavior outcomes

Spinal cord injury (SCI) results in a pathophysiologycharacterized by multiple locomotor and sensory defi-cits, resulting in altered nociception and hyperalgesia.SCI triggers an early and prolonged inflammatoryresponse, with increased interleukin-1blevels. Transientchanges are observed in subunit populations of thetranscription factor nuclear factor-jB (NF-jB). Therewere decreases in neuronal c-Rel levels and inverseincreases in p65 and p50 levels. There were nochanges in neuronal p52 or RelB subunits after SCI atany time point tested. Similarly, SCI had no effect onoligodendroglial levels of any NF-jB subunit. Therewere significant early increases in COX-2 and induciblenitric oxide synthase mRNA and protein levels afterSCI. We used synthetic double-stranded ‘‘decoy’’ deox-yoligonucleotides containing selective NF-jB proteindimer binding consensus sequences. Decoys targetingthe p65/p50 binding site on the COX-2 promoterdecreased SCI-induced cell losses, NF-jB p65/p50DNA-binding activity, and COX-2 and iNOS protein lev-els. NF-jB p65/p50 targeted decoys improved earlylocomotor recovery after moderate but not severe SCI,yet ameliorated SCI-induced hypersensitization afterboth moderate and severe SCI. To determine whetherchanges in GABA activity played a role in decreasedhypersensitivity after SCI and p65/p50 targeted decoy,we countedg-aminobutyric acid (GABA)-containingneurons in laminae 1–3. There were significantly moreGABAergic neurons in the p65/p50 targeted decoy-treated group at the level of injury

The Effect of Minocycline on Motor Neuron Recovery and Neuropathic Pain in a Rat Model of Spinal Cord Injury

Objective : Minocycline, a second-generation tetracycline-class antibiotic, has been well established to exert a neuroprotective effect in animal models and neurodegenerative disease through the inhibition of microglia. Here, we investigated the effects of minocycline on motor recovery and neuropathic pain in a rat model of spinal cord injury.Methods : To simulate spinal cord injury, the rats' spinal cords were hemisected at the 10th thoracic level (T10). Minocycline was injected intraperitoneally, and was administered 30 minutes prior surgery and every second postoperative day until sacrifice 28 days after surgery. Motor recovery was assessed via the Basso-Beattie-Bresnahan test. Mechanical hyperalgesia was measured throughout the 28-day post-operative course via the von Frey test. Microglial and astrocyte activation was assessed by immunohistochemical staining for ionized calcium binding adaptor molecule 1 (lba1) and glial fibrillary acidic protein (GFAP) at two sites: at the level of hemisection and at the 5th lumbar level (L5).Results : In rats, spinal cord hemisection reduced locomotor function and induced a mechanical hyperalgesia of the ipsilateral hind limb. The expression of lba1 and GFAP was also increased in the dorsal and ventral horns of the spinal cord at the site of hemisection and at the L5 level. Intraperitoneal injection of minocycline facilitated overall motor recovery and attenuated mechanical hyperalgesia. The expression of lba1 and GFAP in the spinal cord was also reduced in rats treated with minocycline.Conclusion : By inhibiting microglia and astrocyte activation, minocycline may facilitate motor recovery and attenuate mechanical hyperalgesia in individuals with spinal cord injuries