In vivo testing of a bioresorbable phosphate‐based optical fiber

Optical fibers have recently attracted a noticeable interest for biomedical applications because they provide a minimally invasive method for in vivo sensing, imaging techniques, deep‐tissue photodynamic therapy or optogenetics. The silica optical fibers are the most commonly used because they offer excellent optical properties, and they are readily available at a reasonable price. The fused silica is a biocompatible material, but it is not bioresorbable so it does not decompose in the body and the fibers must be ex‐planted after in vivo use and their fragments can present a considerable risk to the patient when the fiber breaks. In contrast, optical fibers made of phosphate glasses can bring many benefits because such glasses exhibit good transparency in ultraviolet‐visible and near‐infrared regions, and their solubility in water can be tailored by changing the chemical composition. The bioresorbability and toxicity of phosphate glass–based optical fibers were tested in vivo on male laboratory rats for the first time. The fiber was spliced together with a standard graded‐index multi‐mode fiber pigtail and an optical probe for in vitro pH measurement was prepared by the immobilization of a fluorescent dye on the fiber tip by a sol‐gel method to demonstrate applicability and compatibility of the fiber with common fiber optics.      

Constraints on the biological recovery of the Bohemian Forest lakes from acid stress

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Carbon footprint of rice production under biochar amendment – a case study in a Chinese rice cropping system

As a controversial strategy to mitigate global warming, biochar application into soil highlights the need for life cycle assessment before large‐scale practice. This study focused on the effect of biochar on carbon footprint of rice production. A field experiment was performed with three treatments: no residue amendment (Control), 6 t ha^?1 yr^?1 corn straw (CS) amendment, and 2.4 t ha^?1 yr^?1 corn straw‐derived biochar amendment (CBC). Carbon footprint was calculated by considering carbon source processes (pyrolysis energy cost, fertilizer and pesticide input, farmwork, and soil greenhouse gas emissions) and carbon sink processes (soil carbon increment and energy offset from pyrolytic gas). On average over three consecutive rice‐growing cycles from year 2011 to 2013, the CS treatment had a much higher carbon intensity of rice (0.68 kg CO₂‐C equivalent (CO₂‐C_e) kg^?1 grain) than that of Control (0.24 kg CO₂‐C_e kg^?1 grain), resulting from large soil CH₄ emissions. Biochar amendment significantly increased soil carbon pool and showed no significant effect on soil total N₂O and CH₄ emissions relative to Control; however, due to a variation in net electric energy input of biochar production based on different pyrolysis settings, carbon intensity of rice under CBC treatment ranged from 0.04 to 0.44 kg CO₂‐C_e kg^?1 grain. The results indicated that biochar strategy had the potential to significantly reduce the carbon footprint of crop production, but the energy‐efficient pyrolysis technique does matter.     

Purine nucleoside-mediated protection of chemical hypoxia-induced neuronal injuries involves p42/44 MAPK activation

Hypoxia in brain may lead to cell death by apoptosis and necrosis. Concomitant is the formation of purine nucleosides, e.g. adenosine, a powerful endogenous neuroprotectant. Despite vigorous studies, many aspects of the mechanisms involved in purine-based protection are still unclear. In this study, we wanted to investigate the effect of purine nucleosides on cellular responses to chemical hypoxia. O(2)-sensitive neuronal pheochromocytoma (PC12)-cells, which are widely used as a model system for sympathetic ganglion-like neurons, were subjected to chemical hypoxia induced with rotenone, an inhibitor of mitochondrial complex I. Adenosine and its relatives guanosine and inosine were tested for their neuroprotective capability to improve neurite outgrowth and viability. In addition, cell lysates were analyzed for mitogen-activated-protein-kinases (MAPK) activation by anti-active and anti-total MAPKinase immunoblotting. Adenosine, guanosine and inosine significantly inhibited the loss of viability after hypoxic insult. In combination with NGF, purine nucleosides also partially rescued neurite outgrowth. The MEK-1/-2 inhibitor PD098059 inhibited purine nucleoside-mediated protection up to 85.23% and also markedly decreased neurite formation induced by NGF and purine nucleosides in hypoxic cells. Immunoblot analysis revealed a strong activation of MAPKinase upon incubation of cells with adenosine, guanosine or inosine. In combination with NGF an additive effect was observed. Results suggested that activation of the MAPKinase pathway plays a vital role in purine nucleoside-mediated protection of neuronal cells following hypoxic insult.     

Monospecific inhibitors show that both mannan-binding lectin-associated serine protease-1 (MASP-1) and -2 Are essential for lectin pathway activation and reveal structural plasticity of MASP-2

The lectin pathway is an antibody-independent activation route of the complement system. It provides immediate defense against pathogens and altered self-cells, but it also causes severe tissue damage after stroke, heart attack, and other ischemia reperfusion injuries. The pathway is triggered by target binding of pattern recognition molecules leading to the activation of zymogen mannan-binding lectin-associated serine proteases (MASPs). MASP-2 is considered as the autonomous pathway-activator, while MASP-1 is considered as an auxiliary component. We evolved a pair of monospecific MASP inhibitors. In accordance with the key role of MASP-2, the MASP-2 inhibitor completely blocks the lectin pathway activation. Importantly, the MASP-1 inhibitor does the same, demonstrating that MASP-1 is not an auxiliary but an essential pathway component. We report the first Michaelis-like complex structures of MASP-1 and MASP-2 formed with substrate-like inhibitors. The 1.28 Å resolution MASP-2 structure reveals significant plasticity of the protease, suggesting that either an induced fit or a conformational selection mechanism should contribute to the extreme specificity of the enzyme.     

Subcellular localization of components of the dystrophin glycoprotein complex in cultured retinal muller glial cells

The dystrophin glycoprotein complex (DGC) is a membrane-associated protein complex binding extracellular matrix (ECM) molecules, such as laminin and forming a bridge towards the cytoskeleton. The molecular composition of the DGC is cell type dependent and it is involved in cell adhesion and motility. Here we present immunocytochemical localization of beta-dystroglycan, the central member of the DGC, utrophin and Dp71f, the spliced 71 kDa dystrophin protein product of the DMD gene, in cultured retinal Muller glial cells. It is shown that beta-dystroglycan and utrophin are colocalized in clusters in all parts of Muller cells including the lamellipodium and leading edge of migrating cells. As a contrast, Dp71f labels are distinct from beta-dystroglycan and confined to the perinuclear cytoplasm of Muller cells indicating that Dp71f is not a member of the DGC in cultured Muller cells.     

Identification of an X-chromosomal locus and haplotype modulating the phenotype of a mitochondrial DNA disorder

Mitochondrial DNA (mtDNA) mutations are a major cause of human disease. A large number of different molecular defects ultimately compromise oxidative phosphorylation, but it is not clear why the same biochemical defect can cause diverse clinical phenotypes. There is emerging evidence that nuclear genes modulate the phenotype of primary mtDNA disorders. Here, we define an X-chromosomal haplotype that interacts with specific MTND mutations to cause visual failure in the most common mtDNA disease, Leber hereditary optic neuropathy. This effect is independent of the mtDNA genetic background and explains the variable penetrance and sex bias that characterizes this disorder.     

DNA-free recombinant SV40 capsids protect mice from acute renal failure by inducing stress response, survival pathway and apoptotic arrest

Viruses induce signaling and host defense during infection. Employing these natural trigger mechanisms to combat organ or tissue failure is hampered by harmful effects of most viruses. Here we demonstrate that SV40 empty capsids (Virus Like Particles-VLPs), with no DNA, induce host Hsp/c70 and Akt-1 survival pathways, key players in cellular survival mechanisms. We postulated that this signaling might protect against organ damage in vivo. Acute kidney injury (AKI) was chosen as target. AKI is critical, prevalent disorder in humans, caused by nephrotoxic agents, sepsis or ischemia, via apoptosis/necrosis of renal tubular cells, with high morbidity and mortality. Systemic administration of VLPs activated Akt-1 and upregulated Hsp/c70 in vivo. Experiments in mercury-induced AKI mouse model demonstrated that apoptosis, oxidative stress and toxic renal failure were significantly attenuated by pretreatment with capsids prior to the mercury insult. Survival rate increased from 12% to >60%, with wide dose response. This study demonstrates that SV40 VLPs, devoid of DNA, may potentially be used as prophylactic agent for AKI. We anticipate that these finding may be projected to a wide range of organ failure, using empty capsids of SV40 as well as other viruses.