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| 1 | Lipopolysaccharide inhibits or accelerates biomedical titanium corrosion depending on environmental acidity显示文摘Titanium and its alloys are routinely used as biomedical implants and are usually considered to be corrosion resistant under physiological conditions. However, during inflammation, chemical modifications of the peri-implant environment including acidification occur. In addition certain biomolecules including lipopolysaccharide(LPS), a component of Gram-negative bacterial cell walls and driver of inflammation have been shown to interact strongly with Ti and modify its corrosion resistance. Gram-negative microbes are abundant in biofilms which form on dental implants. The objective was to investigate the influence of LPS on the corrosion properties of relevant biomedical Ti substrates as a function of environmental acidity. Inductively coupled plasma mass spectrometry was used to quantify Ti dissolution following immersion testing in physiological saline for three common biomedical grades of Ti(ASTM Grade 2, Grade 4 and Grade 5). Complementary electrochemical tests including anodic and cathodic polarisation experiments and potentiostatic measurements were also conducted. All three Ti alloys were observed to behave similarly and ion release was sensitive to p H of the immersion solution. However, LPS significantly inhibited Ti release under the most acidic conditions(p H 2), which may develop in localized corrosion sites, but promoted dissolution at p H 4–7, which would be more commonly encountered physiologically.The observed pattern of sensitivity to environmental acidity of the effect of LPS on Ti corrosion has not previously been reported. LPS is found extensively on the surfaces of skin and mucosal penetrating Ti implants and the findings are therefore relevant when considering the chemical stability of Ti implant surfaces in vivo. | Fei Yu Owen Addison Stephen J Baker Alison J Davenport | 2015 | International Journal of Oral Science2015，7，3： | 5 |
| 2 | Dying by fire: noncanonical functions of autophagy proteins in neuroinflammation and neurodegeneration显示文摘Neuroinflammation and neurodegeneration are key components in the establishment and progression of neurodegenerative diseases including Alzheimer's Disease(AD). Over the past decade increasing evidence is emerging for the use of components of the canonical autophagy machinery in pathways that are characterized by LC3 lipidation yet are distinct from traditional macro-autophagy. One such pathway that utilizes components of the autophagy machinery to target LC3 to endosomes, a process termed LC3-associated endocytosis(LANDO), has recently been identified and regulates neuroinflammation. Abrogation of LANDO in microglia cells results in a propensity for elevated neuroinflammatory cytokine production. Using the well-established 5 xFAD model of AD to interrogate neuroinflammatory regulation, impairment of LANDO through deletion of a key upstream regulator Rubicon or other downstream autophagy components, exacerbated disease onset and severity, while deletion of microglial autophagy alone had no measurable effect. Mice presented with robust deposition of the neurotoxic AD protein β-amyloid(Aβ), microglial activation and inflammatory cytokine production, tau phosphorylation, and aggressive neurodegeneration culminating in severe memory impairment. LANDO-deficiency impaired recycling of receptors that recognize Aβ, including TLR4 and TREM2. LANDO-deficiency alone through deletion of the WD-domain of the autophagy protein ATG16 L, revealed a role for LANDO in the spontaneous establishment of age-associated AD. LANDO-deficient mice aged to 2 years presented with advanced ADlike disease and pathology correlative to that observed in human AD patients. Together, these studies illustrate an important role for microglial LANDO in regulating CNS immune activation and protection against neurodegeneration. New evidence is emerging that demonstrates a putative linkage between pathways such as LANDO and cell death regulation via apoptosis and possibly necroptosis. Herein, we provide a review of the use of the autophagy machinery in non-canonical mechanisms that alter immune regulation and could have significant impact in furthering our understanding of not only CNS diseases like AD, but likely beyond. | Alexis D.Rickman Addison Hilyard Bradlee L.Heckmann | 2022 | Neural Regeneration Research2022，17，2： | 3 |
| 3 | Chronic peripheral inflammation: a possible contributor to neurodegenerative diseases显示文摘The contribution of chronic peripheral inflammation to the pathogenesis of neurodegenerative diseases is an outstanding question. Sustained activation of the peripheral innate and adaptive immune systems occurs in the context of a broad array of disorders ranging from chronic infectious diseases to autoimmune and metabolic diseases. In addition, progressive systemic inflammation is increasingly recognized during aging. Peripheral immune cells could potentially modulate the cellular brain environment via the secretion of soluble molecules. There is an ongoing debate whether peripheral immune cells have the potential to migrate into the brain under certain permissive circumstances. In this perspective, we discuss the possible contribution of chronic peripheral inflammation to the pathogenesis of age-related neurodegenerative diseases with a focus on microglia, the resident immune cells of the brain parenchyma. | Patrick Süβ Addison J.Lana Johannes C.M.Schlachetzki | 2021 | Neural Regeneration Research2021，16，9： | 3 |
| 4 | Safety testing of tebufenczide, a new molt-inducing insecticide, for effects on nontarget forest显示文摘 | Addison J A | 1996 | Soil Invertebrates Ecotoxicology and Environmental Safety1996，，33： | 2 |
| 5 | Compartment syndrome after closure of the anterolateral thigh flap donor site:a report of two cases显示文摘 | Addison PD Lannon D Neligan PC | 2008 | Ann Plast Surg2008，60，6： | 1 |
| 6 | Exponential in- creases of the brominated flame retardants, polybrominated diphenyl ethers, in the Canadian Arctic from 1981 to 2000 显示文摘 | Ikonomou M G Rayne S Addison R F | 2002 | Environmental Science & Technology2002，36，9： | 1 |
| 7 | Synthesis,structure,and spectroscopic properties of copper(Ⅱ) compounds containing nitrogen sulfur donor ligands--The crystal and molecular-structure of aqua copper(Ⅱ) perchlorate显示文摘 | Addison A W Rao T N Reeddijk J | 1984 | J Chem Soc Dalton Trans1984，1349，： | 1 |
| 8 | Safety testing of tebufenozide, a new molt - inducing insecticide,for effects on nontarget forest soil invertebrates显示文摘 | Addison J A | 1996 | Eeo- toxicology and Environmental Safety1996，33，： | 1 |
| 9 | Pyrophos-phateinhibits mineralization of osteoblast cultures by binding to-mineral,up - regulating osteopontin,and nhibiting alkaline phos-phatase activity显示文摘 | Addison WN Azari F S rensen ES | 2007 | J Biol Chem2007，282，15： | 1 |
| 10 | A novel nonlinear car-Following model显示文摘 | Addison P S Lowd J | 1998 | Chaos1998，8，4： | 1 |
| 11 | Surgical results and pathological find- ings in the oculopharyngeal dystropy syndrome 显示文摘 | Jordan DR Addison DJ | 1993 | Canadian Journal of Ophthalmology1993，28，： | 1 |
| 12 | Type- 1I collagen markers in osteoarthritis:what do they indicate? 显示文摘 | Henrotin Y Addison S Kraus V | 2007 | Curr Opin Rheumatol2007，19，5： | 1 |
| 13 | Chaotic response of a short journal bearing 显示文摘 | Brown R D Drummond G Addison P S | 2000 | Proceedings of the IMECH E Part J Journal of Engineering Tribology2000，214，4： | 1 |
| 14 | Gestational diabe tes and the offspring: Implications in the development of the car- di0renal metabolic syndrome in offspring 显示文摘 | Garcia- Vargas L Addison SS Nistala R | 2012 | Cardiorenal Med2012，2，2： | 1 |
| 15 | Optic neuropathy secondary to linezolid for multidrug-resistant mycobacterial spinal tuberculosis显示文摘 | Agrawal R Addison P Saihan Z | 2015 | Ocul Immunol Inflamm2015，23，1： | 1 |
| 16 | Localiza tion of the herpes simplex virus type 1 major capsid pro tein VP5 to the cell nucleus requires the abundant scaf folding protein VP22a显示文摘 | Nicholson P Addison C Cross A M | 1994 | J Gen Virol1994，75，5： | 1 |
| 17 | Sacral colpopexy is the preferred treatment for vaginal vault prolapse in selected patients显示文摘 | Addison WA Bump RC Cundiff GW | 1996 | J Gynecol Tech1996，2，： | 1 |
| 18 | The CXC chemokine receptor 2,CXCR2,is the putative receptor for ELR+CXC chemokine-induced angiogenic activity 显示文摘 | Addison CL Daniel TO Burdick MD | 2000 | J Immunol2000，165，9： | 1 |
| 19 | Analysis and Modeling of Traffic Flow under Variable Speed Limits 显示文摘 | HEYDECKER B G ADDISON J D | 2011 | Transportation Research Part C2011，19，： | 1 |
| 20 | Urgent and early cholecystectomy for acute gall bladder disease 显示文摘 | Addison NV | 1988 | Br J Surg1988，75，1： | 1 |
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