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Economics in Cooperative Culture
Latest Issue in Print (and Digital)
Free Articles Published Online
Economics in Cooperative Culture—Issue #175
Our new Communities issue on Economics in Cooperative Culture was mailed to subscribers on June 1. You can subscribe now or order a sample and we'll ship you a copy today!
Economics in cooperative culture—the focus of our Summer issue—is expressed in myriad forms. From cohousing developments to gift-economy activist camps, from spiritual communities to mobile home parks, from income-sharing communities to intentional neighborhoods, people across a wide range of economic circumstances and approaches are discovering the benefits of cooperative economics. Their stories suggest new ways of "stewarding our home" and transitioning into a more inclusive and sustainable future.
Articles Featured Online. The following articles from our current issue have been posted in our blog.
Economics in Cooperative Culture, #175 Contents by Chris Roth
Economics in cooperative culture—the focus of our Summer issue—is expressed in myriad forms.
Towards a Joyful Economics by Helen Zuman
From Gift Circles in Brooklyn to the sharing economy at an ecovillage-based collective house, the author explores practical applications of Sacred Economics.
The Gift Economy of Standing Rock by Murphy Robinson
The principles of indigenous culture informed the Water Protectors' camps: generosity, compassion, and collective survival took precedence.
Also in This Issue
- Publisher's Note—Transforming Economics by Sky Blue
- Notes from the Editor—"Stewarding Our Home": a Place for Everyone by Chris Roth
- Participatory Budgeting in an Income-Sharing Community by Adder Oaks
- Servant Leadership in Cooperative Business: Stirring It Up at East Wind Nut Butters by Sumner Nichols
- Community as Economic Engine by Laird Schaub
- Economy, Community, and Place by Lindsay Hagamen
- A New Economy: Connections of Affection by Helen Iles
- Towards a Relationship Economy at Port Townsend EcoVillage by Viki Sonntag
- Home Ownership Is Dead! Long Live the Permanent Real Estate Cooperative! by Janelle Orsi
- Mobile Home Parks: A Fast and Inexpensive Path to Cohousing by William Noel
- Business Co-ops as a Prelude to Intentional Community by Werner Kontara
- Community Is the Best Medicine: A guide to cooperative living on a disability income by Lily Silver
- Exemplars: An Introduction by Paul Freundlich
- Living Out a Gift Economy in Community with Others by Tina Dunn (with input from others in the Jesus Christian community)
- Economics and Cooperation in Community: The Ultimate Contest by Dan Schultz
- Let All Money in the World Become Everyone's Money: Towards a Society Where All People Can Share Money by Yoshifumi Nakano (called Nakanon)
- Mixing Sociability and Utility: A Recipe for Community Connection by Annie Raser-Rowland
- An Invitation to Single Men: Consider Cohousing by Carolyn Schlam
- Sunflower Cohousing en France by Martin Prosser
- How to Create New Nature Reserves by Dr. Adrian Cooper
- Creating Cooperative Culture—Together Resilient: Why This Book? Thoughts on Building Community in the Age of Climate Disruption by Sky Blue
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Since 1972, Communities has been the primary resource for information, issues, and ideas about intentional communities in North America – from urban co-ops to cohousing groups to ecovillages to rural communes. Communities now also focuses on creating and enhancing community in the workplace, in nonprofit or activist organizations, and in neighborhoods, with enhanced coverage of international communities as well. We explore the joys and challenges of cooperation in its many dimensions.
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Riley – Mamiya 645Posted: November 25, 2014 Filed under: Mamiya 645 | Tags: 120 film, Ektar 100, English Cocker Spaniel, film photography, Mamiya, medium format photography, photography 10 Comments
My loyal hunting partner, Riley.
Mamiya 645, Kodak Ektar 100
Autumn trees – Mamiya 645Posted: November 17, 2014 Filed under: Mamiya 645 | Tags: 120 film, Ektar 100, film photography, Mamiya, medium format photography, photography 4 Comments
While grouse hunting in October in northern Minnesota, I created this image of birch trees against the fall foliage by purposely panning the camera vertically hand-held. I think it was about a 1/2 sec exposure with fairly fast panning. I only shot one of these and didn't know how much blurring would occur. The resulting image has a really interesting look that is not quite what I expected, and is different than what I've gotten doing similar shots with a digital camera.
Shot with my Mamiya 645, of which I have not yet written a detailed review. Nice camera though. Info to come.
Shot on Kodak Ektar 100, developed and scanned by Precision Camera (see previous post). The image below is a crop of part of the same image to show the detail of the very interesting and pleasing blur. I could probably crop a whole series of interesting images from this one shot.
While I'm at it, why not crop in tighter to show you the film grain captured in the scan:
Another Nordeast stroll with the Rolleicord IIIPosted: November 14, 2014 Filed under: Rolleicord III | Tags: 120 film, Acros, black & white film, film photography, fuji film, medium format photography, photography, Rolleicord 2 Comments
OK, blog – I'm back.
Shot on Fuji Neopan Acros 100 film with the Rolleicord III.
You'll recognize this location if you've read this blog before. It's an area in NE Minneapolis where I sometimes have a little time to walk around while my son is in a class. For me this is an unbeatable location for looking for interesting shapes and compositions. A perfect way to spend an hour on a nice evening is to load up a medium format camera and walk around slowly looking for those twelve exposures to strike my eye. Having a full hour to shoot twelve exposures is a fantastic exercise in constraint, patience and focus – though when it comes to shooting film that can actually seem like a lot of shots to allow yourself in an hour.
If I'm in the mood for shooting sharp images with a camera I'm fully comfortable with, I usually find myself reaching for the Rolleicord. Of the cameras I own, it can't be beat for reliability, sharp optics, solid feel – it's a camera that builds confidence.
Developed and scanned by Precision Camera and Video in Austin, TX. This is the first time I've tried Precision, and I'm pleased with the results of the scans. The black and white scans are extremely sharp, though there are a lot of dust spots to clean up (I actually think this is good though, because I think some other shops use dust removal software that results in softer images – in many cases I'd rather do some dust spotting in Lightroom or Photoshop in exchange for the sharpest possible scan where you can really see the film grain when you zoom in). I also had them do a couple rolls of color and my initial reaction is that they're a great value for high resolution scans. I've had some experience now with several labs for developing and scanning, and I think I'll write a little post soon about my experiences and a bit of a comparison.

subset: commoncrawl


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Purpose Chemokine CX3CL1 and its receptor CX3CR1 in the lumbar spinal-cord play crucial assignments in pain handling. CFA shot. Mechanical allodynia and thermal hyperalgesia had been examined with von Frey Hargreaves and lab tests lab tests, respectively. The expressions of CX3CL1, CX3CR1 and p38 mitogen-activated proteins kinase (MAPK) had been quantified with Traditional western blots. Meropenem cell signaling The discharge of IL-1, TNF- and IL-6 were evaluated with ELISA. Recombinant CX3CL1 or control IgG had been after that injected through intrathecal catheters in the EA-treated CFA model rats. The behavioral checks, p38 MAPK activation and cytokine launch were then evaluated. Results EA significantly inhibited inflammatory pain induced by CFA for 3 days. In the mean time, EA downregulated the manifestation of CX3CL1 but not CX3CR1 in the lumbar spinal cord of the CFA rats. Besides, activation of p38 MAPK and the launch of pain-related cytokines (IL-1, IL-6 and TNF-) were inhibited by EA. Intrathecal injection of CX3CL1 mainly reversed the analgesic effect of EA treatment and re-activated p38 MAPK signaling, and resulted in pro-inflammatory cytokines increase in acupuncture-treated rats. Summary Our findings indicate that EA alleviates inflammatory pain via modulating CX3CL1 signaling in lumbar spinal Meropenem cell signaling cord, revealing a potential mechanism of anti-nociception of EA in inflammatory pain. 0.05 vs CFA+EA, em P /em 0.01 vs CFA+EA; n=10 in each group. Abbreviations: CFA, total Freunds adjuvant; EA, electroacupuncture. EA treatment suppressed the cleavage of CX3CL1, but not the manifestation of CX3CR1 In order to transmit biological signals, CX3CL1 combines with its receptor CX3CR1 after cleaving from neuronal membrane into a soluble form. We used Western blot to analyze the effects of CFA and EA on CX3CL1 cleavage. On the 1st day after the modeling, CFA led to a rapid upregulation of CX3CL1 content material in lumbar spinal RDX cord ( em P /em 0.05 vs Control), while both EA and sham EA reversed this effect (Number 3A). Three days after modeling, CX3CL1 manifestation in CFA group further improved ( em P /em 0.01 vs Control); while EA treatment still kept the level of CX3CL1 as low as Control ( em P /em 0.01 vs CFA), sham EA no longer suppressed CX3CL1 expression ( em P /em 0.01 vs CFA+EA, Number 3B). The manifestation of CX3CR1, however, was not affected by either CFA injection or EA treatment at two time points (Number 3C Meropenem cell signaling and ?andD),D), indicating that CX3CL1 instead of CX3CR1 could be the regulative target for EA treatment in CFA-induced pain model. Open in a separate windowpane Number 3 Manifestation of CX3CL1 and CX3CR1 in the lumbar spinal cord. Notes: (A) The manifestation of CX3CL1 in CFA group improved 1 day after modeling. (B) The CX3CL1 level in CFA group was upregulated significantly, but decreased to be as low as the Control in CFA+EA group at day time 3 after modeling, sham EA did not prevent upregulation of CX3CL1 at day time 3. (C and D) The manifestation of CX3CL1 receptor CX3CR1 was not affected by CFA or EA treatment. * em P /em 0.05 vs Control, ** em P /em 0.01 vs Control; ## em P /em 0.01 vs CFA; em P /em 0.01 vs CFA+EA; n=6 in each group. Abbreviations: CFA, total Freunds adjuvant; EA, electroacupuncture; GAPDH, glyceraldehyde-3-phosphate dehydrogenase. EA treatment reversed the CFA-increased p38 MAPK phosphorylation and cytokines launch p38 MAPK and cytokines are crucial in the downstream of CX3CL1/CX3CR1 signaling pathway and perform important tasks in pain modulation. As the Western blot analyses illustrated, the total amounts of p38 MAPK did not show any difference among four groups at 24 and 72 hrs after CFA modeling (Figure 4A). However, as seen in Figure 4B, the phosphorylation of p38 MAPK was significantly elevated in CFA group at 72 hrs after modeling ( em P /em 0.01 vs Control), but went back to the control level after EA treatment at 72 hrs ( em P /em 0.01 vs CFA). Unlike EA treatment, sham EA did not prevent p38 MAPK from activating, the expression of Meropenem cell signaling phosph-p38 MAPK markedly increased in CFA+sham EA group ( em P /em 0.01 vs CFA+EA). Open in a separate window Figure 4 EA blocks the activation of p38 MAPK and the release of cytokines in spinal cord. Meropenem cell signaling Notes: (A) The total amount of spinal cord p38 MAPK was not changed by either CFA modeling or real/sham EA treatments. (B) CFA activated the phosphorylation of p38 MAPK on the first and third day after modeling, EA inhibited the activation of p38 MAPK at day 3 after modeling, sham EA failed to suppress p38 MAPK activation at day 3. (CCE) EA suppressed the release of pro-inflammatory cytokines (IL-1, IL-6, TNF-) on the day 3 after CFA injection, sham EA exerts no effect on suppressing cytokine release. * em P /em 0.05 vs Control, ** em P /em 0.01 vs Control; ## em P /em 0.01 vs CFA; em P /em 0.01 vs CFA+EA; n=6 in each group. Abbreviations: p38 MAPK, p38 mitogen-activated protein kinase; phosph-p38 MAPK, phosphorylated p38 MAPK; CFA, complete Freunds adjuvant; EA, electroacupuncture. The ELISA assay further demonstrated that at 3 days after modeling, CFA led to an.
We describe a strategy for analyzing axonal transport of cytosolic proteins
We describe a strategy for analyzing axonal transport of cytosolic proteins (cps) using photoactivatable GFppaGFpwith modifications of standard imaging components that can be retroactively fitted to a conventional epifluorescence microscope. h, during which period several axons could be analyzed and imaged. these methods ought to be easy to look at by most laboratories and could also be helpful for monitoring cp motion in additional cell types. Intro Almost all proteins inside a neuron are synthesized in the perikarya and transferred into axons and synapses via axonal transportation. Transported cargoes consist of membranous organelles, cytoskeletal CPs and elements. Early pulse-chase MCC950 sodium cost radiolabeling research showed that, although membranous organelles had been transferred in an interest rate course known as fast axonal MCC950 sodium cost transportation quickly, cytoskeletal and cytosolic (or soluble) proteinsdefined right here as proteins without membrane-spanning or membrane-anchoring domainsmoved with prices that were many purchases of magnitude slower in an organization called sluggish axonal transportation (evaluated in refs.1,2). CPs are conveyed while discrete radiolabeled waves that are transported more than times within long axons slowly; this motion can be incompatible with diffusion, which decays more than time3C6 exponentially. This rate course of sluggish axonal transport can be called sluggish component-b (or SCb). Although radiolabeling research characterized the entire nature of transportation, the motion could not become visualized by these procedures. With advancements in live imaging, axonal transportation of discrete vesicles and specific cytoskeletal polymers was visualized, resolving many mechanistic information on this movement7C9. However, in the case of cytosolic cargoes, their inherent solubility precluded visualization of their overall dynamics, and molecular mechanisms dictating the transport of cytosolic cargoes remained poorly defined. We recently resolved the transport behavior of CPs by tagging them with photoactivatable vectors and visualizing the kinetics of the population by live imaging10. In this protocol, we describe the experimental and other technical details of this strategy. These methods use imaging components that can be easily attached to a conventional epifluorescence microscope and that involve simple image analysis MCC950 sodium cost tools MCC950 sodium cost that can be adopted by most laboratories. Although our concentrate is on sluggish axonal transportation of CPs, in rule, these methods may be used to visualize/analyze the flexibility of CPs in virtually any cell type with a comparatively toned morphology (Ptk-2 cells, for example) plus they can also be helpful for biophysical research of diffusion within different cellular compartments. Assessment with other strategies These research had been originally influenced by tests from Anthony Browns lab FSCN1 (Ohio State College or university) that visualized the axonal transportation of neurofilaments. The writers used a typical setup (without dual source of light illuminator), as well as the photoactivation and visualization had been sequential, separated with a few mere seconds11. Even though the sequential imaging set up referred to by Trivedi (EXFO X-cite), which includes an ultrastable DC light. 7. Attach a high-speed shutter to obtain pictures after photoactivation (we make use of Wise Shutter). 8. Assemble the filtration system wheel using the GFP excitation filtration system (HQ 480/40). That is detached through the GFP filtration system cube. Inside our case, we only use two positions within this wheeleither the GFP filtration system throughout a photoactivation test or an open up placement when imaging some other wavelength. Therefore, extremely high-speed switching can be unnecessary (we make use of an Olympus filtration system steering wheel U-FWR). 9. Put in a neutral denseness filtration system (we make use of Zeiss ND filter systems) in the filtration system slider (given IX2-RFAW). We typically decrease the event light to 12%. As mentioned above, the strength of the event light is additional reduced by ~20% while going right through the IX2-RFAW prism. 10. Assemble the revised GFP cube the following; this is an adjustment of a typical off-the-shelf GFP cube arranged (U-"type":"entrez-nucleotide","attrs":"text message":"N41001″,"term_identification":"1164599″,"term_text message":"N41001″N41001, Chroma). Initial, detach the excitation filtration system as well as the dichroic reflection. Place the excitation filtration system in the filtration system wheel inside the visualization insight pathway (discover Stage 8). Replace the typical dichroic reflection (Q505lp, Chroma) using the T495pxr (Chroma). The emission filtration system (HQ535/50) remains the same. Make sure that the filter systems/dichroics are oriented appropriately. Remember that optical parts are manufactured with accuracy, and extreme.
Supplementary MaterialsWangJBC2005Sup. feature of the Golgi apparatus in most eukaryotic cells
Supplementary MaterialsWangJBC2005Sup. feature of the Golgi apparatus in most eukaryotic cells is the stack of flattened cisternal membranes with dilated rims (1). The major functions of the Golgi apparatus are thought to be modification Bibf1120 kinase inhibitor and sorting of newly synthesized membrane and secretory proteins and lipids. The ordered structure of this organelle is thought to reflect the requirement for the enzymes and sorting machinery to be compartmentalized to allow a specific series of modifications and sorting reactions to be carried out (2). The mechanism that organizes Golgi cisternae into stacks is usually, as a result, of central importance to understanding Golgi working. Proteins involved with stacking Golgi cisternae had been first discovered using cell-free assays that mimicked the cell cycle-dependent disassembly and reassembly from the Golgi equipment (3). Termed Golgi reassembly stacking protein (GRASPs),1 they consist Bibf1120 kinase inhibitor of Knowledge65 (4) and Knowledge55 (5), the quantity discussing their obvious molecular mass (in kDa) on SDS-PAGE. Antibodies to GRASPs inhibited the restacking of produced cisternae recently, as do soluble types of these protein, but didn't have an effect on the reformation from the cisternae themselves. Knowledge65 was implicated in cisternal stacking displays the area framework of Knowledge65 also, which comprises an N-terminal Knowledge area (the schematic tag potential phosphorylation sites. the schematic tag caspase-3 cleavage sites. and purified sequentially on amylose or glutathione columns accompanied by a nickel column (in each set), or the invert (in each set). Equal levels of proteins from each purification stage had been examined by immunoblotting for Knowledge65 or the label. Remember that, in and and (6). Dynal beads had been covered with different Knowledge65 fragments by cross-linking and incubated in the current presence of interphase or mitotic cytosols. Representative pictures for some from the constructs are proven in Fig. 4and quantitation for every one of the constructs is proven in Fig. 4and and above schematics at above schematics at or acquired no effect on the ability of GRASP65 to oligomerize (Fig. 5and = quantity of cell profiles counted). Note that the GRASP domain name inhibits fragmentation during mitosis but only when localized to the Golgi by the N-terminal myristoylation transmission. and and and data not shown) or quantitative (Fig. 6with and data (Figs. 3 and ?and4)4) suggesting that the lack of mitotic regulation of the GRASP domain name helps prevent the breakdown and dispersal of Golgi fragments during mitosis. Conversation Through mapping experiments we have been able to dissect the GRASP65 protein into two functional domains. The N-terminal, or GRASP domain name, is usually a dimer that is involved in trans-oligomerization. The C-terminal, or SPR domain name, regulates this trans-oligomerization through phosphorylation by mitotic kinases. In the absence of the SPR domain name, the GRASP domain name forms trans-oligomers, but these are not mitotically regulated. Beads coated with the GRASP domain name still aggregate but cannot be broken up by mitotic kinases. Cells stably expressing the GRASP domain name have bigger mitotic Golgi clusters during mitosis, again, consistent with a lack of mitotic regulation. Perhaps the most intriguing and unexpected result is usually Bibf1120 kinase inhibitor that GRASP65 dimers form higher order oligomers more efficiently when the regulatory SPR domain name is removed (Fig. 3, and and supplemental Fig. 1). Hence, in glycerol gradients, the full-length GRASP65 comprises a mixture of different forms, from dimers to higher order oligomers. When pooled fractions of dimers or oligomers are rerun around the gradients, the original pattern is obtained, showing that the various forms are interconvertible readily. In marked comparison, however, the Knowledge area forms oligomers with small Rabbit polyclonal to HHIPL2 proof any dimers in the gradient. Furthermore, when pooled fractions of the oligomers had been rerun in the gradient, just oligomers had been found, attesting with their stability. These oligomers were resistant to treatment with mitotic kinases also. These data therefore claim that the SPR area prevents the Knowledge area from forming steady oligomers normally. A possible cause is the have to breakdown Knowledge65 oligomers during mitosis, in order that cisternal unstacking may appear. The nature from the interaction between Knowledge area dimers may preclude immediate phosphorylation being a.
Data Availability StatementAll versions described within this ongoing function were implemented
Data Availability StatementAll versions described within this ongoing function were implemented in Python. sturdy to evolutionary reduction through mutations to both expression of specific genes, also to the network itself. This robustness points out an apparent paradox of bet-hedgingwhy will it persist in environments where natural selection necessarily functions to remove it? The structure of the underlying molecular mechanism, itself subject to selection, can sluggish the evolutionary loss of bet-hedging to ensure a survival mechanism against environmental catastrophes even when they are rare. Critically, these properties, taken together, have serious implications for the use of treatment-holidays to combat bet-hedging-driven resistant disease, as the effectiveness of breaks from treatment will ultimately become determined by the structure Avibactam manufacturer of the GP mapping. 2011), from your unicellularbacteria (Veening 2008), Avibactam manufacturer fungi (Levy 2012), or malignancy cells (Gupta 2011)through bugs (Danforth 1999; Hopper 1999), vegetation (Childs 2010), and even aspects of human being development (Tonegawa 1983). Importantly, this intercellular variance has been observed actually in homogeneous and constant environments, suggesting that aspects of organismal phenotype may be stochastically determined. In environments that fluctuate unpredictably, this phenomenon can Avibactam manufacturer serve as a survival mechanism by increasing the likelihood that at least some offspring are well-adapted to future environments. Thus, nongenetic, nonenvironmentally-driven variation in phenotypes has been termed (2011) for a discussion of what evolutionary phenomena can be considered bet-hedging]. Oscillatory environments are common in a range of ecological settings, including fluctuating climates, immuneCpathogen interactions, or cyclic hypoxia within tumors, and the range of phenotypic traits that are thought to display stochastic determination is just as broad. Bet-hedging can Avibactam manufacturer offer a survival mechanism in the event of rare catastrophic environmental change. An important clinical example is that of persister cells that arise stochastically within isogenic populations of infectious bacteria such as (Balaban 2004; Lewis 2006; Veening 2008). These cells, which constitute a small fraction of the population [? ?12004; Lewis 2006; Nikaido 2009), and are implicated in the dormancy of chronic diseases, such as tuberculosis, which can be suppressed but not eradicated (Zhang 2012). Novel treatment strategies capable of effectively killing persister cells are desperately needed, and this need will continue to grow with the increasing incidence of resistance to our presently most effective antibiotics. In cancer, bet-hedging has been minimally studied; however, a number of aspects of disease course suggest that bet-hedging mechanisms may be important for understanding how tumors evade therapy. Significant regression of tumors post-therapy leads to a period of remission, followed by the regrowth of aggressive, therapy-resistant lesions. These dynamics can be explained by the clonal model of cancer (Greaves and Maley 2012), wherein recurring drug-resistant cells are those that have stochastically Mouse monoclonal to BLK acquired resistance mechanisms through genetic mutation. However, the high frequency of tumor recurrence in many cancers suggests that therapeutic escape cannot be based solely on mutational luck. Experimental results have shown evidence of transitory resistance (Kurata 2004; Yano 2005) indicative from the lifestyle of a little drug-resistant subpopulation that re-establishes a drug-sensitive tumor cell population. Latest experiments have determined the lifestyle of such populations of tumor persister cells inside a cell type of EGFR+ nonsmall cell lung tumor (Sharma 2010), indicating that bet-hedging may are likely involved in the introduction of tumor medication level of resistance (Ramirez 2016). Therefore, a knowledge of bet-hedging in regular and irregular ((2013), aswell as others (Thattai and Vehicle Oudenaarden 2004; Leibler and Kussell 2005; Wolf 2005), possess demonstrated the selective benefit of bet-hedging strategies in stochastically fluctuating conditions mathematically. Displaying that fitness Avibactam manufacturer can be maximized when the likelihood of individuals taking particular phenotypes matches the probability of the surroundings selecting for your phenotype, so long as fluctuations aren't sluggish that version through hereditary mutation may appear sufficiently, roughly fast that no people of any phenotype may survive and reproduce. Further theoretical function by Botero (2015) considers when bet-hedging can provide a larger fitness benefit than (2009). Nevertheless, this windowpane isn't indefinite as drug-insensitive cells shall revert to a delicate condition, and likely perish in the current presence of a medication. Charlebois (2011) explored this trend through a numerical model that includes switching from a drug-insensitive to a drug-sensitive phenotype as the stochastic rest from circumstances of high to low gene manifestation. This latter.
Supplementary MaterialsS1 Table: Forward and reverse primer sequence used in the
Supplementary MaterialsS1 Table: Forward and reverse primer sequence used in the experiments. in animal and human studies. We hypothesized that AZM modulates post-MI inflammation and enhances cardiac recovery. Methods and results Male WT mice (C57BL/6, 6C8 weeks aged) were treated with Rabbit Polyclonal to SSTR1 either oral AZM (160 mg/kg/day) or automobile (control) beginning 3 days ahead of MI and continuing to time 7 post-MI. We noticed a significant decrease in mortality with AZM therapy. AZM-treated mice demonstrated a significant reduction in pro-inflammatory (Compact disc45+/Ly6G-/F4-80+/Compact disc86+) and upsurge in anti-inflammatory (Compact disc45+/Ly6G-/F4-80+/Compact disc206+) macrophages, lowering the pro-inflammatory/anti-inflammatory macrophage ratio in the heart and peripheral blood vessels as evaluated by stream immunohistochemistry and cytometry. Macrophage adjustments were connected with a substantial drop in boost and pro- in anti-inflammatory cytokines. Mechanistic tests confirmed the power of AZM to change macrophage response towards an anti-inflammatory condition under hypoxia/reperfusion tension. Additionally, AZM treatment was connected with a distinct reduction in neutrophil count number because of apoptosis, a known indication for moving macrophages on the anti-inflammatory phenotype. Finally, AZM treatment improved cardiac recovery, scar tissue size, and angiogenesis. Bottom line Azithromycin has a cardioprotective function in the first stage post-MI through attenuating irritation and improving cardiac recovery. Post-MI treatment and individual translational research are warranted to examine the healing applications of AZM. Launch Acute myocardial infarction (MI) is certainly a leading reason behind mortality and morbidity under western culture [1]. MI provokes a deep coordinated inflammatory response, an activity mediated by inflammatory bone tissue marrow (BM) and peripheral bloodstream (PB) cells, which includes been from the advancement of end stage center failure (HF), a frequent problem post-MI [1] extremely. The peri-infarct area demonstrates dynamic mobile changes with the infiltration of various inflammatory cells including neutrophils, monocytes, and macrophages [2]. Monocytes infiltrate the peri-infarct zone and differentiate into macrophages, which play an important role in the initial inflammatory as well as the following reparatory phases [3]. Two dominant patterns of macrophage activation are found: pro-inflammatory/classically activated macrophages (M1-like) and anti-inflammatory/alternatively activated/reparative macrophages (M2-like), with different cell markers and DAPT biological activity gene expression profiles [2]. In mice, the initial exaggerated inflammatory response may actually confer long-term harm because reductions in the initial recruitment of inflammatory monocytes reduce infarct size and prevent adverse cardiac remodeling [4, 5]. Pro-inflammatory macrophages trigger inflammation, damage of extra cellular matrix (ECM) [6], production of reactive oxygen/ nitrogen species and pro-inflammatory cytokines (IL-6, TNF-, and IL-1) [7]. In contrast, DAPT biological activity anti-inflammatory macrophages promote ECM repair, angiogenesis, and production of anti-inflammatory cytokines (IL-4, IL-10, and IL-13) [8, 9]. Azithromycin (AZM), a clinically approved macrolide antimicrobial agent, has an excellent security profile in humans [10]. AZM modulates the inflammatory response through macrophage polarization towards reparative state [11, 12], as exhibited in models of inflammation and tissue injury such as spinal cord injury [13], lung contamination [14], and stroke [15]. In these clinically relevant scenarios, AZM reduces the production of pro-inflammatory cytokines (IL-6 and IL-12) and increases that of anti-inflammatory cytokines (IL-10) [12]. Additionally, AZM significantly decreased the expression of iNOS and pro-inflammatory macrophage receptor (CCR7) while increasing arginase activity and anti-inflammatory macrophage receptors (MR and CD23) [12]. In an ischemic stroke model, which induces a similar sterile inflammatory response to MI, AZM shifted macrophages from your pro-inflammatory to the reparative state leading to inhibition of blood brain barrier injury and improvement in neurological recovery [15]. Similarly, in a retinal ischemia/reperfusion experimental model, AZM was protective against neuronal injury. This protection was attributed to the anti-inflammatory properties of AZM, as evidenced by the reduction in MMP-9/2 expression and activity [16]. Furthermore to its immunomodulatory properties, AZM is normally DAPT biological activity well tolerated, achieves a broad therapeutic index, and provides well characterized pharmacodynamic and pharmacokinetic properties [10]. Here, we offer the first proof that AZM.
and mutations are generally and simultaneously detected in B cell malignancies.
and mutations are generally and simultaneously detected in B cell malignancies. aggressive form, distinguished by constitutive activation of the canonical NF-B transcription GSK343 novel inhibtior factor family and by poor patient survival and response to the standard treatment regimen of R-CHOP (Lenz and Staudt, 2010). NF-B transcription factors are normally activated by two important receptors for microbes on B cells, the B cell antigen receptor (BCR) and the TLRs, and serve as essential inducers of normal B cell survival, growth, and differentiation (Thome, 2004; Gerondakis and Siebenlist, 2010; Hayden and Ghosh, 2012). Somatic mutations in and occur in 39% of cases of ABC-DLBCLs, with a single L265P amino acid substitution accounting for 75% of the mutations (Ngo et al., 2011). The same mutation occurs in almost 100% of Waldenstr?m macroglobulinemia (WM), 47% of IgM monoclonal gammopathy of undetermined significance, and 3C10% of chronic lymphocytic leukemia (Puente et al., 2011; Wang et al., 2011; Treon et al., 2012; Xu et al., 2013). MYD88 is an essential cytoplasmic GSK343 novel inhibtior adaptor protein, downstream from most TLRs and the IL-1/18 receptor, required to activate the IL-1 receptorCassociated kinases (IRAKs) and NF-B (Akira and Takeda, 2004). MYD88 has two unique domains. A Toll/IL-1R domain name (TIR) promotes homotypic and heterotypic GSK343 novel inhibtior multimerization of MYD88 proteins upon recruitment to dimerized TIR domains in the cytoplasmic tail of TLRs that have been engaged by their microbial ligands (Vyncke et al., 2016). A death domain name forms a helical multimeric signaling complex known as the Myddosome comprising six MYD88 molecules, four IRAK4 molecules, and four IRAK2 molecules (Akira and Takeda, 2004; Lin et al., 2010). The mutation in the TIR area is forecasted to trigger allosteric adjustments in two binding areas and provides been shown to market multimerization with wild-type MYD88 and spontaneous formation from the MYD88-IRAK signaling complicated, resulting in raised NF-B activity (Ngo et al., 2011; Avbelj et al., 2014; Vyncke et al., 2016). When presented into mature mouse B cells by retroviral transduction, is enough to start T and mitogen cell indie B cell proliferation that's terminated after many cell divisions, partly by reviews inhibition of NF-B (Wang et al., 2014). Recently, a mouse model bearing a conditional allele continues to be described to build up lymphoproliferative disease with periodic change into clonal lymphomas (Knittel et al., 2016). Conversely, knockdown of MYD88 kills ABC-DLBCL cell lines, establishing these tumors are dependent on MYD88 activation for success (Ngo et al., 2011). Somatic mutations in take place in 21% of ABC-DLBCLs (Davis et al., 2010). Compact Dynorphin A (1-13) Acetate disc79B and Compact disc79A associate with membrane immunoglobulin noncovalently, portion as the signal-transducing subunits from the BCR via an immunoreceptor tyrosine-based activation theme (ITAM) in the Compact disc79B and Compact disc79A cytoplasmic tails (Reth and Wienands, 1997). Upon antigen binding, both tyrosines in each ITAM are phosphorylated by LYN and various other SRC-family GSK343 novel inhibtior kinases, offering a docking site for the matched SH2 domains of SYK, activating SYK, and initiating the intracellular signaling cascade (Cambier et al., 1994). 85% of mutations alternative the 1st ITAM tyrosine residue at position 196 (Y196) to another amino acid, most frequently histidine (Davis et al., 2010). Unlike mutations, ITAM mutations do not spontaneously activate NF-B in ABC-DLBCL cell lines (Lenz et al., 2008; Davis et al., 2010). Instead, ITAM mutations cause elevated surface BCR expression, probably by inhibiting Lyn-mediated receptor internalization, resulting in higher surface BCR manifestation on ABC-DLBCLs but not in additional tumors absent for mutations (Davis et al., 2010). In mice having a targeted mutation substituting alanine in place of both tyrosine residues in the CD79B ITAM, the mature B cells displayed more BCRs on their surface, had delayed BCR internalization after antigen binding, and experienced exaggerated BCR signaling to calcium, extracellular signal-regulated kinase (ERK), and AKT but normal signaling to NF-B (Gazumyan et al., 2006). Consequently, it is speculated the likely part of mutation in the pathogenesis of ABC-DLBCL is definitely by permitting B cells to respond inappropriately to BCR activation by foreign or self-antigens (Rui et al., 2011). However this hypothesis remains to be tested experimentally. One third of ABC-DLBCLs bearing the mutation also have.
Background Influenza A disease mutates rapidly, making antiviral vaccines and therapies
Background Influenza A disease mutates rapidly, making antiviral vaccines and therapies directed against virus-encoded focuses on ineffective. viral proteins, such as for example oseltamivir, zanamivir, rimantadine and amantadine, have been certified for treatment of influenza [1]. Nevertheless, as influenza disease undergoes mutation extremely quickly and may evolve medication level of Mouse monoclonal to HER-2 resistance, the antiviral drugs can become ineffective during a flu outbreak [2,3]. Recently, host factors exploited by influenza virus have attracted increasing interest because therapeutics targeting these cellular factors may inhibit viral replication independent of the antigenic properties of the virus. Therefore, identification of host factors required for viral replication and development of anti-viral agents targeting host factors is a promising strategy for reducing the viral resistance [4-6]. Recently, several research groups have identified a variety of host cell factors that are important for influenza virus replication by using genome-wide RNA interference screenings in conjunction with other integrative genomics strategies [7-11]. These findings provide a global view of the cellular processes that are exploited by influenza viruses and highlighted potential targets which may be used in antiviral research. The influenza A virus genome is composed of eight segments of negative-sense, single-stranded RNA, which encodes 11 proteins [10]. Hemagglutinin (HA) and neuraminidase (NA) are critical for viral entry and release, respectively, and viral polymerase, composed of three subunits, PA, PB1, and PB2, is responsible for replication and transcription. Following initial interaction of its HA with its N-acetylneuraminic (sialic) acid receptor on the cell surface, the virus enters the cell by receptor-mediated endocytosis. Upon endosomal acidification, the HA protein undergoes conformational changes and WIN 55,212-2 mesylate kinase inhibitor mediates fusion between the viral envelope and endosomal membrane. The acidic environment of the endosome also triggers the disassembly of the viral core and the release of the viral ribonucleoprotein (vRNP) into the cytoplasm [12]. The vRNPs are then rapidly imported WIN 55,212-2 mesylate kinase inhibitor into the nucleus to catalyze viral genome replication and RNA transcription [13]. Subsequently, newly formed vRNPs, in association with other viral proteins are exported into the cytoplasm and transported to the cell membrane for budding and launch. Transcriptional profiling reveals a variety of sponsor factors had been induced upon influenza pathogen infection [14]. These viral inducible elements might play important or inhibitory jobs in the viral lifecycles, such as for example viral admittance, vRNP trafficking, transcription, viral set up and budding [9]. Nevertheless, the function and regulatory systems of the sponsor factors remains unfamiliar mainly. We here record a sponsor element, lysosome-associated membrane glycoprotein 3 (Light3) WIN 55,212-2 mesylate kinase inhibitor is mixed up in post-entry phases of influenza A pathogen infection. We discovered that Light3 was up-regulated upon influenza A pathogen infection significantly. Knockdown of Light3 manifestation by RNA disturbance inhibits viral replication in the first stage, recommending that WIN 55,212-2 mesylate kinase inhibitor LAMP3 might perform a significant role in influenza existence cycles. Results Light3 can be induced upon influenza A pathogen infection Influenza A virus infection induces multiple host gene expression. Interestingly, many of the up-regulated host factors appear to function by facilitating virus replication [9]. To investigate the dynamic host gene profile upon influenza A virus infection response, we used DNA microarray technology to determine global mobile mRNA amounts at different period factors post viral disease. Quickly, A549 cells had been contaminated with influenza A/PR/8/34 pathogen at a multiplicity of disease (MOI) of 0.5. After that, total RNA had been ready at 4 h, 12 h, 24 h, and 48 h post-infection (p.we.), and had been put through global gene manifestation evaluation by microarray potato chips (Capitalbio human being genome oligo array assistance, data not demonstrated). Notably, Light3, known as DC-LAMP also, TSC403 or Compact disc208 [15], was discovered to become being among the most upregulated genes significantly. Upon A/PR/8/34 pathogen infection, Light3 mRNAs had been activated a 45.2 fold at 24 h p.we., and a 34.7 fold at 48 h p.we., respectively (Shape ?(Figure1A).1A). However, the mRNA degrees of two additional Light protein family, LAMP1 and LAMP2, were not altered at any time points indicated, suggesting that LAMP3 may be specifically stimulated by viral contamination. To confirm the gene chip data, we used RT-PCR to detect the mRNA level of LAMP1, LAMP2, and LAMP3 at different time points post influenza A virus infection. Consistently, LAMP3, but not LAMP1 and LAMP2, is significantly induced upon influenza A virus infection (Physique ?(Figure1B).1B). Finally, we decided the protein.
Supplementary Materials [Supplementary Data] ddp262_index. formation assists tethering preceding membrane fusion.
Supplementary Materials [Supplementary Data] ddp262_index. formation assists tethering preceding membrane fusion. By increasing this scholarly research to four additional known COG-deficient individuals, we present the 1st comparative evaluation on problems in transportation right now, golgi and glycosylation ultrastructure in these individuals. The noticed biochemical and structural abnormalities correlate with the severe nature from PR-171 kinase inhibitor the mutation, with the COG4 mutant being the mildest. All together our results indicate that intact COG complexes are required to maintain Golgi dynamics and its associated functions. According to the current CDG nomenclature, this newly identified deficiency is designated CDG-IIj. INTRODUCTION The Golgi apparatus is an important relay station in the secretory pathway as it plays a pivotal role in targeting proteins and lipids to distinct post-Golgi compartments (1). During transit through the Golgi apparatus, most of the newly synthesized secretory and membrane-bound proteins undergo major modifications, mainly involving different types of glycosylation. One of these, polarity (3). A tightly regulated organization of transport is required in order to mediate cargo transit as well as to maintain the organization. The exact mechanism of this transit is still not clarified, though it will most be a mix of the vesicular transportation model most likely, which implicates set cisternae with vesicles moving cargo ahead and recycling escaped protein to previously cisternae or the ER (4C7) as well as the cisternal maturation model. In the second option model, the cisternae mature PR-171 kinase inhibitor for the gene coupled with a PR-171 kinase inhibitor deletion for the maternal allele. Tests performed upon this patient's fibroblasts yielded identical defects albeit much less severe as within the cells from the previously referred to COG-deficient individuals. Furthermore, we present an up to date overview of the various mutations identified so far where we try to correlate for the very first time the respective medical phenotypes with the severe nature in glycosylation and trafficking problems as well much like the Golgi integrity using transmitting electron microscopy (TEM). Our Gata6 evaluation underscores the high need for an intact COG complicated in both intra-Golgi trafficking as well as the maintenance of the standard morphology from the Golgi apparatus. Furthermore, we provide novel insights in the steady-state localization of both full and partial complexes with implications on the action mechanism of the complex. With this study, the number of patients harbouring mutations in individual COG genes rises to ten, which is about one-third of the total number of CDG-II cases in which a mutation has been identified making mutations one of the most frequent causes of CDG-II. Furthermore, given the insights that the different individual research possess generated on COG complicated working and development, we are actually at a spot where a assessment of most mutant subunits along different requirements reveals more particular or even while yet unknown features of not merely the full complicated, but of different subunits and subcomplexes also. RESULTS Hereditary and molecular evaluation of COG4 The recognition of many CDG type II sufferers harbouring mutations in specific subunits from the octameric COG complicated fostered a solid fascination with the functional function this Golgi tethering complicated has in the glycosylation procedure. By immediate sequencing from the genes within a cohort of unsolved CDG-II sufferers, we determined a novel individual carrying a apparently homozygous C T stage mutation at placement 2185 in the genomic DNA encoding the gene (Fig.?1A). The mutation had not been discovered after sequencing of over 100 alleles of the randomly chosen Western european control population. On the proteins level, this mutation changes an extremely conserved arginine 729 (Fig.?1B) right into a tryptophan residue (p.R729W). Open up in another window Body?1. Hereditary and molecular characterization of the described COG4 patient. (A) Sequencing revealed a heterozygous C T missense mutation in the patient and the absence of this mutation in the mother. The fluorescence hybridization (FISH) image shows the deletion of fosmid G24P85580E2 (red) around the maternal allele, whereas the control subtelomeric 16q fosmid (green) shows a normal signal. A schematic representation of the mutations present in the patient is usually given, PR-171 kinase inhibitor the green and red asterisk around the maternal allele indicate, respectively, the last heterozygous SNP and the first hemizygous SNP in the patient, the black asterisk around the paternal allele indicates the position of the missense mutation, green regions indicate genes ( ? : sense/ ? : antisense/bars indicate the location of each gene) and intergenic regions that are present in the patient, the white and grey regions around the maternal allele indicate, respectively, the known deleted region and the region made up of the proximal breakpoint. (B) Alignment of the COG4 sequence of different species shows an absolute conservation of this residue..
Background Appendiceal malignancies are uncommon and contain carcinoid, mucocele, pseudomyxoma peritonei
Background Appendiceal malignancies are uncommon and contain carcinoid, mucocele, pseudomyxoma peritonei (PMP), goblet cell carcinoma, lymphoma, and adenocarcinoma histologies. situ hybridization (Seafood) or CISH]. Outcomes Profiling across all appendiceal malignancy histological subtypes for IHC exposed: 97% BRCP, 81% MRP1, 81% COX-2, 71% MGMT, 56% TOPO1, 5% PTEN, 52% EGFR, 40% ERCC1, 38% SPARC, 35% PDGFR, 35% TOPO2A, 25% RRM1, 21% TS, 16% cKIT, and 12% for TLE3. NGS exposed mutations in the next genes: 50.4% and could be considered. General, appendiceal malignancies have related patterns within their molecular profile to pancreatic malignancies (can we state this, any statistical evaluation done?) and also have differential manifestation from colorectal malignancies. These findings show the necessity to assess patient examples for patterns in marker manifestation and alteration, to be able to better understand the molecular biology and formulate a customized treatment approach in these hard to treat malignancies (supported with a give from Caris Existence Sciences). (HER-2/CEP17 probe; HER-2/CEP17 percentage 2.2 was considered Necrostatin 2 S enantiomer supplier amplified), (EGFR/CEP7 probe EGFR/CEP7 percentage 2, or 15 EGFR copies per cell in 10% of analyzed cells was considered amplified), (Best2/CEP17 probe; Best2A/CEP17 percentage 2.0 was considered amplified), (cMET/CEP7 probe; cMET/CEP7 percentage 5 was regarded as amplified). and position had been more recently examined by chromogenic hybridization (INFORM HER-2 Dual ISH DNA Probe Cocktail; commercially obtainable cMET and chromosome 7 Drill down probe; Ventana), and utilized the same rating system for FISH. Mutational evaluation Sanger sequencing Before the option of CLIA qualified NGS, mutation evaluation by Sanger sequencing included chosen parts of genes and was performed through the use of M13-connected PCR primers made to amplify targeted sequences. PCR items had been bi-directionally sequenced using the BigDye Terminator v1.1 chemistry, analyzed using the 3730 DNA Analyzer (Applied Biosystems). Series traces had been examined using Mutation Surveyor software program v3.25 (Soft Genetics). Up coming era sequencing (NGS) Direct series evaluation was performed on genomic DNA isolated from FFPE tumor examples using the Illumina MiSeq system. Typical sequencing depth was 1,000. Particular parts of 47 genes had been amplified using the Illumina TruSeq Amplicon Malignancy Hotspot panel. Total info on thresholds and particular reagents can be found at: http://www.carismolecularintelligence.com (20). The variant contact was predicated on nomenclature described from the ACMGG. Mutations had been defined as medically actionable if the mutation was one that there can be an authorized agent open to focus on, actually if the agent is definitely authorized to get a different tumor type, aswell as any medical trial predicated on that alteration. Statistical evaluation The patient human population and profiling data had been characterized using regular descriptive statistics. When you compare data over the subtypes, organizations with significantly less than five instances were not regarded as. For chemotherapy proteins biomarkers, overexpression or reduction in at least 60% of examples in a specific subtype had been considered medically significant (mean chosen as cutoff). Outcomes The instances had been classified into histologic subtypes, making use of info in pathology reviews and following pathology overview of H&E slides, ahead of evaluation of molecular SCK patterns in the test outcomes. Nearly all instances had been adenocarcinomas, at 57% [317] of the full total instances (hybridization An individual neuroendocrine case was determined with a rise in EGFR duplicate quantity, out of 43 instances examined. No amplifications had been identified in Best2A (n=24), HER2 (n=246), or cMET (n=194) (data not really demonstrated). Gene sequencing Patterns in most the genomic modifications had been different across subtypes. The adenocarcinomas got higher rate of recurrence of modifications in in comparison to all the subtypes (and modifications. Modifications in the PI3 kinase pathway (modifications in PMP. mutations had been determined in 3 of 8 adenocarcinomas examined. Notably, additional targetable mutations had been found in specific instances, including three cKIT mutations (two mucinous and one neuroendocrine), an mutation, and a mutation. Desk 3 Rate of recurrence of genomic modifications (either Sanger or following era sequencing) by histologic subtype. Genes without mutations determined in hot areas interrogated included: and mutations (65%, 47%, and 83%, respectively, in comparison to just 9% in neuroendocrine and 7% in signet band cell adenocarcinomas). Notably all subtypes, aside from PMP, harbored mutations. Just mucinous adenocarcinomas harbored mutations, in support of mucinous adenocarcinomas and adenocarcinomas harbored mutations (a restricted number of instances had been examined). mutations had been bought at a considerably higher percent in adenocarcinomas, in comparison to all the subtypes (P 0.001), and was found between Necrostatin 2 S enantiomer supplier 5C10% in three subtypes (Mucinous, adenocarcinoma, and signet band) rather than in two subtypes (neuroendocrine and PMP). While was bought at 22% in adenocarcinomas, Necrostatin 2 S enantiomer supplier it had been discovered at 10% in every subtypes. mutations had been discovered in 8% of adenocarcinomas, in 2% of mucinous adenocarcinomas rather than identified in virtually any various other subtypes. Debate Molecular profiling of appendiceal malignancies suggests several treatment options. Remedies based on the IHC appearance of these protein in appendiceal adenocarcinomas are the usage of 5-FU (low TS) which may be coupled with irinotecan (because of high TOPO1). Gemcitabine (low RRM1) along with taxanes such as for example paclitaxel, albumin-bound paclitaxel, docetaxel.
Background MicroRNAs (miRNAs) regulate a whole lot of physiological and pathological
Background MicroRNAs (miRNAs) regulate a whole lot of physiological and pathological procedures, including myocardial ischemia/reperfusion. siRNA-Smad7. Summary Inhibiting miR-92a can attenuate myocardiocyte apoptosis induced by hypoxia/reoxygenation by focusing on as a focus on for miR-92a. Appropriately, we also analyzed the possible participation of in the protecting actions of miR-92a. Components and Strategies Cell Tradition The H9c2 cells (ventricular myocardiocyte, rat in source; Cell Bank from the Chinese language Academy of Sciences, Shanghai, China) had been seeded at a denseness of 2104 cells/cm2 in 6-well plates and cultured in Dulbeccos altered Eagles moderate (DMEM, Sigma, St. Louis, MO, USA) made up of 10% (v/v) fetal bovine serum (FBS, HyClone, Logan, UT, USA) inside a humidified atmosphere of 95% air flow and 5% CO2 at 37C. Transient Transfection with Oligonucleotides Transfection was completed using Lipofectamine 2000 (Invitrogen, Carlsbad, CA, USA). The percentage of oligonucleotide vs. the Lipofectamine 2000 transfection reagent was 15. MiR-92a imitate, inhibitor and matched up unfavorable control (NC) had been synthesized by GenePharma, Shanghai, China. For RNA disturbance, cells had been transiently transfected having a siRNA particular for or NC (GenePharma). All buy 1032823-75-8 transfections had been completed after 12-h serum hunger, and lasted for 48-h before the H/R tests. H/R in H9c2 Cardiomyocytes Hypoxia was induced by revealing the cells to 1% O2, 94% N2, and 5% CO2 for 24 h utilizing a modular incubator (Model 3131, Forma Scientific, Marietta, OH, USA). Reoxygenation (95% air flow, 5% CO2, 37C) lasted for 12 h. Cells under normoxia through the entire tests had been included like a control. All tests had been repeated 3 x. Quantitative Real-time Polymerase String response (qRT-PCR) Total RNA was extracted using Trizol reagent (Invitrogen). Bulge-loop miRNA qRT-PCR primer units (one RT primer and a set of qRT-PCR primers for every set) particular for miR-17, miR-18a, miR-19a, miR-20a, miR-19b and miR-92a had been created by RiboBio (Guangzhou, China). MiRNAs had been change transcribed using the stem-loop RT primer. The primers for Smad7 had been also created by RiboBio. qRT-PCR was completed to examine the manifestation of particular miRNAs or mRNA on the Rotor-Gene 3,000 real-time DNA recognition system (Corbett Study, Sydney, Australia) using SYBR Green (Qiagen, Shanghai, China). All examples had been analyzed in triplicate. Gene manifestation was dependant on comparing the info against the typical curve, and normalized against U6. Dedication of Cell Damage and Apoptosis Structural integrity of cultured H9c2 cardiomyocytes was examined by calculating the focus of lactate dehydrogenase (LDH) and malonaldehyde (MDA) in the tradition press by ELISA using a computerized biochemical analyzer (Model 7150, Hitachi, Tokyo, Japan). Apoptosis was recognized by annexinV-FITC/propidium iodide (AV/PI) dual staining (Bender MedSystems, Burlingame, CA, USA). DNA Constructs and Reporter Gene Assays To examine whether miR-92a regulates the manifestation of 3-UTR. For luciferase reporter tests, the 3UTR from the gene was amplified by PCR from rat genomic DNA and cloned into psiCHECK-2 (Promega) between your missing the putative miR-92a binding series buy 1032823-75-8 was used like a mutated control. 293T cells had been co-transfected with psiCheck2 made up of the 3-UTR as well as the miR-92a imitate using Lipofectamine 2000 (Invitrogen). Co-transfection with non-targeting unfavorable control RNA was performed like a control. The buy 1032823-75-8 cells had been harvested 24 h buy 1032823-75-8 after transfection for luciferase activity utilizing a dual luciferase reporter assay package (Promega) on the luminometer (Lumat LB9507). Immunocytochemistry Cultured H9c2 cardiomyocytes had been set in 4% paraformaldehyde and permeabilized with 0.1% Triton. Cells had been clogged with 3% BSA and incubated with 1000-collapse diluted main antibody against SMAD7 (ab90085; Abcam; Cambridge, MA, USA) over night, and stained with fluorochrome- conjugated supplementary antibody for another 60 min. Cells had been installed in Vectashield mounting moderate made up of 4,6-diamidino-2-phenylindole (DAPI) to visualize nuclei. Pictures had been captured utilizing a fluorescence laser beam scanning confocal microscope (FV1000, Olympus, Tokyo, Japan). Traditional western Blotting Assays Cells had been gathered in RIPA lysis buffer (Bioteke Co, Beijing, China) made up of 1 mM phenylmethylsulfonyl fluoride and centrifuged at 12,000g for 15 min at 4C. Entire cell lysate was utilized for SMAD7 recognition. Cytosolic and nuclear fractions Angpt1 had been prepared using regular nuclear and cytoplasmic removal reagents (Thermo Scientific, Rockford, IL, USA). Proteins concentration was assessed using the Bio-Rad technique. Examples (20 g proteins) had been separated by 10% SDS-PAGE and used in a nitrocellulose membrane. The membranes had been clogged with 5% nonfat dairy in TBST buffer (100 mM.


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Metal Sonic (Project M)
License: MIT
Game Version: Project M
Downloads: 2,659
Followers: 3
Version 3.0 for Project M Project M
Released on 2016-11-02
Balances and buffs. (See video below) Slightly polished models. Changed NAirSpecial to what it should've been.
Version 2.0 for Project M Project M
Released on 2016-06-08
- Revamped Metal Sonic models + Classic Metal Sonic (alt)
- Updated cosmetics and SFX for BrawlEx.
- New Fair, DownTilt, Dair, and DashJab. the rest of the moves are tweaked.
- Better spot-dodge and fallspeed.
- "Easter egg" on Classic Metal Sonic. (Hint: winpose)
- Fully optimized for Subspace Emissary.
Version 1.1 for Project M Project M
Released on 2016-03-26
- BrawlEx compatible files added.
- New Neo Metal Sonic model by Nibroc-Rock for Final Smash & All-Star Trophy only.
- Slightly polished Metal Sonic & fanchars paletteswaps, along with better CSP/CSS/BPs.
- Majority of the moves have been tweaked and nerfed a bit. (See UpSpecial)
- Better Wavedashing and Dash-Dancing added.
- New Classic Mode ending screens for Brawl and PM. (Wolf replacement version)
- Third jab's A+Y and A+B is now Up+A and Down+A.
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text:
- This event has passed.
"Meet the Telescopes" with the Astronomy Volunteers
September 27, 2019 @ 1:30 pm - 3:00 pmFree
Learn about different types of telescopes and the advantages of each design. Acadia Astronomy Volunteers will be available to introduce you to the scopes.
Weather dependent. Check our Facebook page for information on cancellations due to weather.


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Power Shell is an initial attack for Koopas. It can attack all ground enemies with the same attack power as Shell Toss. This move is only available to the player as normal enemy Koopa Troopas cannot perform this move. Kooper is the original owner who starts off with this ability. Though, as of Paper Mario: The Thousand-Year Door, a new Koopa introduced known as the Shady Koopa can perform it while it's flipped over. Koopley, the father of Koops, mentions on teaching this ability to his son to after Hooktail was defeated when the player revisits Petalburg later in the game. Though he finds out a little after his dialogue that Koops already knew how to use it before the events of raiding Hooktail Castle.
Notable Koopas who can perform Power ShellEdit
- Kooper
- Kent C. Koopa
- Koops
- Shellshock (or Shady Koopa. Only when flipped on his back.)
- Koopley (Possibly)


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Blue Badge Discover Manchester Walk
Come and join in, it's absolutely FREE! Here at Social Circle we make it our business to offer you the best of what Manchester has to offer. Our selection of walks enable tou to come along and explore this great city, and meet new people in Manchester along the way.
A pub romp through politics and Manchester on Karl Marx's birthday. Lots of Engels and Marx in the city but much more too. Ends with the Champagne Socialist quiz.
*Please check website for updated times and meeting points as they are subject to change*
"Manchester Guided Tours are the largest and friendliest group of official tour guides in the city! Let us show you Manchester's hidden gems and secret corners. Our knowledgable and professional guides will bring Manchester's fascinating past to life".


text: About Lisa: Lisa Ephraim started in the BME Program at UConn in 2006 and as an Academic Advisor for Biomedical Engineering students in 2007. Lisa earned her BA in Psychology from Eastern Connecticut State University. She advises all levels of undergraduates including Honors students and Pre-Medical/Pre-Dental students. She also assists the BME Department with a variety of Undergraduate Program duties including admissions, promotion of BME activities, scholarships, course scheduling, etc. She gains great satisfaction from advising her students and helping them become successful in industry and graduate school. She is also the Advisor for the UConn student chapters of Global Brigades and MEDLIFE.


text: Welcome to the Jungle. The purpose of the small claims court system is to allow people to resolve their disputes themselves without paying the fees of an attorney. The rules of small claims courts are different from county to county in Indiana, and sometimes from township to township. In some situations, the system works well and individuals are able to obtain a fair result. In others, individuals feel lost or overwhelmed by the court process, especially if the other party is represented by an attorney. Any business organization is required to be represented by an attorney if the matter in controversy involves over $1,500. My advice is to at least speak to an attorney before your scheduled hearing to decide whether you should proceed on your own, and if so, how to do so.


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Shillong 17 th August 2016: The Shillong Sports Association is delighted to confirm that Gionee, one of the world's top mobile phone manufacturers, will be the principal sponsor for the 2016 edition of Meghalaya's leading football competition.
The Shillong Premier League will now be known as the Gionee Shillong Premier League and the first match will kick off on 18 th August with 8 teams competing this year namely, Langsning SC, MLP FT, Malki Sports Club, Nangkiew Irat, Nongkrem FC, Royal Wahingdoh FC, Rangdajied United FC, and Shillong Lajong FC. Team Captains of all the teams were present in a press conference which was organised in the city today.
The first match will be played between Nongkrem and Meghalaya Police on 18 th August at 3:30PM while the defending Champions of the League, Shillong Lajong FC will play their first game on the 22 nd August against Rangdajied United FC.
Speaking on the new season, SSA General Secretary Mr.B.Diengdoh said, "I am very pleased that Gionee has come on board as the main sponsor this year of the Shillong Premier League. The support from Gionee will surely benefit the growth of football in the state of Meghalaya. I would like to wish all the participating teams all the very best for the league and I expect a very high quality competition this year."
Founded in 2002 with a determination to pursue professionalism and innovation, Gionee has already partnered with two exciting sports teams in India – top flight football club Shillong Lajong FC (since 2014-15) and Indian Premier League T20 cricket franchise Kolkata Knight Riders (since 2015) – and the association with the Gionee Shillong Premier League will provide an avenue for the growth of football in Meghalaya.
As a further indication of its commitment to the uplift of sports in the North East and country as a whole, Mr. Nomit Joshi, AGM Marketing, Gionee said, "Shillong Premier League is a popular contested football tournament that resonates with our target audience. Football is a way of life for the people of North East and we plan to be partners in this journey with them. Plus this is a natural extension of our existing association with the premier club of the North East – Shillong Lajong FC. Wishing everyone involved with the league the very best of luck. I personally look forward to watching a few games soon."


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[19 Jun 2015 | Friday]
Fear Not, 25
~ The Widow in Zarephath Knew Peace ~
God does not want His children living in fear. "Grace and peace be multiplied to you in the knowledge of God and of Jesus our Lord, as His divine power has given to us all things that pertain to life and godliness, through the knowledge of Him who called us by glory and virtue" (2 Peter 1:2-3).
"Fear not," or its equivalent, is recorded many times in Scripture—ALN will post one "fear not" each week during this calendar year.
This Week's Verse ~ "And Elijah said to her [a widow in Zarephath], 'Do not fear; go and do as you have said, but make me a small cake from it first, and bring it to me; and afterward make some for yourself and your son. For thus says the Lord God of Israel: "The bin of flour shall not be used up, nor shall the jar of oil run dry, until the day the Lord sends rain on the earth"'" (1 Kings 17:13-14).
The Foundation Of Peace ~ "The Lord is my light and my salvation; whom shall I fear? The Lord is the strength of my life; of whom shall I be afraid" (Psalm 27:1).
The Solution If You Lack Peace ~ "Great peace have those who love Your law, and nothing causes them to stumble" (Psalm 119:165). "You will keep him in perfect peace, whose mind is stayed on You" (Isaiah 26:3). "Be anxious for nothing, but in everything by prayer and supplication, with thanksgiving, let your requests be made known to God; and the peace of God, which surpasses all understanding, will guard your hearts and minds through Christ Jesus" (Philippians 4:6-7).
Summary ~ "No Christ = No Peace" versus "Know Christ = Know Peace"
~ Robert Lloyd Russell, ABUNDANT LIFE NOW
(1) The current TOP 10 ALN posts are listed at the very bottom of this home page.
(2) There is an INDEX of all ALN posts accessed by scrolling down the left column.
(3) You may LINK to any ALN posts on your own blog or website.
(4) You may COPY any ALN post, but please credit ALN as the source by prominently displaying the following statement: Reprinted from "Abundant Life Now," a free blog which offers inspiring moments, thought-provoking comments, and solid Biblical insight at http://RobertLloydRussell.blogspot.com/ .


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Professional-beauty tools manufacturer Olivia Garden has launched its free Hair Brush Guide App, which allows users to find the brush that matches their hair's length, type, texture and/or desired hairstyle.
The Olivia Garden Hair Brush Guide App—marketed as a first of its kind—is available in HD on iPhones, iPads and Androids.
Once users download the app, they're prompted for their hair type, whether straight, wavy or curly. Using curly hair as an example, the next prompt inquires about the user's hair thickness, such as thick/coarse, regular or fine. Next, it prompts for hair length, either short, medium or long. The user is then prompted to enter the desired hairstyle: straight, volume/soft curls, updo, detangling or touch-up. The final prompt supplies the suggested Olivia Garden brush based on the collected input.
"We are excited to launch our new Hair Brush Guide App," says Anne Maza, vice president of sales and marketing for Olivia Garden. "This revolutionary app makes it easy for consumers to identify the brush that is ideal for their specific hair type and desired hairstyle. It takes the guesswork out of picking the No. 1 must-have tool in your beauty arsenal."
[Image courtesy of Olivia Garden]


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United States District Court, D. Maine
June 30, 2018
CALEB B., Plaintiffv.NANCY A. BERRYHILL, Acting Commissioner of Social Security, Defendant
H. Rich III United States Magistrate Judge
plaintiff challenges an administrative law judge's
("ALJ's) finding that, for purposes of his Social
Security Disability ("SSD") and Supplemental
Security Income ("SSI") claims, he was not
disabled prior to April 16, 2015, and seeks remand on the
basis of the submission of evidence that he argues is new and
material, see Motion To Remand on Behalf of
Plaintiff [] ("Motion for Remand") (ECF No. 24)
and, in the alternative, on the basis that the ALJ erred in
evaluating both the medical opinion evidence and his
statements concerning his symptoms and limitations,
see Itemized Statement of Specific Errors
("Statement of Errors") (ECF No. 15) at 6-13. For
the reasons that follow, I conclude that the evidence that
the plaintiff proffers is neither new nor material and that
the ALJ committed no reversible error in weighing the opinion
evidence or in assessing the plaintiff's statements.
Hence, I recommend that the court deny the Motion To Remand
and affirm the commissioner's decision.
The ALJ's Decision
to the commissioner's sequential evaluation process, 20
C.F.R. §§ 404.1520, 416.920; Goodermote v.
Sec'y of Health & Human Servs., 690 F.2d 5, 6
(1st Cir. 1982), the ALJ found, in relevant part, that the
plaintiff met the insured status requirements of the Social
Security Act through December 31, 2014, Finding 1, Record at
22; that, since his alleged onset date of disability, January
17, 2013, he had the severe impairments of multiple sclerosis
("MS"), cervical/lumbar degenerative disc
disease, psoriatic arthritis, major depressive disorder, and
cognitive disorder, Finding 3, id.; that, prior to
April 16, 2015, the date on which he became disabled, he did
not have an impairment or combination of impairments that met
or medically equaled the criteria of any impairment listed in
Appendix 1 to 20 C.F.R. Part 404, Subpart P (the
"Listings"), Finding 4, id.; that, prior
to April 16, 2015, he had the residual functional capacity
("RFC") to perform sedentary work as defined in
20 C.F.R. §§ 404.1567(a) and 416.967(a) except that
he could lift/carry up to 10 pounds frequently and
occasionally, sit for two hours at a time for a total of six
hours in an eight-hour workday, stand for one hour at a time
for a total of two to three hours in an eight-hour workday,
walk for 15 to 30 minutes at a time for a total of two to
three hours in an eight-hour workday, perform up to
occasional overhead reaching-pushing-pulling bilaterally and
up to occasional pushing-pulling of foot controls
bilaterally, needed a handrail for occasional climbing of
stairs, could not climb ladders/scaffolds, could occasionally
stoop, balance, and kneel, could not crouch or crawl, could
have up to occasional exposure to moving mechanical parts but
no exposure to unprotected heights or dangerous machinery,
could drive occasionally but do no commercial driving, could
have no exposure to extreme cold/heat, and had a limitation
in concentration/persistence/pace with an ability to
understand, carry out, and remember only simple tasks, and a
limitation in social functioning requiring object-oriented
tasks with only up to occasional work-related interaction
with the general public, Finding 5, id. at 23; that,
considering his age prior to April 16, 2015 (a younger
individual), education (at least high school), work
experience (transferability of skills immaterial), and RFC,
there were jobs existing in significant numbers in the
national economy that he could have performed, Findings 7-10,
id. at 27; and that he, therefore, had not been
disabled at any time through December 31, 2014, his date last
insured, for purposes of his SSD claim or at any time prior
to April 16, 2015, for purposes of his SSI claim, filed on
December 18, 2013, Finding 14, id. at 29. The
Appeals Council declined to review the decision, id.
at 1-3, making the decision the final determination of the
commissioner, 20 C.F.R. §§ 404.981, 416.1481;
Dupuis v. Sec'y of Health & Human Servs.,
869 F.2d 622, 623 (1st Cir. 1989).
Motion for Sentence Six Remand
Applicable Legal Standard
Sentence six of 42 U.S.C. § 405(g) provides:
The court may . . . at any time order additional evidence to
be taken before the Commissioner of Social Security, but only
upon a showing that there is new evidence which is material
and that there is good cause for the failure to incorporate
such evidence into the record in a prior proceeding[.]
42 U.S.C. § 405(g).
a request for a sentence six remand concerns "new
evidence . . . tendered after the ALJ decision."
Mills v. Apfel, 244 F.3d 1, 5 (1st Cir. 2001)
(citation and internal quotation marks omitted). Sentence six
allows for a "pre-judgment remand" and obviates a
ruling on the existing administrative decision based on the
existence of good cause for remanding for further evidentiary
proceedings. See, e.g., Seavey v. Barnhart,
276 F.3d 1, 13 (1st Cir. 2001); Freeman v. Barnhart,
274 F.3d 606, 610 (1st Cir. 2001).
On a
cautionary note, the First Circuit has observed that
"Congress plainly intended that remands for good cause
should be few and far between, that a yo-yo effect be avoided
- to the end that the process not bog down and unduly impede
the timely resolution of social security appeals."
Evangelista v. Sec'y of Health & Human
Servs., 826 F.2d 136, 141 (1st Cir. 1987). Thus,
prejudgment remand is only appropriate where there is good
cause for the claimant's failure to introduce the
evidence at the administrative hearing and the evidence in
question is new and "material, " as in
"necessary to develop the facts of the case
fully[.]" Id. at 139.
evidence of an infirmity or impairment is not automatically
material. The party seeking remand must show that the
evidence is not merely cumulative and that consideration of
the evidence is essential to a fair hearing, see
id.; in other words, that the earlier decision
"might reasonably have been different" had the
evidence been considered by the commissioner, id. at
140 (citation and internal quotation marks omitted). There is
a temporal concern, as well. The evidence must be material to
the issue of "the claimant's condition during the
time period for which benefits were denied[, ]" as
opposed to the development of a new disability. Tirado v.
Bowen, 842 F.2d 595, 597 (2d Cir. 1988).
plaintiff seeks a sentence six remand on the basis that,
although he requested that the ALJ incorporate his file from
a prior unsuccessful claim for disability benefits into the
record in this case, and the ALJ assured his counsel that she
had the prior file, she neither included the file in the
record nor referred to it in the instant decision.
See Memorandum of Law in Support of Motion To Remand
on Behalf of Plaintiff [] ("Remand Memo") (ECF
No. 24-1), attached to Motion To Remand, at 2-6. He appends
to his motion 243 pages of documents that he represents
constitute the prior claim file. See id. at 1; Exh.
One ("Prior Claim File") (ECF No. 24-2) to Motion
To Remand.
plaintiff contends that the prior file is both new and
material and that he has shown good cause for its omission
from the record before the ALJ. See Remand Memo at
2-6; Reply in Support of Motion To Remand on Behalf of
Plaintiff [] ("Remand Reply") (ECF No. 27) at
1-5. The commissioner disputes that any of these tests is
met. See Defendant's Response to Plaintiff's
Motion for Remand Pursuant to Sentence Six of 42 U.S.C.
§ 405(g) ("Remand Response") (ECF No. 26) at
2-8. I agree that the plaintiff has failed to demonstrate
either the newness or the materiality of the proffered
documents. Because each of these shortcomings is
independently fatal to his bid for remand pursuant to section
six, I do not reach the question of whether he has shown good
cause for the omission of the prior claim file from the
Newness of Old Claim File
As the
commissioner observes, see id. at 3, the prior claim
file is not "new" in that the documents contained
therein were considered in connection with an adverse ALJ
decision dated November 29, 2012, which became
administratively final when the plaintiff filed no appeal of
the Appeals Council's December 6, 2013, denial of his
request for review, see Record at 98-107, 113-16.
plaintiff responds that:
Because the commissioner refused to agree to his request to
supplement the record before this court with the contents of
the prior claim file, his only recourse was to file the
instant motion. See Remand Reply at 1-2 (describing
motion as "the only appropriate procedural mechanism
for requesting that the Court consider providing relief on
the basis of evidence that was presented to the ALJ
and nevertheless not considered by the ALJ or included in the
administrative record filed with the Court") (emphasis
in original).
2. The
ALJ had an affirmative duty to develop the record, and her
failure to do so requires remand. See id. at 2.
3. The
longitudinal history contained in the prior claim file was
relevant to the instant claims. See id.
None of
these arguments bears on the "newness" of the
prior claim file.
In any
event, although neither side cites caselaw for the
proposition that a prior claim file does or does not meet the
"newness" standard for purposes of a sentence six
remand, my research reveals that at least one court has
addressed the issue, concluding that it does not. In that
case, as here, the claimant contended that evidence from her
prior claim file "was wrongfully withheld from the
administrative record by the [c]ommissioner and . . .
constitutes new evidence material to the matter of her mental
retardation on this claim." Crist v. Astrue,
No. 8:06-cv-1587-T-26TBM, 2008 WL 821934, at *6 (M.D. Fla.
Mar. 26, 2008). The court rejected that argument, concluding,
"Simply stated, the records from Plaintiff's prior
claim are not 'new evidence' in contemplation of
the new evidence standard discussed above[.]").
Id. at *8. See also, e.g., Sullivan v.
Finkelstein, 496 U.S. 617, 626 (1990) ("The sixth
sentence of § 405(g) plainly describes an entirely
different kind of remand [from a sentence four remand],
appropriate when the district court learns of evidence
not in existence or available to the claimant at the time
of the administrative proceeding that might have changed
the outcome of that proceeding.") (footnote omitted)
(emphasis added). The prior claim file was both in existence
and available to the plaintiff at the time of the
administrative proceeding.
On the
showing made, the plaintiff fails to demonstrate that the
evidence was "new."
Materiality of Old Claim File
assuming that the prior claim file qualified as
"new" for purposes of sentence six, the
plaintiff's motion for remand pursuant thereto would
founder on the materiality prong of the analysis.
plaintiff argues that the claim file is material because:
1. The
ALJ relied primarily on the testimony of medical expert of
John A. Pella, M.D., at hearing on March 17, 2016, (ii) Dr.
Pella testified that, prior to April 2015, the
plaintiff's cognitive defect was
"'mild'" and "'the other
issues [we]re primarily subjective[, ]'" and (iii)
a report of a neuropsychological evaluation and testing
completed at the Brain Clinic of Central Maine ("Brain
Clinic") in April 2011, contained in the prior claim
file, provided an objective diagnosis of a cognitive disorder
and indicated that the plaintiff "'demonstrated
weaknesses and/or impairments in some aspects of mental
processing speed, complex attention skills, and sustained
attention skills.'" Remand Memo at 4-5 (quoting
Prior Claim File at Page ID ## 779-80).
2. The
ALJ gave "'little probative weight'" to
the opinions of treating neurologist James Stevenson, M.D.,
who expressly referenced the April 2011 Brain Clinic
evaluation as a basis for those opinions. Id. at 5
(quoting Record at 26).
3. The
prior claim file contained (i) May 2011 opinions of Dr.
Stevenson that were consistent with his later opinions, as
well as Dr. Stevenson's contemporaneous treatment
records, and (ii) an August 2012 opinion of treating
physician Timothy T. Goltz, M.D., that the plaintiff had
greater limitations than assessed by the ALJ, precluding the
performance of the full range of work even at the sedentary
level, as well as Dr. Goltz's contemporaneous treatment
records. See id.; see also, e.g., Prior
Claim File at 678-80 (medical source opinion (physical) of
Dr. Goltz dated August 1, ...
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text:
UiB joins Aurora network
The University of Bergen has joined the Aurora network, a pan-European university network, which has a special focus on diversity, improving teaching and the student experience.
On 21 October 2016, the Aurora network was launched in Amsterdam by nine European universitites, after an initiative by the VU University Amsterdam. The University of Bergen (UiB) is proud to be one of the founding members of this exciting new network, which aims to work for diversity in academia, improving teaching and enhancing the student experience, as well as helping to solve global challenges through research. Aurora will be a valuable addition to the other international university and student exchange networks that UiB is already a member of.
The founding of Aurora follows a 30 year old trend of establishing European university networks, which began with the Coimbra Group in 1985 and the Network of Universities from the Capitals of Europe (Unica) in 1990. This was a direct result of the initiation of European funding programmes that led to closer interaction between institutions, something which has only strengthened over the decades following.
Recent years has seen a rise in small networks, such as Universitas 21 in 1997, the League of European Research Universities (Leru) in 2002 and the Guild of Research Intensive Universities in June 2016, to which Aurora adds another dimension. This development can be attributed to the changing missions of universities during the past 15 years.


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Menu Plan for the week of June 7, 2013: Wednesday's Recipes
Pesto Pasta Salad with Grilled Chicken
Cooking time: 25 minutes for menu Cooking schedule: see below for instructions
This is a variation on the traditional Pasta with Pesto Sauce, with feta and olives giving it a bit of Greek flair.
Pesto Pasta Salad with Grilled Chicken
Total time: 25 minutes
This is not the prettiest salad, pesto usually isn't... But the taste is wonderful: the feta and Greek Olives adding just the right amount of contrast to the chicken and pasta.
- 2 chicken breasts, boneless, skinless
- Marinade for chicken breasts:
- 1 tbs Worcestershire Sauce
- 1 tbs olive oil
- 1 tbs red wine vinegar
- 1 tsp dried basil
- Pasta Salad:
- 1 1/4 cup (4.2oz, 125gr) pasta: gemelli, fusilli, penne
- 3oz (90gr) cherry tomatoes about 1/2 cup before slicing
- 3oz (90gr) feta
- 1/2 cup Greek or Kalamata olives
- 2 tbs fresh snipped chives
- Dressing:
- 2 tbs Greek or plain yogurt
- 4 tbs pesto
- 1 tbs salad olive oil
- Cook pasta according to package instructions.
- Chicken Breasts
- Mix Worcestershire, vinegar, basil and oil in a small bowl.
- Pour over chicken and allow to marinate a few minutes.
- Cut tomatoes in half.
- Cut feta into small cubes or crumble.
- Pit olives, if needed, and cut in half or thirds.
- Snip chives.
- Cook chicken, either on barbecue grill or nonstick skillet, 7 - 10 minutes per side, or until done.
- When done, remove and slice.
- To finish:
- In pasta bowl, mix pesto, oil and yogurt.
- When pasta is done drain, rinse lightly with cool water, drain well and add to pesto in bowl. Toss to coat.
- Add chicken, tomatoes, olives, feta and chives, toss gently to combine and serve.
Note: If using leftover chicken, cut into bite-size pieces and add to pasta.
Fresh Fruit
Your choice.... peaches?
Cooking schedule: 25 minutes
Pit olives if needed, cut


text:
Last Sunday, while we were watching the London Marathon on TV, I couldn't stop thinking about our last trip to London, of which I haven't told you everything yet. But, please, don't think I've forgotten about it. Of course I haven't! I have actually been editing the rest of the pictures and committed to my tumblr and instagram accounts, where you will be able to find more pictures. I know, I know! I am hung up on the photography for blogs world, which I find fascinating. I still have so much to learn…
But let's get back to the point, that is, our trip… As you were able to read, the first two days we mostly hung around Westminster, St Paul's Cathedral and the Southbank.
On the weekend, it was the markets' turn. We felt like going to Portobello, which is one of the biggest antique markets in the world, and also one of the most famous markets in London. In addition to antiques, you will also be wondering around food, clothes and many other varied stalls. To get there we decided to take a walk first through Hyde Park, from where we headed to Notting Hill. Then we took Portobello Road, from which the market takes its name. We walked the whole street, up and down, until Ladbroke Grove. And we did buy, of course we did!
In the afternoon we walked in the opposite direction, determined not to use any means of transport but our very own legs. There is nothing better than to walk, walk and walk around London. From Marble Arch we crossed along Oxford Street until we reached Oxford Circus. Then we walked around Carnaby Street and Chinatown. This was our unplanned itinerary. And this was also a soiree devoted to our friends living in London (it was so great to see you again!).
We ended up crossing the Thames River one more time and we did the Southbank walk up to London Bridge once more. But this time it was at night and through the sights of the London lights. We had dinner at Bill's Clink Street, and after that we walked back again up to Hyde Park, believe it or not. London is just such a magnificent scenery that it was worth wearing out our shoes and forget about our Oyster card.
Sunday was cloudy and rainy, but we still decided to cross Hyde Park up to Hyde Park Corner.
We discovered by chance Shepherd's Market, a very pretty and picturesque small square with a variety of boutiques, restaurants and Victorian pubs. It is very close to Piccadilly Circus, in the heart of London's Mayfair.
From Piccadilly we went up Regent Street, one of my favourite streets in London, as it is one of the first places I went to the very first time I set foot in this city. I still remember the feeling: I was astonished by its impressive architecture.
We had the typical Sunday brunch at Heddon Street Kitchen, one of Gordon Ramsay Group restaurants. I promise I will tell you about this experience very soon.
Some more shopping in Oxford Street… and back to the hotel to pick up our luggage and go back to the airport. We took the Heathrow Express from Paddington, which I hardly recommend as it makes the travel a lot shorter and quicker, but mainly thanks to the workers, because thanks to them, we were able to fly as we had left the bag which had our passports in, on the train! We are very forgetful, it's true, but I think that what happened was that we wanted to remain in England. We are comforted with the idea of coming back soon as we always manage to find the perfect excuse to be back again.


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So far 2017 has been an incredible year for Orlando in the real estate market and the sales of houses and homes. The Orlando real estate market reports and overviews all point to the same statistics and conclusions: all numbers are up and the trend will continue for the remainder of the 2017 year! The statistics show that it is a seller's market in the Orlando Metropolitan area and in every other city that comprises what is known as Central Florida: Lake Mary, Winter Park, Sanford, Clermont, Altamonte Springs, Apopka, Mount Dora, Kissimmee and Maitland. Add in the demand for houses that's currently seen in Downtown Orlando and the expanding UCF (University of Central Florida) areas and one can easily say that there has never been a better time to put your Central Florida home on the market. Sunny skies are the forecast for the rest of this year and early 2018. So let's take a look at the statistics.
2017 Statistics For Orlando Real Estate and Home Sales
Average Sale Price –
The average (or median) sale price of homes sold in Orlando over the year has risen to just under $223,000. This is an increase of roughly 10% over last year and just over 7% compared to just a couple of months ago in June of 2017. Consider these facts:?the average price of a home sold in Central Florida has increased now for 71 consecutive months. The average sale price of a house sold in Orlando is almost 93% higher than it was back in July of 2011.
It is important to note that the average sale price of a single family house was actually over $243,000. The reason that the average "home" sale was reported at $223,000 was that condominium sales were included. The price of condos sold in Orlando did also show an increase of roughly 12% to around $110,000.
Average Home Listing Price –
The average listing price in June of 2017 for a Central Florida home just a bit under $270,00. This reflects an increase of almost 8% the average home listing price a year ago (June of 2016).
Price Per Square Foot –
The average price per square foot for a home sold in Orlando was $133. This is an increase of 10% when compared to the average price per square foot just last year.
Home Sales –
According to the most recent ORRA reports, the sales of Orlando houses increased by over 8% when compared on a monthly basis to last year. As an example, June of 2017 showed a total of 3,837 houses were sold and an 8% increase when compared to June of 2016.
New Listings –
There were a total of 4,629 new homes and houses listed last month. This reflects a 10%?increase when compared to June of 2016.
New Contracts –
There were a total of 3,421 new sales contracts written on homes and houses this past June. This reflects an incredible 27%?increase when compared to June of 2016.
Pending Contracts –
Almost 5,900 pending contracts on houses were reported for June 2017. An increase of a little over 7% when compared to June of 2016.
Inventory of Orlando Houses For Sale –
The start of July 2017 showed a total listing inventory of available homes and houses for sale of 9,141. This reflects a decease of roughly -14% in comparison to the home inventory documented in June of 2016. Again, compared to June of 2016, the Central Florida market reflected over a -12% decrease in single family homes and a -22% decrease in condos for sale. However, there was an overall increase of inventory for sale of over 4% compared to the previous month (May of 2017). In other words, the inventory of available homes for sale in Orlando continued its ongoing trend but it was the smallest decrease that we've seen so far in 2017.
Selling Price vs. Listing Price –
The average home?sold in Central Florida and Orlando during July of 2017 showed that the home sold for 97.5% of its listing price. This is slightly above the 96.9% seen in June.
Interest Rate –
The average interest rate for a house purchased with a mortgage so far in 2017 is at 3.98%.
A Seller's Market Exists in Orlando and Central Florida For Homes & Houses
What do all these statistics mean to you? They show that currently the real estate market in Central Florida and Metro Orlando represent a seller's market. In fact, many realtors and experts are saying that there has never been a better environment and time to sell your house quickly and for more than ever before! With the typical home selling for almost 98% of the listing price and on the market for less than four weeks, now is the best time to place your home on the market.
Talk To Lynda First!
If you going to place your Central Florida home or your house on the market, we urge you to call Lynda Miller today at (407) 620-2924 or contact her Online now. With over 20 years of experience in the Orlando real estate market, Lynda's clients all say it best: Lynda sold their homes faster and for more money than they had anticipated.
If you are trying to decide whether or not this is the right time to list your home on the market, again we urge you to talk to Lynda Miller first.?Find out why Linda?was selected as one of Orlando's Top 100 Realtors by Orlando Magazine for 2017 for yourself. Let Lynda help you sell your home quicker and for more, as she's done for so many other satisfied home owners. There is a difference in Central Florida's realtors and Lynda truly is a Real Estate All-Star Agent!