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From the initiative of some of the world's best sailors, the Star Sailors League (SSL), launched an international circuit of regattas in January 2013. This new league has been built on the existing circuit of over 220 International Star regattas around the world, using a unified world ranking, created based on the ATP World Tour
, established by tennis players in 1972. Drawing on this inspiration from tennis, the SSL also awards substantial prize money to the best-ranked sailors.
Find out more on the Star Sailors League website here
3-7 May 2016
Hamburg, Germany
December 2016
Nassau, Bahamas
The full list of upcoming events can be found here
View the full skipper ranking here
Star Sailors League Final - America to have most competitors in Nassau
by Alex D'Agosta on 24 Nov 2013
Brian Faith and Mark Menedelblatt in action Carlo Borlenghi ©
With the largest number of sailors ranked in the Star Sailors League (551), America will have the most competitors taking part in the inaugural Star Sailors League Final, hosted by the Nassau Yacht Club, 3-8 December.
Mark Mendelblatt (15th) with Brian Fatih (13th) are the SSL Ranking leader in the stars and stripes contingent. They will fight hard against fellow American and former Star World Champion, George Szabo (19th) who will be racing with Craig Moss (29th), and Augie Diaz (16th) together with John von Schwarz (15th). These three well known teams will also face two unexpected wild-card entries: the youngest in the SSL Final fleet, Tomas Hornos (39th) with his crew Joshua Revkin (138th), and the sailing celebrity Paul Cayard together with Austin Sperry (37th). Mark Strube (32th) will be crewing for Eivind Melleby.
Mark Mendelblatt, has an enviable racing record in small boats and Olympic classes and a triumph in the Louis Vuitton Cup in 2007, aboard Emirates Team New Zealand as strategist. However, Mark is still very much in love with the Star: he demonstrated it winning the 86th edition of the prestigious Bacardi Cup in Miami, ahead of Star legends, Lars Grael and Xavier Rohart. You can feel his commitment to this class in his words: 'It is very nice to be able to still sail the Star at the highest level, even though we are no longer an Olympic class. The system of using all Star regattas around the world to determine the rankings, then having the grand final, is a great way of bringing the top sailors together each year.'
Paul Cayard spent the most of his career in America's Cup, Olympic Games campaign and multiple round the world race, but the Star class has been a lifelong passion for him. Of all his sailing accomplishments, he counts his 1988 Star Class World championship, as his most prized victory. More recently Cayard represented USA in the Star Class for the 2004 Athens Olympic Games. Cayard also approved the whole format of the Star Sailors League: 'I think it is a fantastic agenda and if there is one class in our sport that should host the 'Masters' each year it is the Star Class.'
George Szabo, former Star World Champion, can't wait to sail again in the beautiful scenery of the Bahamas: 'Nassau is one of the best sailing racetracks in the world. If you like skiing moguls, you will love sailing there. The waves, scenery, people, and sailing are just fantastic.'
This unique event, chock full of champions, is also a rare opportunity for a promising young Tomas Hornos, former Snipe World Champion, to emerge among the sailing aces: 'I'm currently sailing Stars, Etchells and J70s. I think the SSL Final will be extremely competitive and with the new format it will be exciting to see how the last day unfolds. My goal is to take advantage of this opportunity and learn as much as I can from the really talented group of sailors gathered.'
Star Sailors website
If you want to link to this article then please use this URL: www.sail-world.com/116982
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Big fan of superhero and never get enough of them as home decoration. Now, you probably can add one more collection to your superhero furniture. Industrial designer Burak Doğan has designed a series of wall-mounted shelves that pay homage to beloved heroes and heroines – Superman, Captain America, Wonder Woman, and the S.H.I.E.L.D. Each has its iconic logos reproduced as eye-catching planks that have plenty of space for your favorite comics and graphic novels. However, we don't have any information about where you can purchase those shelves. Check on Burak's behance's page if you have more questions about those fancy superhero shelves.
Tag Archives: shelf design
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Microcap or Microvolume? Great price for a great play. The silence is deafening. What's the problem here? Everything else is up?
Sentiment: Strong Buy
sit tight champ
stock went up a couple of times over the past week when most biotechs were getting clobbered
this is not a high vol stock so when the shorts have to scamper you will be all smiles
This is a Biotech stock if you sell now you ain't got a clue.
Sitting on my 2000 shares and wont touch them for a while.
I'm with you, frankie.
Patience is the key. We will be rewarded in Q4 this year.
agreed looking to get in more at these levels or lower its a steal sit tight and do not add to downward pressure by selling on panic or too early!!!!


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Ozone is a pulmonary irritant known to cause oxidative stress, inflammation and tissue injury. Evidence suggests that macrophages play a role in the pathogenic response; however, their contribution depends on the mediators they encounter in the lung which dictate their function. In these studies we analyzed the effects of ozone-induced oxidative stress on the phenotype of alveolar macrophages (AM). Exposure of rats to ozone (2 ppm, 3 h) resulted in increased expression of 8-hydroxy-2′-deoxyguanosine (8-OHdG), as well as heme oxygenase-1 (HO-1) in AM. Whereas 8-OHdG was maximum at 24 h, expression of HO-1 was biphasic increasing after 3 h and 48–72 h. Cleaved caspase-9 and beclin-1, markers of apoptosis and autophagy, were also induced in AM 24 h post-ozone. This was associated with increased bronchoalveolar lavage protein and cells, as well as matrix metalloproteinase (MMP)-2 and MMP-9, demonstrating alveolar epithelial injury. Ozone intoxication resulted in biphasic activation of the transcription factor, NFκB. This correlated with expression of monocyte chemotactic protein -1, inducible nitric oxide synthase and cyclooxygenase -2, markers of proinflammatory macrophages. Increases in arginase-1, Ym1 and galectin-3 positive anti-inflammatory/wound repair macrophages were also observed in the lung after ozone inhalation, beginning at 24 h (arginase-1, Ym1), and persisting for 72 h (galectin-3). This was associated with increased expression of pro-surfactant protein-C, a marker of Type II cell proliferation and activation, important steps in wound repair. These data suggest that both proinflammatory/cytotoxic and anti-inflammatory/wound repair macrophages are activated early in the response to ozone-induced oxidative stress and tissue injury.
Ozone is a highly reactive oxidant that induces lung injury and impairs pulmonary mechanics (Uysal and Schapira, 2003). Toxicity is initiated by ozone-induced peroxidation of polyunsaturated fatty acids in membrane lipids and in lung lining fluid, resulting in the generation of reactive oxygen species, and a mixture of lipid ozonation products including lipoperoxyl radicals, hydroperoxides, malonydialdehyde, isoprostanes and alkenals such as 4-hydroxy-nonenal (Mustafa, 1990; Pryor et al., 1996; Kafoury et al., 1999; Rahman et al., 2002). These reactive products cause oxidative stress in the lung. This leads to damage to the respiratory epithelium, disruption of alveolar epithelial barrier function, edema and inflammation (Hollingsworth et al., 2007; Al-Hegelan et al., 2011).
Evidence suggests that inflammatory macrophages accumulating in the lung in response to ozone-induced injury contribute to oxidative stress and pulmonary toxicity [reviewed in (Hollingsworth et al., 2007; Laskin et al., 2011)]. Thus, following exposure to products released from ozone-injured epithelial cells, lung macrophages are classically activated to release cytotoxic/proinflammatory mediators including reactive oxygen and nitrogen species, and tumor necrosis factor-alpha (TNFα) which promote tissue injury. This is supported by findings that blocking macrophages or cytotoxic mediators they release protects against ozone-induced lung injury (Pendino et al., 1995; Cho et al., 2001; Fakhrzadeh et al., 2002; Toward and Broadley, 2002; Fakhrzadeh et al., 2004a; Fakhrzadeh et al., 2004b). Accumulating data indicate that macrophages also play a protective role following ozone-induced lung injury, clearing oxidized products and cellular debris (Ishii et al., 1998; Dahl et al., 2007). They also augment lung antioxidant activity and release mediators that suppress inflammation and initiate wound repair (Reinhart et al., 1999; Dahl et al., 2007; Backus et al., 2010). It appears that these activities are mediated by a distinct subpopulation of macrophages that is alternatively activated (Byers and Holtzman, 2011; Laskin et al., 2011). The present studies demonstrate that oxidative stress caused by inhalation of ozone leads to activation of both cytotoxic/proinflammatory and anti-inflammatory/wound repair macrophages in the lung. Moreover, their appearance overlaps suggesting that processes of tissue injury and repair are initiated early in the pathogenic response to ozone.
Female specific pathogen-free Wistar rats (200–225 g) were obtained from Harlan Laboratories (IN). Animals were housed in filter top microisolation cages and maintained on food and water ad libitum. All animals received humane care in compliance with the institution's guidelines, as outlined in the Guide for the Care and Use of Laboratory Animals, published by the National Institutes of Health. Animals were exposed in groups of 4 to ultra-pure air (Messer Gas, Allentown, PA) or 2 ppm ozone for 3 h in a whole body Plexiglas chamber. Ozone was generated from oxygen gas via an ultraviolet-light ozone generator (Gilmont Instruments, Barrington, IL) and mixed with air. Concentrations inside the chamber were monitored using a Photometric ozone analyzer (model 400E, Teledyne Instruments, City of Industry, CA).
Animals were euthanized 3–72 h after exposure to air or ozone by intraperitoneal injection of Nembutal (250 mg/kg). The lung was perfused in situ via the portal vein with 50 ml of warm (37°C) perfusion medium (25 mM HEPES, 0.5 mM EGTA, 4.4 mM NaHCO3 in HBSS, pH 7.3), followed by perfusion with Ca+2/Mg+2 -free HBSS (22 mM HEPES, 4.2 mM NaHCO3, pH 7.3) at a rate of 22 ml/min. Previous studies demonstrated that lung perfusion had no significant effect on the number of inflammatory cells in the lung (unpublished observations). For collection of bronchoalveolar lavage (BAL) fluid, the trachea was cannulated, and the lung lavaged by slowly instilling and withdrawing 10 ml cold PBS. BAL was centrifuged (300 x g, 10 min) and supernatants collected for measurement of protein content using a BCA Protein Assay kit (Pierce Biotechnologies Inc., Rockford, IL) with bovine serum albumin (BSA) as the standard. Lungs were excised and BAL cells recovered by lavage with an additional 40 ml (4 x 10 ml) of warm HBSS. Cells were combined with those recovered in the first 10 ml lavage, washed (300 × g, 10 min, 4°C) three times with HBSS containing 2% fetal bovine serum and then counted using a hemocytometer. Viability, as determined by trypan blue dye exclusion, was >98%. For cell differentials, slides were prepared using a Cytospin 4 (Shandon, Cheshire, England), and stained with Giemsa (Labchem Inc., Pittsburgh, PA). A total of 300 cells were counted by light microscopy.
Following lung perfusion, the left bronchus was clamped and the largest lobe of the lung inflated in situ via the trachea with PBS containing 3% paraformaldehyde. After 4 h on ice, the tissue was transferred to 50% ethanol. Histological sections (4 μm) were prepared and stained with hematoxylin and eosin. The extent of inflammatory changes including macrophage and neutrophil localization, alterations in alveolar epithelial barriers, and edema were assessed blindly by a board certified veterinary pathologist (Sherritta Ridgely, DVM). Images were also acquired at high resolution using an Olympus VS120 Virtual Microscopy System, scanned using VS-ASW version 2.4 software and viewed using OlyVIA version 2.4 software (Center Valley, PA). Lung sections from three rats per treatment group were evaluated.
Nuclear extracts were prepared using a kit from Active Motif (Carlsbad, CA). Five μg of nuclear protein samples were used in duplicate to quantify NFκB activity using the TransAM NFκB transcription factor assay kit (Active Motif).
Total mRNA was extracted using an RNeasy Mini kit (Qiagen, Valencia, CA). mRNA was reverse-transcribed using a High Capacity cDNA Reverse Transcription kit (Applied Biosystems, Foster City, CA) according to the manufacturer's protocol. Standard curves were generated using serial dilutions of pooled cDNA samples. Real time PCR was performed using SYBR Green PCR Master Mix (Applied Biosystems) on a 7900HT thermocycler. All PCR primers were generated using Primer Express 3.0 software (Applied Biosystems). Samples from 3 animals per treatment group were pooled for analysis and quantified relative to GAPDH mRNA expression. Forward and reverse primer sequences were Monocyte chemotactic protein (MCP)-1: CCA CTC ACC TGC TGC TAC TCA T, TCT CCA GCC GAC TCA TTG G; inducible nitric oxide synthase (iNOS): GGA TTT TCC CAG GCA ACC A, TCC ACA ACT CGC TCC AAG ATC; GAPDH: CCT GGA GAA ACC TGC CAA GTA T, CTC GGC CGC CTG CTT.
Tissue sections were deparaffinized. After antigen retrieval using citrate buffer (10.2 mM sodium citrate, 0.05% Tween 20, pH 6.0) and quenching of endogenous peroxidase with 3% H2O2 for 15 min, sections were incubated with goat serum (2–10%, room temperature, 1 h) to block nonspecific binding. This was followed by overnight incubation at 4°C with rabbit polyclonal antibody to hemeoxygenase (HO)-1 (1:200; Enzo Life Sciences, Plymouth Meeting, PA), caspase-9 (1:100; Cell Signaling (Danvers, MA), beclin-1 (1:200; Abcam, Cambridge, MA), matrix metalloproteinase (MMP)-2 (1:600; Abcam), iNOS (1:50; Santa Cruz Biotechnology Inc., Santa Cruz, CA), cyclooxygenase (COX)-2 (1: 400; Abcam), Ym1 (1:200; Stem Cell Technologies, Vancouver, Canada), pro surfactant protein (SP)-C (1:500; Millipore, Billerica, MA), or mouse monoclonal antibody to 8-hydroxy-2′-deoxyguanosine (8-OHdG) (1:500; Abcam), arginase I (1:50; BD Biosciences, Rockville, MD), galectin-3 (1:400; R & D Systems, Minneapolis, MN), or appropriate IgG controls. Sections were then incubated with biotinylated secondary antibody (Vector Labs, Burlingame, CA) for 30 min at room temperature. Binding was visualized using a Peroxidase Substrate Kit DAB (Vector Labs). Sections from three rats per treatment group were analyzed.
BAL protein (2 μg) was fractionated on 10% SDS-PAGE or 4–12% gradient Tris-bis gels (Bio Rad, Hercules, CA) and transferred to polyvinylidene fluoride membranes (PVDF, 0.45 μm pore size; Millipore, Billerica, MA). Non-specific binding was blocked by incubation of the blots for 1 h at room temperature with 5% non-fat dry milk in 0.1% TBS-T buffer (0.02 M Tris-base, 0.137 M sodium chloride, 0.1 % Tween-20). Blots were incubated overnight at 4°C with rabbit polyclonal antibody to MMP-2 (1:2000, Abcam) or MMP-9 (1:1000, Abcam). After 4 washes in 0.1% TBS-T buffer, blots were incubated with anti-rabbit (1:20,000) HRP-conjugated secondary antibody (Cell Signaling, Danvers, MA) for 1 h at room temperature. Bands were visualized using an ECL or ECL+ detection system (GE, Healthcare Bio-Science Corp, Piscataway, NJ).
All experiments were repeated at least 3 times. Data were analyzed using student's t-test; a p value of ≤0.05 was considered statistically significant.
Ozone is a potent pulmonary irritant known to cause oxidative stress (Bocci, 2006; Ciencewicki et al., 2008; Yang and Omaye, 2009). Consistent with this activity, we observed a time-related increase in the DNA oxidation product, 8-OHdG in alveolar macrophages, as well as epithelial cells, which was most notable 24 h after ozone exposure (Figure 1). Subsequently 8-OHdG levels declined. The antioxidant HO -1 also increased in alveolar macrophages following ozone exposure, however this response was biphasic, occurring initially at 3 h and then again at 48–72 h (Figure 1). Oxidative stress has been linked to necrotic cell death, as well as to apoptosis and autophagy (Kirichenko et al., 1996; Kosmider et al., 2010; Li et al., 2010; Ryter and Choi, 2010; Jin et al., 2012). Following ozone inhalation, a rapid (within 3 h) and persistent (up to 48 h) increase in expression of cleaved caspase-9 was observed in alveolar macrophages (Figure 1), suggesting initiation of stress-induced mitochondrial apoptosis (Hu et al., 2006). A persistent increase in expression of beclin-1, a marker of autophagy (Cao and Klionsky, 2007; Kang et al., 2011), was also noted. However, this response was delayed, relative to cleaved caspase-9, and not evident until 24 h post-exposure. Alveolar epithelial cell cytotoxicity was also observed after ozone intoxication, as reflected by increased protein and inflammatory cell accumulation in BAL (Figure 2). Whereas protein levels increased within 3 h and remained elevated for 48 h, cell number increased more gradually, reaching maximum levels after 24–72 h. Differential analysis revealed that the majority (>97%) of BAL cells were macrophages at all post-exposure times.
Histologic sections were next examined to further assess ozone-induced structural and inflammatory changes in the lung. Ozone intoxication resulted in neutrophilic infiltration into the lung in peribronchiolar regions, along with patchy, mild thickening of alveolar septa and increased numbers of macrophages in the tissue (Figure 3). These effects were time-related becoming most prominent 48 h after exposure.
Matrix metalloproteinases including MMP-2 and MMP-9 have been reported to disrupt tight junctions, a process thought to be important in ozone-induced alveolar epithelial damage and lung hyperpermeability (Kenyon et al., 2002; Feng et al., 2011; Triantaphyllopoulos et al., 2011). After ozone exposure, levels of MMP-2 and MMP-9 were increased in BAL at 3–24 h, and 3–12 h, respectively (Figure 4). MMP-2 expression was also observed in histologic sections in alveolar macrophages which was most notable 24 h after ozone inhalation (Figure 4).
We next analyzed the consequence of ozone-induced oxidative stress in alveolar macrophages. NF-κB is a redox sensitive transcription factor that plays a key role in regulating macrophage production of cytotoxic and proinflammatory mediators (Hanada and Yoshimura, 2002). We found that NF-κB p65 activity increased rapidly in alveolar macrophages following ozone exposure (Figure 5). This was evident within 3 h and was followed by a decrease at 6 h, and a secondary increase at 12 h which persisted for 48 h. In contrast, no significant changes were observed in alveolar macrophage NF-κB p50 nuclear binding activity.
Activation of NF-κB in macrophages culminates in the production of proinflammatory/cytotoxic proteins including MCP-1, iNOS and COX-2, each of which has been implicated in tissue injury (Zhao et al., 1998; Fakhrzadeh et al., 2002; Sung et al., 2002; Tsatsanis et al., 2006; Murugan and Peck, 2009). A marked increase in MCP-1 mRNA expression was detected in alveolar macrophages after ozone inhalation; this response was biphasic, initially peaking at 12 h and then at 72 h (Figure 6). A biphasic increase in iNOS mRNA was also evident at 6 h and 48 h post ozone exposure. This was associated with increased iNOS protein expression in alveolar macrophages, which was most notable 24 h after ozone (Figure 7). Within 3 h of ozone exposure, increased expression of COX-2 protein was also observed in alveolar macrophages; this persisted for 48 h before returning to control levels (Figure 7).
Evidence suggests that alternatively activated macrophage subpopulations play a role in suppressing inflammation and initiating wound repair after acute injury (Byers and Holtzman, 2011). Arginase-1, Ym-1 and galectin-3 are markers of alternatively activated macrophages (MacKinnon et al., 2008; Nair et al., 2009; Feola et al., 2010; Gibbons et al., 2011). A time-related increase in expression of each of these proteins was observed in alveolar macrophages following ozone inhalation (Figure 8). Interestingly, this was evident within 3 h of exposure. Whereas arginase-1 and Ym-1 positive macrophages remained prominently in the tissue for 24 h before declining, galectin-3 positive cells persisted for at least 72 h after ozone exposure; galectin-3 positive macrophages were also significantly enlarged and exhibited a foamy appearance. These markers of alternatively activated macrophages were not detectable in lung sections from control animals. The presence of alternatively activated alveolar macrophages was correlated with a rapid (within 3 h) and persistent increase in pro-SP-C expression, an indicator of Type II cell proliferation and activation, important steps in tissue repair (Figure 9).
Ozone is a highly reactive molecule that directly or indirectly through the generation of free radicals, oxidizes proteins, lipids and DNA. The resulting oxidation products, together with reactive species produced by inflammatory cells, play a key role in ozone-induced tissue injury (Mustafa, 1990; Pryor et al., 1996; Kafoury et al., 1999; Rahman et al., 2002). The present studies demonstrate that lung macrophages are highly sensitive to ozone-induced oxidative stress, developing into subpopulations displaying classically and alternatively activated phenotypes. Evidence suggests that these macrophage subpopulations play distinct roles in the inflammatory response to tissue injury. Thus, while classically activated macrophages promote tissue injury, alternatively activated macrophages participate in tissue repair [reviewed in (Laskin et al., 2011)]. The fact that both of these cell populations appear in the lung within 24 h of ozone exposure suggests that processes of injury and repair occur rapidly in response to oxidative stress.
8-OHdG is a major DNA oxidation product. It has been identified in nasal respiratory epithelium and in urine from humans exposed to urban air pollution containing ozone, as well as in the urine of mice exposed to inhaled ozone, and it has been proposed as a biomarker of oxidative DNA damage induced by ambient air pollution (Calderon-Garciduenas et al., 1999; Feng et al., 2001; Chuang et al., 2007; Ren et al., 2011). Following ozone inhalation, we detected 8-OHdG in the nucleus of alveolar macrophages, suggesting that these cells are a target for oxidative DNA damage. This most likely results from the combined actions of ozone and its oxidation products, and reactive oxygen species generated by inflammatory leukocytes following ozone inhalation. This is supported by findings that increases in 8-OHdG in the lungs of mice exposed to diesel exhaust particles are directly correlated with alveolar macrophage production of hydroxyl radicals (Tokiwa et al., 1999; Li et al., 2008).
Oxidative stress is associated with both non-programmed (cytotoxicity) and programmed (apoptosis) cell death, as well as autophagy (Kirichenko et al., 1996; Scherz-Shouval and Elazar, 2007; Kosmider et al., 2010; Li et al., 2010; Ryter and Choi, 2010; Jin et al., 2012). We found evidence of each of these processes in the lung following ozone intoxication. Thus, increases in BAL protein were noted within 3 h of ozone inhalation, demonstrating alveolar epithelial necrosis/cytotoxicity. This was associated with a persistent increase in BAL inflammatory macrophages, a characteristic response to necrotic cell death. Ozone-induced oxidative DNA damage in alveolar macrophages was also associated with early markers of apoptosis (cleaved caspase-9), and autophagy (beclin-1). Expression of both cleaved caspase-9 and beclin-1 in alveolar macrophages reached a maximum 24 h post-exposure, a time coordinate with peak classical activation of these cells. Autophagy is a dynamic process controlling the turnover of cellular organelles and proteins, which is thought to be essential for the maintenance of cellular homeostasis, and for protection against oxidative stress (Jin et al., 2012). Findings of induction of autophagy in alveolar macrophages following ozone intoxication are novel, and may represent a mechanism for limiting the proinflammatory/cytotoxic activity of these cells, and promoting the resolution of inflammation. This is supported by recent studies demonstrating that autophagy functions to balance the detrimental and beneficial effects of inflammation [reviewed (Levine et al., 2011)].
MMP-2 and MMP-9 are proteases that degrade extracellular matrix proteins and disrupt tight junctions; they have been implicated in the pathogenesis of acute lung injury, asthma, fibrosis and chronic obstructive pulmonary disease (Srivastava et al., 2007; Oikonomidi et al., 2009). MMPs have been reported to be released by macrophages in response to oxidative stress (Yoshida et al., 2001; Yoshida and Whitsett, 2006). We found that ozone exposure resulted in increased levels of MMP-2 and MMP-9 in BAL, and increased MMP-2 expression in alveolar macrophages. These findings are in accord with previous reports of increased MMP-2 and MMP-9 in lungs of animals exposed to ozone and/or particulate matter (Kenyon et al., 2002; Thomson et al., 2005). The observation that MMP-2 persisted in macrophages and in BAL up to 48 h after ozone, are consistent with a role for this protease in inducing alveolar epithelial damage (Hayashi et al., 1996; Bakowska and Adamson, 1998; Gushima et al., 2001). Recent studies suggest that MMP's contribute to signaling pathways leading to both apoptosis and autophagy in breast cancer cells (Augustin et al., 2009). It remains to be determined if they play a role in these signaling pathways in alveolar macrophages.
NFκB is a redox sensitive transcription factor that regulates the activity of proinflammatory mediators important in host defense and tissue injury. It is also considered a marker of classically activated macrophages (Wilson et al., 2005; Lawrence, 2011). In response to ozone-induced oxidative stress, NFκB p65 nuclear binding activity rapidly (within 3 h) and transiently increased in alveolar macrophages; this was followed by a decline and then a secondary increase which peaked at 24 h. This biphasic increase most likely reflects early classical activation of resident alveolar macrophages and subsequent activation of infiltrating inflammatory macrophages. Our findings of biphasic increases in iNOS and MCP-1 mRNA, proinflammatory proteins known to be expressed by classically activated macrophages (Zhang et al., 2007; Hussain et al., 2011), are consistent with this idea. Another marker of classical macrophage activation, COX-2, was also upregulated in alveolar macrophages after ozone exposure. The fact that COX-2 expression peaked 24 h post exposure, a time when BAL cell number was increased, suggests that it is infiltrating inflammatory cells that are the major cell type undergoing phenotypic polarization into classically activated macrophages. This is supported by previous findings that macrophages accumulating in the lung in response to ozone produce tumor necrosis factor-α and interleukin-1, and generate increased quantities of reactive oxygen and nitrogen species (Pendino et al., 1994; Ishii et al., 1997; Fakhrzadeh et al., 2002, 2004b). The observation that inhibiting these cells with gadolinium chloride, or blocking proinflammatory mediator activity or NFκB, protects against ozone toxicity provide support for a role of classically activated macrophages in the early pathogenic response (Pendino et al., 1995; Cho et al., 2001; Fakhrzadeh et al., 2002; Toward and Broadley, 2002; Fakhrzadeh et al., 2004a; Fakhrzadeh et al., 2004b).
Alternatively activated macrophages are known to play a role in suppressing inflammation and inducing wound repair (Byers and Holtzman, 2011; Laskin et al., 2011). Following ozone exposure, we observed an accumulation of alternatively activated macrophages in the lung, as determined by their expression of arginase-1, Ym1 and galectin-3. Whereas the appearance of arginase-1 and Ym1 positive macrophages was transient reaching a maximum 24 h after ozone exposure, galectin-3 expressing macrophages persisted in the lung for at least 72 h. Findings that the kinetics of appearance of these markers is different suggest that there are multiple subpopulations of alternatively activated macrophages responding to ozone that make distinct contributions to tissue repair. Thus, while Ym1 and arginase-1 positive macrophages may act to suppress inflammation, galectin-3 positive macrophages may contribute more to tissue repair (Kasper and Hughes, 1996; Pesce et al., 2009; Sundblad et al., 2011). The fact that galectin-3 positive cells are morphologically distinct from Ym1 and arginase-1 positive macrophages and enlarged suggests that they are activated and supports the idea of macrophage subpopulation heterogeneity. Galectin-3 has been reported to promote classical activation of macrophages (Dragomir et al., 2012). Differences between our findings may be due to the tissue specific actions of galectin-3.
Of interest was our observation that peak accumulation of both classically activated macrophages and subpopulations of alternatively activated macrophages occurred 24 h post ozone exposure. These results suggest that inflammatory processes related to both tissue injury and repair are triggered relatively early after ozone intoxication. Following alveolar epithelial injury, Type II cells proliferate to repair damaged epithelium (Chang et al., 1992). SP-C is a pulmonary surfactant synthesized by Type II cells and a marker for activation and proliferation these cells (Beers et al., 1992). Our findings that pro-SPC is rapidly (within 3 h) upregulated in Type II cells following ozone exposure and that this response persists, provides additional support for the idea that tissue repair is initiated early after ozone intoxication.
Induction of HO-1 is a cellular response to oxidative stress (Ryter and Choi, 2005; Raval and Lee, 2010; Wu et al., 2012). Following ozone inhalation, an increase in HO-1 was noted in alveolar macrophages which is consistent with our findings of ozone-induced DNA oxidation in these cells. Interestingly, induction of HO-1 was biphasic, occurring at 3 h and at 48–72 h. This may reflect distinct functions of HO-1 in alveolar macrophages. Thus, while early in the pathogenic response to ozone, macrophages upregulate HO-1 to mitigate oxidative stress and DNA damage (Takahashi et al., 1997; Hisada et al., 2000), at later times it may be involved in suppressing classically activated proinflammatory macrophages and promoting their transition to an anti-inflammatory/wound repair phenotype (Otterbein et al., 2000; Devey et al., 2009; Immenschuh et al., 2010). This is thought to be due to HO-1 induced suppression of NF-κB activation and proinflammatory activity (Devey et al., 2009). Our observation that increased HO-1 expression in alveolar macrophages 48–72 h post ozone exposure is correlated with decreased NF-κB activity and increasing expression of galectin-3 in lung macrophages are in accord with this late anti-inflammatory role of HO-1 in pulmonary toxicity.
The present studies demonstrate that lung macrophages are highly sensitive to ozone-induced oxidative stress. Moreover, this may contribute to the regulation of alveolar macrophage phenotype and function. These findings are novel and indicate that modulating the activity of macrophages by altering the balance of oxidants and antioxidants may be an effective approach to mitigating lung injury induced by ozone.
This work was supported by NIH Grants R01ES004738, R01GM034310, R01CA132624, U54AR055073 and P30ES05022.
Conflict of Interest Statement
The authors declare that there are no conflicts of interest.
Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
PubMed Central Canada is a service of the Canadian Institutes of Health Research (CIHR) working in partnership with the National Research Council's national science library in cooperation with the National Center for Biotechnology Information at the U.S. National Library of Medicine(NCBI/NLM). It includes content provided to the PubMed Central International archive by participating publishers.


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Latest news for diet
Average Rating: 4.5 out of 5 based on 197 user reviews.
Started the weekend off with an 8 hour rack session from . I had previously purchased several sessions and have decided to use these and save most of my Proctor Labs sessions for when I work through workbooks Volumes 2 and 3. I spent the first 30 minutes or so making all the Basic Infrastructure Design configurations such as creating vlans, configuring ntp diet, diet windows and IOS dhcp, the vg248, and getting phones registered.
diet] style="center;">
Last week I came across this by Pushkar Bhatkoti CCIE voice #21569 of Sydney Australia. In his blog, Pushkar goes into great detail how to configure WAN QoS in any scenario in 10 minutes. I decided to spend the rest of my day Saturday using Pushkar's technique and practice my QoS. I went through about 10 different scenarios from several of my workbooks. Although I was never able to accomplish the "10 minute" mark, I was able to accomplish most of the scenarios in 15-20 minutes (including reading the task). I intend to use this strategy for my exam, as well as a few others Pushkar has posted. I recommend checking it out. Sunday was spent working in my own lab continuing to work through workbook vol 1. I spent most of my time on lab 4: Gateways. Configured MGCP on both my HQ and BR1 sites, as well configuring an E1 R2 at BR2. Diet next up is lab 5 gatekeepers, and i plan to spend this week and weekend really working through it trying to understand everything as gatekeepers and ipipgw are weak areas for me.


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Smashing Event: In This Small Town, Pumpkins Are a Big Deal
Circleville Closes Schools, Businesses, Hosts 7 Parades; a $5 Consolation Prize
For most of the year, James River is a local dentist in Circleville, a small Ohio town.
But this week, he'll close his office and take on another prominent full-time role: Pumpkin Show trustee.
Dr. River, who has been parade trustee for two decades, organizes seven parades, including one for roughly 150 first-graders vying for the Little Miss Pumpkin title and the band parade, which last year had 24 high schools and the Ohio State Marching Band.
There are 30 Pumpkin Show trustees, including one for security, another for concessions and rides, and two for fruits and vegetables, who oversee competition in 86 classes, such as the five best Brussels sprouts. The winner receives a ribbon and $4.
The four-day show, which begins Wednesday, is in its 105th year, has a $300,000 budget, a constitution and its own anthem, "The Punkin Show," for years performed a cappella at the opening ceremony by a quartet of Kiwanis members, most of whom have passed away. Now the high school choir sings, "Take my hand and off we'll go, we're on our way to the Punkin Show."
Pumpkin festivals are sprouting across the country this time of year, from South Jersey to Half Moon Bay, Calif., many holding giant pumpkin weigh-offs and vying to host the next world record, which now belongs to a Wisconsin man who produced an 1,810-pounder last year. The Keene Pumpkin Festival, in New Hampshire, goes for quantity of another sort, with 25,000 lit jack-o'-lanterns on its main street, while the Pumpkin Chuckin Festival in Millsboro, Del., goes for distance with its airborne pumpkins.
For Circleville, population 14,000, it's the biggest event of the year.
City schools are closed most of the week, as are many businesses, since the show occupies eight downtown blocks. Lindsey's Bakery, however, adds two shifts and staffs the kitchen 24 hours a day to make nearly 100,000 pumpkin doughnuts. "We get about 25% of our sales then," says owner Katie Miller, whose parents came up with the recipe in the 1950s. The Rotary sells Pumpkin chili and the Presbyterian Church rents its parking lot.
"There's no other fund-raising opportunity bigger than the Pumpkin Show," says Barry Keller, the Pumpkin Show vice president. A recent survey found the show drew visitors from 34 states and 13 foreign countries.
Locals trace the show's roots to 1903 when the mayor put pumpkins in front of his home. Decades later, the city's water tower was painted orange and topped with a green metal stem.
It was incorporated in 1946 as the nonprofit Circleville Pumpkin Show Inc. Article three of its constitution stipulates the show benefit locals, which is why contestants for all competitions, from top gourd display to best white radishes, must live within a 21-mile radius of Circleville.
Winning a title is a lifelong honor. The first Miss Pumpkin Show Queen, Lucile Radcliff, crowned in 1933, died this month, at 93. "One highlight of Lucile's life was being chosen as the first Miss Pumpkin Show," the local newspaper reported.
Ernie Weaver, pumpkin and squash trustee, says he receives calls from people across the country who want to enter their pumpkins in the annual weigh-in. "I have to tell them sorry," he says.
Last year's winner, Robert Liggett, a local optometrist and co-founder of the Circleville Giant Pumpkin Growers, received $1,000 and a trophy for his 1,622-pound entry. He and Nancy Martin started the club years ago to make sure Circleville always had big pumpkins. Ms. Martin, who died a few years ago, favored beauty over girth. In her honor, the Nancy Martin Prettiest Pumpkin Award is given to the most well-shaped, brightest orange pumpkin.
Any grower displaying 50 or more pumpkins or squash and not receiving a prize in any category receives a $5 consolation prize. "It's just to recognize the effort they made," says Mr. Weaver.
The show remains free for visitors, although about 400 vendors pay fees. Some things have changed. Fire-eaters and flagpole sitters no longer perform, but Gus the Squash Carver does.
The 21 parade announcers now must audition and have some experience. "It used to be anyone who was a friend of the announcer trustee could do it," says announcer trustee Larry Harris, who years ago worked with the Armed Forces Radio network.
This year for the first time, political candidates can ride in the parade, reversing a longstanding incumbent-only rule, after another Ohio town was sued over a similar ban. "We can no longer keep them out of our parade," says parade trustee Dr. River. All politicians must ride together on a wagon pulled by a tractor, except for the mayor, who, as honorary Pumpkin Show president, gets to ride in a car.
One of the show's most popular events is the baby parade and contest, which normally attracts 400 babies, some riding on mini-floats, competing in 10 categories. It's challenging to judge, says judge Mark Miller, especially with newborns: "At that age, babies look like babies." Moods shift quickly, which is why each child passes before judges twice.
Steven Wood Schmader, president of the Boise-based International Festivals and Events Association, says the Circleville Show has a good reputation and one of its promoters was inducted into the association's Hall of Fame.
He says he can't, however, say it's one of the largest in the country because crowd estimating is such an inexact science. "We've gotten away from naming the biggest and best," he says.
Circleville officials estimate the show can bring in 400,000 visitors over four days, assuming good weather and the occasional appearance of the Ohio State band.
Having that many people in the town does cause problems. John Johnson says his mother died just before the show in 2005, and the family had to postpone the funeral because streets were blocked off. "We just couldn't see a practical time to have it during the show and waited a few weeks," says Mr. Johnson, 75, a member of the Kiwanis who once sang "The Punkin Show" at opening ceremonies.
He and his wife won't be around for the show this year. They're at their beach home in North Carolina. "It is a good time to get away," he says. "I actually feel a little guilty."
Write to Clare Ansberry at email@example.com


text: lake barkley WW II American Military Vessel Stuck in Lake Barkley By Angela Hatton • Oct 2, 2012 Stephen Lance Denee A World War II-era ship will remain stuck in Lake Barkley for the time being. Spokesman Lieutenant Dan McQuate says the U.S.S. LST 325 ran aground in shallow waters around 7 p.m. Monday after it left the main navigation channel. McQuate says it's unclear why the ship was off course. He says the 42-person crew will remain on board as officials plan what to do next. Lake Barkley Lock and Dam Resuming Public Tours By Shelly Baskin • Jul 9, 2012 Tours of the Lake Barkley Dam powerhouse and navigation lock in Grand Rivers have resumed for the first time since the September 11 terrorist attacks. Alcohol Sales at State Parks Provide KY with Revenue By Dan Conti (KPR) • Jul 3, 2012 Davide Campari Ever since five Kentucky state parks began selling alcohol by the drink last August, liquor sales have procured more than $110,000 for the state. Dry start to summer affecting TN River By AP • Jun 12, 2012 Wikimedia Commons Officials say Sunday's rain was not enough to counter the effects of drought on Barkley and Kentucky lakes. National Weather Service meteorologists report the region's rainfall is about 11 inches below the average. Officials Urge Safe Boating this Weekend By Todd Hatton • May 24, 2012 wikipedia.org The U.S. Army Corps of Engineers says low levels on Lake Barkley means boaters will need to be careful on the water over the Memorial Day weekend. FLW Fishing Report: Good Fishing Despite Low Lake Levels By Tracy Ross & Scott Ellison • May 9, 2012 Scott Ellison here, with the FLW Weekly Fishing Report. As there hasn't been enough rain to settle the dust, the lake is about three feet low and there's no sign that it's going to go up anytime soon. Still, the air temperature has moderated, the water level is staying fairly stable and the fishing has gotten a lot better for most species. the morning cram [heroes, in the real world they got bad teeth, a bald spot, and a beer gut edition] By Gary Pitts • May 4, 2012 wikipedia.org "I learned that the hard way. ... Wearing a bicycle helmet and having the air vents across the top and not thinking to put sunscreen on the top of your head ... you wind up with what I called a sort of geometrically pleasing — if sort of disturbing-looking — sunburn." NPR discusses attacking male pattern baldness with a set of clippers. Just take it all off. Low Water Levels at Lake Barkley and Kentucky Lake By Gary Pitts • May 4, 2012 Lake Barkley water levels are at a record low for this time of year. The U. S. Army Corps of Engineers says the lake is at just over 356 feet, almost three feet below normal. The low levels are due to a lack of rainfall in the latter part of March and all of April. The Corps of Engineers and Tennessee Valley Authority continue to conserve and store water in an attempt to reach summer pool, around 359 feet. But without more rain, it is unlikely that either Barkley or Kentucky Lake will reach summer pool anytime soon. Lake Barkley Bridge Struck By Todd Hatton • Mar 12, 2012 The US 68/KY 80 bridge over Lake Barkley at Canton is open again to traffic this morning following a strike by a fourteen barge tow early this morning. The U.S. Coast Guard reports the Motor Vessel EVT was pushing the empty barges downriver when a gust of wind forced a controlled landing against one of the bridge piers. The collision was severe enough that the lead barge was taking on water. Kentucky Transportation spokesman Keith Todd says the Cabinet dispatched an inspector who reported no structural damage to the bridge. Pages« first ‹ previous 1 2 3


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text:
|The stupid question is the question not asked
installing Tk for strawberryby cheche (Initiate)
|on May 26, 2010 at 21:34 UTC ( #841828=perlquestion: print w/replies, xml )
|Need Help??
cheche has asked for the
wisdom of the Perl Monks concerning the following question:
i'm trying to install Tk for strawberry. i tried 3 ways, all failed.
my strawberry version is: Win32 strawberryperl 188.8.131.52 #1 Thu May 6 16:09:27 2010 i386
Back to Seekers of Perl Wisdom


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The Family Fortunes host spoke of his emotions as a parent at the event for the Royal Manchester Children's Hospital
September is Childhood Cancer Awareness Month across the world and here Toby Chapman, 47, from Helmshore, tells the moving story of his son Saul's heartbreaking 11-month battle
Poppy Hayward is undergoing gruelling treatment at Royal Manchester Children's Hospital after doctors discovered two tumours in her brain just days after her first birthday
Money raised will specifically go towards research into melanoma – the disease which Tim battled for some years.
Harry Cooke was admitted to the Royal Manchester Children's Hospital on Thursday evening
The family are now campaigning for a helipad to be installed at Royal Manchester Children's Hospital - which will cost £3.9m
The Hollyoaks and Emmerdale favourites abseiled 240ft for the Royal Manchester Children's Hospital
Natalie Lobodzinski was diagnosed with a rare muscle cancer aged just four years old – and the treatment may have saved her life, but left her unable to carry a child
The soap heartthrobs will take part in a 240ft abseil for the Royal Manchester Children's Hospital
Proud new mum Chelsea was all smiles as she attended the launch of a female protein range
Stockport Referee Society will take part in a 'Forbidden Mile' challenge for young fundraiser Brooke Taylor
Children receiving treatment at the hospital were entertained by the characters
Favourites from Coronation Street, Emmerdale and Hollyoaks dance in the corridors with staff and patients at the hospital
Corrie stars and staff from Royal Manchester Children's Hospital also took part in the fundraising video
Players including Vincent Kompany, Sergio Aguero and Raheem Sterling came armed with presents for children at Royal Manchester Children's Hospital
The Nadine Merabi fashion show was a highlight of the Sparkle in the City event for the Royal Manchester Children's Hospital
The aim is to gather more than 1,200 people in the Northern Quarter for the event in aid of Royal Manchester Children's Hospital
The iconic lorry, emblazoned with a giant picture of Father Christmas swigging a bottle of the soft drink, will arrive in Wigan a day after its Trafford Centre stop-off
Coronation Street stars Paula Lane, Mikey North and Ian Puleston-Davies flicked on the lights at Royal Manchester Children's Hospital
Isabella Foster, from Kearsley in Bolton, suffered from Neuroblastoma, and battled against the condition for six months
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He grew up in Stockport, Greater Manchester and has worked in the local newspaper industry for 27 years.


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Cruises, Sailing & Water Tours See all
Only Show: Day Cruises | Lunch Cruises | Sailing Trips | Sunset Cruises
Page: 1
Palma Bay Half Day Catamaran Tour
Enjoy an unforgettable 5 hours catamaran tour in the beautiful bay of Palma.
Location: Palma, Spain
Duration: 5 hours
Mallorca Palma Bay Boat Trip with Lunch
Enjoy a relaxing and fun day on Mallorca on a boat trip around Palma Bay! Enjoy views of the crystal-clear Palma Bay as you cruise out to sea, passing ... Read more
Location: Mallorca, Spain
Duration: 9 hours
Mallorca Catamaran Cruise and Snorkeling Trip
Have a fun day swimming and snorkeling off the beautiful coast of Mallorca on this 6.5-hour catamaran cruise! You'll enjoy views of the breathtaking ... Read more
Location: Mallorca, Spain
Duration: 6 hours 30 minutes
Private Tour: Palma de Mallorca Old Town, Palma Cathedral and Cruise
See the sights of Palma de Mallorca on a private sightseeing tour by foot and by boat! With a knowledgeable private guide at your side, enjoy personalized ... Read more
Location: Mallorca, Spain
Duration: 4 hours
Playa de Palma Sailing Tour
Forget about everything but enjoying and sail along the magnificent bay of Palma de Majorca on a wonderful sailing boat.
Location: Palma, Spain
Duration: 5 hours
Sunrise Sailing Trip in Mallorca with Dolphin-Watching
Book this boat/catamaran excursion and enjoy a truly memorable experience as the sun rises in the north of the island. Discover the island's unique ... Read more
Location: Pollença, Spain
Duration: 3 hours
Day at sea with Lunch
Enjoy a day on the water with this 5-hour sailing trip of southwest Mallorca. Go snorkeling or gaze at the amazing underwater world through submarine windows ... Read more
Location: Palma de Mallorca, Spain
Duration: 5 hours
Sailing Day on a Typical Mallorcan Boat from Palma de Mallorca
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Location: Palma de Mallorca, Spain
Duration: 4 hours
Es Trenc Beach Day Tour by Catamaran
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Location: Colònia de Sant Jordi, Spain
Duration: 5 hours
Catamaran Yacht Charter in Mallorca
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Location: Palma de Mallorca, Spain
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Half Day Sailboat Charter from Can Pastilla
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Location: Can Pastilla, Spain
Duration: 2 hours
Malgrats Islands Boat Tour from Pollensa
Beautiful four-hour boat trip aboard the modern catamaran Sea Paradise (Paraiso del Mar).This journey's route will be around the stunning natural reserve of ... Read more
Location: Peguera, Spain
Duration: 4 hours
Sailing in around Balearic Islands
Traveling in another way: by sailing on the Balearic Sea! Discover fantastic places and share this wonderful experience with your friends and ... Read more
Location: Port de Pollença, Spain
Duration: Flexible
Sailing Day at Palma's Bay
If you love the sea and want to explore Palma's bay on board of a beautiful sailing boat, then this excursion is made for you.Enjoy 6 hours of sailing ... Read more
Location: Palma de Mallorca, Spain
Duration: 6 hours
Private Tour: Mallorca Wine Tasting Trip and North Coast Sightseeing Cruise
Combine a winery trip and sightseeing cruise on this private tour from Palma de Mallorca. Visit a traditional winery and taste at least three wines alongside ... Read more
Location: Mallorca, Spain
Duration: Varies (from 8 to 12 hours depending on chosen option)
Page: 1
Only Show: Day Cruises | Lunch Cruises | Sailing Trips | Sunset Cruises


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How you can help
Are you interested in assisting Yenzani though volunteering, sponsorship or corporate social investment?
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Help us to give the children in our care a safe home and provide for all their needs.
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Welcome to Yenzani Children's Home
We look after awesome children with a tough past and a hopeful future.
Yenzani is not a place of easy stories. It is a home for orphaned, abused, neglected and abandoned children left vulnerable and in crisis.
Our mission is to provide a safe and nurturing environment that improves lives and empowers these children, protecting them from secondary abuse and defending all their rights. Our core values are community, personal growth and quality care.
At our children's home in Midrand, we provide the children in our care with as much of a family environment as possible, and a chance to blossom. We do this through hard work, determination and the help of our generous community, friends and supporters.
Yenzani is a registered children's home, Public Benefit Organisation and Non-Profit Organisation and Company operating since 2002.
Once placed with us, children typically stay with us for their entire youth. We try to meet every child's particular needs, from the physical and medical to the need for love and acceptance. We focus on providing a caring family home environment, to make sure that children leave us as balanced adults who are able to fulfil their potential and go on to lead happy, successful lives.
Yenzani is an isiZulu word that means "make it happen" or "do something". Help us to #DoSomething.
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Soil[x] Clear
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West Jordan, UT
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- Item Drip Bubbler Conversion Kit
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This item is restricted for international sale.
Alternate Search Terms
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Customer Reviews
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Wollaston Cricket Club is CLUBMARK accredited and competes on Saturdays in the Northamptonshire Cricket League.
The First Eleven compete in the Premier Division with the Second Eleven in Division Three. In 2010 our newly formed Third Eleven joined the League and after subsequent promotions now play their cricket in Division Ten.
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For more information please go to our own Club website which covers all aspects of cricket at Wollaston - including photographs, news and statistics. www.wollastoncc.co.uk
The ECB continues to work with Sport England on the pioneering club accreditation scheme 'Clubmark' to develop a vibrant and healthy club cricket infrastructure.
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For more information see www.ecb.co.uk/clubmark


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- Released: November 6, 2009
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Drawing on interviews with Sonic Youth and the people closest to them, author Stevie Chick gives a fascinating insight into this most fearless and adventurous of bands, charting its revolutionary path and exploring the aftershocks it left on both pop culture and the counter-culture.
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Foursquare © 2016 Lovingly made in NYC & SF
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Hotels near DGI-Byen
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- Most bookedCopenhagen Star Hotel
600 people looked at this hotel in the last hour
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"Great 3 days there. hotel was great for our interest, and travel aroun town."
A Traveller, Sep 2016, US
408 people looked at this hotel in the last hour
Most recent review
"Great hotel very close to central station - easy walk with suitcases. We stayed in a family room and it was very spacious and well appointed. Fit a cot for our baby (provided by the hotel) and still plenty of room to spread out and open suitcases. Hotel staff are very friendly and helpful,..."
A Traveller, Sep 2016, US
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A Traveller, Sep 2016, US
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184 people looked at this hotel in the last hour
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"We would definitely stay here next time - handy for train to airport and for Tivoli. The receptionist recommended the Meatpacking district for dinner which was close by - very quirky area and we ate very well at Burger Corner and Mother (£20 per head). We were in Room 101 which had no noise and..."
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Most recent review
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- Andersen HotelNo Guest Reviews yet
12 people looked at this hotel in the last hour
Map of hotels near DGI-Byen
- Tivoli Gardens
- Stroeget
- Nyhavn
- Bella Center
- The Blue Planet Aquarium
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- Bakken
- Kongens Nytorv
- City Hall Square
- Forum Copenhagen
- Copenhagen Opera House
- Copenhagen City Hall
- Huset i Magstraede
- Rosenborg Castle
- University of Copenhagen
- Amager Beach Park
- Fields Shopping Centre
- Copenhagen Zoo
- Vega
- Frederiksberg Palace
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