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control panel layout redesign
This project received 5 bids from talented freelancers with an average bid price of $140 USD.Get free quotes for a project like this
Project BudgetN/A
Total Bids5
Project Description
We are seeking someone who can take our existing control panel and re-design the layout. This will include FULL integration to our existing system, and must include all features and future features we will be exhibiting.
I am on a short deadline for this project, so the deadline will be 72 for FULL implementation and a maximum of 24 hours from acceptance of project for the preview.
Link: [url removed, login to view]
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pass: testaccount
There are 3 access levels which enable/disable options, (regular user, business owner, site admin)
You are responsible for the changes in layout to make it clean, easy to use and professional. All PHP work is already complete, and if any changes need to be made to accommodate your new design, we have a PHP programmer on staff to handle that.
- existing functionality must be simple/easy to use
- future features must be ready to be implemented (section must be made for them)
-> these include ability to add eCommerce packages, view invoices/billing, and a few others
- CSS/XHTML only, NO TABLES PERMITTED
- must be integrated into existing page, cannot have its own full page design
- deadline of 72 hours is EXTREMELY STRICT, if you do not meet it, another designer will be chosen
- unlimited revisions, must work until satisfied with project
Maximum of 50% milestone to be made up front, and deadlines ARE EXTREMELY STRICT. IF YOU CANNOT MEET THEM DO NOT BID.
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Well, that's the way some interviews go.
I had asked to meet Britain's most unconventional publisher because this week marks a departure for his privately owned, central London-based company (Dennis Publishing, what else?), which produces a sheaf of best-selling computer magazines, aimed at both the user and the trade.
After a year of careful analysis and research, the company is diversifying into the mainstream with Maxim, a glossy monthly for men. This will attempt to capitalise on the success of GQ, Esquire, Loaded, FHM, XL and, most recently, Men's Health, which are proving that around half a million men will buy general interest publications that do not simply rely on the traditional male areas of sport, music and news/politics.
Maxim invades the traditional women's magazine agenda (oral sex, how to pull a rich spouse, careers and cookery), gives it a sex change and adds in a bit of rough. This is quite deliberate: the company headhunted the accomplished editor Gill Hudson (formerly of New Woman and Company) to finesse the £1.25m project into a commercial product, aimed uncompromisingly at heterosexual men.
"We own the computer market, now we'll steal someone else's lollipop. It's a growing market," Dennis observes, as he empties his pockets in preparation for a photograph, throws me his immaculate wallet (so there are no unsightly bulges) and dabs his face with a laundered handkerchief. "Double-breasted suits are most difficult to shoot," he tells the photographer with the assurance of a man who knows every last jot about the editorial game.
All the while he is talking nineteen to the dozen, spinning out jokes and ideas. Hudson is told about his latest editorial idea: a feature on the contents of celebrities' fridges. Dennis says his are crammed full of food that his staff eat; the only thing he draws the line at is Jaffa Cakes (I think this is a joke).
Felix Dennis is streetwise. Twenty-four years ago, he was one of three defendants in the longest obscenity trial in British legal history - the Oz trial. He was accused, along with co-editors Richard Neville and Jim Anderson, with conspiring to produce a magazine "which would corrupt the morals of children and other young persons" by publishing Schoolkids' Oz, a mix of smutty jokes and drawings.
When the saga ended and the sentences were quashed, Dennis edited a final edition of the now broken Oz and then speeded to build himself several publishing fortunes, here and in the United States.
Having been once pursued by the courts, he assures me that he would never sue a journalist for libel, though he is scathing of the low standards of the British press compared with the fact-checking energy that goes into the best American products. (Like many British magazines, Maxim is produced with a small permanent staff of seven and buttressed with contributors.)
Dennis is the genuine article, a bustling entrepreneur who does everything in his distinctively brash and energetic way: he talks about his Roller and his latest purchase, a beautiful villa on Mustique, built by David Bowie. He hands me the estate agent's brochure. This complements his main residence, a historic Warwickshire manor house and estate.
Dennis is as swift to acknowledge that the idea was brought to him by two magazine experts, Mat Snow and Lloyd Bradley, as he is to talk openly about his personal life: no point the News of the World staking out the Warwickshire spread from which he mainly operates, at arm's length from his managers.
Snow and Bradley had failed to interest EMAP Metro in the proposition, so they took it to Dennis. "It was a sound concept, they're talented guys. But we didn't feel either of them was the editor", says Dennis. "They're brilliant, but the biggest prima donnas who ever walked the planet. Magazines are about teamwork."
Mat Snow, who left after the first full dummy of the magazine was devised last May and is now editor of successful music magazine MoJo, replies: "We only met Felix three times. He is a charming man. He didn't rip us off. I'm hurt about the prima donna thing."
The basic aim is to interest the unashamedly red-blooded male, who may well be in his thirties rather than his twenties. Eric Fuller, the publishing director recruited to expand the company, says that the men's market is clearly growing, but that the existing magazines "had a very narrow editorial agenda".
The magazine is smaller than a traditional monthly. It is printed on high-quality paper, and is designed to fit into briefcases for an easy read on the train or Tube. "Classy," says Fuller. "They don't want to feel embarrassed about taking it home."
Gill Hudson says that it is well known that men often read women's magazines. They don't want psychobabble, but straight and real insights into, for example, women's views about sex. (Accordingly, one article is devoted to women discussing oral sex, encounter group-style.)
It also has 15 cartoons. This is Dennis's editorial contribution to the mix. An instinctive entertainer, he wants readers to have a laugh. The title emerged at a board meeting.
The company states publicly that it is aiming for sales of 50,000 by the end of the year, but this is modest for a magazine that has slapped a seductive woman in a skimpy black dress on a bright pink cover.
I read over to Mat Snow the magazine's main storylines. He groaned. "They are all the ones we tried to exclude on the grounds that they are naff." But then he cheered up and repeated what Dennis had said to me the day before. "If it's a success, I can say it's my idea. If it's a failure, I can say they should have listened to me." If it succeeds, then Felix Dennis will be launching more titles aimed at the general reader. Going mainstream.
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TNA stars tweets about his injury
James Storm of Beer Money made the announcement on his Twitter page that he's been diagnosed with a partial separation of his shoulder. He had been working through the pain, but doctors have told him that he should take it easy or else he'd be out of the ring for four to six weeks. That would take him out of TNA's Bound for Glory.
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NBR Trifecta is finest township project by NBR Group, is an outstanding investment opportunity bedspread by the nature tranquility. NBR Trifecta is HNDTA converted and DTCP approved and enclosed by educational institutions, Tech Park and abundance of greenery. NBR Trifecta plots are available in distinct dimensions and pre-launched booking is open just for 1100/-per sq.ft at convenient location. NBR Trifecta is equipped with all the modern amenities reflects the sign of prosperity and luxury. Mail us at email@example.com » for more queries.
NBR Trifecta Highlights Just 5 kilometers from Sarjapur Close to Delhi Public School Close to Chikka Tirupathi Just 45 minutes from Bangalore International Airport 80 acres township
For prelaunch booking, call 8088678678 and for more details browse http://www.nbrdevelopers.com/nbr-trifecta/


text:
The goal of this study is to delay the progression of word-finding problems in patients with Alzheimer's Disease (AD). The paradox of attempting to restore that which has begun to decline in AD is that patients with AD - by definition - have impairments in explicit memory, making new learning problematic. The current approach is novel in that it attempts to strengthen connections that have not yet been lost, making them more resistant to loss as the disease progresses. This study capitalizes on the finding that patients with AD continue to read words well into the course of the disease by strengthening the connections between objects and their written names. While the study is specific in its targeting of word-finding problems, a successful outcome would bode well for other studies aimed at prevention, rather than reversal, of declining cognitive functions in dementia. Patients with mild cognitive impairment (MCI) and mild AD whose naming of pictures has just begun to show signs of decline will practice naming pictures in two conditions. In one condition, they will view the pictures and repeat their names;in the other condition they will view the pictures with their written names, then read and transcribe the names. Naming of pictures trained in each of these conditions will be compared, at three time intervals post-training, with naming of pictures tested before the study but never trained. It is predicted that the pairing of the picture with its written name, combined with the motor task of transcribing the name, will result in a greater ability to name the picture at a later date than simple practice viewing the picture and repeating the name. Generalization of this better preserved naming ability to novel exemplars, contexts and tasks, is also predicted.
During the early stages of AD, when patients are still living at home and functioning within the normal family setting, one of the greatest challenges to normal living is difficulty communicating caused in part by the inability to access the appropriate words. The successful delay of such word finding problems - the goal of the proposed study - would have significant consequences for the quality of life of patients with early AD, and for their families and caregivers.


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Hotel Avon Ruby
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Elephanta Caves / Departure
... about what they are eating and how to order. One is a merchant marine - working on huge container ships. He speaks excellent English, and has just obtained his visa to enter the USA. So excited to sit and talk with us!
We figure the final day is the best one to risk eating in this quality of restaurant. We spend a mere fraction of what we spent for lunch the day before at Ali Babba Restaurant.
We return to ...
Delhi to Mumbai
... I thought I was choosing for the two of us but no, just me. When Doug got his meal, I swapped the sauces. There was little difference in the taste overall so I don't know why one was considered more "bland" than the other.
There was no entertainment on the flight which was fine – it was only a 2 hour flight which went quickly.
Mumbai !!!
We landed early in Mumbai and ...
Dharavi Slum - The land of opportunity
... as ever and residents could actually be 1.5 million, no one really knows. Human rights organisations fought for years for the legal residents to have what other non slum residents have as standard. I don't know how long it will last, this land is worth an arm and a leg to the government and they want it, they don't want 'slums'.
We met out wonderful guide Adnan at 9 o'clock at a train station just 10 minutes down the road. We were given a meeting a point and Lee ...
Mumbai-bai India
... thinks that Hampi is one the most amazing places he has ever seen. He has no desire to return to the North of India, specifically Varanasi. And he can appreciate that Goa was the wrong season. Definitely more good than bad!
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The ordeal is over
... Islands - Enjoying a day out and traditional lunch with Bangalorian friends - Strolling around the opulent, gaudy and glitzy palace at Mysore - Being rowed around Kerala's sleepy backwaters - Making new friends and meeting up to indulge in junk food at Goa Favourite place: Amritsar - the golden temple is still a magical and spiritual experience and the border closing ceremony is intense, hilarious and outrageous whilst being full of national pride (it's hard to imagine how ...


text:
Interleukin-1, tumor necrosis factor-alpha, and transforming growth factor-beta 1 and integrative meniscal repair: influences on meniscal cell proliferation and migration
DOI: 10.1186/ar3515
© Riera et al.; licensee BioMed Central Ltd. 2011
Received: 26 September 2011
Accepted: 16 November 2011
Published: 16 November 2011
Interleukin-1 (IL-1) and tumor necrosis factor-α (TNF-α) are up-regulated in injured and osteoarthritic knee joints. IL-1 and TNF-α inhibit integrative meniscal repair; however, the mechanisms by which this inhibition occurs are not fully understood. Transforming growth factor-β1 (TGF-β1) increases meniscal cell proliferation and accumulation, and enhances integrative meniscal repair. An improved understanding of the mechanisms modulating meniscal cell proliferation and migration will help to improve approaches for enhancing intrinsic or tissue-engineered repair of the meniscus. The goal of this study was to examine the hypothesis that IL-1 and TNF-α suppress, while TGF-β1 enhances, cellular proliferation and migration in cell and tissue models of meniscal repair.
A micro-wound assay was used to assess meniscal cell migration and proliferation in response to the following treatments for 0, 24, or 48 hours: 0 to 10 ng/mL IL-1, TNF-α, or TGF-β1, in the presence or absence of 10% serum. Proliferated and total cells were fluorescently labeled and imaged using confocal laser scanning microscopy and the number of proliferated, migrated, and total cells was determined in the micro-wound and edges of each image. Meniscal cell proliferation was also assessed throughout meniscal repair model explants treated with 0 or 10 ng/mL IL-1, TNF-α, or TGF-β1 for 14 days. At the end of the culture period, biomechanical testing and histological analyses were also performed. Statistical differences were assessed using an ANOVA and Newman-Keuls post hoc test.
IL-1 and TNF-α decreased cell proliferation in both cell and tissue models of meniscal repair. In the presence of serum, TGF-β1 increased outer zone cell proliferation in the micro-wound and in the cross section of meniscal repair model explants. Both IL-1 and TNF-α decreased the integrative shear strength of repair and extracellular matrix deposition in the meniscal repair model system, while TGF-β1 had no effect on either measure.
Meniscal cell proliferation in vivo may be diminished following joint injury due to the up-regulation of inflammatory cytokines, thereby limiting native cellular repair of meniscal lesions. Therefore, therapies that can promote meniscal cell proliferation have promise to enhance meniscal repair and improve tissue engineering strategies.
The menisci are C-shaped fibrocartilaginous tissues located between the femoral condyles and tibial plateau in the knee. They provide load bearing capabilities, lubrication, proprioception, joint congruity and joint stability for normal biomechanical function of the knee joint [1–4]. Damage to and loss of function of the menisci through sports-related [5] or degenerative tears are associated with pain and degradative changes in the knee joint that ultimately lead to osteoarthritis (OA) [6–11]. Approximately two-thirds of patients with meniscal tears develop radiographic knee OA within 5 to 15 years of injury [12]. Partial excisions and total meniscectomies for the treatment of meniscal tears are strongly associated with articular cartilage loss and the progression of OA [6–11]. Therefore, current orthopaedic practice aims to preserve meniscal integrity and restore function.
The success of clinical repairs depends on a number of factors including age, time to surgery, and the type and location of the meniscal tear. In general, repairs involving the outer one-third of the meniscus, the vascularized "red-red zone", have the highest likelihood of success [13]. Repairs are less favorable in the inner two-thirds of the meniscus, the avascular "white-white zone" [13, 14]. However, in vitro studies of integrative repair suggest that the intrinsic repair capabilities of the outer and inner zones are similar, supporting the hypothesis that the in vivo presence of vasculature aids in the repair of the outer zone [15]. Nonetheless, differences in extracellular matrix and cell composition between the inner and outer zones may also influence repair. The outer zone contains fibroblast-like cells [16, 17] that produce predominantly type I collagen [18–20]. The inner zone consists of fibrochondrocyte-like cells [16, 17], both type I and II collagen [18, 20], and increased aggrecan content relative to the outer zone [14]. Meniscal plugs from the outer zone inserted into inner zone tissue demonstrate enhanced healing, suggesting that repair capability is related to the intrinsic healing potential of the outer region, rather than the vasculature alone [21].
The integrative repair of meniscal lesions is associated with increased cell accumulation in the repair site [22–27]. However, the respective roles of cell proliferation and migration in integrative repair, and the influence of soluble mediators on these processes are not fully understood. An in vivo canine model consisting of a fibrin clot surgically inserted into an avascular meniscal defect showed that the clot functioned as a scaffold for cell migration and a chemotactic stimulus for cell proliferation [28]. Furthermore, cells can migrate into an acellular meniscal plug in vivo and remodel the tissue [29]. An important factor that may strongly influence meniscal repair is the inflammatory environment within the joint. The inflammatory cytokines interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNF-α) are up-regulated in injured and OA knee joints [30–33]. In addition, IL-1 and TNF-α decrease integrative meniscal repair in vitro by increasing matrix metalloproteinase (MMP) activity, sulfated glycosaminoglycan (S-GAG) release, and nitric oxide (NO) production, while simultaneously decreasing cell accumulation and tissue formation at the meniscal repair interface, and ultimately compromising the shear strength of repair [23–27, 34]. Initial acute exposure to IL-1 for 1 to 3 days potently suppresses meniscal repair for at least 28 days [27], suggesting that the initial inflammatory environment in a joint post-injury may have long-term degenerative effects. In addition, IL-1 and TNF-α activate other degradative and pro-inflammatory pathways in the meniscus and other joint tissues [30, 31, 35–37].
While many of the potentially negative effects of IL-1 and TNF-α on meniscal repair have been established at the molecular and tissue levels, the specific effects of these proinflammatory cytokines on meniscal cell migration and proliferation are currently unclear, and several in vitro studies have reported conflicting results. In one study, different concentrations of IL-1 caused increased cell migration as compared to controls in bovine meniscal cells isolated from the outer and middle meniscal zones [38]. Conversely, studies with porcine meniscal repair model tissue explants treated with either IL-1 or TNF-α show decreased cell accumulation in the repair interface without a decrease in cell viability, potentially due to a reduction in cell proliferation and/or migration at the repair site [23, 25–27].
Anabolic growth factors have been studied as therapeutics to enhance healing of meniscal injuries. The anabolic growth factor transforming growth factor-β1 (TGF-β1) has been shown to increase meniscal cell proliferation in several in vitro models, including monolayer, explant culture, and meniscal cells seeded on poly-L-lactide (PLLA) scaffolds and three-dimensional collagen sponges [39–43]. In vitro meniscal repair model explants treated with TGF-β1 showed increased cell accumulation in the repair interface and increased integrative repair [24, 44]. In the presence of IL-1, TGF-β1 increased the interfacial shear strength of repair compared to IL-1 alone, overcoming some of the potent catabolic effects of IL-1 [24]. Bovine meniscal cells transduced with vectors expressing TGF-β1 and seeded into the avascular inner zone of the meniscus showed increased cellularity and proteoglycan and collagen synthesis [45]. Furthermore, meniscal cells treated with either 10 or 100 ng/mL TGF-β1 showed marked changes in cell morphology, resulting in a phenotype more similar to fibroblast-like cells [39].
The goal of this study was to investigate the effects of the inflammatory cytokines IL-1 and TNF-α, and the growth factor TGF-β1 on proliferation and migration during cell-mediated repair of the meniscus. We hypothesized that IL-1 and TNF-α suppress cellular proliferation and migration of both inner and outer zone meniscal cells, while TGF-β1 enhances cell proliferation and migration of both inner and outer zone cells, in cell and tissue models of meniscal repair. We assessed cell migration and proliferation using a micro-wound assay with isolated inner and outer zone meniscal cells treated with IL-1, TNF-α or TGF-β1. Cells were fluorescently labeled to identify newly proliferated and total cells and were imaged over time to assess the contribution of proliferated and migrated cells to wound healing. Additionally, cell proliferation was assessed in inner and outer zone meniscal repair model explants [15, 23, 25–27, 34] treated with IL-1, TNF-α or TGF-β1 for 14 days. Meniscus healing was investigated by mechanical testing of the repair model explants to determine the interfacial shear strength and histology was performed to visualize tissue repair and cell viability.
Materials and methods
Meniscal cell isolation
Medial menisci were aseptically isolated from the knee joints of skeletally mature, two- to three-year-old female pigs obtained from a local abattoir. The menisci were trimmed to remove all ligamentous and synovial tissue and separated into the inner two-thirds and outer one-third zones [14]. Meniscal cells from the inner and outer zones were enzymatically isolated from the tissue by sequential digestion with 1,320 PUK/mL pronase (Calbiochem, San Diego, CA, USA) followed by 0.4% collagenase type I (Worthington, Lakewood, NJ, USA) for three hours, as previously described [46]. After enzymatic isolation, the cells were filtered through a 70 μm filter (BD Biosciences, Bedford, MA, USA) and washed three times in Dulbecco's Modified Eagle's Medium high glucose (DMEM with 4.5 g/L D-glucose; Invitrogen, Carlsbad, CA, USA) containing 1,000 units/mL penicillin/streptomycin and 2.5 μg/mL amphotericin B (Invitrogen). Cells were resuspended at a concentration of 1 × 106 cells/mL in culture media composed of DMEM, 10% heat inactivated fetal bovine serum (FBS; HyClone, Logan, UT, USA), 0.1 mM non-essential amino acids (Invitrogen), 10 mM 4-(2-hydroxyethyl)-1-piperazineethanesulfonic acid buffer solution (HEPES; Invitrogen), 100 units/mL penicillin/streptomycin, and 37.5 μg/mL L-ascorbic acid 2-phosphate (Sigma-Aldrich, St. Louis, MO, USA). Cells were seeded at a final concentration of 2 × 106 cells per well in a two-well chambered coverglass slide (Nalge Nunc International, Rochester, NY, USA) that was coated overnight with 50 μg/mL bovine type I collagen (Trevigen, Gaithersburg, MD, USA) in phosphate buffered saline (PBS; Mediatech, Manassas, VA, USA). Cells were incubated for 72 hours at 37°C/5% CO2.
Micro-wounding of meniscal cells
Treatments for micro-wounding experiments
0, 1%, 5%, 10%
Hyclone (Logan, UT, USA)
Recombinant porcine IL-1α
0, 0.1 ng/mL, 1 ng/mL, 10 ng/mL
R & D Systems (Minneapolis, MN, USA)
Recombinant porcine TNF-α
0, 0.1 ng/mL, 1 ng/mL, 10 ng/mL
R & D Systems (Minneapolis, MN, USA)
Porcine TGF-β1
0, 0.1 ng/mL, 1 ng/mL, 10 ng/mL
R & D Systems(Minneapolis, MN, USA)
10% Serum and factors
10% Serum
Hyclone (Logan, UT, USA)
10% Serum + 10 ng/mL IL-1
see above
10% Serum + 10 ng/mL TNF-α
see above
10% Serum + 10 ng/mL TGF-β1
see above
Cells were visualized and photographed using a laser scanning confocal microscope (LSM 510, Carl Zeiss, Inc., Thornwood, NY, USA). To visualize proliferated cells, an excitation wavelength of 488 nm was used and fluorescence was collected at 505 to 530 nm. Total cells were detected by excitation at 543 nm and fluorescence was collected at >585 nm. In order to visualize a single cell layer, an optical slice of 15 μm was utilized. For each sample, the micro-wound was centered in the field of view and four images at different vertical positions along the scratch were obtained.
Micro-wounding image analysis
The confocal images were exported as separate green and red channel images from the Zeiss LSM Image Browser software (Carl Zeiss, Inc.). Collected images were analyzed using a custom Matlab (MathWorks, Natick, MA, USA) script. Briefly, each of the four green and red channel images for each sample was thresholded using optimal threshold values that were determined for the green and red channels individually. These images were then converted to a binary image to identify labeled cells. Images were sub-divided into 32 32-pixel regions and the number of cells within each region was counted. Cell counts from all regions were summed across the four images to yield the total number of cells (red) and the total number of proliferating cells (green) for each sample. The total number of migrating cells that did not proliferate was the difference between the two channels. To assess cell migration and proliferation in the micro-wound, cell counts were averaged across the two center strips and to assess cell proliferation at the edge, cell counts from the green channel images were averaged across the four peripheral strips at the far left and right edges of the image. The total cell counts at the edges were also measured on Day 0 images to establish the starting cell density for each meniscal cell population. All data are expressed as a percentage of the starting cell density.
In the micro-wounding assay, all cells that accumulate in the gap have migrated into the wound from the edge. Therefore, all cells that are described as proliferated in the gap have in fact both migrated and proliferated. However, the order in which these cellular activities occurred could not be assessed. Cells that are described as migrated have, therefore, only migrated into the wound and did not proliferate.
Meniscal repair model system
A previously described meniscal repair model system [15, 23–27] was used to assess in vitro integrative meniscal repair (n = four or more per treatment group, all from different animals). Cylindrical 5 mm biopsy punches (Miltex, York, PA, USA) were harvested perpendicular to the femoral surface of the meniscus from the inner two-thirds and outer one-third of the tissue. Explants were cut parallel to the meniscal surface with a scalpel to a uniform thickness of 2.5 mm using a custom-made cutting block. To simulate a full-thickness tear, a 3 mm biopsy punch (Miltex) was utilized to make a concentric core in the explant, which was removed and immediately reinserted in the original orientation. Explants were placed in a 24-well plate with DMEM containing 1,000 units/mL penicillin/streptomycin for one hour at 37°C/5% CO2. Explants were incubated in the culture media described above for isolated meniscal cells. For cell proliferation experiments, all media included 10 μM EdU. Explants were randomly assigned to one the following treatment groups: control, 10 ng/mL IL-1α, 10 ng/mL TNF-α or 10 ng/mL TGF-β1. Media were changed every 3 days, and explants were cultured for a total of 14 days at 37°C/5% CO2.
Cell proliferation analyses in meniscal repair explants
On Day 14, explants were transected vertically to allow visualization of cells throughout the cross section. Explants were labeled using a modified protocol based on the Click -iT™ EdU Alexa Fluor® 488 Imaging Kit. Briefly, explants were fixed with 3.8% formaldehyde for 30 minutes, permeabilized with 0.5% Triton X-100 for 30 minutes, and tagged with the Alexa Fluor dye to label all proliferated cells. To stain all cells, explants were washed in TE, pH 7.4, stained for 30 minutes in the dark with 1 μM Syto® 82 nucleic acid stain, and then washed three times with TE.
Cells were visualized and photographed using a confocal laser scanning microscope as described above for the micro-wounding assay. Images were collected more than 50 μm into the face of the sample to ensure that cells damaged during transection were excluded [50]. Two images per location were collected from the outer ring, inner core and repair interface for both the surface and cross section of the explants.
Meniscal repair model explant image analysis
Data were collected from different areas of the surface and cross-section of the meniscal repair model explants. Measured areas were outlined in Zeiss LSM image browser (Carl Zeiss). The surface interface included a 50 μm region on either side of the interface, inclusive of the interface, at the surface of the tissue. The surface region of the tissue included images from both the inner core and outer ring that were outside this defined interface region. For cross section images, the tissue was divided into three distinct layers based on distance from the surface and cell morphology. The first 50 μm from the surface was defined as the "superficial zone," the next 100 μm was defined as the "middle zone," and the next 300 μm was termed the "deep zone." The cross section interface included a 50 μm region on either side of the interface, inclusive of the interface, for each of these three layers. The cross section of the tissue included images of the cross section from both the inner core and outer ring that were outside the defined interface region.
Confocal images were exported as separate green and red channel images and saved as TIFF files. The images were gray-scaled using Adobe Photoshop and processed using Scion Image (Scion Corp., Frederick, MD, USA) to invert, subtract background by removing 2D streaks, and smooth. Optimal threshold values were determined for the green and red channels individually. Proliferated cells (green) and total cell (red) counts were obtained using intensity thresholds of 75 and 40, respectively, and a minimum particle size of five. Cell counts were obtained for each of the defined regions in the surface and cross sectional planes. Percent cell proliferation was calculated by dividing the number of proliferated cells (green) by the number of total cells (red) in each sample and multiplying by 100 percent.
Biomechanical testing to assess shear strength of repair
On Day 14, shear strength of repair between the outer ring and inner core of meniscal repair explants was measured with a push-out test [15, 23–27] using an Electroforce (ELF) 3200 materials testing system (Bose-EnduraTEC Corporation, Eden Prairie, MN, USA). Briefly, explants were centered in a custom-made apparatus, such that the 3 mm inner core was centered over a 4 mm concentric hole in the bottom of the dish. A 2 mm diameter rod attached to a load cell displaced the inner core at a rate of 0.0833 mm/s until the inner core was dislodged from the outer ring. The force required for displacement was recorded over time. Following the push out test, the inner core was imaged using a digital video camera (Sony Electronics, Park Ridge, NJ, USA) with a 94-mm video lens (Infinity, Boulder, CO, USA) to measure the inner core thickness using LabVIEW Vision Builder AI (National Instruments Corporation, Austin, TX, USA). Shear strength of repair (in kPa) was calculated by dividing the peak force measured during the push out test by the surface area of the interface.
Histological staining of meniscal explants
On Day 12 of the meniscal repair model explant culture, 0.05% nitroblue tetrazolium chloride (NBT; Invitrogen) was added to the explant culture media for histological analyses. NBT is a cell-permeable compound that is reduced by live cells to form a blue formazan product that remains stable to histological processing and paraffin embedding and has been documented as a live cell marker for chondrocytes [51, 52]. At Day 14, explants were fixed overnight in 4% paraformaldehyde (Electron Microscopy Sciences, Hatfield, PA, USA), containing 100 mM sodium cacodylate trihydrate (Electron Microscopy Sciences), pH 7.4 at 4°C. Samples were dehydrated in EtOH, infiltrated with xylene, and paraffin embedded. Sections were stained with 0.02% aqueous fast green (Sigma-Aldrich) to label collagens and Accustain Safranin O solution (Sigma-Aldrich) to identify proteoglycans.
Statistical analyses
Statistical analyses were performed using Statistica 7.0 (StatSoft Inc., Tulsa, OK, USA). A factorial analysis of variance (ANOVA) and the Newman-Keuls post hoc test were performed to determine significant differences (α = 0.05) and the interactive effect of time and treatment in the micro-wounding experiments. In the meniscal repair model explant studies, the interactive effect of treatment and tissue zone (inner and outer) in the surface images and push-out test and of treatment, tissue zone and cross section layer (superficial, middle, and deep) in the cross section images were also determined using a factorial ANOVA and Newman-Keuls post-hoc test.
The effects of serum on inner and outer zone micro-wound repair
In outer zone meniscal cells, 10% serum increased the total number of cells in the wound (Figure 1D, P < 0.005) and the percentage of proliferated cells in both the wound (P < 0.01) and at the edge (P < 0.005), as compared to all other treatments. On average, treatment with 10% serum for 48 hours resulted in a six-fold increase in the total number of cells in the wound and in the proliferated cells at both the edge and in the wound (P < 0.01). In addition, there was an effect of time in the outer zone cells, with the total number of cells (P < 0.005) and the proliferated cells in the wound being greatest at 48 hours (P < 0.01). No differences were detected in cells that migrated but did not proliferate in the wound of outer zone cells.
The effects of IL-1 on inner and outer zone micro-wound repair
In the outer zone meniscal cells, IL-1 treatment caused a significant decrease in the number of proliferated cells in the wound, as compared to control (Figure 2D, P < 0.05). However, IL-1 did not have a significant effect on the total cell numbers in the wound, migrated cells in the wound, or the proliferated cells at the edge in the outer zone meniscal cells.
The effects of TNF-α on inner and outer zone micro-wound repair
In the outer zone cells, there was a trend towards decreased proliferation at the edge (Figure 3D, P = 0.17) and in the wound (P = 0.46) with TNF-α treatment but these changes were not significant. TNF-α treatment did not alter the total number of cells in the wound or the number of cells that had migrated but not proliferated in the wound.
The effects of TGF-β1 on inner and outer zone micro-wound repair
On the other hand, in the outer zone cells 0.1 ng/mL TGF-β1 increased cell accumulation (Figure 4C). This concentration of TGF-β1 also significantly increased the total cell number in the wound of the outer zone cells, as compared to the control and 1 ng/mL TGF-β1 treatment groups (Figure 4D, P < 0.05). However, TGF-β1 treatment of outer zone cells did not alter the percentage of proliferated cells in the wound, proliferated cells at the edge, or the number of cells that had migrated into the wound but not proliferated.
The effects of IL-1, TNF-α, and TGF-β1 in the presence of serum on inner and outer zone micro-wound repair
In the outer zone cells, TGF-β1 treatment at 48 hours significantly increased cell proliferation in the wound compared to all other treatments (Figure 5D, P < 0.05). In addition, TGF-β1 treatment also promoted cell proliferation at the edge (P < 0.05). Furthermore, total cells (P < 0.05) and proliferated cells in the wound (P < 0.005) increased over time. There was no effect on cell migration into the wound of outer zone cells with the different factors in the presence of serum.
The effects of IL-1 on cellular proliferation in meniscal repair model explants
The effects of TNF-α on cellular proliferation in meniscal repair model explants
Cellular proliferation at the meniscal tissue surface (Figure 6B, C), surface interface (Figure 7B, C), cross-section (Figure 8B, C), and cross-section interface (Figure 9B, C) were decreased in the presence of TNF-α in both inner and outer meniscal repair explants. TNF-α strongly inhibited cell proliferation at the tissue surface (Figure 6E, P < 0.00005) and the surface interface (Figure 7E, P < 0.005) in explants from both zones. Furthermore, TNF-α reduced cell proliferation throughout the cross-section (Figure 8E, P < 0.000005) and cross-section interface (Figure 9E, P < 0.000005). There was also a significant effect of cross-section layer with the superficial layer containing significantly more proliferated cells than the middle and deep layers (Figure 8E, P < 0.0005). In addition, there was an interactive effect of TNF-α and cross-section layer (P < 0.00005).
The effects of TGF-β1 on cellular proliferation in meniscal repair model explants
In both the inner and outer meniscal repair explants, TGF-β1 treatment did not appear to alter cellular proliferation at the meniscal tissue surface (Figure 6B, C), surface interface (Figure 7B, C), cross-section (Figure 8B, C), or cross-section interface (Figure 9B, C). In both inner and outer zone explants, TGF-β1 had no effect on cellular proliferation in meniscal repair model explants at the tissue surface (Figure 6F), the surface interface (Figure 7F), or the cross-section interface (Figure 9F). However, overall TGF-β1 increased cellular proliferation in the tissue cross-section (Figure 8F, P < 0.05). While there was a significant decrease in cellular proliferation throughout the depth of the meniscus cross-section (Figure 8F, P < 0.005), TGF-β1 most noticeably up-regulated proliferation in the middle and deep layers.
The effects of IL-1, TNF-α, and TGF-β1 on the shear strength of integrative repair
The effects of IL-1, TNF-α and TGF-β1 on tissue repair and cell viability
Our results demonstrate that the proinflammatory cytokines IL-1 and TNF-α decreased cell proliferation in both cell and tissue models of meniscal repair. In the presence of serum, the anabolic growth factor TGF-β1 increased outer zone cell proliferation in the micro-wound and in the cross section of meniscal repair model explants. Furthermore, both IL-1 and TNF-α decreased the integrative shear strength of repair and extracellular matrix deposition in the meniscal repair model system, while TGF-β1 had no effect on either measure. Therefore, our results support our hypothesis that the inhibition of cell accumulation and integrative repair by IL-1 and TNF-α is likely due to suppression of cellular proliferation but not migration of cells into meniscal micro-wounds. These results suggest that in vivo, meniscal cell proliferation may be diminished following joint injury due to the up-regulation of inflammatory cytokines, thereby limiting native cellular repair of meniscal lesions. Therefore, therapies that can promote meniscal cell proliferation have promise to enhance meniscal repair and improve tissue engineering strategies.
Serum has been shown to promote proliferation in many cell types, including chondrocytes [53, 54]. Likely growth factors present in the serum promoted healing of the micro-wound [55]. However, inner and outer zone cells exhibited distinct responses in the micro-wound assay. The inner zone cells showed increased cell proliferation in response to 5% and 10% serum, while outer zone cells were only stimulated by 10% serum. The inner zone cells may be more sensitive to serum stimulation due to the lack of prior exposure to the contents of the vasculature in the context of the meniscus [14]. In addition, for inner zone cells, the percentage of cells that migrated but did not proliferate decreased over time, suggesting that the cells are migrating into the wound and then proliferating to repair the defect.
IL-1 treatment suppressed cell proliferation but increased migration in inner zone cells at the wound, although the enhanced migration was insufficient to overcome the suppression of proliferation in order to repair the micro-wound. On the other hand, IL-1 treatment of outer zone cells decreased proliferation but did not alter cell migration into the micro-wound. In other studies, outer and middle zone meniscal cells that grew out of bovine menisci over two to three weeks showed increased chemotaxis in response to four hours of 1 to 100 ng/mL IL-1 [38]. In this study, we did not assess the chemotactic response of the porcine meniscal cells but the differences in our results may be due to the differences in exposure time to IL-1. In the presence of serum, IL-1 treatment of inner zone cells suppressed total cell accumulation and proliferation but had no effect on migration. These experimental conditions are most similar to our explant growth conditions, and the results of these experiments are consistent. In porcine articular chondrocytes, F-actin content is increased after 1 hour of 10 ng/mL IL-1, showing punctate staining at the periphery but this effect is not observed after 12 hours of IL-1 treatment [56]. In tenocytes treated with 100 pM IL-1β for five days, proliferation rate was unchanged; however, actin filaments were disrupted while microtubule structure was unchanged [57]. In addition, chondrocytes treated with exogenous NO, a downstream mediator of IL-1 signaling, showed inhibition of chondrocyte migration and disruption of actin filament assembly [54]. Therefore, disruption of the actin cytoskeleton may be contributing to the IL-1 mediated suppression of proliferation observed in our injury models.
The effect of TNF-α in suppression of proliferation was not as robust as that observed with IL-1, consistent with our previous observations of the different potencies of equal concentrations of IL-1 and TNF-α on meniscal repair [25]. In addition, TNF-α had no effect on the migration of meniscal cells after micro-wounding. TNF-α treatment of human umbilical vein endothelial cells (HUVECs) caused microtubule bundling [58]; perhaps this reorganization prevents cellular proliferation in response to TNF-α. Furthermore, in the presence of serum, TNF-α treatment of inner zone cells suppressed total cell accumulation and proliferation but had no effect on migration, consistent with our explant experiments.
Similar to our results with TGF-β1 treatment, in other studies using isolated rabbit meniscal cells cultured in 10% FBS and equivalent concentrations of TGF-β1, there was no effect of TGFβ1on cell proliferation at 48 hours [59]. TGF-β1 has been shown to increase F-actin levels in isolated chondrocytes [60] and increase actin extensions and lamellar ruffling in agarose embedded chondrocytes [61]. In other studies, 3T3 fibroblasts treated with TGF-β1 did not migrate or proliferate and contained stabilized microtubules [62], consistent with the overall effects observed in this study.
In the micro-wounding experiments, overall the responses of the cells at the site of the injury and away from the wound were similar for the different treatments. These data suggest that the effect of the cytokines were stronger than any local factors that may be released in response to the wound. However, IL-1 treatment of outer zone cells and TNF-α treatment of inner cells resulted in differential responses between the cells at the site of the wound and at the edge. In these conditions, local factors produced by the wounded cells [63] may have altered the global response to the cytokine treatment [64], resulting in different responses of the cells at the site of the injury and those away from the wound.
The cellular proliferation measured in meniscal repair model explants in this study is consistent with results from previous studies. In particular, using fresh or frozen meniscal plugs in avascular sheep meniscal injuries treated with 50 ng/mL TGF-β1 for eight weeks also demonstrated no difference in cell density or proliferation but cells further from the tissue surface proliferated in response to TGF-β1 [65]. In addition, our data are consistent with an in vivo canine model in which superficial layer cells appeared to be the most active in wound repair of meniscal tissue plugs [29]. Taken together, these results suggest that the superficial cells of the meniscus may be integral in initiating and modulating the repair response.
The decreased cellular proliferation by IL-1 and TNF-α correlates with the decreased integrative shear strength of repair. In addition, these data are consistent with our previous studies that have shown that IL-1 and TNF-α suppressed integrative meniscal repair and decreased cell accumulation in the repair interface [23, 25]. Additionally, the general lack of an effect on cell proliferation in response to TGF-β1 treatment is consistent with the mechanical testing data. Previously, we have shown that 1 ng/mL TGF-β1 promoted integrative repair but 10 ng/mL TGF-β1 did not [24]. In adult bovine meniscal repair explants, 10 ng/mL TGF-β3 increased the shear strength of repair at eight weeks but not four weeks [44], suggesting that longer times in culture may be necessary to see the beneficial effects of TGF-β1 on meniscal repair. Scaffolds containing TGF-β3 increased chemotaxis of cells and articular cartilage regeneration in a rabbit model, as compared to scaffolds without TGF-β3 [66], suggesting differential responses of cells to the different isoforms of TGF-β. Interestingly, the outer zone explants showed increased shear strength of repair in the TNF-α and TGF-β1 treatment groups, as compared to inner zone explants. This result is similar to the two-week time point in a previous study, but these differences disappeared over extended culture periods [15].
Cell viability was not altered by any of the treatments in this study, suggesting that the decreased repair in the presence of IL-1 and TNF-α was not due to induction of cell death by these cytokines. The inner zone control samples stained more strongly for proteoglycans than the outer zone samples, reflecting the intrinsic composition of the meniscal tissue [14]. Histological staining revealed the presence of a predominantly collagen-rich matrix bridging the interface in control and TGF-β1 treated samples, whereas reparative tissue was largely absent in IL-1 and TNF-α treated explants. New protein synthesis, in particular collagen deposition [67] and cross-linking [68, 69], are required for successful integrative repair in cartilage repair model systems.
While isolated inner and outer zone cells demonstrated different responses to the various treatments, cells of the inner and outer zone meniscal repair model explants exhibited similar responses. Recently, isolated outer zone cells have also been shown to migrate faster and have lower adhesion strength than inner zone cells in response to electric fields [70]. These data suggest that the sub-populations of cells in the meniscus are inherently different but these differences may be masked by the extracellular matrix in explant culture. Isolated cells lack natural cellular morphology and contact with native extracellular matrix components, whereas explants maintain the cells in the context of the extracellular matrix and associated signaling molecules. Important differences have been noted in the ability of cells to move through two-dimensional and three-dimensional culture systems, particularly due to the barriers presented by collagen networks [71]. In a recent study, fetal, juvenile and adult bovine meniscal cells showed similar proliferation rates and migration abilities in a monolayer micro-wound model. However, fetal and juvenile meniscal repair model explants showed improved repair strength over time while adult explants did not improve [44], further showing the capacity of these two model systems to reveal different information.
These model systems provide valuable information on the cellular response of the meniscus to inflammatory cytokines and growth factors, allowing a careful study of proliferation, migration and matrix deposition under well-controlled environmental conditions. These studies will help to inform future in vivo studies on mechanisms to promote meniscal repair. However, the direct translatability of these studies to in vivo applications is limited by the fact that the joint environment is more complicated, including the presence of many different cell and tissue types and a variety of inflammatory factors that are produced in the joint following meniscal injury. In addition, altered metabolism in all joint tissues and altered mechanical loading effects must be considered for successful in vivo studies.
There are few in vivo meniscal repair studies that have assessed cell migration and proliferation and extracellular matrix deposition. Several animal models of avascular meniscal tears have shown that either autologous or allogenic chondrocytes in a scaffold are necessary for the formation of reparative matrix tissue in the lesion and integration of cells into the native meniscus [72–74]. Animals treated with scaffolds alone resulted in increased cellularity of fibroblast-like cells at the edges of the lesion but no repair tissue in the interface [74]. Adipose-derived mesenchymal stem cells (ASCs) placed in rabbit avascular meniscal lesions prior to suturing, increased the healing rate and yielded an increase in the cellularity of meniscal fibrochondrocytes in the repair tissue [75]. Alternatively, several in vivo studies have demonstrated the need for a vascular supply to promote healing of meniscal lesions, inducing proliferation of vessels, endothelial cells and mesenchymal cells, and resulting in fibrovascular scar tissue repair [13, 76]. However, proliferation of endothelial cells by vascular endothelial growth factor (VEGF) coated sutures was not sufficient to promote healing of meniscal lesions in the avascular region of sheep menisci [77]. The importance of meniscal cell migration and proliferation in meniscal healing is evidenced by a study showing that donor cells from fresh meniscal allografts in the goat do not survive but the host cells migrate into the allograft and repopulate the transplant [78]. In addition, in canine menisci containing devitalized meniscal plugs, cells migrate across the bridging tissue and into the interface, ultimately migrating into the devitalized plugs, remodeling the matrix, and filling the interface with a hyaline-fibrocartilage matrix [29].
Cell migration and/or proliferation are necessary for endogenous meniscal healing and repair. In order to repair a meniscal tear, cells must repopulate the wound and synthesize new extracellular matrix to achieve integrative repair. However, if cells are not able to fill in the gap, as in the presence of inflammatory cytokines, synthesis of reparative tissue and integrative repair cannot occur. Additionally, IL-1 treatment up-regulates MMP activity that promotes the catabolism of the meniscal extracellular matrix [24, 26, 27, 34]. Therefore, a variety of strategies, including blocking proinflammatory cytokines [25], inhibiting MMP activity [26, 79], and/or using anabolic growth factors [24] to increase matrix synthesis and promote cellular proliferation, may be required to promote meniscal healing following an injury and to increase the success of tissue engineering constructs.
In conclusion, we have shown that the inflammatory cytokines IL-1 and TNF-α suppress the proliferation of meniscal cells and suppress integrative meniscal repair, while TGF-β1 overall does not alter the proliferation of cells or meniscal repair. In inner zone meniscal cells, migration is increased by IL-1 treatment but not enough to overcome the suppression of proliferation and fill the micro-wound. However, all other factors did not alter cellular migration independent of proliferation. Therefore, the suppression of cellular proliferation by IL-1 and TNF-α may prevent integrative repair of meniscal lesions by decreasing cell accumulation in the wound, and consequently diminishing the available cell population that can mediate the synthesis of reparative tissue. Therefore, strategies that promote the proliferation of meniscal cells may be able to enhance integrative repair following injury and promote the success of tissue engineered constructs.
analysis of variance
- ASCs:
adipose-derived mesenchymal stem cells
bovine serum albumin
Dulbecco's Modified Eagle's Medium
- EdU:
fetal bovine serum
4-(2-hydroxyethyl)-1-piperazineethanesulfonic acid
human umbilical vein endothelial cells
matrix metalloproteinase
nitroblue tetrazolium chloride
nitric oxide
phosphate buffered saline
sulfated glycosaminoglycan
tris ethylenediaminetetraacetic acid
- TGF-β1:
transforming growth factor-beta 1
- TNF-α:
tumor necrosis factor-alpha
vascular endothelial growth factor.
This study was supported by the Arthritis Foundation, NIH Grants AR50245, AG15768, AR48182, AR48852, and AR55434, and the VA Rehabilitation Research Service. We thank John Finan for Matlab programming assistance. We also thank Robert Nielsen, Kwadwo Owusu-Akyaw, and Karsyn Bailey for technical assistance.
Authors' Affiliations
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This article is published under license to BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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Product Description
Red Maple - Acer rubrum
As it name may suggest, the Red Maple is red all year. During spring it will brighten up your garden with red flowers, in summer its new grown twigs are red, during fall its foliage has a reddish mixture of autumn colours and in the winter small red buds decorate the leafless tree. This tree is the perfect choice for any garden that could use a splash of colour. The Red Maple has a naturally rounded canopy and can grow up to 90 feet. This species of maple is also known as Swamp Maple, Water Maple or Soft Maple - referring to the fact that this tree flourishes in moist areas. However a little drought will not harm the Red Maple in the least, making this tree both beautiful and easy to keep.
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text: A Virginia school district is using a student-centered approach to teaching math, in which students use problem-solving and reasoning to complete problems. The changes -- introduced to help students prepare for new Standards of Learning math tests -- are in place in elementary and middle schools. The teaching strategy also requires students to explain how they arrived at their answers.


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Apologies to Paul Simon, but when I looked at the long list of design ideas I compiled while at the International Builders' Show in Orlando, I thought I'd try to mention 50 of them—a nice round num
Because windows involve both the interior and exterior of the home, installing them can involve a lot of planning. How they look from inside and outside, as well as how the client feels about their privacy, are important considerations. To maximize energy conservation and make the home as comfortable as possible, the right tools and equipment are needed to install and reframe your clients' new windows.
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Photo gallery
Hotel Za' Maria
Get an overview of this hotelRomantic Caronia hotel in Canneto di Caronia with free breakfast
Located in Canneto di Caronia, this romantic hotel is 2.7 mi (4.4 km) from Civic Museum of Ceramics and within 6 mi (10 km) of Castle of Caronia and Sea View Park. Caronia Seafront and Window on the Sea are also within 6 mi (10 km).
Hotel Features
A restaurant, an outdoor pool, and a bar/lounge are available at this hotel. Free buffet breakfast is provided, as well as free WiFi in public areas, free self parking, and free train station pick-up. Additionally, coffee/tea in a common area, a meeting room, and dry cleaning are onsite.
Room Amenities
All 38 rooms offer free WiFi, balconies, and LCD TVs with satellite channels. Minibars, room service, and hair dryers are among the other amenities available to guests.Information missing or incorrect? Tell us!Opens in a new window
Hotel Za' Maria
Hotel Amenities
Hotel Amenities
The hotel offers a restaurant. A bar/lounge is on site where guests can unwind with a drink. A complimentary breakfast is offered. Public areas are equipped with complimentary high-speed wireless Internet access.
This romantic hotel also offers an outdoor pool, multilingual staff, and coffee/tea in a common area. For a surcharge, a roundtrip airport shuttle (available on request) is offered to guests. Complimentary self parking is available on site.
- Babysitting or childcare (surcharge)
- Airport transportation (surcharge)
- Total number of rooms - 38
- Number of floors - 4
- Bar/lounge
- Dry cleaning/laundry service
- Elevator/lift
- Express check-in
- Express check-out
- Front desk (limited hours)
- Laundry facilities
- One meeting room
- Restaurant
- Safe-deposit box at front desk
- Free self parking
- Free train station pickup
- Beach umbrellas
- Beach sun loungers
- Beach towels
- Outdoor pool
- Coffee/tea in common areas
- Wedding services
- Free newspapers in lobby
- Free breakfast
- Free WiFi
- Multilingual staff
- Television in common areas
Available in all rooms: Free WiFi
Available in some public areas: Free WiFi
Free self parking
Room Amenities
- Balcony
- Air conditioning
- Phone
- Minibar
- Daily housekeeping
- Private bathroom
- Free toiletries
- Hair dryer
- Bidet
- Slippers
- Shower/tub combination
- Satellite TV service
- In-room safe
- Desk
- Free WiFi
- Room service (limited hours)
- Free cribs/infant beds
- Connecting/adjoining rooms available
- Rollaway/extra beds (surcharge)
Where to Eat
Guests are offered a complimentary buffet breakfast.
Terrazza Sul Mare - This restaurant specializes in Mediterranean cuisine and serves breakfast, lunch, and dinner. Guests can order drinks at the bar and enjoy alfresco dining (weather permitting).
Room service (during limited hours) is available.
Nearby Things to Do
Recreational amenities at the hotel include an outdoor pool.
The recreational activities listed below are available either on site or nearby; fees may apply.
- Sailing nearby
- Scuba diving nearby
- Windsurfing nearby
- Scooter/moped rentals nearby
- Bicycle rentals nearby
Hotel Policies
Check-in time starts at 11 AM
Special check-in instructions:
Check-out time is noon
Payment types
Children and extra beds
- Children are welcome.
- Rollaway/extra beds are available.
- Free cribs (infant beds)!
- Pets allowed
You need to know
Extra-person charges may apply and vary depending on property policy.
Government-issued photo identification and a credit card or cash deposit are required at check-in for incidental charges.
Special requests are subject to availability upon check-in and may incur additional charges. Special requests cannot be guaranteed.
- Resort fee
Optional extras
- Airport shuttle fee: EUR 75.00 per vehicle (one way)
- Rollaway beds are available for an additional fee
Hotel Name
- Hotel Za' Maria
- Hotel Za' Maria Caronia
- Za' Maria
- Za' Maria Caronia
- Hotel Za Maria Sicily, Italy - Canneto Di Caronia
We should mention
All guests, including children, must be present at check-in and show their government-issued photo ID card or passport. Cash transactions at this property cannot exceed EUR 2999.99, due to national regulations. For further details, please contact the property using information in the booking confirmation. A resort fee is included in the total price displayed. The property has connecting/adjoining rooms, which are subject to availability and can be requested by contacting the property using the number on the booking confirmation.


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Community Photos
New photos added Today Feb 24, 2017
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WHO: Chuck Berry
AKA: The Father of Rock 'n' Roll
CLAIM TO FAME: Chuck Berry took St. Louis' signature sound of the blues, turned it inside out, amplified it and created the worldwide cultural phenomenon known as rock 'n' roll. Beatle John Lennon once said, "If you tried to give rock 'n' roll another name, you might call it Chuck Berry."
NEIGHBORHOOD: Grew up in The Ville neighborhood; resides in Ladue and his Berry Park country estate on the outskirts of St. Louis.
HIGH SCHOOL: Sumner High School (NOTE TO JEN: He never graduated.)
PASSION: The 90-year-young guitar star is a life-long Cardinals baseball fan.
HONORS: His skills as a songwriter and musician, as well as his contributions to American culture have been acknowledged with a Grammy Lifetime Achievement Award, a Kennedy Center Honors Award, addition to the Nashville Songwriters Association International Hall of Fame and was the first artist inducted into the Rock 'n' Roll Hall of Fame. He also has a star on the Hollywood Walk of Fame. Fittingly, Chuck's St. Louis star shines at the entrance to Blueberry Hill, The Loop restaurant and night spot where he thrilled audiences during more than 200 legendary live shows.
MORE: John Lennon speaks about Chuck's musical influence and his son Julian and Chuck sing "Johnny B. Goode" on this clip: http://www.youtube.com/watch?v=5YcPtitpLkk The iconic status of Chuck Berry and his music was a highlight of the original "Back to the Future" movie. Check out the classic film clip at http://www.youtube.com/watch?v=S1i5coU-0_Q.