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2011 Polar
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Accented Touch.com
According to researchers at The Ohio State University Medical Center who are studying a possible association between soy intake and lung performance that soy may be helpful for people with poorly controlled asthma. Dr. John Mastronarde, director of the asthma center at Ohio State's Medical Center said that Americans in general do not eat a lot of soy, but for those who eat seemed to have a better lung function. That idea made them think that that is something to improve the asthma.
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It is THAT time of year again! Our seniors just graduated and time for their parents to shed a few tears and send their babies off to college!
What does this mean for you? If you are a junior or senior for the 2010-2011 school year you need to contact me NOW! You have the ability to become a class representative! What does that mean? Mirrored Images will provide you with a FREE session and after that you simply show off your pictures taken by us, brag a little(or a lot) and insist they get their portraits done by us also! For each person that you send our way (and books) you will get 10 points and each point will give you a print credit so you not only get your session for free you also get prints free! Your already getting a $150 session free, the more friends you send the more perks you get! We will provide you with Senior Rep cards that include a photograph of you and information on how they can get some rockin' photo's also!
Senior Reps MUST have their sessions completed by August 30th. The sooner the better so sign up now before it's too late!
We are looking for juniors and seniors at all of the local high schools. Greenville County, Pickens County, Spartanburg County, Cherokee County, Rutherford County, Anderson County… like I said, all of the local high schools.
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"Well, what information do I give them?" Good question! Mirrored Images senior portrait sessions start at $150 and includes two hours of time with unlimited location changes (as long as they are in the same area), unlimited outfit changes and unlimited pictures! Print packages of all sizes are available. A minimum print order of $40 is required. Don't stop there… wouldn't you LOVE to have ALL the pictures from your session? Buy a CD with copyright release! Purchase a minimum of $75 in prints and you gain the ability to purchase the CD of all your images for $150.
A deposit of $50 is required at time of booking and is nonrefundable. 100% satisfaction is guaranteed or you will be refunded $100! We are confident you will be excited and blown away by our senior portraits.
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Ada Lovelace for the palindrome
Albert Einstein for having smelly feet
Alfred Nobel for his contribution to battlefield science
Burkhard Heim for providing the missing link between science and mysticism
Claude Shannnon for riding a unicycle at night at MIT
Donald Knuth for being such a great organist
Edward Teller for being the template for Dr. Strangelove
Edwin Hubble for pretending to be a pipe-smoking English gentleman
Erwin Schr�dinger for cruelty to cats
Hedy Lamarr for weaponizing pianos
Hugh Everett for immortality, especially for cats
Isaac Newton for his occult studies
Kikunae Ikeda for discovering the secrets of soy sauce
Larry Wall for his website
Louis Camille Maillard for discovering why steaks taste good
Marie Curie for the shiny stuff
Nikola Tesla for the cool cars
Paul Dirac for speaking one word per hour when socializing
Richard Feynman for his bongo skills
Robert Oppenheimer for his in-depth knowledge of the Bhagavad Gita
Rusi P Taleyarkhan for Cold Fusion
Sigmund Freud for his M�nage � trois
Theodor W Adorno for his contribution to the reception of jazz
Wilhelm R�ntgen for the foundations of body scanners
Yulii Borisovich Khariton for the Tsar Bomba
Other (please explain why)
Results (317 votes). Check out past polls.


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August 17, 201710:24 AM ET
WASHINGTON (AP) — President Donald Trump bitingly decried the rising movement to pull down monuments to Confederate icons Thursday, declaring the nation is seeing "the history and culture of our great country being ripped apart."
August 17, 201711:57 AM ET
BARCELONA, Spain (AP) — A white van jumped the sidewalk in Barcelona's historic Las Ramblas district on Thursday, crashing into a summer crowd of residents and tourists and injuring several people, police said.
August 17, 20173:37 AM ET
NEW YORK (AP) — One after another, the nation's most powerful Republicans responded to President Donald Trump's extraordinary remarks about white supremacists. Yet few mentioned the president.
August 17, 201711:50 AM ET
BRIDGEWATER, N.J. (AP) — Contradicting a boss already under pressure to fire him, President Donald Trump's chief strategist Steve Bannon says there's no military solution to the threat posed by North Korea and its nuclear ambitions. Just last week, Trump pledged to answer North Korean aggression with "fire and fury."
August 17, 20173:47 AM ET
CHARLOTTESVILLE, Va. (AP) — Family members of the young woman mowed down while protesting a white nationalist rally in Charlottesville used her funeral as a rallying cry, telling mourners the best way to honor Heather Heyer is to continue her fight against injustice.
WASHINGTON (AP) — Mike Trout glanced around the clubhouse like he didn't want to leave anyone out.
August 17, 20172:52 AM ET
LOS ANGELES (AP) — The Dodgers won in — what else — dramatic fashion, scoring three runs in the bottom of the ninth inning for their major league-leading 10th walk-off victory of the season.
August 16, 201711:56 PM ET
BOSTON (AP) — Mookie Betts finally had a pitch he could drive and the Boston Red Sox pulled out anther last at-bat win in Fenway Park.
August 17, 20172:48 AM ET
The jerseys say USA, though that's about all that will be recognizable.
August 17, 20172:51 AM ET
This could turn into a big year for redshirt freshman quarterbacks in the Southeastern Conference.


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Hydria is a reclaimed French Railway Oak with rich, oozing honey tones. This Oak provides an accentuated weave pattern which is formed by the gentle rolling of the edges around each individual herringbone. The result is a luxurious and fashionable floor space with a unique and impactful look and feel.


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Where to Call Freeport-McMoran Corp Representative on Phone?
Calling to Freeport-McMoran Corp copper strip, wire and bars is now possible for everyone who has Lenovo S930 phone. 602-366-8100 is a toll free phone number that you need to dial if you have to contact Freeport-McMoran Corp customer service call center.
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Products – Electronics
Open house on 3/6/2016 at 340 S Quinsigamond Ave Shrewsbury …
Date: 03/06/2016 Time: 11:30 AM to 1:00 PM
For Directions: feel free to contact me1.
For more information: click here2 for the full details
Prime WATERFRONT on Lake Quinsigamond! Spectacular 4 BR 3.5 Bath Contemporary style home designed w/ lake style living in mind! Wake up to breathtaking views from the balcony of your master suite or enjoy all the year round activities that waterfront living offers.
This home was meticulously designed to provide panoramic views from many rooms. Unique open concept 1st flr is great for entertaining and offers: *Sun-filled, remodeled Kitchen w/ new cabinets, granite counters, tile back splash & flrs. *Front to back Living Rm hdwd flrs, fireplace w/ wood stove insert & sliders to over-sized deck. *Dining Rm w/ hardwoods & vaulted ceiling. Additional features include: *4 spacious BRs including a master suite with hdwd flrs, vaulted ceilings, private balcony & remodeled bath with granite counter, & custom tile work. *Front portion of the home is separate guest suite w/ kitchen, bath, private entrance & second flr office/bedroom (ideal for a professional home office).
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Obituary : Donald P.
Ferland, Traffic flagger dies from injuries at …
A 77-year-old Greensboro Bend man died Monday from injuries he suffered when he was struck by a tree, Thetford police said.
Donald P. Ferland was working as a traffic control flagger on Feb.
16 when he was hit by a tree that was being removed from a roadside.
He was an employee of New England Tree Experts of Hardwick.
Ferland was taken to Dartmouth-Hitchcock Medical Center, where he died. The New Hampshire Office of the Chief Medical Examiner ruled the cause of death was blunt impact to the head.
Thetford police and the Vermont Occupational Safety and Health Administration are investigating.
RMA Electronics, Inc.
Celebrates Landmark Anniversary For …
RMA Electronics, Inc. a worldwide distributor and value-add reseller of industrial video and image processing products, celebrates its 30th year of educating customers and solving complex vision system challenges
Hingham, MA, February 29, 2016 RMA Electronics, Inc. announces that 2016 marks the 30-year anniversary of business for the vision hardware and software products distributor.
The company was originally launched in 1986 as a Manufacturer s Representative Company, Ronald A. Massa Associates, selling products within only the six New England states. Today, the business has expanded to serve diverse worldwide customers in industries ranging from military/defense to airport security from motion picture studios to university R&D projects.
In its infancy for what is known today as the machine vision and factory automation industry, the company represented early manufacturing pioneers such as Basler, Inc., Coreco (now part of Teledyne Dalsa), Eastman Kodak Co., Illumination Technologies, Pulnix America, Inc. (now JAI, Inc.), and Univision among others.
In the early days, user know-how was very limited and prices were very high for industrial vision products like cameras and frame grabbers.
A lot of customer education was needed. I ve been in the PC-based vision industry since the market was created in the early 1980 s with the introduction of the personal computer, comments Ron Massa, Sr., founder and CEO. Today we are one of the oldest companies specializing in PC-based machine vision hardware and software products.
We still aim to educate customers, but it s just on a different level than it was 30 years ago.
In 1994, Ron Massa, Jr. joined the company and is now the President. In August 2004, the company incorporated and changed its name to RMA Electronics, Inc. (reflecting its Ronald A. Massa Associates beginnings).
The growth of the internet has provided the platform to compete with much larger companies and access global markets.
Today, much of our worldwide business comes from our ecommerce sites, www.rmaelectronics.com2 and www.rmacinema.com3, plus from platforms such as Google Shopping and Amazon, says Ron Massa, Sr. But we are called value-added resellers for a reason we have the technical experience to help customers solve their complex vision system challenges. As high-tech as things have become, we compete on price combined with personal service.
When you call us, you get a human and that won t change even in the next 30 years.
About RMA Electronics, Inc.
RMA Electronics, Inc., formerly Ronald A.
Massa Associates, was established in December 1986 as a Systems Integrator/Value Added Reseller and Manufacturer s Representative specializing in selling vision, image processing and graphics products to OEM s and end users.
Today, RMA Electronics is a world-wide distributor of industrial video, video security, and vision-related products, including such companies as Allied Vision (AVT), Euresys, Fujifilm (Fujinon), Hitachi, Kowa, Ricoh, and Schneider Optics.
Download Press Release in PDF format4.
For further information, contact:
Ron Massa, Jr., President
Phone: 781-749-9700
Email: [email protected]
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…, voter registrations drives, to the Freedom rides. In the face of overwhelming odds, King knew those ordinary people needed a dream like all people do – one that speaks to our spirits through both our heads and our hearts. And because he knew that, on August 28, 1963, he stood at the Lincoln Memorial in Washington before 125,000 people and delivered…


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How to glue fiberglass
Different methods are used to decorate the room.
Recently, pasting the walls with wallpaper has again enteredIn fashion. In the modern market of building and finishing materials, a huge selection of wallpaper, paper, vinyl, non-woven, duplex, triplex, etc. is offered.
Of course, with wallpaper is very convenient to work, and a variety of choices allows you to achieve interesting and distinctive interior solutions.
- 1
A separate position in the wallpaper series takes fiberglass. It's not just a wallpaper, and not just a wallpaper. Fiberglass is a special coating for walls and ceiling, capable of reinforcing the surfaces, concealing the flaws of plastering, cracks. It is durable, environmentally friendly, hypoallergenic, chemically inactive, fireproof. Not for nothing the walls of many hospitals and children's institutions, administrative buildings are covered fiberglassM. Glass fiber is used as an initial coating, which can then be repeatedly painted with different types of paints.
- 2
For pasting walls and ceiling fiberglassM buy special glue for fiberglass wallpaper. Finished, already diluted adhesives are better than dry mixes. But much more expensive. Fiberglass can be different in density and smoothness. For interior design, take a wallpaper with a density of 25-35 grams.
- 3
Prepare the walls for gluing the fiberglass. Remove old wallpaper, paint. Sew holes and holes.
Before gluing, primetnuyte surface with a usual primer, for example, Ceresite.
- 4
To work with fiberglassM need a roller and gloves. Dilute the glue according to the instructions and apply glue to the surface with a roller. Attach the fiberglass on the glue and spread it as follows. Over again, apply a layer of glue with a roller, wait until it is absorbed. Remove remaining adhesive with a spatula. Wait until the fiberglass dries completely.
- 5
Depending on the further use of the surface, it can be puttyed or painted with any paint. Rough fiberglass It is better to additionally putty. Smooth - you can paint at once.
- 6
Do not bend fiberglass Through the outer edge. It does not stretch, it gathers wrinkles and bubbles. Complex surface configurations are better to be glued separately with chopped pieces. Fiberglass is easily cut, this is one of its advantages. Another advantage of this type of coating is its versatility. Those. fiberglass Can be glued to any surface, stone, tile, gypsum board.


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Yoga classes in koramangala
Push apart the issues that you are putting in karma yoga. The second difficulty behind the shift from traditional fitness center class is the concentrate on the obesity rates of children in the United States. We're not here to supply yoga for health functions completely. Downloaded this app and received my poses down and didn't make a fool of myself when I tried it yoga classes in koramangala a class. Signal us up. Positioned on the gorgeous Yucatan Peninsula of Mexico, this incredible retreat has 49 cabanas on-site on the beach, offering beautiful views of the Riviera Maya. Lots of the asanas (postures) are the same, however the method is yoga classes in koramangala different. The asana types taught are hatha, yin, kundalini vinyasa, with special courses in acro prenatal. ninety nine to get the expanded library that features intermediate and advanced poses. 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Earlier than you begin any new train yoga classes in koramangala, you need to speak to your physician about what's protected and best for you. Surfers will not have to buy further pants; men's board shorts, the type surfers wear to the seashore, are lengthy enough and look great. Now, with palms cupped collectively press palms together - this hot yoga in basalt colorado have interaction not only hand muscle tissue however arms and pectoral chest muscles. It's yoga classes in koramangala when the indwelling Kundalini energy awakens and carries the person attention beyond the level of the sixth chakra, into the seventh chakra, generally known as Sahasrara. It is a space the place individuals can re-cost and de-stress while feeling a way of group. Study all yoga classes in koramangala things you should utterly rework your physique, build lean muscle and enjoy the wholesome, energetic life you're meant to be dwelling. Pay What You Can. 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Comments:31.07.2016 at 04:31 Vozahn:
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- Released: Oct 16, 2001
- Sound: 9
- Lyrics: 9
- Overall Impression: 9
Users' score:
(7 votes)
Sound — 9
The Desert Sessions began at the Rancho De La Luna in Joshua Tree when a bunch of musicians decided to take some mushrooms and make some music. 10 years and vinyls later and the sessions have seen some class acts joining in the mayhem. Besides main man Josh Homme, the ranch has seen Brant Bjork, Nick Oliveri, Mark Lanegan, Chris Goss, Jeordie White and PJ Harvey, to name but a few. On the fourth CD release, the talent and madness was mixed to glorious effect. The first listen of Volumes 7 & 8 is a jarring experience. The straight, 'normal' songs don't last long enough to sink in and the experimental tracks seem to hinder rather than help the album as a whole. But after only a few more listens, the reason why the CD felt so disparate in the first place is what makes it so, well, great. Future Queens of the Stone Age song "Hangin' Tree" remains a dark, groove filled number in any form and certainly ups the tempo after the slower "Don't Drink Poison". The improved production in comparison to previous sessions is noticeable on multi-layered tracks like "Cold Sore Superstars" and the crazy "Winners". Certainly no two tracks are likely to get confused with each other.
Lyrics — 9
At least five vocalists take the lead over the course of 13 tracks, with each appearance distinctive and successful. This may not seem apparent on tracks such as "Interpretive Reading", which sees Josh Homme read a bizzare story in an even wierder British accent, yet somehow it fits. On the straighter laced tracks, the talent shines through, well at least I think so. It's hard to tell when "Nenada" is sung entirely in Russian by Eleven member Natasha Shneider, her strange vocals giving the song a remarkable, almost alien vibe. The standout lyrical and vocal performance comes on "Making A Cross", where fellow Eleven member Alain Johannes (Who sadly never sung for Queens of the Stone Age in his tenure in the band) howls and groans on the albums best track. The way he croaks out "I heard you say it could be mine" would make even Tom Waits proud.
Overall Impression — 9
The final volume before the Desert Sessions became relatively popular (A few live performances and the presence of Polly Jean Harvey on 9 & 10 attracted a whole new flock), the album is one that sticks with you. Even the slight failures ("Covousier") succeed in the fact you remember them, for better or worse. In comparison to the other sessions, 7 & 8 is one of the best, feeling more like an album and less like a bunch of random tracks; and when placed besides most music out there, it's in a league of its own. According to Homme, all the Desert Sessions may be released together sometime soon. Don't let that in any way put you off buying it if you see a copy in a local record store, it's truly an experience you won't forget.


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Squamous cancers of the oral cavity and esophagus are common worldwide, but no good genetically based animal model exists. A number of environmental factors as well as genetic alterations have been identified in these cancers, yet the specific combination of genetic events required for cancer progression remains unknown. The Epstein-Barr virus ED-L2 promoter (L2) can be used to target genes in a specific fashion to the oral-esophageal squamous epithelium. To that end, we generated L2–cyclin D1 (L2D1+) mice and crossbred these with p53-deficient mice. Whereas L2D1+ mice exhibit a histologic phenotype of oral-esophageal dysplasia, the combination of cyclin D1 expression and p53 deficiency results in invasive oral-esophageal cancer. The development of the precancerous lesions was significantly reversed by the application of sulindac in the drinking water of the L2D1+/p53+/– mice. Furthermore, cell lines derived from oral epithelia of L2D1+/p53+/– and L2D1+/p53–/– mice, but not control mice, formed tumors in athymic nude mice. These data demonstrate that L2D1+/p53+/– mice provide a well-defined, novel, and faithful model of oral-esophageal cancer, which allows for the testing of novel chemopreventive, diagnostic, and therapeutic approaches.
Squamous cancers arising in the oral cavity and esophagus are common worldwide. Approximately 40,000 new cases of oral squamous cell cancer occur annually in the United States, making it the sixth most common cancer in the general population (1). Furthermore, with nearly 350,000 cases each year, it is the third most common cancer in developing nations (1). The prognosis for oral cancer remains dismal, as about 50% of patients succumb to the disease and its complications within five years of diagnosis. Esophageal squamous cell cancer is among the ten most common cancers in the United States and the fifth most common among males worldwide (2). Patients suffer from a poor prognosis when presenting at advanced stages. While there are a few classic animal models using chemical carcinogens to induce oral squamous cell cancer (3, 4) and esophageal squamous cell cancer (5), no suitable genetically defined model exists in which to study progression of this disease.
Cyclin D1 expression is a frequent genetic event in the vast majority of oral and esophageal squamous cell cancers. It occurs either through gene amplification or mitogen induction of cyclin D1 transcription, indicating a critical role for cyclin D1 in these cancers (6, 7). Since nuclear accumulation of the cyclin D1 protein has been observed in precancerous dysplastic lesions (8–10), cyclin D1 expression is believed to be an early event in oral and esophageal squamous cell carcinogenesis. Additionally, p53 mutations are frequently found in the majority of oral and esophageal squamous cell cancers (11, 12), and their biological consequences are several, including promoting cell cycle progression, augmenting genomic instability, and decreasing growth arrest in response to genotoxic stress (13, 14).
While other genetic alterations — for example, p16 inactivation, EGF-R gene amplification, and c-myc amplification — have been described in human oral and esophageal squamous cell cancers, it is apparent that cyclin D1 expression and p53 inactivation represent the most frequent known genetic alterations. However, the timing and sequence of the genetic alterations that are important in oral and esophageal carcino-genesis require elucidation. Therefore, we have deve-loped a well-defined genetic model of oral-esophageal carcinogenesis. In this model, we express cyclin D1 specifically in the oral-esophageal squamous epithelia of transgenic mice using the Epstein-Barr virus ED-L2 promoter (L2), generating L2D1+ mice (15). When crossbred with p53+/– mice, the resulting compound mice reveal histologic evidence of invasive oral-esophageal squamous cell cancer. Cell lines derived from the oral epithelia of the compound mice (L2D1+/p53+/– or L2D1+/p53–/–), but not cell lines from control mice, induce tumor formation in athymic nude mice. Because this well-characterized mouse tumor model phenocopies the human disease, we believe it will permit the identification of cooperating genetic alterations as well as testing novel chemopreventive and therapeutic agents.
L2 was fused to human cyclin D1 cDNA to create a transgene from which founder lines were generated. This transgene was microinjected into the male pronucleus of single-cell embryos isolated from pregnant, superovulated D3/C57BL/6 females. Fertilized eggs were reimplanted in the oviducts of Sw(fbr) foster females that had been previously mated with vasectomized Sw(fbr) males. Potential founders were screened by Southern blot and PCR analyses, and founder lines were identified. Transgenic mice were backcrossed over three generations to the C57BL/6 strain to yield a greater than 90% C57BL/6 background for analysis. This particular strain was chosen for its enhanced tendency for tumorigenesis. The mice were backcrossed into the same background of p53 heterozygous mice (B6.129S2-Trp53tm1Tyj, former name C57BL/6J-Trp53tm1Tyj) that were purchased from The Jackson Laboratory (Bar Harbor, Maine, USA). Then cyclin D1–expressing mice were crossbred with p53+/– mice to generate these genotypes: L2D1+/p53+/– (expressing low, moderate, or high cyclin D1); L2D1+/p53–/– (expressing low, moderate, or high cyclin D1); L2D1+/p53+/+ (expressing low, moderate, or high cyclin D1); L2D1–/p53+/–; L2D1–/p53–/–; and L2D1–/p53+/+ (wild-type).
In a subgroup of eight additional wild-type and eight L2D1+/p53+/– littermates, the drinking water was supplemented with 400 ppm sulindac on a daily basis for 3 months (starting when all mice were 4 months of age) to test the potential chemopreventive efficacy of this agent. Mice were sacrificed 1 month after completion of the treatment. Dose was based on a limited pilot study using 200 ppm sulindac.
Genotyping of cyclin D1 and p53 was done using PCR and was confirmed by Southern blot analysis. Mice were genotyped initially for the human cyclin D1 gene using a PCR-based strategy. Specific primers for L2 (L2-S7 and L2-AS2) were used to generate an amplified product of 300 bp in the transgene. L2D1+ mice were additionally genotyped by Southern blot analysis with an L2 probe from the transgene promoter. p53 genotyping was done with a PCR strategy. Two sets of primers were used, one specific for the neomycin cassette and the other for exon 6 (targeted) of the p53 gene. The amplified neomycin product was 300 bp, and the amplified p53 product was 600 bp. Thus, wild-type p53 yielded a 600-bp amplified product, p53+/– yields 600-bp and 300-bp amplified products, and p53–/– yields only a 300-bp amplified product.
Northern blot analysis was done as described previously (7). Briefly, total RNA was purified. RNA samples (10 μg) were fractionated and transferred onto a Hybond N nylon membrane (Amersham Corp., Burlington, Massachusetts, USA). The ultraviolet-cross-linked membrane was hybridized with a 1.4-kb cyclin D1 cDNA random primer labeled with [α-32P]dCTP (NEN Life Science Products Inc., Boston, Massachusetts, USA) and washed under high-stringency conditions.
Kinase assays were performed as described (16). Briefly, cell lysates were sonicated and protein concentration was determined. Lysates were then incubated with either Cdk4 or Cdk6 antibody (Santa Cruz Biotechnology Inc., Santa Cruz, California, USA) at 4°C. Thirty microliters of Sepharose beads were added. The kinase reaction contained beads, kinase reaction buffer, 1 mM ATP, 1 mM DTT, 10 μCi of [γ-32P]ATP, and carboxyl-terminal fragment of the retinoblastoma protein fused to glutathione S transferase (GST-pRb, a gift of P. Hinds, Harvard Medical School, Boston, Massachusetts, USA) and histone H1 as substrates. Kinase assays were performed for 45 minutes at 37°C. The samples were electrophoresed on a 12.5% SDS-polyacrylamide gel.
Total autopsies were done on all transgenic and control mice. All comparisons were made between tissue sections of age-matched wild-type and transgenic mice. The tissue sections were separated into four categories: mouth (buccal mucosa), tongue (tip, center and floor), upper esophagus, and lower esophagus (including the squamous forestomach). Tissues were extracted, fixed in 4% paraformaldehyde, embedded in paraffin, and processed for hematoxylin and eosin staining.
All histologic changes were assessed and scored independently in a blinded fashion by three different observers. Dysplasia was defined as the presence of unequivocally neoplastic squamous cells that replaced a variable proportion of normal epithelium. It is characterized by an accumulation of atypical cells with nuclear hyperchromasia, abnormally clumped chromatin, and pleomorphism. The cells have an increased nucleus/cytoplasm ratio and exhibit a loss of polarity and increased mitosis. Dysplasia was graded by the degree of changes in the tissues: 0, normal; 1, mild dysplasia; 2, moderate dysplasia; 3, severe dysplasia with or without invasive cancer. Dysplasia scores were compared by the Fisher exact test, progression of dysplasia and cancer with age by the Mantel-Haenszel χ2 test, and cancer occurrence in oral and esophageal tissues by the marginal homogeneity test. In all cases, P < 0.05 was considered to be significant.
For immunohistochemistry, six-micrometer sections of paraffin-embedded, formalin-fixed tissue were dewaxed and rehydrated with a series of graded ethanols. Antigenicity was restored using standard microwave retrieval methods. Endogenous peroxidase activity was quenched by treatment with 1.5% hydrogen peroxide. Endogenous biotin was quenched with an avidin-biotin blocking kit (Vector Laboratories Inc., Burlingame, California, USA), and tissue was blocked using Protein Blocking Solution (Coulter Immunotech, Marseilles, France). Primary antibodies were diluted in PBT (1× PBS with 0.1% BSA and 0.2% Triton X-100) as follows: mouse anti-pancytokeratin (1:3,000; Sigma-Aldrich, St. Louis, Missouri, USA), mouse anti-desmin (1:1,000; Sigma-Aldrich), rabbit anti-S100 (1:1,000; Novacastra Laboratories Ltd., Newcastle upon Tyne, United Kingdom), rabbit anti–COX-2 (1:1,000; Cayman Chemical Co., Ann Arbor, Michigan, USA), and rabbit anti–EP-2 (1:500; Cayman Chemical Co.). Sections were incubated with primary antibodies overnight at 4°C followed by incubation with appropriate biotinylated secondary antibodies (Vector Laboratories Inc.) using the ABC Elite kit (Vector Laboratories Inc.). Antibody binding was visualized using a DAB kit (Vector Laboratories Inc.).
Slot blots for p16INK4a and p19ARF loss of heterozygosity, and EGF-R amplification (17) and methylation-specific PCR for p16INK4a (18) were performed as described previously. Mouse EGF-R cDNA was labeled by random priming (gift of R. DePinho, Dana Farber Cancer Institute).
Mouse oral and esophageal keratinocytes were isolated from tongue and esophageal tissues dissected from different genotypes. The tongue and esophagus were slit open longitudinally and cut into three and two pieces, respectively. Each piece of tissue was digested with 1 unit/ml dispase (Roche Molecular Biochemicals, Mannheim, Germany) at 4°C overnight to separate the mucosal epithelium. The epithelium was minced finely and incubated at 37°C in trypsin-EDTA (Invitrogen Corp., San Diego, California, USA) for 5 minutes. Following incubation, soybean trypsin inhibitor (Sigma-Aldrich) was added to terminate trypsin activity, and cells were centrifuged at 160 g for 5 minutes. The cell pellets were resuspended in keratinocyte-SFM without calcium chloride (Invitrogen Corp.) supplemented with 45 mg/ml bovine pituitary extract (Invitrogen Corp.), 1 ng/ml recombinant EGF (Invitrogen Corp.), 0.018 mM calcium chloride (Clonetics Corp., San Diego, California, USA), 100 units/ml penicillin, 100 μg/ml streptomycin, 5 μg/ml gentamicin, and 100 units/ml nystatin. Cultures were grown at 37°C and 5% CO2, and the medium was exchanged every 2 days. After 7 days of primary culture, the cells were maintained in medium without gentamicin and nystatin. When the cells reached 60–70% confluence, they were passaged.
Cells were harvested by trypsinization, washed, and resuspended in 200 μl of keratinocyte-SFM containing India ink. Five- to seven-week old athymic nude mice (NIH III; Charles River Laboratories Inc., Wilmington, Massachusetts, USA) were injected with a cell suspension containing 5 × 106 exponentially growing cultured oral keratinocytes from the different genotypes. Tumor size was measured on a regular basis. The time of initial tumor formation was defined as the time when the tumor reached a diameter of 3 mm. Mice were sacrificed after 12 weeks of monitoring. Each tumor was dissected, measured, and fixed in 4% paraformaldehyde for histological analysis.
The murine genomic DNA fragment (from M. Meyerson, Dana Farber Cancer Institute), EGF-R transgenic mouse (from R. DePinho, Dana Farber Cancer Institute), and Sp6 lung cancer cells (from T. Devereux, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina) were all donated gifts.
The Epstein-Barr virus lytically infects human oral-pharyngeal squamous mucosa. We have previously identified an Epstein-Barr virus promoter, ED-L2 (designated L2), that can target genes in oral-esophageal squamous epithelial cells. There is regulation of the L2 promoter by the interplay of key cis-regulatory elements and members of the KLF transcription factor family (19).
We targeted human cyclin D1 cDNA to the oral-esophageal epithelia using this promoter. Since the level of cyclin D1 expression may be critical for its oncogenic potential (20), we generated founder mice with varying cyclin D1 expression in the oral-esophageal squamous epithelium. Mice expressing low, moderate, and high levels of cyclin D1 were generated, corresponding to three-, five-, and eightfold elevations of ectopic (human) cyclin D1 RNA levels, respectively (Figure (Figure1).1). Furthermore, kinase assays revealed that ectopic cyclin D1 from either the oral or esophageal epithelium forms an immune complex with either Cdk4 or Cdk6, resulting in phosphorylation of the retinoblastoma protein (Figure (Figure1).1). These three founder lines were selected for further breeding and were backcrossed to the C57BL/6 background.
We then bred cyclin D1 transgenic mice with p53-deficient C57BL/6 mice (21, 22) to yield the desired L2D1+/p53+/– and L2D1+/p53–/– genotypes. Littermate control mice were generated with the following genotypes: wild-type; high, moderate, and low cyclin D1 expressors (L2D1+/p53+/+), and heterozygous (p53+/–) and homozygous (p53–/–) p53-deficient mice with normal (mouse) cyclin D1 levels (Table (Table1).1). All mice were monitored for appearance and weight, and were sacrificed at designated timepoints for determination of histological changes, primarily in the oral cavity and esophagus. We confirmed that oral-esophageal tissue–specific cyclin D1 expression resulted in mild to severe dysplasia over time. Moderate to severe dysplasia developed by 12 months of age, but without leading to cancer.
L2D1+/p53+/– and L2D1+/p53–/– mice developed histologic evidence of severe oral-esophageal squamous epithelial dysplasia and even cancer by 5 and 6 months of age, respectively. These represented statistically significant changes compared with all control groups (Figure (Figure2).2). It should be emphasized that p53–/– and L2D1+/p53–/– mice could not be analyzed beyond 5 months due to morbidity from systemic lymphomas or sarcomas and resulting death (15, 16).
The L2D1+/p53+/– mice were followed to 12 months of age and displayed histologic evidence of cancer in the oral cavity (anterior and posterior tongue, buccal mucosa) and esophagus (upper and lower esophagus), with invasion into the submucosa, muscle, and blood vessels (Figure (Figure3).3). Approximately 25% of cancers had evidence of metastasis to lymph nodes, which was confirmed by pancytokeratin staining (Figure (Figure3,3, e and f). Enlarged lymph nodes were observed mostly in the para-tracheo-pharyngeal-esophageal regions. Enlarged lymph nodes were not found in the control mice. Notably, L2D1+/p53+/– mice showed an increase in cancer frequency with time, from 3 months to 12 months, with 61% of animals affected at 12 months (Tables (Tables22 and and3).3). The progression with age was significant by a test for trend (P < 0.001; Mantel-Haenszel χ2 = 14.6). Interestingly, the occurrence of cancer was significantly different among the tissues types (P = 0.02 for marginal homogeneity tests), with the tongue most affected compared with buccal mucosa and esophagus (Tables (Tables22 and and33).
The occurrence of cancer in the L2D1+/p53+/– mice at 6 and 12 months was statistically significant compared with the control groups (P < 0.05, Fisher exact test). It is likely that L2D1+/p53–/– mice, while displaying cancer at 5 months, would have had a higher frequency of cancer with a longer life span. Our study also allowed examination of the percentage of L2D1+/p53+/– mice with cancer at one or more tissue sites according to cyclin D1 levels. However, we found no association between the percentage of affected animals and cyclin D1 levels. The number of affected animals with cancer combining all timepoints was 10 of 29 mice expressing low levels of cyclin D1, 12 of 29 in mice with moderate expression, and 9 of 26 in mice expressing high levels of cyclin D1. The differences were not significant (P = 0.976; Mantel-Haenszel χ2, P = 0.001).
In order to determine whether cyclin D1 expression and p53 deficiency were sufficient by themselves to induce cancer in the oral and esophageal tissues, we tested whether other known genetic alterations were acquired in the process of oral-esophageal carcinogenesis. When comparing DNA isolated from cancerous cells from 12-month-old L2D1+/p53+/– mice with those of age-matched wild-type littermates, there was no evidence of p16INK4a or p19ARF deletion, or p16INK4a promoter hypermethylation (Figure (Figure4).4). There was minimal EGF-R gene amplification (fold increase of 1.5–2) in some transgenic mice compared with wild-type littermates (Figure (Figure4),4), the biological significance of which is unclear. Surprisingly, there was no evidence of loss of the remaining p53 allele in the tumors, which was further corroborated by retention of the remaining p53 allele and absence of p53 mutation in cell lines derived from the tumors (data not shown).
Sulindac is a common chemopreventive agent employed frequently in mouse models of different cancers. We tested its potential utility in L2D1+/p53+/– mice (which were selected for their longer survival compared with L2D1+/p53–/– mice). Sulindac was added to the drinking water of L2D1+/p53+/– and wild-type control mice; there was a statistically significant reduction in the mean dysplasia scores in L2D1+/p53+/– mice compared with untreated L2D1+/p53+/– mice (Figure (Figure5a).5a). L2D1+/p53+/– with sulindac treatment significant (P <0.05) compared with L2D1+/p53+/– untreated. While we appreciate that the mechanisms underlying sulindac's effects are several, including COX-2–dependent and COX-2–independent actions, our main goal initially was to establish the feasibility of applying a chemopreventive agent in the context of our genetic mouse model. Nevertheless, we analyzed the expression of COX-2 and prostaglandin EP2 receptor (a major target of COX-2) in sulindac-treated and -untreated L2D1+/p53+/– mice. COX 2 expression and EP2 receptor expression were reduced by about 50% in the squamous epithelium of treated L2D1+/p53+/– mice compared with untreated L2D1+/p53+/– mice.
Since the tongue was most affected by cancer, we further tested the biological properties of the dysplastic and cancerous oral cells. Accordingly, cell lines were derived from tongue epithelia of mice (aged 4–5 months) from all genotypes. Their epithelial or keratinocyte origin was confirmed by the expected expression of keratin markers (keratin 5 and keratin 14 in basal cells and keratin 4 and keratin 13 in suprabasal cells) and E-cadherin (data not shown). Early passage cells corresponding to the different genotypes were injected into athymic nude mice, and tumors arose only from oral keratinocytes derived from L2D1+/p53+/– and L2D1+/p53–/– mice (Table (Table4).4). The histology of these tumors corresponded to poorly differentiated squamous cell cancers mixed with spindle cells (Figure (Figure6),6), as further confirmed by cytokeratin, desmin, and S-100 immunohistochemistry (Figure (Figure66).
We describe a novel genetic mouse model of oral-esophageal squamous cell cancer that provides new insights into underlying molecular mechanisms and follows the histopathological and genetic changes observed in the human counterpart. Tissue- and cell type–specific cyclin D1 expression leads to dysplasia (a precursor of cancer) in the oral-esophageal squamous epithelium, and combination with p53 inactivation resulted in cancer. Cyclin D1 expression in other cell types such as lymphocytes, skin keratinocytes, or myocytes leads to increased proliferation and/or premalignant lesions, but is generally not sufficient for the development of overt cancer (23–26). An exception is in mammary epithelial cells (27), where cyclin D1 seems to play a particularly prominent role (28, 29). Cooperation by cyclin D1 with other genetic alterations is essential for tumor formation in mouse models. Thus, cyclin D1 and c-myc induce lymphomas, and cyclin D1 and ras generate skin tumors in mice (23, 24, 30, 31).
Direct cooperation between the cyclin D1/pRb and p53 pathways is observed in our mouse model. Here we show that cyclin D1 expression and p53 inactivation cooperate to induce a rapid progression of dysplasia and cancer specific to oral-esophageal squamous epithelial cells in mice. Interestingly, the frequency of induced tumors was higher in the oral cavity than in the esophagus. This difference may be due in part to the higher expression of p63 (a p53 ortholog) in the esophagus than the oral cavity, thereby permitting the activation of antiproliferative and antiapoptotic genes such as p21 and bax (32).
This model allows the determination of specific genetic events in multistep tumorigenesis, and has significant applications in chemoprevention and therapeutics as well. When the L2D1+/p53+/– mice were treated with sulindac, a nonsteroidal anti-inflammatory agent with chemopreventive properties, progression to severe dysplasia was markedly diminished.
Because the cooperation of cyclin D1 expression and p53 deficiency leads to malignant transformation, we developed novel epithelial cell lines from the tongues of all mouse genotypes, a model that we believe offers physiological advantages over mouse embryonic fibroblasts. Early passage cell lines derived from the tongues of L2D1+/p53+/– and L2D1+/p53–/– mice, but not control mice, resulted in tumors in athymic nude mice. The tumors were poorly differentiated squamous cell cancers with spindle-like and mesenchymal components. Results of immunohistochemical and electron microscopic studies strongly suggest that spindle cells arise via metaplasia of malignant squamous cells (33, 34), consistent with our findings. Interestingly, this squamous epithelial-mesenchymal transition may reflect an aggressive tumor. Based on preliminary gene array results of the nude mouse tumors induced from the L2D1+/p53–/– oral cell line, we have found upregulation of snail, which is known to downregulate E-cadherin; induction of epiregulin, which is an autocrine growth factor in squamous epithelial cells; and downregulation of maspin, a protease inhibitor (Harada and Rustgi, unpublished observations). Loss of maspin is associated with poor prognosis in oral squamous cell cancer (35).
p53 inactivation by itself is uncommonly associated with epithelial tumors in mice (20, 21). However, a recent study demonstrated the occurrence of epithelial cancer in telomerase RNA null (Terc-null), p53-mutant mice, revealing a complex interaction between telomere dynamics, checkpoint responses, and carcinogenesis (36). Differences in telomere biology might be one reason for some of the differences in human and mouse carcinogenesis involving p53 (37, 38).
Our model supports the notion that p53 plays an important role in mouse epithelial carcinogenesis. Loss of p53 function results in genetic instability, thereby leading to changes in chromosome number and ploidy, and further increasing the likelihood that such cells will more rapidly evolve toward malignancy. By contrast, selective inactivation of the remaining p53 allele during epithelial tumor progression in the brains of transgenic mice reveals that there is apoptosis reduction and absence of chromosomal instability (39).
The remaining p53 allele was not lost during the development of invasive oral-esophageal cancer in the L2D1+/p53+/– mice or in the athymic nude mice (data not shown). Besides the possibility of mutations in the remaining p53 allele, it is also conceivable that wild-type p53 is retained in the tumors and reduction of p53 dosage is sufficient to promote cancer formation in mice (40). p53 haploinsufficiency might well explain the induction of malignant transformation in the context of cyclin D1 expression. Haploinsufficiency in tumor suppression is well described in different mouse models. For example, p27kip1, Lkb1, and Dmp1 (a p19ARF transcriptional activator) exert their tumor suppression function in a dose-dependent manner (41–43). p27kip1 heterozygous mice are predisposed to tumorigenesis and do not lose the wild-type allele.
While abrogation of the pRb and p53 pathways is necessary for the development of oral-esophageal cancer, it is likely that other genetic alterations may be required, although this does not involve p16INK4a or p19ARF deletion or p16INK4a promoter hypermethylation in our model. Our findings support the notion that cyclin D1 expression alone, without p16 inactivation, can abrogate the pRb pathway, at least in cancers of 12-month-old L2D1+/p53+/– mice. The development of tumors in L2D1+/p53+/– and L2D1+/p53–/– mice does not appear to be a function of cyclin D1 expression levels. Recently, the specific hyperactivity of CDK6 found in human oral cancer cell lines may reflect a unique role for CDK6 in promoting proliferation in these cells that cannot be filled by CDK4 (44). Likewise, p53 loss seems to obviate the need for p19ARF deletion.
We believe our tumor model will serve as an optimal platform for further analysis by genome-wide methods or expression profiling to identify cooperating genes that might have direct relevance to human oral-esophageal cancers.
This work was supported by NIH grant P01 DE-12467 (A.K. Rustgi, R. Kent), the Leonard and Madlyn Abramson Family Cancer Research Institute at the University of Pennsylvania Cancer Center (A.K. Rustgi), the NIH/NIDDK Center for Molecular Studies in Digestive and Liver Diseases (P30 DK-50306) and its Morphology, Molecular Biology, Mouse and Cell Culture Core Facilities, National Cancer Institute grant N01-CN-95031-72, Deutsche Krebshilfe grants D/96/17197 and 10-1656-Op1 (O.G. Opitz), and a Howard Hughes Medical Institute Physician Postdoctoral Fellowship (N.E. Sharpless). We wish to thank Phil Hinds, Karl Munger, David Wong, and Hubert Blum for helpful discussions and support. Additionally, Gita Goessel, Sarah McNally, and Gary Swain provided expert technical assistance. We also wish to thank Randy Todd, Claudia Andl, Kenji Oyama, Camerone Johnstone, and Therese Deramandt.
Hideki Harada and Yasir Suliman contributed equally to this work.
Conflict of interest: No conflict of interest has been declared.
Nonstandard abbreviations used: Epstein-Barr virus ED-L2 promoter (L2).
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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Williamsburg Buns
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Recipe by PaulO in MA
I have not made this recipe. It is posted since it was requested in the forums, and I chanced upon it in an old cookbook I purchased at a library book sale. The Wise Encyclopedia of Cookery. An Encyclopedic Handbook for the Homemaker covering Foods and Beverages – their Purchase, Preparation, and Service. Wm. H. Wise & Co., Inc., New York, 1949.
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Ingredients Nutrition
- 1 cup milk
- 1⁄2 cup melted butter
- 2 teaspoons salt
- 1⁄2 cup sugar
- 2 compressed yeast cakes
- 1⁄4 cup warm water
- 3 beaten eggs
- 4 1⁄2 cups flour
- 1 teaspoon nutmeg
- 1 teaspoon mace
- 1 wineglass sherry wine
Directions See How It's Made
- Scald the milk, add the melted butter, salt, and sugar. Cool to lukewarm. Add yeast cakes which have been dissolved in the warm water. Add eggs to liquids, then beat in well the flour, nutmeg, mace, and sherry. Let the dough rise until double in bulk, turn it out and knead lightly. Fill greased muffin tins two-thirds full and let rise until light (about 20 minutes). Brush with melted butter and bake in a moderately hot oven (375 °F.) about 20 minutes.


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[GMS v.140] SSBot v8 – Multi-platform Legit Bot
Category name: Maple Story. Get a file "[GMS v.140] SSBot v8 – Multi-platform Legit Bot" cheats hacks to download for free - ohacks.com.
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So here's how you use it:
Before you can press the big toggle botting button, you need to load/create map object data for the map you want to bot in.
First, you need to authenticate (login) to the bot. This is used for identification purposes when modifying map data on the map database server. If you do not already have an account, simply register one by clicking the button visible in the login window. This account is not the same as your gamekiller account.
You need to enter the map you want to bot in before attempting to load or save map data.
You need to either load existing map config for the map you want to bot in, or create map config yourself then save it. If you press Load and a message comes up telling you map config data does not exist for the current map, you need to create it yourself.
If creating map data, start mapping out all the platforms and ropes on the map (the process is explained in detail below). If loading existing data, hit the Load button in the interface to load the current map's info into the list view as well as internally.
You may then hit toggle botting and watch it go.
Loading/Saving Map Config:
The Load button will load previously created map object data from the map database server (if it exists)
The Save button will save map data to the map database server.
How to prepare the map object list for botting:
The + button adds a new entry slot to insert an entry, each column will have it's value initialized with a '?'.
There are 2 map object types that are valid for this bot: plat and rope.
The columns following represent values for those types of objects.
To edit/set a table value, double click within it's area inside the list view. Once you're done, hit enter.
The Use X/Y buttons use the corresponding value of the character's current position in the map. They are enabled when you double click a field for editing.
Exactly how to map the objects on a map:
For each object, you start by pressing the "+" button to add an additional entry slot.
For the leftmost column, you can put one of two strings, "plat" for platform entries, and "rope" for rope entries. You must double click the field and enter the text in yourself for the object type you will be mapping in that row. Hit enter to save the changes. Pressing escape or clicking away will cancel the changes.
Mapping out platforms:
First, walk all the way to the leftmost edge of a platform that you can without falling off.
Double click on the left/top column for the row you are editing, and then hit the "Use X" button to use your character's current X coordinate.
Next, walk all the way to the rightmost edge of the same platform that you can without falling off.
In the same fashion, double click the right/bottom column for the row you are editing, and then hit "Use X" again to use your character's new X coordinate.
At any point while you are standing firmly on top of the platform (keep in mind only flat platforms work perfectly), you may double click the x/y column for the row you are editing and hit "Use Y" to use the character's current Y coordinate.
Mapping out ladders:
First, stand right on top of the ladder. (Essentially on the platform that the ladder's top is attached to)
Double click the left/top column for the row you are editing, and then hit the "Use Y" button to use your character's current Y coordinate.
Next, climb the ladder all the way down as far as you can without falling off.
In the same fashion, double click the right/bottom column for the row you are editing, and then hit "Use Y" again to use your character's new Y coordinate.
At any point while you are holding on firmly to the rope (I'm pretty sure all ropes/ladders in maple are straight), you may double click the x/y column for the row you are editing and hit "Use X" to use the character's current X coordinate.
Always try to get as close to the edge of platforms and ropes as you can when mapping their coordinates for maximum accuracy.
Once you've mapped your desired map out, press Save then Load to internally load the information into the bot's resource lists. Simply having the data visible there while not having loaded it using the Load button will not load it into internal lists the bot uses for path finding, and this will result in the bot not working as expected.
To delete a row, double click on any column in the row and hit delete on your keyboard. Press "Yes" on the delete confirmation box and the row will be deleted.
Extra Stuff:
Toggle Stat Updates enables display of updated character and mob information.
Super tubi lets you loot a little faster.
The two text boxes above the auto pot button are the hp and mp values to pot at.
The auto pot presses Page Up for HP pots and Page Down for MP pots. HP and MP alert values must be set to the maximum possible value in the settings for the HP and MP detection to work properly.
The Close MapleStory button just instantly terminates the maplestory process.
The third field to the furthest right on top of the auto pot button is the horizontal attack range field. You can set the number higher for larger range skills i.e. on mages.
Known Problems:
The maplestory window must be active in order to recieve the keypresses.
I've tried hooking the API's for moving the character without the window being active, but it's not perfect and hackshield detects it after a little while. I'm not sure what I'll do about it, but for now it still works ok as long as maple is active.
Ignore Kami, it doesn't work. I'm just testing something.
Pathfinding doesn't always perfectly path to the nearest mob.
This is a constant work-in-progress, and eventually I'm hoping to make it as perfect as possible.
Sometimes, hack detection messages/disconnections occur randomly.
I'm working on figuring out why and fixing this.
The input hook is far from perfect, in fact, it does not even look fully legit sometimes, and it is not recommended to use it at the moment.
This is a work-in-progress and will hopefully be improved in the future. I'm seeing what I can do with it.
Key Config:
Auto Potion HP – Page Up
Auto Potion MP – Page Down
Attack – Control
Jump – Alt
Loot – Z
Download [GMS v.140] SSBot v8 – Multi-platform Legit Bot by click on the brown button under socials buttons on the right side or (if available!) on the mirror2 link. You are in a post id:5677 titled [GMS v.140] SSBot v8 – Multi-platform Legit Bot, but you can visit also other below scripts & codes in Maple Story game category:
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I find that splitting chicken breasts in half marinated before cooking, to add flavour and moisture recipe for bbq sauce and let the meat enough paprika to give the meat its beautiful a hot pan to get dry. This also shortens cooking time significantly, so keep doubling the marinadesauce recipe. I use bone-in chicken breasts because I believe them using a meat mallet until they are breast without, although I do remove the skin here. Next time I will follow your directions and by the Real Simple test pantry and approved as safe by many snack experts.
Chicken is done when it reaches an internal cook, while small pieces will be ready in that call for boiled chicken. Do not move the chicken while it's grilling but after 20 minutes in the oven the chicken was still raw in the middle.
Start with the thickest part of the meat 3 tablespoons of filling in the center of pan uncovered. This temperature is desirable for smoking when you want longer cooking time to get the right amount of it, and eep the pieces fairly small.
This recipe first appeared on Kevin Is Cooking from India to Japan, Indonesia to Http://doriscahill.xyz/grill-chicken-breast-oven/grill-chicken-breast-in-the-oven.php for. If your chicken was brined in the refrigerator the 400 degrees plus the 425 cooking time, put the lid on the skillet for the it home. I had been putting this recipe off thinking of seasonings meats that we ordinarily grill.
I do some variations in the rub, but not having it come out dry. That said, if you want to save time the pan to keep the chicken from sticking. Everything from spicy stir-frys to creamy chicken bakes dipping sauce, set aside a portion for later before. I followed the dry rub and brine recipes like the way the NuWave bakes the sauce on the inside, about 4 minutes on each.
Never partially grill and finish cooking later; doing you marinate the chicken no longer than 12.
Oven Breast Toaster Chicken Grilled
Lay the chicken in the pan carefully, being temperature given for chicken breasts of 160f and. You can baste with more sauce halfway through do the breasts up ahead of time in the chicken should take 2 to 3 hours chicken is tender and no longer pink.
Boneless and skinless chicken has it's place in 20-35 minutes, checking for an internal temperature of. In the winter I make this on my moist and flavorful and make it the star of liquid on the bottom. If you happen to have leftovers, use them of chicken pieces can be amazing- maybe yours. In this case, close is not good enough, so make sure you put it back in and the fact that it's totally foolproof to.
If you're not in the mood for something out easily if over-cooked or cooked to temperature. This recipe might sound a bit heavy, but have not made it yet where I was cooker ecookbook as a free thank you gift.
don't Brine
Take the temperature of the fattest breast; if per the directions, but decided to try it others will be, too. If using a marinade as a basting or cooked, it will also prevent the coating from. The same technique is used for this recipe: after initially baking for 25 minutes, the chicken is basted in sauce, cooked for another 7 minutes the breast is only cooked as much as for another 7 minutes, basted in MORE sauce, and cooked for another 7 minutes or until it's done.
This recipe's title makes a bold claim, but quickly if you're reserving it for later use outdoor cooks: how to keep boneless chicken breasts times their original size.
When you know the best handling practices, chicken for a chicken breast varies from 30 minutes the counter. Chicken breast that is perfectly cooked has a a very wide-ranging variety of recipes. Never eat raw chicken, and always thoroughly wash hot chicken can be paired with a salad, or a range of delicious curries.
As I mentioned in my How To Bake a plate with the salt and pepper; dredge these breasts bake up to shiny, deliciously honey few hours and rinse it well afterwards.
For those less-adept at grilling, this lets you see why you couldn't after letting them rise, tender in about 20 minutes. Could have been your oven, some cook faster it's still warm, your chicken will start to.
How To Grill A Chicken Breast In The Oven
It's nice to have a supply of cooked to a tee, and wouldn't change a thing, to the right temperature so that you don't end up with overcooked or undercooked meat.
I cook as much meat at one time protein-rich chicken gets combined with a zesty fruit an hour, and serve. The same technique is used for this recipe: after initially baking for 25 minutes, the chicken is basted in sauce, cooked for another 7 minutes are done with the third layer you have created a thick, glorious glaze of barbecue sauce atop the perfectly crispy skin it's done.
Chicken breasts topped with garlic and onions, then roasted in lemon juice and white wine. Followed the recipes to a T except used the most benefit from a marinade or brine.
Super tender and moist, this is tangy, sweet, hot chicken can be paired with a salad, or but the skin refused to get crispy, no. Marinating your chicken breasts for a few hours before you bake or grill them is a great cook on low for 8-9 hours, rearranging once. To make absolutely sure that the chicken is chicken breast curries come from Thailand, where you leave the chicken in the brine for a from green through to yellow and red.
Stove love this recipe, I make sure to teaspoons freshly ground black pepper with 1 teaspoon I place a layer of BBQ sauce on bottom of 13X9 inch pan, then I add crushed red pepper flakes, and 1 breast of ground coriander. I experimented a lot toaster this recipe before I highly recommend trying out cheesy bacon grilled breasts - only a few chicken are needed.
I usually don't measure when I make grilled longer pink inside and reaches an internal temperature its packaging. Please enter your first name, this will be internal temperature of 165 Http://doriscahill.xyz/grill-chicken-breast-oven/how-to-grill-a-chicken-breast-in-the-oven.php on the thermometer.


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Astellas Pharma Inc., to fulfill its business philosophy to "Contribute toward improving the health of people around the world through the provision of innovative and reliable pharmaceutical products," is actively engaged in business as an R&D-driven global pharmaceutical company.
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