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Northwest High School teacher and Justin resident Gwen Hilliard has received more than her share of bad news lately.
This Justin...
This Justin Weekly – Friday, January 25, 2013
EVANS RESIGNS AS CITY MANAGER - Justin City Administrator and recently-appointed City Manager Mike Evans has announced he is retiring, and today is his last day. The city council held a special meeting Wednesday night to name a possible interim, but they decided to use a search firm to choose a city manager. City Secretary Kim Strange said the council has not yet chosen the search firm, but when they do, the firm will most likely provide the city with an interim city manager. Voters approved the city manager position in last November's general election, and Evans was appointed as city manager by the council in December.
Lewisville man arrested for murder of Justin resident
Flower Mound police arrested Anthony Tri Huynh, 40, Saturday in connection with the shooting death of Justin resident Lamont White, 54 on Jan. 1 in Flower Mound. Police say Huynh shot White, who had parked outside a commercial building in the 500 block of Flower Mound Road after leaving his workplace in Lewisville. They believe Huynh followed White and possibly used a strobe feature on his flashlight to get White to pull off into the parking lot. Lewisville police had arrested Huynh Saturday in connection with another shooting that day outside the Suburban Extended Stay Hotel. An investigator noticed that Huynh's vehicle matched the description of the vehicle used in the Jan. 1 shooting. Officers recovered the weapon believed to have been used in both shootings. Huynh has been charged with murder, aggravated assault with a deadly weapon and unlawful possession of a firearm by a felon and remains in the Denton County Jail with bond set at $1.5 million.
This Justin Weekly – Jan. 11, 2013
EDC DIRECTOR WANTED - Justin's Economic Development Corporation Type A and B boards voted Wednesday to advertise for the position of EDC executive director. The director's job has been vacant following the resignation of Chantal Kirkland last September. Justin City Council member David Speicher attended Wednesday's meeting and suggested that the boards consider combining the position of EDC director with the city manager position approved by voters last November.
News Headlines
Conservation district selling tree seedlings
January 17, 2013The Denton County Soil and Water Conservation District has 14 species of tree seedlings available for purchase through its annual tree sale.
Huynh charged in Justin man's murder
January 17, 2013A Lewisville man was arrested last weekend in connection with the murder of a Justin man earlier this month.
Cherishing the memories of Mom
January 17, 2013Having a girls' only weekend, listening to bedtime stories, riding horses every day, giving each other a break from reality, becoming closer and closer to my mom. Someone you thought you would never lose; this was my life until I lost my mom.
Sales tax strong to begin 2013
January 17, 2013The City of Justin received some good economic news to begin the new year: sales tax revenue was up 34.57 percent in January compared to a year ago.
Justin Sports
Texans Baseball to hold clinic
January 17, 2013Northwest Texans Baseball is having a Spring Training Clinic for area youth 4-6 p.m. Saturday, Feb. 9 at the Northwest High School indoor facility, located on the west side of the high school near the tennis courts. This clinic is for 2nd-6th graders.
JYA signups almost over
January 17, 2013The Justin Youth Association is accepting online sign-ups for the Spring Season through Saturday, Jan. 19.
NHS to hold softball clinic
January 17, 2013Northwest High School will hold a softball clinic for grades 3-6 9 a.m.-noon Saturday, Jan. 19 at the NHS indoor facility.
Texans chase down Panthers, 55-42
December 20, 2012The Northwest Texans closed out their non-district schedule with a 55-42 win over the Paschal Panthers Tuesday.
Justin Education
Joli McGrew graduates
January 17, 2013Joli McGrew of Justin graduated Magna Cum Laude from Eastern Oregon University during the 2011-12 academic year.
Honor Rolls
January 17, 2013The following students made 90 percent or better in all subjects for the second six weeks.
Northwest Notes for Thursday, January 10, 2013
January 10, 2013Northwest High School teacher Gwen Hilliard was named the KLTY and CareNow Teacher of the Month.
Northwest Notes for Thursday, January 3, 2013
January 3, 2013Construction is underway for the Cosmetology Academy salon at James M. Steele Accelerated High School in Roanoke.
Jeannette Hensley Huey
January 17, 2013Jeannette Hensley Huey, 73, of Denton, died Jan. 4, 2013, at Longmeadow Care Center in Justin. Funeral was Jan. 7 at Towne North Baptist Church in Denton.
Freeman Eugene Robinson
January 17, 2013Freeman Eugene Robinson, 60, died Monday, Dec. 31, 2012, at his home in Justin.
Bertha LaRue Faulkner
January 17, 2013Bertha LaRue Faulkner, 92, of Justin, died Thursday, Jan. 3, 2013, at Longmeadow Care Center. Graveside service was held at Eakin Cemetery at Ponder Jan. 5 with Rev. Kim Broadstreet officiating.
Steven "Chris" Pepper
January 17, 2013Steven "Chris" Pepper, 59, of Denton died Friday, Dec. 21, 2012. Funeral was Sunday, Dec. 23, 2012, at the First Baptist Church in Justin with Rev. Kim Broadstreet officiating.
Community Calendar
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Calendar developed and supported by Kieran O'Shea


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Lectures and Special Events
Fascinating lectures, debates, and programs on scientific and cultural topics that range from the fossil-hunting to climate change.
March 11, 2015
Join author Melanie L. J. Stiassny on an epic, oceanic journey, in this third installment of the Natural Histories series.
March 14, 2015
Join Brock Fenton and Nancy Simmons as they discuss their new book and present these fascinating nocturnal creatures in a new light.
March 21, 2015
Join us as we explore the special relationship between Earth and the Sun.
March 25, 2015 - March 27, 2015
Join us for a very special event as iconic choreographer Karole Armitage premieres a new dance production about climate change and its cultural context created specifically for the Museum's Milstein Hall of Ocean Life.
May 21, 2015
Frans de Waal will explore the similarities between humans and other primates in power politics, transmission of knowledge and habits, empathy, and sense of fairness.
February 14, 2015
Sold Out - Celebrate Valentine's Day with a unique NYC experience only at the Hayden Planetarium!
February 10, 2015
Sold out - A panel of noted Darwin experts will mark the Museum's historic online publication of this entire 30,000 item corpus by speaking on the collection's never-before-published treasures.
January 22, 2015
Spend an evening with Neil deGrasse Tyson as he reviews headline stories in the Universe, drawn from breaking news in 2014.
January 12, 2015
Sold out - The American Museum of Natural History and The Carter Center invite you to explore the innovative collaborative approaches being developed around the world to combat disease.
December 4, 2014
Experience the thrill of the next step in human space exploration as NASA's new Orion spacecraft launches on its inaugural test flight!
Stay informed about Museum news and research, events, and more!

subset: commoncrawl


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Crahan Denton Movies and Career Information
Mar 20, 1914
Mar 20, 1914
Crahan Denton was an American stage and television actor.
He was born in Seattle, Washington, United States.
From 1945 until his death in 1966, Denton starred in many films, including The Great St. Louis Bank Robbery, The Parent Trap, Birdman of Alcatraz, To Kill a Mockingbird, and Bus Riley's Back in Town. He was also a guest star on many television shows, including Bonanza, Alfred Hitchcock Presents, Gunsmoke, Have Gun Will Travel, and The Fugitive.
In 1960, he also co-starred in an unsold pilot titled, "Mountain Man" about a Rocky Mountain fur trading station in the 1840s.
Denton made two guest appearances on the CBS courtroom drama series Perry Mason, including the role of murder victim Frank Jarrett in the 1960 episode, "The Case of the Nimble Nephew."
In 1966, Denton died after suffering a heart attack in Piedmont, California.
- Crahan Denton Movies before 2014
- Hud 1963
- To Kill a Mockingbird (1962) 1962
- Great St. Louis Bank Robbery
- Young One (1960)
- Birdman of Alcatraz (1962)


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This Boudoir Session in San Francisco was fun, frisky and unforgettable. As a 10-year anniversary gift to her husband, my client wanted to surprise him with a portfolio of elegant and timeless boudoir portraits. Their wedding was a low-key backyard celebration, followed by time together abroad in the Peace Corp. She had never had the pleasure of professional hair and make-up, special wardrobe pieces to feel radiant in or professional photography to capture her unique beauty. It was time, she decided, to treat both herself and her beloved husband to this experience. We had a blast! Her good friend offered her home as the location which had fabulous natural light and architecture. Music played, champagne flowed and lingerie, high heels and sparkly jewels lined all the surfaces. Not only was this a great decision as a gift for her husband, but for herself, as well. These sessions are unforgettable and empowering. With wardrobe consultations, pro hair/make-up and lots of laughter, boudoir sessions are liberating. Congrats on your anniversary! You are beautiful inside and out…Christina. Thanks to Maria Lee Makeup for an incredible job on hair/make-up artistry. Here's our lovely client's every day look:
Annie and Layman's intimate City Hall wedding in San Francisco was romantic and memorable. Although they couple has been together for quite some time, they wanted to make their relationship official, in front of their closest friends. San Francisco is their beloved home so it was the perfect choice to celebrate their nuptials at the iconic City Hall. The world class architecture and ambiance makes for incredible photographs, and I'm so glad they enjoyed their experience. After making some portraits there, the entire wedding party jumped into a limo to stop by some special spots around San Francisco. The first location was Red's Java House along the Embarcadero. Everyone was hungry for their well known chili dogs and fries, a perfect post-wedding snack! Off we went to the Palace of Fine Arts to capture the elegant lines of the buildings and tranquil atmosphere. To end the day, Annie and Layman wanted to see the sunset under the Golden Gate Bridge from Crissy Field. A perfect end to a perfect day.
This was my first time EVER photographing a proposal photo session! Warren called me with his request with the calmest demeanor possible. He loved Iris and wanted to surprise her with a ring before she went to Asia on a holiday trip. I don't remember the last time I was so nervous. What was wrong with me? I photograph highly emotional events on a monthly basis, but a proposal? AHHH! Warren's reassuring mood gave me confidence and of course I agreed. We met at San Francisco Internationl Airport where he was preparing. The ring was placed in a funny coal sack, it being close to Christmas. Warren had a small speaker system to broadcast their favorite song and a set of questions on white boards he was going to display. I hid behind some plant and started sweating. Then….action! Warren gave me the thumbs up and started the song. She entered with bustling fellow travelers but was stopped in her tracks when she realized what was happening. Her reaction was priceless. A crowd quickly formed , cellphones recording the big moment. She said yes. What an adorable couple, and what a romantic groom you are, Warren! Thanks for this memory, I will treasure it always.
LOVE IT! Thanks for everything, Christina! I hide my nervousness well.


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SANTA CLARA –- Safety Eric Reid was ruled out of Sunday's season finale against the Arizona Cardinals due to a concussion, the team announced Friday afternoon.
When it was time for the 49ers to make their original cuts to 53 players, special teams absorbed the biggest hits.
Gunners C.J. Spillman and Darryl Morris were released.
Negative rumors band the team together; 49ers defense adjusts and responds in the second half; Brad Seely's special teams unit comes up big.
Programming note: Watch 49ers Press Conference Live Monday at Noon on Comcast SportsNet Bay Area, or streaming liv


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This location is shown only to members
Khem Raj will enlighten us all with how embedded Linux developers can make use of OpenEmbedded and Yocto.
We also have Jeffrey Osier-Mixon scheduled to participate to answer some questions via video chat.
Jeff Osier-Mixon is the community manager for the Yocto Project. He
has been working with open source embedded systems tools for 20 years.
Jeff occasionally maintains a blog and calendar of open source
conferences at http://jefro.net/blog
Very good presentation. Liked all the discussion from attendees. Came away more knowledgeable about Yocto
June 14, 2012
Great overview of Yocto by Khem, with a very interactive discussion with lots of Q&A!
June 14, 2012
Interesting content and project. Looking forward to migrating to Yocto from regular Openembedded. The questions really killed the flow the of the presentation and didn't provide any interesting information. Waiting till the end to take questions would have really helped.
June 14, 2012
The slides for Kehm's talk are available: http://files.meetup.com/1590495/yocto-oe.pdf
June 14, 2012
Hi all - we may be able to arrange a hands-on walkthrough. If there is wide interest, I'll keep in touch with Khem & Kevin to try to set one up later in the summer.
June 12, 2012
Hi Qirfiraz, Yes, hands-on labs of course are always valuable, but, this is a talk, not training. Also, sorry, since this is a "meetup", and is all about meeting in-person, we won't be recording the talk. I hope you can catch another one.
June 11, 2012
Seems like an interesting talk but I think a hands-on lab will be more suitable, for developers who want to start participating in Yocto Project. Unfortunately, I will be out of the country, and it will be great if someone records the talk and post for later viewing.
June 11, 2012
We just grab a coffee and speak French. Some people have been coming every week for months... it creates a kind of warmth to the group.
— Rafaël, started French Conversation Group
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From Wikipedia, the free encyclopedia - View original article
Library resources about Immune system |
The immune system is a system of biological structures and processes within an organism that protects against disease. To function properly, an immune system must detect a wide variety of agents, known as pathogens, from viruses to parasitic worms, and distinguish them from the organism's own healthy tissue. In many species, the immune system can be classified into subsystems, such as the innate immune system versus the adaptive immune system, or humoral immunity versus cell-mediated immunity.
Pathogens can rapidly evolve and adapt, and thereby avoid detection and neutralization by the immune system; however, multiple defense mechanisms have also evolved to recognize and neutralize pathogens. Even simple unicellular organisms such as bacteria possess a rudimentary immune system, in the form of enzymes that protect against bacteriophage infections. Other basic immune mechanisms evolved in ancient eukaryotes and remain in their modern descendants, such as plants and insects. These mechanisms include phagocytosis, antimicrobial peptides called defensins, and the complement system. Jawed vertebrates, including humans, have even more sophisticated defense mechanisms,[1] including the ability to adapt over time to recognize specific pathogens more efficiently. Adaptive (or acquired) immunity creates immunological memory after an initial response to a specific pathogen, leading to an enhanced response to subsequent encounters with that same pathogen. This process of acquired immunity is the basis of vaccination.
Disorders of the immune system can result in autoimmune diseases, inflammatory diseases and cancer.[2][3] Immunodeficiency occurs when the immune system is less active than normal, resulting in recurring and life-threatening infections. In humans, immunodeficiency can either be the result of a genetic disease such as severe combined immunodeficiency, acquired conditions such as HIV/AIDS, or the use of immunosuppressive medication. In contrast, autoimmunity results from a hyperactive immune system attacking normal tissues as if they were foreign organisms. Common autoimmune diseases include Hashimoto's thyroiditis, rheumatoid arthritis, diabetes mellitus type 1, and systemic lupus erythematosus. Immunology covers the study of all aspects of the immune system.
Immunology is a science that examines the structure and function of the immune system. It originates from medicine and early studies on the causes of immunity to disease. The earliest known reference to immunity was during the plague of Athens in 430 BC. Thucydides noted that people who had recovered from a previous bout of the disease could nurse the sick without contracting the illness a second time.[4] In the 18th century, Pierre-Louis Moreau de Maupertuis made experiments with scorpion venom and observed that certain dogs and mice were immune to this venom.[5] This and other observations of acquired immunity were later exploited by Louis Pasteur in his development of vaccination and his proposed germ theory of disease.[6] Pasteur's theory was in direct opposition to contemporary theories of disease, such as the miasma theory. It was not until Robert Koch's 1891 proofs, for which he was awarded a Nobel Prize in 1905, that microorganisms were confirmed as the cause of infectious disease.[7] Viruses were confirmed as human pathogens in 1901, with the discovery of the yellow fever virus by Walter Reed.[8]
Immunology made a great advance towards the end of the 19th century, through rapid developments, in the study of humoral immunity and cellular immunity.[9] Particularly important was the work of Paul Ehrlich, who proposed the side-chain theory to explain the specificity of the antigen-antibody reaction; his contributions to the understanding of humoral immunity were recognized by the award of a Nobel Prize in 1908, which was jointly awarded to the founder of cellular immunology, Elie Metchnikoff.[10]
The immune system protects organisms from infection with layered defenses of increasing specificity. In simple terms, physical barriers prevent pathogens such as bacteria and viruses from entering the organism. If a pathogen breaches these barriers, the innate immune system provides an immediate, but non-specific response. Innate immune systems are found in all plants and animals.[11] If pathogens successfully evade the innate response, vertebrates possess a second layer of protection, the adaptive immune system, which is activated by the innate response. Here, the immune system adapts its response during an infection to improve its recognition of the pathogen. This improved response is then retained after the pathogen has been eliminated, in the form of an immunological memory, and allows the adaptive immune system to mount faster and stronger attacks each time this pathogen is encountered.[12]
Innate immune system | Adaptive immune system |
Response is non-specific | Pathogen and antigen specific response |
Exposure leads to immediate maximal response | Lag time between exposure and maximal response |
Cell-mediated and humoral components | Cell-mediated and humoral components |
No immunological memory | Exposure leads to immunological memory |
Found in nearly all forms of life | Found only in jawed vertebrates |
Both innate and adaptive immunity depend on the ability of the immune system to distinguish between self and non-self molecules. In immunology, self molecules are those components of an organism's body that can be distinguished from foreign substances by the immune system.[13] Conversely, non-self molecules are those recognized as foreign molecules. One class of non-self molecules are called antigens (short for antibody generators) and are defined as substances that bind to specific immune receptors and elicit an immune response.[14]
Microorganisms or toxins that successfully enter an organism encounter the cells and mechanisms of the innate immune system. The innate response is usually triggered when microbes are identified by pattern recognition receptors, which recognize components that are conserved among broad groups of microorganisms,[15] or when damaged, injured or stressed cells send out alarm signals, many of which (but not all) are recognized by the same receptors as those that recognize pathogens.[16] Innate immune defenses are non-specific, meaning these systems respond to pathogens in a generic way.[14] This system does not confer long-lasting immunity against a pathogen. The innate immune system is the dominant system of host defense in most organisms.[11]
Several barriers protect organisms from infection, including mechanical, chemical, and biological barriers. The waxy cuticle of many leaves, the exoskeleton of insects, the shells and membranes of externally deposited eggs, and skin are examples of mechanical barriers that are the first line of defense against infection.[14] However, as organisms cannot be completely sealed from their environments, other systems act to protect body openings such as the lungs, intestines, and the genitourinary tract. In the lungs, coughing and sneezing mechanically eject pathogens and other irritants from the respiratory tract. The flushing action of tears and urine also mechanically expels pathogens, while mucus secreted by the respiratory and gastrointestinal tract serves to trap and entangle microorganisms.[17]
Chemical barriers also protect against infection. The skin and respiratory tract secrete antimicrobial peptides such as the β-defensins.[18] Enzymes such as lysozyme and phospholipase A2 in saliva, tears, and breast milk are also antibacterials.[19][20] Vaginal secretions serve as a chemical barrier following menarche, when they become slightly acidic, while semen contains defensins and zinc to kill pathogens.[21][22] In the stomach, gastric acid and proteases serve as powerful chemical defenses against ingested pathogens.
Within the genitourinary and gastrointestinal tracts, commensal flora serve as biological barriers by competing with pathogenic bacteria for food and space and, in some cases, by changing the conditions in their environment, such as pH or available iron.[23] This reduces the probability that pathogens will reach sufficient numbers to cause illness. However, since most antibiotics non-specifically target bacteria and do not affect fungi, oral antibiotics can lead to an "overgrowth" of fungi and cause conditions such as a vaginal candidiasis (a yeast infection).[24] There is good evidence that re-introduction of probiotic flora, such as pure cultures of the lactobacilli normally found in unpasteurized yogurt, helps restore a healthy balance of microbial populations in intestinal infections in children and encouraging preliminary data in studies on bacterial gastroenteritis, inflammatory bowel diseases, urinary tract infection and post-surgical infections.[25][26][27]
Inflammation is one of the first responses of the immune system to infection.[28] The symptoms of inflammation are redness, swelling, heat, and pain, which are caused by increased blood flow into tissue. Inflammation is produced by eicosanoids and cytokines, which are released by injured or infected cells. Eicosanoids include prostaglandins that produce fever and the dilation of blood vessels associated with inflammation, and leukotrienes that attract certain white blood cells (leukocytes).[29][30] Common cytokines include interleukins that are responsible for communication between white blood cells; chemokines that promote chemotaxis; and interferons that have anti-viral effects, such as shutting down protein synthesis in the host cell.[31] Growth factors and cytotoxic factors may also be released. These cytokines and other chemicals recruit immune cells to the site of infection and promote healing of any damaged tissue following the removal of pathogens.[32]
The complement system is a biochemical cascade that attacks the surfaces of foreign cells. It contains over 20 different proteins and is named for its ability to "complement" the killing of pathogens by antibodies. Complement is the major humoral component of the innate immune response.[33][34] Many species have complement systems, including non-mammals like plants, fish, and some invertebrates.[35]
In humans, this response is activated by complement binding to antibodies that have attached to these microbes or the binding of complement proteins to carbohydrates on the surfaces of microbes. This recognition signal triggers a rapid killing response.[36] The speed of the response is a result of signal amplification that occurs following sequential proteolytic activation of complement molecules, which are also proteases. After complement proteins initially bind to the microbe, they activate their protease activity, which in turn activates other complement proteases, and so on. This produces a catalytic cascade that amplifies the initial signal by controlled positive feedback.[37] The cascade results in the production of peptides that attract immune cells, increase vascular permeability, and opsonize (coat) the surface of a pathogen, marking it for destruction. This deposition of complement can also kill cells directly by disrupting their plasma membrane.[33]
Leukocytes (white blood cells) act like independent, single-celled organisms and are the second arm of the innate immune system.[14] The innate leukocytes include the phagocytes (macrophages, neutrophils, and dendritic cells), mast cells, eosinophils, basophils, and natural killer cells. These cells identify and eliminate pathogens, either by attacking larger pathogens through contact or by engulfing and then killing microorganisms.[35] Innate cells are also important mediators in the activation of the adaptive immune system.[12]
Phagocytosis is an important feature of cellular innate immunity performed by cells called 'phagocytes' that engulf, or eat, pathogens or particles. Phagocytes generally patrol the body searching for pathogens, but can be called to specific locations by cytokines.[14] Once a pathogen has been engulfed by a phagocyte, it becomes trapped in an intracellular vesicle called a phagosome, which subsequently fuses with another vesicle called a lysosome to form a phagolysosome. The pathogen is killed by the activity of digestive enzymes or following a respiratory burst that releases free radicals into the phagolysosome.[38][39] Phagocytosis evolved as a means of acquiring nutrients, but this role was extended in phagocytes to include engulfment of pathogens as a defense mechanism.[40] Phagocytosis probably represents the oldest form of host defense, as phagocytes have been identified in both vertebrate and invertebrate animals.[41]
Neutrophils and macrophages are phagocytes that travel throughout the body in pursuit of invading pathogens.[42] Neutrophils are normally found in the bloodstream and are the most abundant type of phagocyte, normally representing 50% to 60% of the total circulating leukocytes.[43] During the acute phase of inflammation, particularly as a result of bacterial infection, neutrophils migrate toward the site of inflammation in a process called chemotaxis, and are usually the first cells to arrive at the scene of infection. Macrophages are versatile cells that reside within tissues and produce a wide array of chemicals including enzymes, complement proteins, and regulatory factors such as interleukin 1.[44] Macrophages also act as scavengers, ridding the body of worn-out cells and other debris, and as antigen-presenting cells that activate the adaptive immune system.[12]
Dendritic cells (DC) are phagocytes in tissues that are in contact with the external environment; therefore, they are located mainly in the skin, nose, lungs, stomach, and intestines.[45] They are named for their resemblance to neuronal dendrites, as both have many spine-like projections, but dendritic cells are in no way connected to the nervous system. Dendritic cells serve as a link between the bodily tissues and the innate and adaptive immune systems, as they present antigen to T cells, one of the key cell types of the adaptive immune system.[45]
Mast cells reside in connective tissues and mucous membranes, and regulate the inflammatory response.[46] They are most often associated with allergy and anaphylaxis.[43] Basophils and eosinophils are related to neutrophils. They secrete chemical mediators that are involved in defending against parasites and play a role in allergic reactions, such as asthma.[47] Natural killer (NK cells) cells are leukocytes that attack and destroy tumor cells, or cells that have been infected by viruses.[48]
Natural killer cells, or NK cells, are a component of the innate immune system which does not directly attack invading microbes. Rather, NK cells destroy compromised host cells, such as tumor cells or virus-infected cells, recognizing such cells by a condition known as "missing self." This term describes cells with low levels of a cell-surface marker called MHC I (major histocompatibility complex) – a situation that can arise in viral infections of host cells.[35] They were named "natural killer" because of the initial notion that they do not require activation in order to kill cells that are "missing self." For many years it was unclear how NK cells recognize tumor cells and infected cells. It is now known that the MHC makeup on the surface of those cells is altered and the NK cells become activated through recognition of "missing self". Normal body cells are not recognized and attacked by NK cells because they express intact self MHC antigens. Those MHC antigens are recognized by killer cell immunoglobulin receptors (KIR) which essentially put the brakes on NK cells.[49]
The adaptive immune system evolved in early vertebrates and allows for a stronger immune response as well as immunological memory, where each pathogen is "remembered" by a signature antigen.[50] The adaptive immune response is antigen-specific and requires the recognition of specific "non-self" antigens during a process called antigen presentation. Antigen specificity allows for the generation of responses that are tailored to specific pathogens or pathogen-infected cells. The ability to mount these tailored responses is maintained in the body by "memory cells". Should a pathogen infect the body more than once, these specific memory cells are used to quickly eliminate it.
The cells of the adaptive immune system are special types of leukocytes, called lymphocytes. B cells and T cells are the major types of lymphocytes and are derived from hematopoietic stem cells in the bone marrow.[35] B cells are involved in the humoral immune response, whereas T cells are involved in cell-mediated immune response.
Both B cells and T cells carry receptor molecules that recognize specific targets. T cells recognize a "non-self" target, such as a pathogen, only after antigens (small fragments of the pathogen) have been processed and presented in combination with a "self" receptor called a major histocompatibility complex (MHC) molecule. There are two major subtypes of T cells: the killer T cell and the helper T cell. In addition there are suppressor T cells which have a role in modulating immune response. Killer T cells only recognize antigens coupled to Class I MHC molecules, while helper T cells only recognize antigens coupled to Class II MHC molecules. These two mechanisms of antigen presentation reflect the different roles of the two types of T cell. A third, minor subtype are the γδ T cells that recognize intact antigens that are not bound to MHC receptors.[51]
In contrast, the B cell antigen-specific receptor is an antibody molecule on the B cell surface, and recognizes whole pathogens without any need for antigen processing. Each lineage of B cell expresses a different antibody, so the complete set of B cell antigen receptors represent all the antibodies that the body can manufacture.[35]
Killer T cells are a sub-group of T cells that kill cells that are infected with viruses (and other pathogens), or are otherwise damaged or dysfunctional.[52] As with B cells, each type of T cell recognizes a different antigen. Killer T cells are activated when their T cell receptor (TCR) binds to this specific antigen in a complex with the MHC Class I receptor of another cell. Recognition of this MHC:antigen complex is aided by a co-receptor on the T cell, called CD8. The T cell then travels throughout the body in search of cells where the MHC I receptors bear this antigen. When an activated T cell contacts such cells, it releases cytotoxins, such as perforin, which form pores in the target cell's plasma membrane, allowing ions, water and toxins to enter. The entry of another toxin called granulysin (a protease) induces the target cell to undergo apoptosis.[53] T cell killing of host cells is particularly important in preventing the replication of viruses. T cell activation is tightly controlled and generally requires a very strong MHC/antigen activation signal, or additional activation signals provided by "helper" T cells (see below).[53]
Helper T cells regulate both the innate and adaptive immune responses and help determine which immune responses the body makes to a particular pathogen.[54][55] These cells have no cytotoxic activity and do not kill infected cells or clear pathogens directly. They instead control the immune response by directing other cells to perform these tasks.
Helper T cells express T cell receptors (TCR) that recognize antigen bound to Class II MHC molecules. The MHC:antigen complex is also recognized by the helper cell's CD4 co-receptor, which recruits molecules inside the T cell (e.g., Lck) that are responsible for the T cell's activation. Helper T cells have a weaker association with the MHC:antigen complex than observed for killer T cells, meaning many receptors (around 200–300) on the helper T cell must be bound by an MHC:antigen in order to activate the helper cell, while killer T cells can be activated by engagement of a single MHC:antigen molecule. Helper T cell activation also requires longer duration of engagement with an antigen-presenting cell.[56] The activation of a resting helper T cell causes it to release cytokines that influence the activity of many cell types. Cytokine signals produced by helper T cells enhance the microbicidal function of macrophages and the activity of killer T cells.[14] In addition, helper T cell activation causes an upregulation of molecules expressed on the T cell's surface, such as CD40 ligand (also called CD154), which provide extra stimulatory signals typically required to activate antibody-producing B cells.[57]
Gamma delta T cells (γδ T cells) possess an alternative T cell receptor (TCR) as opposed to CD4+ and CD8+ (αβ) T cells and share the characteristics of helper T cells, cytotoxic T cells and NK cells. The conditions that produce responses from γδ T cells are not fully understood. Like other 'unconventional' T cell subsets bearing invariant TCRs, such as CD1d-restricted Natural Killer T cells, γδ T cells straddle the border between innate and adaptive immunity.[58] On one hand, γδ T cells are a component of adaptive immunity as they rearrange TCR genes to produce receptor diversity and can also develop a memory phenotype. On the other hand, the various subsets are also part of the innate immune system, as restricted TCR or NK receptors may be used as pattern recognition receptors. For example, large numbers of human Vγ9/Vδ2 T cells respond within hours to common molecules produced by microbes, and highly restricted Vδ1+ T cells in epithelia respond to stressed epithelial cells.[51]
A B cell identifies pathogens when antibodies on its surface bind to a specific foreign antigen.[60] This antigen/antibody complex is taken up by the B cell and processed by proteolysis into peptides. The B cell then displays these antigenic peptides on its surface MHC class II molecules. This combination of MHC and antigen attracts a matching helper T cell, which releases lymphokines and activates the B cell.[61] As the activated B cell then begins to divide, its offspring (plasma cells) secrete millions of copies of the antibody that recognizes this antigen. These antibodies circulate in blood plasma and lymph, bind to pathogens expressing the antigen and mark them for destruction by complement activation or for uptake and destruction by phagocytes. Antibodies can also neutralize challenges directly, by binding to bacterial toxins or by interfering with the receptors that viruses and bacteria use to infect cells.[62]
Evolution of the adaptive immune system occurred in an ancestor of the jawed vertebrates. Many of the classical molecules of the adaptive immune system (e.g., immunoglobulins and T cell receptors) exist only in jawed vertebrates. However, a distinct lymphocyte-derived molecule has been discovered in primitive jawless vertebrates, such as the lamprey and hagfish. These animals possess a large array of molecules called Variable lymphocyte receptors (VLRs) that, like the antigen receptors of jawed vertebrates, are produced from only a small number (one or two) of genes. These molecules are believed to bind pathogenic antigens in a similar way to antibodies, and with the same degree of specificity.[63]
When B cells and T cells are activated and begin to replicate, some of their offspring become long-lived memory cells. Throughout the lifetime of an animal, these memory cells remember each specific pathogen encountered and can mount a strong response if the pathogen is detected again. This is "adaptive" because it occurs during the lifetime of an individual as an adaptation to infection with that pathogen and prepares the immune system for future challenges. Immunological memory can be in the form of either passive short-term memory or active long-term memory.
Newborn infants have no prior exposure to microbes and are particularly vulnerable to infection. Several layers of passive protection are provided by the mother. During pregnancy, a particular type of antibody, called IgG, is transported from mother to baby directly across the placenta, so human babies have high levels of antibodies even at birth, with the same range of antigen specificities as their mother.[64] Breast milk or colostrum also contains antibodies that are transferred to the gut of the infant and protect against bacterial infections until the newborn can synthesize its own antibodies.[65] This is passive immunity because the fetus does not actually make any memory cells or antibodies—it only borrows them. This passive immunity is usually short-term, lasting from a few days up to several months. In medicine, protective passive immunity can also be transferred artificially from one individual to another via antibody-rich serum.[66]
Long-term active memory is acquired following infection by activation of B and T cells. Active immunity can also be generated artificially, through vaccination. The principle behind vaccination (also called immunization) is to introduce an antigen from a pathogen in order to stimulate the immune system and develop specific immunity against that particular pathogen without causing disease associated with that organism.[14] This deliberate induction of an immune response is successful because it exploits the natural specificity of the immune system, as well as its inducibility. With infectious disease remaining one of the leading causes of death in the human population, vaccination represents the most effective manipulation of the immune system mankind has developed.[35][67]
Most viral vaccines are based on live attenuated viruses, while many bacterial vaccines are based on acellular components of micro-organisms, including harmless toxin components.[14] Since many antigens derived from acellular vaccines do not strongly induce the adaptive response, most bacterial vaccines are provided with additional adjuvants that activate the antigen-presenting cells of the innate immune system and maximize immunogenicity.[68]
The immune system is a remarkably effective structure that incorporates specificity, inducibility and adaptation. Failures of host defense do occur, however, and fall into three broad categories: immunodeficiencies, autoimmunity, and hypersensitivities.
Immunodeficiencies occur when one or more of the components of the immune system are inactive. The ability of the immune system to respond to pathogens is diminished in both the young and the elderly, with immune responses beginning to decline at around 50 years of age due to immunosenescence.[69][70] In developed countries, obesity, alcoholism, and drug use are common causes of poor immune function.[70] However, malnutrition is the most common cause of immunodeficiency in developing countries.[70] Diets lacking sufficient protein are associated with impaired cell-mediated immunity, complement activity, phagocyte function, IgA antibody concentrations, and cytokine production. Additionally, the loss of the thymus at an early age through genetic mutation or surgical removal results in severe immunodeficiency and a high susceptibility to infection.[71]
Immunodeficiencies can also be inherited or 'acquired'.[14] Chronic granulomatous disease, where phagocytes have a reduced ability to destroy pathogens, is an example of an inherited, or congenital, immunodeficiency. AIDS and some types of cancer cause acquired immunodeficiency.[72][73]
Overactive immune responses comprise the other end of immune dysfunction, particularly the autoimmune disorders. Here, the immune system fails to properly distinguish between self and non-self, and attacks part of the body. Under normal circumstances, many T cells and antibodies react with "self" peptides.[74] One of the functions of specialized cells (located in the thymus and bone marrow) is to present young lymphocytes with self antigens produced throughout the body and to eliminate those cells that recognize self-antigens, preventing autoimmunity.[60]
Hypersensitivity is an immune response that damages the body's own tissues. They are divided into four classes (Type I – IV) based on the mechanisms involved and the time course of the hypersensitive reaction. Type I hypersensitivity is an immediate or anaphylactic reaction, often associated with allergy. Symptoms can range from mild discomfort to death. Type I hypersensitivity is mediated by IgE, which triggers degranulation of mast cells and basophils when cross-linked by antigen.[75] Type II hypersensitivity occurs when antibodies bind to antigens on the patient's own cells, marking them for destruction. This is also called antibody-dependent (or cytotoxic) hypersensitivity, and is mediated by IgG and IgM antibodies.[75] Immune complexes (aggregations of antigens, complement proteins, and IgG and IgM antibodies) deposited in various tissues trigger Type III hypersensitivity reactions.[75] Type IV hypersensitivity (also known as cell-mediated or delayed type hypersensitivity) usually takes between two and three days to develop. Type IV reactions are involved in many autoimmune and infectious diseases, but may also involve contact dermatitis (poison ivy). These reactions are mediated by T cells, monocytes, and macrophages.[75]
It is likely that a multicomponent, adaptive immune system arose with the first vertebrates, as invertebrates do not generate lymphocytes or an antibody-based humoral response.[1] Many species, however, utilize mechanisms that appear to be precursors of these aspects of vertebrate immunity. Immune systems appear even in the structurally most simple forms of life, with bacteria using a unique defense mechanism, called the restriction modification system to protect themselves from viral pathogens, called bacteriophages.[76] Prokaryotes also possess acquired immunity, through a system that uses CRISPR sequences to retain fragments of the genomes of phage that they have come into contact with in the past, which allows them to block virus replication through a form of RNA interference.[77][78] Offensive elements of the immune systems are also present in unicellular eukaryotes, but studies of their roles in defense are few.[79]
Pattern recognition receptors are proteins used by nearly all organisms to identify molecules associated with pathogens. Antimicrobial peptides called defensins are an evolutionarily conserved component of the innate immune response found in all animals and plants, and represent the main form of invertebrate systemic immunity.[1] The complement system and phagocytic cells are also used by most forms of invertebrate life. Ribonucleases and the RNA interference pathway are conserved across all eukaryotes, and are thought to play a role in the immune response to viruses.[80]
Unlike animals, plants lack phagocytic cells, but many plant immune responses involve systemic chemical signals that are sent through a plant.[81] Individual plant cells respond to molecules associated with pathogens known as Pathogen-associated molecular patterns or PAMPs.[82] When a part of a plant becomes infected, the plant produces a localized hypersensitive response, whereby cells at the site of infection undergo rapid apoptosis to prevent the spread of the disease to other parts of the plant. Systemic acquired resistance (SAR) is a type of defensive response used by plants that renders the entire plant resistant to a particular infectious agent.[81] RNA silencing mechanisms are particularly important in this systemic response as they can block virus replication.[83]
Another important role of the immune system is to identify and eliminate tumors. The transformed cells of tumors express antigens that are not found on normal cells. To the immune system, these antigens appear foreign, and their presence causes immune cells to attack the transformed tumor cells. The antigens expressed by tumors have several sources;[85] some are derived from oncogenic viruses like human papillomavirus, which causes cervical cancer,[86] while others are the organism's own proteins that occur at low levels in normal cells but reach high levels in tumor cells. One example is an enzyme called tyrosinase that, when expressed at high levels, transforms certain skin cells (e.g. melanocytes) into tumors called melanomas.[87][88] A third possible source of tumor antigens are proteins normally important for regulating cell growth and survival, that commonly mutate into cancer inducing molecules called oncogenes.[85][89][90]
The main response of the immune system to tumors is to destroy the abnormal cells using killer T cells, sometimes with the assistance of helper T cells.[88][91] Tumor antigens are presented on MHC class I molecules in a similar way to viral antigens. This allows killer T cells to recognize the tumor cell as abnormal.[92] NK cells also kill tumorous cells in a similar way, especially if the tumor cells have fewer MHC class I molecules on their surface than normal; this is a common phenomenon with tumors.[93] Sometimes antibodies are generated against tumor cells allowing for their destruction by the complement system.[89]
Clearly, some tumors evade the immune system and go on to become cancers.[94] Tumor cells often have a reduced number of MHC class I molecules on their surface, thus avoiding detection by killer T cells.[92] Some tumor cells also release products that inhibit the immune response; for example by secreting the cytokine TGF-β, which suppresses the activity of macrophages and lymphocytes.[95] In addition, immunological tolerance may develop against tumor antigens, so the immune system no longer attacks the tumor cells.[94]
Paradoxically, macrophages can promote tumor growth [96] when tumor cells send out cytokines that attract macrophages, which then generate cytokines and growth factors that nurture tumor development. In addition, a combination of hypoxia in the tumor and a cytokine produced by macrophages induces tumor cells to decrease production of a protein that blocks metastasis and thereby assists spread of cancer cells.
Hormones can act as immunomodulators, altering the sensitivity of the immune system. For example, female sex hormones are known immunostimulators of both adaptive[97] and innate immune responses.[98] Some autoimmune diseases such as lupus erythematosus strike women preferentially, and their onset often coincides with puberty. By contrast, male sex hormones such as testosterone seem to be immunosuppressive.[99] Other hormones appear to regulate the immune system as well, most notably prolactin, growth hormone and vitamin D.[100][101]
When a T-cell encounters a foreign pathogen, it extends a vitamin D receptor. This is essentially a signaling device that allows the T-cell to bind to the active form of vitamin D, the steroid hormone calcitriol. T-cells have a symbiotic relationship with vitamin D. Not only does the T-cell extend a vitamin D receptor, in essence asking to bind to the steroid hormone version of vitamin D, calcitriol, but the T-cell expresses the gene CYP27B1, which is the gene responsible for converting the pre-hormone version of vitamin D, calcidiol into the steroid hormone version, calcitriol. Only after binding to calcitriol can T-cells perform their intended function. Other immune system cells that are known to express CYP27B1 and thus activate vitamin D calcidiol, are dendritic cells, keratinocytes and macrophages.[102][103]
It is conjectured that a progressive decline in hormone levels with age is partially responsible for weakened immune responses in aging individuals.[104] Conversely, some hormones are regulated by the immune system, notably thyroid hormone activity.[105] The age-related decline in immune function is also related to decreasing vitamin D levels in the elderly. As people age, two things happen that negatively affect their vitamin D levels. First, they stay indoors more due to decreased activity levels. This means that they get less sun and therefore produce less cholecalciferol via UVB radiation. Second, as a person ages the skin becomes less adept at producing vitamin D.[106]
The immune system is affected by sleep and rest,[107] and sleep deprivation is detrimental to immune function.[108] Complex feedback loops involving cytokines, such as interleukin-1 and tumor necrosis factor-α produced in response to infection, appear to also play a role in the regulation of non-rapid eye movement (REM) sleep.[109] Thus the immune response to infection may result in changes to the sleep cycle, including an increase in slow-wave sleep relative to REM sleep.[110]
When suffering from sleep deprivation, active immunizations may have a diminished effect and may result in lower antibody production, and a lower immune response, than would be noted in a well-rested individual. Additionally, proteins such as NFIL3, which have been shown to be closely intertwined with both T-cell differentiation and our circadian rhythms, can be affected through the disturbance of natural light and dark cycles through instances of sleep deprivation, shift work, etc. As a result these disruptions can lead to an increase in chronic conditions such as heart disease, chronic pain, and asthma.[111]
In addition to the negative consequences of sleep deprivation, sleep and the intertwined circadian system have been shown to have strong regulatory effects on immunological functions affecting both the innate and the adaptive immunity. First, during the early slow-wave-sleep stage, a sudden drop in blood levels of cortisol, epinephrine, and norepinephrine induce increased blood levels of the hormones leptin, pituitary growth hormone, and prolactin. These signals induce a pro-inflammatory state through the production of the pro-inflammatory cytokines interleukin-1, interleukin-12, TNF-alpha and IFN-gamma. These cytokines then stimulate immune functions such as immune cells activation, proliferation, and differentiation. It is during this time that undifferentiated, or less differentiated, like naïve and central memory T cells, peak (i.e. during a time of a slowly evolving adaptive immune response). In addition to these effects, the milieu of hormones produced at this time (leptin, pituitary growth hormone, and prolactin) support the interactions between APCs and T-cells, a shift of the Th1/Th2 cytokine balance towards one that supports Th1, an increase in overall Th cell proliferation, and naïve T cell migration to lymph nodes. This milieu is also thought to support the formation of long-lasting immune memory through the initiation of Th1 immune responses.[112]
In contrast, during wake periods differentiated effector cells, such as cytotoxic natural killer cells and CTLs, peak in order to elicit an effective response against any intruding pathogens. As well during awake active times, anti-inflammatory molecules, such as cortisol and catecholamines, peak. There are two theories as to why the pro-inflammatory state is reserved for sleep time. First, inflammation would cause serious cognitive and physical impairments if it were to occur during wake times. Second, inflammation may occur during sleep times due to the presence of melatonin. Inflammation causes a great deal of oxidative stress and the presence of melatonin during sleep times could actively counteract free radical production during this time.[113][114]
Overnutrition is associated with diseases such as diabetes and obesity, which are known to affect immune function. More moderate malnutrition, as well as certain specific trace mineral and nutrient deficiencies, can also compromise the immune response.[115][page needed]
Foods rich in certain fatty acids may foster a healthy immune system.[116] Likewise, fetal undernourishment can cause a lifelong impairment of the immune system.[117]
The immune response can be manipulated to suppress unwanted responses resulting from autoimmunity, allergy, and transplant rejection, and to stimulate protective responses against pathogens that largely elude the immune system (see immunization) or cancer.
Immunosuppressive drugs are used to control autoimmune disorders or inflammation when excessive tissue damage occurs, and to prevent transplant rejection after an organ transplant.[35][118]
Anti-inflammatory drugs are often used to control the effects of inflammation. Glucocorticoids are the most powerful of these drugs; however, these drugs can have many undesirable side effects, such as central obesity, hyperglycemia, osteoporosis, and their use must be tightly controlled.[119] Lower doses of anti-inflammatory drugs are often used in conjunction with cytotoxic or immunosuppressive drugs such as methotrexate or azathioprine. Cytotoxic drugs inhibit the immune response by killing dividing cells such as activated T cells. However, the killing is indiscriminate and other constantly dividing cells and their organs are affected, which causes toxic side effects.[118] Immunosuppressive drugs such as cyclosporin prevent T cells from responding to signals correctly by inhibiting signal transduction pathways.[120]
Cancer immunotherapy covers the medical ways to stimulate the immune system to attack cancer tumours.
Larger drugs (>500 Da) can provoke a neutralizing immune response, particularly if the drugs are administered repeatedly, or in larger doses. This limits the effectiveness of drugs based on larger peptides and proteins (which are typically larger than 6000 Da). In some cases, the drug itself is not immunogenic, but may be co-administered with an immunogenic compound, as is sometimes the case for Taxol. Computational methods have been developed to predict the immunogenicity of peptides and proteins, which are particularly useful in designing therapeutic antibodies, assessing likely virulence of mutations in viral coat particles, and validation of proposed peptide-based drug treatments. Early techniques relied mainly on the observation that hydrophilic amino acids are overrepresented in epitope regions than hydrophobic amino acids;[121] however, more recent developments rely on machine learning techniques using databases of existing known epitopes, usually on well-studied virus proteins, as a training set.[122] A publicly accessible database has been established for the cataloguing of epitopes from pathogens known to be recognizable by B cells.[123] The emerging field of bioinformatics-based studies of immunogenicity is referred to as immunoinformatics.[124] Immunoproteomics is the study of large sets of proteins (proteomics) involved in the immune response.
The success of any pathogen depends on its ability to elude host immune responses. Therefore, pathogens evolved several methods that allow them to successfully infect a host, while evading detection or destruction by the immune system.[125] Bacteria often overcome physical barriers by secreting enzymes that digest the barrier, for example, by using a type II secretion system.[126] Alternatively, using a type III secretion system, they may insert a hollow tube into the host cell, providing a direct route for proteins to move from the pathogen to the host. These proteins are often used to shut down host defenses.[127]
An evasion strategy used by several pathogens to avoid the innate immune system is to hide within the cells of their host (also called intracellular pathogenesis). Here, a pathogen spends most of its life-cycle inside host cells, where it is shielded from direct contact with immune cells, antibodies and complement. Some examples of intracellular pathogens include viruses, the food poisoning bacterium Salmonella and the eukaryotic parasites that cause malaria (Plasmodium falciparum) and leishmaniasis (Leishmania spp.). Other bacteria, such as Mycobacterium tuberculosis, live inside a protective capsule that prevents lysis by complement.[128] Many pathogens secrete compounds that diminish or misdirect the host's immune response.[125] Some bacteria form biofilms to protect themselves from the cells and proteins of the immune system. Such biofilms are present in many successful infections, e.g., the chronic Pseudomonas aeruginosa and Burkholderia cenocepacia infections characteristic of cystic fibrosis.[129] Other bacteria generate surface proteins that bind to antibodies, rendering them ineffective; examples include Streptococcus (protein G), Staphylococcus aureus (protein A), and Peptostreptococcus magnus (protein L).[130]
The mechanisms used to evade the adaptive immune system are more complicated. The simplest approach is to rapidly change non-essential epitopes (amino acids and/or sugars) on the surface of the pathogen, while keeping essential epitopes concealed. This is called antigenic variation. An example is HIV, which mutates rapidly, so the proteins on its viral envelope that are essential for entry into its host target cell are constantly changing. These frequent changes in antigens may explain the failures of vaccines directed at this virus.[131] The parasite Trypanosoma brucei uses a similar strategy, constantly switching one type of surface protein for another, allowing it to stay one step ahead of the antibody response.[132] Masking antigens with host molecules is another common strategy for avoiding detection by the immune system. In HIV, the envelope that covers the virion is formed from the outermost membrane of the host cell; such "self-cloaked" viruses make it difficult for the immune system to identify them as "non-self" structures.[133]
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Australia's BIGGEST Weddings & Party Sale STARTS NOW! Hurry, while stock lasts! >Shop Now
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Ross is a census-designated place (CDP) in Ross Township, Butler County, Ohio, United States. The population was 1,971 at the 2000 census. It was laid out by Dr. Benjamin Franklin Clark on February 1, 1817, as Venus, which became corrupted as "Venice", a name found on some maps. It received a post office, called Ross, on July 3, 1834. [edit] Research Tips


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These "best of" Hubble telescope photos are amazing (smithsonianmag.com)
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[–]MarshallBanana 1 point2 points3 points 2 years ago (0 children)
You may want to read the rules in the sidebar, and repost this somewhere more appropriate.
[–]expertunderachiever 1 point2 points3 points 2 years ago (0 children)
That website is annoying. Forcing a full page refresh to show a new image is so fucking Web 1.0. Whoever is the webmaster/script monkey for that website should be punched in the nads.
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How are things such as the Cat's Eye Nebula discovered in 1786? How could they possibly identify something like that and distinguish it from others?
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Hello and welcome, pranksters! If you try any of the pranks listed on this site, you really should come and tell us how it went on the forums here. We're always looking for a good laugh
Here are 15 funny school pranks you can try:
- make the sounds and/or looks as if your, u know, turned on, as the teacher talks, like the grunting and the sighing type noises and the breathing and if the teacher ask you whats wrong, then u can say "oh i was just enjoying the pleasure of your teaching until you stopped, please continue". I wouldnt suggest doing it more than once or maybe twice
- tap your pen, pencil or hands on the desk making a beat to every word the teacher says, and u can really get into by goin "yeah" or "oh yeah' or "c'mon" or something between their words or sentences
- have a bunch of tiny paper scraps, like really tiny and put them in a thin straight line and move your nose over the line sniffing in like your inhaling (or actually inhale if u dont mind it goin up there)
- here's another good teacher prank – if there happens to be a roll of duct tape near your desk or table while the teacher is just up front talking, grap the tape and hold it under your desk and rip it off loudly. Also, you can try to keep it silent and take long pieces and hang then from your desk and make like a spiderman web or something. As the teacher keeps talking just hold the tape under your desk and keep pulling off pieces. If its the loud noise, the whole class will hear and laugh or be distracted, while with the web it starts out with the neighbors then eventually everyone else will look at eachother or in your direction asking whats goin' on. Or if nobody tells the teacher or they never notice, just leave it hanging there when class is done
- i have a shitload of pranks, bu i have a real funny one you can use at school. if a lot of the class get to class early, take the nail out of the hinges, and shut the door. the teacher walks into the class, and pulls the door off its hinges. this will be a guaranteed way to destroy a day's worth of class.
- Ask the pricipal if he could let you swith two class rooms to teach the teachers a lessen. and the take pictures of the classroom. and the night that is planed ask for keys from the pricipal and go into the classroom and swich the classrooms to look like each other and when the teachers come in they will get frusterated and every one else should laph and the next nighe swith the class rooms back.
- Say you have a bladder problem and ask to go to the bathroom and if you want when you come back and the teacher ask say you had an accident and go to the office
- when you have a sub or ure ussuall teacher who loves to talk or was in military or something keep asking stupid ??? that they have to answer get several ppl to join in wasting all of class best to do in a subject you hate
- hang the teacher's chair on the wall or on the blackboard, this is a good prank on teachers
- play football/baseball with old sandwiches
- explode a dung-bomb before class and when the teacher comes in gather all your classmates and protest that the teacher is forcing you to study in such unhuman conditions
- hide someone under the desk that's most in the back of class…and make him make weird and funny noises and lett the teacher clearly see that no one is making them…it really scares them,believe me ,it was tested in my class
- gett a tampon..pour red paint into it and stick it on a door…alsow tested..it really pisses them off
- go from class to class and sing carols…and ask for money….be offended when u're not given and asked to get out…tested
- at random times or when it's too quiet…start making funnt noises or act like u have spasms….return to normal and act like nothing happened when the teachers turns to see what's wrong
If you have some more funny high school pranks, post them in the comments.


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Yesterday has gone, Today is new-born and young Thank you God. Let's go!


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BY LANANH NGUYEN and LAURA HURST
LONDON (Bloomberg) -- Ineos Group Holdings SA is shutting the 210,000 barrel-a-day Grangemouth oil refinery and petrochemical site before a strike this weekend that could halt 45 percent of the UK's crude production.
The company is progressively stopping units before a 48-hour industrial action planned by Unite union workers, scheduled to begin on Oct. 20 at 7 a.m. local time.
"We're currently going through a safe shutdown of the site," Richard Longden, a spokesman for Ineos, said by phone from London today. "The units will be brought to a cold status by the time the strike action starts."
Grangemouth workers held a two-day strike in April 2008 that cut North Sea oil output and disrupted fuel supplies across Scotland. The site supplies power and steam to BP Plc's neighboring Kinneil processing plant, which handles oil from the company's Forties Pipeline System (FPS) gathered from more than 80 offshore fields. FPS is scheduled to load 387,000 barrels a day of crude in October, according to a shipping program obtained by Bloomberg news.
Union representatives and Ineos will meet today for talks mediated by the UK's Advisory, Conciliation and Arbitration Service after discussions ended yesterday without resolution, Unite said in a statement last night. The discussions are scheduled for 1 p.m. in Glasgow, Scotland today, according to the UK Department of Energy and Climate Change.
"We're in touch with Ineos to establish the possible impact of the shutdown," Robert Wine, a London-based spokesman for BP, said today by phone. Operations at the Kinneil plant will depend on the outcome of negotiations between Ineos and the union, he said.
Forties output averaged 382,000 barrels a day this year, according to loading programs obtained by Bloomberg News. The UK's average crude production was 850,000 barrels a day this year, data from the International Energy Agency show. Forties is the most abundant of four crude grades that make up the Dated Brent benchmark used to price more than half the world's crude. The others are Brent, Oseberg and Ekofisk.
"We have been monitoring the situation very closely," Cameron Ramos, a spokesman for the Department of Energy and Climate Change, said today by phone from London. "This isn't something that has come as a surprise."
The Grangemouth refinery is jointly owned by Ineos Group Holdings SA and PetroChina Co Ltd, while Ineos is the sole owner of the petrochemical site.
Oil producers lost about 50 million pounds ($80 million) a day in the 2008 outage, reducing the country's tax revenue by at least 25 million pounds a day, according to Oil & Gas U.K., an industry group that represents offshore producers.
"Brent prices may soon have to deal with potential disruption in North Sea production if a planned strike at the Grangemouth refinery, which plays a key role in the supply of Forties crude, goes ahead," JBC Energy GmbH, a researcher in Vienna, said today in a note.
Brent crude fell 59 cents, or 0.5 percent, to $110.45 a barrel as of 10:11 a.m. London time today on the ICE Futures Europe exchange.
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Fred Thin the Movie by Happy-Potato
- Movie
- Rated E
- 3,237 Views
Plenty more like this here!
Contemplating Reiko Reiko is a perfectly normal red-eyed, pointy-eared, sadistic little demon girl.
Author Comments
Little Reiko gets mercilessly pelted with snowballs. Poor kid.
This is part of the Contemplating Reiko series of comics and cartoons from TaintedInk.com.
Rated 5 / 5 stars
even better
that was soooo cute and i luv'd how that li'l bitch died hehe
Rated 5 / 5 stars
love this vid
dude, does the older sis have a girlfriend?? If not, Im single cause my ex just dumbed me.
Rated 5 / 5 stars
lmao that was freakin hilarious and brutal,.. she has a sister? totally cool. hope there are more with the older sis in it.. should make some funny & brutal events
Rated 5 / 5 stars
she has a sister?!
woah are there gonna be more with her sis?? lol i like this one, i though she was gonna put a weapon in the snowball but this is way better...are her parents like this?


text:
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Bridgeport Pools has been proudly serving Mid-Michigan for 53 years. We offer our customers a full line of above ground pools and spas to fit every family.
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Dogs for Sale in Daytona Beach, Florida
(1 - 15 of 401)-
$950 Standard poodle puppy
Standard Poodle · Ormond Beach, FL -
$400 fkkls High Quality Maltese Puppies available
Maltese · Edgewater, FL… , they are akc reg and very smart pets , plz text at (856) 376-0051 for details. -
$500 mbabga french bulldog for sale
French Bulldog · Lake Mary, FL -
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French Bulldog · Daytona Beach, FL -
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Rhodesian Ridgeback · Daytona Beach, FL… , I have puppies that need to go to a loving home.. They have all their vaccines and have... -
$950 Standard poodle pups
Standard Poodle · Ormond Beach, FL -
$700 bnhh M/F french bull dog Puppies for sale
French Bulldog · Daytona Beach, FLbnhh… , please contact us for more information by text to 908 379-3576, Thanks -
$500 JhJgr-gorgeous Male And Female Yorkie puppies
Yorkshire Terrier · Daytona Beach, FL… , Pls txt directly at (321) 270-4484 for more info and pics -
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Bulldog · Daytona Beach, FL… ..,.,send me your email address via text or contact me via text (901) 729 - 9553 -
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American Bulldog · Daytona Beach, FL -
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American Cocker Spaniel · Lake Mary, FL… .These pets are brought up in the house with us and have been looked after well. All of the ... -
$400 gafsgxv pug pups available for sale to lovely homes
Pug · Debary, FL… , for more information text us your email on 757- 750 -1570 -
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Wolverton Drive
Almost all errands require a car.
A few nearby public transportation options.
Flat as a pancake, minimal bike lanes.
Score Details
Wolverton Drive has a Walk Score of 18 out of 100. This location is a Car-Dependent neighborhood so almost all errands require a car.
This location is in Fort Wayne.
Nearby schools include Cornerstone Daycare Learning Center, Northrop High School and Northcrest Elementary School.
The closest grocery stores are Sam's Club, Walmart on Coldwater and Country Kitchen Sweetart Inc.
Nearby coffee shops include BURGER KING®, Starbucks and Banh Mi Barista. Nearby restaurants include Texas Roadhouse, Richards Restaurant Inc and Don Hall's Guesthouse.
Wolverton Drive is near Franke Park, Gren Park and Indiana University-Purdue University - Fort Wayne.
There are minimal bike lanes and the terrain is flat as a pancake. Wolverton Drive is somewhat bikeable, there is minimal bike infrastructure.
Explore how far you can travel by car, bus, bike and foot from Wolverton Drive.
Wolverton Drive has some transit which means a few nearby public transportation options.
Bus lines:
21 Glenbrook / Coldwater / Dupont Road
0.1 mi
4 Wells/Ludwig
0.5 mi
6 Franke Park
0.8 mi
8 Glenbrook / Northrop
0.9 mi
View all Fort Wayne apartments on a map.
Popular apartment searches include pool, hardwood floor and fireplace. View all Fort Wayne apartments and rentals.
This location is in the city of Fort Wayne, IN. Fort Wayne has an average Walk Score of 28 and has 253,691 residents.


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From the Publisher
"Sex is fun, but so many books about erotic intimacy are dull. This book, though, is a party. If you're interested in sex (you are), and you are looking for ways to make it better (who isn't?), this is a must-buy." —Douglas Brown, author of Just Do It


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The lighting effect you used here was executed well and strongly reminds me of chiaroscuro. Was that in your mind when you made this piece? Regardless, this is excellently done (as always!). It does lend itself toward the wonder of creation. That theme keeps coming back to me today (you're the third, actually), so I guess it's a sign toward something.
Anyway, fantastic work, and good luck on your future works!


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Jeff "Apple Grumble" Werner. We decided to make name tags for our 12 guests based on what each were contributing. Designed by Jane in Illustrator using Helvetica and Rosewood, printed on Tobias' inkjet under the dinner table.
Follow Jeff Werner Jeff_Werner Member since 2005
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July 17th, 2011, 07:14 PM | #1 |
2006 Yamaha Rhino Mods Trade
2006 Yamaha Rhino Sport Edition
1600 miles/178 hours Snorkel Relocated radiator Clutch work done Dragonfire dual exhaust Dynatek cdi Dynatek coil Upgraded cv cages in the front All cvs have just been regreased Front differential was serviced New wheel bearings front and rear New brake pads in the front Has a rear bumper on it Rhino lined bed, cage, and bumper There are scratches bumps and bruises on it, its a Rhino! There is about $2000 in upgrades in this machine $6500 cash with stock wheels or will sell the wheels and tires in pictures for extra Will trade for srt4, diesel truck, bmw, audi, mercedes, gsxr, etc. or ? Call/text 262 four nine seven 45eight three |
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EchoLogistics received 96 entries from 26 designers. View this project »
It has been a pleasure to work in this project. Best Regards G. Gernet
Project | Category | Award | Time left | Entries |
Need someone to Design a T-Shirt Design from our Sketch | Clothing | $550 | Complete | 6 |
Echo Website Design | Small Website (uncoded) | $1000 | Complete | 96 |
Name your own price, then watch as dozens of participants submit ideas and choose your favorite. Our 100% money-back guarantee makes it risk-free!
Let us match you up with one of our very best Creatives and work 1-to-1 in complete privacy. You'll have all of the same tools and features as our regular projects!


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Contains letters with exhibition organizers Pontus Hulten, Jennifer Gough-Cooper, and Jacques Caumont regarding exhibition loans and research.
Marcel Duchamp Exhibition Records : VIII. Palazzo Grassi, "Marcel Duchamp," 1993 : A. Correspondence
Subseries A. Correspondence
1991-1993, n.d.Scope and Content Note ArrangementAlphabetical by correspondent.
Box | Folder | Author/Title | Date |


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Patrol Cobry (Amiga)
100 point score based on reviews from various critics. ...
5 point score based on user ratings. |
Not an American user?
Patrol Cobry is a timed puzzle-solving game. The player takes control of a chopper and moves blocks in the devastated by earthquake city to gain access to medical laboratory base in search for a cure for the outbreak. The blocks have been contaminated and must be properly neutralized. The neutralization is done by dropping a block from a height to another block of the same color. The combined blocks are changing to green and cannot be moved again. The pilot may use of two additional objects to neutralize the contaminated blocks: bombs (destroying the object underneath) and two types of transformers (neutralizing side blocks or side and bottom blocks). The pilot must avoid a chemical gas and toxic drops, damaging the engine of the chopper. The passage of time is represented in the form of fuel consumption. The fuel can be supplemented by collecting the oil containers. After earning 20 thousand points the player receives an additional helicopter.Patrol Cobry includes two additional mini games:
- Pionier - an enhanced clone of classic Minesweeper, with the difficulty levels in the form of military ranks and the possibility of switching off and on the time indicator and the scanner machine.
- Skoczek - a puzzle board game, where the player must cover the board by moving the chess horse figure and standing only once on each field.
Alternate Titles
- "Skoczek" -- Game included
- "Pionier" -- Game included
User Reviews
There are no reviews for this game.
The Press Says
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There are currently no topics for this game.
PC version
Despite the technical requirements for the MS-DOS version listed on the cover and mentioned in the manual of the Amiga version, there is no proof the game was ever released on IBM PC.
Karsa Orlong (69218) added Patrol Cobry (Amiga) on Apr 26, 2014
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Hey there Roxy Fans! Welcome to the spring semester! I'm
glad to be back. If you're a frequent visitor to the Stone Writing Center, you
may think that you're now so awesome at writing (you're welcome) that you don't
need us! Remember that even the best writers need help. This is why we're here.
We're here for those days when you just need another set of eyes to look at
your fabulous draft or when you have no idea how to start. That's our job.
1. Sometimes you need confirmation
that your ideas are as amazing as you think they are. We can totally help with
6. And finally, at the end of this
messy process that we call writing, we want to remind you to…
2. And sometimes you need someone to
drag you out of the black hole that you've dug for yourself and reassure you
that you can be an awesome writer!
3. Have you ever sat down to start a
paper and had no idea where to begin? Outlines are great for finding your way,
and we can help with those!
4. Formatting can be hard! We can
help you figure out which font not to
use, among other things. (Don't listen to Jerry, it doesn't.)
5. We're also really good at deciding
which word sounds the best in your sentence. (Please just call them eggs, you're
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We'll be here when you need to start the
process all over again. We can't wait to help you this semester! Come see us – White
Library, 4th floor. See you next time the sun is up, the breeze is
cool, and the waves roll into view. 'Til then, hang ten!


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Comfort Suites At Woodbridge
Comfort Suites At Woodbridge in Avenel
Comfort Suites At Woodbridge
Hotel Guest Reviews of the Comfort Suites At Woodbridge
Our hotel ratings and reviews are from real hotel guests. Priceline.com ensures that its reviews are guests-only by proactively sending hotel surveys to customers after they've completed their hotel stays. In the post-stay surveys, priceline.com hotel customers are asked a number of questions about their stay and the hotel. On a scale of 1-10 with 10 being the best, the survey asks guests to rate their overall experience and specifically rate the hotel's cleanliness, staff and location. Priceline.com does not allow site visitors to post unsolicited hotel reviews.Sort by: All Travelers | Business Traveler(3) | Solo Traveler(4) | Traveling as Couple(2) | Family with Young Children(3) | Family with Teens(3)
Alison from Harrisburg, PA
January 4, 2015
Family Traveling with Teens
January 4, 2015
Family Traveling with Teens
friendly staff, cleanliness
quality of eggs on breakfast buffet below average
Kevin from Springfield, MA
November 13, 2013
Family Traveling with Teens
November 13, 2013
Family Traveling with Teens
It's not my first time staying there. The hotel is very conveniently located and very clean. Most of all like that they have a microwave and refrig.
Verified Hotel Guest from Melville, NY
July 29, 2013
Family Traveling with Teens
July 29, 2013
Family Traveling with Teens
size of room
a lot of their lights in the room did not work including TV remote.
Reviews of Comfort Suites At Woodbridge
(1 - 3 of 3 family with teens reviews)
See all 15 reviews by date
(1 - 3 of 3 family with teens reviews)
See all 15 reviews by date
from $77
- Fairfield Inn & Suites By Marriott Woodbridge from $76 (0mi)
- Horizon Inn from $69 (0.7mi)
- Hollywood Motel from $37 (1.0mi)
- La Mirage Avenel (1.0mi)
- Americana Motel from $31 (1.1mi)
- Woodbridge, NJ (1.9 mi)
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- Iselin, NJ (3.0 mi)
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- Carteret, NJ (5.5 mi)
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- Westfield, NJ (8.6 mi)
- South Plainfield, NJ (9.3 mi)
- Edison, NJ (10.5 mi)
- Plainfield, NJ (10.8 mi)
- Irvington, NJ (13.2 mi)
- Summit, NJ (13.5 mi)
- New Brunswick, NJ (13.7 mi)
- Newark, NJ (13.8 mi)
- Piscataway, NJ (14.0 mi)
- Staten Island, NY (14.4 mi)
- South River, NJ (14.5 mi)
- East Brunswick, NJ (14.7 mi)
Most Popular Guest-Rated Hotels in Avenel
Most Popular Business-Friendly Hotels in Avenel
- Comfort Suites At Woodbridge
- Holiday Inn Express Woodbridge
- Fairfield Inn & Suites By Marriott Woodbridge