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Triumph the Insult Comic Dog
Triumph the Insult Comic Dog is a puppet character puppeteered and voiced by Robert Smigel, best known for mocking celebrities in an Eastern European accent.
As his name indicates, Triumph's comedic style is almost exclusively insult comedy.
A Rottweiler, Triumph often puffs a cigar, which usually falls out of his mouth when he starts talking.
He debuted in 1997 on NBC's "Late Night with Conan O'Brien" and also appeared on "The Tonight Show with Conan O'Brien" from time to time, as well as the short-lived "TV Funhouse", TBS's "Conan", and Adult Swim's "The Jack and Triumph Show".
Smigel and Triumph have been ejected from several events for Triumph's antics, including Westminster (three times), the Honolulu line for auditions for "American Idol", and the 2004 Democratic National Convention (while shooting an aborted movie project).
Triumph filmed a number of segments during the 2004 US presidential election cycle.
In November 2003, in the early days of the 2004 U.S. presidential primary campaign, Triumph was the "lead guest" on "The Tonight Show with Jay Leno" the same night that Democratic candidate John Kerry also appeared on the show.
Kerry made a dramatic entry, riding his Harley-Davidson motorcycle onto the stage; but Triumph, in characteristic style, poked fun at him with a series of scathingly rude remarks, to Kerry's evident discomfort.
(Among his jibes: "The poop I made in the dressing room had more heat than John Kerry!")
In July and August 2004, Triumph followed up with visits to both major parties' national conventions.
During the Democratic National Convention in Boston (from which he was ejected), Triumph and Michael Moore attempted to crash Bill O'Reilly's set.
O'Reilly, having his makeup applied at the time, shouted, "If I have to come out there, Insult Dog, you're gonna be talking a lot higher than you are now."
He also gained entry to the Republican convention in New York, and even debated actor Ron Silver during the wrap-up on MSNBC.
In September 2008, Triumph traveled to St. Paul, Minnesota to attend that year's Republican National Convention, where he filed a series of reports as he joked around with delegates inside the hall and protesters in the streets outside the convention.
He also conducted a 6½-minute interview (at a hotel across the street) with independent candidate Ralph Nader.
In October 2008, Triumph made an appearance at Hofstra University in Hempstead, NY during the final presidential debate between John McCain and Barack Obama.
He interviewed and made jokes with political party supporters and with other members of the press, including the host of Fox News Channel's "On the Record with Greta Van Susteren", making a surprise appearance on her show with Mr. Met, the McCain-supporting mascot of the New York Mets.
He starred in the short-lived Adult Swim series "The Jack and Triumph Show" with Jack McBrayer.
It premiered on February 20, 2015, and lasted until April 3, 2015.
In February 2016, Triumph starred in "Triumph's Election Special 2016", sponsored by Hulu and Funny or Die, traveling on the election trail.
The program went on to be nominated for an Emmy for Outstanding Writing for a Variety Special.
In November 2016, after the election of Donald Trump as president, Triumph appeared on "The Late Show with Stephen Colbert" to discuss Trump's victory.
In 1999, Pets.com filed a lawsuit against "Late Night" and Robert Smigel after Triumph repeatedly accused the company's sock puppet mascot as being a "rip-off" of Triumph on several TV shows, print media and internet, and after Pets.com sent lawsuit threats and cease and desist letters to Robert Smigel claiming "unfair competition, dilution and potentially tortious interference with contract in violation of federal and state laws".
However, the bankruptcy and closing of the company during the dot-com bust of 2000 ended the lawsuit.
During an episode of Saturday Night Live, Triumph humped the Pets.com dog in a bathroom as an act of revenge.
Triumph's 2003 album, "Come Poop with Me", was released by Warner Bros. Records, and featured adult comedy and songs, plus a bonus DVD of live performances by Triumph.
The album was nominated for a Grammy Award for Best Comedy Album.
Appearing with Triumph on the album and the DVD were singer-actor Jack Black, comic actor Adam Sandler, "Saturday Night Live" cast members Maya Rudolph and Horatio Sanz; Blackwolf the Dragonmaster—a real-life fantasy/gaming fan who had once been targeted by Triumph during an infamous encounter with "Star Wars" fans; and Conan O'Brien.
On August 10, 2004, NBC released a DVD, "Late Night with Conan O'Brien: The Best of Triumph, the Insult Comic Dog" featuring select Triumph appearances from "Late Night".
Transplant rejection
Transplant rejection occurs when transplanted tissue is rejected by the recipient's immune system, which destroys the transplanted tissue.
Transplant rejection can be lessened by determining the molecular similitude between donor and recipient and by use of immunosuppressant drugs after transplant.
The first successful organ transplant, performed in 1954 by Joseph Murray, involved identical twins, and so no rejection was observed.
Otherwise, the number of mismatched gene variants, namely alleles, encoding cell surface molecules called major histocompatibility complex (MHC), classes I and II, correlate with the rapidity and severity of transplant rejection.
In humans MHC is also called human leukocyte antigen (HLA).
Though cytotoxic-crossmatch assay can predict rejection mediated by cellular immunity, genetic-expression tests specific to the organ type to be transplanted, for instance AlloMap Molecular Expression Testing, have a high negative predictive value.
Transplanting only ABO-compatible grafts (matching blood groups between donor and recipient) helps prevent rejection mediated by humoral immunity.
Because very young children (generally under 12 months, but often as old as 24 months) do not have a well-developed immune system, it is possible for them to receive organs from otherwise incompatible donors.
This is known as ABO-incompatible (ABOi) transplantation.
Graft survival and patient mortality is approximately the same between ABOi and ABO-compatible (ABOc) recipients.
While focus has been on infant heart transplants, the principles generally apply to other forms of solid organ transplantation.
The most important factors are that the recipient not have produced isohemagglutinins, and that they have low levels of T cell-independent antigens.
UNOS regulations allow for ABOi transplantation in children under two years of age if isohemagglutinin titers are 1:4 or below, and if there is no matching ABOc recipient.
Studies have shown that the period under which a recipient may undergo ABOi transplantation may be prolonged by exposure to nonself A and B antigens.
Furthermore, should the recipient (for example, type B-positive with a type AB-positive graft) require eventual retransplantation, the recipient may receive a new organ of either blood type.
Limited success has been achieved in ABO-incompatible heart transplants in adults, though this requires that the adult recipients have low levels of anti-A or anti-B antibodies.
Kidney transplantation is more successful, with similar long-term graft survival rates to ABOc transplants.
Rejection is an adaptive immune response via cellular immunity (mediated by killer T cells inducing apoptosis of target cells) as well as humoral immunity (mediated by activated B cells secreting antibody molecules), though the action is joined by components of innate immune response (phagocytes and soluble immune proteins).
Different types of transplanted tissues tend to favor different balances of rejection mechanisms.
An animal's exposure to the antigens of a different member of the same or similar species is "allostimulation", and the tissue is "allogenic".
Transplanted organs are often acquired from a cadaver (usually a host who had succumbed to trauma), whose tissues had already sustained ischemia or inflammation.
Dendritic cells (DCs), which are the primary antigen-presenting cells (APCs), of the donor tissue migrate to the recipient's peripheral lymphoid tissue (lymphoid follicles and lymph nodes), and present the donor's "self" peptides to the recipient's lymphocytes (immune cells residing in lymphoid tissues).
Lymphocytes include two classes that enact adaptive immunity, also called specific immunity.
Lymphocytes of specific immunity T cells—including the subclasses helper T cells and killer T cells—and B cells.
The recipient's helper T cells coordinate specific immunity directed at the donor's "self" peptides or at the donor's Major histocompatibility complex molecules, or at both.
When memory helper T cells' CD4 receptors bind to the MHC class II molecules which are expressed on the surfaces of the target cells of the graft tissue, the memory helper T cells' T cell receptors (TCRs) can recognize their target antigen that is presented by the MHC class II molecules.
The memory helper T cell subsequently produces clones that, as effector cells, secrete immune signalling molecules (cytokines) in approximately the cytokine balance that had prevailed at the memory helper T cell's priming to memorize the antigen.
As the priming event in this instance occurred amid inflammation, the immune memory is pro-inflammatory.
As a cell is indicated by the prefix "cyto", a cytotoxic influence destroys the cell.
Alloreactive killer T cells, also called cytotoxic T lymphocytes (CTLs), have CD8 receptors that dock to the transplanted tissue's MHC class I molecules, which display the donor's self peptides.
(In the living donor, such presentation of "self" antigens helped maintain "self" tolerance.)
Thereupon, the T cell receptors (TCRs) of the killer T cells recognize their matching epitope, and trigger the target cell's programmed cell death by apoptosis.
Developed through an earlier "primary exposure" that primed specific immunity to the "nonself" antigen, a transplant recipient can have specific antibody crossreacting with the donor tissue upon the transplant event, a "secondary exposure".
This is typical of minor blood group exposure (e.g.
Kell) following allogenic blood transfusion or trauma during pregnancy.
At secondary exposure, these crossreactive antibody molecules interact with aspects of innate immunity—soluble immune proteins called complement and innate immune cells called phagocytes—which inflames and destroys the transplanted tissue.
Secreted by an activated B cell, then called plasma cell, an antibody molecule is a soluble immunoglobulin (Ig) whose basic unit is shaped like the letter "Y": the two arms are the Fab regions, while the single stalk is the Fc region.
Each of the two tips of Fab region is the paratope, which binds a matching molecular sequence and its 3D shape (conformation), altogether called epitope, within the target antigen.
The IgG's Fc region also enables opsonization by a phagocyte, a process by which the Fc receptor on the phagocyte—such as neutrophils in blood and macrophages in tissues—binds the antibody molecule's FC stalk, and the phagocyte exhibits enhanced uptake of the antigen, attached to the antibody molecule's Fab region.
When the paratope of Ig class "gamma" (IgG) binds its matching epitope, IgG's Fc region conformationally shifts and can host a complement protein, initiating the complement cascade that terminates by punching a hole in a cell membrane.
With many holes so punched, fluid rushes into the cell and ruptures it.
Cell debris can be recognized as damage associated molecular patterns (DAMPs) by pattern recognition receptors (PRRs), such as Toll-like receptors (TLRs), on membranes of phagocytes, which thereupon secrete proinflammatory cytokines, recruiting more phagocytes to traffic to the area by sensing the concentration gradient of the secreted cytokines (chemotaxis).
Initiated by preexisting humoral immunity, "hyperacute rejection" manifests within minutes after transplant, and if tissue is left implanted brings systemic inflammatory response syndrome.
Of high risk in kidney transplants is rapid clumping, namely agglutination, of red blood cells (RBCs or erythrocytes), as an antibody molecule binds multiple target cells at once.
While kidneys can routinely be obtained from human donors, most organs are in short supply leading to consideration of xenotransplants from other species.
Pigs are especially likely sources for xenotransplants, chosen for the anatomical and physiological characteristics they share with humans.
However, the sugar galactose-alpha-1,3-galactose (αGal) has been implicated as a major factor in hyperacute rejection in xenotransplantation.
Unlike virtually all other mammals, humans and other primates do not make αGal, and in fact recognize it as an antigen.
During transplantation, xenoreactive natural antibodies recognize αGal on the graft endothelium as an antigen, and the resulting complement-mediated immune response leads to a rejection of the transplant.
Developing with formation of cellular immunity, "acute rejection" occurs to some degree in all transplants, except between identical twins, unless immunosuppression is achieved (usually through drugs).
Acute rejection begins as early as one week after transplant, the risk being highest in the first three months, though it can occur months to years later.
Highly vascular tissues such as kidney or liver often host the earliest signs—particularly at endothelial cells lining blood vessels—though it eventually occurs in roughly 10 to 30% of liver transplants, and 10 to 20% of kidney transplants.
A single episode of acute rejection can be recognized and promptly treated, usually preventing organ failure, but recurrent episodes lead to "chronic rejection".
It is believed that the process of acute rejection is mediated by the cell mediated pathway, specifically by mononuclear macrophages and T-lymphocytes.
Histology of acute rejection is defined by dense lymphocytic cellular infiltrate as well as vasculitis of organ donor vessels.
The term "chronic rejection" initially described long-term loss of function in transplanted organs via fibrosis of the transplanted tissue's blood vessels.
This is now "chronic allograft vasculopathy", however, leaving "chronic rejection" referring to rejection due to more patent aspects of immunity.
Chronic rejection explains long-term morbidity in most lung-transplant recipients, the median survival roughly 4.7 years, about half the span versus other major organ transplants.
In histopathology the condition is "bronchiolitis obliterans", which clinically presents as progressive airflow obstruction, often involving dyspnea and coughing, and the patient eventually succumbs to pulmonary insufficiency or secondary acute infection.
Airflow obstruction not ascribable to other cause is labeled bronchiolitis obliterans syndrome (BOS), confirmed by a persistent drop—three or more weeks—in "forced expiratory volume" (FEV) by at least 20%.
BOS is seen in over 50% of lung-transplant recipients by 5 years, and in over 80% by ten years.
First noted is infiltration by lymphocytes, followed by epithelial cell injury, then inflammatory lesions and recruitment of fibroblasts and myofibroblasts, which proliferate and secrete proteins forming scar tissue.
Generally thought unpredictable, BOS progression varies widely: lung function may suddenly fall but stabilize for years, or rapidly progress to death within a few months.
Risk factors include prior acute rejection episodes, gastroesophageal reflux disease, acute infections, particular age groups, HLA mis-matching, lymphocytic bronchiolitis, and graft dysfunction (e.g., airway ischemia).
One principal reason for transplant rejection is non-adherence to prescribed immunosuppressant regimens.
This is particularly the case with adolescent recipients, with non-adherence rates near 50% in some instances.
Diagnosis of acute rejection relies on clinical data—patient signs and symptoms but also calls on laboratory data such as blood or even tissue biopsy.
The laboratory pathologist generally seeks three main histological signs: (1) infiltrating T cells, perhaps accompanied by infiltrating eosinophils, plasma cells, and neutrophils, particularly in telltale ratios, (2) structural compromise of tissue anatomy, varying by tissue type transplanted, and (3) injury to blood vessels.
Tissue biopsy is restricted, however, by sampling limitations and risks/complications of the invasive procedure.