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The antigens that trigger the pathogenic immune response in rheumatoid arthritis (RA) remain unknown. Until recently it was assumed that either viral or microbial antigens, or joint-specific antigens were the target of arthritogenic T and B lymphocytes in RA. Consequently, murine models of arthritis are induced by immunization with either joint-specific antigens such as type II collagen or microbial products such as streptococcal cell wall. In the K/B×N T-cell receptor transgenic mouse model arthritis is caused by a systemic autoimmune response to the ubiquitously expressed glycolytic enzyme glucose-6-phosphate isomerase (G6PI). The autoreactive transgenic T cells recognize G6PI and provide help for the production of arthritogenic IgG antibodies against G6PI. More recently it was shown that G6PI immunization induces severe symmetrical peripheral polyarthritis in genetically unaltered DBA/I mice. In that model CD4+ T cells are necessary not only for the induction but also for the effector phase of arthritis. Here we review the pathomechanisms that lead from systemic autoreactivity to arthritis in these models, consider the relevance of anti-G6PI immune reactivity for RA, and discuss the insights into the pathogenesis of RA and possibly other autoimmune conditions that can be gained from these models.
Keywords:arthritis; CD4+ T lymphocytes; DBA/I mice; FCγ receptors; glucose-6-phosphate-isomerase
The aetiology of rheumatoid arthritis (RA), which affects approximately 1% of the population, remains obscure. There is considerable evidence suggesting that RA is an autoimmune disease in which autoreactive lymphocytes trigger macrophages, synoviocytes and other effector cells that mediate synovitis and the destruction of cartilage and bone [1-7].
B and T lymphocytes in rheumatoid arthritis and experimental models
Approximately two-thirds of RA patients produce rheumatoid factors – autoantibodies that are directed against IgG [8]. Because of this strong and diagnostically relevant association, B lymphocytes were long suspected to be the main culprits in RA pathogenesis [1,8]. RA susceptibility and severity are strongly associated with certain HLA-DR haplotypes in Caucasians [9]. The discovery of this linkage led to a more T-cell centred view [3,9-13] because antigen presentation to T lymphocytes is the only known immunological function of MHC class II molecules such as HLA-DR. The difficulty in detecting cellular immune responses against autoantigens in RA patients [14-16], together with the failure of some T-cell directed immunomodulatory treatment strategies [17-22] and impressive successes of therapeutic tumour necrosis factor (TNF)-α blockade in RA, appeared to implicate macrophages as the major effector cells in the clinically overt stages of RA [7,23].
Most recently, however, two different lines of evidence reassert the importance of T cells. First, a large clinical trial [24] showed clear clinical benefits from treating active RA by blocking T-cell costimulation and activation. Second, a spontaneous point mutation in the gene encoding an Src homology 2 (SH2) domain of ZAP-70, a key signal transduction molecule in T cells, causes chronic autoimmune arthritis in mice that resembles human RA in many respects [25]. Moreover, the pathogenic importance of B lymphocytes is again becoming appreciated [26,27], partly because depletion of these cells has been shown to be a successful treatment for RA patients [28]. Taken together, a consensus is beginning to emerge that many different cell types, both from the innate and the adaptive immune systems, are crucial to the pathogenesis of RA [4].
Arthritogenic cartilage antigens?
Although some autoantibodies, such as rheumatoid factors that recognize IgG and antibodies against citrullinated antigens, have diagnostic significance [8,29,30], the autoantigen(s) that are recognized in chronic inflammatory arthritides such as RA are unknown [5,16,22,31,32]. Collagen type II (CII) is the major protein in articular cartilage. It is a candidate autoantigen for RA because antibodies and perhaps T cells against CII occur in patients with RA [5,33-35] and because it is arthritogenic in animals [36]. Collagen-induced arthritis (CIA) has thus become the most intensively studied murine model for human inflammatory arthritides [37].
Autoantibodies are important players in CIA. Adoptive transfer of either polyclonal IgG antibodies purified from the sera of arthritic mice [38-40] or combinations of monoclonal antibodies against CII [41] can induce arthritis even in mouse strains that are not susceptible to actively induced CIA [38]. This form of adoptively transferred arthritis has been called CII antibody-induced arthritis [42]. Antibodies against CII are also found in the blood and joints of some RA patients [33,34,43,44]. In contrast, the role of T lymphocytes in the pathogenesis of CIA is less clear. Collagen-specific proinflammatory T cells can be demonstrated in the blood and synovial fluid of mice with CIA [45]. However, most attempts to induce CIA in mice by T-cell transfer have been unsuccessful [46] and CD4-deficient mice develop CIA with unaltered incidence and severity [47]. Mice lacking α/β T cells are resistant to CIA, whereas γ/δ T cells are neither necessary nor protective. A single report on CIA, albeit at reduced severity as compared with wild-type littermates, in rag-deficient DBA/1 mice [48] has not been corroborated by others to date. Taken together, the question regarding how T cells operate in the pathogenesis of CIA has not yet been answered definitively.
CII-specific T cells have also been difficult to demonstrate in the blood or synovial fluid of RA patients [15,49-51]. Moreover, attempts to treat RA by inducing T-cell tolerance to CII have yielded disappointing results [18,19,22,52]. Taken together, there is little solid evidence that CII or any other single joint-specific antigen such as collagen type XI [53], gp39 [54], cartilage oligomeric matrix protein [55], or cartilage proteoglycan (aggrecan) [56] is a diagnostically or pathogenetically significant autoantigen in all RA patients. Given the complexity and clinical and pathological diversity of RA, it seems more likely that different autoantigens are important in different subsets of RA patients.
Arthritogenic noncartilagenous antigens?
Some noncartilagenous antigens have been used to induce and study arthritis in mice and rats [37]. These are either various microbial compounds with adjuvant effects and/or antigenic properties as in adjuvant arthritis, CpG induced arthritis, or streptococcal cell wall induced arthritis [57-61]; or antigens directly injected into the joints of experimental animals following systemic immunization (antigen-induced arthritis) [62,63]. These arthritides are not the subject of this review because the inciting noncartilagenous antigens are non-self antigens. The importance of noncartilagenous self-antigens to the pathophysiology of arthritis had not been considered until recently.
Autoreactivity against a systemically expressed antigen causes symmetrical peripheral polyarthritis in TCR transgenic K/B×N mice
A T-cell receptor (TCR)-transgenic mouse model of arthritis has challenged the concept that arthritis necessarily results from an autoimmune attack against joint-specific antigens. When C57BL/6 mice expressing a transgene-encoded TCR recognizing amino acids 41–61 of bovine ribonuclease bound to the MHC molecule I-Ak (the 'KRN' receptor) were inadvertently crossed with diabetes-susceptible NOD mice, all of the F1 offspring (the K/B×N mice) spontaneously developed peripheral symmetrical polyarthritis [64]. Arthritis in the K/B×N mice resembles RA in that it symmetrically affects the small peripheral joints. In contrast to RA, the distal interphalangeal joints are regularly affected in K/B×N mice, there are no systemic manifestations, the mice do not produce rheumatoid factors, and the arthritis does not remit [64]. Thus, K/B×N mice spontaneously develop peripheral polyarthritis that resembles human RA in many clinical and pathological respects. This surprising finding induced intense research into the pathophysiology of arthritis in the K/B×N mice.
KRN T cells and I-Aβg7 molecules are necessary for the induction but not the effector phase of arthritis in K/B×N mice
Both the KRN TCR and one copy of the NOD I-Aβg7 MHC molecule are necessary for development of arthritis in K/B×N mice. Neither KRN TCR transgenic C57BL/6 mice nor the F1 from crosses of the transgene-expressing C57BL/6 mice with strains other than the I-Aβg7-bearing NOD mice develop arthritis. KRN T cells proliferate in response to I-Aβg7APC in the absence of experimentally added antigens [65]. Importantly, Th cells are only necessary in the induction phase of arthritis. Once the pathogenesis has passed a certain point, Th cells are dispensable. Treatment with anti-CD4 antibodies is ineffective if it is started less than 5 days before the onset of arthritis. What, then, are the effector mechanisms that induce arthritis in K/B×N mice? Using adoptive transfer experiments and a variety of knockout mice, Mathis and colleagues [65] demonstrated that immunoglobulin is responsible for arthritis induction in K/B×N mice. Transfer of serum (as little as 100 μl) or IgG antibodies from arthritic K/B×N mice induced arthritis in recipient mice of different strains, even in rag-2-/- mice that lack T and B lymphocytes [65]. What do these autoantibodies recognize?
The pathogenic autoantibodies recognize a ubiquitously expressed glycolytic enzyme
Quite surprisingly, the target antigen recognized by both the transgenic T cells and the pathogenic autoantibodies was not joint-specific but the ubiquitously expressed glycolytic enzyme glucose-6-phosphate isomerase (G6PI, or GPI) [66]. G6PI, also known as phosphohexose isomerase, catalyzes the interconversion of fructose-6-phosphate and glucose-6-phosphate [67]. It is an essential glycolytic enzyme, expressed by all cells, and G6PI deficiency is lethal at the two-cell stage [68].
Arthritis can be induced in recipient mice by transfer of polyclonal IgG1 or combinations of at least two different monoclonal IgG1 antibodies against G6PI [69]. Mice that lack the activating FcγRIII are less susceptible to arthritis induced by transfer of K/B×N serum than are normal mice, pointing to FcγRIII+ effector cells in arthritis pathogenesis [70,71]. K/B×N serum transfer arthritis in mice that lack the inhibitory FcγRII has been reported to be similar [70,71] or more severe than in wild-type littermates [72].
Complement, neutrophils and mast cells are all indispensable for arthritis development
In the K/B×N transfer arthritis IgG1 antibodies against G6PI induce several different effector functions of the innate immune system; the alternative pathway of the complement cascade is triggered, resulting in chemotactic activity (but not the membrane attack complex) [70,71]. Neutrophils [73] and mast cells [74] are both required as effector cells to mediate joint destruction.
IL-1 is important but neither TNF-α or IL-6 is needed for arthritis development in K/B×N mice
In contrast to RA in humans and most other murine models of arthritis, neither TNF-α or IL-6 is needed for arthritis development in K/B×N mice [75,76]. TNF-α is an important mediator of joint destruction in RA and several murine models of it [7]. Therefore, the K/B×N model yielded another surprising finding when it turned out that TNF-α blockade had no effect on the development and progression of arthritis [75]. Moreover, K/B×N serum induced arthritis in mice that were deficient for both TNF receptor-1 and TNF receptor-2, or lymphotoxin-α with the same incidence and severity as in normal littermates [76]. In that same study a somewhat reduced incidence of arthritis was noted upon serum transfer in TNF-α-deficient mice obtained from one particular colony as compared with wild-type controls. However, that difference was not found with TNF-α-deficient mice obtained from a different colony [76]. Similarly, and again in contrast to previous findings in other murine models of arthritis [77], IL-6 deficiency had no influence on the development of K/B×N serum transfer arthritis [76].
Taken together, the above findings indicate that recognition of a ubiquitously expressed self-antigen by T cells that bear a transgenically encoded receptor and escape negative selection in the thymus [78] induces an arthritogenic autoantibody response, which then triggers innate immune effector mechanisms to induce arthritis.
Autoreactivity against G6PI in the pathogenesis of RA?
This perplexing and informative model raises the question of whether autoreactivity against G6PI is relevant to the pathogenesis of human RA or other chronic inflammatory arthritides. One initial report [79] indicated that IgG antibodies against G6PI were detectable at low dilution (1:50) in the serum of 64% of RA patients but not in control individuals.
However, a number of other investigators did not find increased levels of α-G6PI antibodies in the serum of patients with RA [80-83], collagen tissue disease [81-83], or other chronic arthritides [81,83,84]. Moreover, the commercial G6PI preparation used in the initial study was found to be contaminated with other proteins, and RA sera contained antibodies against some of these other proteins [81]. Taken together, these findings indicate that antibodies against G6PI are not diagnostic markers for RA. An interesting further twist in the story was added by a recent report. van Gaalen and coworkers [85] found that whereas only one of 55 RA patients who did not have systemic manifestations of the disease produced antibodies against G6PI, seven of 22 patients with systemic manifestations (nodules or vasculitis) and 12 of 13 patients with Felty's syndrome had detectable α-G6PI antibodies in their sera [85]. Thus, the possibility remains that antibodies against G6PI occur frequently in Felty's syndrome. However, it is currently not yet clear whether the increased seropositivity is specific for antibodies against G6PI or a sign of generally dysregulated autoantibody production in patients with Felty's syndrome, and the data must be independently confirmed. Another group [86] compared α-G6PI antibody titres in serum and synovial fluid and found increased concentrations of α-G6PI antibodies in the synovial fluid of RA patients. Taken together, the currently available data argue against a pathogenic role for anti-G6PI immune responses in RA.
Are the immunological events that induce arthritis in the K/B×N model relevant to RA?
Even if G6PI is not a relevant autoantigen to RA pathogenesis, the question remains of whether the immunological events that lead to the development of arthritis in the K/B×N model are involved in human RA. Both experimental and clinical data strongly support the possibility that autoreactivity against systemically expressed autoantigens may result in organ-specific autoimmune disease.
Systemic autoreactivity causes peripheral neuritis in TCR transgenic mice
The K/B×N model is not the only transgenic model in which organ-specific autoimmunity develops as a consequence of systemic self-reactivity of T cells. Oono and coworkers [87] produced transgenic mice that express Eα52–68 covalently bound to the I-Ab molecule as their only MHC peptide complex. These mice spontaneously develop a CD4+ Th cell dependent peripheral nervous system-specific autoimmune disease. Neuritis in these TCR transgenic mice shares many of the histopathological features found in experimental autoimmune neuritis, including demyelination and axon degeneration [87]. Serum from these transgenic mice did not stain peripheral nerves and could not transfer the disease to other animals [87].
Autoantibodies against systemically expressed autoantigens are diagnostically important in organ-specific autoimmune diseases
There are several clinical examples of autoantibodies against systemically expressed autoantigens that are highly sensitive and specific diagnostic markers for certain organ-specific autoimmune diseases. These include the anti-Jo-1 autoantibodies that bind to and inhibit activity of histidyl-tRNA synthetase, and the autoantibodies that recognize proteasomes that are found in different but overlapping subsets of myositis patients [88-90]; the antimitochondrial antibodies (AMA-2) that recognize the E2 subunit of mitochondrial pyruvate dehydrogenise [91], which are found in patients with primary biliary cirrhosis; the autoantibodies against proteinase 3 (c-ANCAs) in Wegener's granulomatosis [92]; and, of course, the rheumatoid factors that recognize IgG antibodies [8]. All of these autoantibodies are directed against systemically expressed autoantigens, yet they are highly specific and sensitive markers for the respective diseases. However, their pathogenic significance remains unknown, partly because of the lack of suitable animal models.
Systemic autoreactivity causes severe peripheral symmetrical polyarthritis in genetically unaltered mice
To bridge the gap between the potentially very informative yet rather artificial transgenic mouse models and the situation in patients, we considered whether a systemic immune response against G6PI could induce joint-specific pathology in genetically unaltered mice. Of several inbred strains tested, DBA/1 mice, the same inbred strain of mice that is also susceptible to CIA, develop severe symmetrical peripheral polyarthritis arthritis following one single immunization with recombinant human or murine G6PI in adjuvant [93] (Fig. 1). The incidence of arthritis upon immunization is in excess of 90%, and the time course is uniform and highly predictable. Clinical signs of arthritis are first visible 9 days after immunization; the arthritis then rapidly progresses, reaches its maximum at about day 14 after immunization, and then slowly resolves. The pattern of joints affected is similar to but not identical to that observed in RA; wrists, metacarpal joints, proximal and distal interphalangeal joints are affected at the front limbs, and the tarsal, ankle and knee joints at the rear limbs. Neither the spine, nor the hip, elbow, or shoulder were affected in any of the animals analyzed [93]. Histologically, there are no further signs of inflammation past day 21. Instead, reorganization and fibrosis become visible. Importantly, there were no pathological findings in any other organs apart from the joints. The sudden onset, and high incidence and severity of arthritis distinguishes this model from CIA. The spontaneous remission of G6PI-induced arthritis in genetically unaltered DBA/1 mice is one important clinical difference from the transgenic K/B×N model. This allows for the study of the immunological mechanisms that modulate the autoimmune response and induce remission of the disease.
Figure 1. (a, b) Front and (c, d) hind limbs from DBA/1 mice that had been immunized with glucose-6-phosphate isomerase (G6PI) subcutaneously (panels b and d) or administered phosphate-buffered saline subcutaneously (panels a and c) 14 days earlier. From [93], © 2004. The American Association of Immunologists, Inc. Reprinted with permission.
Continuous requirement for Th cells in the pathogenesis of G6PI-induced arthritis
Th cells are needed throughout the effector cells in G6PI-induced arthritis in normal mice. Depletion of CD4+ cells immediately after immunization prevents arthritis. More importantly, depletion of CD4+ cell on days 11 and 14 (i.e. when clinical symptoms are at their maximum) induces rapid remission of arthritis both clinically and histologically [93]. Thus, in G6PI-induced arthritis in normal mice, CD4+ cells are not only important in the induction but also throughout the effector phase of the disease. This is in contrast to the K/B×N model, in which Th cells are only necessary to provide help to B cells that produce the arthritogenic antibodies against G6PI. Once these antibodies are produced, T cells are no longer necessary for arthritis development in the K/B×N model, and transfer of serum or antibodies from arthritic K/B×N mice [66,69] can transfer arthritis to naïve recipients of almost any mouse strain. Similarly, CIA can be transferred by antibodies or serum [38-41] and it can be induced even in the absence of CD4+ cells [47,48].
IgG antibodies are necessary but not sufficient for G6PI-induced arthritis in normal mice
DBA/1 mice that lack the FcγR common γ chain and thus cannot signal through the activating FcγRI and FcγRIII are protected from G6PI-induced arthritis. In addition, mice that lack the inhibitory FcγRIIB develop severe and prolonged G6PI-induced arthritis (Fig. 2) [93]. Therefore, IgG antibodies and FcγR+effector cells are necessary for the development of G6PI-induced arthritis. Nevertheless, arthritis cannot be induced in naïve recipients by transfer of serum or antibodies from arthritic DBA/1 mice [93]. It is currently unclear why G6PI-induced arthritis cannot be transferred with serum from arthritic animals; it is possible that the antibodies present in the serum some 14 days after immunization lack the necessary affinity for G6PI. Thus, unlike the CIA and K/B×N models, both CD4+ T cells and antibodies are necessary for the development of G6PI-induced arthritis, and neither transfer of T cells nor transfer of antibodies alone can induce arthritis in recipient mice. TNF-α is indispensable for the development of G6PI-induced arthritis in normal mice; treatment of mice with the soluble p75 TNF receptor (etanercept) completely prevents the development of arthritis [93].
Figure 2. Arthritis scores of (■) DBA/1 wild-type, (●) DBA/1 FcγR common γ-chain deficient, and (▲) DBA/1 FcγRIIB deficient mice. Data are presented as mean clinical scores ± standard error of the mean only for those mice that developed arthritis. Arthritis incidence was 10/11 in DBA/1 wild-type, 8/24 in DBA/1 FcγR common γ-chain deficient, and 16/16 in DBA/1 FcγRIIB deficient mice. From [93], © 2004. The American Association of Immunologists, Inc. Reprinted with permission.
Taken together, the above findings indicate that G6PI-induced arthritis in genetically unaltered mice provides a reliable and robust model in which the induction, effector phase and modulation of organ-specific disease induced by systemic autoimmunity can be dissected and therapeutically targeted. Thus, G6PI-induced arthritis narrows the gap between the TCR transgenic K/B×N model and the situation in patients. Some of the major clinical and immunological similarities and differences between CIA, the K/B×N model and G6PI-induced arthritis are summarized in Table 1. Several important questions remain unanswered.
Table 1. Clinical and pathological characteristics of different arthritis models in mice
Why the joint?
It is currently unclear why systemic autoreactivity against the ubiquitously expressed glycolytic enzyme G6PI specifically induces arthritis, with no other symptoms of organ-specific or systemic autoimmune disease. Interestingly, although GPI is ubiquitously expressed in the body, the immune response against GPI appears to initiate in the draining lymph nodes of peripheral joints in K/B×N mice [94]. The reasons for this early localized immune response are currently unclear but these findings suggest that something unique to the joints initiates a local immune response to a systemic autoantigen. This contention is further supported by positron emission tomography studies [95,96] that demonstrate rapid localization of adoptively transferred antibodies against G6PI to the peripheral joints of the recipient mice.
It is known that cationic antigens such as G6PI bind well to cartilage [62,97]. However, systemically expressed antigens such as G6PI are not only presented in the joint, and not every cationic antigen induces arthritis upon immunization. Immune complexes are a critical component in the pathogenesis of K/B×N serum transfer arthritis [96,98] and for G6PI-induced arthritis in normal mice (unpublished observations). G6PI deposits, together with IgG and C3, are detectable in the joints of arthritic mice in the K/B×N serum transfer model [98]. G6PI–IgG immune complexes are also visible in the glomeruli of arthritic K/B×N mice. In contrast to the joints, however, the immune complexes in the kidney were not colocalized with C3 [98]. It is has therefore been suggested that G6PI–immunoglobulin immune complex trigger the complement cascade exclusively in the joints. This would be explained by the absence of membrane-bound C3 inhibitors from chondrocytes [98]. The question remains as to why only a particular pattern of joints is arthritic in the K/B×N model and in G6PI-induced arthritis. Furthermore, immune complex diseases do not necessarily induce erosive arthritis. Systemic lupus erythematosus provides a classical example; there, the immune complex induces glomerulonephritis but not erosive arthritis.
Why G6PI?
Currently, there is no mechanistic explanation for the association between autoantibodies against certain systemically expressed antigens and particular autoimmune diseases [8,88-92]. Similarly, it is not clear why G6PI becomes the target of an arthritogenic autoimmune response in K/B×N and DBA/1 mice. In addition to its function as a glycolytic enzyme, G6PI can be secreted and serves a variety of other physiological functions [99]. G6PI is identical to neuroleukin, a neurotrophic factor for spinal and sensory neurones [100,101], which is associated with terminal sprouting; autocrine motility factor [102], which stimulates motility via a receptor-mediated pathway [103]; and maturation factor, which mediates the differentiation of human myeloid leukemic HL-60 calls to terminal monocytic cells [104].
A receptor for G6PI, namely gp78, has been identified. Gp78 is a transmembrane protein, a RING finger-dependent ubiquitin protein ligase (E3) of the endoplasmatic reticulum [105,106]. It remains to be investigated whether one or more of these physiological functions of G6PI contribute to its immunogenicity and arthritogenicity.
The search for arthritogenic autoantigens has long focused on joint-specific antigens. The TCR transgenic K/B×N model of arthritis and more recently G6PI-induced arthritis in genetically unaltered mice have demonstrated that a noncartilagenous systemically expressed self-antigen can be the target of an arthritogenic immune response. Although the two models exhibit clinical and pathophysiological differences, a complex interplay between cells and effector mechanisms of both the adaptive and innate immune system is necessary in each model. Whereas autoreactivity against G6PI does not seem to play a role in RA, there are well known clinical examples of autoantibodies that are directed against autoantigens that are systemically expressed but pathognomonic for organ-specific diseases, and the possibility that arthritis may be induced by systemic autoreactivity remains interesting and plausible. G6PI-induced arthritis provides a model in which both the induction and modulation of arthritis induced by autoreactivity against noncartilagenous antigens can be studied.
Competing interests
The author(s) declare that they have no competing interests.
CIA = collagen-induced arthritis; CII = collagen type II; G6PI = glucose-6-phosphate isomerase; IL = interleukin; MHC = major histocompatibility complex; RA = rheumatoid arthritis; TCR = T-cell receptor; Th = T helper; TNF = tumour necrosis factor.
The authors' work on G6PI-induced arthritis has been supported by the DFG (SFB 421 TPC2), the BMBF (Kompetenznetz Rheuma) and the IZKF Jena.
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Wipke BT, Wang Z, Nagengast W, Reichert DE, Allen PM: Staging the initiation of autoantibody-induced arthritis: a critical role for immune complexes.
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text:
eBay glossary
eBay acronyms
A-Z index
Discover the world of eBay sites. From quirky collectibles to the latest fashions, toy cars to real vehicles, and much more, eBay specialty sites offer you an almost endless choice of items to purchase—and many different ways to shop, bid and buy.
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text:
I want to set different tab size/soft tab for different language.
such as
tab size 4 for php with tab
tab size 2 for ruby with soft tab
Could I do this in sublime text?
while self.living? do
mistake = Mistake.new
self.learn_from!(mistake) unless mistake.fatal?
facelessuser wrote:Yes, I think I heard that code runs better if it is prettier.
Grant wrote:For some reason I think that this can be done using the same kind of settings file in your User directory; something like "PHP.sublime-settings". I haven't tried it yet, and there's a very good chance that I'm wrong.
while self.living? do
mistake = Mistake.new
self.learn_from!(mistake) unless mistake.fatal?
{ "tabSize" : 2,
"translateTabsToSpaces" : true
First, make sure your sublime-settings file is in the same directory as the corresponding tmPreferences file.
Users browsing this forum: Google [Bot], olivierlacan, Yahoo [Bot] and 23 guests


text:
The Official
Click here to download Appendix BB -- Experimental Kiteboarding Competition Rules.
David TILLETT (AUS), Chairman of the ISAF Racing Rules Committee, said, "ISAF is delighted to introduce the Experimental Kiteboarding Competition Rules. These Experimental Rules provide a great starting point for competition in this exciting new area of our sport. I would like to thank the members of the group that developed these rules, and in particular Dick Rose, Chairman of the Racing Rules Working Party, and Kamen Fillyov, Chairman of the Windsurfing Committee, for their work in producing the Experimental Rules."
The ISAF Council welcomed kiteboarding into the ISAF family in November 2008, when it approved the International Kiteboarding Association as an ISAF International Class Association at the ISAF Annual Conference in Madrid.


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The Swimovate Poolmate Pro watch brings revolutionary technology to life. With multiple language options and motion sensors, this watch automatically monitors the motion of your arm as you're swimming and counts your laps for you.
Great Product!
I've used the Swimnovate Pro for eight major swim sessions and, in general I am very pleased with its performance. The watch collects a lot of data which can be effectively used with the software to analyze each session. The software also provides cumulative summary data for analysis. I initially had some difficulty using the software on my Mac, but I have been able to successfully resolve all of the issues, and the staff support for this product is very professional, competent, highly responsive, and always willing to help!I think this product is badly needed by swimmers at all levels, and will be further refined in the future, but it's a great start!
Ronnie G.
Corinth, Texas
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Great Swim Watch
This is my second watch (I lost my previous one). I use it to keep track of my distances in practice. About 10,000 yds a week, mostly freestyle. For me is 100% accurate in freestyle. As expected it has trouble with unusual drills and kick only sets.The support PC/MAC software still needs some improvement but it works fine. It allows editing of the data. It keeps track of the workouts and provides a lot of statistics and it is all in your computer. Software support from the manufacturer has been outstanding.On my wish list I would add start/stop button with tactile feedback, larger digits, and to keep the displayed just completed set time a little longer (10sec?)
Thousand Oaks, CA
Great Watch
I have used this watch for over a year now and it is great. I swim every other day and have logged over 400,000 yards. The very few errors it had I can trace to stopping mid lap to adjust my goggles, or an unusually long turn (resting), or changing stroke at mid lap. It is great having the exact speed of each of your sets, so you can easily see your improvement over time. Also no more guessing how far or fast you went.The numbers are hard to read under low light conditions in the middle of a fast practice. But then my eyesight is not what it used to be. There is no problem outdoors in daylight.
Failed on 3 basic levels
I swim a mile a day and wanted to find a way to keep track of my laps without having to constantly repeat my lap count in my head as I swam. I read multiple reviews and decided that this was the watch to buy. I swim just 2 basic strokes, freestyle and breast. After a week's trial, the watch consistently off by 8-10 laps on the count. I tried, as suggested, lengthening my glide after my turns, but this made no difference. Problem #2: I downloaded the software to my Mac (OS 10.7.2) and attached the watch pad. The program did identify that the pad was attached, but I could not get it to upload any of the watch's data after multiple attempts. Problem #3: after only 1 week, the watch already lost 4 minutes of time. A watch should, at a minimum, keep accurate time. I do appreciate the easy return that SwimOutlet.com provided me. I would definitely buy from them again.
Eric S.
Solon, OH
Great Watch
Overall a good watch and amazingly accurate on laps and strokes. I have only tested it extensively on freestyle stroke, but looked to be just as accurate on all the other strokes when I did a couple of laps of each. Really helpful for swimming longer sets and keeping your lap count.At the end of a lap you can push the stop button and see your swim time for a few seconds, then it automatically switches over to the total time you have been resting and keeps counting until you push start to begin counting your next swim. I have found that I need to lift up my tinted goggles to see the display in an indoor pool, which I do not need to do with a Timex watch. Would not be a problem with clear goggles, and may not have this problem outdoors, but have not tried it, yet. Software is easy to use. Wish the watch would show lap speed vs strokes for each lap, instead of the averages over long sets, but still a nice tool to check your overall efficiency and track improvements.
Wilmington, NC
Review of Swmovate Pro
Obtaining true data to improve your swim stroke and timing has beendifficult to generate in the past. This watch provides real-time feedback on your swim laps. Rather than depending on a heart monitor or general "feel", this watch provides the user timing, distance, interval information &efficiency and records it . If you want to see how you are improving, this watch will provide the data.
Germantown TN
PoolMate Watch
Good watch to track your training. However, i would love if the screen had lights as when you swim in the evenings it is difficult to read the numbers on the screen.
watch ok but pod does not work
The watch functions although my counts and its tend to differ but that may be my lack of concentration. The pod to link to my computer arrived nonfunctions; they have shipped a replacement but it has not arrived.I would like the product better if it had a mode to allow it to be more easily used with an endless pool rather than relying on a lap turn.
raleigh, n.c.
This watch is Awsome and when used with water proof MP3 makes your workout seem effortless and u really dont want to get out of the water because time flyes.......
Kevin S.
North Miami, FL
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Swimovate was founded in 2007 by triathletes in the United Kingdom. These triathletes were tired of always forgetting how many laps they had swum and the difficulty with trying to keep track. There were gadgets available, but the only ones on the market were manual devices that required you to push a button; if you forget to count your laps most likely you will forget to push a button.
The triathletes turned their problem into a solution when they invented the Swimovate Pool-Mate, which can only be accurately described as a swimming computer. The Swimovate Pool-Mate measures and tracks lap with a state-of-the-art motion sensor, allowing you to swim hassle free.
The Swimovate team continues to bring you dynamic, innovative electronic training products at an affordable price while maintaining an impeccable customer service performance.


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- Equipment World - http://www.equipmentworld.com -
ISO tackles heavy equipment recycling
Posted By Tom Jackson On January 6, 2009 @ 2:57 pm In Construction News | No Comments
The International Organization for Standardization has developed a new standard for recycling used heavy equipment. [1] According to the news release: "it is essential that eventual recovery issues are already taken into account during the design phase, along with safety, emissions, fuel consumption and other design considerations."
Article printed from Equipment World: http://www.equipmentworld.com
URL to article: http://www.equipmentworld.com/iso-tackles-heavy-equipment-recycling/
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[1] new standard for recycling used heavy equipment. : http://www.iso.org/iso/pressrelease.htm?refid=Ref1186
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Classical CD Reviews
"Remembranza" – Remembrance of Latin Sounds – Rosa Antonelli, piano – Albany
Published on September 15, 2013
"Remembranza" – Remembrance of Latin Sounds – Rosa Antonelli, piano – Albany TROY1388, 76:00 *****:
This collection of works by Astor Piazzolla, Heitor Villa-Lobos, Ernesto Nazareth, Enrique Granados and Issac Albéniz is best described as slow moving, even sleepy, yet expertly recreated by Argentinian pianist Rosa Antonelli.
She has performed extensively in Latin America, Europe and the U.S. (specifically Lincoln Center and Carnegie Hall). She has made several CDs and has held seminars and lectures. Her poetic approach has won praise from various critics.
Argentinian composer Piazzolla's La Ultima Greia describes the sadness of a woman who works in a cabaret. His El Mundo de los Dos is a hymn of love and is a tango lento. The lovely Adiós Nonino was written by Piazzolla on the death of his father. In Imperial, Piazzolla expresses the majestic Palace at Versailles. As you can see, these are not your customary tangos.
Brazilian composer Villa Lobos' contribution to this survey of Latin sounds includes: Poema Singelo and Valse Da Dor (a lyrical, but melancholic waltz). Brazilian Nazareth's Odeón – Tango Brasilero reflects the milieu of theaters, hotels and cinemas he performed in when he was young.
Granados and Albéniz were Spanish composers. Granados' great work was Goyescas, a spectacular piano solo composition made up of many shorter pieces. Quejas ó La Maja y el Ruisenor is taken from Goyescas and is one of the more popular sections. Granados' Allegro de Concierto has color and is brilliant. It is a finger-busting virtuoso piece.
Albeniz's Suite Espanola contains two items played here: Granada (Serenata) with its nostalgic expression influenced by flamenco style; and Cadiz, inspired by a religious song. Following the neo-romantic fashion, L'Automne Waltz (not part of the suite) is languid and low-spirited.
There you have it. Spanish and Latin remembrances somewhat forlorn and at times elegiac. The recorded sound is excellent, as are most Albany Records releases. If you are deep into this type of music, then you have a perfect choice.
—Zan Furtwangler
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Intel preps 22nm Chief River notebook platform with USB 3.0
updated 09:05 am EDT, Mon November 1, 2010
Intel Chief River to run 22nm mobile, get USB 3
Intel has given notebook manufacturers the first details of its next notebook platform after Huron River, mainboard developers claimed on Monday. Chief River would support the 22 nanometer processors based on Intel's future Ivy Bridge architecture and would have native USB 3.0 support. Digitimes was told the design would enter mass production in September 2011, although it wouldn't ship until January 2012, likely arriving at CES.
The update may be the first mobile platform from Intel to officially support USB 3.0. Apple has blamed Intel as at least partly responsible for holding up USB 3.0, since its decision not to support the much faster port technology early on has left companies either having to use third-party chipsets or else skip the connectors altogether. Macs have had the option of FireWire 800 to soften the blow, but most Windows PCs without special USB 3.0 support have been left to USB 2.0.
In the nearer term, Intel is expected to mass-produce its Oak Trail ultramobile platform starting from December. The design is key to hopes for both Intel and Microsoft to have real Atom-based competitors to tablets using ARM chips, such as the iPad and the Samsung Galaxy Tab. Purported insiders said, however, that Intel might also focus it on the "sleek netbook" category for extremely thin portables rather than just slates.
Shortly after Oak Trail, Intel is expected to ship Cedar Trail in the spring. It should mark one of the first major speed upgrades after dual-core by going to a 32 nanometer process and adding much faster, DirectX 10-capable integrated graphics.


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September 21, 2012 Published ~ 3 years ago.
Obama Nominee Would Be First Black Woman To Join Washington DC Trial Court In 30 Years
Over half of Washington, DC's residents are black, yet an African-American woman has not served on the federal trial court that presides over the District of Columbia since 2003, when former Chief Judge Norma Holloway Johnson stepped down from the federal bench. Yesterday, President Obama took the first step towards rectifying this by nominating Sentencing Commission member Ketanji Brown Jackson to a seat on the United States District Court for the District of Columbia. If confirmed, Jackson will be the first black woman to join this court in over thirty years, when Judge Johnson took the bench. President Clinton also nominated a black woman, Rhonda Fields, to the same court, but she was not confirmed by the GOP-controlled Senate.
September 21, 2012 Published ~ 3 years ago.
Rick Perry Wants To Replace Planned Parenthood With Crisis Pregnancy Centers That Don't Provide Health Services
When Texas Republicans cut off Planned Parenthood from the state's Women's Health Program — losing millions in federal funds and endangering access to health care for women in the program — Gov. Rick Perry (R) promised to keeping the program going with only state funds and without Planned Parenthood.
Now it's clear what groups he wants to include in the program for low-income women instead: anti-abortion crisis pregnancy centers that do not provide the same women's health services. In fact, the Women's Health Program doesn't even cover pregnant women, so there is no clear reason why crisis pregnancy centers should be included.
Perry laid out his idea earlier this week at the opening of a new crisis pregnancy center in Houston, according to RH Reality Check:
"The Source for Women clinics, in fact, will be part of Texas's own Women's Health Program, and Planned Parenthood will not be," Perry told the crowd. […]
Despite the fact that the Source currently provides only limited, pregnancy-related medical care and STI screenings, Gov. Perry is holding up the ideologically-motivated crisis pregnancy center as the future of comprehensive reproductive medical care for low-income Texas women. He even told the crowd gathered on Tuesday that Texas is excited about helping them spread their beliefs.
"The opening of this latest medical center will enable you to spread your message," he said, "and do your vital work, on a significantly larger scale in the years to come."
The Source's CEO Cynthia Wenz told RH Reality Check that they will provide pap smears and some forms of contraception in order to participate in the Women's Health Program, but no "abortifacients" will be provided. At crisis pregnancy centers, though, that term can be misconstrued to apply to almost all forms of hormonal birth control and even intrauterine devices (IUDs) — the most effective form of birth control.
September 21, 2012 Published ~ 3 years ago.
Republican Rep: Obama 'has helped jump start a new Ottoman Empire'
Speaking on the House floor Friday afternoon, Rep. Louie Gohmert (R-TX) claimed President Obama's foreign policy in the Middle East was "a massive beginning of a new Ottoman Empire that [he] can take great credit for." Gohmert continued, "This president is trying to buy affection from people who are bullies, who are radical Islamists, who want to destroy us." The Texas Republican has a history of Islamophobic behavior. Watch the clip:
– Greg Noth
September 21, 2012 Published ~ 3 years ago.
Lady Gaga's Record Label Wants Her To Lose Weight
Well, this is discouraging. Lady Gaga's label has apparently decided that, rather than ordering costumes for the singer's tour that suit her body, or letting her decide what she looks good and comfortable in, the pop singer needs to lose weight:
Executives at Universal Music Group saw recent pictures of the singer bulging out of her too-tight clothes and were forced to order a better-fitting wardrobe for the remainder her of her world tour, according to a RadarOnline report. "The tight, skimpy outfits weren't doing anything for Gaga's new fuller figure, so Universal ordered more flattering and better fitting costumes for the rest of the tour," a source told the gossip site.
They allegedly told the "Born This Way" singer to lay off her favorite high-calorie foods, pizza and pasta. "Gaga has an incredible appetite for Italian food, which stems largely from her roots. It's very easy on tour to get hooked on a diet of pizza and pasta because they are comfort foods—and when you are away from home you always long for something that reminds you of where you came from," the source said. "She loves to eat, but because of her tiny frame it shows if she doesn't work out as much as normal. Executives told her to quit gorging on her favorite foods."
Did they like her better when Gaga was talking about being on the so-called Drunk Diet promoted by her then-boyfriend Luc Carl? Are some of the stranger things she's worn during her time in the public eye actually less attractive than the sight of her with curves? There's something pretty depressing about an environment where it's easier for a woman to get away with wearing a dress made of raw meat than a body mass index that's outside what the corporate definition of acceptable.
September 21, 2012 Published ~ 3 years ago.
Backed By $20 Million From Coal, House Members Approve Polluter Giveaway
In the House of Representatives' final act before its two-month vacation, House Republicans approved 233-175 a pro-coal package on Friday that dismantles or delays an array of public health protections. H.R. 4309 may be named for the fictitious "war on coal," but it rolls back protections in the Clean Water and Clean Air Acts, blocking EPA carbon pollution standards and fuel efficiency standards.
In a year where fossil fuel groups have pledged to spend hundreds of millions of dollars, the House GOP's last act before November is a symbolic gesture for coal, that risks Americans' health and even the coal industry itself.
Over their careers, the 233 members who voted for the Big Coal package have received more than $20 million over their careers from coal — according to an analysis of OpenSecrets.org data and additional analysis by Oil Change International. The 175 members who voted against undermining public health have just $8 million in career coal contributions. In just the 2012 cycle, the Big Coal votes have taken $4.5 million more than those voting against the bill.
Like today's vote, campaign contributions from the coal and coal-dependent utilities industries break clearly across partisan lines: House Republicans have raised almost $20 million from coal and utilities industries, double the $10.2 million by Democrats. Coal mining companies alone have contributed $4.4 million to House Republicans over their careers, nearly five times the amount to Democratic members.
* Based on data from OpenSecrets.org with additional analysis by Oil Change International. Oil Change International has purchased, analyzed, and refined this data from the Center for Responsive Politics.
September 21, 2012 Published ~ 3 years ago.
'End Of Watch' And The Rise Of The Latino Cop
End of Watch, Training Day writer David Ayer's third directorial effort after Harsh Times and Street Kings, is being advertised as a violent, aggressive movie that pits cops against cartels. To a certain extent, it is that: forks are shoved in eyes, cops go toe to toe with gang-bangers, and gold-plated guns are confiscated from vehicles. But those elements of the movie exist mostly to sell a much more subtle and interesting picture, a story about an exceedingly close friendship between two cops that also helps shift police dramas away from the monochromatic relationship between black cops and white cops and between white cops and black communities.
The cops in question are Brian Taylor (Jake Gyllenhaal) and Mike Zavala (Michael Peña), who we meet shortly after they're cleared in a shooting incident and return to their work patrolling the streets of South Central Los Angeles. Rather than being detectives or the leaders of special squads, Brian and Mike are beat cops, a designation that means most of what they have to do is mosey around in their police cruiser in between minor bouts of community management and small acts of heroism—Mike fights a cantankerous older gang banger who's been harassing his mailman to get the man to stop and charges into a burning building to rescue two young children, with Brian right behind him. Their stops in various Los Angeles homes veer between humor and horror, from the fisticuffs to the discovery of illegal immigrants locked in a back room. But their conversations, frequently about women, are the best part of the movie.
Mike is married to Gabby, his high school girlfriend, who he credits with marching him off to the police academy in the first place. And while he jokes with Brian that what Brian really needs is to find someone who will cook and won't sleep with his friends and occasionally makes fun of Brian for complaining about being single and sexually successful, Mike clearly loves his wife, telling Brian "I don't want to be with anyone else." Brian has more direction and education than his partner does: a former Marine, when we meet him, he's taking an elective film class as part of his pre-law courses. And his discontent with his dating life stems from a desire for a real connection. "First date: dinner and a respectful kiss," Brian tells Mike. "Second date: dinner and full carnal knowledge. Third date: dinner and awkward silences when I try to talk about anything of merit." End of Watch may be a tough-guy movie, but it's one that argues that strength and tenderness aren't incompatible, and that really loving a woman is more fun and more honorable than suffering through the company of one you couldn't possibly respect.
When Brian finds that woman, a smart, sweet scientist named Janet (an excellent Anna Kendrick), it's Mike he turns to for a model. Peña's been a cop before, in Oliver Stone's World Trade Center, a role that similarly emphasized his character's relationship with his family over action. There, he was Will Jimeno, an officer new to the Port Authority police force, who finds himself trapped under the rubble of the North Tower on September 11 with a senior officer, John McLoughlin (Nicolas Cage). It's the memory of Jimeno's heavily pregnant wife Allison (Maggie Gyllenhaal), who spends the day alternating between Will's family and her own, that helps him keep talking and alive as they wait for rescue. In End of Watch, Mike provides Brian, who seems unmoored in the expanse of Los Angeles, with a surrogate family. Brian may joke about the number of quinceañeras Mike drags him to, but he takes Janet to one on an early date, behaving beautifully to the birthday girl, joining the family on the floor for the Macarena. At Janet and Brian's wedding, Mike promises to take care of Janet, and Gabby gives Janet a primer on how to build a successful marriage with a cop. It's not Mike's streetwise instincts or some sort of flashy, violent charisma, like Alonzo Harris's in Training Day, that bind him and Brian so closely together: it's his sense of how to maintain a family, to be a solid, stable man, that makes Brian turn to Mike for guidance.
That subtlety doesn't characterize the section of the film that follows the Latino gang members who end up Mike and Brian's antagonists through a series of little confrontations—a noise complaint, a traffic stop, Brian's hunches—rather than by conspiracy or aggressive escalation. There are glints of humor in a argument between a young cop, Orozco (America Ferrera) and one of the gang members, heated by unspoken but implied lesbianism on both sides, or Brian's asking another gang member why he goes by the name Big Evil. But watching the gang members psych themselves up for a hit in a profanity-laced tirade that has none of the cleverness of Bunk and McNulty investigating a murder in The Wire has none of the charm of watch Brian pretend to be a Latina teenager and to have Mike respond by mocking the white, yuppie girls, Brian goes out with. I understand the desire to make sure that the gang subplot doesn't step on the relationship between Mike and Brian that is the real core of the movie, but the gap between Ayer's innovations within the cop format and his by-the-numbers portrait of Mexican gangs and the cartels that sometimes pull their strings is obvious.
And at the conclusion of End of Watch, the movie becomes more what it was advertised to be than what it actually, and compellingly, mostly is. I could watch Gyllenhaal and Peña tool around in a car for two hours, talking each other into manhood. But studios will have their blood and bullets. And giving it to them to keep the two men mostly at the center of the frame and in the front seat of their cruiser is worth the tradeoff.
September 21, 2012 Published ~ 3 years ago.
STUDY: Low-Income Smokers In New York Spend A Quarter Of Their Income On Cigarettes
Although cigarette taxes are a very effective way to encourage people to stop smoking — as well a potential source of important revenue for some cash-strapped states — a new study suggests that they also work to highlight income inequality among American smokers.
New York places a $4.35 tax on each pack of cigarettes, the highest rate in the country, and researchers used data from the state health department to calculate how much money its residents are spending on cigarettes each year. They found that that smokers in New York who earn less than $30,000 a year spent an average of 23.6 percent of their annual income on cigarettes, while the state's wealthier smokers — defined as those earning over $60,000 a year — spent an average of just 2.2 percent of their earnings to support their smoking habit.
Because of this discrepancy, researchers pointed out that this tax may be disproportionately straining low-income New Yorkers:
"Although high cigarette taxes are an effective method for reducing cigarette smoking, they can impose a significant financial burden on low-income smokers," Matthew Farrelly and his co-authors wrote in the conclusion of their paper, which was published this month in Plos One, an online, peer-reviewed journal. […]
The low-income now spend twice as much of their earnings on cigarettes as they did in 2003, when the state imposed a tax of $1.50 [compared to the current $4.35 tax] on each pack.
The researchers concluded that to make the cigarette tax less regressive, the state should spend more of the resulting revenue on programs that help low-income smokers quit the habit, although both the researchers and the health department say this would be a challenge.
The study acknowledged that low-income populations tend to have higher percentages of smokers, highlighted by the fact that smoking rates among low-income New Yorkers did not decline at all between 2003 and 2010, even though smoking rates dropped by about 20 percent among all income groups during the same period. According to 2010 figures from the Centers for Disease Control, 28.9 percent of adults below the poverty level were smokers, a full 10 points higher than the rate for the adult population at or above the poverty level. Anti-smoking advocacy groups have also noted the correlation between smoking and income level, pointing out that encouraging lower-income Americans to quit smoking can help save states money on their Medicaid program expenditures, since approximately 10 to 20 percent of all Medicaid funds — totaling more than $30 billion each year — is spent on costs related to smoking-related illnesses.
But as the researchers noted, states could attempt to combat some of these issues by choosing to use the revenue generated by their cigarette taxes to invest in programs to help lower smoking rates among low-income populations. Turning a smoking habit into a bigger financial investment may deter some smokers, but cigarette taxes only represent one part of a broader public health strategy that should also include preventative education and support programs.
September 21, 2012 Published ~ 3 years ago.
Latino And Black Law Enforcement Groups Endorse Colorado Marijuana Initiative
Two national law enforcement organizations representing black and Latino police officers announced their support yesterday for the ballot initiative to legalize marijuana in Colorado.
The endorsements by Blacks in Law Enforcement of America and the National Latino Officers Association of Amendment 64, which proposes to regulate marijuana like alcohol, were accompanied by a letter signed by law enforcement officials from around Colorado:
As police officers, judges, prosecutors, corrections officials and others who have labored to enforce the laws that seek to prohibit marijuana use, and who have witnessed the abysmal failure of this current criminalization approach, we stand together in calling for new laws that will effectively regulate marijuana in a manner similar to alcohol. […]
As law enforcement professionals, we especially want voters to understand that responsible regulation will allow us to do our jobs more effectively and safely. When we change our marijuana laws, police officers will no longer have to waste time on low-level marijuana arrests. As public safety is our primary concern, we look forward to the passage of this initiative, which will allow our criminal justice system to focus on protecting the public from violent crime. […]
Controlling marijuana through a regulated system will fundamentally assist in keeping the substance away from juveniles. Illegal dealers have no incentive to check IDs or avoid selling to juveniles, but under state regulation for adult use, licensed marijuana entities will face penalties and consequences that will effectively deter underage sales. Indeed, a recent study from Columbia University shows that teens currently find it easier to purchase illegal marijuana than age-regulated alcohol.
Other groups that have already endorsed the initiative include the Colorado/Montana/Wyoming NAACP Conference, the Colorado Democratic Party and the Colorado Criminal Defense Bar. Initiatives to legalize marijuana are also on the November ballot in Washington and Oregon.
In a recent poll by the Denver Post, more than half of likely voters said they support the measure. But opposition to the bill is mounting, now that a group funded primarily by strip-mall magnate Melvin Sembler, who was the fundraising chair for Mitt Romney in 2008, has launched a campaign to drive down support for the measure. Sembler and his wife Betty once oversaw a chain of drug abuse treatment centers for teens, at which allegations have emerged of beatings, rape and psychological abuse.
September 21, 2012 Published ~ 3 years ago.
New Research Debunks Republican Talking Point On Higher Education Tuition
To hear Republicans tell it, the constantly rising cost of higher education is attributable to increases in federal financial aid. House Republicans even made this argument to justify cutting Pell Grants in their fiscal year 2013 budget.
However, a new study by the Federal Reserve Bank of New York found that, at least in the last several years, tuition increases have been driven not by rising financial aid but by decreasing state budgets:
After 2007, the group of states with the most funding cuts (Group 1) also has the highest growth in tuition in each year, with an average annual growth rate of 3.4 percent in tuition. Our analysis suggests that over this period, a 10 percent decline in public funding for Group 1 is associated with an average annual increase of 3.1 percent in tuition at public institutions. This compares with an increase of 1.2 percent in public institution tuition for a 10 percent decline in public funding in our full sample over the same period (2007-11). That is, we observe an economically meaningful relationship between public funding and public institution tuition changes but mainly since the recession began and especially for the group of states with larger higher education funding cuts. […]
In the public discourse, federal funding is often blamed for driving up tuition. However, our analysis suggests that public schools are increasing tuition as a way to make up for decreasing state and local appropriations for higher education, and that deeper cuts in public funding may be associated with correspondingly greater tuition hikes.
The Republican budget would reduce Pell Grants for one million students, even though 70 percent of Pell Grants recipients last year came from households with incomes under $30,000.
September 21, 2012 Published ~ 3 years ago.
Paris Hilton Apologizes for Anti-Gay Rant
Normally, I would pay absolutely no attention to anything Paris Hilton says, except that her anti-gay meltdown yesterday and her apology today are a perfect example of how the media's learned to process offense. The hotel heiress found herself in headlines again after a New York taxi driver clandestinely taped her speaking with a friend in a cab, in itself a totally gross thing to do, no matter how gross whatever he captured is. And the exchange between Hilton and her friend is both unattractive and ignorant:
"Say I log into Grindr, someone that's on Grindr can be in that building and it tells you all the locations of where they are and you can be like, 'Yo, you wanna fuck?' and he might be on like, the sixth floor," the friend explains. "Ewww. Eww. To get fucked?" Hilton replies. "Gay guys are the horniest people in the world. They're disgusting. Dude, most of them probably have AIDS." "I would be so scared if I were a gay guy," she adds. "You'll like, die of AIDS."
Of course, she's apologized immediately, releasing a statement through GLAAD:
As anyone close to me knows, I always have been and always will be a huge supporter of the gay community. I am so sorry and so upset that I caused pain to my gay friends, fans and their families with the comments heard this morning. I was having this private conversation with a friend of mine who is gay and our conversation was in no way towards the entire gay community. It is the last thing that I would ever want to do and I cannot put into words how much I wish I could take back every word.HIV/AIDS can hurt anyone, gay and straight, men and women. It's something I take very seriously and should not have been thrown around in conversation. Gay people are the strongest and most inspiring people I know.
Everyone involved here benefits. Hilton gets herself back in the headlines, and doing something that makes her look comparatively classy: apologizing and praising the resiliency of gay people is an upgrade from getting thrown out of Nelson Mandela Bay Stadium for smoking pot, or turned away from Japan for drug convictions. GLAAD gets its position as the arbiter of publicly (or in this case, privacy-violated ) expressed speech about LGBT people and its role as a redemption engine reaffirmed. And anyone who falls into the category of people who still care about Paris Hilton's opinion and felt harmed by her speech gets reassured she doesn't actually mean it. I suppose it's a good thing that these mechanisms exist. I just wish the standards for making amends were higher, and produced more meaningful results than publicist-brokered apology statements. If we're going to make famous people go through the motions of bringing their attitudes in line with what's publicly acceptable, we might as well get more meaningful commitments or donations of time and energy out of them than that.
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Gary Farmer
|Gary Farmer
June 12, 1953
Ohsweken, Ontario
Gary Dale Farmer (born June 12, 1953) is a Canadian actor and musician. He is a member of the First Nations.
Farmer was born in Ohsweken, Ontario into the Cayuga Nation and Wolf Clan[1] of the Haudenosaunee/Iroquois Confederacy.[2][3][4] Farmer attended Syracuse University and Ryerson Polytechnic University, where he studied photography and film production.[4]
His first major role was on the CBC's Spirit Bay. He subsequently played police captain Joe Stonetree on the syndicated TV series Forever Knight, and Chief Tom in the CBC first nations TV series The Rez. Farmer is best known for his role as spiritual Native American guide Nobody in Dead Man. Farmer reprised the role for a cameo in Ghost Dog: The Way of the Samurai, also directed by Jim Jarmusch. He also was the publisher of Aboriginal Voices magazine, one of the Founders of the Aboriginal Voices radio network, and is an avid supporter of native media projects in film, radio, television and the internet. He has won numerous awards and nominations from many native film festivals, and Canadian film awards.
Farmer has performed in both the film and television adaptations of Tony Hillerman's novels. He played "Cowboy" Albert Dashee (Hopi) in the 1991 film The Dark Wind, and Captain Largo (Navajo) in the television adaptations of Coyote Waits (2003) and A Thief of Time (2004). He was nominated for Independent Spirit Awards for his roles in the movies Powwow Highway, Dead Man, and Smoke Signals. Farmer also played the role of Fagin in Twist, the 2003 independent adaptation of the Charles Dickens classic. He also played Deputy Bob in Demon Knight. Two of his latest major roles were Henry Colville, with Kris Kristofferson, in Disappearances (2006) and Jack in Jimmy P: Psychotherapy of a Plains Indian (2013) by Arnaud Desplechin.
He also has a blues band called Gary Farmer and the Troublemakers. The band has released two CDs, Love Songs and Other Issues in 2007 and Lovesick Blues in 2009.
He recorded the audiobook version of Louise Erdrich's 2012 novel The Round House, winner of the 2012 National Book Award for Fiction.
External links[edit]


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Shilo Adds Director/Creative Director Ash Thorp
Bi-coastal design-driven production company adds prolific director, designer, illustrator and artist amid growth stage.
Bi-coastal design-driven production company adds prolific director, designer, illustrator and artist amid growth stage.
Web-slinging spiders, terrifying toys and super-creepy mysteries all team up on store shelves for this week's home entertainment releases on Blu-Ray and DVD.
SIGGRAPH 2014 will offer presentations on more than 15 of the biggest current and upcoming studio productions, including 'X-Men: Days of Future Past,' 'Gravity,' 'How to Train Your Dragon 2' and 'Teenage Mutant Ninja Turtles.'
Visual effects supervisor Everett Burrell joins shade VFX; company recently completed projects for Jon Favreau's 'Chef,' Sony's 'The Amazing Spider-Man 2,' and Disney's 'Million Dollar Arm.'
MPC Vancouver teams up with director Marc Webb and Sony Pictures Imageworks VFX Supervisor Jerome Chen to complete more than 300 shots for 'The Amazing Spider-Man 2.'
The veteran Imageworks visual effects supervisor walks us through the production of Sony's highly anticipated second Spider-Man offering.
Sony Pictures unveils a peek at its forthcoming summer's tentpole, The Amazing Spider-Man 2, during Wednesday night's festivities in New York's Times Square.
Hans Zimmer to work with Pharrell Williams, Johnny Marr, Michael Einziger, and Dave Stewart to create music for The Amazing Spider-Man 2, directed by Marc Webb.


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Panasonic Viera 37-inch LCD HDTV with iPod Dock, now $412
6ave.com's Sick Deal of the Day is the Panasonic Viera X2 Series 37-inch LCD HDTV with iPod Dock (model no. TC-L37X2) on sale for $412, which is $237 off its regular price of $649, and about $28 less than the next best price we have seen this combo for. Features include a maximum video resolution of 1366 x 768, a 16:9 aspect ratio, built-in HDMI and PC inputs, and a universal dock that supports all iPod models. FREE shipping has also been included with this deal, and sales tax applies for residents of New York and New Jersey.
The larger JVC 46-inch 1080p LCD HDTV can be found today at Newegg.com, and has been reduced from $999.99 down to only 699.99, with FREE ground delivery included. Priced at $659 is the Panasonic Viera TC-L37D2 37-inch 1-0-p LED LCD HDTV, which is on sale this week at BHphotovideo.com and also includes FREE shipping. Display your HDTV in style with the 50-inch Flat Panel HDTV Stand, available today at Amazon.com and has gone from $349.99 down to $202.10 with FREE shipping included.


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Allen Americans beat Arizona, 4-3, in shootout on Wednesday
Here is the press release:
Prescott Valley, Arizona – The Allen Americans are on the road for a three game set this week, starting with a meeting with the Arizona Sundogs on Wednesday evening before a pair of back-to-back contests against Denver this weekend.
A testy first period saw a mix of very physical hockey and several fights before play settled down. Arizona opened the scoring late in the period when Pascal Morency lit the lamp at 17:32 with the assist going to Jake Hauswirth. Allen answered back in the final seconds of the first period to tie the game on a Trevor Ludwig goal at 19:39, assisted by Anthony Maiani and Daryl Bootland. The score remained tied at the first intermission with Arizona holding the edge in shots for the period at 14-9.
The second period opened quickly for both clubs with each scoring in the opening minute of play. Arizona struck first when Jake Hauswirth fired a shot past Steve Silverthorn from the slot off a pass from Derek LeBlanc just 33 seconds in. Arizona followed their goal with an immediate penalty that Allen's Scotty Howe's made quick work of, scoring to tie the game 25 second later in his first game back from the IR. Tyler Ludwig earned the assist on the Howes goal for Allen. Kyle Hood gave Arizona back the lead with a wrist shot from the left faceoff circle, assisted by Jeff Kyrzakos and Mario Larocque at 16:49. The Americans answered back within seconds once again when Scotty Howes earned his second marker of the night. Howes one-timed a shot past Adam Russo from the top of the crease off passes from Jamie Schaafsma and Tyler Ludwig at 17:33. Allen outshot Arizona in the middle frame 15-12 for a two period total 26-24 in favor of the Sundogs.
The third period was the only scoreless one in regulation, with both sides having opportunities but neither able to close the deal. Allen outshot Arizona through the third period 10-8 for a three period total of 34-34. Neither team was able to net the game winner in extra time, so the game went to shootout.
In the shootout, the lone scorer of the ten shooters was Allen's Daryl Bootland who earned his 9th goal of the season along with his 3rd game winner on the year. With the victory in Arizona, the Allen Americans move past Wichita, back into first place in the Central Hockey League standings.
The Allen Americans make the trek to Denver to face the Cutthroats in a pair of back-to-back games Friday and Saturday. The puck drop is scheduled for 8:05PM CST Friday and Saturday night.


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Alan Simpson is not only co-chairman of a presidential fiscal commission whose leaders offered a way out of the nation's deficit.
He's also, along with fellow co-chairman Erskine Bowles, a member of the board of TheCanKicksBack, a nonprofit group promoting the opposite of kicking the can down the road (motto: "The debt is too damn high.")
And the retired Republican senator from Wyoming has some Gangnam-styled advice for young people about what they can do about the deficit:
"Stop Instagramming your breakfast."
"Start using those precious media skills" to sign up people for TCKB.
He also has a warning for what Congress will do with the nation's money if someone doesn't do something about it: "These old coots will clean out the Treasury before you'll get there."