technology:antibodies

  • danah boyd : When Good Intentions Backfire – Data & Society : Points
    https://points.datasociety.net/when-good-intentions-backfire-786fb0dead03

    I find it frustrating to bear witness to good intentions getting manipulated, but it’s even harder to watch how those who are wedded to good intentions are often unwilling to acknowledge this, let alone start imagining how to develop the appropriate antibodies. Too many folks that I love dearly just want to double down on the approaches they’ve taken and the commitments they’ve made. On one hand, I get it — folks’ life-work and identities are caught up in these issues.

    I’ve never met an educator who thinks that the process of educating is easy or formulaic. (Heck, this is why most educators roll their eyes when they hear talk of computerized systems that can educate better than teachers.) So why do we assume that well-intended classroom lessons — or even well-designed curricula — might not play out as we imagine? This isn’t simply about the efficacy of the lesson or the skill of the teacher, but the cultural context in which these conversations occur.

    In many communities in which I’ve done research, the authority of teachers is often questioned. Nowhere is this more painfully visible than when well-intended highly educated (often white) teachers come to teach in poorer communities of color. Yet, how often are pedagogical interventions designed by researchers really taking into account the doubt that students and their parents have of these teachers? And how do we as educators and scholars grapple with how we might have made mistakes?

    From the outside, companies like Facebook and Google seem pretty evil to many people. They’re situated in a capitalist logic that many advocates and progressives despise. They’re opaque and they don’t engage the public in their decision-making processes, even when those decisions have huge implications for what people read and think. They’re extremely powerful and they’ve made a lot of people rich in an environment where financial inequality and instability is front and center. Primarily located in one small part of the country, they also seem like a monolithic beast.

    As a result, it’s not surprising to me that many people assume that engineers and product designers have evil (or at least financially motivated) intentions. There’s an irony here because my experience is the opposite. Most product teams have painfully good intentions, shaped by utopic visions of how the ideal person would interact with the ideal system. Nothing is more painful than sitting through a product design session with design personae that have been plucked from a collection of clichés.

    Most products and features that get released start with good intentions, but they too get munged by the system, framed by marketing plans, and manipulated by users. And then there’s the dance of chaos as companies seek to clean up PR messes (which often involves non-technical actors telling insane fictions about the product), patch bugs to prevent abuse, and throw bandaids on parts of the code that didn’t play out as intended. There’s a reason that no one can tell you exactly how Google’s search engine or Facebook’s news feed works. Sure, the PR folks will tell you that it’s proprietary code. But the ugly truth is that the code has been patched to smithereens to address countless types of manipulation and gamification (e.g., SEO to bots). It’s quaint to read the original “page rank” paper that Brin and Page wrote when they envisioned how a search engine could ideally work. That’s so not how the system works today.

    Powerful actors have always tried to manipulate the news media, especially State actors. This is why the fourth estate is seen as so important in the American context. Yet, the game has changed, in part because of the distributed power of the masses. Social media marketers quickly figured out that manufacturing outrage and spectacle would give them a pathway to attention, attracting news media like bees to honey. Most folks rolled their eyes, watching as monied people played the same games as State actors. But what about the long tail? How do we grapple with the long tail? How should journalists respond to those who are hacking the attention economy?

    In short, I keep thinking that we need more well-intended folks to start thinking like hackers.

    Think just as much about how you build an ideal system as how it might be corrupted, destroyed, manipulated, or gamed. Think about unintended consequences, not simply to stop a bad idea but to build resilience into the model.

    As a developer, I always loved the notion of “extensibility” because it was an ideal of building a system that could take unimagined future development into consideration. Part of why I love the notion is that it’s bloody impossible to implement. Sure, I (poorly) comment my code and build object-oriented structures that would allow for some level of technical flexibility. But, at the end of the day, I’d always end up kicking myself for not imagining a particular use case in my original design and, as a result, doing a lot more band-aiding than I’d like to admit.

    #Hacker #Freaks #Résilience #danah_boyd

  • A vaccine that could block mosquitoes from transmitting malaria
    http://theconversation.com/a-vaccine-that-could-block-mosquitoes-from-transmitting-malaria-105

    For some decades, researchers have being working on a novel idea called a “transmission-blocking vaccine.” This vaccine is different from traditional vaccines that protect the recipient from getting the disease. Here, the vaccine blocks the transmission of the parasite that causes malaria from an infected human host to mosquitoes.

    When a human receives such a vaccine, specific antibodies are generated in the blood. When a mosquito bites and ingests the blood of an infected human, both the parasite and antibody are taken up into the mosquito’s stomach. Once inside the mosquito, the antibody attaches to the parasite and inhibits its development. This prevents the mosquito from transmitting the disease to another person.

    The concept is bold but has not yet been tested in large-scale trials.

    #paludisme #vaccin #moustiques

  • Ah ! On le savait bien qu’il y a avait complot vegan !

    A Tick Bite Could Make You Allergic to Meat—and It’s Spreading
    http://news.nationalgeographic.com/2017/06/tick-bite-meat-allergy-spreading-spd

    “You’re walking through the woods, and that tick has had a meal of cow blood or mammal blood,” explained Cosby Stone, an allergy and immunology fellow at Vanderbilt University. “The tick, carrying Alpha-Gal, bites you and activates your allergy immune system.”

    From this, your body creates Alpha-Gal antibodies and, from that point on, the body is wired to fight Alpha-Gal sugar molecules. The majority of people who develop Alpha-Gal allergy syndrome realize their illness after eating meat, which is rife with Alpha-Gal. The sugar is also present in some medications that use gelatins as stabilizers.

    #tique #allergie #viande

  • Le lien entre Zika et maladie neurologique est prouvé - France Inter
    http://www.franceinter.fr/depeche-le-lien-entre-zika-et-maladie-neurologique-est-prouve

    Il existe bien un lien entre le virus Zika et le syndrome de Guillain-Barré. Une première étude vient d’être publiée par une équipe de l’Institut Pasteur à Paris, publiée dans la revue médicale The Lancet. Elle démontre le lien certain entre maladie neurologique grave et virus zika provoqué, lui, par une piqûre de moustique.

    • Guillain-Barré Syndrome outbreak associated with Zika virus infection in French Polynesia: a case-control study - The Lancet
      http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(16)00562-6/abstract

      Summary
      Background
      Between October, 2013, and April, 2014, French Polynesia experienced the largest Zika virus outbreak ever described at that time. During the same period, an increase in Guillain-Barré syndrome was reported, suggesting a possible association between Zika virus and Guillain-Barré syndrome. We aimed to assess the role of Zika virus and dengue virus infection in developing Guillain-Barré syndrome.

      Methods
      In this case-control study, cases were patients with Guillain-Barré syndrome diagnosed at the Centre Hospitalier de Polynésie Française (Papeete, Tahiti, French Polynesia) during the outbreak period. Controls were age-matched, sex-matched, and residence-matched patients who presented at the hospital with a non-febrile illness (control group 1; n=98) and age-matched patients with acute Zika virus disease and no neurological symptoms (control group 2; n=70). Virological investigations included RT-PCR for Zika virus, and both microsphere immunofluorescent and seroneutralisation assays for Zika virus and dengue virus. Anti-glycolipid reactivity was studied in patients with Guillain-Barré syndrome using both ELISA and combinatorial microarrays.

      Findings
      42 patients were diagnosed with Guillain-Barré syndrome during the study period. 41 (98%) patients with Guillain-Barré syndrome had anti-Zika virus IgM or IgG, and all (100%) had neutralising antibodies against Zika virus compared with 54 (56%) of 98 in control group 1 (p<0·0001). 39 (93%) patients with Guillain-Barré syndrome had Zika virus IgM and 37 (88%) had experienced a transient illness in a median of 6 days (IQR 4–10) before the onset of neurological symptoms, suggesting recent Zika virus infection. Patients with Guillain-Barré syndrome had electrophysiological findings compatible with acute motor axonal neuropathy (AMAN) type, and had rapid evolution of disease (median duration of the installation and plateau phases was 6 [IQR 4–9] and 4 days [3–10], respectively). 12 (29%) patients required respiratory assistance. No patients died. Anti-glycolipid antibody activity was found in 13 (31%) patients, and notably against GA1 in eight (19%) patients, by ELISA and 19 (46%) of 41 by glycoarray at admission. The typical AMAN-associated anti-ganglioside antibodies were rarely present. Past dengue virus history did not differ significantly between patients with Guillain-Barré syndrome and those in the two control groups (95%, 89%, and 83%, respectively).

      Interpretation
      This is the first study providing evidence for Zika virus infection causing Guillain-Barré syndrome. Because Zika virus is spreading rapidly across the Americas, at risk countries need to prepare for adequate intensive care beds capacity to manage patients with Guillain-Barré syndrome.

      Funding
      Labex Integrative Biology of Emerging Infectious Diseases, EU 7th framework program PREDEMICS. and Wellcome Trust.

  • Study: cannabis compound might have use as an HIV drug (Wired UK)
    http://www.wired.co.uk/news/archive/2013-05/1/cannabis-hiv-drug

    The way it works is by interaction with the cannabinoid type-2 (CB2) receptor in white blood cells, specifically the macrophages. Macrophages are one of many types of white blood cell in humans. While the main cells, the lymphocytes, do the bulk of the work in fighting infection by tracking down and destroying germs with antibodies, macrophages form a kind of backup part of the immune system — attracted to damaged cells, they surround and engulf them while also alerting lymphocytes of new dangers.

    Macrophages have an unpleasant weakness, though, in that they are one of the first types of cells to be infected by HIV when it enters the body. The virus can live inside macrophages for days, weeks or months, travelling around the body, infecting other cells and acting as an extremely effective pollinator of HIV.

    Stopping the HIV virus from infecting macrophages is one method researchers are investigating, as it would dramatically curtail the speed at which the infection progresses and would give time for other antiretrovirals to help keep it at bay, or even remove it.

    The CB2 receptor in macrophages is stimulated normally when THC enters the bloodstream, so nothing unusual there. However, it appears that macrophages that have their CB2 receptor stimulated are stronger when it comes to fighting and weakening the HIV-1 virus.

    This was discovered when the research team from the Temple University School of Medicine in Philadelphia infected macrophages with the HIV-1 virus, before then exposing cell cultures to one of three types of synthetic THC that specifically target the CB2 receptor. Comparing these cell cultures after seven days against a control group revealed a clear decrease in the rate of HIV-1 infection. Effectively, the macrophages had become stronger at keeping the HIV-1 virus out.

    ...

    An added benefit of targeting only the CB2 receptor is that its only affect is to stimulate the macrophages — the psychoactive component of THC is experienced when the CB1 receptor gets targeted. Synthetic THC compounds can be produced to only target the CB2 receptor in this way. THC has also been shown in studies not to suppress the immune systems of those who take it, meaning that the findings could provide hints at a future drug that, in combination with other methods, could be used for suppressing the HIV-1 virus.

    The study has been published in The Journal of Leukocyte Biology.

  • Israelis find possible cure for malaria
    http://www.israeltoday.co.il/NewsItem/tabid/178/nid/23552/Default.aspx

    The body’s immune system sends antibodies to combat the disruptive proteins, but the Plasmodium parasite is able to use one type of protein to keep the antibodies busy while producing a different protein to continue the infection.

    The Israeli researchers have unlocked the unique DNA sequence that allows the Plasmodium parasite to do this.

    #recherche #paludisme #santé #malaria

  • An Engineered Doomsday - NYTimes.com
    http://www.nytimes.com/2012/01/08/opinion/sunday/an-engineered-doomsday.html?nl=todaysheadlines&emc=tha211

    Defenders of the research in Rotterdam claim it will provide two major benefits for protecting global health. First, they say the findings could prove helpful in monitoring virus samples from infected birds and animals. If genetic analysis found a virus somewhere that was only one or two mutations away from going airborne, public health officials would then know to bear down aggressively in that area to limit human contact with infected poultry and ramp up supplies of vaccines and medicines.

    But it is highly uncertain, even improbable, that the virus would mutate in nature along the pathways prodded in a laboratory environment, so the benefit of looking for these five mutations seems marginal.

    A second postulated benefit is that the engineered virus can be used to test whether existing antiviral drugs and vaccines would be effective against it and, if they come up short, design new drugs and vaccines that can neutralize it. But genetic changes that affect transmissibility do not necessarily change the properties that make a virus susceptible to drugs or to the antibodies produced by a vaccine, so that approach may not yield much useful new information.

    We cannot say there would be no benefits at all from studying the virus. We respect the researchers’ desire to protect public health. But the consequences, should the virus escape, are too devastating to risk.

    #H5N1 #sciences&democratie

  • #Cuba makes #cancer breakthrough — New Internationalist
    http://www.newint.org/blog/majority/2011/11/14/cuba-makes-cancer-breakthrough

    Cuban medical authorities have released CimaVax-EGF, the result of a 25-year research project at Havana’s Center for Molecular Immunology.
    (...)
    The #vaccine (...) can turn aggressive later-stage lung cancer into a manageable chronic disease by creating antibodies. These antibodies battle it out with the proteins that cause uncontrolled cell proliferation.

    l’article se demande si les #pharma vont réussir à poser des #brevets sur cette découverte cubaine, ou si Cuba va réussir à le vendre à l’étranger.

    Pour un papier scientifique voir http://www.ncbi.nlm.nih.gov/pubmed/20387330