About this “feminism” and [some of] the conservative women and their views regarding Aplin, motherhood and children. But most of all about why I don't understand how a whole column about "the bad about the leftish women bashing Palin" can turn out to be bashing the leftish women, when the whole point and main argument in the column is "why women need to not bash other women". Hallå?!
And if I get the energy to translate it all to English I will but now I have to write something in Swedish since I will go absolutely crazy if I don’t comment this in the Swedish newspaper Svenska dagbladet.
”Därför är framgångsrika högerkvinnan Palin från arbetarklassen så provocerande. Hon visar att det feministiska vänsterprojektet inte behövs för att hjälpa kvinnor att bli jämställda. Kvinnor kan erövra makten alldeles av sig själva. En hockeymamma från landet, som aldrig gått på genuskurs och aldrig hört talas om Underordningen kan ta sig fram i maktens korridorer. With a little help from family and friends. I USA är sådant fullt möjligt. Där lämnas människorna i fred i sina hem, byar, småstäder och del- stater, skyddade av konstitutionen mot statens klåfingrighet. Jämställdhetsministrar och genuspedagoger lyser med sin frånvaro. Ändå är USA världsledande på kvinnor med makt i samhället. Sådant svider i skinnet på genus-Sverige. Därför ska Palin fulas ut. Annars kan ju svenska hockeymammor få för sig att de kan bli något, av egen kraft. Och en framtida svensk Sarah Palin kan få för sig att lägga ner alla onödiga och dyra genusprojekt.”
Allvarligt talat, vad i hela friden babblar Fru Claesson om? Eler ja, det vet jag ju men jag kan säga så här; Sverige behöver fler kvinnor som arbetar som inte tar ut 13 månaders mammaledighet själva och lämnar männen åt jobbet. Däremot är det en lögn att det är så himla bra i USA med mammor. Det är sant att det finns fler kvinnor i näringslivet och inom företagen. Det är däremot inte så att dessa kvinnor har tid med sina barn. (Och senast jag läste Fru Claesson sa hon tydligt att ”barnen behöver sina mammor” så i all ärlighet måste man nog kräva viss KONSEKVENSANALYS av debattören.)
Och att säga att USA är jämställt (min fetstil i citatet) är att vara sjukt vindögd och naivt lurad. Eller i och för sig, man kan ju definiera om jämställd förstås. Går det med demokrati kan det väl gå med jämställdhet också. Och så får man jättegärna ta en anomali och framhäva som ett exempel på normalitet. Det är bara det att det inte riktigt ger samma smak av sanning som man skulle vilja.
Kortfattat om Sverige och USA och kvinnor med barn.
I USA är det inte ovanligt att gå tillbaka till jobbet efter 5 veckor när du som kvinna fött barn OM du nu går tillbaka till jobbet vill säga....
I Sverige är det inte ovanligt att stanna hemma HELA föräldraledigheten när du som kvinna fött barn.
I USA är det en brytpunkt, även för medelklassfamiljer, att ha två barn och stanna hemma eftersom barnomsorg är så otroligt dyrt. Så, om du är höginkomstagare och kvinna OCH VILL JOBBA kan du ju hyra en nanny som tar hand om barnen (vilket Fru Claesson i detta inlägg verkar tycka är bra, i sina gamla inlägg tycker hon det är dåligt: ”män kan inte ta hand om barn, enbart kvinnor har dessa genetiska förutsättningar”) men det innebär inte att kvinnorna har bra kontakt med sina barn, eller papporna för den delen heller.
Vore det inte bättre om man hittade ett mellanläge som vore bäst för såväl barn som vuxna? Att tro att man "väljer" när det är 2 månader (om jag är snäll nu) eller vara hemmafru är lite naivt och stor tilltro till "fritt val". Att tro att arbetsgivaren inte tar hänsyn till att du som 25-40 årig kvinna utan barn inte kan tänkas ta ut 13 månader och sen större delen av alla VABdagar är även det lite naivt.
Således är inget av länderna särskilt underunderbart för jämnställt men åtminstone så kan man i Sverige säga att vi har ett val.
Kortfattat från min sida, jag börjar bli redigt förbannand över att det hela tiden är en lösning för ”kvinnor och familjesaker” att man köper in tjänster utifrån snarare än att ”den andra partnern” ska ta och kompromissa och fördela.
Fast mest av allt är jag förbannad på att vissa skribenter ändrar åsikt, ljuger och förenklar verkligheten och därmed omöjliggör en diskussion. (jag skulle så himla gärna vilja ha en sansad diskussion om Vad man kan förvänta sig av sitt liv om man nu får barn?! Både som pappa och som mamma. Och de som tror att dom kan göra EXAKT samma saker och prioriteringar som utan barn kanske inte skulle ha dom där telningarna...... just a thought....)
ok, have to go now and will try and translate this soon enough. but at the moment I am just so... ehh... upset that I can't make that happen.
Sciencey blog with emotions, sometimes too personal, it's venting ;)
Monday, September 15, 2008
Tuesday, September 09, 2008
Exchanging Sundin for Lidström?
I don’t know.... why would you want to move away from your team since 15 years in order to go to.... their worst fiend?!?!?
I would have understood Vancouver (yes, playing with Näslund and the other 4 swedes would be a thrill, especially Näslund). I would have understood Detroit (hey Stanley Cup now I can finally touch you. Oh, and I’ll follow in the footsteps of Salming.) But Canadiens? Really?
I know he did his first time in NHL in Quebec Nordiques (1990, first European to be first over all first drafted in the NHL) but that team morphed into Colorado Avalanche, not Montreal Canadians. Although I guess they spoke French too... and came from the same province... But Montreal? The team and city that Toronto hates. The francophones and their interesting architecture. The rivalry.
Yeah, if nothing else; why would you want to trade to a team who will not win the Stanley cup either? And you get the kicker of being hated by the whole old city. I mean, this is not even considering that he could have traded in the early summer and given The Maple Leafs a shot at getting some new talent and some money. But no… wait until it is like three weeks to the first game and not decide.
Sometimes I hope that the last season was the last season. Period.
At least then I could wear my number 13 shirt with leafs on the chest with pride. Now? I might just go for that Red Wings team. After all they have more Swedes than most teams have together…. And their shirts looks more fitted than the huge number 13 in my closet.
But I will miss the first love. Always.
I would have understood Vancouver (yes, playing with Näslund and the other 4 swedes would be a thrill, especially Näslund). I would have understood Detroit (hey Stanley Cup now I can finally touch you. Oh, and I’ll follow in the footsteps of Salming.) But Canadiens? Really?
I know he did his first time in NHL in Quebec Nordiques (1990, first European to be first over all first drafted in the NHL) but that team morphed into Colorado Avalanche, not Montreal Canadians. Although I guess they spoke French too... and came from the same province... But Montreal? The team and city that Toronto hates. The francophones and their interesting architecture. The rivalry.
Yeah, if nothing else; why would you want to trade to a team who will not win the Stanley cup either? And you get the kicker of being hated by the whole old city. I mean, this is not even considering that he could have traded in the early summer and given The Maple Leafs a shot at getting some new talent and some money. But no… wait until it is like three weeks to the first game and not decide.
Sometimes I hope that the last season was the last season. Period.
At least then I could wear my number 13 shirt with leafs on the chest with pride. Now? I might just go for that Red Wings team. After all they have more Swedes than most teams have together…. And their shirts looks more fitted than the huge number 13 in my closet.
But I will miss the first love. Always.
Friday, September 05, 2008
TLR, PPR, cytokines and signaling
I am a microbiologist. The last couple of weeks however (ah, who am I kidding – lots of months of my post doc stint) I have been trying to become more of an immunologist. Let’s just say that I have never really been a fan of signaling pathways. And what is immunology? That’s right, signaling and reactions to that (inflammation and activation of different parts of the immune system).
My latest thing is TLRs*… or really, trying to figure out why this TLR # is involved in this, and why it isn’t. The hypothesis was “it should be a better outcome, let’s just try it”. The outcome turned out to be the complete opposite. (Not really surprising to anyone who has done those “this is the last control experiment, let’s just confirm the hypothesis”.) Don’t get me wrong. I am all fun and games about this since it means that I might have discovered something really new. Then again there is always this thing that I have misunderstood something. Since we are talking about TLR, PPR**, PAMP***, MyD88****, NfKb***** and the lots of the rest of the proinflammatory cytokines - and last but not least T cell activation and MCH recognition – this is not at all something impossible.
Personally I find it interesting that my reaction to signal pathways (let’s be honest here – mainly immunology and T cells, CD4, CD8, TLR, Il12, Il1, TNF-a and all the other abbreviations and letters that immunologist throw around for fun) is similar to the majority of adolescent students when presented with math and math problems. “I can’t do this. Huu… let’s run away and not think about it. Really, who need this anyway.”
Anyone with a brain can see though that this approach isn’t really helping me get any closer to finishing the paper/project and understanding the bigger picture. Hence, what to do? Well, I guess the drawing I am doing at the moment with the nice little receptor on the cell membrane getting attacked by parts of TLR# activation parts from the bacteria is one way. The other? Use the lovely [true] immunologists who scurry around me in the corridor of the Big Institute.
Here is one of the pictures I am trying to interpret and build on…. Can someone say “black box” and “we don’t know if this is an indirect activation or a direct activation of NfKb”… but sure enough, it is interesting. To a point.
(courtesy of wikipedia and not really a picture I am using but it seems better to use this one due to copyright and journals etc...)
*Toll like receptors, membrane spanning receptors that recognize structurally conserved molecules derived from microbes once they have breached physical barriers such as the skin or intestinal tract mucosa, and activate immune cell responses. They are believed to play a key role in the innate immune system and are conserved in all vertebrates as well as invertebrates. (Even in some part as smaller molecules in bacteria and plants – although not complete and functional.)
Some of these TLRs are found on macrophages, monocytes and dendritic cells and are receptors for interleukins…. And this is in part why they are called TLRs, they give rise to a signal cascade and in the end usually cytokines are produced. There are 13 known TLRs, numbered TLR1 – TRL13.
TLRs got their name (and was discovered) partly by Christiane Nüsslein-Volhard who received the Nobel prize in 1996.
Personally, I read about her when she started the Christiane Nüsslein-Volhard foundation in 1994 to support German female Scientists with children… it is mainly childcare and stipends to facilitate some kind of maternity leave and having children as a researcher without a stay at home wife.
**Pattern recognition receptor; are proteins/receptors expressed on the surface of cells of the immune system.They recognize molecules that are produced by pathogens (and shared between many speices) although different from molecules made by the host as well as molecules produce by cellular stress. TLRs are a type of PPRs, although all PPRs aren’t TLRs.
***Pathogen-associated molecular patterns, are molecular motifs that are found on pathogens. TLRs, and other PPRs, recognize these PAMPs. LPS would be a typical PAMP from a Gram negative bacteria. Lipoteichoic acid (try pronouncing that if you can) and peptidoglycan would be typical Gram postivie PAMPs. And then of course viral and bacterial DNA and RNA are PAMPs as well.
****Myeloid differentiation primary response gene (88); a universal protein that is used by all TLRs (except TLR3 which is a tad bit different and therefore is called the MyD88indepoendent activation pathway) to activate the transcription factor NfkB.
My personal note would be, an important part of the signaling pathway I am trying to understand. There are interesting deficient mice … and MyD88, as far as I understand, is important to apoptosis and pretty much lots of cell signaling.
*****nuclear factor-kappa B is a transcription factor that is found in almost all animal cell types. It is involved in cellular response to stimuli like cytokines (my thing at the moment), bactieral and viral antigens and stress. NF-κB plays a key role in regulating the immune response to infection.
So, back to drawing the signal pathway and trying to get why on earth removal of one TLR would make the outcome worse… it seems a little counter intuitive at the moment, I must say.
My latest thing is TLRs*… or really, trying to figure out why this TLR # is involved in this, and why it isn’t. The hypothesis was “it should be a better outcome, let’s just try it”. The outcome turned out to be the complete opposite. (Not really surprising to anyone who has done those “this is the last control experiment, let’s just confirm the hypothesis”.) Don’t get me wrong. I am all fun and games about this since it means that I might have discovered something really new. Then again there is always this thing that I have misunderstood something. Since we are talking about TLR, PPR**, PAMP***, MyD88****, NfKb***** and the lots of the rest of the proinflammatory cytokines - and last but not least T cell activation and MCH recognition – this is not at all something impossible.
Personally I find it interesting that my reaction to signal pathways (let’s be honest here – mainly immunology and T cells, CD4, CD8, TLR, Il12, Il1, TNF-a and all the other abbreviations and letters that immunologist throw around for fun) is similar to the majority of adolescent students when presented with math and math problems. “I can’t do this. Huu… let’s run away and not think about it. Really, who need this anyway.”
Anyone with a brain can see though that this approach isn’t really helping me get any closer to finishing the paper/project and understanding the bigger picture. Hence, what to do? Well, I guess the drawing I am doing at the moment with the nice little receptor on the cell membrane getting attacked by parts of TLR# activation parts from the bacteria is one way. The other? Use the lovely [true] immunologists who scurry around me in the corridor of the Big Institute.
Here is one of the pictures I am trying to interpret and build on…. Can someone say “black box” and “we don’t know if this is an indirect activation or a direct activation of NfKb”… but sure enough, it is interesting. To a point.
(courtesy of wikipedia and not really a picture I am using but it seems better to use this one due to copyright and journals etc...)
*Toll like receptors, membrane spanning receptors that recognize structurally conserved molecules derived from microbes once they have breached physical barriers such as the skin or intestinal tract mucosa, and activate immune cell responses. They are believed to play a key role in the innate immune system and are conserved in all vertebrates as well as invertebrates. (Even in some part as smaller molecules in bacteria and plants – although not complete and functional.)
Some of these TLRs are found on macrophages, monocytes and dendritic cells and are receptors for interleukins…. And this is in part why they are called TLRs, they give rise to a signal cascade and in the end usually cytokines are produced. There are 13 known TLRs, numbered TLR1 – TRL13.
TLRs got their name (and was discovered) partly by Christiane Nüsslein-Volhard who received the Nobel prize in 1996.
Personally, I read about her when she started the Christiane Nüsslein-Volhard foundation in 1994 to support German female Scientists with children… it is mainly childcare and stipends to facilitate some kind of maternity leave and having children as a researcher without a stay at home wife.
**Pattern recognition receptor; are proteins/receptors expressed on the surface of cells of the immune system.They recognize molecules that are produced by pathogens (and shared between many speices) although different from molecules made by the host as well as molecules produce by cellular stress. TLRs are a type of PPRs, although all PPRs aren’t TLRs.
***Pathogen-associated molecular patterns, are molecular motifs that are found on pathogens. TLRs, and other PPRs, recognize these PAMPs. LPS would be a typical PAMP from a Gram negative bacteria. Lipoteichoic acid (try pronouncing that if you can) and peptidoglycan would be typical Gram postivie PAMPs. And then of course viral and bacterial DNA and RNA are PAMPs as well.
****Myeloid differentiation primary response gene (88); a universal protein that is used by all TLRs (except TLR3 which is a tad bit different and therefore is called the MyD88indepoendent activation pathway) to activate the transcription factor NfkB.
My personal note would be, an important part of the signaling pathway I am trying to understand. There are interesting deficient mice … and MyD88, as far as I understand, is important to apoptosis and pretty much lots of cell signaling.
*****nuclear factor-kappa B is a transcription factor that is found in almost all animal cell types. It is involved in cellular response to stimuli like cytokines (my thing at the moment), bactieral and viral antigens and stress. NF-κB plays a key role in regulating the immune response to infection.
So, back to drawing the signal pathway and trying to get why on earth removal of one TLR would make the outcome worse… it seems a little counter intuitive at the moment, I must say.
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