Cryptic Elliptic
12.20.2003
in boston
I have been in Boston visiting Ed for the past few days. I return Tuesday.
A few interesting links while I'm gone:
Happy holidays.
I have been in Boston visiting Ed for the past few days. I return Tuesday.
A few interesting links while I'm gone:
- A news article in Nature on a WHO program that may move flu vaccine design into the twenty-first century. (The recombination methods currently used to design vaccine strains are, as I understand them, fundamentally no different than those used in 1950s-era genetics.)
- Also in Nature, a nice article on pharmacogenetics which notes that pharmacogenetics (and pharmacogenomics) is the field that may produce the earliest public health benefits of the Human Genome Project.
- Somewhat more frivolously, I point you towards Ed's review of Return of the King. Also, you should check out Lord of the Tchotchke, a very amusing piece by Erin Dailey (who writes recaps for Television Without Pity, which anyone who likes their pop culture with large amounts of snarkiness should enjoy).
Happy holidays.
12.15.2003
nabokov
More substantive posts later, but for now I am up to great things (well, baking, laundering, writing Penn Bowl questions, and convincing my parents to watch Lord of the Rings). However, I have to post the following, which comes from the foreword of Invitation to a Beheading.
A few notes:
More substantive posts later, but for now I am up to great things (well, baking, laundering, writing Penn Bowl questions, and convincing my parents to watch Lord of the Rings). However, I have to post the following, which comes from the foreword of Invitation to a Beheading.
My favorite author (1768-1849) once said of a novel now utterly forgotten "Il a tout pour tous. Il fait rire l'enfant et frissoner la femme. Il donne a l'homme du monde un vertige salutaire et fait rever ceux qui ne revent jamais." Invitation to a Beheading can claim nothing of the kind. Old men will hurriedly turn from it to regional romances and the lives of public figures. No clubwoman will thrill. The evil-minded will perceive in little Emmie a sister of little Lolita, and the disciples of the Viennese witch-doctor will snigger over it in their grotesque world of communal guilt and progresivnoe education. But (as the author of Discours sur les ombres said in reference to another lamplight): I know (je connais) a few (quelques) readers who will jump up, ruffling their hair.
A few notes:
- The quote in French translates to something like this (my poor translation): "It has everything for everyone. It makes the infant laugh and the woman shudder. It gives to the man of the world a healthy giddiness and causes to dream those who never dream." Compare to Babelfish's take: "It has all for all. It makes laugh the child and frissoner the woman. It gives has the society man a giddiness salutary and made rever those which never revent."
- Ah, the favorite author. It's not clear who is meant; an interesting examination of some possible candidates is available here.
- The author of Discours sur les ombres (Discourse on Shadows) is Pierre Delalande, the creation of the author. Gennedy Barabtalo suggests that Delalande is the old French sage who is referred to by Fyodor Godunov-Cherdyntsev (protagonist of The Gift) as the author of a text he wishes to adapt. (I suggest that any Nabokovophile--surely there's a better word--check out the fascinating Nabokov site hosted by Penn State.)
12.08.2003
silliness
From my cell biology practice final:
From my genetics class (evolutionary genetics lecture):
professor: So you get random chromosome mixing. Which is like ... if I have two bags of something--let's say balls--and I can pick out red ones and blue ones, what is the likelihood that I would get two blue balls?
class: Hee.
professor (later on in lecture): And then we come back to the blue balls.
class: Hee hee.
professor: What? Is something funny?
class: Hee hee hee!
professor: I don't get it. What's so funny about blue balls?
student: Nothing is funny about blue balls.
Protein Fundamentals is quite dour by comparison.
From my cell biology practice final:
The receptor for FPF (flatulence promoting factor) also binds a second ligand, UBP (undercooked bean-derived peptide). Binding of the two ligands has differential effects, neither of which can be discussed in polite company.
From my genetics class (evolutionary genetics lecture):
professor: So you get random chromosome mixing. Which is like ... if I have two bags of something--let's say balls--and I can pick out red ones and blue ones, what is the likelihood that I would get two blue balls?
class: Hee.
professor (later on in lecture): And then we come back to the blue balls.
class: Hee hee.
professor: What? Is something funny?
class: Hee hee hee!
professor: I don't get it. What's so funny about blue balls?
student: Nothing is funny about blue balls.
Protein Fundamentals is quite dour by comparison.
12.07.2003
helper T cells gone wild
Over at Crescat Sententia, Beth Plocharczyk reports some interesting medical news about the use of "ringworms" in treating autoimmune ulcerative colitis. [I have absolutely no idea why she calls them ringworms, as the organisms are whipworms (Trichuris suis), a type of nematode. Ringworm, as you probably know, is a fungus.] Unfortunately (and mystifyingly), her post fails to mention in any depth the reasons that people are even considering such a treatment. Since these reasons are fascinating and should be mentioned, I will elaborate.
First, it's important to understand what parts of the immune system are coming into play here. All hematopoietic cells begin as pluripotent hematopoietic stem cells (HSCs) in bone marrow, which then differentiate into common lymphoid progenitors or common myeloid progenitors (you can forget about the myeloid precursors for now). The lymphoid progenitors differentiate into either B cells or T cells. Effector B cells secrete antibodies, while T cells can differentiate into several types of effector cells: cytotoxic T cells, which kill their infected target cells; and TH1 and TH2 cells (helper T cells), which stimulate other immune cells to respond to infection. Basically, TH1 cells stimulate cell-mediated immunity, whereas TH2 cells stimulate humoral immunity.* Pathologically speaking, improper TH2 responses have been implicated in allergies and asthma, while improper TH1 responses have been linked to autoimmune diseases like MS.
In recent years, a very interesting theory called the "hygiene hypothesis" has arisen. First proposed in the mid-1990s, the hygiene hypothesis postulates that there is a balance between TH1 and TH2 responses in the body that must be maintained. Failure to properly stimulate TH1 cells through lack of exposure to pathogens (bacteria, viruses, parasites, etc.) can lead to TH2 overactivity and asthma or allergies. So far as I can tell, the original statement of the hypothesis assumed that TH2 responses always dominate TH1 responses; however, this no longer seems to be the standard viewpoint. Here we come to the relevance of the original article: various forms of colon problems (including the infamous inflammatory bowel disease) are thought to arise from overactive TH1 responses. Inducing a TH2 immune response may serve to balance the immune system and downregulate the TH1 response, providing relief from symptoms. If you're interested in this particular case, check out the Weinstock study (published in the American Journal of Gastroenterology).
It will be interesting to see if the hygiene hypothesis is therapeutically relevant. Asthma and MS are two of the most high-profile disorders whose etiology includes immune and environmental factors. MS, as you probably know, is incurable at present, and cases of asthma have skyrocketed in recent years. If the hygiene hypothesis can be used to develop new therapies for these diseases, the benefits could be immense. TH1/TH2 imbalance may also play a role in several less well-known diseases, the most interesting of which (to me, at least) is pre-eclampsia, a life-threatening immune reaction that occurs in some pregnant women. There's an interesting review on the subject by Saito and Sakai that's worth checking out.
*The consequences of inducing cell-mediated immunity versus humoral immunity can be profound; a good example of this is infection with Mycobacterium leprae, which lives in macrophage vesicles and causes leprosy. The only effective reaction to infection with M. leprae is cell-mediated immunity, which involves the activation of macrophages. When TH2 cells induce humoral immunity, the antibodies produced by B cells can't reach the bacteria (because they're inside macrophages) and thus are not effective. Tuberculoid leprosy (the survivable kind) is induced when cell-mediated immunity is favored, whereas fatal lepromatous leprosy occurs when humoral immunity is favored.
Over at Crescat Sententia, Beth Plocharczyk reports some interesting medical news about the use of "ringworms" in treating autoimmune ulcerative colitis. [I have absolutely no idea why she calls them ringworms, as the organisms are whipworms (Trichuris suis), a type of nematode. Ringworm, as you probably know, is a fungus.] Unfortunately (and mystifyingly), her post fails to mention in any depth the reasons that people are even considering such a treatment. Since these reasons are fascinating and should be mentioned, I will elaborate.
First, it's important to understand what parts of the immune system are coming into play here. All hematopoietic cells begin as pluripotent hematopoietic stem cells (HSCs) in bone marrow, which then differentiate into common lymphoid progenitors or common myeloid progenitors (you can forget about the myeloid precursors for now). The lymphoid progenitors differentiate into either B cells or T cells. Effector B cells secrete antibodies, while T cells can differentiate into several types of effector cells: cytotoxic T cells, which kill their infected target cells; and TH1 and TH2 cells (helper T cells), which stimulate other immune cells to respond to infection. Basically, TH1 cells stimulate cell-mediated immunity, whereas TH2 cells stimulate humoral immunity.* Pathologically speaking, improper TH2 responses have been implicated in allergies and asthma, while improper TH1 responses have been linked to autoimmune diseases like MS.
In recent years, a very interesting theory called the "hygiene hypothesis" has arisen. First proposed in the mid-1990s, the hygiene hypothesis postulates that there is a balance between TH1 and TH2 responses in the body that must be maintained. Failure to properly stimulate TH1 cells through lack of exposure to pathogens (bacteria, viruses, parasites, etc.) can lead to TH2 overactivity and asthma or allergies. So far as I can tell, the original statement of the hypothesis assumed that TH2 responses always dominate TH1 responses; however, this no longer seems to be the standard viewpoint. Here we come to the relevance of the original article: various forms of colon problems (including the infamous inflammatory bowel disease) are thought to arise from overactive TH1 responses. Inducing a TH2 immune response may serve to balance the immune system and downregulate the TH1 response, providing relief from symptoms. If you're interested in this particular case, check out the Weinstock study (published in the American Journal of Gastroenterology).
It will be interesting to see if the hygiene hypothesis is therapeutically relevant. Asthma and MS are two of the most high-profile disorders whose etiology includes immune and environmental factors. MS, as you probably know, is incurable at present, and cases of asthma have skyrocketed in recent years. If the hygiene hypothesis can be used to develop new therapies for these diseases, the benefits could be immense. TH1/TH2 imbalance may also play a role in several less well-known diseases, the most interesting of which (to me, at least) is pre-eclampsia, a life-threatening immune reaction that occurs in some pregnant women. There's an interesting review on the subject by Saito and Sakai that's worth checking out.
*The consequences of inducing cell-mediated immunity versus humoral immunity can be profound; a good example of this is infection with Mycobacterium leprae, which lives in macrophage vesicles and causes leprosy. The only effective reaction to infection with M. leprae is cell-mediated immunity, which involves the activation of macrophages. When TH2 cells induce humoral immunity, the antibodies produced by B cells can't reach the bacteria (because they're inside macrophages) and thus are not effective. Tuberculoid leprosy (the survivable kind) is induced when cell-mediated immunity is favored, whereas fatal lepromatous leprosy occurs when humoral immunity is favored.
12.05.2003
oh, surely this is me
I am anti-quiz, but this one amused me. Especially since Ed came out as Dreyer. I simply must go get King, Queen, Knave now. I would, however, respect this quiz a lot more if it had Charles Kinbote as one of the possible outcomes for the male version.
Martha Dreyer
The Nabokovian Woman Quiz
brought to you by Quizilla
I am anti-quiz, but this one amused me. Especially since Ed came out as Dreyer. I simply must go get King, Queen, Knave now. I would, however, respect this quiz a lot more if it had Charles Kinbote as one of the possible outcomes for the male version.
Martha Dreyer
The Nabokovian Woman Quiz
brought to you by Quizilla
12.02.2003
more proof that high school was useless
I just realized that pretty much everything I learned about bacteria in high school has now been proven incorrect. Bacteria don't have eukaryote-like cytoskeletons! Oops, wait, they do--bacteria can express one tubulin homologue (FtsZ) and three actin homologues. Bacteria don't have organelles! Oops, wait, they do--researchers at UIUC discovered acidosomes in bacteria (published in Nature at the end of last June--citation may follow if I feel less lazy).
I just realized that pretty much everything I learned about bacteria in high school has now been proven incorrect. Bacteria don't have eukaryote-like cytoskeletons! Oops, wait, they do--bacteria can express one tubulin homologue (FtsZ) and three actin homologues. Bacteria don't have organelles! Oops, wait, they do--researchers at UIUC discovered acidosomes in bacteria (published in Nature at the end of last June--citation may follow if I feel less lazy).
12.01.2003
cute mutants
(warning: not about X-Men)
I think that one of the most wonderful benefits of being a developmental biologist must be the opportunity to come up with charming names for genes or mutant phenotypes. This is not to say that clever names are the sole provenance of dev biologists, but they do seem to get more opportunities to name things. A few especially cute ones for your delectation (more can be found at the clever gene names website:
sunday driver: a Drosophila kinesin-I receptor, the lack of which causes axonal jams. Other mutants that disrupt axonal transport include redtape, roadblock, and gridlock.
sonic hedgehog: one of the best known amusingly named mutants due to its importance in signaling. The name derives from the phenotype of shh Drosophila embryos, which are covered with pointy denticles.
one-eyed pinhead: a zebrafish mutant with exactly the phenotype you'd expect. The mutation is in the Nodal pathway.
bag-of-worms: probably my favorite mutant, but I shouldn't admit this. This is a C. elegans mutant (the mutation is in the egg-laying gene Egl1) that cannot lay eggs. Progeny hatch inside mutant worms and eat their way out.
cerberus: a head-inducing factor in Xenopus--when ectopically expressed, it produces two-headed embryos. Normally, it antagonizes Nodal, BMP-4, and Xwnt-8.
nanog: a gene expressed in stem cells that is necessary for pluripotency. Named for the Tir'na'Nog, the land of youth and immortality in Celtic mythology.
(warning: not about X-Men)
I think that one of the most wonderful benefits of being a developmental biologist must be the opportunity to come up with charming names for genes or mutant phenotypes. This is not to say that clever names are the sole provenance of dev biologists, but they do seem to get more opportunities to name things. A few especially cute ones for your delectation (more can be found at the clever gene names website:
sunday driver: a Drosophila kinesin-I receptor, the lack of which causes axonal jams. Other mutants that disrupt axonal transport include redtape, roadblock, and gridlock.
sonic hedgehog: one of the best known amusingly named mutants due to its importance in signaling. The name derives from the phenotype of shh Drosophila embryos, which are covered with pointy denticles.
one-eyed pinhead: a zebrafish mutant with exactly the phenotype you'd expect. The mutation is in the Nodal pathway.
bag-of-worms: probably my favorite mutant, but I shouldn't admit this. This is a C. elegans mutant (the mutation is in the egg-laying gene Egl1) that cannot lay eggs. Progeny hatch inside mutant worms and eat their way out.
cerberus: a head-inducing factor in Xenopus--when ectopically expressed, it produces two-headed embryos. Normally, it antagonizes Nodal, BMP-4, and Xwnt-8.
nanog: a gene expressed in stem cells that is necessary for pluripotency. Named for the Tir'na'Nog, the land of youth and immortality in Celtic mythology.
