Hemoglobin!
11:44 AM
Hemoglobin has become my entire life. I have a biochemistry exam approaching far more rapidly than I'd like, and it's all about protein structure and function. In the context of this class, most of the specific proteins are members of the globin family and immunoglobulins. I've taken immunology so I have a bit of a grasp on immunoglobulins, but the extent of my prior knowledge of hemoglobin is the one and a half cardiac lectures I had in physiology that mostly consisted of learning how to read an EKG.
Shirt: old shirt
Vest: thrifted
Jacket: Anne Klein
Skirt: thrifted
My roommate recently went to a clothing exchange (I stayed home and studied) and came back with a box full of clothes. A lot of the clothes she found were surprisingly high quality. The vest, jacket, and tie are all from the clothing exchange. The tie I'm wearing is actually a belt re-purposed as a tie, because I liked the pattern and it was short enough for me to tie into a tie. Even though I now have almost enough blazers to wear one every day of the work week, I'm still on the lookout for a tweed blazer because my fall aesthetic is "Professor Indiana Jones" mixed with a bit of Henry Higgins.
A discussion about hemoglobin wouldn't be complete without a discussion of hemoglobinopathies, which leads me to my discussion point today. A hemoglobinopathy is a genetic condition that results in abnormal structure of the protein hemoglobin. One of the most important hemoglobinopathies for public health is sickle cell disease. A single nucleotide change in a gene coding for part of hemoglobin results in one amino acid (glutamic acid) being substituted by another (valine). Red blood cells become less elastic and form a sickle shape, which can block blood flow and cause tissue death.
Sickling of the red blood cells occurs in those who have both copies of the sickle cell trait. Those who only carry one copy do not have the severe symptoms those with both copies have (unless in a low oxygen environment, like exercising a lot or being on top of a mountain) but do have resistance to malaria. The malaria resistance conferred by being heterozygous for the sickle cell trait is advantageous enough to allow for maintenance of the mutation in the population. This is why people from areas where malaria is endemic are more likely to have sickle cell disease.
I find this interesting mostly because of the maintenance of a potentially fatal mutation in a population. If there is enough of an advantage conferred by a mutation, even if it may be fatal in some cases, then that mutation may never be bred out of the population. So, unless and until malaria is eradicated, I think it is unlikely that sickle cell disease will be eradicated. This is one example of the co-evolution of host and pathogen that I find incredibly interesting, and one day when I'm not consumed by midterms and projects, I'd like to look into more examples of similar occurrences.
I find this interesting mostly because of the maintenance of a potentially fatal mutation in a population. If there is enough of an advantage conferred by a mutation, even if it may be fatal in some cases, then that mutation may never be bred out of the population. So, unless and until malaria is eradicated, I think it is unlikely that sickle cell disease will be eradicated. This is one example of the co-evolution of host and pathogen that I find incredibly interesting, and one day when I'm not consumed by midterms and projects, I'd like to look into more examples of similar occurrences.
FACT OF THE DAY!
Yoshinori Ohsumi won the 2016 Nobel Prize in Physiology or Medicine. Dr. Ohsumi won the Nobel for his research on the underlying mechanisms of autophagy, a process for cellular component recycling and degradation. He identified the genes necessary for autophagy.
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