So on Thursday night, a certain Dr. Beth of Not To Be Trusted With Knives sent me an email to inform me about a blog-o-awesomeness that a friend of hers had passed on. That blog is known as Dissertation Haiku, a site where one submits a haiku summary of their Ph.D. dissertation. The thought being that haiku are short and sweet, while dissertations are the antithesis of that.
Of course, being the nerdy doctors that we are, we decided that we both needed to submit haiku to said site. But, before we do that, we decided we would first offer them up to you, our loyal readers.
I present to you, my haiku:
Spatial Poisson Mixtures Are
My Bitch Forever
And Beth’s haiku (which can be found in its original form here):
Boozing rat mommies
Make baby rat bones so weak
Poor baby rat bones
Compare the shortness and sweetness of these haiku, to a not-as-short and not-as-sweet scientific summary of what we actually did (below). Clearly the haiku are superior in every way.
Multivariate Spatial Poisson Mixtures With Application In Disease Source Classification.
Gastrointestinal disease (GID) data obtained from the Canadian Institute for Health Information (CIHI) provides motivation to extend Mixture Model (MM) literature in order to classify disease based on infection source. Specically, MMs are employed to classify GID data as foodborne or waterborne. This work will account for spatially indexed disease using two methods. In the first case, independent conditionally autoregressive spatial priors will be assigned to the log linear term of each of the mixture components (one per disease source). The second case investigates a nonindependence assumption. These two models (identified as the IMCAR and MCAR models) are contrasted with the standard CAR spatial model described by Besag et al, 1991. All models are compared via simulation study, with application to Alberta GID data (1992-1998).
The Effects of Prenatal Alcohol Exposure on Endochondral Bone Development in the Fetal Rat
The objective of my thesis was to determine if prenatal alcohol exposure has specific effects on bone development, in addition to its effects on general growth, in the fetal rat. Maternal alcohol intake during pregnancy is known to result in impairments in general growth and skeletal development, but it was unknown if alcohol’s effects on skeletal development resulted from generalized growth retardation or effects specific to bone. The studies in my thesis were designed to test the hypotheses that (1) prenatal alcohol exposure affects skeletal development at doses of alcohol lower than those required to affect general growth (assessed by fetal body weight and length), (2) skeletal sites differ in their sensitivity to the effects of prenatal alcohol exposure and (3) prenatal alcohol exposure disrupts the morphology of the growth plate of the fetal tibia. My research showed that alcohol’s effects on long bone development are independent of alcohol’s effects on general growth, occurring at doses lower than the doses which affect general growth, and that alcohol may affect the later, rather than the earlier, stages of long bone development. As well, I demonstrated that prenatal alcohol exposure disrupts specific histological stages of the developing fetal tibia. As there is increasing evidence to suggest that the intrauterine environment may influence long-term bone health, the effects of prenatal ethanol exposure on fetal skeletal development could potentially increase the offspring’s risk of osteoporosis later in life.