Paper instructions:
1) Appropriately focuses topic on a specific area. Describes one or more aspects of molecular pathogenesis of disease in more detail.
2) Prepares clear and well-organized outline, using appropriate format, correct spelling, etc.
3) Outlines recent advances in the field/subject/area: for example, new approaches, models, drug trials, mechanistic insights. Describes one or more research studies or clinical trials from literature.
4) Add five new annotated references from good quality sources.
2) Prepares clear and well-organized outline, using appropriate format, correct spelling, etc.
3) Outlines recent advances in the field/subject/area: for example, new approaches, models, drug trials, mechanistic insights. Describes one or more research studies or clinical trials from literature.
4) Add five new annotated references from good quality sources.
—Annotation of the references (#4 above) should address the following questions:
• What is the purpose or hypothesis of the study and why was it important to test?
• What specific techniques / reagents / strategies are used to test the hypothesis?
• What are the major conclusions of the study?
• What is the significance?
• What is the purpose or hypothesis of the study and why was it important to test?
• What specific techniques / reagents / strategies are used to test the hypothesis?
• What are the major conclusions of the study?
• What is the significance?
2014-2015 Syllabus
Appendix D : PRE – PRESENTATION OUTLINE PART B WITH ANNOTATED REFERENCES
An example of a Pre-Presentation Outline Part B with Annotated References is given below .
Note that your outline should be more polished with additional details and more in-depth
descriptions of the underlying basis of disease than that presented in the Pre -Presentation
Outline Part A. At least five references should be included. To annotate each reference,
provide the following information under each reference:
x What is the purpose or hypothesis of the study and why was it important to test?
x What specific techniques / reagents / strategies are used to test the hypothesis?
x What are the major conclusions of the study?
x What is the significance?
An example of a Pre-Presentation Outline Part B with Annotated References is given below .
Note that your outline should be more polished with additional details and more in-depth
descriptions of the underlying basis of disease than that presented in the Pre -Presentation
Outline Part A. At least five references should be included. To annotate each reference,
provide the following information under each reference:
x What is the purpose or hypothesis of the study and why was it important to test?
x What specific techniques / reagents / strategies are used to test the hypothesis?
x What are the major conclusions of the study?
x What is the significance?
The outline should be in the “bullet” format as show n below in the example.
PRE – PRESENTATION OUTLINE AND ANNOTATED BIBLIOGRAPHY EXAMPLE
Title: Stevens-Johnson Syndrome
Presenter: Ben Chen
Etiology-Molecular Understanding:
x Stevens-Johnson Syndrome, or SJS (and the more serious form of the disease, toxic epidermal
necrosis, or TEN), are considered type IV hypersensitivities (delayed T- cell mediated
hypersensitivities).
x SJS’s patho -mechanism involves HLA (human leukocyte antigens) – restricted presentation of a
drug or its metabolites for T-cell activation, specifically the activation of cytotoxic T lymphocyte
(CD 8+) responses as well as natural kil ler (NK) cells; this mechanism is strongly supported by
genetic associations between certain HLA alleles and specific drug -induced forms of SJS.
x Because the number of infiltrating inflammatory cells is too few to explain the widespread
epidermal necrosis in SJS, other key mediators have been demonstrated in the disease, primarily
Fas-FasL, perforin/granzyme B, and primarily, granulysin.
Title: Stevens-Johnson Syndrome
Presenter: Ben Chen
Etiology-Molecular Understanding:
x Stevens-Johnson Syndrome, or SJS (and the more serious form of the disease, toxic epidermal
necrosis, or TEN), are considered type IV hypersensitivities (delayed T- cell mediated
hypersensitivities).
x SJS’s patho -mechanism involves HLA (human leukocyte antigens) – restricted presentation of a
drug or its metabolites for T-cell activation, specifically the activation of cytotoxic T lymphocyte
(CD 8+) responses as well as natural kil ler (NK) cells; this mechanism is strongly supported by
genetic associations between certain HLA alleles and specific drug -induced forms of SJS.
x Because the number of infiltrating inflammatory cells is too few to explain the widespread
epidermal necrosis in SJS, other key mediators have been demonstrated in the disease, primarily
Fas-FasL, perforin/granzyme B, and primarily, granulysin.
Genetic Markers and Predisposition to SJS:
x The highly variable HLA polymorphism provides diverse interaction between different kinds of
drug antigens.
x The strong association between HLA alleles and SJS (and subsequent ethnic specificity) was first
found in a study of Han Chinese in 2004, with 100% of carbamazepine (CBZ) -induced SJS patients
carrying the HLA -B *1502 allele; this allele is relatively absent from northeast Asians and
Caucasians and seems uniquely limited to Han Chinese ancestral Asians.
x Other studies of southeast Asian populations have shown high prevalence of this seemingly
ethnic -specific allele in inciden ces of CBZ- induced SJS (another 100% found in a study of Thais).
x For allopurinol -induced SJS, HLA -B *1501 is a genetic marker that has shown strong association
in studies of Taiwanese and Thais. Once more, an ethnic component has been implicated, with
the allele showing low frequency in Caucasians.
x For abacavir -induced SJS, HLA -B *5701 has been shown to be an excellent predictor of sensitivity
Date Created/Revised: __ 7/24/14__ By: _______ Page 31
2014-2015 Syllabus
x The highly variable HLA polymorphism provides diverse interaction between different kinds of
drug antigens.
x The strong association between HLA alleles and SJS (and subsequent ethnic specificity) was first
found in a study of Han Chinese in 2004, with 100% of carbamazepine (CBZ) -induced SJS patients
carrying the HLA -B *1502 allele; this allele is relatively absent from northeast Asians and
Caucasians and seems uniquely limited to Han Chinese ancestral Asians.
x Other studies of southeast Asian populations have shown high prevalence of this seemingly
ethnic -specific allele in inciden ces of CBZ- induced SJS (another 100% found in a study of Thais).
x For allopurinol -induced SJS, HLA -B *1501 is a genetic marker that has shown strong association
in studies of Taiwanese and Thais. Once more, an ethnic component has been implicated, with
the allele showing low frequency in Caucasians.
x For abacavir -induced SJS, HLA -B *5701 has been shown to be an excellent predictor of sensitivity
Date Created/Revised: __ 7/24/14__ By: _______ Page 31
2014-2015 Syllabus
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