This course presents a challenging multi-dimensional perspective on the causes of human disease and mortality. The course focuses on analyses of major causes of mortality in the US since 1900: cancer, cardiovascular and cerebrovascular diseases, diabetes, and infectious diseases. Students create analytical models to derive estimates for historically variant population risk factors and physiological rate parameters, and conduct analyses of familial data to separately estimate inherited and environmental risks. The course evaluates the basic population genetics of dominant, recessive and non-deleterious inherited risk factors.

Students perform an activity similar to the childhood “telephone” game in which each communication step represents a biological process related to the passage of DNA from one cell to another. This game tangibly illustrates how DNA mutations can happen over several cell generations and the effects the mutations can have on the proteins that cells need to produce. Next, students use the results from the “telephone” game (normal, substitution, deletion or insertion) to test how the mutation affects the survivability of an organism in the wild. Through simple enactments, students act as “predators” and “eat” (remove) the organism from the environment, demonstrating natural selection based on mutation.

Students learn about mutations to both DNA and chromosomes, and uncontrolled changes to the genetic code. They are introduced to small-scale mutations (substitutions, deletions and insertions) and large-scale mutations (deletion duplications, inversions, insertions, translocations and nondisjunctions). The effects of different mutations are studied as well as environmental factors that may increase the likelihood of mutations. A PowerPoint® presentation and pre/post-assessments are provided.

In this seminar you will curate information on the types of mutation that best help you learn the information. A comparison of how harmful different types of mutation can be will generate a deeper understanding of each type. You will explore examples of authentic mutations and choose one to communicate your findings.StandardsBIO.B.2.2.1 Describe how the processes of transcription and translation are similar in all organisms.BIO.B.2.2.2 Describe the role of ribosomes, endoplasmic reticulum, Golgi apparatus, and the nucleus in the production of specific types of proteins.BIO.B.2.3.1 Describe how genetic mutations alter the DNA sequence and may or may not affect phenotype (e.g., silent, nonsense, frame-shift).

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Venous malformations are the most common vascular anomaly around the world. Extensive malformations cause pain, bleeding, anatomic distortion, and organ dysfunction. Current therapies are invasive and rarely curative, making it necessary to develop new treatment options. To that end, researchers examined one molecular mechanism known to lead to venous malformations, the interaction between endothelial and smooth muscle cells. The researchers screened 5 patients with the mutation known to cause venous malformations. Malformations with that mutation showed lower expression of platelet-derived growth factor beta and alpha-smooth muscle actin. In addition, mutant endothelial cells showed enhanced cell viability and motility, and decreased tube formation. These conditions could be reversed in vitro by rapamycin, which, experiments showed, worked by inhibiting the AKT-mTOR pathway. This pathway could therefore be an important target for disrupting the formation of venous malformations..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"RNF43 is an enzyme frequently mutated in many forms of cancer. Under normal circumstances, the protein is known to inhibit canonical Wnt signaling, which regulates various aspects of cell development and disease. What remains controversial, however, is the function of a part of the protein known as the “protease-associated” (PA) domain. To find out, researchers recorded the effects of RNF43 without this domain in human cells. They discovered that the PA domain is not essential for RNF43 to block Wnt signaling. Rather, the PA domain’s job is to regulate levels of RNF43 on the cell surface, which is achieved through the pro-Wnt protein RSPO1. Understanding how RSPO1 behaves when RNF43 lacks its PA domain could be informative, as it could refine the perceived role of RNF43 mutations in human disease..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"One of the key oncogenic drivers in patients with non-small-cell lung cancer is rearrangements to the anaplastic lymphoma kinase, or ALK, gene. Inhibitors of this gene have led to promising responses in patients, but the gene rearrangements complicate treatment efforts by facilitating the emergence of drug resistance. To help overcome this, researchers are turning to the drug ceritinib. Results from the recent phase 2 ASCEND-9 study showed that ceritinib can lead to effective treatment responses when similar drugs like alectinib stop working. Ceritinib is a selective oral ALK inhibitor that’s been approved for treating patients with metastatic ALK-positive non-small-cell lung cancer. The drug has demonstrated significant and meaningful improvements in progression-free survival in global phase 3 trials compared to chemotherapy. However, the efficacy and safety of ceritinib in patients who’ve grown resistant to the ALK inhibitor alectinib hasn’t been clear..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

Hank talks about population genetics, which helps to explain the evolution of populations over time by combing the principles of Mendel and Darwin, and by means of the Hardy-Weinberg equation.

Chapters:
1. Population Genetics
2. Population
3. Allele Frequency
4. 5 Factors
a) Natural Selection
b) Natural Selection/Random Mating
c) Mutation
d) Genetic Drift
e) Gene Flow
5. Hardy-Weinberg Principle
6. Hardy-Weinberg Equilibrium
7. Hardy-Weinberg Equation

Psychology is designed to meet scope and sequence requirements for the single-semester introduction to psychology course. The book offers a comprehensive treatment of core concepts, grounded in both classic studies and current and emerging research. The text also includes coverage of the DSM-5 in examinations of psychological disorders. Psychology incorporates discussions that reflect the diversity within the discipline, as well as the diversity of cultures and communities across the globe.Senior Contributing AuthorsRose M. Spielman, Formerly of Quinnipiac UniversityContributing AuthorsKathryn Dumper, Bainbridge State CollegeWilliam Jenkins, Mercer UniversityArlene Lacombe, Saint Joseph's UniversityMarilyn Lovett, Livingstone CollegeMarion Perlmutter, University of Michigan

By the end of this section, you will be able to:Explain the basic principles of the theory of evolution by natural selectionDescribe the differences between genotype and phenotypeDiscuss how gene-environment interactions are critical for expression of physical and psychological characteristics

Through this concluding lesson and its associated activity, students experience one valuable and often overlooked skill of successful scientists and engineers communicating your work and ideas. They explore the importance of scientific communication, including the basic, essential elements of communicating new information to the public and pitfalls to avoid. In the associated activity, student groups create posters depicting their solutions to the unit's challenge question accurate, efficient methods for detecting cancer-causing genes using optical biosensors which includes providing a specific example with relevant equations. Students are also individually assessed on their understanding of refraction via a short quiz. This lesson and its associated activity conclude the unit and serve as the culminating Go Public phase of the Legacy Cycle, providing unit review and summative assessment.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Antibody treatments such as cetuximab are powerful against colorectal cancer, but colorectal cancer cells are known to develop resistance to these drugs in large part due to to overactivation or mutation of the gene KRAS. To understand how KRAS might give rise to cetuximab resistance, researchers treated two types of lab-grown cells with the antibody, normal cancer cells and cancer cells containing a mutated KRAS gene. They then monitored the effects on AMPK, an enzyme that is toxic to various cancer cells. KRAS mutation impaired this AMPK-based defense, enabling mutant cancer cells to outlive normal cancer. Exposing cells with drugs known to activate AMPK, such as metformin, recovered the anti-cancer defense, overcoming the centuximab resistance induced by a mutated KRAS gene. That same mechanism was observed in colorectal tumors grafted onto mice. The results indicate that targeting AMPK could be a powerful therapeutic strategy, possibly boosting anti-cancer defenses in patients with colorectal cancer..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

Students are introduced to the unit challenge discovering a new way to assess a person's risk of breast cancer. Solving this challenge requires knowledge of refraction and the properties of light. After being introduced to the challenge question, students generate ideas related to solving the challenge, and then read a short online article on optical biosensors that guides their research towards solving the problem.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Researchers have taken a significant step towards personalizing the treatment of cancer. Using DNA sequencing, they’ve developed a way to scan blood samples for mutations in circulating tumor DNA -- small bits of genetic material that are released as cancer cells die. The genomic reservoir contained in this DNA is representative of nearly all tumors carried by a patient, providing the foundation needed for comprehensive genetic profiling. Such profiling may help clinicians select the most appropriate therapies for a given patient. The genetic mutations giving rise todrivingthat drive cancer development often differ markedly among individuals. Interventions that match a patient’s unique genetic profile offer great promise, but obtaining tumor tissue for genetic testing can be invasive, and risky and sometimes impossible. To bypass these limitations, the researchers established a way to enrichextract, sequence, and analyze circulating tumor DNA..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.