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:

"Immune checkpoints are an effective way that cancers evade the immune system, but they're not the only one. In the case of pancreatic ductal carcinoma, or PDAC, tumor fibrosis also plays an important role. To understand how fibrosis might translate to poor outcomes among patients with PDAC, researchers examined the ARF6-AMAP1 molecular pathway, which research suggests is activated during fibrosis. Findings revealed that AMAP1 correlated with elevated expression of PD-L1, a molecule that tumor cells present on their surface to elude attack by the immune system. AMAP1 was also linked to elevated fibrosis. Consistently, silencing AMAP1 in a mouse model of human PDAC reduced PD-L1 and fibrosis in their tumors. Suppressing the ARF6-AMAP1, therefore, could be one way to ensure that PDAC tumors can’t hide from immune defenses, offering the prospect of more effective immunotherapies for patients with pancreatic ductal carcinoma..."

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

Software testing gets a bad rap for being difficult, time-consuming, redundant, and above all – boring. But in fact, it is a proven way to ensure that your software will work flawlessly and can meet release schedules.

In a two-course series, we will teach you automated software testing in an inspiring way. We will show you that testing is not as daunting a task as you might think, and how automated testing will make you a better developer who programs excellent software.

This second course builds upon the first course’s material. It covers more advanced tools and techniques and their applications, now utilizing more than just JUnit. Key topics include Test-Driven Development, state-based and web testing, combinatorial testing, mutation testing, static analysis tools, and property-based testing.

This is a highly practical course. Throughout the lessons, you will test various programs by means of different techniques. By the end, you will be able to choose the best testing strategies for different projects.

Biology is designed for multi-semester biology courses for science majors. It is grounded on an evolutionary basis and includes exciting features that highlight careers in the biological sciences and everyday applications of the concepts at hand. To meet the needs of today’s instructors and students, some content has been strategically condensed while maintaining the overall scope and coverage of traditional texts for this course. Instructors can customize the book, adapting it to the approach that works best in their classroom. Biology also includes an innovative art program that incorporates critical thinking and clicker questions to help students understand—and apply—key concepts.

By the end of this section, you will be able to:Describe the different types of variation in a populationExplain why only heritable variation can be acted upon by natural selectionDescribe genetic drift and the bottleneck effectExplain how each evolutionary force can influence the allele frequencies of a population

By the end of this section, you will be able to:Discuss the different types of mutations in DNAExplain DNA repair mechanisms

By the end of this section, you will be able to:Describe how cancer is caused by uncontrolled cell growthUnderstand how proto-oncogenes are normal cell genes that, when mutated, become oncogenesDescribe how tumor suppressors functionExplain how mutant tumor suppressors cause cancer

By the end of this section, you will be able to:Describe how cancer is caused by uncontrolled cell growthUnderstand how proto-oncogenes are normal cell genes that, when mutated, become oncogenesDescribe how tumor suppressors functionExplain how mutant tumor suppressors cause cancer

This series of instructional videos was created by Camosun College for a Canadian edition of the OpenStax "Concepts of Biology" open textbook as part of the BC Open Textbook Project. The lectures are taught by Charles Molnar, a Biology instructor at Camosun College. The videos are accompanied by transcripts.

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:

"Cancer cells are abnormal cells that rapidly proliferate and often find ways to evade the immune system’s attempts to stop them. Such cells often overexpress the genes MYC and ARF6 and have a mutated version of the KRAS gene. These changes are inextricably linked and result in significant resistance to cancer therapies. KRAS activates MYC gene expression and possibly promotes the translation of the messenger RNA for both MYC and ARF6. Then MYC induces expression of genes related to mitochondrial formation and energy production. Meanwhile, ARF6 protects the mitochondria from oxidation-induced injury. ARF6 may also promote cancer invasion, metastasis, and immune evasion. Thus, KRAS, MYC, and ARF6 cooperate to help cancer spread and to avoid the immune system and immune-based treatments. These harmful associations are common in pancreatic cancer and can be strengthened by mutations in other genes like TP53..."

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:

"Alpha-1 antitrypsin deficiency (AATD)-mediated liver disease is a form of toxic inflammation associated with the retention of mutant alpha-1 antitrypsin within cells. Patients with this disease typically show fibrosis and cirrhosis of the liver. Unfortunately, the mechanism of AATD-mediated liver disease is not well understood. To gain some insight, researchers recently explored the role of extracellular vesicles in the progression of AATD-mediated liver disease. They isolated vesicles from the plasma of individuals with both AATD and liver disease and compared them with vesicles from healthy individuals in terms of cytokine and chemokine expression as well as miRNA expression. Vesicles from individuals with AATD were shown to activate hepatic stellate cells in vitro, which is believed to be one of the first steps of fibrosis. a process mediated by the NF-κB and JAK/STAT signaling pathways..."

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

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.