This class analyzes complex biological processes from the molecular, cellular, extracellular, and organ levels of hierarchy. Emphasis is placed on the basic biochemical and biophysical principles that govern these processes. Examples of processes to be studied include chemotaxis, the fixation of nitrogen into organic biological molecules, growth factor and hormone mediated signaling cascades, and signaling cascades leading to cell death in response to DNA damage. In each case, the availability of a resource, or the presence of a stimulus, results in some biochemical pathways being turned on while others are turned off. The course examines the dynamic aspects of these processes and details how biochemical mechanistic themes impinge on molecular/cellular/tissue/organ-level functions. Chemical and quantitative views of the interplay of multiple pathways as biological networks are emphasized. Student work culminates in the preparation of a unique grant application in an area of biological networks.

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 physical and chemical immune barriersExplain immediate and induced innate immune responsesDiscuss natural killer cellsDescribe major histocompatibility class I moleculesSummarize how the proteins in a complement system function to destroy extracellular pathogens

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:

"Acetaminophen (N-acetyl-p-aminophenol, APAP) is a commonly used over-the-counter analgesic and antipyretic, but an overdose can cause severe liver damage or even liver failure, and the therapies for such acetaminophen-induced liver injury (AILI) are limited. To search for new treatment targets, researchers recently investigated the roles of the IL-33/ST2 cytokine signaling pathway in a mouse AILI model. Compared to wild-type mice, IL-33-knockout mice had worse hepatotoxicity after acetaminophen overdose, as indicated by greater hepatocyte necrosis, DNA accumulation, and type I IFN production, suggesting that IL-33 signaling normally has a protective effect. Further investigation in liver cell lines revealed that the binding of IL-33 with its receptor ST2 enhanced the interaction of Beclin-1 with the STING C-terminus..."

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:

"The protein IFNα can reduce growth and promote apoptosis of cancer cells by stimulating genes such as PML, whose deficiency is linked to tumorigenesis, but the contributions of different PML isoforms to the anticancer effects remain unclear. Given that PML-II positively regulates genes that are induced during the type I IFN response, researchers recently investigated whether and how PML-II participates in IFNα-induced cell death using a cervical cancer cell line. In cells with PML-II deletion (siPML-II), death during IFNα stimulation was reduced, and IFNα-induced ISG54 mRNA expression was attenuated. In addition, silencing PML-II decreased the expression of TRAIL and PUMA during IFNα stimulation, indicating that the extrinsic and intrinsic apoptosis pathways were blunted..."

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:

"Toll-like receptors (TLRs) are a highly conserved family of pattern recognition receptors that play a critical role in innate immunity. They evolved before the adaptive immune system, making them an indispensable first line of defense. TLRs are highly studied, and understanding their signaling is critical for developing treatments for autoimmune and chronic inflammatory disorders. But while kinases and E3 ubiquitin ligases are widely known TLR signaling effectors, another pathway is less well-characterized. Phosphatases are important regulators of TLR signaling through NF-κB, type I interferons, and mitogen-activated protein kinases. TLRs activate several pathways through phosphorylation, and thus an interplay must exist between kinases and phosphatases to tightly regulate TLR signaling. Many phosphatases have roles in TLR signaling, including classical protein tyrosine phosphatases and serine/threonine phosphatases..."

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:

"The COVID-19 pandemic, caused by the virus SARS-CoV-2, has spread rapidly since 2019. COVID-19 symptoms are mild in some patients but severe and even life-threatening in others and there are still no reliable treatments for severe COVID-19. In a recent study, researchers investigated the factors related to COVID-19 severity in hospitalized patients with mild or severe illness. Specifically, they investigated the patients’ immune characteristics and signaling pathways involving immune proteins called IFN-Is. Compared with healthy controls, patients with COVID-19 had lower counts of many types of immune cells but higher counts of Th17 cells in their blood and the differences were more drastic in patients with severe disease. In addition, individuals with severe COVID-19 had much lower levels of IFN-I signaling molecules than healthy controls..."

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

In our resource, we highlight the role of the viral non-structural proteins and their role in blocking host interferon signaling of the innate immune system.  In addition, we also describe the host immune response specifically the cytokine signaling clouds in the variation in severity of patients living with COVID-19.  Finally, we apply these latest peer-reviewed research on host immune response to SARS-CoV-2 in the context of integrated immunology framework linked with three-dimensional learning in life science education and topics on social justice dimensions of vaccination access in global health.  Through the social justice lens and global health perspectives, we provide an innovative framework to engage undergraduates in the field of integrated immunology and developmental biology in both remote and hybrid-flexible (HyFlex) learning settings.

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:

"Phosphorylated STAT1 (P-STAT1) is an important mediator of interferon-induced antiviral immunity. During interferon signaling, P-STAT1 dimerizes and accumulates in the nucleus with the help of the protein importin to affect gene transcription and elicit immune responses. In a positive feedback loop, P-STAT1 also induces further STAT1 expression, thereby increasing the cytoplasmic levels of unphosphorylated STAT1 (U-STAT1), a protein that regulates apoptotic cell death. However, the impact of U-STAT1 on the P-STAT1-mediated immune response is unclear. To learn more, researchers recently cotransfected cells with wild-type P-STAT1 and a permanently unphosphorylated U-STAT1 mimic. Interestingly, the U-STAT1 mimic prevented nuclear accumulation of P-STAT1 during interferon gamma (IFNγ) stimulation, but it didn’t impair downstream P-STAT1 signaling, indicating that some P-STAT1 could still enter the nucleus to exert its effects..."

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