The course covers basic concepts of biomedical engineering and their connection with the spectrum of human activity. It serves as an introduction to the fundamental science and engineering on which biomedical engineering is based. Case studies of drugs and medical products illustrate the product development-product testing cycle, patent protection, and FDA approval. It is designed for science and non-science majors.

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:

"Coordinated signaling between HER-family receptors and c-Met has been demonstrated to drive breast cancer in some patients. Although combination therapies targeting HER and c-Met can be very effective in some of these patients, no clinical data has supported an approval for this drug combination in breast cancer. In a recent study, researchers examined the ability of a new clinical test to identify potentially responsive patients. The test, called the CELsignia Multi-Pathway Signaling Function Test, uses an impedance biosensor loaded with a patient’s live tumor cells to quantify cell signaling responses in real time. Using this test, the researchers identified patients whose HER2-negative breast tumors had hyperactive coordinated HER1, HER2, HER3/4, and c-Met signaling, despite having normal expression levels of these receptors on their tumor cells. These results indicated that the identified patients might be responsive to HER-/c-Met-targeting combination therapy..."

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 ligand protein PD-L1 on tumor cells can bind to the receptor protein PD-1 on T cells. This binding negatively regulates T cells to suppress immunity, facilitating large-scale tumor growth. Antibody drugs have been designed to block cell-surface PD-L1/PD-1 binding, but they’re not very effective, possibly because tumor cells can secrete extracellular vesicles (EVs) that express PD-L1. The PD-L1 on EVs can also induce immunosuppression, leading to drug resistance. EV PD-L1 plays tumor-promoting roles in many cancers, such as breast cancer, prostate cancer, and melanoma, and unlike cell-surface PD-L1, which isn’t expressed stably enough to be reliable, EV PD-L1 may be a useful biomarker. Because of its location, EV PD-L1 may also be a good treatment target. For example, drugs preventing EV release have been shown to activate antitumor responses in melanoma cells and to reduce prostate tumor growth and increase anti-PD-L1 efficacy against colon cancer in mice..."

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:

"Gene regulation plays a critical role in human development and disease, including cancer. Genes are regulated by a family of proteins called transcription factors. One such molecule is GLI3, a member of the "Hedgehog" signaling pathway. GLI3 can switch genes ON (such as in development and cancer) and switches gene expression OFF in Hedgehog signaling. This central molecule is important for tissue development in the brain and lungs and for the development and activation of immune cells such as B, T and NK cells. GLI3 is upregulated in many cancers, promoting growth, angiogenesis, and tumor cell proliferation and migration, but interestingly, in certain cancers, GLI3 has an anti-tumor role. and its pro-cancerous role can be modulated by GLI3-targeting microRNA. Understanding GLI3-mediated signaling will clarify its roles in disease, development, and cancer, laying the foundation to target this critical molecule in immune and cancer therapies..."

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:

"Autophagy is a critical process in healthy human cells that removes excess organelles and substances while generating energy. But in cancer cells, autophagy can either feed growing tumors—literally supplying energy—or suppress them by clearing out cancer-promoting substances. Recently, researchers examined this process in non-small cell lung cancer (NSCLC) and focused on GNIP1, a TRIM family protein. Other TRIM proteins have been associated with autophagy previously, but this is the first autophagy study to examine GNIP1. GNIP1 expression was elevated in tumor cells from NSCLC patients, and clinically, it was associated with poor prognosis and survival time. Induced overexpression of GNIP1 in cultured NSCLC cells increased the cancerous behaviors proliferation and migration. Additional cell culture experiments indicated that GNIP1 did this by enhancing autophagy. Specifically, GNIP1 mediated the breakdown of the VPS34 complex, an autophagy inhibitor..."

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

An integrated course stressing the principles of biology. Life processes are examined primarily at the molecular and cellular levels. Intended for students majoring in biology or for non-majors who wish to take advanced biology courses.

Students are given a problem about a relatively new treatment for cancer, Gleevec, and asked to apply and synthesize what they have learned about cell signaling and the eukaryotic cell cycle to explain why this targeted treatment works to prevent cell division with fewer side effects than traditional chemotherapeutic agents.

Student teams learn about engineering design of green fluorescent proteins (GFPs) and their use in medical research, including stem cell research. They simulate the use of GFPs by adding fluorescent dye to water and letting a flower or plant to transport the dye throughout its structure. Students apply their knowledge of GFPs to engineering applications in the medical, environmental and space exploration fields. Due to the fluorescing nature of the dye, plant life of any color, light or dark, can be used unlike dyes that can only be seen in visible light.

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:

"Tumor cells reprogram cellular energy metabolism to power their rapid proliferation. One important energy source for tumors is the amino acid glutamine, making glutamine metabolism a promising target for tumor treatment. However, glutamine is also important for proper immune cell function. Tumor cells can potentially outcompete immune cells for glutamine, tipping the scales of immunity in their favor. Certain intrinsic signaling programs may also help partition glutamine within tumor cells while causing immune cells to rely more heavily on glucose. Among immune cells, the tumor-induced glutamine shortage reduces the activity of cancer-fighting T effector cells. It may also disrupt the balance of other immune cell types such as macrophages, but it’s unclear whether the net effects are pro- or anti-tumor..."

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:

"Gallbladder cancer (GBC) is becoming increasingly common, especially in American Indian and Southeast Asian populations. Early GBC can be successfully removed with surgery, but advanced GBC has a poor prognosis . and the existing treatments have many side effects. To explore better therapies, researchers recently investigated the anti-GBC effects of penfluridol, an antipsychotic drug with anticancer activity. In vitro, penfluridol (PF) strongly inhibited the replication and invasion of three GBC cell lines, confirming its anti-GBC potential, but it also dramatically increased glucose consumption via glycolysis, which is a hallmark of cancer. Specifically, penfluridol activated the AMPK/PFKFB3 glycolysis pathway. However, inhibiting glycolysis, particularly the AMPK/PFKFB3 pathway (with Compound C, CC) solved this problem enhancing penfluridol’s GBC-killing effects. The same synergistic effects were observed in mouse tumor models in vivo..."

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 gut microbiota plays a critical role in various human cancers. But how can these microbes affect cancers that develop relatively far from the gut? In the case of prostate cancer, new research points to the use of antibiotics. Antibiotics are known to cause gut dysbiosis, which is associated with multiple disorders. In mice with prostate cancer, researchers found that gut dysbiosis caused by antibiotics was linked to tumor growth. Mice given broad-spectrum antibiotics (Abx) showed increased tumor growth compared to control mice (NC). Antibiotics exposure also increased Proteobacteria abundance in mouse guts, a sign of dysbiosis. The mechanism behind these findings could be a leaky gut. Under dysbiosis, a leaky gut barrier allowed the release of lipopolysaccharide (LPS) – an inflammation-inducing factor – into the circulation, which then reached the prostate tumor..."

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 HHEX plays multiple roles in development, gene expression, and cancer suppression. For example, it can inhibit breast cancer and prostate cancer cell migration and invasion, which are important processes for cancer spread, but whether and how HHEX affects lung cancer cell motility remain unknown. To learn more, a new study investigated HHEX’s functions in human non-small cell lung cancer cells and control cells. According to an analysis of published datasets, HHEX expression was reduced in lung cancer cells, and low HHEX expression was associated with reduced overall survival in patients. In lung cancer cell lines, silencing HHEX accelerated wound gap closure and increased protrusion formation, indicating increased migration ability, while HHEX overexpression had the opposite effects..."

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:

"Cancer is among the leading causes of death worldwide. Although effective treatments are available in some cases, cancer cells can become resistant to therapeutic intervention. A new strategy, therapeutic hyperthermia, exploits cancer cells’ heat shock response to make them more sensitive to treatment. In combination with treatments such as radiotherapy and chemotherapy, heat is applied to patients’ tissues to sensitize cancer cells to treatment. Unfortunately, although this treatment is promising, our understanding of how cells sense and adapt to elevated temperature is limited. Recently, researchers used live-cell microscopy and mathematical modeling to examine a human breast cancer cell line after exposure to a range of temperatures. Their results showed that elevated temperatures affected a major signaling pathway, NF-κB, which regulates cell proliferation, apoptosis and the immune response..."

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:

"Cancer occurs when the body’s cells corrupt normal growth pathways. One such pathway is the Hedgehog/Glioma-associated oncogene (HH/GLI) pathway. While the pathway is critical for normal development and health in mammals, uncontrolled activation of the pathway can contribute to cancer development. HH/GLI signaling has been implicated in a wide variety of cancers, making it an attractive target for cancer therapies, but side effects and drug resistance have limited the use of HH/GLI pathway inhibitors, and improved treatment strategies are needed. A new review examines HH/GLI signaling in the context of immunosuppression and immune evasion. Critically, HH/GLI signaling can impair the immune response against a tumor. Here, the pathway drives the formation of regulatory T cells and immune checkpoints, which effectively inhibit the anti-tumoral immune response. But at the same time, the HH/GLI pathway interacts with pro-inflammatory signals to promote the division and survival of cancer cells..."

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:

"Researchers have identified a gene important to the growth and spread of gastric cancer, opening the door to new understanding of this deadly disease. The gene, known as SIX1, has been implicated in disease progression in several cancers, but its link to gastric cancer wasn’t clear. This ambiguity prompted researchers at China Medical University to take a closer look at the role of SIX1 in gastric cancer cells. The team started by measuring SIX1 protein expression in gastric tumors and adjacent non-tumor tissue collected from 208 patients. They found high levels of SIX1 in nearly half the tumor samples and virtually none in the non-cancerous tissue – a pattern suggesting that SIX1 is an important biomarker for gastric cancer. This notion was supported by the finding that patients with higher levels of SIX1 had more advanced disease than those with moderate SIX1 expression..."

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

This video lesson is on the details of cancer cell growth. How do cancer cells grow? How does chemotherapy fight cancer (and cause negative side effects)? The answers lie in cell division. George Zaidan explains how rapid cell division is cancer’s "strength" -- and also its weakness.

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:

"Radiation is one of the most powerful cancer therapies especially for glioblastoma, an aggressive and hard-to-treat form of brain cancer But growing evidence suggests that radiation can actually increase the invasiveness of glioblastoma A new study outlines how this unintended consequence can happen The process begins with the protein EMMPRIN Glioblastoma cells release tiny sacs filled with EMMPRIN into their microenvironment which are then taken up by specialized nerve cells called astrocytes EMMPRIN causes astrocytes to secrete matrix metalloproteinases, or MMPs MMPs are degradative proteins that promote the growth and spread of glioblastoma and other cancers This EMMPRIN-MMP pathway, the team found, goes into overdrive when zapping glioblastoma with gamma rays More radiation means more EMMPRIN, more MMPs, and therefore more invasive glioblastoma Understanding this effect is crucial to developing safe and more effective therapies that shut down glioblastoma cells once and for all.."

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:

"Adoptive cell therapy is a powerful anticancer strategy in which patients are administered extra immune cells. Often, the cells are engineered to express chimeric antigen receptors (CARs) that recognize specific cancer cell proteins (antigens), enabling cancer targeting. The strength of the anticancer effect depends on structures within the CARs called costimulatory domains. One such domain, 4-1BB, activates the NFκB signaling pathway, but the relationship between the amount of antigen present and the strength of the elicited response isn’t well described. To help, researchers recently developed a mathematical model of NFκB signaling induced by a 4-1BB-containing CAR. Simulations revealed that the degree of NFκB pathway activation differed in response to different antigen concentrations, but the timing was consistent. The model performed well even when the input parameters were changed, suggesting its reliability under different conditions..."

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:

"Organoids are 3-dimensional structures built in the laboratory from human pluripotent stem cells (hPSCs) to mimic human tissues and organs and have paved the way for research into new disease treatments that would never have been possible with traditional approaches. One field that is notably benefiting from the use of organoids is cancer research, particularly the study of glioma, the most common type of tumor originating in the brain. Poor outcomes are often associated with glioma because of its rapid growth and resistance to chemotherapy, but cerebral organoids hold promise for the development of novel treatments for this type of cancer, as they can be used as valuable tools to track tumor development and screen new drugs. Human cerebral organoids can also be grown from a patient’s own tissues for the creation of personalized cancer treatments, and they can be genetically engineered to study how common gene mutations affect tumor cells..."

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:

"Gastric cancer remains difficult to treat, but a better understanding of its mechanism might lead to better therapies. An inflammatory state characterized by neutrophil activity is known to promote gastric cancer progression. However, it’s unclear how neutrophil extracellular traps (NETs) in the tumor immune microenvironment influence tumor growth. To learn more, researchers recently analyzed NET formation in gastric cancer. Serum NET markers were elevated in patients with gastric cancer, and higher NET marker levels were associated with worse survival. In addition, more NETs formed in gastric cancer tissues than in adjacent normal tissues. In vitro, a hypoxic environment (like that in tumors) caused gastric cancer cells to release neutrophil-recruiting factors. Hypoxia also triggered the cytoplasmic translocation of HMGB1 in gastric cancer cells and subsequent HMGB1 release. This extracellular HMGB1 then activated the TLR4/p38 MAPK pathway in neutrophils to induce NET formation..."

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