The year is 2050 and your once-idyllic beachfront vacation home is now flooded up to the second story. The crab your family has enjoyed every Christmas for as long as you can remember has now become an endangered species. The oceans have changed. In Earth 540, Oceanography for Educators, we explore the mechanisms that lead to sea level rise and ocean acidification. We strive to understand how natural processes such as ocean currents, the gulf-stream, tides, plate tectonics, and the Coriolis Effect, affect our oceans and ocean basins. We then predict how man-made issues such as climate change and overfishing will affect our beloved waters and our livelihoods. Want to see into the future? Then this course is for you!

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:

"Once considered little more than “cell dust”, exosomes are receiving much deserved attention from the research community. Exosomes are tiny sacs whose job includes clearing the cell of certain lipids, proteins, and nucleic acids. But researchers are learning that exosomes are also crucial to signaling and communication between cells. A new review explores various ways exosomes help coordinate the metabolism of lipids in the body. Some of the most promising research describes what happens when exosomes’ ability to synthesize, transport, and degrade lipids is compromised. In some cases, that can lead to disorders such as atherosclerosis, cancer, obesity, and Alzheimer’s disease. Understanding how exosomes orchestrate metabolic activities could clue researchers in on new ways to diagnose and treat related diseases..."

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.

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:

"Stroke is the leading cause of death worldwide. Scientists are finding that mitochondrial abnormalities play a central role in stroke. A recent study suggests that deactivating the protein SIAH2 could help mitochondria and the brain cells they power survive stroke in mice. Oxygen deprivation, which makes stroke fatal, activates SIAH2. Once activated, SIAH2 signals the breakdown of mitochondrial and cellular proteins key to survival. Aiming to curb this damage, researchers switched off the gene controlling SIAH2 formation in mouse neurons. and observed what happened after artificially inducing stroke. They found that without SIAH2, neurons suffered low damage during stroke. preserving the machinery that keeps mitochondria alive and well. Understanding how this switch operates in humans is crucial. as it could lead to drugs that target SIAH2 and help reduce the mortality of stroke..."

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 most common cause of blindness is abnormalities in vascularization - blood vessel formation or distribution. Better understanding how vascularization is regulated will help guide the development of new treatments for eye disease. In a recent study, researchers focused on a signaling pathway that regulates angiogenesis and metabolism. The transcription factor HIF-1α regulates vascular endothelial growth factor (VEGF), directing the cellular response to lack of oxygen. Unfortunately, although polypyrimidine tract-binding protein-associated splicing factor (PSF) is known to regulate HIF-1α, how HIF-1α signals are terminated remains unclear. Using mouse models of hypoxia, researchers examined how PSF affects HIF-1α-mediated cellular energy production, migration, and proliferation. They found that PSF prevented excess vascularization and corrected abnormal VEGF expression in mice with oxygen-induced retinopathy..."

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:

"Insufficient blood supply to the brain and a resulting oxygen shortage are collectively referred to as hypoxic ischemia (HI). During HI, accumulation of the neurotransmitter glutamate (Glu) in synapses can lead to neuron damage. Another neurotransmitter, NAAG, can help protect brain cells during HI by binding to the Glu receptor mGluR3 and preventing excess Glu signaling, but exactly how NAAG helps maintain synaptic networks isn’t clear. To learn more, researchers recently examined NAAG/Glu signaling and synaptic plasticity in the brains of newborn pigs subjected to HI via carotid artery clamping. The levels of NAAG and mGluR3 increased during HI, especially after 12–24 h, and then decreased, consistent with an initial anti-Glu defense mechanism. Next, the researchers inhibited the NAAG-degrading enzyme in piglets to increase brain NAAG levels..."

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:

"Glioblastoma is a highly vascularized and aggressive type of brain tumor. S100A4 is a protein that drives vascularization and contributes to the aggressiveness of other malignancies via proteins like NMIIA (non-muscle myosin IIA). The role of the S100A4/NMIIA axis in glioblastoma was recently explored in a study examining samples from glioblastoma patients and a cultured cell line. S100A4 and NMIIA were upregulated in both pseudopalisading (Ps) and non-Ps perinecrotic lesions. S100A4(+)/HIF-1α(+) glioblastoma cells were found near non-Ps perinecrotic lesions, and when close to vascular-rich areas, these cells had elevated mRNA expression of vascular endothelial growth factor A (VEGFA). S100A4(+)/HIF-1α(-) glioblastoma cells were specifically recruited to the surface of pre-existing host vessels in vascular-rich areas..."

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:

"Colorectal cancer (CRC) is a common cancer affecting approximately 4% of people. CRC arises through multiple genetic events and can affect intestinal homeostasis. Healthy intestinal epithelium acts as a physical barrier separating the intestinal microbiota from the host. The barrier is formed by tightly linked intestinal epithelial cells (IECs), which constantly self-renew, shed, and actively communicate with the microbiota. Signaling pathways affecting intestinal cell fate and homeostasis may therefore alter functions related to intestinal barrier homeostasis and even cause cancer. One critical signaling pathway involved in CRC development is KRAS. KRAS family proteins are involved in IEC proliferation, self-renewal, differentiation, adhesion, and apoptosis, and KRAS mutations occur in 45% of CRC patients, with most mutations locking the protein in an active conformation..."

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:

"Heterotopic ossification (HO) is the growth of bone where it doesn’t belong, such as in muscle tissue HO is most often observed after joint surgery in patients with severe trauma and can cause swelling, pain, nerve compression, and other complications While effective treatment and prevention strategies are currently lacking researchers are beginning to zero in on the molecular pathways that trigger HO It all starts with hypoxia, a state of oxygen deprivation that accompanies tissue damage Hypoxia activates the protein HIF-1α In certain patients, HIF-1α acts as a gateway to HO in at least three ways By stimulating proteins that lay the groundwork for new bone and cartilage By promoting blood vessel formation And by suppressing a protein that normally limits bone growth Drugs that reduce hypoxia or block HIF-1α could therefore prove powerful helping to stop HO early in its development.."

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

This brief investigation has students observe the phenomena of fish illness in the Chesapeke Bay and make predications based on data on the cause of the illness and the connection to the greater environmental issue at hand. AP Content Connection:  Living WorldB. Natural Biogeochemical Cycles (Carbon, nitrogen, phosphorus, sulfur, water, conservation of matter)

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:

"Lung cancer, one of the most common cancers, is the leading cause of cancer-related death. Therefore, better understanding of this disease is needed. GSK3 proteins have been reported to play roles in tumor development, but the specific mechanisms are unclear. To learn more, a new study investigated the function of the GSK3 isoform GSK3α in non-small-cell lung cancer (NSCLC). GSK3α expression was significantly upregulated in patients with NSCLC, and patients with high GSK3α expression had shorter overall survival (OS) times than patients with low expression. In vitro, overexpressing GSK3α in NSCLC cells promoted protumor processes such as proliferation, migration, invasion, and colony formation, while silencing GSK3α exerted the opposite effects. To achieve its effects, GSK3α activated the HIF1α/VEGFA signaling pathway and regulated the stability of HIF1α, a protein induced by hypoxic environments like those around tumors, via the PHD-pVHL pathway..."

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:

"Hypoxia is a condition in which bodily tissue is starved of oxygen. This lack of oxygen is common to many diseases, including cancer and stroke. Now, growing evidence suggests that hypoxia may activate immune cells, stimulating inflammation and possibly secondary injury. The role of programmed death-ligand 1, or PD-L1, in this process has attracted much attention recently. Normally, PD-L1 works like a “brake” on the immune system, keeping the immune response under control, but cancers can hotwire PD-L1 to make immune cells idle while tumor cells grow and multiply. Research shows that both persistent and intermittent hypoxia can trigger the overexpression of PD-L1 in various cells. These effects are closely related to the activity of HIF-1α, a protein critical to the body’s response to hypoxia. HIF-1α regulates PD-L1 expression by acting directly on the promoter region of the PD-L1 gene. As a result, PD‐L1 expression helps reduce autoimmune damage and maintain peripheral tolerance..."

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