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:

"Bone morphogenetic protein receptor 2 (BMPR2) is a member of an embryonic signaling cascade that is involved in lung development, but in mature tissue it plays key roles in both cancer and neurological disease. In cancer BMPR2 regulates cell survival signaling events independent of BMP type 1 receptors or the Smad-1/5 transcription factor. BMPR2 contributes to neurological disease when its signaling pathway is overactivated, and BMPR2 stabilizes microtubules. However, it is not yet known if BMPR2 regulates microtubules in cancer cells or what effect that would have on cell survival. To examine this, researchers recently inhibited BMPR2 signaling in lung cancer cell culture and found that it destabilized microtubules. This destabilization led to the activation of lysosomes, which then further decreased BMPR2 signaling. This likely sensitizes cancer cells to cell death via lysosomal permeability. These results demonstrate novel mechanisms by which BMPR2 regulates survival in 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:

"Crohn’s disease is an incredibly painful inflammatory bowel disease that frequently reoccurs after treatment. The growth of a certain type of abdominal fat has been associated with Crohn's disease recurrence. This fat, called mesenteric adipose tissue, is tucked up against the membrane connecting the intestines to the abdominal wall. Microbes can escape the intestines in Crohn's disease and may affect the mesenteric fat. Recently, researchers explored this relationship by investigating the mesenteric microbiome of patients with Crohn’s disease. Crohn’s disease patients had distinct mesenteric microbiomes, host gene expression patterns, and metabolites compared to controls. To explore the specifics, the researchers isolated bacterial strains from the mesenteric microbiome of these patients. In a mouse model of colitis, introducing a mixture of five of the isolated bacterial strains made disease symptoms worse. One of these strains, _A..."

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:

"Bone morphogenetic proteins (BMPs) regulate cell-fate decisions during embryonic development. But after birth, dysfunctional BMP expression is linked to some human diseases, like carcinomas. In lung cancer, BMPs are reactivated and suppress AMPK signaling. Mitochondrial stress activates AMPK to a ‘normal’ level, where it promotes cancer cell survival, but AMPK can induce cell death if ‘hyperactivated.' BMPs inhibit LKB1, a kinase that can hyperactivate AMPK, making BMPs a potential therapeutic target. So, researchers tested two BMP inhibitors as a combination treatment with mitochondrial targeting agents. In lung cancer cell lines that express LKB1, the combination treatment activated AMPK and suppressed cell growth. The combination treatment was increasing nuclear localization of the aptly named apoptosis inducing factor (AIF) in these cells, an effect that depended on LKB1 expression..."

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:

"For the first time, scientists have figured out how to grow and extend the life of primary airway epithelial cells from newborns and young children. These cells line our nasal passages and lungs, protecting us from pathogens, and controlling our immune responses to allergens. Differences in these cells may help explain why certain infants develop wheezing and asthma later in life, but studying them has been challenging because they are difficult to obtain in babies and usually die in culture after dividing a few times. Now, researchers at Children’s National Medical Center in Washington, D.C. and George Washington University have devised a way to reprogram pediatric airway epithelial cells so that they survive, creating a new model to study respiratory disorders that take hold early in life. The team collected airway epithelial cells from 23 donors, including newborns, infants and young children..."

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:

"Insulin resistance and its progression to type 2 diabetes mellitus is an important public health concern. Both endoplasmic reticulum (ER) stress and reduced levels of the regulatory protein PGC-1α have been implicated in insulin resistance, but little is known about any interactions between them in this context. A recent study used cultured human skeletal muscle cells and mouse experiments to examine these potential interactions. In both cultured cells and mice, induced ER stress led to a decrease in PGC-1α and an increase in expression of ATF4, a transcription factor. To see if ATF4 was influencing PGC-1α expression, researchers increased ATF4 expression without ER stress, which also decreased PGC-1α expression, and reducing ATF4 before inducing ER stress blocked the drop in PGC-1α. ER stress activated mTOR, a major regulatory protein, and reduced levels of CRTC2, which is a transcription co-activator that increases PGC-1α transcription..."

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:

"Epigenetic DNA modifications, like methylation, heritably alter gene expression without changing the genetic code. Aberrant epigenetic alterations and dysregulated methylation often drive cancer development. Identifying such alterations could lead to new cancer biomarkers or treatment targets. Colorectal cancer in particular could benefit from epigenetic biomarkers, as it is the third deadliest cancer globally and has limited early detection methods. In a recent study, researchers screened methylation databases of colorectal cancer patients, and they honed in on HAND2, a transcription factor whose promotor region was frequently methylated in these patients. In the lab, experiments demethylating HAND2 reverted its expression in cultured colorectal cancer cells. Demethylation of HAND2 inhibited pro-cancer behavior — proliferation, invasion, and migration — in these cells. HAND2 demethylation also suppressed tumor growth relative to controls in tumor xenograft experiments..."

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

The course applies molecular biology and reverse genetics approaches to the study of apoptosis, or programmed cell death (PCD), in Drosophila cells. RNA interference (RNAi), or double stranded RNA-mediated gene silencing, will be used to inhibit expression of candidate apoptosis-related genes in cultured Drosophila cells. Teams of 2 or 3 students will design and carry out experiments to address questions about the genes involved in the regulation and execution of PCD in this system. Some projects involve the use of DNA damaging agents or other cytotoxic chemicals or drugs to help understand the pathways that control a cell’s decision to undergo apoptosis. Instruction and practice in written and oral communication are provided.

Designed for students without previous experience in techniques of cellular and molecular biology, this class teaches basic experimental techniques in cellular and molecular neurobiology. Experimental approaches covered include tissue culture of neuronal cell lines, dissection and culture of brain cells, DNA manipulation, synaptic protein analysis, immunocytochemistry, and fluorescent microscopy.

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:

"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.

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:

"Extracellular vesicles (EVs) function in many physiological events ranging from normal cellular activity to pathogenic processes. Some EVs prepared in vitro have exhibited therapeutic effects in preclinical models of immune or neurodegenerative disease. In a recent study, researchers generated EVs enriched with HSPB8 (small heat shock protein B8) in vitro from oligodendroglia (OLs). HSPB8 protects cells from oxidative stress-mediated cell death by supporting autophagic activity and could be carried by EVs. Both the native OL-EVs and the HSPB8-enriched OL-EVs were internalized by a microglial cell line and primary mixed neural cultures without inducing cell death. The HSPB8-enriched OL-EVs increased the endogenous production of HSPB8 mRNA. Both EV subsets helped maintain cellular homeostasis during chronic inflammation by increasing autophagic vesicle 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:

"Scientists at the University of Wisconsin have demonstrated that, in male rats, nitrous oxide impairs axon regeneration after multiple types of injuries. Importantly, their results could point toward a possible mechanism. Reporting in the journal Anesthesiology, the authors discuss the effects of nitrous oxide in four model systems: an in vitro evaluation of axon regeneration following a sciatic nerve injury, in vivo tests of regeneration following a sharp spinal cord or an optic nerve injury, and a test of functional recovery after a blunt spinal cord injury. In most experiments, a group of male rats received either a single 70-percent dose of nitrous oxide for two hours, a series of 80-percent doses, or no gas, and were injured or not, in the case of the controls. In some experiments, the rats also received folic acid supplementation, which helps spur axonal recovery. All experiments showed that nitrous oxide reduced the amount of axonal recovery following an injury..."

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:

"Human respiratory diseases are one of the most common causes of death worldwide. Culture models play an important role in medical research, but the models of human airway are limited. Immortalized airway cells are a potential model, but they do not differentiate well in culture, and thus their physiology may not reflect the physiology of native epithelium. Induced pluripotent stem cells (iPSCs) tend to lose epigenetic modifications, which are important for studies of environmentally-induced airway disorders. Primary HAE cells collected from patients are an accurate model, which retains epigenetic marks, but until recently, their biggest limitation was a limited proliferative lifespan in culture. Several conditionally reprogrammed cell (CRC) HAE models have been developed which allow for longer proliferation and differentiation of airway epithelium. Each CRC model is slightly different and has unique methodologies that need to be considered during the experimental design phase..."

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:

"Despite being the standard treatment for lung cancers, immune checkpoint inhibitors (ICIs) are often less effective for patients with EGFR mutations. And these mutations are far from uncommon; 40% of lung adenocarcinoma (LUAD) patients have them, but one protein that might play a role in this process is ARID1A. A recent study examined ARID1A expression in a cohort of LUAD patients with or without EGFR mutations. Overall, low ARID1A expression corresponded to increased immune cell infiltration and longer survival times. The data also suggested that ICIs were more effective for LUAD patients with EGFR mutations if they had low ARID1A expression. Mechanistic experiments in cultured EGFR-mutated LUAD cells suggested that reducing ARID1A expression inhibited autophagy. Autophagy is a normal process in healthy cells, but it helps cancer cells evade the immune system. Specifically, reduced ARID1A expression decreased autophagy by activating the EGFR/PI3K/Akt/mTOR 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:

"Heart attacks are dangerous events that lead to a massive loss of heart cells, called cardiomyocytes. The catastrophic damage can be treated by generating cardiomyocytes from stem cells and transplanting them into the heart. The stem cells can then proliferate in the space before becoming new cardiomyocytes by differentiating and maturing. But little is known about how macrophages from the injury site impact stem cell-derived cardiomyocytes. To learn more, researchers cultured these stem cells, called induced pluripotent stem cells (iPSCs), with macrophages of several subtypes. Macrophages start in a non-polarized phenotype (M0) and then can polarize between pro-inflammatory (M1) and anti-inflammatory (M2) phenotypes. The pro-inflammatory M1 phenotype macrophages were likely to be found at the injury site, and they inhibited iPSC differentiation and maturation..."

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:

"Oncogenic PIM kinases and the tumor suppressor LKB1 regulate cell growth and metabolism in different directions. LKB1 suppresses tumorigenesis largely by phosphorylating and activating the energy sensing kinase AMPK. Anti-oncogenic PIM inhibitors also increase AMPK phosphorylation. However, the exact mechanism by which PIM inhibition affects AMPK remains unclear. A recent study explored the potential PIM-LKB1 interaction related to AMPK phosphorylation in prostate (PC3) and breast (MCF7) cancer cells. Inhibition of activity (by DHPCC9 or AZD1208) or expression (by triple knockout, TKO) of all three PIM kinases increases AMPK phosphorylation. These effects are LKB1-dependent, suggesting that PIM kinases regulate AMPK via LKB1. Additional assays confirmed that PIM kinases phosphorylate LKB1 to inactivate it, identifying LKB1 as a novel PIM substrate. In a chick embryo xenograft model, LKB1 knockout increased tumorigenic growth of prostate 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:

"Sepsis is a life-threatening overreaction of the immune system to infection. Sepsis causes damage to vascular endothelial cells, which play an important role in maintaining vascular function. Treatment strategies that restore vascular endothelial cell function after sepsis are desperately needed. Pericyte-derived microvesicles (PMVs) have had therapeutic effects in other disorders and may be useful in sepsis treatment. To evaluate the potential treatment utility of PMVs, researchers combined experiments in rats and cultured vascular endothelial cells. PMVs were able to protect lung tissue and improve pulmonary function of septic rats. PMVs were also protective of cellular function in the cell culture model. Through subsequent experiments, the researchers determined that PMV absorption was mediated by the cell-surface protein CD44. and that PMVs restored vascular function by delivering the signaling molecule CTGF and activating the ERK1/2- STAT3 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:

"Osteoarthritis is a painful degradation of joint cartilage. Therapies that boost cartilage's limited ability to repair using adipose tissue-derived stem cells (ASCs) have shown promise in cell culture and animal studies, but that success has not carried over to clinical trials. This variability in clinical trials may come down to how the cells are cultured prior to implantation. To test this, a recent study examined a co-culture system combining ASCs taken from the fat pad behind the patella and cartilage cells (chondrocytes). Co-cultured ASCs and chondrocytes had higher expression of cartilage-associated genes than expected, and the effect was larger in cultures with a lower ratio of ASCs to chondrocytes. This gene expression change likely reflects changes in the ASCs and would suggest that the ASCs are starting to make the molecular changes needed to repair damaged cartilage, but increased expression in the chondrocytes, rather than the ASCs, cannot be ruled out without further experiments..."

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:

"Metabolic syndrome is becoming increasingly common among humans and domestic animals and is thought to be linked to dysfunction in adipose tissue components, including adipose progenitor stem cells (ASCs). The proteins PTP1B and LMPTP have been implicated in the development of metabolic disorders, but their roles in adipogenic differentiation of ASCs and modulation of mitochondrial dynamics in these cells remain unclear. To clarify this issue, a recent study treated ASCs from metabolically impaired horses with PTP1B and LMPTP inhibitors in vitro. Both selective inhibitors enhanced the differentiation of ASCs into adipose cells and increased the expression of PPARγ, a master adipogenesis regulator, while the LMPTP inhibitor increased the expression of adiponectin, which helps protect against metabolic disorders. The compounds also improved antioxidant defense and altered mitochondrial bioenergetics..."

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:

"Acute lung injury/acute respiratory distress syndrome (ALI/ARDS) is a deadly illness characterized by persistent lung inflammation. This inflammation is commonly triggered by the bacterial endotoxin lipopolysaccharide (LPS). LPS activates the synthesis and release of inflammatory cytokines by binding TLR4 (toll-like receptor 4), which activates NF-κB (nuclear factor-κB). To understand the exact signaling mechanisms, researchers focused on two potentially involved proteins, ezrin and ROCK (Rho-associated coiled-coil containing protein kinase). Ezrin is a cross-linking protein that has been previously implicated in the activation of TLR4 signaling during LPS challenge, and ROCK is a kinase that may regulate the activity of ezrin-related proteins via phosphorylation. In cultured pulmonary alveolar epithelial cells, LPS induced ezrin phosphorylation, but this could be inhibited by blocking RhoA/ROCK..."

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