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:

"Pain is useful. It’s a natural mechanism for protecting the body in humans and other animals. However, pain that is chronic and persists longer than it should is considered a disease. Research has revealed that pain is often the result of an important interplay between the immune system and the nervous system. When the body produces an inflammatory response to injury, or disease, inflammation can activate [pain circuits], sensitize them, and lead to increased and ongoing pain. Now, using nanosized particles of medicine that momentarily switch inflammation off, researchers have discovered new clues as to how chronic pain unfolds and how it might be relieved. The team began by inducing immune-based chronic pain in rats. They did so surgically by constricting the right sciatic nerve with loosely tied sutures, causing swelling and inflammation through the infiltration of white blood cells, immune cells including monocytes that become macrophages..."

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.

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:

"Cirrhosis is a chronic disease involving permanent scarring of the liver And it's currently the 11th leading cause of death worldwide In its most advanced form, the disease impairs kidney function, causing what’s known as hepatorenal syndrome While inflammation is believed to play a role in cirrhosis No studies have examined the link between inflammation and hepatorenal syndrome until now Researchers from Spain tracked inflammation responses in 161 patients hospitalized for advanced cirrhosis Patients who developed hepatorenal syndrome showed a much stronger inflammatory response than those without the disease The relatively small patient sample means that these results should be interpreted with caution But the findings could still provide meaningful clues for treating patients with cirrhosis Helping doctors identify potential targets for slowing disease progression Solé et al..."

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:

"Today's obesity epidemic is driven by increased consumption of foods that are high in fat and low in soluble fiber, which alters the makeup of the gut microbiome. These changes also vary by age and sex, causing differences in susceptibility to obesity. Unfortunately, most animal studies compare diets that vary in both fat and fiber, making it difficult to determine which has an effect. Now, a new study suggests that fiber could play the more prominent role. The authors of the study profiled the microbial community in mice fed diets varying in either fiber or fat, but not both. 16S rRNA sequencing revealed that changes in fiber accounted for most of the variance in microbes. While these changes were age- and sex-specific, they were not dependent on dietary fat. Although further studies are needed to fully understand these effects, the results suggest that in animal obesity studies, the choice of control diet matters..."

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:

"Sometimes viruses release RNA into the host’s cytosol, and detecting that RNA is a critical part of the host’s antiviral immune response. But cells need to have a set of brakes to regulate these responses, otherwise they can trigger harmful overproduction of type I interferon proteins. The kinase MST4 is one part of this ‘braking’ system. Previous work found that MST4 limits damaging inflammatory responses by adding a phosphate group to the adaptor protein TRAF6. But researchers wanted to know how MST4 might regulate type I interferon production. So, in a recent study, they determined that MST4 also competes with another TRAF protein, TRAF3, to bind MAVS. MAVS is a key antiviral signaling protein, and when MST4 binds it instead of TRAF3, type I interferon production is slowed. They also found that MST4 facilitated interactions between MAVS and the ubiquitin ligase Smurf1, which encouraged degradation of MAVS..."

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:

"Metabolic syndrome is a combination of cardiovascular risk factors including obesity, hypertension, hyperglycemia, and insulin resistance. Although its effects on entire organ systems are well-studied, researchers are beginning to appreciate the importance of thinking smaller. Mesenchymal stem/stromal cells (MSCs) in tissues like fat are able to self-renew and differentiate into many lineages, giving them powerful roles in regulating the immune response and angiogenesis. However, in individuals with metabolic syndrome, MSCs can become senescent, impairing their function and causing inflammation. Recently, researchers evaluated the effect of metabolic syndrome on extracellular vesicles (EVs) – membrane-bound vesicles secreted by MSCs. Using EVs collected from fat-derived MSCs in pigs, they found that micro-RNAs in EVs were altered by metabolic syndrome, some of which targeted senescence-associated genes..."

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 a large reduction in AIDS-related deaths as a result of HIV antiretroviral programs, the global incidence of HIV has only decreased by 16% in the past 10 years. One hotspot is in South Africa, where young women in particular face high rates of HIV infection. In a recent study, researchers followed up on their previous observation that female genital tract (FGT) inflammation increases HIV risk by evaluating the relationship between FGT inflammation and microbial function in 113 young South African women at high risk of HIV infection. Using metaproteomics to characterize a total of 3,186 microbial and human proteins from vaginal wall swabs, they found that women with elevated FGT inflammation had increased non-optimal bacteria and decreased lactobacilli. Reduced cell wall organization and peptidoglycan biosynthesis were also associated with high FGT inflammation 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:

"For people with diabetes, the dangers of high blood sugar are long established. Now, scientists have uncovered additional components in the blood that can worsen the disease. In a new article in the Journal of Physiology, researchers report that microparticles shed from cells under diabetic conditions have unique inflammatory properties that may help explain the multiple organ vascular dysfunction that’s common to the disease. Microparticles have been increasingly recognized as important biomarkers in various health conditions. But most prior reports have relied on in vitro studies to evaluate particle function. Because in vitro experiments can’t fully replicate physiological conditions, defining exactly how microparticles affect disease progression has been tricky. This prompted researchers to look at the link between microparticles and diabetes-induced vascular dysfunction in vivo, in the microvessels of streptozotocin-induced diabetic rats..."

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:

"Dental caries are the most common health condition worldwide and can progress to pulpitis, a painful dental pulp infection. Odontoblasts at the pulp-dentin interface fight against these conditions by preventing bacterial invasion. In other pathological conditions, mitochondrial DNA (mtDNA)-related cell stress activates the cGAS-STING pathway, which contributes to inflammation, but whether mtDNA and cGAS-STING signaling are involved in caries- and pulpitis-associated odontoblast inflammation is unknown. A recent study used molecular techniques to investigate this possibility in patient tissues and an odontoblast-like cell line. cGAS and STING levels were elevated in human caries and pulpitis tissues, and the levels increased as inflammation worsened. In the cell line, the inflammation-inducing bacterial product liposaccharide (LPS) increased the expression of cGAS-STING pathway proteins, suggesting pathway activation, but silencing STING diminished some inflammation-related changes..."

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:

"Synovitis is one of the most common and serious musculoskeletal diseases in horses, causing osteoarthritis and lameness. While available pharmaceutical treatments can reduce joint pain and inflammation, they are expensive and unable to prevent disease progression. Recently, researchers have started looking toward fibroblast-like synoviocytes (FLS) for the development of new treatment options. FLS are cells that produce lubricating proteins to protect cartilage from injury, But they lose their protective features and begin to produce inflammatory chemicals in horses with synovitis and ultimately cause the failure of the FLS mitochondrial machinery, cell death, and joint degeneration. A team of researchers thus transferred healthy mitochondria from immune cells into FLS to determine whether doing so could restore FLS function. They found decreases in cell proliferation and death after mitochondrial transfer as well as a reduction in the production of inflammatory proteins..."

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

This course focuses on the fundamentals of tissue and organ response to injury from a molecular and cellular perspective. There is a special emphasis on disease states that bridge infection, inflammation, immunity, and cancer. The systems approach to pathophysiology includes lectures, critical evaluation of recent scientific papers, and student projects and presentations.
This term, we focus on hepatocellular carcinoma (HCC), chronic-active hepatitis, and hepatitis virus infections. In addition to lectures, students work in teams to critically evaluate and present primary scientific papers.

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:

"Could doctors one day prescribe electrical stimulation to fight a bacterial infection? Work by an interdisciplinary team of researchers at AIMES suggests that might be possible. In line with the Goals of the United Nations’ 2030 Agenda, researchers at AIMES are dedicated to promoting “Good Health and Well-Being” by achieving a better understanding of bacterial infections and the body’s defenses against them. Some of their latest findings reveal a new aspect of host–pathogen interactions. In addition to the cascade of chemical signals that are activated when bacteria invade, the body might also conduct electrical signals across nerves—enabling the infected organ to call distant parts of the body to action. The team uncovered this form of “biological telecommunication” by studying rats with kidney infections caused by strains of E. coli. Within as little as 4 hours of infection, they could detect an immune response all the way in the spleen..."

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:

"Vascular leakage is excessive permeability of blood vessel walls. It’s an inflammatory process associated with illnesses like septic shock and lung injury induced by ischemia or reperfusion. While the mechanism of vascular leakage has remained unclear,a new study suggests that microparticles derived from platelets and endothelial cells could play critical roles. In rats, injection of these microparticles induced pulmonary vascular leakage and lung injury. The microparticles acted synergistically, with endothelial microparticles (EMP) causing platelet buildup, more platelet microparticle (PMP) formation, and further vascular leakage. Experiments showed that certain microRNA (miR) cargo in the microparticles seemed to control the mechanism of injury. Inhibiting miR-155 in endothelial microparticles and miR-126 in platelet microparticles alleviated the effects of the two types of microparticles on vascular leakage and 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:

"Hepatocellular carcinoma (HCC) is the most common form of primary liver cancer. One of the distinguishing features of HCC tumors is their dense network of blood vessels. This makes Angiopoetin-2, a protein that promotes vessel formation in tumors, an attractive target for fighting HCC. In a recent study, researchers discovered a novel route HCC tumors use to release Angiopoetin-2. Test-tube experiments revealed that tumor cells wrapped Angiopoetin-2 in tiny sacs called exosomes. and delivered them to cells derived from human umbilical cord, which boosted blood vessel formation. Gene editing allowed the team to knock out the gene controlling Angiopoetin-2, which, once delivered, significantly reduced the generation of new lifelines from healthy cells. The results point to a new way of disrupting tumor growth. and could lead to new therapies for cancer of the liver and other organs..."

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:

"Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disorder, affecting over 25% of adults worldwide. It causes inflammation and other health conditions, including hepatocellular carcinoma (HCC), a leading cause of cancer-related death. Recently, researchers have looked toward the use of senolytic drugs as a promising treatment. Senolytic drugs selectively target aging cells that no longer divide, which are associated with NAFLD-induced HCC. In a recent study, mice were given low-dose diethylnitrosamine (DEN) and a high-fat diet (HFD) to induce NAFLD-induced HCC. These and normal (CTL) mice were treated with a mixture of two senolytic drugs, dasatinib and quercetin (D+Q). Unexpectedly, the D+Q cocktail had no effect or even worsened liver disease progression in the mice and slightly increased liver damage and tumor generation. The drug cocktail also did not reduce the number of aging cells in the mouse liver, as indicated by the genetic marker p16..."

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:

"Succinate is a metabolite and extracellular signal transductor with complex, but largely inflammatory, roles in the human body. Circulating succinate is elevated in patients with obesity and type 2 diabetes and has been linked to numerous complications. Both human cells and gut bacteria generate succinate, but how microbial succinate production impacts circulating levels and host health remains unclear. In a recent study, combined evidence from human patients and mice point to intestinal succinate as a key factor in obesity-related metabolic disturbances. Specifically, gut microbiota is identified as a relevant source of the high levels of circulating succinate found in obesity. However, modulation of intestinal flora dysbiosis of obese mice with succinate-consuming bacteria as a probiotic might reduce circulating succinate levels. Odoribacter laneus was a particularly promising candidate for this purpose. O..."

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 pancreatitis, which affects more than 34 out of every 100,000 people, is usually mild. However, some cases worsen rapidly, leading to hospitalization and even death. Acute pancreatitis is promoted by the enzyme heparanase and appears to be regulated by the gut microbiota, but the mechanisms and potential interplay of these factors are unknown. A recent study investigated these issues in mice with caerulein (Cn)-induced acute pancreatitis. Compared with wild-type (WT) mice, heparanase-overexpressing (Hpa-Tg) mice exhibited worse disease with neutrophil infiltration and had a different gut microbiota composition, but microbiota depletion and microbiota transfer between the groups attenuated heparanase’s aggravating effect, indicating that the effect was gut microbiome-dependent..."

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 – life-threatening organ dysfunction caused by infection – is a major cause of death in intensive care units. Inflammation and coagulation are known to build off of each other to contribute to sepsis pathogenesis. Unfortunately, the detailed mechanisms behind signaling in sepsis are incompletely understood. In a new study, researchers evaluated signaling pathways using human cell lines and a mouse model of sepsis. They found that inhibiting phosphorylation of the Tyr705 site on STAT3 (pY-STAT3) reduced inflammation. In septic mice, pY-STAT3 inhibition reduced proinflammatory factors, coagulation, lung injury, and vascular leakage, improving the sepsis survival rate. Inhibiting pY-STAT3 decreased LPS-induced cytokine production by macrophages, protecting pulmonary endothelial cells from damage, and procoagulant factors were downregulated by pY-STAT3 inhibition. Although further studies are needed to translate these findings to the clinic..."

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:

"Phospholipid scramblase 1 (PLSCR1) is the most studied member of its protein family and has a complex array of suggested functions. While PLSCR1 was first described as a plasma membrane protein, it has subsequently been found in other cellular compartments and implicated in numerous cellular pathways including apoptosis, intracellular trafficking of membrane proteins, and pro-inflammatory events. PLSCR1 interacts with various effectors, mediators, and regulators that then contribute to distinct cellular processes. While most PLSCR1 interactors are thought to be cell-type specific, the mechanisms of PLSCR1's regulatory functions are often shared. But not all PLSCR1 interactors are endogenous in origin; PLSCR1 also interacts with exogenous viral proteins. These interactions regulate viral uptake and spread in both pro- and anti-viral ways..."

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