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:

"Pulmonary arterial hypertension is a relatively rare but serious condition – in fact, 60 percent of patients don’t live more than 5 years after diagnosis. Most treatment of the disease involves dilating the arteries to lower pressure. But increasingly, research suggests inflammation may be behind the condition – and newer therapies are on the horizon. A review of pulmonary arterial hypertension from this immunological perspective -- including specialized information for anesthesiologists -- is now available from the journal Anesthesiology. Pulmonary hypertension is defined as a resting mean pulmonary artery pressure of 25 millimeters of mercury or higher. Pulmonary arterial hypertension is a type of pulmonary hypertension that mainly affects the blood vessels in the lung. Cases can be idiopathic, hereditary, or associated with infections or a variety of autoimmune or other systemic conditions. The disease is progressive and cannot be cured..."

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

This learning object describes the inflammatory response - a series of local cellular and vascular responses which are triggered when the body is injured or invaded by micro-organisms or antigen.

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:

"Farmed chickens often suffer from intestinal inflammation which negatively affects their feed intake, digestion, and growth performance. The gut microbial community has a known close relationship with growth performance, but how, or if, this microbiota influences intestinal inflammation is not yet known. To test this, researchers examined the microbiota in young chickens, focusing on the jejunum section of the gut. They found that 7-week-old chickens with high body weight tended to have a microbiota dominated by gram-positive bacteria, like Lactobacilli. But lower-body-weight chickens had a microbiota dominated by gram-negative bacteria, like Escherichia-Shigella. Gram-negative bacteria carry endotoxin (lipopolysaccharide), and consequently, these lower body weight chickens had more of it in their bloodstream. These elevated lipopolysaccharide levels activated inflammatory cytokines in the jejunum, causing damage to the gut barrier..."

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:

"Chronic cerebral hypoperfusion (CCH) drives the secondary brain injury found in some central nervous system (CNS) diseases. Certain CNS diseases can be exacerbated by a dysregulated microbiota-gut-brain axis through metabolites like short chain fatty acids (SCFAs). But is there a relationship between gut dysbiosis and CCH, and does maintaining SCFA metabolism by restoring the gut microbiota protect against CCH? To answer these questions, a recent study examined the effects of fecal microbiota transfer (FMT) on a rat model of CCH. CCH was induced with bilateral common carotid artery occlusion (BCCAO). BCCAO caused cognitive impairment, impaired gut function, altered gut microbiota, and reduced SCFA levels. However, the transfer of a balanced microbiota to BCCAO rats reduced these symptoms. Specifically, a rebalanced microbiota improved gut motility and barrier functions. It also led to higher levels of hippocampal SCFAs and reduced neuroinflammation in response to lipopolysaccharide..."

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:

"Epimedii Folium (EF) is a popular herbal medicine for bone fracture and joint disease. Unfortunately, EF can cause idiosyncratic drug-induced liver injury (IDILI). But the risk factors and mechanisms are not well understood. A new study investigated the liver-damaging effects of the EF compound Icariside I and its effects on the NLRP3 inflammasome a sensor and trigger of inflammatory signals that’s been implicated in IDILI. In cell culture, NLRP3 inflammasome activation by ATP or Nigericin was enhanced by Icariside I. But there was no effect when the inflammasome was activated by SiO2, poly(I:C), or cytosolic lipopolysaccharide. Icariside I alone doesn’t induce mitochondrial reactive oxygen species, a key component of liver damage, but it increases their production after activation by ATP or Nigericin. In an IDILI-susceptible mouse model, the administration of Icariside I induced liver damage, but mice pre-treated with an NLRP3 inhibitor showed no signs of liver damage..."

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:

"Chronic rhinosinusitis is one of the most common diseases among humans, affecting approximately 12% of the adult population globally. It is characterized by inflammation of the nasal cavity and sinuses, causing facial pressure and pain as well as long-term loss of smell. Benign masses called nasal polyps can also develop and cause chronic nasal obstruction, but the exact cause of this disease is unknown. Recent research has indicated that toxins produced by the bacterium _Staphylococcus aureus_, particularly enterotoxin B (SEB), may play an important role. SEB is thought to stimulate the immune system by activating proteins such as toll-like receptor 2 and pro-inflammatory cytokines and by causing reactive oxygen species production and endoplasmic reticulum stress. This inflammatory response may then disrupt the integrity of the epithelial cells in the nose and sinuses..."

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:

"Atherosclerosis is a chronic inflammatory process where lipids accumulate along the arterial wall. One key protein in atherosclerosis development is AIBP (Apolipoprotein A-I binding protein). AIBP exists both inside and outside cells, but only secreted AIBP is well characterized in atherosclerosis. A recent study found that AIBP is highly expressed in human and mouse atherosclerotic lesions and that the AIBP was concentrated within the inner membrane of macrophage mitochondria. Macrophages are immune cells that can have pro- or anti-inflammatory phenotypes. The interplay between these phenotypes plays a pathogenic role in atherosclerosis. In this study, blocking the production of AIBP in bone marrow aggravated atherosclerosis and increased macrophage infiltration in a mouse model. This bone-marrow-specific AIBP deficiency increased the cleavage of the protein PINK1 (PTEN-induced putative kinase 1)..."

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:

"Myocardial infarction (MI), also known as a heart attack, is a common but serious cardiac emergency. The severity and mortality of MI are related to overactivation of immune cells called neutrophils. Specifically, excessive activation of a process called neutrophil degranulation appears to impair MI recovery. During degranulation, molecules that can help fight pathogens and repair tissue damage are released from cytoplasmic granules. This is normally beneficial, but too much degranulation can aggravate MI-related injury. Four main types of granules are released: primary/azurophilic, secondary/specific, tertiary/gelatinase, and secretory granules. These granule types are synthesized and released at different times and contain different mixtures of molecules. For example, primary granules contain the enzyme MPO, excess levels of which can impair ventricular healing and function after MI, while secondary granules contain NGAL, which can increase the risk of plaque formation and promote inflammation and fibrosis..."

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:

"Peptide hormones are important signaling molecules within the body. One such peptide is the secreted protein augurin, which is encoded by the gene Ecrg4, whose expression has been reported in a wide range of human tissues. The product of the gene Ecrg4, the augurin precursor ECRG4, has been predicted to be cleaved to originate different peptides. Augurin is implicated in a variety of processes, including tumorigenesis, inflammation, and infection. It is also involved in the regulation of the hypothalamo-pituitary adrenal axis and in osteoblast differentiation. Augurin is implicated in the modulation of well-known signaling cascades, including NF-kB, PI3K/Akt/mTor, Wnt-beta catenin, and apoptosis pathways, however, the molecular mechanisms underlying its action remain largely unexplored. Given its involvement in health and disease, augurin is an attractive target for the discovery of new therapeutic agents for human pathologies..."

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:

"Mutations in the gene tp53 are often detected in the early stages of colitis-associated colorectal cancer (CAC). The development of CAC is facilitated by gut microbiota disruption (dysbiosis) and chronic intestinal inflammation, but whether tp53 mutations are linked to this dysbiosis and inflammation remains unclear. To learn more, a recent study examined zebrafish larvae with a tp53 mutation. The mutant fish exhibited intestinal inflammation that was due to gut microbiota disruption. confirming the link between tp53 and these pathological changes. Overall, gut microbiome diversity was decreased, while pathogenic Aeromonas bacteria were abnormally abundant, aggressively colonizing the gut. Further investigation revealed that the gut dysbiosis in the mutants induced inflammation by disrupting sialic acid metabolism. Supporting this finding, inhibition of the sialic acid-releasing enzyme sialidase alleviated the pathologies in mutant zebrafish larvae..."

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:

"Inflammation in the brain is a hallmark of many neurodegenerative diseases, including Alzheimer’s and Huntington’s disease. One of the key orchestrators of neuroinflammation is IL-6, a cytokine secreted by brain-resident cells called astrocytes. While low levels of IL-6 support neurons and synapses in the brain higher levels of IL-6 are produced in response to injury or infection, triggering a series of proinflammatory signaling cascades. Unfortunately, how astrocytes regulate IL-6 expression remains unclear. A recent study evaluated signaling pathways involved in IL-6 gene regulation, including β-catenin, TCFs/LEF, C/EBP, and NF-κB. Using human astrocytes, researchers silenced or overexpressed the signaling proteins and measured IL-6 levels. They found that TCF/LEF induces IL-6 in the presence of ATF2, while β-catenin inhibits IL-6 by interacting with TCF/LEF. Interestingly, neither of these signaling pathways is known to regulate IL-6 in other cell types..."

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