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:

"Estrogen receptor α, or ERα, is believed to play a central role in controlling inflammation. Research suggests that ERα does that by regulating anti-inflammatory signaling in the microglia, the only immune cells that reside in the brain. Now, a new study confirms ERα’s beneficial role in the brains of mice. The work explored one mechanism believed to prime ERα to fight inflammation, the attachment of a phosphoryl group to a specific amino acid in ERα’s structure -- a process known as “phosphorylation”. To test that mechanism, researchers blocked the phosphorylation of ERα in microglia from mice. That absence, it turned out, compromised the cells’ defenses against inflammation – leaving mice vulnerable to negative effects. For example, some mice with blocked ERα phosphorylation were obese and showed weakened motor skills. Further study could help explain how phosphorylated ERα regulates brain immunity and inflammation in brain 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:

"Krill oil is rich in polyunsaturated fatty acids which numerous studies have shown to be effective in reducing intestinal inflammation like that associated with inflammatory bowel disease, or IBD. But exactly how krill oil helps has remained unclear. Now, researchers have discovered a few mechanisms that might explain krill oil’s anti-inflammatory effects. Test-tube experiments showed that krill oil suppressed the NF-κB and NOD signaling pathways, which are critical to the innate immune response. Krill oil also enhanced the killing capacity of macrophages, bacteria-fighting cells that help reduce inflammation. In pigs, krill oil reduced the abundance of Rickettsiales, pathogenic bacteria found in humans and livestock. Computational analyses also revealed distinct microbial signatures associated with adding krill oil to the diet..."

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:

"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:

"Bone marrow-derived endothelial progenitor cells, or EPCs, help repair damage to blood vessel walls and can actually be transplanted from healthy donors into patients with cardiovascular disorders. Unfortunately, transplanted EPCs tend to be rejected by host immune cells. Now, researchers have discovered one promising way to prime EPCs for improved acceptance in the body. The method relies on the molecule TNFα, one of the main mediators of EPC activation. TNFα interacts with two receptors, TNFR1 and TNFR2, in opposing ways. While TNFα-TNFR1 signaling provokes inflammation and cell death. TNFα-TNFR2 signaling leads to cell survival, activation, and proliferation. Interestingly, treating EPCs with a small amount of TNFα significantly up-regulated protective TNFR2 expression and increased their immunosuppressive function without increasing the expression of TNFR1 or other molecular markers of injury that typically accompany transplant rejection..."

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:

"Meniscal tears are one of the most frequent knee injuries and the most common pathology leading to arthroscopic surgery in the United States. It’s no surprise, then, that there’s been a lot of research into how repairing these injuries affects joint kinematics and biomechanics. But meniscal injury also causes changes on the microscopic scale, in the joint microenvironment. Tracking these changes could provide important clues into the cellular processes that promote the development of conditions like post-traumatic osteoarthritis. Researchers from the NYU Langone Orthopedic Center are using synovial fluid biomarkers to take a closer look at this link. The team evaluated 41 patients undergoing arthroscopic surgery to treat a symptomatic, unilateral meniscal injury. Synovial fluid samples were collected at the time of surgery from both the operative and contralateral knee. The concentrations of 10 synovial fluid biomarkers were then compared between knees..."

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:

"Traumatic brain injury (TBI) is a leading cause of death and disability worldwide. TBI’s mechanism is complex, but it may involve a particular type of cell death called pyroptosis, especially among brain cells known as microglia. Mesenchymal stem cells (MSCs), such as the stem cells in umbilical cords, have recently been found to regulate pyroptosis, but it’s unclear whether transplanted MSCs could help alleviate pyroptosis after TBI. To find out, researchers recently administered human umbilical cord MSCs and the MSC-secreted protein TSG-6 into the brains of mice with induced TBI. Both the MSCs and the TSG-6 protein alleviated neurological deficits in the TBI mice. They also reduced inflammatory molecule expression and inhibited microglial pyroptosis in the cerebral cortex. The MSCs’ beneficial effects were weakened when TSG-6 expression was inhibited, confirming the importance of this molecule..."

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:

"Targeted therapy with BRAF and MEK inhibitors has significantly improved the outcomes of patients with BRAF-mutated metastatic melanoma. Unfortunately, a combination of genetic and epigenetic events can create resistance to such treatment, causing most patients to relapse. A new study suggests that this resistance could be due to dysregulation of the miR-146a-5p-regulated NFκB signaling network. Initial experiments showed the gene COX2 to be largely regulated by miR-146a-5p and NFκB. Further experiments involved manipulating miR-146a-5p/COX2 in vitro and in 3D cultures of treatment-resistant tumors explanted from patients undergoing therapy, which demonstrated that miR-146a-5p expression increased drug sensitivity and reduced COX2 expression. Tumor cells’ susceptibility to therapy could be significantly enhanced by decreasing COX2 expression through forced miR-146a-5p expression or by inhibiting COX2 expression with the drug celecoxib..."

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