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Complement - Springer Nature

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Last Updated: 03 September 2022

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Complement C3a Receptor (C3aR) Mediates Vascular Dysfunction, Hippocampal Pathology, and Cognitive Impairment in a Mouse Model of VCID

A substantial number of dementia cases are due to vascular involvement in cognitive decline and dementia secondary to chronic mild-moderate cerebral ischemia. Any genetic deficiency of the complement C3a receptor or its pharmacological inhibition in rodents protects against cerebral ischemia in rodents, while others have blamed C3aR in Alzheimer's disease pathogenesis in rodent transgenic models. In male C57BL/6 wild-type and C3aR-knockout mice, we used the bilateral common carotid artery stenosis model to produce VCID. BCAS resulted in decreased CBF and increased HA, WMD, and neurovascular inflammation in WT compared to C3aR2212/u2212 mice. In addition, C3aRu2212/u2212 mice had improved cognitive function on NOR and MWM relative to WT controls. C3aR axis overactivation causes neurovascular inflammation contributing to poor VCID results that are mitigated by C3aR deletion.

Source link: https://doi.org/10.1007/s12975-022-00993-x


The Role of Complement in HSCT-TMA: Basic Science to Clinical Practice

Hematopoietic stem cell transplantation-associated thrombotic microangiopathy is a common complication that occurs post-HSCT and is connected with significant morbidity and mortality if not quickly identified and treated. For HSCT-TMA genesis, three endothelial cell damage genes u201d are required, a genetic blueprint or existing injury, an endothelial cell-damaging regiment, and further insulting remarks are all required. Patients with HSCT-TMA may also be seen simultaneously with these unusual diagnoses and treatment, which may only contribute to confusion and diagnosis. HSCT-TMA can be treated, or even prevented, by removing or enhancing triggering u201d, and new studies have also found the effectiveness of complement-targeted therapies in this patient population. To raise patient outcomes, greater knowledge of TMA post-HSCT is urgently needed; the aim of this paper is to clarify current understanding, demonstrate roots of complement biology, and provide simple methods to aid in the early detection, implementation, and monitoring of HSCT-TMA.

Source link: https://doi.org/10.1007/s12325-022-02184-4


Optimal Regional Insurance Provision: Do Federal Transfers Complement Local Debt?

If effective federal transfers rise with a region's debt level, we estimate the two insurance plans are complements. The paper's key findings are twofold: first, under DIE shocks, federal transfers, and local debt act as complements in implementing the asymmetric information optimum; second, under the DTP shocks, act as complements with observable production of IPGs but substitutes with observable investment on the IPGs.

Source link: https://doi.org/10.1007/s00712-022-00779-7


On joins of a clique and a co-clique as star complements in regular graphs

0̆3bc u03bc of G u03bc of G 0 0gular graphs G that acknowledge the vertex set partition such that one of the induced subgraphs is the join of an e-vertex clique and a t -vertex co-clique, as one of the induced subgraphs is the joining of an e-vertex clique and a t -vertex co-clique in this t u03bc q u03bc of G u03bc of bc u03bc of G t c t p t graft t a t a t e and t clique and a t vertex clique and a t a t vertex co-vertex subgraphs For the remaining probability, we can determine the geometry of a putative counterexample and compare its appearance to a particular 2-class block style.

Source link: https://doi.org/10.1007/s10801-022-01115-4


On the spectrum of Schur complements of 2D elastic clusters joined by rigid edge modes and hybrid domain decomposition

Here we give estimates on the common condition number of the clusters obtained by interconnecting the Schur complements of square elastic subdomains by the average rigid body modes of adjacent edges. Clusters compiling m0̆0d7m m square subdomains are increasing proportionally to m, according to the angle of subdomains' u2019 Schur complements.

Source link: https://doi.org/10.1007/s00211-022-01307-x


Invariant surface glycoprotein 65 of Trypanosoma brucei is a complement C3 receptor

ISG65 of T. brucei, a complement component 3, is a receptor for complement component 3. In vivo, they provide the crystal structure of T. bruce ISG65 in a complex with complement C3d and show that ISG65 is involved in reducing trypanosome susceptibility to C3-mediated clearance. African trypanosomes are extracellular pathogens of mammals and are attracted to mammals' adaptive and innate immune systems. Trypanosomes evade the adaptive immune response through antigenic variation, but no information is known about how they interact with elements of the innate immune response, including complement. We also show that C3 contributes to the prevention of trypanosomes during early infection in a mouse model, as well as evidence that ISG65 was instrumental in reducing trypanosome susceptibility to C3-mediated clearance. Trypanosomes in ISG65 have developed a C3 receptor that reduces the downstream effects of C3 deposition on disease control.

Source link: https://doi.org/10.1038/s41467-022-32728-9


Mild Hypothermia Alleviates Complement C5a-Induced Neuronal Autophagy During Brain Ischemia–Reperfusion Injury After Cardiac Arrest

Mild hypothermia shields against brain I/R injury following ROSC, but the mechanisms have not been fully understood. After ROSC, we found that HT greatly reduced serum NSE, S100, C5a, and C5a, as well as neurologic deficit scores, TUNEL-positive cells, and autophagic vacuoles in the pig brain cortex. Following ROSC or neuronal oxygen deprivation/reoxygenation, pigs' C5aR1 mRNA and the C5a, C5aR1, Beclin 1, LC3-III, and cleaved caspase-3 proteins were noticeably reduced, while P62 protein and NI3K/Akt/mTOR pathway-related proteins were significantly reduced, with pigs. C5a could bind to C5aR1 to induce neuronal autophagy during the brain I/R syndrome, which was associated with the blocked PI3K/Akt/mTOR pathway, according to our results. By regulating the C5aR1 interaction and the PI3K/Akt/mTOR pathway, which may be one of the neuroprotective mechanisms underlying I/R injury, it may be able to reduce C5a-induced neuronal autophagy. After ROSC or neuronal oxygen deprivation/reoxygenation, the C5a receptor 1 mRNA and the C5a, C5aR1, LC3-II, and cleaved caspase-3 proteins were significantly reduced in pigs, although P62 protein and the PI3K/Akt/mTOR pathway-related proteins were dramatically reduced. Graph 5a mRNA and cleaved caspase-3 proteins were significantly reduced in pigs Proposed device by which the HT shields against brain I/R injury by repressing C5aC5aR1-induced excess autophagy. A C5a that may interact with C5aR1 to activate mTOR, most likely via the PI3K-AKT route, which may lead to autophagy activation. To protect against brain I/R injury, HT can help with complement activation and then reduce C5a-induced autophagy.

Source link: https://doi.org/10.1007/s10571-022-01275-8

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions