Background: There is extensive interest in understanding how neighborhood socioeconomic status (nSES) may affect cancer incidence or survival. However, variability regarding items included and approaches used to form a composite nSES index presents challenges in summarizing overall associations with cancer. Given recent calls for standardized measures of neighborhood sociodemographic effects in cancer disparity research, the objective of this systematic review was to identify and compare existing nSES indices studied across the cancer continuum (incidence, screening, diagnosis, treatment, survival/mortality) and summarize associations by race/ethnicity and cancer site to inform future cancer disparity studies.
Methods: Using PRISMA guidelines, peer-reviewed articles published between 2010 and 2019 containing keywords related to nSES and cancer were identified in PubMed.
Results: Twenty-four nSES indices were identified from 75 studies. In general, findings indicated a significant association between nSES and cancer outcomes (n = 64/75 studies; 85.33%), with 42/64 (65.63%) adjusting for highly-correlated individual SES factors (e.g., education). However, the direction of association differed by cancer site, race/ethnicity, and nSES index.
Conclusions: This review highlights several methodologic and conceptual issues surrounding nSES measurement and potential associations with cancer disparities. Recommendations pertaining to the selection of nSES measures are provided, which may help inform disparity-related disease processes and improve the identification of vulnerable populations in need of intervention.
Nicotinic acetylcholine receptors expressed by striatal interneurons inhibit striatal activity and control striatal-dependent behaviors
- Acetylcholine is an important modulator of striatal activity and it is vital to controlling striatal-dependent behaviors, including motor and cognitive functions. Despite this significance, the mechanisms determining how acetylcholine impacts striatal signaling are still not fully understood. In particular, little is known about the role of nicotinic acetylcholine receptors (nAChRs) expressed by striatal interneurons. In the present study, we used fluorescent in situ hybridization (FISH) to determine which neuronal types express the most prevalent beta2 nicotinic subunit in the mouse striatum. Our data support a common view that nAChR expression is mostly restricted to striatal interneurons. Surprisingly though, cholinergic interneurons (CINs) were identified as a population with the highest expression of beta2 nicotinic subunit.
- To investigate the functional significance of beta2-containing nAChRs in striatal interneurons, we deleted them by injecting the AAV-Cre vector into the striatum of beta2-flox/flox male mice. The deletion led to alterations in several behavioral domains, namely to an increased anxiety-like behavior, decrease in sociability ratio, deficit in discrimination learning and increased amphetamine-induced hyperlocomotion and c-Fos expression in mice with beta2 deletion. Further colocalization analysis showed that the increased c-Fos expression was present in both medium spiny neurons and presumed striatal interneurons.
- The present study concludes, that despite being relatively rare, beta2-containing nAChRs are primarily expressed in striatal neurons by CINs and play a significant role in behavior.SIGNIFICANCE STATEMENTA large variety of nicotinic acetylcholine receptors are expressed in the striatum, a brain region that is crucial in the control of behavior. The complexity of receptors with different functions is hindering our understanding of mechanisms through which striatal acetylcholine modulates behavior. We focused on the role of a small population of beta2-containing nicotinic acetylcholine receptors.
- We identified neuronal types expressing these receptors and determined their impact in the control of explorative behavior, anxiety-like behavior, learning and sensitivity to stimulants. Additional experiments showed that these alterations were associated with an overall increased activity of striatal neurons. Thus, the small population of nicotinic receptors represents an interesting target for a modulation of response to stimulant drugs and other striatal-based behavior.
IL-17 Receptor C Signaling Controls CD4 + T H 17 Immune Responses and Tissue Injury in Immune-Mediated Kidney Diseases
Background: IL-17A-producing CD4+ T helper (THe.g., CD4+ T cell subsets, remains to be elucidated.
Methods: Crescentic GN (nephrotoxic nephritis) was induced in IL-17A, IFNγ, and Foxp3 triple-reporter mice for sorting of renal CD4+ T cell subsets and subsequent single-cell RNA sequencing. Moreover, we generated THH+CD45RBhigh T cell transfer colitis model.
<strong class=”sub-title”> Results: </strong> We identified a specific expression of the IL-17 receptor A/C complex on CD4<sup>+</sup> T<sub>H</sub>17 cells. Single-cell RNA sequencing of T<sub>H</sub>17 cells revealed the activation of the IL-17 receptor signaling pathway in experimental crescentic GN. Disruption of the IL-17RC signaling pathway in CD4<sup>+</sup> T cells and, most importantly, specifically in CD4<sup>+</sup> T<sub>H</sub>17 cells, potentiates the IL-17 cytokine response and results in an accelerated course of experimental crescentic GN. Comparable results were observed in experimental models of psoriasis and colitis.
<strong class=”sub-title”> Conclusions: </strong> Our findings indicate that IL-17 receptor C signaling has a previously unrecognized function in the regulation of CD4<sup>+</sup> T<sub>H</sub>17 cells and in the control of organ-specific autoimmunity and might provide new insights into the development of more efficient anti-T<sub>H</sub>17 treatment strategies.
Recombinant Human HGF Protein, Untagged, CHO-10ug |
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| QP10665-CHO-10ug | EnQuireBio | 10ug | 241.2 EUR |
Recombinant Human HGF Protein, Untagged, CHO-1mg |
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| QP10665-CHO-1mg | EnQuireBio | 1mg | 5343.6 EUR |
Recombinant Human HGF Protein, Untagged, CHO-2ug |
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| QP10665-CHO-2ug | EnQuireBio | 2ug | 186 EUR |
Recombinant Mouse CD14 Protein, His, CHO-10ug |
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| QP11301-HIS-CHO-10ug | EnQuireBio | 10ug | 708 EUR |
Recombinant Mouse CD14 Protein, His, CHO-2ug |
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| QP11301-HIS-CHO-2ug | EnQuireBio | 2ug | 294 EUR |
Chinese Hamster Ovary Cell (CHO) host cell Proteins (HCPs) ELISA kit, 96 tests |
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| 800-140-CHO | Alpha Diagnostics | 1 kit | 1000.8 EUR |
CHO-PEG-CHO |
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| abx085042-20kDa1g | Abbexa | 20 kDa; 1 g | 510 EUR |
CHO-PEG-CHO |
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| abx085042-2kDa1g | Abbexa | 2 kDa; 1 g | 477.6 EUR |
CHO-PEG-CHO |
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| abx085042-34kDa1g | Abbexa | 3.4 kDa; 1 g | 510 EUR |
CHO-PEG-CHO |
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| abx085042-5kDa1g | Abbexa | 5 kDa; 1 g | 510 EUR |
CHO-PEG-CHO,10K |
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| 33-HO004004-10K | Biochempeg |
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CHO-PEG-CHO,1K |
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| 33-HO004004-1K | Biochempeg |
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CHO-PEG-CHO,20K |
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| 33-HO004004-20K | Biochempeg |
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CHO-PEG-CHO,2K |
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| 33-HO004004-2K | Biochempeg |
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CHO-PEG-CHO,3.4K |
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| 33-HO004004-3.4K | Biochempeg |
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CHO-PEG-CHO,4K |
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| 33-HO004004-4K | Biochempeg |
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CHO-PEG-CHO,5K |
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| 33-HO004004-5K | Biochempeg |
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CHO antibody |
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| 20R-CG004 | Fitzgerald | 1 ml | 678 EUR |
mPEG-CHO |
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| abx085008-035kDa1g | Abbexa | 0.35 kDa; 1 g | 577.2 EUR |
mPEG-CHO |
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| abx085008-075kDa1g | Abbexa | 0.75 kDa; 1 g | 610.8 EUR |
mPEG-CHO |
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| abx085008-30kDa1g | Abbexa | 30 kDa; 1 g | 610.8 EUR |
CHO antibody |
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| 70R-CG003 | Fitzgerald | 1 mg | 3010.8 EUR |
Slit2, CHO |
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| PR15085 | Neuromics | 50 ug | 553.2 EUR |
HGF CHO |
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| PR27049 | Neuromics | 2 ug | 229.2 EUR |
Spoligotyping Kit with Primers and Controls |
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| IM9701 | Mapmygenome | each | 1620 EUR |
Anti-CHO HCP |
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| 3G-0016 | Cygnus Technologies | 1 ml | 400.8 EUR |
Anti-CHO HCP |
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| 3G-0016-AF | Cygnus Technologies | 1 mg | 2295.6 EUR |
Anti-CHO HCP |
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| 3G-0016-AFB | Cygnus Technologies | 1 mg | 4143.6 EUR |
Adenosine A 2A receptor controls the gateway of the choroid plexus
The choroid plexus (CP) is one of the key gateways regulating the entry of peripheral immune cells into the CNS. However, the neuromodulatory mechanisms of maintaining its gateway activity are not fully understood. Here, we identified adenosine A2A receptor (A2AR) activity as a regulatory signal for the activity of CP gateway under physiological conditions. In association with a tightly closed CP gateway, we found that A2AR was present at low density in the CP.
The RNA-seq analysis revealed that the A2AR antagonist KW6002 affected the expression of the cell adhesion molecules’ (CAMs) pathway and cell response to IFN-γ in the CP. Furthermore, blocking or activating A2AR signaling in the CP resulted in a decreased and an increased, respectively, expression of lymphocyte trafficking determinants and disruption of the tight junctions (TJs). Furthermore, A2AR signaling regulates the CP permeability. Thus, A2AR activity in the CP may serve as a therapeutic target for remodeling the immune homeostasis in the CNS with implications for the treatment of neuroimmunological disorders.