Systematic review of neighborhood socioeconomic indices studied across the cancer control continuum

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.

Controls Kit. Baculovirus controls.

K26 AB Vector LLC 1 Kit 295 EUR

PlasmoTest™ Controls

pt-ctr2 InvivoGen FR 200 tests 122.85 EUR

Primer Set for PCR Controls

MBS412588-025mL MyBiosource 0.25mL 140 EUR

Primer Set for PCR Controls

MBS412588-5x025mL MyBiosource 5x0.25mL 430 EUR

Rat Anti-KLH IgM with controls

KT-568 Kamiya Biomedical Company 96 tests 778 EUR

Rat Anti-KLH IgG with controls

KT-570 Kamiya Biomedical Company 96 tests 778 EUR

NATtrol GI Controls (12 x 0.2 mL)

NATGIC-BIO Zeptometrix 12 x 0.2 mL 487 EUR

NATtrol RP Controls (12 x 0.25 mL)

NATRPC-NNS Zeptometrix 12 x 0.25 mL 501 EUR

CO‐Oximeter Calibration Verification Controls

CVC223 RNA Medical each 396 EUR

Spoligotyping Kit with Primers and Controls

IM9701 Mapmygenome each 1620 EUR

Leptospira IFA IgG Pos/Neg Human Controls

LE-GC Fuller Laboratories each 60 EUR

Leptospira IFA IgM Pos/Neg Human Controls

LE-MC Fuller Laboratories each 60 EUR

NATtrol Respiratory Panel 2 (RP2) Controls (Ea)

NATRPC2-BIO Zeptometrix Ea 550.46 EUR

Coxiella burneti IFA Human IgG Pos/Neg Controls

Q-GC Fuller Laboratories each 60 EUR

Coxiella burneti IFA Human IgM Pos/Neg Controls

Q-MC Fuller Laboratories each 60 EUR

Rickettsia typhi IFA IgG Human Pos/Neg Controls

RT-GC Fuller Laboratories each 60 EUR

Rickettsia typhi IFA IgM Human Pos/Neg Controls

RT-MC Fuller Laboratories each 60 EUR

Zika IgM/IgG Control Pack (IgM,IgG & Negative Controls, 0.25mL)

0801020 Zeptometrix 0.25mL 66 EUR

Zika IgM/IgG Control Pack (IgM,IgG & Negative Controls, 0.25mL)

801020 Zeptometrix 0.25mL 66 EUR

Rickettsia rickettsii IFA Human IgG Pos/Neg Controls

RR-GC Fuller Laboratories each 60 EUR

Rickettsia rickettsii IFA Human IgM Pos/Neg Controls

RR-MC Fuller Laboratories each 60 EUR

Eppendorf Centrifuge 5430 lid rotary knob controls - EACH

E5427000660 Scientific Laboratory Supplies EACH 3586.22 EUR

NATtrol Respiratory Panel 2.1 (RP2.1) Controls (12 x 0.3mL)

NATRPC2.1-BIO Zeptometrix 12 x 0.3mL 529 EUR

NATtrol Meningitis/Encephalitis (ME) Controls (12 x 0.2 mL)

NATMEC-BIO Zeptometrix 12 x 0.2 mL 447 EUR

Calibration Verification Controls (BG, Electrolyte, Metabolite Analyzers)

CVC123 RNA Medical each 565 EUR

Nitrated egg ovalbumin protein for ELISA or controls (in PBS)

NITT16-N Alpha Diagnostics 100 ug 300 EUR

CHO Control Antigen

F063 Cygnus Technologies 50 ul 262.8 EUR

Eppendorf Centrifuge 5430 lid rotary knob controls- IVD Only - EACH

E5427000666 Scientific Laboratory Supplies EACH 4325.4 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.

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