Yam Code
Sign up
Login
New paste
Home
Trending
Archive
English
English
Tiếng Việt
भारत
Sign up
Login
New Paste
Browse
Perioperative neurocognitive disorders (PND) are characterized by deficits in cognitive functions in the elderly following anesthesia and surgery. Effective clinical interventions for preventing this disease are limited. Growing evidence demonstrates that activation of NOD-like receptor protein3 (NLRP3) inflammasome is involved in neurodegenerative diseases. We therefore hypothesized that activation of NLRP3 inflammasome is linked to neuroinflammation and the subsequent cognitive impairments that occurred in an animal model of PND. In this study, 18-month-old C57BL/6 mice were subjected to an exploratory laparotomy under isoflurane anesthesia to mimic clinical human abdominal surgery. For interventional studies, mice received NLRP3 specific inhibitor MCC950 (10 mg/kg) or the vehicle only intraperitoneally. Behavioral studies were performed at 6 and 7 d after surgery using open field and fear conditioning tests, respectively. Interleukin-1β (IL-1β), interleukin-18 (IL-18), tumor necrosis factor-α (TNF-α), ionized calcium-binding adaptor molecule-1 (IBA1) positive cells, glial fibrillary acidic protein (GFAP) positive cells, NLRP3, apoptosis-associated speck-like protein containing a CARD (ASC), and cleaved caspase-1 were measured at 3 days post-surgery. Brain-derived neurotrophic factor (BDNF) and postsynaptic density protein 95 (PSD95) were measured at 7 days post-surgery. Our data indicates that surgery-induced cognitive impairments were associated with significant increases in IL-1β, IL-18, TNF-α, NLRP3, ASC, cleaved caspase-1, IBA1-positive cells and GFAP-positive cells, and decreases in BDNF and PSD95 expression in the hippocampus. Notably, administration with MCC950 attenuated inflammatory changes and rescued surgery-induced cognitive impairments. Our study suggests that surgery induces neuroinflammation and cognitive deficits that are partly attributed to the activation of NLRP3 inflammasome in the hippocampus of aged mice. PD-1 inhibitors have been used to revive exhausted T cell responses in non-small cell lung cancer (NSCLC) and other malignancies. CXCR5+ T follicular helper (Tfh) cells are characterized by constitutive high PD-1 expression and have been associated with the formation of tertiary lymphoid structures and implicated in antitumor immunity. In this study, we investigated the effect of PD-1 and PD-1 inhibition on CXCR5+ CD4 T cells. Data showed that CXCR5+ CD4 T cells in both healthy subjects and NSCLC patients presented markedly higher PD-1 expression than CXCR5- CD4 T cells. Both CXCR5- and CXCR5+ CD4 T cells from NSCLC patients presented higher PD-1 expression than their counterparts in healthy subjects. PD-1+ CXCR5+ CD4 T cells were functional, could express IL-21, IL-10, and CXCL13 upon stimulation, demonstrated auxiliary effects toward CD8 T cell-mediated IFN-γ production and proliferation, and promoted IgM and IgG production. However, the potency of PD-1+ CXCR5+ CD4 T cells was lower than the potency of PD-1- CXCR5+ CD4 T cells. PD-1 blocking could significantly enhance the effector functions of PD-1+ CXCR5+ CD4 T cells. Overall, this study demonstrated that PD-1+ CXCR5+ CD4 T cells could promote CD8 T cell and B cell inflammation and could be modulated by PD-1 inhibition. The prevalence of type 2 diabetes mellitus (DM) is increasing in the children population. It is well known that inflammation contributes to the type 2 DM pathogenesis. Interleukin 38 (IL-38) is one newly identified anti-inflammatory factor. Therefore, we investigated whether the expression level of IL-38 is associated with type 2 DM in the children and the underlying mechanism. Children with recently diagnosed type 2 diabetes mellitus were recruited and studied. The healthy subjects without glucose metabolism abnormalities were used as controls. The IL-38 expression level was determined by quantitative PCR and ELISA (Enzyme-linked immunoassay). Statistic analysis showed that the IL-38 level was significantly associated with type 2 DM and insulin resistance in the children. The patients were then divided into two groups, one group sensitive to insulin therapy while the other resistant to insulin therapy. Data showed that the IL-38 was highly expressed in the group sensitive to insulin therapy. In the mice model, overexpressing the IL-38 could suppress the expression of IL-36, a pro-inflammatory factor, and also the diabetes development. Thus our results showed that higher IL-38 was associated with the increased insulin sensitive in children with type 2 DM and inhibited T2DM development in the mouse model through suppressing the function of IL-36. V.Age prediction can help identify skeletal remains by limiting the search range for a missing person. Although age prediction methods based on odontology and anthropology are frequently used in the forensic field, DNA methylation is particularly promising age-predictive biomarker. In this study, we generated genome-wide DNA methylation profiles of bone samples from 32 identified skeletal remains with an age at death ranging from 31 to 96 years. Only 12 provided more than 800 K quality-filtered CpG methylation values using Illumina's Infinium MethylationEPIC BeadChip array. Methylation ages of the bone samples calculated using a recently developed skin & blood clock composed of 391 CpG sites were found to be very similar to their actual ages (MAD = 6.4 years). However, the low success rate in methylation profiling of bone DNA samples may prevent researchers from applying the array to this type of samples. Therefore, we selected a set of CpG sites that would enable age prediction based on only a few CpG sites in bone DNA samples. Nineteen age-associated CpG marker candidates were selected from 720 K quality-filtered CpG values of 21 male skeletal remain samples. Because age signatures for blood, such as markers on the ELOVL2, FHL2, KLF14 and TRIM59 genes, had showed strong age associations in 12 bone samples, we further tested the age association of the 5 well-known markers in a blood-based model and the 13 out of 19 CpG markers from the array of 21 bone samples with an independent set of 30 skeletal remain samples using SNaPshot multiplex based on single nucleotide primer extension. https://www.selleckchem.com/products/nt157.html Four CpG sites on TMEM51, TRIM59, ELOVL2, and EPHA6 genes showed moderate or weak correlations between methylation and age, which suggests further investigation of these markers to predict the age of bones.
Paste Settings
Paste Title :
[Optional]
Paste Folder :
[Optional]
Select
Syntax Highlighting :
[Optional]
Select
Markup
CSS
JavaScript
Bash
C
C#
C++
Java
JSON
Lua
Plaintext
C-like
ABAP
ActionScript
Ada
Apache Configuration
APL
AppleScript
Arduino
ARFF
AsciiDoc
6502 Assembly
ASP.NET (C#)
AutoHotKey
AutoIt
Basic
Batch
Bison
Brainfuck
Bro
CoffeeScript
Clojure
Crystal
Content-Security-Policy
CSS Extras
D
Dart
Diff
Django/Jinja2
Docker
Eiffel
Elixir
Elm
ERB
Erlang
F#
Flow
Fortran
GEDCOM
Gherkin
Git
GLSL
GameMaker Language
Go
GraphQL
Groovy
Haml
Handlebars
Haskell
Haxe
HTTP
HTTP Public-Key-Pins
HTTP Strict-Transport-Security
IchigoJam
Icon
Inform 7
INI
IO
J
Jolie
Julia
Keyman
Kotlin
LaTeX
Less
Liquid
Lisp
LiveScript
LOLCODE
Makefile
Markdown
Markup templating
MATLAB
MEL
Mizar
Monkey
N4JS
NASM
nginx
Nim
Nix
NSIS
Objective-C
OCaml
OpenCL
Oz
PARI/GP
Parser
Pascal
Perl
PHP
PHP Extras
PL/SQL
PowerShell
Processing
Prolog
.properties
Protocol Buffers
Pug
Puppet
Pure
Python
Q (kdb+ database)
Qore
R
React JSX
React TSX
Ren'py
Reason
reST (reStructuredText)
Rip
Roboconf
Ruby
Rust
SAS
Sass (Sass)
Sass (Scss)
Scala
Scheme
Smalltalk
Smarty
SQL
Soy (Closure Template)
Stylus
Swift
TAP
Tcl
Textile
Template Toolkit 2
Twig
TypeScript
VB.Net
Velocity
Verilog
VHDL
vim
Visual Basic
WebAssembly
Wiki markup
Xeora
Xojo (REALbasic)
XQuery
YAML
HTML
Paste Expiration :
[Optional]
Never
Self Destroy
10 Minutes
1 Hour
1 Day
1 Week
2 Weeks
1 Month
6 Months
1 Year
Paste Status :
[Optional]
Public
Unlisted
Private (members only)
Password :
[Optional]
Description:
[Optional]
Tags:
[Optional]
Encrypt Paste
(
?
)
Create New Paste
You are currently not logged in, this means you can not edit or delete anything you paste.
Sign Up
or
Login
Site Languages
×
English
Tiếng Việt
भारत