Yam Code
Sign up
Login
New paste
Home
Trending
Archive
English
English
Tiếng Việt
भारत
Sign up
Login
New Paste
Browse
Resolving momentum degrees of freedom of excitons, which are electron-hole pairs bound by the Coulomb attraction in a photoexcited semiconductor, has remained an elusive goal for decades. In atomically thin semiconductors, such a capability could probe the momentum-forbidden dark excitons, which critically affect proposed opto-electronic technologies but are not directly accessible using optical techniques. Here, we probed the momentum state of excitons in a tungsten diselenide monolayer by photoemitting their constituent electrons and resolving them in time, momentum, and energy. We obtained a direct visual of the momentum-forbidden dark excitons and studied their properties, including their near degeneracy with bright excitons and their formation pathways in the energy-momentum landscape. These dark excitons dominated the excited-state distribution, a surprising finding that highlights their importance in atomically thin semiconductors.Plant roots determine carbon uptake, survivorship, and agricultural yield and represent a large proportion of the world's vegetation carbon pool. Study of belowground competition, unlike aboveground shoot competition, is hampered by our inability to observe roots. We developed a consumer-resource model based in game theory that predicts the root density spatial distribution of individual plants and tested the model predictions in a greenhouse experiment. Plants in the experiment reacted to neighbors as predicted by the model's evolutionary stable equilibrium, by both overinvesting in nearby roots and reducing their root foraging range. We thereby provide a theoretical foundation for belowground allocation of carbon by vegetation that reconciles seemingly contradictory experimental results such as root segregation and the tragedy of the commons in plant roots.Blindness affects 40 million people across the world. A neuroprosthesis could one day restore functional vision in the blind. We implanted a 1024-channel prosthesis in areas V1 and V4 of the visual cortex of monkeys and used electrical stimulation to elicit percepts of dots of light (called phosphenes) on hundreds of electrodes, the locations of which matched the receptive fields of the stimulated neurons. Activity in area V4 predicted phosphene percepts that were elicited in V1. We simultaneously stimulated multiple electrodes to impose visible patterns composed of a number of phosphenes. The monkeys immediately recognized them as simple shapes, motions, or letters. These results demonstrate the potential of electrical stimulation to restore functional, life-enhancing vision in the blind.Definitive hematopoietic stem and progenitor cells (HSPCs) arise from the transdifferentiation of hemogenic endothelial cells (hemECs). The mechanisms of this endothelial-to-hematopoietic transition (EHT) are poorly understood. We show that microRNA-223 (miR-223)-mediated regulation of N-glycan biosynthesis in endothelial cells (ECs) regulates EHT. miR-223 is enriched in hemECs and in oligopotent nascent HSPCs. miR-223 restricts the EHT of lymphoid-myeloid lineages by suppressing the mannosyltransferase alg2 and sialyltransferase st3gal2, two enzymes involved in protein N-glycosylation. https://www.selleckchem.com/products/cnqx.html ECs that lack miR-223 showed a decrease of high mannose versus sialylated sugars on N-glycoproteins such as the metalloprotease Adam10. EC-specific expression of an N-glycan Adam10 mutant or of the N-glycoenzymes phenocopied miR-223 mutant defects. Thus, the N-glycome is an intrinsic regulator of EHT, serving as a key determinant of the hematopoietic fate.Plants and animals detect pathogen infection using intracellular nucleotide-binding leucine-rich repeat receptors (NLRs) that directly or indirectly recognize pathogen effectors and activate an immune response. How effector sensing triggers NLR activation remains poorly understood. Here we describe the 3.8-angstrom-resolution cryo-electron microscopy structure of the activated ROQ1 (recognition of XopQ 1), an NLR native to Nicotiana benthamiana with a Toll-like interleukin-1 receptor (TIR) domain bound to the Xanthomonaseuvesicatoria effector XopQ (Xanthomonas outer protein Q). ROQ1 directly binds to both the predicted active site and surface residues of XopQ while forming a tetrameric resistosome that brings together the TIR domains for downstream immune signaling. Our results suggest a mechanism for the direct recognition of effectors by NLRs leading to the oligomerization-dependent activation of a plant resistosome and signaling by the TIR domain.As human populations spread across the world, they adapted genetically to local conditions. So too did the resident microorganism communities that everyone carries with them. However, the collective influence of the diverse and dynamic community of resident microbes on host evolution is poorly understood. The taxonomic composition of the microbiota varies among individuals and displays a range of sometimes redundant functions that modify the physicochemical environment of the host and may alter selection pressures. Here we review known human traits and genes for which the microbiota may have contributed or responded to changes in host diet, climate, or pathogen exposure. Integrating host-microbiota interactions in human adaptation could offer new approaches to improve our understanding of human health and evolution.Natural selection can promote or hinder a population's evolvability-the ability to evolve new and adaptive phenotypes-but the underlying mechanisms are poorly understood. To examine how the strength of selection affects evolvability, we subjected populations of yellow fluorescent protein to directed evolution under different selection regimes and then evolved them toward the new phenotype of green fluorescence. Populations under strong selection for the yellow phenotype evolved the green phenotype most rapidly. They did so by accumulating mutations that increase both robustness to mutations and foldability. Under weak selection, neofunctionalizing mutations rose to higher frequency at first, but more frequent deleterious mutations undermined their eventual success. Our experiments show how selection can enhance evolvability by enhancing robustness and create the conditions necessary for evolutionary success.
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