0.2mL 8_Strip PCR Tube Caps
- Known as:
- 0.2mL 8_Strip PCR test kit Tube Caps
- Catalog number:
- C-028-O
- Product Quantity:
- 125 ea
- Category:
- -
- Supplier:
- Bioner
- Gene target:
- 0.2mL 8_Strip PCR Tube Caps
Related genes to: 0.2mL 8_Strip PCR Tube Caps
- Gene:
- CAPS NIH gene
- Name:
- calcyphosine
- Previous symbol:
- -
- Synonyms:
- CAPS1, MGC126562
- Chromosome:
- 19p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1990-05-31
- Date modifiied:
- 2016-07-18
Related products to: 0.2mL 8_Strip PCR Tube Caps
Related articles to: 0.2mL 8_Strip PCR Tube Caps
- This article presents a novel tool to quantify potential air quality co-benefits of local climate action and an analysis applying it to a large sample of cities across European and neighbouring countries. The tool estimates the effects of local actions tackling greenhouse gas (GHG) emissions associated with two sectors, namely residential buildings and transport, on air quality. It estimates emission changes associated with GHG mitigation actions described in city climate action plans (CAPs) for five key air pollutants, namely fine particulate matter (PM ), nitrogen oxides (NOx), sulphur dioxide (SO ), ammonia (NH ) and volatile organic compounds (VOC). The analysis applies the tool to evaluate potential impacts of local climate action for 494 cities on ambient air pollutant emissions, based on 531 CAPs submitted to the Covenant of Mayors for Climate and Energy (CoM) initiative. The results demonstrate that GHG mitigation actions are often synergic with air pollution control strategies, offering significant air quality co-benefits. The magnitude and type of benefits depend on the sector and pollutant considered. Nevertheless, some actions may pose risks for air quality. There are risks of increasing, for example, ammonia emissions through a transport fuel switch and, more significantly, fine particulate matter emissions if solid biomass for heating in the residential sector is promoted. Therefore, context-specific data and case-by-case tailored analyses are needed to support the adequate integration of GHG mitigation and air quality policies at city level, avoiding potential trade-offs and maximizing synergies. - Source: PubMed
Publication date: 2026/05/26
Monforti-Ferrario FabioValentini LuanaBastos JoanaBaldi Marta GiuliaPisoni Enrico - Passive muscle stiffness is a key determinant of musculoskeletal function and is influenced by structural components such as titin, connective tissue, and fascia. However, the effects of joint position, muscle depth, and sex on quadriceps passive stiffness remain unclear. To investigate the passive stiffness of the rectus femoris (RF) and vastus lateralis (VL) under different joint configurations, muscle depths, and between sexes using shear wave elastography (SWE). Thirty-six healthy young adults (18 men and 18 women) participated in this randomized crossover study. Passive stiffness was assessed in four positions of knee flexion: supine with 60° (SUP60), supine with 20° (SUP20), sitting with 60° (SIT60), and sitting with 20° (SIT20). SWE measurements (m/s) were obtained from 30 regions of interest (ROIs) per muscle, categorized into superficial, intermediate, and deep levels. Data were analyzed using Generalized Estimating Equations (GEE). A significant effect of position was observed, with higher stiffness values in the SUP60 condition for both RF and VL (p < 0.001). Superficial regions consistently exhibited greater stiffness compared to intermediate and deep regions across all positions (p < 0.001). Additionally, men demonstrated significantly higher stiffness values than women (p < 0.001). Significant interactions were found between position and muscle, as well as position and depth. Quadriceps passive stiffness is influenced by joint position, muscle depth, and sex. The SUP60 position elicits the highest stiffness, while superficial muscle regions are consistently stiffer. These findings highlight the non-uniform mechanical behavior of the quadriceps and may have implications for clinical assessment, rehabilitation, and exercise prescription. Clinical trial registration: This study was registered at Clinicaltrials.gov in June 06th, 2023. Register number NCT05905406. Link to access https//clinicaltrials.gov/study/NCT05905406. - Source: PubMed
Publication date: 2026/09/11
de Souza Ribeiro Victor Hugode Jesus Ferreira Leandro GomesGeremia Jeam Marcelde Souza Baptista RobertoBabault Nicolasde Cássia Marqueti RitaDurigan João Luiz Quagliotti - Multimodal interventions-combining physical activity, cognitive training, a healthy diet and social interaction-represent the most evidence-based approach to slowing cognitive decline in older adults living at home. This article reviews the mechanisms, risk factors, assessment tools and validated programs, in order to equip healthcare professionals to implement personalised and sustainable strategies. - Source: PubMed
Publication date: 2026/08/21
Laplaud AmbreMorier ElsaBoujut ArnaudUlmer ZékyaGueugneau NicolasManckoundia Patrick - - Source: PubMed
Publication date: 2026/10/01
Lu Qin-Jian - Intronic GGGGCC repeat expansions in C9orf72 cause amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). This expansion supports a non-canonical form of translational initiation known as repeat-associated non-AUG (RAN) translation to produce toxic dipeptide repeat proteins that contribute to neurodegeneration. Here, we find that the efficiency of RAN translation and its dependency on the 5' 7-methylguanosine mRNA cap are variable across cell types, with both rodent neurons and human iNeurons favoring cap-independent RAN translation from two distinct repeats (CGG and GGGGCC) across multiple reading frames. Treatment with an eIF4E inhibitor that blocks cap-dependent translation enhances RAN translation specifically in neurons. Intriguingly, cap-independent RAN translation exhibits less reliance on near-cognate codons for initiation than cap-dependent RAN translation. This finding led us to identify a surprising global alteration in neuronal start codon stringency as a contributor to the relatively higher cap-independent RAN translation in this cell type. This effect correlates with cytoplasmic redistribution of eIF1 in neurons and is reversed with overexpression of the eukaryotic initiation factor eIF5, which relaxes start codon stringency and preferentially enhances cap-dependent RAN translation. Together, these findings reveal several neuron-specific features of translational regulation that favor cap-independent RAN translation with implications for nucleotide repeat expansion disorder pathogenesis. - Source: PubMed
Wieland Clare MWright Shannon EWilley SydneyPurwar IshitaGrudzien Samantha JKrans AmyLaimon Erinn LAsher Melissa JIsaacs Adrian MGarner Amanda LTodd Peter K