Ac_ albumine hum GLOX
- Known as:
- Ac_ albumine hum GLOX
- Catalog number:
- BI 1012
- Product Quantity:
- 4mg/2ml
- Category:
- -
- Supplier:
- P.A.R.I.S
- Gene target:
- Ac_ albumine hum GLOX
Related genes to: Ac_ albumine hum GLOX
- Gene:
- HPDL NIH gene
- Name:
- 4-hydroxyphenylpyruvate dioxygenase like
- Previous symbol:
- GLOXD1
- Synonyms:
- MGC15668, 4-HPPD-L
- Chromosome:
- 1p34.1
- Locus Type:
- gene with protein product
- Date approved:
- 2005-07-26
- Date modifiied:
- 2016-03-16
Related products to: Ac_ albumine hum GLOX
Related articles to: Ac_ albumine hum GLOX
- This study systematically investigates the laser surface hardening (LSH) behavior of two medium carbon steels-the low alloy 42CrMo4 and the plain carbon C45-using a 4 kW high power diode laser (HPDL). The influence of laser parameters (power: 3.0-3.8 kW; scanning speed: 10-16 mm/s), post-laser quenching medium (oil vs. air), and, critically, the initial material condition (normalized "raw" vs. quenched and tempered "Q&T") on the case hardening depth (CHD) was evaluated. Hardness profiles defined the CHD at a threshold of 392 HV1, and microstructural analysis was conducted via optical microscopy. The results demonstrate that prior conventional Q&T heat treatment of 42CrMo4 enhances the subsequent laser-hardened depth by approximately 27% compared to laser treatment of the normalized material under identical parameters, providing a quantitative basis for process optimization. For Q&T 42CrMo4, the quenching medium had an insignificant effect on CHD, with air cooling proving equally effective as oil across the tested parameter range, offering an empirically validated route for sustainable processing. In contrast, C45 exhibited a substantially lower and less parameter-sensitive CHD, constrained by its inherent low hardenability. This comparative analysis underscores that hardening depth in 42CrMo4 is linearly controllable via energy input, whereas for C45 it is hardenability-limited. This work establishes that an integrated approach combining conventional bulk heat treatment with diode laser hardening using air cooling offers a highly effective, controllable, and sustainable surface engineering route for high-performance alloy steels. - Source: PubMed
Publication date: 2026/03/03
Lazov LyubomirTeirumnieks EdmundsMuiznieks GatisLeitans ArmandsČapek JiříTrojan KarelProdanov ProdanYankov EmilTeirumnieks NormundsRēvalds RitvarsAdijāns Imants - Endothelin-1 (ET-1) increased bone resorption during orthodontic tooth movement (OTM) in animal models, suggesting potential clinical applications for accelerating OTM. However, the molecular mechanisms by which ET-1 regulates the expression of genes involved in OTM in human periodontal ligament (hPDL) cells remain unexplored. This study investigated the effect of ET-1 on vascular endothelial growth factor () and cyclooxygenase-2 () expression and PGE2 production in hPDL cells. - Source: PubMed
Publication date: 2026/02/21
Unmanatakoon SupachaiSuttamanatwong Supaporn - Genetic analyses have identified biallelic variants in the () gene as the cause of a neurodegenerative disease that resembles the primary coenzyme Q10 (CoQ10) deficiency syndromes. HPDL is structurally similar to the well-studied 4-hydroxyphenyl pyruvate dioxygenase (HPPD), an iron(II)/α-ketoacid-dependent enzyme. HPPD is known to catalyze the second step in the tyrosine metabolism, the oxidative conversion of 4-hydroxyphenylpyruvate (4-HPP) to homogentisic acid (HGA). Hereditary HPPD deficiencies result in high blood tyrosine levels (tyrosinemia type III), which are associated with neurological symptoms such as mental retardation and ataxia. In 2021, 4-hydroxymandelate (4-HMA) was identified as the long-sought intermediate of the biosynthetic pathway from tyrosine to CoQ10. CoQ10 is an important electron shuttle needed in mitochondria for ATP production. Interestingly, HPDL was shown to be able to catalyze the oxygen-dependent reaction of 4-HPP to 4-HMA. Both 4-HPA and 4-HBz occur in the CoQ10 biosynthetic pathway of mammals. CoQ10 has been suspected to be necessary for correct neuronal function, a link to the neurodegenerative HPDL variants. Here, we present a bioinorganic model that can mimic this potential role of HPDL in the conversion of 4-hydroxyphenylpyruvic acid (4-HPA) to 4-hydroxybenzaldehyde (4-HBz). We used fully synthetic iron(III)-hydroxido and iron(IV)-oxido complexes with a ligand of the pentapyridyl-type to study the interconversion of 4-HPA to 4-HBz from a bioinorganic point of view. We show that while an iron(IV)-oxido species, as it occurs in HPPD, is capable of performing the first reaction step from 4-HPA to 4-HMA, an iron(III)-hydroxido species is capable of the transformation of 4-HMA to 4-HBz. - Source: PubMed
Publication date: 2026/03/10
Lindlar Niko S WStucka RolfGutenthaler-Tietze Sophie MGutenthaler-Tietze JonathanSenderek JanDaumann Lena J - Fibroblast activation is essential for tissue repair following injury; however, prolonged activation drives pathological fibrosis. Idiopathic pulmonary fibrosis (IPF), a progressive and age-associated lung disease, is characterized by aberrant fibroblast activation, with increasing evidence implicating senescent and near-senescent fibroblasts in its pathogenesis. However, the underlying mechanisms remain poorly defined. In this study, we investigated whether histone modification is involved in TGF-β1 treated lung fibroblasts and contributes to the fibrotic phenotype. Human IMR90 lung fibroblasts at low and high population doubling levels (LPDL and HPDL), as well as primary IPF fibroblasts, were used in this study. In response to TGF-β1, both LPDL and HPDL fibroblasts upregulated profibrotic genes, including α-smooth muscle actin (α-SMA) and Collagen type III alpha 1 (Col3A1). Compared with LPDL fibroblasts, HPDL fibroblasts exhibited a delayed and sustained p38 MAPK response. Pharmacological inhibition of p38 MAPK significantly reduced α-SMA and Col3A1 expression in both TGF-β1-stimulated fibroblasts and primary IPF cells. Mechanistically, TGF-β1-induced expression of α-SMA and Col3A1 was mediated by histone H4K16 acetylation (H4K16ac), which was enriched at gene promoter regions and attenuated by p38 MAPK inhibition. These findings suggest that a p38 MAPK-dependent epigenetic mechanism is involved in fibroblast activation, supporting the therapeutic potential of p38 MAPK inhibition for treating age-related fibrotic diseases such as IPF. - Source: PubMed
Publication date: 2026/03/03
Zhu ShanZhou Jennifer QWang KanGuo Ming-LeiSanders Yan Y - This study examined the effects of type I collagen, alone and in combination with poly I:C-a toll-like receptor 3 (TLR3) agonist-on matrix metalloproteinase-13 (MMP-13) expression and wound healing in human periodontal ligament (hPDL) fibroblasts. - Source: PubMed
Publication date: 2026/02/14
Namwad RatthawutChaiyaraksa PitchayaDhanesuan NiradaTiranathanagul Siriluck