PLGF 1
- Known as:
- PLGF 1
- Catalog number:
- CYT-419
- Product Quantity:
- 2µg
- Category:
- -
- Supplier:
- Prospecbio
- Gene target:
- PLGF 1
Ask about this productRelated genes to: PLGF 1
- Gene:
- PGF NIH gene
- Name:
- placental growth factor
- Previous symbol:
- PGFL
- Synonyms:
- PLGF, PlGF-2, PlGF, SHGC-10760, D12S1900, PIGF
- Chromosome:
- 14q24.3
- Locus Type:
- gene with protein product
- Date approved:
- 1994-01-14
- Date modifiied:
- 2016-05-20
Related products to: PLGF 1
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- To evaluate the effectiveness of Fetal Medicine Foundation-based first-trimester preeclampsia (PE) screening using maternal factors, mean arterial pressure, uterine artery Doppler and pregnancy-associated plasma protein-A, without placental growth factor (FMF-UtA-PAPPA), versus the maternal history approach (National Institute for Health and Care Excellence criteria - NICE approach), when implemented in a public non-academic setting with a predominantly East Asian population. - Source: PubMed
Ho Suet YinLee Linus Lin TaiChan Lin Wai - Placental growth factor (PGF) is associated with the progression of hepatocellular carcinoma (HCC), but current research on this relationship remains limited. This study aims to establish a pathomics model for predicting PGF expression levels in H&E-stained HCC sections, and to explore its prognostic relevance and underlying molecular mechanisms. - Source: PubMed
Chen LongZhang XushengLiu KejunMa WeihuDing LingLiang ShicaiWang XueboChen Bendong - This study aimed to evaluate the effect of progesterone (P4) supplementation during the first follicular wave and delayed induced luteolysis with only one PGF (PGF) treatment on d 6 of the modified 5d-CoSynch protocol on ovarian dynamics, serum P4 concentrations, and estrus expression of Holstein heifers. Heifers were pre-synchronized with a PGF on experimental d -2 (pre-PGF) and treated with GnRH on d 0 to induce a first follicular wave of the estrous cycle. On d 0, heifers were randomly assigned (n = 34/treatment) to one of 3 treatments (G5PP-P4, G5PP and G6P). Heifers in the G5PP-P4 had an P4 intravaginal insert placed on d 0 that was removed on d 5. Heifers in G5PP and G5PP-P4 received 2 PGF on d 5 and d 6 (PGF-1 and PGF-2, respectively). Heifers in the G6P received only one PGF on d 6 (PGF-1). Only heifers that had luteolysis and ovulation between pre-PGF and 2 d after GnRH were considered in the first follicular wave and used in the study (G5PP-P4, n = 25; G5PP, n = 29; and G6P, n = 25). Ovarian ultrasound was performed on d -2, 0, 2, 3, at the time of PGF-1 (d 5 for G5PP-P4 and G5PP, and d 6 for G6P), 24h after PGF-1, and then every 12h until ovulation. Additionally, ovarian ultrasound was also performed on d 5 in heifers in the G6P group. Blood was collected on d -2, every day from GnRH until PGF-1, and every 12h after PGF-1 until ovulation or 144h after PGF-1. Heifers supplemented with P4 had greater serum P4 from d 1 to d 5 than heifers not supplemented. Heifers in G5PP-P4 had slower follicular growth and smaller dominant follicles (DF) at PGF-1, and G6P heifers had the largest DF at PGF-1. By 36 and 48 h after PGF-1, all heifers in G5PP-P4 and G5PP, respectively, had serum P4 ≤ 0.45 ng/mL, whereas only 80% of heifers in G6P reached this threshold by 48 h. Treatment did not affect the proportion of heifers with functional CL at PGF-1, expressing estrus, and ovulating after PGF-1. However, despite a shorter interval from PGF-1 to ovulation, the ovulatory follicle was older and larger in G6P heifers at PGF-1 compared with those in the other treatments. In summary, not supplementing P4 and administering only one PGF on d 6 of the first follicular wave of dairy heifers altered the ovulation time but resulted in a similar proportion of heifers with ovulation at the end of the protocol. However, our results suggest that a single PGF dose on d 6 after GnRH may not be as efficient in promoting luteolysis as 2 PGF administrations on d 5 and 6. The impact of adopting these changes on fertility in a timed-AI protocol for dairy heifers such as a 5d-CoSynch still requires further investigation. - Source: PubMed
Publication date: 2026/04/20
Leão Iago M RAnta-Galván EverardoEl Azzi Marcelo SValdés-Arciniega TeresitaMartins João Paulo N - Oxidative stress (OS), derived from an imbalance between reactive oxygen species (ROS) accumulation and impaired antioxidant defense, is a recognized cause of atherothrombosis, through a complex interaction between low-grade inflammation and platelet activation. Lipid peroxidation, as reflected by the urinary excretion of 8-iso-Prostaglandin F2α (8-iso-PGF), is central in the pathogenesis of atherosclerosis. This biochemical abnormality has been observed in patients with cardiovascular risk factors, including diabetes mellitus, obesity, cigarette smoking, hypercholesterolemia, hypertension, atrial fibrillation, and in clinical settings associated with aging, such as acute and chronic cardiovascular diseases and chronic kidney disease. Despite the treatment with acetylsalicylic acid or with any other antithrombotic drugs, patients may undergo recurrent events due to the complex nature of atherothrombosis. A large body of evidence supports the relationship between OS and less-than-expected response to aspirin. Several disease-modifying agents and antioxidant supplementation, as well as modulation of the primary metabolic abnormalities driving lipid peroxidation, have been shown to reduce urinary 8-iso-PGF excretion. Overall, these observations pave the way for potential therapeutic approaches able to target these mechanisms, resulting in the reduction of atherothrombosis progression. This will be an overview of the significance of 8-iso-PGF in the pathogenesis of atherothrombosis and as a potential mechanism-based biomarker of cardiovascular events. - Source: PubMed
Publication date: 2026/04/09
Simeone PaolaLiani RossellaLattanzio StefanoFrezza MaurizioAlfonsetti MargheritaCipollone FrancescoSantilli Francesca - Stillbirth remains a major global health challenge, particularly in low- and middle-income countries. Angiogenic imbalance, characterized by elevated soluble fms-like tyrosine kinase-1 (sFlt-1) and reduced placental growth factor (PlGF), is implicated in placental dysfunction, yet few studies have examined the association between the sFlt-1:PlGF ratio and stillbirth. - Source: PubMed
Publication date: 2026/04/01
Lee Mi-Sun SEum Ki-DoChristiani David C