Pig VEGF-A ELISA
- Known as:
- Pig VEGF-A Enzyme-linked immunosorbent assay test
- Catalog number:
- kt-32008
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Kamiya biomedical company
- Gene target:
- Pig VEGF- ELISA
Ask about this productRelated genes to: Pig VEGF-A ELISA
- Gene:
- FLT1 NIH gene
- Name:
- fms related tyrosine kinase 1
- Previous symbol:
- FLT
- Synonyms:
- VEGFR1
- Chromosome:
- 13q12.3
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2019-04-23
- Gene:
- FLT4 NIH gene
- Name:
- fms related tyrosine kinase 4
- Previous symbol:
- -
- Synonyms:
- VEGFR3, PCL
- Chromosome:
- 5q35.3
- Locus Type:
- gene with protein product
- Date approved:
- 1991-10-25
- Date modifiied:
- 2016-10-05
- Gene:
- KDR NIH gene
- Name:
- kinase insert domain receptor
- Previous symbol:
- -
- Synonyms:
- FLK1, VEGFR, VEGFR2, CD309
- Chromosome:
- 4q12
- Locus Type:
- gene with protein product
- Date approved:
- 1991-07-10
- Date modifiied:
- 2019-04-23
- Gene:
- NRP1 NIH gene
- Name:
- neuropilin 1
- Previous symbol:
- -
- Synonyms:
- NRP, VEGF165R, CD304
- Chromosome:
- 10p11.22
- Locus Type:
- gene with protein product
- Date approved:
- 1998-12-23
- Date modifiied:
- 2016-10-05
- Gene:
- NRP2 NIH gene
- Name:
- neuropilin 2
- Previous symbol:
- -
- Synonyms:
- VEGF165R2
- Chromosome:
- 2q33.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-12-23
- Date modifiied:
- 2015-09-01
Related products to: Pig VEGF-A ELISA
Related articles to: Pig VEGF-A ELISA
- Background Increased peripheral inflammation and astrogliosis, as assessed by glial fibrillary acidic protein (GFAP) associates with worse cognition. GFAP, however, does not provide brain spatial information. F-SMBT-1, a tracer that binds to overexpressed MAO-B in reactive astrogliosis, may help overcome this limitation. Neuroprotective growth factors (e.g. BDNF, VGF, VEGFA, VEGFD, IGF1R and IGFBP7) usually accompany astrogliosis and could mediate the pathways between AD pathology and cognitive impairment. We evaluated the relationships among peripheral inflammatory markers, growth factors, astrogliosis, and cognitive function and explored whether the relationship of astrogliosis with cognition could be mediated by these growth factors. Methods In a sample of older adults without dementia, we evaluated the relationship of astrogliosis with overall and domain-specific cognitive performance (verbal memory, visual memory, executive function and attention). C-PiB and F-SMBT-1 radiotracers were used to assess Aβ status and astrogliosis, respectively. The NULISAseq CNS disease panel was used to assess GFAP, markers of peripheral inflammation and selected growth factors. We used multivariable robust linear regression models to test the relationship of peripheral inflammation and astrogliosis and cognition. Later, we ran causal mediation analyses stratified by Aβ status to address the effects of BDNF and IGFR1 on the relationship between astrogliosis and cognition. Results Ninety-four non-demented participants were included (mean age: 68 ± 7 yrs, 52% women, 89%, White); among them, 76 were classified as A- and 18 as A+. F-SMBT-1 binding in precuneus was higher among A+ individuals. Also, among A+ individuals, regional F-SMBT-1 binding was associated with worse verbal and visual memory and executive function. Lastly, we found that IGFR1 but not BDNF significantly mediated (suppressed) the association of F-SMBT-1 with worse visual memory, but only among A+ individuals (p<.0001). Conclusion In this non-demented population of older adults with low levels of Aβ pathology and neuroinflammation, astrogliosis related with worse cognitive functions, but only among A+ individuals. Further, IGFR1 may play a suppressive role decreasing by more than 50% the effect of astrogliosis on worse visual memory. - Source: PubMed
Publication date: 2026/07/31
Ramirez-Tirado Laura-AlejandraCohen Ann DLopresti Brian JIkonomovic Milos DGogola AlexandraMatan CristyZeng XuemeiKarikari Thomas KLopez Oscar LSnitz Beth EShaaban C ElizabethVillemagne Victor L - The TSC complex, formed by the binding of TSC2 with TSC1 and TBC1D7, plays an important role in the onset of endometrial-related diseases through the TSC-mTORC1 axis. However, the relationship between these proteins and adenomyosis has not been determined thus far. Here, we aimed to investigate the expression of TSC proteins in adenomyosis and determine the correlation between TSC expression and clinicopathologic parameters in patients with adenomyosis. 21 patients (age range, 40-50 years) with histologically diagnosed adenomyosis who underwent hysterectomy for nonendometrial disease were enrolled in this study. Specimens of healthy endometria were obtained from 21 patients (age range, 38-53 years) with cervical carcinoma in situ who underwent laparoscopy. The participants were interviewed via a standard questionnaire consisting of items pertaining to sociodemographic characteristics and reproductive history. The severity of dysmenorrhea and menorrhagia was quantified by means of the visual analogue scale and the menstrual pictogram, and preoperative hemoglobin levels were determined. Samples of serum and endometrial tissue were collected, TSC and VEGF expression was determined via immunofluorescence, and VEGF expression in the serum was quantified via ELISA. We found that, in patients with adenomyosis, TSC expression was significantly decreased during the secretory phase. Endometrial TSC1 and TSC2 expression was correlated with menstrual volume. Additionally, high levels of VEGFD increased the likelihood of moderate-to-severe menorrhagia in adenomyosis patients. Our results suggest that TSC is associated with clinical symptoms such as menorrhagia. In addition, VEGFD may be a potential quantitative predictor of the severity of menorrhagia in patients with adenomyosis. - Source: PubMed
Publication date: 2026/07/21
Gu Ni-HaoLuo Liu-JingYang Nai-PingYang Ye-PingLi Guo-JingOu-Yang JingWei Chen-XuanLin YuSun FengYang Si-QinXu Hong - Blood group antigens are well known for their importance in transfusion medicine and transplant compatibility; however, their biological role extends beyond these functions and includes associations with the risk of several diseases. In this study, we investigated the relationship between ABO blood groups and the circulating levels of 73 different molecules. - Source: PubMed
Publication date: 2026/06/19
Di Salvo AlessiaMotisi ChiaraBulati MatteoScola LetiziaBalistreri Carmela Rita - In endurance athletes, cardiovascular oxygen delivery is the primary limitation to performance. While the focus of athletes and regulatory bodies has been on hemoglobin and red blood cells, the increased oxygen-delivering capacity resulting from training is also a consequence of the expanded blood volume, which requires vascular adaptation. Angiogenesis-the formation of new blood vessels from pre-existing ones-is an understudied area in exercise physiology due to the need for invasive procedures. Among the vascular endothelial growth factors, VEGF-A and VEGF-D are the most potent angiogenic inducers and thus candidates for doping purposes. VEGF expression can be stimulated by several external factors, of which oxygen deprivation and its mimics are the most significant in the context of doping. A controlled overexpression of VEGF-A or VEGF-D, and the resulting blood vessel formation, could directly increase vascular space and indirectly increase blood volume and athletic ability. A master regulatory gene such as HIF-1α would be a preferred target over any single growth factor, as it would affect red blood cell production and vascular expansion synchronously. Currently available compounds may already be misused, with potential unintended consequences, including the aggravation of inflammatory diseases or tumor progression. Due to the ease of implementation and difficulty of detection, angiogenic doping and possible detection strategies deserve to be studied further. - Source: PubMed
Publication date: 2026/05/21
Lehto SofieSima SetarehKünnapuu JaanaIljukov SergeiJeltsch Michael - Lipedema is a chronic adipose tissue disorder characterized by disproportionate fat accumulation, pain, microvascular dysfunction, and low-grade inflammation. Although low-carbohydrate, high-fat (LCHF) dietary approaches are increasingly used in clinical practice, their longer-term associations with vascular, lymphatic, and immunometabolic pathways in lipedema remain insufficiently understood. This preliminary exploratory study evaluated clinical outcomes and circulating mediators during a 7-month LCHF dietary intervention. Twenty-four women with lipedema (median age: 39 years) underwent a 7-month individualized, calorie-restricted LCHF diet under medical supervision. Outcomes included body mass index (BMI), leg volume, and adipose tissue pain assessed using a visual analogue scale (VAS). Fasting serum samples collected at baseline and follow-up were analyzed for angiogenic, inflammatory, endothelial, and lipid mediators using Luminex assays and liquid chromatography-tandem mass spectrometry (LC-MS/MS). The intervention was associated with significant reductions in BMI, leg volume, and adipose tissue pain ( < 0.001). These changes were accompanied by increased vascular endothelial growth factor A (VEGF-A), vascular endothelial growth factor D (VEGF-D), and angiopoietin-2 (Ang-2), together with decreased pro-inflammatory cytokines and endothelial adhesion molecules. Several endocannabinoid-related lipid mediators, including oleoyl ethanolamide (OEA), arachidonoyl ethanolamide (AEA), and palmitoyl ethanolamide (PEA), also decreased. Baseline OEA and AEA concentrations, as well as reductions in OEA over time, were associated with greater BMI reduction. Change in interleukin-8 (IL-8) showed a nominal association with leg volume reduction, while pain improvement was associated with decreases in P-selectin and VEGF-A and increases in interleukin-13 (IL-13). A 7-month calorie-restricted LCHF dietary intervention in women with lipedema was associated with clinical improvement and changes in circulating vascular, inflammatory, and lipid mediators. These findings reflect systemic changes accompanying the intervention; however, causal relationships and specific mechanisms cannot be established. - Source: PubMed
Publication date: 2026/04/28
Chachaj AngelikaFleszar MariuszLewandowski ŁukaszFortuna PaulinaMaciejewska GabrielaSowicz MonikaAdaszyńska AgnieszkaJakobsche-Policht UrszulaKrzystek-Korpacka MałgorzataSzuba AndrzejJeziorek Małgorzata