Introduction: Burning wounds are common afflictions; However, conservative wound care frequently lead to poor compliance with physical treatment and disability in patients with deep burns. As a result, regenerative biological materials, which are more effective for tissue repair, are in particular for the deep burns of the second degree. A new spray formulation of basic fibroblast growth factors (BFGF) has been produced by synthesizing fibroblast growth factor proteins. In this post-marketing surveillance study (PMS), we evaluated the safety and efficacy of BFGF and compared indirectly this formulation with cultured epidermal autografts (CEA) to treat deep-degree burns.
Materials and methods: A total of 3173 patients treated in 15 hospitals were used for BFGF PMS in South Korea for six years. A total of 1630 patients with second degree burns were selected to evaluate adverse events (AES) of BFGF treatments. The efficiency was evaluated according to the periods until the re-epithelialization and the clinical utility of BFGF was indirectly compared to that of CEAs.
Results: AES occurred in 37 patients (2.3%) and included the pain at the application site (1.7%) and contact dermatitis (0.6%). All AES were light and were evaluated as probably unrelated to BFGF. The average delay of re-epithelialization was 8 days; This period of time was significantly longer after major burns (9.7 days) after minor (7.8 days) or moderate burns (7.9 days). The most treated burn wounds (99.8%) have been evaluated as improved. The indirect comparison comprised 534 patients using the same inclusion criteria for CEA patients (N = 35). The BFGF treatment has shown superior efficiency compared to CEA by significantly reducing the average day on demand (5.4% versus 8.8 days) and re-epithelialization time (7.1% against 13.7 days).
Conclusion: Our study has shown that BFGF is a convincing regenerative treatment with competitive clinical efficiency and security for deep-degree burns and a reduction in treatment time, which should reduce medical costs, particularly for patients with patients with burns of second.
Fibroblast growth factor-23 as early marker of the CKD-mineral bone disorder in dogs: preliminary inquiry
Objectives: To examine the relationship between the fibroblast growth factor-23, the severity of chronic diseases and mineral metabolic disorders associated with chronic kidney disease in dogs.
Materials and methods: Fifteen chronic kidney control dogs were included retrospectively. The growth factor of serum fibroblast – the concentration and other phosphate metabolite parameters have been compared between the controls and every step of the international renal interest company. A multiple regression analysis was performed to determine the predictors of the fibroblast growth factor-23.
Results: The concentrations of the growth of serum fibroblasts-23 have been significantly higher in dogs with stages of IRIS 2, 3 and 4 chronic renal disease than those in dogs in the control group and with the stage. 1 and increase the severity of chronic renal disease. Compared to control dogs, serum parathyroid hormone is considerably increased from increased serum phase 2 and phosphorus concentrations in dogs with stages 4. In dogs with phase 2, growth levels of fibroblasty-23 have increased significantly in hyperphosphatemia relative to those with normophosphatemia. While eight of 26 (30.8%) of dogs with hyperparathyroidism developed by floor 2 (intact parathyroid hormone> 8.5 ng / l), 19 (73.1%) dogs with floor 2 had raised the factor Fibroblast growth-23 over the reference range (> 528 pg / ml). Log Creatinine, intact housing Parathyroid hormone and total accommodation housing total and phosphorus were independent predictors of the log-fibroblast-23 growth factor.
Safety and efficacy of basic fibroblast growth factors for deep second-degree burn patients
Targeting drugs against the fibroblast growth factor factor (s) of cell signaling
Background: Fibroblast growth factor (FGF) The family is composed of 23 highly regulated monomeric proteins regulating a plethora of development and pathophysiological processes, including tissue repair, wound healing, angio-ogeis and the Embryonic development. FGF FGF Growth Factor Receiver Binding (FGFR), a tyrosine kinase re-cek, is facilitated by a glycosaminoglycan, heparin. FGFR activated phosphorylate Tyrosine kinase residues that mediate the induction of downstream signaling pathways, such as Ras-Mapk, PI3K-AKT, PLCγ and STAT. The dysregulation of the FGF / FGFR signaling occurs frequently in cancer due to genes amplification, FGF activation mutations, chromosomal rearrangers, integration and oncogenic fusions. The aberrant FGFR signaling also affects organogenesis, embryonic development, tissue homeostasis and has been associated with cell proliferation, angiogenesis, cancer and other physiological changes.
Objective: This comprehensive review will discuss the biology, chemistry and functions of FGFS and its current applications for healing, diabetes, remedy and regeneration of fabrics and diseases of foie gras. In addition, specific aberrations of the FGFR signaling and the drugs that target FGFR and facilitate the mitigation of various disorders, such as cancer, are also discussed in detail.
Description: FGF-2 Bovine purified from bovine pituitary is a single, glycosylated, polypeptide chain having a molecular mass of 16kDa.;The basic-FGF is purified by proprietary chromatographic techniques.
Description: A sandwich quantitative ELISA assay kit for detection of Bovine Fibroblast Growth Factor 2, Basic (FGF2) in samples from serum, plasma, tissue homogenates, cell lysates, cell culture supernates or other biological fluids.
Description: A sandwich quantitative ELISA assay kit for detection of Bovine Fibroblast Growth Factor 2, Basic (FGF2) in samples from serum, plasma, tissue homogenates, cell lysates, cell culture supernates or other biological fluids.
Conclusion: The inhibitors of the FGFR signaling are promising medicines in the treatment of several types of cancers. The clinical benefits of FGF / FGFR targeting therapies are hindered due to the activation of other RTK signaling mechanisms or mutations that abolish drug inhibitor activity on FGFR. Thus, the development of drugs with different action mechanisms for FGF / FGFR targeting therapies is the recent goal of several preclinical and clinical studies.
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