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Fibroblast Growth Factor 2* ; Humans ; Pilot Projects*

PURPOSE: The production of basic fibroblast growth factor (bFGF) which is known to have a strong angiogenic activity in gastric cancer, was evaluated. METHODS: Using alkaline phosphoatase - labelled, synthetic oligonucleotide probe of bFGF genes, the expression of the gene was evaluated in 9 fresh advanced gastric cancer tissues by using in-situ hybridization. RESULTS: In-situ hybridization of bFGF mRNA showed a positive reaction in 8 of 9 patients. CONCLUSION: Basic fibroblast growth factor is expressed in 88% of gastric cancer tissues. In view of the profuse expression of angiogenic growth factor, future therapeutic targeting for angiogenesis could be reasonable in patients with gastric cancer.
Fibroblast Growth Factor 2 ; Humans ; RNA, Messenger ; Stomach Neoplasms*

PURPOSE: We investigated the effect of basic fibroblast growth factor (bFGF) on the vascularization rate of Medpor(R), a synthetic polyethylene orbital implant. METHODS: Medpor(R), pretreated or untreated with bFGF (25 ng/ml), was inserted into one eye of 18 New Zealand white rabbits and removed at 1, 2, and 4 weeks after implantation, and stained with hematoxylineosin and Masson's trichrome. Degree of vascularization was classified into zone 1 (2 (1.6~3.0 mm ingrowth), zone 3 (3.1~4.5 mm ingrowth), and zone 4 (>or=4.6 mm ingrowth). RESULTS: One and two weeks after implantation, the percentage of the vascularization area were 56.25% and 68.75% in bFGF-untreated group, while those of bGFG-treated group were 75% and 80.56% respectively, but there were no statistical difference between bFGF-untreated and treated group. However, four weeks after implantation it was significantly higher in bFGF-treated group (84.38%) than in bFGFuntreated group (66.25%) (P<0.05). CONCLUSIONS: BFGF enhanced more and early fibrovascular ingrowth of Medpor(R).
Fibroblast Growth Factor 2* ; Orbit* ; Orbital Implants ; Polyethylene* ; Rabbits

OBJECTIVE: To investigate the correlation of serum bFGF level with MDS typing, serum IL-32 and prognosis. METHODS: A total of 62 patients with myelodysplastic syndromes admitted in our hospital from April of 2014 to April of 2017 were enrolled in MDS group. And 50 healthy people who received healthy physical examination in our hospital were selected as the control group at the same period. According to the type of disease, the MDS group was divided into 4 subgroups: A, B, C, D. the serum levels of bFGF, and IL-32 were detected, and the prognosis of patients with different MDS types was evaluated. RESULTS: The serum levels of bFGF and IL-32 in 4 subgroups of MDS were higher than those in the control group (P<0.05). the serum level of bFGF and IL-32 was not significanty different between subgroup A and B (P>0.05), and the serum levels bFGF and IL-32 also was no significantly different between subgroup C and D (P>0.05), but the serum levels of bFGF and IL-32 in subgroup C and D were significantly higher than those in subgroup A and B (P<0.05). The total efficiency of clinical treatment was not significantly different between subgroup A and B (P>0.05),but significantly higher than that in the other 2 subgroups (P<0.05). CONCLUSION The serum levels of bFGF and IL-32 in MDS patients were significantly higher than that in the normal controls, while the serum levels of bFGF and IL-32 in RAEB and RAEB-t subtypes were significantly higher than that in RA and RAS. The changes of serum bFGF and IL-32 levels are positively correlative.
Fibroblast Growth Factor 2 ; Humans ; Interleukins ; Myelodysplastic Syndromes ; Prognosis

Pfeiffer syndrome is a rare autosomal dominant disorder characterized by coronal craniosynostosis, brachycephaly, mid-facial hypoplasia, and broad and deviated thumbs and great toes. Pfeiffer syndrome occurs in approximately 1:100,000 live births. Clinical manifestations and molecular genetic testing are important to confirm the diagnosis. Mutations of the fibroblast growth factor receptor 1 (FGFR1) gene or FGFR2 gene can cause Pfeiffer syndrome. Here, we describe a case of Pfeiffer syndrome with a novel c833_834GC>TG mutation (encoding Cys278Leu) in the FGFR2 gene associated with a coccygeal anomaly, which is rare in Pfeiffer syndrome.
Acrocephalosyndactylia ; Craniosynostoses ; Live Birth ; Molecular Biology ; Receptor, Fibroblast Growth Factor, Type 1 ; Receptor, Fibroblast Growth Factor, Type 2 ; Thumb ; Toes

OBJECTIVETo observe the alteration of fibroblast growth factor 10 (Fgf10) and fibroblast growth factor receptor 2 (Fgfr2b) signal in mouse embryonic palate after dexamethasone and vitamin B12 exposure.

METHODSDams were divided teratogenetic group, antagomistic group and control group and were respectively injected dexamethasone, dexamethasone and vitamin B12, and normal sodium. Dams were killed and fetus was collected at embryo 12.5 and 13.5 day. The expression of Fgf10 and Fgfr2b and mesenchymal cells proliferation of mouse embryonic by western blotting and BrdU assay were checked.

RESULTSFgf10 and Fgfr2b expression was down-regulated and mesenchymal cells proliferation was inhibited significantly after dexamethasone exposure. After vitamin B12 treatment, Fgf10 and Fgfr2b expression did not restore, but cells proliferation was recovered.

CONCLUSIONDexamethasone and vitamin B12 affected the expression of Fgf10 and Fgfr2b of mouse embryonic palate and mesenchyme cells proliferation, but the change was disaccord.

Apert syndrome is an uncommon congenital disorder characterized by malformation of the skull in association with symmetrical syndactyly of both hands and feet. This syndrome is autosornal dominant. The original description was presented by Apert in 1906. Since then more than 200 cases have been reported in the world. Recently, we experienced a case of newhorn male infant with congenital anomalies of the skull and extremities. Molecular biologically, he was found to have Ser252Try mutation in the FGFR2 exonIIIa. A brief review of literature was made.
Acrocephalosyndactylia ; Congenital, Hereditary, and Neonatal Diseases and Abnormalities ; Extremities ; Fibroblast Growth Factors* ; Fibroblasts* ; Foot ; Hand ; Humans ; Infant ; Male ; Receptor, Fibroblast Growth Factor, Type 2* ; Receptors, Fibroblast Growth Factor* ; Skull ; Syndactyly

PURPOSE: To investigate the effects of commodified growth factor products used clinically on fibrovascular ingrowth into porous polyethylene orbital implants. METHODS: Porous polyethylene orbital implant sheets (Medpor(R)) soaked with Nepidermin (Easyef(R)), Trafermin (Fiblast(R)), and normal saline were implanted into the backs of 18 Sprague-Dawley rats. The degree of fibrovascular ingrowth as observed using a light microscope was compared 1 and 2 weeks after implantation and was calculated as a percentage of the fibrovascular ingrowth length. RESULTS: One week after implantation, the percentage of fibrovascular ingrowth length was 25.33 +/- 5.43%, 22.56 +/- 5.30%, and 21.78 +/- 4.66% in the Easyef(R)-, Fiblast(R)- and normal saline-soaked groups. The degree of fibrovascularization was higher in the Easyef(R)-soaked group than in the other groups (p = 0.020, 0.012). Two weeks after implantation, the degree of fibrovascularization was 98.33 +/- 5.00%, 100.00 +/- 0.00%, and 95.89 +/- 4.57%, which was significantly higher in the Easyef(R)-, and Fiblast(R)-soaked groups than in normal saline-soaked group (p = 0.019, <0.001). CONCLUSIONS: Commodified growth factor products used in other areas selectively enhanced fibrovascular ingrowth to a greater degree and earlier in ophthalmic plastic and reconstructive surgery.
Epidermal Growth Factor ; Fibroblast Growth Factor 2 ; Orbital Implants* ; Plastics ; Polyethylene* ; Rats, Sprague-Dawley

OBJECTIVETo investigate the effects of bioactive glasses (BG) including 45S5 and nano-58S on proliferation, angiogenic markers vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) secretion and gene expression of human dental pulp cells (HDPC).

METHODSHDPC of 4th passage were cultured in Dulbecco's modified Eagle's medium (DMEM) which contained 0.1 g/L 45S5 or nano-58S ionic dissolution products. Meanwhile HDPC were cultured in DMEM without BG as control group. Proliferation of the cells was evaluated with methyl thiazolyl tetrazolium (MTT) assay on day 1, 2, 3. Quantitative real-time PCR and quantitative sandwich enzyme immunoassays were used to test VEGF and bFGF gene expression and protein secretion of HDPC on day 1, 2, 3.

RESULTSThe relative growth rate (RGR) of 45S5 and nano-58S groups were (134.5 ± 5.0)% and (146.3 ± 19.8)%, which was significantly different from that of control group (P < 0.05). The quantity of VEGF secretion of two experimental groups were (189.29 ± 4.64) and (216.18 ± 14.67) ng/L, respectively, significantly higher than that of the control group [(159.03 ± 11.69) ng/L] (P < 0.05). Furthermore, the nano-58S group secreted much more VEGF than 45S5 group (P < 0.05).bFGF secretion of HDPC was also enhanced by both 45S5 and nano-58S bioactive glasses. The VEGF gene expression of 45S5 and nano-58S on day 1 were (1.70 ± 0.19) and (1.63 ± 0.42), while the bFGF gene expressin on day 3 were (1.49 ± 0.02) and (2.30 ± 0.04), all significantly higher than that of control group (P < 0.05).

CONCLUSIONSBioactive glasses can enhance the proliferation, VEGF and bFGF secretion and gene expression of human dental pulp cells. Compared with 45S5, nano-58S showed a higher activation.

OBJECTIVEThis study aimed to investigate the effects of hirudin on the expression of transforming growth factor (TGF-β1) and basic fibroblast growth factor (bFGF) in human gingival fibroblasts (HGFs) in vitro, as well to explore its func- tion in the mechanism of gingival remodeling.

METHODSAfter culturing was performed with classic tissue-explant method, HGFs were derived from normal gingival and gingival hyperplasia tissues followed by orthodontic treatments with different concentrations of hirudin. The mRNA and protein expression levels of TGF-β1 and bFGF were respectively detected by real time quantity polymerase chain reaction and immunocytochemistry.

RESULTSCompared with normal HGFs, TGF-β1 expression promoted collagen synthesis of fibroblasts, whereas bFGF collagen synthesis was decreased in hyperplasia HGFs without hirudin (P < 0.05). Hirudin significantly upregulated the expression levels of bFGF but downregulated TGF-β1 in hyperplasia HGFs (P < 0.05).

CONCLUSIONOrthodontic force may influence the balance of collagen synthesis and degradation in HGFs. Hirudin may modulate the balance of HGF collagen metabolism, thereby promoting gingival remodeling.