Diabetic foot ulcer (DFU) is a leading cause of high-level amputation in DM patients, with a low wound healing rate and a high incidence of infection. Vascular endothelial growth factor (VEGF) plays an important role in diabetes mellitus (DM) related complications. This study aims to explore the VEGF expression and its predictive value for prognosis in DFU, in order to provide basis for the prevention of DFU related adverse events. We analyzed 502 patients, with 328 in healing group and 174 in non-healing/recurrent group. The general clinical data and laboratory indicators of patients were compared through Spearman correlation analysis, ROC analysis and logistic regression analysis. Finally, the independent risk factors for adverse prognosis in DFU patients were confirmed. Spearman analysis reveals a positive correlation between the DFU healing rate and ABI, VEGF in wound tissue, and positive rate of VEGF expression, and a negative correlation with DM duration, FPG, HbA1c, TC, Scr, BUN, and serum VEGF. Further logistic regression analysis finds that the DM duration, FPG, HbA1c, ABI, serum VEGF, VEGF in wound tissue, and positive rate of VEGF expression are the independent risk factors for adverse prognosis in DFU (p < 0.05). DM duration, FPG, HbA1c, ABI, serum VEGF, VEGF in wound tissue, and positive rate of VEGF expression are the independent risk factors for prognosis in DFU patients. Patients with these risk factors should be screened in time, which is of great significance to prevent DFU related adverse events and improve outcomes.

BACKGROUND: Migration of keratinocyte plays an essential role in wound healing. The proprietary platelet-rich plasma from human blood, named as self-growth colony (SGC), functions in stimulating migration of wounded keratinocytes. In addition, the growth factors, including VEGF, being enriched in SGC could account for this function. Scutellarin, an active phytochemical from root of Scutellaria barbata D. Don, has been proposed to have various pharmacological functions; however, the activity in epidermal skin cells is yet to be explored. Here, the role of scutellarin in potentiating the functionality of SGC to promote the regeneration of wounded keratinocyte was probed.
METHODS: Molecular docking and ultrafiltration-based LC-MS were performed to verify the binding between scutellarin and VEGF, which potentiated the VEGF-mediated functions. Scratch assay, performed on cultured keratinocytes, was to analyze the treatments of SGC and scutellarin in the process of wound healing. Western blot analysis was to confirm the involvement of signaling cascades in observed effects.
RESULTS: We have identified the binding of scutellarin with VEGF. The binding accounted for the potentiation role of scutellarin in skin regeneration, as triggered by SGC. The co-treatment of scutellarin and SGC onto scratched keratinocyte cultures was able to enhance the process of wound healing, that is, scutellarin showed a potentiating effect to SGC. In addition, the potentiation of scutellarin was shown to be mediated by phosphorylation of VEGF receptor-2 (VEGFR2) and mitogen-activated protein kinase (MAPK) signaling.
CONCLUSIONS: These findings support the application of scutellarin as an enhancing agent in potentiating the SGC-mediated wound healing.

OBJECTIVE: We aimed to observe and investigate the clinical significance of vascular endothelium growth factor (VEGF) levels in exhaled breath condensate (EBC) from patients with acute respiratory distress syndrome (ARDS).
METHODS: An improved EcoScreen condenser was used to collect EBC from 31 ARDS patients on mechanical ventilation and from 22 healthy subjects. Serum and EBC VEGF levels were analyzed with ELISA. VEGF levels in the EBC of patients with different grades of lung injuries were analyzed. The correlation between VEGF levels and clinical indicators was analyzed.
RESULTS: Serum and EBC VEGF levels were linearly and positively correlated with a correlation coefficient of 0.694 (P< 0.01). The VEGF level in the EBC of ARDS patients was significantly lower than that in the control group (P< 0.01). The VEGF level in the EBC of the mild ARDS group was higher than that in the moderate-severe ARDS group (P< 0.01). The VEGF level in the EBC of the survival group was higher than that in the mortality group. The VEGF level in the EBC of ARDS patients was positively correlated with PaO2/FiO2 and PaO2 and was negatively correlated with lung injury score (LIS) and A-aDO2/PaO2.
CONCLUSIONS: The changes in VEGF levels in the EBC of ARDS patients can Respiratory Medicine, reflect the severity of lung injury. Therefore, VEGF level in EBC can be used as an auxiliary index for judging the severity and prognosis of ARDS patients.

OBJECTIVE: This study was to investigate the impact of ranibizumab on the level of intercellular adhesion molecule type 1 (ICAM-1) in the vitreous of eyes with PDR.
METHODS: This is an interventional case-control study. A total of 82 eyes from 82 patients who had undergone vitreous surgery for the treatment of retinal disorders were included. Twenty-two eyes with PDR received an intravitreal ranibizumab injection (IVR) 3-7 days before vitrectomy and were grouped as \'PDR with recent IVR\' or Group 1. Sixteen eyes with PDR received IVR more than 7 days before vitrectomy and were grouped as \'PDR with remote IVR\' or Group 2. Twenty-two matched PDR eyes did not receive IVR before vitrectomy and were grouped as \'PDR without IVR\' or Group 3. Finally, 22 eyes from 22 patients with idiopathic macular pucker (IMP) served as the \'non-diabetic control\' group, or Group 4. Vitreous samples were obtained at the time of vitrectomy from all eyes, and the levels of vascular endothelium growth factor (VEGF) and ICAM-1 were analysed using ELISA.
RESULTS: PDR without IVR (Group 3) had the highest vitreous VEGF concentration; the difference was significant compared with those in the PDR with recent IVR (Group 1), PDR with remote IVR (Group 2) and the non-diabetic control group (Group 4) (p < 0.001). Group 2 had a lower vitreous VEGF level than Group 1 (p = 0.041). Group 1 had the highest vitreous ICAM-1 levels (p < 0.001 versus. Groups 2, 3 and 4); Group 2 had a lower vitreous ICAM-1 level than Group 3 (p = 0.028).
CONCLUSIONS: The vitreous fluid level of ICAM-1 was significantly increased within 1 week of IVR administration, but markedly decreased after a week of administration in eyes with PDR. This suggests that leucostasis, vascular leakage and endothelial dysfunction may be amplified in the early days after IVR, but that a therapeutic effect of IVR in these processes may appear after 1 week of ranibizumab administration in eyes with PDR.

Pim-3 is a member of the provirus integration site for Moloney murine leukemia virus (Pim) family proteins that exhibit serine/threonine kinase activity. Similar to the other Pim kinases (Pim-1 and Pim-2), Pim-3 is involved in many cellular processes, including cell proliferation, survival, and protein synthesis. Although Pim-3 is expressed in normal vital organs, it is overexpressed particularly in tumor tissues of endoderm-derived organs, including the liver, pancreas, and colon. Silencing of Pim-3 expression can retard in vitro cell proliferation of hepatocellular, pancreatic, and colon carcinoma cell lines by promoting cell apoptosis. Pim-3 lacks the regulatory domains similarly as Pim-1 and Pim-2 lack, and therefore, Pim-3 can exhibit its kinase activity once it is expressed. Pim-3 expression is regulated at transcriptional and post-transcriptional levels by transcription factors (e.g., Ets-1) and post-translational modifiers (e.g., translationally-controlled tumor protein), respectively. Pim-3 could promote growth and angiogenesis of human pancreatic cancer cells in vivo in an orthotopic nude mouse model. Furthermore, a Pim-3 kinase inhibitor inhibited cell proliferation when human pancreatic cancer cells were injected into nude mice, without inducing any major adverse effects. Thus, Pim-3 kinase may serve as a novel molecular target for developing targeting drugs against pancreatic and other types of cancer.

OBJECTIVE: To study the effect of Buflomedil on the morphological repair on crush injury of sciatic nerve and also the expression of vascular endothelial growth factor (VEGF).
METHODS: Rat sciatic nerves were crushed by pincers. All of the 400 Sprague Dawley rats were randomly divided into: Sham-operated; saline; saline + VEGF-antibody; Buflomedil; and Buflomedil + VEGF antibody groups. The expression of VEGF in dorsal root ganglia (DRGs), following crush injury to sciatic nerves, was studied by RT-PCR, immunohistochemistry. The effects of Buflomedil on expression of VEGF and repair of neural pathology were also evaluated.
RESULTS: VEGF mRNA was significantly increased in Buflomedil and Buflomedil + VEGF-antibody groups, compared with other groups. The number of VEGF-positive neurons was significantly increased in the Buflomedil and the saline groups. Besides, Buflomedil also caused less pathological changes in DRGs.
CONCLUSIONS: The vasoactive agent Buflomedil may decrease the pathological lesion and improve the functional rehabilitation of peripheral nerves, which may correlate to upregulation of the expression of VEGF, following crush injury to the peripheral nerves.

OBJECTIVE: To investigate retinal vascular endothelial growth factor (VEGF) level and retinal cells apoptosis in the early stage of diabetic NOD mouse retina.
METHODS: Animals were divided into non-diabetes group, (control) (2-, 4-, 6-, 8- and 12-week sub-groups, n=30) and diabetes group (2-, 4-, 6-, 8- and 12-week sub-groups, n=30). Enzyme-linked immunosorbent assay (ELISA) was performed to detect VEGF level in both serum and retina. Transmission electron microscope method was used to examine retinal cell apoptosis.
RESULTS: Compared with the control group, VEGF levels in serum and retina were increased significantly in the NOD group (12 weeks: 4.9±0.4µg/g vs 0.19±0.1µg/g in serum sample, P<0.01; 165±9µg/g vs 17±5µg/g in retinal sample, P<0.01). There exists a positive correlation between serum VEGF and retinal VEGF levels in the early diabetic NOD mice (γ=0.9902, P=0.001). The number of the cells apoptosis in the ganglion cells and endothelium can also been found increased significantly in the NOD group (P<0.01).
CONCLUSIONS: The high VEGF expression may be contributed to increased retinal cells apoptosis. Many factors associated with retinal VEGF expression might involve in the early diabetes stage.