Chronic foot wounds are a leading cause of morbidity and hospitalization for patients with diabetes. Negative pressure wound therapy (NPWT) is known to promote healing of diabetic foot wounds, but the underlying molecular mechanisms remain elusive. We propose to gain molecular insights into the wound healing promoting signals underlying the effects of NPWT on diabetic foot wounds in humans. We assessed 30 patients with diabetic foot ulcers. Of these cases, 15 were treated with NPWT, while 15 patients were treated with traditional gauze therapy. Granulated tissue was harvested before and after treatment in both patient groups and histologically analyzed with hematoxylin & eosin as well as Masson's trichrome staining methods. Immunohistochemistry and Western blot analysis was performed to evaluate expression of basic fibroblast growth factor (bFGF) and extracellular signal-regulated kinase (ERK)1/2, previously associated with promoting cellular growth and/or wound healing. Unlike controls, the wounds in the NPWT-treated diabetic patients developed characteristic features of granulated tissue with increased collagen deposition. Immunohistochemical analysis also revealed an increase in bFGF levels in NPWT-treated patients. Western blot analysis further showed a significant up-regulation of bFGF and phosphorylated ERK1/2 protein levels in the NPWT-treated diabetic patients vs. controls. Our studies reveal that NPWT is associated with an up-regulation of bFGF and ERK1/2 signaling, which may be involved in promoting the NPWT-mediated wound healing response.
The aim of this study was to explore the clinical value of ultrasonic monitoring in the assessment of pulmonary recruitment and the best positive end-expiratory pressure (PEEP).Between January 2015 and June 2017, 40 patients with acute respiratory distress syndrome in our hospital were randomly divided into 2 groups: ultrasound group (ULS group; n = 20) and oxygenation group (OXY group; n = 20). The PEEP incremental method was used to perform recruitment maneuvers. Ultrasound scoring and the oxygenation method were used to evaluate the pulmonary recruitment endpoint. The best PEEP was chosen by ultrasound scoring and the oxygenation method after achieving the pulmonary recruitment endpoint and sustaining it for 15 minutes.The oxygenation index, PEEP, peak airway pressure (Ppeak), mean airway pressure (Pmean), and dynamic compliance (Cdyn) in the OXY group were significantly lower than those in the ULS group (P < .05) at the pulmonary recruitment endpoint; however, there was no statistical significance in the mean arterial blood pressure (MAP) or heart rate (HR) (P > .05). The best PEEPs in the OXY and ULS groups were 13.1 ± 3.1 and 15.7 ± 4.2 cmH2O, respectively, with a significant difference between the 2 groups (t = 2.227, P = .016). Compared with the basal state, the Cdyn, oxygenation index, Pmean, and Ppeak in both groups significantly increased after pulmonary recruitment (P < .05). Furthermore, the Cdyn and oxygenation index in the ULS group were significantly higher than those in the OXY group after pulmonary recruitment (P < .05). The HR in both groups significantly increased, and the MAP significantly decreased. Two hours after recruitment, the HR and MAP returned to near basal levels without a significant difference between the 2 groups (P > .05).Lung ultrasound can be used to detect the endpoint of lung recruitment and the best PEEP, with good effects on lung compliance and oxygenation improvement.
BackgroundReports on the association between growth hormone deficiency (GHD) and cardiovascular risk factors in children are limited. We aim to investigate the effect of different doses of recombinant human growth hormone (rhGH) therapy on blood lipid and carotid intima-media thickness (cIMT) in Chinese GHD children.MethodsNinety children, including sixty isolated GHD children and thirty healthy children, were enrolled. GHD children were randomly divided into two groups (A and B) according to the rhGH dose given: group A received 0.23 mg/kg/week and group B received 0.35 mg/kg/week for 12 months. The TC, TG, LDL-C, HDL-C, and cIMT at baseline and after treatment were measured.ResultsThe height, weight, and height velocity improved significantly over 12 months of rhGH therapy in all GHD children. At baseline, GHD children in both the treatment groups showed significantly higher total cholesterol (TC), triglyceride (TG), low-density lipoprotein-cholesterol (LDL-C), cIMT, and lower high-density lipoprotein-cholesterol (HDL-C) than healthy children (all P≤0.033). After the 12-month rhGH therapy, a significant decrease in the TC, TG, LDL-C, and cIMT, as well as a significant increase in the HDL-C (P≤0.046), was observed in the GHD children, with change in the group B being even more marked.ConclusionsThe RhGH replacement therapy in GHD children can improve both the blood lipid profile and carotid intima-media thickness, with higher-dose rhGH therapy showing superior effects.
Aims: Whether pioglitazone (PIO), a peroxisome proliferator-activated receptor-gamma agonist, increases the risk of developing bladder cancer has been debated for several years. The aim of this study was to investigate the in vitro effects of PIO on normal urothelial transitional epithelium (NUTE) cells and bladder cancer (J82) cells to further evaluate the risk.Methods: NUTE cells were obtained from Sprague-Dawley rats. NUTE and J82 cells were treated with different concentrations of PIO for various time periods. Cell proliferation was tested by the MTT assay. Cell apoptosis was evaluated by flow cytometry. The expressions of p53, cyclin D1, Bcl-2, and Bax were determined by qRT-PCR and western blots.Results: After 24 hours, the treatment of NUTE cells with 10 μmol/L PIO led to morphological changes, without changes in J82 cells. Moreover, PIO inhibited the proliferation and induced apoptosis of NUTE cells, but not J82 cells, in a time- and dose-dependent manner. However, PIO did not alter the growth of cells from other tissues. In addition, treatment with PIO for up to 72 hours did not result in changes in the expressions of p53, cyclin D1, Bcl-2, and Bax in NUTE cells and J82 cells. Interestingly, PIO significantly downregulated the protein levels of p53 and cyclin D1 in J82 cells, but not NUTE cells after more than 192 hours of treatment.Conclusions: PIO did not promote malignant alterations of NUTE cells or stimulate proliferation of J82 cells. PIO decreased the expression of p53 and cyclin D1 in J82 cells after long-term culture, which suggested that PIO may be helpful for diabetic patients with bladder cancer.
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