Objective To investigate the effect of self-designed closed negative pressure drainage combined with sponge dressings on refractory wounds.Methods Sixty patients with phase III-IV pressure ulcers were randomly divided into experiment group and control group in equal number.The self-designed closed negative pressure drainage combined with sponge dressing was applied in the experiment group and in the control group the conventional dressings were used.The two groups were compared in terms of hyperplasia of fresh granulation tissue,time for filling the defect and the healing time and the medical expense.Results Compared to the control group,the time for hyperplasia of fresh granulation tissue,the time for filling the defect and the healing time in the experiment group were all significantly shorter,and the medical expense of the experiment group was significantly less(all P<0.01). Conclusion The self-designed closed negative pressure drainage combined with sponge dressings in the treatment of phase III-IV refractory pressure ulcers may effectively shorten the healing time,improve the curative effects and reduce the economic burden of patients.

The Hedgehog (Hh) signalling pathway is essential for cellular proliferation and differentiation during embryonic development.Gain and loss of function of Hh signalling are known to result in an array of craniofacial malformations.To determine the critical period for Hh pathway antagonist-induced frontal bone hypoplasia,we examined patterns of dysmorphology caused by Hh signalling inhibition.Pregnant mice received a single oral administration of Hh signalling inhibitor GDC-0449 at 100 or 150 mg·kg-1 body weight at preselected time points between embryonic days (E)8.5 and 12.5.The optimal teratogenic concentration of GDC-0449 was determined to be 150 mg·kg-1.Exposure between E9.5 and E10.5 induced frontal bone dysplasia,micrognathia and limb defects,with administration at E10.5 producing the most pronounced effects.This model showed decreased ossification of the frontal bone with downregulation of Hh signalling.The osteoid thickness of the frontal bone was significantly reduced.The amount of neural crest-derived frontal bone primordium was reduced after GDC-0449 exposure owing to a decreased rate of cell proliferation and increased cell death.

OBJECTIVE： To design and synthesize N-aroyl substituted indoline-3-acetic acid derivatives and evaluate their in vitro hypoglycemic activity. METHODS： Using indoline derivative 2-[5-（benzyloxy）-1-（4-chlorobenzoyl）-2-methyl-1H-inclol-3-yl]acetic acid （GY3） as leading compound， 4-（benzyloxy）phenyl hydrazine hydrochloride and methyl 4-oxopentanoate as raw material， 8 kinds of N-aroyl （3-hydroxybenzoyl， 3-cyanobenzoyl， 4-nitrobenzoyl， 4-methylsulfonylbenzoyl， 4-acetamidobenzoyl， 3-acetylaminobenzoyl， isoniacyl and pyridine-2-formyl） substituted indoline-3-acetic acid derivatives were synthesized via 4 steps reactions： Fischer indole cyclization， reduction， amidation and hydrolyzation. The human hepatoma HepG2 cell lines were used to investigate the glucose consumption activity of the target compounds. RESULTS： Totally 8 various N-aroyl substituted indoline-3-acetic acids were synthesized and their structures were confirmed by mass spectrum（MS）， nuclear magnetic resonance 1H-NMR and 13C spectrum. Under the condition of 1.0 μmol/L， the percentage of glucose- promoting consumption of the synthesized compounds on HepG2 cells was 5.4％-9.1％. 2-[（2R， 3S）-5-benzyloxy-2-methyl-1-（4-methylsulfonyl benzoyl）-2，3-dihydro-indole-3-yl] acetic acid showed the best hypoglycemic activity. The percentage of glucose- promoting consumption was （9.1±1.81）％， which was close to that of positive control metformin [（10.58±1.68）％]， but less potent than that of leading compound GY3[（12.15±0.78）％]. CONCLUSIONS： Different electron-withdrawing substituents are introduced into N-aroyl aromatic rings of dihydroindole compounds， such as cyano， nitro， methyl sulfonyl； hypoglycemic activity decreases in varying degrees and is weaker than halogen substituents.

The Hedgehog (Hh) signalling pathway is essential for cellular proliferation and differentiation during embryonic development. Gain and loss of function of Hh signalling are known to result in an array of craniofacial malformations. To determine the critical period for Hh pathway antagonist-induced frontal bone hypoplasia, we examined patterns of dysmorphology caused by Hh signalling inhibition. Pregnant mice received a single oral administration of Hh signalling inhibitor GDC-0449 at 100 mg•kg or 150 mg•kg body weight at preselected time points between embryonic days (E)8.5 and 12.5. The optimal teratogenic concentration of GDC-0449 was determined to be 150 mg•kg. Exposure between E9.5 and E10.5 induced frontal bone dysplasia, micrognathia and limb defects, with administration at E10.5 producing the most pronounced effects. This model showed decreased ossification of the frontal bone with downregulation of Hh signalling. The osteoid thickness of the frontal bone was significantly reduced. The amount of neural crest-derived frontal bone primordium was reduced after GDC-0449 exposure owing to a decreased rate of cell proliferation and increased cell death.
Administration, Oral ; Anilides ; pharmacology ; Animals ; Bone Diseases, Developmental ; chemically induced ; Cell Proliferation ; drug effects ; physiology ; Female ; Frontal Bone ; abnormalities ; Hedgehog Proteins ; antagonists & inhibitors ; Limb Deformities, Congenital ; chemically induced ; Mice ; Micrognathism ; chemically induced ; Osteogenesis ; drug effects ; Pregnancy ; Pyridines ; pharmacology ; Signal Transduction ; drug effects