N,N-Dimethylglycine (DMG) is a glycine derivative, and its sodium salt (DMG-Na) has been demonstrated to possess various biological activities, including immunomodulation, free radical scavenging, and antioxidation, collectively contributing to the stability of tissue and cellular functions. However, its direct effects and underlying mechanisms in wound healing remain unclear. In this study, a full-thickness excisional wound model was established on the dorsal skin of mice, and wounds were treated locally with DMG-Na. Wound healing progression was assessed by calculating wound closure rates. Histopathological analysis was conducted using hematoxylin-eosin (HE) staining, and keratinocyte proliferation, migration, and differentiation were evaluated using CCK-8 assays, scratch wound assays, and quantitative reverse transcription PCR (qRT-PCR). Inflammation-related cytokine expression in keratinocytes was analyzed via ELISA and qRT-PCR. Results revealed that DMG-Na treatment significantly accelerated wound healing in mice and improved overall wound closure quality. The wound healing rates on days 3, 6, and 9 were 49.18%, 68.87%, and 90.55%, respectively, with statistically significant differences compared to the control group ( P<0.05). DMG-Na treatment downregulated the mRNA levels of keratinocyte differentiation markers while enhancing cell proliferation and migration ( P<0.05). Furthermore, DMG-Na decreased the secretion of LPS-induced keratinocyte inflammatory cytokines, including IL-1β, IL-6, IL-8, TNF-α, and CXCL10 ( P<0.05). These findings indicate that DMG-Na regulates inflammatory responses and promotes keratinocyte proliferation and migration, thereby facilitating the healing of skin wounds.
Animals ; Wound Healing/drug effects* ; Mice ; Cell Proliferation/drug effects* ; Keratinocytes/drug effects* ; Cell Movement/drug effects* ; Cell Differentiation/drug effects* ; Glycine/pharmacology* ; Skin/injuries* ; Male

OBJECTIVETo establish a method for determining 2, 4-D butylate in serum by gas chromatography (GC)and to provide a basis for the diagnosis and treatment of clinical poisoning.

METHODSSerum 2, 4-D butylate level was determined by the following steps: mixing serum (0.5 ml)with trichloromethane (2.0 ml), adequately shaking for extraction, standing for 5 min, centrifuging at 4 000 rpm for 10 min, blow-drying the trichloromethane layer with nitrogen, adding ethanol (50 µl)to a certain volume, adding the sample (1.0 µl), and performing GC with a hydrogen flame ionization detector.

RESULTSSerum 2, 4-D butylate level showed a linear relationship within 5∼40 µg/ml, with a regression equation of y = 1 831.6.4x-899.4 (r = 0.999 2); the minimum detectable concentration was 1.0 µg/ml. The recovery rate was 88.7%∼103.0% (relative standard deviation (RSD) 3.8%∼5.0%). The intra-day RSD and inter-day RSD were 3.87-4.92% and 3.33%∼5.34%, respectively.

CONCLUSIONThis determination method is simple, efficient, and accurate and provides a good means for rapid diagnosis and treatment of 2, 4-D butylate poisoning.

Chromatography, Gas ; methods ; Humans ; Serum ; chemistry ; Thiocarbamates ; blood

Objective To investigate the clinical feature of Acinetobacter baumannii and to provide the basis for clinical rational use of anti-microbial agents.Methods ATB system was used to identify Acinetobacter baumanii, and antimicrobial resistance was determined by Kirby-Bauer method.The results were analyzed by Whonet 5.4 soft-ware.Results A total of the 358 strains Acinetobacter baumannii were isolated,91.62% were from sputum and throat swab.The main departments was ICU(52.23%);In 358 strains Acinetobacter baumannii,217 strains were multi-drug resistant strains(60.61%).The drug resistance to polymyxin B was the lowest 0% followed by minocy-cline 19.8% and cefoperazone/sulbactam 9.8%, the next was netilmicin 21.1% and meropenem 41.5%. Conclusion Acinetobacter baumannii shows multi-drug resistance, especially in ICU.Anti-microbial agents should be the rational use according to the results of drug susceptibility in order to reduce and control the incidence of noso-comial infections.