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Objective:To investigate and analyze the distribution of pathogens and to explore the related risk factors of infections in burn patients in order to provide theoretical basis for effective prevention and treatment of wound infections in burn patients.Methods:A total of 245 burn patients, admitted to the PLA 926 Hospital from January 2016 to December 2020, were selected. The pathogens and antimicrobial susceptibility of the wound secretions were tested and the clinical data of burn patients were collected. The risk factors of burn wound infection were screened by single factor comparison method and multivariate logistic regression.Results:Among the 245 burn patients, 184 patients were with bacterial infections, the infection rate was 75.10% (184/245), and 79 patients were multi-drug resistant, accounting for 42.93%(79/184). A total of 367 strains of pathogens were isolated from wound secretions in the 184 patients, among which 72 (19.62%, 72/367) strains were gram-positive bacteria, mainly Staphylococcus aureus (11.44%, 42/367), 283 (77.11%, 283/367) strains were gram-negative bacteria, mainly Pseudomonas aeruginosa (20.16%, 74/367) and Acinetobacter baumannii (19.89%, 73/367), and 12 (3.27%, 12/367) strains were fungi, mainly Aspergillus (1.91%, 7/367). The results of drug sensitivity tests showed that the pathogens of burn patients were highly resistant to common antibiotics. Monofactor analysis showed that age(χ 2=8.629, P=0.013), burn area (χ 2=21.504, P=0.002), wound depth (χ 2=17.139, P=0.000), hypovolemic shock (χ 2=21.112, P=0.000) and length of hospital stay (χ 2=21.967, P=0.000) were the related risk factors for wound infections. Multivariate logistic regression analysis showed that ages below 4 years old or over 69 years old ( OR=8.414,95% CI:2.971-23.830, P=0.000), burn area>30% ( OR=5.672,95% CI:1.029-31.272, P=0.046), Ⅲ degree wound ( OR=4.069,95% CI:1.396-11.858, P=0.010), length of hospital stay≥15 days ( OR=2.593,95% CI:1.091-6.162, P=0.031) were the independent risk factors of wound infections in burn patients. Conclusions:The incidence of wound infection and multi-drug resistance is relatively high in burn patients, and the pathogens are mainly gram-negative bacteria. Age, burn area, burn wound depth and length of hospital stay are the high-risk factors for wound infections, and taking effective preventive measures according to risk factors can reduce the occurrence of wound infections and hospital infections.
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Enlarged facial pores remain a common skin concern. Its occurrence is mainly associated with increased sebum production, skin aging (skin laxity and decreased skin elasticity) , increased hair follicle size and other factors, and current treatments for enlarged facial pores mainly target these factors. This review retrospectively summarizes current common treatments, including oral antiandrogens, topical retinoids, chemical peels, lasers, radiofrequency and focused ultrasound. The increasing development of photoelectric devices offers newer and more reliable choices.
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<p><b>OBJECTIVE</b>To investigate the protective effects of small dose of dopamine on the intestinal mucosa of scalded rats in shock stage.</p><p><b>METHODS</b>Wistar rats inflicted by 30% TBSA of III degree scalding were employed as the model. The rats were pre-placed with cardiac catheter before and were resuscitated intravenously after injury. The scalded rats were treated by routine (control) and small dose of dopamine (3 micro g.kg(-1).min(-1)), respectively. The changes of rat serum levels of diamine oxidase (DAO), malondialdehyde (MDA) and lactic acid (LA) were observed after treatment. And the pathomorphological changes of the intestine were scored.</p><p><b>RESULTS</b>The general condition of the rats with dopamine treatment in shock stage was better than that in control group. The rat serum levels of MDA, LA and DAO decreased obviously, especially during 3 to 12 postburn hours (PBHs) after treatment by small dose of dopamine. The pathomorphological scoring of ileum in dopamine treating group was better than that in control.</p><p><b>CONCLUSION</b>The intestinal mucosa of severely scalded rats in shock stage could be well protected by small dose of dopamine.</p>
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Animals , Male , Rats , Burns , Pathology , Disease Models, Animal , Dopamine , Pharmacology , Intestinal Mucosa , Physiology , Protective Agents , Pharmacology , Rats, WistarABSTRACT
Objective To investigate the role of bacterial DNA in systemic inflammatory response syndrome (SIRS). Methods A total of 100 mice of Kunming species were divided into ten groups: E.coli DNA (30, 20, 10, 5 and 1 mg/kg ), 30 mg/kg of CT DNA, 60Co DNA, DNased DNA, organic residue of DNA extraction and sterile water control. The last two were pre-treated with D-galactoamine (600 mg/kg intra peritoneally). Animals were administratively injected via tail vein. General physical condition and the death rate of mice were observed within 48 h. Results ①Obvious lethal effect of double strand E.coli DNA on mice were observed with a dose-effect correlation, LD50=11.51 mg/kg. ②NO difference in death rate was found in the group of 30 mg/kg E.coli DNA with or without 60Co irradiation (10/10 and 8/10,P>0.05). ③No rats died in the group of DNased DNA, organic residue of DNA extraction and calf thymic DNA (0/10). Conclusion Bacterial DNA may play an important role in the development of SIRS.
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AIM: To investigate whether the bacterial DNA participates in SIRS and its possible mechanism. METHODS: Escherichia coli genomic DNA (EC DNA) was extracted and purified from Escherichia coli 25922 by alkaline lysis method. Mortality of mice challenged with EC DNA and the changes of TNF-? and IL-6 in rat serum were observed. ANA-1 cells were cultured in vitro, after the cells were stimulated by different concentrations of EC DNA and LPS, the level of TNF-? and IL-6 in supernatant were tested. Meanwhile,expression of TLR9 and TLR4 on cell surface was measured. Activation of NF-?B was also observed. RESULTS: The lethal effect of EC DNA on mice with an obvious dose-effect relationship was observed. The death happened within 24 hours. Calf thymus DNA and DNase I-treated EC DNA did not lead to mice to die. The changes of serum TNF-? and IL-6 in rats induced by EC DNA and LPS were similar, but TNF-? peak level of EC DNA group appeared 1 hour earlier than that of LPS group. In vitro, large amount of TNF-? and IL-6 were released from ANA-1 cells stimulated by EC DNA. High expression of TLR9 and TLR4 was observed on surfaces of THP-1 cells. In particularly, LPS induced strong activation of NF?B. The results suggested other pathway possibly took part in the signal transduction inducea by EC DNA. CONCLUSION: EC DNA has the abilities to lead to death of mice, and induces serum TNF-? and IL-6 level to increase in rats and ANA-1 cells to release cytokines in vitro. High expression of TLR9 and TLR4, strong activation of NF-?B may be its important molecular mechanism, but other pathway probably exists to play an important role.