Effect of ultrasound-guided stellate ganglion block on perioperative inflammatory responses and postoperative recovery of gastrointestinal function in patients undergoing gastrointestinal surgery / 中华麻醉学杂志

Objective To investigate the effect of ultrasound-guided stellate ganglion block ( SGB) on perioperative inflammatory responses and postoperative recovery of gastrointestinal function in patients un-dergoing gastrointestinal surgery. Methods Fifty-five American Society of Anesthesiologists physical classⅠ-Ⅲpatients of both sexes, aged 18-64 yr, weighing 50-75 kg, undergoing elective gastrointestinal sur-gery, were divided into SGB group ( n=18) and control group ( C group, n=37) using a random number table method. Ultrasound-guided SGB was conducted with 0. 5％ ropivocaine 7 ml at the left C6 level in SGB group. The equal volume of normal saline was given under ultrasound guidance at the same site in C group. Peripheral venous blood samples were collected at 5 min before SGB and 2, 4 and 24 h after SGB for deter-mination of plasma tumor necrosis factor-α ( TNF-α) , interleukin ( IL)-1β and IL-6 concentrations by en-zyme-linked immunosorbent assay. The increased level of leukocyte count ( leukocyte count at 24 h after SGB-leukocyte count at 24 h before SGB) was recorded. The recovery time of bowel sounds and anal or sto-ma exhaust time were also recorded. Results Compared with C group, the concentrations of TNF-αat 2 h after SGB and IL-1βat 2, 4 and 24 h after SGB were significantly decreased, the increased level of leuko-cyte count was decreased, and the recovery time of bowel sounds and anal or stoma exhaust time were short-ened in SGB group ( P<0. 05) . Conclusion Ultrasound-guided SGB can reduce perioperative inflammato-ry responses and promote the recovery of postoperative gastrointestinal function in the patients undergoing gastrointestinal surgery.

Feasibility of developing HAP risk warning model in critically ill patients based on genomic copy number polymorphisms of DEFA1/DEFA3 / 中华麻醉学杂志

Objective To evaluate the feasibility of developing hospital acquired pneumonia (HAP) risk warning model in critically ill patients based on genomic copy number polymorphisms (CNPs) of the genes encoding human neutrophil peptides 1-3 (DEFA1/DEFA3).Methods Seventy-seven HAP patients (group HAP) and 109 non-HAP patients of matched age and sex in intensive care unit (ICU) (group NHAP) were enrolled in the study.The genomic CNPs of DEFA1/DEFA3 was determined by realtime quantitative polymerase chain reaction after extracting DNA from peripheral blood samples.The source of patients,condition of endotracheal intubation within 24 h after admission to ICU,Acute Physiology Score,Acute Physiology and Chronic Health Evaluation Ⅱ score,Sequential Organ Failure Assessment score,mechanical ventilation time,length of hospital and ICU stay and outcomes were obtained.The predictive model was developed using logistic regression through combining DEFA1/DEFA3 copy numbers and clinical characteristics (Acute Physiology Score and source of emergency) within 24 h after admission to ICU.The receiver operating characteristic curve was used to evaluate the predictive efficacy of the model.Results The copy numbers of DEFA1/DEFA3 were significantly lower in HAP group than in NHAP group (P ＜0.05).The area under the receiver operating characteristic curve of the predictive model developed through combining the DEFA1/DEFA3 copy numbers with clinical characteristics was 0.789 (95％ CI 0.724-0.854) when the model was used for predicting HAP.Conclusion CNPs of DEFA1/DEFA3 can be used to develop the HAP risk warning model in critically ill patients.

Association of single nucleotide polymorphism in exon of transient receptor potential melastatin 2 gene with sepsis / 浙江大学学报·医学版

To investigate the association between single nucleotide polymorphism (SNP) in the 11th exon of transient receptor potential melastatin 2 (TRPM2) gene with the susceptibility and outcome of sepsis.A total of 119 septic patients and 112 normal subjects were enrolled from the First Affiliated Hospital, Zhejiang University School of Medicine. Among 119 septic patients, 62 died (fatal group) and 57 survived (survival group) within 28 days of disease onset. The genotypes of these individuals were detected using TaqMan allelic discrimination assays, and its correlations with susceptibility and outcome of sepsis were analyzed.There was no significant difference in genotype frequencies and allelic frequencies of TRPM2 SNP rs1556314 between septic patients and the controls (all>0.05). And no significant difference in genotype frequencies and allelic frequencies of TRPM2 SNP rs1556314 was observed between the survivors and fatal cases of septic patients (all>0.05).The TRPM2 SNP rs1556314 does not have significant association with sepsis, but this result need to be confirmed by large scale studies.

Correlation of human β-defensin 1 gene polymorphism with fungal susceptibility to severe sepsis / 中华创伤杂志

Objective To investigate the correlation between gene polymorphism within human β defensin 1 (DEFB1) and fungal susceptibility to severe sepsis through case-control association study.Methods A total of211 patients with severe sepsis in ICU were enrolled in the present case control study. Sepsis in this study was diagnosed according to the definition of American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference in 1992 and 2002. Based on the development of fungal infection during ICU stay, all 211 patients were divided into fungal infection group (Group Ⅰ) and control group (Group C). Alleles and genotypes of-1816A/G, -390A/T, -52A/G, -44C/G and-20A/G within DEFB1 gene were assayed in all 211 patients by means of DNA direct sequencing, Allele-specific PCR amplifications or high-throughput site-specific TaqMan assay. Genetic analysis was employed to calculate the distribution frequency of haplotypes. The correlation between the genomic variations (allele,genotype and haplotype) and fungal infection was analyzed by Chi-square test or Fisher's exact test.Odds ratio (OR) was employed to reflect the correlation degree of genetic factor with fungal susceptibility to severe sepsis. Results Group Ⅰ enrolled 80 patients, of whom 43 pstients were male, at age of (60.81 ± 18.30) years. Group C enrolled 131 patients, of whom 80 patients were male, at mean age of (60.42 ± 17.03) years. No significant difference was found between two groups in aspect of gender and age (P＞0.05). The genetic locus of -1816A/G, -390A/T, -52A/G, -44C/G and -20A/G of both groups were in agreement with Hardy Weinberg equilibrium. No significant difference was found between two groups in the distribution of allelic frequencies and genotype frequencies (P ＞0.05). No significant difference was found in the distribution frequency of four common haplotypes of the above five genetic locus such as AAACG, ATGCA, GTGGG and ATACG (all P ＞ 0.05). Conclusions Genetic locus of -1816A/G, -390A/T, -52A/G, -44C/G and-20A/G within DEFB1 gene have no correction with fungal infections in severe sepsis, suggesting that DEFB1 gene polymorphism may not serve as a key genetic marker for the predisposition to fungal infection in severe sepsis.