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Objective:To investigate the effect of symptom management theory(SMT)-based nursing care for the prevention of postoperative abdominal distension in patients with primary hepatocellular carcinoma.Methods:A total of 80 primary hepatocellular carcinoma patients in the Second Affiliated Hospital of Wenzhou Medical University from May 2016 to May 2019 were assigned to the experimental group and the control group according to the admission time, there were 40 cases in each group. The patients in the control group received routine postoperative nursing care, while the patients in the experimental group added SMT-based intervention. The postoperative first exhaust time and defecation time were recorded; the abdominal distension degree after 1, 3, 7 days of surgery were evaluated. In addition, the symptom distress was assessed by The Symptom Module Specific to Primary Liver Cancer (TSM-PLC).Results:The postoperative first exhaust time and defecation time were (69.08±11.44), (78.80±15.54) h in the experimental group, which were significantly lower than those in the control group (76.03±12.26), (86.03±13.48) h, the differences were statistically significant ( t=2.62, 2.22, both P<0.05). After 3, 7 days of surgery, the abdominal distension degrees were significantly alleviated in the experimental group compared to the control group, the differences were statistically significant ( Z =2.31, 2.34, both P<0.05). After 7 days of surgery, the abdominal distension, weight loss, fever symptom scores in TSM-PLC were 1.80±0.28, 0.76±0.21, 0.48±0.19 in the experimental group, which were significantly lower than those in the control group 2.16±0.31, 0.93±0.25, 0.74±0.20, the differences were statistically significant ( t=5.38, 3.27, 5.90, all P<0.05). Conclusions:SMT-based intervention can promote the recovery of postoperative gastrointestinal function and alleviate abdominal distension symptom distress of patients with primary hepatocellular carcinoma.
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<p><b>OBJECTIVE</b>To assess the associations of death receptor DR4 and DR5 gene polymorphisms with Crohn's disease (CD).</p><p><b>METHODS</b>A total of 295 CD patients and 490 healthy controls were recruited. Three single nucleotide polymorphisms (SNPs) of the DR4 (rs13278062, rs20575) and DR5 (rs1047266) genes were determined with a SNaPshot method. Unconditional logistic regression analysis was carried out for determining the allelic and genotypic differences of the three SNPs between CD patients and the controls, as well as the influence of the DR4 and DR5 gene polymorphisms on the clinical features of CD patients. Linkage disequilibrium and haplotype analysis were calculated by haplotype 4.2 and R language software. A gene-gene interaction model was established to analyze whether the three SNPs can exert a synergistic effect on the susceptibility to CD.</p><p><b>RESULTS</b>The mutant allele (T) and genotype (GT+TT) of DR4 (rs13278062) were increased among CD patients compared to the controls (37.12% vs. 32.04%, P = 0.040, 95%CI: 1.010-1.550; 62.71% vs. 54.90%, P = 0.032, 95%CI: 1.028-1.855, respectively). However, the allelic and genotypic frequencies of DR4 (rs20575) and DR5 (rs1047266) did not differ between the two groups (all P > 0.05). Based on the Montreal Classification Standards, the CD patients were stratified by locations and behaviors of the disease. After multiple comparison correction (P < 0.0125), compared to ileocolonic CD patients respectively, the mutant allele (T) and genotype (GT+TT) of the rs13278062 polymorphism were significantly increased in colonic CD patients (41.04% vs. 25.64%, P = 0.002, 95%CI: 0.315-0.778; 66.04% vs. 41.03%, P = 0.001, 95%CI: 0.196-0.655, respectively) and terminal ileum CD patients (41.44% vs. 25.64%, P = 0.002, 95%CI: 0.311-0.762; 74.77% vs. 41.03%, P < 0.001, 95%CI: 0.126-0.437, respectively). In comparison to penetrating CD patients, the mutant allele (T) and genotype (GT+TT) of DR4 (rs13278062) were significantly decreased in stricturing CD patients (32.29% vs. 48.91%, P = 0.007, 95%CI: 0.300-0.828; 57.29% vs. 86.96%, P = 0.001, 95%CI: 0.078-0.520, respectively). A similar conclusion was drawn for the mutant genotype (GT+TT) of DR4 (rs13278062) in non-stricturing, non-penetrating CD patients (58.82% vs. 86.96%, P = 0.001, 95%CI: 0.086-0.536). Haplotype analysis indicated that the CT haplotype formed by rs20575 and rs13278062 was increased in CD patients compared to the controls (37.1% vs. 31.8%, P = 0.029, OR=1.279, 95%CI: 1.022-1.600). The outcome of a gene-gene interaction model indicated that the mutant genotype (GT+TT) of DR4 (rs13278062) and mutant genotype (CT+TT) of DR5 (rs1047266) may play a negatively synergistic role in CD patients (B = - 0.483, OR = 0.617, P = 0.030).</p><p><b>CONCLUSION</b>The rs13278062 polymorphism of the DR4 gene not only can confer an increased risk for CD, but may also influence the location of the lesions and the disease behaviors. The CT haplotype formed by rs20575 and rs13278062 may be an independent risk factor for CD. Furthermore, the mutant genotype (GT+TT) of DR4 (rs13278062) and mutant genotype (CT+TT) of DR5 (rs1047266) may exert a negative synergistic effect on CD.</p>
Subject(s)
Adult , Female , Humans , Male , Middle Aged , Crohn Disease , Genetics , Epistasis, Genetic , Genetic Predisposition to Disease , Genotype , Haplotypes , Polymorphism, Single Nucleotide , Receptors, TNF-Related Apoptosis-Inducing Ligand , GeneticsABSTRACT
Objective To identify the risk factors of Burkholderia cenocepacia associated nosocomial lower respiratory tract infections (NLRTIs),and to investigate the drug resistance of Burkholderia cenocepacia strains.Methods A total of 138 patients with Burkholderia cenocepacia associated NLRTIs and 40 patients with non-Burkholderia cenocepacia associated NLRTIs were enrolled in the study.All patients were collected from the Second Affiliated Hospital of Wenzhou Medical University during January 2009 and December 2012.Clinical data and results of drug sensitivity tests were retrospectively reviewed.Chi-square test and Logistic regression analysis were performed to identify the risk factors of Burkholderia cenocepacia associated NLRTIs.Results Logistic regression analvsis showed that combination use of 2 or more antimicrobial agents,mechanical ventilation,stay in intensive care unit (ICU) for more than two weeks,use of antacid H2 antagonist and deep venous puncture were the independent risk factors of Burkholderia cenocepacia associated NLRTIs (OR =6.315,5.957,5.254,4.585 and 2.017,P ＜0.05).Burkholderia cenocepacia strains were sensitive to levofloxacin,ceftazidime and sulfamethoxazole; More than 40％ strains were resistant to cefotaxime,ceftriaxone,cefepime,aztreonam and tetracycline; And nearly 100％ strains were resistant to gentamicin,amikacin and tobramycin.Conclusion Burkholderia cenocepacia associated NLRTIs are more likely to occur in patients with combination use of 2 or more antimicrobial agents,mechanical ventilation,and those who stay in ICU for more than two weeks,or received antacid and deep venous punctures,and most Burkholderia cenocepacia strains are multiple drug resistant.
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Objective To investigate the correlations of extracellular matrix and hepatic ultramicrostructural changes with clinical manifestations in patients with mild chronic hepatitis B (CHB).Methods Patients with chronic HBV infections were enrolled and were divided into mild CHB group (n=66) and HBV carrier group (n=10).Serum samples were collected from patients, and serum HBV markers, HBV DNA load and liver fibrosis indexes were measured.All subjects received liver biopsy, and the tissue samples were observed by light microscope and electron microscope.T test and χ2 test were performed for measurement data and enumeration data, respectively.Spearman test was used for ranked data.Results The differences on ALT and AST levels between mild CHB group and HBV carrier group were significant (t=12.42, 7.06, P＜0.05), but there was no significant difference on HBV DNA load between two groups (t=0.24, P ＞ 0.05).Serum liver fibrosis indexes (hyaluronic acid, type Ⅲ collagen,type Ⅳ collagen and laminin protein) in mild CHB group were not significantly higher than those in HBV carrier group (t=0.45, 0.95, 0.76 and 1.21, P ＞0.05).In mild CHB group, there were 33 patients with ≥G2 and ≥S2, but in HBV carrier group were only 2 patients (χ2=4.17, P ＜ 0.05).Seventeen patients in mild CHB group were with S3-4, while that was not observed in HBV carrier group (χ2=4.75, P ＜0.05).In mild CHB group, hepatic ultramicrostrutural changes on fat storing cell, collagen protein and portal area were correlated with fibrosis grades, and the correlation coefficients were 0.351, 0.675 and 0.301, respectively (P=0.004, 0.000 and 0.014).Conclusion Electron microscope is of higher sensitivity than light microscope in observing hepatic ultramicrostructural changes, which is effective in evaluating the severity of mild CHB.
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Objective To evaluate the therapeutic effects of recombinant expression plasmid containing hepatocyte growth factor (HGF) and augmenter of liver regeneration (ALR) on rats with hepatic fibrosis. Methods Ninety Sprague-Dawley rats, which had been established into hepatic fibrosis models, were equally divided into 6 groups: blank group, pcDNA3.1 therapy group,pcDNA3.1-HGF therapy group, pcDNA3. 1-ALR therapy group, pcDNA3.1-HGF and pcDNA3. 1-ALR combined therapy group, and pcDNA3. 1-HGF-ALR therapy group. Zero point one μmol of blank or plasmid was injected into model rats in each group by tail vein once a day for 3 days. Model rats in blank group didn't receive any treatment. Additional 10 rats were chosen as control group, which were not given any interference during the experiment. All rats were sacrificed 4 days after end of treatment. Liver tissues were reserved for observing pathologic changes after HE staining and detecting proliferating cell nuclear antigen (PCNA) and c-jun by immunohistochemistry. Measurement data were compared by single-factor analysis of variance. Comparison between groups was done by SNK test. Enumeration data were analyzed by Fisher's exact test. Results In blank group and pcDNA3.1 therapy group, hyperplasia of fibrous connective tissue was very obvious, false lobules were formed. There was no significant difference between these two groups (x2 =0. 317,P= 1. 000).In the 4 remaining groups, hepatic fibrosis all achieved different degree of amelioration, and the therapeutic effect of pcDNA3.1-HGF-ALR was optimal. In control group, the expressions of PCNA and c-jun in liver tissues were low, with absorbance value of 8.6±1.9 and 3.2 ± 1.2, respectively. In blank group and pcDNA3. 1 therapy group, the expressions of PCNA and c-jun were obviously increased, with absorbance value of 24. 1±3.0, 24.5±4.3 and 23.8±3.1, 24.9±4.2, respectively,which were significant different from control group (all P＜0.01). In the 4 remaining groups, the expressions of PCNA were all obviously increased, and expressions of c-jun were all obviously decreased. The maximum change scope was observed in pcDNA3. 1-HGF-ALR therapy group.Conclusions The recombinant expression plasmid pcDNA3. 1-HGF-ALR can effectively ameliorate experimental hepatic fibrosis of rats. The anti-fibrosis effects are achieved probably by up-regulating PCNA expression and down-regulating c-jun expression.