Objective Nutrition becomes a focus to professionals as an important factor during the development of pressure ulcers.However, there is no evidence for the effectiveness of eternal nutrition support for pressure ulcer prevention .This research aimed to evaluate the effectiveness of eternal nutrition support for pressure ulcer prevention and provide evidence for patients with the risk of pressure ulcer . Methods Key words such as pressure ulcer prevention,eternal nutritional supportwere used to search information in the Cochrane Library , JBI Database of Systematic Reviews , MEDLINE, Web of Science, EMbase, CBMdisc, CNKI and Wanfang Database to collect randomized controlled trials (RCTs).The quality of RCTs was critically appraised and data were extracted by 3 reviewers independently .Meta-analyses were conducted for the eligible RCTs using RevMan 5.0 software, and Stata12.0 software was applied to detect bias or sensitivity analysis to determine the source of heterogeneity if necessary . Results 7 RCTs were includ-ed, among which 1 RCT was excluded by sensitivity analysis .6 RCTs ( n=1553 ) were finally included for meta analysis ( n=728 in trail group, n=825 in control group), and all the patients were given oral nutrition support for 7days to 26 weeks.The results showed that the ulcer incidence in the intervention group reduced by 16%in comparison to the control group (P=0.006).The protein and energy intake in intervention group were higher than those in control group , and the length of stay in hospital was shortened by 16 days. No significant difference was found in the albumin values . Conclusion The enteric nutrition support can reduce the incidence of pressure ulcer obviously with the highest level of evidence , IA .

Objective To explore the application of quantitative DNA analysis in differential diagnosis of benign and malignant breast masses to aid the surgery plan formation.Methods Four hundred and eighty-eight patients with breast mass were enrolled into this study.Tissues of breast mass in patients were gained by fine-needle aspiration puncture.Two sections were made from each sample,one was stained by Papanicolaou for regular cytology analysis and another was stained with Feulgen for quantitative DNA analysis.Pathological results were confirmed in each case after surgery.Results One hundred and sixty-four cases were classified as patients with benign neoplasm,while the other 324 cases were classified as malignant neoplasm,according to the pathological examination results.The sensibility and specificity were 91.4%(296/324) and 92.7%(152/164) for regular cytological method,90.1%(292/324) and 100.0%(164/164) for quantitative DNA analysis method.Meanwhile the positive predictive and negtive value of quantitative DNA analysis was 100.0%(292/292) and 83.7%(164/164),of which regular cytological methods were 96.1%(296/308) and 84.4%(152/180).Conclusion The quantitative DNA analysis might assistant differential diagnosis of benign and malignant breast tumor.

Objective:To investigate the clinical characteristics of E. coli peritoneal dialysis-associated peritonitis (PDAP) and the risk factors for its occurrence and treatment failure.Methods:The clinical data of patients with episodes of PDAP in four general hospitals in Jilin Province from 2013 to 2019 were retrospectively reviewed. According to the pathogenic bacteria, the patients were divided into E. coli and non- E. coli groups. The incidence of E. coli PDAP in the last seven years was calculated and the clinical characteristics were compared between two PDAP groups. Logistic regression was used to analyze the risk factors for the occurrence and treatment failure of E. coli PDAP. Results:A total of 693 PDAP episodes/cases were enrolled in this study, including 100 episodes/cases in the E. coli group and 593 episodes/cases in the non- E. coli group. The incidence rate of E. coli PDAP in the four hospitals showed a decreasing trend during 2013 to 2019. Compared with the non-E.coli group, the proportion of diabetic patients and the average blood albumin levels in the E. coli group were lower ( χ2=5.006, Z=-2.992, P<0.05), while the proportion of refractory peritonitis was higher, and the duration of antibiotic therapy was longer ( χ2=6.350, Z=-2.779, P<0.05). Multivariate Logistic regression analysis showed that history of PDAP ( OR=1.577, 95% CI: 1.015-2.448) and low baseline serum albumin level ( OR=0.958, 95% CI: 0.923-0.995) were independent risk factors for the development of E. coli PDAP, while concomitant diabetes was an independent protective factor for E. coli PDAP ( OR=0.538, 95% CI: 0.330-0.876). Moreover, long-term dialysis was an independent risk factor for treatment failure of E. coli PDAP ( OR=1.047, 95% CI: 1.018-1.076). Conclusion:The incidence rate of E. coli PDAP in study institutions has declined in the past 7 years, but the rate of refractory PDAP is still high. The history of PDAP and low blood albumin level are independent risk factors for the occurrence of E. coli PDAP, while concomitant diabetes is an independent protective factor for the occurrence of E. coli PDAP. Long-term dialysis is an independent risk factor for treatment failure of E. coli PDAP.

Our previous works disclosed the contributing role of macrophage migration inhibitory factor (MIF) and dopaminergic inhibition by lysine dimethyltransferase G9a/Glp complex in peripheral nerve injury-induced hypersensitivity. We herein propose that the proinflammatory cytokine MIF participates in the regulation of neuropathic hypersensitivity by interacting with and suppressing the descending dopaminergic system. The lumbar spinal cord (L-SC) and ventral tegmental area (VTA) are two major locations with significant upregulation of MIF after chronic constriction injury (CCI) of the sciatic nerve, and they display time-dependent changes, along with a behavioral trajectory. Correspondingly, dopamine (DA) content shows the reverse characteristic change to MIF with a time-dependent curve in post-surgical behavior. The levels of both MIF and DA are reversed by the MIF tautomerase inhibitor ISO-1, and a negative relationship exists between MIF and DA. The reversed role of ISO-1 also affects tyrosine hydroxylase expression. Furthermore, CCI induces Th promoter CpG site methylation in the L-SC and VTA areas, and this effect could be abated by ISO-1 administration. G9a/SUV39H1 and H3K9me2/H3K9me3 enrichment within the Th promoter region following CCI in the L-SC and VTA was also decreased by ISO-1. In cultured dopaminergic neurons, rMIF enhanced the recruitment of G9a and SUV39H1, followed by an increase in H3K9me2/H3K9me3. These molecular changes correspondingly exhibited alterations in Th promoter CpG site methylation and pain behaviors. In summary, MIF functions as a braking factor in curbing dopaminergic descending inhibition in peripheral nerve injury-induced hypersensitivity by mediating Th gene methylation through G9a/SUV39H1-associated H3K9 methylation.