Objective To evaluate the effect of nurse-led follow-up on medication adherence and quality of life for breast cancer patients receiving adjuvant hormonal therapy.Methods A randomized controlled trial was conducted with 157 patients in the intervention group and 154 in the control group.A self-design web-database medication monitoring platform was designed for managing patients such as texting,reminding and mailing.Participants were randomized to follow-up care as usual(yearly outpatient clinic visits) or nurse-led telephone follow-up(monthly consultation with structured intervention).Telephone follow-up was performed by four trained breast care nurses (BCN) and consisted of a semi-structured interview including managing the side-effects of endocrine therapy,compliance with hormonal therapy and an open discussion of these issues.Patients' medication adherence and quality of life were evaluated by Morisky Medication Adherence Questionnaire(MAQ) and FACT-B at baseline and 3,6 18 and 24 months,respectively.Results The Nurse-led telephone follow-up did not significantly improve the quality of life(P＞0.05).MAQ score in the intervention group was significantly greater than that in the control group(P＜0.05) at 3,6,18 and 24 months.Conclusion Nurse-led follow-up using computer-based monitoring system can improve patients' medication adherence,but there is no obvious increase in quality of life.

Nine hundred and forty nine general physicians in Beijing urban area received surgical skill assessment in 2008.The assessment results of five surgical skills (taking out stitches,changing dressings,skin suture,knot with gloves and wearing isolation gown) were analyzed with the relations of different gender,age,educational background,professional title,specialty,hospital grade,length of service and times of test taking.The average score of the total assessment was 71.The score was lower in the practitioners who were male,older than 50 years,higher educational background,lower professional tide,more than 2 times of test taking,and who were specialized in traditional Chinese medicine,ophthalmology and otorhinolaryngology and emergency medicine.Results suggest that the levels of surgical skills in general practitioners are generally low and periodical training is needed.

This paper is a follow-up study of 329 children in factory-run nurseries in urban Shanghai. The investigation lasted for a period of one year for each index-child, focusing on the conditions of nutrition, development and diseases of the children of various ages.Comparison between nutritionl findings and RDA of China disclosed that calorie intake of most of the index-child groups were 80-85% of RDA, the only exception being the 6-12 months group where the average calorie intake showed 90%. Protein intake of all groups was over 80% of RDA. Fe intake was lower than RDA, except for 18-month-old and over.Weight and height of the children were compared with the anthropo-metric data established in 1985 (1985 data) for Shanghai children under six years of age. It was found that the average weight and height appeared differently according to their age. Average weight of children under one year old was slightly higher than 1985 data, while average height was lower than 1985 data once the children reached 10 months old. Average weight, however, became lower than the 1985 data after the children were two years old. Over 60% of the index between 6-18 months old suffered from anemia (IDA).Accordingly, it is requested that calorie and iron intake should be supplemented.

Objective:To explore the application of linkage teaching model between hospitals and colleges based on integration of theory and practice in the course of pediatric nursing skills.Methods:Two undergraduate classes of pediatric nursing in a college in 2017 were selected as the experimental group and the control group by random sampling. The experimental group adopted the combined teaching method of colleges and hospitals based on the integration of truth and practice, while the control group adopted the traditional teaching method. The results of skill operation assessment were compared between the two groups, and the results were evaluated by the self-designed teaching effect evaluation questionnaire.Results:The results of the combined nursing skills teaching in colleges and universities were higher in the experimental group (91.24±3.01) than that in the control group (87.33±2.96), the difference was statistically significant ( t value was 5.027, P<0.05). The evaluation score of teaching effect of the experimental group was 62.61 ± 2.94, which was significantly higher than that of the control group (49.67 ± 7.79) ( t value was 7.965, P<0.05). Conclusions:The combined teaching mode of colleges and hospitals based on the integration of theory and practice is beneficial to improve students′ comprehensive quality and learning effect, further shorten the gap between college theory and clinical practice, and is an effective form of pediatric nursing education.

Objective:To investigate the signaling pathway of inhibiting macrophage phagocytosis of TIR domain-containing protein encoded by Escherichia coli (TcpC) N-terminal ubiquitin ligase active fragments of uropathogenic Escherichia coli. Methods:Bioinformatics software was used to analyze the amino acid sequences and the function of TcpC N-terminal ubiquitin ligase active fragments as well as the functional sites. PCR was performed to amplify tcpc-330, tcpc-450 and tcpc-510 genes and a prokaryotic expression system was constructed to express the target proteins. The recombinant proteins rTcpC-N110, rTcpC-N150 and rTcpC-N170 were purified by Ni-NTA affinity chromatography. LPS in the recombinant proteins was removed by Detoxi-gel chromatography. The expression of MyD88 at protein and mRNA levels in macrophages incubated with rTcpC-N110, rTcpC-N150, rTcpC-N170 or rTcpC-TIR was detected by Western blot and qRT-PCR. The activation of NF-κB signal pathway and the levels of proinflammatory factors in macrophages incubated with the above TcpC protein fragments were measured by Western blot and ELISA, respectively. Results:Cys12, Trp104 and Trp106 in the N-terminal fragment of TcpC were crucial amino acids in maintaining its ubiquitin ligase activity. The target recombinant proteins rTcpC-N110, rTcpC-N150 and rTcpC-N170 were successfully expressed and purified. After Detoxi-gel chromatography, rTcpC-N110, rTcpC-N150 and rTcpC-N170 extracts were undetectable for LPS. TcpC ubiquitin ligase fragments inhibited the expression of MyD88 at protein level, but not affect its expression at mRNA level in macrophages. LPS-induced phosphorylation of NF-κB signaling pathway-related proteins p50 and p65 was significantly inhibited in macrophages treated with TcpC ubiquitin ligase fragments. Moreover, LPS-induced production of pro-inflammatory factors was also significantly inhibited.Conclusions:The recombinant proteins rTcpC-N110, rTcpC-N150 and rTcpC-N170 could inhibit the expression of MyD88 at protein level and suppress the activation of NF-κB signaling pathway, suggesting that they were closely related to the inhibition of innate immune activity of macrophages.

Objective:To investigate the role of TcpC in uropathogenic Escherichia coli (UPEC)-induced cystitis in mice and to preliminarily analyze the pathogenic mechanism. Methods:C57BL/6 mice were injected with 10 9 CFU wild-type UPEC CFT073 (CFT073 wt) or tcpc gene-deleted mutant (CFT073 Δ tcpc) from urethra into bladder to construct the mouse model of cystitis. The mice were sacrificed 3 d after infection and the bladders were taken to observe the gross pathological changes. Histopathological changes in bladder tissues were observed after HE staining. Immunohistochemistry was used to detect TcpC in bladder tissues. Bacterial loads in urine samples of UPEC-infected mice were counted by tenfold dilution method, and the presence of tcpc gene in the genomic DNA of bacteria from the bladder and urine samples of CFT073 wt-infected mice was measured by PCR. Real-time quantitative RT-PCR (qRT-PCR) and Western blot were performed to detect the expression of TcpC at mRNA and protein levels in macrophages after CFT073 wt infection. The influence of UPEC strains on the activation of NF-κB signaling pathway in macrophages were determined by Western blot. The levels of proinflammatory factors and the bacterial and cell activity after infecting macrophages with UPEC strains were detected by ELISA, laser confocal microscope and fluorescence microscope, respectively. Results:Compared with the mice with CFT073 Δ tcpc infection, CFT073 wt-infected mice had significantly enlarged bladder and severe neutrophil infiltration and abundant TcpC in bladder tissues. The number of bacteria in the urine of CFT073 wt-infected mice was significantly greater than that of the CFT073 Δ tcpc group. PCR results showed that the bacteria in bladder or urine were CFT073 wt. The expression of TcpC at both mRNA and protein levels in macrophages increased significantly after CFT073 wt infection. Moreover, in CFT073 wt-infected macrophages, the expression of IκBα was promoted and the phosphorylation of p65 and the production of proinflammatory factors were suppressed. TcpC was instrumental in the survival and invasion of CFT073 wt in macrophages. Conclusions:TcpC expression increased significantly in mice with CFT073 wt-induced cystitis. TcpC inhibited the activation of NF-κB signaling pathway and the production of proinflammatory factors in macrophages to improve the survival rate of CFT073 wt, which was closely related to the pathogenesis and immune evasion of UPEC.

Non-suicidal self-injury(NSSI)is a behavior that occurs most often in adolescents.Previous studies showed that this behavior has the addictive related characteristics.Interestingly,the addictive nature of NSSI behavior can be assessed using Ottawa selfinjury inventory(OSI),the higher addiction score indicates the more serious NSSI behavior.From the psychological mechanism,different models show that the addictive feature of NSSI behavior may be related to the behavioral reinforcement mechanism and the interaction mechanism of emotion,cognition,and behavior of susceptible individuals.From the neurobiological mechanisms,opioid and dopamine may mediate the addiction characteristics of NSSI,and the brain reward circuit originated in the midbrain system may play a key role.From the perspective of treatment,current psychotherapy may have advantages in alleviating NSSI behavior,while therapeutic drugs and non-invasive neural regulation of substance use disorders may improve NSSI behavior via alleviating behavioral addiction.In conclusion,NSSI may be an addictive disorder,which needs further verification in the future studies.

Objective:To investigate whether the hypervirulent Klebsiella pneumoniae (hvKP) induces liver abscess through activating NLRP3 inflammasome. Methods:K1-hvKP and K35-non-hvKP bacterial suspensions were intraperitoneally injected into C57BL/6 mice to establish the models of liver abscess. Human peripheral blood neutrophils were sorted by immunomagnetic beads with CD45 + and Gr-1 + , and the purity was detected by flow cytometry. The concentrations of capsular polysaccharide of K1-hvKP and K35-non-hvKP were detected by total carbohydrate assay kit. The expression of IL-18 and IL-33 by neutrophils at mRNA and protein levels was detected by real-time fluorescence quantitative PCR and ELISA, respectively. The activation of NLRP3 inflammasome in neutrophils was detected by Western blot. Neutrophil extracellular trap formation (NETosis) was observed under confocal laser scanning microscope. Results:The C57BL/6 mice with K1-hvKP infection had significantly serious liver abscess as compared with the K35-non-hvKP-infected mice. The purity of human neutrophils was more than 95%. The concentration of capsular polysaccharide in K1-hvKP was significantly higher than that in K35-non-hvKP. Compared with K35-non-hvKP, K1-hvKP significantly promoted the neutrophils to express IL-18 and IL-33 at both mRNA and protein levels, enhanced the activation of NLRP3 and induced NETosis.Conclusions:This study suggested that hvKP could promote NETosis by activating NLRP3 inflammasome to cause liver abscess.