Survey of Rehabilitation Nursing Management of Neurogenic Bladder and Clinical Application of Intermittent Catheterization in Guangdong, China / 中国康复理论与实践

Objective:To investigate the knowledgement and clinical application of neurogenic bladder and intermittent catheterization among nurses in Guangdong. Methods:From December, 2020 to January, 2021, 241 nurses in Guangdong were investigated with a questionnaire designed by ourselves. Results:The score was low in understanding the neurogenic bladder rehabilitation nursing management and intermittent catheterization through self-assessment. The awareness was deficient in the complication and risk management of neurogenic bladder. Although there were a lot of patients with dysuria in clinical practice, 67.2% of nurses still used indwelling catheter, and only 24.1% used intermittent catheterization. Only 9.9% nurses thought that patients with dysuria were treated positively by doctors. Most of nurses would like to participate in the training and nursing alliance in neurogenic bladder rehabilitation nursing management and intermittent catheterization, and manage patients with neurogenic bladder after discharge. Conclusion:The knowledge of guidelines related with neurogenic bladder and intermittent catheterization among nurses is insufficient, and is not applied in clinical practice. More work should be done to improve the knowledge and standardization of management of neurogenic bladder.

Alterations in thymocyte populations under conditions of endotoxin tolerance / 中华医学杂志(英文版)

BACKGROUND@#Endotoxin tolerance (ET) is a protective phenomenon in which pre-treatment with a tolerance dose of lipopolysaccharide (LPS) leads to dramatically elevated survival. Accumulating evidence has shown that peripheral T cells contribute to the induction of ET. However, what happens to T cell development in the thymus under ET conditions remains unclear. The purpose of this study was to analyze the alterations in thymocyte populations (double-positive [DP] and single-positive [SP] cells) under ET conditions.@*METHODS@#Mice were intraperitoneally injected with LPS at a concentration of 5 mg/kg to establish an LPS tolerance model and were divided into two groups: a group examined 72 h after LPS injection (72-h group) and a group examined 8 days after LPS injection (8-day group). Injection of phosphate-buffered saline was used as a control (control group). Changes in thymus weight, cell counts, and morphology were detected in the three groups. Moreover, surface molecules such as CD4, CD8, CD44, CD69, and CD62L were analyzed using flow cytometry. Furthermore, proliferation, apoptosis, cytokine production, and extracellular signal-regulated kinase (ERK) pathway signaling were analyzed in thymocyte populations. The polymorphism and length of the T-cell receptor (TCR) β chain complementarity-determining region 3 (CDR3) were analyzed using capillary electrophoresis DNA laser scanning analysis (ABI 3730).@*RESULTS@#Thymus weight and cell counts were decreased in the early stage but recovered by the late stage in a murine model of LPS-induced ET. Moreover, the proportions of DP cells (control: 72.130 ± 4.074, 72-h: 10.600 ± 3.517, 8-day: 84.770 ± 2.228), CD4+ SP cells (control: 15.770 ± 4.419, 72-h: 44.670 ± 3.089, 8-day: 6.367 ± 0.513), and CD8+ SP cells (control: 7.000 ± 1.916, 72-h: 34.030 ± 3.850, 8-day: 5.133 ± 0.647) were obviously different at different stages of ET. The polymorphism and length of TCR β chain CDR3 also changed obviously, indicating the occurrence of TCR rearrangement and thymocyte diversification. Further analysis showed that the expression of surface molecules, including CD44, CD69, and CD62L, on thymocyte populations (DP and SP cells) were changed to different degrees. Finally, the proliferation, apoptosis, cytokine production, and ERK pathway signaling of thymocyte populations were changed significantly.@*CONCLUSION@#These data reveal that alterations in thymocyte populations might contribute to the establishment of ET.

Overexpresssion of NDUFA4 induces epithelial-mesenchymal transition of human colorectal cancer cells / 医学研究生学报

Objective The role and action mechanisms of NADH dehydrogenase 1 alpha subcomplex 4 (NDUFA4) in the development of human colorectal cancer (CRC) are not yet clarified. This article aims to study the effect of overexpressed NDUFA4 on the epithelial-mesenchymal transition (EMT) of human CRC cells. Methods The recombinant plasmid NDUFA4 (p-NDUFA4) and control plasmid (p-Cont) were transiently transfected into human CRC HCT116 cells. The expression of NDUFA4 in the cells was determined by real-time PCR and Western blot respectively, and the migration ability of the cells detected by Transwell migration and wound healing assays. The expression levels of MMP2, MMP9 and CXCR4 in the cells were measured by qRT-PCR, and those of Twist, Snail, E-cadherin and Vimentin by Western blot and by immunofluorescence assay, respectively. Results Compared with the p-Cont group, the human CRC HCT116 cells of the p-NDUFA4 group showed significantly up-regulated expressions of NDUFA4 mRNA ([0.96±0.15]% vs [1.94±0.08]%, P<0.05) and NDUFA4 protein ([0.06±0.05]% vs [1.07±0.12]%, P<0.05), increased in vitro migration ability ([29.51±3.17]% vs [54.36±4.08]%, P<0.01) and migrated cell rate ([0.99±0.12]% vs [1.85±0.10]%, P<0.01), elevated expression levels of MMP2, MMP9, CXCR4, N-cadherin,Vimentin, Snail and Twist, but down-regulated level of E-cadherin (P<0.05). Conclusion Overexpressed NDUFA4 promotes the epithelial-mesenchymal transition of human colorectal cancer cells.

5, 7, 2', 4', 5'-Pentamethoxyflavanone regulates M1/M2 macrophage phenotype and protects the septic mice / 中国天然药物

Flavonoids have been reported to exert protective effect against many inflammatory diseases, while the underlying cellular mechanisms are still not completely known. In the present study, we explored the anti-inflammation activity of 5, 7, 2', 4', 5'-pentamethoxyflavanone (abbreviated as Pen.), a kind of polymethoxylated flavonoid, both in vitro and in vivo experiments. Pen. was showed no obvious toxicity in macrophages even at high dosage treatment. Our results indicated that Pen. significantly inhibited both mRNA and protein level of proinflammatory cytokines, IL-1β, IL-6, TNF-α and iNOS, which was characteristic expressed on M1 polarized macrophages. These effects of Pen. were further confirmed by diminished expression of CD11c, the M1 macrophage surface marker. Further researches showed that the mechanism was due to that Pen. downregulated the activity of p65, key transcription factor for M1 polarization. On the other hand, Pen. also enhanced M2 polarization with upregulation of anti-inflammatory factors and increase of M2 macrophage surface markers, which lead to the balance of M1 and M2 macrophages. Moreover, in vivo research verified that Pen. treatment alleviated LPS-induced sepsis in mice by increasing survival rate, decreasing inflammatory cytokines and improving lung tissue damage. In summary, our results suggested that Pen. modulated macrophage phenotype via suppressing p65 signal pathway to exert the anti-inflammation activity.