Objective:To explore the influence of continuous care on cognitive function and quality of life of AD patients.Methods:A total of 76 patients with AD admitted to our hospital from January 2019 to January 2020 were prospectively selected and randomly divided into 2 groups by simple number random table method. The control group (38 cases) received routine nursing care and the observation group (38 cases) received continuous nursing care based on routine nursing. Mini-mental State Examination (MMSE), Quality of Life-Alzheimer′s Disease (QOL-AD), Barthel Index (BI) and Activity of Daily Living scale (ADL) scores were compared between the two groups.Results:The MMSE score of the observation group before nursing was 11.26±1.40, 11.28±1.35 in the control group, and the difference between the two groups was not statistically significant ( t value was 0.063, P>0.05).After nursing, MMSE score of patients in the observation group after nursing was 21.03±2.46, significantly higher than that of the control group 18.66±2.32 ( t value was 4.321, P<0.05). After nursing, the QOL-AD strongest items, stronger items, ordinary items, weak items scores in the post-nursing observation group were 10.70±1.22, 14.34±1.33, 10.44±1.08, 10.53±1.31, and 43.17±2.66, respectively. All of them were significantly higher than the control group (7.26±0.78, 9.37±0.90, 7.44±0.69, 7.48±0.74, 30.27±2.25), the difference between the two groups was statistically significant ( t value was 12.496-22.825, all P<0.05). After nursing, the BI score of the observation group was 68.06±16.51, which was significantly higher than that of the control group 51.04±15.56, the difference between the two groups was statistically significant ( t value was 7.018, P<0.05). The ADL score of the observation group was 16.19±7.22, which was significantly lower than that of the control group 20.52±8.79, the difference between the two groups was statistically significant ( t value was 22.347, P<0.05). Conclusion:Continuous nursing care for AD patients can improve cognitive function, improve quality of life, and improve the ability of daily life of patients.

Objective: This study aimed to investigate the relationship between the genetic variation of CD55 promoter and the risk of esophageal cancer. Methods: A total of 700 esophageal cancer patients recruited between April 2008 and December 2012 at Tangshan Grongren Hospital and Tangshan Renmin Hospital, and 700 frequency matched controls were randomly selected from a pool of cancer free subjects recruited from a nutritional survey. Genotypes of CD55 rs2564978 polymorphism among all subjects were conducted by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). The OR and 95%CI were calculated by non-conditional Logistic regression to evaluate the association of CD55 rs2564978T/C polymorphism with the risk of esophageal cancer. Results: The average age of cases and control was (60.04±9.19) and (59.21±9.98) years old. Compared with CD55 rs2564978 TT carriers, the individuals with CC genotype had a significantly higher risk of esophageal cancer (OR=1.94, 95%CI:1.42-2.66) . When stratified by sex, this genetic variation affected the risk of esophageal cancer among both males (OR=1.92, 95%CI:1.37-2.70) and females (OR=2.34, 95%CI:1.04-5.27). When stratified by age, the CD55 rs2564978 CC was associated with the susceptibility of developing esophageal cancer among younger individuals (OR=1.79, 95%CI:1.19-2.68) and older people (OR=2.32, 95%CI:1.41-3.83).When stratified by drinking status, CC genotype carriers increase the risk of esophageal cancer when drinking (OR=1.93, 95%CI:1.03-3.63) or not drinking (OR=1.95, 95%CI:1.36-2.80). When stratified by smoking status, CC genotype was associated with the risk of esophageal cancer among non-smokers (OR=1.79, 95%CI: 1.13-2.83), light smokers (less than 30 packs/year, OR=1.86, 95%CI:1.31-2.64) and heavy smokers (more than 30 packs/year, OR=2.67, 95%CI:1.28-5.57). Gene-environmental interaction analysis showed that CD55 rs2564978T/C polymorphism interacted with smoking status to increase the risk of esophageal cancer. Conclusion CD55 rs2564978 polymorphism effects on the risk of esophageal cancer.

Objective To discuss the controversial role of breast milk in late-onset group B Streptococcus (GBS) infections.Methods This study reported a case of recurrent late-onset GBS sepsis with the suspicion of breast milk transmission in an extremely preterm infant born at 22+6 weeks who was treated at the University of Hong Kong-Shenzhen Hospital in September 2016.Literatures about late-onset GBS cases associated with contaminated breast milk were reviewed to investigate whether GBS could be transmitted through breast milk.Results (1) Case report:A breast-fed extremely preterm infant born at 22+6 gestational weeks suffered from GBS sepsis along with meningitis for the first time on 100 d.The mother was negative for rectovaginal GBS screening.Breast milk wasn't tested as no signs of mastitis were found.The neonate recovered from the first GBS sepsis after 14 days of antibiotic treatment,then returned to breastfeeding.On 126 d,GBS sepsis reoccurred in this baby.Fresh breast milk culture yielded GBS which was identical with the GBS strains isolated from the neonatal blood in antimicrobial susceptibility.After recovery from the second episode,the baby was partially breastfed again without further relapses of late-onset GBS sepsis.(2) Literature review:64 cases of late-onset GBS infections that transmitted via breast milk were retrieved from PubMed,while no Chinese cases had been reported.Clinical data of the 65 cases (including this case) were reviewed and the results revealed that contaminated breast milk was associated with late-onset GBS infections.The reported relapse rate of GBS infections transmitted via breast milk was 25％ for two episodes and 7％ for three episodes.Conclusions GBS contaminated breast milk could potentially cause late-onset GBS sepsis in infants and further studies are required to identify the underlying mechanisms.

OBJECTIVETo investigate the effect and its possible mechanism of interleukin-17 (IL-17) on invasion and metastasis of human colon cancer cells.

METHODSIL-17 was added into the culture media of human colon cancer cells SW480 and LOVO. Cells were divided into 4 groups: SW480 control group (SW480 cells), LOVO control group (LOVO cells), SW480 experiment group (50 μg/L IL-17+SW480 cells), and LOVO experiment group (50 μg/L IL-17+LOVO cells). Cell growth was measured by CCK-8 assay. The proliferation rate(%)=[(Aexperiment group-Ablank)/(Acontrol group-Ablank)]×100%). The ability of cell invasion and migration was measured by transwell assay. Real time-PCR was used to detect mRNA expression of VEGF and MMP-9. Western blot was performed to detect protein expression of STAT3, p-STAT3, VEGF and MMP-9. Enzyme-linked immunosorbent assay (ELISA) was applied to measure the protein content of VEGF and MMP-9 in the supernatant.

RESULTSAfter cultivation for 24, 48 and 72 hours, CCK-8 assay revealed that the proliferation rate of SW480 was 1.18%±0.07%, 1.42%±0.09%, and 1.62%±0.08%; the proliferation rate of LOVO was 1.13%±0.02%, 1.32%±0.05% and 1.73%±0.02% in experiment group. Transwell experiments showed that after cultivation with IL-17 for 24 hours, number of invasion cell in experimental groups (SW480: 34.00±0.45, LOVO: 41.60±0.51) was higher as compared to corresponding control groups (SW480: 4.53±0.14; LOVO: 3.67±0.33) with significant differences (SW480: t=-76.026, P=0.001; LOVO: t=-81.580, P=0.005). The number of migration cell in experimental groups (SW480: 36.40±0.51, LOVO: 46.40±0.68) was higher as compared to corresponding control groups (SW480: 7.83±0.69; LOVO: 6.67±0.48) with significant differences (SW480: t=-51.542, P=0.003; LOVO: t=-49.265, P=0.005). Real-time PCR results revealed that after cultivation with IL-17 for 24 hours, VEGF and MMP-9 mRNA relative expression levels in experimental groups (SW480: VEGF:1.53±0.12, MMP-9: 2.44±0.23; LOVO: VEGF: 2.96±0.35, MMP-9: 3.38±0.55) were higher than those in control groups (both 1) with significant differences (VEGF: t=3.799, P=0.043; MMP-9: t=5.254, P=0.039). Western blot illustrated that after cultivation with IL-17 for 24 hours, STAT3, p-STAT3, VEGF and MMP-9 proteins relative expression levels in experimental groups were significantly higher that those in control groups (SW480:STAT3: t=3.233, P=0.023; p-STAT3: t=3.954, P=0.032; VEGF: t=3.201, P=0.025; MMP-9: t=3.154, P=0.029; LOVO: STAT3: t=3.788, P=0.012; p-STAT3: t=2.662, P=0.040; VEGF: t=4.118, P=0.035; MMP-9: t=4.268, P=0.030). ELISA indicated that content of VEGF and MMP-9 in the supernatant of experimental groups (SW480: VEGF 5 491.41±63.22, MMP-9: 21.43±1.35. LOVO: VEGF: 8 631.46±129.59, MMP-9: 178.32±3.20) were higher than those in control groups (SW480: VEGF:4 456.32±87.56, MMP-9:18.57±2.44. LOVO: VEGF: 8 122.38±108.66, MMP-9: 163.22±6.89) with significant differences (SW480: VEGF: t=6.993, P=0.037; MMP-9: t=5.587, P=0.040. LOVO: VEGF: t=7.013, P=0.044; MMP-9: t=6.762, P=0.043).

CONCLUSIONIL-17 may be able to activate STAT3 signal transduction pathway in vitro through up-regulation of VEGF and MMP-9 expression, thereby enhancing the invasion and migration of colon cancer SW480 and LOVO cells.

Cell Cycle ; Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; Colonic Neoplasms ; pathology ; Humans ; Interleukin-17 ; pharmacology ; Matrix Metalloproteinase 9 ; metabolism ; Neoplasm Invasiveness ; Real-Time Polymerase Chain Reaction ; STAT3 Transcription Factor ; metabolism ; Signal Transduction ; Up-Regulation ; Vascular Endothelial Growth Factor A ; metabolism