Aim To investigate the effects of saponin of sea cucumber ( SSC ) on the blood pressure in obese mice. Methods C57BL/KsJ(db/db) mice were ran-domized into 3 groups ( 8 mice each ): model group, low-dose SSC group and high-dose SSC group. Normal C57BL/KsJ mice were used as control. The low and high SSC groups were fed on basal diets incorporated with 0. 02% and 0. 04% SSC. Different treatments were administered for 6 weeks and arterial pressure was measured in the third and sixth weeks. The abundance of renal ACE, ACE2 and REN mRNA was detected by real time PCR . Results Compared with control group, the blood pressure of model group mice was ob-viously raised ( P<0. 01 ) . Low-dose SSC group mice showed lower blood pressure than model group without statistically significant differences, and the blood pres-sure of high-dose SSC group mice was similar to that of control group and significantly lower than model group. ( P<0. 05 ) There were no remarkable differences a-bout ACE and REN mRNA among the groups, howev-er, ACE2 mRNA level was significantly increased in high-dose SSC group. Conclusion SSC plays a vital role in decreasing blood pressure, which probably re-lates to the regulating function of renin-angiotensin sys-tem( RAS) .

AIM: To study the effects of insulin on the proliferation and function of osteoblasts and the relationship between insulin post-receptor change in osteoblasts and osteoblastic cell growth.METHODS: The effects of different levels of insulin on osteoblasts were assessed by MTT colorimetry.Osteocalcin in medium was measured by RIM.IGF-1 mRNA expression levels were determined by RT-PCR.The concentrations of free IGF-1 protein in serum-free medium were measured by ELISA.In addition,the protein level and phosphorylated protein of P~(44/42)MAPK were determined by Western blotting analysis.RESULTS: Insulin enhanced the proliferation of osteoblasts,depending on its dose and exposure time.Insulin at concentration of 10~(-7) mol/L showed the strongest effect,and the action attained the plateau phase beyond 96 h.The best concentration that stimulated synthesis of osteocalcin by insulin was 10~(-7) mol/L.When the insulin concentration beyond 10~(-7) mol/L,the osteocalcin concentration was decreased.Exposure time had no effect on insulin-stimulated synthesis of osteocalcin of osteoblastic cells.When the concentration of insulin reaches 10~(-6) mol/L,the IGF-1 mRNA expression stimulated by insulin was also decreased.The concentrations of free IGF-1 protein in insulin-stimulated groups were all higher than that in control group(P0.05).Insulin acute stimulation rapidly induced the activity of tyrosine phosphorylation of P~(44/42)MAPK.The degree of tyrosine phosphorylation of P~(44/42)MAPK was increased step by step along with the increasing doses of insulin from 0 to 10~(-7) mol/L(P

Objective:To analyze the research status and development trend of pediatrician competence in China and abroad, for reference in promoting the pediatrician competence research in the country.Methods:Literature review on pediatric resident′s competency was made using CNKI, WanFang and PubMed databases, ranging from their establishment up to December 25, 2019. A descriptive statistical analysis was made on the literatures′ publication year, publication area, research object and application area among others, using Excel 2019 and EndnoteX8.Results:A total of 199 Chinese documents and 262 English documents were finally retrieved. From 2009, the number of publications increased year by year, of which the Pediatrics has topped the rest, followed by Academic Medicine and Chinese Journal of Medical Education Research. The publishing institutions were mostly universities and affiliated hospitals, among which the Children′s Hospital of Chongqing Medical University topped the rest. The keyword of the highest frequency was education and the researches focus on the competency application and modelling. Conclusions:The pediatric healthcare system is paying greater attention on competence researches, but China has not yet established an appropriate pediatric resident competency model fitting local conditions. Meanwhile, the researches are plagued by such setbacks as excessive concentration of resources, simple methods and lack of empirical studies. It is recommended to broaden the explorations in this regard so as to identify pediatric resident competency development models fitting China′s conditions.

Objective:To analyze the risk factors of acute kidney injury (AKI) in hospitalized patients with infective endocarditis (IE), construct prediction model, and discuss its predictive value.Methods:The clinical data of 402 adult inpatients diagnosed with IE admitted to the Affiliated Hospital of Qingdao University from January 2010 to January 2020 were retrospectively analyzed. The patients were divided into the AKI group and the non-AKI group. The clinical data, such as gender, age, presence of diabetes, basic estimated glomerular filtration rate (eGFR), laboratory indexes at admission, involvement of valves, presence of sepsis, medication during hospitalization, surgery and outcome of the two groups were compared. Multivariate Logistic regression analysis was used to screen the risk factors of AKI in IE inpatients. A predictive model was constructed, and receiver operating characteristic (ROC) curve was used to analyze the predictive value of the model.Results:A total of 290 patients with IE were enrolled, including 198 non-AKI patients and 92 AKI patients. The incidence of AKI was 31.7%. Among the 92 AKI patients, 46 patients were at AKI stage 1 (50.0%), while 46 patients were at AKI stage 2 and stage 3 (50.0%). Compared with the non-AKI group, patients in the AKI group were older [years old: 64 (55, 71) vs. 55 (46, 63)], and had lower basic eGFR (mL·min -1·1.73 m -2: 64.6±13.6 vs. 82.9±19.5), higher proportion of diabetic and incidence of sepsis (16.3% vs. 8.6%, 38.0% vs. 13.1%), more frequent use of angiotensin converting enzyme inhibitors/angiotensin Ⅱ receptor antagonists (ACEI/ARB), diuretics and non-steroidal anti-inflammatory drugs (NSAIDs; 25.0% vs. 15.2%, 82.6% vs. 63.1%, 58.7% vs. 24.2%), more abnormal urine test results (hematuria or proteinuria, 35.9% vs. 22.7%), higher pathogen culture negative rate (73.9% vs. 51.5%), lower Gram positive (G +) cocci infection rate and surgery rate (22.8% vs. 40.4%, 60.9% vs. 81.8 %), with significant differences (all P < 0.05). There were no significant differences in the gender, number and location of involved valves, and laboratory indexes at admission between the two groups. Compared with the non-AKI group, the inpatient mortality rate of the AKI group was higher (30.4% vs. 8.6%, P < 0.01), and the inpatient mortality rate of patients with AKI stage 2 and stage 3 was significantly higher than that of patients with AKI stage 1 (43.5% vs. 17.4%, P < 0.01). In multivariate Logistic regression analysis, the lower basic eGFR [hazard ratio ( HR) = 0.136, 95% confidence interval (95% CI) was 0.066-0.280], sepsis ( HR = 6.100, 95% CI was 2.394-15.543), demand for NSAIDs ( HR = 2.990, 95% CI was 1.184-7.546) and radiocontrast agent ( HR = 3.153, 95% CI was 1.207-8.238) were independent risk factors for AKI in hospitalized patients with IE (all P < 0.05). A prediction model was constructed based on the above risk factors, and ROC curve analysis showed that the area under the ROC curve (AUC) of prediction model for AKI was 0.888 (95% CI was 0.833-0.943, P < 0.01) with sensitivity of 86.4% and specificity of 80.9%. Conclusions:In the IE-susceptible population, low basic eGFR, sepsis, the need for NSAIDs and contrast agent are independent risk factors to AKI. The predictive model constructed by the above risk factors has certain predictive value for the occurrence of AKI in the IE inpatients.

Objective:To explore the protective effect and mechanism of scutellarin (Scu) on sepsis associated-acute kidney injury (SA-AKI).Methods:① In vivo experiment: 36 male C57BL/6 mice were divided into normal saline (NS) control group, lipopolysaccharide (LPS) induced SA-AKI model group (LPS group), 20 mg/kg Scu control group (Scu 20 control group), and 5, 10, 20 mg/kg Scu pretreatment groups by random number table with 6 mice in each group. The SA-AKI model was reproduced by intraperitoneal injection of 10 mg/kg LPS. The NS control group was injected with NS intraperitoneally. The Scu pretreatment groups were intraperitoneally injected with different doses of Scu every day before LPS injection for 1 week. Scu 20 control group was injected with 20 mg/kg Scu for 1 week. After 24 hours of LPS treatment, mice in each group were sacrificed, kidney tissues were collected, and kidney injury was detected by hematoxylin-eosin (HE) staining. Western blotting was used to detect the protein expression levels of nuclear factor-κB (NF-κB) signaling pathway related molecules, apoptosis-related proteins and cysteine-rich protein 61-connective tissue growth factor-nephroblastoma overexpressed gene 1 (CCN1). ② In vitro experiment: human renal tubular epithelial cell line HK-2 was cultured in vitro and used for experiment when the cells fused to 80%. In the cells without LPS treatment and after 100 g/L LPS treatment, pcDNA3.1-CCN1 and small interfering RNA (siRNA) CCN1 sequence were transfected to overexpress and inhibit CCN1 expression, respectively, to observe whether CCN1 was involved in NF-κB signaling pathway activation and apoptosis. In addition, 100g/L LPS and 20 μmol/L Scu were added into HK-2 cells transfected with and without CCN1 siRNA to investigate the mechanism of protective effect of Scu on LPS-induced HK-2 cells injury. Results:① The results of in vivo experiment: the renal function of SA-AKI mice induced by LPS was significantly decreased, and had kidney histological damage and severely damaged renal tubules. Scu could alleviate renal function and histological damage in a dose-dependent manner. Western blotting results showed Scu could reduce the protein expression of NF-κB signaling pathway related molecules and CCN1 in the renal tissue, and had a significant alleviating effect on apoptosis, indicating that CCN1 was involved in NF-κB signaling pathway activation and apoptosis. ② The results of in vitro experiment: in HK-2 cells not treated with LPS, CCN1 overexpression had no effect on apoptosis related protein and pro-inflammatory factors of NF-κB signaling pathway. In HK-2 cells treated with LPS, overexpression of CCN1 significantly inhibited the mRNA expressions of interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α) and monocyte chemoattractant protein-1 (MCP-1), with significant differences as compared with cells stimulated only by LPS [IL-1β mRNA (2 -ΔΔCT): 3.20±0.57 vs. 4.88±0.69, TNF-α mRNA (2 -ΔΔCT): 2.99±0.44 vs. 5.00±0.81, MCP-1 mRNA (2 -ΔΔCT): 2.81±0.50 vs. 5.41±0.75, all P < 0.05], and the apoptosis-related protein was significantly down-regulated. However, when siRNA was used to inhibit the expression of CCN1, the mRNA expressions of pro-inflammatory factors were significantly increased as compared with cells stimulated only by LPS [IL-1β mRNA (2 -ΔΔCT): 6.01±1.13 vs. 4.88±0.69, TNF-α mRNA (2 -ΔΔCT): 5.15±0.86 vs. 5.00±0.81, all P < 0.05], and apoptosis-related protein was significantly up-regulated. In the LPS-induced HK-2 cells, the mRNA expressions of pro-inflammatory factors were significantly down-regulated after Scu treatment as compared with cells stimulated only by LPS [IL-1β mRNA (2 -ΔΔCT) : 2.55±0.50 vs. 6.15±1.04, TNF-α mRNA (2 -ΔΔCT): 2.58±0.40 vs. 3.95±0.52, MCP-1 mRNA (2 -ΔΔCT): 2.64±0.44 vs. 6.21±0.96, all P < 0.05], and apoptosis-related protein was also significantly reduced. When the expression of CCN1 was inhibited by siRNA, the protective effect of Scu on cells was weakened, which showed that the mRNA expressions of pro-inflammatory factors in cells was significantly up-regulated compared with the cells without inhibition of CCN1 expression [IL-1β mRNA (2 -ΔΔCT): 5.34±0.76 vs. 2.55±0.50, TNF-α mRNA (2 -ΔΔCT): 3.66±0.54 vs. 2.58±0.40, MCP-1 mRNA (2 -ΔΔCT): 5.15±0.79 vs. 2.64±0.44, all P < 0.05], and the expression of apoptosis related protein was also significantly up-regulated. Conclusions:Scu could protect the renal function in SA-AKI mice, and the protective effect is associated with NF-κB signaling pathway and CCN1. Thus, Scu could alleviate LPS-induced kidney injury by regulating the NF-κB signaling pathway.