1-[(Z)-(5-Methyl-2-pyrid­yl)iminiometh­yl]-2-naphtholate

In the zwitterionic title compound, C17H14N2O, the dihedral angle between the naphthalene and pyridine ring systems is 3.56 (9)° and an intra­molecular N—H⋯O hydrogen bond generates an S(6) ring. In the crystal, mol­ecules are linked by C—H⋯O inter­actions

Protective effect of catalpol on isoproterenol-induced myocardial injury in Wistar rats

The neuroprotective effects of catalpol had been well demonstrated in many studies. Nevertheless, little work was done to investigate the cardioprotective effects of catalpol. This study was designed to explore whether catalpol protected myocardium against isoproterenol (ISO)-induced myocardial injury through attenuating oxidative stress and suppressing inflammation. Histopathological changes were assessed by hematoxylin and eosin staining. Results show that catalpol could effectively suppress the histopathological changes including myocardial structure damage and leucocyte infiltration. Oxidative stress and antioxidant status were also analysed. Results show that catalpol could significantly attenuate the increase of myocardial malondialdehyde (MDA) and renew the activities of superoxide dismutase (SOD). Furthermore, the results of real time reverse transcription polymerase chain reaction (RT-PCR) and Western-blot analysis showed that catalpol could inhibit the upregulation of the expressions of tumor necrosis factor-β (TNF-β) and interleukin-1β (IL-1β) caused by ISO. In conclusion, our data suggest that catalpol had a protective effect against ISO-induced cardiotoxicity in rat, by maintaining endogenous antioxidant enzyme activities and alleviating inflammatory response. This study provides novel insights that catalpol treatment could be an approach for the prevention of ischemic heart disease.Key words: Catalpol, isoproterenol, inflammation, oxidative stress, myocardial injury

The effect of personalized intervention on the cognitive function of elderly inpatients

目的  对住院老年患者进行早期认知功能护理干预，评价其效果。方法  2013年1月—2015年1月入院老年科病房的120名患者，运用MMSE量表对其认知功能进行评价，观察干预效果。结果  MMSE总分及MMSE量表中时间定向、短期记忆及插画条目干预后有改善（P＜0.05），地点定向、语言记忆、注意力、物品命名、语言复述、阅读能力、语言能力及语言表达条目改善不明显（P＞0.05）。 结论  个性化的认知干预能够延缓和改善患者认知功能障碍，提高老年患者的生活质量。Objectives: To assess the effect of the early cognitive function nursing intervention on the cognitive function of elderly inpatients. Methods: A total of 120 elderly inpatients in geriatrics ward were rolled from January 2013 to January 2015, and we evaluate the cognitive function of them and gave personalized intervention to them by MMSE scale. Results: The total score of MMSE was increased (P＜0.05); The entries of time orientation, short-term memory and illustration were improved significantly after three-month intervention (P＜0.05); The entries of place orientation, language, memory, attention, article name, repeat language, reading skills, language skills and language were not improved significantly. Conclusions:  Personalized cognitive intervention could improve the cognitive dysfunction and the quality of life of elderly patients

Influence of inverter-interfaced renewable energy generators on directional relay and an improved scheme

Renewable energy sources (RESs) are typically interfaced to the grid using power electronics which can cause their fault current characteristics to display significant low frequency harmonics and unbalanced sequence impedances. Such current characteristics can lead to the operation failure of fault component based directional relays. To demonstrate the influence of inverter-interfaced renewable energy generators (IIREGs) on directional relays in detail, analytical expressions for the IIREG equivalent positive- and negative-sequence superimposed impedances are derived in this paper. Considering various factors, the angular characteristics of the sequence superimposed impedances are investigated. Based on these attributes, it can be concluded that fault component based directional relays may be unable to operate in some circumstances. A novel high-frequency impedance-based protection scheme is proposed to manage the adaptability problem by determining the fault direction due to a stable impedance angle. The theoretical analysis and the proposed scheme are tested and verified through real time digital simulation (RTDS) simulation and field testing data

Overexpression of MYCT1 Inhibits Proliferation and Induces Apoptosis in Human Acute Myeloid Leukemia HL-60 and KG-1a Cells in vitro and in vivo

MYC target 1 (MYCT1), a direct target gene of c-Myc, is a novel candidate tumor suppressor gene first cloned from laryngeal squamous cell carcinoma. The downregulation of MYCT1 has been reported to be associated with carcinogenesis. However, the role of MYCT1 in the development and progress of acute myeloid leukemia (AML) remains unknown and requires further investigation. In this study, we first found that the expression level of MYCT1 was significantly lower in the bone marrow (BM) derived from AML patients than that from healthy individuals. The low expression of MYCT1 in AML BM may be due to the hypermethylation in its promoter. MYCT1 expression was strongly associated with French–American–British classifications of AML. The low expression level of MYCT1 was more often observed in patients of M1, M5 and M6 types. In vitro, lentiviral particles carrying the complete CDS of MYCT1 gene were used to mediate the forced overexpression of MYCT1 in two AML cell lines, HL-60 and KG-1a. MYCT1 overexpression significantly inhibited cell proliferation, arrested cell cycle at G0/G1 phase, and downregulated the expression of cyclins D and E. Moreover, MYCT1 overexpression triggered apoptosis in AML cells, which was accompanied by enhanced cleavage of caspase-3 and -9, upregulated expression of B-cell lymphoma 2 (Bcl-2)-associated X protein (Bax), and downregulated Bcl-2. Finally, in BALB/c nude mice bearing xenograft tumors generated by HL-60 and KG-1a cells, we noted that the intratumoral injection of MYCT1 lentivirus repressed tumor growth and led to massive apoptosis. In summary, our results reveal that MYCT1’s promoter is hypermethylated and its expression is downregulated in the BM of AML patients. MYCT1 plays a tumor-suppressive role, and it may serve as a promising target for the genetic therapeutic strategy in treating AML

Modulation of epithelial sodium channel in human alveolar epithelial cells by lipoxin A4 through AhR-cAMP-dependent pathway

Purpose: To investigate the effect of lipoxin A4 (LXA4) on the expressions of protein and mRNA of alveolar epithelial sodium channel (ENaC) in normal and lipopolysaccharide (LPS)-stimulated A549 cells.Methods: A549 cell-lines were randomized into 11 groups (N = 8) and treated. EnaC level was evaluated by Western blot. Total RNA was extracted and reverse-transcribed and then levels of ENaC mRNA, cGMP and cAMP in the cells were determined.Results: LXA4 (10-7mol/L) increased the expressions of α-subunit of ENaC relative to LPS group. In addition, LXA4 significantly up-regulated the expression of mRNAs of α, β and γ subunits of ENaC (p < 0.01). The level of cAMP was increased in LXA4 group, but significantly reduced in LPS group relative to control group (p < 0.05). However, treatment with LXA4 annulled the increased cAMP concentration, compared with LPS group (p < 0.05)Conclusion: These results show that LXA4 influences ENaC up-regulation in normal and LPS stimulated A549 alveolar epithelial cells.Keywords: Acute lung injury, Alveolar epithelial sodium channel, Lipoxin A4, AhR, cAMP, cGM