Objective To investigate the change of plasma ghrelin level and explore the related factors of ghrelin alteration in elderly hypertensive patients with psychological distress. Methods A total of 300 elders, who were screened with Hamilton Anxiety Scale (HAMA), Hamilton Rating Scale for Depression (HAMD), and the Symptom Checklist-90 (SCL-90) for psychological stress and somato-psychological manifestations respectively, were divided into hypertension group (n=148) and non-hypertension group (n=152). Their blood samples were collected to measure the plasma level of ghrelin and total cortisol on the same day. Results The incidences of anxiety and depression were 27.7% and 11.7%, respectively, in all the enrolled elders. However, the rates of psychological distress, particularly anxiety, were significantly higher in the hypertensive elders than in the non-hypertensive ones (43.2% vs. 12.5%). Anxiety was positively related to the cortisol level but negatively related to the plasma ghrelin level, and the latter two were negatively correlated with each other. Conclusion Chronic increase of plasma cortisol induced by long-term anxiety can lead to the reduction of ghrelin level, which then adversely affects blood pressure in elders with psychological distress. Therefore, ghrelin might be a selective antihypertensive medicine for hypertensive elders with anxiety.

Interferon (IFN)-mediated pathways are a crucial part of the cellular response against viral infection. Type III IFNs, which include IFN-λ1, 2 and 3, mediate antiviral responses similar to Type I IFNs via a distinct receptor complex. IFN-λ1 is more effective than the other two members. Transcription of IFN-λ1 requires activation of IRF3/7 and nuclear factor-kappa B (NF-κB), similar to the transcriptional mechanism of Type I IFNs. Using reporter assays, we discovered that viral infection induced both IFN-λ1 promoter activity and that of the 3'-untranslated region (UTR), indicating that IFN-λ1 expression is also regulated at the post-transcriptional level. After analysis with microRNA (miRNA) prediction programs and 3'UTR targeting site assays, the miRNA-548 family, including miR-548b-5p, miR-548c-5p, miR-548i, miR-548j, and miR-548n, was identified to target the 3'UTR of IFN-λ1. Further study demonstrated that miRNA-548 mimics down-regulated the expression of IFN-λ1. In contrast, their inhibitors, the complementary RNAs, enhanced the expression of IFN-λ1 and IFN-stimulated genes. Furthermore, miRNA-548 mimics promoted infection by enterovirus-71 (EV71) and vesicular stomatitis virus (VSV), whereas their inhibitors significantly suppressed the replication of EV71 and VSV. Endogenous miRNA-548 levels were suppressed during viral infection. In conclusion, our results suggest that miRNA-548 regulates host antiviral response via direct targeting of IFN-λ1, which may offer a potential candidate for antiviral therapy.
3' Untranslated Regions ; Adult ; Antiviral Agents ; pharmacology ; therapeutic use ; Base Sequence ; Down-Regulation ; drug effects ; Female ; Hep G2 Cells ; Hepatitis B, Chronic ; drug therapy ; metabolism ; pathology ; Humans ; Interferon Regulatory Factor-3 ; metabolism ; Interferon Regulatory Factor-7 ; metabolism ; Interleukins ; antagonists & inhibitors ; genetics ; metabolism ; Leukocytes, Mononuclear ; metabolism ; Male ; MicroRNAs ; metabolism ; Middle Aged ; NF-kappa B ; metabolism ; Poly I-C ; pharmacology ; therapeutic use ; Promoter Regions, Genetic ; RNA Interference ; RNA, Small Interfering ; metabolism

OBJECTIVETo observe the effect of oversized occluder on endothelialization post percutaneous closure of experimental atrial septal defect (ASD) in dogs.

METHODSASD was established with the help of transthoracic echocardiography in 18 dogs. ASD size was (6.0 ± 0.2) mm. Dogs were randomly divided into normal size group (implanted with 8 mm occlude, n = 9) and oversized group (implanted with 12 mm occluder, n = 9). Dogs were randomly killed at 3, 6 and 14 months after percutaneous closure. The endothelialization process on device surface was observed by scanning electron microscope.

RESULTSFour animals died around 1 month post procedure. Microscopic sections from normal group showed nearly complete endothelialization at 3 months after device implantation and complete endothelialization at 6 and 14 months after device implantation. While microscopic sections showed lack of endothelialization at 3 months post implantation, nearly endothelialization at 6 months, and complete endothelialization at 14 months after device implantation in oversized group.

CONCLUSIONIncomplete endothelialization of occluder surface is observed at 6 months after implantation of an oversized ASD occluder device in this model.

Animals ; Dogs ; Echocardiography ; Heart Septal Defects, Atrial ; diagnostic imaging ; therapy ; Percutaneous Coronary Intervention ; Septal Occluder Device

Objective To observe the effect of oversized occluder on endothelialization post percutaneous closure of experimental atrial septal defect ( ASD) in dogs.Methods ASD was established with the help of transthoracic echocardiography in 18 dogs.ASD size was ( 6.0 ±0.2 ) mm.Dogs were randomly divided into normal size group ( implanted with 8 mm occlude , n =9 ) and oversized group (implanted with 12 mm occluder, n =9).Dogs were randomly killed at 3, 6 and 14 months after percutaneous closure.The endothelialization process on device surface was observed by scanning electron microscope.Results Four animals died around 1 month post procedure.Microscopic sections from normal group showed nearly complete endothelialization at 3 months after device implantation and complete endothelialization at 6 and 14 months after device implantation.While microscopic sections showed lack of endothelialization at 3 months post implantation , nearly endothelialization at 6 months, and complete endothelialization at 14 months after device implantation in oversized group.Conclusion Incomplete endothelialization of occluder surface is observed at 6 months after implantation of an oversized ASD occluder device in this model.