Generation of human induced pluripotent stem cell line (XWHNi004-A) from a male with APOE gene mutation.

Genetic polymorphism of apolipoprotein E (APOE) confers differential susceptibility to Alzheimer's disease (AD), and APOE ɛ4 variants is the most powerful risk factor for this disease. Here, we report the generation of a human induced pluripotent stem cell (iPSC) line carrying the APOE ɛ4/ɛ4 genotype from peripheral blood mononuclear cells (PBMCs) isolated from a male with a family history of AD utilizing non-integrative Sendai virus vector. The iPSC maintains their original genotype, highly express endogenous pluripotency markers, displays a normal karyotype, and retains the ability to differentiate into cells representative of the three germ layers.

Molecular mechanism of CAIF inhibiting myocardial infarction by sponging miR­488 and regulating AVEN expression.

In recent years, the global incidence and mortality of myocardial infarction (MI) has increased and become one of the important diseases threatening public health. Long non­coding (lnc)RNAs are a type of ncRNA that serve critical roles in the progression of various types of disease. The present study aimed to investigate the effect and mechanism of lncRNA cardiac autophagy inhibitory factor (CAIF) on cardiac ischemia/reperfusion (I/R) injury. CAIF was downregulated in the myocardium of I/R rats and cardiomyocytes treated with hydrogen peroxide (H2O2). Further experiments demonstrated that CAIF overexpression inhibited I/R­induced cardiac infarction and apoptosis in vivo. CAIF decreased H2O2­induced apoptosis and oxidative stress of cardiomyocytes. Mechanistically, CAIF sponged microRNA (miR)­488­5p; this interaction was confirmed by rescue experiments. Moreover, miR­488­5p targeted apoptosis and caspase activation inhibitor (AVEN) and inhibited its expression. In summary, the present data identified a novel CAIF/miR­488­5p/AVEN signaling axis as a key regulator of myocyte apoptosis, which may be a potential therapeutic target for the treatment of MI.

The Beneficial Effects of Saffron Extract on Potential Oxidative Stress in Cardiovascular Diseases.

Saffron is commonly used in traditional medicines and precious perfumes. It contains pharmacologically active compounds with notably potent antioxidant activity. Saffron has a variety of active components, including crocin, crocetin, and safranal. Oxidative stress plays an important role in many cardiovascular diseases, and its uncontrolled chain reaction is related to myocardial injury. Numerous studies have confirmed that saffron exact exhibits protective effects on the myocardium and might be beneficial in the treatment of cardiovascular disease. In view of the role of oxidative stress in cardiovascular disease, people have shown considerable interest in the potential role of saffron extract as a treatment for a range of cardiovascular diseases. This review analyzed the use of saffron in the treatment of cardiovascular diseases through antioxidant stress from four aspects: antiatherosclerosis, antimyocardial ischemia, anti-ischemia reperfusion injury, and improvement in drug-induced cardiotoxicity, particularly anthracycline-induced. Although data is limited in humans with only two clinically relevant studies, the results of preclinical studies regarding the antioxidant stress effects of saffron are promising and warrant further research in clinical trials. This review summarized the protective effect of saffron in cardiovascular diseases and drug-induced cardiotoxicity. It will facilitate pharmacological research and development and promote utilization of saffron.

Long non-coding RNAE330013P06 promotes progression of breast cancer with type 2 diabetes.

BACKGROUND: In previous research, we found diabetes rather than obesity was an independent risk factor of breast cancer. However, why diabetes could lead to increased risk of breast cancer patients remains elusive. Long non-coding RNAE330013P06 has been shown to be upregulated in diabetes, and long non-coding RNAs generally promote progression of cancer. METHODS: About 200 specimens of breast patients were obtained in previous clinical trial; 34 samples diagnosed as type 2 diabetes in breast cancer patient were enrolled in this research. Blood samples from 36 patients diagnosed as breast cancer without diabetes; 35 diabetic patients and 35 healthy peoples were obtained as control. All blood samples were measured by quantitative real-time PCR (qRT-PCR). Invasion and migration were tested by Transwell assay. Cell proliferation assay was tested by CCK-8. Protein analysis was determined by Western blot. RESULTS: Compared with breast cancer patients without diabetes, diabetic patients without breast cancer and healthy peoples, LncRNAE330013P06 was upregulated in breast cancer patient with diabetes. Furthermore, of 34 breast patients, high LncRNAE330013P06 expression was significantly associated with family history, tumor-node-metastasis stage and lymph node metastasis. E33 promoted cancer cell growth in vitro via downregulation of P53. CONCLUSION: Upregulation of LncRNAE330013P06 driven by type 2 diabetes is one of the factors which promoted progression of breast cancer.

A cadaveric study on sacroiliac joint injection.

The scope of this study was to explore the possibility as well as the feasibility of sacroiliac joint injection following simple X-ray clip location. For the cadaveric study, 10 fixed sacroiliac joint (SIJ) sectional specimens, 4 dried cadaveric pelvises and 21 embalmed adult cadaveric pelvises were dissected, followed by an injection of contrast agent into the joint. The irrigation of the agent was observed through CT scanning. For the radiologic study, 188 CT scans of ankylosing spondylitis patients (143 male, 45 female) were collected from 2010 to 2012, in Nanfang Hospital. What was measured was (1) Distance between the posterior midline and sagittal synovium; (2) Length of the sagittal synovium; (3) Distance between the midpoint of the sagittal synovium and posterior superior iliac spine; and (4) Distance between the superficial skin vertical to the sagittal synovium point were measured. For the practice-based study: 20 patients (17 males and 3 females) with early ankylosing spondylitis, from Nanfang Hospital affiliated with Southern Medical University were recruited, and sacroiliac joint unguided injections were done on the basis of the cadaveric and radiologic study. Only the inferior 1/3(rd) portion parallel to the posterior midline could be injected into since the superior 2/3(rd) portion were filled with interosseous ligaments. Thirteen of the 20 patients received successful injections as identified by CT scan using the contrast agent. Sacroiliac joint injection following simple X-ray clip location is possible and feasible if the operation is performed by trained physicians familiar with the sacroiliac joint and its surrounding anatomic structures.

4-Hydroxynonenal promotes growth and angiogenesis of breast cancer cells through HIF-1α stabilization.

4-Hydroxynonenal (4-HNE) is a stable end product of lipid peroxidation, which has been shown to play an important role in cell signal transduction, while increasing cell growth and differentiation. 4-HNE could inhibit phosphatase and tensin homolog (PTEN) activity in hepatocytes and increased levels have been found in human invasive breast cancer. Here we report that 4-HNE increased the cell growth of breast cancer cells as revealed by colony formation assay. Moreover, vascular endothelial growth factor (VEGF) expression was elevated, while protein levels of hypoxia inducible factor 1 alpha (HIF-1α) were up-regulated. Sirtuin-3 (SIRT3), a major mitochondria NAD+-dependent deacetylase, is reported to destabilize HIF-1α. Here, 4-HNE could inhibit the deacetylase activity of SIRT3 by thiol-specific modification. We further demonstrated that the regulation by 4-HNE of levels of HIF-1α and VEGF depends on SIRT3. Consistent with this, 4-HNE could not increase the cell growth in SIRT3 knockdown breast cancer cells. Additionally, 4-HNE promoted angiogenesis and invasion of breast cancer cells in a SIRT3-dependent manner. In conclusion, we propose that 4-HNE promotes growth, invasion and angiogenesis of breast cancer cells through the SIRT3-HIF-1α-VEGF axis.