Dietary, Metabolic, and Potentially Environmental Modulation of the Lysine Acetylation Machinery

Healthy lifestyles and environment produce a good state of health. A number of scientific studies support the notion that external stimuli regulate an individual's epigenomic profile. Epigenetic changes play a key role in defining gene expression patterns under both normal and pathological conditions. As a major posttranslational modification, lysine (K) acetylation has received much attention, owing largely to its significant effects on chromatin dynamics and other cellular processes across species. Lysine acetyltransferases and deacetylases, two opposing families of enzymes governing K-acetylation, have been intimately linked to cancer and other diseases. These enzymes have been pursued by vigorous efforts for therapeutic development in the past 15 years or so. Interestingly, certain dietary components have been found to modulate acetylation levels in vivo. Here we review dietary, metabolic, and environmental modulators of the K-acetylation machinery and discuss how they may be of potential value in the context of disease prevention

Comparison of supercritical and near-critical carbon dioxide extraction of carotenoid enriched wheat bran oil

Supercritical and near-critical carbon dioxide (CO2) extraction were carried out to extract oil from wheat bran. The extraction temperatures for supercritical and near-critical CO2 were 35 - 45°C and 25 - 30°C, respectively. The applied pressure was ranging from 10 to 30 MPa for both supercritical and near-critical CO2 extraction. The extraction was performed in a semi batch process with a CO2 flow rate of 26.81 g/min for 1.5 h. The oil obtained from wheat bran at different extraction conditions was quantitatively measured to  investigate the solubility of oil at supercritical and near-critical CO2. The highest solubility was found at near-critical condition. The fatty acid compositions of wheat bran oil were measured by gas chromatography (GC). Linoleic, palmitic, oleic and γ-linolenic acid were the major fatty acids of wheat bran oil. Total carotenoid was measured spectrophotometerically. Highest yield of total carotenoid was found at 45°C and 30 MPa.Key words: Supercritical and near-critical carbon dioxide, wheat bran oil, total carotenoid

Low-temperature formation of epitaxial graphene on 6H-SiC induced by continuous electron beam irradiation

It is observed that epitaxial graphene forms on the surface of a 6H-SiC substrate by irradiating electron beam directly on the sample surface in high vacuum at relatively low temperature (similar to 670 degrees C). The symmetric shape and full width at half maximum of 2D peak in the Raman spectra indicate that the formed epitaxial graphene is turbostratic. The gradual change of the Raman spectra with electron beam irradiation time increasing suggests that randomly distributed small grains of epitaxial graphene form first and grow laterally to cover the entire irradiated area. The sheet resistance of epitaxial graphene film is measured to be similar to 6.7 k Omega/sq.open4

HP1γ Sensitizes Cervical Cancer Cells to Cisplatin through the Suppression of UBE2L3

Cisplatin is the most frequently used agent for chemotherapy against cervical cancer. However, recurrent use of cisplatin induces resistance, representing a major hurdle in the treatment of cervical cancer. Our previous study revealed that HP1γ suppresses UBE2L3, an E2 ubiquitin conjugating enzyme, thereby enhancing the stability of tumor suppressor p53 specifically in cervical cancer cells. As a follow-up study of our previous findings, here we have identified that the pharmacological substances, leptomycin B and doxorubicin, can improve the sensitivity of cervical cancer cells to cisplatin inducing HP1γ-mediated elevation of p53. Leptomycin B, which inhibits the nuclear export of HP1γ, increased cisplatin-dependent apoptosis induction by promoting the activation of p53 signaling. We also found that doxorubicin, which induces the DNA damage response, promotes HP1γ-mediated silencing of UBE2L3 and increases p53 stability. These effects resulted from the nuclear translocation and binding of HP1γ on the UBE2L3 promoter. Doxorubicin sensitized the cisplatin-resistant cervical cancer cells, enhancing their p53 levels and rate of apoptosis when administered together with cisplatin. Our findings reveal a therapeutic strategy to target a specific molecular pathway that contributes to p53 degradation for the treatment of patients with cervical cancer, particularly with cisplatin resistance

Viral and serological kinetics in Zika virus-infected patients in South Korea

Abstract Zika virus is a mosquito-borne flavivirus that causes clinical symptoms similar to those observed in dengue and chikungunya virus infections. The Korea Centers for Disease Control and Prevention initiated laboratory testing using a real-time reverse transcription-polymerase chain reaction in January 2016. More than 1,000 suspected cases of infection were tested and nine were confirmed as imported cases of Zika virus infection from January to July 2016. The travel destinations of the infected individuals were Brazil, Philippines, Viet Nam, Guatemala, Puerto Rico, and the Dominican Republic. Phylogenetic analysis based on the partial envelope gene indicated that the viruses belonged to the Asian genotype circulating in South America. We further investigated the duration for which the viral RNA and virus-specific antibodies were detectable after the symptom onset. After the day of symptom onset, Zika virus was detectable until 6 days in serum, 14 days in urine and saliva, and 58 days in semen. Immunoglobulin M against Zika virus was detected as early as 2 days after the symptom onset and was maintained at these levels until 41 days, whereas Immunoglobulin G was detectable from 8 days after the symptom onset and was maintained until 52 days. These findings would help diagnostic laboratories improve their testing programs for Zika virus infection

HDAC8 Deacetylates HIF-1α and Enhances Its Protein Stability to Promote Tumor Growth and Migration in Melanoma

Melanoma is the most lethal type of skin cancer, and it causes more than 55,000 deaths annually. Although regional melanoma can be surgically removed, once melanoma metastasizes to other regions of the body, the survival rate drops dramatically. The current treatment options are chemotherapy, immunotherapy, and targeted therapy. However, the low response rate and the development of resistance necessitate the search for a novel therapeutic target in melanoma. Hypoxia-inducible factor-1 α (HIF-1α) is overexpressed in melanoma and plays a crucial role in driving malignant transformation in cancer cells. Here, we identified that histone deacetylase 8 (HDAC8) enhances the protein stability of HIF-1α. HDAC8 directly binds to and deacetylates HIF-1α, thereby promoting its protein stability. This, in turn, upregulates the transcriptional activity of HIF-1α and promotes the expressions of its target genes, such as hexokinase 2 (HK2) and glucose transporter 1 (GLUT1). The inhibition of HDAC8 suppresses the proliferation and metastasis of melanoma cells. Furthermore, HDAC8 is correlated with HIF1A expression and poor prognosis in samples from patients with melanoma. These findings uncover a novel epigenetic mechanism that maintains HIF-1α stability and implicates the potential of HDAC8 inhibitors for melanoma therapy