The opportunity of membrane technology for hydrogen purification in the power to hydrogen (P2H) roadmap: a review.

The global energy market is in a transition towards low carbon fuel systems to ensure the sustainable development of our society and economy. This can be achieved by converting the surplus renewable energy into hydrogen gas. The injection of hydrogen (⩽10% v/v) in the existing natural gas pipelines is demonstrated to have negligible effects on the pipelines and is a promising solution for hydrogen transportation and storage if the end-user purification technologies for hydrogen recovery from hydrogen enriched natural gas (HENG) are in place. In this review, promising membrane technologies for hydrogen separation is revisited and presented. Dense metallic membranes are highlighted with the ability of producing 99.9999999% (v/v) purity hydrogen product. However, high operating temperature (⩾300 °C) incurs high energy penalty, thus, limits its application to hydrogen purification in the power to hydrogen roadmap. Polymeric membranes are a promising candidate for hydrogen separation with its commercial readiness. However, further investigation in the enhancement of H2/CH4 selectivity is crucial to improve the separation performance. The potential impacts of impurities in HENG on membrane performance are also discussed. The research and development outlook are presented, highlighting the essence of upscaling the membrane separation processes and the integration of membrane technology with pressure swing adsorption technology.

Crosslinked PEG and PEBAX Membranes for Concurrent Permeation of Water and Carbon Dioxide.

Membrane technology can be used for both post combustion carbon dioxide capture and acidic gas sweetening and dehydration of natural gas. These processes are especially suited for polymeric membranes with polyether functionality, because of the high affinity of this species for both H2O and CO2. Here, both crosslinked polyethylene glycol diacrylate and a polyether-polyamide block copolymer (PEBAX 2533(©)) are studied for their ability to separate CO2 from CH4 and N2 under single and mixed gas conditions, for both dry and wet feeds, as well as when 500 ppm H2S is present. The solubility of gases within these polymers is shown to be better correlated with the Lennard Jones well depth than with critical temperature. Under dry mixed gas conditions, CO2 permeability is reduced compared to the single gas measurement because of competitive sorption from CH4 or N2. However, selectivity for CO2 is retained in both polymers. The presence of water in the feed is observed to swell the PEG membrane resulting in a significant increase in CO2 permeability relative to the dry gas scenario. Importantly, the selectivity is again retained under wet feed gas conditions. The presence of H2S is observed to only slightly reduce CO2 permeability through both membranes.

Aberrant Methylation Changes Detected in Cutaneous Squamous Cell Carcinoma of Immunocompetent Individuals.

In order to elucidate the role of epigenetic alterations in the development of cutaneous squamous cell carcinoma (SCC), we analyzed both gene-specific promoter hypermethylation and repetitive sequence hypomethylation in cutaneous SCC as well as normal skin tissue samples. We showed that methylation of DAPK1 and CDH13 was associated with cutaneous SCC. While methylation frequency of DAPK1 was increased from sun-protected normal skin, sun-exposed normal skin, perilesional to lesional tissues, methylation of CDH13 was almost exclusively detected in cutaneous SCC tissues. Further, methylation of DAPK1 and CDH13 was neither correlated with the presence of HPV nor with the presence of p53 mutations in lesional skin tissues. Finally, we detected trend of reduced methylation level of repetitive sequences from sun-protected, sun-exposed normal skin samples to perilesional, and lesional tissues from SCC patients. We conclude that both gene-specific hypermethylation and repetitive sequence hypomethylation are present in cutaneous SCC tissue samples; these epigenetic changes might represent an independent pathway in the development of cutaneous SCC.

Hypermethylation of CCND2 May Reflect a Smoking-Induced Precancerous Change in the Lung.

It remains unknown whether tobacco smoke induces DNA hypermethylation as an early event in carcinogenesis or as a late event, specific to overt cancer tissue. Using MethyLight assays, we analyzed 316 lung tissue samples from 151 cancer-free subjects (121 ever-smokers and 30 never-smokers) for hypermethylation of 19 genes previously observed to be hypermethylated in nonsmall cell lung cancers. Only APC (39%), CCND2 (21%), CDH1 (7%), and RARB (4%) were hypermethylated in >2% of these cancer-free subjects. CCND2 was hypermethylated more frequently in ever-smokers (26%) than in never-smokers (3%). CCND2 hypermethylation was also associated with increased age and upper lobe sample location. APC was frequently hypermethylated in both ever-smokers (41%) and never-smokers (30%). BVES, CDH13, CDKN2A (p16), CDKN2B, DAPK1, IGFBP3, IGSF4, KCNH5, KCNH8, MGMT, OPCML, PCSK6, RASSF1, RUNX, and TMS1 were rarely hypermethylated (<2%) in all subjects. Hypermethylation of CCND2 may reflect a smoking-induced precancerous change in the lung.

DNA methylation changes in normal liver tissues and hepatocellular carcinoma with different viral infection.

Hepatocellular carcinoma (HCC) is known to be associated with both HBV and HCV. While epigenetic changes have been previously reported to be associated with hepatocellular carcinoma (HCC), whether the epigenetic profile of HBC associated HCC differs from that of HCV-associated HCC is unclear. We analyzed DNA methylation of ten genes (APC, CCND2, CDKN2A, GSTP1, HOXA9, RARB, RASSF1, RUNX, SFRP1, and TWIST1) using MethyLight assays on 65 archived liver tissue blocks. Three genes (APC, CCND2, and GSTP1) were frequently methylated in normal liver tissues. Five genes (APC, CDKN2A, HOXA9, RASSF1, and RUNX) were significantly more frequently methylated in malignant liver tissues than normal liver tissues. Among HCC cases, HOXA9, RASSF1 and SFRP1 were methylated more frequently in HBV-positive HCC cases, while CDKN2A were significantly more frequently methylated in HCV-positive HCC cases. Our data support the hypothesis that HCC resulting from different viral etiologies is associated with different epigenetic changes.

DNA hypermethylation of tumors from non-small cell lung cancer (NSCLC) patients is associated with gender and histologic type.

BACKGROUND: We previously identified a number of genes which were methylated significantly more frequently in the tumor compared to the non-cancerous lung tissues from non-small cell lung cancer (NSCLC) patients. Detection of methylation profiles of genes in NSCLC could provide insight into differential pathways to malignancy and lead to strategies for better treatment of individuals with NSCLC. METHODS: We determined the DNA methylation status of 27 genes using quantitative MethyLight assays in lung tumor samples from 117 clinically well-characterized NSCLC patients. RESULTS: Hypermethylation was detected in one of more of the genes in 106 (91%) of 117 cases and was detected at high levels (percentage methylation reference (PMR)> or =4%) in 79% of NSCLC cases. Methylation of APC, CCND2, KCNH5 and, RUNX was significantly more frequent in adenocarcinomas compared to squamous cell carcinomas (SCC), while methylation of CDKN2A was more common in SCC. Hypermethylation of KCNH5, KCNH8, and RARB was more frequent in females compared to males. Hypermethylation of APC and CCND2 was inversely associated with proliferation score assessed by Ki-67 level. CONCLUSIONS: Our findings of differential gene hypermethylation frequencies in tumor tissues from patients with adenocarcinoma or squamous cell cancers and in females compared to males suggests that further investigation is warranted in order to more fully understand the potential disparate pathways and/or risk factors for NSCLC associated with histologic type and gender.

DNA methylation in tumor and matched normal tissues from non-small cell lung cancer patients.

We used MethyLight assays to analyze DNA methylation status of 27 genes on 49 paired cancerous and noncancerous tissue samples from non-small cell lung cancer (NSCLC) patients who underwent surgical resection. Seven genes (RARB, BVES, CDKN2A, KCNH5, RASSF1, CDH13, and RUNX) were found to be methylated significantly more frequently in tumor tissues than in noncancerous tissues. Only methylation of CCND2 and APC was frequently detected in both cancerous and noncancerous tissues, supporting the hypothesis that the methylation of these two genes is a preneoplastic change and may be associated with tobacco smoking exposure. Methylation of any one of eight genes (RASSF1, DAPK1, BVES, CDH13, MGMT, KCNH5, RARB, or CDH1) was present in 80% of NSCLC tissues but only in 14% of noncancerous tissues. Detection of methylation of these genes in blood might have utility in monitoring and detecting tumor recurrence in early-stage NSCLC after curative surgical resection.

Detection of hypermethylated genes in women with and without cervical neoplasia.

BACKGROUND: DNA methylation changes are an early event in carcinogenesis and are often present in the precursor lesions of various cancers. We examined whether DNA methylation changes might be used as markers of cervical intraepithelial neoplasia (CIN) and invasive cervical cancer (ICC). METHODS: We used methylation-specific polymerase chain reaction (PCR) to analyze promoter hypermethylation of 20 genes, selected on the basis of their role in cervical cancer, in 319 exfoliated cell samples and matched tissue biopsy specimens collected during two studies of Senegalese women with increasingly severe CIN and ICC (histology negative/atypical squamous cells of undetermined significance [ASCUS] = 142, CIN-1 = 39, CIN-2 = 23, CIN-3/carcinoma in situ [CIS] = 23, ICC = 92). Logic regression was used to determine the best set of candidate genes to use as disease markers. All statistical tests were two-sided. RESULTS: Similar promoter methylation patterns were seen in genes from exfoliated cell samples and corresponding biopsy specimens. For four genes (CDH13, DAPK1, RARB, and TWIST1), the frequency of hypermethylation increased statistically significantly with increasing severity of neoplasia present in the cervical biopsy (P<.001 for each). By using logic regression, we determined that the best panel of hypermethylated genes included DAPK1, RARB, or TWIST1. At least one of the three genes was hypermethylated in 57% of samples with CIN-3/CIS and in 74% of samples with ICC but in only 5% of samples with CIN-1 or less. The estimated specificity of the three-gene panel was 95%, and its sensitivity was 74% (95% confidence interval [CI] = 73% to 75%) for ICC and 52% (95% CI = 49% to 55%) for CIN-3/CIS. By extrapolation, we estimated that, among Senegalese women presenting to community-based clinics, detection of the DAPK1, RARB, or TWIST1 hypermethylated gene would reveal histologically confirmed CIN-3 or worse with a sensitivity of 60% (95% CI = 57% to 63%) and a specificity of 95% (95% CI = 94% to 95%). CONCLUSIONS: Aberrant promoter methylation analysis on exfoliated cell samples is a potential diagnostic tool for cervical cancer screening that potentially may be used alone or in conjunction with cytology and/or human papillomavirus testing.