Significance of gasification during oxy-fuel combustion of a lignite char in a fluidised bed using a fast UEGO sensor

In oxy-fuel combustion, fuel is combusted in a mixture of O₂ and recycled flue gas, i.e. the N₂ is replaced by CO₂ with the O₂ supplied from an air separation unit. The resulting gas consists largely of steam and CO2, which would be ready for sequestration when dried. In this work, the rate of reaction of particles of lignite char, typically 1200 μm diameter, in a fluidised bed reactor was determined using mixtures of O₂ with either CO₂ (“oxy-fuel”) or N₂. A universal exhaust-gas oxygen (UEGO) sensor enabled rapid measurements of the oxygen partial pressures in the off-gas, representing a novel application of this type of sensor. It was found that the rate of combustion of the particles in oxy-fuel is much more sensitive to temperature than in the equivalent O₂ and N₂ mixture. This is because for bed temperatures >∼1000 K particle combustion in mixtures of N₂ and O₂ is rate controlled by external mass transfer, which does not increase significantly with temperature. In contrast, using oxy-fuel, as the temperature increases, gasification by the high concentrations of CO₂ present becomes increasingly significant. At low temperatures, e.g. ∼1000 K, rates of combustion in oxy-fuel were lower than those in mixtures of O₂ and N₂ containing the same mole fraction of O₂ owing, primarily, to the lower diffusivities of O2 in CO₂ compared to O₂ in N₂ under conditions at which external mass transfer is still a significant factor in controlling the rate of reaction. At higher temperatures, e.g. 1223 K, oxy-fuel combustion rates were significantly higher than those in O₂ and N₂. The point at which oxy-fuel combustion becomes more rapid than in mixtures of O₂ and N₂ depends not only on temperature but also on the ratio of O₂ to CO₂ or N₂, respectively. A numerical model was developed to account for external mass transfer, changes in the temperature of the particle and for the effect of gasification under oxy-fuel conditions. The model confirmed that, at high temperatures, the high concentration of CO₂ at the surface of the burning particle in the oxy-fuel mixture led to an increase in the overall rate of carbon conversion via CO₂ + C → 2CO, whilst the rate of reaction with O₂ was limited by mass transfer. Good agreement was observed between the rates predicted by the numerical model and those observed experimentally.Financial support from the Engineering and Physical Sciences Research Council (Grant reference number: EP/G063265/1) and the Consejo Nacional de Ciencia y Tecnología (CONACYT) is also acknowledged.This is the author accepted manuscript. The final version is available from Elsevier via http://dx.doi.org/10.1016/j.fuel.2014.10.02

Role of simian virus 40 in cancer incidence in solid organ transplant patients

Transplant recipients have an increased risk of developing cancer in comparison with the general population. We present here data on cancer development in transplanted subjects who received organs from donors whose DNA was previously examined for the genomic insertion of Simian Virus 40 (SV40). Active follow-up of 387 recipients of solid organs donated by 134 donors, not clinically affected by cancer, was performed through the National Transplant Center (NTC). The average length of follow-up after transplant was 671±219 days (range 0–1085 days). Out of 134 proposed donors, 120 were utilised for organ donation. Of these, 12 (10%) were classified as positive for SV40 genomic insertion. None of the 41 recipients of organs from SV40 positive donors developed a tumour during the follow-up. In all, 11 recipients of organs given by SV40 negative donors developed a tumour (cancer incidence: 0.015 per year). In conclusion, cancer rates observed in our study are comparable to what reported by the literature in transplanted patients. Recipients of solid organs from SV40 positive donors do not have an increased risk of cancer after transplant. The role of SV40 in carcinogenesis in transplanted patients may be minimal

Thirty-five year mortality following receipt of SV40- contaminated polio vaccine during the neonatal period

Early poliovirus vaccines, both inactivated and live attenuated, were inadvertently contaminated with simian virus 40 (SV40), a monkey virus known to be oncogenic for newborn hamsters. Although large epidemiologic studies have not identified an elevated cancer risk in persons who received SV40-contaminated vaccines, fragments of SV40 DNA have recently been identified in certain human tumours. We report the follow-up of a cohort of 1073 persons, unique because they received SV40-contaminated poliovirus vaccines as newborns in 1961–63. A previous report of the status of these subjects as of 1977–79 identified 15 deaths, none due to cancer. The present study utilized the National Death Index to identify deaths in the cohort for the years 1979–96. Expected deaths were calculated from Cleveland area sex-, age-, race- and year-specific mortality rates. Increased mortality from all causes was not found. 4 deaths from cancer were found compared to 3.16 expected (P= 0.77). However, 2 deaths from testicular cancer occurred, compared to 0.05 expected (P= 0.002), which may be a chance finding due to multiple comparisons. There were 2 deaths due to leukaemia, a non-significant finding, and no deaths due to tumours of the types putatively associated with SV40. Although these results are, for the most part, consistent with other negative epidemiologic investigations of risks from SV40-contaminated vaccines, further study of testicular cancer may be warranted, and it will be important to continue monitoring this cohort which is now reaching middle-age. © 2001 Cancer Research Campaig

Characterization of highly frequent epitope-specific CD45RA(+)/CCR7(+/- )T lymphocyte responses against p53-binding domains of the human polyomavirus BK large tumor antigen in HLA-A*0201+ BKV-seropositive donors

Human polyomavirus BK (BKV) has been implicated in oncogenic transformation. Its ability to replicate is determined by the binding of its large tumor antigen (LTag) to products of tumor-suppressor genes regulating cell cycle, as specifically p53. We investigated CD8+ T immune responses to BKV LTag portions involved in p53 binding in HLA-A*0201+ BKV LTag experienced individuals. Peptides selected from either p53-binding region (LTag(351–450 )and LTag(533–626)) by current algorithms and capacity to bind HLA-A*0201 molecule were used to stimulate CD8+ T responses, as assessed by IFN-γ gene expression ex vivo and detected by cytotoxicity assays following in vitro culture. We observed epitope-specific immune responses in all HLA-A*0201+ BKV LTag experienced individuals tested. At least one epitope, LTag(579–587); LLLIWFRPV, was naturally processed in non professional antigen presenting cells and induced cytotoxic responses with CTL precursor frequencies in the order of 1/20'000. Antigen specific CD8+ T cells were only detectable in the CD45RA+ subset, in both CCR7+ and CCR7- subpopulations. These data indicate that widespread cellular immune responses against epitopes within BKV LTag-p53 binding regions exist and question their roles in immunosurveillance against tumors possibly associated with BKV infection

Detection of oncogenic virus genomes and gene products in lung carcinoma

We investigated a series of 122 cases of small cell lung carcinomas and non-small cell lung carcinomas for the presence of several viruses that are known to be oncogenic in humans. Thus, viral genomes (DNA) and/or RNA transcripts and/or proteins of human papillomaviruses (HPV) 16, 18, 31, 33, 51, Epstein–Barr virus (EBV), human herpesvirus 8 (HHV-8), human cytomegalovirus (HCMV) and simian virus 40 (SV40) were investigated on tissue sections (prepared in tissue microarrays) with different techniques of immunohistochemistry and in situ hybridisation. None of the cases displayed a single positive tumour cell for all the viruses tested whatever the technique applied. Of note, in five cases of tumours with lymphoid infiltrates, we detected scattered EBV (EBER)-positive bystander lymphocytes. In three cases, a faint nuclear staining was found with the anti-latent nuclear antigen/LANA1 (HHV-8) antibody. These cases were checked by PCR with two sets of primers (orf 26 and orf 75) and remained negative for this latter virus. Taken together, our data strongly suggest that the conventional human oncogenic viruses (HPV, EBV, HCMV, HHV-8 and SV40) are unlikely to play some role in the development of lung carcinomas

Epigenetic mechanisms in virus-induced tumorigenesis

About 15–20% of human cancers worldwide have viral etiology. Emerging data clearly indicate that several human DNA and RNA viruses, such as human papillomavirus, Epstein–Barr virus, Kaposi’s sarcoma-associated herpesvirus, hepatitis B virus, hepatitis C virus, and human T-cell lymphotropic virus, contribute to cancer development. Human tumor-associated viruses have evolved multiple molecular mechanisms to disrupt specific cellular pathways to facilitate aberrant replication. Although oncogenic viruses belong to different families, their strategies in human cancer development show many similarities and involve viral-encoded oncoproteins targeting the key cellular proteins that regulate cell growth. Recent studies show that virus and host interactions also occur at the epigenetic level. In this review, we summarize the published information related to the interactions between viral proteins and epigenetic machinery which lead to alterations in the epigenetic landscape of the cell contributing to carcinogenesis

Chronic Viral Infection and Primary Central Nervous System Malignancy

Primary central nervous system (CNS) tumors cause significant morbidity and mortality in both adults and children. While some of the genetic and molecular mechanisms of neuro-oncogenesis are known, much less is known about possible epigenetic contributions to disease pathophysiology. Over the last several decades, chronic viral infections have been associated with a number of human malignancies. In primary CNS malignancies, two families of viruses, namely polyomavirus and herpesvirus, have been detected with varied frequencies in a number of pediatric and adult histological tumor subtypes. However, establishing a link between chronic viral infection and primary CNS malignancy has been an area of considerable controversy, due in part to variations in detection frequencies and methodologies used among researchers. Since a latent viral neurotropism can be seen with a variety of viruses and a widespread seropositivity exists among the population, it has been difficult to establish an association between viral infection and CNS malignancy based on epidemiology alone. While direct evidence of a role of viruses in neuro-oncogenesis in humans is lacking, a more plausible hypothesis of neuro-oncomodulation has been proposed. The overall goals of this review are to summarize the many human investigations that have studied viral infection in primary CNS tumors, discuss potential neuro-oncomodulatory mechanisms of viral-associated CNS disease and propose future research directions to establish a more firm association between chronic viral infections and primary CNS malignancies

Significance of gasification during oxy-fuel combustion of a lignite char in a fluidised bed using a fast UEGO sensor

In oxy-fuel combustion, fuel is combusted in a mixture of O2 and recycled flue gas, i.e. the N2 is replaced by CO2 with the O2 supplied from an air separation unit. The resulting gas consists largely of steam and CO2, which would be ready for sequestration when dried. In this work, the rate of reaction of particles of lignite char, typically 1200 μm diameter, in a fluidised bed reactor was determined using mixtures of O2 with either CO2 ("oxy-fuel") or N2. A universal exhaust-gas oxygen (UEGO) sensor enabled rapid measurements of the oxygen partial pressures in the off-gas, representing a novel application of this type of sensor. It was found that the rate of combustion of the particles in oxy-fuel is much more sensitive to temperature than in the equivalent O2 and N2 mixture. This is because for bed temperatures >∼1000 K particle combustion in mixtures of N2 and O2 is rate controlled by external mass transfer, which does not increase significantly with temperature. In contrast, using oxy-fuel, as the temperature increases, gasification by the high concentrations of CO2 present becomes increasingly significant. At low temperatures, e.g. ∼1000 K, rates of combustion in oxy-fuel were lower than those in mixtures of O2 and N2 containing the same mole fraction of O2 owing, primarily, to the lower diffusivities of O2 in CO2 compared to O2 in N2 under conditions at which external mass transfer is still a significant factor in controlling the rate of reaction. At higher temperatures, e.g. 1223 K, oxy-fuel combustion rates were significantly higher than those in O2 and N2. The point at which oxy-fuel combustion becomes more rapid than in mixtures of O2 and N2 depends not only on temperature but also on the ratio of O2 to CO2 or N2, respectively. A numerical model was developed to account for external mass transfer, changes in the temperature of the particle and for the effect of gasification under oxy-fuel conditions. The model confirmed that, at high temperatures, the high concentration of CO2 at the surface of the burning particle in the oxy-fuel mixture led to an increase in the overall rate of carbon conversion via CO2 + C → 2CO, whilst the rate of reaction with O2 was limited by mass transfer. Good agreement was observed between the rates predicted by the numerical model and those observed experimentally