Primary endothelial sarcoma of the thoracic aorta

Primary malignant tumors of the aorta are extremely rare. The case of a 64-year-old woman who presented with peripheral embolism to both femoropopliteal arteries is reported. The search for a source revealed a polypoid lesion severely narrowing the lumen of the distal thoracic aorta. Differential diagnosis included thrombus and primary aortic tumor. Extirpation of the tumorous lesion was performed. Histologic examination revealed intimal aortic sarcoma of endothelial cell origin. Although the liver was the only site of suspected metastases at the time of operation, during the 18-month follow-up until the patient's death, generalized metastatic spread had developed. This case report thus demonstrates the generally poor prognosis of this rare variety of aortic sarcoma, in particular when symptoms have already occurred.     

Integrating a Top-Gas Recycling and CO2 Electrolysis Process for H2-Rich Gas Injection and Reduce CO2 Emissions from an Ironmaking Blast Furnace

Introducing CO₂ electrochemical conversion technology to the iron-making blast furnace not only reduces CO₂ emissions, but also produces H₂ as a byproduct that can be used as an auxiliary reductant to further decrease carbon consumption and emissions. With adequate H₂ supply to the blast furnace, the injection of H₂ is limited because of the disadvantageous thermodynamic characteristics of the H₂ reduction reaction in the blast furnace. This paper presents thermodynamic analysis of H₂ behaviour at different stages with the thermal requirement consideration of an iron-making blast furnace. The effect of injecting CO₂ lean top gas and CO₂ conversion products H₂–CO gas through the raceway and/or shaft tuyeres are investigated under different operating conditions. H₂ utilisation efficiency and corresponding injection volume are studied by considering different reduction stages. The relationship between H₂ injection and coke rate is established. Injecting 7.9–10.9 m³/tHM of H₂ saved 1 kg/tHM coke rate, depending on injection position. Compared with the traditional blast furnace, injecting 80 m³/tHM of H₂ with a medium oxygen enrichment rate (9%) and integrating CO₂ capture and conversion reduces CO₂ emissions from 534 to 278 m³/tHM. However, increasing the hydrogen injection amount causes this iron-making process to consume more energy than a traditional blast furnace does.     

Interferon regulatory factor 6 is necessary, but not sufficient, for keratinocyte differentiation

Regulation of epidermal proliferation and differentiation is critical for maintenance of cutaneous homeostasis. Interferon Regulatory Factor 6 (Irf6)-deficient mice die perinatally and exhibit ectopic proliferation and defective epidermal differentiation. We sought to determine whether these disruptions of epidermal function were cell autonomous, and used embryonic Irf6(-/-) keratinocytes to understand the specific role of Irf6 in keratinocyte proliferation and differentiation. In the absence of Irf6, keratinocytes exhibited a heterogeneous phenotype with the presence of large cells. Irf6(-/-) keratinocytes displayed increased colony-forming efficiency compared with wild-type cells, suggesting that Irf6 represses long-term proliferation. Irf6 was present at low levels in wild-type keratinocytes in culture, and upregulated after induction of differentiation in vitro, along with upregulation of markers of early differentiation. However, Irf6(-/-) keratinocytes did not express markers of terminal differentiation. Overexpression of Irf6 in wild-type keratinocytes was insufficient to induce expression of markers of differentiation under growing conditions. Together, these results indicated that Irf6 is necessary, but not sufficient, for keratinocyte differentiation. Finally, using a transgenic mouse expressing Lac-Z under the regulation of an enhancer element 9.7 kb upstream of the Irf6 start site, we demonstrated that this element contributes to the regulation of Irf6 in the epidermis and keratinocytes in culture.     

Systemic protection by antioxidants against UVL-induced erythema

An antioxidant supplemented diet provided marked systemic protection against ultraviolet light mediated erythema in hairless mice. Among the individual constituents of the diet, butylated hydroxytoluene was most effective whereas glutathione and vitamins C and E afforded negligible protection. The mixture of antioxidants, and butylated hydroxytoluene individually, demonstrated diminished, but significant, protection when applied topically. The safety of this systemic photoprotectant and its clinical relevance at present is unknown.     

Wirtsbereichsverhalten der Bakteriophagen T3 und T7 an Escherichia coli K12-Stämmen

The closely related phages T3 and T7 exhibit different growth patterns on Escherichia coli W host cells (E. coli K12 derivatives). T7 grows normally while T3 does not adsorb. T3h_w mutants displaying a T7-like host range were isolated and described.     

Marker chromosome genomic structure and temporal origin implicate a chromoanasynthesis event in a family with pleiotropic psychiatric phenotypes

Small supernumerary marker chromosomes (sSMC) are chromosomal fragments difficult to characterize genomically. Here, we detail a proband with schizoaffective disorder and a mother with bipolar disorder with psychotic features who present with a marker chromosome that segregates with disease. We explored the architecture of this marker and investigated its temporal origin. Array comparative genomic hybridization (aCGH) analysis revealed three duplications and three triplications that spanned the short arm of chromosome 9, suggestive of a chromoanasynthesis‐like event. Segregation of marker genotypes, phased using sSMC mosaicism in the mother, provided evidence that it was generated during a germline‐level event in the proband's maternal grandmother. Whole‐genome sequencing (WGS) was performed to resolve the structure and junctions of the chromosomal fragments, revealing further complexities. While structural variations have been previously associated with neuropsychiatric disorders and marker chromosomes, here we detail the precise architecture, human life‐cycle genesis, and propose a DNA replicative/repair mechanism underlying formation.     

Merging models of hepatitis C virus pathogenesis

Chronic hepatitis C virus (HCV) infection is one of the major causes for development of liver cirrhosis and end-stage liver disease. This article reviews two contrasting models of HCV pathogenesis, discusses the merits of each, and presents a rationale for combining the two models into one. Any successful model of HCV pathogenesis must explain how the characteristic features of cirrhosis and end-stage liver disease arise. These features include the loss of hepatocyte function (low serum albumin and reduced clotting ability); the presence of regenerative nodules; and the deposition of excessive extracellular matrix material, especially collagen (fibrosis), which is associated with the transformation of the liver sinusoids to capillary-like structures leading to portal hypertension. A successful model should explain several observations about the rate of disease progression. HCV is characterized by slow progression of fibrogenesis and, importantly, cirrhosis seems to develop only after a long latency (and only in a subset of patients). Among the prognostic factors of disease progression, the age at infection with the HCV virus and the presence of fibrosis appear to be highly relevant in predicting the development of progressive fibrosis. Traditional models of HCV pathogenesis propose that fibrogenesis is the predominant process. Fibrogenesis is induced by activation of fibrogenic cells, such as stellate cells, which results in excessive collagen deposition. By altering the normal architecture and vasculature, the collagen bands finally lead to cirrhosis and loss of organ function. Activation of stellate cells is induced by inflammation, cytokine signaling, and possibly by hepatocyte apoptosis. The telomere model of HCV pathogenesis suggests that hepatocyte damage plays an essential role in the development of cirrhosis. According to this model, hepatocyte damage leads to increased cell turnover, and to the accelerated shortening of hepatocyte telomeres. Critical telomere shortening leads to hepatocyte senescence, loss of hepatocyte function, exhaustion of hepatocellular regeneration, and to a greatly enhanced fibrotic response to injury. This review summarizes both models and presents evidence that these models are not mutually exclusive but rather can be merged into a comprehensive pathogenesis model that outlines the pathway of HCV-induced cirrhosis.     

Peptide-mediated broad-spectrum plant resistance to tospoviruses

Plant viruses have a significant impact on agronomic losses worldwide. A new strategy for engineering virus-resistant plants by transgenic expression of a dominant interfering peptide is presented here. This peptide of 29 aa strongly interacts with the nucleocapsid proteins (N) of different tospoviruses. Transgenic Nicotiana benthamiana lines expressing the peptide fused to a carrier protein were challenged with five different tospoviruses that have a nucleocapsid protein interacting with the peptide. In the transgenic plants, strong resistance to tomato spotted wilt virus, tomato chlorotic spot virus, groundnut ring spot virus, and chrysanthemum stem necrosis virus was observed. This therefore demonstrates the feasibility of using peptide "aptamers" as an in vivo tool to control viral infection in higher plants.