Celadonite and smectite formation in the Úrkút Mn-carbonate ore deposit (Hungary)

Synsedimentary and early diagenetic oxygen levels are estimated by evaluating celadonitesmectite formation in marine Jurassic black shale-hosted manganese-carbonates. Celadonite formed under suboxic-dysaerobic conditions, Al-rich Fe-smectite formed at suboxic-anaerobic conditions, and nontronite formed at anoxic-anaerobic conditions during sedimentary burial. A genetic pathway by direct precipitation from solution is proposed for the enormous mass of celadonite, based on mineral and textural evidence. Lamination of the manganese ore is independent of clay-mineral composition and was given by a series of mineralized microbial Ferich biomats

Growth and mass wasting of volcanic centers in the northern South Sandwich arc, South Atlantic, revealed by new multibeam mapping

New multibeam (swath) bathymetric sonar data acquired using an EM120 system on the RRS James Clark Ross, supplemented by sub-bottom profiling, reveals the underwater morphology of a not, vert, similar 12,000 km2 area in the northern part of the mainly submarine South Sandwich volcanic arc. The new data extend between 55° 45′S and 57° 20′S and include Protector Shoal and the areas around Zavodovski, Visokoi and the Candlemas islands groups. Each of these areas is a discrete volcanic center. The entirely submarine Protector Shoal area, close to the northern limit of the arc, forms a 55 km long east–west-trending seamount chain that is at least partly of silicic composition. The seamounts are comparable to small subaerial stratovolcanoes in size, with volumes up to 83 km3, indicating that they are the product of multiple eruptions over extended periods. Zavodovski, Visokoi and the Candlemas island group are the summits of three 3–3.5 km high volcanic edifices. The bathymetric data show evidence for relationships between constructional volcanic features, including migrating volcanic centers, structurally controlled constructional ridges, satellite lava flows and domes, and mass wasting of the edifices. Mass wasting takes place mainly by strong erosion at sea level, and dispersal of this material along chutes, probably as turbidity currents and other mass flows that deposit in extensive sediment wave fields. Large scale mass wasting structures include movement of unconsolidated debris in slides, slumps and debris avalanches. Volcanism is migrating westward relative to the underlying plate and major volcanoes are asymmetrical, being steep with abundant recent volcanism on their western flanks, and gently sloping with extinct, eroded volcanic sequences to their east. This is consistent with the calculated rate of subduction erosion of the fore-arc

Surgical treatment for pulmonary metastases from esophageal carcinoma after definitive chemoradiotherapy: Experience from a single institution

<p>Abstract</p> <p>Background</p> <p>Surgical treatment for pulmonary metastases is known to be a safe and potentially curative procedure for various primary malignancies. However, there are few reports regarding the prognostic role of surgical treatment for pulmonary metastases from esophageal carcinoma, especially after definitive chemoradiotherapy (CRT).</p> <p>Methods</p> <p>We retrospectively reviewed 5 patients who underwent surgical treatment for pulmonary metastases from esophageal carcinoma at our institution. The primary treatment for esophageal carcinoma was definitive CRT, and a complete response (CR) was achieved in all patients.</p> <p>Results</p> <p>The surgical procedure for pulmonary metastases was wedge resection, and pathological complete resection was achieved in all 5 patients. The disease free interval after definitive CRT varied from 7 to 36 months, with a median of 19 months. There were no perioperative complications, but postoperative respiratory failure occurred in 1 patient. The postoperative hospital stay varied from 4 to 7 days, with a median of 6 days. Three patients are now alive with a good performance status (PS) and are disease free. The other 2 patients died of primary disease. The overall survival after surgical treatment varied from 20 to 90 months, with a median of 29 months.</p> <p>Conclusions</p> <p>Surgical treatment should be considered for patients with pulmonary metastases from esophageal carcinoma who previously received CRT and achieved a CR, because it provides not only a longer survival, but also a good postoperative PS for some patients.</p

A study of lymph node ratio in stage IV colorectal cancer

which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Background: The finding of metastasis in colorectal cancer, stage IV disease, has a major impact on prognosis and treatment strategy. Known important factors include the extent of the metastasis and the patients &apos; performance status. The lymph node factors are of known importance in earlier cancer stages but less described in metastatic disease. The aim of the study was to evaluate lymph node status and ratio as prognostic markers in stage IV colorectal cancer. Methods: The study was retrospective and assessing all patients operated, with bowel resection, for an initial stage IV colorectal cancer during 1999–2003 (n = 136). Basic demographic data as well as given treatment was assessed. The Lymph node ratio (LNR), the quota between the number of lymph node metastasis and assessed lymph nodes, was calculated. LNR groups were created by ratio thirds, 3 equally sized groups. The analysis was made by LNR group and by eligibility for chemotherapy with cancer specific survival as outcome parameter. Results: The median survival (CSS) for the entire group was 431 days with great variability. For the patients eligible for chemotherapy it ranged from 791 days in LNR-group 1 to 433 days for th

DNA methylation-associated inactivation of TGFβ-related genes DRM/Gremlin, RUNX3, and HPP1 in human cancers

The transforming growth factor β (TGFβ)-signalling pathway is deregulated in many cancers. We examined the role of gene silencing via aberrant methylation of DRM/Gremlin and HPP1, which inhibit TGFβ signalling, and RUNX3, which facilitates TGFβ-signalling, of all genes that are thought to be tumour suppressors, are aberrantly expressed, and are thus thought to have important role in human cancers. We examined DRM/Gremlin mRNA expression in 44 cell lines and the promoter methylation status of DRM/Gremlin, HPP1, and RUNX3 in 44 cell lines and 511 primary tumours. The loss of DRM/Gremlin mRNA expression in human cancer cell lines is associated with DNA methylation, and treatment with the methylation inhibitor-reactivated mRNA expression (n=13). Methylation percentages of the three genes ranged from 0–83% in adult tumours and 0–50% in paediatric tumours. Methylation of DRM/Gremlin was more frequent in lung tumours in smokers, and methylation of all three genes was inversely correlated with prognosis in patients with bladder or prostate cancer. Our results provide strong evidence that these TGFβ-related genes are frequently deregulated through aberrant methylation in many human malignancies

The clinical potential of antiangiogenic fragments of extracellular matrix proteins

Neovasculature development is a crucial step in the natural history of a cancer. While much emphasis has been placed on proangiogenic growth factors such as VEGF, it is clear that endogenous angiogenesis inhibitors also have critical roles in the regulation of this process. Recent research has identified several cryptic fragments of extracellular matrix/vascular basement membrane proteins that have potent antiangiogenic properties in vivo. It has become apparent that many of these fragments signal via interactions with endothelial integrins, although multiple downstream effector pathways have been implicated and endostatin, the first non-collagenous domain of collagen XVIII, influences an intricate signalling network. The activity of these molecules in animal models suggests that they may have significant clinical activity; however, results of phase I/II trials with endostatin were disappointing. Many possible reasons can be found for the failure of these studies. Weaknesses in trial design, endostatin administration regimen and patient selection are identifiable, and importantly the lack of a clearly defined antiangiogenic mechanism for endostatin hindered assessment of biologically effective dose. Additionally, in vivo immunological and proteolytic function-neutralising mechanisms may have negated endostatin's actions. Lessons learned from these studies will aid the future clinical development of other antiangiogenic extracellular matrix protein fragments