MR447: Seasonal Water Table and Temperature Relationships in Calcareous Till and Residual Soils of Central Maine

Water table depths and soil temperatures were monitored for four growing seasons in six calcareous till pedons developed on gently rolling to level till plains in Corinth and Exeter, Maine. These soils are part of a new catena that supports potato production in southeastern Penobscot County. Three of these coarse-loamy to fine-loamy pedons are moderately well drained Oxyaquic Eutrudepts taxadjuncts in potato fields, and three are somewhat poorly drained Aquic Dystric Eutrudepts in predominantly deciduous forest. Soil morphology, hydrologic data, and a,a dipyridyl applications support the described subgroup classification of each pedon, along with the udic moisture regime. Despite a smooth, glaciated landscape that would suggest the presence of extensive lodgment till, five observation sites lacked a densic contact and one contained residuum (saprolite) in the substratum. Apparent water tables in the SPD very deep soils, as well as oxyaquic hydrology in the deep soils on 0 to 3 percent slopes, suggest the more permeable subglacial melt-out till predominating, rather than lodgment till in all of these pedons. Growing season concepts were compared based on frost-free season at 0 and -2.2° C thresholds, soil temperatures in the plow layer, soil temperature at 50 cms and well-water temperature. The commencement of the growing season in the spring did not differ much across all five concepts. However, in the fall there was a 4- to 8-week lag between the air or shallower soil-temperature growing-season concepts and the deeper soil or well-water-temperature growing-season concepts. Daytime air temperature during the first 2 years of monitoring differed significantly between spring and fall seasons, but not between field and forest sites within each season.https://digitalcommons.library.umaine.edu/aes_miscreports/1027/thumbnail.jp

The Deglaciation of Maine, USA

The glacial geology of Maine records the northward recession of the Late Wisconsinan Laurentide Ice Sheet, followed by development of a residual ice cap in the Maine-Québec border region due to marine transgression of the St. Lawrence Lowland in Canada. The pattern of deglaciation across southern Maine has been reconstructed from numerous end moraines, deltas and submarine fans deposited during marine transgression of the coastal lowland. Inland from the marine limit, a less-detailed sequence of deglaciation is recorded by striation patterns, meltwater channels, scattered moraines and waterlain deposits that constrain the trend of the ice margin. There is no evidence that the northern Maine ice cap extended as far south-west as the Boundary Mountains and New Hampshire border. Newly-obtained radiocarbon ages from marine and terrestrial ice-proximal environments have improved the chronology of glacial recession in Maine. Many of these ages were obtained by coring late-glacial sediments beneath ponds and lakes. Data from this study show that the state was deglaciated between about 14.5 and 11.0 ka BP (14C years). The coastal moraine belt in southern Maine was deposited by oscillatory ice-margin retreat during the cold pre-Bølling time. Rapid ice recession to northern Maine then occurred between 13 and 11 ka BP, during the warmer Bølling/Allerød chronozones. Radiocarbon-dated pond sediments in western and northern Maine show lithologic evidence of Younger Dryas climatic cooling and persistence of the northern ice cap into Younger Dryas time. A large discrepancy still exists between radiocarbon ages of deglaciation in coastal south-western Maine and the timing of ice retreat indicated by New England varve records in areas to the west. Part of this problem may stem from the uncertainty of reservoir corrections applied to the radiocarbon ages of marine organics

Deletion mapping of chromosome 16q in hepatocellular carcinoma

Hepatocellular carcinoma (HCC) frequently shows an allelic imbalance (AI) on chromosome 16q. In order to define the commonly affected regions on chromosome 16q, we assessed AI studies in 41 HCCs using a panel of 37 microsatellite markers. Thirty-five cases (85%) showed AI at one or more loci. Among the 35 cases with AI, 21 cases showed multiple AI, suggesting the wide scope of deletion on the long arm of chromosome 16, and the remaining 14 cases showed partial AI. Detailed deletion mapping identified two independent commonly deleted regions on this chromosome arm. These included the D16S3106 locus and D16S498 locus. In conclusion, we have demonstrated frequent AI on 16q in HCCs and identified two loci with frequent AI, which may harbour new tumour suppressor genes.ope

Mutation analysis of the Fanconi anaemia A gene in breast tumours with loss of heterozygosity at 16q24.3

The recently identified Fanconi anaemia A (FAA) gene is located on chromosomal band 16q24.3 within a region that has been frequently reported to show loss of heterozygosity (LOH) in breast cancer. FAA mutation analysis of 19 breast tumours with specific LOH at 16q24.3 was performed. Single-stranded conformational polymorphism (SSCP) analysis on cDNA and genomic DNA, and Southern blotting failed to identify any tumour-specific mutations. Five polymorphisms were identified, but frequencies of occurrence did not deviate from those in a normal control population. Therefore, the FAA gene is not the gene targeted by LOH at 16q24.3 in breast cancer. Another tumour suppressor gene in this chromosomal region remains to be identified. © 1999 Cancer Research Campaig

Segmentation of corpus callosum using diffusion tensor imaging: validation in patients with glioblastoma

Abstract Background This paper presents a three-dimensional (3D) method for segmenting corpus callosum in normal subjects and brain cancer patients with glioblastoma. Methods Nineteen patients with histologically confirmed treatment naïve glioblastoma and eleven normal control subjects underwent DTI on a 3T scanner. Based on the information inherent in diffusion tensors, a similarity measure was proposed and used in the proposed algorithm. In this algorithm, diffusion pattern of corpus callosum was used as prior information. Subsequently, corpus callosum was automatically divided into Witelson subdivisions. We simulated the potential rotation of corpus callosum under tumor pressure and studied the reproducibility of the proposed segmentation method in such cases. Results Dice coefficients, estimated to compare automatic and manual segmentation results for Witelson subdivisions, ranged from 94% to 98% for control subjects and from 81% to 95% for tumor patients, illustrating closeness of automatic and manual segmentations. Studying the effect of corpus callosum rotation by different Euler angles showed that although segmentation results were more sensitive to azimuth and elevation than skew, rotations caused by brain tumors do not have major effects on the segmentation results. Conclusions The proposed method and similarity measure segment corpus callosum by propagating a hyper-surface inside the structure (resulting in high sensitivity), without penetrating into neighboring fiber bundles (resulting in high specificity)

Translocator protein is a marker of activated microglia in rodent models but not human neurodegenerative diseases

Microglial activation plays central roles in neuroinflammatory and neurodegenerative diseases. Positron emission tomography (PET) targeting 18 kDa Translocator Protein (TSPO) is widely used for localising inflammation in vivo, but its quantitative interpretation remains uncertain. We show that TSPO expression increases in activated microglia in mouse brain disease models but does not change in a non-human primate disease model or in common neurodegenerative and neuroinflammatory human diseases. We describe genetic divergence in the TSPO gene promoter, consistent with the hypothesis that the increase in TSPO expression in activated myeloid cells depends on the transcription factor AP1 and is unique to a subset of rodent species within the Muroidea superfamily. Finally, we identify LCP2 and TFEC as potential markers of microglial activation in humans. These data emphasise that TSPO expression in human myeloid cells is related to different phenomena than in mice, and that TSPO-PET signals in humans reflect the density of inflammatory cells rather than activation state.Published versionThe authors thank the UK MS Society for financial support (grant number: C008-16.1). DRO was funded by an MRC Clinician Scientist Award (MR/N008219/1). P.M.M. acknowledges generous support from Edmond J Safra Foundation and Lily Safra, the NIHR Senior Investigator programme and the UK Dementia Research Institute which receives its funding from DRI Ltd., funded by the UK Medical Research Council, Alzheimer’s Society, and Alzheimer’s Research UK. P.M.M. and D.R.O. thank the Imperial College Healthcare Trust-NIHR Biomedical Research Centre for infrastructure support and the Medical Research Council for support of TSPO studies (MR/N016343/1). E.A. was supported by the ALS Stichting (grant “The Dutch ALS Tissue Bank”). P.M. and B.B.T. are funded by the Swiss National Science Foundation (projects 320030_184713 and 310030_212322, respectively). S.T. was supported by an “Early Postdoc.Mobility” scholarship (P2GEP3_191446) from the Swiss National Science Foundation, a “Clinical Medicine Plus” scholarship from the Prof Dr. Max Cloëtta Foundation (Zurich, Switzerland), from the Jean et Madeleine Vachoux Foundation (Geneva, Switzerland) and from the University Hospitals of Geneva. This work was funded by NIH grants U01AG061356 (De Jager/Bennett), RF1AG057473 (De Jager/Bennett), and U01AG046152 (De Jager/Bennett) as part of the AMP-AD consortium, as well as NIH grants R01AG066831 (Menon) and U01AG072572 (De Jager/St George-Hyslop)

Analysis of the 10q23 chromosomal region and the PTEN gene in human sporadic breast carcinoma

We examined a panel of sporadic breast carcinomas for loss of heterozygosity (LOH) in a 10-cM interval on chromosome 10 known to encompass the PTEN gene. We detected allele loss in 27 of 70 breast tumour DNAs. Fifteen of these showed loss limited to a subregion of the area studied. The most commonly deleted region was flanked by D10S215 and D10S541 and encompasses the PTEN locus. We used a combination of denaturing gradient gel electrophoresis and single-strand conformation polymorphism analyses to investigate the presence of PTEN mutations in tumours with LOH in this region. We did not detect mutations of PTEN in any of these tumours. Our data show that, in sporadic breast carcinoma, loss of heterozygosity of the PTEN locus is frequent, but mutation of PTEN is not. These results are consistent with loss of another unidentified tumour suppressor in this region in sporadic breast carcinoma. © 1999 Cancer Research Campaig

Building an immune-mediated coagulopathy consensus: early recognition and evaluation to enhance post-surgical patient safety

Topical hemostats, fibrin sealants, and surgical adhesives are regularly used in a variety of surgical procedures involving multiple disciplines. Generally, these adjuncts to surgical hemostasis are valuable means for improving wound visualization, reducing blood loss or adding tissue adherence; however, some of these agents are responsible for under-recognized adverse reactions and outcomes. Bovine thrombin, for example, is a topical hemostat with a long history of clinical application that is widely used alone or in combination with other hemostatic agents. Hematologists and coagulation experts are aware that these agents can lead to development of an immune-mediated coagulopathy (IMC). A paucity of data on the incidence of IMC contributes to under-recognition and leaves many surgeons unaware that this clinical entity, originating from normal immune responses to foreign antigen exposure, requires enhanced post-operative vigilance and judicious clinical judgment to achieve best outcomes