Book Reviews

Reviews of the following books: Maine: A Bicentennial History by Charles E. Clark; History, Records, Recollections of Gray, Maine by George T. Hill; History of the Town of Burlington, Penobscot County, Maine from Settlement to 1975 by Alan H. Hawkins; Charlie York: Maine Coast Fisherman by Harold B. Cliffor

Cytolytic T Lymphocytes Specific for Tumors and Infected Cells from Mice with a Retrovirus-induced Immunodeficiency Syndrome.

LP-BM5 retrovirus complex-infected C57BL/6 mice develop immunodeficiency, somewhat analogous to AIDS, termed murine AIDS (MAIDS). After secondary stimulation with syngeneic B-cell lymphomas from LP-BM5-infected mice, C57BL/6 mice produced vigorous CD8+ cytotoxic T lymphocytes specific for MAIDS-associated tumors. An anti-LP-BM5 specificity was suggested because spleen and lymph node cells from LP-BM5-infected mice served as target cells in competition assays, and cells from LP-BM5, but not ecotropic, virus-infected mice functioned as secondary in vitro stimulators to generate cytotoxic T lymphocytes to MAIDS tumors

Clinical and molecular genetic features of pulmonary hypertension in patients with hereditary hemorrhagic telangiectasia

BACKGROUND: Most patients with familial primary pulmonary hypertension have defects in the gene for bone morphogenetic protein receptor II (BMPR2), a member of the transforming growth factor beta (TGF-beta) superfamily of receptors. Because patients with hereditary hemorrhagic telangiectasia may have lung disease that is indistinguishable from primary pulmonary hypertension, we investigated the genetic basis of lung disease in these patients. METHODS: We evaluated members of five kindreds plus one individual patient with hereditary hemorrhagic telangiectasia and identified 10 cases of pulmonary hypertension. In the two largest families, we used microsatellite markers to test for linkage to genes encoding TGF-beta-receptor proteins, including endoglin and activin-receptor-like kinase 1 (ALK1), and BMPR2. In subjects with hereditary hemorrhagic telangiectasia and pulmonary hypertension, we also scanned ALK1 and BMPR2 for mutations. RESULTS: We identified suggestive linkage of pulmonary hypertension with hereditary hemorrhagic telangiectasia on chromosome 12q13, a region that includes ALK1. We identified amino acid changes in activin-receptor-like kinase 1 that were inherited in subjects who had a disorder with clinical and histologic features indistinguishable from those of primary pulmonary hypertension. Immunohistochemical analysis in four subjects and one control showed pulmonary vascular endothelial expression of activin-receptor-like kinase 1 in normal and diseased pulmonary arteries. CONCLUSIONS: Pulmonary hypertension in association with hereditary hemorrhagic telangiectasia can involve mutations in ALK1. These mutations are associated with diverse effects, including the vascular dilatation characteristic of hereditary hemorrhagic telangiectasia and the occlusion of small pulmonary arteries that is typical of primary pulmonary hypertension

Recovery of the Historical SN1957D in X-rays with Chandra

SN1957D, located in one of the spiral arms of M83, is one of the small number of extragalactic supernovae that has remained detectable at radio and optical wavelengths during the decades after its explosion. Here we report the first detection of SN1957D in X-rays, as part of a 729 ks observation of M83 with \chandra. The X-ray luminosity (0.3 - 8 keV) is 1.7 (+2.4,-0.3) 10**37 ergs/s. The spectrum is hard and highly self-absorbed compared to most sources in M83 and to other young supernova remnants, suggesting that the system is dominated at X-ray wavelengths by an energetic pulsar and its pulsar wind nebula. The high column density may be due to absorption within the SN ejecta. HST WFC3 images resolve the supernova remnant from the surrounding emission and the local star field. Photometry of stars around SN1957D, using WFC3 images, indicates an age of less than 10**7 years and a main sequence turnoff mass more than 17 solar masses. New spectra obtained with Gemini-South show that the optical spectrum continues to be dominated by broad [O III] emission lines, the signature of fast-moving SN ejecta. The width of the broad lines has remained about 2700 km/s (FWHM). The [O III] flux dropped precipitously between 1989 and 1991, but continued monitoring shows the flux has been almost constant since. In contrast, radio observations over the period 1990-2011 show a decline rate inf the flux proportional to t**-4, far steeper than the rate observed earlier, suggesting that the primary shock has overrun the edge of a pre-SN wind.Comment: 28 pages, including 3 tables and 7 figures, accepted for publication in Ap

Cop1 constitutively regulates c-Jun protein stability and functions as a tumor suppressor in mice

Biochemical studies have suggested conflicting roles for the E3 ubiquitin ligase constitutive photomorphogenesis protein 1 (Cop 1; also known as Rfwd2) in tumorigenesis, providing evidence for both the oncoprotein c-Jun and the tumor suppressor p53 as its targets. Here we present what we believe to be the first in vivo investigation of the role of Cop1 in cancer etiology. Using an innovative genetic approach to generate an allelic series of Cop1, we found that Cop1 hypomorphic mice spontaneously developed malignancy at a high frequency in the first year of life and were highly susceptible to radiation-induced lymphomagenesis. Further analysis revealed that c-Jun was a key physiological target for Cop1 and that Cop1 constitutively kept c-Jun at low levels in vivo and thereby modulated c-Jun/AP-1 transcriptional activity. Importantly, Cop1 deficiency stimulated cell proliferation in a c-Jun-dependent manner. Focal deletions of COP1 were observed at significant frequency across several cancer types, and COP1 loss was determined to be one of the mechanisms leading to c-Jun upregulation in human cancer. We therefore conclude that Cop1 is a tumor suppressor that functions, at least in part, by antagonizing c-Jun oncogenic activity. In the absence of evidence for a genetic interaction between Cop1 and p53, our data strongly argue against the use of Cop1-inhibitory drugs for cancer therapy

Results of the Cooperative Uniform Soybean Tests, 1947 Part I. North Central States

United States Department of Agriculture, Agricultural Research Administration; Bureau of Plant Industry, Soils, and Agricultural Engineering, Division of Forage Crops and Diseases Cooperating with State Agricultural Experiment Station

Results of the Cooperative Uniform Soybean Tests, 1946 Part I. North Central States

United States Department of Agriculture, Agricultural Research Administration; Bureau of Plant Industry, Soils, and Agricultural Engineering, Division of Forage Crops and Diseases Cooperating with State Agricultural Experiment Station

Results of the Cooperative Uniform Soybean Tests, 1945. Part I. North Central States

United States Department of Agriculture Agricultural Research Administration Bureau of Plant Industry, Soils, and Agricultural Engineering, Division of Forage Crops and Diseases Cooperating with State Agricultural Experiment Station