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  • 1
    Publication Date: 2015-09-30
    Description: We report the development of a potent, selective histone deacetylase 6 (HDAC6) inhibitor. This HDAC6 inhibitor blocks growth of normal and transformed cells but does not induce death of normal cells. The HDAC6 inhibitor alone is as effective as paclitaxel in anticancer activity in tumor-bearing mice.
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
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  • 2
    Publication Date: 2016-01-29
    Description: Analytical Chemistry DOI: 10.1021/acs.analchem.5b03696
    Print ISSN: 0003-2700
    Electronic ISSN: 1520-6882
    Topics: Chemistry and Pharmacology
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  • 3
    Publication Date: 2014-05-06
    Description: In resprouting species, fire-induced topkill causes a reduction in height and leaf area without a comparable reduction in the size of the root system, which should lead to an increase in the efficiency of water transport after fire. However, large plants undergo a greater relative reduction in size, compared with small plants, so we hypothesized that this enhancement in hydraulic efficiency would be greatest among large growth forms. In the ecotone between long-leaf pine ( Pinus palustris Mill.) savannas and wetlands, we measured stomatal conductance ( g s ), mid-day leaf water potential ( leaf ), leaf-specific whole-plant hydraulic conductance ( K L.p ), leaf area and height of 10 species covering a range of growth forms in burned and unburned sites. As predicted, K L.p was higher in post-fire resprouts than in unburned plants, and the post-fire increase in K L.p was positively related to plant size. Specifically, large-statured species tended to undergo the greatest relative reductions in leaf area and height, and correspondingly experienced the greatest increases in K L.p . The post-fire increase in K L.p was smaller than expected, however, due to a decrease in absolute root hydraulic conductance (i.e., not scaled to leaf area). The higher K L.p in burned sites was manifested as an increase in g s rather than an increase in leaf . Post-fire increases in g s should promote high rates of photosynthesis for recovery of carbohydrate reserves and aboveground biomass, which is particularly important for large-statured species that require more time to recover their pre-fire size.
    Print ISSN: 0829-318X
    Electronic ISSN: 1758-4469
    Topics: Agriculture, Forestry, Horticulture, Fishery, Domestic Science, Nutrition
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  • 4
    Publication Date: 2014-06-04
    Description: We have prepared L- and D-deoxypolypeptides (DOPPs) by selective reduction of appropriately protected polyhistidines with borane, reducing the carbonyl groups to methylenes. The result is a chiral polyamine, not amide, with a mainly protonated backbone and chirally mounted imidazolylmethylene side chains that are mostly unprotonated at neutrality because of the...
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
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  • 5
    Publication Date: 1997-01-17
    Description: Familial combined hyperlipidemia (FCHL) is a common inherited lipid disorder, affecting 1 to 2 percent of the population in Westernized societies. Individuals with FCHL have large quantities of very low density lipoprotein (VLDL) and low density lipoprotein (LDL) and develop premature coronary heart disease. A mouse model displaying some of the features of FCHL was created by crossing mice carrying the human apolipoprotein C-III (APOC3) transgene with mice deficient in the LDL receptor. A synergistic interaction between the apolipoprotein C-III and the LDL receptor defects produced large quantities of VLDL and LDL and enhanced the development of atherosclerosis. This mouse model may provide clues to the origin of human FCHL.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Masucci-Magoulas, L -- Goldberg, I J -- Bisgaier, C L -- Serajuddin, H -- Francone, O L -- Breslow, J L -- Tall, A R -- HL 21006/HL/NHLBI NIH HHS/ -- HL 54591/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1997 Jan 17;275(5298):391-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Columbia University, 630 West 168 Street, New York, NY 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8994037" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apolipoprotein C-III ; Apolipoproteins B/blood ; Apolipoproteins C/*genetics ; Apolipoproteins E/blood ; Arteriosclerosis/etiology ; Carrier Proteins/genetics ; Cholesterol/blood ; Cholesterol Ester Transfer Proteins ; Cholesterol, HDL/blood ; Cholesterol, LDL/blood ; Cholesterol, VLDL/blood ; Diet ; *Disease Models, Animal ; Disease Susceptibility ; Female ; *Glycoproteins ; Humans ; *Hyperlipidemia, Familial Combined/blood/genetics ; Hyperlipoproteinemia Type IV/genetics ; Lipoproteins/blood ; Lipoproteins, VLDL/blood ; Male ; Mice ; Mice, Inbred C57BL ; *Mice, Transgenic ; Receptors, LDL/*genetics/metabolism ; Transgenes ; Triglycerides/blood
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
    Publication Date: 1990-08-17
    Description: Primary and secondary hypertriglyceridemia is common in the general population, but the biochemical basis for this disease is largely unknown. With the use of transgenic technology, two lines of mice were created that express the human apolipoprotein CIII gene. One of these mouse lines with 100 copies of the gene was found to express large amounts of the protein and to be severely hypertriglyceridemic. The other mouse line with one to two copies of the gene expressed low amounts of the protein, but nevertheless manifested mild hypertriglyceridemia. Thus, overexpression of apolipoprotein CIII can be a primary cause of hypertriglyceridemia in vivo and may provide one possible etiology for this common disorder in humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ito, Y -- Azrolan, N -- O'Connell, A -- Walsh, A -- Breslow, J L -- HL 36461/HL/NHLBI NIH HHS/ -- HL33435/HL/NHLBI NIH HHS/ -- HL33714/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1990 Aug 17;249(4970):790-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Rockefeller University, New York, NY 10021.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2167514" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apolipoprotein C-III ; Apolipoproteins C/blood/*genetics ; Chylomicrons/blood ; Cloning, Molecular ; DNA Restriction Enzymes/metabolism ; DNA, Recombinant/metabolism ; *Gene Expression ; Humans ; Hypertriglyceridemia/blood/*genetics ; Lipoproteins, VLDL/blood ; Mice ; Mice, Inbred C57BL ; Mice, Inbred CBA ; Mice, Transgenic ; Nucleic Acid Hybridization ; RNA, Messenger/genetics ; Triglycerides/blood
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
    Publication Date: 1989-04-07
    Description: Low-density lipoprotein (LDL) concentrations correlate with risk of coronary heart disease, and genetic variation affecting LDL levels influences atherosclerosis susceptibility. The principal LDL protein is apolipoprotein B (apoB); apoB is not exchangeable between lipoprotein particles and there is only one apoB per LDL particle. Plasma LDL therefore consists of two populations, one containing apoB derived from the maternal and one from the paternal apoB alleles. Products of the apob gene with high or low affinity for the MB-19 monoclonal antibody can be distinguished, and this antibody was used to identify heterozygotes with allele-specific differences in the amount of apoB in their plasma. A family study confirmed that the unequal expression phenotype was inherited in an autosomal dominant manner and was linked to the apob gene locus. Significant apoB genetic variation affecting plasma LDL levels may be more common than previously appreciated.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gavish, D -- Brinton, E A -- Breslow, J L -- HL32435/HL/NHLBI NIH HHS/ -- HL33714/HL/NHLBI NIH HHS/ -- HL36461/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1989 Apr 7;244(4900):72-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Rockefeller University, New York 10021.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2565046" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Aged ; *Alleles ; Apolipoproteins B/blood/*genetics ; Binding Sites, Antibody ; Child ; Child, Preschool ; Genetic Linkage ; Genotype ; Humans ; Lipoproteins, LDL/blood/*genetics ; Pedigree ; Phenotype ; Polymorphism, Restriction Fragment Length
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1996-05-03
    Description: As a species the mouse is highly resistant to atherosclerosis. However, through induced mutations it has been possible to develop lines of mice that are susceptible to this disease. For example, mice that are deficient in apolipoprotein E, a ligand important in lipoprotein clearance, develop atherosclerotic lesions resembling those observed in humans. These lesions are exacerbated when the mice are fed a high-cholesterol, high-fat, Western-type diet. Other promising models are mice that are deficient in the low density lipoprotein receptor and transgenic mice that express human apolipoprotein B and transdominant mutant forms of apolipoprotein E. These models are now being used to study the pathogenesis of atherosclerotic lesions, as well as the influence of genetics, environment, hormones, and drugs on lesion development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Breslow, J L -- New York, N.Y. -- Science. 1996 May 3;272(5262):685-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Biochemical Genetics and Metabolism, Rockefeller University, New York, 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8614828" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apolipoproteins B/deficiency/genetics ; Apolipoproteins E/deficiency/genetics ; *Arteriosclerosis/etiology/genetics/metabolism ; Cholesterol, Dietary/administration & dosage ; Dietary Fats/administration & dosage ; *Disease Models, Animal ; Genetic Predisposition to Disease ; Humans ; Mice ; Mice, Inbred Strains ; Mice, Knockout ; Mice, Transgenic ; Mutation ; Receptors, LDL/deficiency/genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
    Publication Date: 1978-07-14
    Description: Cultured skin fibroblasts from patients with cystic fibrosis (CF) are more resistant to dexamethasone toxicity than are normal cells. We now report that, when fibroblasts cultured from obligate CF heterozygotes are exposed to dexamethasone, they have an intermediate survival compared to normal and homozygous CF cells. When dexamethasone survival was tested on cells from four patients undergoing amniocentesis, cells from a woman at risk of producing a child with CF showed significant dexamethasone resistance, similar to that of fibroblasts derived from lnown CF homozygotes; the other amniotic cell specimens showed dexamethasone sensitivity similar to that of normal skin fibroblasts. These data suggest that the dexamethasone resistance previously observed in skin fibroblasts may also be useful in the prenatal diagnosis of CF.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Breslow, J L -- Epstein, J -- Fontaine, J H -- Forbes, G B -- New York, N.Y. -- Science. 1978 Jul 14;201(4351):180-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/663650" target="_blank"〉PubMed〈/a〉
    Keywords: Amniotic Fluid/cytology ; Cell Survival/drug effects ; Cystic Fibrosis/diagnosis/genetics/*physiopathology ; Dexamethasone/*toxicity ; Drug Resistance ; Female ; Heterozygote ; Homozygote ; Humans ; Pregnancy ; Prenatal Diagnosis
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1978-05-26
    Description: Risk factors for disease consist of (i) personal habits, such as cigarette smoking and excessive alcohol consumption, and (ii) bodily characteristics, such as hypertension and high serum cholesterol. Progress in identifying and quantifying risk factors is opening the way to the prevention of disease and maintenance of health. Systematic, controlled trials of intervention against risk factors are beginning to produce evidence on the extent of success in reducing both the factors and the mortality from associated diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Breslow, L -- New York, N.Y. -- Science. 1978 May 26;200(4344):908-12.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/644333" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Arteriosclerosis/etiology ; Coronary Disease/etiology/*prevention & control ; Disease/*etiology ; Female ; Humans ; Hypercholesterolemia/complications ; Hypertension/complications ; Lung Neoplasms/etiology ; Male ; Middle Aged ; *Preventive Medicine ; *Probability ; *Risk ; Smoking/complications
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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