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Query: UMLS:C1332347 (ADH)
 2,230 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two inbred lines of Drosophila melanogaster extracted from a laboratory cage population and homozygous for the AdhS allele of alcohol dehydrogenase (Adh) showed almost a twofold difference in specific activity. Analysis of generations derived from these lines showed that the genetic variation in ADH activity was controlled by additive gene action. There was no evidence of directional dominance or of non-allelic interactions. Although the Adh structural gene is on the second chromosome there was a significant effect of the X chromosome, indicating the action of modifying genes.
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PMID:Genetical variation for enzyme activity in a population of Drosophila melanogaster. II. Aspects of the inheritance of alcohol dehydrogenase activity in Adhs/s flies. 81 Apr 63

Four inbred lines, two homozygous AdhS/S and two homozygous AdhF/F, were extracted from a laboratory cage population of Drosophila melanogaster and crossed in all combinations. Directional dominance for low ADH activity was present and confined to AdhF/S heterozygotes. The remaining genetical differences between the four lines for ADH activity were due to additive genetical variation. The frequency of the AdhS allele in the population was 0-89. The observed directional dominance for low ADH activity in AdhF/S heterozygotes corresponded to the general direction of selection for ADH activity within the population.
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PMID:Genetical variation for enzyme activity in a population of Drosophila melanogaster. III. Dominance relationships for alcohol dehydrogenase activity. 81 Apr 64

Fifteen highly inbred lines extracted by sib-mating from the laboratory cage population, "Texas", of Drosophila melanogaster were crossed in a half-diallel mating design. Female progeny were assayed individually for ADH activity at 25 degrees and 35 degrees C and for total protein. At 25 degrees C there was considerable additive genetical variation and the dominance variation was attributable to specific parents and to specific crosses at random in the diallel table. The character total protein also showed considerable additive variation but less dominance variation. Largely independent gene action was shown by the characters ADH activity and total protein. There were strong genotype-environment interactions for heat-stability. At 35 degrees C most of the genetical variation was additive and mainly due to modifier loci. It was concluded that at 25 degrees C dominance was ambidirectional and almost complete. This genetical architecture was compatible with a past history of stabilising selection for ADH activity in the "Texas" population.
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PMID:Genetical variation for enzyme activity in a population of Drosophila melanogaster. V. The genetical architecture, as shown by diallel analysis, of alcohol dehydrogenase (ADH) activity. 677 Dec 36

Despite modern therapy, one third to one half of patients who get breast cancer will eventually die from it. This disconcerting circumstance has focused attention on prevention, and preventing breast cancer will require a much better understanding of the biological abnormalities underlying its development and progression. Many studies into the mechanisms of invasive breast cancer evolution have evaluated presumed precursor lesions (e.g. proliferative disease without atypia, atypical ductal hyperplasia, and ductal carcinoma in-situ) for genetic alterations known to occur in fully developed invasive carcinomas. This approach has shed some light on events which may be important in early malignant transformation, including the observations that overexpression of the c-erbB-2 oncogene and mutations of the p53 tumor suppressor gene are present in significant subsets of DCIS, but not PDWA or ADH. Although this approach is limited by our incomplete knowledge of cancer genetics, there is still a great deal to learn about breast cancer evolution by evaluating cancer-associated genes in potential precursor lesions using established techniques such as immunohistochemistry and in situ hybridization.
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PMID:Immunohistochemical studies of early breast cancer evolution. 781 82

Early breast neoplasia may be defined in many ways. Any non-invasive or invasive but nonmetastatic breast cancer qualifies as early neoplasia in the sense that they are non-lethal. Before we can prevent lethal breast cancer, we must gain a better understanding of the biological abnormalities underlying its development and progression. Many studies into the mechanisms of breast cancer evolution have evaluated potential precursor lesions (e.g., proliferative disease without atypia [PDWA], atypical ductal hyperplasia [ADH], and ductal carcinoma in situ [DCIS]) for genetic alterations known to occur in fully developed invasive carcinomas. This approach has shed some light on events which may be important in early malignant transformation, including the observations that overexpression of the c-erbB-2 oncogene and mutations of the p53 tumor suppressor gene are present in significant subsets of DCIS, but not PDWA or ADH. This approach is limited by our incomplete knowledge of cancer genetics. However, there is more to learn by evaluating known cancer-associated genes in potential precursor lesions using established techniques such as immunohistochemistry and in situ hybridization. Until recently, technology could not detect unknown genetic abnormalities in microscopic lesions such as PDWA, ADH, or DCIS. Now, PCR-based techniques have the theoretical ability to detect novel tumor promoter and suppressor genes in clinical samples of these very small lesions. For example, suppressor-type genes may be detected using comprehensive mapping probes to identify loss of heterozygosity in PCR-amplified DNA extracted from a few hundred cells microdissected from either fresh or archival tissue.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Biomarkers in early breast neoplasia. 800 90

Aggressiveness is an ancestral behavior common to all animal species. Its neurophysiological mechanisms are similar in all vertebrates. Males are generally more aggressive than females. In this review, aggressive behavior in rodents, monkeys, and man and the role of testosterone and brain serotonin levels have been considered. Interspecific aggressiveness in rats has been studied considering the mouse-killing behavior; the neonatal androgenization of females increases adult mouse-killing as does the administration of testosterone in adults. Intraspecific aggressiveness was studied by putting two or more male rats (or mice) in the same cage; the condition of subjection or dominance is influenced by testosterone. In monkeys, testosterone is related to aggressiveness and dominance and, during the mating season, increases in testosterone levels and aggressive attitude are observed. In men, higher testosterone levels were obtained in perpetrators of violent crimes, in men from the army with antisocial behaviors, in subjects with impulsive behaviors, alcoholics and suicidals, in athletes using steroids, and during competitions. Aggressive and dominant behavior are distinguished. Testosterone influences both of these, even if man is usually inclined to affirm his power without causing physical damage. Testosterone receptors are mainly in some hypothalamic neurons, where it is aromatized into estrogens, which determine the increase in aggressiveness. A relation between testosterone levels and diencephalic serotonin has been shown: in fact, the lack of serotonin increases aggressive behaviors both in animals and man. Testosterone also increases ADH levels in the medial amygdala, lateral hypothalamus, and preoptical medial area, involved in aggressive behaviors.
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PMID:Testosterone and aggressiveness. 1579 10

By comparison of mass spectra from a small cohort of nipple aspiration fluids (NAF), we previously discovered a panel of five candidate breast cancer biomarkers among them an unidentified 4.7 kD peptide BF5. The purposes of the present study were to verify the presence of BF5 in an independent cohort; to determine the protein identity of BF5; and to provide insight into the biology of BF5 production and elevation in tumor-associated NAF. We prospectively collected bilaterally matched NAF from patients with unilateral Stage I/II breast cancer (IBC-31), ductal carcinoma in situ (DCIS-6), atypical ductal hyperplasia (ADH-5), and presumed healthy women who came to routine mammography and had a normal exam (31). Following the consolidation of its cancer-associated expression on SELDI-mass spectrometry, BF5 was isolated by gel electrophoresis and sequenced by tandem mass spectrometry. BF5 was elevated in 15-25% of women with IBC, DCIS, or ADH vs. 0% of controls. This elevation was restricted to the affected breasts. BF5 was identified as 41/42-aa C-terminal peptide of alpha1-antitrypsin (AAT), the principle inhibitor of serine protease neutrophile elastase. The full length AAT showed a consistent expression pattern as C-41/42, and C-41/42 can be generated in vitro by MMP-7 cleavage. In conclusion, elevated C-41/42 is likely the result of elevated AAT synthesis, and the activity of specific MMPs present within the tumor. As other C-terminal fragments of AAT are reported to function as tumor-derived suppressors to the host immune-system, elevated C-41/42 may also be predictive of a poor outcome.
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PMID:A unique proteolytic fragment of alpha1-antitrypsin is elevated in ductal fluid of breast cancer patient. 1990 53