Imminent Geologic and Hydrologic Hazards on Fort Ord BLM Land

The Bureau of Land Management acquired 7,500 acres of land as part of the re-use of the decommissioned Fort Ord Army base. A variety of geologic hazards exist on the landscape including gully erosion, mass wasting, and decaying earthen dams. This short report highlights a few critical areas that deserve closer evaluation and remediation. Of particular concern are decaying earthen dams and mass wasting of tall stream banks that may impact BLM infrastructure or adjacent urban development. (Document contains 13 paGES)

Electrochemical studies of lipophilic ion transport through BLM. The influence of sterols on its transport

Cyclic voltammetry was employed to study the influence of sterols on the lipophilic ion transport through the BLM. The mole fraction of the sterols (cholesterol, oxidized cholesterol). as referred to total lipid, was varied in a range of 0-0.8. Data demonstrate that a thin-layer model is suitable to this BLM system. By this model, the number of charges transported per lipophilic ion, the concentration of the ion in the membrane bulk phase and the aqueous/membrane phase partition coefficient could be calculated. These parameters proved that sterols had an obvious influence on the lipophilic ion transport. Cholesterol had a stronger influence on the ion transport than oxidized cholesterol. Its incorporation into egg lecithin membranes increased the partition coefficient beta of the ion up to more than 3-fold. Yet, oxidized cholesterol incorporated into egg lecithin membranes only increased the beta up to less than 2-fold, and the beta had no great variation at different oxidized cholesterol mole fractions. The higher beta obtained was partly due to the trace amount of solvent existing in the core of the lipid bilayers. At the different sterol mole fractions, combining the change of beta with the change of peak current, we also concluded that sterols had somewhat inhibiting effect on the ion transport at the higher sterols mole fraction (>0.4). These results are explained in terms of the possible change of dipole potential of the membrane produced by sterols and the decrease of the membrane fluidity caused by the condensation effect of sterols and the thinning effect caused by sterols. The substituting group (in the oxidized cholesterol) had some inhibiting effects on the ion transport at higher mole fractions (oxidized cholesterol mole fraction >0.4).

Peut-on être blâmé pour ses croyances? : le déontologisme épistémique face au problème de l'involontarisme doxastique

Peut-on parfois être blâmé pour ses croyances ? Selon les partisans du déontologisme épistémique, la pratique ordinaire consistant à blâmer et critiquer les gens pour leurs croyances est tout à fait légitime. Toutefois, d’autres philosophes soutiennent que malgré son omniprésence dans la vie de tous les jours, le blâme doxastique n’est jamais approprié. En effet, selon l’argument à partir de l’involontarisme doxastique, nous ne pouvons jamais être blâmés pour nos croyances puisque (1) nous pouvons être blâmés pour une croyance seulement si elle est sous notre contrôle volontaire et (2) nos croyances ne sont jamais sous notre contrôle volontaire. Le but de ce mémoire est de déterminer si les déontologistes peuvent répondre de manière convaincante à cet argument. Autrement dit, pouvons-nous parfois être blâmés pour nos croyances malgré ce qu’en disent les anti-déontologistes, ou faut-il leur donner raison et rejeter la pratique du blâme doxastique ? Pour répondre à cette question, je commence par clarifier l’argument anti-déontologiste en précisant la teneur de sa thèse centrale : l’involontarisme doxastique. Par la suite, je passe en revue différentes stratégies qui ont été proposées par des représentants du déontologisme pour défendre le blâme doxastique contre cet argument. Devant l’échec de ces réponses, je suggère une défense alternative du déontologisme selon laquelle l’involontarisme doxastique n’est pas incompatible avec le blâme doxastique. Si cette réponse est concluante, alors nous n’avons pas à donner raison aux anti-déontologistes : nous pouvons parfois être blâmés pour nos croyances.

Topo IIIalpha and BLM act within the Fanconi anemia pathway in response to DNA-crosslinking agents

The Bloom protein (BLM) and Topoisomerase IIIalpha are found in association with proteins of the Fanconi anemia (FA) pathway, a disorder manifesting increased cellular sensitivity to DNA crosslinking agents. In order to determine if the association reflects a functional interaction for the maintenance of genome stability, we have analyzed the effects of siRNA-mediated depletion of the proteins in human cells. Depletion of Topoisomerase IIIalpha or BLM leads to increased radial formation, as is seen in FA. BLM and Topoisomerase IIIalpha are epistatic to the FA pathway for suppression of radial formation in response to DNA interstrand crosslinks since depletion of either of them in FA cells does not increase radial formation. Depletion of Topoisomerase IIIalpha or BLM also causes an increase in sister chromatid exchanges, as is seen in Bloom syndrome cells. Human Fanconi anemia cells, however, do not demonstrate increased sister chromatid exchanges, separating this response from radial formation. Primary cell lines from mice defective in both Blm and Fancd2 have the same interstrand crosslink-induced genome instability as cells from mice deficient in the Fancd2 protein alone. These observations demonstrate that the association of BLM and Topoisomerase IIIalpha with Fanconi proteins is a functional one, delineating a BLM-Topoisomerase IIIalpha-Fanconi pathway that is critical for suppression of chromosome radial formation.

Functional analysis of BLAP75, a BLM-associated protein

Bloom syndrome (BS) is an autosomal recessive disorder characterized by dwarfism, immunodeficiency, impaired fertility, and most importantly, early development of a broad range of cancers. The hallmark of BS cells is hyper-recombination, characterized by a drastically elevated frequency of sister chromatid exchange (SCE). BLM, the gene mutated in BS, encodes a DNA helicase of the RecQ protein family. BLM is thought to participate in several DNA transactions and to interact with many proteins involved in DNA replication, recombination, and repair. However, the precise function of BLM and the BLM-dependent anti-tumor mechanism remain obscure. ^ A novel protein, BLAP75 (BLM-associated polypeptide, 75KD), was identified to form an evolutionarily conserved complex with BLM and DNA topoisomerase IIIα (Topo IIIα). Our work demonstrates that loss of BLAP75 destabilized BLM and Topo IIIα proteins. BLAP75 colocalized with BLM in subnuclear foci in response to DNA damage and the recruitment of BLM to these foci was BLAP75-dependent. Moreover, depletion of BLAP75 by siRNA resulted in an elevated SCE rate similar to cells depleted of BLM by siRNA. In addition, RNAi-mediated silencing of BLAP75 greatly diminished cell viability. This cellular deficiency was rescued by expression of wild type BLAP75 but not BLAP75 with mutated conserved domain III, which abrogated the interaction between BLAP75, BLM and Topo IIIα, suggesting that the integrity of BLM-Topo IIIα-BLAP75 complex might be critical for cell survival. Finally, I found that BLAP75 was phosphorylated during mitosis and upon various DNA-damaging agents, implying that BLAP75 might also function in mitosis and DNA damage response. ^ Taken together, this study has defined BLAP75 as an integral component of the BLM complex to maintain genome stability. Our findings provide insights into the molecular mechanisms of the BLM helicase pathway and tumorigenesis process associated with these mechanisms. ^

The DNA Helicase Activity of BLM Is Necessary for the Correction of the Genomic Instability of Bloom Syndrome Cells

Bloom syndrome (BS) is a rare autosomal recessive disorder characterized by growth deficiency, immunodeficiency, genomic instability, and the early development of cancers of many types. BLM, the protein encoded by BLM, the gene mutated in BS, is localized in nuclear foci and absent from BS cells. BLM encodes a DNA helicase, and proteins from three missense alleles lack displacement activity. BLM transfected into BS cells reduces the frequency of sister chromatid exchanges and restores BLM in the nucleus. Missense alleles fail to reduce the sister chromatid exchanges in transfected BS cells or restore the normal nuclear pattern. BLM complements a phenotype of a Saccharomyces cerevisiae sgs1 top3 strain, and the missense alleles do not. This work demonstrates the importance of the enzymatic activity of BLM for its function and nuclear localization pattern.

Land management systems : BLM faces risks in completing the Automated Land and Mineral Record System : report to the Chairman and Ranking Minority Member, Subcommittee on Interior and Related Agencies, Committee on Appropriations, House of Representatives /

"B-271929"--P. 1.

Utah BLM statewide wilderness environmental impact statement : draft /

Vol. 1 includes index.

Land management systems : status of BLM's actions to improve information technology management : report to the Subcommittee on Interior and Related Agencies, Committee on Appropriations, House of Representatives /

"B-284472"--P. 3.

BLM intensive wilderness inventory, Utah : final decision on wilderness study areas.

Cover title.

Opportunity and challenge : the story of BLM /

Mode of access: Internet.