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Communicator, Dec. 2006, San Jose State University, Department Of Kinesiology Dec 2006

Communicator, Dec. 2006, San Jose State University, Department Of Kinesiology

Communicator (Kinesiology)

Volume 19, Issue 2


Communicator, Oct. 2006, San Jose State University, Department Of Kinesiology Oct 2006

Communicator, Oct. 2006, San Jose State University, Department Of Kinesiology

Communicator (Kinesiology)

Volume 19, Issue 2


Thermal Stress On Intertidal Limpets: Long-Term Hindcasts And Lethal Limits, Mark Denny, Luke Miller, Christopher Harley Apr 2006

Thermal Stress On Intertidal Limpets: Long-Term Hindcasts And Lethal Limits, Mark Denny, Luke Miller, Christopher Harley

Faculty Publications

When coupled with long-term meteorological records, a heat-budget model for the limpet, Lottia gigantea, provides a wealth of information regarding environmental and topographic controls of body temperature in this ecologically important species. (1) The maximum body temperature predicted for any site (37.5°C) is insufficient to kill all limpets, suggesting that acute thermal stress does not set an absolute upper limit to the elevation of L. gigantea on the shore. Therefore, the upper limit must be set by behavioral responses, sublethal effects or ecological interactions. (2) Temperatures sufficient to kill limpets are reached at only a small fraction of ...


Dna Damage Responses In Progeroid Syndromes Arise From Defective Maturation Of Prelamin A, Michael Sinensky, Y. Liu, A. Rusinol, Y. Wang, Y. Zou Jan 2006

Dna Damage Responses In Progeroid Syndromes Arise From Defective Maturation Of Prelamin A, Michael Sinensky, Y. Liu, A. Rusinol, Y. Wang, Y. Zou

Michael Sinensky

The genetic diseases Hutchinson-Gilford progeria syndrome (HGPS) and restrictive dermopathy (RD) arise from accumulation of farnesylated prelamin A because of defects in the lamin A maturation pathway. Both of these diseases exhibit symptoms that can be viewed as accelerated aging. The mechanism by which accumulation of farnesylated prelamin A leads to these accelerated aging phenotypes is not understood. Here we present evidence that in HGPS and RD fibroblasts, DNA damage checkpoints are persistently activated because of the compromise in genomic integrity. Inactivation of checkpoint kinases Ataxia-telangiectasia-mutated (ATM) and ATR (ATM- and Rad3-related) in these patient cells can partially overcome their ...


Farnesylated Lamins, Progeroid Syndromes And Farnesyl Transferase Inhibitors, Michael Sinensky, A. E. Rusinol Jan 2006

Farnesylated Lamins, Progeroid Syndromes And Farnesyl Transferase Inhibitors, Michael Sinensky, A. E. Rusinol

Michael Sinensky

Three mammalian nuclear lamin proteins, lamin B1, lamin B2 and the lamin A precursor, prelamin A, undergo canonical farnesylation and processing at CAAX motifs. In the case of prelamin A, there is an additional farnesylation-dependent endoproteolysis, which is defective in two congenital diseases: Hutchinson-Gilford progeria (HGPS) and restrictive dermopathy (RD). These two diseases arise respectively from defects in the prelamin A substrate and the enzyme (ZmpSte24) that processes it. Recent work has shed light on the roles of the lamin proteins and the enzymes involved in their farnesylation-dependent maturation. Other experimental work, including mouse model studies, have examined the possibility ...


Farnesylated Lamins, Progeroid Syndromes And Farnesyl Transferase Inhibitors, Michael Sinensky, A. E. Rusinol Jan 2006

Farnesylated Lamins, Progeroid Syndromes And Farnesyl Transferase Inhibitors, Michael Sinensky, A. E. Rusinol

Faculty Publications

Three mammalian nuclear lamin proteins, lamin B1, lamin B2 and the lamin A precursor, prelamin A, undergo canonical farnesylation and processing at CAAX motifs. In the case of prelamin A, there is an additional farnesylation-dependent endoproteolysis, which is defective in two congenital diseases: Hutchinson-Gilford progeria (HGPS) and restrictive dermopathy (RD). These two diseases arise respectively from defects in the prelamin A substrate and the enzyme (ZmpSte24) that processes it. Recent work has shed light on the roles of the lamin proteins and the enzymes involved in their farnesylation-dependent maturation. Other experimental work, including mouse model studies, have examined the possibility ...


Interpolation Of Tracking Data In A Fluid Environment, Y Tremblay, Scott A. Shaffer, S L. Fowler, C E. Kuhn, B I. Mcdonald, M J. Weise, C -A Bost, H Weimerskirch, D E. Crocker, M E. Goebel, D P. Costa Jan 2006

Interpolation Of Tracking Data In A Fluid Environment, Y Tremblay, Scott A. Shaffer, S L. Fowler, C E. Kuhn, B I. Mcdonald, M J. Weise, C -A Bost, H Weimerskirch, D E. Crocker, M E. Goebel, D P. Costa

Faculty Publications

Interpolation of geolocation or Argos tracking data is a necessity for habitat use analyses of marine vertebrates. In a fluid marine environment, characterized by curvilinear structures, linearly interpolated track data are not realistic. Based on these two facts, we interpolated tracking data from albatrosses, penguins, boobies, sea lions, fur seals and elephant seals using six mathematical algorithms. Given their popularity in mathematical computing, we chose Bézier, hermite and cubic splines, in addition to a commonly used linear algorithm to interpolate data. Performance of interpolation methods was compared with different temporal resolutions representative of the less-precise geolocation and the more-precise Argos ...


A Database For The Study Of Marine Mammal Behavior: Gap Analysis, Data Standardization, And Future Directions, Scott A. Shaffer, D P. Costa Jan 2006

A Database For The Study Of Marine Mammal Behavior: Gap Analysis, Data Standardization, And Future Directions, Scott A. Shaffer, D P. Costa

Faculty Publications

A relational database that contained published information on the diving behavior and/or movement patterns of marine mammals was compiled to facilitate a modeling effort of the Effects of Sound on the Marine Environment (ESME) program. A total of 448 references from reports, books, and peer-reviewed journal articles were obtained. The metadata describing each animal studied, location of the study, and equipment used were entered into the database as well as empirical data describing the diving behavior and movement patterns of each animal. In total, the database contained 1815 entries from 51 different marine mammal species or subspecies. The majority ...


Validation Of Water Flux And Body Composition In Glaucous Gulls (Larus Hyperboreus), Scott A. Shaffer, Gabrielsen, G.W., Verreault, J, Costa, D.P Jan 2006

Validation Of Water Flux And Body Composition In Glaucous Gulls (Larus Hyperboreus), Scott A. Shaffer, Gabrielsen, G.W., Verreault, J, Costa, D.P

Faculty Publications

Water influx rates (WIR) measured with tritiated water dilution were compared with direct measures of water and energy intake in glaucous gulls (Larus hyperboreus). Total body water (TBW) measured isotopically was also compared with TBW determined by body composition analysis (BCA) of the same birds. Seventeen wild gulls were captured and studied in outdoor enclosures at Ny-Ålesund, Svalbard, in July 2002. Gulls were hand-fed known quantities of Arctic cod (Boreogadus saida) or given water on the basis of one of four experimental treatments: (A) fasting, (B) fish only, (C) water only, or (D) fish and water. Water and energy content ...


Dna Damage Responses In Progeroid Syndromes Arise From Defective Maturation Of Prelamin A, Michael Sinensky, Y. Liu, A. Rusinol, Y. Wang, Y. Zou Jan 2006

Dna Damage Responses In Progeroid Syndromes Arise From Defective Maturation Of Prelamin A, Michael Sinensky, Y. Liu, A. Rusinol, Y. Wang, Y. Zou

Faculty Publications

The genetic diseases Hutchinson-Gilford progeria syndrome (HGPS) and restrictive dermopathy (RD) arise from accumulation of farnesylated prelamin A because of defects in the lamin A maturation pathway. Both of these diseases exhibit symptoms that can be viewed as accelerated aging. The mechanism by which accumulation of farnesylated prelamin A leads to these accelerated aging phenotypes is not understood. Here we present evidence that in HGPS and RD fibroblasts, DNA damage checkpoints are persistently activated because of the compromise in genomic integrity. Inactivation of checkpoint kinases Ataxia-telangiectasia-mutated (ATM) and ATR (ATM- and Rad3-related) in these patient cells can partially overcome their ...