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Review of Waite, Kevin, West of Slavery: The Southern Dream of a Transcontinental Empire
(The Civil War Monitor, 0021-07) Zander, Cecily N.
As an historian of the Civil War’s westernmost reaches, I have been eagerly anticipating the publication of Kevin Waite’s West of Slavery: The Southern Dream of a Transcontinental Empire. Waite’s book is a significant achievement of scholarship, building on older literatures of slavery, western expansion, and nineteenth-century imperialism while advancing a newer body of work grappling with alternative forms of coercive and unfree labor in the United States, the borderlands, the significance of the American West to the Civil War, and the interconnected relationship between the West and South during the Civil War era. Waite reveals not only the ways in which Southerners and slaveholders imagined the Southwest, but also examines the lasting consequences of those pro-slavery imperial visions for a region most Americans do not associate with slaveholding.
The elongin B ubiquitin homology domain
(Elsevier, 1999) Brower, Christopher S.; Shilatifard, Ali; Mather, Timothy; Kamura, Takumi; Takagi, Yuichiro; Haque, Dewan; Treharne, Annemarie; Foundling, Stephen I.; Conaway, Joan Weliky; Conaway, Ronald C.
Mammalian Elongin B is a 118-amino acid protein composed of an 84-amino acid amino-terminal ubiquitin-like domain and a 34-amino acid carboxyl-terminal tail. Elongin B is found in cells as a subunit of the heterodimeric Elongin BC complex, which was originally identified as a positive regulator of RNA polymerase II elongation factor Elongin A and subsequently as a component of the multiprotein von Hippel-Lindau tumor suppressor and suppressor of cytokine signaling complexes. As part of our effort to understand how the Elongin BC complex regulates the activity of Elongin A, we are characterizing Elongin B functional domains. In this report, we show that the Elongin B ubiquitin-like domain is necessary and sufficient for interaction with Elongin C and for positive regulation of Elongin A transcriptional activity. In addition, by site-directed mutagenesis of the Elongin B ubiquitin-like domain, we identify a short Elongin B region that is important for its interaction with Elongin C. Finally, we observe that both the ubiquitin-like domain and carboxyl-terminal tail are conserved in Drosophila melanogaster and Caenorhabditis elegans Elongin B homologs that efficiently substitute for mammalian Elongin B in reconstitution of the transcriptionally active Elongin ABC complex, suggesting that the carboxyl-terminal tail performs an additional function not detected in our assays.
Germany’s PDS: Between East and West
(International Institute of Political Science, 2002) Olsen, Jonathan
As with other communist successor parties, Germany's Party of Democratic Socialism (PDS) enjoyed a political comeback in the mid-1990s. The PDS's success can be explained by many eastern German voters' disenchantment with the social, cultural, and economic effects of reunification as well as by the distinctive regional and fragmented character of the German Political Party System that allows the PDS, as the self-proclaimed defender of "eastern interests," disproportionate political influence. The PDS is faced with a dilemma, however. In the long-term it will have to become a true all-German party of the left if it wishes to survive electorally. Yet in becoming an all-German party the PDS risks losing the distinctive eastern identity that has been so essential to its success hitherto.
A molecular basis for stabilization of the von hippel-lindau (VHL) tumor suppressor protein by components of the VHL ubiquitin ligase
(Elsevier, 2002) Kamura, Takumi; Brower, Christopher S.; Conaway, Ronald C.; Conaway, Joan Weliky
The multiprotein von Hippel-Lindau (VHL) tumor suppressor (CBCVHL, Cul2-ElonginBC-VHL) and SCF (Skp1-Cul1/Cdc53-F-box protein) complexes are members of structurally related families of E3 ubiquitin ligases that use a heterodimeric module composed of a member of the Cullin protein family and the RING finger protein Rbx1 (ROC1/Hrt1) to activate ubiquitylation of target proteins by the E2 ubiquitin-conjugating enzymes Ubc5 and Cdc34. VHL and F-box proteins function as the substrate recruitment subunits of CBCVHLand SCF complexes, respectively. In cells, many F-box proteins are short lived and are proposed to be ubiquitylated by an autocatalytic mechanism and destroyed by the proteasome following assembly into SCF complexes. In contrast, the VHL protein is stabilized by interaction with the Elongin B and C subunits of CBCVHL in cells. In this report, we have presented direct biochemical evidence that unlike the F-box protein Cdc4, which is ubiquitylated in vitro by Cdc34 in the context of the SCF, the VHL protein is protected from Ubc5-catalyzed ubiquitylation following assembly into the CBCVHL complex. CBCVHL is continuously required for negative regulation of hypoxia-inducible transcription factors in normoxic cells and of SCF complexes, many of which function only transiently during the cell cycle or in response to cellular signals. Our findings provide a molecular basis for the different modes of cellular regulation of VHL and F-box proteins and are consistent with the known roles of CBCVHL.
Human error: The principal cause of skydiving fatalities
(Society for Human Performance in Extreme Environments, 2003) Hart, Christian L.; Griffith, James D.
Between 1993 and 2001, 308 people died while participating in civilian recreational skydives in the United States. Using a database generated by the United States Parachute Association, the authors of the present study conducted an analysis to determine the proportion of fatalities that were due to human error. The results of the analysis indicated that human error was the principal cause in 86% of the cases. Methods for reducing human error fatalities are suggested.
Identification of mammalian mediator subunits with similarities to yeast mediator subunits srb5, srb6, med11, and ROX3
(Elsevier, 2003) Sato, Shigeo; Tomomori-Sato, Chieri; Banks, Charles A.S.; Sorokina, Irina; Parmely, Tari J.; Kong, Stephanie E.; Jin, Jingji; Cai, Yong; Lane, William S.; Brower, Christopher S.; Conaway, Ronald C.; Conaway, Joan Weliky
The Mediator is a multiprotein coactivator required for activation of RNA polymerase II transcription by DNA binding transactivators. We recently identified a mammalian homologue of yeast Mediator subunit Med8 and partially purified a Med8-containing Mediator complex from rat liver nuclei (Brower, C. S., Sato, S., Tomomori-Sato, C., Kamura, T., Pause, A., Stearman, R., Klausner, R. D., Malik, S., Lane, W. S., Sorokina, I., Roeder, R. G., Conaway, J. W., and Conaway, R. C. (2002) Proc. Natl. Acad. Sci. U. S. A. 99, 10353–10358). Analysis of proteins present in the most highly purified Med8-containing fractions by tandem mass spectrometry led to the identification of many known mammalian Mediator subunits, as well as four potential Mediator subunits exhibiting sequence similarity to yeast Mediator subunits Srb5, Srb6, Med11, and Rox3. Here we present direct biochemical evidence that these four proteins are bona fide mammalian Mediator subunits. In addition, we identify direct pairwise binding partners of these proteins among the known mammalian Mediator subunits. Taken together, our findings identify a collection of novel mammalian Mediator subunits and shed new light on the underlying architecture of the mammalian Mediator complex.
A mammalian homolog of drosophila melanogaster transcriptional coactivator intersex is a subunit of the mammalian Mediator Complex
(Elsevier, 2003) Sato, Shigeo; Tomomori-Sato, Chieri; Banks, Charles A.S.; Parmely, Tari J.; Sorokina, Irina; Brower, Christopher S.; Conaway, Ronald C.; Conaway, Joan Weliky
The multiprotein Mediator complex is a coactivator required for transcriptional activation of RNA polymerase II transcribed genes by DNA binding transcription factors. We previously partially purified a Med8-containing Mediator complex from rat liver nuclei (Brower, C. S., Sato, S., Tomomori-Sato, C., Kamura, T., Pause, A., Stearman, R., Klausner, R. D., Malik, S., Lane, W. S., Sorokina, I., Roeder, R. G., Conaway, J. W., and Conaway, R. C. (2002) Proc. Natl. Acad. Sci. U. S. A. 99, 10353–10358). Analysis of proteins present in the most highly enriched Mediator fractions by tandem mass spectrometry led to the identification of several new mammalian Mediator subunits, as well as several potential Mediator subunits. Here we identify one of these proteins, encoded by the previously uncharacterized AK000411 open reading frame, as a new subunit of the mammalian Mediator complex. The AK000411 protein, which we designate hIntersex (human Intersex), shares significant sequence similarity with the Drosophila melanogaster intersex protein, which has functional properties expected of a transcriptional coactivator specific for the Drosophila doublesex transactivator. In addition, we show that hIntersex assembles into a subcomplex with Mediator subunits p28b and TRFP. Taken together, our findings identify a new subunit of the mammalian Mediator and shed new light on the architecture of the mammalian Mediator complex.
Stanniocalcin-1 is a naturally occurring L-channel inhibitor in cardiomyocytes: relevance to human heart failure
(2003-07-01) Sheikh-Hamad, David; Bick, Roger; Gang-Yi, Wu; Monster Christensen, Birgitte; Razeghi, Peter; Poindexter, Brian; Taegtmeyer, Heinrich; Wamsley, Ann; Padda, Ranjit; Entman, Mark; Nielsen, Soren; Youker, Keith
Cardiomyocytes of the failing heart undergo profound phenotypic and structural changes that are accompanied by variations in the genetic program and profile of calcium homeostatic proteins. The underlying mechanisms for these changes remain unclear. Because the mammalian counterpart of the fish calcium-regulating hormone stanniocalcin-1 (STC1) is expressed in the heart, we reasoned that STC1 might play a role in the adaptive-maladaptive processes that lead to the heart failure phenotype. We examined the expression and localization of STC1 in cardiac tissue of patients with advanced heart failure before and after mechanical unloading using a left ventricular assist device (LVAD), and we compared the results with those of normal heart tissue. STC1 protein is markedly upregulated in cardiomyocytes and arterial walls of failing hearts pre-LVAD and is strikingly reduced after LVAD treatment. STC1 is diffusely expressed in cardiomyocytes, although nuclear predominance is apparent. Addition of recombinant STC1 to the medium of cultured rat cardiomyocytes slows their endogenous beating rate and diminishes the rise in intracellular calcium with each contraction. Furthermore, using whole cell patch-clamp studies in cultured rat cardiomyocytes, we find that addition of STC1 to the bath causes reversible inhibition of transmembrane calcium currents through L-channels. Our data suggest differential regulation of myocardial STC1 protein expression in heart failure. In addition, STC1 may regulate calcium currents in cardiomyocytes and may contribute to the alterations in calcium homeostasis of the failing heart. Stanniocalcin-1 (STC1) is a homodimeric glycoprotein hormone involved in calcium regulation in bony fish (8), where elevation of serum calcium triggers the release of STC1 from the corpuscles of Stannius (23), organs associated with the kidneys (26). On circulation in the gill and intestine, STC1 inhibits calcium flux from the aquatic environment through these organs, thus maintaining normal calcium concentrations in the blood (15, 24). In mammals, STC1 is expressed in multiple organs, including the heart, skeletal muscle, brain, thyroid, spleen, thymus, parathyroid, lung, kidney, pancreas, small intestine, colon, placenta, ovary, testes, and prostate (4, 5, 22). The wide expression of STC1 suggested that it might function in an autocrine and/or paracrine manner, whereas its localization to the heart and skeletal muscle suggested a role in myocyte function. Through the evolutionary process from fish to mammals, STC1 appears to have maintained its functional role in calcium regulation, because mammalian STC1 appears to be involved in calcium homeostasis in the normal physiology of the gut (16) and in the adaptive response of brain cells to ischemic injury (28). Because cardiomyocyte calcium homeostasis demonstrates a wide range of abnormalities in patients with heart failure (2, 9, 11, 13, 17, 21), we hypothesized that myocardial expression of STC1 may be relevant to calcium homeostasis in the failing heart. Our current data suggest differential expression of STC1 protein in cardiomyocytes and blood vessel walls of failing hearts and are consistent with a potential role for STC1 in cardiomyocyte calcium homeostasis.
Satisfaction with campus police services: A community policing initiative
(Project Innovation Austin LLC, 2004) Griffith, James D.; Hueston, Harry; Wilson, Eddie; Moyers, Casey; Hart, Christian L.
Problem: Higher education has seen dramatic increases in student enrollments, diversity and crime rates during the past 25 years. These changes have created the need for new approaches from campus law enforcement agencies. There has been a movement toward community oriented policing (COP) policies and practices by campus police departments to address these changes. A vital step as part of a comprehensive COP strategy is to gather information from its community members. Method: This study collected survey responses from 557 students at a mid-sized university on information regarding victimization, contact with campus police, satisfaction with campus police services, and overall feeling of safety. Results: There was a low crime rate on campus and those that were a victim of crime did tend to report it to a university official. Students were highly satisfied with campus police services and felt safe on campus. Conclusions: This survey represents an initial step toward developing a foundation for a community policing initiative. Implications of the findings are discussed.
A mammalian mediator subunit that shares properties with saccharomyces cerevisiae mediator subunit CSE2
(Elsevier, 2004) Tomomori-Sato, Chieri; Sato, Shigeo; Parmely, Tari J.; Banks, Charles A.S.; Sorokina, Irina; Florens, Laurence; Zybailov, Boris; Washburn, Michael P.; Brower, Christopher S.; Conaway, Ronald C.; Conaway, Joan Weliky
The multiprotein Mediator complex is a coactivator required for activation of RNA polymerase II transcription by DNA bound transcription factors. We previously identified and partially purified a mammalian Mediator complex from rat liver nuclei (Brower, C.S., Sato, S., Tomomori-Sato, C., Kamura, T., Pause, A., Stearman, R., Klausner, R.D., Malik, S., Lane, W.S., Sorokina, I., Roeder, R.G., Conaway, J.W., and Conaway, R.C. (2002) Proc. Natl. Acad. Sci. U. S. A. 99, 10353–10358). Analysis by tandem mass spectrometry of proteins present in the most highly purified rat Mediator fractions led to the identification of a collection of new mammalian Mediator subunits, as well as several potential Mediator subunits including a previously uncharacterized protein encoded by the FLJ10193 open reading frame. In this study, we present direct biochemical evidence that the FLJ10193 protein, which we designate Med25, is a bona fide subunit of the mammalian Mediator complex. In addition, we present evidence that Med25 shares structural and functional properties with Saccharomyces cerevisiae Mediator subunit Cse2 and may be a mammalian Cse2 ortholog. Taken together, our findings identify a novel mammalian Mediator subunit and shed new light on the architecture of the mammalian Mediator complex.
AT1A-mediated activation of kidney JNK1 and SMAD2 in obstructive uropathy: Preservation of kidney tissue mass using candesartan
(American Physiological Society, 2004-09-01) Wamsley-Davis, Ann; Padda, Ranjit; Truong, Luan D.; Tsao, Chun Chui; Zhang, Ping; Sheikh-Hamad, David
Literature suggests the involvement of the renin-angiotensin system and transforming growth factor (TGF)-β in the renal injury that follows chronic ureteric obstruction. SMAD proteins and the JNK1 cascade are essential components of TGF-β signaling machinery, and recent data suggest cooperative interaction between JNK1 and SMAD proteins in TGF-β-mediated gene expression. We used a rat model of chronic unilateral ureteric obstruction to study the effects of candesartan, an AT1A-receptor blocker, on tissue morphology and the activities of JNK1 and SMAD2 protein in the kidney. Ureteric obstruction for 28 days leads to interstitial fibrosis, tubule atrophy, and marked activation of SMAD2 and JNK1, without significant change in p38 kinase or ERK. Candesartan treatment, however, attenuated the chronic tubulointerstitial injury in obstructed kidneys and was associated with significant preservation of kidney tissue mass. Furthermore, treatment with candesartan diminished JNK1 activity and downregulated SMAD2 protein and activity in obstructed kidneys. In conclusion, obstructed kidneys showed chronic tubulointerstitial injury, which was associated with JNK1 and SMAD2 activation. The renoprotective effects afforded by AT1A-receptor blockade in obstructive uropathy are consistent with attenuation of JNK1- and SMAD2-mediated renal injury. Obstruction of urine flow complicates many human diseases, such as prostate hypertrophy, abdominopelvic malignancies, and retroperitoneal fibrosis. It is characterized by infiltration of mononuclear inflammatory cells, predominantly macrophages, and is accompanied by activation of cytokines, growth factors, and mediators of apoptosis, the net result of which is the deletion of tubular cells by apoptosis and replacement of renal parenchyma with fibrous tissue. If left untreated, chronic kidney obstruction leads to loss of functional renal parenchyma, and ultimately, the development of kidney failure. Numerous reports implicate the renin-angiotensin system in the pathogenesis of ureteric obstruction, and inhibition of the rennin-angiotensin system, using either angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers, has been shown to attenuate the renal injury that follows ureteric obstruction (19, 23, 37). Activation of the kidney renin-angiotensin system occurs immediately after urteric obstruction, with resultant vasoconstriction and salt and water retention (14). These hemodynamic changes are followed by the activation of a number of cytokines (6, 9, 20, 21, 36, 50), some of which have been directly linked to angiotensin II, such as monocyte chemotactic protein-1 (MCP-1) (20) and transforming growth factor-β (TGF-β) (22), which appears to play a key role in the genesis of the ensuing fibrosis (32). TGF-β signaling is initiated after ligand binding to the TGF-β receptor (15, 33), leading to phosphorylation of SMAD2 or SMAD3 (1, 47, 53). SMAD proteins represent a group of transcription factors involved in gene regulation downstream of the TGF-β receptor. A heteromeric SMAD proteins complex is formed (7), resulting in translocation of the complex to the nucleus (1, 31, 47), where it can interact with transcription factors directly (7), or indirectly (27), to regulate gene expression. It was recently reported that JNK pathway (25, 51), which targets the activation of c-Jun and activated transcription factor-2 (ATF-2) (8, 12, 16, 26), is stimulated rapidly by TGF-β in human fibrosarcoma cells and that JNK activity is essential for TGF-β-induced fibronectin production (17). Furthermore, it was also suggested that SMAD proteins and the JNK1 pathway interact cooperatively in TGF-β signaling (17). These observations assume particular importance, in light of recent data that implicate JNK1 in the development of cell apoptosis after ischemia and UV irradiation in a variety of tissues (2, 3). Apoptosis is a crucial component in the pathogenesis of ureteric obstruction (5, 49). Based on these observations, we hypothesized that JNK1 may be a key contributor to the development of renal injury and fibrosis in obstructive uropathy, and thus renal protection after AT1A-receptor blockade in obstructive uropathy may be related to the downregulation of JNK1 and SMAD proteins. Consistent with this hypothesis, our data suggest activation of SMAD2 and JNK1 signaling in obstructed kidneys in a manner that is AT1A dependent. AT1A- receptor blockade using candesartan downregulates JNK1 and SMAD2, decreases tissue fibrosis, and leads to tissue preservation in obstructed kidneys.
Collegiate skydivers: Do they fear death?
(Individual Differences Association, Inc, 2005) Griffith, James D.; Hart, C. Lanier
Skydiving is considered to be among the most dangerous sporting activities in the world. Each time a skydiver exits an aircraft, they essentially face death. Although there is a relatively high risk of death compared to other sports, a large number of individuals participate in this activity in a recreational capacity. The present study compared 54 collegiate skydivers (high-risk) and 54 college students who never made a skydive (low-risk) on death anxiety. Death anxiety was measured using the Collett-Lester Fear of Death Scale (Lester & Abdel-Khalek, 2003). The analyses revealed that skydivers had lower levels of death anxiety on three of the four dimensions. This finding is in opposition of studies that have found that individuals working in death-risk occupations (e.g., police officer, firefighter) had higher death anxiety scores compared to control groups. Possible explanations for these divergent findings include the extent to which individuals have personal control over death-risk situations and self-esteem enhancement.
Responses to the sports inventory for pain among BASE jumpers
(University of South Alabama, 2006) Griffith, James D.; Hart, Christian L.; Goodling, Morgan; Kessler, Jill; Whitmire, Andy
BASE jumping is considered to be among the most dangerous sporting activities in the world. Individuals involved in this activity jump off of four different types of fixed objects that include buildings, antennas, spans (e.g., bridges), and edges (e.g., cliffs). There are many similarities between skydiving and BASE jumping, but there are distinct differences that force BASE jumpers to deal with more hazards in less time resulting in a much smaller margin of error necessary to make a successful jump. Although there is a high risk of injury and death compared to more traditional sports, no studies have examined how these extreme sport participants perceive pain. A total of 134 BASE jumpers were categorized on the basis of experience (low, medium, high) and completed the Sports Inventory for Pain (Meyers, Bourgeois, Stewart, & LeUnes, 1992) that measured six dimensions of pain coping styles. Multivariate analyses revealed significant differences on five of the six dimensions. In each significant finding, there was a similar pattern such that experienced BASE jumpers used more conservative pain coping styles than inexperienced participants as conceptualized by the instrument. It is argued that more conservative responses among experienced jumpers are associated with a greater awareness of the risk factors involved in BASE jumping and a higher level of self-preservation.
Managerial beliefs about the behavioral cues of deception
(Individual Differences Association, Inc, 2006) Hart, Christian L.; Hudson, Lucas P.; Fillmore, Derek G.; Griffith, James D.
Lies and deception occur regularly in the workplace during the application and interview process, as excuses for failures and missed deadlines, or as excuses for absenteeism. Undoubtedly, this workplace deception results in tremendous financial losses for companies. Generally, people believe that they can use behavioral cues to detect when others are lying to them. This study examined the behavioral cues that managers use to detect when others are lying. Managers (N = 120) completed a survey in which they indicated the degree to which ten separate behavioral cues increase, decrease, or stay the same when people lie to them. For the most part, managers held incorrect beliefs about the behavioral changes that typically accompany lying. The managers' beliefs about lying behavior were compared to the beliefs held by non-managerial employees. The results of this comparison indicated that managers and non-managers hold similar incorrect beliefs about the behavioral changes that occur when people lie, although managers are more confident in their ability to detect lies.
Teaching grant writing with service learning
(International Society for Exploring Teaching and Learning, 2006) Griffith, James D.; Hart, Christian L.; Goodling, Morgan M.
Grant writing experience can be a valuable asset for students completing masters-level degree programs across a variety of disciplines. A service learning grant writing project was incorporated in a multidisciplinary program evaluation course as part of a writing requirement. Twelve students served as “ghost writers” and wrote grant proposals to foundations for community organizations. Projects were assessed by ratings provided by faculty across departments who served as judges. Qualitative data was collected from students and organizational sponsors that showed high levels of satisfaction from both groups and an awareness of reciprocity of benefit from service learning were observed in both groups. Benefits and limitations of the pedagogical technique are discussed.
Arginyltransferase, its specificity, putative substrates, bidirectional promoter, and splicing-derived isoforms
(Elsevier, 2006) Hu, Rong-Gui; Brower, Christopher S.; Wang, Haiqing; Davydov, Ilia V.; Sheng, Jun; Zhou, Jianmin; Tae Kwon, Yong; Varshavsky, Alexander
Substrates of the N-end rule pathway include proteins with destabilizing N-terminal residues. Three of them, Asp, Glu, and (oxidized) Cys, function through their conjugation to Arg, one of destabilizing N-terminal residues that are recognized directly by the pathway’s ubiquitin ligases. The conjugation of Arg is mediated by arginyltransferase, encoded by ATE1. Through its regulated degradation of specific proteins, the arginylation branch of the N-end rule pathway mediates, in particular, the cardiovascular development, the fidelity of chromosome segregation, and the control of signaling by nitric oxide.We show that mouse ATE1 specifies at least six mRNA isoforms, which are produced through alternative splicing, encode enzymatically active arginyltransferases, and are expressed at varying levels in mouse tissues. We also show that the ATE1 promoter is bidirectional, mediating the expression of bothATE1 and an oppositely oriented, previously uncharacterized gene. In addition, we identified GRP78 (glucose-regulated protein 78) and protein-disulfide isomerase as putative physiological substrates of arginyltransferase. Purified isoforms of arginyltransferase that contain the alternative first exons differentially arginylate these proteins in extract from ATE1 / embryos, suggesting that specific isoforms may have distinct functions. Although the N-end rule pathway is apparently confined to the cytosol and the nucleus, and although GRP78 and protein-disulfide isomerase are located largely in the endoplasmic reticulum, recent evidence suggests that these proteins are also present in the cytosol and other compartments in vivo, where they may become N-end rule substrates.
Ironic effects of mental control in problem solving: Evidence for the implementation of ineffective strategies
(McNeese State University, 2006) Hart, Christian L.; Randell, Joe A.
The ironic effect of intending to solve problems was examined in this study. Previous research has demonstrated ironic effects of mental control for numerous behavioral and cognitive processes. In this study, subjects were either asked to solve problems, or they were asked to solve the same problems as quickly and efficiently as possible. Based on previous demonstrations of ironic effects of mental control, it was expected that those exercising the greatest mental control would have the poorest performance. Results indicated that those subjects trying to solve problems quickly and efficiently actually solved fewer problems and committed more errors than those who were not intended to work quickly and efficiently. Furthermore, there is evidence that this ironic effect of mental control in problem solving was associated with the use of different strategies. The use of ineffective strategies is suggested as one explanation for the ironic effects of mental control.
MEKK3-mediated signaling to p38 kinase and TonE in hypertonically stressed kidney cells
(American Physiological Society, 2006-10-01) Padda, Ranjit; Wamsley-Davis, Ann; Gustin, Michael C.; Ross, Rebekah; Yu, Christina; Sheik-Hamad, David
Mitogen-activated protein kinase (MAPK) cascades contain a trio of kinases, MAPK kinase kinase (MKKK) → MAPK kinase (MKK) → MAPK, that mediate a variety of cellular responses to different signals including hypertonicity. The signaling response to hypertonicity is conserved across evolution from yeast to mammals in that it involves activation of p38/SAPK. However, very little is known about which upstream protein kinases mediate activation of p38 by hypertonicity in mammals. The MKKKs, MEKK3 and MEKK4, are upstream regulators of p38 in many cells. To investigate these signaling proteins as potential activators of p38 in the hypertonicity response, we generated stably transfected MDCK cells that express activated versions of MEKK3 or MEKK4, utilized RNA interference to deplete MEKK3, and employed pharmacological inhibition of p38 kinase. MEKK3-transfected cells demonstrated increased betaine transporter (BGT1) mRNA levels and upregulated tonicity enhancer (TonE)-driven luciferase activity under isotonic (basal) and hypertonic conditions compared with empty vector-transfected controls; small-interference RNA-mediated depletion of MEKK3 downregulated the activity of p38 kinase and decreased the expression of BGT1 mRNA. p38 Kinase inhibition abolished the effects of MEKK3 activation on BGT1 induction. In contrast, the response to hypertonicity in MEKK4-kA-transfected cells was similar to that observed in empty vector-transfected controls. Our data are consistent with the existence of an input from MEKK3 →→ p38 kinase →→ TonE. Many organisms, including bacteria, yeast, plants, and animals, adapt to sustained hypertonic stress by the preferential accumulation of compatible organic osmolytes (56). In water-deprived mammals, for example, the extracellular osmolality of the kidney medulla may exceed 4,000 mosmol/kgH2O (38). Roughly one-half of the prevailing medullary interstitial solutes consist of urea, whereas the other half is composed of NaCl (15). Urea easily equilibrates across biological membranes and does not cause water shift between the intracellular and extracellular compartments. However, NaCl remains confined to the extracellular space, owing to the action of the Na-K-ATPase. An increase in the extracellular concentration of NaCl contributes to dehydration of the intracellular milieu (hypertonic stress), and restoration of intracellular volume in hypertonically stressed kidney cells requires the induction of a group of genes that lead to the accumulation of organic osmolytes intracellulary [BGT1 for betaine transporter (54), SMIT for inositol transporter (55), taurine transporter (49), and the aldose reductase enzyme (AR), which catalyze the reduction of d-glucose to the organic solute sorbitol (3)]. The transcriptional “machinery” that drives the expression of these genes [SMIT, BGT1, taurine transporter, and AR] under hypertonic conditions is similar (13, 19, 36, 44) and involves interaction between the cis-element [tonicity enhancer (TonE) (36), also known as osmotic response element (ORE) (13); referred to herein as TonE] and transcription factor TonE binding protein [TonEBP; (37), also known also as ORE binding protein (OREBP) (24) as well as NFAT5 (34); referred to herein as TonEBP]. Activation of TonE-mediated gene expression by hypertonicity is not unique to kidney cells [Madin-Darby canine kidney (MDCK) (36); rabbit kidney papillary epithelial cells (PAP-HT25) (25); mouse inner medullar collecting duct cells (mIMCD) (48)], as it has been shown to occur in neurons (35), human liver-derived HepG2 (41), Chang liver, Cos-7, and HeLa cells (24). Deletion of the TonEBP gene in mice blocks the expression of TonE-mediated gene expression in the kidney medulla almost completely, as evidenced by the diminished expression of the BGT1, SMIT, and AR genes. Remarkably, mice lacking TonEBP show atrophy of the renal medulla, which contains smaller cells and displays increased apoptosis (33). While transcriptional control of hypertonicity-induced genes in mammalian cells is reasonably well characterized, the signaling pathways leading to TonE-mediated gene expression need further delineation. In yeast, the adaptation to osmotic stress is dependent on the p38 MAPK homolog high-osmolarity glycerol 1 (HOG1) (7). Similarly, the induction of TonE-mediated gene expression in mammalian cells is p38 kinase dependent (41, 46) but requires cooperative action of Fyn, the catalytic subunit of PKA and the DNA damage-inducible kinase ATM (reviewed in Ref. 47). While ERK and JNK are induced by hypertonicity, the significance of their activation is not clear, as JNK and ERK do not appear to have an effect on TonE-mediated gene expression (reviewed in Ref. 47). In the current experiments, we sought to determine upstream signaling molecules in the p38 kinase cascade that “drive” the expression of hypertonicity-induced genes (represented by the betaine transporter BGT1) and affect TonE-mediated gene expression in kidney cells. The activity of p38 kinase is dependent on MAPK kinases (MKKs) and their activators, the MAPK kinase kinases (MKKKs; see review in Ref. 52). MEK kinase 1 (MEKK1; 1 of the MKKKs) is linked to JNK activation, whereas MEKK2 is linked to JNK and ERK activation (reviewed in Ref. 27). On the other hand, MEKK3 may activate ERK, JNK, and p38, whereas MEKK4 may activate JNK and p38 kinase (27). Hence, we hypothesized that MEKK3 and/or MEKK4 are likely mediators of p38 kinase activation in kidney cells under hypertonic conditions. Our data are consistent with the existence of MEKK3 → → → p38 kinase input to drive TonE-mediated gene expression.
Evaluation of the race card strategy: The importance of supporting evidence
(Boise State University, 2007) Hart, Christian L.; Lopez, Edward P.; Griffith, James D.
The role that racial issues play in the courtroom has been studied in terms of the effect of salient racial variables on juror perceptions and decision- making. However, no prior research examined the effects of using charges of racial bias by police officers as a criminal defense strategy. The “race card” strategy can be defined as the introduction of salient racial variables in an attempt to sway attitudes and beliefs of jurors or judges. In these two experiments, subjects reviewed fictional criminal case summaries in which the race card strategy was or was not used. Furthermore, evidence supporting the defendant claims of racial bias was introduced in some of the cases. The results indicated that when a defendant claimed arrest because of racial bias by the arresting officer, those claims resulted in significant reductions in juror perceptions of guilt. However, claims of racial bias were only effective when the defense produced further evidence supporting claims of racist attitudes or behaviors by the arresting officer
Ironic effects of attempting to remember
(North American Journal of Psychology, 2007) Hart, Christian L.; Randell, Joe A.; Griffith, James D.
In this study, ironic effects of intentional memory processes were explored. Ironic effects have previously been demonstrated in a number of mental control domains such as sleep onset, anxiety, and physical behavior. In this study, it was determined that ironic effects of mental control do occur when individuals apply greater cognitive effort toward the memorization of a word list. Specifically, individuals trying the hardest to remember information were later able to recall less information than those who were not trying as hard to encode and store information. It was further determined that the conditions that give rise to these ironic effects in the memory domain are associated with heightened cognitive workload. Finally, we demonstrated that while elevated intention to remember results in less than optimal recall, this heightened intention is still more effective than no intent. Thus it appears that ironic effects of attempting to remember vary with the level of mental control over mnemonic processing. A theoretical perspective linking ironic effects of mental control with the implementation of ineffective strategies is discussed.

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