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Although the Flemish Cap played a pivotal role in the opening of the North Atlantic, the tectonic history of this continental ribbon has been poorly constrained owing to insufficient seismic coverage. In this study, we present 13 newly acquired seismic reflection profiles over the Flemish Cap, on which seismic reflectors show highly variable seismic facies both on and beneath the top acoustic basement, with exceptional imaging of layered crustal structure. The upper crust is primarily characterized by transparent, chaotic amplitude reflectivity. The lower crust, particularly on the flanks of the cap, exhibits relatively bright and coherent reflection packages interpreted as Appalachian orogenic fabrics based on onshore–offshore correlations from pre-rift plate reconstructions. Extensional systems within the continental crust of the Flemish Cap record a transitional stage between Paleozoic orogenic collapse and pre-Jurassic rifting. The crustal architecture associated with Mesozoic rifting of the Flemish Cap is also mapped and the interpreted distinct rift domains display along-strike variations. Overall, the complex tectonic history of the Flemish Cap involved dominantly ductile deformation during the Paleozoic orogenic stage, multiple deformation styles (primarily ductile and brittle–ductile) during the orogen-to-rift transitional stage and brittle deformation during the major Jurassic–Cretaceous rifting stage. [ABSTRACT FROM AUTHOR]

Lifelong learning plays a central role in the lives of clinical psychologists. As psychological science advances and evidence-based practices develop, it is critical for clinical psychologists to not only maintain their competencies but to also evolve them. In this article, we discuss lifelong learning as a clinical, ethical, and scientific imperative in the myriad dimensions of the clinical psychologist’s professional life, arguing that experience alone is not sufficient. Attitude is also important in lifelong learning, and we call for clinical psychologists to adopt an intellectually humble stance and embrace “a beginner’s mind” when approaching new knowledge and skills. We further argue that clinical psychologists must maintain and refresh their critical-thinking skills and seek to minimize their biases, especially as they approach the challenges and opportunities of lifelong learning. We intend for this article to encourage psychologists to think differently about how they approach lifelong learning.

I INTRODUCTION Commercial surrogate-motherhood contracts should be legally enforceable, despite the vociferous and prevalent opposition to them. We shall, in particular, argue here that they do not involve the commodification [...]

The theory on changing customer perception of product and service quality in disjoint markets serviced by a single sales-support team is considered. Tests are applied to study a firm that serves non-overlapping markets, namely display distributors, photographic materials distributors and custom trade show booth designers. It is shown that quality perception can be controlled regardless of market category.

In 2008 The Joint Commission issued a Sentinel Event Alertthat further defined “behaviors that undermine a culture of safety,” stating that “intimidating and disruptive behaviors” can result in medical errors that affect patient care and safety. The American College of Physician Executives found that more than 95% of respondents encountered “disturbing . . . and potentially dangerous” behaviors on a regular basis. The purpose of this study is to evaluate the effectiveness of a professional development program on unprofessional physician behaviors using the B29™, a reliable and valid tool to assess workplace behaviors.

The bacterium Xylella fastidiosa is a major agricultural pest. Some strains of the microbe cause Pierce's disease, a serious problem for grapevines in the United States and Central America. Other [...]

Collaborating on projects ranging from monitoring soil's water retention to finding genes associated with worm resistance in cows, the agricultural research agencies of the United States and Brazil are discovering [...]

The article focuses on building a law practice centered around core values, exemplified by Kim Wright's journey and her establishment of a practice aligning with her values. Topics include evolving legal practices, global systems change, and the integration of personal values into legal documents and consulting services.

Gas-phase carbonylation of dimethyl ether (DME) to methyl acetate (MA) was investigated on ferrierite (FER) zeolite having different Si/Al molar ratios of 10.4–12.5 as well as high crystallinity synthesized by using various zeolite seed materials such as MOR, ZSM-5 and USY. The enhanced crystallinity of the FER prepared by simply using FER seeds (denoted as FER@FER) having newly formed mesopore structures was responsible for an increased amount of active Brønsted acid sites, which resulted in a higher MA productivity of 2.94 mmol gcath−1with MA selectivity of above 99%. The highly crystalline FER@FER revealed the suppressed deposition of aromatic coke precursors due to the presence of fewer defect sites. Compared to other zeolite seed-derived FER zeolites, the lesser amount of defect sites (extra-framework Lewis acid Al species, EFAL) on the FER@FER was successfully controlled through a recrystallization process. The active Brønsted acid sites for the DME carbonylation reaction mainly originated from the preferential formation of stable tetrahedral Al sites (especially the T2 sites of the Al–O–Si–O–Al framework of FER) on the 8- and 10-membered ring channels of the FER@FER. On those stable T2 sites having proper acid strength, the adsorbed methyl intermediates formed by the dissociation of DME can be transformed to acetyl adsorbates by a relatively faster CO insertion rate on the vicinal Brønsted acid sites, which results in a high catalytic stability and activity of the highly crystalline FER@FER.

Mammalian NIMA-like kinase-1 (NEK1) is a dual-specificity kinase highly expressed in mouse germ cells during prophase I of meiosis. Loss of NEK1 induces retention of cohesin on chromosomes at meiotic prophase I. Timely deposition and removal of cohesin is essential for accurate chromosome segregation. Two processes regulate cohesin removal: a non-proteolytic mechanism involving WAPL, sororin, and PDS5B and direct cleavage by separase. Here, we demonstrate a role for NEK1 in the regulation of WAPL loading during meiotic prophase I, via an interaction between NEK1 and PDS5B. This regulation of WAPL by NEK1-PDS5B is mediated by protein phosphatase 1 gamma (PP1γ), which both interacts with and is a phosphotarget of NEK1. Taken together, our results reveal that NEK1 phosphorylates PP1γ, leading to the dephosphorylation of WAPL, which, in turn, results in its retention on chromosome cores to promote loss of cohesion at the end of prophase I in mammals.

The blood-brain barrier (BBB) poses a unique challenge for drug delivery to the central nervous system (CNS). The BBB consists of a continuous layer of specialized endothelial cells linked together by tight junctions, pericytes, nonfenestrated basal lamina, and astrocytic foot processes. This complex barrier controls and limits the systemic delivery of therapeutics to the CNS. Several innovative strategies have been explored to enhance the transport of therapeutics across the BBB, each with individual advantages and disadvantages. Ongoing advances in delivery approaches that overcome the BBB are enabling more effective therapies for CNS diseases. In this review, we discuss: (1) the physiological properties of the BBB, (2) conventional strategies to enhance paracellular and transcellular transport through the BBB, (3) emerging concepts to overcome the BBB, and (4) alternative CNS drug delivery strategies that bypass the BBB entirely. Based on these exciting advances, we anticipate that in the near future, drug delivery research efforts will lead to more effective therapeutic interventions for diseases of the CNS.

Before I get into the real topic of my 'bloggish' type of editorial, I must admit that in preparing this piece I read and re-read many of the previous 'Beyond [...]

Glioblastoma multiforme (GBM) is the most frequent malignant and aggressive type of glioma. Most cases of GBM present as a single solitary solid tumor; however, there are rare instances in which it may present as a cystic lesion. Here, we report an even rarer case of GBM presenting as bilateral multicystic lesions, mimicking infectious etiology. Our case highlights the importance of identifying clinical features of cystic GBM to ensure early diagnosis and treatment. A literature review was conducted in PubMed, looking at the common characteristics and treatment options for cystic GBM.

A personal narrative is presented which explores the author's experience as a woman lawyer, her discovery of practising law's alternative and collaborative way, and her observation of the destructive conflict between people.

Regionally constrained 3D gravity inversion results on the Orphan Basin-Flemish Cap and the Irish Atlantic conjugate continental margins are compared to investigate crustal structure, early rifting history and geological evolution of this part of the North Atlantic. The full-crustal density anomaly distributions provide some of the first depth images of how rifted structures compare along and across these conjugate margins. Broad similarities in crustal structure are identified with some noticeable differences, linked to rifting and crustal stretching processes. Extreme crustal thinning (stretching factors >3.5) is indicated beneath much of the southern Porcupine Basin, the western half of West Orphan Basin, the eastern half of Jeanne d'Arc Basin, the southeastern half of East Orphan Basin and in pockets beneath Rockall Basin. This appears to have resulted in the serpentinization (and possible exhumation) of mantle lithosphere on the Irish Atlantic and Flemish Cap margins but not beneath Orphan Basin. A simple evolution model is proposed for the early stages of rifting between the margins. It is suggested that ancient orogenic sutures played an important role in controlling the northward migration of rifting and the rotation and displacement of Flemish Cap out of Orphan Basin. [ABSTRACT FROM AUTHOR]

A study was conducted to evaluate the effect of monochromatic light on sexual maturity, production performance, and egg quality of laying hens. A total of 144 14-week-old Hy-Line Brown chickens were reared in cages and illuminated under four different light treatment groups with three replicates (12 birds per replication, n = 12) for 14 to 60 weeks. A 60 W incandescent light bulb (IL) was used as a control, and white light (WL), blue light (BL), and red light (RL) were produced using light emitting diode lamps. The four light treatment groups each had an intensity of 20 lux. A significant delay in laying was observed when pullets were reared under BL compared to all the other light treatments. By contrast, pullets reared under RL laid significantly earlier than those under IL and BL. Hens reared under RL produced significantly higher number of eggs than those under IL and BL, and hens reared under WL produced more eggs than those under BL from 18 to 60 weeks. Feed intake was significantly increased when birds were reared under RL compared to WL and BL. The egg weight was significantly higher in BL compared to WL and RL from 41 to 50 weeks. The FCR was significantly increased when birds were reared under RL compared to other light treatments from 31 to 40 weeks and from 18 to 60 weeks. By contrast, birds reared under RL exhibited significantly increased egg shell thickness compared to birds reared under IL and BL. The ovary weight of laying pullets grown under WL was significantly higher compared to other treatments at 16 weeks of age. It is concluded that birds reared under RL matured earlier, increased egg production and egg shell thickness, but feed conversion rate was not improved under RL.

Glutamate carboxypeptidase II (GCPII) in the central nervous system is referred to as the prostate-specific membrane antigen (PSMA) in the periphery. PSMA serves as a target for imaging and treatment of prostate cancer and because of its expression in solid tumor neovasculature has the potential to be used in this regard for other malignancies as well. An overview of GCPII/PSMA in cancer, as well as a discussion of imaging and therapy of prostate cancer using a wide variety of PSMA-targeting agents is provided.

It has been recognized that Gastrodia elata Bl (GE), an oriental herb medicine, ameliorates various neurological disorders, that GE modulates the monoaminergic and GABAergic systems, and that GE possess antioxidant activities. We examined whether GE affects methamphetamine (MA)-induced striatal dopaminergic toxicity in mice. Treatment with MA (7.5 mg/kg, i.p. × 4) resulted in significant decreases in behavioural activity (as shown by locomotor activity and rota rod performance), dopamine level, tyrosine hydroxylase (TH) activity, and TH protein expression (as evaluated by immunocytochemistry and western blot analysis). In addition, MA treatment showed significant increases in lipid peroxidation [as evaluated by 4-hydroxy-2-nonenal (4-HNE) expression and malondialdehyde formation], protein oxidation (as shown by protein carbonyl expression and its formation), and reactive oxygen species (ROS) formation. Treatment with GE significantly attenuates MA-induced behavioural and dopaminergic impairments, and oxidative stresses in a dose-dependent manner. Our results suggest that GE treatment shows anti-dopaminergic effects in response to MA insult via, at least in part, inhibiting oxidative stresses in the striatum of the mice.

It has been demonstrated that 5-HT1A receptors play an important role in the pathophysiology of schizophrenia. Because Gastrodia elata Bl (GE) modulates the serotonergic system, we examined whether GE could affect phencyclidine (PCP)-induced abnormal behavior in mice. Repeated treatment with PCP increased immobility time, while it decreased social interaction time and recognition memory. PCP-induced abnormal behaviors were significantly attenuated by GE, and these effects were comparable to those of 8-OH-DPAT, a 5-HT1A receptor agonist. Furthermore, GE-mediated effects were counteracted by WAY 100635, a 5-HT1A receptor antagonist. Our results suggest that the antipsychotic effects of GE are, at least in part, mediated via activation of 5-HT1A in mice.

Cocaine, as an indirect dopamine agonist, induces selective behavioral and physiological events such as hyperlocomotion and dopamine release. These changes are considered as consequences of cocaine-induced molecular adaptation such as CREB and c-Fos. Recently, methanolic extracts from licorice was reported to decrease cocaine-induced dopamine release and c-Fos expression in the nucleus accumbens. In the present study, we investigated the effects of liquiritigenin (LQ), a main compound of licorice, on acute cocaine-induced behavioral and molecular changes in rats. LQ attenuated acute cocaine-induced hyperlocomotion in dose-dependent manner. In addition, LQ inhibited CREB phosphorylation and c-Fos expression in the striatum and the nucleus accumbens induced by acute cocaine. Results provide strong evidence that LQ effectively attenuates the acute behavioral effects of cocaine exposure and prevents the induction of selective neuroadaptive changes in dopaminergic signaling pathways. Further investigation of LQ from licorice extract might provide a novel therapeutic strategy for the treatment of cocaine addiction.

It has been suggested that GABAergic neurotransmission can modulate cocaine dependence and seizure activity. Since Gastrodia elata Bl (GE), an oriental herb agent, has been shown to enhance GABAergic transmission, we examined whether GE affects cocaine-induced seizures, conditioned place preference (CPP), and behavioral sensitization in mice. Treatment with GE (500 or 1000 mg/kg, p.o.) significantly delayed seizure onset time and significantly shortened seizure duration induced by cocaine (90 mg/kg, i.p.). In addition, cocaine (15 mg/kg, i.p.)-induced CPP was significantly attenuated by GE in a dose-dependent manner. However, GE did not significantly alter behavioral sensitization induced by cocaine (15 mg/kg, i.p.). In order to understand whether GABAergic receptors are implicated in GE-mediated pharmacological action in response to cocaine, GABAA receptor antagonist bicuculline and GABAB receptor antagonist SCH 50911 were employed in the present study. GE-mediated attenuations on the cocaine-induced seizures and CPP were significantly reversed by bicuculline (0.25 or 0.5 mg/kg, i.p.), but not by SCH 50911 (1.5 or 3.0 mg/kg, i.p.). Therefore, our results suggest that GE attenuates cocaine-induced seizures and CPP via, at least in part, GABAA receptor activation.

The chemokine system represents a diverse group of G protein-coupled receptors responsible for orchestrating cell recruitment under both homeostatic and inflammatory conditions. Chemokine receptor 9 (CCR9) is a chemokine receptor known to be central for migration of immune cells into the intestine. Its only ligand, CCL25, is expressed at the mucosal surface of the intestine and is known to be elevated in intestinal inflammation. To date, there are no reports of small-molecule antagonists targeting CCR9. We report, for the first time, the discovery of a small molecule, CCX282-B, which is an orally bioavailable, selective, and potent antagonist of human CCR9. CCX282-B inhibited CCR9-mediated Ca(2+) mobilization and chemotaxis on Molt-4 cells with IC(50) values of 5.4 and 3.4 nM, respectively. In the presence of 100% human serum, CCX282-B inhibited CCR9-mediated chemotaxis with an IC(50) of 33 nM, and the addition of α1-acid glycoprotein did not affect its potency. CCX282-B inhibited chemotaxis of primary CCR9-expressing cells to CCL25 with an IC(50) of 6.8 nM. CCX282-B was an equipotent inhibitor of CCL25-directed chemotaxis of both splice forms of CCR9 (CCR9A and CCR9B) with IC(50) values of 2.8 and 2.6 nM, respectively. CCX282-B also inhibited mouse and rat CCR9-mediated chemotaxis. Inhibition of CCR9 with CCX282-B results in normalization of Crohn's disease such as histopathology associated with the TNF(ΔARE) mice. Analysis of the plasma level of drug associated with this improvement provides an understanding of the pharmacokinetic/pharmacodynamic relationship for CCR9 antagonists in the treatment of intestinal inflammation.

The article describes a method for measuring the local drag coefficient on a long cylinder which exhibits vortex-induced vibration (VIV). A comparison of measured and predicted local drag coefficient is presented. Results showed that large confidence bounds on the estimated drag coefficient values in the region toward the top of the pipe. Due to uncertainty, the strain and drag coefficient results near the top of the pipe should be disregarded.

The article presents an analysis of experiments where the response amplitude and the non-dimensional frequency of flexible cylinder vortex-induced vibrations show significant trends with increasing Reynolds number. Experiments include the High-Mode tests conducted in the Ocean Basin at Marintek, the Lake Seneca tests conducted at the Naval Surface Warfare Center acoustic test facility and the Steel Catenary Rise tests conducted at Marintek. The experiments showed changes in the amplitude of vibration over the duration of a single test.

Background: Decreases in drinking behavior prior to treatment onset often occur in pharmacotherapy trials for alcohol dependence. We propose that these decreases are associated with both trait and state factors operating before initiation of treatment to influence participants’ expectation or perception of future treatment outcome. While trait factors typically include personality traits, state factors can include readiness to change and severity of drinking at screening. Understanding the characteristics of changes in drinking early in the process of entering treatment can improve clinical trials and outcomes. Our goal was to evaluate drinking behavior before initiating a randomized, double‐blind pharmacotherapy clinical trial for alcohol dependence.

A strategy for controlling the location of gold nanoparticles within block copolymer domains through varying the surface coverage of gold nanoparticles by end-attached polymer ligands is described. Gold nanoparticles coated by short thiol end functional polystyrene homopolymers (PS-SH) (Mn 3.4 kg/mol) are incorporated into a poly(styrene-b-2-vinylpyridine) diblock copolymer template (PS-b-P2VP) (Mn 196 kg/mol), the P2VP block of which has a more favorable interaction with a bare gold particle surface than does the PS block. The areal chain density of the PS-SH ligands on gold particles is varied by changing the mole ratio of PS-SH chains to gold atoms. It is found that the areal density of PS chains on the gold particles is critical to controlling their location in block copolymer templates. PS-coated gold nanoparticles with PS chain areal density higher than 1.6 chains/nm2are dispersed in PS domains of PS-b-P2VP while they are segregated along the interface between PS and P2VP domains of PS-b-P2VP for PS chain areal density <1.3 chains/nm2. Even at extremely low grafting densities of polymer ligands, gold nanoparticles can be stabilized in solution, and self-assembly of these nanoparticles can be controlled within the block copolymer template.

DNA is a powerful and versatile tool for nanoscale self-assembly. Several researchers have assembled nanoparticles and colloids into a variety of structures using the sequence-specific binding properties of DNA. Until recently, however, all of the reported structures were disordered, even in systems where ordered colloidal crystals might be expected. We detail the experimental approach and surface preparation that we used to form the first DNA-mediated colloidal crystals, using 1 μm diameter polystyrene particles. Control experiments based on the depletion interaction clearly indicate that two standard methods for grafting biomolecules to colloidal particles (biotin/avidin and water-soluble carbodiimide) do not lead to ordered structures, even when blockers are employed that yield nominally stable, reversibly aggregating dispersions. In contrast, a swelling/deswelling-based method with poly(ethylene glycol) spacers resulted in particles that readily formed ordered crystals. The sequence specificity of the interaction is demonstrated by the crystal excluding particles bearing a noninteracting sequence. The temperature dependence of gelation and crystallization agree well with a simple thermodynamic model and a more detailed model of the effective colloidal pair interaction potential. We hypothesize that the surfaces yielded by the first two chemistries somehow hinder the particle−particle rolling required for annealing ordered structures, while at the same time not inducing a significant mean-force interaction that would alter the self-assembly phase diagram. Finally, we observe that particle crystallization kinetics become faster as the grafted-DNA density is increased, consistent with the particle−particle binding process being reaction, rather than diffusion limited.

Antagonism of the bradykinin B1 receptor represents a potential treatment for chronic pain and inflammation. Novel antagonists were designed that display low-nanomolar affinity for the human bradykinin B1 receptor and good bioavailability in the rat.

Based on information of the nucleotide sequence obtained from rat genome clones, a new CYP3A (CYP3A62) cDNA was isolated from the cDNA library of a rat liver. The CYP3A62 cDNA was 1746 base pairs (bp) in length, which included 1491 bp of an open reading frame and 93 bp and 209 bp of the respective 5'- and 3'-noncoding regions. Amino acid sequence deduced from CYP3A62 cDNA shared the highest similarity with rat CYP3A9 (79.9%) among human and rat CYP3A forms previously reported. CYP3A62 mRNA and protein were consistently detected in small intestines as well as livers. CYP3A62 was a major form in small intestines of both sexes but was a female-predominant form in livers of adult rats. CYP3A62 in both tissues of male and female rats were clearly enhanced by the treatment with dexamethasone. These expression profiles resembled those of CYP3A9. Despite clear detection of CYP3A62, no detectable levels of CYP3A1 and CYP3A2 proteins, as well as those of mRNAs, were found in the intestinal tract. Therefore, CYP3A62 may play major roles together with CYP3A9 and CYP3A18 in endogenous or exogenous detoxification at the absorption site.

Objectives/HypothesisCoccidioidomycosis is a fungal disease endemic to semiarid regions in the southwestern United States, northern Mexico, and parts of South America. Although this is primarily a pulmonary disease, approximately 0.5% to 1.0% of infected individuals develop disseminated disease affecting skin, subcutaneous tissue, bone, joints, and meninges. The objectives of the study were to present three cases of head and neck manifestations of disseminated coccidioidomycosis and to review the literature of head and neck presentations, diagnosis, and treatment of this potentially life‐threatening disease.

Meiotic recombination plays a key role in the maintenance of sequence diversity in the human genome. However, little is known about the fine–scale distribution and processes of recombination in human chromosomes, or how these impact on patterns of human diversity. We have therefore developed sperm typing systems that allow human recombination to be analysed at very high resolution. The emerging picture is that human crossovers are far from randomly distributed but instead are targeted into very narrow hot spots that can profoundly influence patterns of haplotype diversity in the human genome. These hot spots provide fundamental information on processes of human crossover and gene conversion, as well as evidence that they can violate basic rules of Mendelian inheritance.

This paper reports 1) the increase in expression of CYP1A2 in mutant Nagase analbuminemic rats (NARs), 2) the role of globulin binding of azosemide in circulating blood in its urinary excretion and hence its diuretic effects in NARs, and 3) the significantly faster renal (CL(R)) and nonrenal (CL(NR)) clearances of azosemide in NARs. Azosemide (mainly metabolized via CYP1A2 in rats), 10 mg/kg, was intravenously administered to control rats and NARs. Northern and Western blot analyses revealed that the expression of CYP1A2 increased approximately 3.5-fold in NARs as compared with control. The plasma protein binding of azosemide in control rats and NARs was 97.9 and 84.6%, respectively. In NARs, plasma protein binding (84.6%) was due to binding to alpha- (82.6%) and beta- (68.9%) globulins. In NARs, the amount of unchanged azosemide excreted in 8-h urine was significantly greater (37.7 versus 21.0% of intravenous dose) than that in control rats due to an increase in intrinsic renal active secretion of azosemide. Accordingly, the 8-h urine output was significantly greater in NARs. The area under the plasma concentration-time curve of azosemide was significantly smaller (505 versus 2790 microg. min/ml) in NARs because of markedly faster CL(R) (7.36 versus 0.772 ml/min/kg, secondary to a significant increase in urinary excretion of azosemide and intrinsic renal active secretion). Additionally, CL(NR) was significantly faster (12.4 versus 3.05 ml/min/kg, because of approximately 3.5 fold increase in CYP1A2) in NARs compared with control. Based on in vitro hepatic microsomal studies, the intrinsic M1 [a metabolite of azosemide; 5-(2-amino-4-chloro-5-sulfamoylphenyl)-tetrazole] formation clearance was significantly faster (67.0% increase) in NARs than that in control rats, and this supports significantly faster CL(NR) in NARs. Renal sensitivity to azosemide was significantly greater in NARs than in control rats with respect to 8-h urine output (385 versus 221 ml/kg) and 8-h urinary excretions of sodium, potassium, and chloride. This study supports that in NARs, binding of azosemide to alpha- and beta-globulins in circulating blood play an important role in its diuretic effects.

Phenobarbital (PB) induction ofCYP2Bgenes is mediated by translocation of the constitutively active androstane receptor (CAR) to the nucleus. Interaction of CAR with p160 coactivators and enhancement of CAR transactivation by the coactivators have been shown in cultured cells. In the present studies, the interaction of CAR with the p160 coactivator glucocorticoid receptor-interacting protein 1 (GRIP1) was examined in vitroand in vivo. Binding of GRIP1 to CAR was shown by glutathione S-transferase (GST) pull-down and affinity DNA binding. N- or C-terminal fragments of GRIP1 that contained the central receptor-interacting domain bound to GST-CAR, but the presence of ligand increased the binding to GST-CAR of only the fragments containing the C-terminal region. In gel shift analysis, binding to CAR was observed only with GRIP1 fragments containing the C-terminal region, and the binding was increased by a CAR agonist and decreased by a CAR antagonist. Expression of GRIP1 enhanced CAR-mediated transactivation in cultured hepatic-derived cells 2–3-fold. In hepatocytes transfected in vivo, expression of exogenous GRIP1 alone induced transactivation of theCYP2B1PB-dependent enhancer 15-fold, whereas CAR expression alone resulted in only a 3-fold enhancement in untreated mice. Remarkably, CAR and GRIP1 together synergistically transactivated the enhancer about 150-fold, which is approximately equal to activation by PB treatment. In PB-treated mice, expression of exogenous CAR alone had little effect, expression of GRIP1 increased transactivation about 2-fold, and with CAR and GRIP, a 4-fold activation was observed. In untreated mice, expression of GRIP resulted in nuclear translocation of green fluorescent protein-CAR. These results strongly suggest that a p160 coactivator functions in CAR-mediated transactivation in vivoin response to PB treatment and that the synergistic activation of CAR by GRIP in untreated animals results from both nuclear translocation and activation of CAR.

Tumor necrosis factor-alpha (TNF-alpha), a cytokine secreted by inflammatory cells, has been implicated in several inflammatory disease states. (E)-2(R)-[1(S)-(Hydroxycarbamoyl)-4-phenyl-3-butenyl]-2'-isobutyl-2'-(methanesulfonyl)-4-methylvalerohydrazide (Ro 32-7315), is a potent, orally active inhibitor of the TNF-alpha convertase (TACE), an enzyme responsible for proteolytic cleavage of the membrane bound precursor, pro-TNF-alpha. Ro 32-7315 inhibited a recombinant form of TACE (IC(50) = 5.2 nM) with selectivity over related matrix metalloproteinases. In a cellular assay system, THP-1 cell line, and in human and rat whole blood, Ro 32-7315 significantly reduced lipopolysaccharide (LPS)-induced TNF-alpha release with IC(50) values of 350 +/- 14 nM (n = 5), 2.4 +/- 0.5 microM (n = 5), and 110 +/- 18 nM (n = 5), respectively. Oral administration of Ro 32-7315 to Wistar rats caused a dose-dependent inhibition of LPS-induced release of systemic TNF-alpha with an ED(50) of 25 mg/kg. Treatment (days 0-14) of Allen and Hamburys hooded rats with Ro 32-7315 (2.5, 5, 10, and 20 mg/kg, i.p., twice daily) significantly reduced adjuvant-induced secondary paw swelling (42, 71, 83, and 93%, respectively) as compared with the vehicle group. In the Ro 32-7315-treated group, the reduced paw swelling was associated with improved lesion score and joint mobility. Furthermore, in a placebo-controlled, single-dose study, Ro 32-7315 given orally (450 mg) significantly suppressed ex vivo, LPS-induced TNF-alpha release in the whole-blood samples taken from healthy male and female volunteers (mean inhibition of 42% over a 4-h duration, n = 6). These data collectively support the potential use of such a compound for the oral treatment of inflammatory disorders.

Salsolinol (SAL), a novel dopaminergic catechol tetrahydroisoquinoline neurotoxin, has been speculated to contribute to the etiology of Parkinson's disease and neuropathology of chronic alcoholism. Our previous studies have demonstrated that SAL induces strand scission in X174 supercoiled DNA and oxidative base modification in calf thymus DNA in the presence of cupric ion. We now report that treatment of rat pheochromocytoma (PC12) cells with SAL causes reduced viability, which was exacerbated by Cu(2+). The copper chelator bathocuproinedisulfonic acid ameliorated cytotoxicity induced by SAL and Cu(2+). N-Acetyl-L-cysteine and reduced glutathione protected against SAL- plus Cu(2+)-mediated PC12 cell death. Cells exposed to SAL underwent apoptosis, as revealed by characteristic morphological and biochemical changes. SAL treatment resulted in increased levels of Bax with a concomitant decrease in expression of Bcl-x(L). Furthermore, SAL rapidly activated c-Jun N-terminal kinase, whereas the activity of extracellular signal-regulated protein kinase remained unchanged. Transfection with Bcl-x(L) or Bcl-2 led to protection against SAL-mediated PC12 cell death. Although SAL alone could cause apoptotic death in PC12 cells, cells treated with SAL together with Cu(2+) became necrotic. Cells exposed to both SAL and Cu(2+) exhibited higher levels of intracellular reactive oxygen species, malondialdehyde, and 8-oxo-7,8-dihydro-2'-deoxyguanosine than did those treated with SAL alone. These results suggest that copper accelerates redox cycling of SAL, leading to massive production of reactive oxygen species, which can divert the SAL-induced cell death to necrosis.

BACKGROUND: Inflammatory bowel disease (IBD) is a chronic inflammation of the gastrointestinal tract caused by an abnormal and uncontrolled immune response to one or more normally occurring gut constituents. AIM: Given the effects of transforming growth factor beta1 (TGF-beta1) on both the immune system and extracellular matrix, we postulated that alterations in TGF-beta signalling in intestinal epithelial cells may play an important role in the development of IBD. METHODS: TGF-beta signalling was inactivated in mouse intestine by expressing a dominant negative mutant form of the TGF-beta type II receptor under the control of the mouse intestinal trefoil peptide (ITF)/TFF3 promoter. Transgenic mice (ITF-dnRII) developed spontaneous colitis presenting with diarrhoea, haematochezia, and anal prolapse when not maintained under specific pathogen free (SPF) conditions. Under SPF conditions we induced colitis by mixing dextran sodium sulphate (DSS) in drinking water to examine the significance of loss of TGF-beta signalling in the pathogenesis of IBD. RESULTS: Transgenic mice showed increased susceptibility to DSS induced IBD, and elicited increased expression of major histocompatibility complex class II, generation of autoantibodies against intestinal goblet cells, and increased activity of matrix metalloproteinase in intestinal epithelial cells compared with wild-type littermates challenged with DSS. CONCLUSIONS: Deficiency of TGF-beta signalling specifically in the intestine contributes to the development of IBD. Maintenance of TGF-beta signalling may be important in regulating immune homeostasis in the intestine

The underlying cause of the selective death of the nigral dopaminergic neurons in Parkinson's disease is not fully understood. Tetrahydrobiopterin (BH4) is synthesized exclusively in the monoaminergic, including dopaminergic, cells and serves as an endogenous and obligatory cofactor for syntheses of dopamine and nitric oxide. Because BH4 contributes to the syntheses of these two potential oxidative stressors and also undergoes autoxidation, thereby producing reactive oxygen species, it was possible that BH4 may play a role in the selective vulnerability of dopaminergic cells. BH4 given extracellularly was cytotoxic to catecholamine cells CATH. a, SK-N-BE(2)C, and PC12, but not to noncatecholamine cells RBL-2H3, CCL-64, UMR-106-01, or TGW-nu-1. This was not caused by increased dopamine or nitric oxide, because inhibition of their syntheses did not attenuate the damage and BH4 did not raise their cellular levels. Dihydrobiopterin and biopterin were not toxic, indicating that the fully reduced form is responsible. The toxicity was caused by generation of reactive oxygen species, because catalase, superoxide dismutase, and peroxidase protected the cells from the BH4-induced demise. Furthermore, thiol agents, such as reduced glutathione, dithiothreitol, beta-mercaptoethanol, and N-acetylcysteine were highly protective. The BH4 toxicity was initiated extracellularly, because elevation of intracellular BH4 by sepiapterin did not result in cell damage. BH4 was spontaneously released from the cells of its synthesis to a large extent, and the release was not further enhanced by calcium influx. This BH4-induced cytotoxicity may represent a mechanism by which selective degeneration of dopaminergic terminals and neurons occur.

The 2-(4-nitrophenylsulfonyl)ethoxycarbonyl (Nsc) group is an alternative to Fmoc for N^α-protection in solid-phase peptide synthesis. Nsc-amino acids may be particularly suitable for automatic synthesizers, in which the amino acids are stored in solution, and the incorporation of residues prone to racemization such as Cys and His. Owing to the hydrophilicity of the Nsc group, these derivatives are useful for the preparation of protected peptides in convergent solid-phase peptide synthesis strategies.

A key event in deflagellation or deciliation is the severing of the nine outer-doublet axonemal microtubules at a specific site in the flagellar transition zone. Previous genetic analysis revealed three genes that are essential for deflagellation in Chlamydomonas. We have now identified the first of these products, Fa1p, a protein required for Ca(2+)-dependent, axonemal microtubule severing. Genetic mapping and the availability of a tagged allele allowed us to physically map the gene to the centromere-proximal domain of the mating-type locus. We identified clones of Chlamydomonas genomic DNA that rescued the Ca(2+)-dependent axonemal microtubule severing defect of fa1 mutants. The FA1 cDNA, obtained by RT-PCR, encodes a novel protein of 171 kDa, which is predicted to contain an amino-terminal coiled-coil domain and three Ca(2+)/calmodulin binding domains. By western analysis and subcellular fractionation, the FA1 product is enriched in flagellar-basal body complexes. Based on these observations and previous studies, we hypothesize that a Ca(2+)-activated, Ca(2+)-binding protein binds Fa1p leading ultimately to the activation of axonemal microtubule severing.

Published plate reconstructions have provided insights regarding the formation of the North Atlantic, in which the motion of the Porcupine Bank, on the Irish Atlantic margin, underlain by orogenic pre‐rift crustal basement terranes, is investigated and restored. Previous reconstructions of the Porcupine Bank mainly relied on potential field data rather than seismic constraints and failed to reveal the role of inherited crustal terranes during rifting and subsequent crustal deformation. In this study, five deformable plate tectonic models with distinct structural inheritance trends are established in GPlates by adjusting a previously published restoration model for the North Atlantic. For each model, driving factors such as the inclusion of the Orphan Knoll, the Flemish Cap poles of rotation, and the motion of the eastern border of the Porcupine Basin are also considered. To assess the validity of deformable plate models, crustal thickness estimates obtained from gravity inversion and seismic data modeling are compared with those calculated via deformable plate models. The preferred deformable plate model proposes the subdivision of the Porcupine Bank into four blocks with each block experiencing poly‐phased rotation and shearing prior to the final continental breakup, implying strong inheritance and segmentation of the Porcupine Bank and Porcupine Basin. The reconstructed paleo‐positions of the Flemish Cap and Porcupine Bank within deformable regions reveal evolving conjugate relationships during rifting, which are assessed using regional seismic transects from both margins. Finally, extensional obliquity between both margins is quantitatively restored, showing time‐variant orientations due to the rotation and shearing of associated continental blocks. The Porcupine Bank experienced rotation and shearing during oblique rifting, strongly influenced by the inherited Caledonian suturesCrustal thickness between the Flemish Cap‐Porcupine Bank pair is quantitatively restored over time based on the deformable plate modelExtension obliquity between the Porcupine Bank and Flemish Cap varies over time, accompanied by segmentation of the Porcupine Basin The Porcupine Bank experienced rotation and shearing during oblique rifting, strongly influenced by the inherited Caledonian sutures Crustal thickness between the Flemish Cap‐Porcupine Bank pair is quantitatively restored over time based on the deformable plate model Extension obliquity between the Porcupine Bank and Flemish Cap varies over time, accompanied by segmentation of the Porcupine Basin

VINCENT GABRIELSEN. The Naval Aristocracy of Hellenistic Rhodes. Aarhus: Aarhus University Press, 1997; dist. Oakville, Conn.: David Brown Book Company. Pp. 254. $30.00 (US). Reviewed by E. E. RiceDONALD DENOON, ed., with STEWART FIRTH, JOCELYN LINNEKIN, MALAMA MELEISEA, and KAREN NERO. The Cambridge History of the Pacific Islanders. New York: Cambridge University Press, 1997. Pp. xvi, 518. $79.95 (US). Reviewed by Judith A. BennettCHRISTOPHER TYERMAN. The Invention of the Crusades. Toronto: University of Toronto Press, 1998. Pp. ix, 170. $16.95 (CDN)> paper. Reviewed by Norman HousleyROBIN FRAME. Ireland and Britain, 1170–1450. London and Rio Grande: Hambledon Press, 1998. Pp. xix, 332. $60.00 (US). Reviewed by Karl S. BottigheimerSIDNEY POLLARD. Marginal Europe: The Contribution of Marginal Lands since the Middle Ages. New York: Clarendon Press, Oxford University Press, 1997. Pp. 327. $108.00 (CDN). Reviewed by Michael PalairetNICHOLAS WRIGHT. 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