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PubMed1985

Management of an infant with prenatal ultrasound diagnosis of upper airway obstruction.

We report a case in which a cervical teratoma was diagnosed antenatally in the mid third trimester. In anticipation of potential upper airway obstruction, resources were mobilized to the operating room at the time of the planned cesarean section. The neonate was unable to breathe, but his airway was secured without delay. There was no evidence of cerebral anoxia initially or at one year follow-up. As prenatal diagnosis by ultrasound becomes more refined, the otolaryngologist will play an increasing role in perinatal decision making and anticipated emergencies at the time of delivery. Airway obstruction of various causes will be the most urgent problem.

Airway Obstruction↗
PubMed1997

The sticking probability of a hydrogen atom on icy mantle.

In the present work, we investigate the sticking process of a hydrogen atom on the surface of dust grains. As a realistic model for the icy mantle of dust grains, we produced slab-shaped amorphous water ice with infinite area by classical molecular dynamics (MD) computational simulation using two-dimensional periodic boundary condition. The resulting amorphous water ice slabs at 10 K and 70 K were found to be in good agreement with the experimental high-density and low-density amorphous water ice, respectively. Then, we investigated the dynamical behaviors of an impinging H atom on the surface of it by MD simulations. The sticking probabilities of incident H atoms with several initial temperatures on 10 K and 70 K ice were obtained. It was found that most of H atoms colliding with the 10 K ice stuck on the surface of it. After having stuck, the impinging H atoms diffused on the surface of ice and became trapped in one of potential wells on the surface. The mobility of a H atom on the surface of the amorphous water ice was found to depend only upon the temperature of ice.

Computer Simulation↗
PubMed2001

Androgen receptor signalling: comparative analysis of androgen response elements and implication of heat-shock protein 90 and 14-3-3eta.

Androgen receptor (AR) signalling was analysed using as models the cysteine-rich secretory protein-1 (CRISP-1) and CRISP-3 gene promoters, which are differentially regulated by androgen in vivo and contain multiple potential androgen response elements. Using electrophoretic mobility shift assay, we identified several elements with differing affinities for the AR at positions -3706, -1270, -1253 and -350 of the CRISP-1 promoter and at positions -369 and -349 of the CRISP-3 promoter. The strongest binding was observed for the -1253 element of CRISP-1. In transactivation assays using a PC-3 cell line stably transfected with the AR (PC-3/AR), the -1253 element placed as two or four copies upstream of the TK minimal promoter yielded a strong induction of luciferase reporter gene activity in the presence of the androgen methyltrienolone (R1881). In the context of the CRISP promoters a 2-fold induction by R1881 was measured for the CRISP-3 upstream region whereas only limited effects were noted for the CRISP-1 upstream region. The androgenic stimulation of the p(-1253 ARE)(4x)-TK-luciferase reporter construct was dose-dependently inhibited by geldanamycin and radicicol, two compounds that selectively interact with the chaperone protein, heat-shock protein 90. Cotransfection with an expression vector for the 14-3-3eta protein markedly enhanced the androgen-dependent stimulation. These results emphasize the influence of promoter context on androgen regulation and the importance of AR-associated proteins.

14-3-3 Proteins↗
PubMed2000

Dexamethasone-enhanced sensitivity of mouse hippocampal HT22 cells for oxidative stress is associated with the suppression of nuclear factor-kappaB.

Glucocorticoids (GCs) exacerbate various insults to the hippocampus but the exact molecular mechanisms of this GC activity is not known. GCs can suppress the activity of the redox-sensitive nuclear factor NF-kappaB, which potentially serves neuroprotective functions. Employing electrophoretic mobility shift assays and transfection assays using a NF-kappaB-dependent reporter plasmid, we demonstrate that the increased oxidative stress sensitivity of clonal mouse hippocampal HT22 cells caused by GCs is associated with the suppression of NF-kappaB. GCs increased the expression of IkappaBalpha, the physiological inhibitor of NF-kappaB. Downregulation of NF-kappaB activity after overexpression of a dominant-negative mutant form of IkappaBalpha results in an increased sensitivity to oxidative stress. We conclude that the suppression of the basal NF-kappaB activity contributes to the enhanced vulnerability of neuronal cells to oxidative stress caused by GCs.

Animals↗
PubMed2003

Multiple roles of oxidants in the pathogenesis of asbestos-induced diseases.

Exposure to asbestos causes cellular damage, leading to asbestosis, bronchogenic carcinoma, and mesothelioma in humans. The pathogenesis of asbestos-related diseases is complicated and still poorly understood. Studies on animal models and cell cultures have indicated that asbestos fibers generate reactive oxygen and nitrogen species (ROS/RNS) and cause oxidation and/or nitrosylation of proteins and DNA. The ionic state of iron and its ability to be mobilized determine the oxidant-inducing potential of pathogenic iron-containing asbestos types. In addition to their capacity to damage macromolecules, oxidants play important roles in the initiation of numerous signal transduction pathways that are linked to apoptosis, inflammation, and proliferation. There is strong evidence supporting the premise that oxidants contribute to asbestos-induced lung injury; thus, strategies for reducing oxidant stress to pulmonary cells may attenuate the deleterious effects of asbestos.

Animals↗
PubMed2005

Synthesis and characterization of electron-deficient pentacenes.

[structure: see text]. Halogen functional groups on pentacene can be used both as synthetic handles for further functionalization as well as to tune the pi-stacking in these systems. The halogenated pentacene derivatives described here (X = Br, X' = H, and X = X' = F) are all stable and soluble, with reduction potentials significantly lower than that of the parent functionalized pentacene (X = X' = H). The bromopentacenes could be further elucidated to pentacene nitriles, further decreasing the acene's reduction potential, while the charge-carrier mobility in the fluorinated systems was shown to scale with the degree of fluorine substitution.

Journal Article↗
PubMedDate not supplied

Biotic diversity of Natchez Trace State Forest, western Tennessee.

We carried out a multiple-scale assessment of biotic resources within Natchez Trace State Forest (NTSF) in western Tennessee, focusing on the relation between biotic communities and seven previously developed ecological land types (ELT, based on topography and soils). We wanted to test the functional ability of ELTs for biodiversity stewardship. Woody and herbaceous flora as well as herpetofauna and avifauna communities had substantial differences between upland and lowland forests. However, none of the faunal communities distinguished among upland ELTs. In addition, herbaceous taxa also failed to distinguish upland ELTs. The results suggest the present use of ELTs at NTSF will not be a helpful guide to land stewardship focusing on biodiversity. The disturbance history of the Forest and the mobility of animals are given as potential explanations for a poor relationship between abiotic ELTs and the resident biota.

Animals↗
PubMed1997

Feedback regulation of extracellular ATP-stimulated phosphoinositide hydrolysis by protein kinase C-alpha in bovine glomerular endothelial cells.

In glomerular endothelial cells, extracellular ATP stimulates a phospholipase C with subsequent hydrolysis of polyphosphoinositides and an increase in cytosolic free Ca2+ concentration ([Ca2+]i). Short-term (30 min) pretreatment of endothelial cells with 12-O-tetradecanoylphorbol 13-acetate (TPA), a potent activator of protein kinase C (PKC), decreases the ATP-stimulated phosphoinositide degradation and Ca2+ mobilization. However, this inhibition was lost after incubating the cells for four hours with TPA. Longer-term pretreatment (10 to 48 hr) even potentiated ATP-induced phosphoinositide breakdown and Ca2+ mobilization. In addition, pretreating the cells for 30 minutes with the specific PKC inhibitor Ro 31-8220 dose-dependently increased ATP-stimulated phosphoinositide hydrolysis, thus clearly indicating a regulatory role for PKC in the inositol lipid signaling pathway in glomerular endothelial cells. By using specific antibodies recognizing the different PKC isoenzymes, it is observed that glomerular endothelial cells express five isoenzymes: PKC-alpha, -delta, -epsilon, -zeta and -theta. No PKC-beta, -gamma, -eta and -mu isoenzymes were detected. On exposure to TPA, a complete depletion of PKC-alpha is observed within four hours. In contrast, PKC-epsilon was more resistant to phorbol ester, and even after 48 hours of TPA treatment, only 60% of PKC-epsilon was down-regulated. PKC-theta decreased very slowly from the cytosol (47% left after 24 hr of phorbol ester treatment) and translocated to the Triton X100-insoluble fraction. Moreover, PKC-delta and PKC-zeta were not significantly affected by 48 hours of phorbol ester incubation. Thus, only PKC-alpha is depleted with a kinetic that corresponds to the loss of feedback inhibition of ATP-stimulated phosphoinositide turnover. In the next step, [Ca2+]i changes were measured in single cells loaded with Fura-2 after microinjection of neutralizing PKC isoenzyme-specific antibodies. Injection of antibodies specific for PKC-alpha potently increased Ca2+ mobilization in response to ATP stimulation when compared to cells injected with buffer only or antibodies specific for PKC-epsilon. These results provide evidence that PKC-alpha mediates feedback inhibition of ATP-stimulated phosphoinositide hydrolysis in glomerular endothelial cells.

Adenosine Triphosphate↗
PubMed2003

RNA truncation by premature polyadenylation attenuates human mobile element activity.

Long interspersed elements (LINE-1s, also called L1s) are the only active members of the autonomous, non-long terminal repeat (LTR) retrotransposon family, which reshapes mammalian genomes in many different ways. LINE-1 expression is low in most differentiated cells but high in some cancer cells, in testis and during embryonic development. To minimize the negative impact on their hosts' genomes, many mobile elements strategically limit their amplification potential, particularly in somatic cells. Here we show that the A-rich coding strand of the human LINE-1 contains multiple functional canonical and noncanonical polyadenylation (poly(A)) signals, resulting in truncation of full-length transcripts by premature polyadenylation. This attenuation lowers the rate of retrotransposition in assays using HeLa cells. It probably also increases the negative effects of LINE-1 insertions into genes.

Animals↗
PubMed2000

The frequency and proliferative potential of megakaryocytic colony-forming cells (Meg-CFC) in cord blood, cytokine-mobilized peripheral blood and bone marrow, and their correlation with total CFC numbers: implications for the quantitation of Meg-CFC to predict platelet engraftment following cord blood transplantation.

CFC numbers have shown to correlate with success of engraftment and speed of neutrophil recovery following cord blood (CB) transplantation. To investigate whether the number of Meg-CFC in a CB stem cell preparation might correlate with time to platelet engraftment, we evaluated the frequency of Meg-CFC among all CFC types in 134 CB, 21 adult bone marrow (BM) and 52 cytokine-mobilized peripheral blood (PB) stem cell preparations. The correlation of Meg-CFC with the total number of CFC and mixed cell-CFC was also assessed. The frequency of Meg-CFC was highest in CB and correlated significantly with total CFC numbers (mean 20.8%, correlation coefficient (r) 0.84, P = 0.0001) compared with Meg-CFC from mobilized PB (mean 13.1%, r = 0.29, P = 0.07) and BM (mean 4%, r = 0. 39, P = 0.13). In addition, mixed-cell CFC numbers in CB were highly correlated with the total number of Meg-CFC (r = 0.7, P = 0.0001). No such correlations were found with mobilized PB or BM. We conclude that, based on the high degree of correlation between Meg-CFC and non-Meg-CFC numbers in CB, no additional information concerning time to platelet engraftment would be gained by routinely performing Meg-CFC assays in addition to non-Meg-CFC assays. The fact that CB Meg-CFC and mixed-cell CFC are strongly correlated suggests that CB Meg-CFC are more primitive than their counterparts in BM and PB and may reflect the number of stem cells in CB. Bone Marrow Transplantation (2000).

Adult↗
PubMed2002

A single nucleotide polymorphism in the proximal IFN-gamma promoter alters control of gene transcription.

Interferon-gamma (IFN-gamma) is an important cytokine that regulates cellular immune responses to intracellular pathogens and neoplasia. Regulation of IFN-gamma expression is stringently controlled at the transcriptional level. In this report we describe two novel single nucleotide polymorphisms (SNPs); one, at -179 in the promoter, occurs in 4% of African Americans. This SNP represents a guanidine to thymidine transition and creates a potential AP-1 binding element. Electrophoretic mobility shift analysis reveals a unique complex binding to an oligonucleotide containing the variant -179T but not to the -179G using nuclear extracts from human peripheral blood T cells. In reporter gene assays, T cell lines transfected with the variant -204(179T) IFN-gamma promoter show a six to 13-fold induction of luciferase activity in response to TNF-alpha over the common -204(179G) construct. The -179T allele identified in the proximal IFN-gamma promoter confers TNF-alpha inducibility and may prove important in human immune disorders and responsiveness to pathogens.

Animals↗
PubMedDate not supplied

Cyclin K as a direct transcriptional target of the p53 tumor suppressor.

Cyclin K, a newly recognized member of the "transcription" cyclin family, may play a dual role by regulating CDK and transcription. Using cDNA microarray technology, we found that cyclin K mRNA was dramatically increased in U373MG, a glioblastoma cell line deficient in wild-type p53, in the presence of exogenous p53. An electrophoretic mobility-shift assay showed that a potential p53-binding site (p53BS) in intron 1 of the cyclin K gene could indeed bind to p53 protein. Moreover, a heterologous reporter assay revealed that the p53BS possessed p53-dependent transcriptional activity. Colony-formation assays indicated that overexpression of cyclin K suppressed growth of T98G, U373MG and SW480 cells. The results suggested that cyclin K may play a role in regulating the cell cycle or apoptosis after being targeted for transcription by p53.

Adenoviridae↗
PubMed2002

Identification of the interferon regulatory factor 5 gene (IRF-5) as a direct target for p53.

Interferon regulatory factors (IRFs) regulate transcription of interferon genes through DNA sequence-specific binding to these targets. Using a differential display method for examining gene expression in p53-defective cells infected with adenovirus containing wild-type p53, we found that expression of interferon regulatory factor 5 (IRF-5) mRNA was increased in the presence of exogenous p53. An electrophoretic mobility-shift assay showed that a potential p53 binding site (p53BS) detected in exon 2 of the IRF-5 gene could in fact bind to p53 protein. Moreover, a heterologous reporter assay revealed that the p53BS possessed p53-dependent transcriptional activity. Expression of IRF-5 was induced in p53+/+ cells (MCF7 and NHDF), but not inp53-/- cells (H1299) when DNA was damaged by gamma-irradiation, UV-radiation, or adriamycin treatment in a wild-type p53-dependent manner. These results suggest that IRF-5 is a novel p53-target, and that it might mediate the p53-dependent immune response.

Amino Acid Sequence↗
PubMed1997

Splinting osseointegrated implants and natural teeth in rehabilitation of partially edentulous patients. Part I: laboratory and clinical studies.

A significant clinical consideration in the restoration of partial edentulism with implant and tooth-supported prostheses is whether implants and natural teeth abutments should be splinted, and if so, in what manner. This article presents a review of laboratory and clinical studies related to splinting. Stress analysis studies reveal high stress concentration around the implant neck when rigidly connected to teeth. This was not borne out in in vivo studies in short-span bridges. While stress absorbing elements have been advocated to redistribute and reduce stress concentration away from the implant neck where bone resorption is often seen, finite element analysis and photo-elastic studies demonstrate that such stress absorbing elements may be effective only when their resiliency is in the same order of magnitude as the periodontal ligament. Clinical studies reporting life table statistics in combined implant and tooth restorations do not show adverse effects of splinting teeth to implants. These studies, however, are mostly short-term reports on survival with results that are as yet inconclusive. The issue of connecting with rigid or non-rigid connectors remains unresolved with a growing body of information favouring retrievable short-span rigid connection to non-mobile teeth. Root intrusion is a potential clinical hazard of non-rigid connection.

Bone Resorption↗
PubMed1995

Metabotropic glutamate receptor (mGluR)-mediated potentiation of cyclic AMP responses does not require phosphoinositide hydrolysis: mediation by a group II-like mGluR.

Metabotropic glutamate receptors (mGluRs) in the CNS are coupled to a variety of second messenger systems, the best characterized of which is activation of phosphoinositide hydrolysis. Recently, we found that activation of mGluRs in rat brain slices by the selective mGluR agonist 1-aminocyclopentane-1S,3R-dicarboxylic acid (1S,3R-ACPD) potentiates cyclic AMP (cAMP) responses elicited by activation of other receptors coupled to Gs. It has been suggested that mGluR-mediated potentiation of cAMP responses is secondary to activation of phosphoinositide hydrolysis. However, preliminary evidence suggests that this is not the case. Therefore, we designed a series of experiments to test more fully the hypothesis that mGluR-mediated potentiation of cAMP responses is secondary to phosphoinositide hydrolysis. Inhibitors of both protein kinase C and intracellular calcium mobilization failed to antagonize 1S,3R-ACPD-stimulated potentiation of cAMP responses. Further, coapplication of phorbol esters and 1S,3R-ACPD induced a cAMP response that was greater than additive. Finally, (RS)-3,5-dihydroxyphenylglycine, a selective agonist of mGluRs coupled to phosphoinositide hydrolysis, failed to potentiate cAMP responses, whereas (2S,1'R,2'R,3'R)-2-(2,3-dicarboxycyclopropyl)glycine, an mGluR agonist that does not activate mGluRs coupled to phosphoinositide hydrolysis, elicited a robust potentiation of cAMP responses. In total, these data strongly suggest that mGluR-mediated potentiation of cAMP responses is not secondary to activation of phosphoinositide hydrolysis and is likely mediated by a group II mGluR.

Animals↗
PubMed2003

Cardiac progenitor cells from adult myocardium: homing, differentiation, and fusion after infarction.

Potential repair by cell grafting or mobilizing endogenous cells holds particular attraction in heart disease, where the meager capacity for cardiomyocyte proliferation likely contributes to the irreversibility of heart failure. Whether cardiac progenitors exist in adult myocardium itself is unanswered, as is the question whether undifferentiated cardiac precursor cells merely fuse with preexisting myocytes. Here we report the existence of adult heart-derived cardiac progenitor cells expressing stem cell antigen-1. Initially, the cells express neither cardiac structural genes nor Nkx2.5 but differentiate in vitro in response to 5'-azacytidine, in part depending on Bmpr1a, a receptor for bone morphogenetic proteins. Given intravenously after ischemia/reperfusion, cardiac stem cell antigen 1 cells home to injured myocardium. By using a Cre/Lox donor/recipient pair (alphaMHC-Cre/R26R), differentiation was shown to occur roughly equally, with and without fusion to host cells.

Animals↗
PubMed1999

The Epstein-Barr virus latency BamHI-Q promoter is positively regulated by STATs and Zta interference with JAK/STAT activation leads to loss of BamHI-Q promoter activity.

In Epstein-Barr virus (EBV)-associated tumors in nonimmunocompromised patients, EBV gene expression is highly restricted. EBV-encoded nuclear antigen (EBNA)-1 is expressed, whereas the immunogenic and proliferative EBNAs are not. This pattern of EBNA expression is generated by usage of the BamHI-Q promoter (Qp). We have determined that the JAK/STAT pathway positively regulates Qp activity. In transient-transfection assays, a Qp-CAT reporter was activated by cotransfected JAK-1 and by treatment of cells with the cytokine IL-6. The ability of Qp to bind signal transducer and activator of transcription (STAT) proteins was directly demonstrated by electrophoretic mobility-shift assay, and mutation of potential STAT-binding sites reduced Qp responsiveness to Janus kinase (JAK)-1. Consistent with a role for STATs in Qp function, Qp using Burkitt's lymphoma Rael cells and cultured nasopharyngeal carcinoma (NPC) cells contained nuclear STAT protein. We investigated whether the inability to maintain EBV-positive NPC cell lines in culture was related to Qp activity. Passaging of the NPC cell line HK666 led to activation of expression of BZLF1, which encodes Zta and loss of Qp function. Transient expression assays linked Zta expression to the down-regulation of Qp. Cotransfection of Zta reduced Qp activity in reporter assays. This negative regulation required Zta DNA-binding activity. We provide evidence that Zta up-regulation of p53 leads to p53-mediated interference with JAK/STAT activation of Qp. The data imply that JAK/STAT signaling has a role in EBV-associated malignancies.

B-Lymphocytes↗