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PubMed2002

Particle accelerators in the hot spots of radio galaxy 3C 445, imaged with the VLT.

Hot spots (HSs) are regions of enhanced radio emission produced by supersonic jets at the tip of the radio lobes of powerful radio sources. Obtained with the Very Large Telescope (VLT), images of the HSs in the radio galaxy 3C 445 show bright knots embedded in diffuse optical emission distributed along the post-shock region created by the impact of the jet into the intergalactic medium. The observations reported here confirm that relativistic electrons are accelerated by Fermi-I acceleration processes in HSs. Furthermore, both the diffuse emission tracing the rims of the front shock and the multiple knots demonstrate the presence of additional continuous re-acceleration processes of electrons (Fermi-II).

Journal Article↗

PubMed2002

Electron acceleration by a wake field forced by an intense ultrashort laser pulse.

Plasmas are an attractive medium for the next generation of particle accelerators because they can support electric fields greater than several hundred gigavolts per meter. These accelerating fields are generated by relativistic plasma waves-space-charge oscillations-that can be excited when a high-intensity laser propagates through a plasma. Large currents of background electrons can then be trapped and subsequently accelerated by these relativistic waves. In the forced laser wake field regime, where the laser pulse length is of the order of the plasma wavelength, we show that a gain in maximum electron energy of up to 200 megaelectronvolts can be achieved, along with an improvement in the quality of the ultrashort electron beam.

Journal Article↗

PubMed2004

Accelerated biodegradation of cement by sulfur-oxidizing bacteria as a bioassay for evaluating immobilization of low-level radioactive waste.

Disposal of low-level radioactive waste by immobilization in cement is being evaluated worldwide. The stability of cement in the environment may be impaired by sulfur-oxidizing bacteria that corrode the cement by producing sulfuric acid. Since this process is so slow that it is not possible to perform studies of the degradation kinetics and to test cement mixtures with increased durability, procedures that accelerate the biodegradation are required. Semicontinuous cultures of Halothiobacillus neapolitanus and Thiomonas intermedia containing thiosulfate as the sole energy source were employed to accelerate the biodegradation of cement samples. This resulted in a weight loss of up to 16% after 39 days, compared with a weight loss of 0.8% in noninoculated controls. Scanning electron microscopy of the degraded cement samples revealed deep cracks, which could be associated with the formation of low-density corrosion products in the interior of the cement. Accelerated biodegradation was also evident from the leaching rates of Ca(2+) and Si(2+), the major constituents of the cement matrix, and Ca exhibited the highest rate (up to 20 times greater than the control rate) due to the reaction between free lime and the biogenic sulfuric acid. Leaching of Sr(2+) and Cs(+), which were added to the cement to simulate immobilization of the corresponding radioisotopes, was also monitored. In contrast to the linear leaching kinetics of calcium, silicon, and strontium, the leaching pattern of cesium produced a saturation curve similar to the control curve. Presumably, the leaching of cesium is governed by the diffusion process, whereas the leaching kinetics of the other three ions seems to governed by dissolution of the cement.

Betaproteobacteria↗

PubMed1970

Accelerated Cytopathology in HeLa Cells Induced by Reovirus and Cycloheximide.

The addition of the protein inhibitor cycloheximide, at concentrations which suppress virus replication, to HeLa cell monolayers infected with reovirus type 2 results in the appearance of accelerated cytopathic effects (CPE). At high multiplicity of infection, CPE appeared after a lag period of 2 to 3 hr and increased progressively, until by 12 hr the entire monolayer had rounded and sloughed off. During this same period, both the uninfected cycloheximide-treated and untreated virus-infected controls exhibited no CPE. The phenomenon is affected by the kind of cell species employed and can be reversed if the antibiotic is removed within 1 hr after exposure. The evidence obtained through studies in which specific metabolic inhibitors and direct biochemical analyses were used suggests that the accelerated CPE observed in cycloheximide-treated reovirus-infected cells is the consequence of the combined inhibition of the synthesis of both cellular protein and ribonucleic acid. The accelerated CPE is also induced in the antibiotic-treated cells by reovirus serotypes 1 and 3.

Journal Article↗

PubMed1992

Penicillin treatment accelerates middle ear inflammation in experimental pneumococcal otitis media.

Most Streptococcus pneumoniae strains are killed by very low concentrations of penicillin and other beta-lactam antibiotics, yet middle ear inflammation and effusion persist for days to weeks after treatment in most cases of pneumococcal otitis media. To study the effect of beta-lactam antibiotic treatment on pneumococci and the middle ear inflammatory response during pneumococcal otitis media, we measured concentrations of pneumococci, inflammatory cells, and lysozyme in middle ear fluid (MEF) by using the chinchilla model. Procaine penicillin G given intramuscularly 12 and 36 h after inoculation of pneumococci into the middle ear caused a significant acceleration in the MEF inflammatory cell concentration compared with that in untreated controls, with a significant peak in the inflammatory cell concentration 24 h after pneumococcal inoculation. The lysozyme concentration in MEF also increased more rapidly in treated than in control animals. Viable pneumococci were not detected in MEF after the second dose of penicillin, but the total pneumococcal cell concentration remained unchanged for at least 45 days. Therefore, penicillin treatment accelerated middle ear inflammation while killing pneumococci, but treatment did not accelerate clearance of the nonviable pneumococcal cells from MEF. Further studies will need to define the contribution of these responses to acute and chronic tissue injury.

Animals↗

PubMed1999

Decay-accelerating factor and cytoskeleton redistribution pattern in HeLa cells infected with recombinant Escherichia coli strains expressing Dr family of adhesins.

Escherichia coli strains expressing Dr fimbriae are able to enter epithelial cells by interacting with a complement-regulatory protein, decay-accelerating factor. This model of bacterial internalization, with a well-characterized bacterial ligand and host receptor, provides a unique opportunity to investigate the early stages of invasion. We used immunofluorescence staining techniques to examine the distribution of receptor and cytoskeletal proteins in HeLa cells infected with E. coli recombinant strains that expressed Dr family of adhesins: Dr, Dr-II, F1845, AFA-I, and AFA-III. A major rearrangement of decay-accelerating factor was found at the adherence sites of recombinant strains expressing Dr, Dr-II, and F1845 adhesins. The changes in the distribution of receptor were significantly smaller on HeLa cells infected with E. coli bearing AFA-I or AFA-III afimbrial adhesins. Receptor aggregation was associated with the redistribution of cytoskeleton-associated proteins such as actin, alpha-actinin, ezrin, and occasionally tropomyosin. Purified Dr fimbriae coated on polystyrene beads were capable of triggering clustering of receptor and accumulating actin at the adhesion sites of beads to HeLa cells. Using scanning and transmission electron microscopic techniques, we have shown that beads coated with Dr fimbriae, as opposed to beads coated with bovine serum albumin, were enwrapped by cellular microvilli and ultimately internalized into HeLa cells. This indicates that interaction of Dr fimbriae with decay-accelerating factor is associated with redistribution of receptor and is sufficient to promote bacterial internalization.

Actins↗

PubMed2003

Inhibition of gamma interferon decreases bacterial load in peritonitis by accelerating peritoneal fibrin deposition and tissue repair.

Bowel perforation can lead to significant bacterial spillage, which may then cause septic peritonitis, characterized by a systemic inflammatory response and organ dysfunction. There are several reports that have shown that the development of peritoneal adhesions is dependent on inflammatory cytokine levels and that these adhesions can reduce bacterial spread, possibly by sealing off the cecum in the cecal ligation and puncture (CLP) model of septic peritonitis. There have not, however, been any studies that have utilized a strategy to accelerate tissue repair in order to seal off the injured cecum and reduce bacterial spread as well as ameliorate systemic inflammation. In the present study, we demonstrate that the administration of anti-gamma interferon (IFN-gamma) antibody (1.2 mg/kg of body weight, intravenously) accelerated tissue repair via increased fibrin deposition 12 and 24 h after CLP in rats. This increase in fibrin deposition was associated with peritoneal adhesion 24 h after CLP and a reduction in bacterial load compared to the bacterial load of rats given irrelevant antibody. Plasma fibrin levels, however, were not altered after IFN-gamma antibody administration, suggesting that the inhibition of IFN-gamma activity specifically increased fibrin deposition to the site of injury. Furthermore, plasma interleukin-6, used as a marker of systemic inflammatory response, was reduced in CLP rats given IFN-gamma antibody compared to that found in those given irrelevant antibody. These results suggest that the early inhibition of IFN-gamma activity in the CLP model is beneficial by accelerating fibrin deposition in cecal tissue to prevent bacterial spread and reduce the systemic inflammatory response. Importantly, increased fibrin deposition in the ceca was not associated with increased plasma fibrin whereas the latter may have detrimental effects associated with coagulation disorders.

Animals↗

PubMed1974

Acceleration of dextransucrase activity of Streptococcus mutans by secretory immunoglobulin A.

The effect of immunoglobulins on the activity of dextransucrase purified from Streptococcus mutans strain HS-6 is described. When human salivary immunoglobulin A (IgA) or colostral IgA, either natured or denatured, was incubated with dextransucrase, the rate of the dextran synthesis was markedly accelerated, whereas human serum IgA or IgG neither accelerated nor inhibited the enzyme activity. The results suggest that a portion unique for secretory IgA, the secretory component, might be related to the enzyme acceleration. On the other hand, specific rabbit antiserum against the dextransucrase inhibited completely dextran synthesis by the enzyme.

Animals↗

PubMed2003

The human cytomegalovirus UL82 gene product (pp71) accelerates progression through the G1 phase of the cell cycle.

As viruses are reliant upon their host cell to serve as proper environments for their replication, many have evolved mechanisms to alter intracellular conditions to suit their own needs. For example, human cytomegalovirus induces quiescent cells to enter the cell cycle and then arrests them in late G(1), before they enter the S phase, a cell cycle compartment that is presumably favorable for viral replication. Here we show that the protein product of the human cytomegalovirus UL82 gene, pp71, can accelerate the movement of cells through the G(1) phase of the cell cycle. This activity would help infected cells reach the late G(1) arrest point sooner and thus may stimulate the infectious cycle. pp71 also induces DNA synthesis in quiescent cells, but a pp71 mutant protein that is unable to induce quiescent cells to enter the cell cycle still retains the ability to accelerate the G(1) phase. Thus, the mechanism through which pp71 accelerates G(1) cell cycle progression appears to be distinct from the one that it employs to induce quiescent cells to exit G(0) and subsequently enter the S phase.

Animals↗

PubMed2004

Tumorigenesis by human herpesvirus 8 vGPCR is accelerated by human immunodeficiency virus type 1 Tat.

Human herpesvirus 8 (HHV-8), also called Kaposi's sarcoma (KS) herpesvirus, can cause KS but is inefficient. Untreated human immunodeficiency virus type 1 (HIV-1) coinfection is a powerful risk factor. The HHV-8 chemokine receptor, vGPCR (ORF74), activates NF-kappaB and NF-AT, and their levels of activation are synergistically increased by HIV-1 Tat. Transgenic vGPCR mice develop KS-like tumors. A cell line derived from one such tumor expresses vGPCR and forms tumors in nude mice. Here we show that transfection of DNA encoding HIV-1 tat (but not a transactivation-defective mutant) into these tumor cells increases NF-kappaB and NF-AT activation levels and accelerates tumor formation. Tumorigenesis was also accelerated when Tat DNA was transfected into normal cells and the transfected cells were mixed with the tumor cells and injected into a single site. Tumorigenesis was also increased when the two cell types were injected at separate sites, suggesting that tumorigenesis is accelerated by Tat through soluble factors.

Animals↗

PubMed2005

Adenovirus exploits the cellular aggresome response to accelerate inactivation of the MRN complex.

Results reported here indicate that adenovirus 5 exploits the cellular aggresome response to accelerate inactivation of MRE11-RAD50-NBS1 (MRN) complexes that otherwise inhibit viral DNA replication and packaging. Aggresomes are cytoplasmic inclusion bodies, observed in many degenerative diseases, that are formed from aggregated proteins by dynein-dependent retrograde transport on microtubules to the microtubule organizing center. Viral E1B-55K protein forms aggresomes that sequester p53 and MRN in transformed cells and in cells transfected with an E1B-55K expression vector. During adenovirus infection, the viral protein E4orf3 associates with MRN in promyelocytic leukemia protein nuclear bodies before MRN is bound by E1B-55K. Either E4orf3 or E4orf6 is required in addition to E1B-55K for E1B-55K aggresome formation and MRE11 export to aggresomes in adenovirus-infected cells. Aggresome formation contributes to the protection of viral DNA from MRN activity by sequestering MRN in the cytoplasm and greatly accelerating its degradation by proteosomes following its ubiquitination by the E1B-55K/E4orf6/elongin BC/Cullin5/Rbx1 ubiquitin ligase. Our results show that aggresomes significantly accelerate protein degradation by the ubiquitin-proteosome system. The observation that a normal cellular protein is inactivated when sequestered into an aggresome through association with an aggresome-inducing protein has implications for the potential cytotoxicity of aggresome-like inclusion bodies in degenerative diseases.

Acid Anhydride Hydrolases↗

PubMed1995

Ras transformation results in an elevated level of cyclin D1 and acceleration of G1 progression in NIH 3T3 cells.

Ectopic overexpression of v-H-Ras protein in NIH 3T3 cells resulted in cellular transformation and an acceleration of G1 progression of these cells. A shortened G1 phase was found to be associated with an increased level of cyclin D1 but not cyclin E protein. Using an antisense blocking method, reduced synthesis of cyclin D1 in v-H-Ras transformants resulted in a slower G1 progression rate of these cells. Although constitutive overexpression of cyclin D1 in NIH 3T3 cells accelerated G1 progression, cells remained untransformed. Furthermore, inhibition of cyclin D1 synthesis greatly impaired the soft-agar cloning efficiency of v-H-Ras transformants. These results suggest that increased expression of cyclin D1 is necessary but not sufficient for the transforming activity of v-H-Ras. Similar effect on cell cycle progression was also observed in Raf-transformed cells. In addition to cyclin D1, cyclin E protein was found to be elevated in Src transformants. This may account for the further shortening of the G1 phase of these cells. Activation of an additional Ras-independent pathway was suggested to be responsible for the further acceleration of the G1 phase in Src transformants.

3T3 Cells↗

PubMed1999

Accelerated mammary tumor development in mutant polyomavirus middle T transgenic mice expressing elevated levels of either the Shc or Grb2 adapter protein.

The Grb2 and Shc adapter proteins play critical roles in coupling activated growth factor receptors to several cellular signaling pathways. To assess the role of these molecules in mammary epithelial development and tumorigenesis, we have generated transgenic mice which individually express the Grb2 and Shc proteins in the mammary epithelium. Although mammary epithelial cell-specific expression of Grb2 or Shc accelerated ductal morphogenesis, mammary tumors were rarely observed in these strains. To explore the potential role of these adapter proteins in mammary tumorigenesis, mice coexpressing either Shc or Grb2 and a mutant form of polyomavirus middle T (PyV mT) antigen in the mammary epithelium were generated. Coexpression of either Shc or Grb2 with the mutant PyV mT antigen resulted in a dramatic acceleration of mammary tumorigenesis compared to parental mutant PyV mT strain. The increased rate of tumor formation observed in these mice was correlated with activation of the epidermal growth factor receptor family and mitogen-activated protein kinase pathway. These observations suggest that elevated levels of the Grb2 or Shc adapter protein can accelerate mammary tumor progression by sensitizing the mammary epithelial cell to growth factor receptor signaling.

Adaptor Proteins, Signal Transducing↗

PubMed1976

Comparison of intravenous oxytocin and prostaglandin E2 for accelerating labour.

In a prospective study of 52 consecutive women who required acceleration of labour intravenous prostaglandin E2 (PGE2) was used as the oxytocic agent. These mothers were matched for age, parity, height, gestational age, initial cervical dilatation, and station and position of the fetal head with 52 women whose labours were accelerated with oxytocin; both drugs were equally effective. Acceleration to delivery intervals, second-stage durations, the number of assisted deliveries, and Apgar scores were similar regardless of the oxytocic used. Although PGE2 compares well with oxytocin, it offers no further advantages and is more expensive and less well tried than oxytocin.

Adolescent↗

PubMed1991

Short chain fatty acids in the terminal ileum accelerate stomach to caecum transit time in the rat.

We have previously shown that infusion of triglycerides and long chain fatty acids into the ileum of humans and rats delays small bowel transit time. The present studies have investigated the effect on the stomach to caecum transit time of a baked bean meal of the ileal infusion of 20 mM, 50 mM, and 100 mM acetic, butyric, hexenoic, and caprylic acids in rats. After an 18 hour fast either a control or a short chain fatty acid (SCFA) solution (pH 6.5) was infused into the ileum for 30 minutes (0.3 ml/hour). A test meal was given by gavage and the infusion continued for a further 150 minutes. The arrival of the meal in the colon was signalled by a rise in the exhaled hydrogen concentration. Acetic acid (20 mM, 50 mM, 100 mM), butyric acid (100 mM), and caprylic acid (100 mM) produced a significant acceleration of transit which was inversely proportional to SCFA chain length. In a separate experiment, infusion of 100 mM acetic acid, the most potent SCFA, into an isolated ileal Thirty-Vella loop failed to accelerate transit of the test meal. Our results suggest that SCFAs accelerate transit via a local enteric reflex.

Acetates↗

PubMed1988

Accelerated idioventricular rhythm of infundibular origin in patients with a concealed form of arrhythmogenic right ventricular dysplasia.

Five apparently healthy people (aged 16-47) presented with recurrent episodes of accelerated idioventricular rhythm characterised by left bundle branch block and right axis deviation. Clinical history, physical findings, basic electrocardiogram, chest x ray, and blood tests were within normal limits in all. Holter monitoring, exercise stress test, and electrophysiological study (in three patients) showed that accelerated idioventricular rhythm was mainly bradycardia dependent, easily suppressed by effort and overdrive pacing, and originated from the outflow tract of the right ventricle. The mechanism could be enhanced automaticity. Data from cross sectional echocardiography (in all patients) and from haemodynamic evaluation (in three) identified structural or wall motion abnormalities of the right ventricle or both without appreciable dilatation of the ventricle. Biopsy specimens of the right ventricular endomyocardium showed fibrosis in one patient, fibrosis and fatty infiltration in the second, and pronounced fatty infiltration in the third. These results show that some patients with accelerated idioventricular rhythm have right ventricular abnormalities that are typical of the localised and concealed forms of arrhythmogenic right ventricular dysplasia.

Adolescent↗

PubMed2006

MDM2 SNP309 accelerates colorectal tumour formation in women.

Recent studies have shown that the G-allele of MDM2 SNP309 (T/G) in the p53 tumour suppressor pathway can accelerate tumorigenesis and alter the risk of various cancers in women and not in men. In this report, data are presented from two independent groups of patients that suggest that the G-allele of SNP309 accelerates colorectal tumour formation only in women, and that lend further support to the model that primarily female-specific hormones, such as oestrogen, could either directly or indirectly allow for the G-allele of SNP309 to accelerate tumour formation in women.

Adult↗

PubMed1987

Accelerated irradiation of cervical node metastases.

Accelerated irradiation combining electron beam and cobalt sources was carried out in 34 patients with large involved nodes fixed to the cervical structures (N3). Concomitant boost technique was used to reduce the overall duration of treatment from 7 to 5 weeks while maintaining the standard 70-Gy tumor dose. The first part of treatment consisted of conventional cobalt irradiation, 50 Gy delivered to the whole neck over 5 weeks. The accelerated schedule, carried out over 4 weeks, delivered an additional 1 Gy/day to the node through a circular and lateral electron beam field, for a total dose of 70 Gy to the enlarged node. In the case of an identified primary the tumor site was also boosted to the 70-Gy total dose. The rate of acute skin reactions was acceptable and there were no major mucosal complications. At the end of irradiation, 62% of patients experienced complete clinical regression; 41% subsequently had cervical recurrences. Early cervical fibrosis was limited to the over-treated area. The concomitant boost technique is a good way to accelerate irradiation without decreasing the total dose or increasing the immediate complication rate.

Adolescent↗