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A Gallagher

Publications and source records attributed to A Gallagher.

At least 37 records · Page 2Linked to original sources
PubMed2000

Model of particle growth in silane discharges

The growth of silicon particles in the neutral plasma region of pure silane, rf capacitively coupled, steady-state discharges is calculated with a homogeneous, plasma-chemistry model. Plasma conditions are typical of those used in hydrogenated amorphous silicon (a-Si:H) device production. SiH3 and SiH-3 grow into particles by the step-by-step addition of silicon atoms, primarily due to reactions with SiH3. Attrition of growing Si(x)H(z)(m) radicals and ions with z charges, which are "particles" for large x, occurs by diffusion of neutral and positively charged radicals to the electrodes. Rate coefficients for electron, ion, radical, and silane collisions with the Si(x)H(z)(m) for x=1-10(5) are estimated from detailed considerations of the literature and relevant physics. Self-consistent anion, cation (n(+)), and electron (n(e)) densities and charge fluxes are used, and charge neutrality is maintained. Typically n(+)/n(e) congruent with100, which causes a large fraction of neutral particles and thereby a major particle flux into the growing a-Si:H film. The density of visible particles (x>10(4)) varies many orders of magnitude with relatively minor changes in discharge power, pressure, and electrode gap. This parameter dependence agrees with experiment, and by adjusting collision parameters within a reasonable range the calculated particle densities can be brought into exact agreement with experiment. An additional result of the model, which has not yet been detected, is that Si(x)H(m) clusters with 3<x<30 are continuously deposited into growing films, and for typical conditions yield a very significant fraction (1-10 %) of total film growth.

Journal Article↗
PubMed2000

Precursors of literacy delay among children at genetic risk of dyslexia.

This paper reports the literacy skills of 63 children selected as being at genetic risk of dyslexia compared with 34 children from families reporting no history of reading impairment. Fifty-seven per cent of the at-risk group were delayed in literacy development at 6 years compared with only 12% of controls. The "unimpaired" at-risk group were not statistically different from controls on most cognitive and language measures at 45 months, whereas the literacy-delayed group showed significantly slower speech and language development, although they did not differ from controls in nonverbal ability. Letter knowledge at 45 months was the strongest predictor of literacy level at 6 years. In addition, early speech and language skills predicted individual differences in literacy outcome and genetic risk accounted for unique variance over and above these other factors. The results are discussed in terms of an interactive developmental model in which semantic and phonological skills support early reading acquisition.

Child↗
PubMed1999

Detection of Epstein-Barr virus (EBV) genomes in the serum of patients with EBV-associated Hodgkin's disease.

DNA from malignant cells is present in the serum/plasma of cancer patients and DNA from this source is amenable to analysis by polymerase chain reaction (PCR). In the present study, we evaluated whether Epstein-Barr virus (EBV) DNA is present in the serum of patients with EBV-associated Hodgkin's disease (HD). Using conventional PCR, EBV DNA was detected in serum from 30/33 patients with EBV-associated HD but in only 6/26 patients with non-EBV-associated disease (p < 0.001). Samples from healthy individuals were negative and only 5/12 infectious mononucleosis samples were positive. Real-time quantitative PCR was subsequently employed to determine the concentration of EBV DNA present in serum; among positive samples the level ranged from 1 to 705 copies per 125 microliter of serum. Post-treatment samples from 5/14 cases with EBV-associated HD contained detectable EBV DNA; analysis of this small group of cases suggests that positivity in post-treatment samples correlates with risk factors indicative of a poor prognosis. Overall, our results are consistent with the notion that DNA from Reed-Sternberg cells is present in the serum of HD patients, and further suggest that serum EBV should be evaluated as a prognostic marker. Int. J. Cancer (Pred. Oncol.) 84:442-448, 1999.

Adult↗
PubMed1999

The porcine calcitonin receptor promoter directs expression of a linked reporter gene in a tissue and developmental specific manner in transgenic mice.

We have investigated the transcriptional regulation of the porcine calcitonin (CT) receptor (pCTR) promoter in transgenic mice. A construct containing 2.1 kb pCTR 5' flanking region, fused to a beta-galactosidase (lacZ) gene, was employed for the production of transgenic mice. At 11.5 days of development lacZ expression was observed in the embryonic brain and spinal cord. By 15.5 days post fertilization, lacZ expression was detected in the developing mammary gland, external ear, cartilage primordium of the humerus, and anterior naris (nostril). RT-PCR on RNA from these fetal tissues showed endogenous mouse CTR (mCTR) expression. In neonatal and adult transgenics, lacZ expression was silenced, except in brain, spinal cord, and testis (adults only). Endogenous mCTR gene expression and pCTR promoter activity were corepressed in the same tissues from adult mice. No pCTR promoter activity was detected in the kidney or bone of transgenic animals. This suggests that additional DNA sequences may be required for pCTR promoter activity in these tissues. From these results, we conclude that the pCTR promoter is active only in tissues expressing endogenous mCTR. Many of the these tissues represent previously unknown sites of CTR gene expression. Finally, the developmental regulation of pCTR/mCTR in tissues such as breast and cartilage primordium suggests that CTRs may play a role in the morphogenesis of these tissues.

Aging↗
PubMed1999

Aberrant neurofilament phosphorylation in sensory neurons of rats with diabetic neuropathy.

Aberrant neurofilament phosphorylation occurs in many neurodegenerative diseases, and in this study, two animal models of type 1 diabetes--the spontaneously diabetic BB rat and the streptozocin-induced diabetic rat--have been used to determine whether such a phenomenon is involved in the etiology of the symmetrical sensory polyneuropathy commonly associated with diabetes. There was a two- to threefold (P < 0.05) elevation of neurofilament phosphorylation in lumbar dorsal root ganglia (DRG) of diabetic rats that was localized to perikarya of medium to large neurons using immunocytochemistry. Additionally, diabetes enhanced neurofilament M phosphorylation by 2.5-fold (P < 0.001) in sural nerve of BB rats. Neurofilaments are substrates of the mitogen-activated protein kinase (MAPK) family, which includes c-jun NH2-terminal kinase (JNK) or stress-activated protein kinase (SAPK1) and extracellular signal-regulated kinases (ERKs) 1 and 2. Diabetes induced a significant three- to fourfold (P < 0.05) increase in phosphorylation of a 54-kDa isoform of JNK in DRG and sural nerve, and this correlated with elevated c-Jun and neurofilament phosphorylation. In diabetes, ERK phosphorylation was also increased in the DRG, but not in sural nerve. Immunocytochemistry showed that JNK was present in sensory neuron perikarya and axons. Motoneuron perikarya and peroneal nerve of diabetic rats showed no evidence of increased neurofilament phosphorylation and failed to exhibit phosphorylation of JNK. It is hypothesized that in sensory neurons of diabetic rats, aberrant phosphorylation of neurofilament may contribute to the distal sensory axonopathy observed in diabetes.

Animals↗
PubMed1999

Neurotrophin-3 reverses nerve conduction velocity deficits in streptozotocin-diabetic rats.

The ability of neurotrophin-3 (NT-3) to reverse established nerve disorders was investigated in the peripheral neuraxis of streptozotocin-diabetic rats. Sciatic sensory and motor nerve conduction velocity deficits established after 2 months of diabetes were completely normalized by one further month of treatment with either NT-3 or insulin. None of these conduction velocity changes were associated with altered mean axonal caliber in the sciatic nerve. In the dorsal and ventral roots, mean axonal caliber was significantly decreased after 8 weeks of diabetes (both P < 0.05). Subsequently, one month of insulin, but not NT-3, treatment increased mean axonal caliber to age-matched control values. NT-3 treatment was also without effect on the significant (both P < 0.05) decrease in phosphorylated heavy neurofilament (NFH) subunits seen in dorsal and ventral roots of 12 week diabetic rats. In the sural nerve, diabetes attenuated a maturation-associated increase in mean axonal caliber over the first 8 weeks of diabetes, and induced atrophy between weeks 8 and 12 that was ameliorated by both NT-3 and insulin treatment. Reductions in sural nerve axonal caliber were associated with a tendency for elevation of both phosphorylated NFH levels in large fibers and the ratio of phosphorylated to nonphosphorylated NFH that was attenuated by NT-3. These data demonstrate that NT-3 corrects established sciatic nerve conduction deficits in diabetic rats in a manner independent of changes in axonal caliber in this nerve. Further, although NT-3 was without effect on decreases in axonal caliber and NFH subunit phosphorylation in the spinal roots, reversal of axonal caliber deficits in peripheral nerves of sensory fibers may involve NT-3-mediated normalization of aberrant neurofilament phosphorylation.

Animals↗
PubMed1998

Lack of involvement of known oncogenic DNA viruses in Epstein-Barr virus-negative Hodgkin's disease.

Epstein-Barr virus (EBV) is associated with around one-third of cases, but young adult cases are rarely EBV associated. In this study, known oncogenic DNA viruses, including human adenoviruses, papovaviruses and the human herpesviruses-6 (HHV-6) and -8 (HHV-8) were not detected in Hodgkin's disease lesions. These results suggest that an as yet unidentified infectious agent is involved in the pathogenesis of non-EBV-associated Hodgkin's disease.

Adolescent↗
PubMed1998

Nitric oxide inhibits lipopolysaccharide-induced apoptosis in pulmonary artery endothelial cells.

Our group recently reported that cultured sheep pulmonary artery endothelial cells (SPAECs) became resistant to lipopolysaccharide (LPS)-induced apoptosis several days after constitutive synthesis of nitric oxide (NO) after adenoviral (Ad) transfer of inducible NO synthase (iNOS) or exposure to the NO donor S-nitroso-N-acetylpenicillamine (SNAP) (E. Tzeng, Y.-M. Kim, B. R. Pitt, A. Lizonova, I. Kovesdi, and T. R. Billiar. Surgery 122: 255-263, 1997). In the present study, we confirmed this observation by establishing stable transfectants after retroviral gene transfer [replication-deficient retrovirus (DFG)] of human iNOS (DFG-iNOS) SPAECs and then used all three approaches (Ad, DFG, and SNAP) to determine underlying mechanisms of this phenomenon. Continuous endogenous production of NO in itself did not cause apoptosis as assessed by phase-contrast microscopy, nuclear morphology, and internucleosomal DNA fragmentation. Prolonged (72-96 h) synthesis of NO, however, after DFG- or replication-deficient adenovirus (Ad. CMV)-iNOS or SNAP (100 microM, 96 h) inhibited LPS-induced apoptosis. The kinetics of such protection suggested that NO may be inducing other gene products. Ad-mediated transfer of manganese superoxide dismutase (MnSOD) decreased the sensitivity of wild-type SPAECs to LPS-induced apoptosis. MnSOD, however, was not induced in an NG-monomethyl-L-arginine (L-NMMA)-sensitive time-dependent fashion after Ad.CMV-iNOS. Other inducible genes that may be affected by NO and that may protect against potential oxidant-mediated LPS-induced apoptosis including 70-kDa heat shock protein, heme oxygenase-1, metallothionein, and Bcl-2 also were not elevated in an L-NMMA-sensitive, time-dependent fashion. Although the candidate gene product underlying NO-induced protection remains unclear, we did note that prolonged synthesis of NO inhibited LPS-induced activation of an interleukin-1beta-converting enzyme-like cysteine protease (cysteine protease protein-32-like) in a dithiothreitol-sensitive fashion, suggesting that S-nitrosylation of an important downstream target of convergence of apoptotic signals may contribute to the sensitivity of SPAECs to LPS.

Adenoviridae↗
PubMed1997

Evaluation of joint medical and nursing notes with preprinted prompts.

OBJECTIVE: To determine the views of doctors and nurses about two recent innovations in the structure of case notes: the use of preprinted prompts and the use of joint medical and nursing notes. DESIGN: Questionnaire survey of all doctors and nurses working on the children's wards. SETTING: Children's wards in a district general hospital. MAIN OUTCOME MEASURES: Whether or not respondents wanted to return to traditional notes; positive and negative aspects of the two innovations. RESULTS: There was an 81% response rate. 45 of 48 respondents (94%) did not want to return to traditional notes. Positive features of joint notes that were identified included: promotes team work (21/48 respondents), improves access to information (14/48), and reduces duplication (14/48). Negative features included uncertainty about identity of writer (8/48) and incompletely filled in sheets (7/48). Positive features of preprinted prompts included: less information omitted (29/48), easier to read and find information (28/48), and quicker to write (21/48). Negative features included: not enough space (19/48) and clerking too mechanical (16/48). CONCLUSION: Advantages of both innovations outweighed their disadvantages to the extent that only three out of 48 respondents wanted to return to writing traditional notes.

Adult↗