Carpenter, D, Meadows, HJ, Brough, S, Chapman, G, Clarke, C, Coldwell, M, Davis, R, Harrison, D, Meakin, J, McHale, M, Rice, SQJ, Tomlinson, WJ, Wood, M & Sanger, GJ 1999, 'Site-specific splice variation of the human P2X4 receptor', Neuroscience Letters, vol. 273, no. 3, pp. 183-186.
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Cook, JW, Cardarelli, MG & Pate, JW 1999, 'Traumatic aortic rupture: Recent outcome with regard to neurologic deficit - Discussion', ANNALS OF THORACIC SURGERY, vol. 67, no. 4, pp. 964-965.
Gurbuz, AT, Weiman, DS & Pate, JW 1999, 'Traumatic injury to the thoracic aorta', The Annals of Thoracic Surgery, vol. 68, no. 3, pp. 1116-1117.
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Harris, LM 1999, 'Mood and Prospective Memory', Memory, vol. 7, no. 1, pp. 117-127.
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This study considered the relationship between mood states, prospective memory, and retrospective memory among a non-clinical sample of undergraduate students. Multiple regression analyses with simultaneous entry of variables were undertaken to examine the unique contributions of the alternate memory test and the emotional states to memory test performance. As expected, retrospective free recall performance and anxiety made unique and significant contributions to performance on the prospective memory task. However, only prospective memory performance emerged as a significant predictor of retrospective free recall. It is suggested that none of the mood measures emerged as a significant predictor of retrospective memory performance because they do not account for unique variance. In contrast, the relationship between anxiety and prospective memory appears to be due to factors uniquely associated with anxiety, and unrelated to depression.
Harris, LM, Robinson, J & Menzies, RG 1999, 'Evidence for fear of restriction and fear of suffocation as components of claustrophobia', Behaviour Research and Therapy, vol. 37, no. 2, pp. 155-159.
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Recent investigations of the aetiology and treatment of specific phobias have focussed on clarifying the concerns underlying phobic anxiety. It has been proposed that claustrophobic fear is comprised of separable confinement and suffocation components. This paper presents data from 78 general medical outpatients undergoing magnetic resonance imaging (MRI) scans in two major teaching hospitals. The findings support the two factor structure of claustrophobia, in that exposure to confinement reduced confinement subscale scores, but did not influence suffocation scores. Copyright (C) 1998 Elsevier Science Ltd.
Izatt, L, Greenman, J, Hodgson, S, Ellis, D, Watts, S, Scott, G, Jacobs, C, Liebmann, R, Zvelebil, MJ, Mathew, C & Solomon, E 1999, 'Identification of germline missense mutations and rare allelic variants in the ATM gene in early-onset breast cancer', Genes Chromosomes and Cancer, vol. 26, no. 4, pp. 286-294.
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Epidemiological studies have shown an increased risk of breast cancer in obligate ataxia telangiectasia (A-T) heterozygotes. We analyzed 100 samples from young breast cancer patients for mutations in ataxia-telangiectasia mutated (ATM), the gene responsible for the autosomal recessive condition, A- T, to determine whether A-T heterozygosity predisposes such individuals to develop breast cancer. These patients were selected from families with a moderate or absent family history of breast cancer and included a subset of 16 radiosensitive patients. Forty-four germline sequence variants were detected by fluorescent chemical cleavage of mismatch of RT-PCR products. These included seven rare variants found in nine patients (three described for the first time), but no truncating mutations. Although three variants were detected in the radiosensitive subset, this was not statistically significant compared to the nonradiosensitive group. One variant, G2765S, is likely to be a missense mutation, but the other six variants probably represent rare polymorphisms. However, five of the seven rare germline variants detected showed loss of heterozygosity of the wild-type ATM allele for one or more markers close to the ATM locus in matched tumor DNA. This high rate of somatic inactivation of ATM may indicate either that these rare variants play a role in breast cancer development or alternatively that a neighboring tumor suppressor gene is important for tumorigenesis. We found germline truncating ATM mutations to be rare in these young breast cancer patients and therefore they are unlikely to play a role n the etiology of their disease.
Izatt, L, Greenman, J, Hodgson, S, Ellis, D, Watts, S, Scott, G, Jacobs, C, Liebmann, R, Zvelebil, MJ, Mathew, C & Solomon, E 1999, 'Identification of germline missense mutations and rare allelic variants in the ATM gene in early‐onset breast cancer', Genes, Chromosomes and Cancer, vol. 26, no. 4, pp. 286-294.
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Izatt, L, Greenman, J, Hodgson, S, Ellis, D, Watts, S, Scott, G, Jacobs, C, Liebmann, R, Zvelebil, MJ, Mathew, C & Solomon, E 1999, 'Identification of germline missense mutations and rare allelic variants in theATM gene in early-onset breast cancer', Genes, Chromosomes and Cancer, vol. 26, no. 4, pp. 286-294.
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Menzies, RG, Onslow, M & Packman, A 1999, 'Anxiety and Stuttering', American Journal of Speech-Language Pathology, vol. 8, no. 1, pp. 3-10.
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Onslow, M & Packman, A 1999, 'The Early Stuttering Intervention Debate: Generating Light and Heat', Advances in Speech Language Pathology, vol. 1, no. 2, pp. 143-145.
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Onslow, M & Packman, A 1999, 'The Lidcombe Programme and Natural Recovery: Potential Choices of Initial Management Strategies for Early Stuttering', Advances in Speech Language Pathology, vol. 1, no. 2, pp. 113-121.
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We have attempted to contribute to the current debate about the timing of early stuttering intervention by focusing on empirical information about the Lidcombe Programme and natural recovery. We have attempted to summarise that information in such a way to assist clinicians in making scientifically informed decisions about the timing of intervention. However, we have not made any specific clinical recommendations, in the belief that the decision about timing early intervention is ultimately a value judgment, and while it is best that such judgments are informed by science, the malung of the judgment itself is beyond the limits of science. Perhaps our readers will agree with us about the value of having empirical data underpinning decisions about what to do with cases of early stuttering in clinics. For our part, we are certain that our colleagues and ourselves are more accountable about the timing of intervention when we can yoke such judgments to what science says of the matter. At the level of the value of science in the development of our clinical profession, there are other, extensive arguments. But that topic is for another time and place. Here we have dealt with day-to-day clinical matters. In going about our task, we have conceptualised spontaneous recovery-from our clinical perspective-as a management strategy. In our view, existing literature on the timing of early intervention has had the effect of presenting the issue as a problem, and part of our attempted contribution has been to restate the issue instead as a choice between two initial management strategies. Looking at the matter that way, we find that the following conclusions, which we have summarised in Table 1, appear justified. After natural recovery there is virtually zero stuttering, probably for many years, with a success rate of somewhere between 30 to 90%. We do not know how much clinical time natural recovery will require, and we do not know how much calendar time it will require, and we ...
Onslow, M & Packman, A 1999, 'Treatment Recovery and Spontaneous Recovery From Early Stuttering', Journal of Speech, Language, and Hearing Research, vol. 42, no. 2, pp. 398-402.
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Packman, A & Onslow, M 1999, 'Fluency disruption in speech and in wind instrument playing', Journal of Fluency Disorders, vol. 24, no. 4, pp. 293-298.
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Packman, A & Onslow, M 1999, 'Treating Early Stuttering', American Journal of Speech-Language Pathology, vol. 8, no. 1, pp. 94-95.
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Poulton, R, Menzies, RG, Craske, MG, Langley, JD & Silva, PA 1999, 'Water trauma and swimming experiences up to age 9 and fear of water at age 18: a longitudinal study', Behaviour Research and Therapy, vol. 37, no. 1, pp. 39-48.
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A small number of retrospective studies on the etiology of specific fears have obtained findings consistent with a biological (non-associative) explanation of fear acquisition. Unfortunately, reliance on imperfect memory to recall conditioning events which occurred many years earlier limits the conclusions that can be drawn from such data. The present investigation attempts to overcome this methodological shortcoming by examining the relationship between water trauma (i.e. conditioning) and water skills (e.g. swimming) before the age of 9 and the presence of water fear and phobia at age 18 in a longitudinal birth cohort. We found no evidence of a relationship between water confidence and water trauma up to the age of 9 and fear of water at age 18. Similar findings were obtained for water phobia at age 18 with the exception that study members who were less able to immerse themselves in water with confidence at age 9 were more likely to report water phobia at age 18. Associative and non-associative explanations of these findings were discussed. Copyright (C) 1998 Elsevier Science Ltd.
Walton, LJ, Franklin, IJ, Bayston, T, Brown, LC, Greenhalgh, RM, Taylor, GW & Powell, JT 1999, 'Inhibition of Prostaglandin E 2 Synthesis in Abdominal Aortic Aneurysms', Circulation, vol. 100, no. 1, pp. 48-54.
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Background —There is no treatment proven to limit the growth of abdominal aortic aneurysms, in which the histological hallmarks include inflammation and medial atrophy, with apoptosis of smooth muscle cells and destruction of elastin. Methods and Results —Aneurysm biopsies were used for explant cultures, the preparation of smooth muscle cell cultures, and isolation of macrophages. Tissue macrophages stained strongly for cyclooxygenase 2. Prostaglandin E 2 (PGE 2 ) concentrations in aneurysm tissue homogenates, conditioned medium from explants, and isolated macrophages were 49±22 ng/g, 319±38 ng/mL, and 22±21 ng/mL, respectively. PGE 2 inhibited DNA synthesis and proliferation in normal aortic smooth muscle cells (IC 50 , 23.2±3.8 and 23.6±4.5 ng/mL, respectively). In smooth muscle cells derived from aneurysmal aorta, PGE 2 also caused cell death, with generation of oligonucleosomes. Conditioned medium from the mixed smooth muscle and monocyte cultures derived from explants also had potent growth-inhibitory effects, and fractionation of this medium showed that the growth-inhibitory molecule(s) coeluted with PGE 2 . In explants, indomethacin 10 μmol/L or mefenamic acid 10 μmol/L abolished PGE 2 secretion and significantly reduced IL-1β and IL-6 secretion. In a separate case-control study, the expansion of abdominal aortic aneurysms was compared in 15 patients taking nonsteroidal anti-inflammatory drugs and 63 control subjects; median growth rates were 1.5 and 3.2 mm/y, respectively,
White, SL, Shanske, S, McGill, JJ, Mountain, H, Geraghty, MT, DiMauro, S, Dahl, HM & Thorburn, DR 1999, 'Mitochondrial DNA mutations at nucleotide 8993 show a lack of tissue‐ or age‐related variation', Journal of Inherited Metabolic Disease, vol. 22, no. 8, pp. 899-914.
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AbstractTwo pathogenic mitochondrial DNA mutations, a T‐to‐G substitution (8993T>G) and a T‐to‐C substitution (8993T>C), at nucleotide 8993 have been reported. We describe 13 pedigrees with mitochondrial DNA mutations at nucleotide 8993; 10 pedigrees with the 8993T>G mutation and three with the 8993T>C mutation. Prenatal diagnosis of the nucleotide 8993 mutations is technically possible. However, there are three major concerns: (i) that there is variation in mutant loads among tissues; (ii) that the mutant load in a tissue may change over time; and (iii) that the genotype–phenotype correlation is not clearly understood. We have used the 13 pedigrees to determine specifically the extent of tissue‐ and age‐related variation of the two mutations at nucleotide 8993 in the mitochondrial DNA. The tissue variation was investigated by analysing two or more different tissues from a total of 18 individuals. The age‐related variation of the mutation was investigated by comparing the amount of both mutations in blood taken at birth and at a later age. No substantial tissue variation was found, nor was there any substantial change in the proportion of either mutation over periods of 8–23 years in the four individuals studied. In addition, we noted that two features were remarkably common in families with nucleotide 8993 mutations, namely (i) unexplained infant death (8 cases in 13 pedigrees), and (ii) de novo mutations (5 of the 10 8993T>G pedigrees).
Zeegers, MPA, Tan, FES, Verhagen, AP, Weijenberg, MP & van den Brandt, PA 1999, 'Elevated risk of cancer of the urinary tract for alcohol drinkers: a meta-analysis', Cancer Causes and Control, vol. 10, no. 5, pp. 445-451.
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