Biomedical subjects
Publications and source records attributed to K Walker.
1. Fatigue is a real symptom of HIV infection, and up to two thirds of clients with HIV report symptoms of depression. 2. Depression and fatigue, besides being closely related in HIV cases, have an adverse effect on quality of life. 3. Treating depression and underlying causes of fatigue will improve the quality of life for patients with HIV, who now have an extended life span.
Often unrecognised and untreated, clinical depression exacts a high toll in terms of social, emotional and economic damage. Nurses are well placed to observe the early symptoms of depression and ensure that appropriate treatment is obtained.
OBJECTIVE: To evaluate the ability of nucleic acid amplification techniques to detect Rhodococcus equi in equine buffy coat, blood, and tracheal wash fluid and to differentiate between virulent and avirulent strains of the bacteria. SAMPLE POPULATION: Blood anticoagulated with EDTA and tracheal wash fluid from healthy horses. PROCEDURE: Logarithmic dilutions of virulent and avirulent strains of R equi were added to equine buffy coat and tracheal wash fluid samples. The DNA was extracted and amplified by polymerase chain reaction (PCR), using primers specific for the 16S ribosomal subunit gene and the virulence plasmid of R equi. RESULTS: PCR with 16S ribosomal subunit primers amplified a 441-bp segment of DNA from virulent and avirulent strains of R equi, but not from samples containing other species of bacteria. The virulence plasmid primers amplified an 875-bp segment of DNA from virulent strains of R equi, but not from avirulent R equi, or from other species of bacteria. Virulent strains of R equi could be identified by PCR and differentiated from avirulent strains within 12 to 24 hours after sample collection, with as few as 10 to 100 organisms present. CONCLUSIONS: PCR can be used to rapidly and accurately identify R equi in equine blood and tracheal wash fluid samples and can differentiate between virulent and avirulent strains of the organism. CLINICAL RELEVANCE: Because PCR can confirm a diagnosis of R equi infection in horses more rapidly and specifically than use of standard culture techniques, extrapolation of this assay to soil and fecal samples could be useful in epidemiologic studies and studies of environmental disinfection or decontamination.
Thrombopoietin (TPO) is a hematopoietic factor involved in the regulation of megakaryocytopoiesis. Full length recombinant human TPO (332 residues) has been expressed in BHK cells and purified to homogeneity using conventional means. Peptide, disulfide, and glycosylation mapping of human TPO from residues 1 to 246 has been carried out using liquid chromatography-electrospray mass spectrometry (LC-ESMS). A modification of the ramped orifice method of Carr and co-workers [Carr et al. (1993) Protein Sci. 2, 183-196] is employed, providing additional information for assignment of the LC-ESMS chromatograms. With the modification, b- and y-series peptide ions are produced via front-end CID which confirms the mass-based assignments. The results of our analysis of TPO indicate that the amino acid sequence of TPO 1-246 is as expected from the transfected cDNA with complete cleavage of the signal peptide. Two unique disulfides are formed between the four cysteines in the cytokine domain of TPO: Cys7-Cys151 and Cys29-Cys85. The glycosylation map indicates the position, occupancy, and structures of the N- and O-glycans in TPO 1-246. In addition, site specific structural characterization of the PNGase F-liberated N-glycans has been performed following purification by high-pH anionic exchange chromatography with pulsed amperometric detection (HPAEC-PAD); the results corroborate the LC-ESMS data. The N-glycans are of the complex type with the core-fucosylated disialylated biantennary and trisialylated triantennary structures predominating. The O-glycans are of the mucin type with the monosialylated and disialylated GalGalNAc-S/T structures predominating. Furthermore, we propose that the C-terminal domain of TPO be further divided into two domains on the basis of sequence homology among the cloned sequences and glycosylation/structural features: an N-glycan domain (154-246) and an O-glycan domain (247-332).
The present study investigated the development of hyperthermia and thermal and mechanical hyperalgesia following i.c.v. injections of E. coli lipopolysaccharide (LPS) in rats. LPS increased core temperature and this was prevented by i.c.v. administration of HOE 140, a kinin B2 receptor antagonist or by indomethacin i.c.v. or i.v. B1 receptor antagonists had no effect. LPS induced thermal and mechanical hyperalgesia which was reversed by i.c.v. HOE 140 and indomethacin i.c.v. and i.v., but not by B1 receptor antagonists. These results indicate that injections of endotoxin to the CNS induces hyperthermia and hyperalgesia and that kinins, acting on centrally located B2 receptors, and prostanoids are involved.
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1. E. coli lipopolysaccharide (LPS) produced a dose-dependent (dose range: 0.02-150 micrograms) increase in rat core temperature that was maximal 6 h after intracerebroventricular (i.c.v.) administration. LPS (200 ng) increased core temperature by 1.0 +/- 0.2 degrees C, 6 h following administration, as compared to vehicle-treated controls (-0.2 +/- 0.2 degrees C). 2. LPS-induced (200 ng) hyperthermia was prevented by co-administration of the bradykinin (BK) B2 receptor antagonist, Hoe 140 (10 and 30 pmol, i.c.v.) or by indomethacin (10 nmol, i.c.v.). 3. Systemic administration of Hoe 140 at doses up to 1 mumol kg-1, s.c., did not attenuate LPS-induced (200 ng, i.c.v.) hyperthermia. However, LPS hyperthermia was significantly reduced by systemic administration of indomethacin (1 mumol kg-1, i.v.). 4. Co-administration of the selective B1 receptor antagonists, [des-Arg9, Leu8]BK (0.1 - 1 nmol, i.c.v.) or [des-Arg10] Hoe 140 (0.1 - 1 nmol, i.c.v.), did not prevent LPS-induced hyperthermia. 5. It is concluded that the development of hyperthermia following central administration of endotoxin requires activation of central, but not peripheral bradykinin B2 receptors. The formation of kinins within the CNS may be an important initial component of CNS inflammation following infection.
One of the strategies identified by the NHS to achieve improvements in the health status of the Scottish population is to implement health promotion programmes through the general medical practitioner service. Grampian Local Health Council undertook a survey of Grampian residents to identify factors which might encourage greater public participation in such programmes. The results which are analysed and discussed in this paper show that factors identified by the public include: a preference for doctors to carry out health checks; the need for public education on the roles of different health professionals; the need for information on health checks and their benefits to be supplied in advance; a choice of appointment times and the offer of a follow-up appointment to discuss test results. These results are of interest to health professionals as they are likely to contribute to higher levels of patient involvement in health promotion programmes.
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Kinins, including bradykinin and kallidin, are peptides that are produced and act at the site of tissue injury or inflammation. They induce a variety of effects via the activation of specific B1 or B2 receptors that are coupled to a number of biochemical transduction mechanisms. In the periphery the actions of kinins include vasodilatation, increased vascular permeability and the stimulation of immune cells and peptide-containing sensory neurones to induce pain and a number of neuropeptide-induced reflexes. Mechanisms for kinin synthesis are also present in the CNS where kinins are likely to initiate a similar cascade of events, including an increase in blood flow and plasma leakage. Kinins are potent stimulators of neural and neuroglial tissues to induce the synthesis and release of other pro-inflammatory mediators such as prostanoids and cytotoxins (cytokines, free radicals, nitric oxide). These events lead to neural tissue damage as well as long lasting disturbances in blood-brain barrier function. Animal models for CNS trauma and ischaemia show that increases in kinin activity can be reversed either by kinin receptor antagonists or by the inhibition of kinin production. A number of other central actions have been attributed to kinins including an effect on pain signalling, both within the brain (which may be related to vascular headache) and within the spinal dorsal horn where primary afferent nociceptors can be stimulated. Kinins also appear to play a role in cardiovascular regulation especially during chronic spontaneous hypertension. Presently, however, direct evidence is lacking for the release of kinins in pathophysiological conditions of the CNS and it is not known whether spinal or central neurones, other than afferent nerve terminals, are sensitive to kinins. A more detailed examination of the effects of kinins and their central pharmacology is necessary. It is also important to determine whether the inhibition of kinin activity will alleviate CNS inflammation and whether kinin receptor antagonists are useful in pathological conditions of the CNS.
This study aimed to test the Differential Experience Hypothesis which suggests mothers and fathers interact differently with their child. The forms and functions of parents' language in interaction with their 2-2.5-year-old child were investigated across four different interactional settings within the home and for each parent separately. The results, supporting the differential experience hypothesis, suggest that differences do exist between mothers' and fathers' conversational styles. However, the findings indicate that gender is not the only influencing factor. The situations in which interaction occurs also appear to have an effect on the style of interaction irrespective of the sex of the parent (context hypothesis).
This paper addresses a research project currently in progress. It is a postmodern ethnographic and (auto)biographical undertaking that simultaneously redraws the methodological and theoretical boundaries of conventional ethnographic work while it engages a 'praxis' oriented approach to working collaboratively and creatively with nurses from both clinical practice and academia. Only the broadest parameters of this 'project of possibility' are outlined--to do otherwise would be antithetical to its participatory, processual and provisional character. It is an unprecedented venture between those who think and write about the culture of clinical nursing and those who actually live it on a daily basis.
Nurses have long anguished over how best to assess performance in clinical practice. The 'competency' movement appears to have provided a solution to this problem. In this paper I undertake a 'radical hermeneutic' interrogation of the cultural text of clinical practice doubled with a poststructuralist interpretation of the literal text of the Australian competency project. Through this work I attempt to expose some of the deeply embedded assumptions that underwrite the competency movement and amplify the problems posed by an uncritical appropriation of competency based training and assessment in nursing education.
'Telling' our lives as they happen to us is an extremely pervasive activity in our social world. Through the stories which suture together the multiple ways we can make sense of a life as a nurse, is woven the fabric of a culture. Clinical nursing culture is, as yet, poorly understood and little theorised. By appropriating narrative as a research technology I suggest that we might be better placed to first articulate, and then critique, the complexity and diversity of clinical practice through a postmodern poetics and politics of orality.
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To determine if dog galanin is a potent inhibitor of dog insulin secretion we determined its primary structure from its cloned cDNA, evaluated its expression in celiac ganglia and determined its effect on islet hormone secretion. The predicted amino acid sequence differs from the other known species of galanin by three to six amino acids in the C-terminal half of the molecule. In situ hybridization revealed the presence of dog progalanin mRNA in every neuronal cell body in the dog celiac ganglion. The predicted dog galanin peptide was synthesized and infused i.v. at 0.25, 2.5, 25 or 250 pmol/kg/min. It potently inhibited insulin secretion, less potently inhibited pancreatic somatostatin release and stimulated glucagon secretion, similar to the effects of porcine galanin in the dog. In summary, dog galanin is expressed in the neuronal cell bodies that innervate the pancreas and the sequence of the dog galanin preserves the potent insulin inhibitory part of the galanin molecule. These data support the hypothesis that galanin is a sympathetic neurotransmitter in dog pancreas.
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