Publications by authors named "Worton K"

Background: Enhancing the quality of therapeutic engagement between nurse and service user is related to positive impact on care, safety, and recovery outcomes. Achieving improved therapeutic engagement remains challenging in the acute mental health inpatient setting, characterised by complex social processes and contextual features that constrain behaviour change. The Therapeutic Engagement Questionnaire is an evidence-based tool co-produced with service users and nurses to improve therapeutic engagement.

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A strong association exists between the quality of nurse-service user therapeutic relationship and care outcomes on acute mental health inpatient wards. Despite evidence that service users desire improved therapeutic engagement, and registered mental health nurses recognize the benefits of therapeutic relationships, such interactions remain sub-optimal. There is a dearth of evidence on factors influencing implementation of interventions to support and encourage therapeutic engagement.

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Successful chemotherapeutic treatment of drug-responsive cancers can be compromised by the acquisition of drug resistance. Standard remission induction therapy for childhood acute lymphoblastic leukemia includes L-asparaginase, since the leukemic cells lack asparagine synthetase (AS) activity and require exogenous asparagine. We have used the Chinese hamster ovary cell line N3, which lacks AS activity, as a model to examine a novel mechanism involved in the development of drug resistance in acute lymphoblastic leukemia.

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Using a histochemical peroxidase technique, under conditions that preferentially stain erythrocytes, we have shown changes in the microcirculation of villi of neonatal mice infected with murine rotavirus. Between 18 and 48 h postinfection (PI), throughout all areas of the small intestine there occurred, sequentially, a marked ischemia and atrophy of villi. By 72 h PI, villi had recovered their normal height and showed incipient hyperemic microcirculation.

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The anatomy of the microcirculation of intestinal villi from the upper, middle, and lower small intestine of neonatal mice from 8 to 14 days old was studied using a histochemical peroxidase technique that specifically stained erythrocytes. Over 8-14 days, there was little chronological variation between the same regions of gut; the exception was the lower intestine, which, in younger mice, was noticeably less well perfused with erythrocytes. Vascular beds in the middle and lower intestine comprised a hairpin loop with cross-connections.

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Nitrogen mustard (N2M) treatment of rabbits induced neutropenia, and, in ligated ileal loops, it inhibited fluid secretion induced by salmonella or by cholera toxin (CT). Pretreatment of rabbits with indomethacin almost abolished salmonella-induced fluid secretion and significantly reduced that induced by CT. Similar effects of N2M and indomethacin on fluid secretion induced by salmonella, but not by CT, have been reported by other workers and used to implicate prostaglandins, from the salmonella-induced inflammation, as mediators of fluid secretion.

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Leucocyte influx into rabbit ileal loops, induced by strains of Salmonella typhimurium of different virulence, was assessed with 111Indium-labelled leucocytes. Strains fell into two groups on the basis of their leucotactic potential: "virulent" strains (which induced fluid secretion) caused a dose-dependent leucocyte influx; strains which did not induce fluid secretion failed to induce a significant leucocyte influx. Fluid secretion was never observed in the absence of leucocyte influx, but leucocyte influx per se did not induce fluid secretion.

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The abilities of six strains of Salmonella typhimurium to associate with rabbit ileal mucosa have been measured in vitro. Two were "virulent" strains (TML and W118 which are invasive and inducers of fluid secretion in rabbit ileal loops); four were "avirulent" (LT7, M206 and SL1027 which are invasive but induce negligible fluid secretion, and Thax-1 which is neither invasive nor an inducer of fluid secretion). A special organ-culture apparatus was designed to expose only the luminal surface of the mucosa to organisms.

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To investigate further the pathophysiology of rotavirus-induced diarrhea, changes in specific activities of eight relevant intestinal enzymes [alkaline phosphatase, thymidine kinase, lactase, maltase, sucrase, Na+,K+-adenosine triphosphatase (ATPase), adenylate and guanylate cyclases] were measured following infection of suckling mice with murine rotavirus (epizootic diarrhea of infant mouse strain) and compared with age-matched control mice. The concentration of lactose within the lumen of the gastrointestinal tract during infection was also measured. During the course of infection, activities of alkaline phosphatase and lactase decreased, whilst the activity of thymidine kinase increased.

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Seven-day-old mice were infected orally with murine rotavirus (EDIM) and regions of the gut examined at 24 h intervals up to 7 days by electron microscopy. Structural changes were correlated with data on viral antigen production, thymidine kinase activity, and clinical signs of diarrhea. No pathological changes were detected in the colon.

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Six strains of Salmonella typhimurium (W118, TML, SL1027, LT7, M206 and Thax 1) of different virulence were examined for the presence of antigens which react with antibodies to cholera toxin (anti-CT). A fluorescent-antibody-labelling technique employing anti-CT was used to analyse antigen expression. A rapid increase in the proportion of cells producing a CT-related antigen was demonstrated in cells in early log phase (1-4 h growth) followed by a rapid decline during mid-late log phase in each of the six strains.

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Targeting of cytotoxic T cells to cell-bound antigens has previously been reported using bispecific antibodies. In this report we document a novel targeting system whereby cytotoxic T helper (Thc) cells were targeted to a B cell lymphoma by means of an anti-idiotypic antibody (anti-Id), specific for the surface immunoglobulin of the B cell, coupled to the carrier protein keyhole limpet hemocyanin (KLH). In this system the anti-Id-KLH complex bound to the Id determinant of the surface immunoglobulin of the B cell lymphoma.

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