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F Roberts

Publications and source records attributed to F Roberts.

At least 19 recordsLinked to original sources
PubMed1998

Evidence for the shikimate pathway in apicomplexan parasites.

Parasites of the phylum Apicomplexa cause substantial morbidity, mortality and economic losses, and new medicines to treat them are needed urgently. The shikimate pathway is an attractive target for herbicides and antimicrobial agents because it is essential in algae, higher plants, bacteria and fungi, but absent from mammals. Here we present biochemical, genetic and chemotherapeutic evidence for the presence of enzymes of the shikimate pathway in apicomplexan parasites. In vitro growth of Toxoplasma gondii, Plasmodium falciparum (malaria) and Cryptosporidium parvum was inhibited by the herbicide glyphosate, a well-characterized inhibitor of the shikimate pathway enzyme 5-enolpyruvyl shikimate 3-phosphate synthase. This effect on T. gondii and P. falciparum was reversed by treatment with p-aminobenzoate, which suggests that the shikimate pathway supplies folate precursors for their growth. Glyphosate in combination with pyrimethamine limited T. gondii infection in mice. Four shikimate pathway enzymes were detected in extracts of T. gondii and glyphosate inhibited 5-enolpyruvyl shikimate 3-phosphate synthase activity. Genes encoding chorismate synthase, the final shikimate pathway enzyme, were cloned from T. gondii and P. falciparum. This discovery of a functional shikimate pathway in apicomplexan parasites provides several targets for the development of new antiparasite agents.

3-Phosphoshikimate 1-Carboxyvinyltransferase↗
PubMed1998

Covered lives and seamless systems: nursing workforce development and integration in Arizona's managed-care environment.

Responding to demands that nursing leaders conduct business in creative proactive ways, the authors of this department share the work of The Robert Wood Johnson Foundation's national program, Colleagues in Caring: Regional Collaboratives for Nursing Work Force Development. The purpose of this initiative is to enhance regional and state collaborative planning and implement actions and policies to address the rapid changes occurring in the United States nursing labor market. This department, edited by Mary Fry Rapson, PhD, RN, CS, National Program Director and Rebecca B. Rice, EdD, RN, National Deputy Director, presents the ongoing work of the program, highlighting the work of the 20 individual collaboratives. Regional approaches to the expected program outcomes and specific challenges and opportunities that are unique to each region's environment are included.

Arizona↗
PubMed1995

From a regulatory lens: a perspective on the delegation of nursing activities to unlicensed assistive personnel.

Along with the reforming of health care, nursing services and related regulatory approaches are concurrently adapting. As the health care environment changes, the number and preparation of individuals who perform health-related activities has increased dramatically. Heightened interest is expressed at both ends of the nursing care delivery spectrum, unlicensed and advanced nursing practice. Boards of nursing, the States' regulatory arm over the profession, pay particular attention to public health and safety issues attached to the delegation of nursing tasks to unlicensed assistive personnel (UAPs). Equally important to the appropriate use of delegation is the provision of adequate supervision of those who are serving in the role of "delegatee." Mechanisms exist in a number of states whereby professional nurses can ascertain the level of competence of a UAP and feel assured that safe and appropriate care can be delegated. It is the role of the professional nurse to provide the required supervision, once a nursing activity is delegated. Nurse practice acts should not be used as barriers to escape required and prudent alterations to the traditional delivery of nursing care. Conversely, these same acts should not be manipulatively circumvented solely in the name of cost containment and as a needed response to "health care reform." As health care reforms, humanity would be best served with public or patient safety and protection as a guiding principle.

Facility Regulation and Control↗
PubMed1994

Evaluation of Mesalt dressings and continuous wet saline dressings in ulcerating metastatic skin lesions.

The care of chronic ulcerating metastatic skin lesions is not well established or supported by research. Because these cancerous lesions may be present for many years, patients and their caregivers are confronted with ongoing dressing care to control and prevent odor, bleeding, drainage, and infection. Eleven patients in this study compared Mesalt dressings (Sancella Incorporated, Oakville, Ontario, Canada) with continuous wet saline dressings using a crossover design. Results indicated that Mesalt dressings received significantly higher ratings when compared with continuous wet saline dressings for ease of application and odor control and were significantly preferred by patients. No significant differences were found for ease of removal and comfort of the dressing. Neither were there any significant differences in the occurrence of clinical infection, number of dressing changes, and time spent for the care of the lesion. Mesalt dressings were more expensive than continuous wet saline dressings, but benefits may outweight the costs.

Aged↗
PubMed1985

Histamine-induced excitation of spontaneously active medullary neurones in the rat brain is mediated by H2-receptors. A microiontophoretic study using H1- and H2-agonists and antagonists.

The effects of histamine, applied by microiontophoresis onto spontaneously-active medullary neurones were investigated in the rat. Histamine caused current-dependent excitation of these neurones, an action that is at variance with previous studies in the cat. The nature of the receptor mediating these effects was examined using a number of agonists with differing potencies at peripheral H1- and H2-receptors. The precursor of histamine, L-histidine and the metabolite, N-telemethylhistamine did not mimic the effects of histamine while the H2-agonist, 4-methylhistamine caused similar but weaker excitation. The extent of excitations produced by the H1-agonists, 2-pyridylethylamine, 2-methylhistamine and 2-thiazolylethylamine could be related to their activity at H2-receptors. Metiamide was ineffective in antagonising responses to histamine and related agonists as was mepyramine. The H2-antagonist ranitidine, however, proved a good antagonist of responses to histamine and the H1- and H2-agonists, despite an unrelated excitatory action which may be linked to inhibition of cholinesterase. It is concluded that the excitatory effects of microiontophoretically-applied histamine and the agonists on medullary neurones in the rat is probably a result of activation of H2-receptors.

Animals↗
PubMed1983

Histamine and the hypothalamus.

The chemical tools that could be used to examine the function of histamine in the brain are considered together with the evidence linking histamine specifically with the hypothalamus. The distribution of histamine and the enzymes responsible for its synthesis and metabolism is consistent with there being both mast cells and histaminergic nerve terminals within the hypothalamus. Iontophoresis, mepyramine binding and histamine-stimulated adenylate cyclase studies suggest that both histamine H1- and H2- receptors are present in the hypothalamus. In addition, intracerebroventricularly injected histamine receptor agonists and antagonists affect many functions associated with the hypothalamus such as cardiovascular control, food intake, body temperature control, and pituitary hormones whose release is mediated via the hypothalamus, such as corticotropin, growth hormone, thyroid stimulating hormone, prolactin, gonadotropins and vasopressin. However, only in the case of thyroliberin release, prolactin release, body fluid control and blood pressure control is there evidence yet that such effects are mediated via histamine receptors actually in the hypothalamus. The effects of enzyme inhibitors suggest endogenous histamine may be involved in the physiological control of thyroid stimulating hormone, growth hormone and blood pressure, and the effects of receptor antagonists support a role for endogenous histamine in prolactin control. Otherwise, there is little evidence for a physiological role for endogenous, as against exogenous, histamine whether it be from histaminergic terminals or mast cells. In addition, few studies have tried to distinguish possible effects on presynaptic receptors, postsynaptic receptors, hypothalamic blood vessels or the hypophyseal portal blood vessels. It is concluded that although there is good evidence now linking histamine and the hypothalamus more specific studies are required, for instance using microinjection or in vitro techniques and the more specific chemical tools now available, to enable a clearer understanding of the physiological role of histamine in the hypothalamus.

Adrenocorticotropic Hormone↗
PubMed1980

A comparison of the in vivo uptake of [3H]GABA into rat celebral cortex and dorsal medulla following topical application.

The penetration of [3H]GABA and [14C]sucrose from the dorsal surface of the rat medulla and cerebral cortex was studied in vivo. The levels of both declined exponentially from the surface of both regions and were decreased by raised potassium levels and the presence of GABA uptake inhibitors. Inhibition of GABA metabolism increased the amounts of 3H recovered particularly after long incubation periods. More [3H]GABA and [14C]sucrose was tken up into the cerebral cortex than the medulla, and more [3H]GABA than [14C]sucrose was taken up in both regions.

Animals↗
PubMed1979

The effect of depolarizing potassium concentrations on the efflux of GABA from rat dorsal medulla in vivo and from slices and synaptosomes.

The efflux of [3H]GABA from the dorsal surface of adult rat medulla overlying the dorsal column nuclei (DCN) was found not be influenced by increasing the concentration of potassium in the superfusing solution to 40 mequiv. Similarly, raised potassium was found not to influence the efflux from slices of the dorsal region of the caudal medulla containing the dorsal column nuclei. This lack of effect of raised potassium is not thought to be due to lack of GABAergic terminals in this region because there is good pharmacological evidence for their presence and bacause both electrical stimulation and 100 microM veratridine increased the efflux of [3H]GABA from such slices. Also, 40 mequiv potassium was found to increase the efflux of both endogenous and [3H]GABA from crude synaptosome preparations of this region without influencing the efflux of [14C]sucrose or [3H]leucine. This release of [3H]GABA was calcium-dependent, and was similar whether produced by 20, 40 of 60 mequiv potassium and occurred whether eos or AOAA was used to inhibit GABA metabolism. Release from synaptosomes could also be induced with 100 microM veratridine. Raised potassium was additionally found to prevent the increased efflux from slices produced by electrical stimulation and to increase the efflux from slices prepared from the brains of rats 14 days old. It is suggested that the astrocytic swelling produced by raised potassium concentration restricts the diffusion of GABA away from depolarized terminals.

Aminooxyacetic Acid↗
PubMed1978

The anticonvulsant action of L-2,4-diaminobutyric acid.

The GABA uptake inhibitor, L-2,4-diaminobutyric acid (L-DABA) was examined for potential anticonvulsant activity in mice. Given intracerebroventricularly (i.c.v., 2 mumoles) L-DABA almost doubled the CD50 of picrotoxin and 3-mercaptopropionate (3-MP), a glutamate decarboxylase inhibitor--the convulsants being administered 15 min after the L-DABA. The anticonvulsant effect was not observed after 40 min. L-DABA given i.p (5 mmoles/kg) was also anticonvulsant against 3-MP but given i.p. or i.c.v. had no anticonvulsant action against strychnine. The D-isomer of DABA, less active as an inhibitor of GABA uptake, had no anticonvulsant activity against 3-MP and nor did three other inhibitors of GABA uptake, namely nipecotic acid, cis-1,3-aminocyclohexane carboxylic acid (ACHA) and beta-alanine. Possible mechanisms of the anticonvulsant action of L-DABA are discussed.

3-Mercaptopropionic Acid↗