The educational preparation of nurses in a developing economy and patient mortality.

BACKGROUND: Most studies have reported that higher levels (baccalaureate degree) of educational attainment by nurses are associated with lower levels of patient mortality. Researchers working in developed economies (e.g. North America and Europe) have almost exclusively conducted these studies. The value of baccalaureate nurse education has not been tested in countries with a developing economy. METHOD: A retrospective observational study conducted in seven hospitals. Patient mortality was the main outcome of interest. Anonymized data were extracted from nurses and patients from two different administrative sources and linked using the staff identification number that exists in both systems. We used bivariate logistic regression models to test the association between mortality and the educational attainment of the admitting nurse (responsible for assessment and care planning). RESULTS: Data were extracted for 11 918 (12, 830 admissions) patients and 7415 nurses over the first 6 months of 2015. The majority of nurses were educated in South Asia and just over half were educated to at least bachelor degree level. After adjusting for confounding and clustering, nurse education was not found to be associated with mortality. IMPLICATIONS FOR NURSING AND HEALTH POLICY: Our observations may suggest that in a developing economy, the academic level of nurses' education is not associated with a reduction in patient mortality. Findings should be interpreted with considerable caution but do challenge widely held assumptions about the value of baccalaureate-prepared nurses. Further research focused on nursing education in developing economies is required to inform health policy and planning.

Implementing a nursing systems framework in a developing country.

AIM: To test the effect on patient mortality of implementing a nursing systems framework across a national health system. BACKGROUND: There have been five previous observational studies that have tested the effect of a nursing systems framework on clinical outcomes for patients. Implementation of a nursing systems framework in the health system of a developing country has not been evaluated. DESIGN: Quasi-experimental (before and after) study. METHOD: A nursing systems framework consisting of six themes: (i) Professionalisation; (ii) Education; (iii) Structure; (iv) Quality of nursing care; (v) An academic health system; and (vi) Communication (Professional), was implemented across the national health system of Qatar in March 2015. Routine administrative data were extracted (March 2014-February 2016) for elective admissions. Our primary and secondary outcomes were, respectively, all cause mortality at discharge and readmission to hospital (within 28 days of discharge). We split the data into two time periods: before (March 2014-February 2015) and after (March 2015-February 2016) the implementation of the nursing systems framework. Multivariable regression modelling was used to examine the effect of the framework on patient mortality, after adjusting for key confounding variables (patient age, episode acuity, intensive care admission and length of stay). FINDINGS: Data were extracted for 318 548 patients (year 1 = 130 829; year 2 = 187 725). After adjusting for confounding, there was a significant association between the implementation of the nursing systems framework, mortality and readmission. CONCLUSION AND IMPLICATIONS FOR NURSING POLICY AND PRACTICE: Our observations suggest that the implementation of a nursing systems framework may be important in improving outcomes for patients in emerging health systems.

Determining the efficacy of dietary phytochemicals in cancer prevention.

Accumulating data suggest that dietary phytochemicals have the potential to moderate deregulated signalling or reinstate checkpoint pathways and apoptosis in damaged cells, while having minimal impact on healthy cells. These are ideal characteristics for chemopreventive and combination anticancer strategies, warranting substantial research effort into harnessing the biological activities of these agents in disease prevention and treatment. However, this requires further investigation into their mode of action and novel approaches to the development of reliable biomarkers.

Oscillations in NF-kappaB signaling control the dynamics of gene expression.

Signaling by the transcription factor nuclear factor kappa B (NF-kappaB) involves its release from inhibitor kappa B (IkappaB) in the cytosol, followed by translocation into the nucleus. NF-kappaB regulation of IkappaBalpha transcription represents a delayed negative feedback loop that drives oscillations in NF-kappaB translocation. Single-cell time-lapse imaging and computational modeling of NF-kappaB (RelA) localization showed asynchronous oscillations following cell stimulation that decreased in frequency with increased IkappaBalpha transcription. Transcription of target genes depended on oscillation persistence, involving cycles of RelA phosphorylation and dephosphorylation. The functional consequences of NF-kappaB signaling may thus depend on number, period, and amplitude of oscillations.

Strong linear- k valence-band mixing at semiconductor heterojunctions.

This paper examines linear- k terms in the gamma(8) valence-band Hamiltonian for heterostructures of zinc-blende-type semiconductors. In bulk crystals such terms are known to be extremely small, due to their origin as relativistic perturbations from d and f orbitals. However, in heterostructures there is a nonvanishing contribution from p orbitals. This contribution is an order of magnitude larger than the corresponding bulk term, and it should give rise to an optical anisotropy comparable to (although smaller than) that seen in recent experiments on the quantum-well Pockels effect.

A paradox of cerebral hyperperfusion in the face of cerebral hypotension: the effect of perfusion pressure on cerebral blood flow and metabolism during normothermic cardiopulmonary bypass.

BACKGROUND: The purpose of this study was to determine the impact of perfusion pressure on cerebral blood flow (CBF) and metabolism during normothermic cardiopulmonary bypass (CPB) and after weaning. MATERIALS AND METHODS: Two groups of mongrel dogs were studied (Group A, CPB perfusion at 50 mm Hg, n = 6; and Group B, CPB perfusion at 100 mm Hg, n = 6). All animals underwent 2 h of normothermic bypass at cardiac indexes >2.1 L/min/m2 and were weaned from pump, maintained at pressures >75 mm Hg, and followed for an additional 2 h. RESULTS: In both groups CBF increased over 85% from baseline, in proportion to the hemodilution during the initiation of CPB. Intracranial pressure increased moderately in both groups during CPB, compromising CBF at 1 h in Group A, but not in Group B. The Group A cerebral metabolic rate for oxygen (CMRO2), however, remained unchanged as the percentage of oxygen extraction increased to compensate for the decreased CBF. During recovery, temperature, mean arterial pressure, and cerebral perfusion pressure were not significantly different between the two groups. However, the CBF, percentage of oxygen extracted, and CMRO2 were significantly lower in Group A. CONCLUSIONS: Normothermic CPB initiated with a crystalloid prime and performed at the lower end of a 50-70 mm Hg perfusion window resulted in a highly significant increase in CBF in order to compensate for hemodilution, while at the same time reduced the perfusion pressure available to supply the increased CBF. Together, these two events create a hemodynamic paradox of hyperperfusion in the face of hypotension. The reduction in CMRO2 in Group A is yet to be explained but seems to remain coupled to CBF and could represent a previously undescribed protective mechanism of hibernating cerebral tissue, similar to the phenomena of ischemic preconditioning in the heart, where cerebral tissue is stimulated to lower metabolism in response to inadequate CBF.

Septo-optic dysplasia associated with polyendocrine dysfunction.

Septo-optic dysplasia (SOD) is a rare congenital disease that has been described in association with hypothalamic dysfunction. A case of polyendocrine dysfunction is described in a 22 year-old white female with septo-optic dysplasia. Findings included atrophic optic nerves, a cavum septum pellucidum and a small pituitary gland detected by magnetic resonance imaging. The patient had central diabetes insipidus, Hashimoto's thyroiditis, and gestational diabetes mellitus. A review of the literature is presented. A careful and detailed endocrine evaluation is needed in patients with SOD.

Response of canine coronary collateral vessels to ergonovine and alpha-adrenergic stimulation.

The ability of moderately well-developed coronary collateral vessels to undergo vasoconstriction in response to alpha-adrenergic stimulation and to ergonovine was studied. Studies were performed in 15 dogs 4-16 wk after embolic occlusion of the left anterior descending coronary artery had been performed to stimulate collateral vessel growth. Interarterial collateral flow was measured as retrograde flow from the cannulated left anterior descending coronary artery, while microvascular collateral flow was measured as continuing tissue flow determined with radioactive microspheres administered during the retrograde flow collection. Studies were performed after beta-adrenergic blockade with propranolol. Neither cardiac sympathetic nerve stimulation nor alpha 1-adrenergic stimulation with phenylephrine caused significant change in retrograde blood flow or myocardial tissue flow. The selective alpha 2-adrenergic agonist, B-HT 933, decreased tissue flow in the collateral-dependent region but did not significantly alter retrograde flow. Although these data indicate that intramural microvascular collateral communications are capable of vasoconstriction in response to alpha 2-adrenergic stimulation, the larger interarterial collaterals are unresponsive to alpha-adrenergic influences. However, under the conditions of the experiment, adrenergic activity did not appear to influence collateral function, since neither alpha 1-adrenergic blockade with prazosin nor alpha 2-adrenergic blockade with rauwolscine altered collateral flow. Ergonovine, 0.2-0.8 microgram.kg-1.min-1, caused a 22 +/- 4% decrease in retrograde flow (P less than 0.01) but did not alter microvascular collateral flow. Thus, of the agents tested, only ergonovine caused vasoconstriction of the large interarterial coronary collateral vessels.

Vasoconstriction of canine coronary collateral vessels with vasopressin limits blood flow to collateral-dependent myocardium during exercise.

This study was performed to test the hypothesis that active constriction of coronary collateral vessels can worsen hypoperfusion of collateral-dependent myocardium during exercise. Studies were performed in seven adult mongrel dogs in which intermittent followed by permanent occlusion of the left circumflex coronary artery produced an area of collateral-dependent myocardium without gross evidence of infarct. Myocardial blood flow was determined with microspheres while measurement of aortic and distal coronary pressures allowed calculation of collateral and small vessel resistance at rest and during treadmill exercise. The ability of collateral vessel constriction to limit blood flow was assessed by infusion of vasopressin during exercise. During control conditions, blood flow in the collateral zone underwent a subnormal increase during exercise in comparison with the normal zone (1.74 +/- 0.27 versus 2.50 +/- 0.40 ml/min/g, respectively, p less than 0.05). Infusion of vasopressin in a dose that caused no change in normal zone flow (0.01 microgram/kg/min i.v.) produced a 30 +/- 5% further decrease in flow to the collateral zone (p less than 0.01). This decrease in collateral zone flow resulted from a 48 +/- 14% increase in transcollateral resistance in response to vasopressin infusion (p less than 0.01), as well as a 40 +/- 9% increase in small vessel resistance in the collateral zone (p less than 0.01). These data demonstrate that active constriction of both collateral vessels and coronary resistance vessels can contribute to hypoperfusion of collateral-dependent myocardium during exercise.

Pathogenesis of retinal dystrophy in the Royal College of Surgeons rat.

The Royal College of Surgeons (RCS) rat is an animal with genetically transmitted progressive retinal dystrophy. We compared histopathologically the RCS rat retina with normal age-matched control retinas (Long-Evans rats) using light and scanning electron microscopy. Retinal degeneration begins with alteration of the rod outer segments. There is a progressive involvement of the entire retina, with all layers affected by 45 days. The three-dimensional view obtained with scanning electron microscopy provides another perspective on the pathogenetic changes of the RCS retina.

Effect of atrial natriuretic peptide on coronary collateral blood flow.

This study was carried out to examine the effects of atrial natriuretic peptide on coronary collateral blood flow. Studies were performed in nine adult mongrel dogs 3.4 months after embolic occlusion of the left anterior descending coronary artery had been performed to stimulate collateral vessel growth. At the time of study the anterior descending coronary artery was cannulated to allow estimation of interarterial collateral flow from measurements of retrograde blood flow. Injection of radioactive microspheres during retrograde flow collection allowed simultaneous determination of continuing tissue flow for evaluation of microvascular collateral communications. Atrial natriuretic peptide in doses of 20 and 200 micrograms administered into the left atrium resulted in 17 +/- 3.0% and 34 +/- 4.5% increases in retrograde flow, respectively (each p less than 0.01). Tissue flow in the collateral dependent myocardial region did not change in response to atrial natriuretic peptide. After the larger dose of atrial natriuretic peptide, the administration of nitroglycerin (10 micrograms/kg into the left atrium) caused no further increase of retrograde blood flow, and no further decrease of collateral vascular resistance. These data indicate that atrial natriuretic peptide causes vasodilation of moderately well-developed interarterial coronary collateral vessels.

Antibody response of mice to lactate dehydrogenase-elevating virus during infection and immunization with inactivated virus.

BALB/c and Swiss mice were infected with lactate dehydrogenase-elevating virus (LDV) or immunized with glutaraldehyde-inactivated or ether-extracted virus and their plasma was monitored for anti-LDV IgG and IgM levels by ELISA and indirect fluorescent antibody staining, for neutralizing antibodies, for sensitized antibody-virus complexes, for immune complexes, and for total plasma IgG and IgM. In infected mice, anti-LDV IgM was transiently formed during the first 2 weeks post infection (p.i.) but only at a low level. Anti-LDV IgG was produced in a biphasic manner with an initial peak at about 10 days p.i. and a secondary rise reaching a maximum level 30-80 days p.i. which was retained throughout the persistent phase of infection. The concomitant appearance of comparable levels of low molecular weight immune complexes suggests that most anti-LDV IgG was complexed with LDV proteins. Also, as early as 10 days p.i., infectious antibody-LDV complexes developed, which were neutralizable by rabbit anti-mouse IgG, whereas antibodies that neutralize the infectivity of exogenously added LDV appeared only 1-2 months p.i. Throughout infection, most of the anti-LDV IgG was directed to VP-3, the envelope glycoprotein of LDV, which was found to exist in at least 10 distinct forms ranging in molecular weight from 24 to 42 kDa. Anti-LDV IgG levels as high as those observed in infected mice developed in mice immunized with inactivated LDV. Antibodies to glutaraldehyde-inactivated LDV were also mainly directed to VP-3, but exhibited no neutralizing activity. The polyclonal B cell activation associated with a persistent LDV infection and the formation of immune complexes were not observed in mice immunized with inactivated virus.