Miracle-dz/UniFAR-FTUs huggingface dataset:
Focus groups as a tool for critical social research in nurse education.

Focus groups are now widely adopted in qualitative health and social research, and have been increasingly used as a data-collection technique in nursing research. The focus group is not a new method, but its uses and procedures have been considerably revised in recent years. The aim of this paper is to present an overview of the focus group as a research tool in social science literature, followed by a more considered discussion on the use of focus groups in contemporary critical social science. It draws on this work to illustrate the potential of focus groups to address some of the political issues in social research, in particular the balance of power between researcher and researched, and the empowerment of under-represented groups. Advantages of the method in connecting the researcher with group perspectives and experiences that may be unexplored by other methods of data collection are discussed, and the 'collective conscience' is put forward as an appropriate resource in data analysis. It argues that the application of focus-group techniques can build on experiences and principles of working with or participating in groups. Focus groups are particularly applicable to research in nurse education, for involving diverse stakeholders in curriculum evaluation and development, and in ongoing appraisals of the student's perceptions of their experience, for which universities have tended to rely on survey approaches and structured questionnaires. The article ends by drawing some conclusions from the health and social research literature to inform nursing education research using focus groups.
Structure-Function Investigation of the Interaction of 1- and 2-Substituted 3-Hydroxypyridin-4-ones with 5-Lipoxygenase and Ribonucleotide Reductase*

The structural and physiochemical properties of 3-hydroxypyridin-4-one chelators (HPOs) which influence inhibition of the iron-containing metalloenzymes ribonucleotide reductase (RR) and 5-lipoxygenase (5-LO) have been investigated. HPOs with substituents at the 1- and 2-positions of the pyridinone ring have been synthesized, and their inhibitory properties compared with those of desferrioxamine (DFO). Varying the alkyl substituents does not affect the affinity constant of these ligands for iron(III), but permits a systematic investigation of the effect of hydrophobicity and molecular shape on inhibitory properties. The inhibition of RR was monitored, indirectly by measuring tritiated thymidine incorporation into DNA and directly by the quantification of the EPR signal of the enzyme tyrosyl radical. 5-LO inhibition was examined spectrophotometrically, measuring the rate of linoleic hydroperoxide formation by soybean lipoxygenase. The results indicate that the substituent size introduced at the 2-position of the HPO ring is critical for determining inhibition of both enzymes. Large substituents on the 2-position, introduce a steric factor which interferes with accessibility to the iron centers. These studies have identified chelators such as 1,6-dimethyl-2-(N-4′,N-propylsuccinamido)methyl-3-hydroxypyridin-4-one (CP358), which causes only a 10% inhibition of 5-LO after 24 h of incubation at 110 μm IBE (iron-binding equivalents) in comparison to simple dialkyl HPOs such as Deferiprone (CP20) which cause up to 70% inhibition. Using EPR spectroscopy, CP358 inhibits RR at a slower rate than CP20, while chelating intracellular iron(III) at a similar rate, a finding consistent with an indirect inhibition of the tyrosyl radical. However, hepatocellular iron is mobilized at a faster rate by CP358 (P < 0.001). These findings demonstrate that it is possible to design bidentate HPOs which access intracellular iron pools rapidly while inhibiting non-heme iron-containing enzymes relatively slowly, at rates comparable to DFO. It is anticipated that such compounds will possess a superior therapeutic safety margin to currently available bidentate HPOs.
Biochemical Characterization and Physiological Properties of Escherichia coli UDP-N-Acetylmuramate:l-Alanyl-γ-d-Glutamyl-meso- Diaminopimelate Ligase

ABSTRACT The UDP-N-acetylmuramate:l-alanyl-γ-d-glutamyl-meso-diaminopimelate ligase (murein peptide ligase [Mpl]) is known to be a recycling enzyme allowing reincorporation into peptidoglycan (murein) of the tripeptide l-alanyl-γ-d-glutamyl-meso-diaminopimelate released during the maturation and constant remodeling of this bacterial cell wall polymer that occur during cell growth and division. Mpl adds this peptide to UDP-N-acetylmuramic acid, thereby providing an economical additional source of UDP-MurNAc-tripeptide available for de novo peptidoglycan biosynthesis. The Mpl enzyme from Escherichia coli was purified to homogeneity as a His-tagged form, and its kinetic properties and parameters were determined. Mpl was found to accept tri-, tetra-, and pentapeptides as substrates in vitro with similar efficiencies, but it accepted the dipeptide l-Ala-d-Glu and l-Ala very poorly. Replacement of meso-diaminopimelic acid by l-Lys resulted in a significant decrease in the catalytic efficacy. The effects of disruption of the E. coli mpl gene and/or the ldcA gene encoding the ld-carboxypeptidase on peptidoglycan metabolism were investigated. The differences in the pools of UDP-MurNAc peptides and of free peptides between the wild-type and mutant strains demonstrated that the recycling activity of Mpl is not restricted to the tripeptide and that tetra- and pentapeptides are also directly reused by this process in vivo. The relatively broad substrate specificity of the Mpl ligase indicates that it is an interesting potential target for antibacterial compounds.
Human Septal Chondrocyte Redifferentiation in Alginate, Polyglycolic Acid Scaffold, and Monolayer Culture

Objectives/Hypothesis Tissue engineering laboratories are attempting to create neocartilage that could serve as an implant material for structural support during reconstructive surgery. One approach to forming such tissue is to proliferate chondrocytes in monolayer culture and then seed the expanded cell population onto biodegradable scaffolds. However, chondrocytes are known to dedifferentiate after this type of monolayer growth and, as a result, decrease their production of cartilaginous extracellular matrix components such as sulfated glycosaminoglycans. The resultant tissue lacks the biomechanical properties characteristic of cartilage. The objective of the study was to determine whether different culture systems could induce monolayer‐expanded human septal chondrocytes to redifferentiate and form extracellular matrix.
The respiratory development of Atlantic salmon. I. Morphometry of gills, yolk sac and body surface

During development from larva to juvenile in Atlantic salmon, Salmo salar, there is a change in the anatomical potential for gas exchange among gills, body skin and yolk sac as the larvae resorb yolk, grow and develop gills. Newly hatched Atlantic salmon have poorly developed gills but do have a high skin area to mass ratio and a large well-vascularized yolk sac. Cutaneous surfaces accounted for over 95 % of the total area available for respiration in newly hatched Atlantic salmon (body mass 0.032­0.060 g). The branchial contribution to total area increased rapidly, however, so that by the end of yolk absorption (body mass 0.19­0.23 g) it constituted 22 % of the total area and overtook cutaneous surface area between 5 and 6 g wet body mass. Harmonic mean diffusion distance across the skin increased through development from 20 µm at hatch (14 µm across the yolk sac) to 70 µm in an 11 g fish. Diffusion distances across both the filaments and lamellae of the gills decreased through development, from 3.7 to 2.4 µm for lamellae and from 14.5 to 10.8 µm for filaments. The total anatomical diffusion factor (ADF, mass-specific surface area per unit diffusion distance) remained constant over early development and appeared to be higher than in adult fish. The distribution of ADF changed over early development from 50 % yolk sac, 42 % body surface and 8 % branchial in newly hatched fish to 68 % branchial and 32 % cutaneous at the end of yolk resorption. Generally, early post-hatch development of gills, ADF and some cutaneous surfaces showed high mass exponents. After yolk resorption (body mass 0.2 g), however, these coefficients were lower and closer to unity. The change in scaling at the end of yolk resorption in this study may reflect the completion of larva to juvenile metamorphosis in Atlantic salmon. Comparison between our data and values in the literature suggests that the timing of gill development is related more to developmental stage than to body size.
Parasite Antigen-Driven Basophils Are a Major Source of IL-4 in Human Filarial Infections

Basophil contribution to the IL-4 pool in filarial infections was assessed using PBMC from 20 patients with active filarial infections and from 9 uninfected subjects. Patient basophils released histamine in response to Brugia malayi Ag (BmAg). They also released IL-4 within 2 h after exposure to BmAg, as assessed by intracellular cytokine flow cytometry. This IL-4 induction was Ag specific, as IL-4 was not detected in BmAg-exposed basophils obtained from uninfected subjects. Although there were, on average, 64 times more CD4+ T cells than basophils in the peripheral circulation of filaria-infected patients, the absolute numbers of basophils and CD4+ T cells producing IL-4 per 100,000 PBMC were equivalent (geometric mean: 16 IL-4-producing basophils/100,000 PBMC vs 22 IL-4-producing CD4+ T cells/100,000 PBMC). Basophils also released IL-4 in response to both low and high concentrations of BmAg, whereas CD4+ T cells released IL-4 only after incubation with a high concentration of BmAg, raising the possibility that basophils, due to their lower threshold for activation, may actually release IL-4 more frequently than CD4+ T cells in vivo. Furthermore, IL-4 production in vitro by Ag-stimulated purified basophils or CD4+ T cells provided evidence that basophils release greater quantities of IL-4 per cell than CD4+ T cells in response to BmAg. These results suggest that, when Ag-specific IgE is present in a filaria-infected individual, basophils function to amplify the ongoing Th2 response by releasing IL-4 in greater amounts and possibly more frequently than CD4+ T cells in response to filarial Ag.
[Epidemiological study on the incidence of inflammatory bowel disease in 4 Spanish areas. Spanish Group on the Epidemiological Study of Inflammatory Bowel Disease].

BACKGROUND The incidence of inflammatory bowel disease (IBD) shows marked geographical variations. The aim of this study was to determine and compare the incidence of IBD in four Spanish areas: Sabadell (Northeast), Vigo (Northwest), Mallorca island and Motril (South). PATIENTS AND METHODS Prospective survey based on inception cohorts over a two-years period (1 October 1991 to September 1993). Subjects were the patients resident in these areas and diagnosed of IBD according to a standard protocol for case ascertainment and definition. RESULTS Altogether 328 cases were identified, of whom 191 were diagnosed as ulcerative colitis (UC), 135 as Crohn's disease (CD) and 2 as indeterminate colitis. The overall adjusted incidence rate per 100,000 persons between ages 15-64 years of UC and CD were respectively 9.8 and 5.2 in Sabadell, 7.7 and 5.0 in Vigo, 7.8 and 5.8 in Mallorca and 4.3 and 6.5 in Motril. The Incidence rate ratio showed no significant differences for either conditions among these areas. The global adjusted incidence rate of UC in Spanish areas (8.0; IC 95%: 6.3-9.7) was significantly lower to that of Northern European countries while that of CD (5.5; IC 95%: 4.1-6.9) was between that of Northern and Southern Europe with no significant differences. CONCLUSIONS The incidence of IBD did not show differences among the Spanish areas, and rates are between 2 and 6 times higher than those previously reported. The incidence of UC is significantly lower than that observed in the North of Europe, while for CD the incidence is between that of Northern and Southern Europe.
The principal rapamycin-sensitive p70(s6k) phosphorylation sites, T-229 and T-389, are differentially regulated by rapamycin-insensitive kinase kinases

Mitogen-induced activation of p70(s6k) is associated with the phosphorylation of specific sites which are negatively affected by the immunosuppressant rapamycin, the fungal metabolite wortmannin, and the methylxanthine SQ20006. Recent reports have focused on the role of the amino terminus of the p85(s6k) isoform in mediating kinase activity, with the observation that amino-terminal truncation mutants are activated in the presence of rapamycin while retaining their sensitivity to wortmannin. Here we show that the effects of previously described amino- and carboxy-terminal truncations on kinase activity are ultimately reflected in the phosphorylation state of the enzyme. Mutation of the principal rapamycin-targeted phosphorylation site, T-389, to an acidic residue generates a form of the kinase which is as resistant to wortmannin or SQ20006 as it is to rapamycin, consistent with the previous observation that T-389 was a common target of all three inhibitors. Truncation of the first 54 residues of the amino terminus blocks the serum-induced phosphorylation of three rapamycin-sensitive sites, T-229 in the activation loop and T-389 and S-404 in the linker region. This correlates with a severe reduction in the ability of the kinase to be activated by serum. However, loss of mitogen activation conferred by the removal of the amino terminus is reversed by additional truncation of the carboxy-terminal domain, with the resulting mutant demonstrating phosphorylation of the remaining two rapamycin-sensitive sites, T-229 and T-389. In this double-truncation mutant, phosphorylation of T-229 occurs in the basal state, whereas mitogen stimulation is required to induce acute upregulation of T-389 phosphorylation. The phosphorylation of both sites proceeds unimpaired in the presence of rapamycin, indicating that the kinases responsible for the phosphorylation of these sites are not inhibited by the macrolide. In contrast, activation of the double-truncation mutant is blocked in the presence of wortmannin or SQ20006, and these agents completely block the phosphorylation of T-389 while having only a marginal effect on T-229 phosphorylation. When the T-389 site is mutated to an acidic residue in the double-truncation background, the activation of the resulting mutant is insensitive to the wortmannin and SQ20006 block, but interestingly, the mutant is activated to a significantly greater level than a control in the presence of rapamycin. These data are consistent with the hypothesis that T-389 is the principal regulatory phosphorylation site, which, in combination with hyperphosphorylation of the autoinhibitory domain S/TP sites, is acutely regulated by external effectors, whereas T-229 phosphorylation is regulated primarily by internal mechanisms.
Review on gendered perspective of households participation in agricultural activities in Ethiopia

Gender is a crosscutting issue that attracts the attention of development professionals, policy makers and politicians. It is due to the fact that in any development, interventions involvement of women has become compulsory. To this end, considering the roles of men and women is very important, and gender roles vary across culture. In Ethiopia where agriculture is the backbone of the economy, the participation of women in the field is very high. Though men are taking the lion’s share in agricultural production, the contribution of women has also been an undeniable fact. Rural Ethiopian women must work up to twice as many hours per day compared to men, since they are primarily responsible for their households, including gathering firewood and water, cooking, cleaning, and providing child care. The contribution of women to agricultural and food production is significant but it is impossible to verify empirically the share produced by women. This paper re-affirms that women make essential contributions to agriculture and rural enterprises across the developing world. But there is much diversity in women’s roles and over-generalization undermines policy relevance and planning. Key words: Gender, women, gender role, agricultural extension.
A Single Polymorphism Disrupts the Killer Ig-Like Receptor 2DL2/2DL3 D1 Domain12

Genetic polymorphisms found in the killer Ig-like receptor (KIR), two domains, long cytoplasmic tail 2/3 (KIR2DL2/3) locus are responsible for the differential binding of KIR2DL2/3 allelic products with their HLA-C ligands and have been associated with the resolution of hepatitis C infection. In our study, a KIR CD3ζ fusion-binding assay did not detect any interaction between the KIR2DL2*004 extracellular domain and several putative KIR2DL2/3 ligands. To determine the amino acid polymorphism(s) responsible for the KIR2DL2*004 phenotype, we mutated the polymorphic residues of full-length KIR and expressed them in human Jurkat cells. Flow cytometry analysis failed to detect the surface expression of receptors containing a threonine at position 41 (T41), a polymorphism specific to KIR2DL2*004. Confocal microscopy showed that receptors containing T41 were retained inside the cell and had a perinuclear localization, possibly indicating that their extracellular domain was misfolded. Most KIR2DL2/3 alleles possess an arginine at position 41 (R41), and we predicted through molecular modeling and demonstrated by mutagenesis that R41 most likely interacts with the nearby residues Y77 and D47. Interaction between these residues would maintain C strand contact with the C′ and F strands of the D1 domain β-sheet. Furthermore, R41 and Y77 are conserved in the C and F strand amino acid alignments of Ig-like superfamily members, and may therefore be necessary for the structural integrity of other immune response proteins. Our data indicate that the extracellular T41 polymorphism encoded by the KIR2DL2*004 allele most likely results in misfolding of the D1 domain and complete intracellular retention of the receptor.
Increased mucosal tumour necrosis factor α production in Crohn’s disease can be downregulated ex vivo by probiotic bacteria

Background and aims: Tumour necrosis factor α (TNF-α) plays a key role in the pathogenesis of intestinal inflammation in Crohn’s disease. The effect of bacteria on TNF-α release by intestinal mucosa was investigated. Methods: Ileal specimens were obtained at surgery from 10 patients with Crohn’s disease (ileal stricture) and five disease controls undergoing right hemicolectomy (caecal cancer). Mucosal explants from each specimen were cultured for 24 hours with either non-pathogenic Escherichia coli, Lactobacillus casei DN-114001, L bulgaricus LB10, or L crispatus (each study contained blank wells with no bacteria). Tissue and bacterial viability was confirmed by lactate dehydrogenase (LDH) release and culture. Concentrations of TNF-α were measured in supernatants and the phenotype of the intestinal lymphocytes was analysed by flow cytometry. Results: Coculture of mucosa with bacteria did not modify LDH release. Release of TNF-α by inflamed Crohn’s disease mucosa was significantly reduced by coculture with L casei or L bulgaricus; changes induced by L crispatus or E coli were not significant. The effect of L casei and L bulgaricus was not prevented by protease inhibitors. Coculture with L casei and L bulgaricus reduced the number of CD4 cells as well as TNF-α expression among intraepithelial lymphocytes from Crohn’s disease mucosa. None of the bacteria induced changes in non-inflamed mucosa. Conclusions: Probiotics interact with immunocompetent cells using the mucosal interface and modulate locally the production of proinflammatory cytokines.
Cardiorespiratory events in infants with gastroesophageal reflux symptoms: Is there any association?

Cardiorespiratory (CR) events (apnea, bradycardia, oxygen desaturation) and gastroesophageal reflux (GER) symptoms often coexist in infants admitted to Neonatal Intensive Care Unit, leading to over‐prescription of drugs and delayed discharge. We aimed to evaluate the relationships between CR and GER events.
Dissecting the species–energy relationship

Environmental energy availability can explain much of the spatial variation in species richness. Such species–energy relationships encompass a diverse range of forms, and there is intense debate concerning which of these predominate, and the factors promoting this diversity. Despite this there has been relatively little investigation of whether the form, and relative strength, of species–energy relationships varies with (i) the currency of energy availability that is used, and (ii) the ecological characteristics of the constituent species. Such investigations can, however, shed light on the causal mechanisms underlying species–energy relationships. We illustrate this using the British breeding avifauna. The strength of the species–energy relationship is dependent on the energy metric used, with species richness being more closely correlated with temperature than the Normalized Difference Vegetation Index, which is a strong correlate of net primary productivity. We find little evidence, however, for the thermoregulatory load hypothesis that high temperatures enable individuals to invest in growth and reproduction, rather than thermoregulation, increasing population sizes that buffer species from extinction. High levels of productive energy may also elevate population size, which is related to extinction risk by a negative decelerating function. Therefore, the rarest species should exhibit the strongest species–energy relationship. We find evidence to the contrary, together with little support for suggestions that high-energy availability elevates species richness by increasing the numbers of specialists or predators.
Prompt Recovery of Damaged Adrenal Medullae Induced by Salinomycin

The morphologic changes in the adrenal medullae of rats treated with an ionophore antibiotic, salinomycin, are described. Male rats of approximately 7 wk of age were treated orally with a single dose of salinomycin at 80 mg/kg body weight. Following this treatment, the adrenal glands were examined, using immunohistochemistry, for neurofilament, laminin, fibronectin, and S-100 protein; the glands were also examined using transmission electron microscopy. One hour after the treatment, a karyopyknosis was observed in the clusters of affected chromaffin cells in which the neurofilament, laminin, and fibronectin were present. The lesions became progressively conspicuous between hours 5 and 10. Ultimately, the outcome was cell lysis. Five hours after salinomycin treatment, unaffected chromaffin cells strongly stained to tyrosine hydroxylase. At 10 hr, new chromaffin cells, which were irregular in shape with electron-dense cytoplasm (dark cell), that were strongly stained for tyrosine hydroxylase appeared at the basement membrane site of the necrotic clusters, and these cells contained very few immature catecholamine granules of less than 80 nm. At 17 hr, the catecholamine granules increased in number and size to about 200 nm. The newly formed chromaffin cells grew within the clusters to fill in the medulla by 24 hr, and cytoplasmic granules progressively increased in number and size. The interstitial tissue was seen to be edematous at 5 hr. New capillaries were found in the adrenal medullae of both control and salinomycin-treated rats. The protruding chromaffin cells (protruding cells), which we previously described in normal rats, were also observed in salinomycin-treated rats, which suggests that holocrine secretion is performed in the adrenal medullae. The results indicated that the rat adrenal medullae have the ability to make a rapid recovery after an insult by salinomycin.