Miracle-dz/UniFAR-FTUs huggingface dataset:
TÜRKİYE’DE KURAM/MODELE DAYALI HEMŞİRELİK ARAŞTIRMALARININ İNCELEMESİ

Exploration of Theory/Model Based Nursing Research In Turkey Nursing discipline consists of three basic elements: theory, research and practice. These elements contribute to development of nursing science in mutual interaction. The purpose of this study was to investigate the quality and quantity of researches performed by nurses in our country based on theory and model. For this purpose, database of The Council of Higher Education and full texts articles available on-line were screened. There are 48 studies carried out by nurses in Turkey between 1995-2010 based on theory/model. The most commonly theory/model used by nurses is Orem’s Self-Care Deficit Nursing Theory in Nursing. As a result, the use of theor/model in nursing researches in our country is limited and it was observed that there was no standardization in using theories/models. It is recommended that theory/model-based nursing researches should be supported and that standardization regarding how to use theories/ models in researches should be identified.
Richer milk for sons but more milk for daughters: Sex‐biased investment during lactation varies with maternal life history in rhesus macaques

Lactation represents the greatest postnatal energetic expenditure for human and non‐human primate females, and the ability to sustain the costs of lactation is influenced by a mother's physical condition. This is especially true for young mothers that initiate reproduction shortly after adolescence. These mothers have fewer bodily reserves available for lactation and face tradeoffs between reproduction and their own growth. Milk synthesis among captive rhesus macaques (Macaca mulatta) was investigated at the California National Primate Research Center from 2005 to 2007 (N = 114). Rhesus macaques produced low energy density milk typical of the primate order, but there was substantial individual variation among mothers in both milk energy density and yield. As a consequence, the available milk energy (AME), the product of milk energy density and milk yield, to support infant growth, development, and activity, varied tenfold among mothers. Primiparous mothers (N = 40) had fewer bodily resources, as measured by mass and body mass index, available for lactation than did multiparous mothers (N = 74) and showed poorer lactational performance. Mothers of sons produced milk of higher energy density, especially primiparous mothers, but lower milk yield, such that AME was the same for sons and daughters. Although AME from the mother was the same for sons and daughters, there was significant sexual dimorphism in infant mass. These data indicate that selection has likely favored sex‐specific regulation of growth and development that is not necessarily contingent on greater maternal investment. Am. J. Hum. Biol. 2009. © 2009 Wiley‐Liss, Inc.
Three aspects in the treatment of acute exacerbations of chronic obstructive pulmonary disease: the rôle of nebulised magnesium, the risks of oxygen and the utility of the CRB-65 score

Chronic Obstructive Pulmonary Disease (COPD) is one of the commonest long-term conditions worldwide. It is characterised by chronic airflow limitation, pathological changes in the lung and significant extra-pulmonary manifestations. The treatment of an acute exacerbation of COPD (AECOPD), involves glucocorticoids and bronchodilators supplemented by antibiotics if needed. In-hospital, oxygen, which has potential risks as well as benefits, and additional respiratory support can be given if the patient deteriorates. Clinicians need to decide which treatment to provide and who can be safely discharged. This has led to the advent of scoring systems to define severity in COPD This thesis examines the evidence base for the use of magnesium in airways disease and presents the results of the first randomised double-blind placebo-controlled trial using nebulised magnesium in the treatment of AECOPD. 116 patients were randomised, but after 3 nebulisations over 90 minutes, there was no significant difference in FEV1 compared to placebo (p=0.67). In a second study, the CRB65 score was retrospectively assigned to a cohort of patients presenting to the emergency department with AECOPD, using data collected from a previous audit. Patients with a CRB65 score of 0 or 1 had a low risk of in-hospital and 30- day mortality and could be considered for discharge, whereas those with scores between 2-4 required admission with mortality increasing with the score. The CRB65 score showed a similar utility in AECOPD as it does in pneumonia. Finally, 18 subjects with stable but severe COPD were randomised in a crossover study to two nebulisations with salbutamol and ipratropium over 15 minutes with a five minute interval between nebulisations, using air or oxygen as the driving gas. When oxygen was used there was a 3.1mmHg difference (p<0.001) at 35 minutes, compared to air, illustrating the potential risks of repeated nebulisations to those with severe COPD.
Promoting Mental Health in Early Childhood Programs Serving Families From Low-income Neighborhoods

Although the majority of young children growing up in low-income communities will not experience mental health problems, a proportion of children will develop problems that can be painful for families and costly to society. There is growing consensus that preventive interventions in the first 5 years of life are the most cost-effective strategy for reducing children's mental health problems. The purposes of this article are to (a) present the case for providing health promotion and preventive interventions to economically disadvantaged parents of young children as standard practice in early childhood programs and (b) describe the feasibility and utility of incorporating mental health promotion services in child care centers serving low-income families using the Chicago Parent Program (CPP) as an example. The CPP is an evidence-based intervention designed in collaboration with low-income, ethnic minority parents to promote positive parenting skills and reduce behavior problems in young children. J Am Psychiatr Nurses Assoc, 2007; 13(5), 313-320. DOI: 10.1177/1078390307306996
Cardiac sarcoidosis

: Cardiac sarcoidosis is a rare but life-threatening condition, requiring a high degree of clinical suspicion and low threshold for investigation to make the diagnosis. The cardiac manifestations include heart failure, conducting system disease, and arrhythmias predisposing to sudden cardiac death. A number of investigations are available to assist in making the diagnosis. The diagnosis may be made from the clinical history and evidence of inflammation on imaging modalities in the active phase and evidence of myocardial scarring in the chronic phase.
Transmembrane Segments Prevent Surface Expression of Sodium Channel Nav1.8 and Promote Calnexin-dependent Channel Degradation*

The voltage-gated sodium channel (Nav) 1.8 contributes substantially to the rising phase of action potential in small dorsal root ganglion neurons. Nav1.8 is majorly localized intracellularly and its expression on the plasma membrane is regulated by exit from the endoplasmic reticulum (ER). Previous work has identified an ER-retention/retrieval motif in the first intracellular loop of Nav1.8, which prevents its surface expression. Here we report that the transmembrane segments of Nav1.8 also cause this channel retained in the ER. Using transferrin receptor and CD8α as model molecules, immunocytochemistry showed that the first, second, and third transmembrane segments in each domain of Nav1.8 reduced their surface expression. Alanine-scanning analysis revealed acidic amino acids as critical factors in the odd transmembrane segments. Furthermore, co-immunoprecipitation experiments showed that calnexin interacted with acidic amino acid-containing sequences through its transmembrane segment. Overexpression of calnexin resulted in increased degradation of those proteins through the ER-associated degradation pathway, whereas down-regulation of calnexin reversed the phenotype. Thus our results reveal a critical role and mechanism of transmembrane segments in surface expression and degradation of Nav1.8.
Tratamiento nutricional del fallo intestinal y potenciales mecanismos de estimulación

Severe forms of intestinal failure represent one of the most complex pathologies to manage, in both children and adults. In adults, the most common causes are chronic intestinal pseudo-obstruction and severe short bowel syndrome following large intestinal resections, particularly due to massive mesenteric ischemic, within the context of cardiopathies occurring with atrial fibrillation. The essential management after stabilizing the patient consists in nutritional support, either by parenteral or enteral routes, with tolerance to oral diet being the final goal of intestinal adaptation in these pathologies. Surgery may be indicated in some cases to increase the absorptive surface area. Parenteral nutrition is an essential support measure that sometimes has to be maintained for long time, even forever, except for technique-related complications or unfavorable clinical course that would lead to extreme surgical alternatives such as intestinal transplantation. Hormonal therapy with trophism-stimulating factors opens new alternatives that are already being tried in humans.
Normal and Friedreich Ataxia Cells Express Different Isoforms of Frataxin with Complementary Roles in Iron-Sulfur Cluster Assembly*

Friedreich ataxia (FRDA) is an autosomal recessive degenerative disease caused by insufficient expression of frataxin (FXN), a mitochondrial iron-binding protein required for Fe-S cluster assembly. The development of treatments to increase FXN levels in FRDA requires elucidation of the steps involved in the biogenesis of functional FXN. The FXN mRNA is translated to a precursor polypeptide that is transported to the mitochondrial matrix and processed to at least two forms, FXN42–210 and FXN81–210. Previous reports suggested that FXN42–210 is a transient processing intermediate, whereas FXN81–210 represents the mature protein. However, we find that both FXN42–210 and FXN81–210 are present in control cell lines and tissues at steady-state, and that FXN42–210 is consistently more depleted than FXN81–210 in samples from FRDA patients. Moreover, FXN42–210 and FXN81–210 have strikingly different biochemical properties. A shorter N terminus correlates with monomeric configuration, labile iron binding, and dynamic contacts with components of the Fe-S cluster biosynthetic machinery, i.e. the sulfur donor complex NFS1·ISD11 and the scaffold ISCU. Conversely, a longer N terminus correlates with the ability to oligomerize, store iron, and form stable contacts with NFS1·ISD11 and ISCU. Monomeric FXN81–210 donates Fe2+ for Fe-S cluster assembly on ISCU, whereas oligomeric FXN42–210 donates either Fe2+ or Fe3+. These functionally distinct FXN isoforms seem capable to ensure incremental rates of Fe-S cluster synthesis from different mitochondrial iron pools. We suggest that the levels of both isoforms are relevant to FRDA pathophysiology and that the FXN81–210/FXN42–210 molar ratio should provide a useful parameter to optimize FXN augmentation and replacement therapies.
The human obesity epidemic, the mismatch paradigm, and our modern “captive” environment

In the distant past obesity in humans was rare and likely caused by metabolic dysregulation due to genetic or disease‐related pathology. External factors precluded the ability of most people to overeat or under exert. Socio‐cultural obesity came about due to the rareness of obesity and its difficulty to achieve. What is rare becomes valuable and what is difficult to achieve becomes a badge of prestige. The modern human obesity epidemic would appear to represent a third class of obesity: environmental obesity. Much like the captive environments which humans construct for the captive/companion animals in our care, the modern human environment has greatly decreased the challenges of life that would restrict food intake and enforce exertion. And like us, our captive/companion animal populations are also experiencing obesity epidemics. A further concern is that maternal obesity alters maternal signaling to offspring, in utero through the placenta and after birth through breast milk, in ways that perpetuate an enhanced vulnerability to obesity. Molecules such as leptin, produced by adipose tissue and placenta, have significant developmental effects on brain areas associated with feeding behavior. Leptin and other cytokines and growth factors are found in breast milk. These molecules have positive effects on gut maturation; their effects on metabolism and brain development are unclear. Placenta and brain also are hotspots for epigenetic regulation, and epigenetic changes may play significant roles in the later vulnerability to obesity and to the development of a diverse array of diseases, including heart disease, hypertension, and noninsulin‐dependent diabetes. Am. J. Hum. Biol., 2012. © 2012 Wiley Periodicals, Inc.
Mesencephalic Astrocyte-derived Neurotrophic Factor (MANF) Has a Unique Mechanism to Rescue Apoptotic Neurons*

Mesencephalic astrocyte-derived neurotrophic factor (MANF) protects neurons and repairs the Parkinson disease-like symptoms in a rat 6-hydroxydopamine model. We show a three-dimensional solution structure of human MANF that differs drastically from other neurotrophic factors. Remarkably, the C-terminal domain of MANF (C-MANF) is homologous to the SAP domain of Ku70, a well known inhibitor of proapoptotic Bax (Bcl-2-associated X protein). Cellular studies confirm that MANF and C-MANF protect neurons intracellularly as efficiently as Ku70.
A Novel Pleckstrin Homology Domain-containing Protein Enhances Insulin-stimulated Akt Phosphorylation and GLUT4 Translocation in Adipocytes

Protein kinase B/Akt protein kinases control an array of diverse functions, including cell growth, survival, proliferation, and metabolism. We report here the identification of pleckstrin homology-like domain family B member 1 (PHLDB1) as an insulin-responsive protein that enhances Akt activation. PHLDB1 contains a pleckstrin homology domain, which we show binds phosphatidylinositol PI(3,4)P2, PI(3,5)P2, and PI(3,4,5)P3, as well as a Forkhead-associated domain and coiled coil regions. PHLDB1 expression is increased during adipocyte differentiation, and it is abundant in many mouse tissues. Both endogenous and HA- or GFP-tagged PHLDB1 displayed a cytoplasmic disposition in unstimulated cultured adipocytes but translocated to the plasma membrane in response to insulin. Depletion of PHLDB1 by siRNA inhibited insulin stimulation of Akt phosphorylation but not tyrosine phosphorylation of IRS-1. RNAi-based silencing of PHLDB1 in cultured adipocytes also attenuated insulin-stimulated deoxyglucose transport and Myc-GLUT4-EGFP translocation to the plasma membrane, whereas knockdown of the PHLDB1 isoform PHLDB2 failed to attenuate insulin-stimulated deoxyglucose transport. Furthermore, adenovirus-mediated expression of PHLDB1 in adipocytes enhanced insulin-stimulated Akt and p70 S6 kinase phosphorylation, as well as GLUT4 translocation. These results indicate that PHLDB1 is a novel modulator of Akt protein kinase activation by insulin.
Acondroplasia: diagnóstico clínico precoce

rEsUMO A acondroplasia e uma sindrome genetica que afeta a ossificacao endocondral, sendo uma das causas de nanismo. Acomete um recem-nascido em cada oito a dez mil nascimentos. Embora o defeito genetico tenha carater autossomico dominante, cerca de 85% dos casos resultam de novas mutacoes. Os portadores da acondroplasia apresentam caracteristicas clinicas tipicas como macrocefalia, baixa estatura, membros curtos com predominio do segmento proximal e limitacao da extensao dos cotovelos. Entretanto, essas caracteristicas clinicas no periodo neonatal podem passar despercebidas dos pais e pediatras, uma vez que os recem-nascidos normais apresentam os membros curtos em relacao ao tronco, o que dificulta a observacao dessa desproporcao. No presente estudo de caso, registra-se um caso tipico de acondroplasia diagnosticado imediatamente apos o nascimento. Palavras-chave. Acondroplasia; nanismo; recem-nascido
Influence of body fat and level of physical activity on rate‐pressure product at rest in preschool children

The rate‐pressure product (RPP) has strong correlation with the maximal oxygen consumption and is an indicator of myocardium stress being considered as the best indirect method to measure myocardial oxygen consumption. However, to the best of our knowledge, no studies have addressed in preschool children. The aim of this study was to analyze the influence of percentage of body fat (%BF) and physical activity (PA) patterns on RPP at Rest (RPPrest) as a marker of cardiac load in Preschool children.
Clinical characteristics of cytomegalovirus infection in rheumatic diseases: multicentre survey in a large patient population.

OBJECTIVE To survey and elucidate the clinical characteristics of CMV infection in rheumatic disease patients. METHODS A detailed questionnaire survey on CMV infection was carried out against rheumatic disease patients hospitalized in member hospitals, and the obtained clinical and/or laboratory data were analysed. RESULTS Out of 7377 patients, 151 were diagnosed as having CMV infection. The underlying diseases ranged broadly, but SLE, microscopic polyangiitis, and dermatomyositis were the most common. Four were diagnosed histopathologically, and the others via positive CMV antigenaemia. In addition to oral corticosteroid for all but one patient, 81 were treated with pulsed methylprednisolone (MPSL), 64 with cyclophosphamide (CYC) and 36 with other immunosuppressants. Forty-four had a fatal outcome, for which presence of clinical symptoms, other infectious complications, lymphopenia, an older age (>59.3 yrs) and the use of pulsed MPSL were significant risk factors (P < 0.05) by univariate analysis. Multivariate analysis retained the first three (P < 0.05). The CMV antigenaemia count was significantly higher for the symptomatic than asymptomatic [10.1 (0.0-2998.0) vs 4.0 (1.3-1144.4)/10(5) PMNs, respectively, P < 0.05; threshold count: 5.6/10(5) PMNs]. No treatment benefit by anti-viral agent was observed as for survival. CONCLUSION CMV infection was mostly diagnosed by antigenaemia, and occurred among patients under strong immunosuppressive therapy using pulsed MPSL and/or immunosuppressants. Lymphopenia, presence of symptoms and other infections are significant risk factors for a poor outcome and pulsed MPSL and an older age may predict it. Patients were prone to be symptomatic with anti-genaemia count over 5.6/10(5) PMNs.
Selective Translational Control of the Alzheimer Amyloid Precursor Protein Transcript by Iron Regulatory Protein-1*♦

Iron influx increases the translation of the Alzheimer amyloid precursor protein (APP) via an iron-responsive element (IRE) RNA stem loop in its 5′-untranslated region. Equal modulated interaction of the iron regulatory proteins (IRP1 and IRP2) with canonical IREs controls iron-dependent translation of the ferritin subunits. However, our immunoprecipitation RT-PCR and RNA binding experiments demonstrated that IRP1, but not IRP2, selectively bound the APP IRE in human neural cells. This selective IRP1 interaction pattern was evident in human brain and blood tissue from normal and Alzheimer disease patients. We computer-predicted an optimal novel RNA stem loop structure for the human, rhesus monkey, and mouse APP IREs with reference to the canonical ferritin IREs but also the IREs encoded by erythroid heme biosynthetic aminolevulinate synthase and Hif-2α mRNAs, which preferentially bind IRP1. Selective 2′-hydroxyl acylation analyzed by primer extension analysis was consistent with a 13-base single-stranded terminal loop and a conserved GC-rich stem. Biotinylated RNA probes deleted of the conserved CAGA motif in the terminal loop did not bind to IRP1 relative to wild type probes and could no longer base pair to form a predicted AGA triloop. An AGU pseudo-triloop is key for IRP1 binding to the canonical ferritin IREs. RNA probes encoding the APP IRE stem loop exhibited the same high affinity binding to rhIRP1 as occurs for the H-ferritin IRE (35 pm). Intracellular iron chelation increased binding of IRP1 to the APP IRE, decreasing intracellular APP expression in SH-SY5Y cells. Functionally, shRNA knockdown of IRP1 caused increased expression of neural APP consistent with IRP1-APP IRE-driven translation.
Electrostatic Compensation Restores Trafficking of the Autosomal Recessive Retinitis Pigmentosa E150K Opsin Mutant to the Plasma Membrane*

Rhodopsin is the rod photoreceptor G protein-coupled receptor responsible for capturing light. Mutations in the gene encoding this protein can lead to a blinding disease called retinitis pigmentosa, which is inherited frequently in an autosomal dominant manner. The E150K opsin mutant associated with rarely occurring autosomal recessive retinitis pigmentosa localizes to trans-Golgi network membranes rather than to plasma membranes of rod photoreceptor cells. We investigated the molecular mechanisms underlying opsin retention in the Golgi apparatus. Electrostatic calculations reveal that the E150K mutant features an overall accumulation of positive charges between helices H-IV and H-II. Human E150K and several other closely related opsin mutants were then expressed in HEK-293 cells. Spectral characteristics and functional biochemistry of each mutant were analyzed after reconstitution with the cis-retinoid chromophore. UV-visible spectra and rhodopsin/transducin activation assays revealed only minor differences between the purified wild type control and rhodopsin mutants. However, partial restoration of the surface electrostatic charge in the compensatory R69E/E150K double mutant rescues the plasma membrane localization of opsin. These findings emphasize the fundamental importance of electrostatic interactions for appropriate membrane trafficking of opsin and advance our understanding of the pathophysiology of autosomal recessive retinitis pigmentosa due to the E150K mutation.
Cytomegalovirus infection induces T‐cell differentiation without impairing antigen‐specific responses in Gambian infants

Cytomegalovirus (CMV) infection induces profound differentiation of T cells, and is associated with impaired responses to other immune challenges. We therefore considered whether CMV infection and the consequent T‐cell differentiation in Gambian infants was associated with impaired specific responses to measles vaccination or polyclonal responses to the superantigen staphylococcal enterotoxin B (SEB). While the concentration of undifferentiated (CD27+ CD28+ CCR7+) T‐cells in peripheral blood was unaffected by CMV, there was a large increase in differentiated (CD28− CD57+) CD8 T‐cells and a smaller increase in differentiated CD4 cells. One week post‐vaccination, the CD4 cell interferon‐γ (IFN‐γ) response to measles was lower among CMV‐infected infants, but there were no other differences between the cytokine responses, or between the cytokine or proliferative responses 4 months post‐vaccination. However, the CD8 T cells of CMV‐infected infants proliferated more in response to SEB and the antibody response to measles correlated with the IFN‐γ response to CMV, indicating that CMV infection actually enhances some immune responses in infancy.
Value of fluorodeoxyglucose positron emission tomography in characterizing clinically‐significant thyroid carcinomas

Background: Despite the rising incidence of thyroid incidentalomas, their clinical significance remains unclear. The present study aimed to determine whether fluorodeoxyglucose positron emission tomography (FDG‐PET) is associated with a significantly higher risk of clinically‐significant thyroid carcinoma (CSC) in incidentalomas than other non‐functional imaging modalities.