Miracle-dz/UniFAR-FTUs huggingface dataset:
Provoking Allergens and Treatment of Anaphylaxis in Children and Adolescents: Data From the Anaphylaxis Registry of German-Speaking Countries

S Hompes, A Kohli, K Nemat. Pediatr Allergy Immunol. 2011;22(6):568–574 To characterize provoking allergens, clinical features, accompanying factors, and treatment modalities for children presenting with anaphylaxis. Data were analyzed from the anaphylaxis registry of German - speaking countries, which included 197 reported anaphylactic reactions from children and adolescents between 2006 and 2009. This database is based on an online questionnaire for providers of allergy specialty care in Germany, Austria, and Switzerland. The questionnaire included demographic data, clinical symptoms, the cause of reaction, accompanying or possible aggravating …
Staff Expectations on Implementing New Electronic Applications in a Changing Organization

This study was undertaken to describe staff expectations prior to implementation of new electronic applications in a changing organization. Changes are a part of human existence; changes based on implementation of technology and information and communication technology are taking place in the health care sector globally. The Swedish public health care and social care sector is taking a similar path. A qualitative approach with group interviews of 23 staff divided in 5 groups was performed. Latent content analysis was used to analyze the transcribed interviews. The theme, taking standpoint today in relation to the past, emerged from 3 areas of discussion: “distance holding,” “ruled by the organization,” and “health care development in the future. ” New restraints on staff affect the caregiving process. Managers should consider whether a particular change is revolutionary or evolutionary and act in the change process according to the possible psychological impact of the change.
Helicobacter pylori and the Risk of Colonic Adenomas

Aims: Previous studies have found a positive association between Helicobacter pylori infection and colorectal adenomas. The aim of the present study was to examine this association while taking possible confounding factors into account. Methods: 98 serum samples were available from 182 patients with colorectal adenomas who entered a case-control study of colorectal adenomas and diet. The H. pylori status in patients was compared with a hospital control group and a population control group. Results: H. pylori IgG antibodies were more common in colorectal polyp patients compared with either control group, the prevalence being 79% in cases compared with 62% in both control groups. The corresponding RR was 1.4 (0.76–2.6) compared with hospital controls and 2.1 (1.1–3.9) compared with population controls. After adjusting for possible confounding variables the association between H. pylori status and adenoma risk was even more marked. There was an RR of 1.6 (0.80–3.4) compared with hospital controls and an RR of 2.6 (1.3–5.4) compared with population controls, the latter association being statistically significant. Conclusion: These findings suggest a statistically significant association between H. pylori infection and colorectal polyps. A possible mechanism might be increased gastrin levels in H. pylori-infected subjects which exhibit a trophic effect on colonic mucosa.
An Analysis of Restructuring Orientation to Enhance Nurse Retention

The nursing shortage has received much media attention; however, something that contributes to it—nurse turnover—has not received the same attention. Facilities spend time and money to train new employees only to have them leave within a few months. Staff morale, money, time, and quality of care are all affected by nurse turnover. The fact that it often occurs so soon after one takes a position makes it pertinent to look at the process of transition into the new position, namely, the orientation program. This article examines the turnover statistics, costs, rationale, and orientation programs that have proven positive results. It is hoped that the findings can assist health care facilities to replicate successful orientation programs and reduce nurse turnover.
Sexual outcome following female genital cancer treatment : a critical review of methods of investigation and results

Abstract Information about changes in sexual functioning after medical treatment is not being provided routinely by doctors. The inadequate information about possible effects of diseases and therapeutic interventions in patients' sexual functioning is also reflected in the scarce amount of empirical research available on this issue. This review summarizes investigations dealing with the sexual functioning of gynaecological cancer patients.
Clinical librarians, a new tribe in the UK: roles and responsibilities.

AIMS The aims of this research were to determine the background, education, training experience, roles and responsibilities of practising Clinical Librarians (CL) in the UK. This paper reports the findings of a survey undertaken in 2007 at the third Clinical Librarian conference. This research builds on research undertaken by Harrison and Sargeant in 2002 and Ward in 2004, and can be considered as part of a longitudinal study of the role of the CL in the UK. OBJECTIVES The objectives of the research were to define and gain a broad understanding of the role of the CL in the UK highlighting similarities and differences amongst the professionals and provide evidence for a baseline of skills and activities for the CL role. The type of sampling used was Judgmental. RESULTS/ANALYSIS: Results/analysis detail the skills and activities undertaken by CLs. Searching for information for Clinicians was the activity most frequently undertaken. Developing good relationships with other healthcare professionals was considered essential. Two-thirds of the respondents held a postgraduate library qualification. CONCLUSIONS Crucially a new model for the UK CL role is derived drawing on the findings of this study and the existing literature.
Ingestão dietética de cálcio e adiposidade em mulheres adultas

OBJETIVO: Avaliar a ingestao de calcio dietetico e sua correlacao com parâmetros de adiposidade em mulheres adultas, residentes em Diamantina (MG). METODOS: Foram determinados, em cinquenta mulheres adultas, o indice de massa corporal, a circunferencia da cintura, a relacao cintura-quadril e o percentual de gordura corporal. A ingestao dietetica de calcio foi avaliada por meio de recordatorio de 24 horas e de um questionario de frequencia de consumo. Os alimentos do questionario foram divididos em tres grupos: 1) laticinios, 2) vegetais fontes de calcio, 3) redutores da biodisponibilidade de calcio. Foram calculados os escores I, II e III de frequencia de consumo, correspondentes aos grupos 1, 2 e 3 de alimentos. RESULTADOS: Aproximadamente 42,0% das mulheres apresentou indice de massa corporal >25Kg/m2, sendo 26,0% com algum grau de obesidade; 90,0% apresentou excesso de gordura corporal, sendo 42,0% com risco para doencas metabolicas. A ingestao media diaria de calcio representou 43,8% da Ingestao Adequada e nao diferiu entre aquelas com indice de massa corporal 25kg/m2. Os escores I e II foram significativamente inferiores aquele dos alimentos que interferem na biodisponibilidade deste nutriente (p 0,05). CONCLUSAO: A baixa ingestao de calcio pode ter contribuido para a ausencia de correlacao entre as variaveis estudadas. Associacoes entre a ingestao de calcio e parâmetros de adiposidade ainda permanecem pouco claras e devem ser objeto de pesquisas adicionais.
Alterations of CaMKII after hypoxia‐ischemia during brain development

Transient brain hypoxia‐ischemia (HI) in neonates leads to delayed neuronal death and long‐term neurological deficits. However, the underlying mechanisms are incompletely understood. Calcium‐calmodulin‐dependent protein kinase II (CaMKII) is one of the most abundant protein kinases in neurons and plays crucial roles in synaptic development and plasticity. This study used a neonatal brain HI model to investigate whether and how CaMKII was altered after HI and how the changes were affected by brain development. Expression of CaMKII was markedly up‐regulated during brain development. After HI, CaMKII was totally and permanently depleted from the cytosol and concomitantly deposited into a Triton‐insoluble fraction in neurons that were undergoing delayed neuronal death. Autophosphorylation of CaMKII‐Thr286 transiently increased at 30 min of reperfusion and declined thereafter. All these changes were mild in P7 pups but more dramatic in P26 rats, consistent with the development‐dependent CaMKII expression in neurons. The results suggest that long‐term CaMKII depletion from the cytosolic fraction and deposition into the Triton‐insoluble fraction may disable synaptic development, damage synaptic plasticity, and contribute to delayed neuronal death and long‐term synaptic deficits after transient HI.
Minimal role for activating transcription factor 3 in the oligodendrocyte unfolded protein response in vivo

To further our goal of identifying and characterizing the functions of major components of the unfolded protein response (UPR) in oligodendrocytes, the gene encoding the activator of transcription factor 3 protein (ATF3) has been ablated in mice expressing mutant forms of the Proteolipid protein 1 (Plp1) gene and the phenotype of double mutants characterized at several levels. Mature oligodendrocytes in Plp1 mutant mice undergo UPR‐induced cell stress, induce ATF3 expression and exhibit a greater propensity to die by apoptosis, which is consistent with pro‐death function of ATF3 proposed from in vitro studies. However, we find that the absence of ATF3 has no effect on the levels of apoptosis in Plp1 mutants. Furthermore, we find that oligodendrocyte function appears normal in Atf3−/− mice and that motor coordination and neural communication are similarly unaffected. Accordingly, we conclude that ATF3, at best, plays a minor role in UPR signaling and its expression is more likely induced by the UPR as a secondary event in oligodendrocytes that is unrelated to cell death.
NSCL‐1 and ‐2 control the formation of precerebellar nuclei by orchestrating the migration of neuronal precursor cells

During embryonic development post‐mitotic neurons of the precerebellar neuroepithelium, migrate from the rhombic lip to the ventral part of the neural tube to form the precerebellar nuclei of the pons and medulla oblongata. In this study, we show that neural basic helix‐loop‐helix transcription factors NSCL‐1 and ‐2 are expressed in all cells of the anterior extramural migration stream (aes), which forms the precerebellar nuclei. The combined inactivation of NSCL‐1 and ‐2 led to a complete absence of the pontine nuclei and a strong reduction in the reticulotegmental nuclei. We demonstrate that NSCL‐1/2 were required for a sustained expression of the netrin receptor and cell guidance molecule Dcc in the aes. Unc5H3, a second netrin receptor, which serves as a stop signal for migratory cells was up‐regulated in NSCL‐1/2 deficient cells, which ceased migration and accumulated ectopically. Furthermore, we observed a massive increase of apoptosis in cells of the aes in the absence of NSCL‐1/2, which together with the arrest of migration might explain the virtually complete loss of aes‐derived structures in NSCL‐1/2 mutant mice. We conclude that NSCL‐1/2 maintain migration and survival of cells in the aes.
Kir4.1 channels regulate swelling of astroglial processes in experimental spinal cord edema

In glial cells, inwardly rectifying K+ channels (Kir) control extracellular [K+]o homeostasis by uptake of K+ from the extracellular space and release of K+ into the microvasculature. Kir channels were also recently implicated in K+‐associated water influx and cell swelling. We studied the time‐dependent expression and functional implication of the glial Kir4.1 channel for astroglial swelling in a spinal cord edema model. In this CNS region, Kir4.1 is expressed on astrocytes from the second postnatal week on and co‐localizes with aquaporin 4 (AQP4). Swelling of individual astrocytes in response to osmotic stress and to pharmacological Kir blockade were analyzed by time‐lapse‐two‐photon laser‐scanning microscopy in situ. Application of 30% hypotonic solution induced astroglial soma swelling whereas no swelling was observed on astroglial processes or endfeet. Co‐application of hypotonic solution and Ba2+, a Kir channel blocker, induced prominent swelling of astroglial processes. In Kir4.1−/− mice, however, somatic as well as process swelling was observed upon application of 30% hypotonic solutions. No additional effect was provoked upon co‐application with Ba2+. Our experiments show that Kir channels prevent glial process swelling under osmotic stress. The underlying Kir channel subunit that controls glial process swelling is Kir4.1, whereas changes of the glial soma are not substantially related to Kir4.1.
Effects of super-hard rice bread blended with black rice bran on amyloid β peptide production and abrupt increase in postprandial blood glucose levels in mice

Alzheimer’s disease and type 2 diabetes are very serious diseases with the latter having been suggested to cause the former. We prepared super-hard rice bread blended with black rice bran (SRBBB), which contained a high amount of resistant starch that showed strong inhibitory activities against β-secretase and acetylcholinesterase even after heating. Black rice bran showed greater β-secretase inhibitory activity (3.6-fold) than Koshihikari rice. The bran contained more oleic acid and anthocyanin, meaning that it is potentially a biofunctional food with a high antioxidant capacity. Furthermore, aged mice, which were fed a SRBBB diet for four weeks, showed lower amyloid β 40 peptide in the blood than mice fed a commercial diet (p < 0.01). Additionally, their initial blood glucose levels (BGLs) after 12 weeks of being fed SRBBB were significantly lower than those in the control group. Taken together, our results indicate SRBBB shows promise for inhibiting not only amyloid β production, but also abrupt increases in postprandial BGLs. Graphical abstract Characterization of amyloid β-40 protein species with ELISA method.
Course of multiple sclerosis

The course of multiple sclerosis was monitored by means of a long‐term prospective study. This paper reports on first results from this study, covering 102 patients who were monitored for 2 years or more and examined regularly. It is attempted to quantify the extent of the worsening or improvement in the patients’clinical status over the period of observation using regression analysis techniques. The severity of the disease did not correlate to the period of observation in 15% of the cases, these displaying no progression with regard to the clinical signs. In most cases (32%) a description of the disease progression was possible by means of a linear regression line, 21% had a parabolic and 23.5% an increasingly progressive course. For nine patients a second or third degree polynomial regression curve could be used to describe the course of the disease. The individual progression of the disease as estimated using the linear regression coefficient did not correlate with the individual relapse rate (on average 1.1 per year), nor with the age of the patient, the severity of the multiple sclerosis, the duration of the illness or with the previous course of the disease.
Loss of cardiolipin in palmitate‐treated GL15 glioblastoma cells favors cytochrome c release from mitochondria leading to apoptosis

Unlike oleate and linoleate, palmitate induced mitochondrial apoptosis in GL15 glioblastoma cells. Decrease in membrane potential in a subpopulation of mitochondria of palmitate‐treated cells was revealed using the 5,5′,6,6′‐tetrachloro‐1,1′,3,3′‐tetraethylbenzimidazolylcarbocyanine iodide probe. The diminished ability to reduce a tetrazolium salt indicated an impairment of mitochondrial function. Up to 50% cytochrome c (cyt c) was detached from the inner mitochondrial membrane and released outside mitochondria in palmitate‐treated cells, whereas no release was detected after oleate and linoleate treatments. Cyt c release into the cytosol was followed by caspase 3 activation. Released cyt c and caspase 3 activity were not affected by neutral and acid sphingomyelinase inhibitors and by the inhibitor of serine palmitoyltransferase cycloserine, indicating that apoptosis was independent of the ceramide pathway, nor the mitochondrial pro‐apoptotic AIF or Bcl‐2/Bax factors appeared to be involved in the effect. Utilization of palmitate by GL15 cells altered phospholipid composition. Cardiolipin (CL), the lipid involved in cyt c interaction with the inner mitochondrial membrane, was decreased and highly saturated. This produced an imbalance in hydrophilic/hydrophobic interactions underlying the anchorage of cyt c, by weakening the hydrophobic component and facilitating detachment of the protein and activation of downstream processes. The primary role of CL was explored by supplying GL15 with exogenous CL through a fusion process of CL liposomes with cell plasma membrane. Fused CL moved to mitochondria, as detected by nonylacridine orange probe. Enrichment of mitochondrial membranes with CL prior to palmitate treatment of cells caused decreased cyt c release and caspase 3 activity.
Quercetin inhibits advanced glycation end product formation via chelating metal ions, trapping methylglyoxal, and trapping reactive oxygen species

Physiological concentration of Mg2+, Cu2+, and Zn2+ accelerated AGE formation only in glucose-mediated conditions, which was effectively inhibited by chelating ligands. Only quercetin (10) inhibited MGO-mediated AGE formation as well as glucose- and ribose-mediated AGE formation among 10 polyphenols (1–10) tested. We performed an additional structure-activity relationship (SAR) study on flavanols (10, 11, 12, 13, and 14). Morin (12) and kaempherol (14) showed inhibitory activity against MGO-mediated AGE formation, whereas rutin (11) and fisetin (13) did not. These observations indicate that 3,5,7,4′-tetrahydroxy and 4-keto groups of 10 are important to yield newly revised mono-MGO adducts (16 and 17) and di-MGO adduct (18) having cyclic hemiacetals, while 3′-hydroxy group is not essential. We propose here a comprehensive inhibitory mechanism of 10 against AGE formation including chelation effect, trapping of MGO, and trapping of reactive oxygen species (ROS), which leads to oxidative degradation of 18 to 3,4-dihydroxybenzoic acid (15) and other fragments. Graphical abstract Inhibitory mechanism of quercetin against glucose-, ribose-, and MGO-mediated AGE formation and structures of MGO-quercetin adducts were elucidated.
Increased APLP1 expression and neurodegeneration in the frontal cortex of manganese‐exposed non‐human primates

Chronic manganese (Mn) exposure produces a neurological syndrome with psychiatric, cognitive, and parkinsonian features. Gene expression profiling in the frontal cortex of Cynomologous macaques receiving 3.3–5.0 mg Mn/kg weekly for 10 months showed that 61 genes were increased and four genes were decreased relative to controls from a total of 6766 genes. Gene changes were associated with cell cycle regulation, DNA repair, apoptosis, ubiquitin‐proteasome system, protein folding, cholesterol homeostasis, axonal/vesicular transport, and inflammation. Amyloid‐β (Aβ) precursor‐like protein 1, a member of the amyloid precursor protein family, was the most highly up‐regulated gene. Immunohistochemistry confirmed increased amyloid precursor‐like protein 1 protein expression and revealed the presence of diffuse Aβ plaques in Mn‐exposed frontal cortex. Cortical neurons and white matter fibers from Mn‐exposed animals accumulated silver grains indicative of on‐going degeneration. Cortical neurons also exhibited nuclear hypertrophy, intracytoplasmic vacuoles, and apoptosis stigmata. p53 immunolabeling was increased in the cytoplasm of neurons and in the nucleus and processes of glial cells in Mn‐exposed tissue. In summary, chronic Mn exposure produces a cellular stress response leading to neurodegenerative changes and diffuse Aβ plaques in the frontal cortex. These changes may explain the subtle cognitive deficits previously demonstrated in these same animals.
Dysregulation of intracellular calcium homeostasis is responsible for neuronal death in an experimental model of selective hippocampal degeneration induced by trimethyltin

Trimethyltin (TMT) intoxication is considered a suitable experimental model to study the molecular basis of selective hippocampal neurodegeneration as that occurring in several neurodegenerative diseases. We have previously shown that rat hippocampal neurons expressing the Ca2+‐binding protein calretinin (CR) are spared by the neurotoxic action of TMT hypothetically owing to their ability to buffer intracellular Ca2+ overload. The present study was aimed at determining whether intracellular Ca2+ homeostasis dysregulation is involved in the TMT‐induced neurodegeneration and if intracellular Ca2+‐buffering mechanisms may exert a protective action in this experimental model of neurodegeneration. In cultured rat hippocampal neurons, TMT produced time‐ and concentration‐dependent [Ca2+]i increases that were primarily due to Ca2+ release from intracellular stores although Ca2+ entry through Cav1 channels also contributed to [Ca2+]i increases in the early phase of TMT action. Cell pre‐treatment with the Ca2+ chelator, 1,2‐bis(2‐aminophenoxy)ethane‐N,N,N′,N′‐tetraacetic acid tetrakis(acetoxymethyl ester) (2 μM) significantly reduced the TMT‐induced neuronal death. Moreover, CR+ neurons responded to TMT with smaller [Ca2+]i increases. Collectively, these data suggest that the neurotoxic action of TMT is mediated by Ca2+ homeostasis dysregulation, and the resistance of hippocampal neurons to TMT (including CR+ neurons) is not homogeneous among different neuron populations and is related to their ability to buffer intracellular Ca2+ overload.
MAPKAP kinase 2‐deficiency prevents neurons from cell death by reducing neuroinflammation – relevance in a mouse model of Parkinson’s disease

The inflammatory response in the brain is closely associated with the pathogenesis of degenerative neurological disorders. A role for the p38 stress‐activated protein kinase/MAPK‐activated protein kinase 2 (MK2) axis in inflammation and apoptosis is well documented. Here, we provide evidence that neurodegeneration can be prevented by eliminating MK2. In primary mesencephalic neuron‐glia co‐cultures dopaminergic neurons from MK2‐deficient (MK2−/−) mice were significantly more resistant to lipopolysaccharide‐induced neurotoxicity compared with cells from wild‐type mice. This neuroprotection in MK2‐deficient cultures was associated with a reduced inflammatory response, especially with reduced production of the inflammatory mediators tumor necrosis factor alpha, keratinocyte‐derived chemokine, interleukin‐6, and nitric oxide (NO). Interestingly, in primary neuron‐enriched cell cultures p38 MAPK, but not MK2, also participates in NO‐mediated neuronal cell death. In the MPTP mouse model for Parkinson’s disease, MK2‐deficient mice show a reduced neuroinflammation and less degeneration of dopaminergic neurons in the substantia nigra after MPTP lesion compared with wild‐type mice. In conclusion, our results reveal that MK2 does not directly participate in neuronal cell death, but indirectly contributes to neurodegeneration by the production of neurotoxic substances, such as NO or tumor necrosis factor alpha, from activated glia cells.