bluuebunny/crossref_metadata_2025_split huggingface dataset:
Medication use as a risk factor for inpatient falls in an acute care hospital: a case‐crossover study
Authors: Shuto Hideki , Imakyure Osamu , Matsumoto Junichi , Egawa Takashi , Jiang Ying , Hirakawa Masaaki , Kataoka Yasufumi , Yanagawa Takashi 
Published: January 2010

WHAT IS ALREADY KNOWN ABOUT THIS SUBJECT • Benzodiazepines, antidepressants, antipsychotic agents, anti‐arrhythmic agents, opioid analgesics and antihypertensive agents including α‐receptor antagonists and β‐receptor antagonists, but not angiotensin II receptor antagonists, have been implicated as risk factors for falls among community dwelling elderly people, and those in aged care hospitals and nursing homes. WHAT THIS STUDY ADDS • Using a case‐crossover design, the study's findings provide the first evidence suggesting that newly initiating treatment using an angiotensin II receptor antagonist, candesartan, or etizolam, biperiden and zopiclone may be potential risk factors for falls in acute hospitals.AIMS The present study aimed to evaluate the associations between medication use and falls and to identify high risk medications that acted as a trigger for the onset of falls in an acute care hospital setting.METHODS We applied a case‐crossover design wherein cases served as their own controls and comparisons were made within each participant. The 3‐day period (days 0 to −2) and the 3‐day periods (days −6 to −8, days −9 to −11 and days −12 to −14) before the fall event were defined as the case period and the control periods, respectively. Exposures to medications were compared between the case and control periods. Odds ratios (OR) and 95% confidence intervals (CI) for the onset of falls with respect to medication use were computed using conditional logistic regression analyses.RESULTS A total of 349 inpatients who fell during their hospitalization were recorded on incident report forms between March 2003 and August 2005. The initial use of antihypertensive, antiparkinsonian, anti‐anxiety and hypnotic agents as medication classes was significantly associated with an increased risk of falls, and these ORs (95% CI) were 8.42 (3.12, 22.72), 4.18 (1.75, 10.02), 3.25 (1.62, 6.50) and 2.44 (1.32, 4.51), respectively. The initial use of candesartan, etizolam, biperiden and zopiclone was also identified as a potential risk factor for falls.CONCLUSIONS Medical professionals should be aware of the possibility that starting a new medication such as an antihypertensive agent, including candesartan, and antiparkinsonian, anti‐anxiety and hypnotic agents, may act as a trigger for the onset of a fall.
Rapid isolation of translocation breakpoints in chronic myeloid and acute promyelocytic leukaemia
Authors: Bartley Paul A. , Martin‐Harris Michael H. , Budgen Bradley J. , Ross David M. , Morley Alexander A. 
Published: January 2010

SummaryIsolation and sequencing of the translocation breakpoint in chronic myeloid leukaemia‐(CML) and acute promyelocytic leukaemia (APML) may help to elucidate the mechanism of translocation and provide a molecular marker for monitoring of minimal residual disease. Amplification across the translocation breakpoint was performed in samples from 91 patients with CML and 15 patients with APML using single‐tube multiplex polymerase chain reaction (PCR) involving 308 primers for CML and 40 primers for APML. Nonspecific amplification was removed by a modification of PCR, termed sequential hybrid primer PCR (SHP‐PCR), which involved two sequential rounds of PCR, each of which used a low concentration of a specially designed hybrid primer. The resultant amplified material was sequenced. The method as finally developed was simple quick and robust. The translocation breakpoint was successfully isolated and sequenced in all 106 samples. The strategy of highly multiplexed PCR followed by SHP‐PCR is thus an effective method for isolating the translocation breakpoint in CML and APML. It may also be applicable to other haematological disorders characterised by translocation, deletion or inversion.
A prostacyclin agonist with thromboxane inhibitory activity for airway allergic inflammation in mice
Authors: Hayashi M. , Koya T. , Kawakami H. , Sakagami T. , Hasegawa T. , Kagamu H. , Takada T. , Sakai Y. , Suzuki E. , Gelfand E. W. , Gejyo F. 
Published: January 2010

SummaryBackground
ONO‐1301 is a novel drug that acts as a prostacyclin agonist with thromboxane A2 (TxA2) synthase inhibitory activity. We investigated the effect of ONO‐1301 on development of airway allergic inflammation.Methods
Mice sensitized and challenged to ovalbumin (OVA) received ONO‐1301, OKY‐046 (TxA2 synthase inhibitor), beraprost, a prostacyclin receptor (IP) agonist, ONO‐1301 plus CAY10449 (selective IP antagonist) or vehicle during the challenge period. Twenty‐four hours after the OVA challenge, airway hyperresponsiveness (AHR) to methacholine was assessed and bronchoalveolar lavage was performed. Lung specimens were excised for goblet cell staining and analysis of lung dendritic cells (DCs). Bone marrow‐derived dendritic cells (BMDCs) were generated, in the presence or absence of drugs, for analysis of DC function.Results
Mice that received ONO‐1301 showed significantly lower AHR, airway eosinophilia, T‐helper type 2 cytokine levels, mucus production and lung DCs numbers than vehicle‐treated mice. These effects of ONO‐1301 were mostly reversed by CAY10449. BMDCs treated with ONO‐1301 alone showed lower DC functions, such as expression of costimulatory factors or stimulation to spleen T cells.Conclusions
These data suggest that ONO‐1301 may suppress AHR and airway allergic inflammation through modulation of DCs, mainly mediated through the IP receptor. This agent may be effective as an anti‐inflammatory drug in the treatment of asthma. Cite this as: M. Hayashi, T. Koya, H. Kawakami, T. Sakagami, T. Hasegawa, H. Kagamu, T. Takada, Y. Sakai, E. Suzuki, E. W. Gelfand and F. Gejyo, Clinical & Experimental Allergy, 2010 (40) 317– 326.
Airway smooth muscle proliferation and survival is not modulated by mast cells
Authors: Kaur D. , Hollins F. , Saunders R. , Woodman L. , Sutcliffe A. , Cruse G. , Bradding P. , Brightling C. 
Published: January 2010

SummaryBackground
Airway smooth muscle (ASM) hyperplasia and mast cell localization within the ASM bundle are important features of asthma. The cause of this increased ASM mass is uncertain and whether it is a consequence of ASM–mast cell interactions is unknown.Objective
We sought to investigate ASM proliferation and survival in asthma and the effects of co‐culture with mast cells.Methods
Primary ASM cultures were derived from 11 subjects with asthma and 12 non‐asthmatic controls. ASM cells were cultured for up to 10 days in the presence or absence of serum either alone or in co‐culture with the human mast cell line‐1, unstimulated human lung mast cells (HLMC) or IgE/anti‐IgE‐activated HLMC. Proliferation was assessed by cell counts, CFSE assay and thymidine incorporation. Apoptosis and necrosis were analysed by Annexin V/propidium iodide staining using flow cytometry and by assessment of nuclear morphology using immunofluorescence. Mast cell activation was confirmed by the measurement of histamine release.Results
Using a number of techniques, we found that ASM proliferation and survival was not significantly different between cells derived from subjects with or without asthma. Co‐culture with mast cells did not affect the rate of proliferation or survival of ASM cells.Conclusion
Our findings do not support a role for increased airway smooth proliferation and survival as the major mechanism driving ASM hyperplasia in asthma. Cite this as: D. Kaur, F. Hollins, R. Saunders, L. Woodman, A. Sutcliffe, G. Cruse, P. Bradding and C. Brightling, Clinical & Experimental Allergy, 2010 (40) 279– 288.
Childhood asthma and early life exposure to indoor allergens, endotoxin and β(1,3)‐glucans
Authors: Bertelsen R. J. , Lødrup Carlsen K. C. , Carlsen K.‐H. , Granum B. , Doekes G. , Håland G. , Mowinckel P. , Løvik M. 
Published: January 2010

SummaryBackground
Divergent results have been reported regarding early life exposure to indoor environmental agents and the risk of asthma and allergic sensitization later in life.Objective
To assess whether early exposure to indoor allergens, β(1,3)‐glucans and endotoxin modifies the risk of allergic diseases at 10 years of age.Methods
The concentrations of mite, cat and dog allergens, endotoxin and β(1,3)‐glucans were determined in dust from the homes of 260 two‐year‐old children with lung function measured at birth (tidal flow volume loops) in the Environment and Childhood Asthma study in Oslo. At 10 years, the health status was assessed in a follow‐up study including a structured interview of the parents and an extended clinical examination.Results
Cat and dog keeping at 2 years of age was reported in 6.5% and 5.5% of the families, respectively. Mite allergens were detected in only 4/260 dust samples. The adjusted odds ratio for asthma at age 10 was 1.20 (95% confidence interval: 1.01–1.43) and 1.22 (1.02–1.46) for bronchial hyperresponsiveness (BHR) per 10 μg/g dust increase in cat allergen exposure at 2 years of age. No association was seen with allergic sensitization. Moreover, endotoxin and β(1,3)‐glucan exposure did not modify the risk of asthma or allergic sensitization. None of the measured environmental factors were associated with lung function at 10 years of age or a relative change in lung function from birth.Conclusion
In a community with a low prevalence of pet keeping and low mite allergen levels, exposure to cat allergens early in life increased the risk of late childhood asthma and BHR, but not the risk of allergic sensitization. No risk modification was seen for dog allergens, endotoxin and β(1,3)‐glucans. Cite this as: R. J. Bertelsen, K. C. Lødrup CarlsenK.‐H. Carlsen, B. Granum, G. Doekes, G. Håland, P. Mowinckel and M. Løvik, Clinical & Experimental Allergy, 2010 (40) 307– 316.
Processing‐dependent and ‐independent pathways for recognition of iodinated contrast media by specific human T cells
Authors: Keller M. , Lerch M. , Britschgi M. , Tâche V. , Gerber B. O. , Lüthi M. , Lochmatter P. , Kanny G. , Bircher A. J. , Christiansen C. , Pichler W. J. 
Published: January 2010

SummaryBackground
One to three percent of patients exposed to intravenously injected iodinated contrast media (CM) develop delayed hypersensitivity reactions. Positive patch test reactions, immunohistological findings, and CM‐specific proliferation of T cells in vitro suggest a pathogenetic role for T cells. We have previously demonstrated that CM‐specific T cell clones (TCCs) show a broad range of cross‐reactivity to different CM. However, the mechanism of specific CM recognition by T cell receptors (TCRs) has not been analysed so far.Objective
To determine how T cells specifically recognize CM.Methods
CM‐specific TCCs were generated from human blood of three CM‐allergic patients and a specific TCR was transfected into a mouse T cell hybridoma. Functional analysis such as proliferation assays, IL‐2 secretion assays, and calcium influx experiments were performed using irradiated, glutaraldehyde‐fixed, CM‐pre‐incubated, human leucocyte antigen (HLA)‐DR‐matched or ‐mismatched antigen‐presenting cells (APCs), and HLA‐blocking antibodies.Results
We identified two mechanisms of T cell stimulation: some TCCs and the transfectant reacted to CM independent of uptake by APCs because proliferation/IL‐2 secretion occurred in the presence of glutaraldehyde‐fixed APCs, and intracellular calcium increased within seconds after drug addition. Other TCCs required functional APCs, compatible with uptake and presentation of CM on MHC‐class II molecules, as implied by three findings: (1) glutaraldehyde fixation of APCs abrogated presentation; (2) CM could not be washed away from CM‐pre‐incubated APCs; and (3) the optimal pulsing time was 10–20 h. Because allogeneic, MHC‐matched, CM‐pulsed APCs could induce proliferative responses as well, the ability of CM uptake and presentation is not unique to APCs from patients with CM‐induced delayed hypersensitivity.Conclusion
Our data suggest that CM may be stimulatory for T cells either by direct binding to the MHC–TCR complex or by binding after uptake and processing by APCs. This questions the assumed inert nature of CM. Cite this as: M. Keller, M. Lerch, M. Britschgi, V. Tâche, B. O. Gerber, M. Lüthiuthi, P. Lochmatter, G. Kanny, A. J. Bircher, C. Christiansen and W. J. Pichler, Clinical & Experimental Allergy, 2010 (40) 257–268.
Experimental hookworm infection: a randomized placebo‐controlled trial in asthma
Authors: Feary J. R. , Venn A. J. , Mortimer K. , Brown A. P , Hooi D. , Falcone F. H. , Pritchard D. I. , Britton J. R. 
Published: January 2010

SummaryBackground
Epidemiological studies suggest that hookworm infection protects against asthma, and therefore that hookworm infection may have a direct or an indirect therapeutic potential in this disease. We now report the first clinical trial of experimental hookworm infection in people with allergic asthma.Objectives
To determine the effects of experimental hookworm infection in asthma.Methods
Thirty‐two individuals with asthma and measurable airway responsiveness to adenosine monophosphate (AMP) were randomized and double blinded to cutaneous administration of either ten Necator americanus larvae, or histamine solution (placebo), and followed for 16 weeks. The primary outcome was the change in provocation dose of inhaled AMP required to reduce forced expiratory volume in 1 s by 20% (PD20AMP) from baseline to week 16. Secondary outcomes included change in several measures of asthma control and allergen skin sensitivity and the occurrence of adverse effects.Results
Mean PD20AMP improved in both groups, more in the hookworm [1.49 doubling doses (DD)] than the placebo group (0.98 DD), but the difference between groups was not significant (0.51 DD; 95% confidence interval: −1.79 to 2.80; P=0.65). There were no significant differences between the two groups for other measures of asthma control or allergen skin sensitization. Infection was generally well tolerated.Conclusions
Experimental infection with ten hookworm larvae in asthma did not result in significant improvement in bronchial responsiveness or other measures of asthma control in this study. However, infection was well tolerated and resulted in a non‐significant improvement in airway responsiveness, indicating that further studies that mimic more closely natural infection are feasible and should be undertaken. Cite this as: J. R. Feary, A. J. Venn, K. Mortimer, A. P Brown, D. Hooi, F. H. Falcone, D. I. Pritchard and J. R. Britton, Clinical & Experimental Allergy, 2010 (40) 299– 306.
Differences in allergy trends between East and West Germany and possible explanations
Authors: Krämer U. , Oppermann H. , Ranft U. , Schäfer T. , Ring J. , Behrendt H. 
Published: January 2010

SummaryBackground
At the time of the German reunification in 1990, manifestations of most allergic diseases were less prevalent in East than in West Germany. It was hypothesized that these East–West differences would diminish with lifestyle and pollution changes in East Germany.Objective
To investigate whether changes in the prevalence of asthma, hayfever, eczema or allergic sensitization in East Germany approached the levels seen in West Germany and to identify possible lifestyle or environmental factors that may influence this.Methods
Between 1991 and 2000, 6‐year‐old children from four areas in East Germany participated in an annual survey. Every 3rd year, a parallel survey was performed in four areas of West Germany. In total, 31 903 children were included. Parents completed a questionnaire regarding lifestyle factors and diagnoses and symptoms of asthma, hayfever and eczema. In sub‐areas, eczema was clinically assessed by a dermatologist. Specific IgE sensitization was determined for 6121 children. Logistic regression was used to analyse differences in time trends and the influence of lifestyle and pollution changes.Results
Lifestyle and pollution changed significantly differently between East and West Germany. The trends in hayfever and in strong (specific IgE >3.5) sensitization against pollen, and particularly birch pollen, were steeper in East than in West Germany. The trend towards marked pollen sensitization was four times stronger (95% confidence interval 1.2–13.9) in East than in West Germany. Increasing numbers of only children, less single‐room heating with fossil fuels and increasing importance of traffic‐related pollution in East Germany partly explained these differences in time trends.Conclusions
Hayfever and sensitization against pollen were the most sensitive allergic manifestations to changes experienced specifically in East Germany. Influences of lifestyle (single‐room heating, living as a single child) were important in explaining different trend developments. Cite this as: U. Krämer, H. Oppermann, U. Ranft, T. Schäfer, J. Ring and H. Behrendt, Clinical & Experimental Allergy, 2010 (40) 289– 298.
Non‐uniqueness with refraction inversion – the Mt Bulga shear zone
Authors: Palmer Derecke 
Published: January 2010

ABSTRACTThe tau‐p inversion algorithm is widely employed to generate starting models with many computer programs that implement refraction tomography. However, this algorithm can frequently fail to detect even major lateral variations in seismic velocities, such as a 50 m wide shear zone, which is the subject of this study.By contrast, the shear zone is successfully defined with the inversion algorithms of the generalized reciprocal method. The shear zone is confirmed with a 2D analysis of the head wave amplitudes, a spectral analysis of the refraction convolution section and with numerous closely spaced orthogonal seismic profiles recorded for a later 3D refraction investigation.Further improvements in resolution, which facilitate the recognition of additional zones with moderate reductions in seismic velocity, are achieved with a novel application of the Hilbert transform to the refractor velocity analysis algorithm. However, the improved resolution also requires the use of a lower average vertical seismic velocity, which accommodates a velocity reversal in the weathering. The lower seismic velocity is derived with the generalized reciprocal method, whereas most refraction tomography programs assume vertical velocity gradients as the default.Although all of the tomograms are consistent with the traveltime data, the resolution of each tomogram is comparable only with that of the starting model. Therefore, it is essential to employ inversion algorithms that can generate detailed starting models, where detailed lateral resolution is the objective.Non‐uniqueness can often be readily resolved with head wave amplitudes, attribute processing of the refraction convolution section and additional seismic traverses, prior to the acquisition of any borehole data. It is concluded that, unless specific measures are taken to address non‐uniqueness, the production of a single refraction tomogram that fits the traveltime data to sufficient accuracy does not necessarily demonstrate that the result is either correct, or even the most probable.
Cytotoxicity and genotoxicity of sodium percarbonate: a comparison with bleaching agents commonly used in discoloured pulpless teeth
Authors: Fernández M. R. , Carvalho R. V. , Ogliari F. A. , Beira F. A. , Etges A. , Bueno M. 
Published: January 2010

Fernández MR, Carvalho RV, Ogliari FA, Beira FA, Etges A, Bueno M. Cytotoxicity and genotoxicity of sodium percarbonate: a comparison with bleaching agents commonly used in discoloured pulpless teeth. International Endodontic Journal, 43, 102–108, 2010.AbstractAim  To evaluate the cytotoxicity and genotoxicity of sodium percarbonate (SPC) in comparison with bleaching agents used on discoloured pulpless teeth.Methodology  The cytotoxicity and genotoxicity of bleaching agents were evaluated both in their pure form as well as at concentrations commonly used in clinical practice. Hydrogen peroxide (HP), carbamide peroxide (CP), sodium perborate (SP) and SPC were diluted in Dulbecco’s modified Eagle’s medium (DMEM) in series. To evaluate the cytotoxicity, the survival of 3T3/NIH mouse fibroblasts was measured photometrically using an 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide assay after a 24 h‐exposure period. Genotoxicity was indicated by micronuclei (MN) formation, and modification of the normal cell was analysed by light microscopy (400×). Statistical analysis was performed by one‐way anova, followed by a multiple‐comparison Tukey post hoc test (P < 0.05).Results  All groups exhibited a dose‐dependent cytotoxicity. However, CP showed a similar cytotoxic effect when compared with DMEM‐untreated control (UC) group. HP and SPC were significantly more cytotoxic than SP. The genotoxicity test showed that SPC and SP had an intermediate rate of MN frequency when compared with the UC group. The mean rate of MN frequency for HP was higher and statistically more significant than for the other groups tested. No difference was observed when CP and UC groups were compared.Conclusions  Sodium percarbonate showed cytotoxicity and genotoxicity similar to those of the other products tested. However, before SPC is used clinically, studies should be conducted to confirm its safety in vivo.
Activated platelets increase proliferation and protein synthesis of human dental pulp–derived cells
Authors: Agis H. , Stampfl B. , Watzek G. , Gruber R. 
Published: January 2010

Agis H, Stampfl B, Watzek G, Gruber R. Activated platelets increase proliferation and protein synthesis of human dental pulp–derived cells. International Endodontic Journal, 43, 115–124, 2010.AbstractAim  To evaluate the impact of activated platelets on the mitogenic expansion of human dental pulp–derived cells (DPC) in vitro.Methodology  The effect of supernatants released from activated platelets (PRS) and the corresponding platelet membranes (MEM) on proliferation and protein synthesis of DPC was evaluated. The contributions of the phosphoinositide 3‐kinase (PI3K)/AKT and mitogen‐activated protein kinase (MAPK) pathways to the response of DPC were assessed using kinase inhibitors. Also examined was whether the presence of calcium hydroxide or the inflammatory mediators tumour necrosis factor alpha, interleukin‐1, interleukin‐6 and lipopolysaccharide of Escherichia coli modulated the expansion of DPC.Results  Physiologic concentrations of PRS and MEM stimulated proliferation and protein synthesis by 18.4‐fold (P < 0.01) and 2.9‐fold (P < 0.01), respectively. This mitogenic expansion was paralleled by activation of AKT and the MAP kinases extracellular signal‐regulated kinase (ERK), c‐Jun N‐terminal kinase (JNK) and p38. Inhibitor studies revealed that the mitogenic response of DPC involved PI3K/AKT, JNK and p38 signalling (P < 0.05). Calcium hydroxide and inflammatory factors did not significantly modulate the mitogenic response of DPC to PRS and MEM.Conclusion  Supernatants released from activated platelets and the corresponding platelet membranes stimulated DPC proliferation and protein synthesis involving PI3K/AKT and MAPK signalling. These findings may serve as a basis for preclinical studies that address the role of activated platelets in dental pulp repair.