bluuebunny/crossref_metadata_2025_split huggingface dataset:
Expression characteristics of ARF1 and SAR1 during development and the de‐etiolation process
Authors: Keskin B. Cevher , Yuca E. , Ertekin Ö. , Yüksel B. , Memon A. R. 
Published: July 2011

AbstractARF1 (ADP‐ribosylation factor 1) and SAR1 (secretion‐associated RAS super family) are involved in the formation and budding of vesicles throughout plant endomembrane systems. The molecular mechanisms of this transport have been studied extensively in mammalian and yeast cells. However, very little is known about the mechanisms of coat protein complex (COP) formation and recruitment of COP‐vesicle cargoes in plants. To provide insights into vesicular trafficking in Pisum sativum L., we investigated mRNA and protein expression patterns of ARF1 and SAR1 in roots and shoots at early growth stages and in the de‐etiolation process. We showed that ARF1 was concentrated mostly in the crude Golgi fractions, and SAR1 was concentrated predominantly in the crude ER fractions of de‐etiolated shoots. ARF1 and SAR1 proteins were several times more abundant in shoots relative to roots. In total protein homogenates, the expression level of SAR1 and ARF1 was higher in shoots of dark‐grown pea plants than light‐grown plants. In contrast, ARF1 was higher in roots of light‐grown pea relative to roots of dark‐grown pea. With ageing, the ARF1 mRNA in roots was reduced, while SAR1 expression increased. Unlike ARF1 transcripts, ARF1 protein levels did not fluctuate significantly in root and shoot tissue during early development. The relative abundance of SAR1 protein in root tissues may suggest a high level of vesicular transport from the ER to the Golgi. Experimental results suggested that white light probably affects the regulation of ARF1 and SAR1 protein levels. On the other hand, short‐term white light affects SAR1 but not ARF1.
Evaluation of dietary stevioside supplementation on anti‐human serum albumin immunoglobulin G, Alpha‐1‐glycoprotein, body weight and thyroid hormones in broiler chickens
Authors: Daneshyar M. , Geuns J. M. C. , Willemsen H. , Ansari Z. , Darras V. M. , Buyse J. G. , Everaert N. 
Published: July 2011

SummarySixty male broiler chickens fed a diet supplemented with 130 mg/kg stevioside (S group) or an unsupplemented diet (C group) from day 1 of age onwards. On day 21 of age, ten birds from either the S (SH) or C (CH) group were injected subcutaneously with 100 μg human serum albumin (HSA) and ten others from either S (SP) or C (CP) group injected with 100 μl phosphate‐buffered saline (PBS) in the same way. There were no significant effect of supplementation nor interaction with age on average body weights, T3 and T4 concentrations of non‐injected chickens. After the primary immunization, α1‐glycoprotein concentrations increased in all treatment groups except the CP group, and were significantly higher in the CH group in relation to the other groups. Fourteen and 18 days after the primary immunization, HSA injected chickens of both dietary treatments had significantly higher anti‐HSA immunoglobulin G (IgG) levels than their PBS injected controls. No effect of stevioside supplementation was observed for IgG level. In conclusion, dietary stevioside inclusion can attenuate the pro‐inflammatory response after stimulation of the innate immune response in broiler chickens.
The antidepressant fluoxetine but not citalopram suppresses synapse formation and synaptic transmission between Lymnaea neurons by perturbing presynaptic and postsynaptic machinery
Authors: Getz Angela , Xu Fenglian , Zaidi Wali , Syed Naweed I. 
Published: July 2011

AbstractDepression is a debilitating mental disorder, and selective serotonin reuptake inhibitors (SSRIs) constitute the first‐line antidepressant treatment choice for the clinical management of this illness; however, the mechanisms underlying their therapeutic actions and side effects remain poorly understood. Here, we compared the effects of two SSRIs, fluoxetine and citalopram, on synaptic connectivity and the efficacy of cholinergic synaptic transmission between identified presynaptic and postsynaptic neurons from the mollusc Lymnaea. The in vitro paired cells were exposed to clinically relevant concentrations of the two SSRIs under chronic and acute experimental conditions, and the incidence of synapse formation and the efficacy of synaptic transmission were tested electrophysiologically and with fluorescent Ca2+ imaging. We demonstrate that chronic exposure to fluoxetine, but not to citalopram, inhibits synapse formation and reduces synaptic strength, and that these effects are reversible following prolonged drug washout. At the structural level, we demonstrate that fluoxetine, but not citalopram, prevents the expression and localization of the presynaptic protein synaptophysin. Acute exposure to fluoxetine substantially reduced synaptic transmission and synaptic plasticity (post‐tetanic potentiation) in established synapses, whereas citalopram reduced synaptic transmission, but not short‐term synaptic plasticity. We further demonstrate that fluoxetine, but not citalopram, directly inhibits voltage‐gated Ca2+ currents in the presynaptic neuron, as well as postsynaptic responsiveness to exogenously applied neurotransmitter. This study provides the first direct evidence that fluoxetine and citalopram exert characteristic, non‐specific side effects that are unrelated to their function as SSRIs, and that fluoxetine is more detrimental to synaptic physiology and structure than citalopram.
Effects of divalent cations on slow unblock of native NMDA receptors in mouse neocortical pyramidal neurons
Authors: Kim Nam‐Kyung , Robinson Hugh P. C. 
Published: July 2011

AbstractThe N‐methyl‐d‐aspartate receptor (NMDAR) exhibits strong voltage‐dependent block by extracellular Mg2+, which is relieved by sustained depolarization and glutamate binding, and which is central to the function of the NMDAR in synaptic plasticity. Rapid membrane depolarization during agonist application reveals a slow unblock of NMDARs, which has important functional implications, for example in the generation of NMDAR spikes, and in determining the narrow time window for spike‐timing‐dependent plasticity. However, its mechanism is still unclear. Here, we study unblock of divalent cations in native NMDARs in nucleated patches isolated from mouse cortical layer 2/3 pyramidal neurons. Comparing unblock kinetics of NMDARs in the presence of extracellular Mg2+or in nominally zero Mg2+, and with Mn2+or Co2+substituting for Mg2+, we found that the properties of slow unblock were determined by the identity of the blocking metal ion at the binding site, presumably by affecting the operation of a structural link to channel gating. The time course of slow unblock was not affected by zinc, or the zinc chelator TPEN [N,N,N′,N′‐tetrakis‐(2‐pyridylmethyl)‐ethylenediamine], while the slower fraction of unblock was reduced by ifenprodil, an NR2B‐selective antagonist. Slow unblock was only weakly temperature dependent, speeding up with rise in temperature with a Q10 of ≈1.5. Finally, using action potential waveform voltage‐clamp, we show that this slow relief from divalent cation block is a prominent feature in physiologically realistic patterns of changing membrane potential.
Excess comorbidities associated with malignant hyperthermia diagnosis in pediatric hospital discharge records
Authors: Li Guohua , Brady Joanne E. , Rosenberg Henry , Sun Lena S. 
Published: July 2011

SummaryBackground:  Case reports have linked malignant hyperthermia (MH) to several genetic diseases.Objective/aim:  The objective of this study was to quantitatively assess excess comorbidities associated with MH diagnosis in pediatric hospital discharge records.Patients and methods:  Data for this study came from the Kids’ Inpatient Database (KID) for the years 2000, 2003, and 2006. The KID contains an 80% random sample of patients under the age of 21 discharged from short‐term, non‐Federal hospitals in the United States, with up to 19 diagnoses recorded for each patient. Using all pediatric inpatients as the reference, we calculated the standardized morbidity ratios (SMRs) and 95% confidence intervals (CIs) for children with MH diagnosis according to major disease groups and specific medical conditions.Results:  Of the 5 916 989 nonbirth‐related hospital discharges studied, 175 had a recorded diagnosis of MH. Compared with the general pediatric inpatient population, children with MH diagnosis were significantly more likely to be diagnosed with diseases of the musculoskeletal system and connective tissue (SMR 5.7; 95% CI: 3.9–7.9), diseases of the circulatory system (SMR 3.3; 95% CI: 2.1–4.8), and congenital anomalies (SMR 3.2; 95% CI: 2.3–4.4). The specific diagnosis that was most strongly associated with MH was muscular dystrophies (SMR 31.3; 95% CI 12.6–64.6).Conclusions:  Diseases of the musculoskeletal system and connective tissue are significantly associated with MH diagnosis in children. Further research is warranted to determine the clinical utility of these comorbidities in assessing MH susceptibility in children.
Impaired antibody memory to varicella zoster virus in HIV‐infected children: low antibody levels and avidity*
Authors: L'Huillier AG , Ferry T , Courvoisier DS , Aebi C , Cheseaux J‐J , Kind C , Rudin C , Nadal D , Hirschel B , Sottas C , Siegrist C‐A , Posfay‐Barbe KM ,   the Pediatric Infectious Diseases,   Group of Switzerland (PIGS),   the Swiss HIV Cohort Study (SHCS) and the Swiss Mother & Child HIV Cohort Study (MoCHiV)
Published: July 2011

ObjectiveHIV‐infected children have impaired antibody responses after exposure to certain antigens. Our aim was to determine whether HIV‐infected children had lower varicella zoster virus (VZV) antibody levels compared with HIV‐infected adults or healthy children and, if so, whether this was attributable to an impaired primary response, accelerated antibody loss, or failure to reactivate the memory VZV response.MethodsIn a prospective, cross‐sectional and retrospective longitudinal study, we compared antibody responses, measured by enzyme‐linked immunosorbent assay (ELISA), elicited by VZV infection in 97 HIV‐infected children and 78 HIV‐infected adults treated with antiretroviral therapy, followed over 10 years, and 97 age‐matched healthy children. We also tested antibody avidity in HIV‐infected and healthy children.ResultsMedian anti‐VZV immunoglobulin G (IgG) levels were lower in HIV‐infected children than in adults (264 vs. 1535 IU/L; P<0.001) and levels became more frequently unprotective over time in the children [odds ratio (OR) 17.74; 95% confidence interval (CI) 4.36–72.25; P<0.001]. High HIV viral load was predictive of VZV antibody waning in HIV‐infected children. Anti‐VZV antibodies did not decline more rapidly in HIV‐infected children than in adults. Antibody levels increased with age in healthy (P=0.004) but not in HIV‐infected children. Thus, antibody levels were lower in HIV‐infected than in healthy children (median 1151 IU/L; P<0.001). Antibody avidity was lower in HIV‐infected than healthy children (P<0.001). A direct correlation between anti‐VZV IgG level and avidity was present in HIV‐infected children (P=0.001), but not in healthy children.ConclusionFailure to maintain anti‐VZV IgG levels in HIV‐infected children results from failure to reactivate memory responses. Further studies are required to investigate long‐term protection and the potential benefits of immunization.
Job creation and labour market flexibility: miracle or mirage on the Polish labour market?
Authors: Ingham Hilary , Ingham Mike 
Published: July 2011

ABSTRACTPoland's post‐communist economic performance has been generally good. However, for many years, its growth was jobless; it exhibited very high unemployment rates and made little progress towards the targets set for EU Member States and accession countries. Unexpectedly, in 2003, the country's labour market began to exhibit a new dynamism, with employment growing strongly and unemployment tumbling. This apparent improvement coincided with a liberalisation of its Labour Code. Unfortunately, the measures introduced to increase flexibility are at variance with the EU's Fixed‐term Work Directive and will likely need to be modified, which may conceivably reverse the recent developments that form the focus of this article.
Azithromycin distinctively modulates classical activation of human monocytes in vitro
Authors: Vrančić M , Banjanac M , Nujić K , Bosnar M , Murati T , Munić V , Stupin Polančec D , Belamarić D , Parnham MJ , Eraković Haber V 
Published: July 2011

BACKGROUND AND PURPOSE Azithromycin has been reported to modify activation of macrophages towards the M2 phenotype. Here, we have sought to identify the mechanisms underlying this modulatory effect of azithromycin on human monocytes, classically activated in vitro.EXPERIMENTAL APPROACH Human blood monocytes were primed with IFN‐γ for 24 h and activated with LPS for 24 h. Azithromycin, anti‐inflammatory and lysosome‐affecting agents were added 2 h before IFN‐γ. Cytokine and chemokine expression was determined by quantitative PCR and protein release by ELISA. Signalling molecules were determined by Western blotting and transcription factor activation quantified with a DNA‐binding ELISA kit.KEY RESULTS Azithromycin (1.5–50 µM) dose‐dependently inhibited gene expression and/or release of M1 macrophage markers (CCR7, CXCL 11 and IL‐12p70), but enhanced CCL2, without altering TNF‐α or IL‐6. Azithromycin also enhanced the gene expression and/or release of M2 macrophage markers (IL‐10 and CCL18), and the pan‐monocyte marker CD163, but inhibited that of CCL22. The Toll‐like receptor (TLR) 4 signalling pathway was modulated, down‐regulating NF‐κB and STAT1 transcription factors. The inhibitory profile of azithromycin differed from that of dexamethasone, the phosphodiesterase‐4 inhibitor roflumilast and the p38 kinase inhibitor SB203580 but was similar to that of the lysosomotropic drug chloroquine. Effects of concanamycin and NH4Cl, which also act on lysosomes, differed significantly.CONCLUSIONS AND IMPLICATIONS Azithromycin modulated classical activation of human monocytes by inhibition of TLR4‐mediated signalling and possible effects on lysosomal function, and generated a mediator expression profile that differs from that of monocyte/macrophage phenotypes so far described.
Medieval Archaeology and Ethnicity: Where are We?
Authors: Curta Florin 
Published: July 2011

AbstractDuring the last few decades, medieval archaeology has considerably grown into a respectable, and much needed academic discipline. Although no systematic reflection exists to date about ethnicity, the topic has dominated the field, primarily because of new claims (especially among German scholars) that ethnicity in the medieval past is beyond the conceptual reach of archaeologists interested in the Middle Ages. The recent contributions are however building upon theories of ethnicity developed in anthropology and sociology to approach the problem from an angle different from both the primordialist and the instrumentalist agendas. Issues of private vs. public, gender and ethnicity, and the role of the archaeological discourse in the construction of nationalist ideologies have been drawn much attention in recent years.
Unfolded proteins and endoplasmic reticulum stress in neurodegenerative disorders
Authors: Doyle Karen M. , Kennedy Donna , Gorman Adrienne M. , Gupta Sanjeev , Healy Sandra J. M. , Samali Afshin 
Published: July 2011

Abstract
Introduction
ER stress and the UPR
ER stress–induced apoptosis
ER stress and autophagy
The UPR and neurodegenerative disease
Future perspectives
The stimuli for neuronal cell death in neurodegenerative disorders are multi‐factorial and may include genetic predisposition, environmental factors, cellular stressors such as oxidative stress and free radical production, bioenergy failure, glutamate‐induced excitotoxicity, neuroinflammation, disruption of Ca2+‐regulating systems, mitochondrial dysfunction and misfolded protein accumulation. Cellular stress disrupts functioning of the endoplasmic reticulum (ER), a critical organelle for protein quality control, leading to induction of the unfolded protein response (UPR). ER stress may contribute to neurodegeneration in a range of neurodegenerative disorders. This review summarizes the molecular events occurring during ER stress and the unfolded protein response and it specifically evaluates the evidence suggesting the ER stress response plays a role in neurodegenerative disorders.
Submerged and transmucosal healing yield the same clinical outcomes with two‐piece implants in the anterior maxilla and mandible: interim 1‐year results of a randomized, controlled clinical trial
Authors: Hämmerle Christoph H. F. , Jung Ronald E. , Sanz Mariano , Chen Stephen , Martin William C. , Jackowski Jochen ,   On behalf of this multicenter study group, Ivanoff Carl‐Johan , Cordaro Luca , Ganeles Jeffrey , Weingart Dieter , Wiltfang Jörg , Gahlert Michael 
Published: July 2011

Abstract
Objectives: To test whether or not transmucosal healing at two‐piece implants is as successful as submerged placement regarding crestal bone levels and patient satisfaction.
Material and methods: Adults requiring implants in the anterior maxilla or mandible in regions 21–25, 11–15, 31–35 or 41–45 (WHO) were recruited for this randomized, controlled multi‐center clinical trial of a 5‐year duration. Randomization was performed at implantation allowing for either submerged or transmucosal healing. Final reconstructions were seated 6 months after implantation. Radiographic interproximal crestal bone levels and peri‐implant soft tissue parameters were measured at implant placement (IP) (baseline), 6 and 12 months. Patient satisfaction was assessed by a questionnaire. A two‐sided t‐test (80% power, significance level α=0.05) was performed on bone‐level changes at 6 and 12 months.
Results: One hundred and twenty‐seven subjects were included in the 12‐month analysis (submerged [S]: 52.5%, transmucosal [TM]: 47.2%). From IP to 6 months, the change in the crestal bone level was −0.32 mm (P<0.001) for the S group and −0.29 mm (P<0.001) for the TM group. From IP to 12 months, bone‐level changes were statistically significant in both groups (S −0.47 mm, P<0.001; TM −0.48 mm, P<0.001). The mean differences of change in the bone levels between the two groups were not statistically significant at either time point, indicating the equivalence of both procedures. For both groups, very good results were obtained for soft tissue parameters and for patient satisfaction.
Conclusions: Transmucosal healing of two‐piece implants is as successful as the submerged healing mode with respect to tissue integration and patient satisfaction within the first 12 months after IP.
To cite this article: Hämmerle CHF, Jung RE, Sanz M, Chen S, Martin WC, Jackowski J, Ivanoff CJ, Cordaro L, Ganeles J, Weingart D, Wiltfang J, Gahlert M. Submerged and transmucosal healing yield the same clinical outcomes with two‐piece implants in the anterior maxilla and mandible: interim 1‐year results of a randomized, controlled clinical trial. Clin. Oral Impl. Res 23, 2012; 211–219.  doi: 10.1111/j.1600‐0501.2011.02210.x
Oral treatment with complement factor C5a receptor (CD88) antagonists inhibits experimental periodontitis in rats
Authors: Breivik T. , Gundersen Y. , Gjermo P. , Taylor S. M. , Woodruff T. M. , Opstad P. K. 
Published: July 2011

Breivik T, Gundersen Y, Gjermo P, Taylor SM, Woodruff TM, Opstad PK. Oral treatment with complement factor C5a receptor (CD88) antagonists inhibits experimental periodontitis in rats. J Periodont Res 2011; 46: 643–647. © 2011 John Wiley & Sons A/SBackground and Objective:  The complement activation product 5a (C5a) is a potent mediator of the innate immune response to infection, and may thus also importantly determine the development of periodontitis. The present study was designed to explore the effect of several novel, potent and orally active C5a receptor (CD88) antagonists (C5aRAs) on the development of ligature‐induced periodontitis in an animal model.Material and Methods:  Three different cyclic peptide C5aRAs, termed PMX205, PMX218 and PMX273, were investigated. Four groups of Wistar rats (n = 10 in each group) were used. Starting 3 d before induction of experimental periodontitis, rats either received one of the C5aRas (1–2 mg/kg) in the drinking water or received drinking water only. Periodontitis was assessed when the ligatures had been in place for 14 d.Results:  Compared with control rats, PMX205‐ and PMX218‐treated rats had significantly reduced periodontal bone loss.Conclusion:  The findings suggest that complement activation, and particularly C5a generation, may play a significant role in the development and progression of periodontitis. Blockade of the major C5a receptor, CD88, with specific inhibitors such as PMX205, may offer novel treatment options for periodontitis.
Topical and intermittent application of parathyroid hormone recovers alveolar bone loss in rat experimental periodontitis
Authors: Tokunaga K. , Seto H. , Ohba H. , Mihara C. , Hama H. , Horibe M. , Yoneda S. , Nagata T. 
Published: July 2011

Tokunaga K, Seto H, Ohba H, Mihara C, Hama H, Horibe M, Yoneda S, Nagata T. Topical and intermittent application of parathyroid hormone recovers alveolar bone loss in rat experimental periodontitis. J Periodont Res 2011; 46: 655–662. © 2011 John Wiley & Sons A/SBackground and Objective:  Periodontitis is characterized by periodontal tissue inflammation and alveolar bone loss. The intermittent administration of parathyroid hormone (PTH), a major regulator of bone remodeling, has been demonstrated to stimulate osteoblastic activity. Although the systemic administration of PTH has been reported to protect against periodontitis‐associated bone loss, the effect of the topical administration of PTH is unclear. In this study, the effect of intermittent administration of PTH on osteoblastic differentiation was examined in cultured calvaria cells and then the effect of topical and intermittent administration of PTH was determined by measuring the recovery of alveolar bone loss after inducing experimental periodontitis in rats.Material and Methods:  Alkaline phosphatase activity and bone nodule formation were measured in fetal rat calvaria cells. Experimental periodontitis was induced by placing nylon ligature around rat maxillary molars for 20 d. After ligature removal (day 0), PTH was topically injected into buccal gingiva three times a week for 10 wk. Micro‐computed tomography analysis and histological examination were performed on days 35 and 70.Results:  Intermittent exposure of PTH in calvaria cells increased alkaline phosphatase activity and bone nodule formation by 1.4‐ and 2.4‐fold, respectively. Ligature procedures induced marked alveolar bone loss around the molars on day 0 and greater bone recovery was observed in the PTH‐treated rats on day 70. An increase in osteoid formation on the surface of alveolar bone was detected in the PTH‐treated rats.Conclusion:  Intermittent treatment with PTH stimulated osteoblastic differentiation in fetal rat calvaria cell cultures, and topical and intermittent administration of PTH recovered alveolar bone loss in rat experimental periodontitis.