bluuebunny/crossref_metadata_2025_split huggingface dataset:
Urinary uric acid : creatinine ratios in healthy Turkish children
Authors: Poyrazoğlu Hakan M. , Düşünsel Ruhan , Yazici Cevat , Durmaz Halil , Dursun İsmail , Şahin Habibe , Gündüz Zübeyde , Gürgöze Metin K. 
Published: July 2009

AbstractBackground:  Determining uric acid : creatinine ratios in random urine samples may be useful to assess the excretion of uric acid in children. Because it was shown that urinary uric acid excretion varies with age and geographic area, it is important to have accurate reference values of uric acid excretion. The aim of the present study was therefore to obtain regional reference values for urinary uric acid : creatinine ratios in healthy Turkish children.Methods:  A total of 1306 children aged 1 month–15 years were analyzed for uric acid and creatinine, and urinary uric acid : creatinine ratios were determined from each sample. The second non‐fasting morning urine samples were taken from all the children. Urine samples were analyzed for uric acid using the uricase method, and for creatinine with the Jaffe reaction.Results:  The mean ± SD and 5th–95th percentiles of urinary uric acid : creatinine ratios (mg/mg) were 1.09 ± 0.48 and 0.27–1.87 at 1–6 months, 0.86 ± 0.41 and 0.19–1.64 at 7–12 months, 0.76 ± 0.32 and 0.32–1.43 at 1–3 years, 0.63 ± 0.29 and 0.20–1.23 at 4–6 years, 0.44 ± 0.24 and 0.14–0.93 at 7–11 years, and 0.30 ± 0.14 and 0.12–0.62 at 12–15 years. Uric acid : creatinine ratios were not significantly different between boys and the girls except at 12–15 years. Girls aged 12–15 years had higher urinary uric acid : creatinine ratio when compared with boys (P < 0.05). There was no correlation between urinary uric acid : creatinine ratio and protein intake.Conclusions:  Urinary uric acid : creatinine ratio changes with age. When assessing urinary uric acid : creatinine ratio, the clinician should consider the age of the child.
Reliability of family history of lifestyle‐related diseases on questionnaire
Authors: Saito Tomohiro , Nanri Seiichiro , Saito Ikuo 
Published: July 2009

AbstractBackground:  Family history of lifestyle‐related diseases is an important risk factor and is widely used in epidemiologic studies. To justify its use the validity of the family history needs to be assessed. The aim of the present study was therefore to examine reliability, that is, consistency in repeated measurements, of the family history obtained on questionnaire.Methods:  A questionnaire survey on the family history of lifestyle‐related diseases was conducted for 438 high school students about students' parents, grandparents, uncles and aunts, twice with a 1 year interval. The questionnaire was filled in by their parents. Discordance between the two questionnaires in age, age at death and a positive history of lifestyle‐related diseases expressed by age at onset by decade age among the family members was examined. Kappa was used as a measure of agreement.Results:  The kappas for relatives were high, mostly >0.7 for hypertension and >0.5 for myocardial infarction, angina pectoris, stroke, diabetes mellitus and hypercholesterolemia. The discordance tended to be higher among grandparents than parents, uncles and aunts. The discordance with regard to relatives was mostly <4% for angina pectoris, myocardial infarction, stroke and diabetes mellitus; for hypertension and hypercholesterolemia the discordance was <6%.Conclusions:  The questionnaire provides a reliable and valid method of collecting family history on relatives of high school students. Thus, family history obtained through questionnaires can be used justifiably as a risk factor for lifestyle‐related diseases among children and youths.
Neutropenia in the acute phase of Kawasaki disease and prevention of coronary artery aneurysm
Authors: Onouchi Zenshiro , Hamaoka Kenji , Ozawa Seiichiro , Sakata Koichi , Kiyosawa Nobuyuki , Ito Hisato 
Published: July 2009

AbstractBackground:  The significance of neutropenia in Kawasaki disease (KD) has not been fully elucidated as yet.Methods:  Subjects were retrospectively sampled from two clinical trials. These patients treated with aspirin alone (ASA) and PolyglobinN‐Bayel (PolyN) given as i.v. immunoglobulin were categorized as ASA‐early (n = 0), ASA‐late (n = 8), PolyN‐early (n = 18), or PolyN‐late (n = 27) based on the therapy administered and the incidence of neutropenia before the 10th day of illness (DI) and after 11 DI. Data regarding the time of onset of neutropenia, and incidence of coronary artery lesion (CAL) formation were obtained. P < 0.05 was considered statistically significant.Results:  No patients in the ASA group exhibited neutropenia within 10 DI. The time of onset of neutropenia in the PolyN‐early group was 8 ± 1.3 DI. That in the PolyN‐late group (19.8 ± 8 DI) was earlier than in the ASA‐late group (26.6 ± 14 DI; P < 0.025). PolyN‐early patients had a lower incidence of CAL formation than ASA‐non patients (patients without neutropenia in the ASA group; P = 0.00019) and ASA‐late patients (P = 0.04). That in the PolyN‐early group tended to be lower than in the PolyN‐late group (P < 0.1).Conclusion:  Early neutropenia indicated that circulating neutrophils within 10 DI may play an indispensable role in the following sequence to CAL formation in KD.
Homozygous variant of UGT1A1 gene mutation and severe neonatal hyperbilirubinemia
Authors: Boo Nem‐Yun , Wong Fei‐Liang , Wang May‐Kay , Othman Ainoon 
Published: July 2009

AbstractBackground:  The aim of the present study was to compare, in a case–control study, the prevalence of nucleotide 211 guanine to adenine (G→A) mutation of uridine diphosphoglucuronosyl transferase (UGT1A1) gene in Malaysian Chinese newborns with and without severe hyperbilirubinemia (total serum bilirubin >250 µmol/L during first 48 h of life or ≥300 µmol/L thereafter), and to determine whether this mutation was a significant risk factor associated with severe hyperbilirubinemia.Methods:  Seventy‐four term infants of Chinese descent admitted with severe hyperbilirubinemia were recruited. Infants without severe hyperbilirubinemia (n = 125) were randomly selected from among healthy Chinese term infants. UGT1A1 nucleotide 211 polymorphism was assayed using the Taqman single nucleotide polymorphism genotyping method. Using gestational age, types of feeds, G6PD mutation, G6PD enzyme levels, and UGT1A1 gene mutation status as independent variables, logistic regression analysis was carried out to determine the significant risk factors associated with severe hyperbilirubinemia.Results:  UGT1A1 gene mutation was significantly more common among hyperbilirubinemic infants (39.2%) than controls (25.6%; P = 0.04). Gestational age (adjusted odds ratio [OR], 0.7; 95% confidence intervals [CI]: 0.5–0.9; P = 0.01), G6PD mutation (adjusted OR, 7.2; 95%CI: 2.7–19.0; P < 0.0001), exclusive breast‐feeding (adjusted OR, 11.7; 95%CI: 2.7–49.9; P = 0.001), and homozygous variant of UGT1A1 gene mutation (adjusted OR, 32.2; 95%CI: 3.8–273.2; P = 0.001) were significant risk factors. Heterozygous variant of UGT1A1 gene mutation, actual levels of G6PD enzyme, and mixed feeding were not.Conclusion:  Homozygous variant of nucleotide 211 G→A mutation of UGT1A1 gene is a significant risk factor associated with severe hyperbilirubinemia among Malaysian Chinese newborns.
Diagnostic quality of Actigraph‐based physical activity cut‐offs for children: What overweight/obesity references can tell?
Authors: Guinhouya Comlavi B. , Apété Géoffroy K. , Hubert Hervé 
Published: July 2009

AbstractBackground:  There is conflicting literature about Actigraph‐based cut‐off points (CoP) that define the lower limit of moderate–to–vigorous physical activity (MVPA) among children. The aim of the present study was to compare the diagnostic quality of Actigraph‐based CoP relative to different body mass index (BMI) classification systems of the weight status of children.Methods:  One hundred and thirteen children aged 8–11 years recruited from three randomly selected elementary schools wore the Actigraph, model 7164 (Actigraph Manufacturing Technology) for 3 days. Five CoP, expressed in counts per minute (c.p.m.; CoP 1000 CoP 2000, CoP 3000, CoP 3200, and CoP 3600) were used to compute their MVPA. The area under the receiver operating characteristic curves (AUC) together with specific indices allowed assessment of the performance of these CoP in reference to overweight/obesity status as defined using BMI‐based criteria from the International Obesity Task Force (IOTF), French References (FR) and World Health Organization (WHO) standards.Results:  Overweight/obesity frequency ranged from 30% to 42%, with no sex‐related difference. All AUC (range, 0.623–0.660) were significantly higher than 0.500 except from those of CoP 1000 and 2000 using the IOTF criteria (0.602 ± 0.058 and 0.601 ± 0.057, respectively) and the FR (0.608 ± 0.060 for CoP 1000). Furthermore, with the WHO standards, all the CoP provided non‐significant AUC (range, 0.566–0.597). According to the IOTF and the FR criteria, respectively, CoP 3600 had the highest probability of correct decision (0.62 and 0.68), the lowest misclassification errors (0.38 and 0.32), the highest validity coefficient (0.21 and 0.29), and the highest expected maximum utility (59 and 83).Conclusion:  When children are classified using BMI‐based criteria, the threshold of 3600 c.p.m. should be more appropriate in discriminating non‐overweight from overweight/obese.
Cilnidipine mediates a neuroprotective effect by scavenging free radicals and activating the phosphatidylinositol 3‐kinase pathway
Authors: Lee Young Joo , Park Kee Hyung , Park Hyun‐Hee , Kim Yun Jin , Lee Kyu‐Yong , Kim Seung Hyun , Koh Seong‐Ho 
Published: July 2009

AbstractWe investigated the neuroprotective effect and mechanisms of action of cilnidipine, a long‐acting, second‐generation 1,4‐dihydropyridine inhibitor of L‐ and N‐type calcium channels, in PC12 cells that were neuronally differentiated by treatment with nerve growth factor (nPC12 cells). To evaluate the effect of cilnidipine on viability, nPC12 cells were treated with several concentrations of this drug before performing viability assays. Free radical levels and intracellular signaling proteins were measured with the fluorescent probe, 2′,7′‐dichlorodihydrofluorescein diacetate and western blotting, respectively. Cell viability was not affected by low concentrations of cilnidipine up to 150 μM, but it was slightly decreased at 200 μM cilnidipine. Following H2O2 exposure, the viability of nPC12 cells decreased significantly; however, treatment with cilnidipine increased the viability of H2O2‐injured nPC12 cells in a concentration‐dependent manner. Treatment with H2O2 resulted in a concentration‐dependent increase in free radical levels in nPC12 cells, and cilnidipine treatment reduced free radical levels in H2O2‐injured nPC12 cells in a dose‐dependent manner. Cilnidipine treatment increased the expression of p85aPI3K (phosphatidylinositol 3‐kinase) phosphorylated Akt, phosphorylated glycogen synthase kinase‐3 (pGSK‐3β), and heat shock transcription factor (HSTF‐1) which are proteins related to neuronal cell survival, and decreased levels of cytosolic cytochrome c, activated caspase 3, and cleaved poly (ADP‐ribose) polymerase (PARP), which are associated with neuronal cell death, in H2O2‐injured nPC12 cells. These results indicate that cilnidipine mediates its neuroprotective effects by reducing oxidative stress, enhancing survival signals (e.g., PI3K, phosphorylated Akt, pGSK‐3β, and HSTF‐1), and inhibiting death signals from cytochrome c release, caspase 3 activation, and PARP cleavage.
Botulinum neurotoxins C, E and F bind gangliosides via a conserved binding site prior to stimulation‐dependent uptake with botulinum neurotoxin F utilising the three isoforms of SV2 as second receptor
Authors: Rummel Andreas , Häfner Kirstin , Mahrhold Stefan , Darashchonak Natallia , Holt Matthew , Jahn Reinhard , Beermann Silke , Karnath Tino , Bigalke Hans , Binz Thomas 
Published: July 2009

AbstractThe high toxicity of clostridial neurotoxins primarily results from their specific binding and uptake into neurons. At motor neurons, the seven botulinum neurotoxin serotypes A–G (BoNT/A–G) inhibit acetylcholine release, leading to flaccid paralysis, while tetanus neurotoxin blocks neurotransmitter release in inhibitory neurons, resulting in spastic paralysis. Uptake of BoNT/A, B, E and G requires a dual interaction with gangliosides and the synaptic vesicle (SV) proteins synaptotagmin or SV2, whereas little is known about the entry mechanisms of the remaining serotypes. Here, we demonstrate that BoNT/F as wells depends on the presence of gangliosides, by employing phrenic nerve hemidiaphragm preparations derived from mice expressing GM3, GM2, GM1 and GD1a or only GM3. Subsequent site‐directed mutagenesis based on homology models identified the ganglioside binding site at a conserved location in BoNT/E and F. Using the mice phrenic nerve hemidiaphragm assay as a physiological model system, cross‐competition of full‐length neurotoxin binding by recombinant binding fragments, plus accelerated neurotoxin uptake upon increased electrical stimulation, indicate that BoNT/F employs SV2 as protein receptor, whereas BoNT/C and D utilise different SV receptor structures. The co‐precipitation of SV2A, B and C from Triton‐solubilised SVs by BoNT/F underlines this conclusion.
Relationship between phosphodiesterase type 4 inhibition and anti‐inflammatory activity of CI‐1044 in rat airways
Authors: Pruniaux Marie‐Pierre , Lagente Vincent , Ouaged Malika , Bertin Bernadette , Moreau François , Julien‐Larose Christine , Rocher Marie‐Noelle , Leportier Christelle , Martin Brigitte , Bouget Anita , Dubuit Jean‐Pierre , Burnouf Catherine , Doherty Annette M. , Bertrand Claude P. 
Published: July 2009

AbstractThe anti‐inflammatory effects of CI‐1044 and of the other selective PDE4 inhibitors rolipram and cilomilast were investigated in Brown‐Norway (BN) rats, against lipopolysaccharide‐induced tumor necrosis factor α (TNFα) production in whole blood and antigen‐induced lung eosinophilia. In vitro, CI‐1044 inhibited TNFα production with an IC50of 0.31 μmbeing equipotent to Cilomilast (IC50 = 0.26 μm) and rolipram (IC50 = 0.11 μm). Given orally, CI‐1044 inhibited ex vivo TNFα production with an ED50value of 0.4 mg/kg after single administration, whereas rolipram (ED50 = 1.4 mg/kg) and cilomilast (ED50 = 1.6 mg/kg) were less potent. In the same ex vivo setting, but given repeatedly, CI‐1044 led to an ED50of 0.5 mg/kg corresponding to a plasma concentration of 82.6 ng/mL (0.22 μm). In vivo, CI‐1044 prevented TNFα release with an ED50of 1 mg/kg p.o. and inhibited ovalbumin‐induced lung eosinophilia following single or repeated oral administration with an ED50of 3.25 and 4.8 mg/kg p.o., respectively, suggesting the absence of pharmacological tolerance. CI‐1044 in this model was equipotent to rolipram (81% inhibition at 10 mg/kg) but better than cilomilast (25% inhibition at 10 mg/kg). Finally, CI‐1044 (10 mg/kg) inhibited inflammatory cell recruitment with a long duration of action (up to 8 h) and was still active when given post‐challenge. Our data show that CI‐1044 is an orally active PDE4 inhibitor that may be used as an anti‐inflammatory therapy in lung inflammatory diseases.
Human liver stem cell‐derived microvesicles accelerate hepatic regeneration in hepatectomized rats
Authors: Herrera M. B. , Fonsato V. , Gatti S. , Deregibus M. C. , Sordi A. , Cantarella D. , Calogero R. , Bussolati B. , Tetta C. , Camussi G. 
Published: July 2009

AbstractSeveral studies indicate that adult stem cells may improve the recovery from acute tissue injury. It has been suggested that they may contribute to tissue regeneration by the release of paracrine factors promoting proliferation of tissue resident cells. However, the factors involved remain unknown. In the present study we found that microvesicles (MVs) derived from human liver stem cells (HLSC) induced in vitro proliferation and apoptosis resistance of human and rat hepatocytes. These effects required internalization of MVs in the hepatocytes by an α4‐integrin‐dependent mechanism. However, MVs pre‐treated with RNase, even if internalized, were unable to induce hepatocyte proliferation and apoptosis resistance, suggesting an RNA‐dependent effect. Microarray analysis and quantitative RT‐PCR demonstrated that MVs were shuttling a specific subset of cellular mRNA, such as mRNA associated in the control of transcription, translation, proliferation and apoptosis. When administered in vivo, MVs accelerated the morphological and functional recovery of liver in a model of 70% hepatectomy in rats. This effect was associated with increase in hepatocyte proliferation and was abolished by RNase pre‐treatment of MVs. Using human AGO2, as a reporter gene present in MVs, we found the expression of human AGO2 mRNA and protein in the liver of hepatectomized rats treated with MVs. These data suggested a translation of the MV shuttled mRNA into hepatocytes of treated rats. In conclusion, these results suggest that MVs derived from HLSC may activate a proliferative program in remnant hepatocytes after hepatectomy by a horizontal transfer of specific mRNA subsets.
Implant surfaces and design (Working Group 4)
Authors: Lang Niklaus P. , Jepsen Søren 
Published: July 2009

AbstractIntroduction: The remit of this working group (4) was to update existing knowledge on the effects of implant surface topography, composition and design on bone integration and re‐osseointegration.Material and methods: Based on five narrative reviews that were performed following a defined search strategy, clinical implications as well as suggestions for further research have been formulated.Results: The results and conclusions of the review processes in the following papers together with the group consensus, clinical implications and directions for future research are presented:  1. Effects of titanium surface topography on bone integration.  2. Effects of implant surface coatings and composition on bone integration (two reviews).  3. Effects of different implant surfaces and designs on marginal bone level alterations.  4. Re‐osseointegration onto previously contaminated implant surfaces.
What impact do systemically administrated bisphosphonates have on oral implant therapy? A systematic review
Authors: Madrid Carlos , Sanz Mariano 
Published: July 2009

AbstractObjectives: The aim of this systematic review is to evaluate, analysing the dental literature, whether:• Patients on intravenous (IV) or oral bisphosphonates (BPs) can receive oral implant therapy and what could be the risk of developing bisphosphonate‐related osteonecrosis of the jaw (BRONJ)?• Osseointegrated implants could be affected by BP therapy.Material and methods: A Medline search was conducted and all publications fulfilling the inclusion and exclusion criteria from 1966 until December 2008 were included in the review. Moreover, the Cochrane Data Base of Systematic Reviews, and the Cochrane Central Register of Controlled Trials and EMBASE (from 1980 to December 2008) were searched for English‐language articles published between 1966 and 2008. Literature search was completed by a hand research accessing the references cited in all identified publications.Results: The literature search rendered only one prospective and three retrospective studies. The prospective controlled non‐randomized clinical study followed patients with and without BP medication up to 36 months after implant therapy. The patients in the experimental group had been on oral BPs before implant therapy for periods ranging between 1 and 4 years. None of the patients developed BRONJ and implant outcome was not affected by the BP medication. The three selected retrospective studies (two case–controls and one case series) yielded very similar results. All have followed patients on oral BPs after implant therapy, with follow‐up ranging between 2 and 4 years. BRONJ was never reported and implant survival rates ranged between 95% and 100%. The literature search on BRONJ including guidelines and recommendations found 59 papers, from which six were retrieved. Among the guidelines, there is a consensus on contraindicating implants in cancer patients under IV‐BPs and not contraindicating dental implants in patients under oral‐BPs for osteoporosis.Conclusions: From the analysis of the one prospective and the three retrospective series (217 patients), the placement of an implant may be considered a safe procedure in patients taking oral BPs for <5 years with regard to the occurrence of BRONJ since in these studies no BRONJ has been reported. Moreover, the intake of oral‐BPs did not influence short‐term (1–4 years) implant survival rates.
Ceramics in implant dentistry (Working Group 1)
Authors: Hobkirk J. A. , Wiskott H. W. A. 
Published: July 2009

AbstractIntroduction: The remit of this working group was to update the existing knowledge base in ceramics in implant dentistry. The reviews from working group 1 formed the basis for this update. Moreover, clinical applications as well as suggestions for further research have been formulated.Materials and methods: The papers in the working group critically reviewed the literature on the topic. Manuscripts were produced on: 1. The performance of ceramic and metal implant abutments supporting fixed implant reconstructions. 2. The viability of ceramic implants as alternatives to titanium implants. 3. The survival and complications of CAD–CAM reconstructions as compared with FDPs which have been fabricated using conventional techniques.Results: The results and conclusions of the review process are presented in the following papers, together with the group consensus statements, clinical implications and directions for future research:Sailer I., Philipp A., Zembic A., Pjetursson B. E., Hämmerle C. H. F., Zwahlen M. A systematic review of the performance of ceramic and metal implant abutments supporting fixed implant reconstructions. Andreiotelli M., Wenz H. J., Kohal R.‐J. Are ceramic implants a viable alternative to titanium implants? A systematic literature review. Harder S., Kern M. Survival and complications of CAD‐CAM vs. conventionally fabricated reconstructions: a systematic review.
Biofilm formation on rat skin wounds by Pseudomonas aeruginosa carrying the green fluorescent protein gene
Authors: Kanno Emi , Toriyabe Souhachi , Zhang Lianbo , Imai Yoshimichi , Tachi Masahiro 
Published: July 2009

Please cite this paper as: Biofilm formation on rat skin wounds by Pseudomonas aeruginosa carrying the green fluorescent protein gene. Experimental Dermatology 2010; 19:154–156.Abstract:  Most chronic wounds are covered by biofilms. However, questions remain about whether biofilms are a causative factor in delayed wound healing and whether the biofilm state contributes to this pathology. The purpose of this study was to develop an experimental model for convenient observation of biofilm formation on skin wounds. Full‐thickness wounds were created on the backs of SD rats. Suspensions of Pseudomonas aeruginosa carrying the gene encoding green fluorescent protein were then applied to the wounds. The wounds were harvested at 8 h, and at 1, 3 and 7 days postwounding for histological and immunohistochemical examinations. Fluorescence microscopy confirmed the presence of a biofilm as early as 8 h. Comparing with non‐infected wounds, epithelialization was not delayed. In conclusion, wound healing of rat acute wounds was unaffected by biofilm formation.