451 resultados para Jens Eder


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Over the last 180 years, several theories concerning the origin of hydranencephaly have been proposed with an emphasis on infectious, aplastic, and vascular etiologies. In this report, we present a case of triplets with fetofetal transfusion syndrome of which 2 fetuses (1 and 2) developed almost similar hydranencephaly, whereas the third exhibited the features of a fetus papyraceus (3). In the monochorial triamniotic placenta, multiple arteriovenous anastomoses were detected, representing a probable route for the transmission of thrombi originating from fetus 3 causing visceral lesions in fetus 2. Hydranencephaly was histologically characterized by necrosis, macrophage invasion, and endothelial proliferation. In addition, polymicrogyria was seen in fetuses 1 and 2. The combination of multiple visceral thromboembolic events and the death of fetus 3 approximately in the 11th week of gestation suggested a vascular thrombotic pathogenesis of hydranencephaly. Polymicrogyria can be considered as postmigratory laminar necrosis. Our findings contribute to the pathogenetic understanding of combined hydranencephaly and polymicrogyria.

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PURPOSE: A systematic review was performed to find evidence for prophylactic administration of antibiotics in relation to treatment of maxillofacial fractures. METHODS: Four studies were retrieved that fulfilled most of the requirements of being randomized controlled clinical trials. RESULTS: An analysis of these studies showed a 3-fold decrease in the infection rate of mandibular fractures in the antibiotic treated groups compared with the control groups. A variety of antibiotics had been used with an apparently uniform effect. A "1-shot" regimen or a 1-day treatment course had a similar or perhaps even better effect than 7 days of treatment. No infections were related to condylar, maxillary, or zygoma fractures. CONCLUSION: A 1-shot or 1-day administration of prophylactic antibiotics seem to be the best documented to reduce infections in the management of mandibular fractures not involving the condylar region.

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AIMS: The experience of using radiofrequency ablation (RFA) for the treatment of arrhythmias in children and adolescents is still limited. This study aimed to review the most recent results of RF ablation in children and adolescents in a highly experienced centre with access to both conventional techniques and non-fluoroscopic electroanatomic mapping (CARTO). METHODS AND RESULTS: A total of 154 consecutive patients younger than 19 years treated with RFA during the period 2000-04 were included. Numbers (%) or median (quartiles) are reported. Age was 15 (12-17) years, 70 (45%) were males. Five patients (3%) had congenital heart disease. RFA was successful in 147/154 patients (95%). Arrhythmia recurrence occurred in 11 patients (7%). Procedure time was 55 (35-90) min and fluoroscopy time was 8.8 (4-19) min. Number of RF applications was 4 (2-10) and number of RF applications >20 s was 2 (1-7). One patient (0.7%) had complicating high-grade atrioventricular block. CARTO was used in 18 RF ablation procedures (11%) performed in 15 patients. CONCLUSION: RF ablation can be undertaken in children and adolescents with a high success rate, few recurrences and complications, very short procedure times, and acceptable fluoroscopy times. Non-fluoroscopic electroanatomic mapping is helpful in selected patients.

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BACKGROUND: Many HIV-infected patients on highly active antiretroviral therapy (HAART) experience metabolic complications including dyslipidaemia and insulin resistance, which may increase their coronary heart disease (CHD) risk. We developed a prognostic model for CHD tailored to the changes in risk factors observed in patients starting HAART. METHODS: Data from five cohort studies (British Regional Heart Study, Caerphilly and Speedwell Studies, Framingham Offspring Study, Whitehall II) on 13,100 men aged 40-70 and 114,443 years of follow up were used. CHD was defined as myocardial infarction or death from CHD. Model fit was assessed using the Akaike Information Criterion; generalizability across cohorts was examined using internal-external cross-validation. RESULTS: A parametric model based on the Gompertz distribution generalized best. Variables included in the model were systolic blood pressure, total cholesterol, high-density lipoprotein cholesterol, triglyceride, glucose, diabetes mellitus, body mass index and smoking status. Compared with patients not on HAART, the estimated CHD hazard ratio (HR) for patients on HAART was 1.46 (95% CI 1.15-1.86) for moderate and 2.48 (95% CI 1.76-3.51) for severe metabolic complications. CONCLUSIONS: The change in the risk of CHD in HIV-infected men starting HAART can be estimated based on typical changes in risk factors, assuming that HRs estimated using data from non-infected men are applicable to HIV-infected men. Based on this model the risk of CHD is likely to increase, but increases may often be modest, and could be offset by lifestyle changes.

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PURPOSE: To characterize the phenotype and map the locus responsible for autosomal recessive inherited ovine microphthalmia (OMO) in sheep. METHODS: Microphthalmia-affected lambs and their available relatives were collected in a field, and experimental matings were performed to obtain affected and normal lambs for detailed necropsy and histologic examinations. The matings resulted in 18 sheep families with 48 cases of microphthalmia. A comparative candidate gene approach was used to map the disease locus within the sheep genome. Initially, 27 loci responsible for the microphthalmia-anophthalmia phenotypes in humans or mice were selected to test for comparative linkage. Fifty flanking markers that were predicted from comparative genomic analysis to be closely linked to these genes were tested for linkage to the disease locus. After observation of statistical evidence for linkage, a confirmatory fine mapping strategy was applied by further genotyping of 43 microsatellites. RESULTS: The clinical and pathologic examinations showed slightly variable expressivity of isolated bilateral microphthalmia. The anterior eye chamber was small or absent, and a white mass admixed with cystic spaces extended from the papilla to the anterior eye chamber, while no recognizable vitreous body or lens was found within the affected eyes. Significant linkage to a single candidate region was identified at sheep chromosome 23. Fine mapping and haplotype analysis assigned the candidate region to a critical interval of 12.4 cM. This ovine chromosome segment encompasses an ancestral chromosomal breakpoint corresponding to two orthologue segments of human chromosomes 18, short and long arms. For the examined animals, we excluded the complete coding region and adjacent intronic regions of ovine TGIF1 to harbor disease-causing mutations. CONCLUSIONS: This is the first genetic localization for hereditary ovine isolated microphthalmia. It seems unlikely that a mutation in the TGIF1 gene is responsible for this disorder. The studied sheep represent a valuable large animal model for similar human ocular phenotypes.

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Avulsion of permanent teeth is the most serious of all dental injuries. The prognosis depends on the measures taken at the place of accident or the time immediately after the avulsion. Replantation is the treatment of choice, but cannot always be carried out immediately. An appropriate emergency management and treatment plan is important for a good prognosis. Guidelines are useful for delivering the best care possible in an efficient manner. The International Association of Dental Traumatology (IADT) has developed a consensus statement after a review of the dental literature and group discussions. Experienced researchers and clinicians from various specialties were included in the group. In cases in which the data did not appear conclusive, recommendations were based on the consensus opinion of the IADT board members. The guidelines represent the current best evidence based on literature research and professional opinion. In this second article of three, the IADT Guidelines for management of avulsed permanent teeth are presented.

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OBJECTIVES: To evaluate whether or not preparation of the implant site with osteotomes instead of drilling may improve peri-implant bone density and/or osseointegration, and whether or not this further improves the predictability of immediate loading of SLA implants. MATERIAL AND METHODS: The second, third, and fourth premolars were extracted in both sides of the mandible in six dogs, and after at least 3 months four SLA implants were inserted into each side of the jaw. In three animals, the implant sites were prepared by means of osteotomes, while standard stepwise drilling was used in the remaining animals. In each side of the jaw, two non-adjacent implants were restored with single crowns 4 days after installation, while the remaining two implants were left without crowns to serve as non-loaded controls. After 2, 4, or 12 weeks of loading, specimens including the implants and surrounding tissues were obtained and processed for histologic analysis of undecalcified sections. RESULTS: All implants placed with osteotomes were lost (five before delivery of the crowns and the rest during the first week after loading). None of the conventionally inserted implants, however, was lost, and histomorphometrical analysis revealed similar soft- and hard peri-implant tissue characteristics at immediately loaded and non-loaded implants at all observation times. Average bone-to-implant contact was 59-72% at immediately loaded implants vs. 60-63% at non-loaded ones. CONCLUSION: Preparation of the implant site by means of osteotomes had a deleterious effect on osseointegration, while immediate loading of single, free-standing, SLA implants following a conventional surgical protocol did not jeopardize their osseointegration.

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Neonates are particularly susceptible to malnutrition due to their limited reserves of micronutrients and their rapid growth. In the present study, we examined the effect of vitamin C deficiency on markers of oxidative stress in plasma, liver and brain of weanling guinea pigs. Vitamin C deficiency caused rapid and significant depletion of ascorbate (P < 0.001), tocopherols (P < 0.001) and glutathione (P < 0.001), and a decrease in superoxide dismutase activity (P = 0.005) in the liver, while protein oxidation was significantly increased (P = 0.011). No changes in lipid oxidation or oxidatively damaged DNA were observed in this tissue. In the brain, the pattern was markedly different. Of the measured antioxidants, only ascorbate was significantly depleted (P < 0.001), but in contrast to the liver, ascorbate oxidation (P = 0.034), lipid oxidation (P < 0.001), DNA oxidation (P = 0.13) and DNA incision repair (P = 0.014) were all increased, while protein oxidation decreased (P = 0.003). The results show that the selective preservation of brain ascorbate and induction of DNA repair in vitamin C-deficient weanling guinea pigs is not sufficient to prevent oxidative damage. Vitamin C deficiency may therefore be particularly adverse during the neonatal period.

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Accumulation of iron probably predisposes the aging brain to progressive neuronal loss. We examined various markers of oxidative stress and damage in the brain and liver of 3- and 24-month-old rats following supplementation with the lipophilic iron derivative [(3,5,5-trimethylhexanoyl)ferrocene] (TMHF), which is capable of crossing the blood-brain barrier. At both ages, iron concentration increased markedly in the liver but failed to increase in the brain. In the liver of TMHF-treated young rats, levels of alpha- and gamma-tocopherols and glutathione (GSH) were also higher. In contrast, the brain displayed unaltered levels of the tocopherols and GSH. Malondialdehyde (MDA) level was also higher in the cerebrospinal fluid (CSF) and the liver but not in the brain. In old rats, the absence of an increase in iron concentration in the brain was reflected by unaltered concentrations of GSH, tocopherols, and MDA as compared to that in untreated rats. In the aging liver, concentrations of GSH and MDA increased with TMHF treatment. Morphological studies revealed unaltered levels of iron, ferritin, heme oxygenase-1 (HO-1), nitrotyrosine (NT), or MDA in the brains of both young and old rats treated with TMHF. In contrast, TMHF treatment increased the level of HO-1 in Kupffer cells, NT in hepatic endothelial cells, and MDA and ferritin in hepatocytes. Although these results demonstrated an increase in the biochemical markers of oxidative stress and damage in response to increasing concentrations of iron in the liver, they also demonstrated that the brain is well protected against dietary iron overload by using iron in a lipid-soluble formulation.

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The aim of this study was to obtain comprehensive data on clinical presentation, microbiology, computed tomography, surgical findings and histology in acute, sub-acute and chronic mastoiditis. We performed a prospective, observational study in children under 16 years of age presenting to our institution during the 2-year period beginning in April 2000. The children were examined and their condition treated in accordance with a standardized protocol elaborated by the paediatric, otolaryngology (ORL) and radiology departments. Thirty-eight patients were hospitalized (22 with acute mastoiditis, seven with sub-acute mastoiditis, nine with chronic mastoiditis). There were 30 complications present in 21 patients (55%). Streptococcus pyogenes was the most common pathogen (7/24 cases), followed by Streptococcus pneumoniae (4/24 cases). Mastoid surgery was performed in 29 patients. Histology of mastoid tissue revealed predominantly acute inflammation in two cases, mixed acute/chronic inflammation in 19 cases and predominantly chronic inflammation in seven cases. Radiologic data were evaluated retrospectively. Spiral, volume-based high-resolution (HR) computed tomography (CT) of the temporal bone had a sensitivity of 100%, specificity of 38%, positive predictive value (PPV) of 50% and negative predictive value (NPV) of 100% in detecting coalescence of mastoid trabeculae. Cranial CT with contrast had a sensitivity of 80%, specificity of 94%, PPV of 80% and NPV of 94% in identifying intra-cranial extension. Conclusion: histological evidence suggests that sub-acute/chronic infection underlies not only sub-acute and chronic mastoiditis, but most cases of acute mastoiditis as well. HR-CT of the temporal bone is effective in ruling out coalescence. Cranial CT is valuable in identifying intra-cranial extension. Cranial and HR-CT are recommended in the examination of children with mastoiditis.

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Voluntary exercise (VE) has a beneficial influence on the heart and mean lifespan. The present study evaluates structural adaptations of cardiomyocytes and their mitochondria due to VE by new, unbiased stereological methods. Female, 7-9-week-old mice were randomly assigned to a control (CG, n = 7) or VE group (EG, n = 7). EG animals were housed in cages with free access to a running wheel and had a mean running distance of 6.7 (1.8) km per day. After 4 weeks, the hearts of all mice were processed for light and electron microscopy. We estimated the number and volume of cardiomyocytes by the disector method and the number and volume of mitochondria by estimation of the Euler number. In comparison to CG, VE did not have an effect on the myocardial volume of the left ventricle (CG: 93 (10), EG: 103 (17) (mm(3))), the number of cardiomyocytes (CG: 2.81 (0.27), EG: 2.82 (0.43) (x10(6))) and their number-weighted mean volume. However, the composition of the cardiomyocytes changed due to VE. The total volume of mitochondria (CG: 21.8 (4.9), EG: 32.2 (4.3) (mm(3)), P < 0.01) and the total number (CG: 3.76 (0.44), EG: 7.02 (1.13) (x10(10)), P < 0.001) were significantly higher in EG than in CG. The mean number-weighted mitochondrial volume was smaller in EG than in CG (P < 0.05). In summary, VE does not alter ventricular volume nor cardiomyocyte volume or number but the oxidative capacity of cardiomyocytes by an increased mitochondrial number and total volume in the left ventricle. These structural changes may participate in the beneficial effects of VE.

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STATEMENT OF PROBLEM: AuTi alloys with 1.6% to 1.7% (wt%) Ti provide sufficient bond strength to veneering ceramics, but the strength of entire metal-ceramic restorations fabricated from these alloys is not known. However, this information is important to assess the clinical performance of such materials. PURPOSE: This in vitro study evaluated the fracture strength and thermal shock resistance of metal-ceramic crowns with AuTi frameworks produced by milling or casting. MATERIAL AND METHODS: Frameworks of the alloy Au-1.7Ti-0.1Ir (wt%) (Esteticor Vision) were produced by milling or casting (test groups). A high-gold alloy (Esteticor Special) was used as the control. The frameworks were veneered with ceramic (VMK 95). Specimens (n=7) were loaded until fracture. Loads at failure (N) were recorded and the mean values statistically evaluated using 1-way analysis of variance and a post hoc Dunnett test (alpha=.05). To assess the crazing resistance of the veneering ceramic, 6 additional crowns of each group were subjected to a thermal shock test. Fractured surfaces were documented by scanning electron microscopy. Coefficients of thermal expansion of the materials used were measured (n=2) to assess the thermal compatibility between alloys and ceramic. RESULTS: The mean fracture strength of the crowns with machined AuTi frameworks (1294 +/- 236 N) was significantly lower (P=.012) than that of the cast AuTi frameworks (1680 +/- 150 N), but statistically not different than the high-gold alloy (1449 +/- 159 N). Bonding failure to the AuTi alloy predominantly occurred at the alloy-oxide interface. For the high-gold alloy, more ceramic residues were observed. In the thermal shock test, crowns with milled AuTi frameworks showed significantly higher thermal shock resistance compared to the other groups. The coefficients of thermal expansion (Esteticor Vision cast: 14.5 microm/m.K; Esteticor Vision milled: 14.3 microm/m.K; Esteticor Special cast: 13.7 microm/m.K) did not correlate with the results of the thermal shock test. CONCLUSION: The in vitro fracture strength of crowns with milled AuTi frameworks is lower than that obtained with cast AuTi frameworks, but comparable to those crowns produced with a high-gold alloy.

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Objective: To assess in vitro the bond strength of a machined surface of a Au-Ti alloy to a veneering ceramic. Method and Materials: Metal strips of the alloy Au 1.7-Ti 0.1-Ir were milled from a semiproduct fabricated by continuous casting and cold forming. For comparison, the same alloy as well as a traditional Au-Pt-Pd-In alloy were used in the as-cast state. Six samples of each group were fabricated for the crack initiation test, according to ISO 9693:1999, by preparing appropriate metal strips that were veneered with ceramic using a standard firing procedure. The crack initiation test was performed in a universal testing machine. Load at fracture was recorded. Means of bond strength were calculated for each group and the results compared by use of a 1-sided Student t test (P < .05). Fracture sites were documented by means of SEM. Results: Bond strength in the 3 groups was in the same order of magnitude. Failure mode was different for both alloys. Failure of the bonding to the Au-Ti alloy predominantly occurred at the alloy-oxide interface, no matter which fabrication process was used. On the Au-Pt-Pd-In alloy, more ceramic residues were observed. Conclusion: The machined alloy Au 1.7-Ti 0.1-Ir provides sufficient bond strength to veneering ceramics, but this has to be proven by a clinical study. (Quintessence Int 2007;38:867-872).

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T lymphocytes lacking the lymph node-homing receptors L-selectin and CCR7 do not migrate to lymph nodes in the steady state. Instead, we found here that lymph nodes draining sites of mature dendritic cells or adjuvant inoculation recruited L-selectin-negative CCR7- effector and memory CD8+ T cells. This recruitment required CXCR3 expression on T cells and occurred through high endothelial venules in concert with lumenal expression of the CXCR3 ligand CXCL9. In reactive lymph nodes, recruited T cells established stable interactions with and killed antigen-bearing dendritic cells, limiting the ability of these dendritic cells to activate naive CD4+ and CD8+ T cells. The inducible recruitment of blood-borne effector and memory T cells to lymph nodes may represent a mechanism for terminating primary and limiting secondary immune responses.