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"text": "\n185377\nFemoral neck fractures in children and the role of early hip decompression in final outcome.\n\nBukva, B\n\nAbramović, D\n\nVrgoč, G\n\nMarinović, M\n\nBakota, B\n\nDučić, S\n\nMiškulin, M\n\nBrdar, R\n\nČoklo, M\n\nGulan, G\n\nBeiträge in Fachzeitschriften\nNone\n26592094.0\n10.1016/j.injury.2015.10.059\nNone\nFemoral neck fractures in children are very rare and account for about 1% of all paediatric fractures. The aim of this retrospective study was to analyse the clinical and radiographic outcome in paediatric femoral neck fracture and to review the role of early decompression of the hip in the final outcome.\n The study was performed at the Department of Paediatric Orthopaedics and Traumatology, University Children's Hospital in Belgrade, Serbia from January 1996 to January 2010. The study included 28 patients, 12 female and 16 male, aged 4-14 years. Patients who were aged over 14 years or who had pathological femoral neck fractures or metabolic disturbances were excluded from the study. The type of neck fracture was determined according to the Delbet and Colonna classification. The patients were treated using different surgical procedures: closed reduction and cast immobilisation, closed reduction and percutaneous fixation with Kirschner wires (K-wires), closed reduction and fixation with cannulated screws and open reduction with Wagner plate stabilisation. The final outcome was evaluated using the clinical outcome (based on the Howorth-Ferguson scale), radiographic outcome and occurrence of complications.\n The median age of patients included in the study was 10.75 years and the average follow up was 9 years. According to the Delbet classification, there was one patient with type I, eight patients with type II, 16 patients with type III and three patients with type IV femoral neck fracture. Based on the Colonna classification, there were 23 displaced and five non-displaced femoral neck fractures. Decompression of the hip was performed in 21 patients. Avascular necrosis (AVN) developed as the main complication in 11 patients. The final outcome was excellent in 14 patients, good in four patients and poor in 14 patients.\n Our study unequivocally confirms the positive effect of urgent treatment on the incidence of AVN as well as on the outcome. We have established a 12-hour interval after injury as an optimal time limit for commencing treatment. Unambiguously positive effects of hip decompression on the incidence of AVN were also noted. We found similar efficiency for open and needle hip decompression.\n Copyright © 2015 Elsevier Ltd. All rights reserved.\n\n\n"
},
{
"text": "\n74674\nClinical evaluation of monitor unit software and the application of action levels.\n\nGeorg, D\n\nNyholm, T\n\nOlofsson, J\n\nKjaer-Kristoffersen, F\n\nSchnekenburger, B\n\nWinkler, P\n\nNystrom, H\n\nAhnesjo, A\n\nKarlsson, M\n\nBeiträge in Fachzeitschriften\nISI:000252201400020\n17904234.0\n10.1016/j.radonc.2007.04.035\nNone\nPURPOSE: The aim of this study was the clinical evaluation of an independent dose and monitor unit verification (MUV) software which is based on sophisticated semi-analytical modelling. The software was developed within the framework of an ESTRO project. Finally, consistent handling of dose calculation deviations applying individual action levels is discussed. MATERIALS AND METHODS: A Matlab-based software ("MUV") was distributed to five well-established treatment centres in Europe (Vienna, Graz, Basel, Copenhagen, and Umeå) and evaluated as a quality assurance (QA) tool in clinical routine. Results were acquired for 226 individual treatment plans including a total of 815 radiation fields. About 150 beam verification measurements were performed for a portion of the individual treatment plans, mainly with time variable fluence patterns. The deviations between dose calculations performed with a treatment planning system (TPS) and the MUV software were scored with respect to treatment area, treatment technique, geometrical depth, radiological depth, etc. RESULTS: In general good agreement was found between calculations performed with the different TPSs and MUV, with a mean deviation per field of 0.2+/-3.5% (1 SD) and mean deviations of 0.2+/-2.2% for composite treatment plans. For pelvic treatments less than 10% of all fields showed deviations larger than 3%. In general, when using the radiological depth for verification calculations the results and the spread in the results improved significantly, especially for head-and-neck and for thorax treatments. For IMRT head-and-neck beams, mean deviations between MUV and the local TPS were -1.0+/-7.3% for dynamic, and -1.3+/-3.2% for step-and-shoot IMRT delivery. For dynamic IMRT beams in the pelvis good agreement was obtained between MUV and the local TPS (mean: -1.6+/-1.5%). Treatment site and treatment technique dependent action levels between +/-3% and +/-5% seem to be clinically realistic if a radiological depth correction is performed, even for dynamic wedges and IMRT. CONCLUSION: The software MUV is well suited for patient specific treatment plan QA applications and can handle all currently available treatment techniques that can be applied with standard linear accelerators. The highly sophisticated dose calculation model implemented in MUV allows investigation of systematic TPS deviations by performing calculations in homogeneous conditions.\n\nWinkler, Peter\n\n\n"
},
{
"text": "\n78285\nEfficacy and safety of gadodiamide (Gd-DTPA-BMA) in renal 3D-magnetic resonance angiography (MRA): a phase II study.\n\nKittner, T\n\nRudolf, J\n\nFages, JF\n\nLegmann, P\n\nAschauer, M\n\nRepa, I\n\nAlvares, MR\n\nSavalegui, I\n\nIttrich, H\n\nGeterud, K\n\nde Kevviler, E\n\nAyuso, J\n\nLockhart, ME\n\nBlum, A\n\nIliasch, H\n\nLeisinger, G\n\nvan Beek, EJ\n\nReid, AW\n\nBrown, JJ\n\nYu, TC\n\nFlamm, SD\n\nDüber, C\n\nJudmaier, W\n\nReimer, P\n\nStiskal, M\n\nKramann, B\n\nWolff, S\n\nBlankenstein, C\n\nBeiträge in Fachzeitschriften\nISI:000251811700019\n17412546.0\n10.1016/j.ejrad.2007.02.034\nNone\nPURPOSE: To determine the most efficacious dose of gadodiamide for three-dimensional (3D) contrast-enhanced (CE) magnetic resonance angiography (MRA) of the renal arteries on a patient level based on the sensitivity in detecting the main hemodynamically relevant (> or =50% or occlusion) renal artery stenosis (RAS) using intra-arterial digital subtraction angiography (IA DSA) as the gold standard. MATERIALS AND METHODS: This prospective, randomized, double-blind, parallel-group, multicenter study included 273 patients referred to IA DSA for suspected RAS. Patients underwent 3D CE MRA after injection of 0.01, 0.05, 0.1, or 0.2mmol/kg of body weight gadodiamide (0.5mmol/ml). The images were assessed for location and degree of RAS by independent blinded readers (MRA: three readers, IA DSA: one reader). Hypothesis testing for a significant trend in sensitivity across dose groups was based on the one-sided Cochran-Armitage style trend test for each independent MRA reader. RESULTS: The lowest dose group (0.01mmol/kg) proved non-efficacious in detecting hemodynamically relevant (i.e., > or =50% or occlusion) RAS. A statistically significant dose trend (p<0.001) was shown for each of the three independent readers. Depending on reader, the sensitivity obtained with 0.05, 0.1, and 0.2mmol/kg was 63.9-86.1%, 75.8-91.4% and 80.6-90.6%, the specificity was 66.7-73.9%, 59.3-75.0%, and 59.3-75.0% and accuracy was 67.8-78.9%, 75.4-77.4%, and 76.3-81.0%, for the three dose groups, respectively. There were eight non-severe adverse events (AEs). Three serious AEs occurring in one patient were judged not related to gadodiamide by the on-site investigator. CONCLUSION: A significant dose trend between the four doses examined was observed. The lowest dose (0.01mmol/kg) differed significantly from those of the other three doses. Based on the analysis of the primary and secondary endpoints, 0.1mmol/kg gadodiamide appears to be the most suitable dose in diagnosing hemodynamically relevant RAS. The present study also demonstrated gadodiamide to be safe and well tolerated.\n\nAschauer, Manuela\n\n\n"
},
{
"text": "\n112092\nModeling of hyaluronan clearance with application to estimation of lymph flow.\n\nRössler, A\n\nFink, M\n\nGoswami, N\n\nBatzel, JJ\n\nBeiträge in Fachzeitschriften\nISI:000292775400014\n21743125.0\n10.1088/0967-3334/32/8/014\nNone\nOne of the important factors in blood pressure regulation is the maintenance of the level of blood volume, which depends on several factors including the rate of lymph flow. Lymph flow can be measured directly using cannulation of lymphatic vessels, which is not clinically feasible, or indirectly by the tracer appearance rate, which is the rate at which macromolecules appear into the blood from the peritoneal cavity. However, indirect lymph flow measurements do not always provide consistent results. Through its contribution to osmotic pressure and resistance to flow, the macromolecule hyaluronan takes part in the regulation of tissue hydration and the maintenance of water and protein homeostasis. It arrives in blood plasma through lymph flow. Lymphatic hyaluronic acid (HA, hyaluronan) concentration is several times higher than that in plasma, suggesting that the lymphatic route may account for the majority of HA found in plasma. Furthermore, circulating levels of HA reflect the dynamic state between delivery to-and removal from-the bloodstream. To develop an accurate estimation of the fluid volume distribution and dynamics, the rate of lymph flow needs to be taken into account and hyaluronan could be used as a marker in estimating this flow. To examine the HA distribution and system fluid dynamics, a six-compartment model, which could reflect both the steady-state relationships and qualitative characteristics of the dynamics, was developed. This was then applied to estimate fluid shifts from the interstitial space via the lymphatic system to the plasma during different physiological stresses (orthostatic stress and the stress of ultrafiltration during dialysis). Sensitivity analysis shows that during ultrafiltration, lymph flow is a key parameter influencing the total HA level, thus suggesting that the model may find applications in addressing the problem of estimating lymph flow. Since the fluid balance between interstitium and plasma is maintained by lymph flow and microvasculature filtration, our novel method of flow estimation may provide an important tool for understanding fluid dynamics during perturbations of the cardiovascular system. Since the fluid balance between interstitium and plasma is maintained by lymph flow and microvasculature filtration, our novel method of flow estimation may provide an important tool for understanding fluid dynamics during perturbations of the cardiovascular system.\n\nGoswami, Nandu\n\nRössler, Andreas\n\n\n"
},
{
"text": "\n123899\nProposed actions are no actions: re-modeling an ontology design pattern with a realist top-level ontology.\n\nSeddig-Raufie, D\n\nJansen, L\n\nSchober, D\n\nBoeker, M\n\nGrewe, N\n\nSchulz, S\n\nBeiträge in Fachzeitschriften\nNone\n23046561.0\n10.1186/2041-1480-3-S2-S2\nPMC3448525\nOntology Design Patterns (ODPs) are representational artifacts devised to offer solutions for recurring ontology design problems. They promise to enhance the ontology building process in terms of flexibility, re-usability and expansion, and to make the result of ontology engineering more predictable. In this paper, we analyze ODP repositories and investigate their relation with upper-level ontologies. In particular, we compare the BioTop upper ontology to the Action ODP from the NeOn an ODP repository. In view of the differences in the respective approaches, we investigate whether the Action ODP can be embedded into BioTop. We demonstrate that this requires re-interpreting the meaning of classes of the NeOn Action ODP in the light of the precepts of realist ontologies.\n As a result, the re-design required clarifying the ontological commitment of the ODP classes by assigning them to top-level categories. Thus, ambiguous definitions are avoided. Classes of real entities are clearly distinguished from classes of information artifacts. The proposed approach avoids the commitment to the existence of unclear future entities which underlies the NeOn Action ODP. Our re-design is parsimonious in the sense that existing BioTop content proved to be largely sufficient to define the different types of actions and plans.\n The proposed model demonstrates that an expressive upper-level ontology provides enough resources and expressivity to represent even complex ODPs, here shown with the different flavors of Action as proposed in the NeOn ODP. The advantage of ODP inclusion into a top-level ontology is the given predetermined dependency of each class, an existing backbone structure and well-defined relations. Our comparison shows that the use of some ODPs is more likely to cause problems for ontology developers, rather than to guide them. Besides the structural properties, the explanation of classification results were particularly hard to grasp for 'self-sufficient' ODPs as compared with implemented and 'embedded' upper-level structures which, for example in the case of BioTop, offer a detailed description of classes and relations in an axiomatic network. This ensures unambiguous interpretation and provides more concise constraints to leverage on in the ontology engineering process.\n\nSchulz, Stefan\n\n\n"
},
{
"text": "\n168391\nMicroscopic Isthmuses and Fibrosis Within the Border Zone of Infarcted Hearts Promote Calcium-Mediated Ectopy and Conduction Block\n\nCampos, FO\n\nShiferaw, Y\n\ndos Santos, RW\n\nPlank, G\n\nBishop, MJ\n\nBeiträge in Fachzeitschriften\nISI:000434407400001\nNone\n10.3389/fphy.2018.00057\nNone\nVentricular tachycardia secondary to myocardial infarction (MI) remain a major cause of sudden death in adults. Premature ventricular complexes (PVCs), the first initiating beats of a portion of these arrhythmias, arise from triggered activity in the infarct border zone (BZ). At the cellular scale, spontaneous calcium release (SCR) events are a known cause of triggered activity and have been reported in cells that survive MI. At the tissue scale, fibrosis has been shown to play an important role in creating the substrate for VT. However, the interplay between SCR-mediated triggered activity and fibrosis upon VT formation in infarcted hearts has not been fully investigated. Here, we conduct in-silico experiments to assess how macroscopic and microscopic anatomical properties of the BZ can create a substrate for SCR-mediated VT formation. To study this question, we employ a stochastic subcellular-scale model of SCR events and action potential to simulate different cardiac preparations. Within 2D sheet models with idealized infarct scars and BZ we show that the probability of PVCs is higher, 55%, in preparations with thin conducting isthmuses (0.2 mm) transcending the scar. In an anatomically-detailed model of the rabbit ventricles with a realistic representation of intramural scars, we show that the heart's protective source-sink mismatch prevents ectopy. Furthermore, we demonstrate that fibrosis disrupts this antiarrhythmic mechanism making PVCs more likely. PVC probability is highest (>= 25%) when fibrosis accounts for 60 and 90% of the BZ in the 2D sheet and the 3D anatomical model, respectively. Above these thresholds, PVC occurrence decreases because of: (1) the reduced number of myocytes in the BZ; (2) conduction block. Block is caused either by disconnection of BZ cells from the myocardium or due to source-sink mismatches at regions of rapid tissue expansion. Moreover, while outward propagation to healthy tissue may fail, PVCs traveling inward through the scar might encounter more favorable loading conditions. These PVCs may exit to the myocardium and reenter back at the region of block. Overall, our findings indicate that thin isthmuses and strands of myocytes interspersed with fibrosis can be arrhythmogenic. Ablation of these microscopic structures may prevent VT formation.\n\nPlank, Gernot\n\n\n"
},
{
"text": "\n183124\nThe stability of carbapenems before and after admixture to PMMA-cement used for replacement surgery caused by Gram-negative bacteria.\n\nSchmid, M\n\nSteiner, O\n\nFasshold, L\n\nGoessler, W\n\nHoll, AM\n\nKühn, KD\n\nBeiträge in Fachzeitschriften\nISI:000565126400001\n32811560.0\n10.1186/s40001-020-00428-z\nPMC7433091\nProsthetic joint infection (PJI) is a serious complication of orthopedic implant surgery. Treatment often includes the use of an antibiotic-loaded Polymethyl methacrylate (PMMA) bone cement spacer. Several antibiotics are commonly used for the preparation of these spacers, but due to the increasing number of infections with resistant Gram-negative bacteria, there is a need for the use of carbapenem antibiotics such as meropenem and imipenem as drugs of last resort. Unfortunately, the reaction heat generated during the preparation of the bone cement can be a major problem for the stability of these antibiotics. In the present study, the stability of meropenem and imipenem was tested before and after the admixture to PMMA bone cements.\n High-performance liquid chromatography with ion-pairing reversed-phase separation and spectrophotometric detection was used for analysis. Stability tests with meropenem and imipenem were performed with antibiotics in solution and solid form at different temperatures (37 °C, 45 °C, 60 °C, 90 °C) and times (30 min, 60 min, 120 min). To test the stability of both antibiotics in PMMA after exposure to the reaction heat during polymerization, three different bone cements were used to generate specimens that contained defined amounts of antibiotics. Reaction heat was measured. The form bodies were mechanically crushed and aliquots were dissolved in ethyl acetate. Samples were prepared for HPLC DAD analysis.\n Meropenem and imipenem showed the highest degradation levels after heat stressed in solution, with maximum levels of 75% and 95%, respectively. In solid form, degradation levels decreased dramatically for meropenem (5%) and imipenem (13%). Stability tests of both carbapenems in bone cement showed that they remained largely stable during PMMA polymerization, with retrieved amounts of about 70% in Palacos® R and Copal® G+V, and between 80 and 90% in Copal® spacem.\n In contrast to the results of meropenem and imipenem in solution, both antibiotics remain stable in solid form and mostly stable in the cement after PMMA polymerization. The low degradation levels of both antibiotics after exposure to temperatures > 100 °C allow the conclusion that they can potentially be used for an application in PMMA cements.\n\n\n"
},
{
"text": "\n2692\nTrace elements in pleural effusions.\n\nDomej, W\n\nKrachler, M\n\nSchlagenhaufen, C\n\nTrinker, M\n\nKrejs, GJ\n\nIrogolic, KJ\n\nBeiträge in Fachzeitschriften\nISI:000073326300006\n9575474.0\n10.1016/S0946-672X(97)80018-1\nNone\nWhen the secretion of pleural fluids exceeds their resorption, liquid (pleural effusion ) will accumulate between the visceral and parietal pleura. Pleural effusions derived from the liquid components of blood are expected to contain trace elements and may, as a sink for trace elements, deprive the body of needed essential elements upon their removal by medical intervention. Consequently, patients may be at risk of drifting into trace-element deficiencies. Because the literature is almost devoid of data about trace elements in effusions, the concentrations of 14 trace elements (Ba, Ca, Cd, Co, Cs, Cu, Mg, Mn, Mo, Pb, Rb, Sn, Sr, Zn) were determined simultaneously by inductively-coupled argon-plasma mass spectrometry (ICP-MS) in effusions from 17 patients. The median values for the concentrations of Rb (209 microgram/kg, range 104-334 microgram/kg) and Cs (1.5 micrograms/kg, range 0.8-2.4 microgram/kg) in the effusions were almost the same as in the sera. The concentrations of Mg (range 15-22 mg/kg), Ca range 52-91 mg/kg), Sr (range 12-37 micrograms/kg), and Ba (range 1.4-18.2 micrograms/kg) were consistently lower in the effusions than in the sera by 18% for Mg, 26% Ca 14% for Sr, and 88% for Ba (percentages based on median in serum as 100%). The concentrations of the essential trace elements Co (range 0.16-0.5 microgram/kg), Cu (130-902 micrograms/kg), Mn (0.2-2.2 micrograms/kg), Mo (0.4-1.5 micrograms/kg), Sn (0.4-1.2 micrograms/kg), and Zn (27-1931 micrograms/kg) in the effusions are generally lower (25-55% based on median) than in the corresponding sera, although a few effusions have higher concentrations of Co, Mn Mo, or Zn than in the sera. The concentrations of Cd (range 0.2-0.5 microgram/kg) in the effusions were approximately the same as in the sera for three patients, considerably lower than in the sera for four patients, and considerably higher for three patients. The concentrations for lead (range 0.6-45 micrograms/kg) in the effusions were generally much higher than in the sera. The effusions were not significantly contaminated with lead-rich erythrocytes. The concentrations of Ca, Cu, and Zn in the effusions correlated positively with the protein concentrations in the effusions. One kilogram of the effusions contain from 10-30% of the trace elements present in the entire volume of serum in circulation.\n\nDomej, Wolfgang\n\nKrejs, Günter Josef\n\n\n"
},
{
"text": "\n2782\nTumor induction by ras and myc oncogenes in fetal and neonatal brain: modulating effects of developmental stage and retroviral dose.\n\nRadner, H\n\nel-Shabrawi, Y\n\nEibl, RH\n\nBrüstle, O\n\nKenner, L\n\nKleihues, P\n\nWiestler, OD\n\nBeiträge in Fachzeitschriften\nISI:A1993ME47000008\n8310796.0\nNone\nNone\nIntroduction into fetal rat brain cells of a replication-defective retroviral vector harboring v-Ha-ras and v-gag-myc rapidly causes the induction of highly malignant undifferentiated neuroectodermal tumors following transplantation into the brains of syngeneic hosts [Wiestler, et al. (1992) Cancer Res. 52: 3760-3767]. In the present study, we have investigated the modulating effect of the developmental stage of neural target cells and of the dose of the retroviral vector used in the grafting experiments. Exposure of fetal cells from embryonic day (E)12 or E14 produced a 100% incidence of malignant neuroectodermal tumors which led to the death of recipient animals after a median latency period of 32 days. A 100-fold reduction of the virus dose from 2.062 x 10(6) to 2.062 x 10(4) focus-forming units/ml resulted in a lower tumor incidence of 25%. Of six neural grafts exposed to v-Ha-ras and v-myc at E16, only one showed evidence of tumorigenesis (low-grade astrocytoma and hemangioma). All other transplants were morphologically normal for observation periods of 26 weeks, indicating a marked loss of transforming activity of ras and myc in more advanced stages of brain development. In retrovirus-exposed donor cells which caused the development of neural tumors in recipient rats, malignant transformation was also evident during culture in vitro, usually after 9-12 days. Oncogene complementation was also studied in the newborn rat brain. After microinjection of the retroviral vector into the brain at postnatal day (P)0, P1 and P3, 5 out of 20 animals (25%) developed a total of seven brain tumors. Histopathologically, three of these neoplasms were malignant neuroectodermal tumors which, in contrast to those induced in fetal brain transplants showed evidence of focal glial and/or neuronal differentiation. In addition, we observed one oligodendroglioma, two hemangiomas and a malignant hemangioendothelioma. These data indicate that neural precursor cells and endothelia of the rat brain represent the major target cells for the complementary action of ras and myc and that the use of target cells from later developmental stages (E16 and postnatal) leads to the induction of both primitive and more differentiated neoplasms.\n\nEl-Shabrawi, Yosuf\n\n\n"
},
{
"text": "\n66698\nDiagnosis of families with familial hypercholesterolaemia and/or Apo B-100 defect by means of DNA analysis of LDL-receptor gene mutations.\n\nWidhalm, K\n\nDirisamer, A\n\nLindemayr, A\n\nKostner, G\n\nBeiträge in Fachzeitschriften\nISI:000245470900018\n17347910.0\n10.1007/s10545-007-0563-5\nNone\nBACKGROUND: One major problem of using hypercholesterolaemia alone as a primary criterion for diagnosing familial hypercholesterolaemia (FH) is that 15-40% of relatives may be misdiagnosed because plasma lipid levels in FH heterozygotes overlap with those in the general population. SETTING: General Hospital/University of Vienna, Department of Pediatrics, Outpatient lipid clinic. METHODS: As a part of the MED-PED (make early diagnosis-prevent early death) project we are currently investigating children, adolescents and their relatives who are suspected to be affected with FH in our out-patient clinic for metabolic diseases using MED-PED inclusion criteria and confirming the diagnosis by means of DNA analysis. PATIENTS: 263 patients with premature atherosclerosis and/or hypercholesterolaemia: 116 children (mean age 11.6 +/- 4.1 years; 57 girls and 59 boys) and 147 adults (64 women, mean age 41.5 +/- 13.7 years; 83 men, mean age 42.8 +/- 10.8 years). RESULTS: 119 patients with mutations have been detected; 56 children with either low density lipoprotein receptor (LDLR) and/or ApoB mutations (27 girls and 29 boys; mean total cholesterol (TC) 275 +/- 71 mg/dl, triglycerides (TG) 101 +/- 57 mg/dl, high-density lipoprotein cholesterol (HDL-C) 49 +/- 12 mg/dl, low-density lipoprotein cholesterol (LDL-C) 198 +/- 67 mg/dl) and one boy with a homozygous. LDLR mutation. A further 62 adults with LDLR and/or ApoB mutations were documented; 33 women (mean age 36.9 +/- 11.1 years; mean TC 283 +/- 76 mg/dl, TG 137 +/- 78 mg/dl, HDL-C 55 +/- 17 mg/dl, LDL-C 210 +/- 67 mg/dl) and 29 men (mean age 45.0 +/- 10.6 years; mean TC 301 +/- 87 mg/dl, TG 163 +/- 112 mg/dl, HDL-C 42 +/- 12 mg/dl, LDL-C 233 +/- 83 mg/dl). In 32 of these subjects (11 children (21%), 21 adults (42%)), serum lipid levels were lower than the diagnostic MED-PED limits adopted, so that they might have been misclassified without an additional DNA analysis. CONCLUSION: In our study, diagnosis of FH and related disorders (ApoB-100 defect) by means of conventional laboratory methods missed at least 21% in children and 42% in adults affected with LDLR and/or ApoB gene mutations. Genetic FH diagnosis provides a tool for specific diagnosis of mutation carrier status.\n\nKostner, Gerhard\n\n\n"
},
{
"text": "\n77011\nThe effect of stress doses of hydrocortisone during septic shock on posttraumatic stress disorder and health-related quality of life in survivors.\n\nSchelling, G\n\nStoll, C\n\nKapfhammer, HP\n\nRothenhäusler, HB\n\nKrauseneck, T\n\nDurst, K\n\nHaller, M\n\nBriegel, J\n\nBeiträge in Fachzeitschriften\nISI:000084523600012\n10628609.0\n10.1097/00003246-199912000-00012\nNone\nOBJECTIVES: The exposure to intense physical and psychological stress during intensive care can result in posttraumatic stress disorder (PTSD) in survivors. Cortisol is a biological stress mediator that can have a protective effect during severe stress. The administration of stress doses of hydrocortisone during treatment in the intensive care unit could theoretically result in a lower incidence of PTSD. We tested this hypothesis in survivors of septic shock. DESIGN: A retrospective case-controlled analysis. SETTING: A 20-bed multidisciplinary intensive care unit of a tertiary-care university hospital. PATIENTS: We identified 27 patients who received standard therapy for septic shock. These patients served as controls and were compared with an equal number of patients who received hydrocortisone in addition to standard treatment. These patients were selected from our database with regard to age (+/-4 yrs), gender, and cause of septic shock to be as similar as possible with control patients. INTERVENTIONS: Patients from the hydrocortisone group had received stress doses of hydrocortisone (100 mg bolus, followed by 0.18 mg/kg/hr) in addition to standard treatment. Patients from the control group received standard protocol-driven treatment only. PTSD was diagnosed with the Posttraumatic Stress Syndrome-10 inventory, a self-report scale for diagnosis of PTSD. Health-related quality of life was measured using the Medical Outcomes Study Short-Form Survey (Medical Outcomes Trust, Boston, MA), which consists of 36 questions. MEASUREMENTS AND MAIN RESULTS: Patients who received hydrocortisone during septic shock had a significantly lower incidence of PTSD than patients who received standard treatment only (5 of 27 vs. 16 of 27; p = .01) and had significantly higher scores on the mental health index of the Medical Outcomes Study Short-Form health-related quality-of-life questionnaire (68 vs. 44 points; p = .009). CONCLUSIONS: Data from this study support the hypothesis that the administration of stress doses of hydrocortisone in doses equivalent to the maximal endocrine secretion rate during septic shock reduces the incidence of PTSD and improves emotional well-being in survivors. This hypothesis should be tested in a prospective randomized trial.\n\nKapfhammer, Hans-Peter\n\nRothenhäusler, Hans-Bernd\n\n\n"
},
{
"text": "\n98818\nMulti-system neurological disease is common in patients with OPA1 mutations.\n\nYu-Wai-Man, P\n\nGriffiths, PG\n\nGorman, GS\n\nLourenco, CM\n\nWright, AF\n\nAuer-Grumbach, M\n\nToscano, A\n\nMusumeci, O\n\nValentino, ML\n\nCaporali, L\n\nLamperti, C\n\nTallaksen, CM\n\nDuffey, P\n\nMiller, J\n\nWhittaker, RG\n\nBaker, MR\n\nJackson, MJ\n\nClarke, MP\n\nDhillon, B\n\nCzermin, B\n\nStewart, JD\n\nHudson, G\n\nReynier, P\n\nBonneau, D\n\nMarques, W\n\nLenaers, G\n\nMcFarland, R\n\nTaylor, RW\n\nTurnbull, DM\n\nVotruba, M\n\nZeviani, M\n\nCarelli, V\n\nBindoff, LA\n\nHorvath, R\n\nAmati-Bonneau, P\n\nChinnery, PF\n\nBeiträge in Fachzeitschriften\nISI:000276046000013\n20157015.0\n10.1093/brain/awq007\nPMC2842512\nAdditional neurological features have recently been described in seven families transmitting pathogenic mutations in OPA1, the most common cause of autosomal dominant optic atrophy. However, the frequency of these syndromal 'dominant optic atrophy plus' variants and the extent of neurological involvement have not been established. In this large multi-centre study of 104 patients from 45 independent families, including 60 new cases, we show that extra-ocular neurological complications are common in OPA1 disease, and affect up to 20% of all mutational carriers. Bilateral sensorineural deafness beginning in late childhood and early adulthood was a prominent manifestation, followed by a combination of ataxia, myopathy, peripheral neuropathy and progressive external ophthalmoplegia from the third decade of life onwards. We also identified novel clinical presentations with spastic paraparesis mimicking hereditary spastic paraplegia, and a multiple sclerosis-like illness. In contrast to initial reports, multi-system neurological disease was associated with all mutational subtypes, although there was an increased risk with missense mutations [odds ratio = 3.06, 95% confidence interval = 1.44-6.49; P = 0.0027], and mutations located within the guanosine triphosphate-ase region (odds ratio = 2.29, 95% confidence interval = 1.08-4.82; P = 0.0271). Histochemical and molecular characterization of skeletal muscle biopsies revealed the presence of cytochrome c oxidase-deficient fibres and multiple mitochondrial DNA deletions in the majority of patients harbouring OPA1 mutations, even in those with isolated optic nerve involvement. However, the cytochrome c oxidase-deficient load was over four times higher in the dominant optic atrophy + group compared to the pure optic neuropathy group, implicating a causal role for these secondary mitochondrial DNA defects in disease pathophysiology. Individuals with dominant optic atrophy plus phenotypes also had significantly worse visual outcomes, and careful surveillance is therefore mandatory to optimize the detection and management of neurological disability in a group of patients who already have significant visual impairment.\n\n\n"
},
{
"text": "\n115632\nModulation of the smooth-muscle L-type Ca2+ channel alpha1 subunit (alpha1C-b) by the beta2a subunit: a peptide which inhibits binding of beta to the I-II linker of alpha1 induces functional uncoupling.\n\nHohaus, A\n\nPoteser, M\n\nRomanin, C\n\nKlugbauer, N\n\nHofmann, F\n\nMorano, I\n\nHaase, H\n\nGroschner, K\n\nBeiträge in Fachzeitschriften\nISI:000087893700022\n10839999.0\n10.1042/0264-6021:3480657\nPMC1221110\nModulation of the smooth-muscle Ca(2+) channel alpha1C-b subunit by the auxiliary beta2a subunit was studied in the HEK 293 (cell line from human embryonic kidney cells) expression system. In addition, we tested whether the alpha1-beta interaction in functional channels is sensitive to an 18-amino-acid synthetic peptide that corresponds to the sequence of the defined major interaction domain in the cytoplasmic I-II linker of alpha1C (AID-peptide). Ca(2+) channels derived by co-expression of alpha1C-b and beta2a subunits exhibited an about 3-fold higher open probability (P(o)) than alpha1C-b channels. High-P(o) gating of alpha1C-b.beta2a channels was associated with the occurrence of long-lasting channel openings [mean open time (tau)>10 ms] which were rarely observed in alpha1C-b channels. Modulation of fast gating by the beta2a subunit persisted in the cell-free, inside-out recording configuration. Biochemical experiments showed that the AID-peptide binds with appreciable affinity to beta2 subunits of native Ca(2+) channels. Binding of the beta2 protein to immobilized AID-peptide was specifically inhibited (K(i) of 100 nM) by preincubation with free (uncoupled) AID-peptide, but not by a corresponding scrambled peptide. Administration of the AID-peptide (10 microM) to the cytoplasmic side of inside-out patches induced a substantial reduction of P(o) of alpha1C-b.beta2a channels. The scrambled control peptide failed to affect alpha1C-b. beta2a channels, and the AID-peptide (10 microM) did not modify alpha1C-b channel function in the absence of expressed beta2a subunit. Our results demonstrate that the beta2a subunit controls fast gating of alpha1C-b channels, and suggest the alpha1-beta interaction domain in the cytoplasmic I-II linker of alpha1C (AID) as a possible target of modulation of the channel. Moreover, our data are consistent with a model of alpha1-beta interaction that is based on multiple interaction sites, including AID as a determinant of the affinity of the alpha1-beta interaction.\n\nGroschner, Klaus\n\n\n"
},
{
"text": "\n120824\nPityriasis Lichenoides et Varioliformis Acuta With Numerous CD30(+) Cells A Variant Mimicking Lymphomatoid Papulosis and Other Cutaneous Lymphomas. A Clinicopathologic, Immunohistochemical, and Molecular Biological Study of 13 Cases.\n\nKempf, W\n\nKazakov, DV\n\nPalmedo, G\n\nFraitag, S\n\nSchaerer, L\n\nKutzner, H\n\n\n\nBeiträge in Fachzeitschriften\nISI:000306008000011\n22472952.0\n10.1097/PAS.0b013e31824f4f66\nNone\nPityriasis lichenoides comprises a clinicopathologic spectrum of cutaneous inflammatory disorders, with the 2 most common variants being pityriasis lichenoides et varioliformis acuta (PLEVA) and pityriasis lichenoides chronica. The aim of the study was to describe 13 cases of a unique PLEVA variant characterized in the conspicuous CD30 component and thus mimicking lymphomatoid papulosis (LyP), a condition currently classified in the spectrum of CD30 lymphoproliferative disorders. The cohort included 10 female and 3 male patients whose ages at diagnosis ranged from 7 to 89 years (mean 41 y; median 39 y). The clinical manifestation was that of PLEVA, with small erythematous macules quickly evolving into necrotic papules. No waxing and waning was seen on follow-up in any of the cases. Histopathologically, typical features of PLEVA were present, but an unusual finding was occurrence of a considerable number of CD30 small lymphocytes as detected immunohistochemically. Over half of the cases also displayed a large number of CD8 cells and showed coexpression of CD8 and CD30 in the intraepidermal and dermal component of the infiltrate. Of the 11 cases of PLEVA studied for T-cell receptor gene rearrangement, 6 evidenced a monoclonal T-cell population, and 5 were polyclonal. Parvovirus B19 (PVB19) DNA was identified in 4 of 10 cases investigated, and positive serology was observed for PVB19 in 2 patients, altogether suggesting that PVB19 is pathogenetically linked to PLEVA at least in a subset of cases. The presence of CD30 lymphocytes and CD8 lymphocytes would be consistent with an inflammatory antiviral response, as CD30, even atypically appearing lymphoid cells have been identified in some viral skin diseases. The main significance of the PLEVA variant is, however, its potential confusion with LyP or some cytotoxic lymphomas. Admittedly, the CD30 PLEVA variant described herein and LyP show considerable overlap if one takes into account all known variations of the 2 conditions recognized in recent years, thus suggesting that LyP and PLEVA may be much more biologically closely related entities than currently thought or can even occur on a clinicopathologic spectrum.\n\n\n"
},
{
"text": "\n131163\nHuman endometrial mesenchymal stem cells modulate the tissue response and mechanical behavior of polyamide mesh implants for pelvic organ prolapse repair.\n\nUlrich, D\n\nEdwards, SL\n\nSu, K\n\nTan, KS\n\nWhite, JF\n\nRamshaw, JA\n\nLo, C\n\nRosamilia, A\n\nWerkmeister, JA\n\nGargett, CE\n\nBeiträge in Fachzeitschriften\nISI:000331208800032\n24083684.0\n10.1089/ten.TEA.2013.0170\nPMC3926142\nPelvic organ prolapse (POP) is defined as the descent of one or more of the pelvic structures into the vagina and includes uterine, vaginal vault, and anterior or posterior vaginal wall prolapse. The treatment of POP may include implantation of a synthetic mesh. However, the long-term benefit of mesh surgery is controversial due to complications such as mesh exposure or pain. The aim of this study was to use a tissue engineering (TE) approach to assess the in vivo biological and biomechanical behavior of a new gelatin/polyamide mesh, seeded with a novel source of mesenchymal stem cells in a subcutaneous rat model of wound repair.\n W5C5-enriched human endometrial mesenchymal stem cells (eMSC) were seeded onto meshes (gelatin-coated polyamide knit) at 100, 00 cells/cm². Meshes, with or without cells were subcutaneously implanted dorsally in immunocompromised rats for 7, 30, 60, and 90 days. Flow cytometry was used to detect DiO labeled cells after explantation. Immunohistochemical assessment of foreign body reaction and tissue integration were conducted. Total collagen and the levels of collagens type III and type I were determined. Uniaxial tensiometry was performed on explanted meshes, originally seeded with and without cells, at days 7 and 90.\n Implanted meshes were well tolerated, with labeled cells detected on the mesh up to 14 days postimplantation. Meshes with cells promoted significantly more neovascularization at 7 days (p<0.05) and attracted fewer macrophages at 90 days (p<0.05). Similarly, leukocyte infiltration was significantly lower in the cell-seeded meshes at 90 days (p<0.05). Meshes with cells were generally less stiff than those without cells, after 7 and 90 days implantation.\n The TE approach used in this study significantly reduced the number of inflammatory cells around the implanted mesh and promoted neovascularization. Seeding with eMSC exerts an anti-inflammatory effect and promotes wound repair with new tissue growth and minimal fibrosis, and produces mesh with greater extensibility. Cell seeding onto polyamide/gelatin mesh improves mesh biocompatibility and may be an alternative option for future treatment of POP.\n\nGold ehem Ulrich, Daniela\n\n\n"
},
{
"text": "\n140958\nPresence of human polyomavirus 6 in mutation-specific BRAF inhibitor-induced epithelial proliferations.\n\nSchrama, D\n\nGroesser, L\n\nUgurel, S\n\nHafner, C\n\nPastrana, DV\n\nBuck, CB\n\nCerroni, L\n\nTheiler, A\n\nBecker, JC\n\nBeiträge in Fachzeitschriften\nISI:000346234300010\n24943872.0\n10.1001/jamadermatol.2014.1116\nNone\nA frequent adverse effect of mutation-specific BRAF inhibitor therapy is the induction of epithelial proliferations including cutaneous squamous cell carcinomas. To date, the only factor identified contributing to their development is the activation of the mitogen-activated signal transduction cascade by mutations in the RAS genes. However, these mutations explain only 60% of the tumors; hence, it is important to identify what is causing the remaining tumors.\n To test for the presence of human papillomaviruses (HPVs) and the recently identified human polyomaviruses (HPyVs), Merkel cell polyomavirus (MCPyV), and trichodysplasia spinulosa-associated polyomavirus (TSPyV), as well as HPyV-6, HPyV-7, HPyV-9, and HPyV-10, in epithelial proliferations occurring after BRAF inhibitor therapy to determine whether these oncogenic viruses may contribute to BRAF inhibitor-induced skin tumors.\n Retrospective study at a university hospital in Austria of epithelial proliferations that developed in patients with melanoma after initiation of treatment with the BRAF inhibitor vemurafenib. Samples were analyzed for (1) presence of the most frequently observed RAS mutations by SNaPshot technology, (2) detection of the viruses by real-time polymerase chain reaction, and (3) presence of capsid proteins of the most abundantly detected virus by immunohistochemical analysis.\n RAS mutational status, as well as HPV and HPyV presence, in BRAF inhibitor-induced epithelial proliferations.\n Eighteen biopsy samples from 6 patients were retrieved from our hospital's archive. We identified RAS mutations in 10 (62%) of the 16 samples with clear results. DNA of HPyV-9, HPyV-10, and TSPyV were virtually absent in the samples. MCPyV DNA was present in 13 of 18 samples, and HPV, HPyV-6, and HPyV-7 DNA were present in all samples. In general, the amount of DNA encoding the latter viruses was rather low, with the exception of HPyV-6 in several samples of 1 individual patient. Notably, the relevance of the presence of HPyV-6 in the epithelial proliferation was underlined by immunohistochemical detection of the core protein VP1 of HPyV-6.\n The presence of both high HPyV-6 DNA load and VP1 protein suggests that polyomaviruses may contribute to the epithelial proliferations observed in patients receiving BRAF inhibitor therapy, albeit the relative impact as compared with that of RAS mutations appears circumstantial.\n\nCerroni, Lorenzo\n\n\n"
},
{
"text": "\n146379\nClinical Course of acute-on-chronic liver failure syndrome and effects on prognosis.\n\nGustot, T\n\nFernandez, J\n\nGarcia, E\n\nMorando, F\n\nCaraceni, P\n\nAlessandria, C\n\nLaleman, W\n\nTrebicka, J\n\nElkrief, L\n\nHopf, C\n\nSolís-Munoz, P\n\nSaliba, F\n\nZeuzem, S\n\nAlbillos, A\n\nBenten, D\n\nMontero-Alvarez, JL\n\nChivas, MT\n\nConcepción, M\n\nCórdoba, J\n\nMcCormick, A\n\nStauber, R\n\nVogel, W\n\nde Gottardi, A\n\nWelzel, TM\n\nDomenicali, M\n\nRisso, A\n\nWendon, J\n\nDeulofeu, C\n\nAngeli, P\n\nDurand, F\n\nPavesi, M\n\nGerbes, A\n\nJalan, R\n\nMoreau, R\n\nGinés, P\n\nBernardi, M\n\nArroyo, V\n\nCANONIC Study Investigators of the EASL-CLIF Consortium\n\nBeiträge in Fachzeitschriften\nISI:000356864800030\n25877702.0\n10.1002/hep.27849\nNone\nAcute-on-chronic liver failure (ACLF) is characterized by acute decompensation (AD) of cirrhosis, organ failure(s), and high 28-day mortality. We investigated whether assessments of patients at specific time points predicted their need for liver transplantation (LT) or the potential futility of their care. We assessed clinical courses of 388 patients who had ACLF at enrollment, from February through September 2011, or during early (28-day) follow-up of the prospective multicenter European Chronic Liver Failure (CLIF) ACLF in Cirrhosis study. We assessed ACLF grades at different time points to define disease resolution, improvement, worsening, or steady or fluctuating course. ACLF resolved or improved in 49.2%, had a steady or fluctuating course in 30.4%, and worsened in 20.4%. The 28-day transplant-free mortality was low-to-moderate (6%-18%) in patients with nonsevere early course (final no ACLF or ACLF-1) and high-to-very high (42%-92%) in those with severe early course (final ACLF-2 or -3) independently of initial grades. Independent predictors of course severity were CLIF Consortium ACLF score (CLIF-C ACLFs) and presence of liver failure (total bilirubin ≥12 mg/dL) at ACLF diagnosis. Eighty-one percent had their final ACLF grade at 1 week, resulting in accurate prediction of short- (28-day) and mid-term (90-day) mortality by ACLF grade at 3-7 days. Among patients that underwent early LT, 75% survived for at least 1 year. Among patients with ≥4 organ failures, or CLIF-C ACLFs >64 at days 3-7 days, and did not undergo LT, mortality was 100% by 28 days.\n Assessment of ACLF patients at 3-7 days of the syndrome provides a tool to define the emergency of LT and a rational basis for intensive care discontinuation owing to futility.\n © 2015 by the American Association for the Study of Liver Diseases.\n\nStauber, Rudolf\n\n\n"
},
{
"text": "\n148929\nRisk Factors for Sternal Wound Infection After Open Heart Operations Vary According to Type of Operation.\n\nMeszaros, K\n\nFuehrer, U\n\nGrogg, S\n\nSodeck, G\n\nCzerny, M\n\nMarschall, J\n\nCarrel, T\n\nBeiträge in Fachzeitschriften\nISI:000372522700037\n26652136.0\n10.1016/j.athoracsur.2015.09.010\nNone\nThis study evaluated whether risk factors for sternal wound infections vary with the type of surgical procedure in cardiac operations.\n This was a university hospital surveillance study of 3, 49 consecutive patients (28% women) from 2006 to 2010 (median age, 69 years [interquartile range, 60 to 76]; median additive European System for Cardiac Operative Risk Evaluation score, 5 [interquartile range, 3 to 8]) after (1) isolated coronary artery bypass grafting (CABG), (2) isolated valve repair or replacement, or (3) combined valve procedures and CABG. All other operations were excluded. Univariate and multivariate binary logistic regression were conducted to identify independent predictors for development of sternal wound infections.\n We detected 122 sternal wound infections (3.8%) in 3, 49 patients: 74 of 1, 57 patients (4.0%) after CABG, 19 of 799 (2.4%) after valve operations, and 29 of 593 (4.9%) after combined procedures. In CABG patients, bilateral internal thoracic artery harvest, procedural duration exceeding 300 minutes, diabetes, obesity, chronic obstructive pulmonary disease, and female sex (model 1) were independent predictors for sternal wound infection. A second model (model 2), using the European System for Cardiac Operative Risk Evaluation, revealed bilateral internal thoracic artery harvest, diabetes, obesity, and the second and third quartiles of the European System for Cardiac Operative Risk Evaluation were independent predictors. In valve patients, model 1 showed only revision for bleeding as an independent predictor for sternal infection, and model 2 yielded both revision for bleeding and diabetes. For combined valve and CABG operations, both regression models demonstrated revision for bleeding and duration of operation exceeding 300 minutes were independent predictors for sternal infection.\n Risk factors for sternal wound infections after cardiac operations vary with the type of surgical procedure. In patients undergoing valve operations or combined operations, procedure-related risk factors (revision for bleeding, duration of operation) independently predict infection. In patients undergoing CABG, not only procedure-related risk factors but also bilateral internal thoracic artery harvest and patient characteristics (diabetes, chronic obstructive pulmonary disease, obesity, female sex) are predictive of sternal wound infection. Preventive interventions may be justified according to the type of operation.\n Copyright © 2016 The Society of Thoracic Surgeons. Published by Elsevier Inc. All rights reserved.\n\nMarsoner, Katharina\n\n\n"
},
{
"text": "\n160333\nAnalysis of the in vitro secretory activity of human pituitary adenomas: modification of corticotropin release from adenoma tissue explant cultures by addition of a human plasma ultrafiltrate bioactive fraction.\n\nZarković, N\n\nHayn, M\n\nPlavsić, V\n\nZarković, K\n\nPaladino, J\n\nHirsl, N\n\nGolubić, J\n\nMikulandra, S\n\nRogić, D\n\nSalzer, B\n\nPokrić, B\n\nSchaur, RJ\n\nTatzber, F\n\nFaulhammer, H\n\nBenko, B\n\nDietrich, W\n\nJurin, M\n\nKorsić, M\n\nBeiträge in Fachzeitschriften\nISI:A1996TV25500005\n8704030.0\nNone\nNone\nThe lack of control of tumour behaviour is manifested in different ways, depending primarily on the type of tumour. This results in numerous problems of tumour diagnosis and therapy. In the case of "benign" tumours, like pituitary adenomas, in vitro studies are often used for evaluation of the tumour. The use of tissue explant cultures of human pituitary adenomas and the comparison of the feature of cultured tumours with their behaviour in vivo showed that corticotropin is released not only from the tumours associated with Cushing's disease, but also from clinically non-functioning tumours. Hence, it was supposed that the release of corticotropin in vivo from non-secreting tumours is probably under the influence of certain neuroendocrine and/or systemic humoral factors. To test this possibility, samples of 22 tumours were cultured in plain culture medium or in the presence of the "human plasma ultrafiltrate bioactive fraction" (tentatively termed as TBP) prepared by anion-exchange chromatography. In the presence of TBP the release of corticotropin was strongly inhibited in adenomas showing relatively high spontaneous secreting activity in vitro (> 200 ng/l in 24 hours), while immunohistochemistry of these tumours indicated accumulation of corticotropin inside the cells. In contrast, TBP stimulated corticotropin release from tumours that showed relatively low basic corticotropin release (< 200 ng/l in 24 hours), with no obvious change in cellular corticotropin immunoreactivity. Such a dual activity of TBP was not observed for 8 samples of adenomas cultured in the presence of surrounding pituitary tissue, probably because TBP did not affect corticotropin secretion by the normal pituitary cells (as indicated by immunohistochemistry). From these results, it appears that TBP could be one of the humoral factors involved in the regulation of corticotropin release from pituitary adenoma tissue. Its possible involvement in the regulation of corticotropin release from normal pituitary tissue, however, is uncertain.\n\nTatzber, Franz\n\n\n"
},
{
"text": "\n160338\nIntake of mercury from fish, lipid peroxidation, and the risk of myocardial infarction and coronary, cardiovascular, and any death in eastern Finnish men.\n\nSalonen, JT\n\nSeppänen, K\n\nNyyssönen, K\n\nKorpela, H\n\nKauhanen, J\n\nKantola, M\n\nTuomilehto, J\n\nEsterbauer, H\n\nTatzber, F\n\nSalonen, R\n\nBeiträge in Fachzeitschriften\nISI:A1995QD43400007\n7828289.0\n10.1161/01.CIR.91.3.645\nNone\nEven though previous studies have suggested an association between high fish intake and reduced coronary heart disease (CHD) mortality, men in Eastern Finland, who have a high fish intake, have an exceptionally high CHD mortality. We hypothesized that this paradox could be in part explained by high mercury content in fish.\n We studied the relation of the dietary intake of fish and mercury, as well as hair content and urinary excretion of mercury, to the risk of acute myocardial infarction (AMI) and death from CHD, cardiovascular disease (CVD), and any cause in 1833 men aged 42 to 60 years who were free of clinical CHD, stroke, claudication, and cancer. Of these, 73 experienced an AMI in 2 to 7 years. Of the 78 decreased men, 18 died of CHD and 24 died of CVD. Men who had consumed local nonfatty fish species had elevated hair mercury contents. In Cox models with the major cardiovascular risk factors as covariates, dietary intakes of fish and mercury were associated with significantly increased risk of AMI and death from CHD, CVD, and any death. Men in the highest tertile (> or = 2.0 micrograms/g) of hair mercury content had a 2.0-fold (95% confidence interval, 1.2 to 3.1; P = .005) age- and CHD-adjusted risk of AMI and a 2.9-fold (95% CI, 1.2 to 6.6; P = .014) adjusted risk of cardiovascular death compared with those with a lower hair mercury content. In a nested case-control subsample, the 24-hour urinary mercury excretion had a significant (P = .042) independent association with the risk of AMI. Both the hair and urinary mercury associated significantly with titers of immune complexes containing oxidized LDL.\n These data suggest that a high intake of mercury from nonfatty freshwater fish and the consequent accumulation of mercury in the body are associated with an excess risk of AMI as well as death from CHD, CVD, and any cause in Eastern Finnish men and this increased risk may be due to the promotion of lipid peroxidation by mercury.\n\nTatzber, Franz\n\n\n"
}
]
}