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        {
            "text": "\n4691\nDifferences in cephalometric and occlusal outcome of cleft palate patients regarding different surgical techniques.\n\nGaggl, A\n\nSchultes, G\n\nFeichtinger, M\n\nSantler, G\n\nMossböck, R\n\nKärcher, H\n\nBeiträge in Fachzeitschriften\nISI:000181093200004\n12553922.0\n10.1016/S1010-5182(02)00142-7\nNone\nIntroduction: The purpose of this study was to assess differences of the long-term results following surgical treatment in patients with cleft palate treated by two different surgical concepts. Patients: Fifty-nine adult patients operated on for cleft palate were examined. Thirty palates were closed by a two stage (Widmaier and Veau) and 29 by a single-stage procedure (Veau's pedicled flap). Methods: Lateral cephalometric and model analysis was performed. In the cephalometric analysis, the vertical and horizontal parameters of the position of maxilla and midface and transverse and sagittal dimensions of the models were compared between the two groups. Results: Model analysis: According to the Bolton analysis the maxillary dental arch was too large in 22 patients in each group. The other patients had mandibular arches that were too large. In 18 patients with two-stage closure and in 9 patients with one-stage closure, a space deficit in the lateral part of the maxilla was observed. Persisting transverse deficits were seen in all patients with two-stage repairs and in, 11 patients with one-stage repairs. The deficit was more severe in the molar area in the first group and almost equally severe in the premolar and the molar regions of the second group. A sagittal deficiency was found more often in patients with two-stage repairs while Angle's class I occlusion was seen more often in patients with one-stage surgery. Lateral cephalometry: Similar SNA-angles were seen in both groups whereas the ANB-angle was greater following two-stage repair. In both patient groups a low inclination of the midface was seen. The vertical dimension of the midface in comparison with the lower face was normal in the one-stage group; in the other group a deficiency of the anterior midface height was registered, Conclusion: There was a more severe growth impairment of the midface in patients with this type of two-stage palatal repair. The horizontal deficiency was similar in both groups. The long-term occlusal result revealed smaller sagittal and transverse deficiencies in patients with this type of single-stage closure. (C) 2002 European Association for Cranio-Maxillofacial Surgery.\n\nKärcher, Hans\n\nSantler, Gert\n\n\n"
        },
        {
            "text": "\n8087\nApolipoproteins and lipoproteins of human plasma: significance in health and in disease.\n\nKostner, GM\n\nBeiträge in Fachzeitschriften\nISI:A1983SA24700001\n6230900.0\nNone\nNone\nWhen DeLalla and Gofman (1954) presented their work "Ultracentrifugal Analysis of Serum Lipoproteins" more than 25 years ago, we were thinking about lipoproteins in terms of density fractions. In the 1970s the electrophoresis concept was pushed by Fredrickson and his colleagues (Fredrickson et al., 1967). There is no doubt that both these lipoprotein research centers have fertilized entire investigations in this field and still have a tremendous impact on our current knowledge. It was, however, not until 1966, when Gustafson, Alaupovic, and Furmann first described the presence of a third lipoprotein family, LpC, that researchers in this area became aware of the dominant role of apolipoproteins in the transport and metabolism of plasma lipids. Lipoprotein density fractions and electrophoretic classes in the mean time have not lost their importance; they still exist and the application of methods yielding those fractions is still going on in lipoprotein laboratories. Yet we need to recognize that the whole lipid transport system is far more complex than was believed some 10 or 20 years ago. Lipoprotein density fractions consist of varying numbers of families; some of them comigrate upon electrophoresis, and the protein moiety of them is mostly composed of nonidentical polypeptides. There are a number of inborn errors of metabolism, for example, ABL, Tangier disease, and enzyme defects, which have taught us a lot about the functions and interplay of the complex apolipoprotein system. In dyslipoproteinemia, abnormal lipoproteins occur in the plasma and apolipoproteins, which are hardly recognized in normal fasting plasma, suddenly become prominent. There still exist, however, apolipoproteins and lipoproteins, one of which certainly is Lp(a), whose function and biological significance remains completely unknown. The structure and the molecular arrangement of lipids and apolipoproteins within a lipoprotein particle has been the subject of intensive investigations, and almost every physicochemical method available has been applied to reveal the morphology of individual lipoproteins in closest detail. Lipoproteins and apolipoproteins have often also served as model substances for cell membranes. After the purification of individual apolipoproteins succeeded in many laboratories and specific antibodies were available, clinical chemists and epidemiologists became interested in this area of research. Apolipoprotein quantification currently is most prominent for the prediction of atherosclerotic risk in preventive medicine.(ABSTRACT TRUNCATED AT 400 WORDS)\n\nKostner, Gerhard\n\n\n"
        },
        {
            "text": "\n63478\nResponse of human NK cells to IL-6 alterations of the cell surface phenotype, adhesion to fibronectin and laminin, and tumor necrosis factor-alpha/beta secretion.\n\nRabinowich, H\n\nSedlmayr, P\n\nHerberman, RB\n\nWhiteside, TL\n\nBeiträge in Fachzeitschriften\nISI:A1993LD91600013\n8496590.0\nNone\nNone\nIn vitro effects of human recombinant IL-6 (1-1000 U/ml) on highly enriched human NK CD3-CD56+ cells (94% +/- 2; mean +/- SEM; n = 8), obtained from PBL were studied. IL-6 induced low levels of NK cell proliferation (7- to 30-fold during 6-day incubation), which was IL-2-independent, because IL-6 did not induce detectable IL-2 production by NK cells. Two-color flow cytometry analysis demonstrated that incubation of NK cells with IL-6 at the optimal concentration of 250 U/ml for 6 days significantly increased the proportion of NK cells expressing the following activation Ag: CD25 (26% +/- 17, mean +/- SEM vs 4% +/- 1 in control, n = 5), CD54 (44% +/- 17 vs 9% +/- 3), HLA-DR (29% +/- 13 vs 12% +/- 4), CD69 (45% +/- 7 vs 12% +/- 3), and CD71 (34% +/- 17 vs 6% +/- 2). The mean fluorescence intensity of these activation Ag was increased as well. IL-6 induced expression of CD49b (alpha-chain of VLA-2, 20% +/- 11 vs 2% +/- 1) and CD49c (alpha-chain of VLA-3, 43% +/- 17 vs 5% +/- 3), which are not expressed on resting NK cells. IL-6 also enhanced the fluorescence intensity of beta 1 integrins, CD49d, CD49e, and CD49f, expressed on NK cells. IL-6-stimulated NK cells showed significantly increased integrin-mediated adhesion to fibronectin- or laminin-coated plates (26 +/- 3 mean % cells adhering +/- SEM vs 15 +/- 4 in control for FN and 19 +/- 1 vs 11 +/- 1 for LM, p < 0.05 for both) as determined in a 3 h binding assay. As assessed by inhibition of adhesion using mAb to the VLA-2, -3, -4, -5, and -6, NK cell adhesion to fibronectin was mediated by VLA-4 and 5, and their adhesion to laminin by VLA-3 and -6. NK cells incubated in the presence of IL-6 were found to produce a factor cytostatic to WEHI-164 clone 13 target cells. This effect was partly, although significantly, blocked by neutralizing antibodies to TNF-alpha or TNF-beta. Our data demonstrate that IL-6 can directly activate human NK cells, but is a less potent NK cell activator, for all activation and functional parameters studied, than IL-2.\n\nSedlmayr, Peter\n\n\n"
        },
        {
            "text": "\n71246\nTemperature-controlled slow pathway ablation for treatment of atrioventricular nodal reentrant tachycardia using a combined anatomical and electrogram guided strategy.\n\nWillems, S\n\nShenasa, H\n\nKottkamp, H\n\nChen, X\n\nHindricks, G\n\nYli-Mäyry, S\n\nHaverkamp, W\n\nWichter, T\n\nRotman, B\n\nBreithardt, G\n\nBorggrefe, M\n\nBeiträge in Fachzeitschriften\nISI:A1996UU20200023\n8809528.0\nNone\nNone\nAIMS: Anatomical and electrogram-guided techniques have been used separately for slow pathway ablation in atrioventricular nodal reentrant tachycardia. The aims of the present study were to analyse electrogram characteristics of target sites and biophysical parameters using a combined anatomical and electrogram-guided technique for temperature-controlled radiofrequency catheter ablation of the slow pathway. METHODS AND RESULTS: Using a temperature-controlled (pre-selected 60 degrees C) catheter system, 53 patients with atrioventricular nodal reentrant tachycardia underwent slow pathway radiofrequency ablation. Mapping was started posteroseptally near the coronary sinus ostium and continued towards the midseptal area if needed. The longest and latest atrial electrograms with an atrioventricular ratio of < or = 0.5 were targeted. After a median of two pulses (mean 2.36 +/- 1.33), atrioventricular nodal reentrant tachycardia was rendered non-inducible in all patients without complications. Successful sites had longer atrial electrograms (78.8 +/- 9.8 vs 67.6 +/- 13.3 ms, P < 0.003) and larger ventricular electrogram amplitudes (92.4 +/- 51.2 vs 63.1 +/- 28.8 mV, P < 0.05) than the failed sites, but had a similar atrioventricular ratio, P-A interval and atrial electrogram amplitude. Overall, an atrial electrogram duration of > or = 70 ms was associated with effective radiofrequency delivery, with 86% sensitivity and 62% specificity. The achieved temperature maximum was 62.3 +/- 9.8 degrees C at successful and 58.8 +/- 9.0 degrees C at unsuccessful sites (ns). There was no significant difference between successful and unsuccessful applications with respect to power output, impedance and total delivery energy. During a pre-discharge study, three patients with inducible atrioventricular nodal reentrant tachycardia underwent a repeat ablation. During 12.3 +/- 2.5 (6-15) months of follow-up, three others had a clinical recurrence of atrioventricular nodal reentrant tachycardia. CONCLUSIONS: The combined approach for slow pathway ablation is highly effective, requiring a low number of radiofrequency pulses. Long atrial activation time seems to be the most powerful predictor of success. Similar catheter tip temperature levels during successful and unsuccessful radiofrequency applications indicate that suboptimal selection of target sites rather than ineffective heating due to poor catheter tissue coupling is responsible for unsuccessful energy delivery.\n\n\n"
        },
        {
            "text": "\n72090\nIn vivo treatment with anti-I-A antibodies: differential effects on Ia antigens and antigen-presenting cell function of spleen cells and epidermal Langerhans cells.\n\nAberer, W\n\nKruisbeek, AM\n\nShimada, S\n\nKatz, SI\n\nBeiträge in Fachzeitschriften\nISI:A1986AYB1700013\n3455705.0\nNone\nNone\nThe in vivo activation of T cells by a variety of antigens can be inhibited by the administration of anti-I-A antibodies (Ab) at the time of antigen priming. This inhibition can partially be explained by the temporary loss of Ia molecules from Ia-bearing antigen-presenting cells (APC) in the spleen. In this study, the effects of i.p. injected monoclonal Ab specific for I-A glycoproteins of different H-2 haplotypes on Ia antigen expression and APC function of spleen cells and epidermal Langerhans cells were compared. It was found that anti-I-A Ab quickly bound to both spleen cell and Langerhans cell Ia antigens. Although spleen cell Ia antigens were modulated and thus temporarily disappeared, Ia antigen expression by epidermal Langerhans cells was not modulated. In functional studies, the capacity of spleen cells and epidermal cells from anti-I-A Ab treated vs control animals to function as APC for antigen-specific, I-A- or I-E-restricted T cell clones was tested. A single injection of anti-I-A Ab completely abolished the APC function of spleen cells as shown in several inbred mouse strains, F1 animals, and with the use of several different Ab and T cell clones. In contrast, Langerhans cell-dependent APC function of epidermal cells remained completely unaltered. Even multiple injections of high doses of Ab never caused any inhibition of Langerhans cell function. Experiments with anti-I-Ak or anti-I-Ad Ab in an (H-2k X H-2d)F1 animal showed abrogation of APC function of spleen cells, but again not of Langerhans cells. Thus in vivo anti-I-A Ab administration appears to differentially affect Ia antigen expression and APC function from spleen and epidermis: Ia antigens are modulated from spleen cells but not from epidermis, and APC function disappears in the spleen but not in the epidermis. The abrogation of splenic but not of Langerhans cell APC function with anti-I-A Ab will facilitate the dissection of the relative contributions of Langerhans cells as compared with other APC in the generation of cutaneous immune responses.\n\nAberer, Werner\n\n\n"
        },
        {
            "text": "\n112954\nEffects of a multifaceted educational program on blood pressure and cardiovascular risk in hypertensive patients: the Austrian herz.leben project.\n\nPerl, S\n\nRiegelnik, V\n\nMrak, P\n\nEderer, H\n\nRakovac, I\n\nBeck, P\n\nKraler, E\n\nStoff, I\n\nWinklehner, S\n\nKlima, G\n\nPieske, BM\n\nPieber, TR\n\nZweiker, R\n\nBeiträge in Fachzeitschriften\nISI:000294718500025\n21857535.0\n10.1097/HJH.0b013e32834aa769\nNone\nObjective Although hypertension is the most prevalent risk factor for cardiovascular and cerebrovascular morbidity and mortality, the level of blood pressure control remains poor. To amplify quality of care in hypertensive patients, a multifaceted program consisting of structured educational programs for both patients and staff, structured documentation and feedback reports with peer comparison, was implemented on a multicentre basis. Main targets were improvement of blood pressure control and reduction of cardiovascular risk. A provisional reimbursement was provided. Methods Patients were eligible for inclusion in the program if office blood pressure was uncontrolled (> 160/95 or > 140/90 mmHg) in addition to elevated cardiovascular risk [> 15% according to the New Zealand Risk Score (NZRS)]. Blood pressure and lipid panels were measured at entry in the program and after 12 months. Patients attended four educational units held by hypertension nurses and physicians. All data were collected in structured documentation sheets and benchmarking reports were provided every 6 months. Results Two thousand and forty-one patients were enrolled in the program within 5 years and 3 months; 54% female, age 62.8 +/- 11.1years, BMI 29.50 +/- 7.88 kg/m(2) (mean +/- SD). To date, 744 patients have been seen at 1-year follow-up. Entry blood pressure was 156.1 +/- 20.8/88.9 +/- 11.1 mmHg. Total cholesterol showed mean levels of 207.0 +/- 46.0mg/dl, low-density lipoprotein 122.3 +/- 41.6 mg/dl, high-density lipoprotein 57.2 +/- 22.4 mg/dl and calculated cardiovascular risk level (NZRS) was 17.28 +/- 8.29%. One year following the educational program, blood pressure was reduced to 139.2 +/- 15.6 (P < 0.001)/82.1 +/- 9.5 mmHg (P < 0.001). NZRS (14.1 +/- 7.2%; P < 0.001) and BMI (29.26 +/- 4.92 versus 29.06 +/- 4.99) also improved significantly. Conclusion This structured educational program showed its ability to improve intermediate outcomes in hypertensive patients. Better blood pressure control and significant reduction of the individual cardiovascular risk profile were achieved. A broad implementation of the program in the management of hypertension seems justified. J Hypertens 29:2024-2030 (C) 2011 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins.\n\nPerl, Sabine\n\nPieber, Thomas\n\nZweiker, Robert\n\n\n"
        },
        {
            "text": "\n118142\nTelethonin deficiency is associated with maladaptation to biomechanical stress in the mammalian heart.\n\nKnöll, R\n\nLinke, WA\n\nZou, P\n\nMiocic, S\n\nKostin, S\n\nBuyandelger, B\n\nKu, CH\n\nNeef, S\n\nBug, M\n\nSchäfer, K\n\nKnöll, G\n\nFelkin, LE\n\nWessels, J\n\nToischer, K\n\nHagn, F\n\nKessler, H\n\nDidié, M\n\nQuentin, T\n\nMaier, LS\n\nTeucher, N\n\nUnsöld, B\n\nSchmidt, A\n\nBirks, EJ\n\nGunkel, S\n\nLang, P\n\nGranzier, H\n\nZimmermann, WH\n\nField, LJ\n\nFaulkner, G\n\nDobbelstein, M\n\nBarton, PJ\n\nSattler, M\n\nWilmanns, M\n\nChien, KR\n\nBeiträge in Fachzeitschriften\nISI:000294950000008\n21799151.0\n10.1161/CIRCRESAHA.111.245787\nPMC3664427\nRATIONALE: Telethonin (also known as titin-cap or t-cap) is a 19-kDa Z-disk protein with a unique ß-sheet structure, hypothesized to assemble in a palindromic way with the N-terminal portion of titin and to constitute a signalosome participating in the process of cardiomechanosensing. In addition, a variety of telethonin mutations are associated with the development of several different diseases; however, little is known about the underlying molecular mechanisms and telethonin's in vivo function.\r\n\r\nOBJECTIVE: Here we aim to investigate the role of telethonin in vivo and to identify molecular mechanisms underlying disease as a result of its mutation.\r\n\r\nMETHODS AND RESULTS: By using a variety of different genetically altered animal models and biophysical experiments we show that contrary to previous views, telethonin is not an indispensable component of the titin-anchoring system, nor is deletion of the gene or cardiac specific overexpression associated with a spontaneous cardiac phenotype. Rather, additional titin-anchorage sites, such as actin-titin cross-links via a-actinin, are sufficient to maintain Z-disk stability despite the loss of telethonin. We demonstrate that a main novel function of telethonin is to modulate the turnover of the proapoptotic tumor suppressor p53 after biomechanical stress in the nuclear compartment, thus linking telethonin, a protein well known to be present at the Z-disk, directly to apoptosis ("mechanoptosis"). In addition, loss of telethonin mRNA and nuclear accumulation of this protein is associated with human heart failure, an effect that may contribute to enhanced rates of apoptosis found in these hearts.\r\n\r\nCONCLUSIONS: Telethonin knockout mice do not reveal defective heart development or heart function under basal conditions, but develop heart failure following biomechanical stress, owing at least in part to apoptosis of cardiomyocytes, an effect that may also play a role in human heart failure.\n\nSchmidt, Albrecht\n\n\n"
        },
        {
            "text": "\n122350\nTranscriptome profiling of primary murine monocytes, lung macrophages and lung dendritic cells reveals a distinct expression of genes involved in cell trafficking.\n\nZaslona, Z\n\nWilhelm, J\n\nCakarova, L\n\nMarsh, LM\n\nSeeger, W\n\nLohmeyer, J\n\nvon Wulffen, W\n\nBeiträge in Fachzeitschriften\nISI:000263726500001\n19149869.0\n10.1186/1465-9921-10-2\nPMC2639356\nBACKGROUND: Peripheral blood monocytes (PBMo) originate from the bone marrow, circulate in the blood and emigrate into various organs where they differentiate into tissue resident cellular phenotypes of the mononuclear phagocyte system, including macrophages (Mphi) and dendritic cells (DC). Like in other organs, this emigration and differentiation process is essential to replenish the mononuclear phagocyte pool in the lung under both inflammatory and non-inflammatory steady-state conditions. While many studies have addressed inflammation-driven monocyte trafficking to the lung, the emigration and pulmonary differentiation of PBMo under non-inflammatory conditions is much less understood.\r\n\r\nMETHODS: In order to assess the transcriptional profile of circulating and lung resident mononuclear phagocyte phenotypes, PBMo, lung Mphi and lung DC from naïve mice were flow-sorted to high purity, and their gene expression was compared by DNA microarrays on a genome-wide scale. Differential regulation of selected genes was validated by quantitative PCR and on protein level by flow cytometry.\r\n\r\nRESULTS: Differentially-expressed genes related to cell traffic were selected and grouped into the clusters (i) matrix metallopeptidases, (ii) chemokines/chemokine receptors, and (iii) integrins. Expression profiles of clustered genes were further assessed at the mRNA and protein levels in subsets of circulating PBMo (GR1- vs GR1+) and lung resident macrophages (alveolar vs interstitial Mphi). Our data identify differentially activated genetic programs in circulating monocytes and their lung descendents. Lung DC activate an extremely diverse set of gene families but largely preserve a mobile cell profile with high expression levels of integrin and chemokine/chemokine receptors. In contrast, interstitial and even more pronounced alveolar Mphi, stepwise downregulate gene expression of these traffic relevant communication molecules, but strongly upregulate a distinct set of matrix metallopetidases potentially involved in tissue invasion and remodeling.\r\n\r\nCONCLUSION: Our data provide new insight in the changes of the genetic profiles of PBMo and their lung descendents, namely DC and Mphi under non-inflammatory, steady-state conditions. These findings will help to better understand the complex relations within the mononuclear phagocyte pool of the lung.\n\nMarsh, Leigh\n\n\n"
        },
        {
            "text": "\n139894\nClinical course of illness in women with early onset puerperal psychosis: a 12-year follow-up study.\n\nKapfhammer, HP\n\nReininghaus, EZ\n\nFitz, W\n\nLange, P\n\nBeiträge in Fachzeitschriften\nISI:000345557300025\n25373118.0\n10.4088/JCP.13m08769\nNone\nTo complete a follow-up analysis at a mean of 12 years after patients had presented with an early onset puerperal psychotic index episode.\n                A retrospective design was used. Patients with puerperal psychosis and onset within 4 weeks after childbirth who had been referred to the Psychiatric Department of the Ludwig Maximilian University of Munich, Munich, Germany, between 1975 and 1995 (maximum: 24 years, minimum: 7 years) were followed up after a mean of 12 years post index episode. Ninety patients were included in the study. Before the index episode, 35 of the patients had previous nonpuerperal psychoses, while 55 patients presented their index episode as the first manifestation of a psychotic illness. Diagnostic evaluation at follow-up was performed by the Structured Clinical Interview for DSM-IV Axis I Disorders according to DSM-IV-TR. Differential rates of risk of psychotic relapse were calculated. Data on some gynecologic variables (postpartum blues, premenstrual tension, psychiatric symptoms triggered perimenstrually, mood symptoms while taking oral contraceptives) were collected. Clinical and psychosocial outcomes were measured by the Global Assessment Scale and Disability Assessment Scale.\n                Patients who presented with major depression and bipolar affective disorder with psychotic features at the initial index episode showed overall diagnostic stability. Many patients with initial brief psychosis (cycloid psychosis) shifted to a clear bipolar affective disorder. The general risk of a psychotic relapse was high (previous psychosis = 0.77 vs first psychotic manifestation = 0.56; not significant). The risk after further pregnancies was 0.57 versus 0.48, respectively (not significant), and the risk regarding at least 1 other psychotic nonindex episode was 0.71 versus 0.44, respectively (P = .015). Gynecologic variables did not significantly discriminate between the groups. In some patients, a possible link to a hormonal susceptibility was discussed. Patients who remained without any further psychotic relapse (n = 24) had a favorable outcome.\n                Puerperal psychosis of an early onset seemed to be of a prevailing affective nature. Brief psychosis (cycloid psychosis) during a puerperal index episode showed a strong link to bipolar affective disorder in the further course of illness. Outcome was excellent in patients without a further psychotic relapse.\n                © Copyright 2014 Physicians Postgraduate Press, Inc.\n\nFitz, Werner\n\nKapfhammer, Hans-Peter\n\nReininghaus, Eva\n\n\n"
        },
        {
            "text": "\n160688\nUnto the third generation: evidence for strong familial aggregation of physicians, psychologists, and psychotherapists among first-year medical and psychology students in a nationwide Austrian cohort census.\n\nTran, US\n\nBerger, N\n\nArendasy, ME\n\nGreitemeyer, T\n\nHimmelbauer, M\n\nHutzler, F\n\nKraft, HG\n\nOettl, K\n\nPapousek, I\n\nVitouch, O\n\nVoracek, M\n\nBeiträge in Fachzeitschriften\nISI:000400583300005\n28468682.0\n10.1186/s12909-017-0921-4\nPMC5415715\nMedical students present higher numbers of physician relatives than expectable from the total population prevalence of physicians. Evidence for such a familial aggregation effect of physicians has emerged in investigations from the Anglo-American, Scandinavian, and German-speaking areas. In particular, past data from Austria suggest a familial aggregation of the medical, as well as of the psychological and psychotherapeutic, professions among medical and psychology undergraduates alike. Here, we extend prior related studies by examining (1) the extent to which familial aggregation effects apply to the whole nation-wide student census of all relevant (eight) public universities in Austria; (2) whether effects are comparable for medical and psychology students; (3) and whether these effects generalize to relatives of three interrelated health professions (medicine, psychology, and psychotherapy).\n                We investigated the familial aggregation of physicians, psychologists, and psychotherapists, based on an entire cohort census of first-year medical and psychology students (n = 881 and 920) in Austria with generalized linear mixed models.\n                For both disciplines, we found strong familial aggregation of physicians, psychologists, and psychotherapists. As compared with previous results, directionally opposite time trends within disciplines emerged: familial aggregation of physicians among medical students has decreased, whilst familial aggregation of psychologists among psychology students has increased. Further, there were sex-of-relative effects (i.e., more male than female physician relatives), but no substantial sex-of-student effects (i.e., male and female students overall reported similar numbers of relatives for all three professions of interest). In addition, there were age-benefit effects, i.e., students with a relative in the medical or the psychotherapeutic profession were younger than students without, thus suggesting earlier career decisions.\n                The familial aggregation of physicians, psychologists, and psychotherapists is high among medical and psychology undergraduates in Austria. Discussed are implications of these findings (e.g., gender equity, feminization of the medical field, ideas for curricular implementation and student counselling), study limitations, and avenues for future research.\n\nÖttl, Karl\n\n\n"
        },
        {
            "text": "\n163619\nChanges of intestinal microbiota composition and diversity in very low birth weight infants related to strategies of NEC prophylaxis: protocol for an observational multicentre pilot study.\n\nKurath-Koller, S\n\nMoissl-Eichinger, C\n\nGorkiewicz, G\n\nKraschl, R\n\nKanduth, C\n\nHopfer, B\n\nUrlesberger, B\n\nResch, B\n\nBeiträge in Fachzeitschriften\nNone\n29152325.0\n10.1186/s40814-017-0195-y\nPMC5678711\nAt the Division of Neonatology, Department of Paediatrics, Medical University Graz, a unique regimen of necrotizing enterocolitis (NEC) prophylaxis in preterm infants showing a < 1500 g birth weight (i.e. very low birth weight, VLBW) is used. The regimen includes oral antibiotic and antifungal therapy and probiotic preparations as well as a standardised feeding regimen. The incidence of NEC in preterm infants treated by this regimen has been shown to be lower, reflecting 0.7% when treatment was initiated on the first day of life, compared to international incidence rates (5.1%). However, the impact of the prophylaxis regimen on the intestinal microbiome is yet unknown.\n                We here report the protocol of an observational multicentre STROBE compliant pilot study in VLBW preterm infants. Research will compare three groups as defined by different NEC prophylaxis regimens. Each centre will provide 20 infants. Stool samples will be collected every 2 days throughout the first 2 weeks of life. Samples will be stored at - 80 °C until 16S-rRNA sequencing. 16S-rRNA genes will be amplified using suitable primers (specific for bacteria, fungi and archaea) and prepared for MiSeq Sequencing. Analyses will be performed using public analysis-pipelines, such as Mothur and Qiime, thus allowing an analysis of high-throughput community sequencing data. Abundance and composition changes in intestinal microbiota will be compared between the groups throughout the first 2 weeks of life.\n                Different surroundings at the three participating study centres, including contacts to care takers and parents, as well as feeding or medication all might influence intestinal microbiota composition and abundance. In the planned sequel study, this should be kept in mind and a more standardised process ought to be established. However, the results obtained from the presented pilot study will display the burden of bias and help to establish a more strict protocol for the future.\n                Trial has been registered with the German Registry for Clinical Trials (registry ID DRKS00009290).\n\nGorkiewicz, Gregor\n\nKurath-Koller, Stefan\n\nMoissl-Eichinger, Christine\n\nResch, Bernhard\n\nUrlesberger, Berndt\n\n\n"
        },
        {
            "text": "\n171330\nPhase-contrast magnet resonance imaging reveals regional, transmural, and base-to-apex dispersion of mechanical dysfunction in patients with long QT syndrome.\n\nBrado, J\n\nDechant, MJ\n\nMenza, M\n\nKomancsek, A\n\nLang, CN\n\nBugger, H\n\nFoell, D\n\nJung, BA\n\nStiller, B\n\nBode, C\n\nOdening, KE\n\nBeiträge in Fachzeitschriften\nISI:000408584300026\n28479515.0\n10.1016/j.hrthm.2017.04.045\nNone\nRegional dispersion of prolonged repolarization is a hallmark of long QT syndrome (LQTS). We have also revealed regional heterogeneities in mechanical dysfunction in transgenic rabbit models of LQTS.\n                In this clinical pilot study, we investigated whether patients with LQTS exhibit dispersion of mechanical/diastolic dysfunction.\n                Nine pediatric patients with genotyped LQTS (12.2 ± 3.3 years) and 9 age- and sex-matched healthy controls (10.6 ± 1.5 years) were subjected to phase-contrast magnetic resonance imaging to analyze radial (Vr) and longitudinal (Vz) myocardial velocities during systole and diastole in the left ventricle (LV) base, mid, and apex. Twelve-lead electrocardiograms were recorded to assess the heart rate-corrected QT (QTc) interval.\n                The QTc interval was longer in patients with LQTS than in controls (469.1 ± 39.4 ms vs 417.8 ± 24.4 ms; P < .01). Patients with LQTS demonstrated prolonged radial and longitudinal time-to-diastolic peak velocities (TTP), a marker for prolonged contraction duration, in the LV base, mid, and apex. The longer QTc interval positively correlated with longer time-to-diastolic peak velocities (correlation coefficient 0.63; P < .01). Peak diastolic velocities were reduced in LQTS in the LV mid and apex, indicating impaired diastolic relaxation. In patients with LQTS, regional (TTPmax-min) and transmural (TTPVz-Vr) dispersion of contraction duration was increased in the LV apex (TTPVz_max-min: 38.9 ± 25.5 ms vs 20.2 ± 14.7 ms; P = .07; TTPVz-Vr: -21.7 ± 14.5 ms vs -8.7 ± 11.3 ms; P < .05). The base-to-apex longitudinal relaxation sequence was reversed in patients with LQTS compared with controls (TTPVz_base-apex: 14.4 ± 14.9 ms vs -10.1 ± 12.7 ms; P < .01).\n                Patients with LQTS exhibit diastolic dysfunction with reduced diastolic velocities and prolonged contraction duration. Mechanical dispersion is increased in LQTS with an increased regional and transmural dispersion of contraction duration and altered apicobasal longitudinal relaxation sequence. LQTS is an electromechanical disorder, and phase-contrast magnetic resonance imaging Heterogeneity in mechanical dysfunction enables a detailed assessment of mechanical consequences of LQTS.\n                Copyright © 2017 Heart Rhythm Society. Published by Elsevier Inc. All rights reserved.\n\nBugger, Heiko Matthias\n\n\n"
        },
        {
            "text": "\n177812\n<i>N</i>-acetylaspartate availability is essential for juvenile survival on fat-free diet and determines metabolic health.\n\nHofer, DC\n\nZirkovits, G\n\nPelzmann, HJ\n\nHuber, K\n\nPessentheiner, AR\n\nXia, W\n\nUno, K\n\nMiyazaki, T\n\nKon, K\n\nTsuneki, H\n\nPendl, T\n\nAl Zoughbi, W\n\nMadreiter-Sokolowski, CT\n\nTrausinger, G\n\nAbdellatif, M\n\nSchoiswohl, G\n\nSchreiber, R\n\nEisenberg, T\n\nMagnes, C\n\nSedej, S\n\nEckhardt, M\n\nSasahara, M\n\nSasaoka, T\n\nNitta, A\n\nHoefler, G\n\nGraier, WF\n\nKratky, D\n\nAuwerx, J\n\nBogner-Strauss, JG\n\nBeiträge in Fachzeitschriften\nISI:000507466100059\n31638418.0\n10.1096/fj.201801323R\nPMC6894082\nN-acetylaspartate (NAA) is synthesized by aspartate N-acetyltransferase (gene: Nat8l) from acetyl-coenzyme A and aspartate. In the brain, NAA is considered an important energy metabolite for lipid synthesis. However, the role of NAA in peripheral tissues remained elusive. Therefore, we characterized the metabolic phenotype of knockout (ko) and adipose tissue-specific (ako) Nat8l-ko mice as well as NAA-supplemented mice on various diets. We identified an important role of NAA availability in the brain during adolescence, as 75% of Nat8l-ko mice died on fat-free diet (FFD) after weaning but could be rescued by NAA supplementation. In adult life, NAA deficiency promotes a beneficial metabolic phenotype, as Nat8l-ko and Nat8l-ako mice showed reduced body weight, increased energy expenditure, and improved glucose tolerance on chow, high-fat, and FFDs. Furthermore, Nat8l-deficient adipocytes exhibited increased mitochondrial respiration, ATP synthesis, and an induction of browning. Conversely, NAA-treated wild-type mice showed reduced adipocyte respiration and lipolysis and increased de novo lipogenesis, culminating in reduced energy expenditure, glucose tolerance, and insulin sensitivity. Mechanistically, our data point to a possible role of NAA as modulator of pancreatic insulin secretion and suggest NAA as a critical energy metabolite for adipocyte and whole-body energy homeostasis.-Hofer, D. C., Zirkovits, G., Pelzmann, H. J., Huber, K., Pessentheiner, A. R., Xia, W., Uno, K., Miyazaki, T., Kon, K., Tsuneki, H., Pendl, T., Al Zoughbi, W., Madreiter-Sokolowski, C. T., Trausinger, G., Abdellatif, M., Schoiswohl, G., Schreiber, R., Eisenberg, T., Magnes, C., Sedej, S., Eckhardt, M., Sasahara, M., Sasaoka, T., Nitta, A., Hoefler, G., Graier, W. F., Kratky, D., Auwerx, J., Bogner-Strauss, J. G. N-acetylaspartate availability is essential for juvenile survival on fat-free diet and determines metabolic health.\n\nAbdellatif, Mahmoud\n\nGraier, Wolfgang\n\nHöfler, Gerald\n\nKratky, Dagmar\n\nMadreiter-Sokolowski, Corina\n\nPessentheiner, Ariane Raphaela\n\nSedej, Simon\n\n\n"
        },
        {
            "text": "\n1765\nMyxofibrosarcoma. Clinicopathologic analysis of 75 cases with emphasis on the low-grade variant.\n\nMentzel, T\n\nCalonje, E\n\nWadden, C\n\nCamplejohn, RS\n\nBeham, A\n\nSmith, MA\n\nFletcher, CD\n\nBeiträge in Fachzeitschriften\nISI:A1996UC90000001\n8604805.0\n10.1097%2F00000478-199604000-00001\nNone\nMyxofibrosarcoma is one of the most common sarcomas in the extremities of elderly patients. We analysed the clinicopathologic features in a series of 75 patients. All patients were adults (range, 22-91 years; median, 66 years) with an approximately equal incidence in men and women. Thirty-five tumors arose in the lower and 25 in the upper extremities, nine on the trunk, two each in the retroperitoneum and the head and neck region, and one each in the pelvis and penis. Forty-eight cases (69.5%) were located in dermal or subcutaneous tissues. Distinctive histologic features included the following: a commonly nodular growth pattern; a myxoid matrix containing elongated, curvilinear capillaries; and fusiform, round or stellate tumor cells with indistinct cell margins, slightly eosinophilic cytoplasm, and hyperchromatic atypical nuclei. These lesions varied from a hypocellular, mainly myxoid, and purely spindle-cell appearance (low-grade neoplasms) to high-grade, pleomorphic (malignant fibrous histiocytoma-like) lesions with multinucleated giant cells, high mitotic activity, and areas of necrosis. Immunohistochemistry in 44 cases revealed only vimentin and occasional actin positivity. Ultrastructurally, tumor cells had a fibroblastic phenotype. DNA flow cytometry and proliferation analysis showed an association between aneuploidy and histologic grade. An average follow-up of 45 months (range, 5-300 months) in 60 cases has revealed local recurrence in 33 cases (54%). Thirteen patients developed metastases, and 13 tumor-related deaths occurred. A short interval to first local recurrence was associated with poor clinical outcome. The rate of local recurrence was independent of histologic grade, but only intermediate and high-grade neoplasms metastasized. The depth of the primary lesion did not influence the incidence of local recurrence. However, in deep-seated neoplasms, the incidence of metastases was higher and the percentage of tumor-related deaths was twice as high as in superficially located lesions, reflecting the fact that deep-seated lesions tended to be higher-grade, larger tumors. Myxofibrosarcoma tends to become progressively higher grade in recurrences, as demonstrated in five cases in our series. The poorly recognized low-grade myxofibrosarcoma is emphasized, as proper diagnosis and treatment and scrupulous follow-up are mandatory to avoid local recurrence and gradual tumor progression to a higher-grade neoplasm that may then metastasize.\n\n\n"
        },
        {
            "text": "\n115568\nIntracellular Ca2+ inhibits smooth muscle L-type Ca2+ channels by activation of protein phosphatase type 2B and by direct interaction with the channel.\n\nSchuhmann, K\n\nRomanin, C\n\nBaumgartner, W\n\nGroschner, K\n\nBeiträge in Fachzeitschriften\nISI:A1997YF13300002\n9348323.0\n10.1085/jgp.110.5.503\nPMC2229392\nModulation of L-type Ca2+ channels by tonic elevation of cytoplasmic Ca2+ was investigated in intact cells and inside-out patches from human umbilical vein smooth muscle. Ba2+ was used as charge carrier, and run down of Ca2+ channel activity in inside-out patches was prevented with calpastatin plus ATP. Increasing cytoplasmic Ca2+ in intact cells by elevation of extracellular Ca2+ in the presence of the ionophore A23187 inhibited the activity of L-type Ca2+ channels in cell-attached patches. Measurement of the actual level of intracellular free Ca2+ with fura-2 revealed a 50% inhibitory concentration (IC50) of 260 nM and a Hill coefficient close to 4 for Ca2+- dependent inhibition. Ca2+-induced inhibition of Ca2+ channel activity in intact cells was due to a reduction of channel open probability and availability. Ca2+-induced inhibition was not affected by the protein kinase inhibitor H-7 (10 microM) or the cytoskeleton disruptive agent cytochalasin B (20 microM), but prevented by cyclosporin A (1 microg/ ml), an inhibitor of protein phosphatase 2B (calcineurin). Elevation of Ca2+ at the cytoplasmic side of inside-out patches inhibited Ca2+ channels with an IC50 of 2 microM and a Hill coefficient close to unity. Direct Ca2+-dependent inhibition in cell-free patches was due to a reduction of open probability, whereas availability was barely affected. Application of purified protein phosphatase 2B (12 U/ml) to the cytoplasmic side of inside-out patches at a free Ca2+ concentration of 1 microM inhibited Ca2+ channel open probability and availability. Elevation of cytoplasmic Ca2+ in the presence of PP2B, suppressed channel activity in inside-out patches with an IC50 of approximately 380 nM and a Hill coefficient of approximately 3; i.e., characteristics reminiscent of the Ca2+ sensitivity of Ca2+ channels in intact cells. Our results suggest that L-type Ca2+ channels of smooth muscle are controlled by two Ca2+-dependent negative feedback mechanisms. These mechanisms are based on (a) a protein phosphatase 2B-mediated dephosphorylation process, and (b) the interaction of intracellular Ca2+ with a single membrane-associated site that may reside on the channel protein itself.\n\nGroschner, Klaus\n\n\n"
        },
        {
            "text": "\n120858\nAntiresorptives overlapping ongoing teriparatide treatment result in additional increases in bone mineral density.\n\nMuschitz, C\n\nKocijan, R\n\nFahrleitner-Pammer, A\n\nLung, S\n\nResch, H\n\nBeiträge in Fachzeitschriften\nISI:000315103200019\n22836585.0\n10.1002/jbmr.1716\nNone\nDuring teriparatide (TPTD) treatment, high levels of bone formation are accompanied by an increase in bone resorption. The aim of this work was to test if coadministration of raloxifene (RAL) or alendronate (ALN) following 9 months of ongoing TPTD therapy would reopen the anabolic window, thereby exerting additional benefit on bone mineral density (BMD). Postmenopausal women (n = 125) with severe osteoporosis on TPTD treatment for 9 months were randomized into three open-label groups for a further 9 months: ALN (70 mg/week) in addition to TPTD; RAL (60 mg/d) in addition to TPTD; or no medication in addition to TPTD. Amino-terminal propeptide of type I procollagen (P1NP) and cross-linked C-telopeptide (CTX), and areal and volumetric BMD at the lumbar spine and hip were assessed. During the combination period, P1NP concentrations did not change on TPTD monotherapy (693% ± 371%, p < 0.0001) and decreased in the ALN (360% ± 153%, p < 0.0001) and RAL (482% ± 243%, p < 0.0001) combination groups; whereas CTX did not change on TPTD monotherapy (283% ± 215%, p < 0.0001), decreased to the starting level in the ALN combination group (17% ± 72%, p = 0.39), and remained elevated in the RAL combination group (179% ± 341%, p < 0.0001). The increase in lumbar spine BMD was 5% ± 6.3% in the ALN and 6% ± 5.2% in the RAL combination groups compared with 2.8% ± 9.3% in the TPTD monotherapy group (p = 0.085 and p = 0.033, respectively). The increase of trabecular lumbar spine BMD for both the ALN and RAL combination groups was superior to TPTD monotherapy. Total hip BMD changes were 4% ± 5.3% for the ALN combination group and 1.4% ± 5.1% for the TPTD monotherapy (p = 0.032), and 1.4% ± 3.4% (p = 0.02) for the RAL combination group. With the exception of no differences in the trabecular compartment of femoral neck, volumetric BMD changes in the ALN combination group for all other comparisons were significantly superior to the two other groups. Our data suggest that ALN when added to TPTD 9 months after initiation of TPTD monotherapy results in a more robust increase in BMD, probably due to a reopening of the anabolic window. The clinical relevance of the BMD increase is unknown.\n\nFahrleitner-Pammer, Astrid\n\n\n"
        },
        {
            "text": "\n130178\nDALI: Vitamin D and lifestyle intervention for gestational diabetes mellitus (GDM) prevention: an European multicentre, randomised trial - study protocol.\n\nJelsma, JG\n\nvan Poppel, MN\n\nGaljaard, S\n\nDesoye, G\n\nCorcoy, R\n\nDevlieger, R\n\nvan Assche, A\n\nTimmerman, D\n\nJans, G\n\nHarreiter, J\n\nKautzky-Willer, A\n\nDamm, P\n\nMathiesen, ER\n\nJensen, DM\n\nAndersen, L\n\nDunne, F\n\nLapolla, A\n\nDi Cianni, G\n\nBertolotto, A\n\nWender-Oegowska, E\n\nZawiejska, A\n\nBlumska, K\n\nHill, D\n\nRebollo, P\n\nSnoek, FJ\n\nSimmons, D\n\nBeiträge in Fachzeitschriften\nISI:000321655900001\n23829946.0\n10.1186/1471-2393-13-142\nPMC3710199\nGestational diabetes mellitus (GDM) is an increasing problem world-wide. Lifestyle interventions and/or vitamin D supplementation might help prevent GDM in some women.\n                Pregnant women at risk of GDM (BMI ≥ 29 (kg/m(2))) from 9 European countries will be invited to participate and consent obtained before 19+6 weeks of gestation. After giving informed consent, women without GDM will be included (based on IADPSG criteria: fasting glucose<5.1 mmol; 1 hour glucose <10.0 mmol; 2 hour glucose <8.5 mmol) and randomized to one of the 8 intervention arms using a 2 × (2 × 2) factorial design: (1) healthy eating (HE), 2) physical activity (PA), 3) HE+PA, 4) control, 5) HE+PA+vitamin D, 6) HE+PA+placebo, 7) vitamin D alone, 8) placebo alone), pre-stratified for each site. In total, 880 women will be included with 110 women allocated to each arm. Between entry and 35 weeks of gestation, women allocated to a lifestyle intervention will receive 5 face-to-face, and 4 telephone coaching sessions, based on the principles of motivational interviewing. The lifestyle intervention includes a discussion about the risks of GDM, a weight gain target <5 kg and either 7 healthy eating 'messages' and/or 5 physical activity 'messages' depending on randomization. Fidelity is monitored by the use of a personal digital assistance (PDA) system. Participants randomized to the vitamin D intervention receive either 1600 IU vitamin D or placebo for daily intake until delivery. Data is collected at baseline measurement, at 24-28 weeks, 35-37 weeks of gestation and after delivery. Primary outcome measures are gestational weight gain, fasting glucose and insulin sensitivity, with a range of obstetric secondary outcome measures including birth weight.\n                DALI is a unique Europe-wide randomised controlled trial, which will gain insight into preventive measures against the development of GDM in overweight and obese women.\n                ISRCTN70595832.\n\nDesoye, Gernot\n\n\n"
        },
        {
            "text": "\n167280\nAcute stimulation of the soluble guanylate cyclase does not impact on left ventricular capacitance in normal and hypertrophied porcine hearts in vivo.\n\nAlogna, A\n\nSchwarzl, M\n\nManninger, M\n\nHamdani, N\n\nZirngast, B\n\nKloth, B\n\nSteendijk, P\n\nVerderber, J\n\nZweiker, D\n\nWestermann, D\n\nBlankenberg, S\n\nMaechler, H\n\nTschöpe, C\n\nLinke, WA\n\nMarsche, G\n\nPieske, BM\n\nPost, H\n\nBeiträge in Fachzeitschriften\nISI:000444288600024\n29727215.0\n10.1152/ajpheart.00510.2017\nNone\nExperimental data indicate that stimulation of the nitric oxide-soluble guanylate cyclase(sGC)-cGMP-PKG pathway can increase left ventricular (LV) capacitance via phosphorylation of the myofilamental protein titin. We aimed to test whether acute pharmacological sGC stimulation with BAY 41-8543 would increase LV capacitance via titin phosphorylation in healthy and deoxycorticosteroneacetate (DOCA)-induced hypertensive pigs. Nine healthy Landrace pigs and 7 pigs with DOCA-induced hypertension and LV concentric hypertrophy were acutely instrumented to measure LV end-diastolic pressure-volume relationships (EDPVRs) at baseline and during intravenous infusion of BAY 41-8543 (1 and 3 μg·kg-1·min-1 for 30 min, respectively). Separately, in seven healthy and six DOCA pigs, transmural LV biopsies were harvested from the beating heart to measure titin phosphorylation during BAY 41-8543 infusion. LV EDPVRs before and during BAY 41-8543 infusion were superimposable in both healthy and DOCA-treated pigs, whereas mean aortic pressure decreased by 20-30 mmHg in both groups. Myocardial titin phosphorylation was unchanged in healthy pigs, but total and site-specific (Pro-Glu-Val-Lys and N2-Bus domains) titin phosphorylation was increased in DOCA-treated pigs. Bicoronary nitroglycerin infusion in healthy pigs ( n = 5) induced a rightward shift of the LV EDPVR, demonstrating the responsiveness of the pathway in this model. Acute systemic sGC stimulation with the sGC stimulator BAY 41-8543 did not recruit an LV preload reserve in both healthy and hypertrophied LV porcine myocardium, although it increased titin phosphorylation in the latter group. Thus, increased titin phosphorylation is not indicative of increased in vivo LV capacitance. NEW & NOTEWORTHY We demonstrate that acute pharmacological stimulation of soluble guanylate cyclase does not increase left ventricular compliance in normal and hypertrophied porcine hearts. Effects of long-term soluble guanylate cyclase stimulation with oral compounds in disease conditions associated with lowered myocardial cGMP levels, i.e., heart failure with preserved ejection fraction, remain to be investigated.\n\nAlbori, Jochen\n\nMächler, Heinrich\n\nManninger-Wünscher, Martin\n\nMarsche, Gunther\n\nZirngast, Birgit\n\nZweiker, David\n\n\n"
        },
        {
            "text": "\n173692\nThe European Registry on Obstetric Antiphospholipid Syndrome (EUROAPS): A survey of 1000 consecutive cases.\n\nAlijotas-Reig, J\n\nEsteve-Valverde, E\n\nFerrer-Oliveras, R\n\nSáez-Comet, L\n\nLefkou, E\n\nMekinian, A\n\nBelizna, C\n\nRuffatti, A\n\nTincani, A\n\nMarozio, L\n\nEspinosa, G\n\nCervera, R\n\nRíos-Garcés, R\n\nDe Carolis, S\n\nLatino, O\n\nLLurba, E\n\nChighizola, CB\n\nGerosa, M\n\nPengo, V\n\nLundelin, K\n\nRovere-Querini, P\n\nCanti, V\n\nMayer-Pickel, K\n\nReshetnyak, T\n\nHoxha, A\n\nTabacco, S\n\nStojanovich, L\n\nGogou, V\n\nVaroudis, A\n\nArnau, A\n\nRuiz-Hidalgo, D\n\nTrapé, J\n\nSos, L\n\nStoppani, C\n\nMartí-Cañamares, A\n\nFarran-Codina, I\n\nEUROAPS Study Group\n\nBeiträge in Fachzeitschriften\nISI:000466455600010\n30772493.0\n10.1016/j.autrev.2018.12.006\nNone\nTo analyse the clinical features, laboratory data and foetal-maternal outcomes, and follow them up on a cohort of 1000 women with obstetric antiphospholipid syndrome (OAPS).\n                The European Registry of OAPS became a registry within the framework of the European Forum on Antiphospholipid Antibody projects and was placed on a website in June 2010. Thirty hospitals throughout Europe have collaborated to carry out this registry. Cases with obstetric complaints related to antiphospholipid antibodies (aPL) who tested positive for aPL at least twice were included prospectively and retrospectively. The seven-year survey results are reported.\n                1000 women with 3553 episodes were included of which 2553 were historical and 1000 were latest episodes. All cases fulfilled the Sydney classification criteria. According to the laboratory categories, 292 (29.2%) were in category I, 357 (35.7%) in IIa, 224 (22.4%) in IIb and 127 (12.7%) in IIc. Miscarriages were the most prevalent clinical manifestation in 386 cases (38.6%). Moreover, the presence of early preeclampsia (PE) and early foetal growth restriction (FGR) appeared in 181 (18.1%) and 161 (16.1%), respectively. In this series, 448 (44.8%) women received the recommended OAPS treatment. Patients with recommended treatment had a good live-birth rate (85%), but worse results (72.4%) were obtained in patients with any treatment (low-dose aspirin (LDA) or low-molecular-weight heparin (LMWH) not on recommended schedule, while patients with no treatment showed a poor birth rate (49.6%).\n                In this series, recurrent miscarriage is the most frequent poor outcome. To avoid false-negative diagnoses, all laboratory category subsets were needed. OAPS cases have very good foetal-maternal outcomes when treated. Results suggest that we were able to improve our clinical practice to offer better treatment and outcomes to OAPS patients.\n                Copyright © 2019 Elsevier B.V. All rights reserved.\n\nMayer-Pickel, Karoline Ilse\n\n\n"
        },
        {
            "text": "\n4804\nImmediate loading of single-tooth implants in the anterior maxilla. Preliminary results after one year.\n\nLorenzoni, M\n\nPertl, C\n\nZhang, K\n\nWimmer, G\n\nWegscheider, WA\n\nBeiträge in Fachzeitschriften\nISI:000182380900007\n12656877.0\n10.1034/j.1600-0501.2003.140207.x\nNone\nAccording to the standard protocol, a load-free healing period is one of the most emphasized requirements for implant integration. Recent studies have encouraged a progressive shortening of the healing period for single-tooth implants and immediate loading has been proposed for the aesthetic zone in the maxilla. The present study evaluated clinical outcomes of immediately loaded FRIALIT-2 Synchro implants 12 months after placement in the maxillary incisal region. In the course of our investigation, nine patients have been treated following an immediate loading protocol. The stepped-screw type implants were inserted with an increasing torque up to 45 Ncm, thus measuring the primary stability of the implants. All implants were immediately restored with unsplinted acrylic resin provisional crowns and the patients provided with occlusal splints. Regular controls were performed at monthly intervals, intraoral radiographs were taken directly after implant placement, 6 and 12 months post insertion. The survival rate, clinical stability (Periotest) and radiographic coronal bone defects (CBD) were evaluated at delivery of the definitive superstructures (CBD 6) and 6 months later (CBD 12). Twelve FRIALIT-2 Synchro stepped screws of 3.8, 4.5 and 5.5 mm diameter and 13 and 15 mm length were placed in the incisal maxillary region. The median Periotest value 6 months post insertion was -2 with a minimum of -5 and a maximum of +2. The mean coronal bone level changes (CBD) at 6 and 12 months were 0.45 and 0.75 mm. No implant failed up to 12 months after insertion, resulting in a 100% survival rate. The presented results showed promising data for immediately loaded single-tooth implants in the anterior maxilla. Periotest values were within the range published for submerged implants. The radiographic coronal bone resorption after 6 and 12 months was even less than evaluated for implants placed in a standard two-stage procedure. It is evident that successful immediate loading protocols require a careful and strict patient selection aimed at achieving the best primary stability and avoiding any excessive functional or non-functional loading. Additional research needs to be done to provide data in situations where problems of poor bone quality, multiple implants or augmentation procedures must be overcome.\n\nLorenzoni, Martin\n\nWegscheider, Walther\n\nWimmer, Gernot\n\n\n"
        }
    ]
}