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- wassergefiltertes Infrarot A (wIRA) (25)
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Wassergefiltertes Infrarot A (wIRA) als spezielle Form der Wärmestrahlung mit hohem Eindringvermögen in das Gewebe bei geringer thermischer Oberflächenbelastung kann die Heilung akuter und chronischer Wunden sowohl über thermische und temperaturabhängige als auch über nicht-thermische und temperaturunabhängige Effekte verbessern. wIRA steigert Temperatur (+2,7°C in 2 cm Gewebetiefe) und Sauerstoffpartialdruck im Gewebe (+32% in 2 cm Gewebetiefe) sowie die Gewebedurchblutung. Diese drei Faktoren sind entscheidend für eine ausreichende Versorgung des Gewebes mit Energie und Sauerstoff und deshalb auch für Wundheilung und Infektionsabwehr.
wIRA vermag Schmerzen deutlich zu mindern (ausnahmslos bei 230 Bestrahlungen) mit bemerkenswert niedrigerem Analgetikabedarf (52–69% niedriger in den Gruppen mit wIRA verglichen mit den Kontrollgruppen) und eine erhöhte Wundsekretion und Entzündung herabzusetzen sowie positive immunmodulierende Effekte zu zeigen. Die Gesamtbeurteilung des Effekts der Bestrahlung wie auch die Wundheilung und das kosmetische Ergebnis (erhoben mittels visueller Analogskalen) waren in der Gruppe mit wIRA wesentlich besser verglichen mit der Kontrollgruppe. wIRA kann sowohl bei akuten als auch bei chronischen Wunden einschließlich infizierter Wunden die Wundheilung beschleunigen (Abnahme der Wundfläche im Median um 90% bei schwerbrandverletzten Kindern bereits nach 9 Tagen in der Gruppe mit wIRA verglichen mit 13 Tagen in der Kontrollgruppe; im Durchschnitt 18 versus 42 Tage bis zum kompletten Wundschluss bei chronischen venösen Unterschenkelulzera) oder bei stagnierender Wundheilung verbessern (mit Erreichen eines kompletten Wundschlusses und Normalisierung des thermographischen Bildes bei zuvor therapierefraktären chronischen venösen Unterschenkelulzera). Nach großen abdominalen Operationen zeigte sich ein Trend zugunsten der wIRA-Gruppe hin zu einer niedrigeren Rate von Wundinfektionen insgesamt (7% versus 15%) einschließlich später Infektionen nach der Entlassung aus dem Krankenhaus (0% versus 8%) und ein Trend hin zu einem kürzeren postoperativen Krankenhausaufenthalt (9 versus 11 Tage).
Selbst der normale Wundheilungsprozess kann verbessert werden.
Die erwähnten Effekte wurden in 6 prospektiven Studien belegt, die meisten mit einem Evidenzgrad von Ia/Ib.
wIRA stellt eine wertvolle Therapieoption dar und kann generell für die Therapie von akuten und chronischen Wunden empfohlen werden.
Wassergefiltertes Infrarot A (wIRA) ist eine spezielle Form der Wärmestrahlung mit hohem Eindringvermögen in das Gewebe und geringer thermischer Belastung der Hautoberfläche.
wIRA steigert deutlich Temperatur, Sauerstoffpartialdruck und Durchblutung im Gewebe und wirkt auch über nicht-thermische zelluläre Effekte.
wIRA mindert indikationsübergreifend Schmerzen (mit relevant weniger Analgetikabedarf), Entzündung und vermehrte Sekretion und fördert Infektionsabwehr und Regeneration.
Entsprechend breit sind die klinischen Anwendungsmöglichkeiten von wIRA.
wIRA ist ein kontaktfreies, verbrauchsmaterialfreies, leicht anzuwendendes, (selbst bei Wunden) als angenehm empfundenes Verfahren mit guter Tiefenwirkung und anhaltendem Wärmedepot.
wIRA ist u.a. einsetzbar zur Verbesserung der Heilung akuter und chronischer Wunden (wobei selbst eine ungestört "normal" ablaufende Wundheilung noch verbessert werden kann: schneller, schmerzärmer), bei Hauterkrankungen (wie vulgären Warzen, Herpes labialis, Herpes Zoster, Sklerodermie, Akne papulopustulosa; aktinischen Keratosen im Rahmen einer Photodynamischen Therapie), zur Resorptionsverbesserung topisch applizierter Substanzen, bei muskuloskeletalen Erkrankungen (wie Arthrosen, Arthritiden, Lumbago, ankylosierender Spondyloarthritis), zur Regeneration nach Sport, beim komplexen regionalen Schmerzsyndrom (CRPS), bei Polyneuropathien und in Kombination mit Strahlentherapie oder Chemotherapie in der Onkologie.
Die infizierte Problemwunde
(2006)
Die erste Ausgabe der Online-Zeitschrift "GMS Krankenhaushygiene Interdisziplinär" der Deutschen Gesellschaft für Krankenhaushygiene (DGKH) innerhalb von German Medical Science behandelt das Thema "Die infizierte Problemwunde". Die Zielsetzung dieser Zeitschrift besteht in der komplexen Darstellung aktueller Themen der Krankenhaushygiene in interdisziplinärer Zusammenarbeit zwischen Hygienikern, Mikrobiologen, Infektiologen und für die jeweilige Thematik relevanten klinischen Fachdisziplinen und ggf. auch mit Experten anderer Fachrichtungen, z.B. Juristen, da rechtliche Aspekte zunehmend Bedeutung erlangen. ...
Correction to: Infection (2020) 48:723–733 https://doi.org/10.1007/s15010-020-01469-6. The original version of this article unfortunately contained a mistake. In this article the authors Dirk Schürmann at affiliation Charité, University Medicine, Berlin, Olaf Degen at affiliation University Clinic Hamburg Eppendorf, Hamburg and Heinz-August Horst at affiliation University Hospital Schleswig–Holstein, Kiel, Germany were missing from the author list. The original article has been corrected.
Attention-deficit/hyperactivity disorder (ADHD) is a common, highly heritable neurodevelopmental disorder. Genetic loci have not yet been identified by genome-wide association studies. Rare copy number variations (CNVs), such as chromosomal deletions or duplications, have been implicated in ADHD and other neurodevelopmental disorders. To identify rare (frequency ≤1%) CNVs that increase the risk of ADHD, we performed a whole-genome CNV analysis based on 489 young ADHD patients and 1285 adult population-based controls and identified one significantly associated CNV region. In tests for a global burden of large (>500 kb) rare CNVs, we observed a nonsignificant (P=0.271) 1.126-fold enriched rate of subjects carrying at least one such CNV in the group of ADHD cases. Locus-specific tests of association were used to assess if there were more rare CNVs in cases compared with controls. Detected CNVs, which were significantly enriched in the ADHD group, were validated by quantitative (q)PCR. Findings were replicated in an independent sample of 386 young patients with ADHD and 781 young population-based healthy controls. We identified rare CNVs within the parkinson protein 2 gene (PARK2) with a significantly higher prevalence in ADHD patients than in controls (P=2.8 × 10(-4) after empirical correction for genome-wide testing). In total, the PARK2 locus (chr 6: 162 659 756-162 767 019) harboured three deletions and nine duplications in the ADHD patients and two deletions and two duplications in the controls. By qPCR analysis, we validated 11 of the 12 CNVs in ADHD patients (P=1.2 × 10(-3) after empirical correction for genome-wide testing). In the replication sample, CNVs at the PARK2 locus were found in four additional ADHD patients and one additional control (P=4.3 × 10(-2)). Our results suggest that copy number variants at the PARK2 locus contribute to the genetic susceptibility of ADHD. Mutations and CNVs in PARK2 are known to be associated with Parkinson disease.
Background: To evaluate clinical outcomes after either immediate or deferred initiation of antiretroviral therapy in HIV-1-infected patients, presenting late with pneumocystis pneumonia (PCP) or toxoplasma encephalitis (TE).
Methods: Phase IV, multicenter, prospective, randomized open-label clinical trial. Patients were randomized into an immediate therapy arm (starting antiretroviral therapy (ART) within 7 days after initiation of OI treatment) versus a deferred arm (starting ART after completing the OI-therapy). All patients were followed for 24 weeks. The rates of clinical progression (death, new or relapsing opportunistic infections (OI) and other grade 4 clinical endpoints) were compared, using a combined primary endpoint. Secondary endpoints were hospitalization rates after completion of OI treatment, incidence of immune reconstitution inflammatory syndrome (IRIS), virologic and immunological outcome, adherence to proteinase-inhibitor based antiretroviral therapy (ART) protocol and quality of life.
Results: 61 patients (11 patients suffering TE, 50 with PCP) were enrolled. No differences between the two therapy groups in all examined primary and secondary endpoints could be identified: immunological and virologic outcome was similar in both groups, there was no significant difference in the incidence of IRIS (11 and 10 cases), furthermore 9 events (combined endpoint of death, new/relapsing OI and grade 4 events) occurred in each group.
Conclusions: In summary, this study supports the notion that immediate initiation of ART with a ritonavir-boosted proteinase-inhibitor and two nucleoside reverse transcriptase inhibitors is safe and has no negative effects on incidence of disease progression or IRIS, nor on immunological and virologic outcomes or on quality of life.
Elliptic flow from nuclear collisions is a hadronic observable sensitive to the early stages of system evolution. We report first results on elliptic flow of charged particles at midrapidity in Au+Au collisions at sqrt(s_NN)=130 GeV using the STAR TPC at RHIC. The elliptic flow signal, v_2, averaged over transverse momentum, reaches values of about 6% for relatively peripheral collisions and decreases for the more central collisions. This can be interpreted as the observation of a higher degree of thermalization than at lower collision energies. Pseudorapidity and transverse momentum dependence of elliptic flow are also presented.
R-flurbiprofen is the non-COX-inhibiting enantiomer of flurbiprofen and is not converted to S-flurbiprofen in human cells. Nevertheless, it reduces extracellular prostaglandin E2 (PGE2) in cancer or immune cell cultures and human extracellular fluid. Here, we show that R-flurbiprofen acts through a dual mechanism: (i) it inhibits the translocation of cPLA2α to the plasma membrane and thereby curtails the availability of arachidonic acid and (ii) R-flurbiprofen traps PGE2 inside of the cells by inhibiting multidrug resistance–associated protein 4 (MRP4, ABCC4), which acts as an outward transporter for prostaglandins. Consequently, the effects of R-flurbiprofen were mimicked by RNAi-mediated knockdown of MRP4. Our data show a novel mechanism by which R-flurbiprofen reduces extracellular PGs at physiological concentrations, particularly in cancers with high levels of MRP4, but the mechanism may also contribute to its anti-inflammatory and immune-modulating properties and suggests that it reduces PGs in a site- and context-dependent manner.
Bipolar disorder (BD) is a highly heritable neuropsychiatric disease characterized by recurrent episodes of mania and depression. BD shows substantial clinical and genetic overlap with other psychiatric disorders, in particular schizophrenia (SCZ). The genes underlying this etiological overlap remain largely unknown. A recent SCZ genome wide association study (GWAS) by the Psychiatric Genomics Consortium identified 128 independent genome-wide significant single nucleotide polymorphisms (SNPs). The present study investigated whether these SCZ-associated SNPs also contribute to BD development through the performance of association testing in a large BD GWAS dataset (9747 patients, 14278 controls). After re-imputation and correction for sample overlap, 22 of 107 investigated SCZ SNPs showed nominal association with BD. The number of shared SCZ-BD SNPs was significantly higher than expected (p = 1.46x10-8). This provides further evidence that SCZ-associated loci contribute to the development of BD. Two SNPs remained significant after Bonferroni correction. The most strongly associated SNP was located near TRANK1, which is a reported genome-wide significant risk gene for BD. Pathway analyses for all shared SCZ-BD SNPs revealed 25 nominally enriched gene-sets, which showed partial overlap in terms of the underlying genes. The enriched gene-sets included calcium- and glutamate signaling, neuropathic pain signaling in dorsal horn neurons, and calmodulin binding. The present data provide further insights into shared risk loci and disease-associated pathways for BD and SCZ. This may suggest new research directions for the treatment and prevention of these two major psychiatric disorders.
HLA-DRB1 and HLA-DQB1 genetic diversity modulates response to lithium in bipolar affective disorders
(2021)
Bipolar affective disorder (BD) is a severe psychiatric illness, for which lithium (Li) is the gold standard for acute and maintenance therapies. The therapeutic response to Li in BD is heterogeneous and reliable biomarkers allowing patients stratification are still needed. A GWAS performed by the International Consortium on Lithium Genetics (ConLiGen) has recently identified genetic markers associated with treatment responses to Li in the human leukocyte antigens (HLA) region. To better understand the molecular mechanisms underlying this association, we have genetically imputed the classical alleles of the HLA region in the European patients of the ConLiGen cohort. We found our best signal for amino-acid variants belonging to the HLA-DRB1*11:01 classical allele, associated with a better response to Li (p < 1 × 10−3; FDR < 0.09 in the recessive model). Alanine or Leucine at position 74 of the HLA-DRB1 heavy chain was associated with a good response while Arginine or Glutamic acid with a poor response. As these variants have been implicated in common inflammatory/autoimmune processes, our findings strongly suggest that HLA-mediated low inflammatory background may contribute to the efficient response to Li in BD patients, while an inflammatory status overriding Li anti-inflammatory properties would favor a weak response.