@phdthesis{Calvano2018,
  author    = {Calvano, Claudia},
  title     = {Funktionelle Bauchschmerzen im Kindesalter},
  school      = {Universit{\"a}t Potsdam},
  pages     = {209},
  year      = {2018},
  abstract  = {Funktionelle Bauchschmerzen des Kindes betreffen die ganze Familie, wobei die Literatur insbesondere die Rolle der Eltern hervorhebt. Bisher wurden die Eltern jedoch prim{\"a}r als „critical behavioral agents" (Palermo \& Eccleston, 2009) gesehen, die einen Einfluss auf die Bauchschmerzen und Beeintr{\"a}chtigung des Kindes aus{\"u}ben. Untersuchungen der psychosozialen Auswirkungen der Bauchschmerzen und der Beeintr{\"a}chtigung des Kindes auf die Eltern wurden bislang vernachl{\"a}ssigt (Palermo \& Eccleston, 2009). Die Dissertation hatte daher zum Ziel, die Rolle der Eltern bei funktionellen Bauchschmerzen umfassend zu betrachten, indem sowohl schmerzbezogene Reaktionen der Eltern, als auch die psychosoziale Belastung der Eltern ber{\"u}cksichtigt und systematisch in Zusammenhang zu den Bauchschmerzen und der Beeintr{\"a}chtigung des Kindes untersucht wurden. Zum anderen sollten durch Interventionsstudien Aussagen {\"u}ber die Ver{\"a}nderbarkeit spezifischer Belastungsmerkmale der Eltern und {\"u}ber das Wechselspiel zwischen der Ebene der Eltern und der Ebene des Kindes erm{\"o}glicht werden. Anhand von vier Studien sollten die Fragen beantworten werden 1) welche Faktoren die {\"a}rztliche Inanspruchnahme beeinflussen und welche besondere Relevanz dabei die Bewertungsprozesse der Eltern besitzen, 2) wie die psychosoziale Belastung der Eltern charakterisiert ist und durch welche Faktoren sie beeinflusst wird, 3) welche Ver{\"a}nderungen im Rahmen einer kindzentrierten verhaltenstherapeutischen Intervention auf Seiten der Eltern zu beobachten sind und 4) wie sich diese Ver{\"a}nderungen seitens der Eltern und seitens des Kindes gegenseitig beeinflussen.},
  language  = {de}
}
@phdthesis{Pellegrino2022,
  author    = {Pellegrino, Antonio},
  title     = {miRNA profiling for diagnosis of chronic pain in polyneuropathy},
  doi       = {10.25932/publishup-58385},
  url       = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus4-583858},
  school      = {Universit{\"a}t Potsdam},
  pages     = {viii, 97, xi},
  year      = {2022},
  abstract  = {This dissertation aimed to determine differential expressed miRNAs in the context of chronic pain in polyneuropathy. For this purpose, patients with chronic painful polyneuropathy were compared with age matched healthy patients. Taken together, all miRNA pre library preparation quality controls were successful and none of the samples was identified as an outlier or excluded for library preparation. Pre sequencing quality control showed that library preparation worked for all samples as well as that all samples were free of adapter dimers after BluePippin size selection and reached the minimum molarity for further processing. Thus, all samples were subjected to sequencing. The sequencing control parameters were in their optimal range and resulted in valid sequencing results with strong sample to sample correlation for all samples. The resulting FASTQ file of each miRNA library was analyzed and used to perform a differential expression analysis. The differentially expressed and filtered miRNAs were subjected to miRDB to perform a target prediction. Three of those four miRNAs were downregulated: hsa-miR-3135b, hsa-miR-584-5p and hsa-miR-12136, while one was upregulated: hsa-miR-550a-3p. miRNA target prediction showed that chronic pain in polyneuropathy might be the result of a combination of miRNA mediated high blood flow/pressure and neural activity dysregulations/disbalances. Thus, leading to the promising conclusion that these four miRNAs could serve as potential biomarkers for the diagnosis of chronic pain in polyneuropathy. Since TRPV1 seems to be one of the major contributors of nociception and is associated with neuropathic pain, the influence of PKA phosphorylated ARMS on the sensitivity of TRPV1 as well as the part of AKAP79 during PKA phosphorylation of ARMS was characterized. Therefore, possible PKA-sites in the sequence of ARMS were identified. This revealed five canonical PKA-sites: S882, T903, S1251/52, S1439/40 and S1526/27. The single PKA-site mutants of ARMS revealed that PKA-mediated ARMS phosphorylation seems not to influence the interaction rate of TRPV1/ARMS. While phosphorylation of ARMST903 does not increase the interaction rate with TRPV1, ARMSS1526/27 is probably not phosphorylated and leads to an increased interaction rate. The calcium flux measurements indicated that the higher the interaction rate of TRPV1/ARMS, the lower the EC50 for capsaicin of TRPV1, independent of the PKA phosphorylation status of ARMS. In addition, the western blot analysis confirmed the previously observed TRPV1/ARMS interaction. More importantly, AKAP79 seems to be involved in the TRPV1/ARMS/PKA signaling complex. To overcome the problem of ARMS-mediated TRPV1 sensitization by interaction, ARMS was silenced by shRNA. ARMS silencing resulted in a restored TRPV1 desensitization without affecting the TRPV1 expression and therefore could be used as new topical therapeutic analgesic alternative to stop ARMS mediated TRPV1 sensitization.},
  language  = {en}
}
@misc{WippertWiebking2018,
  author    = {Wippert, Pia-Maria and Wiebking, Christine},
  title     = {Stress and Alterations in the Pain Matrix},
  series = {Postprints der Universit{\"a}t Potsdam : Humanwissenschaftliche Reihe},
  journal   = {Postprints der Universit{\"a}t Potsdam : Humanwissenschaftliche Reihe},
  number    = {438},
  url       = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus4-412058},
  pages     = {11},
  year      = {2018},
  abstract  = {The genesis of chronic pain is explained by a biopsychosocial model. It hypothesizes an interdependency between environmental and genetic factors provoking aberrant long-term changes in biological and psychological regulatory systems. Physiological effects of psychological and physical stressors may play a crucial role in these maladaptive processes. Specifically, long-term demands on the stress response system may moderate central pain processing and influence descending serotonergic and noradrenergic signals from the brainstem, regulating nociceptive processing at the spinal level. However, the underlying mechanisms of this pathophysiological interplay still remain unclear. This paper aims to shed light on possible pathways between physical (exercise) and psychological stress and the potential neurobiological consequences in the genesis and treatment of chronic pain, highlighting evolving concepts and promising research directions in the treatment of chronic pain. Two treatment forms (exercise and mindfulness-based stress reduction as exemplary therapies), their interaction, and the dose-response will be discussed in more detail, which might pave the way to a better understanding of alterations in the pain matrix and help to develop future prevention and therapeutic concepts},
  language  = {en}
}
@article{WippertWiebking2018,
  author    = {Wippert, Pia-Maria and Wiebking, Christine},
  title     = {Stress and Alterations in the Pain Matrix},
  series = {International Journal of Environmental Research and Public Health},
  volume    = {15},
  journal   = {International Journal of Environmental Research and Public Health},
  number    = {4},
  publisher = {MDPI AG},
  address   = {Basel},
  issn      = {1660-4601},
  doi       = {10.3390/ijerph15040785},
  pages     = {1 -- 11},
  year      = {2018},
  abstract  = {The genesis of chronic pain is explained by a biopsychosocial model. It hypothesizes an interdependency between environmental and genetic factors provoking aberrant long-term changes in biological and psychological regulatory systems. Physiological effects of psychological and physical stressors may play a crucial role in these maladaptive processes. Specifically, long-term demands on the stress response system may moderate central pain processing and influence descending serotonergic and noradrenergic signals from the brainstem, regulating nociceptive processing at the spinal level. However, the underlying mechanisms of this pathophysiological interplay still remain unclear. This paper aims to shed light on possible pathways between physical (exercise) and psychological stress and the potential neurobiological consequences in the genesis and treatment of chronic pain, highlighting evolving concepts and promising research directions in the treatment of chronic pain. Two treatment forms (exercise and mindfulness-based stress reduction as exemplary therapies), their interaction, and the dose-response will be discussed in more detail, which might pave the way to a better understanding of alterations in the pain matrix and help to develop future prevention and therapeutic concepts},
  language  = {en}
}