Publications by authors named "Verena von Bulow"

Article Synopsis
  • Schistosomiasis impacts over 250 million people, especially affecting those aged 10-14 years, leading to uncertain liver damage severity based on the host's age.
  • In a study using male mice of different ages, researchers found that older hosts showed improved outcomes in liver-related issues like inflammation and fibrosis after infection compared to younger hosts.
  • The results highlight the importance of understanding how age influences liver damage and response to schistosomiasis, supporting the need for further research in patients.
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Article Synopsis
  • - Schistosomiasis, caused by parasitic worms, affects over 250 million people and primarily impacts the gastrointestinal tract, triggering a specific immune response linked to the formation of granulomas through its eggs.
  • - A study on hamsters explored the connection between the number of parasitic eggs and the immune response, analyzing egg load and cytokine expression in liver and colon tissues.
  • - Results showed no link between Th1 cytokines and egg load in the liver, while some Th2 cytokines exhibited an unexpected inverse correlation, potentially due to prolonged embryogenesis of eggs in the liver, which didn't occur in the colon.
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Schistosomiasis, a widespread neglected tropical disease, presents a complex and multifaceted clinical-pathological profile. Using hamsters as final hosts, we dissected molecular events following infection in the liver-the organ most severely affected in schistosomiasis patients. Employing tandem mass tag-based proteomics, we studied alterations in the liver proteins in response to various infection modes and genders.

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Schistosomiasis is a parasitic disease affecting more than 250 million people worldwide. The transcription factor c-Jun, which is induced in S. mansoni infection-associated liver disease, can promote hepatocyte survival but can also trigger hepatocellular carcinogenesis.

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Background & Aims: Schistosomiasis is one of the most prominent parasite-induced infectious diseases, affecting more than 250 million people. Schistosoma mansoni causes metabolic exhaustion and a strong redox imbalance in the liver, causing parenchymal damage, and may predispose for cancer. We investigated whether oxidative stress provokes hepatocellular proliferation upon S.

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Article Synopsis
  • Schistosomiasis, a parasitic infection affecting over 200 million people, primarily causes liver-related morbidity through its eggs rather than adult worms.
  • Research methods involved advanced imaging and biochemical techniques on hamster models and human cell lines, validating findings with human biopsies.
  • The study found that the infection leads to lipid and glycogen depletion in the liver, with parasites reprogramming host metabolism, resulting in oxidative stress and DNA damage, indicating a severe impact on liver cells regardless of the immune response.
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Schistosomiasis is one of the most prominent parasite-induced infectious diseases, causing tremendous medical and socioeconomic problems. Current studies have reported on the spread of endemic regions and the fear of development of resistance against praziquantel, the only effective drug available. Among the species, only is classified as a Group 1 carcinogen (definitely cancerogenic to humans), causing squamous cell carcinoma of the bladder, whereas infection with is included in Group 3 of carcinogenic hazards to humans by the International Agency for Research on Cancer (IARC), indicating insufficient evidence to determine its carcinogenicity.

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This review covers basic aspects of histone modification and the role of posttranslational histone modifications in the development of allergic diseases, including the immune mechanisms underlying this development. Together with DNA methylation, histone modifications (including histone acetylation, methylation, phosphorylation, ubiquitination, etc.) represent the classical epigenetic mechanisms.

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Background: Wnt proteins are important for developmental processes and certain diseases. WNT5A is a non-canonical Wnt protein that previously has been shown to play a role in the progression of malignant melanoma. High expression of WNT5A in melanoma tumors correlates to formation of distant metastasis and poor prognosis.

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The transcription factor nuclear factor κB (NF-κB) plays a central role in regulating inflammation in response to several external signals. The TGFβ-associated kinase 1 (TAK1) is an upstream regulator of NF-κB signaling. In TGFβ-stimulated cells, TAK1 undergoes Lys-63-linked polyubiquitination at Lys-34 by TNF receptor-associated factor 6 and is thereby activated.

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Transforming growth factor-beta (TGF-beta) is a multifunctional cytokine that regulates embryonic development and tissue homeostasis; however, aberrations of its activity occur in cancer. TGF-beta signals through its Type II and Type I receptors (TbetaRII and TbetaRI) causing phosphorylation of Smad proteins. TGF-beta-associated kinase 1 (TAK1), a member of the mitogen-activated protein kinase kinase kinase (MAPKKK) family, was originally identified as an effector of TGF-beta-induced p38 activation.

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Excessive and permanent cytokine production in response to bacterial LPS causes cell and tissue damage, and hence organ failure during sepsis. We have previously demonstrated that zinc treatment prevents LPS-induced TNF-alpha expression and production in human monocytes by inhibiting cyclic nucleotide phosphodiesterase (PDE) activity and expression, and subsequent elevation of the cyclic nucleotide cGMP. In the present study, we investigated the molecular mechanism by which cGMP signaling affects the LPS-induced signaling cascade to suppress TNF-alpha transcription and release from monocytes.

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Alpha2HS-glycoprotein/fetuin-A (Ahsg) is a serum protein preventing soft tissue calcification. In trauma and inflammation, Ahsg is down-regulated and therefore considered a negative acute phase protein. Enhancement of Ahsg expression as a protective serum protein is desirable in several diseases including tissue remodelling after trauma and infection, kidney and heart failure, and cancer.

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The trace element zinc affects several aspects of immune function, such as the release of proinflammatory cytokines from monocytes. We investigated the role of cyclic nucleotide signaling in zinc inhibition of LPS-induced TNF-alpha and IL-1beta release from primary human monocytes and the monocytic cell line Mono Mac1. Zinc reversibly inhibited enzyme activity of phosphodiesterase-1 (PDE-1), PDE-3, and PDE-4 in cellular lysate.

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