TY - JOUR
A1 - Ranisch, Robert
T1 - Consultation with Doctor Twitter
BT - consent Fatigue, and the role of developers in digital medical ethics
JF - The American journal of bioethics : ajob
Y1 - 2021
U6 - https://doi.org/10.1080/15265161.2021.1926595
SN - 1526-5161
SN - 1536-0075
VL - 21
IS - 7
SP - 24
EP - 25
PB - Routledge, Taylor & Francis Group
CY - Philadelphia, Pa.
ER -
TY - JOUR
A1 - Henkel, Janin
A1 - Klauder, Julia
A1 - Statz, Meike
A1 - Wohlenberg, Anne-Sophie
A1 - Kuipers, Sonja
A1 - Vahrenbrink, Madita
A1 - Püschel, Gerhard Paul
T1 - Enhanced Palmitate-Induced Interleukin-8 Formation in Human Macrophages by Insulin or Prostaglandin E-2
JF - Biomedicines
N2 - Macrophages in pathologically expanded dysfunctional white adipose tissue are exposed to a mix of potential modulators of inflammatory response, including fatty acids released from insulin-resistant adipocytes, increased levels of insulin produced to compensate insulin resistance, and prostaglandin E-2 (PGE(2)) released from activated macrophages. The current study addressed the question of how palmitate might interact with insulin or PGE(2) to induce the formation of the chemotactic pro-inflammatory cytokine interleukin-8 (IL-8). Human THP-1 cells were differentiated into macrophages. In these macrophages, palmitate induced IL-8 formation. Insulin enhanced the induction of IL-8 formation by palmitate as well as the palmitate-dependent stimulation of PGE(2) synthesis. PGE(2) in turn elicited IL-8 formation on its own and enhanced the induction of IL-8 release by palmitate, most likely by activating the EP4 receptor. Since IL-8 causes insulin resistance and fosters inflammation, the increase in palmitate-induced IL-8 formation that is caused by hyperinsulinemia and locally produced PGE(2) in chronically inflamed adipose tissue might favor disease progression in a vicious feed-forward cycle.
KW - macrophages
KW - insulin
KW - prostaglandin E-2
KW - interleukin-8
KW - inflammation
Y1 - 2021
U6 - https://doi.org/10.3390/biomedicines9050449
SN - 2227-9059
VL - 9
IS - 5
PB - MDPI
CY - Basel
ER -
TY - JOUR
A1 - He, Yangyang
A1 - Würtz-Kozak, Karin
A1 - Kühl, Linn Kristina
A1 - Wippert, Pia-Maria
T1 - Extracellular vesicles
BT - Potential mediators of psychosocial stress contribution to osteoporosis?
JF - International journal of molecular sciences
N2 - Osteoporosis is characterized by low bone mass and damage to the bone tissue’s microarchitecture, leading to increased fracture risk. Several studies have provided evidence for associations between psychosocial stress and osteoporosis through various pathways, including the hypothalamic-pituitary-adrenocortical axis, the sympathetic nervous system, and other endocrine factors. As psychosocial stress provokes oxidative cellular stress with consequences for mitochondrial function and cell signaling (e.g., gene expression, inflammation), it is of interest whether extracellular vesicles (EVs) may be a relevant biomarker in this context or act by transporting substances. EVs are intercellular communicators, transfer substances encapsulated in them, modify the phenotype and function of target cells, mediate cell-cell communication, and, therefore, have critical applications in disease progression and clinical diagnosis and therapy. This review summarizes the characteristics of EVs, their role in stress and osteoporosis, and their benefit as biological markers. We demonstrate that EVs are potential mediators of psychosocial stress and osteoporosis and may be beneficial in innovative research settings.
KW - allostatic load
KW - bone remodeling
KW - microRNA
KW - osteoblast
KW - osteoclast
Y1 - 2021
U6 - https://doi.org/10.3390/ijms22115846
SN - 1422-0067
VL - 22
IS - 11
PB - Molecular Diversity Preservation International
CY - Basel
ER -
TY - JOUR
A1 - Enssle, Jörg
A1 - Weylandt, Karsten-Henrich
T1 - Secure and optimized detection of PNPLA3 rs738409 genotype by an improved PCR-restriction fragment length polymorphism method
JF - BioTechniques : the international journal of life science methods
N2 - The PNPLA3 reference single-nucleotide polymorphism rs738409 has been identified as a predisposing factor for nonalcoholic fatty liver disease. A simple method based on PCR and restriction fragment length polymorphism (RFLP) analysis had been published to detect the nonpathogenic allele PNPLA3 rs738409 variant. The presence of the pathogenic variant was deduced by the indigestibility of the corresponding PCR product with BtsCI recognizing the nonpathogenic allele. However, one cannot exclude that an enzymatic reaction does not occur for other, more trivial, reasons. For safe and secure detection of the pathogenic PNPLA3 rs738409, we have further developed the PCR-restriction fragment length polymorphism method by adding a second restriction enzyme digest, clearly identifying the correct PNPLA3 alleles and in particular the pathogenic variant.
METHOD SUMMARY
The method presented here represents an improved genetic diagnosis of the PNPLA3 rs738409 alleles based on conventional and inexpensive molecular biological methods. We used methodology based on PCR and restriction fragment length polymorphisms and clearly identified both described alleles by the use of two restriction enzymes. Digestion of individuals' specific PNPLA3 PCR fragments with both enzymes in independent reactions clearly showed the PNPLA3 rs738409 genotype.
KW - n-3 polyunsaturated fatty acid therapies
KW - nonalcoholic fatty liver
KW - disease
KW - PCR– RFLP
KW - PNPLA3
KW - rs738409
Y1 - 2021
U6 - https://doi.org/10.2144/btn-2020-0163
SN - 0736-6205
SN - 1940-9818
VL - 70
IS - 6
SP - 345
EP - 349
PB - Future Science Ltd.
CY - London
ER -
TY - JOUR
A1 - Witte, Leonie
A1 - Linnemannstoens, Karen
A1 - Honemann-Capito, Mona
A1 - Groß, Julia Christina
T1 - Visualization and quantitation of Wg trafficking in the Drosophila wing imaginal epithelium
JF - Bio-protocol
N2 - Secretory Wnt trafficking can be studied in the polarized epithelial monolayer of Drosophila wing imaginal discs (WID). In this tissue, Wg (Drosophila Wnt-I) is presented on the apical surface of its source cells before being internalized into the endosomal pathway. Long-range Wg secretion and spread depend on secondary secretion from endosomal compartments, but the exact post-endocytic fate of Wg is poorly understood. Here, we summarize and present three protocols for the immunofluorescencebased visualization and quantitation of different pools of intracellular and extracellular Wg in WID: (1) steady-state extracellular Wg; (2) dynamic Wg trafficking inside endosomal compartments; and (3) dynamic Wg release to the cell surface. Using a genetic driver system for gene manipulation specifically at the posterior part of the WID (EnGal4) provides a robust internal control that allows for direct comparison of signal intensities of control and manipulated compartments of the same WID. Therefore, it also circumvents the high degree of staining variability usually associated with whole-tissue samples. In combination with the genetic manipulation of Wg pathway components that is easily feasible in Drosophila, these methods provide a tool-set for the dissection of secretory Wg trafficking and can help us to understand how Wnt proteins travel along endosomal compartments for short-and long-range signal secretion.
KW - Wingless/Wnt secretion
KW - Morphogen signaling
KW - Drosophila wing imaginal disc
KW - Recycling assay
KW - Extracelluar wingless
KW - Imaginal disc dissection
Y1 - 2021
U6 - https://doi.org/10.21769/BioProtoc.4040
SN - 2331-8325
VL - 11
IS - 11
PB - bio-protocol.org
CY - Sunnyvale, CA
ER -