European journal of clinical investigation
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Eur. J. Clin. Invest. · Nov 2021
TNF-α antagonism rescues the effect of ageing on stroke: Perspectives for targeting inflamm-ageing.
Epidemiologic evidence links ischemic stroke to age, yet the mechanisms that underlie the specific and independent effects of age on stroke remain elusive, impeding the development of targeted treatments. This study tested the hypothesis that age directly aggravates stroke outcomes and proposes inflamm-aging as a mediator and potential therapeutic target. ⋯ This study identifies TNF-α as a causative contributor to the deleterious effect of aging on stroke and points to inflamm-aging as a mechanism of age-related worsening of stroke outcomes and potential therapeutic target in this context. Thus, this work provides a basis for tailoring novel stroke therapies for the particularly vulnerable elderly population.
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Eur. J. Clin. Invest. · Nov 2021
Observational StudySerum antibody response to BNT162b2 after natural SARS-CoV-2 infection.
There is preliminary evidence that individuals with previous SARS-CoV-2 infections exhibit a more pronounced antibody response. However, these assumptions have not yet been supported by data obtained through various CE-marked tests. This study aimed to close this gap. ⋯ Compared with naïve individuals, seropositives after natural SARS-CoV-2 infection presented with a substantially higher antibody response already after dose 1 of BNT162b2, as measured by two CE-marked in vitro diagnostic tests and a sVNT. These results should stimulate discussion and research on whether individuals after previous SARS-CoV-2 infection would benefit from a two-part vaccination schedule or whether these currently much-needed second doses could be saved.
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Eur. J. Clin. Invest. · Nov 2021
Circ_0021087 acts as a miR-184 sponge and represses gastric cancer progression by adsorbing miR-184 and elevating FOSB expression.
Gastric cancer (GC) ranks third among the causes of cancer-related deaths in the world. Circular RNA hsa_circ_0021087 (circ_0021087) plays a repressive role in GC. Nevertheless, the mechanism by which circ_0021087 constrains GC advancement is unclear. ⋯ Circ_0021087 and FOSB were lowly expressed in GC, whereas miR-184 had an opposite result. Circ_0021087 overexpression repressed GC cell proliferation and epithelial-mesenchymal transition (EMT) in xenograft models in vivo and induced GC cell apoptosis, repressed GC cell proliferation, EMT, migration and invasion in vitro. Circ_0021087 could elevate FOSB expression by adsorbing miR-184. MiR-184 mimic reversed the inhibitory influence of circ_0021087 overexpression on GC cell malignancy. Also, FOSB knockdown offset the suppressive impact of miR-184 silencing on GC cell malignancy. In conclusion, circ_0021087 played a repressive influence on GC progression by elevating FOSB expression by adsorbing miR-184, offering a new mechanism for circ_0021087 to inhibit the progression of GC.
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Eur. J. Clin. Invest. · Nov 2021
ReviewQuality of life assessment in amyloid transthyretin (ATTR) amyloidosis.
Amyloid transthyretin (ATTR) amyloidosis is caused by the systemic deposition of transthyretin molecules, either normal (wild-type ATTR, ATTRwt) or mutated (variant ATTR, ATTRv). ATTR amyloidosis is a disease with a severe impact on patients' quality of life (QoL). Nonetheless, limited attention has been paid to QoL so far, and no specific tools for QoL assessment in ATTR amyloidosis currently exist. QoL can be evaluated through patient-reported outcome measures (PROMs), which are completed by patients, or through scales, which are compiled by clinicians. The scales investigate QoL either directly or indirectly, i.e., by assessing the degree of functional impairment and limitations imposed by the disease. ⋯ Scales or PROMs for ATTR amyloidosis would be useful to better characterize newly diagnosed patients and to assess disease progression and response to treatment. The ongoing ITALY (Impact of Transthyretin Amyloidosis on Life qualitY) study aims to develop and validate 2 PROMs encompassing the whole phenotypic spectrum of ATTRwt and ATTRv amyloidosis, that might be helpful for patient management and may serve as surrogate endpoints for clinical trials.