The Supreme Court of the United States has recently been petitioned to revisit legal issues pertaining to the lawfulness of imposing a vaccine mandate on individuals with proof of natural immunity during the COVID-19 pandemic. While the petition accepts that the protection of public health during COVID-19 was an important governmental interest, the petitioners maintain that the imposition of a vaccine mandate on individuals with natural immunity was not 'substantially related' to accomplishing that purpose. In this short report, we outline how some of the petition's general arguments interact with points we raised in a 2022 article in this journal defending natural immunity exemptions, in light of new evidence. In particular, we reflect on new evidence pertaining to differences between vaccine-induced immunity, natural immunity, and so-called 'hybrid' immunity. We suggest that the nuanced nature of this evidence highlights the importance of making fine-grained judgements about proportionality and necessity when considering vaccine mandates. We conclude by claiming that if future pandemics necessitate the imposition of vaccine mandates, then those seeking to justify them should clearly articulate the relevance (and the evidence) for the comparative protection of vaccine-induced, natural, and hybrid immunity.
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http://dx.doi.org/10.1136/jme-2024-110034 | DOI Listing |
J Cancer Res Ther
December 2024
School of Chemistry, Chemical Engineering and Life Sciences, Wuhan University of Technology, Wuhan, China.
Tumor-infiltrating lymphocytes (TILs) are key components of the tumor microenvironment (TME) and serve as prognostic markers for breast cancer. Patients with high TIL infiltration generally experience better clinical outcomes and extended survival compared to those with low TIL infiltration. However, as the TME is highly complex and TIL subtypes perform distinct biological functions, TILs may only provide an approximate indication of tumor immune status, potentially leading to biased prognostic results.
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January 2025
Department of Nutrition, Second Military Medical University, Shanghai, China.
Tamoxifen is an inhibitor of estrogen receptors and was originally developed for breast cancer therapy. Besides, tamoxifen is widely used for Cre-estrogen receptor-mediated conditional knockout in transgenic mice. However, we found that the 3-month feeding of 0.
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January 2025
Innate Immunity Group, Institute of Genetics, HUN-REN Biological Research Centre, 6726 Szeged, Hungary.
Parasitoid elimination in involves special hemocytes, called lamellocytes, which encapsulate the eggs or larvae of the parasitoid wasps. The capsules are melanized, and metabolites of the melanization reaction may play a potential role in parasitoid killing. We have observed a variation in the melanization capacity of different, commonly used strains, such as Canton-S, Oregon-R, and BL5905, BL6326.
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January 2025
Third Department of Obstetrics and Gynecology, University General Hospital "ATTIKON", Medical School, National and Kapodistrian University of Athens, 12462 Athens, Greece.
Chronic inflammation is increasingly recognized as a critical factor in female reproductive health; influencing natural conception and the outcomes of assisted reproductive technologies such as in vitro fertilization (IVF). An essential component of innate immunity, the NLR family pyrin domain-containing 3 (NLRP3) inflammasome is one of the major mediators of inflammatory responses, and its activation is closely linked to oxidative stress. This interaction contributes to a decline in oocyte quality, reduced fertilization potential, and impaired embryo development.
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January 2025
Department of Anatomy and Cell Biology, Carver College of Medicine, University of Iowa, Iowa City, Iowa, USA.
Cystic fibrosis (CF) is caused by mutations in the (). While gene therapy holds promise as a cure, the cell-type-specific heterogeneity of expression in the lung presents significant challenges. Current CF ferret models closely replicate the human disease phenotype but have limitations in studying functional complementation through cell-type-specific CFTR restoration.
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