Publications by authors named "J P Nemmer"
Although p38 MAP Kinase α (p38 MAPKα) is generally accepted to play a central role in the cardiac stress response, to date its function in maladaptive cardiac hypertrophy is still not unambiguously defined. To induce a pathological type of cardiac hypertrophy we infused angiotensin II (AngII) for 2 days via osmotic mini pumps in control and tamoxifen-inducible, cardiomyocyte (CM)-specific p38 MAPKα KO mice (iCMp38αKO) and assessed cardiac function by echocardiography, complemented by transcriptomic, histological, and immune cell analysis. AngII treatment after inactivation of p38 MAPKα in CM results in left ventricular (LV) dilatation within 48 h (EDV: BL: 83.
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- The study investigates how mutations in the filaggrin (FLG) gene affect skin barrier function and its relationship with atopic dermatitis (AD), a condition characterized by inflammation and altered skin.
- Researchers analyzed genetic, gene expression, and microbial data from AD patients with FLG mutations, compared to healthy controls, to understand the biological and microbial interactions occurring in the skin.
- Findings revealed that FLG mutations lead to altered skin gene expression related to barrier dysfunction and inflammation, with specific bacteria (like S. aureus) influencing the skin's microbiome and highlighting 28 key genes linked to AD.
Background: The skin is an organ frequently affected by chronic diseases. Inflammatory, immune-mediated dermatoses such as atopic dermatitis and psoriasis show a high prevalence as well as a significant impact on the quality of life of those affected. In a large proportion of cases, atopic dermatitis is associated with a marked change in microbial colonization of both clinically healthy and affected skin.
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- * Recent studies highlight the importance of Interleukin (IL)-31 and its receptor, with promising results from the IL-31RA antibody nemolizumab for treating conditions like atopic dermatitis.
- * The summary reviews the role of IL-31 in various allergic conditions, detailing its cellular origins, regulatory mechanisms, and its contributions to pruritus, inflammation, and tissue changes.
Energy depletion and lactate are at plateau levels within five minutes of complete ischemic-anoxia in the brain; however, irreversible brain injury has not occurred in this time. Brain free fatty acids (FFA) rise sharply during the first five minutes of ischemic-anoxia, but then continue to rise during the following hour without plateauing. Barbiturate anesthesia preischemia attenuates the FFA rise.
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