Publications by authors named "E Gurevich"

Article Synopsis
  • The study aimed to evaluate the duration of relapsing childhood idiopathic nephrotic syndrome (INS) using data from a large health organization in Israel.
  • Researchers analyzed the medical history of 608 children diagnosed with INS, focusing on corticosteroid use and the other treatments they received.
  • Results showed that while most children entered long-lasting remission by age 11, about 21.6% continued to experience the disease into adulthood, highlighting the need for effective transition to adult healthcare services.
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Article Synopsis
  • * This technique allows for high-resolution color printing with up to 50,000 dots per inch, where the color and saturation can be easily adjusted by altering the nanostructures.
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The tubulointerstitial compartment comprises most of the kidney parenchyma. Inflammation in this compartment (tubulointerstitial nephritis-TIN) can be acute and resolves if the offending factor is withdrawn or may enter a chronic process leading to irreversible kidney damage. Etiologic factors differ, including different exposures, infections, and autoimmune and genetic tendency, and the initial damage can be acute, recurrent, or permanent, determining whether the acute inflammatory process will lead to complete healing or to a chronic course of inflammation leading to fibrosis.

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In rodents with unilateral ablation of neurons supplying dopamine to the striatum, chronic treatment with the dopamine precursor L-DOPA induces a progressive increase of behavioral responses, a process known as behavioral sensitization. This sensitization is blunted in arrestin-3 knockout mice. Using virus-mediated gene delivery to the dopamine-depleted striatum of these mice, we find that the restoration of arrestin-3 fully rescues behavioral sensitization, whereas its mutant defective in c-Jun N-terminal kinase (JNK) activation does not.

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Biological activity of free arrestins is often overlooked. Based on available data, we compare arrestin-mediated signaling that requires and does not require binding to G-protein-coupled receptors (GPCRs). Receptor-bound arrestins activate ERK1/2, Src, and focal adhesion kinase (FAK).

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