Search

The article focuses on Albert Einstein's time at Oxford University and the reasons behind his eventual move to Princeton. Topics include Einstein's deep admiration for British physics and his initial enthusiasm for Oxford, his dissatisfaction with Oxford's academic environment and formality, and his preference for solitude, which ultimately led him to emigrate to the United States.

[CD4.sup.+] T cells play a major role in protective immunity against the blood stage of malaria, but the mechanism of protection is unclear. By adoptive transfer of cloned T cell lines, direct evidence is provided that both [T.sub.H]1 and [T.sub.H]2 subsets of [CD4.sup.+] T cells can protect against Plasmodium chabaudi chabaudi infection. [T.sub.H]1 cells protect by a nitric oxide-dependent mechanism, whereas [T.sub.h] 2 cells protect by the enhancement and accelerated production of specific immunoglobulin G1 antibody., Malaria, principally Plasmodium falciparum malaria, affects 250 to 400 million people and causes more than 1 million deaths annually (1). Vaccine development would be facilitated by a better understanding of [...]

These observations, wrote Einstein, were "the origin of the next great theoretical advance, which had to await, over a hundred years, the coming of Thomas Young." INSIGHTS In 1931, Albert Einstein wrote a foreword to the fourth edition of Isaac Newton's 1704 Opticks, which described Newton's experiments with, and explanations of, phenomena associated with light, including his observations of the colors of thin films. In 2023, the 250th anniversary of Young's birth, the chief lesson of his life for scientists is surely how Young made his greatest discovery, the double-slit experiment. [Extracted from the article]

The article reviews the exhibition "Bedlam: The Asylum and Beyond" at the Wellcome Collection in London, England, on display until January 15, 2017, focusing on the history of treatment of mental illness.

The article reviews the exhibition "Fox Talbot: Dawn of the Photograph," featuring the photography by William Henry Fox Talbot at the Science Museum in London, England until September 11, 2016, including the book "William Henry Fox Talbot: Dawn of the Photograph," by Russell Roberts and Greg Hobson.

The article reviews the exhibition "Ada Lovelace " exhibited at Science Museum in London, England, through March 31, 2016, which will feature color portraits of British mathematician Ada Lovelace.

The article reviews the exhibition "Marks of Genius: Masterpieces from the Collections of the Bodleian Libraries" at the Weston Library at the University of Oxford in England through September 20, 2015, which features books, maps, manuscripts, and artworks.

The article reviews "Forensics: The Anatomy of Crime," an exhibition on the history of forensic science at the Wellcome Collection in London, England February 26-June 21, 2015.

The localization, number, and function of postsynaptic AMPA-type glutamate receptors (AMPARs) are crucial for synaptic plasticity, a cellular correlate for learning and memory. The Hippo pathway member WWC1 is an important component of AMPAR-containing protein complexes. However, the availability of WWC1 is constrained by its interaction with the Hippo pathway kinases LATS1 and LATS2 (LATS1/2). Here, we explored the biochemical regulation of this interaction and found that it is pharmacologically targetable in vivo. In primary hippocampal neurons, phosphorylation of LATS1/2 by the upstream kinases MST1 and MST2 (MST1/2) enhanced the interaction between WWC1 and LATS1/2, which sequestered WWC1. Pharmacologically inhibiting MST1/2 in male mice and in human brain-derived organoids promoted the dissociation of WWC1 from LATS1/2, leading to an increase in WWC1 in AMPAR-containing complexes. MST1/2 inhibition enhanced synaptic transmission in mouse hippocampal brain slices and improved cognition in healthy male mice and in male mouse models of Alzheimer's disease and aging. Thus, compounds that disrupt the interaction between WWC1 and LATS1/2 might be explored for development as cognitive enhancers.