Cybersecurity researchers have uncovered over 40 malicious browser extensions for Mozilla Firefox that are designed to steal cryptocurrency wallet secrets, putting users’ digital assets at risk.
“These extensions impersonate legitimate wallet tools from widely-used platforms such as Coinbase, MetaMask, Trust Wallet, Phantom, Exodus, OKX, Keplr, MyMonero, Bitget, Leap, Ethereum Wallet, and Filfox,” Koi Security researcher Yuval Ronen said.
The large-scale campaign is said to have been ongoing since at least April 2025, with new extensions uploaded to the Firefox Add-ons store as recently as last week.
Germline cells play a key role in the transmission of phenotypes and physiological adaptations to subsequent generations (1). Over a century ago, August Weismann proposed that changes in somatic cells cannot be passed on to germ cells or offspring, a theory known as the Weismann barrier (2). Nevertheless, recent studies have proven that the Weismann barrier is permeable, and information can pass from soma to germline and modulate offspring phenotypes. In the past decade, there has been tremendous interest and progress in understanding how an altered microbiome (dysbiosis) affects different somatic cells that compose body tissues, such as brain, liver, heart, kidney, and lungs (3). Nevertheless, whether gut microbiome dysbiosis can exert an influence on the mammalian germline cells (i.e., gut to germline), and ultimately nonexposed offspring, remains unclear.
To tackle this research question, my colleagues and I established an inducible model of gut microbiota dysbiosis in isogenic male mice, using ad lib nonabsorbable antibiotics (nABX) that cannot cross the epithelial barrier of the gut (4). As expected, 6 weeks of low-dose nABX treatment led to a physiologically significant dysbiosis, which is reversible and gradually normalized to a physiologically healthy gut microbiota after 8 weeks of nABX withdrawal (6 weeks + 8 recovery). The induced dysbiosis after 6 weeks of nABX had no appreciable effects on male body weight, growth, or fertility. No nABx residues were detected in the serum or testes of treated males, which confirmed that any distal tissue responses are gut dysbiosis–induced rather than systemic drug effects.
We then examined physiological changes in the male reproductive system in response to 6 weeks of dysbiosis. Dysbiotic males had smaller testes, lower sperm count, and more abnormally shaped sperm. Histological analysis uncovered a wide range of anatomical abnormalities in testes of dysbiotic males, including increased number of abnormal seminiferous tubules, reduced epithelial thickness, and absence of mitotic compartments, which were not observed in control testes. Testicular metabolomic profiles revealed that testes clustered according to gut microbiota status and exhibited dysregulated sphingolipids, glycerophospholipids, and endocannabinoids, all known to play pivotal roles in germ cell function. Moreover, in dysbiotic male testes, spermatogenesis-regulating genes were misexpressed—most notably leptin, a reproductive hormone, was strongly down-regulated.
Hans Albrecht Bethe was born in Strasbourg, Alsace-Lorraine, on July 2 1906. He attended the Gymnasium in Frankfurt from 1915 to 1924. He then studied at the University of Frankfurt for two years, and at Munich for two and one half years, taking his Ph. D. in theoretical physics with Professor Arnold Sommerfeld in July 1928.
He then was an Instructor in physics at Frankfurt and at Stuttgart for one semester each. From fall 1929 to fall 1933 his headquarters were the University of Munich where he became Privatdozent in May 1930. During this time he had a travel fellowship of the International Education Board to go to Cambridge, England, in the fall of 1930, and to Rome in the spring terms of 1931 and 1932. In the winter semester of 1932–1933,he held a position as Acting Assistant Professor at the University of Tubingen which he lost due to the advent of the Nazi regime in Germany.
Bethe emigrated to England in October 1933 where he held a temporary position as Lecturer at the University of Manchester for the year 1933–1934, and a fellowship at the University of Bristol in the fall of 1934. In February 1935 he was appointed Assistant Professor at Cornell University, Ithaca, N. Y. U.S.A., then promoted to Professor in the summer of 1937. He has stayed there ever since, except for sabbatical leaves and for an absence during World War II. His war work took him first to the Radiation Laboratory at the Massachusetts Institute of Technology, working on microwave radar, and then to the Los Alamos Scientific Laboratory which was engaged in assembling the first atomic bomb. He returned to Los Alamos for half a year in 1952. Two of his sabbatical leaves were spent at Columbia University, one at the University of Cambridge, and one at CERN and Copenhagen.
Incoming information from the retina is channeled into two pathways in the brain’s visual system: one that’s responsible for processing color and fine spatial detail, and another that’s involved in spatial localization and detecting high temporal frequencies. A new study from MIT provides an account for how these two pathways may be shaped by developmental factors.
Newborns typically have poor visual acuity and poor color vision because their retinal cone cells are not well-developed at birth. This means that early in life, they are seeing blurry, color-reduced imagery. The MIT team proposes that such blurry, color-limited vision may result in some brain cells specializing in low spatial frequencies and low color tuning, corresponding to the so-called magnocellular system. Later, with improved vision, cells may tune to finer details and richer color, consistent with the other pathway, known as the parvocellular system.
To test their hypothesis, the researchers trained computational models of vision on a trajectory of input similar to what human babies receive early in life—low-quality images early on, followed by full-color, sharper images later. They found that these models developed processing units with receptive fields exhibiting some similarity to the division of magnocellular and parvocellular pathways in the human visual system. Vision models trained on only high-quality images did not develop such distinct characteristics.