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Millions of carbon credits are generated by overestimating forest preservation, study finds
The majority of carbon offset schemes are significantly overestimating the levels of deforestation they are preventing, according to a study published in Science.
This means that many of the “carbon credits” bought by companies to balance out emissions are not tied to real-world forest preservation as claimed.
An international team of scientists and economists led by the University of Cambridge and VU Amsterdam found that millions of carbon credits are based on crude calculations that inflate the conservation successes of voluntary REDD+ projects.
Genetically engineered pig-to-human liver xenotransplantation
The advent of genetically edited porcine-to-human xenotransplantation has predominantly focused on cardiac and renal applications, with no reported cases of porcine-to-human liver xenotransplantation. This study presents the world’s first successful genetically modified pig auxiliary liver xenotransplantation in a living human, achieving an unprecedented survival of 171 days, and provides valuable insights into the critical factors influencing the procedure’s success.
Strain engineering enhances spin readout in quantum technologies, study shows
Quantum defects are tiny imperfections in solid crystal lattices that can trap individual electrons and their “spin” (i.e., the internal angular momentum of particles). These defects are central to the functioning of various quantum technologies, including quantum sensors, computers and communication systems.
Reliably predicting and controlling the behavior of quantum defects is thus very important, as it could pave the way for the development of better performing quantum systems tailored for specific applications. A property closely linked to the dependability of quantum technologies is the so-called spin readout contrast, which essentially determines how clear it is to distinguish between two different spin states in a system.
Researchers at the Harbin Institute of Technology (Shenzhen), the HUN-REN Wigner Research Center for Physics, Shanghai Institute of Microsystem and Information Technology, Chinese Academy of Sciences and other institutes recently showed that strain engineering (i.e., stretching or compressing materials) could be used to control how quantum defects behave and enhance spin readout contrast in quantum systems.
Immune and Inflammatory Mechanisms of Atherosclerosis*
Several reports demonstrate T and B lymphocyte accumulation in the aortic adventitia in normal (9) and atherosclerotic vessels (9, 85, 86). Adoptive transfer experiments suggest that lymphocytes accumulate in the adventitia through the migration from the adventitial vasa vasorum rather than from the intimal lumen site (9). Local revascularization correlates with an increase in cellular composition within vulnerable regions of human atherosclerotic plaques (Figure 1). In contrast, the inhibition of plaque neovascularization reduces macrophage accumulation and progression of advanced atherosclerosis (87). Recently, investigators have shown that vasa vasorum can penetrate the media, enter atherosclerotic plaques, and come close to the arterial lumen (88). This is an important direct demonstration of the existence of a vascular network connecting the adventitia with the plaque tissue. Thus, we now better understand the role of neovascularization in atherosclerosis (87), but further studies are necessary to elucidate the role of small adventitial vessels in the immune response during this disease.
The presence of antigen-presenting cells and T cells within atherosclerosis-prone artery walls is well documented, but there is little information about local antigen-dependent activation of T cells. It remains to be determined whether elevated numbers of lymphocytes, which have been seen in atherosclerotic vessels, are a consequence of the accelerated recruitment of activated cells from draining lymph nodes or of local antigen-induced proliferation that leads to the increased aortic lymphocyte numbers.
One of the possible sites of T cell activation in aorta may be vascular-associated tertiary lymphoid structures (Figure 1). The lymphoid-like structures are formed in a variety of autoimmune-mediated diseases, such as rheumatoid arthritis or Hashimoto’s thyroiditis. Conglomerates of leukocytes within the adventitia were reported in the early 1970s; however, only in 1997 did Wick et al. (44) name these conglomerates vascular-associated lymphoid tissues (VALTs). These lymphoid structures are formed within advanced atherosclerosis-prone vessels and contain T and B lymphocytes, plasma cells, CD4+/CD3− inducer (LTi) cells, and some MECA-32+ and HECA-452+ microvessels (9, 86, 89). Follicles located close to the arterial external elastic lamina contain proliferating Ki67+ leukocytes, apoptotic cells, and CD138+ plasma cells, showing local B cell maturation and possible humoral immune response in these structures (86). Whether the VALTs in atherosclerosis are beneficial or proatherogenic is still unclear.
Cellular N-Myristoyl Transferases Are Required for Mammarenavirus Multiplication
The mammarenavirus matrix Z protein plays critical roles in virus assembly and cell egress. Meanwhile, heterotrimer complexes of a stable signal peptide (SSP) together with glycoprotein subunits GP1 and GP2, generated via co-and post-translational processing of the surface glycoprotein precursor GPC, form the spikes that decorate the virion surface and mediate virus cell entry via receptor-mediated endocytosis. The Z protein and the SSP undergo N-terminal myristoylation by host cell N-myristoyltransferases (NMT1 and NMT2), and G2A mutations that prevent myristoylation of Z or SSP have been shown to affect the Z-mediated virus budding and GP2-mediated fusion activity that is required to complete the virus cell entry process.
Mitochondrial building block balance linked to age-related inflammation
Research led by the Max Planck Institute for Biology of Aging in Cologne reports that misincorporation of ribonucleotides into mitochondrial DNA (mtDNA) initiates an inflammatory cascade.
Mitochondria support cell survival through metabolic and signaling roles. Conversely, their disruption has been associated with inflammation, cell death and disease.
Innate immune activation through the cGAS-STING-TBK1 pathway can move a cell from short-term defense to a chronic state of alarm. cGAS-STING activity is linked to autoimmune and inflammatory diseases and contributes to senescence and aging, intertwining immune signaling with tissue decline.
