Geochemistry and geochronology of dolerite dykes from the Daba and Dongbo peridotite massifs, SW Tibet: Insights into the style of mantle melting at the onset of Neo-Tethyan subduction

This study reports compositional and whole-rock Sr-Nd isotope data as well as zircon U-Pb geochronological data on dolerite dikes from the Daba and Dongbo ultramafic massifs, southwest Yarlung-Zangbo Suture Zone (YZSZ), Tibet. The 120.6 \ub1 1.6 Ma dolerite dikes from the Daba peridotite exhibit normal mid-ocean ridge basalt (N-MORB)-type normalized mutli-element patterns [(La/Yb)N = 0.43-0.72] with noticeable negative Nb and Th anomalies. They have high initial 87Sr/8624 Sr ratios (87Sr/8625 Sr(i) = 0.70720-0.70788) and high \u3b5Nd(t) values (+7.4 to +7.9). The 125.4 \ub1 1.8 Ma dolerite intrusions within the Dongbo peridotite show N-MORB\u2012type trace element profiles [(La/Yb)N = 0.65-0.84] characterized by apparent negative anomalies in Nb and Th, and mild negative anomalies in Ti (\ub1 Y). They also have high 87Sr/8629 Sr(i) ratios (0.70611-0.70679) and elevated \u3b5Nd(t) values (+7.8 to +8.2). Semi-quantitative La/Yb vs. Dy/Yb modeling demonstrates that the parental magmas of the investigated dolerite dikes derived from more than 20% (cumulative) melting of a (broad) mantle source region that had a spinel-bearing N-MORB\u2013like lherzolitic composition. Our geochemical and isotopic data indicate that the composition of the inferred mantle source was influenced by minor input of subducted crustal material. The petrogenesis of the Daba and Dongbo massifs could be linked to upwelling of an asthenospheric source that caused continental rift and subsequent seafloor spreading, followed by subduction initiation adjacent to a passive margin during the early Cretaceous (~130-120 Ma). Our study provides a more detailed, and perhaps more elegant, hypothesis for the tectono-magmatic evolution of the southwestern YZSZ "ophiolitic" peridotites after their accretion beneath a Neo-Tethyan marginal basin

5G PRS-Based Sensing: A Sensing Reference Signal Approach for Joint Sensing and Communication System

The emerging joint sensing and communication (JSC) technology is expected to support new applications and services, such as autonomous driving and extended reality (XR), in the future wireless communication systems. Pilot (or reference) signals in wireless communications usually have good passive detection performance, strong anti-noise capability and good auto-correlation characteristics, hence they bear the potential for applying in radar sensing. In this paper, we investigate how to apply the positioning reference signal (PRS) of the 5th generation (5G) mobile communications in radar sensing. This approach has the unique benefit of compatibility with the most advanced mobile communication system available so far. Thus, the PRS can be regarded as a sensing reference signal to simultaneously realize the functions of radar sensing, communication and positioning in a convenient manner. Firstly, we propose a PRS based radar sensing scheme and analyze its range and velocity estimation performance, based on which we propose a method that improves the accuracy of velocity estimation by using multiple frames. Furthermore, the Cramer-Rao lower bound (CRLB) of the range and velocity estimation for PRS based radar sensing and the CRLB of the range estimation for PRS based positioning are derived. Our analysis and simulation results demonstrate the feasibility and superiority of PRS over other pilot signals in radar sensing. Finally, some suggestions for the future 5G-Advanced and 6th generation (6G) frame structure design containing the sensing reference signal are derived based on our study

Molecular Mechanisms of snoRNA-IL-15 Crosstalk in Adipocyte Lipolysis and NK Cell Rejuvenation

Obesity, in which the functional importance of small nucleolar RNAs (snoRNAs) remains elusive, correlates with risk for many cancer types. Here, we identify that the serum copies of adipocyte-expressed SNORD46 correlate with body mass index (BMI), and serum SNORD46 antagonizes interleukin-15 (IL-15) signaling. Mechanically, SNORD46 binds IL-15 via G11, and G11A (a mutation that significantly enhances binding affinity) knockin drives obesity in mice. Functionally, SNORD46 blocks IL-15-induced, FER kinase-dependent phosphorylation of platelet glycoprotein 4 (CD36) and monoglyceride lipase (MGLL) in adipocytes, leading to inhibited lipolysis and browning. In natural killer (NK) cells, SNORD46 suppresses the IL-15-dependent autophagy, leading to reduced viability of obese NK. SNORD46 power inhibitors exhibit anti-obesity effects, concurring with improved viability of obese NK and anti-tumor immunity of CAR-NK cell therapy. Hence, our findings demonstrate the functional importance of snoRNAs in obesity and the utility of snoRNA power inhibitors for antagonizing obesity-associated immune resistance

Molecular Mechanisms of snoRNA-lL-15 Crosstalk in Adipocyte Lipolysis and NK Cell Rejuvenation

Obesity, in which the functional importance of small nucleolar RNAs (snoRNAs) remains elusive, correlates with risk for many cancer types. Here, we identify that the serum copies of adipocyte-expressed SNORD46 correlate with body mass index (BMI), and serum SNORD46 antagonizes interleukin-15 (IL-15) signaling. Mechanically, SNORD46 binds IL-15 via G11, and G11A (a mutation that significantly enhances binding affinity) knockin drives obesity in mice. Functionally, SNORD46 blocks IL-15-induced, FER kinase-dependent phosphorylation of platelet glycoprotein 4 (CD36) and monoglyceride lipase (MGLL) in adipocytes, leading to inhibited lipolysis and browning. In natural killer (NK) cells, SNORD46 suppresses the IL-15-dependent autophagy, leading to reduced viability of obese NK. SNORD46 power inhibitors exhibit anti-obesity effects, concurring with improved viability of obese NK and anti-tumor immunity of CAR-NK cell therapy. Hence, our findings demonstrate the functional importance of snoRNAs in obesity and the utility of snoRNA power inhibitors for antagonizing obesity-associated immune resistance

Interaction between pollution and climate change augments ecological risk to a coastal ecosystem

Pollution and climate change are among the most challenging issues for countries with developing economies, but we know little about the ecological risks that result when these pressures occur together. We explored direct effects of, and interactions between, environmental pollution and climate change on ecosystem health in the Bohai Sea region of Northern China. We developed an integrated approach to assess ecological risks to this region under four scenarios of climate change. Although ecological risks to the system from pollution alone have been declining, interactions between pollution and climate change have enhanced ecological risks to this coastal/marine ecosystem. Our results suggest that current policies focused strictly on pollution control alone should be changed to take into account the interactive effects of climate change so as to better forecast and manage potential ecological risks

Well Water Arsenic Exposure, Arsenic Induced Skin-Lesions and Self-Reported Morbidity in Inner Mongolia

Residents of the Bayingnormen region of Inner Mongolia have been exposed to arsenic-contaminated well water for over 20 years, but relatively few studies have investigated health effects in this region. We surveyed one village to document exposure to arsenic and assess the prevalence of arsenic-associated skin lesions and self-reported morbidity. Five-percent (632) of the 12,334 residents surveyed had skin lesions characteristics of arsenic exposure. Skin lesions were strongly associated with well water arsenic and there was an elevated prevalence among residents with water arsenic exposures as low as 5 μg/L-10 μg/L. The presence of skin lesions was also associated with self-reported cardiovascular disease

Tumor-associated Nonmyelinating Schwann Cell-expressed Nuclear Export Signal Mutation of Epidermal Growth Factor Receptor Enhances Malignant Phenotypes of Cancer Cells

One of the major obstacles to treating pancreatic ductal adenocarcinoma (PDAC) is its immunoresistant microenvironment. The functional importance and molecular mechanisms of Schwann cells in PDAC remains largely elusive. We characterized the gene signature of tumor-associated nonmyelinating Schwann cells (TASc) in PDAC and indicated that the abundance of TASc was correlated with immune suppressive tumor microenvironment and the unfavorable outcome of patients with PDAC. Depletion of pancreatic-specific TASc promoted the tumorigenesis of PDAC tumors. TASc-expressed long noncoding RNA (lncRNA) plasmacytoma variant translocation 1