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The winter‐spring precipitation over the Southwestern United States (SWUS) decreased since 1980. It is frequently attributed to Pacific internal decadal variability, but recent studies found anthropogenic aerosols (AA) can also induce a transition to a negative Pacific Decadal Variability (PDV) phase. We revisit the attribution of SWUS drying by quantifying the contributions of anthropogenically forced decadal Pacific Sea Surface Temperatures (SSTs). Applying a low‐frequency component analysis to observations, Community Earth System Model version 2 (CESM2) all‐forcings and single‐forcing large ensembles, we find up to 42% of the observed precipitation trend to be related to the AA‐induced negative PDV‐like pattern, which is driven by the emission shift from the Western to the Eastern Hemisphere. In CESM2, other radiative forcings counteract the influence of AA, but it remains unclear whether the model correctly simulates this balance. This implies that the near‐future trajectories of these forcings, in particular Asian aerosols, are important for projections of SWUS precipitation. Plain Language Summary Water resources of the Southwestern United States (SWUS) rely on winter‐spring precipitation, which has been declining since 1980. To understand the reasons for the decline, we evaluate the impacts of human‐caused Pacific Sea Surface Temperature (SST) changes on SWUS precipitation. We use observations and climate model experiments together with statistical approaches. We find evidence that the shift of aerosol emissions from the Western to the Eastern Hemisphere induced a change in Pacific SSTs that in turn favors a winter‐spring SWUS precipitation decline. Additionally, we showed that other human‐caused factors, such as greenhouse gases, can offset the impact of aerosols. This means that the near‐future SWUS precipitation change depends on the trajectories and the interactions of these various human‐caused factors. Key Points We quantify the role of anthropogenic aerosols in post‐1980 Pacific sea surface temperatures and the U.S. Southwest precipitation decline Internal variability dominates the winter‐spring precipitation trend but aerosols contribute to it through their influence on Pacific SSTs Community Earth System Model version 2 simulates a tug‐of‐war between aerosols and other forcings (e.g., greenhouse gases) and its response to aerosols might be too weak

A novel and an efficient rescue system with a multi-agent simultaneous localization and mapping (SLAM) framework is proposed to reduce the rescue time while rescuing the people trapped inside a burning building. In this study, the truncated signed distance (TSD) based SLAM algorithm is employed to accurately construct a two-dimensional map of the surroundings. For a new and significantly different scenario, information is gathered and the general iterative closest point method (GICP) is directly employed instead of the conventional TSD-SLAM process. Rescuers can utilize a total map created by merging individual maps, allowing them to efficiently search for victims. For online map merging, it is essential to determine the timing of when the individual maps are merged and the extent to which one map reflects the other map, via the weights. In the several experiments conducted, a light-detection and ranging system and an inertial measurement unit were integrated into a smart helmet for rescuers. The results indicated that the map was built more accurately than that obtained using the conventional TSD-SLAM. Additionally, the merged map was built more correctly by determining proper parameters for online map merging. Consequently, the accurate merged map allows rescuers to search for victims efficiently.

This article introduces the Extratropical–Tropical Interaction Model Intercomparison Project (ETIN-MIP), where a set of fully coupled model experiments are designed to examine the sources of longstanding tropical precipitation biases in climate models. In particular, we reduce insolation over three targeted latitudinal bands of persistent model biases: the southern extratropics, the southern tropics, and the northern extratropics. To address the effectof regional energy bias corrections on the mean distribution of tropical precipitation, such as the double intertropical convergence zone problem, we evaluate the quasi-equilibrium response of the climate system corresponding to a 50-yr period after the 100 years of prescribed energy perturbation. Initial results show that, despite a large intermodel spread in each perturbation experiment due to differences in ocean heat uptake response and climate feedbacks across models, the southern tropics is most efficient at driving a meridional shift of tropical precipitation. In contrast, the extratropical energy perturbations are effectively damped by anomalous heat uptake over the subpolar oceans, thereby inducing a smaller meridional shift of tropical precipitation compared with the tropical energy perturbations. The ETIN-MIP experiments allow us to investigate the global implications of regional energy bias corrections, providing a route to guide the practice of model development, with implications for understanding dynamical responses to anthropogenic climate change and geoengineering.

Climate models exhibit substantial inter-model spread in climate sensitivity, typically attributed to uncertainty in cloud feedbacks. In contrast, the influence of clear-sky shortwave absorption (SWA) remains underexplored, despite its substantial uncertainty. Using a single-model framework, we systematically perturb SWA and impose CO₂ quadrupling on distinct mean states that differ in SWA, allowing assessment of its impact on both the mean climate and the CO₂-driven response. Enhanced SWA reduces surface shortwave radiation, leading to Arctic cooling. Under higher SWA, CO₂ forcing drives increased advection of colder Arctic air into the subpolar North Atlantic, enhancing turbulent heat loss and facilitating AMOC recovery. This accelerated recovery amplifies warming in the subpolar North Atlantic, strengthens lapse rate and shortwave cloud feedbacks, and ultimately increases climate sensitivity over time. These findings reveal a previously overlooked pathway by which clear-sky SWA modulates long-term climate feedback, underscoring the need to better constrain SWA in climate models.

Primary microcephaly (MCPH) associated proteins CDK5RAP2, CEP152, WDR62 and CEP63 colocalize at the centrosome. We found that they interact to promote centriole duplication and form a hierarchy in which each is required to localize another to the centrosome, with CDK5RAP2 at the apex, and CEP152, WDR62 and CEP63 at sequentially lower positions. MCPH proteins interact with distinct centriolar satellite proteins; CDK5RAP2 interacts with SPAG5 and CEP72, CEP152 with CEP131, WDR62 with MOONRAKER, and CEP63 with CEP90 and CCDC14. These satellite proteins localize their cognate MCPH interactors to centrosomes and also promote centriole duplication. Consistent with a role for satellites in microcephaly, homozygous mutations in one satellite gene, CEP90, may cause MCPH. The satellite proteins, with the exception of CCDC14, and MCPH proteins promote centriole duplication by recruiting CDK2 to the centrosome. Thus, centriolar satellites build a MCPH complex critical for human neurodevelopment that promotes CDK2 centrosomal localization and centriole duplication. When a cell divides, the chromosomes that contain the genetic blueprint for the cell must be replicated and shared between the two new cells. A structure called the centrosome organizes the cellular machinery that separates the chromosome copies during cell division. At the center of each centrosome are two cylindrical microtubule-based structures called centrioles. Mutations in certain proteins that interact with the centrosome cause a neurodevelopmental disorder called primary microcephaly. People born with microcephaly have unusually small heads and brains. As a result, they may have difficulties with mental tasks. Scientists do not know exactly how these ‘microcephaly-associated’ proteins normally interact with the centrosomes or what they do at the centrosomes, so it is difficult to work out what goes wrong in people with microcephaly. One idea is that the proteins help to duplicate the centrioles before a cell divides. If this duplication does not occur, a cell cannot divide properly; so, people with mutations that interfere with centriole duplication cannot grow enough brain cells. Now, Kodani et al. have examined how these microcephaly-associated proteins work with ‘satellite’ proteins that congregate near the centrosome to duplicate centrioles. The satellite proteins help to recruit four microcephaly-associated proteins to the centrosome, where they are built into a ring. The microcephaly-associated proteins congregate at the centrosome in a particular order, with each protein recruiting the next one in the sequence. Once all four are in place near the centrosome, an enzyme that helps to duplicate the centrioles joins them. Further experiments suggest that mutations that affect one of the satellite proteins—known as CEP90—may cause microcephaly. Future analysis of how microcephaly-associated genes work may reveal the cell biological mechanisms by which centrioles participate in brain development.

Background Sarcopenia is an age‐related progressive loss of muscle mass and function. Sarcopenia is a multifactorial disorder, including metabolic disturbance; therefore, metabolites may be used as circulating biomarkers for sarcopenia. We aimed to investigate potential biomarkers of sarcopenia using metabolomics. Methods After non‐targeted metabolome profiling of plasma from mice of an aging mouse model of sarcopenia, sphingolipid metabolites and muscle cells from the animal model were evaluated using targeted metabolome profiling. The associations between sphingolipid metabolites identified from mouse and cell studies and sarcopenia status were assessed in men in an age‐matched discovery (72 cases and 72 controls) and validation (36 cases and 128 controls) cohort; women with sarcopenia (36 cases and 36 controls) were also included as a discovery cohort. Results Both non‐targeted and targeted metabolome profiling in the experimental studies showed an association between sphingolipid metabolites, including ceramides (CERs) and sphingomyelins (SMs), and sarcopenia. Plasma SM (16:0), CER (24:1), and SM (24:1) levels in men with sarcopenia were significantly higher in the discovery cohort than in the controls (all P < 0.05). There were no significant differences in plasma sphingolipid levels for women with or without sarcopenia. In men in the discovery cohort, an area under the receiver‐operating characteristic curve (AUROC) of SM (16:0) for low muscle strength and low muscle mass was 0.600 (95% confidence interval [CI]: 0.501–0.699) and 0.647 (95% CI: 0.557–0.737). The AUROC (95% CI) of CER (24:1) and SM (24:1) for low muscle mass in men was 0.669 (95% CI: 0.581–0.757) and 0.670 (95% CI: 0.582–0.759), respectively. Using a regression equation combining CER (24:1) and SM (16:0) levels, a sphingolipid (SphL) score was calculated; an AUROC of the SphL score for sarcopenia was 0.712 (95% CI: 0.626–0.798). The addition of the SphL score to HGS significantly improved the AUC from 0.646 (95% CI: 0.575–0.717; HGS only) to 0.751 (95% CI: 0.671–0.831, P = 0.002; HGS + SphL) in the discovery cohort. The predictive ability of the SphL score for sarcopenia was confirmed in the validation cohort (AUROC = 0.695, 95% CI: 0.591–0.799). Conclusions SM (16:0), reflecting low muscle strength, and CER (24:1) and SM (16:0), reflecting low muscle mass, are potential circulating biomarkers for sarcopenia in men. Further research on sphingolipid metabolites is required to confirm these results and provide additional insights into the metabolomic changes relevant to the pathogenesis and diagnosis of sarcopenia.

Background Sarcopenia and osteoporosis frequently co‐occur in the elderly and have common pathophysiological determinants. Slit guidance ligand 3 (SLIT3) has been recently discovered as a novel therapeutic factor against osteoporosis, and a SLIT3 fragment containing the second leucine‐rich repeat domain (LRRD2) had a therapeutic efficacy against osteoporosis. However, a role of SLIT3 in the skeletal muscle is unknown. Methods Skeletal muscle mass, strength, and/or physical activity were evaluated in Slit3−/−, ovariectomized, and aged mice, based on the measurements of muscle weight and grip strength, Kondziella's inverted hanging test, and/or wheel‐running test. Skeletal muscles were also histologically evaluated by haematoxylin and eosin staining and/or immunofluorescence. The ovariectomized and aged mice were intravenously injected with recombinant SLIT3 LRRD2 for 4 weeks. C2C12 cells were used to know cellular effects of SLIT3, such as in vitro myogenesis, fusion, cell viability, and proliferation, and also used to evaluate its molecular mechanisms by immunocytochemistry, immunoprecipitation, western blotting, real‐time PCR, siRNA transfection, and receptor‐ligand binding ELISA. Results Slit3‐deficient mice exhibited decreased skeletal muscle mass, muscle strength, and physical activity. The relative masses of gastrocnemius and soleus were lower in the Slit3−/− mice (0.580 ± 0.039% and 0.033 ± 0.003%, respectively) than those in the WT littermates (0.622 ± 0.043% and 0.038 ± 0.003%, respectively) (all, P < 0.05). Gastrocnemius of Slit3−/− mice showed the reduced number of Type I and Type IIa fibres (all, P < 0.05), but not of Type IIb and Type IIx fibres. SLIT3 activated β‐catenin signalling by promoting its release from M‐cadherin, thereby increasing myogenin expression to stimulate myoblast differentiation. In vitro experiments involving ROBO2 expression, knockdown, and interaction with SLIT3 indicated that ROBO2 functions as a SLIT3 receptor to aid myoblast differentiation. SLIT3 LRRD2 dissociated M‐cadherin‐bound β‐catenin and up‐regulated myogenin expression to increase myoblast differentiation, in a manner similar to full‐length SLIT3. Systemic treatment with SLIT3 LRRD2 increased skeletal muscle mass in both ovariectomized and aged mice (all, P < 0.05). The relative masses of gastrocnemius and soleus were higher in the treated aged mice (0.548 ± 0.045% and 0.033 ± 0.005%, respectively) than in the untreated aged mice (0.508 ± 0.016% and 0.028 ± 0.003%, respectively) (all, P < 0.05). SLIT3 LRRD2 treatment increased the hanging duration of the aged mice by approximately 1.7‐fold (P < 0.05). Conclusions SLIT3 plays a sarcoprotective role by activating β‐catenin signalling. SLIT3 LRRD2 can potentially be used as a therapeutic agent against muscle loss.

Background Sarcopenia is characterized by a progressive decrease in skeletal muscle mass and function with age. Given that sarcopenia is associated with various metabolic disorders, effective metabolic biomarkers for its early detection are required. We aimed to investigate the metabolic biomarkers related to sarcopenia in elderly men and perform experimental studies using metabolomics. Methods Plasma metabolites from 142 elderly men, comprising a sarcopenia group and an age‐matched control group, were measured using global metabolome profiling. Muscle and plasma samples from an aging mouse model of sarcopenia, as well as cell media and cell lysates during myoblast differentiation, were analysed based on targeted metabolome profiling. Based on these experimental results, fatty acid amides were quantified from human plasma as well as human muscle tissues. The association of fatty acid amide levels with sarcopenia parameters was evaluated. Results Global metabolome profiling showed that fatty acid amide levels were significantly different in the plasma of elderly men with sarcopenia (all Ps < 0.01). Consistent with these results in human plasma, targeted metabolome profiling in an aging mouse model of sarcopenia showed decreased levels of fatty acid amides in plasma but not in muscle tissue. In addition, the levels of fatty acid amides increased in cell lysates during muscle cell differentiation. Targeted metabolome profiling in men showed decreased docosahexaenoic acid ethanolamide (DHA EA) levels in the plasma (P = 0.016) but not in the muscle of men with sarcopenia. DHA EA level was positively correlated with sarcopenia parameters such as skeletal muscle mass index (SMI) and handgrip strength (HGS) (P = 0.001, P = 0.001, respectively). The area under the receiver‐operating characteristic curve (AUC) for DHA EA level ≤ 4.60 fmol/μL for sarcopenia was 0.618 (95% confidence interval [CI]: 0.532–0.698). DHA EA level ≤ 4.60 fmol/μL was associated with a significantly greater likelihood of sarcopenia (odds ratio [OR]: 2.11, 95% CI: 1.03–4.30), independent of HGS. The addition of DHA EA level to age and HGS significantly improved the AUC from 0.620 to 0.691 (P = 0.0497). Conclusions Our study demonstrated that fatty acid amides are potential circulating biomarkers in elderly men with sarcopenia. DHA EA, in particular, strongly related to muscle mass and strength, can be a key metabolite to become a reliable metabolic biomarker for sarcopenia. Further research on fatty acid amides will provide insights into the metabolomic changes relevant to sarcopenia from an aging perspective.

The Hadley cell response to globally increasing CO 2 concentrations is spatially complex, with an intensified rising branch and weakened descending branch. To better understand these changes, we examine the sensitivity of the Hadley cell to idealized radiative forcing in different latitude bands. The Hadley cell response is, to first order, governed by the latitudinal structure of the forcing. The strengthening of the upward branch is attributed to tropical forcing, whereas the weakening of the descending branch is attributed to extratropical forcing. These direct radiatively-forced Hadley cell responses are amplified by changes in atmospheric eddy heat transport while being partially offset by changes in gross moist stability and ocean heat uptake. The radiative feedbacks further modulate the Hadley cell response by altering the meridional atmospheric energy gradient. The Hadley cell projections under global warming are thus a result of opposing – and thus compensating – effects from tropical and extratropical radiative forcings.

Climate models are increasingly used to inform water availability projections at regional scales. However, the models’ own runoff sensitivities—the change in runoff per unit change of precipitation or temperature—are often biased, which can degrade their projections of runoff change. Specifically, models tend to underestimate the runoff decline in response to a temperature increase. Here, we conduct a comprehensive analysis with multiple observational datasets, two climate model generations, and large ensemble sampling of internal climate variability to assess these biases and to constrain future runoff projections across major river basins globally. For basins that can be robustly constrained by available observations, the constraint indicates stronger runoff declines than raw model projections. The constrained projections thus indicate more severe impacts of climate change on water resources than indicated by direct climate model output. Global river runoff projections constrained by observations indicate stronger declines in runoff under climate change than raw model outputs, according to a study combining multiple observational datasets, two generations of climate models, and large ensemble sampling of internal variability.