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<i>Operando</i> Unveiling of Hydrogen Spillover Mechanisms on Tungsten Oxide Surfaces

Impaired MC3T3-E1 osteoblast differentiation triggered by oncogenic HRAS is rescued by the farnesyltransferase inhibitor Tipifarnib

Abstract HRAS is a ubiquitously expressed protein and functions as a central regulator of cellular homeostasis. In somatic cells, mutations in this gene cause cancer, while germline mutations trigger a developmental disorder known as Costello syndrome (CS). Among numerous pathologies, adult CS patients develop osteoporosis. Previous studies revealed that HRAS is implicated in bone homeostasis by controlling osteoblast differentiation, adaptation to mechanical strain and repression of RANKL expression in mature osteoblasts, and by regulating osteoclast differentiation. However, the impact of HRAS on osteoblast differentiation is still debatable. In this study, we created stable doxycycline inducible cell lines overexpressing HRAS G12 mutants in MC3T3-E1 preosteoblast cell line and analyzed their impact on osteoblast differentiation. We demonstrated an inhibitory role of HRAS G12S and HRAS G12V mutants on osteogenic differentiation and identified an increased expression of Opn in an HRAS-dependent manner, which directly correlated with impaired osteogenesis, and was rescued by the farnesyl transferase inhibitor Tipifarnib. At the molecular level, Tipifarnib was not able to block HRAS activation, but impaired HRAS localization to the plasma membrane, and inhibited MAPK activation and Opn expression. Thus, HRAS abundance/activation and its potential crosstalk with OPN may be more critical for osteogenic differentiation than previously assumed.

Functionalized Docetaxel Probes for Refined Visualization of Mitotic Spindles by Expansion Microscopy

High-intensity interval training alleviates STZ-induced muscle atrophy by restoration of nuclear positioning defects in C57BL/6 male mice

Reduction-Interrupted Tandem Reaction for General Synthesis of Functional Amino Acids by a Heterogeneous Cobalt Catalyst

Ectomycorrhizal fungal community varies across broadleaf species and developmental stages

Peptide Backbone Editing via Post-Translational O to C Acyl Shift

Anti-tumor efficacy and safety of AEV01 in preclinical glioblastoma and hepatocellular carcinoma models

Helix-Guarded Molecular Clips for Cell-Free DNA Scavenging and Treatment of Systemic Lupus Erythematosus

Revealing the confluences of workplace bullying, suicidality, and their association with depression

Quad-band split ring resonator-based sensor for microwave sensing application

Epidemiological studies on the incidence of papaya ringspot disease under Indian sub-continent conditions

Fecal metabolomics to understand intestinal dysfunction in male dairy beef calves at arrival to the rearing farm

Pentraxin3 exacerbates acute pancreatitis injury by inhibiting oxidative phosphorylation pathway

Molecular mechanisms of CAND2 in regulating SCF ubiquitin ligases

SmartAPM framework for adaptive power management in wearable devices using deep reinforcement learning

Thermokarst lake drainage halves the temperature sensitivity of CH4 release on the Qinghai-Tibet Plateau

Abstract Thermokarst lakes as hot spots of methane (CH4) release are crucial for predicting permafrost carbon feedback to global warming. These lakes are suffering from serious drainage events, however, the impacts of lake drainage on CH4 release remain unclear. Here, synthesizing field drilling, incubation experiments, and carbon composition and microbial communities, we reveal the temperature sensitivities (Q10) and drivers of CH4 release from drainage-affected lakes on the Qinghai-Tibet Plateau. We find that cumulative CH4 release decreases with depth, where 0–30 cm-depth sediment accounts for 97% of the whole release. The Q10 of surface sediment is 2 to 4 times higher than deep layers, but roughly 56% lower than the non-drainage lakes. The response of CH4 release to warming is mainly driven by microbial communities (49.3%) and substrate availability (30.3%). Our study implies that drainage mitigates CH4 release from thermokarst lakes and sheds light on crucial processes for understanding permafrost carbon projections.

Power enhancement of PV arrays in different configurations under different partial shaded condition

A reconfigurable non-linear active metasurface for coherent wave down-conversion

Evaluation the toxic effects of Cobalt-Zinc Ferrite nanoparticles in experimental mice

Abstract Cobalt Zinc ferrite nanoparticles (NPs) were synthesized utilizing the auto-combustion flash method, with the general formula Co1 − xZnxFe2O4 (x = 0,0.35). This study aimed to evaluate the hepato-renal and systemic toxicity of Cobalt Zinc Ferrite nanoparticles (CZF NPs). A total of eighty female mice were utilized to ascertain the median lethal dose (LD50) of CF NPs (100 mg/kg) and CZF NPs (100 mg/kg). Thirty female CD1 mice were placed into three groups, each containing ten animals. In Group 1 (Gp1), mice were administered a 200 µl injection of sterile saline intraperitoneally (i.p.). During a 6-day period, Gp2 and Gp3 received injections of CF NPs and CFZ NPs. On day 14 after injection, hematological, biochemical, and histopathological data were measured. CZF NPs were characterized using X-ray Diffraction Analysis (XRD), Transmission Electron Microscope (TEM) and Vibrating Sample Magnetometer (VSM). There was a significant alteration in the overall body weight of mice injected with CZF NPs. Injections of CF NPs did not significantly alter red blood cells (RBC) counts, hemoglobin concentration (Hb), hematocrit percentage (Hct%), total white blood cells (WBCs), and platelets. However, injections of CZF NPs resulted in an increase in WBC count and a decrease in platelet count. Furthermore, injection of CZF NPs altered the differential leukocyte percentages. The liver and kidney functions in mice injected with CF NPs did not show any notable changes. However, mice treated with CZF NPs had considerable increases in liver and kidney bio-markers. The administration of CF NPS did not modify the histological structure of hepatic and renal tissues; however, the hepatic and renal structures were disrupted in animals injected with CZF NPs. Overall, the findings indicated high toxicity of CZF NPs in the mice used for the experiment.