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Cholelithiasis is a common digestive disease that drives a myriad of adverse complications. The correlation between sarcopenia and various digestive disorders has been extensively researched, whereas its association with cholelithiasis remains unreported. We aimed to investigate the association through prospective and Mendelian randomization (MR) analyses and establish a quantitative score reflecting the impact of sarcopenia‐related markers on cholelithiasis. The prospective study involved 448 627 participants from the UK Biobank. Cox proportional hazard models were employed to investigate the correlation between sarcopenia‐related markers and cholelithiasis. To quantitatively assess cholelithiasis risk, the SARCHO score was derived from a multivariable Cox model. Bidirectional two‐sample MR analysis was conducted to validate the causal association. A total of 16 738 individuals developed cholelithiasis during a median follow‐up of 12 years. Hazard ratios (HRs) of cholelithiasis decreased stepwise over skeletal muscle index tertiles (highest tertile: reference; middle tertile: 1.23, p <.001; lowest tertile: 1.33, p <.001). The tertiles of grip strength showed a similar pattern. Individuals with slow walking pace had a higher risk of cholelithiasis compared to those with normal walking pace (HR 1.23; p <.001). Our SARCHO score better quantifies the risk of cholelithiasis. MR analysis showed a causal relationship between muscle mass and cholelithiasis (OR 0.81; p <.001). No causal effect of cholelithiasis on lean mass was observed. Prospective and MR analyses have consistently demonstrated an increased risk of cholelithiasis in individuals with decreased muscle mass. Additionally, SARCHO score further quantified the cholelithiasis occurrence risk. These findings provide compelling evidence for muscle strengthening in preventing cholelithiasis. [ABSTRACT FROM AUTHOR]

Purpose: This study aims to explore the role of circ_0032704 in sorafenib‐resistant hepatocellular carcinoma (HCC). Methods: The expression of circ_0032704, miR‐514a‐3p, and programmed death‐ligand 1 (PD‐L1) mRNA was detected by quantitative real‐time PCR (qPCR). The expression of multidrug resistant‐related proteins, migration/invasion‐related proteins, exosome‐related proteins, and PD‐L1 protein was detected by western blot. Cell viability was detected by CCK‐8 assay. Cell proliferation, migration, and invasion were assessed by EdU assay, wound healing assay, and transwell assay. The binding between miR‐514a‐3p and circ_0032704 or PD‐L1 was verified by RIP assay, pull‐down assay, and dual‐luciferase reporter assay. Cell‐ or serum‐derived exosomes were isolated and identified by TEM and NTA. Xenograft models were established to determine the effect of circ_0032704 on drug resistance in vivo. Results: Circ_0032704 was overexpressed in sorafenib‐resistant HCC tissues and cells. Circ_0032704 knockdown reduced sorafenib resistance in HCC cells and inhibited cell proliferation, migration, and invasion of sorafenib‐resistant HCC cells, while these effects were reversed by PD‐L1 overexpression. We found that circ_0032704 positively regulated PD‐L1 expression via targeting miR‐514a‐3p. Exosomes with circ_0032704 inhibition reduced sorafenib resistance in HCC cells and inhibited cell proliferation, migration, and invasion of sorafenib‐resistant HCC cells. Exosomes with circ_0032704 inhibition also inhibited tumor growth in vivo. The expression of circ_0032704 in exosomes was stable and possessed diagnostic value. Conclusion: Circ_0032704 enhanced sorafenib resistance in HCC and promoted the malignant development of sorafenib‐resistant HCC. Circ_0032704 could be transported by exosomes, and exosomal circ_0032704 had diagnostic value. [ABSTRACT FROM AUTHOR]

Disruption of disulfide homeostasis during biological processes can have fatal consequences. Excess disulfides induce cell death in a novel manner, termed as "disulfidptosis." However, the specific mechanism of disulfidptosis has not yet been elucidated. To determine the cancer types sensitive to disulfidptosis and outline the corresponding treatment strategies, we firstly investigated the crucial functions of disulfidptosis regulators pan‐cancer at multi‐omics levels. We found that different tumor types expressed dysregulated levels of disulfidptosis regulators, most of which had an impact on tumor prognosis. Moreover, we calculated the disulfidptosis activity score in tumors and validated it using multiple independent datasets. Additionally, we found that disulfidptosis activity was correlated with classic biological processes and pathways in various cancers. Disulfidptosis activity was also associated with tumor immune characteristics and could predict immunotherapy outcomes. Notably, the disulfidptosis regulator, glycogen synthase 1 (GYS1), was identified as a promising target for triple‐negative breast cancer and validated via in vitro and in vivo experiments. In conclusion, our study elucidated the complex molecular phenotypes and clinicopathological correlations of disulfidptosis regulators in tumors, laying a solid foundation for the development of disulfidptosis‐targeting strategies for cancer treatment. [ABSTRACT FROM AUTHOR]

Objective: Metabolic dysfunction‐associated steatotic liver disease (MASLD) affects many populations, and screening out the high‐risk populations at an early stage is a challenge. As a sarcopenia index, the relationship between creatinine to cystatin C ratio (CCR) and MASLD remains unclear. This cross‐sectional, prospective study aimed to explore the relationship between CCR and MASLD. Design Firstly, explored the correlation between CCR and MASLD in cross‐sectional analyses. Then excluded the population with baseeline diagnosis of MASLD and analyzed the association with baseline CCR levels and the onset of MASLD in the population with available follow‐up data. Univariate and multivariate logistic regression analyses were used to calculate odds ratios (ORs) to evaluate the association between CCR levels and MASLD. Patients and Measurements: This study included 368,634 participants from the UK Biobank for cross‐sectional and prospective analyses. The demographic characteristics and laboratory measurements of all participants were obtained from the UK Biobank. MASLD was diagnosed according to the multi‐society consensus nomenclature. Hepatic steatosis was defined as FLI ≥60. Results: We grouped the study participants according to CCR tertiles. In cross‐sectional analyses, participants in CCR tertile 1 had the highest MASLD risk (OR: 1.070, 95% CI: 1.053−1.088, p <.001). And the similar association was observed in the prospective analyses (CCR tertile 1 OR: 1.340, 95% CI: 1.077−1.660, p =.009; CCR tertile 2 OR: 1.217, 95% CI: 1.021−1.450, p =.029, respectively). After stratification by gender, the significant association between CCR and the onset of MASLD was only observed in males (CCR tertile 1 OR: 1.639, 95% CI: 1.160−2.317, p =.005; CCR tertile 2 OR: 1.322, 95% CI: 1.073−1.628, p =.005, respectively). Conclusion: Our results indicated that lower CCR was significantly associated with higher risk of MASLD, based on which predictive models can be developed to screen populations at high risk of developing MASLD. [ABSTRACT FROM AUTHOR]

Background: Cancer metastasis is still a life threat to patients with colorectal cancer (CRC). Brain and muscle ARNT‐like protein 1 (BMAL1) is an important biological proteins that can regulate the behavior of cancer cells and their response to chemotherapy. However, the role of BMAL1 in the tumorigenic phenotype of CRC remains unclear. Here, we aim to investigate the functional role and mechanisms of BMAL1 in CRC. Methods: The mRNA expression of BMAL1 was studied using the Cancer Genome Atlas (TCGA) databases. The protein level in clinical tissues was confirmed by immunohistochemistry (IHC). The effects of BMAL1 on the epithelial‐to‐mesenchymal transition (EMT) and proliferation of CRC cell lines (including BMAL1 overexpressed or silencing cells) were studied by Transwell, wound healing, CCK‐8 and colony formation experiments. A series of experiments were conducted to demonstrate the mechanisms of BMAL1 regulating EMT and cancer proliferation in vitro and in vivo. Results: We found that BMAL1 expression was closely related to the poor prognosis of CRC. BMAL1 overexpression promoted cell proliferation and migration. Mechanistically, we found that BMAL1 may activate the epithelial‐to‐mesenchymal transition (EMT) pathway and induce the β‐catenin release further promotes the expression of oncogene c‐Myc and the migration of colorectal cells by activating MAPK pathway. However, BMAL1 silencing achieved the opposite effect. In addition, blocking MAPK‐signaling pathway with specific inhibitors of ERK1/2 and JNK can also downregulate the expressions of c‐Myc in vitro. Taken together, these results suggested that the BMAL1/ c‐Myc‐signaling pathway may regulate the metastasis of CRC through the JNK/ERK1/2 MAPK‐dependent pathway. Conclusions: Our study showed that BMAL1 promotes CRC metastasis through MAPK‐c‐Myc pathway. These results deepen our understanding of the relationship between BMAL1 and tumorigenic phenotypes, which may become a promising therapeutic target for BMAL1 overexpressing CRC. [ABSTRACT FROM AUTHOR]

The surface ligand environment plays a dominant role in determining the physicochemical, optical, and electronic properties of colloidal quantum dots (CQDs). Specifically, the ligand‐related electronic traps are the main reason for the carrier nonradiative recombination and the energetic losses in colloidal quantum dot solar cells (CQDSCs), which are usually solved with numerous advanced ligand exchange reactions. However, the synthesis process, as the essential initial step to control the surface ligand environment of CQDs, has lagged behind these post‐synthesis ligand exchange reactions. The current PbS CQDs synthesis tactic generally uses lead oxide (PbO) as lead precursor, and thus suffers from the water byproducts issue increasing the surface‐hydroxyl ligands and aggravating trap‐induced recombination in the PbS CQDSCs. Herein, an organic‐Pb precursor, lead (II) acetylacetonate (Pb(acac)2), is used instead of a PbO precursor to avoid the adverse impact of water byproducts. Consequently, the Pb(acac)2 precursor successfully optimizes the surface ligands of PbS CQDs by reducing the hydroxyl ligands and increasing the iodine ligands with trap‐passivation ability. Finally, the Pb(acac)2‐based CQDSCs possess remarkably reduced trap states and suppressed nonradiative recombination, generating a certified record Voc of 0.652 V and a champion power conversion efficiency (PCE) of 11.48% with long‐term stability in planar heterojunction‐structure CQDSCs. [ABSTRACT FROM AUTHOR]

Metasurfaces have an exceptional capacity to manipulate the phase, amplitude, polarization, or spectrum of light. However, unit cells, or meta‐atoms, of metasurfaces are conventionally designed using regular shapes, limiting performance improvement. The utilization of metasurfaces with freeform shaped meta‐atoms for on‐chip ultraspectral imaging is proposed, where the freeform shaped patterns are generated with controllable feature sizes and boundary curvatures for feasible fabrication. These patterns broaden design diversity and enrich metasurface‐unit spectral response with complicated Bloch modes, thus improving spectral imaging performance with enhanced spectrum recovery precision for broadband spectra and smaller center‐wavelength deviation for narrowband spectra. A snapshot on‐chip ultraspectral imaging, with 356 × 436 spectral pixels is experimentally demonstrated. Spectral resolution is state‐of‐the‐art, at 0.5 nm, and mean fidelity of spectral reconstruction for a standard color board reaches 98.78%. These results support future applications in the field of precise intelligent perception. Moreover, the generating method for freeform shaped patterns also benefits for the forward and inverse designs for high‐performance metasurfaces. [ABSTRACT FROM AUTHOR]

Both energy and information are different manifestations of light. Using light to offer the coexistence of sensing, communication, and energy harvesting functionalities, monolithically integrated III‐nitride diode system toward the Internet of Things is dealt with. The III‐nitride receiver is capable to convert optical signals into electronic ones and forward them to the transmitter. The energy harvester generates electricity from light to turn on the transmitter, which, in turn, can transmit information optically to other proximally located devices for analysis or relay the data over longer distances. This monolithic III‐nitride optoelectronic system can simultaneously achieve wireless energy harvesting and communication through light. The truly self‐powered, integrated III‐nitride system is a paradigm change where the previously competing sensing, communication, and energy harvesting operations can be jointly implemented on a single chip. [ABSTRACT FROM AUTHOR]

Multifunctioning InGaN/GaN multi‐quantum well (MQW) diodes can transmit and detect light separately. In particular, MQW diodes have spectral overlap between electroluminescence (EL) and responsivity, conferring the unique ability to detect light emitted by another device sharing an identical MQW structure. Herein, a III‐nitride transmitter and a receiver on a single chip are monolithically integrated, which can establish an asymmetric optical link and significantly reduce material and processing costs. By attaching the chip to the skin with the transmitter emitting toward it, the device can monitor cardiac activity. Heart pulses change blood volume of the vascular bed, which modulates the reflected light. The receiver absorbs that light and converts it into electrical signals. Finally, by integrating a programmed circuit, the biological signals are analyzed. Herein, a feasible approach to monitor heart rate and cardiac‐related pulse information simultaneously is provided. [ABSTRACT FROM AUTHOR]

The integration of III‐nitride electronics and photonics is of great interest toward future computing systems with low power consumption. Multifunctioning multiple quantum well (MQW) diodes can address the challenging issue for on‐chip integration of a light source, which is a key component to drive the photonic circuits. Herein, a transmitter, waveguide, modulator, and receiver are monolithically integrated on a III‐nitride‐on‐silicon platform to perform light emission, transmission, modulation, and detection simultaneously. Both the receiver and modulator exhibit sufficient sensitivity to optical signals from the transmitter, which has an identical InGaN/AlGaN multiple quantum well (MQW) structure because the III‐nitride diode provides spectral overlap between the emission and absorption spectra. On‐chip data communication among these optical components is achieved using light, and the effective wavelength range is from 365 to 385 nm, in which multifunctional devices can be operated. [ABSTRACT FROM AUTHOR]