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Based on the consecutive synoptic magnetic maps, we devise a new method to calculate the solar differential rotation coefficients. This method is very easy to implement and has a high accuracy. Firstly, based on the two-term or three-term differential rotation formula, we simulate a synoptic map CR |$_{n}$| evolves one Carrington Rotation (CR) time only under the effect of the differential rotation, and thereby a stretched synoptic map CR |$_{n*}$| is obtained. Then, through searching the maximum covariance between the maps CR |$_{n*}$| and CR |$_{n+1}$| by the grid search method, the rotation coefficients can be determined. Based on the synoptic maps of CRs 1625 to 2278 (during the years 1975–2023), the two-term coefficients A and B for latitude region between |$\pm 40^{\circ }$| are calculated. The rotation coefficient B shows an obvious 11-yr period. From the time series of B , we find that the Sun usually rotates more differentially in the rising phases of the sunspot cycles than in the falling phases. Moreover, the strong magnetic field corresponds to an increasing of B (note that B has a negative sign) or decreasing of differential. The evolutionary trend of B also indicates that there are several years until the maximum value of B will be reached in solar cycle 25, and the coefficient B will be still in the rising phase in the few coming years. The two-term rotation coefficients for the two hemispheres are also calculated separately, and in the studied time-scale, the largest N–S asymmetry of the rotation rate appeared in October 2007. [ABSTRACT FROM AUTHOR]

Temporary works are necessary to ensure the construction and operation of railways. These works are characterized by their large scale, numerous locations, and long construction periods. However, suitable land resources for such purposes are extremely limited in mountainous railway areas. Additionally, the selection of sites for these works often overlaps with areas affected by debris flow, leading to high potential risks from geological disasters. Taking the Jinjia Gully watershed as an example, this paper explores a method for assessing debris flow risks in single gullies, including the zoning of debris flow danger areas, vulnerability analysis, and risk assessment. Based on the data obtained from field surveys, they utilize ArcGIS and the Analytic Hierarchy Process (AHP), combined with numerical simulations and indoor experiments, to establish a quantitative risk assessment method for large-scale temporary works. The results indicate that (1) the area of debris flow hazard zones decreases with increasing rainfall frequency, and (2) the vulnerability assessment model can not only reflect the types of individual work, structural materials, and construction quality but also the shielding effect of building clusters. In the direction of flow, the shielding effect range of buildings on debris flow accumulation fans is approximately 37.5 times the size of the buildings. In the direction of extension, when the angle between current and rear buildings exceeds 0.674 radians, the shielding effect can be neglected. (3) At a rainfall frequency of p = 5%, more than 80% of large-scale temporary works are in extremely low or low-risk zones, indicating that the study area is at a low risk level. [ABSTRACT FROM AUTHOR]

Background: MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine), original found in synthetic heroin, causes Parkinson's disease (PD) in human through its metabolite MPP+ by inhibiting complex I of mitochondrial respiratory chain in dopaminergic neurons. This study explored whether yeast internal NADH-quinone oxidoreductase (NDI1) has therapeutic effects in MPTP- induced PD models by functionally compensating for the impaired complex I. MPP+-treated SH-SY5Y cells and MPTP-treated mice were used as the PD cell culture and mouse models respectively. The recombinant NDI1 lentivirus was transduced into SH-SY5Y cells, or the recombinant NDI1 adeno-associated virus (rAAV5-NDI1) was injected into substantia nigra pars compacta (SNpc) of mice. Results: The study in vitro showed NDI1 prevented MPP+-induced change in cell morphology and decreased cell viability, mitochondrial coupling efficiency, complex I-dependent oxygen consumption, and mitochondria-derived ATP. The study in vivo revealed that rAAV-NDI1 injection significantly improved the motor ability and exploration behavior of MPTP-induced PD mice. Accordingly, NDI1 notably improved dopaminergic neuron survival, reduced the inflammatory response, and significantly increased the dopamine content in striatum and complex I activity in substantia nigra. Conclusions: NDI1 compensates for the defective complex I in MPP+/MPTP-induced models, and vastly alleviates MPTP-induced toxic effect on dopaminergic neurons. Our study may provide a basis for gene therapy of sporadic PD with defective complex I caused by MPTP-like substance. [ABSTRACT FROM AUTHOR]

Background: MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine), original found in synthetic heroin, causes Parkinson's disease (PD) in human through its metabolite MPP + by inhibiting complex I of mitochondrial respiratory chain in dopaminergic neurons. This study explored whether yeast internal NADH-quinone oxidoreductase (NDI1) has therapeutic effects in MPTP- induced PD models by functionally compensating for the impaired complex I. MPP + -treated SH-SY5Y cells and MPTP-treated mice were used as the PD cell culture and mouse models respectively. The recombinant NDI1 lentivirus was transduced into SH-SY5Y cells, or the recombinant NDI1 adeno-associated virus (rAAV5-NDI1) was injected into substantia nigra pars compacta (SNpc) of mice., Results: The study in vitro showed NDI1 prevented MPP + -induced change in cell morphology and decreased cell viability, mitochondrial coupling efficiency, complex I-dependent oxygen consumption, and mitochondria-derived ATP. The study in vivo revealed that rAAV-NDI1 injection significantly improved the motor ability and exploration behavior of MPTP-induced PD mice. Accordingly, NDI1 notably improved dopaminergic neuron survival, reduced the inflammatory response, and significantly increased the dopamine content in striatum and complex I activity in substantia nigra., Conclusions: NDI1 compensates for the defective complex I in MPP + /MPTP-induced models, and vastly alleviates MPTP-induced toxic effect on dopaminergic neurons. Our study may provide a basis for gene therapy of sporadic PD with defective complex I caused by MPTP-like substance., (© 2024. The Author(s).)

Mucin 1 (MUC1) has been regarded as an ideal target for cancer treatment, since it is overexpressed in a variety of different cancers including the majority of breast cancer. However, there are still no approved monoclonal antibody drugs targeting MUC1. In this study, we generated a humanized MUC1 (HzMUC1) antibody from our previously developed MUC1 mouse monoclonal antibody that only recognizes MUC1 on the surface of tumor cells. Furthermore, an antibody-drug conjugate (ADC) was generated by conjugating HzMUC1 with monomethyl auristatin (MMAE), and the efficacy of HzMUC1-MMAE on the MUC1-positive HER2+ breast cancer in vitro and in 'Xenograft' model was tested. Results from western blot analysis and immunoprecipitation revealed that the HzMUC1 antibody did not recognize cell-free MUC1-N in sera from breast cancer patients. Confocal microscopy analysis showed that HzMUC1 antibody bound to MUC1 on the surface of breast cancer cells. Results from mapping experiments suggested that HzMUC1 may recognize an epitope present in the interaction region between MUC1-N and MUC1-C. Results from colony formation assay and flow cytometry demonstrated that HzMUC1-MMAE significantly inhibited cell growth by inducing G2/M cell cycle arrest and apoptosis in trastuzumab-resistant HER2-positive breast cancer cells. Meanwhile, HzMUC1-MMAE significantly reduced the growth of HCC1954 xenograft tumors by inhibiting cell proliferation and enhancing cell death. In conclusion, our results indicate that HzMUC1-ADC is a novel therapeutic drug that can overcome trastuzumab resistance of breast cancer. HzMUC1-ADC should also be an effective therapeutic drug for the treatment of different MUC1-positive cancers in clinic., (© The Author(s) 2021. Published by Oxford University Press on behalf of the Center for Excellence in Molecular Cell Science, Chinese Academy of Sciences. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)