Objective: The aims of this study were to investigate the association between positive TCT and sex hormone levels and to evaluate the feasibility of change in sex hormone level as a potential predictor of cervical cancer.
Methods: We recruited 910 female participants from the health examination center of a hospital in Guizhou between 2019 and 2023. All participants had undergone both hematologic examinations and cervical cancer screening.
Background: Chronic noise exposure poses a remarkable public health concern, drawing attention to its impacts on the brain. Ferroptosis is involved in several brain-related diseases. However, the role of ferroptosis in the effects of chronic noise on the brain remains elusive.
View Article and Find Full Text PDFThe discovery of MPTP, an industrial chemical and contaminant of illicit narcotics, which causes parkinsonism in humans, non-human primates and rodents, has led to environmental pollutants exposure being convicted as key candidate in Parkinson's disease (PD) pathogenesis. Though MPTP-induced mitochondrial dysfunction and neuroinflammation are mainly responsible for the causative issue of MPTP neurotoxicity, the underlying mechanism involved remains unclear. Here, we reveal a novel signaling mechanism of CDK5-USP30-MAVS regulating MPTP/MPP induced PD.
View Article and Find Full Text PDFBackground: Analysis on the burden of specific types of road injuries (RIs) in the previous Global burden of disease (GBD) studies is lacking. The present work aimed to analyze the burden of three common RIs using the updated data of the GBD 2019, which would inform policy-making.
Methods: Data on cyclist road injuries (CRIs), motorcyclist road injuries (MRIs), and motor vehicle road injuries (MVRIs) were extracted from the GBD 2019.
Front Public Health
September 2022
Background: Gaps remained in the updated information of the firearm violence (FV) burden from a global landscape. Understanding the global burden of FV could contribute to decision-making.
Methods: Data on the FV burden, including physical violence by firearm (PVF), self-harm by firearm (SHF), and unintentional firearm injuries (UFI), were extracted from the Global Burden of Disease 2019.
Background: Secondhand smoke is an important risk factor to breast cancer patients' survival. This article aimed to describe the epidemiological changes of health loss caused by female breast cancer attributable to secondhand smoke from 1990 to 2019.
Methods: Data on breast cancer was derived from the Global Burden of Disease study 2019.
Mitochondrial dysfunction, oxidative stress and misfolded protein aggregation are related to autophagy-lysosomal dysregulation and contribute to the pathogenesis of Parkinson' s disease (PD). ZKSCAN3, a transcriptional repressor, plays a crucial role in autophagy and lysosomal biogenesis. However, the role and modification of ZKSCAN3 in the defection of ALP, along with the molecular mechanism involved in pathogenesis of PD, still remain unclear.
View Article and Find Full Text PDFPoly (ADP-ribose) polymerase 1 (PARP1) is a master regulator of diverse biological processes such as DNA repair, oxidative stress, and apoptosis. PARP1 can be activated by aggregated α-synuclein, and this process in turn exacerbates toxicity of α-synuclein. This circle is closely linked to the evolution of Parkinson's disease (PD) that characterized by progressive neurodegeneration and motor deficits.
View Article and Find Full Text PDFAbnormal accumulation of α-synuclein and mitochondria dynamics dysfunction are considered to be implicated in the pathogenesis of Parkinson's disease. However, the underlying mechanisms how α-synuclein abnormal accumulation causes mitochondrial dynamics dysfunction remains unclear. Here, we demonstrate that dynamin-related protein 1(DRP1) is a substrate for p38 MAPK, mutant α-synuclein overexpression in SN4741 cell caused p38 MAPK activation, p38 MAPK-mediated phosphorylation DRP1 at serine 616 to activate DRP1 and is associated with increased mitochondrial fission, which resulted in mitochondrial dysfunction and neuronal loss.
View Article and Find Full Text PDFBiochem Biophys Res Commun
February 2019
Parkinson's disease (PD) is a progressive neurodegenerative disease characterized by the loss of dopaminergic neurons in the substantia nigra. Prevailing evidence suggests that abnormal autophagy and mitochondrial dysfunction participate in the process of PD. However, many damages of neuronal functions are regulated by intracellular Ca signaling and the contribution of mitochondrial Ca to the process of neurodegeneration is still unclear.
View Article and Find Full Text PDFImpairment in autophagy-lysosomal pathway (ALP) results in accumulation of misfolded proteins and dysfunctional organelles, which is the hallmark of neurodegenerative diseases including Parkinson's disease (PD). Recent studies revealed activated nonreceptor tyrosine kinase Abelson (c-Abl) in PD models and brain specimen of PD patients. Inhibition of c-Abl through pharmacological inhibitors has been shown to enhance ALP function and provide neuroprotective effects in cells and animal models of PD.
View Article and Find Full Text PDFα-synuclein abnormal accumulation and mitochondria dysfunction are involved in the pathogenesis of Parkinson's disease. Selective autophagy of mitochondria (mitophagy) is a crucial component of the network controlling the mitochondrial homeostasis. However, the underlying mechanism that mutant α-synuclein induces mitochondrial abnormality through mitophagy impairment is not fully understood.
View Article and Find Full Text PDFParkinson's disease (PD) is one of the most debilitating neurodegenerative disorders. The etiology of sporadic PD remains unknown. One prominent hypothesis is that impaired mitochondrial function may underlie slow and progressive neurodegeneration.
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