A correlation study between cervical cancer and sex hormones.

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.

Chronic noise exposure induces Alzheimer's disease-like neuropathology and cognitive impairment via ferroptosis in rat hippocampus.

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.

CDK5-USP30 signaling pathway regulates MAVS-mediated inflammation via suppressing mitophagy in MPTP/MPP PD model.

The 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.

Global burden and trends of three common road injuries from 1990 to 2019 and the implications for prevention and intervention.

Background: 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.

Global burden and trends of firearm violence in 204 countries/territories from 1990 to 2019.

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.

Global Trends in Death, Years of Life Lost, and Years Lived With Disability Caused by Breast Cancer Attributable to Secondhand Smoke From 1990 to 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.

Deacetylation of ZKSCAN3 by SIRT1 induces autophagy and protects SN4741 cells against MPP-induced oxidative stress.

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.

Poly (ADP-ribose) polymerase 1 inhibition prevents neurodegeneration and promotes α-synuclein degradation via transcription factor EB-dependent autophagy in mutant α-synucleinA53T model of Parkinson's disease.

Poly (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.

p38 MAPK-DRP1 signaling is involved in mitochondrial dysfunction and cell death in mutant A53T α-synuclein model of Parkinson's disease.

Abnormal 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.

Mitochondrial calcium dysfunction contributes to autophagic cell death induced by MPP via AMPK pathway.

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.

Role of c-Abl-GSK3β Signaling in MPP+-Induced Autophagy-Lysosomal Dysfunction.

Impairment 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.

Phosphorylation of Parkin at serine 131 by p38 MAPK promotes mitochondrial dysfunction and neuronal death in mutant A53T α-synuclein model of Parkinson's disease.

α-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.

Mitochondrial calcium uniporter-mediated inhibition of 1-methyl-4-phenylpyridinium ions neurotoxicity in PC12 cells.

Parkinson'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.