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[GINS1 Enhances Glycolysis, Proliferation and Metastasis in Lung Adenocarcinoma Cells by Activating the Notch/PI3K/AKT/mTORC1 Signaling Pathway].
Zhongguo Fei Ai Za Zhi
October 2024
Medical Laboratory Center, the Affiliated Cancer Hospital of Xinjiang Medical University, Urumqi 830011, China.
Article Synopsis
- * Researchers analyzed GINS1 expression in LUAD tissues compared to healthy controls using various techniques, including bioinformatics, immunohistochemistry, and qRT-PCR, and manipulated GINS1 levels in cancer cell lines to assess its effects on cell proliferation, migration, and invasion.
- * Initial results indicate variations in GINS1 expression between LUAD patients and healthy controls, and ongoing experiments aim to uncover the underlying molecular mechanisms, potentially identifying new therapeutic targets for LUAD treatment
[Mechanism of vitamin D deficiency involvement in the development of pulmonary arterial hypertension related to monocrotaline-induced connective tissue disease in rats].
Zhonghua Yi Xue Za Zhi
November 2024
Department of Rheumatology and Immunology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing210008, China.
To investigating the impact of vitamin D (VitD) deficiency on the jagged 1 protein (Jagged1)/Notch3 signaling pathway in the pulmonary arteries of rats with monocrotaline (MCT)-induced connective tissue disease (CTD)-related pulmonary arterial hypertension (PAH) and to explore the pathological and molecular mechanisms of VitD involvement in the development of CTD-PAH. Twenty-four 7-week-old male Wistar rats were divided into a normal diet group and a VitD-free diet group using random number table, with 12 rats in each group. After 5 weeks of feeding, the rats were further randomly divided into saline and MCT groups, forming group A (normal diet+saline), group B (normal diet+MCT), group C (VitD-free+saline), and group D (VitD-free+MCT), with 6 rats in each group, and the rats were continued to be fed for another 4 weeks.
View Article and Find Full Text PDF[ORY-1001 inhibits glioblastoma cell growth by downregulating the Notch/HES1 pathway suppressing lysine-specific demethylase 1 expression].
Nan Fang Yi Ke Da Xue Xue Bao
August 2024
Medical Sciences Research Center, Department of Neurology, University-Town Hospital of Chongqing Medical University, Chongqing 400000, China.
Objective: To explore the inhibitory effect ORY-1001, a lysine-specific histone demethylase 1 (LSD1) inhibitor, on growth of glioblastoma (GBM) and the underlying mechanism.
Methods: We analyzed LSD1 expressions in GBM and normal brain tissues based on data from TCGA and HPA databases. Female BALB/c mouse models bearing xenografts derived from U87 cells or cells with lentivirus-mediated LSD1 silencing or Notch overexpression were treated with saline or 400 µg/kg ORY-1001 by gavage every 7 days, and GBM formation and survival time of the mice were recorded.
Nailfold capillary measurements correlated to NOTCH3 R544C mutation in preclinical CADASIL patients.
J Neurol Sci
July 2024
Department of Post-Baccalaureate Medicine, College of Medicine, National Chung Hsing University, Taichung, Taiwan; School of Medicine, College of Medicine, National Yang Ming Chiao Tung University, Taipei, Taiwan; Division of Allergy, Immunology, and Rheumatology, Department of Internal Medicine, Taichung Veterans General Hospital, Taichung, Taiwan; Department of Medical Research, Taichung Veterans General Hospital, Taichung, Taiwan; Institute of Biomedical Science and Rong Hsing Research Center for Translational Medicine, National Chung Hsing University, Taichung, Taiwan; Precision Medicine Research Center, College of Medicine, National Chung Hsing University, Taichung, Taiwan. Electronic address:
Article Synopsis
- - The study investigates the relationship between nailfold capillaroscopy measurements and brain changes in patients with CADASIL, a hereditary disease caused by the NOTCH3 mutation.
- - Researchers analyzed data from 69 participants, comparing brain imaging and capillary measurements to identify correlations between structural brain changes and vascular health.
- - Findings showed that individuals with the NOTCH3 mutation had increased white matter hyperintensities, highlighting the potential of capillaroscopy as a useful screening tool for preclinical CADASIL.
[The hereditary vessel disease CADASIL].
Laeknabladid
July 2024
Department of Neurology, University Hospital of Iceland, Reykjavik, Iceland.
Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy (CADASIL) is a hereditary small vessel disease of the brain characterized by progressive white matter lesions, subcortical infarcts, and cognitive decline. This autosomal dominant disorder is caused by mutations in the NOTCH3 gene located on chromosome 19, resulting in the accumulation of granular osmiophilic material within the walls of small arteries and arterioles. Clinically, CADASIL typically manifests in mid-adulthood with recurrent ischemic events, migraine with aura, mood disturbances, and cognitive impairment.
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