The cDNA array technology is a powerful tool to analyze a high number of genes in parallel. We investigated whether large-scale gene expression analysis allows clustering and identification of cellular phenotypes of chondrocytes in different in vivo and in vitro conditions. In 100% of cases, clustering analysis distinguished between in vivo and in vitro samples, suggesting fundamental differences in chondrocytes in situ and in vitro regardless of the culture conditions or disease status. It also allowed us to differentiate between healthy and osteoarthritic cartilage. The clustering also revealed the relative importance of the investigated culturing conditions (stimulation agent, stimulation time, bead/monolayer). We augmented the cluster analysis with a statistical search for genes showing differential expression. The identified genes provided hints to the molecular basis of the differences between the sample classes. Our approach shows the power of modern bioinformatic algorithms for understanding and classifying chondrocytic phenotypes in vivo and in vitro. Although it does not generate new experimental data per se, it provides valuable information regarding the biology of chondrocytes and may provide tools for diagnosing and staging the osteoarthritic disease process.
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http://dx.doi.org/10.1097/BLO.0b013e318047976a | DOI Listing |
Breast Cancer Res
January 2025
Division of Medical Oncology, The Ohio State University Comprehensive Cancer Center, Columbus, OH, USA.
Background: Epidemiological studies associate an increase in breast cancer risk, particularly triple-negative breast cancer (TNBC), with lack of breastfeeding. This is more prevalent in African American women, with significantly lower rate of breastfeeding compared to Caucasian women. Prolonged breastfeeding leads to gradual involution (GI), whereas short-term or lack of breastfeeding leads to abrupt involution (AI) of the breast.
View Article and Find Full Text PDFJ Exp Clin Cancer Res
January 2025
School of Medicine, Chinese PLA General Hospital, Nankai University, Beijing, China.
Background: Glioblastoma multiforme (GBM) exhibits a cellular hierarchy with a subpopulation of stem-like cells known as glioblastoma stem cells (GSCs) that drive tumor growth and contribute to treatment resistance. NAD(H) emerges as a crucial factor influencing GSC maintenance through its involvement in diverse biological processes, including mitochondrial fitness and DNA damage repair. However, how GSCs leverage metabolic adaptation to obtain survival advantage remains elusive.
View Article and Find Full Text PDFEur J Med Res
January 2025
Department of General Surgery, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, 310000, China.
Objectives: SOX10 is crucially implicated in various cancer, yet the regulatory role in pancreatic cancer (PC) remains enigmatic. Underlying molecular mechanisms of SOX10 in PC were explored in our study.
Methods: Relationships between SOX10 and immune landscape were estimated using bioinformatic approaches.
Chin Med
January 2025
Department of Clinical Chinese Pharmacy, School of Chinese Materia Medica, Beijing University of Chinese Medicine, Beijing, 102488, China.
Background: With extended gefitinib treatment, the therapeutic effect in some non-small cell lung cancer (NSCLC) patients declined with the development of drug resistance. Aidi injection (ADI) is utilized in various cancers as a traditional Chinese medicine prescription. This study explores the molecular mechanism by which ADI, when combined with gefitinib, attenuates gefitinib resistance in PC9GR NSCLC cells.
View Article and Find Full Text PDFMol Med
January 2025
Department of Gastroenterology and Medical Research Center, Liaoning Key Laboratory of Research and Application of Animal Models for Environmental and Metabolic Diseases, ShengJing Hospital of China Medical University, SanHao Street No. 36, HePing District, Shenyang, 110000, Liaoning, China.
The lack of knowledge about the mechanism of hyperoxia-induced intestinal injury has attracted considerable attention, due to the potential for this condition to cause neonatal complications. This study aimed to explore the relationship between hyperoxia-induced oxidative damage and ferroptosis in intestinal tissue and investigate the mechanism by which hyperoxia regulates inflammation through ferroptosis. The study systematically evaluated the effects of hyperoxia on oxidative stress, mitochondrial damage, ferroptosis, and inflammation of intestinal epithelial cells both in vitro and in vivo.
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