RNAscope

Background: Regulatory T cells (Tregs) suppress inflammation in atherosclerosis, and therefore have the therapeutic potential to decrease the risk of myocardial infarction and stroke. However, there is currently no method to generate antigen specific Tregs that target atherosclerosis. We therefore engineered Tregs that express a chimeric antigen receptor (CAR) targeting malonaldehyde-modified low-density lipoprotein cholesterol (MDA-LDL), the most common form of oxidized LDL and a key molecular component of atherosclerosis.

Background The critical role for chronic inflammation in the development of thoracic aortic aneurysms and dissections (TAADs) has been recognized in both experimental and clinical settings. However, challenges remain on translating this knowledge to clinical applications. In this study, we tested the hypothesis that TLR-7 signaling triggered by self-RNAs substantiates chronic inflammation, promoting TAAD formation. Methods A mouse TAAD model induced by SMC-specific deletion of Tgfbr1 (Tgfbr1iko) was used.

Abstract Unavailable

Human papillomavirus (HPV)-associated oropharyngeal squamous cell carcinoma is increasing in incidence and is often first diagnosed on a cytology fine needle aspiration (FNA) specimen of metastatic nodal disease of the neck. In the setting of oropharyngeal squamous cell carcinoma, HPV status defines the disease with HPV-associated tumors having better overall prognosis than those that are HPV negative. Furthermore, metastatic squamous cell carcinoma of the neck of unknown origin requires testing for HPV as a positive result suggests an oropharyngeal primary.

Mike May, is a freelance writer and editor with more than 30 years of experience. He earned an MS in biological engineering from the University of Connecticut and a PhD in neurobiology and behavior from Cornell University. He worked as an associate editor at American Scientist, and he is the author of more than 1,000 articles for clients that include GEN, Nature, Science, Scientific American and many others. In addition, he served as the editorial director of many publications, including several Nature Outlooks and Scientific American Worldview.

Rationale DNA damage accumulation is a hallmark of vascular smooth muscle cell (VSMC) ageing. Importantly, VSMC DNA damage accumulation and ageing has been implicated in the progression of cardiovascular disease (CVD), including atherosclerosis and vascular calcification. Chemotherapy drugs used in the treatment of many cancers are known to induce DNA damage in cardiovascular cells and accelerate CVD. Histone deacetylase (HDAC) inhibitors are drugs being investigated for novel treatments of many cancers.

BACKGROUND The long saphenous vein (LSV) is commonly utilised in CABG surgery to facilitate revascularisation. However, over time these grafts develop intimal hyperplasia (IH) and accelerated atherosclerosis, leading to stenosis and occlusion. A common feature of IH is vascular calcification (VC) within the affected vessel. Recently, the matricellular protein osteopontin (OPN) has been implicated in this process at endothelial injury sites in porcine models, but this has not been expanded to humans.

RESULTS We established that eNOS is a high shear stress marker both in healthy and diseased aorta and used this to compare the transcriptional profiles of EC exposed to high shear stress in health and disease. We performed scRNAseq analysis of aorta from Apoe-/- normal diet (ND; intermediate cholesterol) mice and Apoe-/- high fat diet (HFD; high cholesterol) mice. eNOShigh cells were selected for transcriptome analysis (Figure 1A).

The mammalian placenta, which is responsible for bonding between the mother and the fetus, is one of the first organs to develop. Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) infection has caused a great threat to public health and affected almost all the organs including the placenta. Owing to limited available data on vertical transmission and pathological changes in the placenta of SARS-CoV-2 positive patients, we aim to review and summarize histopathological and ultrastructural changes in the placental tissue following SARS-CoV-2 infection.