Ubiquitination-Related Gene Signature, Nomogram and Immune Features for Prognostic Prediction in Patients with Head and Neck Squamous Cell Carcinoma.

The objective of this research was to create a prognostic model focused on genes related to ubiquitination (UbRGs) for evaluating their clinical significance in head and neck squamous cell carcinoma (HNSCC) patients. The transcriptome expression data of UbRGs were obtained from The Cancer Genome Atlas (TCGA) database, and weighted gene co-expression network analysis (WGCNA) was used to identify specific UbRGs within survival-related hub modules. A multi-gene signature was formulated using LASSO Cox regression analysis.

Neoadjuvant Immunotherapy for Head and Neck Squamous Cell Carcinoma: Expecting Its Application in Temporal Bone Squamous Cell Carcinoma.

Temporal bone malignant tumors are characterized by atypical clinical symptoms, and easy recurrence and metastasis. They account for 0.2% of head and neck tumors, and the most common pathological type is squamous cell carcinoma.

TCB-2, a 5-hydroxytryptamine 2A receptor agonist, disrupts prepulse inhibition in the ventral pallidum and nucleus accumbens.

The 5-hydroxytryptamine 2A (5-HT) receptor plays an important role in schizophrenia. The 5-HT receptor is also involved in the regulation of prepulse inhibition (PPI) in rodents. The aim of this study was to determine whether selective 5-HT receptor agonizts or antagonists may alter PPI in rats and to identify the critical brain regions in which the activity of 5-HT receptors regulates PPI.

Activation of dopamine D receptors in the shell of nucleus accumbens triggers conditioned avoidance responses in rats.

Conditioned avoidance responses (CAR) behavior is a classical instrumental response paradigm, which is widely used to study aversive conditioning and defensive motivation behavior. Previous studies have shown that dopamine D and D receptors are involved in CAR behavior; however, it is unclear in which brain regions that dopamine evokes CAR behavior. The aim of the study is to investigate whether dopamine triggers CAR behavior via activating dopamine D or D receptors in the shell of nucleus accumbens or dorsolateral striatum.

Pimavanserin, a 5-hydroxytryptamine 2A receptor inverse agonist, reverses prepulse inhibition deficits in the nucleus accumbens and ventral hippocampus.

Prepulse inhibition (PPI) is disrupted in many neuropsychiatric diseases. Although the inverse agonist of the 5-hydroxytryptamine 2A (5-HT) receptors, pimavanserin, alleviates PPI deficits in rodents, the precise mechanisms and critical brain areas in the reversal effect of 5-HT receptor inverse agonists remain unclear. The present study aimed to investigate the critical brain areas responsible for the reversal effect of the 5-HT receptor inverse agonist on PPI deficits in male mice.

MK212, a 5-hydroxytryptamine 2C receptor agonist, reverses prepulse inhibition deficits in the medial prefrontal cortex and ventral hippocampus.

Prepulse inhibition (PPI) is disrupted in many neuropsychiatric diseases. Molecules such as 5-HT receptor agonists alleviate PPI deficits in rodents; however, the precise mechanisms and critical regions of the brain responsible for the reversal effect of these agonists remain inconclusive. The present study aimed to investigate the areas of the brain critical for the reversal effect of 5-HT receptor agonists on PPI deficits in mice.

Biochanin A Mitigates Atherosclerosis by Inhibiting Lipid Accumulation and Inflammatory Response.

Biochanin A (BCA), a dietary isoflavone extracted from red clover and cabbage, has been shown to antagonize hypertension and myocardial ischemia/reperfusion injury. However, very little is known about its role in atherogenesis. The aim of this study was to observe the effects of BCA on atherosclerosis and explore the underlying mechanisms.

LncRNA kcnq1ot1 promotes lipid accumulation and accelerates atherosclerosis via functioning as a ceRNA through the miR-452-3p/HDAC3/ABCA1 axis.

Kcnq1 overlapping transcript 1 (kcnq1ot1), an imprinted antisense lncRNA in the kcnq1 locus, acts as a potential contributor to cardiovascular disease, but its role in atherosclerosis remains unknown. The aim of this study was to explore the effects of kcnq1ot1 on atherogenesis and the underlying mechanism. Our results showed that kcnq1ot1 expression was significantly increased in mouse aorta with atherosclerosis and lipid-loaded macrophages.

LncRNA-modulated autophagy in plaque cells: a new paradigm of gene regulation in atherosclerosis?

The development of atherosclerosis is accompanied by the functional deterioration of plaque cells, which leads to the escalation of endothelial inflammation, abnormal vascular smooth muscle cell phenotype switching and the accumulation of lipid-laden macrophages within vascular walls. Autophagy, a highly conserved homeostatic mechanism, is critical for the delivery of cytoplasmic substrates to lysosomes for degradation. Moderate levels of autophagy prevent atherosclerosis by safeguarding plaque cells against apoptosis, preventing inflammation, and limiting the lipid burden, whereas excessive autophagy exacerbates cell damage and inflammation and thereby accelerates the formation of atherosclerotic plaques.