Mitochondrial DNA in atherosclerosis: Mechanisms, biomarker potential, and therapeutic perspectives.

Atherosclerosis is a chronic inflammatory disease in which mitochondrial DNA (mtDNA) has emerged as a key contributor to its pathogenesis. We synthesized evidence from experimental and clinical studies showing that mtDNA damage, release, and mutation profoundly affect endothelial cells, macrophages, and vascular smooth muscle cells, thereby driving plaque initiation and progression. By activating immune signaling pathways-including cGAS-STING, NLRP3 inflammasome, and TLR9-mtDNA amplifies inflammation and oxidative stress, exacerbating atherosclerotic lesion development.

Mitochondrial DNA leakage: underlying mechanisms and therapeutic implications in neurological disorders.

Mitochondrial dysfunction is a pivotal instigator of neuroinflammation, with mitochondrial DNA (mtDNA) leakage as a critical intermediary. This review delineates the intricate pathways leading to mtDNA release, which include membrane permeabilization, vesicular trafficking, disruption of homeostatic regulation, and abnormalities in mitochondrial dynamics. The escaped mtDNA activates cytosolic DNA sensors, especially cyclic gmp-amp synthase (cGAS) signalling and inflammasome, initiating neuroinflammatory cascades via pathways, exacerbating a spectrum of neurological pathologies.

Novel insights into molecular patterns of ROS1 fusions in a large Chinese NSCLC cohort: a multicenter study.

ROS proto-oncogene 1, receptor tyrosine kinase (ROS1) rearrangements are a crucial therapeutic target in non-small cell lung cancer (NSCLC). However, there is limited comprehensive analysis of the molecular patterns of ROS1 fusions. This study aimed to address this gap by analysing 135 ROS1 fusions from 134 Chinese NSCLC patients using next-generation sequencing (NGS).

Micronutrient Level Is Negatively Correlated with the Neutrophil-Lymphocyte Ratio in Patients with Severe COVID-19.

Aim: To explore the potential relationship between NLR and micronutrient deficiency in patients with severe COVID-19 infection.

Methods: Sixteen patients were categorized into the mild group (mild COVID-19) and severe group (severe COVID-19) based on the guideline of the management of COVID-19. The lactate dehydrogenase (LDH); superoxide dismutase (SOD), the inflammatory markers (neutrophil lymphocyte ratio (NLR)), erythrocyte sedimentation rate (ESR), c-reactive protein (CRP), selenium (Se), iron (Fe), zinc (Zn), nickel (Ni), copper (Cu), chromium (Cr), cadmium (Cd), arsenic (As), and manganese (Mn) were measured in the blood.

An epigenome-wide DNA methylation study of patients with COVID-19.

In the early 2000s, emerging SARS-CoV-2, which is highly pathogenic, posed a great threat to public health. During COVID-19, epigenetic regulation is deemed to be an important part of the pathophysiology and illness severity. Using the Illumina Infinium Methylation EPIC BeadChip (850 K), we investigated genome-wide differences in DNA methylation between healthy subjects and COVID-19 patients with different disease severities.

CXCL8 chemokine in ulcerative colitis.

Ulcerative colitis (UC) is a major type of inflammatory bowel disease (IBD), which is characterized by diffuse inflammation of the mucosa of the colon and rectum. Abdominal pain, diarrhea, and hematochezia are UC's main clinical manifestations. Pathogenesis of UC has not yet been clearly elucidated, but it is considered to result from dysregulated expressions of molecules engaged in proinflammatory and anti-inflammatory processes.

Clinical Features for Severely and Critically Ill Patients with COVID-19 in Shandong: A Retrospective Cohort Study.

Background: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a novel pathogen, has caused an outbreak of coronavirus disease 2019 (COVID-19) that has spread rapidly around the world. Determining the risk factors for death and the differences in clinical features between severely ill and critically ill patients with SARS-CoV-2 pneumonia has become increasingly important.

Aim: This study was intended to provide insight into the difference between severely ill and critically ill patients with SARS-CoV-2 pneumonia.

LncRNA LINC00511 plays an oncogenic role in lung adenocarcinoma by regulating PKM2 expression via sponging miR-625-5p.

Background: Lung adenocarcinoma (LAC) is the most prominent histological subtype of non-small cell lung cancer (NSCLC) with a high rate of mortality and metastasis. Accumulating evidence has shown that long non-coding RNAs (lncRNAs) play malfunctioning roles in the development of human tumors. Hence, this study aimed to determine the biological function of LINC00511 in LAC and to provide a novel diagnostic and therapeutic target for it.

Thrombin promotes proliferation of human lung fibroblasts via protease activated receptor-1-dependent and NF-κB-independent pathways.

Acute and chronic respiratory diseases are associated with abnormal coagulation regulation and fibrolysis. However, the detailed mechanism by which coagulation regulation and fibrolysis affect the occurrence and development of lung diseases remain to be elucidated. Protease activated receptor-1 (PAR-1), a major high-affinity thrombin receptor, and nuclear factor kappa B (NF-κB), a transcription factor, are involved in cell survival, differentiation, and proliferation.

[Influence of Aconiti Lateralis Radix Praeparata on asthenia cold syndrome rats with whole genome gene expression of liver by gene chip technique].

Objective: To study the influence of Aconiti Lateralis Radix Praeparata on asthenia cold syndrome rats with whole genome gene expression of liver by gene chip technique.

Method: The asthenia cold syndrome rat models were established by administering traditional Chinese medicine raw Gypsum Fibrosum, Gentianae Radix, Phellodendri Chinensis Cortex and Anemarrhenae Rhizoma. After treated with Aconiti Lateralis Radix Praeparata, the rats' liver gene expressions were detected using gene chip.

[Sustained electrical stimulation of Bötzinger complex on phrenic nerve discharges in rabbits].

Aim: To observe the effects of sustained electrical stimulation at Bötzinger complex (Böt. c) on phrenic nerve discharges.

Methods: Sustained electrical stimulation (10--50 microA, 40-100 Hz, 0.

[The locus coeruleus modulates the inspiratory inhibition induced by electrical stimulation of the Bötzinger complex].

Experiments were done on urethane anesthetized adult rabbits. Long-train electrical stimulation was delivered to the Bötzinger complex (Böt.C) to observe the changes in the peak amplitude of integrated phrenic nerve activity.