Clinical Research Directory

Inflammation Severity and miRNA-126 in Trauma

Trauma triggers a complex immune response intended to eliminate danger signals and restore physiological balance. Early post-traumatic inflammation is primarily initiated by damage-associated molecular patterns (DAMPs) and pathogen-associated molecular patterns (PAMPs). In patients with severe trauma, dysregulated inflammation increases susceptibility to infection, systemic inflammatory response syndrome (SIRS), multiple organ dysfunction syndrome (MODS), and mortality. The lungs are particularly vulnerable, and excessive inflammatory activation may lead to acute lung injury (ALI) or acute respiratory distress syndrome (ARDS), conditions characterized by increased vascular permeability, alveolar epithelial injury, surfactant dysfunction, and impaired gas exchange. Pro-inflammatory cytokines, activated neutrophils, reactive oxygen species, and proteases contribute to endothelial and epithelial barrier disruption. Recent evidence also suggests that several microRNAs, including miR-126, may play a regulatory role in pulmonary barrier integrity through modulation of tight-junction proteins and PI3K/AKT-related pathways. Although many components of the trauma-related inflammatory response have been described, the relationship between systemic inflammatory severity and impairment of pulmonary gas exchange remains insufficiently defined in clinical settings. This study aims to investigate the correlation between inflammatory severity markers (C-reactive protein, procalcitonin, IL-6, reactive oxygen derivatives, neutrophil-to-lymphocyte ratio, lactate), imaging findings (flow-mediated dilation by ultrasound), clinical parameters (blood pressure, heart rate, urine output, vasoactive medication requirements), pulmonary gas-exchange measurements (arterial blood gases, PaO₂/FiO₂ ratio), and circulating miRNA-126 levels in trauma patients. The findings may help identify biomarkers that better reflect inflammatory burden and the risk of lung dysfunction following trauma.

Probing the Role of Mitochondrial Oxidative Stress in Impaired Vascular Function Among Young Adults With Early Life Adversity

Adverse childhood experiences (ACEs) represent highly stressful events in the first 18 years of life that include abuse, neglect, and household and community-level dysfunction. Greater exposure to ACEs are associated with greater increases in the risk of cardiovascular diseases and death. Our laboratory has previously observed that vascular function is disrupted in young adults with prior ACE exposure, even though these individuals appear to be healthy clinically (i.e., no classic clinical cardiovascular disease risk factors). There is a need to identify and understand the biological mechanisms underlying these vascular impairments to inform effective interventions to reduce cardiovascular risks the millions of individuals affected by ACEs. The body's response to stress is coordinated across various systems, all of which depend on energy supplied by mitochondria (often referred to as the "powerhouse of cells"). Based on new evidence across multiple physiological systems from our team, our overarching hypothesis is that disruption of mitochondrial function contributes to cardiovascular impairments among young adults with ACEs. Here we propose the initial pilot work necessary to begin to understand these associations, which will directly inform identification of individuals who may be most vulnerable to stress-related cardiovascular risk and the development of interventions to promote cardiovascular-stress resilience. Our aims are to: 1. Determine whether mitochondrial oxidative stress contributes to impaired vascular function among young adults who experienced early life adversity. 2. Determine whether reducing mitochondrial oxidative stress improves the cellular stress and integrated cardiovascular response to laboratory-based psychosocial stress among young adults who experienced early life adversity.

MSC Exosome Therapy for Post-Preeclampsia Endothelial Dysfunction

\--- Why Is This Study Being Done? Women who have preeclampsia during pregnancy face a much higher risk of heart disease later in life. Preeclampsia is a serious pregnancy condition that causes high blood pressure and damages blood vessels. Even after the baby is born, the blood vessels do not fully heal on their own, which can lead to heart problems/cardiovascular years later. This study tests whether a new treatment called exosomes can help repair damaged blood vessels in women who had preeclampsia. Exosomes are tiny particles that come from stem cells and contain healing substances that may help blood vessels work better. \--- What Will Happen in This Study? This study will include 80 women who recently gave birth and had preeclampsia during their pregnancy. Half of the women will receive the exosome treatment through an IV, and half will receive a placebo (a substance with no active treatment). \--- What Will Participants Need to Do? Participants will: * Have blood tests and other health checks * Receive one treatment through an IV * Return for follow-up visits at 1 week after treatment * Have tests to check how well their blood vessels are working Who Can Join This Study? Women who: * Recently gave birth (within 1-2 weeks) * Had preeclampsia during their last pregnancy * Are healthy enough to participate * Can give permission to join the study What Are the Possible Benefits and Risks? The treatment may help repair blood vessel damage and reduce the risk of future heart disease. The exosome treatment appears to be safe based on other studies, but like any medical treatment, there may be side effects. \--- How Long Will the Study Last? The main treatment happens during one visit, with follow-up visits for 1 week to check on participants' health and see if the treatment is working. This research may lead to new ways to protect women's heart health after pregnancy complications.

Th Tl Xb Prescription on Reprogramming of Lipid Metabolism and Endothelial Injury for Cerebral Infarction Patients

This study is a prospective, open-label, randomized control trial. It is planning to include 160 cerebral infarction patients which will be randomized in a 1﹕1 fashion to receive Chinese herbal medicines combined basic medicine treatment, or to receive standard basic medicine treatment within 3 months after inclusion. Follow-up will be performed after the treatment for 3 months to evaluate the incidence and disability rates of limb impairment, language impairment, cognitive impairment, and emotional disorders. The primary outcome is modified Rankin Scale Score, which is measured by the overall distribution from 0 (no symptoms) to 6 (death). The secondary outcome include the Evaluation of Neurological Function Deficit score (National Institute of Health stroke scale scoring) and carotid atherosclerotic plaque score (Crouse scoring system for neck carotid atherosclerotic plaque scoring). Additional outcomes include laboratory indicator to analysis the reprogramming of lipid metabolism and endothelial Injury, Chinese medicine symptom and sign scoring system and biological indicators. The investigators will perform the intention-to-treat analysis for withdrawal and missing data, and estimate the health economic value.