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1.
Clinics (Sao Paulo) ; 78: 100300, 2023.
Article in English | MEDLINE | ID: mdl-37931530

ABSTRACT

OBJECTIVES: To investigate the changes in the coagulation function and hemodynamic parameters in patients with Hemorrhagic Traumatic Shock (HTS) after restrictive fluid resuscitation. METHODS: A total of 139 patients with HTS admitted to our hospital were enrolled, among which 69 HTS patients were divided into the control group and the remaining 70 HTS patients as the observation group. Patients in the control group underwent regular fluid resuscitation, while those in the observation group underwent restrictive fluid resuscitation. RESULTS: During treatment, 70 patients in the observation group had a lower bleeding amount, infusion amount, and blood transfusion volume than those in the control group (p < 0.05). After treatment, patients in the observation group had better hemodynamic parameters and blood coagulation than those in the control group (p < 0.05), and the incidence rate in the observation group was only 12.9%, which was significantly lower than 60.87% in the control group, while the cure rate in the observation group was 100%, which was significantly higher than that in the control group (p < 0.05). CONCLUSIONS: Restrictive fluid resuscitation could remarkably increase the cure rate and reduce the bleeding amount during HTS treatment, thereby benefiting the recovery of the patient's blood coagulation.


Subject(s)
Shock, Hemorrhagic , Shock, Traumatic , Humans , Shock, Traumatic/therapy , Shock, Hemorrhagic/drug therapy , Hemodynamics , Fluid Therapy , Blood Coagulation , Resuscitation
2.
Clinics ; 78: 100300, 2023. tab, graf
Article in English | LILACS-Express | LILACS | ID: biblio-1528425

ABSTRACT

Abstract Objectives To investigate the changes in the coagulation function and hemodynamic parameters in patients with Hemorrhagic Traumatic Shock (HTS) after restrictive fluid resuscitation. Methods A total of 139 patients with HTS admitted to our hospital were enrolled, among which 69 HTS patients were divided into the control group and the remaining 70 HTS patients as the observation group. Patients in the control group underwent regular fluid resuscitation, while those in the observation group underwent restrictive fluid resuscitation. Results During treatment, 70 patients in the observation group had a lower bleeding amount, infusion amount, and blood transfusion volume than those in the control group (p < 0.05). After treatment, patients in the observation group had better hemodynamic parameters and blood coagulation than those in the control group (p < 0.05), and the incidence rate in the observation group was only 12.9%, which was significantly lower than 60.87% in the control group, while the cure rate in the observation group was 100%, which was significantly higher than that in the control group (p < 0.05). Conclusions Restrictive fluid resuscitation could remarkably increase the cure rate and reduce the bleeding amount during HTS treatment, thereby benefiting the recovery of the patient's blood coagulation.

3.
Drug Des Devel Ther ; 16: 1099-1106, 2022.
Article in English | MEDLINE | ID: mdl-35440867

ABSTRACT

Introduction: Endothelial dysfunction (ED) is associated with the progression of sepsis. Ruscogenin (RUS) has shown considerable efficacy in treating ED and sepsis. In the current study, the effects of RUS on sepsis-induced ED were assessed, and the mechanism was explored by focusing on the interactions of RUS with miRs. Methods: Sepsis was induced in mice and in human umbilical vein endothelial cells (HUVECs) using LPS method. Expression profile of miRs responding to sepsis was determined. Symptoms associated with sepsis and ED were examined after treatment with RUS. Changes in mouse survival, arterial structure, systemic inflammation, cell viability, apoptosis, and the miR-146a-5p/NRP2/SSH1 axis were analyzed. Results: Based on the microarray results, miR-146a-5p was selected as the therapeutic target. RUS improved survival rates and arterial structure, suppressed proinflammatory cytokines, down-regulated miR-146a-5p, and up-regulated NPR2 and SSH1 in septic mice. In HUVECs, RUS increased cell viability, suppressed apoptosis, inhibited inflammation, downregulated miR-146a-5p, and increased NRP2 and SSH1 levels. The re-induction of miR-146a-5p-5p impaired the protective effects of RUS on HUVECs. Discussion: Effects of RUS on sepsis-induced impairments in endothelium relied on the suppression of miR-146a-5p.


Subject(s)
MicroRNAs , Sepsis , Animals , Apoptosis , Human Umbilical Vein Endothelial Cells , Humans , Inflammation/chemically induced , Inflammation/complications , Inflammation/drug therapy , Lipopolysaccharides/metabolism , Lipopolysaccharides/pharmacology , Mice , MicroRNAs/metabolism , Phosphoprotein Phosphatases/metabolism , Phosphoprotein Phosphatases/pharmacology , Sepsis/chemically induced , Sepsis/drug therapy , Spirostans
4.
Int Wound J ; 19(3): 679-691, 2022 Mar.
Article in English | MEDLINE | ID: mdl-34414663

ABSTRACT

The development of biologically active multifunctional hydrogel wound dressings can assist effectively to wound regeneration and also has influenced multiple functions on wound injury. Herein, we designed a carbon-based composited injectable silk fibroin hydrogel as multifunctional wound dressing to provide effective anti-bacterial, cell compatibility and in vivo wound closure actions. Importantly, the fabricated injectable hydrogel exhibit sustained drug delivery properties, anti-oxidant and self-healing abilities, which confirm that composition of hydrogel is highly beneficial to tissue adhesions and burn wound regeneration ability. Frequently, designed injectable hydrogel can be injected into deep and irregular burn wound sites and would provide rapid self-healing and protection from infection environment with thoroughly filled wound area. Meanwhile, incorporated carbon nanofillers improve injectable hydrogel strength and also offer high fluid uptake to hydrogel when applied on the wound sites. In vitro MTT cytotoxicity assay on human fibroblast cell lines establish outstanding cytocompatibility of the injectable hydrogel and also have capability to support cell growth and proliferations. In vivo burn wound animal model results demonstrate that the hydrogel dressings predominantly influenced enhanced wound contraction and also promoted greater collagen deposition, granulation tissue thickness and vascularization. This investigation's outcome could open a new pathway to fabricate multifunctional biopolymeric hydrogel for quicker burn wound therapy and effectively prevents microenvironment bacterial infections.


Subject(s)
Burns , Fibroins , Animals , Anti-Bacterial Agents , Bandages , Burns/drug therapy , Fibroins/pharmacology , Fibroins/therapeutic use , Humans , Hydrogels/therapeutic use , Wound Healing
5.
J Int Med Res ; 48(12): 300060520969090, 2020 Dec.
Article in English | MEDLINE | ID: mdl-33284724

ABSTRACT

OBJECTIVE: To investigate the protective effects of the ginsenoside Rh3 on rats subjected to myocardial ischemia-reperfusion (MIR) via its impact on caspase-3 and the p38 mitogen-activated protein kinase (MAPK) pathway. METHODS: Fifteen male Sprague-Dawley rats were randomly categorized into the MIR group (MY group, n = 5), sham surgery group (SS group, n = 5), and ginsenoside Rh3 group (GR group, n = 5). RESULTS: The MY group exhibited the largest myocardial infarctions compared with the GR and SS groups. The GR group exhibited significantly higher cell viability of cardiomyocytes and significantly decreased apoptosis compared with the MY group. Fibrils of infarcted tissue in the GR group were disordered but less swollen, with a more organized fibril orientation than those in the MY group. The GR group showed reduced p-p38 MAPK protein and caspase-3 mRNA expression levels compared with the MY and SS groups. CONCLUSIONS: Rh3 significantly improved myocardial necrosis and caspase-3 levels in myocardial tissues by suppressing the p38 MAPK pathway, thereby inhibiting caspase-3 involvement in apoptosis. Thus, Rh3 was effective in inhibiting the escalated apoptotic pathway in myocardial infarction and can potentially serve as a useful therapeutic agent to rescue myocardial infarction.


Subject(s)
Myocardial Reperfusion Injury , Reperfusion Injury , Animals , Apoptosis , Caspase 3/genetics , Ginsenosides , Male , Myocardial Reperfusion Injury/drug therapy , Myocardial Reperfusion Injury/genetics , Rats , Rats, Sprague-Dawley , Reperfusion Injury/drug therapy , p38 Mitogen-Activated Protein Kinases
6.
Exp Ther Med ; 20(2): 1441-1446, 2020 Aug.
Article in English | MEDLINE | ID: mdl-32742377

ABSTRACT

Sequential invasive-noninvasive ventilation (NIV) improves the outcomes of patients with respiratory failure caused by acute exacerbation of chronic obstructive pulmonary disease (AECOPD); however, there is no clear consensus on the optimal timing of the switch to sequential invasive-NIV in these patients. In the present study, a potential role for the modified Glasgow Coma Scale (GCS) score to guide sequential weaning was investigated. Patients with AECOPD and respiratory failure were prospectively recruited from three study centers (Wenling Hospital Affiliated to Wenzhou Medical University, the First Affiliated Hospital of Wenzhou Medical University and Changsha Central Hospital) between January 1st 2016 and December 31st 2018. Patients were randomly assigned to group A and B, with the switching point for sequential weaning strategy in the two groups being a modified GCS score ≥13 and 10 points, respectively. Each group included 240 patients. Baseline demographic characteristics were comparable in the two groups. The duration of invasive mechanical ventilation (IMV) in group A was significantly shorter than that in group B. However, there were no significant between-group differences with respect to the incidence of re-intubation, ventilator-associated pneumonia, in-hospital mortality or the length of hospital stay. Use of a modified GCS score ≥13 as the switching point for sequential invasive-NIV may help decrease the duration of IMV in patients with AECOPD and respiratory failure.

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