Biomedicine & pharmacotherapy = Biomédecine & pharmacothérapie
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Biomed. Pharmacother. · Dec 2018
Randomized Controlled TrialEffect of intravenous magnesium sulfate on bupivacaine spinal anesthesia in preeclamptic patients.
Magnesium sulfate (MgSO4) is the standard therapy for the treatment of preeclampsia and prevention of eclamptic seizures in labor. This study aimed to determine the effect of the magnesium administered intravenously as a bolus prior to spinal anesthesia on the speed of onset and duration of the spinal anesthesia in preeclamptic women. ⋯ Intravenous MgSO4 can hasten the onset of sensory block, prolong the duration of sensory block, motor block and spinal anesthesia, alleviate postoperative pain, but not hasten the onset of motor block in preeclamptic women undergoing spinal anesthesia without additional side effects. (www.chictr.org.cn, registration number: ChiCTR-IOR-15006856).
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Biomed. Pharmacother. · Dec 2018
Role of bone marrow derived mesenchymal stromal cells and Schwann-like cells transplantation on spinal cord injury in adult male albino rats.
Spinal cord injury is a considerable health impact accompanied with physical, psychological and economic burden. Bone marrow derived mesenchymal stromal cells (BM-MSCs) transplantation was found to produce neuronal regenerative effects. Schwann-like cells differentiated from BM-MSCs have myelin-forming ability. ⋯ Transplantation of BM-MSCs and Schwann-like cells improved the structural and functional alterations of spinal cord injury with better improvement in BM-MSC group.
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Biomed. Pharmacother. · Dec 2018
ReviewAdipokines in critical illness: A review of the evidence and knowledge gaps.
Adipose tissue products or adipokines play a major role in chronic endocrine and metabolic disorders; however, little is known about critical conditions. In this article, the experimental and clinical evidence of alterations of adipokines, adiponectin, leptin, resistin, visfatin, asymmetric dimethylarginine (ADMA), and ghrelin in critical illness, their potential metabolic, diagnostic, and prognostic value, and the gaps in the field have been reviewed. The results showed considerable changes in the concentration of the adipokines; while the impact of adipokines on metabolic disorders such as insulin resistance and inflammation has not been well documented in critically ill patients. ⋯ However, there is no consensus on these findings. Although primary data indicated the role of adipokines in critical illness, further studies are required to clarify whether the reason of these changes is pathophysiological or compensatory. The relationship of pathophysiological background, disease severity, baseline nutritional status and nutrition support during hospitalization, and variations in body fat percentage and distribution with adipokines, as well as the potential prognostic or therapeutic role of these peptides should be further investigated in critically ill patients.
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Biomed. Pharmacother. · Dec 2018
Roles of apoptosis and inflammation in a rat model of acute lung injury induced right ventricular dysfunction.
The effect of intratracheal lipopolysaccharide (LPS) instillation on right ventricular dysfunction in rats was studied with the aim of exploring underlying mechanisms. ⋯ As well as acute lung injury, a single dose of LPS intratracheally instilled can induce pulmonary hypertension at 6 h post-exposure, with obvious right ventricular systolic dysfunction and right ventricular dilation present at 12 h post-exposure, possibly via cardiomyocytes apoptosis and inflammation.
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Biomed. Pharmacother. · Dec 2018
Overexpression of miR-142-3p improves mitochondrial function in cardiac hypertrophy.
Our previous studies have shown that Src homology 2 (SH2) B adaptor protein 1 (SH2B1) plays an important role in cardiac hypertrophy, but the specific mechanism remains to be studied. Through bioinformatics and related research, it is found that miR-14 2-3 p is closely related to SH2B1. Exploring the relationship between miR-14 2-3 p and gene SH2B1 expression is beneficial for the treatment of cardiac hypertrophy. SH2B1 is a key factor regulating energy metabolism, mitochondria are the main organelles of energy metabolism and cardiac hypertrophy are closely related to mitochondrial dysfunction. So it is particularly important to explore the relationship between miR-14 2-3 p and SH2B1 and myocardial mitochondrial function. In this study, we investigated whether overexpression of miR-14 2-3 p can inhibit the expression of gene SH2B1, ameliorate cardiac mitochondrial dysfunction and cardiac hypertrophy. ⋯ When the pressure overload myocardial hypertrophy model was constructed for four weeks, echocardiography revealed that the heart volume, Left ventricular end diastolic diameter(LVIDd), Left ventricular end systolic diameter (LVIDs), Left ventricular posterior wall thickness (LVPWd), Systolic left ventricular posterior wall (LVPWs), Left ventricle (LV) Mass increased, Ejection fraction (EF) % decreased of AB group increased, but transfected with miR-14 2-3 p agomir of AB, these increase was not significant, EF% reduction was not obvious. HE staining showed that the myocardial cross-sectional area of AB group increased significantly, but the miR-14 2-3 p agomir treatment of AB group did not increase significantly. PCR analysis showed that the expression of ANP, BNP,β-MHC mRNA was significantly increased in AB group, but the miR-14 2-3 p agomir treatment of AB group was not significantly increased. Flow cytometry showed that the mitochondrial membrane potential of AB group was significantly reduced, and the miR-14 2-3 p agomir treatment of AB group was not significantly decreased. During AngII-induced cardiomyocyte hypertrophy, ANP, BNP,β-MHC mRNA expression was increased, while these factors was not significantly increased in miR-14 2-3 p mimic treatment group; mitochondrial membrane potential, mitochondrial density and OCR was significantly decreased in AngII treated group, and these were not significantly reduced in miR-14 2-3 p mimic treatment group; CONCLUSIONS: miR-14 2-3 p not only mitigate cardiac hypertrophy by directly inhibit the expression of gene SH2B1, but also can protect mitochondrial function in cardiac hypertrophy of vitro and vivo.