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Desensitization therapy for iodinated contrast media (ICM) aims to induce drug tolerance in patients with a history of severe allergic reactions to ICM in a short time. Currently, there is no widely accepted consensus on inducing desensitization to avoid severe allergic responses to ICM. The clinically successful cases have shown that prophylactic use of antihistamines and glucocorticoids can increase the desensitization effect; repeatedly desensitizing and gradually increasing the dose can be conducive to establishing better tolerance to ICM. Most desensitization effects, including stress resistance, can endure 24-48 h. The mechanisms of desensitization therapy remain unclear, the initial dose, administration interval and dose gradient are largely based on clinical experiences and the reaction of patients. This article reviews the current research progress on ICM-related allergies, desensitization methods and related mechanisms, as well as the benefits and hazards of desensitization, to provide a reference for desensitization treatment of hypersensitivity to ICM .
Subject(s)
Humans , Contrast Media/adverse effects , Consensus , Glucocorticoids , HypersensitivityABSTRACT
To investigate the therapeutic effects of oral osthole on streptozotocin (STZ)-induced type 1 diabetes mellitus(T1DM) mice and explore its internal mechanism. METHODS: The diabetes model induced by STZ was established. Mice were randomly divided into control group, STZ model group, STZ+osthole group (20 mg/kg). Body weight, blood glucose, urine protein, blood urea nitrogen and creatinine were observed to detect renal function. The degree of renal tissue damage was detected by H&E staining and PAS staining, and the degree of renal fibrosis was detected by Sirius Red staining. CD68 and F4/80 immunofluorescence staining was used to observe the infiltration of macrophages in kidney tissue. The mRNA expressive levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) in renal tissue were detected by RT-qPCR. The protein expressive levels of phospho-NF-κB p65, NF-κB p65, IκBα, phospho-IκBα, phospho-p38 and p38 were detected by Western blot in renal tissue. RESULTS: Compared with the STZ model group, the levels of urinary protein, blood urea nitrogen, creatinine were significantly decreased after osthole treatment (P<0.05 or P<0.01). The renal structure disorder, mesangial matrix area, collagen fiber accumulation, and macrophage infiltration were significantly improved (P<0.05 or P<0.01). The expression of mRNA of pro-inflammatory cytokines TNF-α and IL-6 were significantly decreased (P<0.05 or P<0.001). The expression of phospho-NF-κB p65, phospho-IκBα and phospho-p38 were significantly down-regulated (P<0.05 or P<0.01), while the protein expression level of NF-κB p65, IκBα was up-regulated (P<0.05). CONCLUSION: Osthole has a protective effect on kidney injury caused by diabetes and inhibits NF-κB and p38/MAPK signaling pathway.
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AIM: To analyze the effect of influential factors on the estimation of pharmacokinetic parameters of teicoplanin, this study was proposed to develop the population pharmacokinetic (PPK) model of teicoplanin in patients with renal insufficiency. METHODS: A total of 66 routine blood teicoplanin concentration monitoring data were collected from 46 cases with renal insufficiency, and a nonlinear mixed effect modeling program was used to establish one-compartment model with Monolix 2021R1 software. Furthermore, 20 routine blood teicoplanin concentration monitoring data were also collected from the other 20 cases with renal insufficiency, and the external validation of the model was performed by goodness-of-fit parameter method. RESULTS: The one compartment model was an appropriate model for simulating the pharmacokinetics of teicoplanin in patients with renal insufficiency. The typical values of apparent volume of distribution and clearance rate were 148.9 L and 0.13 L/h, respectively. Glomerular filtration rate and body weight, instead of other factors, were the primary variables that affected the elimination of teicoplanin in vivo. CONCLUSION: The population pharmacokinetic model of teicoplanin established in the present study was effective and stable, which could also predict the dynamic change of teicoplanin concentration. As a result, the population pharmacokinetic model could provide references for the rational use of teicoplanin in special populations.
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Cardiac disease is the general term of diseases, caused by damage to the structure or abnormal function of the heart. Its morbidity and mortality have remained high, seriously threatening the lives and health of people. The tyrosine kinase receptor ErbB2 (also known as EGFR2 or HER2) was originally discovered for its oncogenic activity, however, recent studies have found that ErbB2 have protective effects in various heart diseases. Therefore, this article reviews the role and underlying mechanism of ErbB2 in myocardial infarction, myocardial ischemia/reperfusion injury, cardiac hypertrophy, heart failure, doxorubicin-induced cardiotoxic injury and diabetic cardiomyopathy. Furthermore, this article also preliminarily discusses the application prospects, limitations and development directions of ErbB2 as a clinical diagnostic marker and therapeutic target for heart disease.
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OBJECTIVE:To establish a method for the content determination of zolpidem tartrate in microsamples of rat plas-ma. METHODS:Rats were given zolpidem tartrate solution 3 mg/kg intragastrically,and 0.2 ml blood sample were collected and isolated. 50 μl plasma was precipitated by methanol,and the supernatant was determined by HPLC-fluorescence combined with ex-ternal method. Agilent HC-C18 column was used with mobile phase consisted of 0.03 mol/L KH2PO4 solution(containing 0.2% tri-ethylamine)-methanol (33∶67,V/V) at flow rate of 1.0 ml/min. The excitation and emission wavelengths were 254 nm and 390 nm,respectively. The sample size was 20 μl. RESULTS:The linear ranges of zolpidem tartrate in plasma was 2-200 μg/L(r=0.999 7),and the limit of quantification was 2 μg/L. The method recoveries of zolpidem were (96.96 ± 1.35)%-(105.0 ± 5.36)%(RSD=2.20%-4.88%,n=5),and extraction recoveries were (79.72 ± 0.01)%-(80.77 ± 0.02)%(RSD=1.34%-3.90%,n=5). The intra-day and inter-day RSDs were 1.40%-5.10% and 3.22%-9.25%(n=5),respectively. CONCLUSIONS:The method is simple,sensitive and suitable for the content determination of zolpidem tartrate in microsamples of plasma.