The synergistic antimicrobial activities of three natural essential oils (i.e., clove bud oil, cinnamon oil, and star anise oil) with chitosan films were investigated. Cinnamon oil had the best antimicrobial activity among three oils against Escherichia coli , Staphylococcus aureus , Aspergillus oryzae , and Penicillium digitatum . The chitosan solution exhibited good inhibitory effects on the above bacteria except the fungi, whereas chitosan film had no remarkable antimicrobial activity. The cinnamon oil-chitosan film exhibited a synergetic effect by enhancing the antimicrobial activities of the oil, which might be related to the constant release of the oil. The cinnamon oil-chitosan film had also better antimicrobial activity than the clove bud oil-chitosan film. The results also showed that the compatibility of cinnamon oil with chitosan in film formation was better than that of the clove bud oil with chitosan. However, the incorporated oils modified the mechanical strengths, water vapor transmission rate, moisture content, and solubility of the chitosan film. Furthermore, chemical reaction took place between cinnamon oil and chitosan, whereas phase separation occurred between clove bud oil and chitosan.
The aim of this study was to evaluate the pharmacokinetics, safety profile, and pharmacodynamics of gadopiclenol, a new high relaxivity macrocyclic gadolinium-based contrast agent, in healthy subjects and patients with brain lesions. Materials and Methods: This was a single ascending dose phase I/IIa study. Phase I was double-blind, randomized, placebo-controlled and included 54 healthy subjects. In each dose group (0.025, 0.05, 0.075, 0.1, 0.2, and 0.3 mmol/kg), 6 subjects received gadopiclenol and 3 received placebo (NaCl 0.9%) in intravenous injection. Phase IIa was open-label and included 12 patients with brain lesions, 3 per dose group (0.05, 0.075, 0.1, and 0.2 mmol/kg). Concentrations were measured in plasma samples collected before administration and over a 24-hour period postadministration and in urine specimens (phase I) collected until 7 days after administration. A noncompartmental approach was used for pharmacokinetic analysis. Pharmacodynamic assessments included a qualitative evaluation of the visualization of brain structures/lesions and quantitative measurements (signal-to-noise ratio, contrast-to-noise ratio) on magnetic resonance imaging. A clinical and biological safety follow-up was performed up to 7 days after administration for phase I and up to 1 day after administration for phase IIa. Results: In healthy subjects (male, 50%; median age, 26.0 years), the pharmacokinetics of gadopiclenol is considered linear with mean maximum concentration C max values ranging from 248.7 to 3916.4 μg/mL. Gadopiclenol was excreted in an unchanged form via the kidneys, eliminated from plasma with a terminal elimination half-life (t 1/2 ) of 1.5 to 2 hours. There was no difference in the pharmacokinetics between males and females. After administration of gadopiclenol, the contrast enhancement scores in brain structures were improved in all dose groups. Similar rates of related adverse events were observed with gadopiclenol (36.1%) and placebo (33.3%). No clinically significant modifications in biochemistry, hematology, urinalysis, electrocardiogram parameters, and vital signs were reported.In patients (male, 58%; median age, 53.0 years), a similar pharmacokinetic and safety profile was observed, and sufficient contrast enhancement was seen at all tested doses. Conclusions: The pharmacokinetics of gadopiclenol is dose-independent in healthy subjects and patients with brain lesions. Its good safety profile is in line with that reported for other macrocyclic gadolinium-based contrast agents. Preliminary pharmacodynamic results in patients suggest that gadopiclenol is a promising macrocyclic contrast agent with the potential use of lower dose for clinical routine magnetic resonance imaging scans.The study is registered on ClinicalTrials.gov under the trial registration number NCT03603106.
The factors that influence preadipocyte determination remain poorly understood. In the present paper, we report that CREBL2 [CREB (cAMP-response-element-binding protein)-like 2], a novel bZIP_1 protein, is up-regulated during MDI-induced preadipocyte differentiation. During both overexpression and under physiological conditions, CREBL2 interacted and was entirely co-localized with CREB. Overexpression of CREBL2 was sufficient to promote adipogenesis via up-regulating the expression of PPARγ (peroxisome-proliferator-activated receptor γ) and C/EBPα (CCAAT/enhancer-binding protein α) and accelerate lipogenesis accompanied with increased GLUT (glucose transporter) 1 and GLUT4. CREBL2 knockdown restrained adipogenic conversion and lipogenesis. Additionally, depletion of CREB could completely block the effects of overexpressed CREBL2, whereas an increase in CREB could not drive adipogenesis in the absence of CREBL2, indicating that the roles for CREBL2 on adipogenesis were CREB-dependent. Furthermore, siCREBL2 [siRNA (short interfering RNA) against CREBL2] could down-regulate CREB transcriptional activity and suppress CREB phosphorylation. CREB knockdown decreased the CREBL2 protein levels and vice versa. Collectively, the results of the present study indicate that CREBL2 plays a critical role in adipogenesis and lipogenesis via interaction with CREB.
Neurodevelopmental programs are frequently dysregulated in cancer. Semaphorins are a large family of guidance cues that direct neuronal network formation and are also implicated in cancer. Semaphorins have two kinds of receptors, neuropilins and plexins. Besides their role in development, semaphorin signaling may promote or suppress tumors depending on their context. Sema3C is a secreted semaphorin that plays an important role in the maintenance of cancer stem-like cells, promotes migration and invasion, and may facilitate angiogenesis. Therapeutic strategies that inhibit Sema3C signaling may improve cancer control. This review will summarize the current research on the Sema3C pathway and its potential as a therapeutic target.
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