Targeted metabolomic study indicating glycyrrhizin's protection against acetaminophen-induced liver damage through reversing fatty acid metabolism.

The present study aimed to give a short report on a possible mechanism of glycyrrhizin to acetaminophen-induced liver toxicity. Seven-day intraperitoneal administration of glycyrrhizin (400 mg/kg/day) to 2- to 3-month-old male C57BL/6N mice (mean weight 27 g) significantly prevents acetaminophen-induced liver damage, as indicated by the activity of alanine transaminase and aspartate aminotransferase. Metabolomics analysis and principal component analysis (PCA) using ultra-fast liquid chromatography coupled to triple time-of-flight mass spectrometer were performed. PCA separated well the control, glycyrrhizin-treated, acetaminophen-treated, and glycyrrhizin+acetaminophen-treated groups. Long-chain acylcarnitines were listed as the top ions that contribute to this good separation, which include oleoylcarnitine, palmitoylcarnitine, palmitoleoylcarnitine, and myristoylcarnitine. The treatment of glycyrrhizin significantly reversed the increased levels of long-chain acylcarnitines induced by acetaminophen administration. In conclusion, this metabolomic study indicates a significant glycyrrhizin protection effect against acetaminophen-induced liver damage through reversing fatty acid metabolism.

Will a handheld ultrasound scanner be applicable for screening for heart abnormalities in newborns and children?

BACKGROUND: There is significant interest in opportunities to provide echocardiography services for detection of congenital heart disease with portable, or even handheld, devices in remote areas or third world countries where conventional ultrasound systems may not be available. We tested a handheld system (HHS) (SonoHeart, SonoSite Inc, Bothell, Wash) equipped with a broadband, 7- to 4-MHz, miniaturized, curved, linear-array transducer and implemented with an improved directional Doppler flow map. METHODS: All echocardiography scanning was performed in the neonatal nursery, pediatric intensive care department, or pediatric echocardiography laboratory of our institution. We reviewed limited echocardiography view sequences sequentially obtained by the same expert examiner (D.J.S.) in 50 infants and children (age: 1 day to 6 years), with preoperative or postoperative forms of congenital heart disease. Each patient was studied twice, once with a conventional full-feature system (FFS) and then a limited scan with the HHS using similar frequency transducers. The cardiologist (D.J.S.) and blinded research laboratory reviewers (X.L., G.K.M., R.A.R.) read the FFS and HHS image sequences for diagnosis and for grading the quality of the anatomic and flow feature images. The studies were performed and reviewed with the examiner and reviewers blinded to patient diagnosis. RESULTS: The major diagnoses (eg, patent ductus arteriosus, atrio-ventricular (AV) canal, peripheral pulmonary valve stenosis, aortic coarctation, atrial septal defect, ventricular septal defect, preoperative or postoperative tetralogy of Fallot, and mitral regurgitation) were made by both readers, who were unaware of each other's diagnosis results. Furthermore, the average composite HHS cardiac anatomic feature score on a scale of 0 (not visualized) to 3 (visualized precisely) from the parasternal long-axis and 4- or 5-chamber view for cardiac anatomy were 2.67 +/- 0.49 (SD) and 2.50 +/- 0.55, respectively, versus 2.73 +/- 0.45 and 2.55 +/- 0.54 for the FFS. The mean flow feature score, comprising all views, was 2.67 +/- 0.45 (HHS) versus 2.72 +/- 0.48 (FFS). The P values for all above comparisons were >.05. Image quality of the FFS anatomic structures were, thus, not statistically different from the HHS. Although the color cosmetic was different for the HHS directional (nonvelocity) map, only 9% of 150 total findings (including structural abnormalities and flow features, none of which were critical) were missed, whereas the other 91% regurgitant, shunt, stenosis flow features or heart structure were imaged adequately by the HHS in this population. CONCLUSIONS: Implementing high-frequency transducers and programs optimized for tissue and flow imaging on the HHS should provide images of sufficient quality for targeted echocardiography examinations to determine the presence, absence, or status of congenital heart disease in newborns and young children.

Expression of the SET protein in testes of mice at different developmental stages.

SET is a multifunctional protein involved in regulating many biological processes of the cell cycle. It is also a regulator of steroidogenesis in the ovary. However, the expression of SET protein in testis, and its function, still remains ambiguous. In this study, we observed the expression of SET in the testes of mice at different developmental stages, and have discussed its potential function in regulating spermatogenesis and androgen production. Forty-eight male mice at different developmental stages (1 week old as the infancy group; 4 weeks old as the prepubertal group; 12 weeks old as the adult group; over 12 months old as the ageing group) were used. Cellular location of SET protein in the testes was observed by immuno-histochemistry. Expression levels of Set mRNA and SET protein were analyzed by quantitative polymerase chain reaction and Western blotting. SET protein was expressed in spermatogonial cells and spermatocytes; the highest level was mainly in haploid and tetraploid cells of the prepubertal and adult groups, and Leydig cells of the adult and ageing groups. There was a low expression in Sertoli cells. Expression of Set mRNA in the prepubertal group was significantly higher than that in the adult group (P < 0.05), while expression of SET protein was at the highest level in the adult group (P < 0.05). SET protein is mainly expressed in spermatogonial cells and spermatocytes, and poorly expressed in Sertoli cells, suggesting that it is involved in spermatogenesis. Expression of SET protein in Leydig cells suggests a possible role in steroidogenesis.