A Modified Double Eyelid Plastic Surgery Method: Continuous Buried Suture Method Accompanied by Simultaneous Correction of Mild Blepharoptosis.

BACKGROUND: Double eyelid surgery with a buried suture is a popular plastic surgery procedure in Asia owing to the relatively minor scarring and quick recovery associated with it. In this article, we present a new approach involving a continuous single-loop buried suture method, which expands the operating site to the conjunctiva and the aponeurosis-Müller's muscle complex. METHODS: The medical records of 42 patients (80 eyes) who underwent double-eyelid blepharoplasty were retrospectively reviewed. We performed double-eyelid blepharoplasty with a single-knot continuous buried suture method, along with the resection of a small piece of the orbicularis oculi muscle. The formation of a double eyelid was achieved through traction of the aponeurosis-Müller's muscle complex from the medial conjunctiva and penetration of the upper eyelid. RESULTS: The majority of patients achieved the expected cosmetic effect of double eyelid formation after the procedure. In the subsequent follow-up period of 2-30 months, no complications, such as loosing or sagging of the double eyelid or granuloma formation, occurred. The mean recovery time ranged between one and 6 weeks. The pre-operative margin reflex distance (MRD1) was 2.36 ± 0.61 mm, and the post-operative MRD1 was 3.72 ± 0.63 mm, (p < 0.001). The Wilcoxon signed rank test was used for nonparametric, paired comparisons. CONCLUSIONS: We proposed a modified technique involving a continuous buried suture method to create a better cosmetic effect through the formation of a double eyelid and simultaneous correction of mild blepharoptosis. This modified procedure is simple, fast, and effective, with limited adverse effects. LEVEL OF EVIDENCE IV: This journal requires that authors assign a level of evidence to each article. For a full description of these evidence-based medicine ratings, please refer to the Table of Contents or the online Instructions to Authors www.springer.com/00266 .

Glucocorticoids accelerate maturation of the heme pathway in fetal liver through effects on transcription and DNA methylation.

Glucocorticoids are widely used in threatened preterm labor to promote maturation in many organ systems in preterm babies and have significant beneficial effects on morbidity and mortality. We performed transcriptional profiling in fetal liver in a rat model of prenatal glucocorticoid exposure and identified marked gene expression changes in heme biosynthesis, utilization, and degradation pathways in late gestation. These changes in gene expression associated with alterations in DNA methylation and with a reduction in hepatic heme concentration. There were no persistent differences in gene expression, DNA methylation, or heme concentrations at 4 weeks of age, suggesting that these are transient effects. Our findings are consistent with glucocorticoid-induced accelerated maturation of the haematopoietic system and support the hypothesis that glucocorticoids can drive changes in gene expression in association with alterations in DNA methylation.

Maternal obesity has little effect on the immediate offspring but impacts on the next generation.

Maternal obesity during pregnancy has been linked to an increased risk of obesity and cardiometabolic disease in the offspring, a phenomenon attributed to developmental programming. Programming effects may be transmissible across generations through both maternal and paternal inheritance, although the mechanisms remain unclear. Using a mouse model, we explored the effects of moderate maternal diet-induced obesity (DIO) on weight gain and glucose-insulin homeostasis in first-generation (F1) and second-generation offspring. DIO was associated with insulin resistance, hyperglycemia and dyslipidemia before pregnancy. Birth weight was reduced in female offspring of DIO mothers (by 6%, P = .039), and DIO offspring were heavier than controls at weaning (males by 47%, females by 27%), however there were no differences in glucose tolerance, plasma lipids, or hepatic gene expression at 6 months. Despite the relative lack of effects in the F1, we found clear fetal growth restriction and persistent metabolic changes in otherwise unmanipulated second-generation offspring with effects on birth weight, insulin levels, and hepatic gene expression that were transmitted through both maternal and paternal lines. This suggests that the consequences of the current dietary obesity epidemic may also have an impact on the descendants of obese individuals, even when the phenotype of the F1 appears largely unaffected.

Multigenerational programming in the glucocorticoid programmed rat is associated with generation-specific and parent of origin effects.

Exposure to an adverse early life environment is associated with increased cardio-metabolic disease risk, a phenomenon termed "programming." The effects of this are not limited to the exposed first (F1) generation but can be transmissible to a second generation (F2) through male and female lines. Using a three generation animal model of programming by initial prenatal glucocorticoid overexposure we have identified effects on fetal and placental weight in both the F1 and F2 offspring. However, the expression of candidate imprinted genes in the fetus and placenta differed between the F1 and F2, with marked parent-of-origin effects in F2. Since DNA methylation at imprinted genes is maintained at fertilization, they are potential templates for the transmission of programming effects across generations. Although we detected alterations in DNA methylation at differentially methylated regions (DMRs) of the key prenatal growth factor Igf2 in F1 and F2 fetal liver, the changes in DNA methylation at these DMRs do not appear to underlie the transmission of effects on Igf2 expression through sperm. Thus, multigenerational programming effects on birth weight and disease risk is associated with different processes in F1 and F2. These findings have implications for the pathogenesis and future attempts to stratify therapies for the "developmental component" of cardiometabolic disease.

Intergenerational transmission of programmed effects: public health consequences.

Epidemiological studies have shown that the environment experienced in early life can 'programme' susceptibility to later disease. Furthermore, there is increasing evidence that these effects can be transmissible to subsequent generations through non-genomic mechanisms, with profound implications for human populations. Several mechanisms can underpin the intergenerational transmission of the programmed phenotype, including persistence of the abnormal environment across generations, maternal effects and the transmission of epigenetic information through the germline. In this review, we discuss the evidence for these mechanisms in human and animal studies and the potential importance of this field for human health.

Discovery of a novel family of SARS-CoV protease inhibitors by virtual screening and 3D-QSAR studies.

The severe acute respiratory syndrome-associated coronavirus (SARS-CoV) 3C-like protease (3CL(pro) or M(pro)) is an attractive target for the development of anti-SARS drugs because of its crucial role in the viral life cycle. In this study, a compound database was screened by the structure-based virtual screening approach to identify initial hits as inhibitors of SARS-CoV 3CL(pro). Out of the 59,363 compounds docked, 93 were selected for the inhibition assay, and 21 showed inhibition against SARS-CoV 3CL(pro) (IC(50)