In this study, a novel laccase gene (Lcc1) from Ganoderma tsugae was isolated and its functions were characterized in detail. The results showed that Lcc1 has the highest expression activity during mycelium development and fruit body maturation based on the analysis of Lcc1 RNA transcripts at different developmental stages of G. tsugae. To investigate the exact contribution of Lcc1 to mycelium and fruit body development in G. tsugae, Lcc1 transgenic strains were constructed by targeted gene replacement and over-expression approaches. The results showed that the lignin degradation rate in Lcc1 deletion mutant was much lower than the degradation efficiency of the wild-type (WT), over-expression and rescue strains. The lignin degradation activity of G. tsugae is dependent on Lcc1 and the deletion of Lcc1 exerted detrimental influences on the development of mycelium branch. Furthermore, the study uncovered that Lcc1 deletion mutants generated much shorter pale grey fruit bodies, suggesting that Lcc1 contributes directly to pigmentation and stipe elongation during fruit body development in G. tsugae. The information obtained in this study provides a novel and mechanistic insight into the specific role of Lcc1 during growth and development of G. tsugae.

ObjectiveThe aim of this study is to investigate the relationship between anti-Müllerian hormone (AMH) and parameters related to polycystic ovary syndrome (PCOS). MethodsWe measured serum AMH levels in 100 women with PCOS by Rotterdam European Society for Human Reproduction and Embryology criteria. We conducted somatometry, blood test and transvaginal or transrectal ultrasound test. We compared and analyzed AMH and parameters in terms of insulin resistance according to PCOS related phenotypes. We divided phenotypes into four groups by polycystic ovarian morphology (PCOM) and hyperandrogenemia (total testosterone [TT], free testosterone [fT]). ResultsAMH levels ranged from 4.1 to 21.0 ng/mL and the mean level was 10.4 ± 4.1 ng/mL. Signifi cant differences in parameters of insulin resistance were not observed among low (4 to 8 ng/mL), moderate (8 to 12 ng/mL), and high (>12 ng/mL) levels of AMH. Significant differences in AMH were not observed among groups according to PCOS related phenotypes. Weight, body mass index, waist-hip ratio, TT, fT, sex hormone binding globulin, 2-hour insulin and homeostasis model assessment of insulin resistance index were different signifi cantly according to PCOS related phenotypes. TT, ovarian volume and follicle number were positively correlated with AMH. ConclusionIncreased serum AMH levels in PCOS are correlated with TT and PCOM.

Background: To investigate whether obesity with or without metabolic syndrome is prospectively associated with coronary artery calcium (CAC) progression and incident cardiovascular disease events. Methods: A total of 1730 participants from the CARDIA study (Coronary Artery Risk Development in Young Adults) were included (age, 40.1±3.6 years; 38.3% men), who completed computed tomography of CAC at baseline (year 15: 2000–2001) and follow-up (year 20 or 25). Metabolically healthy obesity (MHO) was defined as body mass index≥30 kg/m 2 without any metabolic syndrome components in our main analysis. Sensitivity analyses were conducted for several conditions characterizing 4 metabolic phenotypes. Results: During a mean follow-up of 9.1 years, 439 participants had CAC progression. MHO subjects had a significantly higher risk of CAC progression than their metabolically healthy normal weight counterparts (adjusted hazard ratios [95% CIs] from 1.761 [1.369–2.264] to 2.047 [1.380–3.036]) depending on the definition of MHO adopted. Obesity with unhealthy metabolic profile remained the highest significant risk of CAC progression and cardiovascular disease events whatever the definitions adopted for metabolically unhealthy status. Up to 60% of participants with MHO converted to metabolically unhealthy obesity from year 15 to year 20 or year 25. Further sensitivity analysis showed that MHO throughout carried a similar risk of incident cardiovascular disease events compared with metabolically healthy normal weight throughout. Conclusions: Different metabolic phenotypes of obesity beginning at a young age exhibit distinct risks of CAC progression and subsequent cardiovascular disease events in later midlife. MHO represents an intermediate phenotype between metabolically low- to high-risk obese individuals. REGISTRATION: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT00005130.

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Background & Aims Individuals with high blood pressure (BP) have varying risks of cardiovascular events due to other coexisting factors. We aimed to identify the predictors of long-term absence of coronary artery calcium (CAC) in individuals with high BP, which is an indicator of healthy arterial aging and can guide preventive strategies. Methods We analyzed data from participants with high BP (≥120/80 mm Hg) in the Multi-Ethnic Study of Atherosclerosis who had baseline CAC = 0 and underwent a second CAC scanning after 10 years. We used multivariable logistic regression to evaluate the association between various risk factors for atherosclerotic cardiovascular disease (ASCVD) and long-term CAC = 0. We also calculated the area under the receiver operating characteristic curve (AUC) to predict the phenotype of healthy arterial aging in this population. Results We included 830 participants (37.6% male, mean ± SD age of 59.4 ± 8.7 years). During follow-up, 46.5% of participants ( n = 386) had CAC = 0, and they were younger and had fewer metabolic syndrome components. Adding ASCVD risk factors to the demographic model (age, sex, and ethnicity) moderately increased the predictive value for long-term CAC = 0 (AUC: demographic model + ASCVD risk factors vs. demographic model alone, 0.653 vs. 0.597, p < .001; category net reclassification improvement = 0.104, p = .044; integrated discrimination improvement = 0.040, p < .001). Conclusion In individuals with high BP and initial CAC = 0, over 40% maintained CAC = 0 during a 10-year follow-up, which was associated with fewer ASCVD risk factors. These findings may have implications for preventive strategies in individuals with high BP. Clinical Trial registration number: The MESA was registered at clinical trials. gov as NCT 00005487. KEY MESSAGES Nearly half (46.5%) of individuals with high blood pressure (BP) maintained a long-term absence of coronary artery calcium (CAC) during a 10-year follow-up, and this was associated with a 66.6% lower risk of atherosclerotic cardiovascular disease (ASCVD) events compared to those who developed incident CAC. Individuals with high BP, who are usually assumed to have an increased risk of ASCVD, exhibit significant heterogeneity in their ASCVD risk; those who maintain CAC = 0 have a lower ASCVD risk. Adding overall ASCVD risk factors to demographic information resulted in a moderate improvement in predicting long-term CAC = 0.

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Objective: To investigate the association between preterm birth and cytokine genes (IFN-γ, interleukin (IL)-10) in intrauterine infection and enzyme gene (CYP1A1) in oxidative stress response. Methods: This study involved a case-control study conducted at Ewha Womans University Hospital in Seoul, Korea. Subjects with preterm deliveries (<37 weeks of gestation) and normal controls with term deliveries (≥37 weeks of gestation) were selected from gravidas who had undergone prenatal examinations in the hospital and were followed until infant delivery. The weight, height, and blood samples of each participants were obtained according to standard protocols. We included subjects who gave birth to a singleton infant and had a gestational age between 24 and 42 weeks. Mutiple births, stillbirths, and congenital anomalies were excluded. Finally, 164 gravidas with preterm births and 305 normal controls with term deliveries were enrolled in the present study. Results: Preterm delivery group and term delivery group had significant difference in gestational age and neonatal body weight (P<0.0001).There were no statistically significant association between preterm birth and IFN-γ, IL-10, CYP1A1 genes (P>0.05).

Objective: To determine the accuracy and usefulness of prenatal ultrasonographic and molecular genetic diagnosis in detection of skeletal dysplasia. Methods: This study was based upon data of the 17 cases of skeletal dysplasia diagnosed by prenatal ultrasound and 7 cases by molecular diagnosis performed among the 17 cases and the 2 cases who has familial skeletal dysplasia by molecular diagnosis during the first trimester at Ewha and Eulji University from March 1998 to August 2005. A final diagnosis was sought on the basis of radiographic studies, molecular testing, or both. Results: The mean gestational age at diagnosis was 24.9 weeks (range, 17 to 35 weeks). Nine cases were diagnosed before 24 weeks. A final diagnosis was obtained in 16 cases (94.1%). There was 1 false-positive diagnosis. The antenatal diagnosis was correct in 14 cases (82.4%). The 8 cases were prenatally confirmed and 1 case was postpartum confirmed using molecular genetic testing and accurate antenatal diagnosis and prediction was done. We were able to rule out skeletal dysplasia through chorionic villus sampling during the first trimester in the 2 cases with the family history with skeletal dysplasia. Conclusion: Prenatal diagnosis of skeletal dysplasia can be a considerable diagnostic challenge. However, skeletal dysplasia is correctly diagnosed on the basis of prenatal meticulous ultrasound and antenatal prediction of lethality was highly accurate. Using prenatal molecular diagnosis, skeletal dysplasia can be diagnosed at first trimester of pregnancy and nonlethal skeletal dysplasia can be confirmed when prenatal ultrasound was nonspecific.