Biomedical subjects

Rong Yang

Publications and source records attributed to Rong Yang.

At least 19 recordsLinked to original sources

PubMed2026

CRISPR/Cas9 screening revealed BIRC6-AS1/BIRC6 mediates abiraterone resistance via NHEJ pathway-dependent A20 degradation in prostate cancer.

Abiraterone acetate is a standard-of-care therapy for prostate cancer (PCa). However, resistance frequently emerges, often characterized by the progression to AR-independent phenotypes. Employing a genome-wide CRISPR/Cas9 library screening strategy, we identified 523 long non-coding RNAs (lncRNAs) and 2,183 protein-coding genes as potential candidates associated with abiraterone resistance. Notably, a pair of sense-antisense genes, BIRC6-AS1/BIRC6, was identified as a significant contributor to abiraterone resistance, serving as a critical survival factor in AR-independent contexts. BIRC6-AS1 depletion led to a reduction in both the mRNA and protein levels of BIRC6. Moreover, depletion of either BIRC6-AS1 or BIRC6 enhanced the sensitivity of PCa cells to abiraterone in both in vitro and in vivo settings. Further investigation revealed that BIRC6-AS1 stabilized the mRNA of BIRC6 through interaction with ILF2. Suppression of either BIRC6-AS1 or BIRC6 attenuated non-homologous end joining (NHEJ) repair activity, resulting in the disassembly of 53BP1 foci at DNA damage sites and an increased accumulation of DNA damage, thereby exposing a vulnerability in AR-independent resistant cells. Mechanistically, BIRC6 interacted with A20 and facilitated the K48-linked ubiquitination and subsequent degradation of A20 at the K337 residue. Additionally, A20 knockdown effectively reversed the abiraterone sensitivity induced by BIRC6-AS1 depletion. Collectively, our study provides a landscape of lncRNAs and protein-coding genes associated with abiraterone resistance and suggests that targeting the BIRC6-AS1/BIRC6 axis represents a potential therapeutic strategy to eradicate AR-independent resistant tumors in prostate cancer.

Journal Article↗

PubMed2026

Genetically predicted CXCL16 expression is associated with Parkinson's disease risk and peripheral immune cell dysregulation: a two-sample mendelian randomization study.

BACKGROUND: Parkinson's disease (PD) is a progressive neurodegenerative disorder with limited disease-modifying therapies. PANoptosis, an integrated form of programmed cell death involving apoptosis, pyroptosis, and necroptosis, has been implicated in neuroinflammation-related neurodegeneration. However, the roles of PANoptosis-related genes in PD remain unclear. METHODS: We performed two-sample Mendelian randomization (MR) using cis-eQTL instruments from the eQTLGen Consortium for 30 PANoptosis-related genes, with PD GWAS data from Nalls et al. 2019 as the outcome. Instrumental variables were selected using a hierarchical strategy, with genome-wide significant cis-eQTLs as primary instruments and a relaxed threshold applied only for genes with fewer than three independent SNPs. Sensitivity analyses included MR-Egger, weighted median, MR-PRESSO, MR-RAPS, and leave-one-out analyses. SMR/HEIDI testing and two-step MR mediation using 731 peripheral immune traits were also performed. RESULTS: Genetically predicted higher CXCL16 expression was associated with increased PD risk (OR = 1.115, 95% CI 1.060-1.173, p = 2.4 × 10-5), while higher FADD expression was associated with reduced PD risk (OR = 0.861, 95% CI 0.790-0.939, p = 7.1 × 10-4). CASP1 and IFI27 were nominally significant and considered exploratory. Sensitivity analyses were directionally consistent, although MR-Egger estimates were imprecise. SMR/HEIDI supported CXCL16. Exploratory mediation analysis identified 63/66 candidate immune mediators after FDR correction. CONCLUSION: These findings provide MR-based genetic evidence linking CXCL16 expression to PD risk, with exploratory mediation through peripheral immune phenotypes. The CXCL16-immune cell-PD axis warrants further experimental validation.

Humans↗

PubMed2024

The association between vitamin D receptor gene polymorphism FokI and type 2 diabetic kidney disease and its molecular mechanism: a case control study.

BACKGROUND: The role of the vitamin D receptor single nucleotide polymorphism FOKI (VDR-FOKI) (rs2228570) in genetic susceptibility to type 2 diabetic kidney disease (T2DKD) remains uncertain. This study investigated the relationship between VDR-FOKI and T2DKD within the Chinese Plateau Han population and analyzed the underlying mechanisms. METHODS: A total of 316 subjects were enrolled, including 44 healthy adults, 114 individuals with type 2 diabetes mellitus (T2DM), and 158 patients with T2DKD. According to the 2023 American Diabetes Association Diabetes Guidelines, patients with T2DKD were categorized into low-medium-risk and high-risk groups based on estimates of glomerular filtration rate and urinary albumin-to-creatinine ratio. The VDR-FokI genotypes of all participants were identified using the Taqman probe and classified as homozygous mutant genotypes (C/C or FF), heterozygous mutant genotypes (C/T or Ff), and homozygous wild genotypes (T/T or ff). Plasma levels of malondialdehyde (MDA), glutathione (GSH), and superoxide dismutase activity (SOD) were assessed in T2DKD patients with FF and ff genotypes. Additionally, the levels of plasma VDR, GPX4, and P53 were determined using ELISA, while the relative expressions of VDR mRNA, GPX4 mRNA, and TP53 mRNA in whole blood were measured by RT-qPCR. RESULTS: The T2DM patients with the ff genotype exhibited a 2.93-fold increased likelihood of developing T2DKD compared to those with the FF genotype (ORadjusted = 2.93; 95% CI: 1.142-7.513). Additionally, they were 2.01 times more likely to develop T2DKD than individuals with the FF and Ff genotypes (ORadjusted = 2.01; 95% CI: 1.008-4.006). However, no significant differences in VDR-FokI genotype distribution were observed between the healthy control group and the T2DM group, as well as between the low-medium-risk and high-risk groups of T2DKD. Furthermore, T2DKD patients with the ff genotype had significantly higher plasma levels of MDA compared to those with the FF genotype. In contrast, plasma GSH and SOD content was significantly lower in the ff genotype patients (P < 0.05). Additionally, the GPX4 concentration in ff genotype patients was significantly lower than in FF genotype patients [14.88 (11.32,22.39) vs. 12.76 (8.55,13.75), P = 0.037]. Nevertheless, no statistically significant difference was observed in the expression of VDRmRNA, GPX4mRNA, TP53mRNA, plasma VDR, and plasma P53. CONCLUSIONS: The ff genotype of VDR-FokI is a risk factor for T2DKD, and the potential mechanism may be related to ferroptosis. However, It is not associated with T2DM or the progression of T2DKD.

Humans↗

PubMed2024

Functional analysis of a novel nonsense PPP1R12A variant in a Chinese family with infantile epilepsy.

BACKGROUND: Defects in PPP1R12A can lead to genitourinary and/or brain malformation syndrome (GUBS). GUBS is primarily characterized by neurological or genitourinary system abnormalities, but a few reported cases are associated with neonatal seizures. Here, we report a case of a female newborn with neonatal seizures caused by a novel variant in PPP1R12A, aiming to enhance the clinical and variant data of genetic factors related to epilepsy in early life. METHODS: Whole-exome and Sanger sequencing were used for familial variant assessment, and bioinformatics was employed to annotate the variant. A structural model of the mutant protein was simulated using molecular dynamics (MD), and the free binding energy between PPP1R12A and PPP1CB was analyzed. A mutant plasmid was constructed, and mutant protein expression was analyzed using western blotting (WB), and the interaction between the mutant and PPP1CB proteins using co-immunoprecipitation (Co-IP) experiments. RESULTS: The patient experienced tonic-clonic seizures on the second day after birth. Genetic testing revealed a heterozygous variant in PPP1R12A, NM_002480.3:c.2533 C > T (p.Arg845Ter). Both parents had the wild-type gene. MD suggested that loss of the C-terminal structure in the mutant protein altered its structural stability and increased the binding energy with PPP1CB, indicating unstable protein-protein interactions. On WB, a low-molecular-weight band was observed, indicating that the protein was truncated. Co-IP indicated that the mutant protein no longer interacted with PPP1CB, indicating an effect on the structural stability of the myosin phase complex. CONCLUSION: The PPP1R12A c.2533 C > T variant may explain the neonatal seizures in the present case. The findings of this study expand the spectrum of PPP1R12A variants and highlight the potential significance of truncated proteins in the pathogenesis of GUBS.

Female↗

PubMed2007

Identification of endogenous resolvin E1 and other lipid mediators derived from eicosapentaenoic acid via electrospray low-energy tandem mass spectrometry: spectra and fragmentation mechanisms.

Resolvin E1 (RvE1, 5S,12R,18R-trihydroxy-6Z,8E,10E,14Z,16E-eicosapentaenoic acid) is a novel anti-inflammatory lipid mediator recently found in humans, mice, and fish in vivo. To identify endogenous RvE1 and other eicosapentaenoic acid (EPA)-derived lipid mediators using electrospray low-energy collision-induced dissociation tandem mass spectrometry (MS/MS), the MS/MS product ion spectra of these compounds were correlated with their structures, and the MS/MS fragmentation mechanisms were studied. Deuterium labeling confirmed the proposed correlations and the fragmentation mechanisms. beta-cleavage was observed for RvE1, and beta and gamma cleavages were seen for leukotriene B5; however, alpha-cleavage was more common. The positions and numbers of hydroxyls and double bonds of these lipid mediators can be deduced from the MS/MS spectra. The MS/MS fragmentation generating chain-cut ions involved beta-ene, gamma-ene, or alpha-H-beta-ene rearrangement, depending on the specific structure. The m/z value of a detected chain-cut ion from RvE1 or from an EPA-derived product is equal to the corresponding hypothetical homolytic segment (cc, cm, mc, or mm) with the addition or extraction of up to two hydrogen atoms (H) from hydroxyls or an alpha-carbon; namely, the m/z value of an alpha-cleavage-generated ion is equal to [cc+H], [cm-2H], [mc-H], or [mm]. Wideband activation increased the signal intensities of chain-cut ions, and therefore was better for trace analysis of RvE1 in biological samples. RvE1, LTB5, PGE3, and other EPA-derived lipid mediators were found in trout brain or head-kidney via this approach on the basis of MS/MS spectra and fragmentation mechanisms. Negative ion electrospray low-collision-energy MS/MS spectra provide adequate data to elucidate and identify the structures of RvE1 and other EPA-derived lipid mediators at levels below a few picomoles in trout samples.

Animals↗

PubMed2006

Differential expression of neurotrophins in penises of streptozotocin-induced diabetic rats.

To explore the mechanism of diabetic erectile dysfunction, we studied the distribution of neurotrophins in the penises of diabetic rats, including nerve growth factor (NGF), brain derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), and neurotrophin-4 (NT-4). Male Sprague-Dawley rats were injected with 65 mg/kg streptozotocin to induce diabetes mellitus (DM). The control rats were raised as age-matched control. Eight weeks later, the intercavernous pressure (ICP) of the rats was measured after electrostimulation and before sacrifice. Each peeled penis was divided into 2 parts, one for immunohistochemistry and the other for Western blot analysis. The ICP of the DM group rats was significantly decreased as compared to the vehicle control rats. There were significantly more NGF-positive neurons in the penises of the diabetic rats than in those of the control rats, while the opposite results were observed for BDNF-positive neurons. In the Western blot analysis, the proteins of NGF, NT-3, and NT-4 were all increased, while that of BDNF was decreased in diabetic rats. This is the first study revealing the expression of NT-4 protein in cavernous tissue. The abnormal level of these 4 neurotrophins in cavernous tissue may be one of the factors of the pathogenesis of diabetic ED. The increase of neurotrophins may reflect the degree of cavernous tissue denervation and may represent a compensatory mechanism. The lesion of the retrograde axonal transport of the nerves caused by hyperglycemia may be related to this phenomenon.

Animals↗

PubMed2006

Conformational flexibility and strand arrangements of the membrane-associated HIV fusion peptide trimer probed by solid-state NMR spectroscopy.

The human immunodeficiency virus (HIV) fusion peptide (HFP) is the N-terminal apolar region of the HIV gp41 fusion protein and interacts with target cell membranes and promotes membrane fusion. The free peptide catalyzes vesicle fusion at least to the lipid mixing stage and serves as a useful model fusion system. For gp41 constructs which lack the HFP, high-resolution structures show trimeric protein and suggest that at least three HFPs interact with the membrane with their C-termini in close proximity. In addition, previous studies have demonstrated that HFPs which are cross-linked at their C-termini to form trimers (HFPtr) catalyze fusion at a rate which is 15-40 times greater than that of non-cross-linked HFP. In the present study, the structure of membrane-associated HFPtr was probed with solid-state nuclear magnetic resonance (NMR) methods. Chemical shift and intramolecular (13)CO-(15)N distance measurements show that the conformation of the Leu-7 to Phe-11 region of HFPtr has predominant helical conformation in membranes without cholesterol and beta strand conformation in membranes containing approximately 30 mol % cholesterol. Interstrand (13)CO-(13)CO and (13)CO-(15)N distance measurements were not consistent with an in-register parallel strand arrangement but were consistent with either (1) parallel arrangement with adjacent strands two residues out-of-register or (2) antiparallel arrangement with adjacent strand crossing between Phe-8 and Leu-9. Arrangement 1 could support the rapid fusion rate of HFPtr because of placement of the apolar N-terminal regions of all strands on the same side of the oligomer while arrangement 2 could support the assembly of multiple fusion protein trimers.

Amino Acid Sequence↗

PubMed2006

Resolvin D1, protectin D1, and related docosahexaenoic acid-derived products: Analysis via electrospray/low energy tandem mass spectrometry based on spectra and fragmentation mechanisms.

Resolvin D1 (RvD1) and protectin D1 (Neuroprotectin D1, PD1/NPD1) are newly identified anti-inflammatory lipid mediators biosynthesized from docosahexaenoic acid (DHA). In this report, the spectra-structure correlations and fragmentation mechanisms were studied using electrospray low-energy collision-induced dissociation tandem mass spectrometry (MS/MS) for biogenic RvD1 and PD1, as well as mono-hydroxy-DHA and related hydroperoxy-DHA. The loss of H2O and CO2 in the spectra indicates the number of functional group(s). Chain-cut ions are the signature of the positions and numbers of functional groups and double bonds. The observed chain-cut ion is equivalent to a hypothetical homolytic-segment (cc, cm, mc, or mm) with addition or extraction of up to 2 protons (H). The alpha-cleavage ions are equivalent to: [cc + H], with H from the hydroxyl through a beta-ene or gamma-ene rearrangement; [cm - 2H], with 2H from hydroxyls of PD1 through a gamma-ene rearrangement, or 1H from the hydroxyl and the other H from the alpha-carbon of mono-HDHA through an alpha-H-beta-ene rearrangement; [mc - H], with H from hydroxyl through a beta-ene or gamma-ene rearrangement, or from the alpha-carbon through an alpha-H-beta-ene rearrangement; or [mm] through charge-direct fragmentations. The beta-ene or gamma-ene facilitates the H shift to gamma position and alpha-cleavage. Deuterium labeling confirmed the assignment of MS/MS ions and the fragmentation mechanisms. Based on the MS/MS spectra and fragmentation mechanisms, we identified RvD1, PD1, and mono-hydroxy-DHA products in human neutrophils and blood, trout head-kidney, and stroke-injury murine brain-tissue.

Chromatography, High Pressure Liquid↗

PubMed2006

Bifendate treatment attenuates hepatic steatosis in cholesterol/bile salt- and high-fat diet-induced hypercholesterolemia in mice.

Effects of bifendate, a synthetic intermediate of schisandrin C (a dibenzocyclooctadiene derivative), on liver lipid contents were investigated in experimentally-induced hypercholesterolemia in mice. Hypercholesterolemia was induced by either chronic administration of cholesterol/bile salt or feeding a high-fat diet containing cholesterol and/or bile salt. Hepatic and serum total cholesterol levels were significantly increased (42-268% and 23-124%, respectively) in cholesterol or high-fat diet-treated mice, when compared with control animals receiving vehicle or normal diet. Hepatic triglyceride level was increased (up to 108%), but serum triglyceride level was significantly reduced by 23-63% in hypercholesterolemic mice. Daily administration of bifendate (0.03-1.0 g/kg, i.g.) for 4 days decreased hepatic levels of total cholesterol (9-37%) and triglyceride (10-37%) in hypercholesterolemic mice. Supplementing the high-fat diet with bifendate (0.25%, w/w) caused decreases in hepatic total cholesterol (25-56%) and triglyceride (22-44%) levels following 7 or 14 days of experiment, respectively, when compared with animals fed with high-fat diet not supplemented with bifendate. While fenofibrate treatment decreased both hepatic and serum lipid levels in hypercholesterolemic mice, bifendate treatment did not reduce serum lipid levels. Bifendate and fenofibrate caused an increase (10-41% and 59-98%, respectively) in hepatic index of hypercholesterolemic mice. The results indicate that bifendate treatment can invariably decrease hepatic (but not serum) lipid levels in various mouse models of hypercholesterolemia.

Animals↗

PubMed2006

Effect of iodine intake on thyroid diseases in China.

BACKGROUND: Iodine is an essential component of thyroid hormones; either low or high intake may lead to thyroid disease. We observed an increase in the prevalence of overt hypothyroidism, subclinical hypothyroidism, and autoimmune thyroiditis with increasing iodine intake in China in cohorts from three regions with different levels of iodine intake: mildly deficient (median urinary iodine excretion, 84 microg per liter), more than adequate (median, 243 microg per liter), and excessive (median, 651 microg per liter). Participants enrolled in a baseline study in 1999, and during the five-year follow-up through 2004, we examined the effect of regional differences in iodine intake on the incidence of thyroid disease. METHODS: Of the 3761 unselected subjects who were enrolled at baseline, 3018 (80.2 percent) participated in this follow-up study. Levels of thyroid hormones and thyroid autoantibodies in serum, and iodine in urine, were measured and B-mode ultrasonography of the thyroid was performed at baseline and follow-up. RESULTS: Among subjects with mildly deficient iodine intake, those with more than adequate intake, and those with excessive intake, the cumulative incidence of overt hypothyroidism was 0.2 percent, 0.5 percent, and 0.3 percent, respectively; that of subclinical hypothyroidism, 0.2 percent, 2.6 percent, and 2.9 percent, respectively; and that of autoimmune thyroiditis, 0.2 percent, 1.0 percent, and 1.3 percent, respectively. Among subjects with euthyroidism and antithyroid antibodies at baseline, the five-year incidence of elevated serum thyrotropin levels was greater among those with more than adequate or excessive iodine intake than among those with mildly deficient iodine intake. A baseline serum thyrotropin level of 1.0 to 1.9 mIU per liter was associated with the lowest subsequent incidence of abnormal thyroid function. CONCLUSIONS: More than adequate or excessive iodine intake may lead to hypothyroidism and autoimmune thyroiditis.

Adolescent↗

PubMed2006

Proton-transfer kinetics of photoexcited 7-hydroxy-1-naphthalenesulfonic acid in aqueous formamide solutions.

The monoanion of 7-hydroxy-1-naphthalenesulfonic acid (HNS) undergoes pseudo-first order dissociation and its conjugate base, second order protonation in the lowest excited singlet state. The proton transfer kinetics in water containing formamide up to a mole fraction of about 0.95 have been evaluated as a function of formamide concentration. At mole fractions above 0.95 of formamide, proton-transfer does not measurably occur. At mole fractions below 0.95, steady state and pulsed-source fluorimetries show the rate constant for dissociation to decrease exponentially with increasing mole fraction of formamide. This is believed to be due to penetration and disruption of the aqueous solvent cage of the HNS by formamide, resulting in impairment of the Grotthus proton-transfer mechanism.

Formamides↗

PubMed2006

Identification of differentially expressed genes in human heart with ventricular septal defect using suppression subtractive hybridization.

Ventricular septal defect (VSD) accounts for the largest number of birth congenital heart defects in human, but the genetic programs that control ventricular septation are poorly understood. To identify differentially expressed genes between ventricular septal defect and normal ventricular septum myocardium, we have undertaken suppression subtractive hybridization (SSH) and generated reciprocal cDNA collections of representative mRNAs specific to human heart with ventricular septal defect versus normal control. Following SSH, 1378 clones were sequenced and found to derive from 551 different genes. These predominately expressed genes included genes involved in energy metabolism, cell cycle and growth, cytoskeleton and cell adhesion, LIM protein, zinc finger protein, and development. It is anticipated that further study of genes identified will provide insights into their specific roles in the etiology of VSD, even in cardiac development, aging, and disease.

Adult↗

PubMed2006

Anti-inflammatory actions of neuroprotectin D1/protectin D1 and its natural stereoisomers: assignments of dihydroxy-containing docosatrienes.

Protectin D1, neuroprotectin D1 when generated by neural cells, is a member of a new family of bioactive products generated from docosahexaenoic acid. The complete stereochemistry of protectin D1 (10,17S-docosatriene), namely, chirality of the carbon-10 alcohol and geometry of the conjugated triene, required for bioactivity remained to be assigned. To this end, protectin D1/neuroprotectin D1 (PD1) generated by human neutrophils during murine peritonitis and by neural tissues was separated from natural isomers and subjected to liquid chromatography-tandem mass spectrometry and gas chromatography-mass spectrometry. Comparisons with six 10,17-dihydroxydocosatrienes prepared by total organic and biogenic synthesis showed that PD1 from human cells carrying potent bioactivity is 10R,17S-dihydroxy-docosa-4Z,7Z,11E,13E,15Z,19Z-hexaenoic acid. Additional isomers identified included trace amounts of Delta15-trans-PD1 (isomer III), 10S,17S-dihydroxy-docosa-4Z,7Z,11E,13Z,15E,19Z-hexaenoic acid (isomer IV), and a double dioxygenation product 10S,17S-dihydroxy-docosa-4Z,7Z,11E,13Z,15E,19Z-hexaenoic acid (isomer I), present in exudates. 18O2 labeling showed that 10S,17S-diHDHA (isomer I) carried 18O in the carbon-10 position alcohol, indicating sequential lipoxygenation, whereas PD1 formation proceeded via an epoxide. PD1 at 10 nM attenuated (approximately 50%) human neutrophil transmigration, whereas Delta15-trans-PD1 was essentially inactive. PD1 was a potent regulator of polymorphonuclear leukocyte (PMN) infiltration (approximately 40% at 1 ng/mouse) in peritonitis. The rank order at 1- to 10-ng dose was PD1 approximately PD1 methyl ester >> Delta15-trans-PD1 > 10S,17S-diHDHA (isomer I). 10S,17S-dihydroxy-docosa-4Z,7Z,11E,13E,15Z,19Z-hexaenoic acid (isomer VI) proved > or = PD1 in blocking PMN infiltration, but was not a major product of leukocytes. PD1 also reduced PMN infiltration after initiation (2 h) of inflammation and was additive with resolvin E1. These results indicate that PD1 is a potent stereoselective anti-inflammatory molecule.

Animals↗

PubMed2006

Intelligent inferencing and haptic simulation for Chinese acupuncture learning and training.

This paper presents an intelligent virtual environment for Chinese acupuncture learning and training using state-of-the-art virtual reality technology. It is the first step toward developing a comprehensive virtual human model for studying Chinese medicine. Students can learn and practice acupuncture in the proposed 3-D interactive virtual environment that supports a force feedback interface for needle insertion. Thus, students not only "see" but also "touch" the virtual patient. With high performance computers, highly informative and flexible visualization of acupuncture points of various related meridian and collateral can be highlighted to guide the students during training. A computer-based expert system using our newly proposed intelligent fuzzy petri net is designed and implemented to train the students to treat different diseases using acupuncture. Such an intelligent virtual reality system can provide an interesting and effective learning environment for Chinese acupuncture.

Acupuncture↗

PubMed2006

High doses of bifendate elevate serum and hepatic triglyceride levels in rabbits and mice: animal models of acute hypertriglyceridemia.

AIM: To investigate the effects of bifendate on serum and hepatic lipids level in rabbits and mice. METHODS: Animals were administered bifendate [powdered pill suspended in 0.5% sodium carboxymethylcellulose (CMC)] at increasing doses (0.25-1 g/kg, ig). Blood lipid and apolipoprotein levels were measured using commercially available assay kits. RESULTS: The treatment of rabbits with a single dose of bifendate (0.3 g/kg) caused a time-dependent and biphasic change in serum triglyceride (TG) levels, with the value reaching a maximum (3-fold increase compared to the baseline value) between 24 and 36 h post-dosing. When mice were orally treated with bifendate (0.25-1 g/kg), serum TG levels increased by 39%-76% and 14%-39% at 24 and 48 h post-dosing, respectively. When given at daily doses of 0.25 and 1 g/kg for 4 d, bifendate increased serum TG levels (56%-79%), with concomitant elevations in apolipoprotein A-I and apolipoprotein B levels at 24 h after the last dosing. TG levels were also increased (11%-43%) in liver samples of mice receiving single or multiple doses of bifendate. However, bifendate treatment caused slight reductions in serum and hepatic total cholesterol levels (9%-13%). The hypertriglyceridemia induced by bifendate was ameliorated by fenofibrate but not inositol nicotinate treatment in mice. CONCLUSION: The findings suggest that bifendate treatment at high oral doses can cause an acute elevation in serum and hepatic TG levels.

Animals↗

PubMed2006

[Construction and utilization of the prognostic model of serous ovarian adenocarcinoma].

OBJECTIVE: To analyze the related factors with prognosis in patients with serous ovarian adenocarcinoma and to set up a prognostic model of serous ovarian adenocarcinoma. METHODS: The clinical, pathological and follow-up data of 104 cases with serous ovarian adenocarcinoma were retrospectively analyzed. Kaplan-meier univariate analysis was used to screen the prognostic factors; COX univariate and multivariate analyses were used to determine the risk coefficient of each factors and different layers in each factor. Pearson rank correlation was used to reject the influence of different factors with each other. And the prognostic model of serous ovarian adenocarcinoma was set up based on the result of the above study, which could be used to deduce the survival probability of patients with serous ovarian adenocarcinoma. RESULTS: International Federation of Gynecology and Obstetrics (FIGO) stage (P = 0.0029), histological grade (P = 0.0054), residual disease (P = 0.0000), metastasis of lymph nodes (P = 0.0000) and chemotherapy (P = 0.0000) were the related factors of prognosis in patients with serous ovarian adenocarcinoma, of which FIGO stage was the most important one, followed sequentially by histological grade, metastasis of lymph node, residual disease and chemotherapy (the independent risk coefficient of each factor was 1.3392, 0.9206, 0.7071, 0.6004, 0.4985 in sequence). We set up a prognosis model according to the prognostic index of each factors. The effect of chemotherapy and residual disease on prognosis could be quantified by this model, and the higher the score, the lower the survival probability of patients. CONCLUSIONS: FIGO stage, histological grade, residual disease, metastasis of lymph nodes and chemotherapy are important prognostic factors of serous ovarian adenocarcinoma. This model can be used to estimate the prognosis of patients with serous ovarian adenocarcinoma, and the effect of both chemotherapy and residual disease on the prognosis could be quantified by the model.

Adult↗

PubMed2005

Scanning tunneling microscopy and surface simulation of zinc-blende GaN(001) intrinsic 4x reconstruction: linear gallium tetramers?

Scanning tunneling microscopy images confirm electron diffraction studies that the zinc-blende GaN(001)-4x reconstruction consists of rows aligned along [110] with a spacing along [110] of 4a. Dual-bias imaging shows a 180 degree shift of the corrugation maximum position between the profiles of empty and occupied states, in agreement with surface simulations based on the 4 x 1 linear tetramer model of Neugebauer et al. [Phys. Rev. Lett. 80, 3097 (1998)]. Electronic structure calculations predict a surface band gap of 1.1 eV, close to the measured value of 1.14 eV and the previously predicted value (1.2 eV). Despite the successes of this model, high-resolution images reveal an unexpected 3x periodicity (not seen in diffraction) along the [110] row direction, indicating the need for a 4 x 3 model, and putting into question the existence of linear Ga tetramers.

Journal Article↗

PubMed2005

Comparison between Generalized-Born and Poisson-Boltzmann methods in physics-based scoring functions for protein structure prediction.

Continuum solvent models such as Generalized-Born and Poisson-Boltzmann methods hold the promise to treat solvation effect efficiently and to enable rapid scoring of protein structures when they are combined with physics-based energy functions. Yet, direct comparison of these two approaches on large protein data set is lacking. Building on our previous work with a scoring function based on a Generalized-Born (GB) solvation model, and short molecular-dynamics simulations, we further extended the scoring function to compare with the MM-PBSA method to treat the solvent effect. We benchmarked this scoring function against seven publicly available decoy sets. We found that, somewhat surprisingly, the results of MM-PBSA approach are comparable to the previous GB-based scoring function. We also discussed the effect to the scoring function accuracy due to presence of large ligands and ions in some native structures of the decoy sets.

Chemical Phenomena↗