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Biomedical subjects

Yong Jiang

Publications and source records attributed to Yong Jiang.

At least 19 recordsLinked to original sources

Stage shift, histological differentiation, and survival patterns of lung squamous cell carcinoma versus adenocarcinoma in low-dose CT screening.

BACKGROUND: Whether LDCT-associated stage shift translates into similar survival patterns across lung cancer histologies remains uncertain. We compared stage shift, histological differentiation, tumor characteristics, and survival between lung squamous cell carcinoma (LUSC) and adenocarcinoma (LUAD) in the National Lung Screening Trial. METHODS: Among participants diagnosed with LUSC or LUAD, stage distribution and histological differentiation were compared between LDCT and chest X-ray (CXR) arms. Survival among diagnosed cases was measured from randomization. Multivariable models tested screening arm-by-histology interactions. Screen-detected LDCT tumors were compared by histology. RESULTS: During 6.5 years of median follow-up, 498 LUAD and 249 LUSC cases were diagnosed in the LDCT arm, and 374 and 212, respectively, were diagnosed in the CXR arm. LDCT was associated with higher odds of stage I disease for LUAD (adjusted odds ratio [aOR], 2.48; 95% CI 1.88-3.28) and LUSC (aOR, 1.71; 95% CI 1.17-2.48), without significant interaction (P&#x202f;=&#x202f;0.116). LDCT was associated with lower hazard of lung cancer-specific death among diagnosed LUAD cases (adjusted hazard ratio [aHR], 0.54; 95% CI 0.43-0.66), but not among diagnosed LUSC cases (aHR, 1.04; 95% CI 0.78-1.39; P for interaction<0.001). LUSC had lower screening sensitivity, more frequent detection in annual screening rounds, greater prediagnostic tumor size increase, and fewer well-differentiated stage I tumors than LUAD. CONCLUSION: LDCT was associated with stage shift for both subtypes, but favorable survival patterns among diagnosed cases were mainly observed for LUAD. Lower screening sensitivity, greater prediagnostic tumor size increase, and poorer histological differentiation may help explain why stage shift did not translate into similar survival patterns for LUSC. TRIAL REGISTRATION: ClinicalTrials.gov, NCT00047385.

Humans↗

Gain-of-function PPM1D mutations attenuate ischemic stroke.

Identification of genetic aberrations in stroke, the second leading cause of death worldwide, is of paramount importance for understanding the disease pathogenesis and generating new therapies. Whole-genome sequencing from 10,241 ischemic stroke patients identified eight patients carrying gain-of-function mutations on coding variants in the protein phosphatase magnesium-dependent 1 &#x3b4; (PPM1D) gene. Patients carrying PPM1D mutations exhibit better stroke-related clinical phenotypes, including improvements in peripheral inflammation, fibrinogen, low-density lipoprotein, cholesterol&#xa0;and plateletcrit level. Experimental brain ischemia in Ppm1d-deficient (Ppm1d-/-) mice resulted in enlarged lesions and pronounced neurological impairments. Spatial transcriptomics revealed a distinct Ppm1d-associated gene expression pattern, indicating disrupted endothelial homeostasis during ischemic brain injury. Proteomic analysis demonstrated that differentially expressed proteins in primary brain endothelial cells from Ppm1d-/- mice were significantly enriched in the peroxisome proliferator-activated receptors (PPARs)-mediated metabolic signaling. Mechanistically, Ppm1d deficiency promoted aberrant fatty acid &#x3b2;-oxidation and increased oxidative stress, which impaired endothelial cell function through the PPAR&#x3b1; pathway. A small molecule, T2755, was identified to engage Trp427 and stabilize PPM1D, thereby mitigating ischemic brain injury in mice. Collectively, we find that PPM1D protects against ischemic brain injury and validates its pharmacological stabilizer T2755 as a promising therapy for ischemic stroke. Gain-of-function PPM1D mutations attenuate ischemic cerebral injury. Whole-genome sequencing data of 10,241 ischemic stroke patients from the Third Chinese National Stroke Registry (CNSR-III) identified eight patients with gain-of-function mutations in the protein phosphatase magnesium-dependent 1 &#x3b4; (PPM1D) gene (17q23.2). These mutation carriers displayed improved peripheral inflammation,&#xa0;decreased&#xa0;fibrinogen, low-density lipoprotein, cholesterol&#xa0;and plateletcrit level. Ppm1d-deficient (Ppm1d-/-) mice exhibited exacerbated stroke outcomes, characterized by enlarged infarct volumes, disrupted cerebrovascular architecture, and enhanced neuro-inflammation. Mechanistically, Ppm1d deficiency induced the disturbance of endothelial fatty acid metabolism involving the PPAR&#x3b1; pathway. Through integrated computational modeling, virtual screening, and in vitro validation, T2755 was identified as a small molecule PPM1D stabilizer. Pharmacological PPM1D stabilization with T2755 significantly attenuated ischemic brain injury in murine models.

Aged↗

KSHVbook: An Information-Sharing Database for Kaposi's Sarcoma-Associated Herpesvirus.

Kaposi's sarcoma-associated herpesvirus (KSHV) is a double-stranded DNA virus belonging to the &#x3b3;-herpesvirus subfamily. KSHV is the causative agent of Kaposi's sarcoma (KS), primary effusion lymphoma (PEL), multicentric Castleman's disease (MCD), and KSHV inflammatory cytokine syndrome (KICS). Since its discovery, research on KSHV has rapidly progressed, but existing information platforms relatively lack comprehensiveness and do not provide efficient analysis tools tailored for KSHV. To further promote the research on KSHV more effectively, we have developed KSHVbook (http://www.kshvbook.com), a specialized information-sharing database dedicated to KSHV. This platform offers extensive information on genes, coding sequences, proteins, and the gene regulatory region. Besides, the KSHVbook includes about 35&#x2009;010 transcription factor binding sites (TFBSs), 342&#x2009;010 pairs of KSHV miRNA-host target gene relationships, protein structures predicted by AlphaFold3, qPCR primers, and so on. We also develop analytical tools for viral genome regions, TFBSs, and KSHV miRNA target genes to discover previously unknown biological functions of KSHV. These analytical tools can effectively identify the potential regulatory relationships between host transcription factors and viral genes. Overall, this platform provides a centralized data resource for KSHV research by integrating multiple databases, offering accessible analysis tools, and simplifying data acquisition. The KSHVbook will continue to be updated, and more features can be found on the website.

Herpesvirus 8, Human↗

Equilibrium distributions of dipalmitoyl phosphatidylcholine and dilauroyl phosphatidylcholine in a mixed lipid bilayer: atomistic semigrand canonical ensemble simulations.

Conventional molecular dynamics (MD) simulations are seriously limited by the slow rate of diffusive mixing in their ability to predict lateral distributions of different lipid types within mixed-lipid bilayers using atomistic models. A method to overcome this limitation, using configuration-bias Monte Carlo (MC) "mutation" moves to transform lipids from one type to another in dynamic equilibrium, is demonstrated in binary fluid-phase mixtures of lipids whose tails differ in length by four carbons. The hybrid MC-MD method operates within a semigrand canonical ensemble, so that an equilibrium composition of the mixture is determined by a constant difference in chemical potential (Delta(mu)) chosen for the components. Within several nanoseconds, bilayer structures initiated as pure dipalmitoyl phosphatidylcholine (DPPC) or pure dilauroyl phosphatidylcholine (DLPC) converge to a common composition and structure in independent simulations conducted at the same Delta(mu). Trends in bilayer thickness, area per lipid, density distributions across the bilayer, and order parameters have been investigated at three mixture compositions and compared with results from the pure bilayers at 323 K. The mixtures showed a moderate increase in DPPC acyl tail sites crossing the bilayer midplane relative to pure DPPC. Correlations between lateral positions of the two lipid types within or across the bilayer were found to be weak or absent. While the lateral distribution is consistent with nearly ideal mixing, the dependence of composition on Delta(mu) indicates a positive excess free energy of mixing.

1,2-Dipalmitoylphosphatidylcholine↗

Effect of APOE polymorphisms on early responses to traumatic brain injury.

To investigate the relationship between apolipoprotein E (APOE) polymorphisms and the severity of traumatic brain injury (TBI) in acute stage in the cohort of mainland Chinese patients. We prospectively identified admissions to the two neurosurgical departments for head injury. A total of 110 subjects with TBI (80 males and 30 females, with mean age of 43.87 years) were enrolled from December 2003 to May 2004, and demographic and clinical data were collected. Venous blood was collected from patients with TBI on admission to determine the APOE genotype polymorphisms. The APOE genotyping was performed by means of PCR-RFLP. The deterioration of patients' condition in acute stage (<7 days after TBI) was judged by either of following criteria: decrease of GCS, increase in hematoma volume or delayed hematoma both detected by repeated CT scanning. Chi2-test and logistic regression analyses were done by SPSS. The distributions of APOE genotypes and alleles matched Hardy-Weinberg law. In 110 Chinese patients, 19 subjects presented with deteriorated clinical condition after hospitalization, and seven of 17 patients with APOE epsilon4 (41.2%) had a deteriorated condition which was significantly different from those without APOE epsilon4 (12 of 93 patients, 12.9%, P=0.01). However, neither the presence of epsilon2 nor of epsilon3 was significantly different from those absent of it (P>0.05). Logistic regression analyses showed that APOE epsilon4 was a risk factor (OR=4.836, P=0.011, 95% CI 1.443-16.208) to predispose to clinical deterioration after adjusting for patient age, sex, smoking or not, alcohol-drinking or not, injury severity, injury mechanisms, treatments, and pattern of TBI. This finding suggests that the patients with APOE epsilon4 predispose to clinical deterioration in acute phase after TBI and APOE polymorphisms play a role in early responses to TBI.

Adult↗

Role of AP1 element in the activation of human eNOS promoter by lysophosphatidylcholine.

Human endothelial nitric oxide synthase (eNOS) plays a crucial role in maintaining blood pressure homeostasis and vascular integrity. It, therefore, is very essential to elucidate the regulation of it. In the current study, a red fluorescent protein (RFP) reporter system containing human eNOS promoter was first constructed, being characteristics of real time morphologic and quantitative analysis for the same sample. It was observed by DNA sequence deletion that 68% of the basal activity of the promoter was controlled by the region from -1 to -166 bp, and 32% of it was dependent on the region from -1,033 to -1,600 bp. The mutation of SSRE element (-999 to -994 bp) and wild-type SSRE decoy oligodeoxynucleotides (ODN) did not alter the basal activity and the stimulating activity by lysophosphatidylcholine (LPC). The mutation of upstream AP1 element (-1,530 to -1,524 bp) did not affect the basal activity, but resulted in near 30% reduction in the stimulating activity by LPC. Moreover, wild-type AP1 decoy ODN also remarkably attenuated it. It was proved by EMSA analysis that LPC indeed enhanced the activity of AP1 transcriptional factor binding to AP1 element. However, the role of AP1 was dependent on the presence of SP1, which was proved by the combining mutation of AP1 with SP1. The mutation of downstream AP1 element (-662 to -656 bp) had no influence on the basal and stimulating activities by LPC. These results strongly suggest that the main functional region of the promoter is from -1 bp to -166 bp, that the upstream AP1 participates in the activation of the promoter by LPC on the premise of the presence of SP1, and that the downstream AP1 and SSRE do not involve the basal and stimulating activity by LPC.

Animals↗

Computer simulation model on ultrasonic myocardial backscatter.

Myocardial ultrasonic tissue characterization with integrated backscatter (IB) has been studied in recent years. To evaluate the dynamic characters of the myocardium, dynamic tracing of each unit volume of myocardium is a key point. Thus, a 2D CVIB imaging algorithm based on an auto-tracing method was developed in our previous work. Where, an auto-tracking method was used in CVIB-weighted images so that the POI in each frame throughout the cardiac cycle is automatically traced to reflect the real myocardial tissue movement. It is necessary to validate the auto-tracing method. However, at present there are no appropriate models to support the process. In order to validate the auto-tracing method, two myocardium models have been established to simulate the short and long axis view of echocardiography. The motions of partially ischemic myocardium have been simulated. The models have been used to validate the 2D CVIB imaging methods in the detection of myocardial ischemia. The simulation results show that the auto-tracing algorithm is effective. The model developed in this work provides a tool for studying and developing technologies in myocardial behavior.

Algorithms↗

[High mobility group box-1 protein activates endothelial cells to produce cytokines and has synergistic effect with lipopolysaccharide in inducing interleukin-6 release].

OBJECTIVE: To observe the effects of high mobility group box 1 (HMGB1) protein on the release of cytokines of human umbilic vein endothelial cells (HUVECs) and the expression of interleukin-6 (IL-6) induced by lipopolysaccharide (LPS). METHODS: HUVECs were cultured and then divided into the following groups. (1) Recombinant HMGB1 protein of the terminal concentration of 15 ng/ml was added into the culture fluid of HUVECs, 24 hours later the supernatant was collected to detect the levels of granulocyte/macrophage colony stimulating factor (GM-CSF), interferon-gamma (IFN-gamma), and interleukin-10, IL-12, IL-1beta, IL-2, IL-4, IL-6, and IL-8, by using LiquiChip system. (2) HMGB1 protein of the terminal concentrations of 3, 15, or 75 ng/ml was added into the culture fluid of the HUVECs, 24 hours later the supernatants were collected to detect the level of IL-6. (3) HMGB1 protein of the terminal concentration of 15 ng/ml was added into the culture fluid of HUVECs, 1, 3, 6, 12, and 24 hours after the stimulation the supernatant was collected to detect the level of IL-6. (4) The culture fluid of HUVECs was added with HMGB1 protein of the terminal concentration of 15 ng/ml and/or LPS of the concentration of 10 ng/ml, 24 hours later the supernatant was collected to detect the level of IL-6. Culture fluid not added with HMGB1 protein was used as control in any kind of test. RESULTS: (1) The levels of GM-CSF, IFN-gamma, IL-6, IL-8, and monocyte chemoattractant protein-1 (MCP-1) secreted by the HMGB1 stimulated HUVECs were 5, 7, 4.2, 27.8, 12.8, and 5.4 times that of those control group (all P < 0.01) (2) The levels of IL-6 secreted by the HUVECs stimulated with HMGB1 protein of the concentrations of 3, 15 and 75 ng/ml respectively were 155 pg/ml +/- 33 pg/ml, 901 pg/ml +/- 184 pg/ml, and 1508 pg/ml +/- 379 pg/ml respectively, all significantly higher than that of the control group (32 pg/ml +/- 21 pg/ml, all P < 0.01). (3) Since 3 h after the stimulation of HMGB1 protein the level of IL-6 began to increase gradually. 6, 12, and 24 hours after the stimulation the levels of IL-6 secreted by the HUVEC were 75 pg/ml +/- 22 pg/ml, 453 pg/ml +/- 78 pg/ml, and 901 pg/ml +/- 184 pg/ml respectively, all significantly higher than that of the control group (32 pg/ml +/- 21 pg/ml, all P < 0.01). (4) When the HUVECs were stimulated individually by LPS (10 ng/ml) or HMGB1 (15 ng/ml), the levels of IL-6 increased to 289 pg/ml +/- 42 pg/ml and 901 pg/ml +/- 183.6 pg/ml respectively (both P < 0.01); when the HUVECs were costimulated by LPS and HMGB1, the level of IL-6 increased to 2360 pg/ml +/- 299 pg/ml, which showing that there was a synergistic effect between HMGB and LPS (F = 69.405, P < 0.001). CONCLUSION: HMGB1 activates HUVECs to produce multiple inflammatory cytokines and induces HUVEC to secret IL-6 in a dose- and time-dependent manner. HMGB1 can also act synergistically with LPS in inducing IL-6 release, which may play an important role in the development of sepsis.

Cell Line↗

Cloning and characterization of porcine aquaporin 1 water channel expressed extensively in gastrointestinal system.

AIM: To clone and characterize the porcine aquaporins (AQPs) in the gastrointestinal system. METHODS: A PCR-based cloning strategy and RACE were used to clone full-length AQP coding sequence from reversely transcribed pig liver cDNA. Stopped-flow light scattering and a YFP-based fluorescence method were used to measure the osmotic water permeability of erythrocytes and the stably transfected CHO cells. RT-PCR, Northern blot, and immunohistochemistry were used to determine the gastrointestinal expression and localization of cloned AQPs. Protein expression in transfected cells and red blood cells was analyzed by Western blot. RESULTS: An 813 bp cDNA encoding a 271 amino acid porcine aquaporin (designated pAQP1) was cloned from liver mRNA (pAQP1 has a 93% identity with human AQP1 and contains two NPA motifs conserved in AQP family, one consensus sequence for N-linked glycosylation, and one mercury-sensitive site at cysteine 191). RT-PCR analysis revealed extensive expression of pAQP1 mRNA in porcine digestive glands and gut. Northern blot showed a single 3.0 kb transcript in selected digestive organs. pAQP1 protein was localized at central lacteals of the small intestine, microvessles of salivary glands, as well as epithelium of intrahepatic bile ducts by immunoperoxydase. High osmotic water permeability that is inhibitable by HgCl2 was detected in porcine erythrocytes and CHO cells stably transfected with pAQP1 cDNA. Immunoblot analysis of porcine erythrocytes and pAQP-transfected CHO cells revealed an unglycosylated 28 ku band and larger glycosylated proteins. CONCLUSION: pAQP1 is the first porcine aquaporin that can be molecularly identified so far. The broad distribution of pAQP1 in epithelium and endothelium of porcine digestive organs may suggest an important role of channel-mediated water transport in fluid secretion/absorption as well as in digestive function and pathophysiology of the gastrointestinal system.

Amino Acid Sequence↗

Nanospring behaviour of ankyrin repeats.

Ankyrin repeats are an amino-acid motif believed to function in protein recognition; they are present in tandem copies in diverse proteins in nearly all phyla. Ankyrin repeats contain antiparallel alpha-helices that can stack to form a superhelical spiral. Visual inspection of the extrapolated structure of 24 ankyrin-R repeats indicates the possibility of spring-like behaviour of the putative superhelix. Moreover, stacks of 17-29 ankyrin repeats in the cytoplasmic domains of transient receptor potential (TRP) channels have been identified as candidates for a spring that gates mechanoreceptors in hair cells as well as in Drosophila bristles. Here we report that tandem ankyrin repeats exhibit tertiary-structure-based elasticity and behave as a linear and fully reversible spring in single-molecule measurements by atomic force microscopy. We also observe an unexpected ability of unfolded repeats to generate force during refolding, and report the first direct measurement of the refolding force of a protein domain. Thus, we show that one of the most common amino-acid motifs has spring properties that could be important in mechanotransduction and in the design of nanodevices.

Amino Acid Motifs↗

Prevalence of peripheral arterial disease and its association with smoking in a population-based study in Beijing, China.

OBJECTIVE: Although the prevalence of peripheral arterial disease (PAD) and its association with smoking in Western populations has been extensively studied, little information is available in China. The objective of this study was to determine the age-standardized prevalence of PAD and examine the relationship between smoking, quitting, and PAD in elderly Chinese. METHODS: We conducted a population-based cross-sectional study in an urban Beijing sample of 2334 subjects aged > or =60 years (943 men and 1391 women) in 2001 to 2002. PAD was assessed by symptoms of intermittent claudication (IC) as measured by the WHO/Rose questionnaire and an ankle-arm systolic blood pressure index (AAI) of <0.90. RESULTS: The prevalence of PAD defined by IC was 11.3% (men, 8.0%; women, 13.6%); 15.3% (men, 11.7%; women, 17.7%) by AAI, and 19.8% (men, 14.7%; women, 23.2%) by both criteria. After adjusting for age, gender, marital status, education, alcohol drinking, exercise, body mass index, and histories of hypertension and diabetes mellitus, the odds ratios and 95% confidence intervals of PAD for current smokers vs never smokers were 1.54 (1.12 to 2.11) and 1.28 (0.91 to 1.79) for former smokers (stopped smoking for at least 2 years). There was a dose-response relation between the number of cigarettes smoked and increasing risk of PAD. Quitting for > or =10 years nearly eliminated excess risk associated with smoking. CONCLUSIONS: PAD is common in elderly Chinese and the prevalence is higher in women than in men. About 40% of PAD patients were asymptomatic and unaware of their condition. Cigarette smoking is a major risk factor for PAD, and smoking cessation substantially reduces the risk.

Age Factors↗

A nucleolin-binding 3' untranslated region element stabilizes beta-globin mRNA in vivo.

The normal expression of human beta globin is critically dependent upon the constitutively high stability of its encoding mRNA. Unlike with alpha-globin mRNA, the specific cis-acting determinants and trans-acting factors that participate in stabilizing beta-globin mRNA are poorly described. The current work uses a linker-scanning strategy to identify a previously unknown determinant of mRNA stability within the beta-globin 3' untranslated region (3'UTR). The new determinant is positioned on an mRNA half-stem opposite a pyrimidine-rich sequence targeted by alphaCP/hnRNP-E, a factor that plays a critical role in stabilizing human alpha-globin mRNA. Mutations within the new determinant destabilize beta-globin mRNA in intact cells while also ablating its 3'UTR-specific interaction with the polyfunctional RNA-binding factor nucleolin. We speculate that 3'UTR-bound nucleolin enhances mRNA stability by optimizing alphaCP access to its functional binding site. This model is favored by in vitro evidence that alphaCP binding is enhanced both by cis-acting stem-destabilizing mutations and by the trans-acting effects of supplemental nucleolin. These studies suggest a mechanism for beta-globin mRNA stability that is related to, but distinct from, the mechanism that stabilizes human alpha-globin mRNA.

3' Untranslated Regions↗

Downregulation of human endothelial nitric oxide synthase promoter activity by p38 mitogen-activated protein kinase activation.

Human endothelial nitric oxide synthase (eNOS) plays a crucial role in maintaining blood pressure homeostasis and vascular integrity. eNOS gene expression may be upregulated by a signaling pathway, including PI-3Kgamma--> Jak2--> MEK1 --> ERK1/2--> PP2A. It remains unclear whether other mitogen-activated protein kinase (MAPK) family members, such as JNK, p38 kinase, and ERK5/BMK1, also modulate eNOS gene expression. Our purpose, therefore, is to shed light on the effect of the p38 MAPK signaling pathway on the regulation of eNOS promoter activity. The results showed that a red fluorescent protein reporter gene vector containing the full length of the human eNOS promoter was first successfully constructed, expressing efficiently in ECV304 cells with the characteristics of real time observation. The wild-types of p38alpha, p38beta, p38gamma, and p38delta signal molecules all markedly downregulated promoter activity, which could be reversed by their negative mutants, including p38alpha (AF), p38beta (AF), p38gamma (AF), and p38delta (AF). Promoter activity was also significantly downregulated by MKK6b (E), an active mutant of an upstream kinase of p38 MAPK. The reduction in promoter activity by p38 MAPK could be blocked by treatment with a p38 MAPK specific inhibitor, SB203580. Moreover, the activation of endogenous p38 MAPK induced by lipopolysaccharide resulted in a prominent reduction in promoter activity. These findings strongly suggest that the activation of the p38 MAPK signaling pathway may be implicated in the downregulation of human eNOS promoter activity.

Blotting, Western↗

[Application of two-color infrared fluorescence for detection of protein phosphorylation].

OBJECTIVE: To assess the value of two-color infrared fluorescence imaging system in detecting protein phosphorylation in comparison with chemiluminescent detection. METHOD: The lung tissue homogenate of mice treated with lipopolysaccharide (LPS) for different time lengths were prepared to separate the proteins by SDS-polyacrylamide gel electrophoresis followed by transfer of the proteins onto PVDF membranes. The membranes were incubated with the antibodies against total p42/44 MAPK/phospho-p42/44 MAPK, and then with goat anti-mouse or anti-rabbit secondary antibodies conjugated to Alexa Fluor 680, IRDye 800 or horseradish peroxidase. The blotted proteins were detected and quantified using Odyssey infrared imaging system or chemiluminescent detection. RESULTS: LPS treatment rapidly induced p42/44 MAPK phosphorylation, which reached the peak level 1 h after the treatment and resumed the baseline level at 12 h. Consistent results were obtained by the two detection methods, but two-color infrared fluorescence imaging system showed better sensitivity in detecting the target protein, and was easy to manipulate with good efficiency and capable of analyzing two proteins simultaneously. CONCLUSION: Two-color infrared fluorescence system is a powerful system for detecting phosphorylation of proteins.

Animals↗

[Studies on chemical constituents from roots of Polygala tricornis].

OBJECTIVE: To study the chemical constituents from the roots of Polygala tricornis. METHOD: Compounds were isolated by repeated silica gel column chromatography and their structures were determined by spectral analysis and physicochemical properties. RESULT: Six compounds were isolated from the roots of P. tricornis, and their structures were identified as p-hydroxy benzoic acid (I), glucosyringic acid (II), 1-O-p-coumaroyl-D-glucopyranose (III), cis-coniferin (IV), cis-syringin (V) and vacciniin (VI). CONCLUSION: Compounds I approximately VI were obtained from this plant for the first time.

Benzoates↗

[A study of correlation between the blood supply types of PHcc on spiral CT and the level of VEGF expression in PHcc].

OBJECTIVE: To study the correlation between the blood supply types of primary hepatocellar carcinoma (PHcc) on Spiral CT and the level of vascular endothelial growth factor (VEGF) expression in PHcc for improvement in treatment strategies and prognostication. METHODS: Forty-five cases of PHcc identified by operation and pathology were investigated. Immunohistochemistry staining in SP was performed. The relationships between blood supply types of PHcc on Spiral CT during dual-phase scanning and the expression levels of VEGF in well-differentiated, moderately differentiated and poorly differentiated PHcc were analyzed. RESULTS: There were four blood supply types of PHcc on Spiral CT. Both the strong positive staining and the positive staining were most frequently seen in the hepatic artery blood supply type, and then were frequently in the double blood supply type, i. e. the hepatic arterial supply combining with the portal blood supply type. The positive staining results were rarely seen in the portal blood supply type and poor blood supply type (P<0.001). And with the escalation of the Edmonson- Steiner histological grades, the VEGF expression levels were shown to increase correspondingly (P < 0.05). CONCLUSION: We can ascertain the blood supply type of PHcc and infer the VEGF expression levels that reflect the PHcc angiogenesis condition and the histological grades by means of Spiral CT during dual- phase scanning. Hence this method is useful for the selection of PHcc treatment plans, including anti-angiogenesis and evaluating the prognosis.

Adult↗

[Fingerprint of Polygala tenuifolia by high performance liquid chromatography].

AIM: To study and establish the fingerprint of Polygala tenuifolia by RP-HPLC. METHODS: The fingerprint of P. tenuifolia was built by using Kromasil C18 as column and acetonitrile-0.05% phosphoric acid aqueous in gradient as mobile phase. The flow rate was 1.0 mL x min(-1), and the detecting wavelength was set at 318 nm. Total 14 batches of P. tenuifolia from different habitats were detected, and different commodities and preparative methods were compared. RESULTS: Samples from different habitats were of high similarities, and the qualities of "yuanzhitong" and "yuanzhirou" were better than that of "yuanzhigun", while the fingerprints of P. tenuifolia with different preparative methods have not obvious differences. Moreover, the standard fingerprint of P. tenuifolia was originated from the "Computer Aided Similarity Evaluation" software, and 29 common peaks existed in the fingerprint. Each peak in the fingerprint was separated very well under the above chromatographic condition, with good accuracy, stability and repeatability, satisfied to the requests of fingerprint. CONCLUSION: The RP-HPLC fingerprint method can be used in the quality control of P. tenuifolia.

Chromatography, High Pressure Liquid↗