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Biomedical subjects

P Liu

Publications and source records attributed to P Liu.

At least 127 records · Page 7Linked to original sources
PubMed2000

[Electric maze test in rats after prenatal methylmercury exposure].

To study the changes of rat's learning and memory ability in maze test after prenatal methylmercury exposure, methylmercury in doses of 0, 0.01, 0.05 and 2.00 mg/(kg.d) were fed to pregnant rats at the 6th-9th day after conception. We adopted a Y-shaped electric maze to detect learning and memory ability of the rat offspring. Double blind was used in the experiment. The results showed that the error times and arrival time of all exposure groups were more, and active avoidance ratio of all exposure groups was less than that of control group. The differences were significant(P < 0.05 or P < 0.01). There was no difference between male and female rats. It is concluded that methylmercury could affect the growth and development of central nerve system. The learning and memory ability of rat offspring was greatly damaged.

Animals↗
PubMed2000

[The changes of GFAP and PCNA after human brain contusion: an immunohistochemical study in forensic pathology].

In order to find out changes of GFAP and PCNA after human brain trauma, samples of 38 cases were studied by the immunnohistochemistry method combined with quantitative image analysis. The gray degree and area of PCNA positive cells increased to the maximum at the 4th day and then decreased gradually. GFAP positive cells began to increase significantly 12 hours after contusion, reached the maximum at the 4th day and stayed in high level until the 7th day. These results suggest that: (1) GFAP, PCNA show regular changes with survival time after brain contusion; (2) GFAP and PCNA can be used as time markers of brain contusion from 2-20 days.

Adult↗
PubMed2000

[Analysis of imidacloprid and damanlin by high performance liquid chromatography].

A new method for determination of imidacloprid and damanlin by using HPLC was established. It was carried out on a mu Bondapak C18 column (3.9 mm i.d. x 300 mm) with ACN-MeOH-H2O (60:10:30, V/V) as eluent and detected at 240 nm using photodiode array detector. The results of imidacloprid and damanlin were 3.71% and 15.65% respectively. The standard deviations for imidacloprid and damanlin were 0.88% and 0.76% respectively.

Animals↗
PubMed2000

[Antibacterial and antifungal effects of Agkistrodon halys Pallas: purification of its antibacterial protein--LAO].

This paper reports the venom from Agkistrodon halys Pallas have inhibitory activity against fungi and E. coli by tested in a disc diffusion assay. An antibacterial component--LAO from the venom were purified to homogeneous. It had not only antibacterial effect, but L-amino acid oxidase activity. And its enzymatic specific activity was 808 U/mg. The venom had at least 3 antibacterial components (I, II, III) as determined by acid polyacrilamide gel electrophoresis, LAO is the antibaterial components II.

Agkistrodon↗
PubMed1999

Susceptibility to myocarditis is dependent on the response of alphabeta T lymphocytes to coxsackieviral infection.

Viral myocarditis is an important cause of heart failure and dilated cardiomyopathy. T lymphocytes are implicated in myocardial damage in murine models of coxsackievirus B3 (CVB3) myocarditis. We used knockout mice lacking CD4 (CD4(-/-)), CD8 (CD8(-/-)), both coreceptors (CD4(-/-)CD8(-/-)), or the T-cell receptor beta chain (TCRbeta(-/-)) to address the contribution of T-cell subpopulations to host susceptibility to CVB3 myocarditis. Severity of disease was magnified in CD8(-/-) mice but attenuated in CD4(-/-) mice, consistent with a pathogenic role for CD4(+) lymphocytes. Elimination of both CD4 and CD8 molecules from T lymphocytes by genetic knockout better protected mice from myocarditis, demonstrating that both CD4(+) and CD8(+) T cells contribute to host susceptibility. The same benefit occurred in TCRbeta(-/-) mice, with prolonged survival and minimal myocardial disease observed after CVB3 infection. Elevated interferon-gamma and decreased tumor necrosis factor-alpha expression are associated with attenuated myocardial damage in CD4(-/-)CD8(-/-) mice. These results show that the presence of TCRalphabeta(+) T cells enhances host susceptibility to myocarditis. The severity of myocardial damage and associated mortality are dependent on the predominant T-cell type available to respond to CVB3 infection. One mechanism by which CD4(+) and CD8(+) T-cell subsets influence the pathogenesis of myocarditis may involve specific cytokine expression patterns.

Animals↗
PubMed1999

Determinants of survival and length of survival in adults with Eisenmenger syndrome.

A retrospective study of adults with Eisenmenger syndrome assessed at a tertiary referral center was performed to identify clinical characteristics and establish prognostic determinants. Mortality and cause of death are reported with baseline clinical data correlated with mortality to identify predictors of death. Clinical events during follow-up, including heart failure, atrial arrhythmia, hemoptysis, and syncope were also reviewed. A total of 109 adults with Eisenmenger syndrome (mean +/- SD age 29 +/- 11 years, 43% men) were followed for a median of 6.3 years. Sixty-six patients (61%) had simple cardiac anatomy (13 atrial septal defect, 43 ventricular septal defect, 10 patent ductus arteriosus). The remainder (43 patients) had complex cardiac anatomy (including atrioventricular septal defect, truncus arteriosus, univentricular heart, and transposition of the great arteries). There were 33 deaths and 9 transplantations during follow-up. Median survival was 53 years. Multivariate Cox regression analysis identified age at presentation (hazard ratio [HR] 0.90), supraventricular arrhythmia (HR 3.44), precordial electrocardiogram voltage (HR 1.61/mV increase), and poor New York Heart Association functional class (HR 2.60) as independent predictors of mortality. There is a large variation in the life expectancy for adults with Eisenmenger syndrome. Baseline characteristics associated with increased mortality include younger age at presentation (associated with complex anatomy), functional class, supraventricular arrhythmia, and an electrocardiogram index for right ventricular hypertrophy.

Adult↗
PubMed1999

Evidence of a phenotypically determined ductal cell lineage in mouse salivary glands.

The submandibular salivary gland of mice contains a parenchymal element, the granular duct, which matures peripubertally from the striated ducts. Granular duct cells also differentiate from intercalated ducts in the adult mouse submandibular gland. Using preproNGF-A as a signature protein of mature granular duct cells, this study inquired if phenotypic determination might have occurred earlier than the first signs of cellular differentiation. Results from RT-PCR indicate the presence of preproNGF-A transcripts at all postnatal stages of development of the submandibular glands, as well as in adult sublingual glands. The preproNGF-A transcript was also detected prenatally as early as embryonic day 17 in the submandibular/sublingual complex. Using an antibody directed specifically against the "pre" peptide, immunocytochemistry showed preproNGF-A localized in the granular ducts and striated ducts of the adult submandibular gland. In addition preproNGF-A was detected throughout the first order branches of the intercalated duct system. In the neonatal gland, preproNGF-A was found in the large tubules that differentiate to the striated ducts. The early appearance of preproNGF-A in the histological lineage that sequentially gives rise to striated ducts and then to granular ducts suggests that this lineage is phenotypically determined as early as birth. An undifferentiated stage of the phenotypically determined lineage also appears to be retained in the intercalated duct system to provide progenitors for subsequent differentiation in the adult gland. Throughout development of the sublingual gland, preproNGF-A was detectable in the striated ducts or in their predecessors, suggesting that they may also represent a phenotypically determined cell lineage similar to that of the submandibular gland.

Amino Acid Sequence↗
PubMed1999

Phosphatidic acid increases inositol-1,4,5,-trisphosphate and [Ca2+]i levels in neonatal rat cardiomyocytes.

Phosphatidic acid (PA), which can be synthesized de novo, or as a product of phosphatidylcholine hydrolysis and/or phosphorylation of 1,2-diacylglycerol (DAG), mediates diverse cellular functions in various cell types, including cardiomyocytes. We set out to characterize the effect of PA on intracellular free calcium ([Ca2+]i) and inositol-1,4,5-trisphosphate (IP(3)) levels in primary cultures of neonatal rat cardiomyocytes. Addition of PA led to rapid, concentration and time dependent increases in both IP(3) and [Ca2+]i levels in adherent cells. There was strong correlation in the concentration-response relationships between IP(3) and [Ca2+]i increases evoked by PA. Incubation with the sarcoplasmic reticulum (SR) Ca2+ pump inhibitor, cyclopiazonic acid (CPA), significantly attenuated the PA evoked [Ca2+]i increase but had no significant effect on IP(3) accumulation. The phospholipase C (PLC) inhibitor, D-609, attenuated both IP(3) and [Ca2+]i elevations evoked by PA whereas staurosporine (STS), a potent and non-selective PKC inhibitor, had no significant effect on either. Another PLC inhibitor, U73122, but not its inactive analog, U73343, also inhibited PA evoked increases in [Ca2+]i. Depletion of extracellular calcium attenuated both basal and PA evoked increases in [Ca2+]i. The PLA(2) inhibitors, bromophenylacyl-bromide (BPB) and CDP-choline, had no effect on PA evoked [Ca2+]i responses. Neither the DAG analog, dioctanoylglycerol, nor the DAG kinase inhibitor, R59949, affected PA evoked changes in [Ca2+]i. Taken together, these data indicate that PA, in a manner independent of PKC, DAG, or PLA(2), may enhance Ca2+ release from IP(3) sensitive SR Ca(2+) stores via activation of PLC in neonatal rat cardiomyocytes.

Animals↗
PubMed1999

Spatial organization of EGF receptor transmodulation by PDGF.

Even though the modulation of EGF receptors by PDGF is well documented, it is not known where on the cell surface cross-talk between the two receptor systems takes place. The recent finding that both populations of receptors are concentrated in cell surface caveolae suggestes that the confinement of the two receptors to this space might facilitate their interaction. Here we show that stimulation of PDGF receptors in caveolae with PDGF causes a subpopulation of EGF receptors in the same membrane fraction to become phosphorylated on tyrosine. Coincident with tyrosine phosphorylation, the binding of EGF to its receptor markedly declines. Loss of EGF binding is partially blocked by tyrosine kinase inhibitors. Despite the close proximity of the two receptors in caveolae, we saw no evidence that EGF could stimulated PDGFR tyrosine phosphorylation. These results suggest that these two receptor systems are highly organized in caveolae.

Cell Membrane↗
PubMed1999

Use of hormone replacement therapy among cardiac patients at a Canadian academic centre.

BACKGROUND: Although hormone replacement therapy (HRT) is associated with a reduced risk of coronary artery disease (CAD), use of this treatment among post-menopausal women is not widespread. The authors sought to determine the extent of HRT use in a select population of women at high risk for CAD. METHODS: A cross-sectional survey was performed involving all consecutive post-menopausal women who attended a cardiology clinic in a Toronto teaching hospital between January 1996 and August 1997. A chart review was followed by a telephone interview with the patients or their physicians. The utilization rate of HRT was obtained. Predictors of HRT use were identified using a multivariate logistic regression model. RESULTS: A total of 80 women with risk factors for CAD, symptoms suspicious of CAD or definite CAD diagnosed after cardiac investigations were included in the survey. Information on HRT use or nonuse was documented in 17 (21%) of the charts. Of the 72 women for whom data on HRT were available 16 (22%) were currently using it, 41 (57%) were not, and 15 (21%) had used it in the past. Five women (7%) were receiving HRT but there was no chart documentation. On multivariate analysis, younger women were more likely than older women to use HRT (odds ratio 0.91, 95% confidence interval 0.22-0.96; p < 0.05). Coronary risk profile, CAD diagnosis and history of hysterectomy were not associated with HRT use. Of the 41 women who had never received HRT 10 (24%) had possible contraindications (e.g., breast cancer or deep vein thrombosis); the proportion was similar in the group of women who were current or past users of HRT (29%). INTERPRETATION: Documentation of HRT use in patient charts is lacking. Few women in the study who were at risk for CAD were currently using HRT. The data support the need for better adherence to optimal practices in the management of women at high risk for CAD.

Aged↗
PubMed1999

Generation of humanized mice susceptible to peptide-induced inflammatory heart disease.

BACKGROUND: Dilated cardiomyopathy (DCM) is a major cause of sudden cardiac death. In certain mouse major histocompatibility complex (MHC) backgrounds, myocarditis and inflammatory cardiomyopathy can be triggered by immunization with heart muscle-specific proteins. Similarly, chronic heart disease in humans has been linked to certain HLA alleles, such as HLA-DQ6. However, there is no experimental evidence showing that human MHC class II molecules and peptides derived from human proteins are involved in the pathogenesis of myocarditis and DCM. METHODS AND RESULTS: We generated double CD4- and CD8-deficient mice transgenic for human CD4 (hCD4) and human HLA-DQ6 to specifically reconstitute the human CD4/DQ6 arm of the immune system in mice. Transgenic hCD4 and HLA-DQ6 expression rendered genetically resistant C57BL/6 mice susceptible to the induction of autoimmune myocarditis induced by immunization with cardiac myosin. Moreover, we identified heart-specific peptides derived from both mouse and human alpha-myosin heavy chains capable of inducing inflammatory heart disease in hCD4 and HLA-DQ6 double transgenic mice but not in hCD4 single transgenic littermates. The autoimmune inflammatory heart disease induced by the human heart muscle-specific peptide in hCD4 and HLA-DQ6 double transgenic mice shared functional and phenotypic features with the disease occurring in disease-susceptible nontransgenic mice. CONCLUSIONS: Our data provide the first genetic and functional evidence that human MHC class II molecules and a human alpha-myosin heavy chain-derived peptide can cause inflammatory heart disease and suggest that human inflammatory cardiomyopathy can be caused by organ-specific autoimmunity. The humanized mice generated in this study will be an ideal animal model to further elucidate the pathogenesis of inflammatory heart disease and facilitate the development of rational treatment strategies.

Animals↗
PubMed1999

Tissue expression and immunolocalization of tumor necrosis factor-alpha in postinfarction dysfunctional myocardium.

BACKGROUND: Tumor necrosis factor-alpha (TNF-alpha) is markedly elevated in advanced heart failure. It is not known whether tissue TNF-alpha is elevated in the common setting of myocardial infarction leading to heart failure and what the source of TNF-alpha is. To determine this, we studied the expression and protein localization of TNF-alpha and its 2 main receptors (TNF-R1/R2) in a rat model of large infarction. METHODS AND RESULTS: Male rats were randomized to proximal left anterior descending ligation. The animals were killed on days 1, 3, 10, and 35 after ligation to examine gene expression and protein production of TNF-alpha and TNF-R1/R2 from the infarct, peri-infarct, and contralateral zones of infarcted heart. There was increased TNF-alpha mRNA production throughout the myocardium at day 1, and detectable expression persisted to day 35 after myocardial infarction. The expression of this cytokine is not confined strictly to the infarct or peri-infarct zones but is expressed by cardiac myocytes within the myocardium in the contralateral normal zone. Changes in gene expression are mirrored initially by augmented protein production within the myocytes. Levels of TNF-alpha protein in the infarct and peri-infarct zones rose early to 8- to 10-fold above normal levels and rose to 4- to 5-fold in the contralateral zone. Finally, expression of the TNF-R1 mRNA transcripts was upregulated at days 3 and 10 after ligation in the infarct and peri-infarct zones, suggesting that the signal transduction pathways necessary for TNF-alpha in the heart remain intact as TNF-alpha biosynthesis increases. CONCLUSIONS: TNF-alpha is present early in a model of large myocardial infarction and is sustained into the later stage within the myocardium. Expression of this cytokine is not only confined strictly to the infarct or peri-infarct zone but is expressed by cardiac myocytes within the myocardium contralateral to the infarct. Therefore TNF-alpha production forms a part of an important intrinsic myocardial stress response system to injury.

Animals↗
PubMed1999

Transdermal iontophoretic delivery of methylphenidate HCl in vitro.

Methylphenidate is prescribed orally for Attention Deficit Disorder in children and adults, and for narcolepsy patients. Methylphenidate has a short plasma half-life (1-2 h) and thus needs to be frequently administered for effective therapy. Such therapy has limitations in terms of patient compliance, particularly in young children. For such reasons, the development of a transdermal dosage form of methylphenidate may be useful. This study was undertaken to evaluate the passive and electrically assisted transport (iontophoresis) of methylphenidate from aqueous methylphenidate hydrochloride solutions across excised human skin. A maximum flux of 12.0 micrograms/(cm2 h) of protonated methylphenidate was estimated from the passive transport data at pH 3.5. Iontophoresis significantly enhanced protonated methylphenidate transport as compared with passive delivery. From the present experiments, the efficiency of iontophoretic delivery of methylphenidate was approximately 700 micrograms/(mA h). Based on in vitro skin flux data, the daily dose of 15-40 mg methylphenidate can be achieved using a current density of 0.5 mA/cm2 and a minimum transport area of 2-5 cm2 for 24-h application, or an area of 4-10 cm2 for 12-h (daytime) application. From methylphenidate skin flux values, methylphenidate mobility of 2.2 x 10(-4) cm2/(V s) was estimated, which compares reasonably with its free solution mobility of 6.6 x 10(-4) cm2/(V s).

Administration, Cutaneous↗
PubMed1999

Patterns of failure in endometrial carcinoma stage IB grade 3 and IC patients treated with postoperative vaginal vault brachytherapy.

OBJECTIVE: The vagina is the most common site of locoregional failure in surgical stage IB, IC, and II (occult) endometrial adenocarcinoma. The objective of this study is to evaluate the therapeutic efficacy of vaginal vault brachytherapy alone for surgical stage I patients with high-risk features. MATERIALS AND METHODS: The study group consists of high-risk stage I patients with either stage IB grade (G) 3 or any grade IC disease. From February 1991 to August 1997, 124 patients with endometrial carcinoma were treated postoperatively with high-dose-rate vaginal vault brachytherapy as the only adjuvant treatment. All patients were surgically staged. Among them, 38 patients were identified as high risk. Twelve patients had stage IBG3, 14 had ICG1, 9 had ICG2, and 3 had ICG3 disease. The median age was 67 years (range 41 to 86 years). A dose of 21 Gy in three fractions of 7 Gy each was delivered to a prescription depth of 0.5 cm from the surface of the vaginal applicator using high-dose-rate brachytherapy. RESULTS: The median follow-up was 30 months (range 7 to 91 months). No patient has developed a vaginal or pelvic recurrence. Three patients developed tumor recurrence in the upper abdomen at 11, 18, and 37 months. Two of the three patients with recurrent disease also had history of breast cancer. In one patient, breast cancer was diagnosed 4.8 years prior and in the second 3 years subsequent to the diagnosis of endometrial cancer. The 5-year actuarial overall survival and disease-free survival are 93 and 87%, respectively. There was no treatment-related grade 3 or 4 morbidity observed. CONCLUSIONS: For patients with surgical stage IBG3 and IC, excellent local control and minimal morbidity has been observed with the selective use of vaginal brachytherapy alone. Further studies and longer follow-up are warranted.

Adenocarcinoma↗
PubMed1999

Segmental embolization by ethanol iodized oil emulsion for hepatocellular carcinoma.

The hemodynamic changes of portal vein before and after intra-arterial infusion of ethanol iodized oil emulsion (EIOE) were studied in 4 healthy dogs. Segmental transcatheter arterial embolization (TAE) using EIOE was performed in 55 patients with hepatocellular carcinoma (HCC). Twenty patients subsequently underwent surgery. It was concluded that segmental TAE might lead to double embolization of both hepatic arteries and portal veins. It is a more effective therapeutic method for HCC localized in one or a few segments, as compared with conventional TAE.

Adult↗
PubMed1999

Regulation of osteogenic differentiation of human bone marrow stromal cells: interaction between transforming growth factor-beta and 1,25(OH)(2) vitamin D(3) In vitro.

Bone marrow stromal cells are believed to play a major role in bone formation as a major source of osteoprogenitor cells, however, very little is known about how the osteogenic differentiation of these cells is regulated by systemic hormones and local growth factors. We examined the effects of TGF-beta and its interaction with 1, 25(OH)(2) Vitamin D(3) [1,25(OH)(2)D(3)] on the differentiation and proliferation of human bone marrow stromal cells (hBMSC) in secondary cultures. Alkaline phosphatase (ALP) activity was inhibited by TGF-beta (0.1-10 ng/ml) and increased by 1, 25(OH)(2)D(3) (50 nM), however, co-treatment of TGF-beta and 1, 25(OH)(2)D(3) synergistically enhanced ALP activity with maximal stimulation occurring at about 8 days after treatment. This synergistic effect was independent of proliferation because, in contrast to TGF-beta alone, combined treatment with TGF-beta and 1, 25(OH)(2)D(3) had no effect on hBMSC proliferation. As no synergistic effect was seen with combinations of 1,25(OH)(2)D(3) and other osteotrophic growth factors, including BMP-2, IGF-I, and basic fibroblast growth factor (bFGF), it would seem likely that the synergistic interaction is specific for TGF-beta. The increased ALP activity was due to an enhancement of 1,25(OH)(2)D(3)-induced ALP activity by TGF-beta, rather than vice versa. In contrast, TGF-beta inhibited 1,25(OH)(2)D(3)-induced osteocalcin production. Taken together, these results indicate that TGF-beta and 1,25(OH)(2)D(3) act synergistically to stimulate the recruitment of BMSC to the osteoblast lineage. This interaction may play an important role in bone remodeling.

Adult↗