Search PubMed⌕ Search

Biomedical subjects

J F Li

Publications and source records attributed to J F Li.

At least 19 recordsLinked to original sources
PubMed2006

Self-assembled pattern formation of block copolymers on the surface of the sphere using self-consistent field theory.

The spherical surface is spatially discretized with triangular lattices to numerically calculate the Laplace-Beltrami operator contained in the self-consistent field theory (SCFT) equations using a finite volume method. Based on this method we have developed a spherical alternating-direction implicit (ADI) scheme for the first time to help extend real-space implementation of SCFT in 2D flat space to the surface of the sphere. By using this method, we simulate the equilibrium microphase separation morphology of block copolymers including AB diblocks, ABC linear triblocks and ABC star triblock copolymers occurred on the spherical surface. In general, two classes of microphase separation morphologies such as striped patterns for compositionally symmetric block copolymers and spotted patterns for asymmetric compositions have been found. In contrast to microphase separation morphology in 2D flat space, the geometrical characteristics of a sphere has a large influence on the self-assembled morphology. For striped patterns, several of spiral-form and ring-form patterns are found by changing the ratio of the radius of a sphere to the averaging width of the stripes. The specific pattern such as the striped and spotted pattern with intrinsic dislocations or defects stems from formed periodic patterns due to microphase separation of block copolymers arranged on the curved surface.

Adsorption↗
PubMed2005

Cloning of novel laccase isozyme genes from Trametes sp. AH28-2 and analyses of their differential expression.

Three novel laccase isozyme genes, lacA, lacB, and lacC, have been identified from basidiomycete Trametes sp. AH28-2. These genes display a high similarity with other basidiomycete laccases at the amino acid level. An inferred TATA box and several putative CAAT, MRE, XRE, and CreA consensus sequences were identified in the lacA, lacB, and lacC promoter regions. Different from the TATA boxes of lacA and lacB at about -100, the TATA box of lacC is located at -172. For all the isozymes, copper ion is essential for laccase synthesis in Trametes sp. AH28-2. More interestingly, different aromatic compounds can selectively induce the production of distinct laccase isozymes, with o-toluidine inducing the expression of laccase A (LacA) while 3,5-dihydroxytoluene mainly stimulating the production of laccase B (LacB). Quantitative reverse transcriptase-polymerase chain reaction showed that the accumulation of laccase messenger RNA transcripts is accompanied by the increase of corresponding enzyme activity in cultures. The glucose-repression effect on laccase expression in Trametes sp. AH28-2 was also observed. Furthermore, lower Cu2+ concentration (lower than 0.5 mM) can induce LacA and a novel laccase (LacC), and the latter will disappear when Cu2+ concentration is increased up to 1-2 mM. Upon induction by 3,5-dihydroxytoluene, the ratio of LacA to LacB decreased in the later phase of induction.

Amino Acid Sequence↗
PubMed2003

Conformal miniaturization of domains with low domain-wall energy: monoclinic ferroelectric states near the morphotropic phase boundaries.

A theory is developed for intermediate monoclinic (FE(m)) phases near morphotropic phase boundaries in ferroelectrics of complex oxides. It is based on the conformal miniaturization of stress-accommodating tetragonal domains under the condition of low domain-wall energy density. The microdomain-averaged lattice parameters are determined and attributed to the parameters of an adaptive monoclinic phase. The theory is applied to the temperature, electric field, and compositional dependent FE(m) lattice parameters. The predictions of the theory are rigidly obeyed over the entire FE(m) stability range.

Journal Article↗
PubMed2001

"Norwalk-like viruses". Public health consequences and outbreak management.

"Norwalk-like viruses" (NLVs) cause outbreaks of gastroenteritis and are spread frequently through contaminated food or water. Molecular diagnostics now enables detecting viruses in clinical and environmental specimens, linking of NLV strains causing outbreaks in multiple geographic locations, and tracing them to their sources in contaminated food or water. This report reviews recent advances in NLV detection and provides guidelines and recommendations for investigating NLV-related outbreaks, including specimen collection and disease prevention and control. This report also updates information provided in CDC's previously published, Viral Agents of Gastroenteritis: Public Health Importance and Outbreak Management (MMWR 1990;39 [No. RR-5]: 1-24). These CDC recommendations are intended for public health professionals who investigate outbreaks of acute gastroenteritis but could be useful in academic and research settings as well.

Caliciviridae Infections↗
PubMed2001

Characterization of capsid genes, expressed in the baculovirus system, of three new genetically distinct strains of "Norwalk-like viruses".

"Norwalk-like viruses" (NLVs), members of a newly defined genus of the family Caliciviridae, are the most common agents of outbreaks of gastroenteritis in the United States. Two features of NLVs have hindered the development of simple methods for detection and determination of serotype: their genetic diversity and their inability to grow in cell culture. To assess the immune responses of patients involved in outbreaks of gastroenteritis resulting from infection with NLVs, we previously used recombinant-expressed capsid antigens representing four different genetic clusters, but this panel proved insufficient for detection of an immune response in many patients. To extend and further refine this panel, we expressed in baculovirus the capsid genes of three additional genetically distinct viruses, Burwash Landing virus (BLV), White River virus (WRV), and Florida virus. All three expressed proteins assembled into virus-like particles (VLPs) that contained a full-length 64-kDa protein, but both the BLV and WRV VLPs also contained a 58-kDa protein that resulted from deletion of 39 amino acids at the amino terminus. The purified VLPs were used to measure the immune responses in 403 patients involved in 37 outbreaks of acute gastroenteritis. A majority of patients demonstrated a fourfold rise in the titer of immunoglobulin G to the antigen homologous to the outbreak strain, but most seroconverted in response to other genetically distinct antigens as well, suggesting no clear pattern of type-specific immune response. Further study of the antigenicity of the NLVs by use of VLPs should allow us to design new detection systems with either broader reactivity or better specificity and to define the optimum panel of antigens required for routine screening of patient sera.

Amino Acid Sequence↗
PubMed2000

Hydrogen peroxide induces apoptosis in human hepatoma cells and alters cell redox status.

Direct exposure of human hepatoma cell line SMMC-7721 to hydrogen peroxide (H2O2) can induce apoptosis. Apoptosis induced by H2O2 was inhibited by cycloheximide, actinomycin D, 3-aminobenzamide, EGTA or Zn2+. H2O2 can increase the level of intracellular Ca2+, downregulate GSH levels, slightly induce lipid peroxidation, and lead to change in the ratio of reduced ion components to oxidized ion components of cells. Analysis of flow cytometry indicates that H2O2 decreases the level of Bcl-2. The data indicate that H2O2-induced apoptosis requires new mRNA and protein syntheses; H2O2 can activate Ca2+/Mg2+-dependent endonuclease leading to internucleosomal DNA fragmentation and activation of poly (ADP-ribose) polymerase interfering with the energy metabolism of the cell. The H2O2 downregulation of GSH may be more important for apoptosis than H2O2 induction of lipid peroxidation, and the H2O2 induced changes in redox status of the cell may be among the original events which lead up to other biochemical changes.

Apoptosis↗
PubMed2000

A laser scanning confocal microscopy method. Simultaneous detection of intracellular Ca2+ and apoptosis using Fluo-3 and Hoechst 33342.

OBJECTIVE: To develop a simple and direct method to simultaneously determine apoptotic cells from a treated population of cells and detect the changes of intracellular Ca2+ in these apoptotic cells, in particular single ones, by confocal microscopy. STUDY DESIGN: MGC-803 cells treated with As2O3 were used as the double-staining cell model with Hoechst 33342 as a DNA probe and Fluo-3AM as a Ca2+ indicator. MGC-803 cell apoptosis induced by As2O3 was first demonstrated by DNA ladder in gel electrophoresis. Based on the difference in DNA stainability with Hoechst 33342 and corresponding fluorescence intensity between live and apoptotic cells, apoptotic cells and the changes in intracellular Ca2+ were detected at the same time by confocal microscopy. No necrotic cells in the group treated with As2O3 were found by the trypan blue exclusion test. RESULTS: The results from confocal microscope detection showed that intact and apoptotic cells were successfully recognized and the changes of intracellular Ca2+ in apoptotic and intact cells were simultaneously detected in the same sample. CONCLUSION: We provided a useful method to exactly detect changes in intracellular Ca2+ in apoptotic cells, especially in single ones, by confocal microscopy and to exclude the artifact effect of necrotic and intact cells.

Aniline Compounds↗
PubMed1999

Induction of apoptosis and inhibition of human gastric cancer MGC-803 cell growth by arsenic trioxide.

Arsenic trioxide (As2O3), used to treat human diseases for centuries in traditional Chinese medicine, has been identified as a very effective antileukaemic agent, but its effect on solid tumours which could be more suitable for clinical treatment with arsenic compounds is still unknown. In this study, we investigated the in vitro effect of As2O3 at concentrations of 0.01-1 microM against six human malignant cell lines, MGC-803, HIC, MCF-7, HeLa, BEL-7402 and A549 cells. As2O3 inhibited growth and induced apoptosis in these malignant cells at varying degrees, in a time dose-dependent manner. The most marked effects were seen in the gastric cancer cell line, MGC-803. In contrast, minimal growth inhibition and induction of apoptosis occurred in human embryonic pulmonary cells following treatment with As2O3 found at the same concentrations. Changes in intracellular Ca2+, following As2O3 treatment were measured by Ca2+ sensitive fluorescent probe Indo-1/AM in flow cytometric assays. The increase in intracellular Ca2+ correlated with the sensitivity of these cells to As2O3, possibly indicating that a critical intracellular Ca2+ signal transduction pathway could be involved in As2O3-mediated cell-death and its selectivity. The marked sensitivity of MGC-803 cells in vitro suggests that As2O3 may be a potential antigastric cancer agent.

Antineoplastic Agents↗
PubMed1998

Photodynamic effects of hypocrellin A on three human malignant cell lines by inducing apoptotic cell death.

Hypocrellin A (HA), a lipid-soluble peryloquinone derivative extracted from the fungus Hypocrella bambusae, has been proved to be effective in treating many diseases. In this study, we have examined the photodynamic effects of HA on three different human malignant epithelioid cell lines, i.e., HIC, MGC-803 and HeLa cells. They all respond to photodynamic therapy (PDT) by committing apoptosis or necrosis evidenced by morphological changes, DNA fragmentation and a decrease of mitochondria dehydrogenase activity. The sensitivity order of the three cell lines to cytotoxicity by HA is HIC > MGC-803 > HeLa. The extent of apoptosis is also dependent on light dose, post-treatment time and cell type. Vitamin E can significantly protect cells against cell death, indicating that reactive oxygen species (ROS) play an important role in apoptotic or necrotic cell death. These results may be to some extent instructive for clinical cancer treatment.

Apoptosis↗
PubMed1998

Apoptosis, redifferentiation and arresting proliferation simultaneously triggered by oxidative stress in human hepatoma cells.

The effects of oxidative stress (ascorbic acid-ferrous system) on the proliferation, differentiation and apoptosis of the human hepatoma cell SMMC-7721 were studied. Oxidative stress significantly inhibited cell proliferation and induced morphological differentiation. Whatever the indices related with cell malignancy, such as alpha-fetoprotein and c-glutamyltranspeptidase or the index related with cell differentiation, such as tyrosine-alpha-ketoglutarate transaminase, all inclined evidently to normalization. The tumour's clonogenic potential decreased significantly. Moreover, together with differentiation, the phenomenon of apoptosis was found by the appearance of apoptotic bodies, detached cells, and apoptotic morphological feature. Although, their DNA was not degraded into oligonucleosomal fragmentation, the DNA was cut into larger fragments (about 21.2 kbp) of a size associated with chromatin loops. These findings indicated that oxidative stress can induce both differentiation and apoptosis simultaneously in tumour cells. All the results showed that oxidative stress may initiate the tumour cells reverse transformation. The possible mechanism of the differentiation and apoptosis induced by oxidative stress may be related to the lipid peroxidation of cell membrane.

Apoptosis↗
PubMed1998

[Effects of oxidative stress on the proliferation, differentiation and apoptosis in the human hepatoma cells].

The human hepatoma cells SMMC-7721 were treated with different concentrations of ascorbic acid (50-800 mumol/L) and FeSO4 (2.5-40 mumol/L) system to generate oxidative stress at various degrees. The oxidative stress induced by the system were mainly contributed to hydroxyl radical. All the various degrees of oxidative stress in this study are able to inhibit the proliferation of hepatoma cells. While low levels of oxidative stress may cause hepatoma cells lost some malignant features, such as aggregation of Con-A to the cell surface, alpha-fetoprotein, gamma-glutamyltransepeptidase and tyrosine-alpha-ketoglutarate transaminase, all of the 4 indices tended to cell differentiation, coloning efficiency potential decreased significantly, and apoptotic cells appeared. The numbers of apoptotic cells increased with the increasing of oxidative stress. The apoptotic cells exhibited non-adherent, smaller, chromatin condensed around the periphery of the nucleus in the shape of crescent, nuclear fragmentations but with intact cellular membrane, and DNA degraded to around 21.2 kbp fragment. All of the results showed that there is possibility to inhibit hepatoma cells growth, to promote differentiation and apoptosis, and therefore to initiate reverse transformation via strict regulation of oxidative stress.

Apoptosis↗
PubMed1998

Crosstalk between alpha-1A and alpha-1B adrenoceptors in neonatal rat myocardium: implications in cardiac hypertrophy.

The myocardial effect of alpha-1A adrenoceptor (alpha-1 AR) agonists in neonatal rats are mediated by alpha-1A AR and not by alpha-1B AR, although both receptor subtypes are equally expressed; the functions of alpha-1B AR are not known. Here, we report that alpha-1 B ARs inhibit the activities of alpha-1A ARs in neonatal rat myocardium so that the inactivation of alpha-1 B ARs by chloroethylclonidine (CEC) potentiated the effects of nonselective alpha-1 AR agonist phenylephrine (PE) on myocardial protein synthesis and early gene (c-fos and c-jun) expression. CEC did not modify the hypertrophic effect of angiotensin II. The potentiation of the effects of PE by CEC was associated with a translocation of Ca(++)-dependent protein kinase C (PKC)alpha, which did not occur in the absence of CEC. Alpha-1A AR-selective agonist A61603 was approximately 1000-fold more potent than PE as a positive inotropic agent; it caused the translocation of PKC alpha, which was not affected by CEC. 5-Methylurapidil antagonized the effects of PE and A61603, suggesting that these were mediated via alpha-1A ARs. Alpha-1D AR antagonist BMY 7378 did not modify PE-induced translocation of PKC. CEC potentiated the effects of PE on Ca++ transients in Fura 2-AM-loaded dispersed cardiomyocytes, and this potentiation was prevented by nifedipine. In whole-cell patch-clamp recordings of cultured cardiomyocytes, CEC potentiated the effect of norepinephrine on Ca++ channel currents, which was blocked by 5-methylurapidil. We conclude that alpha-1A ARs are positively and alpha-1B ARs are negatively coupled to nifedipine-sensitive Ca++ channels, possibly via Gi protein, and this antagonistic relationship between alpha-A AR and alpha-1B AR in the neonatal heart might be required physiologically for normal alpha-1 AR-mediated responses and myocardial development.

Animals↗
PubMed1997

Vascular lesions in Chinese patients with transient ischemic attacks.

We studied 96 Chinese patients with TIAs using transcranial Doppler and duplex ultrasonography. We found intracranial stenosis or occlusion in 51% of cases and extracranial disease in 19% of cases. The most common intracranial lesion was stenosis of the terminal internal carotid artery or proximal middle cerebral artery, whereas the most common extracranial lesion was stenosis of the carotid bifurcation.

Adolescent↗
PubMed1996

Effects of vitamin E on the blastogenic response of splenocytes and lipofuscin contents in the hearts and brains of aged mice.

Semipurified diets containing 30 or 500 ppm of dl-alpha-tocopherol (VE) were fed for 12 weeks to young (3-month-old) and old (20-month-old) Swiss mice. We measured the blastogenic response of splenocytes, the serum VE, and the lipofuscin levels in brains and hearts. We found that old mice fed with 500 ppm VE diet had a significantly higher serum VE level and blastogenic response of splenocytes to concanavalin-A (ConA) and lipopolysaccharide (LPS) than those fed with 30 ppm VE diet (p < 0.01). However, the lipofuscin level in the brains and hearts of aged mice declined substantially with the VE supplementation (heart: p < 0.001, brain: p < 0.05). Furthermore, the effects of dietary VE on the serum VE and tissue lipofuscin content in aged mice were much more obvious than in the young animals.

Aging↗
PubMed1996

[Study on the enhancing effect of polyporus polysaccharide, mycobacterium polysaccharide and lentinan on lymphokine-activated killer cell activity in vitro].

The actions of Polyporus polysaccharide (PPS), mycobacterium polysaccharide (MPS) and lentinan (LEN) on lymphokine-activated killer (LAK) cell activity in vitro were investigated in this study. Human peripheral blood mononuclear cells (PBMC) were cultured for 96 hours with medium containing different concentrations of the above-mentioned drugs in combination with recombinant interleukin 2 (rIL-2). Then cell-mediated lysis was determined by 1H-TdR release assay including NK sensitive and NK resistant target cells. The results demonstrated that, when combined with rIL-2 in a certain concentration, all three kinds of polysaccharides could enhance the LAK activity by 42%-56.9%, and reduce the dose of rIL-2 by 50% (P < 0.05-0.01). It suggested that the PPS, MPS and LEN could be used as bioactivity regulators in LAK cell therapy in tumor treatment.

Cytotoxicity, Immunologic↗
PubMed1995

Immunohistochemical localization of transforming growth factor-beta 1 in Kaposi's sarcoma.

Immunohistochemical localization of transforming growth factor beta 1 (TGF-beta 1) was studied in Kaposi's sarcoma (KS) tissues obtained from autopsy and biopsy materials of patients with and without acquired immunodeficiency syndrome (AIDS) or human immunodeficiency virus (HIV) infection. There was no difference in the localization and distribution of TGF-beta 1 in KS tissues regardless of the HIV-1 status of the patients. Rabbit polyclonal antibodies to synthetic peptides, corresponding to the first 30 amino acids of mature TGF-beta 1, anti-LC(1-30), and anti-CC(1-30), were used for localization of intracellular and extracellular TGF-beta 1. An antibody to a peptide corresponding to amino acids 266 to 278 of the TGF-beta 1 precursor sequence anti-Pre(266 to 278) was used to detect the TGF-beta 1 precursor and the latency-associated peptide. Intracellular mature TGF-beta 1 was demonstrated in mononuclear cells, presumably macrophages, within KS tumors but not in spindle-shaped KS cells. Extracellular mature TGF-beta 1 was localized in the basement membranes of blood vessels and fibrous capsules of KS tumors. Intracellular reactivity to anti-Pre was localized in vascular smooth muscle cells and pericytes within the tumor, in variable proportions of spindle-shaped KS cells, and also in macrophage-like cells. These cells appear to be the production sites of TGF-beta 1, which may exert paracrine as well as autocrine proliferative effects.

Acquired Immunodeficiency Syndrome↗
PubMed1995

Advanced glycation endproducts interacting with their endothelial receptor induce expression of vascular cell adhesion molecule-1 (VCAM-1) in cultured human endothelial cells and in mice. A potential mechanism for the accelerated vasculopathy of diabetes.

Vascular cell adhesion molecule-1 (VCAM-1), an inducible cell-cell recognition protein on the endothelial cell surface (EC), has been associated with early stages of atherosclerosis. In view of the accelerated vascular disease observed in patients with diabetes, and the enhanced expression of VCAM-1 in diabetic rabbits, we examined whether irreversible advanced glycation endproducts (AGEs), could mediate VCAM-1 expression by interacting with their endothelial cell receptor (receptor for AGE, RAGE). Exposure of cultured human ECs to AGEs induced expression of VCAM-1, increased adhesivity of the monolayer for Molt-4 cells, and was associated with increased levels of VCAM-1 transcripts. The inhibitory effect of anti-RAGE IgG, a truncated form of the receptor (soluble RAGE) or N-acetylcysteine on VCAM-1 expression indicated that AGE-RAGE-induced oxidant stress was central to VCAM-1 induction. Electrophoretic mobility shift assays on nuclear extracts from AGE-treated ECs showed induction of specific DNA binding activity for NF-kB in the VCAM-1 promoter, which was blocked by anti-RAGE IgG or N-acetylcysteine. Soluble VCAM-1 antigen was elevated in human diabetic plasma. These data are consistent with the hypothesis that AGE-RAGE interaction induces expression of VCAM-1 which can prime diabetic vasculature for enhanced interaction with circulating monocytes.

Animals↗