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Biomedical subjects

Nan Li

Publications and source records attributed to Nan Li.

At least 73 records · Page 4Linked to original sources
PubMed2005

[Surgical treatment of metastatic spinal tumors by anterial approach].

OBJECTIVE: To investigate the efficacy of surgical treatment of the patients with metastatic spinal tumors by anterial decompression and stabilization. METHODS: From December 1997 to December 2003, 93 patients (40 women and 53 men) with metastatic spinal tumors were treated in our department. The locations of the tumor included, thoracic vertebra (53 cases), lumbar vertebra (33 cases), and cervical region (7 cases). The original tumors included lung cancer (21 cases), renal cancer (13 cases), prostate cancer (8 cases), hepatic cancer (5 cases), breast cancer (13 cases), thyroid cancer (5 cases), gastrointestinal tumor (3 cases), and multiple myeloma (8 cases). However, no primary tumor was found in the rest of 17 cases. Among 54 of 93 patients who presented with neurological dysfunction, 16 patients completely paralyzed and others incompletely paralyzed. The follow-up time ranged from 10 to 72 months. RESULTS: Pain was relieved in 87 of 93 patients (93.5%) and neurological function was improved in 47 of the 54 patients. Among 16 completely paralyzed patients, 7 patients experienced a neurological function improvement (from Frankel grade A or B to C or D after decompression). The average amount of blood transfused was 3000 ml. No severe complications were seen in our series. The one-year survival rate was 85% (79 cases). CONCLUSIONS: The integrity of the spinal column structure and neurological function should be considered firstly in the treatment of spinal metastasis. Thorough resection of metastatic tumor and stable internal fixation by anterior approach should be performed when single or two vertebra are involved. In order to alleviate paralysis, promote spinal stability, and improve the quality of life, urgent decompression should be performed on patient with spinal metastasis.

Breast Neoplasms↗
PubMed2005

[Pharmacokinetic study of intraperitoneal chemotherapy with HCPT].

OBJECTIVE: To study the pharmacokinetic of 10-Hydroxycamptothecin HCPT by intraperitoneal administration. METHOD: Six dogs were given HCPT by intraperitoneal perfusion: HCPT 2 mg x kg(-1), dissolved in 300 mL NS. During the course of experiments, peritoneal fluids and blood were sampled using a standardized protocol. The concentration of HCPT in all samples was determined by high performance liquid chromatography (HPLC). RESULT: The area under the curve (AUC) of peritoneal fluids was significantly highly as compared to the AUC of femoral vein and portal vein (P < 0.001). CONCLUSION: These experiments demonstrate that intraperitoneal chemotherapy has significant effect on the pharmacokinetics of IP route of HCPT administration. This method should be a more reasonable chemotherapy for the prevention of recurrence and liver metastasis of gastric cancer, colon cancer and ovary cancer after radical resection.

Animals↗
PubMed2004

Electrochemical study of a new methylene blue/silicon oxide nanocomposition mediator and its application for stable biosensor of hydrogen peroxide.

A novel organic-inorganic nanocomposite of methylene blue (MB) and silicon oxide was synthesized and characterized by TEM, FTIR, and UV-vis. The as-prepared material was able to transfer the electron of the MB to electrode and was different from other SiO2 spheres structurally. It can be used as mediator to construct a biosensor with horseradish peroxidase (HRP) coimmobilized in the gelatine matrix and cross-linked with formaldehyde. The resulting biosensor exhibited fast amperometric response and good stability to hydrogen peroxide (H2O2). The linear range for H2O2 determination was from 1 x 10(-5) to 1.2 x 10(-3) M, with a detection limit of 4 x 10(-6) M based on S/N = 3. Moreover, the lifetime is more than 3 months under dry conditions at 4 degrees C.

Biosensing Techniques↗
PubMed2004

Bone marrow stromal cell-derived growth inhibitor inhibits growth and migration of breast cancer cells via induction of cell cycle arrest and apoptosis.

Genes encoding growth-inhibitory proteins are postulated to be candidate tumor suppressors. The identification of such proteins may benefit the early diagnosis and therapy of tumors. Here we report the cloning and functional characterization of a novel human bone marrow stromal cell (BMSC)-derived growth inhibitor (BDGI) by large scale random sequencing of a human BMSC cDNA library. Human BDGI cDNA encodes a 477-amino acid residue protein that shares high homology with rat and mouse pregnancy-induced growth inhibitors. The C-terminal of BDGI is identical to a novel human pregnancy-induced growth inhibitor, OKL38. BDGI is also closely related to many other eukaryotic proteins, which together form a novel and highly conserved family of BDGI-like proteins. BDGI overexpression inhibits the proliferation, decreases anchorage-dependent growth, and reduces migration of MCF-7 human breast cancer cells, whereas down-regulation of BDGI expression promotes the proliferation of MCF-7 and HeLa cervix epitheloid carcinoma cells. Interestingly, the inhibitory effect of BDGI on MCF-7 cells is more potent than that of OKL38. We demonstrate that BDGI induces cell cycle arrest in S phase and subsequent apoptosis of MCF-7 cells, which is likely to account for the antiproliferative effects of BDGI. This process may involve up-regulation of p27Kip1 and down-regulation of cyclin A, Bcl-2, and Bcl-xL. The inhibitory effect of BDGI on cell proliferation and the induction of apoptosis were also observed in A549 lung cancer cells but not HeLa cells. These results indicate that BDGI might be a growth inhibitor for human tumor cells, especially breast cancer cells, possibly contributing to the development of new therapeutic strategies for breast cancer.

Amino Acid Sequence↗
PubMed2004

Interaction of echinomycin with guanine: electrochemistry and spectroscopy studies.

The interaction of antitumor antibiotic, echinomycin (Echi) with guanine (Gua) was thoroughly investigated by adsorptive transfer stripping cyclic voltammetry, ultraviolet and visible adsorption spectra (UV/Vis) and Fourier-transform infrared spectroscopy (FTIR). Electrochemistry provided a simple tool for verifying the occurrence of interaction between Echi and Gua. Echi could be accumulated from the solution and give well-defined electrochemical signals in 0.1 M phosphate buffer solution (pH 7.0) only when Gua was present on the surface of the electrochemically pretreated glass carbon electrode (GCE), suggesting a strong binding of Echi to Gua. All the acquired spectral data showed that a new adduct between Echi and Gua was formed, and two pairs of adjacent intermolecular hydrogen bonds between the Ala backbone atoms in Echi and Gua (Ala-NH to Gua-N3 and Gua-NH2 to Ala-CO) played a dominating role in the interaction. Electrochemistry coupled with spectroscopy techniques could provide a relatively easy way to obtain useful insights into the molecular mechanism of drug-DNA interactions, which should be important in the development of new anticancer drugs with specific base recognition.

Adsorption↗
PubMed2004

Inhibition of mitochondrial gene transcription suppresses neurotensin secretion in the human carcinoid cell line BON.

Mitochondria, organelles essential for ATP production, play a central role in a number of cellular functions, including the regulation of insulin secretion. Neurotensin (NT), an important regulatory intestinal hormone, has been implicated in fatty acid translocation, gut motility and secretion, and intestinal cell growth; however, mechanisms regulating NT secretion have not been entirely defined. The purpose of this study was to determine the effect of inhibition of mitochondrial gene transcription on NT secretion. BON cells, a novel human carcinoid cell line that produces and secretes NT peptide and expresses the gene encoding NT (designated NT/N), were treated with ethidium bromide (EB; 0.05, 0.1, and 0.4 microg/ml), an inhibitor of DNA and RNA synthesis, or vehicle over a time course (1-4 days). Cells were then stimulated with either ACh (100 microM) or phorbol 12 myristate,13-acetate (PMA, 10 nM) for 30 min. Media and cells were extracted, and NT peptide measured by RIA. Treatment with EB had no effect on BON cell viability or cell cycle distribution over the 4-day course. In contrast, EB treatment produced a dose-dependent reduction of mitochondrial gene expression; however, NT/N gene expression was not altered. Mitochondrial inhibition by EB treatment suppressed NT secretion induced by ACh and PMA, both in a dose-dependent manner. EB-mediated inhibition of NT secretion and mitochondrial gene expression was reversed with removal of EB. Our results demonstrate that inhibition of mitochondrial gene transcription suppresses both ACh- and PMA-stimulated NT release. These findings are the first to demonstrate that mitochondrial function is important for agonist-mediated NT secretion.

Acetylcholine↗
PubMed2004

A novel human dendritic cell-derived C1r-like serine protease analog inhibits complement-mediated cytotoxicity.

Trypsin-like serine proteases are involved in diverse biological processes such as complement activation, tissue remodeling, cellular migration, tumor invasion, and metastasis. Here we report a novel human C1r-like serine protease analog, CLSPa, derived from dendritic cells (DC). The 487-residue CLSPa protein contains a CUB domain and a serine protease domain, possessing characteristic catalytic triad but lacking typical activation/cleavage sequence. It shares great homology with complement C1r/C1s and mannose-associated serine proteases. CLSPa mRNA is widely expressed, especially abundant in placenta, liver, kidney, pancreas, and myeloid cells, which are a major resources of serine proteases. Upon stimulation by agonistic anti-CD40 Ab, TNF-alpha, or LPS, CLSPa mRNA expression was significantly up-regulated in monocytic cells and monocyte-derived immature DC. When overexpressed in 293T cells, CLSPa protein was synthesized into the culture supernatants as a secretory protein, which had an inhibitory effect on complement-mediated cytotoxicity to antibody-sensitized erythrocytes. However, CLSPa itself possesses little protease activity, but it plays an inhibitory role in other active protease catalytic processes. The identification of human CLSPa as a novel Clr-like protein might facilitate future investigation of the regulatory mechanism of CLSPa in complement pathways during inflammation.

Amino Acid Sequence↗
PubMed2004

A novel human phosphatidylethanolamine-binding protein resists tumor necrosis factor alpha-induced apoptosis by inhibiting mitogen-activated protein kinase pathway activation and phosphatidylethanolamine externalization.

The phosphatidylethanolamine (PE)-binding proteins (PEBPs) are an evolutionarily conserved family of proteins with pivotal biological functions. Here we describe the cloning and functional characterization of a novel family member, human phosphatidylethanolamine-binding protein 4 (hPEBP4). hPEBP4 is expressed in most human tissues and highly expressed in tumor cells. Its expression in tumor cells is further enhanced upon tumor necrosis factor (TNF) alpha treatment, whereas hPEBP4 normally co-localizes with lysosomes, TNFalpha stimulation triggers its transfer to the cell membrane, where it binds to Raf-1 and MEK1. L929 cells overexpressing hPEBP4 are resistant to both TNFalpha-induced ERK1/2, MEK1, and JNK activation and TNFalpha-mediated apoptosis. Co-precipitation and in vitro protein binding assay demonstrated that hPEBP4 interacts with Raf-1 and MEK1. A truncated form of hPEBP4, lacking the PE-binding domain, maintains lysosomal co-localization but has no effect on cellular responses to TNFalpha. Given that MCF-7 breast cancer cells expressed hPEBP4 at a high level, small interfering RNA was used to silence the expression of hPEBP4. We demonstrated that down-regulation of hPEBP4 expression sensitizes MCF-7 breast cancer cells to TNFalpha-induced apoptosis. hPEBP4 appears to promote cellular resistance to TNF-induced apoptosis by inhibiting activation of the Raf-1/MEK/ERK pathway, JNK, and PE externalization, and the conserved region of PE-binding domain appears to play a vital role in this biological activity of hPEBP4.

Amino Acid Sequence↗
PubMed2004

KLRL1, a novel killer cell lectinlike receptor, inhibits natural killer cell cytotoxicity.

Natural killer (NK) cell inhibitory receptors play important roles in the regulation of target susceptibility to natural killing. Here, we report the molecular cloning and functional characterization of a novel NK cell receptor, KLRL1, from human and mouse dendritic cells. KLRL1 is a type II transmembrane protein with an immunoreceptor tyrosine-based inhibitory motif and a C-type lectinlike domain. The KLRL1 gene is located in the central region of the NK gene complex in both humans and mice, on human chromosome 12p13 and mouse chromosome 6F3, adjacent to the other KLR genes. KLRL1 is preferentially expressed in lymphoid tissues and immune cells, including NK cells, T cells, dendritic cells, and monocytes or macrophages. Western blot and fluorescence confocal microscopy analyses indicated that KLRL1 is a membrane-associated glycoprotein, which forms a heterodimer with an as yet unidentified partner. Human and mouse KLRL1 are both predicted to contain putative immunoreceptor tyrosine-based inhibitory motifs (ITIMs), and immunoprecipitation experiments demonstrated that KLRL1 associates with the tyrosine phosphatases SHP-1 (SH2-domain-containing protein tyrosine phosphatase 1) and SHP-2. Consistent with its potential inhibitory function, pretreatment of target cells with human KLRL1-Fc fusion protein enhances NK-mediated cytotoxicity. Taken together, our results demonstrate that KLRL1 belongs to the KLR family and is a novel inhibitory NK cell receptor.

Animals↗
PubMed2004

Triptolide (PG-490) induces apoptosis of dendritic cells through sequential p38 MAP kinase phosphorylation and caspase 3 activation.

Dendritic cells (DCs) are the most potent antigen-presenting cells that play crucial roles in the regulation of immune response. Triptolide, an active component purified from the medicinal plant Tripterygium wilfordii Hook F., has been demonstrated to act as a potent immunosuppressive drug capable of inhibiting T cell activation and proliferation. However, little is known about the effects of triptolide on DCs. The present study shows that triptolide does not affect phenotypic differentiation and LPS-induced maturation of murine DCs. But triptolide can dramatically reduce cell recovery by inducing apoptosis of DCs at concentration as low as 10ng/ml, as demonstrated by phosphatidylserine exposure, mitochondria potential decrease, and nuclear DNA condensation. Triptolide induces activation of p38 in DCs, which precedes the activation of caspase 3. SB203580, a specific kinase inhibitor for p38, can block the activation of caspase 3 and inhibit the resultant apoptosis of DCs. Our results suggest that the anti-inflammatory and immunosuppressive activities of triptolide may be due, in part, to its apoptosis-inducing effects on DCs.

Animals↗
PubMed2004

IgSF13, a novel human inhibitory receptor of the immunoglobulin superfamily, is preferentially expressed in dendritic cells and monocytes.

A novel inhibitory receptor of immunoglobin superfamily (IgSF), IgSF member 13 (IgSF13), has been identified from human dendritic cells (DC). IgSF13 is a type I transmembrane protein containing an N-terminal signal peptide, a extracellular region with a single Ig V-like domain, a transmembrane region, and a cytoplasmic tail with two classical immunoreceptor tyrosine-based inhibitory motifs (ITIM), suggesting its inhibitory function. IgSF13 shows significant homology to human CMRF35 and pIgR. IgSF13 gene is mapped to chromosome 17q25.2, very close to that of CMRF35. IgSF13 is preferentially expressed in myelo-monocytic cells, including monocytes, monocyte-derived DC, and monocyte-related cell lines. Upon pervanadate treatment, IgSF13 was hyper-phosphorylated and associated with Src homology-2 domain-containing phosphatases SHP-1 and SHIP, but not SHP-2. The identification of IgSF13 as a novel ITIM-bearing receptor selectively expressed by DC and monocytes suggests that it may be potentially involved in the negative regulation of specific leukocyte population.

Amino Acid Sequence↗
PubMed2004

[The COX regression analysis on the use of corticosteroids in the treatment of SARS].

OBJECTIVE: To explore the effectiveness of corticosteroids (GCS) and to determine how to use it in the treatment of SARS. METHODS: All reported probable cases in Beijing were reviewed. Those who fulfilled the diagnostic criteria with an integrity clinical record were recruited in the study. A database was established and all the clinical data, including patients' personal information, epidemiological history, underlying diseases, clinical manifestations, laboratory tests and therapies after hospitalization, as well as the outcome of the disease, were inputted under a quality control. Unifactor and COX multifactor regression analysis were done. The dose of GCS was all expressed in that of methylprednisolone. RESULTS: 1291 cases were in consistence with the demands mentioned above. Among them, 1084 cases (83.96%) had used GCS and 207 did not in the course of SARS. There was no significant difference of average age (t = -1.08, P = 0.2808) and the time from SARS onset to hospitalization (P = 0.2797) between the two groups. COX regression showed that the risk of fatality in the GCS group was higher than that of those who did not use GCS (RR = 1.334, 95% of CI: 0.588 - 3.026). In the patients with comorbidities, RR was 2.086 (95% of CI: 0.694 - 6.267), and RR was 0.536 (95% of CI: 0.146 - 1.970) in the patients with no comorbidity. In those without any comorbidity, the initial doses, maximal doses, average doses and cumulative doses all showed a 'J' shape change. An appropriate dose could keep RR to be the lowest whereas the doses either higher or lower than it could increase RR. The initial dose with the lowest RR was 80 - 160 mg/d, the maximum 80 - 160 mg/d, the average < 80 mg/d and the cumulative one 1000 - 3000 mg although there was no statistical significance (all P > 0.05). RR was less than 1 in non-comorbidity patients who initiated GCS therapy before the 15th day of the disease. RR was 1.415 (95% of CI: 0.195 - 10.257) in the patients who began to use GCS over this period. Counting from hospitalization, the time of GCS use also showed a 'J' type change of RR. The initiation of GCS from day 5 to 7 had the lowest RR (0.282, 95% of CI: 0.043 - 1.828) and that from day 8 to 14 was 1 (95% of CI: 0.150 - 6.654). CONCLUSION: In the treatment of SARS, GCS seems to be effective. An appropriate dose and a right time of application decrease the risk of death. The use of GCS in SARS patients with comorbidities should be with caution.

Adolescent↗
PubMed2004

Rab7b, a novel lysosome-associated small GTPase, is involved in monocytic differentiation of human acute promyelocytic leukemia cells.

Rab7 is a small Rab GTPase that regulates vesicular traffic from early to late endosomal stages of the endocytic pathway. Here we report the cloning and characterization of a novel Rab7-like GTPase, which shares highest homology with Rab7 and thus is designated as Rab7b. Northern blot analysis shows that Rab7b mRNA is expressed in human heart, placenta, lung, skeletal muscle, and peripheral blood leukocyte. RT-PCR or Western blot analysis of Rab7b expression shows that Rab7b is selectively expressed in monocytes, monocyte-derived immature dendritic cells (DCs), and promyeloid or monocytic leukemia cell lines. In the peripheral blood, Rab7b is specifically detected in CD14(+) cells, but not in CD4(+), CD8(+), CD19(+) or CD56(+) cells. When immature DCs are matured with lipopolysaccharide (LPS), Rab7b expression is gradually downregulated, while Rab7b is upregulated when monocytes are activated by LPS treatments. In acute promyelocytic leukemia (APL) HL-60 and NB4 cell lines, Rab7b expression is upregulated after phorbol myristate acetate (PMA)-induced monocytic differentiation. By immunofluorescence confocal microscopy, we demonstrate that Rab7b is associated with lysosomal organelles. Our data suggest that Rab7b is a lysosome-localized monocytic cell-specific small GTPase, and is involved in PMA-induced APL cell differentiation and possibly in regulation of monocyte functions.

Amino Acid Sequence↗
PubMed2004

Artificial rearing of mouse pups: development of a mouse pup in a cup model.

Artificial rearing of rat pups has been used in the investigation of the neonatal gut. We propose to adapt the model of artificially rearing rat pups for use in mouse pups, thereby allowing the use of transgenic animals for our research. We hypothesized that gastrostomy catheters may be placed successfully into neonatal mouse pups and that the pups may be artificially reared without significant alterations in their growth or intestinal development. Gastrostomy tubes are placed into 5-d-old mouse pups [artificially reared (AR); n = 32], and the mice are fed rodent milk substitute. Littermate pups [maternally reared (MR); n = 22] are used as controls. After 5 d, pups are killed and their organs are harvested. Intestinal villus measurements, protein content, and DNA content are determined. Data are reported as mean +/- SEM, compared with appropriate statistical methods, and significance is determined at P < 0.05. Initial weights and lengths are not different between the two groups, but after 5 d, MR pups weigh more than their AR counterparts (5.0 +/- 0.13 versus 4.1 +/- 0.14 g, MR versus AR; P < 0.01). However, the pups' length and the intestinal villus height-to-width ratios, protein, and DNA content are not different between the MR and AR pups. To our knowledge, this is the first report of artificially rearing mouse pups. Development of this technique will permit nutritional manipulation in neonatal mice, a mammalian model wherein the genome is sequenced and transgenic mutants are available.

Animals↗
PubMed2004

Scaling of directed dynamical small-world networks with random responses.

A dynamical model of small-world networks, with directed links which describe various correlations in social and natural phenomena, is presented. Random responses of sites to the input message are introduced to simulate real systems. The interplay of these ingredients results in the collective dynamical evolution of a spinlike variable S(t) of the whole network. The global average spreading length (s) and average spreading time (s) are found to scale as p(-alpha)ln(N with different exponents. Meanwhile, S(t) behaves in a duple scaling form for N>>N(*): S approximately f(p(-beta)q(gamma)t), where p and q are rewiring and external parameters, alpha, beta, and gamma are scaling exponents, and f(t) is a universal function. Possible applications of the model are discussed.

Disease Transmission, Infectious↗
PubMed2004

Glutamine regulates Caco-2 cell tight junction proteins.

Intestinal epithelial tight junction (TJ) barrier dysfunction may lead to inflammation and mucosal injury. Glutamine (GLN) plays a role in maintenance of intestinal barrier function in various animal models and critically ill humans. Recent evidence from intestinal cell monolayers indicates that GLN maintains transepithelial resistance and decreases permeability. The mechanisms of these effects remain undefined. We hypothesized that GLN affects proteins involved in the intercellular junctional complex. GLN availability was controlled in Caco-2 monolayers by addition to the medium and treatment with methionine sulfoximine (MSO) to inhibit glutamine synthetase (GS). Expression of TJ proteins, claudin-1, occludin, and zonula occluden (ZO)-1 was measured by immunoblotting. Localization of TJ proteins was evaluated by immunofluorescence light microscopy. Structure of TJ was determined by transmission electron microscopy (TEM). Deprivation of GLN decreased claudin-1, occludin, and ZO-1 protein expression and caused a disappearance of perijunctional claudin-1 and a reduction of occludin but had no effect on ZO-1. TEM revealed that MSO-treated cells in the absence of GLN formed irregular junctional complexes between the apical lateral margins of adjoining cells. These findings indicate that TJ protein expression and cellular localization in Caco-2 cell monolayers rely on GLN. This mechanism may similarly relate to GLN-mediated modulation of intestinal barrier function in stressed animals and humans.

Blotting, Western↗