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Biomedical subjects

Ling Wang

Publications and source records attributed to Ling Wang.

At least 145 records · Page 8Linked to original sources
PubMed2003

Biocompatibility and biodegradation of poly(hydroxybutyrate)/poly(ethylene glycol) blend films.

Using chloroform as co-solvent, a series of poly(3-hydroxybutyrate) (PHB) and polyethylene glycol (PEG) blend materials with different ratio ranging from 80 : 20 (wt %) to 20 : 80 (wt %) were prepared by solution blend. The blood-compatibility was evaluated by means of platelet clotting time test and exploring its morphological changes. The results showed that PEG played an important role in resisting platelet adhesion. With the increased addition of PEG, the clotting times became longer and the number of platelet adhesion decreased apparently. All platelets were in discrete state, no pseudopodium had been found and no collective phenomenon had been happened. The cell-compatibility was evaluated via Chinese Hamster Lung (CHL) fibroblast cultivation in vitro. The cells cultured on the matrix spread and proliferated well. With the increase of PEG content in the blend films, the number of live cells became more and more. These results indicated that PHB exhibited satisfying cell-compatibility and the addition of PEG also could improve the cell-compatibility of PHB. The biodegradation experiment indicated that the degradation of PHB/PEG was accelerated by enzyme in vitro and the blending of PEG was favorable to degradation.

Journal Article↗
PubMed2003

Inactivation of the nuclear receptor coactivator RAP250 in mice results in placental vascular dysfunction.

Coactivators constitute a diverse group of proteins that are essential for optimal transcriptional activity of nuclear receptors. In the past few years many coactivators have been identified but it is still unclear whether these proteins interact indiscriminately with all nuclear receptors and whether there is some redundancy in their functions. We have previously cloned and characterized RAP250 (ASC-2/PRIP/TRBP/NRC), an LXXLL-containing coactivator for nuclear receptors. In order to study its biological role, Rap250 null mice were generated by gene targeting. Here we show that genetic disruption of Rap250 results in embryonic lethality at embryonic day (E) 13.5. Histological examination of placentas revealed a dramatically reduced spongiotrophoblast layer, a collapse of blood vessels in the region bordering the spongiotrophoblast, and labyrinthine layers in placentas from Rap250(-/-) embryos. These findings suggest that the lethality of Rap250(-/-) embryos is the result of obstructed placental blood circulation. Moreover, the transcriptional activity of PPAR gamma is reduced in fibroblasts derived from Rap250(-/-) embryos, suggesting that RAP250 is an essential coactivator for this nuclear receptor in the placenta. Our results demonstrate that RAP250 is necessary for placental development and thus essential for embryonic development.

Animals↗
PubMed2003

UV-induced corneal epithelial cell death by activation of potassium channels.

PURPOSE: The purpose of the present study is to determine the role of K+ channel activity as an early event in UV-induced corneal epithelial cell apoptosis. METHOD: Both cell-attached and nystatin-perforated patch-clamping were performed to record K+ channel activity in rabbit corneal epithelial (RCE) and primary cultured rabbit corneal epithelial (PRCE) cells exposed to UV irradiation. On exposure of corneal epithelial cells or intact corneas to UV-C irradiation or treatment of corneal epithelial cells with etoposide, cell apoptosis was determined by DNA fragmentation, ethidium bromide-acridine orange nuclear stain and TdT-mediated dUTP nick-end labeling (TUNEL). RESULTS: In the present study, UV-irradiation-induced corneal epithelial cell apoptosis through activation of a K+ channel in the cell membrane was an early event in response to UV irradiation. UV-C irradiation (42 microJ/cm(2)) activated robust K+ channel activity in RCE and PRCE cells at both the single-channel and whole-cell levels, when measured with the cell-attached and nystatin-perforated patch clamps, respectively. Suppression of UV-irradiation-induced K+ channel activity with the specific K+ channel blocker 4-aminopurydine (4-AP) prevented UV-irradiation-induced apoptosis in the RCE and PRCE cells, loss of the superficial layer of corneal epithelium, and apoptosis in the basal layer corneal epithelium. However, suppression of K+ channel activity did not protect RCE and PRCE cells from etoposide, a topoisomerase II inhibitor, which induced cell death by bypassing the membrane. Furthermore, application of valinomycin, a K+ ionophore, to mimic the effect of mass activation of the K+ channel in RCE and PRCE cells caused cell apoptosis. CONCLUSIONS: The results indicate that UV irradiation induces superactivity of K+ channels in the membrane is an early event mediating signaling transduction and resulting in corneal epithelial cell death in response to UV irradiation.

4-Aminopyridine↗
PubMed2003

UV-induced signaling pathways associated with corneal epithelial cell apoptosis.

PURPOSE: UV-C irradiation of corneal epithelial cells elicits K+ channel activation, which in turn causes them to undergo apoptosis. In the present study, the intermediary role played by mitogen-activated protein kinase (MAPK) signaling pathways in mediating this response was investigated. METHODS: Western blot and kinase assays were used to measure UV-induced activation (i.e., phosphorylation) of c-Jun NH(2)-terminal kinase (JNK)/SEK, extracellular signal-regulated kinase (ERK), and p38. Corneal epithelial apoptosis was determined by measuring caspase 3 activity. RESULTS: UV-irradiation-induced increases in cell membrane K+ channel activity resulted in activations of JNK, SEK upstream of JNK, and caspase 3 downstream of JNK. Suppression of K+ channel activity with specific K+ channel blockers significantly inhibited UV-irradiation-induced activation of JNK cascades. However, suppression of K+ channel activity did not prevent hyperosmotic-stress-induced JNK activation. In addition, UV-irradiation-induced SEK/JNK activation was unaffected by removal of extracellular free Ca2+ with EGTA. CONCLUSIONS: UV-irradiation-induced corneal epithelial cell apoptosis is mediated through activation of the SEK/JNK signaling pathway. Such activation is dependent on increases in K+ channel activity, which play an important role in the early events that result in activation of this pathway.

Animals↗
PubMed2003

Tissue-specific impairment of insulin signaling in vasculature and skeletal muscle of fructose-fed rats.

The relation between insulin resistance/hyperinsulinemia and cardiovascular diseases has attracted much attention. Insulin affects not only glucose metabolism, but also protein synthesis and cell growth. Insulin stimulates both the phosphatidylinositol 3-kinase (PI3-K) and mitogen-activated protein kinase (MAPK) pathways, but the relationship between cardiovascular disease and selective insulin signal pathways is unclear. We investigated the tissue specificity and intracellular signal transduction selectivity of insulin resistance in the vasculature and skeletal muscle of fructose-fed rats (FFR). Sprague-Dawley rats were fed either normal rat chow (control rats) or fructose-rich chow. Normal saline with or without 1,000 (microg/kg) insulin was injected, and then the thoracic aorta or soleus muscle was removed under anesthetization. Insulin-induced tyrosine phosphorylation of insulin receptor beta subunit (IRbeta) and insulin receptor substrate-1 (IRS-1) and tyrosine/threonine phosphorylation of p44/42 MAPK (ERK-1/2) were evaluated. There were no significant differences in the degree of phosphorylation of IRbeta or ERK-1/2 in the thoracic aorta or in the soleus muscle between FFR and controls. However, tyrosine phosphorylation of IRS-1 in the soleus muscle of FFR was significantly reduced to 80% (p<0.001) of that in controls. The results suggest that PI3-K pathway in skeletal muscle is selectively impaired in FFR, and this impairment may induce hyperinsulinemia, which in turn may stimulate the MAPK pathway and lead to atherosclerosis. Thus PI3-K pathway may be one of the factors underlying the onset of cardiovascular disease in patients with insulin resistance.

Animals↗
PubMed2003

Chinese medicine, Jiang-Tang-Ke-Li, improves insulin resistance by modulating muscle fiber composition and muscle tumor necrosis factor-alpha in fructose-fed rats.

Insulin resistance and hyperinsulinemia are common findings in patients with essential hypertension. These impairments in glucose metabolism are commonly associated with diabetes mellitus, hypertension, and dyslipidemia, which are high risk factors of cardiovascular diseases, and recent evidence indicates that they may play a role in the development of coronary artery disease. The aim of this study was to determine the effect of Jiang-Tang-Ke-Li (JTKL), a traditional Chinese medicine used to treat diabetes mellitus in China, on insulin resistance and hypertension in fructose-fed rats (FFR). Systolic blood pressures in the FFR groups were significantly higher than that in the control group, although JTKL had no effect on systolic blood pressure for the last 2 weeks of treatment with the medicine. The average rate of glucose infusion during a glucose clamp, as an index of insulin sensitivity (M value), was significantly lower in the FFR than in the control rats, and treatment with JTKL for 2 weeks significantly increased the M value to that of the control. Treatment with Panax ginseng (PG), a component of JTKL, for 2 weeks also significantly increased the M value of FFR to the control level. The composite ratio of type I fibers in soleus muscle decreased significantly in the FFR compared to that in the control, and treatment with JTKL led to recovery of the composite ratio of type I fibers to the same level as that of the control group. The M value showed a significant positive correlation with the composite ratio of type I fibers and a significant negative correlation with the composite ratio of type II fibers. Tumor necrosis factor (TNF)-alpha levels were significantly higher in the soleus and extensor digitorum longus (EDL) muscles of the FFR than in those of the control rats. Treatment with JTKL for 2 weeks significantly lowered TNF-alpha levels to the control levels. M values showed a significant negative correlation with TNF-alpha in both the soleus and EDL muscles. The results suggest that the Chinese medicine JTKL, which contains PG as one of its valid components, improves insulin resistance by modulating muscle fiber composition and TNF-alpha in skeletal muscles in hypertensive and insulin-resistant FFR.

Animals↗
PubMed2003

[Analysis and identification of transcriptional repression domain of ETO].

OBJECTIVE: To further verify the transcriptional repression domains in ETO and their relationship with histone deacetylase (HDAC). METHODS: Either of the ETO two zinc fingers was mutated respectively by site-directing mutagenesis. The truncation fragments of ETO were amplified by polymerase chain reaction (PCR) and cloned into eukaryotic expression plasmid pFA-CMV. By the means of DNA transfection and analysis of the transcription derived from the promoter of reporter gene, the transcriptional regulation domains of ETO was determined. RESULTS: The expression plasmids carrying truncated ETO and ETO with point mutation at either zinc finger were successfully constructed. Two repression domains were found within ETO, which were located at two zinc finger motifs and 275 - 487 amino acid residues, respectively. CONCLUSION: The transcription repression by ETO was mediated by two separated domains and closely associated with HDAC, which may be used as therapeutic target for acute myeloid leukemia M(2b).

Core Binding Factor Alpha 2 Subunit↗
PubMed2003

[Changes of serum interleukin (IL)-12 and IL-13 in asthmatic patients and regulatory effects of glucocorticoids on them].

OBJECTIVE: To observe the changes of serum interleukin (IL)-12, IL-13 and lung function in asthmatic patients and to evaluate the influence of glucocorticoid on them. METHODS: The serum samples were obtained from (1) 25 asthmatic patients with acute asthma attack before and after one week course of oral prednisone, (2) 20 asthmatic patients in remission stage, and (3) 15 healthy volunteers. Serum IL-12 and IL-13 were determined with sandwich ELISA. Lung ventilatory function forced expiratory volume in one second (FEV(1)) and respiratory impedance airway resistance (R(5)) were measured in all patients. RESULTS: (1) Serum level of IL-12 in asthma attack group was significantly lower than that in asthma remission group (P < 0.05); both were significantly lower than that in normal control group (P < 0.01); in asthma attack group IL-12 level after prednisone treatment was significantly higher than that before treatment (P < 0.01). (2) Serum level of IL-13 in asthma attack group was significantly higher than that in asthma remission group (P < 0.01); both were significantly higher than that in normal control group (P < 0.01); in asthma attack group IL-13 level after prednisone treatment was significantly lower than that before treatment (P < 0.01). Correlation analysis showed that the serum level of IL-12 was positively correlated to FEV(1) and negatively correlated to R(5) and to serum level of IL-13 (r(1) = 0.458, r(2) = -0.516, and r(3) = -0.549, respectively; P < 0.05 and P < 0.01); the serum level of IL-13 was negatively correlated to FEV(1) and positively correlated to R(5) (r(1) = -0.493, and r(2) = 0.528, respectively; P < 0.05). CONCLUSION: The secretion of IL-12 and IL-13 was impaired in asthma with a significant increase in serum level of IL-13 and decrease in serum level of IL-12. Glucocorticoid could downregulate the serum level of IL-13 and upregulate the serum level of IL-12, redress the imbalance of IL-12/IL-13, and improve lung function in asthmatic patients.

Adolescent↗
PubMed2003

[Effect of fluticasone inhalation combined with xiaoqinglong decoction on pulmonary function and serum interleukin-16 level in asthma patients].

OBJECTIVE: To observe the effect of Fluticasone inhalation combined with Xiaoqinglong decoction (XQLD) on pulmonary function and serum interleukin-16 (IL-16) level in asthma patients. METHODS: Fifty-four mild or severe asthma patients were selected and randomly divided into three groups. The treated group was treated with Fluticasone inhalation combined with XQLD, Fluticasone group treated with Fluticasone inhalation, and XQLD group treated with XQLD respectively. Meanwhile ten healthy volunteers were selected as healthy control group. The conventional pulmonary function FEV1 and respiratory impedance R5 were measured before and after 4 weeks treatment. The IL-16 levels were determined by using ELISA. RESULTS: FEV1 were obviously increased and R5 decreased in the three groups after treatment (P < 0.05 or P < 0.01), but the improvement was more significant in the treated group (P < 0.01). Before treatment, serum levels of IL-16 in all the three groups were significantly higher than those in the healthy control group (P < 0.01) and lowered after treatment respectively, the treated group was significantly lower than those of the other two groups (P < 0.05 or P < 0.01). The serum level of IL-16 was negatively correlated with FEV1 and positively with R5(r1 = -0.67, r2 = 0.71, P < 0.01). CONCLUSION: The effects of Fluticasone inhalation combined with XQLD on pulmonary function and serum IL-16 levels were superior to those of Fluticasone inhalation and XQLD alone in asthma patients. So it could become an important therapeutical method in treating mild and severe asthma patients.

Administration, Inhalation↗
PubMed2003

[Clinical application of universal spine system in reconstruction of lumbar sacrum joint after resection of sacrum tumor].

OBJECTIVE: To investigate the operative indications and techniques of the universal spine system (USS) in reconstruction of the stability of the lumbar-sacrum joint after resection of sacrum tumor. METHODS: Nine patients were treated with USS after resection of sacrum tumor. Among them, there were 6 males and 3 females, aged from 34-60 years. The operation could be divided into four main procedures: 1. to resect sacrum tumor; 2. to insert the pedicle screw into the normal pedicle (L3 or L4 or L5) above the region of laminectomy; 3. to insert the lower screw into the iliac plate; 4. to put the rods, bone graft and links. RESULTS: There was no recurrence of sacrum tumor by MRI examination during 7-17 month follow-up. The pains of the lumbar-sacrum joint and the spinal nerve root were relieved obviously. The patients could stand and walked normally. There was no loose screw and no fracture of the screw and the rod. There was no appearance of the enlarged screw passage, the lessened pelvis and lowed L5 spine. CONCLUSION: Reconstruction of the lumbar-sacrum joint by the USS after resection of sacrum tumor is a practical operation clinically. It is characterized by the easy manipulation, few complication and stable fixation.

Adult↗
PubMed2003

[Spatial diversity index analysis on wildlife habitat pattern change in the Liaohe Delta].

Based on the study of land cover change in the Liaohe Delta with GIS and RS, the wildlife habitat pattern was described quantitatively, and the pattern change between 1988 and 1998 was analyzed with spatial diversity index. The results showed that the wildlife habitat pattern had an obvious change during the ten years caused by natural and human disturbance. The area of suitable habitat(Sd > or = 0.35) was becoming smaller and more fragmented, with a deteriorated quality. It was proved that spatial diversity index could reflect the habitat suitability of wildlife, and describe the habitat spatial pattern explicitly. This study would provide a scientific basis for protecting wild animals and their habitats.

Animals↗
PubMed2003

[Study of NMDAR expression in hippocampal CA(1) region in neonatal rats with hypoxic-ischemia].

AIM: To study the expressions of NMDAR in hippocampal CA(1) region after hypoxic-ischemic brain damage(HIBD) in neonatal rats. METHODS: An neonatal rat model with hypoxic-ischemic brain damage was set up. The expression of NMDAR was detected in normal control and hypoxic-ischemic (HI) brain damage group by immunohistochemical staining and in situs hybridization. RESULTS: The number of NR1(+) and NR1 mRNA(+) cells decreased slightly in hippocampal CA(1) region at 2 h after HI. The numbers increased from 24 h to 48 h after HI, and reached maximum at 72 h after HI. CONCLUSION: NR1 expressed in hippocampal CA(1) region of normal neonatal rats, and the expression is up-regulated after HI brain injury.

Animals↗
PubMed2003

[Induction of specific cytotoxic T lymphocytes and humoral immune response by MUC1 DNA vaccine in mice].

AIM: To observe the specific cytotoxic T lymphocyte and humoral immune response induced by MUC1 DNA inmunization in mice. METHODS: Female BALB/c mice were immunized intramuscularly with 100 microg pcDNA3.1-MUC1 3 times at intervals of 3 weeks. Three weeks after the last immunization, tumor challenge experiments were performed by inoculation of MUC1 positive breast cancer cell line EMT6. Both humoral immune response and CTL-specific cytotoxicity were detected by immunohistochemical staining and (51)Cr release assay, respectively. RESULTS: The cytotoxicity of MUC1-specific CTLs to EMT6 target cells showed that the cytotoxic effect was different at various ratio of effector cells to target cells. At ratios of 100:1, 50:1, 25:1 and 12.5:1, the specific lysis in MUC1cDNA group reached 54.1%, 39.8%, 26.4% and 20.1%, while two control groups 13.2%, 10%, 8.2%, 7.2% and 11.7%, 9.8%, 7.7%, 7.0%, respectively. The former was markedly higher than the two latters(P<0.01). MUC1 expression was exhibited to be positive in breast cancer tissue by immunohistochemical staining with BALB/c mouse sera against MUC1 cDNA. There was only 40% tumorigenic rate in MUC1 cDNA immunized group, while there 100% in pcDNA3.1(+) and NS control groups. There was a significant difference between MUC1 cDNA group and control groups (P<0.05). CONCLUSION: Specific CTLs and antibody prodution are elicited by MUC1 DNA inmunization. MUC1 cDNA inmunization partly inhibit the growth of implanted tumor in mice.

Animals↗
PubMed2003

[Anti-mutagenesis effects of total flavonoids of Astragalus].

OBJECTIVE: To investigate the anti-mutagenic action of the total flavonoids of Astragalus (TFA). METHOD: Three groups of concentrations of TFA and one inducer group were used. The anti-mutagenic action of TFA was studied by experiments in vitro and in vivo including miconucleolus assay, semen teraogenesis test and gene mutagenesis of V79/HGPRT. RESULT: TFA did not affect the weight of the mice during the experiment period. The high concentration of TFA could significantly reduce cyclohophamide-induced miconucleolus number and gene mutagenesis of V79/HGPRT compared with inducer group. However, TFA did not make statistic change in the semen teraogenesis induced by mitomycin C. CONCLUSION: TFA has antimutagenesis effect.

Animals↗
PubMed2002

Liver X receptors in the central nervous system: from lipid homeostasis to neuronal degeneration.

Liver X receptors (LXRalpha and -beta) are nuclear receptors abundant in the liver where they are regulators of lipid homeostasis. Both LXRs are also expressed in the brain, but their roles in this tissue remain to be clarified. We examined the brains of mice in which the genes of both LXRalpha and -beta have been disrupted and found several severe abnormalities. One of the most striking features is that the lateral ventricles are closed and lined with lipid-laden cells. In addition, there are enlarged brain blood vessels, especially in the pars reticularis of the substantia nigra and in the globus pallidus. Other features of the brains are excessive lipid deposits, proliferation of astrocytes, loss of neurons, and disorganized myelin sheaths. Electron micrographs revealed that, as mice aged, lipid vacuoles accumulated in astrocytes surrounding blood vessels. Comparison of mRNA profiles in LXR knockout mice and wild-type littermates showed that expression of several LXR target genes involved in cholesterol efflux from astrocytes was reduced. These findings show that LXRs have an important function in lipid homeostasis in the brain, and that loss of these receptors results in neurodegenerative diseases. Further characterization of the role of LXRs in the brain could lead to new insights into the etiology and treatment of some neurodegenerative disorders.

Animals↗
PubMed2002

Accumulation of foam cells in liver X receptor-deficient mice.

BACKGROUND: The nature of some of the target genes for liver X receptors (LXRs)-alpha and -beta, such as sterol regulatory element binding protein-1 and ATP-binding cassette transporter proteins, suggests a pivotal role of these nuclear receptors in the regulation of fatty acid and cholesterol homeostasis. The present study aimed to elucidate the physiological relevance of both LXRs with regard to lipid metabolism and macrophage cholesterol efflux. METHODS AND RESULTS: Mice depleted for LXRalpha, LXRbeta, or both were fed low-fat rodent chow for 18 months before investigations. The combined deficiency of LXRalpha and LXRbeta was linked to impaired triglyceride metabolism, increased LDL and reduced HDL cholesterol levels, and cholesterol accumulation in macrophages (foam cells) of the spleen, lung, and arterial wall. CONCLUSIONS: Our data demonstrate the physiological importance of both LXRs in lipid metabolism and strongly indicate that both LXRs have a protective role against the development of atherosclerosis.

ATP-Binding Cassette Transporters↗
PubMed2002

Estrogen actions in the brain.

Understanding of the mechanisms of estrogen action in the brain has always been poor. Neurons in several brain regions do not harbor estrogen receptor alpha (ERalpha) and yet are estrogen responsive. It was formerly thought that these responses represented indirect actions of estrogen. It is now evident that these neurons express ERbeta and that estrogen receptors have diverse actions in the central nervous system. By clear delineation of the cellular expression and function of the two estrogen receptors, it is likely that, in the future, selective ERalpha and ERbeta ligands will be developed and used for treatment of depression and behavioral disorders and may be useful in preventing degenerative diseases, such as Alzheimer's and Parkinson's disease.

Animals↗