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J Q Zhang

Publications and source records attributed to J Q Zhang.

At least 19 recordsLinked to original sources
PubMed2006

Parallel sequential minimal optimization for the training of support vector machines.

Sequential minimal optimization (SMO) is one popular algorithm for training support vector machine (SVM), but it still requires a large amount of computation time for solving large size problems. This paper proposes one parallel implementation of SMO for training SVM. The parallel SMO is developed using message passing interface (MPI). Specifically, the parallel SMO first partitions the entire training data set into smaller subsets and then simultaneously runs multiple CPU processors to deal with each of the partitioned data sets. Experiments show that there is great speedup on the adult data set and the Mixing National Institute of Standard and Technology (MNIST) data set when many processors are used. There are also satisfactory results on the Web data set.

Algorithms↗
PubMed2006

Loss of heterozygosity at 6p21.3 underlying HLA class I downregulation in gastric cancer.

Human major histocompatibility complex (HLA), located on 6p21.3, encodes for genes involved in antigen processing and presentation. Loss of heterozygosity (LOH) at 6p21.3 may cause downregulated expression of HLA, thus provide tumor cells with an immune-escape tumor phenotype. In the present study, we detected HLA class I expression in gastric cancer and correlated it with LOH at 6p21.3. The expression of HLA class I antigen was analyzed by immunohistochemical procedure in 50 fresh surgically removed gastric cancers and corresponding normal tissues using 5 monoclonal antibodies (mAbs). LOH studies were detected by using 6 microsatellite markers located at 6p21.3, 1 marker located at 6q21 and 2 microsatellite markers flanking the beta2m gene. HLA class I complex was obviously downregulated in gastric cancer compared with corresponding normal tissues (t=4.00, p<0.01). The expression of beta2m gene was also downregulated in tumor, but not concordant with HLA class I surface downregulation. Out of the 50 tumors, 25 (50%) showed LOH of at least one STR marker at 6p21.3 while only 11 (22%) showed LOH of the two markers flanking the beta2m gene. The LOH frequency of D6S105, which is close to HLA-A gene, was the highest in all STR markers studied (34%). Downregulation of HLA class I expression was correlated with loss of chromosomal regions at 6p21.3 (chi-squared = 5.13, p<0.05). Our results suggested that LOH of 6p21.3 contributed to HLA class I downregulated expression in gastric cancer especially at HLA-A locus. LOH of HLA-A gene might be one of the mechanisms underlying the abnormal expression of HLA class I complex.

Chromosome Deletion↗
PubMed2005

Investigation of the kinetics of a TiO2 photoelectrocatalytic reaction involving charge transfer and recombination through surface states by electrochemical impedance spectroscopy.

In this paper, the electrochemical impedance spectroscopy (EIS) mathematical model of TiO2 photoelectrocatalytic (PEC) reactions involving charge transfer and recombination through surface states was developed. The model was used to study the kinetics of photoelectrocatalytic decomposition of salicylic acid. The model simulation results show that the appearance of two distinguishable semicircles in the EIS response depends on the charging of surface state and light intensity. The experimental results demonstrated that similar phenomena to the theoretical simulation results. The model provides a way to obtain the rate constants for the photoelectrochemical reactions of surface states mediating charge transfer and recombination. The applied potential changes not only the recombination rate constant but also the charge-transfer rate constant. Moreover, the experimental EIS results here and those previous published on PEC degradation reactions can be explained by the present model satisfactorily. The relevance of surface states was discussed briefly. The results demonstrated that EIS is a powerful tool for studying the kinetics of PEC decomposition of organic pollutants on TiO2 electrodes.

Journal Article↗
PubMed2005

Lyophilized paclitaxel magnetoliposomes as a potential drug delivery system for breast carcinoma via parenteral administration: in vitro and in vivo studies.

PURPOSE: The study reports in vitro and biological evaluation of lyophilized negatively charged paclitaxel magnetic liposomes as a potential carrier for breast carcinoma via parenteral administration. METHODS: Paclitaxel in magnetoliposomes were extracted by centrifugation and quantified by high-performance liquid chromatography (HPLC). Biological properties were studied using pharmacokinetics, in vivo distribution and cytotoxicity assays, as well as a mouse model of EMT-6 breast cancer. METHODS: Pharmacokinetic studies showed that encapsulation of paclitaxel in magnetoliposomes produced marked difference over the drug in Cremophor EL/ethanol pharmacokinetics, with an increased t(1/2beta) 19.37 h against 4.11 h. For in vivo distribution, paclitaxel concentration of lyophilized magnetoliposomes in the tumor was much higher than that of lyophilized conventional liposomes or Cremophor EL/ethanol, whereas in heart it was much lower than the latter two formulations via s.c. and i.v. administration. Lyophilized paclitaxel magnetic liposomes showed more potency on the therapy of breast cancer than other formulations via s.c. and i.p. administration. CONCLUSIONS: The current study demonstrates that paclitaxel magnetoliposomes can effectively be delivered to tumor and exert a significant anticancer activity with fewer side effects in the xenograft model.

Animals↗
PubMed2003

Lung-targeting microspheres of carboplatin.

Carboplatin (CPt) was incorporated in the gelatin microspheres by the method of emulsion and the drug content determined spectrophotometrically. The arithmetic mean diameter of the microspheres was 13.20 microm with 98% of the microspheres ranging from 5.0 to 28.6 microm. The average carboplatin content was 23.76% and the yield of the microspheres 85.12%. The microspheres were stable for three months when stored at 37 degrees C/RH 75%, showing insignificant change in appearance and drug content. The in vitro release profile of the microspheres could be described by a biexponential equation, and the release t(1/2) was 49.7 min and 92.04% released in 10h; while for the original drug, CPt, under the same conditions, 92.15% released in the first half an hour. Very high lung-targeting efficiency in vivo was proved by the results of targeting parameters. The S-180 lung neoplasm models were established by i.v. cancer cells in mice and the number of pulmonary nodules examined for evaluation of the treatment effect. The results of therapeutic tests showed that the antitumour effects were increased by injection of the microspheres compared with the injection of CPt solution: half of the dose in the microspheres showed comparable effect to the original drug.

Animals↗
PubMed2001

Ultrastructural and biochemical localization of N-RAP at the interface between myofibrils and intercalated disks in the mouse heart.

N-RAP is a recently discovered muscle-specific protein found at cardiac intercalated disks. Double immunogold labeling of mouse cardiac muscle reveals that vinculin is located immediately adjacent to the fascia adherens region of the intercalated disk membrane, while N-RAP extends approximately 100 nm further toward the interior of the cell. We partially purified cardiac intercalated disks using low- and high-salt extractions followed by density gradient centrifugation. Immunoblots show that this preparation is highly enriched in desmin and junctional proteins, including N-RAP, talin, vinculin, beta1-integrin, N-cadherin, and connexin 43. Electron microscopy and immunolabeling demonstrate that N-RAP and vinculin are associated with the large fragments of intercalated disks that are present in this preparation, which also contains numerous membrane vesicles. Detergent treatment of the partially purified intercalated disks removed the membrane vesicles and extracted vinculin and beta1-integrin. Further separation on a sucrose gradient removed residual actin and myosin and yielded a fraction morphologically similar to fasciae adherentes that was highly enriched in N-RAP, N-cadherin, connexin 43, talin, desmin, and alpha-actinin. The finding that N-RAP copurifies with detergent-extracted intercalated disk fragments even though beta-integrin and vinculin have been completely removed suggests that N-RAP association with the adherens junction region is mediated by the cadherin system. Consistent with this hypothesis, we found that recombinant N-RAP fragments bind alpha-actinin in a gel overlay assay. In addition, immunofluorescence shows that N-RAP remains bound at the ends of isolated, detergent-treated cardiac myofibrils. These results demonstrate that N-RAP remains tightly bound to myofibrils and fasciae adherentes during biochemical purification and may be a key constituent in the mechanical link between these two structures.

Animals↗
PubMed2001

Identification, characterization and leucocyte expression of Siglec-10, a novel human sialic acid-binding receptor.

Here we characterize Siglec-10 as a new member of the Siglec family of sialic acid-binding Ig-like lectins. A full-length cDNA was isolated from a human spleen library and the corresponding gene identified. Siglec-10 is predicted to contain five extracellular Ig-like domains and a cytoplasmic tail containing three putative tyrosine-based signalling motifs. Siglec-10 exhibited a high degree of sequence similarity to CD33-related Siglecs and mapped to the same region, on chromosome 19q13.3. The expressed protein was able to mediate sialic acid-dependent binding to human erythrocytes and soluble sialoglycoconjugates. Using specific antibodies, Siglec-10 was detected on subsets of human leucocytes including eosinophils, monocytes and a minor population of natural killer-like cells. The molecular properties and expression pattern suggest that Siglec-10 may function as an inhibitory receptor within the innate immune system.

Amino Acid Sequence↗
PubMed2001

Renin expression at sites of repair in the infarcted rat heart.

Y. Sun, J. Zhang, J. Q. Zhang and K. T. Weber. Renin Expression at Sites of Repair in the Infarcted Rat Heart. Journal of Molecular and Cellular Cardiology (2001) 33, 995-1003. Angiotensin (Ang) II has autocrine and paracrine functions that contribute to structural cardiac remodeling by fibrous tissue following myocardial infarction (MI). The recruitment of angiotensin converting enzyme (ACE) and AngII receptors by inflammatory and fibroblast-like cells involved in tissue repair of the infarcted heart is now well established. On the other hand, the temporal and spatial response and cellular source of renin in infarcted hearts have not been fully elucidated. The relationship between renin synthesis and circulating renin activity have likewise not been addressed. The present study sought to assess the cellular source, spatial distribution and temporal response of renin expression and synthesis in the rat heart following anterior transmural MI, and to determine its relationship to circulating renin activity. At day 3 and weeks 1, 2, 3 and 4 following left coronary artery ligation, the localization and optical density of cardiac renin mRNA was detected by quantitative in situ hybridization; cardiac and circulating renin activity was measured by radioimmunoassay; cells expressing cardiac renin were detected by immunohistochemistry; and injury/repair was assessed by hematoxylin/eosin and collagen-specific picrosirius red staining. Unoperated rats served as normal controls. The authors found: (1) renin mRNA and activity were not detected in either normal control or non-infarcted myocardium, but were expressed at the site of infarction and other sites of repair involving visceral pericardium and endocardium of interventricular septum at all time points; (2) cells expressing renin at day 3 and weeks 1 and 2 were predominantly macrophages, while at weeks 3 and 4, they were primarily myofibroblasts; (3) renin activity in the infarcted myocardium rose progressively over the course of 4 weeks; and (4) circulating renin activity was significantly increased at day 3 and week 1, reached a peak at week 2, declined at week 3 and returned to normal levels at week 4. Thus, renin expression and activity appear at sites of repair in the infarcted rat heart on day 3 and rise progressively thereafter over 4 weeks, independent of circulating renin. Several types of cells are responsible for renin synthesis at these sites; primarily macrophages during the inflammatory phase of repair, and myofibroblasts during the subsequent fibrogenic phase. Cardiac renin production following MI contributes to local AngII generation that regulates tissue repair and structural remodeling following MI.

Actins↗
PubMed2001

Topography and distribution of sympathetic nerve fibers in the rat temporomandibular joint: immunocytochemistry and ultrastructure.

The distribution and fine structure of nerve fibers containing neuropeptide Y (NPY), tyrosine hydroxylase (TH), and vasoactive intestinal polypeptide (VIP) in the temporomandibular joint were investigated by both the avidin-biotin complex method and an indirect immunofluorescence technique. The innervation pattern of NPY- and TH-positive fibers differed from that of VIP-positive fibers. Specifically, the former was distributed in both the superficial and deep sublining layers, while the latter was mostly located in the deep sublining layer. NPY- and TH-immunoreactive fibers were largely confined to vascular elements; occasional fibers were observed in the synovial lining layer close to the joint cavity. More nerves with NPY and TH immunoreactivity were observed close to the upper joint compartment than near the lower compartment NPY and TH immunoreactivity was dramatically reduced in the TMJ of superior cervical ganglionectomized animals, indicating the sympathetic origin of these nerves. NPY immunoreactivity was found only in unmyelinated axons, which were located in the adventitia and adventitia-medial border of arteries or arterioles. Occasionally, axons were near the joint cavity, in areas free of vascular structures. These observations show that abundant sympathetic nerves supply the temporomandibular joint of the rat and provide a morphological basis for the involvement of different neuropeptides in vascular regulatory and modulatory functions in physiological and pathophysiological conditions.

Animals↗
PubMed2001

Effect of exercise and medium-chain fatty acids on postprandial lipemia.

The purpose of this study was to evaluate the effect of medium-chain triglycerides (MCT) with and without exercise on postprandial lipemia (PPL). Subjects were 25 young men and women. Each subject performed three trials: 1) control (fat meal only, 1.5 g fat/kg) 2) MCT (substitution of MCT oil, 30% of fat calories), and 3) MCT + Ex (exercise 12 h before the MCT meal). Before each trial, the subject underwent consistent dietary preparation. Blood was collected on 2 separate days for baseline measurements of postheparin lipases and, in each trial, at 0 h (premeal), at 2, 4, 6, and 8 h after the fat meal for triglycerides and cholesterol ester transfer protein (CETP), and at 8 h for postheparin lipoprotein lipase (LPL) and hepatic lipase activities (HL). ANOVA indicated that the partial substitution of MCT oil to the fat meal did not affect the PPL response. However, the PPL was significantly lower after the MCT + Ex trial vs. the other trials. LPL activity was significantly elevated after all trials compared with baseline, whereas HL was lower in the MCT + Ex trial only. CETP mass was significantly lower at 4 and 8 h than 0 h during all trials but relatively higher in the MCT + Ex trial vs. the nonexercise trials. These results suggest that MCT does not affect the TG response to a fat meal. LPL and CETP are affected by a fat meal with or without exercise, but HL is affected only when exercise is included.

Adult↗
PubMed2001

[A review of brain aromatase].

Aromatase catalyzes the conversion of androgen to estrogen. This enzyme has been primarily localized in the neurons of specific areas of limbic system and hypothalamus of the brain. Astrocytes may also express this enzyme. Studies show that the gene expression of aromatase is driven by multiple tissue-specific exons, and the effective concentration of brain estrogen depends on the expression of brain aromatase. The locally produced estrogen plays an important role in the regulation of synaptogenesis, density of dendritic spine and the expression of neurotrophic factors and/or their receptors. Estrogen can also protect brain cells from the damages of neurotoxins and can greatly improve the deficits of learning and memory resulted from neurodegenerative disorders such as Alzheimer's diseases.

Animals↗
PubMed2001

[Studies on lung targeted niosomes of carboplatin].

AIM: To improve the treatment efficacy and reduce the side effect of carboplatin (CBP), the antitumor drug was incorporated into niosomes (NS). METHODS: Lung targeted niosomes of CBP (CBP-NS) were prepared by the method of hand shaking. The ultraviolet absorption spectrophotometric method was used for the determination of CBP. The method of dynamic dialysis was used for in vitro release of CBP from CBP-NS. The S-180 lung neoplasms models were established by i.v. cancer cells in mice. The number of pulmonary nodules was examined for evaluating the therapeutic efficacy. RESULTS: The data showed that the mean diameter of CBP-NS was 3.72 microns, with a span of 0.66. The entrapment ratio of CBP in CBP-NS was 29.2% and the CBP-NS were stable for three months stored at 3 degrees C-5 degrees C, 15 degrees C-25 degrees C or 37 degrees C (relative humidity 75%). The release profile in vitro could be described by a biexpotential equation. The calculated values of the three targeting parameters indicated that CBP-NS showed good targeting efficiency. The results of therapeutic trials showed that the antitumor effects were significantly increased by injection of CBP-NS compared with CBP in the treatment of mice with lung carcinoma. CONCLUSION: The results indicated that CBP-NS have good targeting efficiency in vivo, and the biodegradable CBP-NS may decrease the side effects of carboplatin and improve its therapeutic efficacy.

Animals↗
PubMed2000

Siglec-9, a novel sialic acid binding member of the immunoglobulin superfamily expressed broadly on human blood leukocytes.

Here we characterize the properties and expression pattern of Siglec-9 (sialic acid-binding Ig-like lectin-9), a new member of the Siglec subgroup of the immunoglobulin superfamily. A full-length cDNA encoding Siglec-9 was isolated from a dibutyryl cAMP-treated HL-60 cell cDNA library. Siglec-9 is predicted to contain three extracellular immunoglobulin-like domains that comprise an N-terminal V-set domain and two C2-set domains, a transmembrane region and a cytoplasmic tail containing two putative tyrosine-based signaling motifs. Overall, Siglec-9 is approximately 80% identical in amino acid sequence to Siglec-7, suggesting that the genes encoding these two proteins arose relatively recently by gene duplication. Binding assays showed that, similar to Siglec-7, Siglec-9 recognized sialic acid in either the alpha2,3- or alpha2, 6-glycosidic linkage to galactose. Using a specific mAb, Siglec-9 was found to be expressed at high or intermediate levels by monocytes, neutrophils, and a minor population of CD16(+), CD56(-) cells. Weaker expression was observed on approximately 50% of B cells and NK cells and minor subsets of CD8(+) T cells and CD4(+) T cells. These results show that despite their high degree of sequence similarity, Siglec-7 and Siglec-9 have distinct expression profiles.

Amino Acid Sequence↗
PubMed2000

Cardiac remodeling by fibrous tissue after infarction in rats.

After transmural myocardial infarction (MI), extensive myocardial remodeling by fibrous tissue appears in both infarcted and noninfarcted myocardium, which contributes to ventricular diastolic dysfunction. In the present study we sought to assess the time course of collagen remodeling in the infarcted rat hearts by detecting spatial and time-dependent cellular events related to collagen synthesis and degradation 2 to 28 days after left coronary artery ligation. In infarcted hearts, and compared with findings in sham-operated and unoperated rat hearts, we found the following: (1) macrophages infiltrated into sites of MI and visceral pericardium on day 2 and gradually disappeared after day 14; (2) myofibroblasts (MyoFb) first appeared at these sites of repair on day 3 and remained abundant thereafter at all time points examined; (3) transforming growth factor-beta1 (TGF-beta1) mRNA was enhanced in infarcted and noninfarcted myocardium on day 2 and remained throughout 28 days; (4) type I and III collagen mRNAs began to increase at and remote to MI on day 3 and remained elevated thereafter; (5) matrix metalloproteinase-1 mRNA was significantly increased at and remote to MI on day 3, declined to the control level on day 7, and remained low thereafter; (6) tissue inhibitor of matrix metalloproteinase (TIMP)-I, -II, and -III mRNAs were markedly elevated at sites of repair on day 3 and sustained throughout 28 days; (7) fibrillar collagen accumulation that was evident at and remote to MI on day 7 continued to accumulate thereafter at each site over 4 weeks. When compared with findings in unoperated rat heart, pericardial fibrosis was evident in both infarcted and noninfarcted heart, and the temporal response of collagen generation/ degradation in pericardium was similar to that in infarcted myocardium. Thus collagen synthesis is activated in both infarcted and noninfarcted rat myocardium after transmural anterior infarction and is persistent throughout the 28-day period of study, whereas early collagen degradation is short lived and inactivated in the fibrogenic phase. Activated TGF-beta1 mRNA expression is accompanied by the appearance of MyoFb and the expression of fibrillar collagens and TIMPs, suggesting that this fibrogenic cytokine may contribute to collagen remodeling in the rat heart after MI.

Actins↗
PubMed2000

Local angiotensin II and transforming growth factor-beta1 in renal fibrosis of rats.

Studies have demonstrated that local angiotensin II (Ang II) generation is enhanced in repairing kidney and that ACE inhibition or AT(1) receptor blockade attenuates renal fibrosis. The localization of ACE and Ang II receptors and their relationship to collagen synthesis in the injured kidney, however, remain uncertain. Using a rat model of renal injury with subsequent fibrosis created with chronic elevations in circulating aldosterone (ALDO), we examined the distribution and binding density of ACE and Ang II receptors in repairing kidneys, as well as their anatomic relationship to transforming growth factor-beta1 (TGF-beta1) mRNA, type I collagen mRNA, collagen accumulation, and myofibroblasts. Two groups of animals (n=7 in each group) were studied: (1) normal rats served as controls, and (2) uninephrectomized rats received ALDO (0.75 microg/h SC) and 1% NaCl in drinking water for 6 weeks. Compared with control rats, in ALDO-treated rats we found (1) significantly (P<0.01) increased blood pressure, reduced plasma renin activity, and increased plasma creatinine levels, (2) diffuse fibrosis in both renal cortex and medulla, (3) abundant myofibroblasts at these sites of fibrosis, (4) significantly increased (P<0.01) binding density of ACE and Ang II receptors (60% AT(1), 40% AT(2)) at the sites of fibrosis, and (5) markedly increased (P<0.01) expression of TGF-beta1 and type I collagen mRNAs at these same sites. Thus, in this rat model of renal repair, the enhanced expression of ACE, Ang II receptors, and TGF-beta1 is associated with renal fibrosis. Ang II generated at the sites of repair appears to have autocrine/paracrine functions in the regulation of renal fibrous tissue formation alone or through its stimulation of TGF-beta1 synthesis.

Aldosterone↗
PubMed1999

Appearance and regression of rat pouch tissue.

Fibrosis, a consequence of tissue repair, can become a final common pathway to organ failure, if progressive. Prevention and regression of organ fibrosis represent targets of considerable interest. The natural fate of fibrosis differs among various tissues being either persistent, progressive or regressive. Cellular and molecular responses involving myofibroblasts (myoFb), a phenotypically transformed fibroblast-like cell of considerable functional diversity, is involved in collagen turnover at sites of repair, where they govern the fate of fibrosis. Insights gained from the natural regression of established fibrous tissue may offer strategies to remove unwanted fibrosis in failing organs. In the present study, we addressed the temporal sequence to various components of collagen synthesis and degradation involved in the appearance and subsequent regression of pouch tissue induced in the rat by subcutaneous injection of air followed by instillation of the phorbol ester croton oil. Pouch tissue was collected on day 2, 4, 10, 14, 21, 28 and 35 (n=6 at each time point). Activities of matrix metalloproteinase-1 (MMP-1) and tissue inhibitor of MMP-1 (TIMP-1) were determined by zymography and reverse zymography, respectively; collagen accumulation by hydroxyproline concentration; gene expression of TIMP-1 or tissue inhibitor of MMP-1, type I collagen and transforming growth factor-beta1 (TGF-beta1) by in situ hybridization; TGF-beta1 concentration by sandwich enzyme-linked immunosorbant assay (ELISA); and myoFb and its phenotypes by immunohistochemistry using antibodies to alpha-smooth muscle actin (alpha-SMA), vimentin or desmin. During pouch tissue formation, we found: (1) pouch weight increased progressively from day 2 to day 14 and then declined progressively thereafter; (2) type I collagen mRNA expression, barely detectable at day 2, increased at day 4, together with tissue hydroxyproline concentration (P<0.05) reaching a peak on day 10, and gradually decreased thereafter in association with declining tissue hydroxyproline concentration; (3) mRNA expression and concentration of TGF-beta1, detectable at day 2, significantly (P<0.05) increased at day 4, reached a peak at day 10, and gradually declined thereafter; (4) MMP-1 activity, low at day 2, increased continually over the course of 35 days; (5) TIMP-1 mRNA, detectable at day 2 and significantly (P<0.05) increased at day 4, gradually decreased thereafter; (6) activity of TIMP-1 increased continuously from day 2 to day 14 and then was markedly reduced thereafter; and (7) myoFb were first observed in pouch tissue at day 4 and became more extensive thereafter with their phenotype changing over time. Early appearing myoFb (day 4, 10, 14, and 21) expressed alpha -SMA and vimentin (VA phenotype), while later appearing cells (day 28 and 35) additionally expressed desmin (VAD phenotype). Thus, in croton oil-induced rat pouch model, the subcutaneous accumulation of pouch tissue hydroxyproline over the course of 10 days is initially associated with a VA-positive myoFb phenotype and its transcription of TGF-beta1, type I collagen and TIMP-1. Beyond day 10, a regression of pouch tissue collagen begins in association with the appearance of a VAD-positive myoFb phenotype and progressive increase in MMP-1 activity as the expression of TIMP-1 and TGF-beta1 are withdrawn. Regression of established fibrosis in failing organs may, therefore, be attainable through manipulation of myoFb phenotype and/or enhanced collagen degradation relative to collagen synthesis.

Animals↗