Biomedical subjects

D He

Publications and source records attributed to D He.

At least 37 records · Page 2Linked to original sources

PubMed2001

Source contributions to ambient concentrations of CO and NOX in the urban area of Beijing.

An emission inventory based on GIS technology was developed in this study, and used to estimate the spatial distribution of the stationary and mobile sources in the urban area of Beijing. The stationary sources were divided into various types of finer classes depending on different usage, stack height and emission factors. The mobile sources were treated as both line sources and area sources. It was shown that total anthropogenic CO and NOX emissions had reached 1.4 million and 233 thousand tons, respectively, and vehicle sources emissions of CO and NOX accounted for 76.8% and 40.2%, respectively, of the total emissions in 1995. ISCST3, a Gaussian dispersion air quality model, was modified at low wind speed condition, and then used to facilitate the study of source contributions to ambient concentrations of CO and NOX in Beijing. The simulation results showed that emissions from the vehicle sources had contributed 76.5% and 68.4% of the total CO and NOX concentrations in urban atmosphere of Beijing in 1995, and were even higher in the city core (86.3% of the CO and 72.0% of the NOX). Therefore, strategies for CO and NOX pollution control will of necessity need to focus on the vehicle sources.

Air Movements↗

PubMed2001

Activation of NF-kappaB by hepatitis B virus X protein through an IkappaB kinase-independent mechanism.

pX, the hepatitis B virus-encoded transcription coactivator, is involved in viral infection in vivo. pX stimulates the activity of several transcription factors including nuclear factor-kappaB (NF-kappaB), but the mechanism of activation is poorly understood. The IkappaB kinase complex (IKK) mediates activation of NF-kappaB in response to various extracellular stimuli, including inflammatory cytokines like tumor necrosis factor and interleukin 1, human T cell lymphoma virus 1 Tax protein, and tumor promoters like phorbol esters. It is not known whether IKK also mediates activation of NF-kappaB by pX. Here we report that IKK was not essential for activation of NF-kappaB by pX. Expression of pX resulted in the degradation of IkappaBalpha in the absence of its phosphorylation at Ser(32) and Ser(36) residues. Although pX stimulated the activity of cotransfected IKK-beta when it was overexpressed, it failed to activate endogenous IKK. Furthermore, expression of pX stimulated NF-kappaB nuclear translocation and transcriptional activity in IKK-gamma-null fibroblast 5R cells. Our data indicate that pX stimulates NF-kappaB activity through a mechanism that is dependent on IkappaBalpha degradation but not on IKK activation.

Cell Line↗

PubMed2001

Role of nitric oxide in the cerebrovascular and thermoregulatory response to interleukin-1 beta.

Central administration of interleukin-1 beta (IL-1 beta) increases cerebral blood flow (CBF) and body temperature, in part, through the production of prostaglandins. In previous studies, the temporal relationship between these effects of IL-1 beta have not been measured. In this study, we hypothesized that the increase in CBF occurs before any change in brain or body temperature and that the cerebrovascular and thermoregulatory effects of IL-1 beta would be attenuated by inhibiting the production of nitric oxide (NO). Adult male rats received 100 ng intracerebroventricular (icv) injection of IL-1 beta, and cortical CBF (cCBF) was measured by laser-Doppler in the contralateral cerebral cortex. A central injection of IL-1 beta caused a rapid increase in cCBF to 133 +/- 12% of baseline within 15 min and to an average of 137 +/- 12% for the remainder of the 3-h experiment. Brain and rectal temperature increased by 0.4 +/- 0.2 and 0.5 +/- 0.2 degrees C, but not until 45 min after IL-1 beta administration. Pretreatment with N(omega)-nitro-L-arginine methyl ester (L-NAME; 5 mg/kg iv) completely prevented the changes in cCBF and brain and rectal temperature induced by IL-1 beta. L-Arginine (150 mg/kg iv) partially reversed the effects of L-NAME and resulted in increases in both cCBF and temperature. These findings suggest that the vasodilatory effects of IL-1 beta in the cerebral vasculature are independent of temperature and that NO plays a major role in both the cerebrovascular and thermoregulatory effects of centrally administered IL-1 beta.

Animals↗

PubMed2001

WAKs: cell wall-associated kinases linking the cytoplasm to the extracellular matrix.

There are only a few proteins identified at the cell surface that could directly regulate plant cell wall functions. The cell wall-associated kinases (WAKs) of angiosperms physically link the plasma membrane to the carbohydrate matrix and are unique in that they have the potential to directly signal cellular events through their cytoplasmic kinase domain. In Arabidopsis there are five WAKs and each has a cytoplasmic serine/threonine protein kinase domain, spans the plasma membrane, and extends a domain into the cell wall. The WAK extracellular domain is variable among the five isoforms, and collectively the family is expressed in most vegetative tissues. WAK1 and WAK2 are the most ubiquitously and abundantly expressed of the five tandemly arrayed genes, and their messages are present in vegetative meristems, junctions of organ types, and areas of cell expansion. They are also induced by pathogen infection and wounding. Recent experiments demonstrate that antisense WAK expression leads to a reduction in WAK protein levels and the loss of cell expansion. A large amount of WAK is covalently linked to pectin, and most WAK that is bound to pectin is also phosphorylated. In addition, one WAK isoform binds to a secreted glycine-rich protein (GRP). The data support a model where WAK is bound to GRP as a phosphorylated kinase, and also binds to pectin. How WAKs are involved in signaling from the pectin extracellular matrix in coordination with GRPs will be key to our understanding of the cell wall's role in cell growth.

Arabidopsis↗

PubMed2001

[Motor vehicle source contributions to air pollutants in Beijing].

Beijing's motor vehicle emission inventory based on GIS technology was developed, and used to estimate the contribution rate of different types of vehicles and different areas of vehicles to the total vehicular emissions in the urban area of Beijing. ISCST3, a gaussian dispersion air quality model, was modified at low wind speed condition, and then used to facilitate the study of the spatial and temporal distribution of CO and NOx concentrations in Beijing. It was shown that vehicle source emissions of CO and NOx accounted for 76.8% and 40.2%, respectively, of the total emissions in 1995. The simulation results also showed that emissions from the vehicle sources had contributed 76.5% and 68.4% of the total CO and NOx concentrations in urban atmosphere of Beijing in 1995, and were even higher at down-town and near the arteries. Therefore, strategies for CO and NOx pollution control will of necessity need to focus on the vehicle sources.

Air Pollutants↗

PubMed2001

[The application of three-dimensional model in the oral and maxillofacial surgery].

OBJECTIVE: To exploit the three-dimensional model technique and apply it in the oral and maxillofacial surgery. METHODS: Using CT and rapid prototype technique to make three-dimentional model and used it for the therapy of the comminuted zygomatic features, jaw bone asymmetry, defects after tumor removal, and implantations. RESULTS: By using three-dimensional models eight patients with comprehensive bone defects had good results. CONCLUSIONS: Three-dimensional models can help surgeons in many ways for the therapy of the oral and maxillofacial deformities.

Adult↗

PubMed2001

[Antisense oligodeoxynucleotide of telomerase gene enhances cisplatin-induced apoptosis in acute myeloid leukemia and chronic myeloid leukemia cells].

OBJECTIVE: To explore the effect of human telomerase reverse transcriptase(hTERT) gene antisense oligodeoxynucleotide (ASODN) on cisplatin-induced apoptosis in cultured primary acute myeloid leukemia (AML) and chronic myeloid leukemia (CML) cells. METHODS: Cell surviving fraction was determined using the trypan blue dye exclusion assay. Apoptosis was detected by DNA gel electrophoresis and flow cytomertric cell cycle analysis. RESULTS: Treatment with cisplatin after 24 hours of exposure of the cells to ASODN significantly reduced the number of viable AML and CML cells. However, there was no difference on AML and CML cells survival between those treated with sense oligodeoxynucleotide (SODN)/cisplatin combination and cisplatin alone. Agarose gel electrophoresis of genomic DNA from the blasts of AML and CML treated with ASODN and cisplatin combination for 72 hours showed typical DNA "ladder", but DNA from AML or CML cells treated with SODN plus cisplatin or cisplatin alone did not. The percentage of apoptotic AML and CML cells treated with cisplatin for 48 or 72 hours after 24 hours of exposure to ASODN (42.68%, 35.72%) was significantly different with that of apoptotic cells treated with SODN plus cisplatin (29.02%, 23.84%) or cisplatin alone (27.53%, 21.02%). CONCLUSION: hTERT ASODN could enhance the cisplatin-induced apoptosis of AML and CML cells.

Acute Disease↗

PubMed2001

[Effect of inhibition of telomerase activity on cisplatin-induced apoptosis in K562 cells].

OBJECTIVE: To explore the effect of human telomerase reverse transcriptase (hTERT) gene antisense oligodeoxynucleotide (ASODN) on telomerase activity and cisplatin-induced apoptosis in K562 cells. METHODS: Telomerase activity was analyzed by using polymerase chain reaction enzyme-linked immunoassay (PCR-ELISA), expression levels of hTERT protein by immunofluorescence and apoptosis by DNA gel electrophoresis and flow cytometry. RESULTS: There was a marked decrease in both the percentage of hTERT protein positive cells and the telomerase activity in ASODN treated cell as compared with that in control and sense oligodeoxynucleotide (SODN)-treated cells; but no difference between the latter two groups. Agarose gel electrophoresis of genomic DNA from K562 cells treated with ASODN and cisplatin combination for 72 h showed typical DNA ladder; neither did DNA from K562 cells treated with SODN plus cisplatin nor cisplatin alone. Apoptosis rates of K562 cells treated with ASODN for 24 h and then with cisplatin for 72 h were significantly increased. There was statistically significant difference in the percentage of apoptotic cells between hTERT ASODN plus cisplatin group and SODN plus cisplatin or cisplatin alone group. CONCLUSION: The hTERT gene ASODN could inhibit telomerase activity of K562 cells whereby it enhanced cisplatin-induced apoptosis of the cells.

Antineoplastic Agents↗

PubMed2001

[Study on some metal elements levels and the T lymphocyte subset of the peripheral lymphocytes in patients with nasopharyngeal carcinomas].

OBJECTIVE: To study some metal elements levels and T lymphocyte subset of the peripheral lymphocytes in patients with nasopharyngeal. METHOD: Metal elements in the patients with nasopharyngeal and normal control were detected by the Atomic Absorption Spectrometer (Flame SHIMATZV.JAPAN). T lymphocyte subset were detected by the flow cytometry (FCM). RESULT: The level of copper was significantly higher and the level of zinc was significantly lower in patients with nasopharyngeal carcinomas than those in normal control group (P < 0.01 and < 0.05 respectively). The number of CD3/CD4 cell in the patients group were less than those in normal group(P < 0.01). CONCLUSION: The results of correlative analysis showed that there was a significant correlationship between the number of CD4 cells and levels of copper in peripheral lymphocytes of the patients group.

Adult↗

PubMed2000

Direct isolation of human central nervous system stem cells.

Stem cells, which are clonogenic cells with self-renewal and multilineage differentiation properties, have the potential to replace or repair damaged tissue. We have directly isolated clonogenic human central nervous system stem cells (hCNS-SC) from fresh human fetal brain tissue, using antibodies to cell surface markers and fluorescence-activated cell sorting. These hCNS-SC are phenotypically 5F3 (CD133)(+), 5E12(+), CD34(-), CD45(-), and CD24(-/lo). Single CD133(+) CD34(-) CD45(-) sorted cells initiated neurosphere cultures, and the progeny of clonogenic cells could differentiate into both neurons and glial cells. Single cells from neurosphere cultures initiated from CD133(+) CD34(-) CD45(-) cells were again replated as single cells and were able to reestablish neurosphere cultures, demonstrating the self-renewal potential of this highly enriched population. Upon transplantation into brains of immunodeficient neonatal mice, the sorted/expanded hCNS-SC showed potent engraftment, proliferation, migration, and neural differentiation.

Animals↗

PubMed2000

alpha-Amylase immobilized on bulk acoustic-wave sensor by UV-curing coating.

A new method for immobilization of alpha-amylase by UV-curing coating is proposed in this paper. The immobilization procedure of UV-curing coating on piezoelectric quartz crystal is simple and convenient, and causes less loss of enzymatic activity. The activity of the immobilized alpha-amylase is monitored by a technique based on bulk acoustic-wave (BAW) sensor. The frequency shift of BAW sensor can reflect the degree of hydrolysis of starch by the immobilized alpha-amylase. It is appropriate for the immobilized alpha-amylase to hydrolyze the soluble starch under pH 7.0 condition, which is similar to that of the free alpha-amylase. Kinetic parameters (the Michaelis constant, K(m), and the maximum initial rate V(max)) of the enzymatic hydrolysis of starch by the immobilized alpha-amylase are estimated by using a linear method of Lineweaver-Burk plot. K(m)=12.7mgml(-1) and V(max)=15.9Hzmin(-1). And the experimental results show that the immobilized alpha-amylase entrapped by the UV-curing coating retains adequate enzymatic activity and can be reused more than 50 times under certain experimental conditions.

Journal Article↗

PubMed2000

Determination of the binding parameters of drug to protein by equilibrium dialysis/piezoelectric quartz crystal sensor.

A novel method, equilibrium dialysis/piezoelectric quartz crystal sensor, applied to determine the binding parameters of diethyldithiocarbamate to human plasma protein is proposed. Based on the investigation of the equilibrium reaction for the binding of drug to protein, the related theoretical equations for this binding were derived. By monitoring the frequency responses of a copper-plated piezoelectric quartz crystal sensor to drug in and out of a dialysis membrane after equilibrium, the binding parameters were determined, i.e., 0.375 micromol g(-1) for beta(p), 6.496 microM for K(dp), 141.99 L mmol(-1) for K(p), and 0.043 for N. These values were in good agreement with reference values. It was found that this method may have application for studying the characteristics of the interaction between other drugs and proteins.

Biosensing Techniques↗

PubMed2000

Transforming growth factor beta -inducible independent binding of SMAD to the Smad7 promoter.

SMAD proteins can mediate transforming growth factor beta (TGF-beta)-inducible transcriptional responses. Whereas SMAD can recognize specific DNA sequences, it is usually recruited to a promoter through interaction with a DNA-binding partner. In an effort to search for TGF-beta-inducible genes, we used a subtractive screening method and identified human Smad7, which can antagonize TGF-beta signaling and is rapidly up-regulated by TGF-beta. In this report, we show that TGF-beta can stabilize Smad7 mRNA and activate Smad7 transcription. The Smad7 promoter is the first TGF-beta responsive promoter identified in vertebrates that contains the 8-bp palindromic SMAD-binding element (SBE), an optimal binding site previously identified by a PCR-based selection from random oligonucleotides by using recombinant Smad3 and Smad4. We demonstrate that on TGF-beta treatment, endogenous SMAD complex can bind to a Smad7 promoter DNA as short as 14 or 16 bp that contains the 8-bp SBE in gel mobility shift and supershift assays. Our studies provide strong evidence that SMAD proteins can bind to a natural TGF-beta responsive promoter independent of other sequencespecific transcription factors. We further show that, whereas recombinant Smad3 binds to the SBE, endogenous or even transfected Smad3 cannot bind to the SBE in the absence of Smad4. These findings have important implications in the identification of target genes of the TGF-beta/SMAD signaling pathways.

Base Sequence↗

PubMed2000

Effects of naloxone on the serum luteinizing hormone level and the number of Fos-positive gonadotropin-releasing hormone neurons in immature female rats.

To examine developmental changes in the number of gonadotropin-releasing hormone (GnRH) neurons activated by an opioid receptor antagonist in female rats, blood sampling and double-labeled immunocytochemistry for Fos and GnRH were performed after the injection of naloxone (NAL) in immature (postnatal d16 and d30) and mature female rats. Three age groups of rats were perfused with 4% paraformaldehyde-PB 90 min after the subcutaneous injection of NAL (2.5 mg/kg) or saline. All tissue incubation and staining for double-labeled immunocytochemistry were simultaneously performed. Although no significant developmental change was observed in the total number of GnRH neurons (p0.05), NAL-induced increases in serum luteinizing hormone (LH) concentrations were much greater in the d16 group than those in the d30 and mature groups (p<0.01). Conversely, Fos-positive GnRH neurons were rarely observed in d16, and some Fos-positive GnRH neurons were observed in the d30 group (p<0.05 vs. saline) and the mature group (p<0.01 vs. saline). These results suggest that opiatergic inhibitory system on GnRH neuron in immature female rats is different from that in mature female rats.

Age Factors↗

PubMed2000

Induction of Alzheimer-specific Tau epitope AT100 in apoptotic human fetal astrocytes.

In Alzheimer's and other neurodegenerative diseases, hyperphosphorylated tau accumulates in affected neuronal and glial cells in the form of paired helical filaments (PHFs). This tau binds antibody AT100, which recognizes the double phosphorylation site (Thr212/Ser214) that is not present in normal biopsy tau. In primary cultures, highly enriched (>98%) in astrocytes of human fetal brain, three polypeptides of 52, 64, and 70 kD showed immunoreactivity with tau antibodies against non-phosphorylated epitopes, accounting for 88, 12, and <1%, respectively, of the total reactivity. All three polypeptides were phosphorylated at the PHF-1 epitope but not at the epitopes Tau-1, 12E8, AT8, and AT100. Treatment of cultures with okadaic acid resulted in apoptosis characterized by the blebbing of the plasma membrane, condensation of nuclear chromatin, and fragmentation of the nucleus. This treatment also resulted in a 3- to 5-fold increase in the content of both tau protein and phosphorylation. The increases were observed in all phosphorylation sites examined, and included the AT100 site. The AT100 site has been proposed to be generated by protein kinase B/Akt and Cdc2. Since okadaic acid can induce an AD-like hyperphosphorylated state of normal tau in primary cultures of human brain cells, a simple cellular model is available permitting study of self-aggregation of tau and phosphorylation events characteristic of neurodegeneration.

Alternative Splicing↗

PubMed2000

CENP-G in neocentromeres and inactive centromeres.

CENP-G is a novel constitutive centromere-specific protein localized to the kinetochore inner plate and subjacent region. It has been identified as associating specifically with the alpha-1 subfamily of alpha-satellite DNA. In the present work, the localization of CENP-G was compared with that of other CENPs by immunofluorescence and fluorescence in situ hybridization. Studies were carried out on four abnormal human centromeres: two neocentromeres and two inactive centromeres. CENP-G was detected in one of the two inactive centromeres but not in the other that shows a partial deletion of the alphoid DNA. Interestingly, CENP-G is also present in neocentromeres, which lack alphoid DNA sequences, and in the human Y chromosome, which lacks the alpha-1 type of satellite DNA. These data provide further evidence that CENP-G may be an essential factor in centromeric function and that in centromeres lacking the alpha-1 subfamily of alphoid DNA, other DNA sequences are able to bind CENP-G.

Aged↗

PubMed2000

Clostridium difficile toxin A causes early damage to mitochondria in cultured cells.

BACKGROUND & AIMS: The mechanism by which Clostridium difficile toxin A causes actin depolymerization and cell rounding involves toxin internalization and subsequent monoglucosylation of the Rho family of proteins. This study explored toxin internalization and effects on mitochondrial function before cell rounding. METHODS: Chinese hamster ovary (CHO) cells were exposed to toxin A, and mitochondrial localization was assayed by confocal microscopy. Mitochondrial function was measured by adenosine triphosphate (ATP) concentration, mitochondrial permeability, and leakage of cytochrome c. RESULTS: Confocal microscopy showed toxin A colocalization with the mitochondrial protein GRP 75 at 5 minutes after toxin exposure. Between 5 and 15 minutes, toxin A caused an 80% diminution in cellular ATP levels; cell rounding and Rho glucosylation commenced between 15 and 30 minutes. Toxin A also resulted in reduction of mitochondrial membrane potential and a 2-3-fold increase in reactive oxygen radicals. Preincubation of CHO cells with the antioxidants butylated hydroxyanisole or butylated hydroxytoluene blocked the toxin A-induced increase in oxygen radicals and diminished cell rounding. Western blot analysis of toxin A-exposed isolated mitochondria showed a direct effect of toxin A on leakage of cytochrome c. CONCLUSIONS: The results show that extensive mitochondrial damage occurs within 15 minutes in CHO cells exposed to toxin A. Diminished ATP concentrations and increased oxygen radicals are likely to contribute to cytotoxicity from this bacterial toxin.

Adenosine Triphosphate↗

PubMed2000

A z gain nonuniformity correction for multislice volumetric CT scanners.

This paper presents a calibration and correction method for detector cell gain variations. A key functionality of current CT scanners is to offer variable slice thickness to the user. To provide this capability in multislice volumetric scanners, while minimizing costs, it is necessary to combine the signals of several detector cells in z, when the desired slice thickness is larger than the minimum provided by a single cell. These combined signals are then pre-amplified, digitized, and transmitted to the system for further processing. The process of combining the output of several detector cells with nonuniform gains can introduce numerical errors when the impinging x-ray signal presents a variation along z over the range of combined cells. These numerical errors, which by nature are scan dependent, can lead to artifacts in the reconstructed images, particularly when the numerical errors vary from channel-to-channel (as the filtered-backprojection filter includes a high-pass filtering along the channel direction, within a given slice). A projection data correction algorithm has been developed to subtract the associated numerical errors. It relies on the ability of calibrating the individual cell gains. For effectiveness and data flow reasons, the algorithm works on a single slice basis, without slice-to-slice exchange of information. An initial error vector is calculated by applying a high-pass filter to the projection data. The essence of the algorithm is to correlate that initial error vector, with a calibration vector obtained by applying the same high-pass filter to various z combinations of the cell gains (each combination representing a basis function for a z expansion). The solution of the least-square problem, obtained via singular value decomposition, gives the coefficients of a polynomial expansion of the signal z slope and curvature. From this information, and given the cell gains, the final error vector is calculated and subtracted from the projection data.

Algorithms↗