Search PubMed⌕ Search

Biomedical subjects

W Gao

Publications and source records attributed to W Gao.

At least 73 records · Page 4Linked to original sources
PubMed2001

[Evaluation on the growth and development of children from gangsan primary school in Kundulun district of Baotou City].

In order to evaluate the growth and development of primary school children and the effect of anemia on body height and weihgt, a routine examination on anthropometry and heomoglobin was carried out among the children from Gangsan Primary School in the Kundulun District of Baotou City, including 580 boys and 561 girls for anthropometry and 579 boys and 560 girls for hemoglobin in the Spring of 2001. The results showed that the growth and development of children were higher than the average results of children published in 1992 National Nutrition Survey, and also higher than the results from the Chinese school children physique development in 1995. The average prevalence of anemia was 26.2%, and the girls suffered from anemia were much higher than the boys (30.9% and 21.8% respectively). The highest prevalence of anemia in boys was in the second grades(29.3% and 28.9%), however, the highest prevalence of anemia in girls was in the second grade(43.2%). Compared with normal children, the children suffered from anemia were in lower height, lower body weight and lower body mass index significantly(P < 0.001); The present study indicated that anemia might have adverse effects on the growth and development of children.

Anemia, Iron-Deficiency↗
PubMed2001

[Characterization of alumina adobe and sintered body of GI-infiltrated ceramic].

OBJECTIVE: This study was conducted to elucidate the mechanism of formation of porous structure by investigating the porosity of the alumina adobe and sintered body of GI-II Infiltrate Ceramic, and its role in strengthening and toughening this kind of ceramic composite. METHODS: The alumina powder size-mass distribution was obtained by BI-XDC powder size analysis device; the open pore parameters of alumina adobe and sintered body were analyzed using the mercury pressure method. Their fracture surfaces were observed under scanning electronic microscope. RESULTS: Fine powder had two main size groups of 0.09-0.1 micron and 0.2-0.5 micron, respectively, and coarse powder, with size between 1.5 to 4.5 microns, occupied the majority of powder mass. Alumina adobe's pores became larger after sintering. The median pore radii of adobe and sintered body were 0.2531 micron and 0.3081 micron, respectively; the average pore radii changed from 0.0956 micron to 0.1102 micron. Under scanning electronic microscope, fine alumina powders were fused partially together and their surfaces were blunted, but coarse powders did not show such phenomena. CONCLUSION: The alumina size distribution contributes to the formation of porous structure of alumina sintered body. This porous structure is not only the shape skeleton but also the mechanical skeleton of GI-II Infiltrated Ceramic. It plays an important role in raising the mechanical properties of this kind of ceramic composite.

Aluminum Oxide↗
PubMed2001

[Study on the photoluminescence spectrum of nickel passivation treatment of porous silicon].

A new method for electrolysis passivation treatment of porous silicom (PS) in NiCl2 is reported in this paper. The photoluminescence (PL) spectra of PS treated in different time is observed, the spectra show that peak intensity is 2.5 times stronger than that without treatment, peak wavelength is 33 nm blue shift when PS is treated properly. The phenomenon caused is that the results of the SiHx change into SiNix when replaced H by Ni on surface of PS.

Chemical Phenomena↗
PubMed2000

Tuberculosis: reasons for diagnostic delay in Auckland.

AIMS: First, to quantify the interval between the onset of symptoms and the start of anti-tuberculous treatment in a series of Auckland tuberculosis patients. Second, to examine the help-seeking behaviour of the patients and the responses of the health-care providers whom they consulted about their symptoms. Third, to identify potentially modifiable reasons for delayed presentation or diagnosis. METHODS: 100 patients with tuberculosis (TB) were interviewed using a questionnaire which sought symptom duration and help-seeking behaviour. The doctors whom they consulted were surveyed about their diagnostic, therapeutic and referral responses. RESULTS: Delayed presentation by patients ('patient delay') was found in smokers, patients who reported cough, patients who hoped their symptoms would go away on their own, and patients reporting fear of what would be found on diagnosis. 'Doctor delay' (the interval from first consultation with a doctor to start of treatment) was longer than that found in most published series and was a more important component of total delay than delayed presentation by patients. Longer doctor delay was found if patients had pre-existing lung disease or consulted multiple doctors, and if doctors did not inquire into past exposure to TB or request a chest X-ray. CONCLUSIONS: Awareness programmes for high-risk communities are needed to encourage early reporting of symptoms. Continuing medical education for general practitioners is needed to encourage vigilance for TB and earlier use of diagnostic tests in patients who have symptoms of TB and are in high-risk groups.

Adolescent↗
PubMed2000

Requirement of the chemokine receptor CXCR3 for acute allograft rejection.

Chemokines provide signals for activation and recruitment of effector cells into sites of inflammation, acting via specific G protein-coupled receptors. However, in vitro data demonstrating the presence of multiple ligands for a given chemokine receptor, and often multiple receptors for a given chemokine, have led to concerns of biologic redundancy. Here we show that acute cardiac allograft rejection is accompanied by progressive intragraft production of the chemokines interferon (IFN)-gamma-inducible protein of 10 kD (IP-10), monokine induced by IFN-gamma (Mig), and IFN-inducible T cell alpha chemoattractant (I-TAC), and by infiltration of activated T cells bearing the corresponding chemokine receptor, CXCR3. We used three in vivo models to demonstrate a role for CXCR3 in the development of transplant rejection. First, CXCR3-deficient (CXCR3(-/)-) mice showed profound resistance to development of acute allograft rejection. Second, CXCR3(-/)- allograft recipients treated with a brief, subtherapeutic course of cyclosporin A maintained their allografts permanently and without evidence of chronic rejection. Third, CXCR(+/+) mice treated with an anti-CXCR3 monoclonal antibody showed prolongation of allograft survival, even if begun after the onset of rejection. Taken in conjunction with our findings of CXCR3 expression in rejecting human cardiac allografts, we conclude that CXCR3 plays a key role in T cell activation, recruitment, and allograft destruction.

Acute Disease↗
PubMed2000

Differential effects of cyclosporine A, methylprednisolone, mycophenolate, and rapamycin on CD154 induction and requirement for NFkappaB: implications for tolerance induction.

BACKGROUND: Recent experimental data indicate that the targeting of the costimulatory molecule CD40-ligand (CD154) may well offer an opportunity for tolerance induction in transplant recipients and patients with autoimmune diseases, although the optimal therapeutic strategy for clinical application of CD154 monoclonal antibody (mAb) is unclear. METHODS: We undertook vascularized heterotopic cardiac allograft transplantation in completely MHC-mismatched mice, treated recipients with CD154 mAb plus various immunosuppressive agents, and performed flow cytometric analysis of CD154 expression by T cells activated in vitro in the presence of corresponding immunosuppressive agents. We also tested the extent to which CD154 induction was NFkappaB-dependent by using NFkappaB/p50-deficient mice as allograft recipients and as source of cells for in vitro studies of CD154 induction, and through use of proteasome inhibitors to block IkappaBalpha degradation and NFKB activation in wild-type mice. RESULTS: Concomitant use of cyclosporin A or methylprednisolone, but not rapamycin or mycophenolate, inhibited CD154 mAb-induced allograft survival. The differential effects of these agents on CD154 mAb-induced tolerance correlated with their capacity to inhibit activation-induced CD154 expression on CD4+ T cells. Full expression of CD154 expression was found to require NF-kappaB activation, and CD154 mAb was ineffective in NF-kappaB/p50 deficient allograft recipients or control mice in which NF-kappaB activation was blocked by proteasome inhibition. CONCLUSIONS: Strategies to use CD154 mAb clinically must take into account the effects of immunosuppressive agents on CD154 induction, which seems to be at least partially NF-kappaB dependent. Our data suggest that ligation of surface-expressed CD154 provides an important signal that modulates T cell activation and thereby contributes to the effects of CD154 mAb, in addition to previously recognized actions involving blockade of CD40/CD154-dependent cell activation and activation-induced cell death.

Animals↗
PubMed2000

In vitro caries inhibition at the enamel margins of glass ionomer restoratives developed for the ART approach.

OBJECTIVES: To assess the ability of conventional glass ionomer cements manufactured specifically for the atraumatic restorative treatment (ART) approach to inhibit the in vitro demineralization of enamel. METHODS: Twenty-four sound permanent premolar teeth, extracted for orthodontic reasons, had cervical cavities (4x2x1. 5mm(3)) prepared in enamel. These were restored with Fuji IX, Fuji IX GP, Ketac-Molar and Compoglass, and then thermocycled 300 times between 5-55 degrees C before being placed in a demineralizing solution (0.1M lactic acid with 1g/l dissolved hydroxyapatite at pH 4.7) for four weeks. Buccolingual planoparallel sections were cut axially through the restorations, and subsequently lapped to approximately 100 microm thickness. The sections were examined with a polarized light microscope, and lesion measurements made using image analysis software. ANOVA and coefficients of variance were used to compare the findings. RESULTS: Compoglass and Ketac-Molar showed significantly less surface erosion than did the other two cements (p<0.0001). Inhibition of enamel demineralization immediately adjacent to the restoration margins was more frequent with the glass ionomer cements (20.5-25.0%) than with Compoglass (13.0%). However, the widths of the inhibition zones varied between materials and sites. CONCLUSIONS: Fluoride ion release from the restorative materials afforded some degree of protection to the adjacent enamel against in vitro demineralization.

Analysis of Variance↗
PubMed2000

Heparin-free hemodialysis in the treatment of hypernatremia in severely burned patients.

BACKGROUND: Hypernatremia in severely burned patients is associated with high morbidity and mortality rates. As the causes of hypernatremia in major burn patients are still not clear, hemodialysis is the method of choice for the treatment. While hemodialysis is effective for the control of hypernatremia, it can cause bleeding complications that may be fatal for burn patients with extensive wounds and potential gastro-intestinal mucosal damage. CLINICAL DATA: In the present study heparin-free hemodialysis in which the heparin is firmly absorbed to the haemofiltration membrane, hemophan, dispensed with systemic use of heparin. In two extensively burned patients with burn area of 100% TBSA and 98% TBSA respectively and hypernatremia with serum sodium concentration as high as 169 and 158 mmol/l respectively, heparin-free hemodialysis was performed five times and three times each. RESULTS: Hypernatremia was satisfactorily corrected with no interference to the coagulation system in the two patients as indicated by clinical observation and biochemical analysis. The patient with burn area of 98% TBSA survived and the patient with burn area of 100% TBSA died of wound coverage failure 6 weeks after injury because of non-availability of autograft. CONCLUSION: Heparin-free hemodialysis is an effective and safe method in the treatment of hypernatremia in extensively burned patients.

Adult↗
PubMed2000

Local alpha-bungarotoxin-sensitive nicotinic receptors in the nucleus accumbens modulate nicotine-stimulated dopamine secretion in vivo.

Nicotinic cholinergic receptors in the ventral tegmental area are required for the accumbal dopamine response to systemic nicotine. In contrast, the role of nicotinic receptors located within the nucleus accumbens itself has not been clarified for systemically administered nicotine. In the present study, in vivo microdialysis of accumbal dopamine secretion and receptor antagonist blockade in both the ventral striatal nucleus accumbens and the midbrain ventral tegmental area were used to evaluate this question. The nicotinic receptor antagonists methyllycaconitine or mecamylamine were delivered through the accumbal dialysis probe, followed by 0.09mg/kg nicotine (i.v.). The alpha7 subunit antagonist methyllycaconitine inhibited 71% of the dopamine response (P<0.01), whereas mecamylamine was completely ineffective. In addition, the classical alpha7 subunit antagonist alpha-bungarotoxin infused into the nucleus accumbens adjacent to the microdialysis probe, significantly reduced dopamine release by 0.065 or 0.09mg/kg nicotine (i.v.; P<0. 05). Combined, these data indicate the involvement of alpha7 subunit-containing nicotinic receptors in the nucleus accumbens. In contrast, local infusion of mecamylamine into the ventral tegmental area effectively blocked nicotine-induced accumbal dopamine release. Simultaneous infusions of methyllycaconitine into the accumbens and mecamylamine into the ventral tegmental area induced greater blockade of nicotine-stimulated dopamine secretion than methyllycaconitine or mecamylamine alone. In conclusion, the present study demonstrates that different types of nicotinic cholinergic receptors, located in the ventral striatal nucleus accumbens (alpha-bungarotoxin sensitive and mecamylamine insensitive) and the midbrain ventral tegmental area (mecamylamine sensitive), may be required for the full effects of nicotine on the mesostriatal dopaminergic pathway. While activation of nicotinic cholinergic receptors in the ventral tegmentum is required for the accumbal dopamine response to systemic nicotine, accumbal nicotinic receptors themselves act as modulators of this response. This fine tuning of the dopamine reward pathway through alpha7 nicotinic cholinergic receptors in the nucleus accumbens may amplify the secretion of dopamine, allowing a subthreshold brain concentration of nicotine to become an effective stimulus for dopamine secretion.

Acetylcholine↗
PubMed2000

Chemokines and their receptors in allograft rejection.

Despite current recognition of over 40 chemokines and more than 18 chemokine receptors, understanding of their role in transplant immunobiology and transplant rejection is extremely limited and fragmentary. Recent literature has demonstrated the presence of chemokines and their receptors in transplants and some studies demonstrate important functional roles.

Animals↗
PubMed2000

Apoptotic cells actively inhibit the expression of CD69 on Con A activated T lymphocytes.

Although apoptosis is commonly viewed as a silent cell death without damage to adjacent tissues, the effect of apoptosis on immunity has been unclear. We have investigated the influence of apoptotic cells on T-cell activation. The K562 or HL-60 human leukemia cell lines that had been induced apoptosis by FTY720 or cycloheximide (CHX) were added into the culture of mouse spleen cells stimulated with Con A. Six to 20 h later, the expression of CD69, an early T-cell activation antigen, was detected using flowcytometry. Living cells and necrotic cells served as control groups. Apoptotic K562 or HL-60 cells induced by either FTY720 or CHX unanimously inhibited CD69 expression on the CD3+ mouse T cells while living and necrotic cells did not. The inhibition was proportional to the number of apoptotic cells and was different in the T-cell subsets, showing a rapid and transient inhibition on the CD3+CD8+ T-cell activation but with a slow and continuous inhibition on CD3+CD8- T-cell activation. In conclusion, the apoptotic cells actively inhibit a T-cell activation that is independent of the cell lines or the apoptotic inducers, indicating that the apoptotic cells dominantly regulate T-cell immunity.

Animals↗
PubMed2000

Permeability barrier disorder in Niemann-Pick disease: sphingomyelin-ceramide processing required for normal barrier homeostasis.

Prior studies have established the requirement for enzymatic hydrolysis of glucosylceramides to ceramide for epidermal barrier homeostasis. In this study, we asked whether sphingomyelin-derived ceramide, resulting from acid-sphingomyelinase activity, is also required for normal barrier function. We showed first, that a subset of Niemann-Pick patients with severe acid-sphingomyelinase deficiency (i.e., <2% residual activity) demonstrate abnormal permeability barrier homeostasis, i.e., delayed recovery kinetics following acute barrier disruption by cellophane tape-stripping. To obtain further mechanistic insights into the potential requirement for sphingomyelin-to-ceramide processing for the barrier, we next studied the role of acid-sphingomyelinase in hairless mouse skin. Murine epidermis contains abundant acid-sphingomyelinase activity (optimal pH 5.1-5.6). Two hours following acute barrier disruption by tape-stripping, acid-sphingomyelinase activity increases 1. 44-fold (p<0.008 versus vehicle-treated controls), an increase that is blocked by a single topical application of the acid-sphingomyelinase inhibitor, palmitoyldihydrosphingosine. Furthermore, both palmitoyldihydrosphingosine and desipramine, a chemically and mechanically unrelated acid-sphingomyelinase inhibitor, significantly delay barrier recovery both 2 and 4 h after acute barrier abrogation. Inhibitor application also causes both an increase in sphingomyelin content, and a reduction of normal extracellular lamellar membrane structures, in the stratum corneum. Both of the inhibitor-induced delays in barrier recovery can be overridden by co-applications of topical ceramide, demonstrating that an alteration of the ceramide-sphingomyelin ratio, rather than sphingomyelin accumulation, is likely responsible for the barrier abnormalities that occur with acid-sphingomyelinase deficiency. These studies demonstrate an important role for enzymatic processing of sphingomyelin-to-ceramide by acid-sphingomyelinase as a mechanism for generating a portion of the stratum corneum ceramides for permeability barrier homeostasis in mammalian skin.

Adolescent↗
PubMed2000

Three lycopodium alkaloid N-oxides from Huperzia serrata.

Three lycopodium alkaloid N-oxides, huperzine J (1), huperzine K (2) and huperzine L (3) were obtained from Huperzia serrata (Thunb.) Trev. Their structures were elucidated by spectroscopic methods and the relative configurations of 1 and 3 were established via NOESY NMR observations; optical rotation values and CD data are presented.

Magnetic Resonance Spectroscopy↗
PubMed2000

Demineralisation and remineralisation of dentine caries, and the role of glass-ionomer cements.

In accordance with the principles of modern operative dentistry, to conserve tooth structure and to use therapeutic restorative materials, an understanding of the carious process in dentine and the biological properties of glass-ionomer cements (GICs) are necessary. Delineation of the outer necrotic from the inner vital and remineralisable carious dentine allows for the preservation of tooth structure. This delineation is not possible when relying on visual and tactile perceptions, but requires the use of a caries detecting dye. GICs are ideal dentine substitutes because of their anticariogenic properties, stable long-term ionic bonding, and ability to assist the process of remineralization. The range of usage of these restorative materials continues to expand with the development of improved products.

Apatites↗
PubMed2000

Heterologous expression of Trypanosoma cruzi trans-sialidase in Leishmania major enhances virulence.

Earlier studies showed that mice primed for a few hours with the trans-sialidase (TS) of Trypanosoma cruzi, the agent of Chagas' disease, become highly susceptible to trypanosomal infection. These studies suggest that TS affects parasite virulence independent of antigenic stimulation. Potentially, TS could enhance or reduce the virulence of heterologous microbes depending on the mechanism of TS action and on the type of immune response elicited by the particular parasite. We tested this hypothesis by expressing heterologous TS in Leishmania major, a protozoan parasite that causes cutaneous leishmaniasis and lacks TS and the TS product alpha2-3-linked sialic acid. Leishmania cells transfected with a T. cruzi TS expression construct made high levels of active enzyme, which was present in the promastigotes and shed into the extracellular milieu. TS expression did not affect L. major binding to and entry into cultured macrophages or its tropism for macrophage infection in vivo. However, TS-expressing L. major exhibited elevated virulence in BALB/c mice, as determined by lesion progression, parasite numbers, and macro- and microscopic examination of cutaneous lesions. Several genetic tests proved that the enhanced virulence was directly attributable to TS expression. The results are consistent with TS functioning to sabotage the mouse immune system to confer a growth advantage on T. cruzi and transgenic L. major. These data suggest that heterologous expression of T. cruzi virulence factors in Leishmania may provide a new approach for dissecting their function in vivo.

Animals↗
PubMed2000

Targeting of the chemokine receptor CCR1 suppresses development of acute and chronic cardiac allograft rejection.

Although mononuclear cell infiltration is a hallmark of cellular rejection of a vascularized allograft, efforts to inhibit rejection by blocking leukocyte-endothelial cell adhesion have proved largely unsuccessful, perhaps in part because of persistent generation of chemokines within rejecting grafts. We now provide, to our knowledge, the first evidence that in vivo blockade of specific chemokine receptors is of therapeutic significance in organ transplantation. Inbred mice with a targeted deletion of the chemokine receptor CCR1 showed significant prolongation of allograft survival in 4 models. First, cardiac allografts across a class II mismatch were rejected by CCR1(+/+) recipients but were accepted permanently by CCR1(-/-) recipients. Second, CCR1(-/-) mice rejected completely class I- and class II-mismatched BALB/c cardiac allografts more slowly than control mice. Third, levels of cyclosporin A that had marginal effects in CCR1(+/+) mice resulted in permanent allograft acceptance in CCR1(-/-) recipients. These latter allografts showed no sign of chronic rejection 50-200 days after transplantation, and transfer of CD4(+) splenic T cells from these mice to naive allograft recipients significantly prolonged allograft survival, whereas cells from CCR1(+/+) mice conferred no such benefit. Finally, both CCR1(+/+) and CCR1(-/-) allograft recipients, when treated with a mAb to CD4, showed permanent engraftment, but these allografts showed florid chronic rejection in the former strain and were normal in CCR1(-/-) mice. We conclude that therapies to block CCR1/ligand interactions may prove useful in preventing acute and chronic rejection clinically.

Acute Disease↗
PubMed2000

Systemic nicotine stimulates dopamine release in nucleus accumbens: re-evaluation of the role of N-methyl-D-aspartate receptors in the ventral tegmental area.

Systemic nicotine stimulates dopamine (DA) release in the nucleus accumbens (NAcc), and N-methyl-D-aspartate (NMDA) receptors in the ventral tegmental area (VTA) appear to be involved. However, it is not known whether the secretion of DA elicited by nicotine depends on the tonic and/or phasic activation of NMDA receptors by glutamate (Glu). To clarify this, in vivo microdialysis was conducted in freely moving, alert rats to measure DA and Glu overflows in the NAcc and Glu in the VTA. Nicotine (0.065, 0.09, or 0.135 mg/kg delivered i.v. at 0.09 mg/kg/60 s via a jugular cannula) dose dependently stimulated NAcc DA secretion (P <.05). However, 0.065 mg/kg nicotine failed to stimulate Glu release in the VTA, whereas higher doses of nicotine (> or =0.09 mg/kg) were effective (P <.05). Administering the competitive NMDA receptor antagonists, 2-amino-5-phosphonopentanoic acid (AP-5; 1 mM) or 0.2 mM cis-4-phosphonomethyl-2-piperidine carboxylic acid (CGS 19755) through the VTA probe, abolished NAcc DA release after 0.065 mg/kg nicotine (P <.01) and reduced the response to 0.09 mg/kg nicotine. Therefore, the NAcc DA response to a relatively low dose of nicotine depends on the tonic activation of NMDA receptors in the VTA. In contrast, infusing 1 mM 2-amino-5-phosphonopentanoic acid or 1 mM 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), an alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA) receptor antagonist, into the NAcc through the microdialysis probe had no effect on NAcc DA secretion in response to 0.09 mg/kg nicotine. These findings, coupled with data showing that Glu secretion in the VTA was stimulated only by higher doses of nicotine, indicate that the phasic release of VTA Glu is involved in the NAcc DA response to higher doses of nicotine (> or =0.09 mg/kg).

2-Amino-5-phosphonovalerate↗