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Biomedical subjects

W Gao

Publications and source records attributed to W Gao.

At least 37 records · Page 2Linked to original sources
PubMed2002

Cancer incidence in Singapore, 1998 to 1999.

The age-standardised incidence rates for all cancers for 1998-1999 were 235.0 per 100,000 in males and 199.8 per 100,000 in females. The corresponding rates for 1993-1997 were 233.1 per 100,000 in males and 198.1 per 100,000 in females. The greatest difference was for breast cancer in females with age-standardised incidence rates increasing from 46.1 to 53.1 cases per 100,000 persons per year between these time periods. There also appears to be a shift of the peak age-specific incidence for breast cancer from premenopausal to postmenopausal years over this period. This suggests that our breast cancer incidence pattern is rapidly becoming more similar to populations in the West.

Adult↗
PubMed2001

The Sma I polymorphism in the von Willebrand factor gene associated with acute ischemic stroke.

The von Willebrand factor (vWF) is a highly multimerized glycoprotein that promotes platelet adhesion and aggregation at a high shear rate, and also acts as a carrier of coagulation factor VIII. vWF has been identified as a risk factor for recurrent myocardial infarction in the general population. It has been reported that two polymorphisms of vWF gene promoter and the Thr789Ala polymorphism in vWF gene are associated with arterial thrombosis. The Sma I polymorphism is located in intron 2 of vWF gene. The relevance of this polymorphism to thrombotic disease was investigated by genotypic identification in two case-control studies: 107 patients with acute ischemic stroke, 49 patients with acute myocardial infarction (AMI), and 113 health controls age- and race-matched for each patient. Twenty-eight (26.2%) of the 107 patients with acute ischemic stroke, 8 (16.3%) of 49 patients with AMI, and 11 (9.7%) of 113 controls were found to be homozygous for CC genotype, respectively. The prevalence of the CC genotype in acute ischemic stroke was significantly higher than that of the normal controls (odds ratio [OR]=3.29, 95% confidence interval [CI]=1.54-7.01,.01>P>.001). However, the prevalence of the CC genotype in AMI was not significantly different from that of the normal controls (OR=1.81, 95% CI=0.68-4.82,.30>P>.20). Plasma vWF:Ag was also determined by enzyme-linked immunosorbent assay (ELISA) on the frozen plasma of 122 subjects. The mean plasma vWF:Ag levels of the controls, patients with acute ischemic stroke, and AMI were 0.468, 0.584, and 0.783 U/ml, respectively. The mean level of plasma vWF:Ag did not differ significantly between controls and patients with acute ischemic stroke (P=.195), but had significantly difference between controls and patients with AMI (P=.001). No association was found between the Sma I polymorphism and vWF plasma levels in controls, patients with acute ischemic stroke, or the AMI group (one-way ANOVA, P=.323, P=.315, P=.96). Results show that the Sma I polymorphism is strongly associated with increased risk of acute ischemic stroke, however, no association was observed between this polymorphism and AMI. This polymorphism of vWF may represent a newly identified risk factor for acute ischemic stroke in Chinese. Whether it is the real functional variant associated with acute ischemic stroke remains to be elucidated.

Acute Disease↗
PubMed2001

IL-7 enhances the survival and maintains the size of naive T cells.

T cells require continual presence of extrinsic signals from their in vivo microenvironment to maintain viability. T cells removed from these signals and placed in tissue culture atrophied and died in a caspase-independent manner. Atrophy was characterized by smaller cell sizes, delayed mitogenic responses, and decreased glycolytic rate. Bcl-2 expression remained constant in vitro despite ongoing cell death, indicating that endogenous Bcl-2 expression is insufficient to explain the life span and size control of lymphocytes in vivo and that cell-extrinsic signals provided may be required to maintain both cell viability and size in vivo. One such signal, IL-7, was found to maintain both the size and survival of neglected T cells in vitro. IL-7 was not unique, because the common gamma-chain cytokines IL-2, IL-4, and IL-15, as well as the gp130 cytokine IL-6, also promoted both T cell survival and size maintenance. IL-7 did not induce resting T cells to proliferate. Instead, IL-7 stimulated neglected T cells to maintain their metabolic rate at levels comparable to freshly isolated cells. The survival and trophic effects of IL-7 could be separated because IL-7 was able to promote up-regulation of Bcl-2 and maintain cell viability independent of phosphatidylinositol 3-kinase and mammalian target of rapamycin activity but was unable to prevent cellular atrophy when phosphatidylinositol 3-kinase and mammalian target of rapamycin were inhibited. These data demonstrate that T cells require the continuous presence of extrinsic signals not only to survive but also to maintain their size, metabolic activity, and the ability to respond rapidly to mitogenic signals.

Animals↗
PubMed2001

Role of calcium, glutamate neurotransmission, and nitric oxide in spreading acidification and depression in the cerebellar cortex.

This study investigated the mechanisms underlying the recently reported fast spreading acidification and transient depression in the cerebellar cortex in vivo. Spreading acidification was evoked by surface stimulation in the rat and mouse cerebellar cortex stained with the pH-sensitive dye neutral red and monitored using epifluorescent imaging. The probability of evoking spreading acidification was dependent on stimulation parameters; greater frequency and/or greater amplitude were more effective. Although activation of the parallel fibers defined the geometry of the spread, their activation alone was not sufficient, because blocking synaptic transmission with low Ca(2+) prevented spreading acidification. Increased postsynaptic excitability was also a major factor. Application of either AMPA or metabotropic glutamate receptor antagonists reduced the likelihood of evoking spreading acidification, but stronger stimulation intensities were still effective. Conversely, superfusion with GABA receptor antagonists decreased the threshold for evoking spreading acidification. Blocking nitric oxide synthase (NOS) increased the threshold for spreading acidification, and nitric oxide donors lowered the threshold. However, spreading acidification could be evoked in neuronal NOS-deficient mice (B6;129S-Nos1(tm1plh)). The depression in cortical excitability that accompanies spreading acidification occurred in the presence of AMPA and metabotropic glutamate receptor antagonists and NOS inhibitors. These findings suggest that spreading acidification is dependent on extracellular Ca(2+) and glutamate neurotransmission with a contribution from both AMPA and metabotropic glutamate receptors and is modulated by nitric oxide. Therefore, spreading acidification involves both presynaptic and postsynaptic mechanisms. We hypothesize that a regenerative process, i.e., a nonpassive process, is operative that uses the cortical architecture to account for the high speed of propagation.

Acids↗
PubMed2001

Beneficial effects of targeting CCR5 in allograft recipients.

BACKGROUND: The chemokine receptor, CCR5, and its three high-affinity ligands, macrophage inflammatory protein- (MIP) 1alpha, MIP-1beta, and regulated on activation normal T cell expressed and secreted (RANTES), are expressed by infiltrating mononuclear cells during the rejection of clinical and experimental organ allografts, although the significance of these molecules in the pathogenesis of rejection has not been established. METHODS: We studied intragraft events in four allograft models. First, we studied cardiac transplants in fully MHC-mismatched mice that were deficient in CCR5 or two of its ligands, MIP-1alpha or RANTES. Second we tested the effects of a neutralizing rat anti-mCCR5 monoclonal antibody on allograft survival. Third we assessed whether a subtherapeutic course of cyclosporine would potentiate enhance survival in CCR5-deficient recipients. Finally, we tested the effect of targeting CCR5 in a class II-mismatched model. RESULTS: Whereas mice deficient in expression of MIP-1alpha or RANTES reject fully MHC-mismatched cardiac allografts normally, CCR5-/- mice, or CCR5+/+ mice treated with a neutralizing mAb to mCCR5, show enhanced allograft survival. MHC class II-disparate mismatched are permanently accepted in CCR5-/- but not CCR5+/+ recipients. Finally, the beneficial effects of targeting of CCR5 are markedly synergistic with the effects of cyclosporine, resulting in permanent engraftment without development of chronic rejection. CONCLUSIONS: We conclude that CCR5 plays a key role in the mechanisms of host T cell and macrophage recruitment and allograft rejection, such that targeting of CCR5 clinically may be of therapeutic significance.

Animals↗
PubMed2001

Lung tumor KRAS and TP53 mutations in nonsmokers reflect exposure to PAH-rich coal combustion emissions.

We determined the TP53 and codon 12 KRAS mutations in lung tumors from 24 nonsmokers whose tumors were associated with exposure to smoky coal. Among any tumors studied previously, these showed the highest percentage of mutations that (a) were G --> T transversions at either KRAS (86%) or TP53 (76%), (b) clustered at the G-rich codons 153-158 of TP53 (33%), and (c) had 100% of the guanines of the G --> T transversions on the nontranscribed strand. This mutation spectrum is consistent with an exposure to polycyclic aromatic hydrocarbons, which are the primary component of the smoky coal emissions. These results show that mutations in the TP53 and KRAS genes can reflect a specific environmental exposure.

Air Pollution, Indoor↗
PubMed2001

Direct-Sun column ozone retrieval by the ultraviolet multifilter rotating shadow-band radiometer and comparison with those from Brewer and Dobson spectrophotometers.

A methodology for direct-Sun ozone retrieval using the ultraviolet multifilter rotating shadow-band radiometer (UV-MFRSR) is presented. Total vertical column ozone was retrieved in three stations: Mauna Loa, Hawaii, in the U.S., and Regina, Saskatchewan, and Toronto, Ontario, in Canada, from direct solar irradiances of the UV-MFRSR at 325-, 305-, 332-, and 311-nm channels (2-nm FWHM). The total uncertainty of ozone retrievals in this study is +/-2.0%. For Mauna Loa the mean ratios of the UV-MFRSR column ozone retrievals to the collocated Dobson and Brewer were 0.998 and 0.986 between May and September of 1999. The mean ratio of UV-MFRSR retrievals to the collocated Brewer retrievals was 1.012 in Toronto between April and August of 1999, and the mean ratio of retrievals of the UV-MFRSR to the collocated Brewer was 0.988 in Regina between June and September of 1999. Total vertical column ozone values for solar zenith angles of >70 degrees were not considered, because of the signal-to-noise ratio and the angular response of the instruments, and were not used in the evaluation. The advantages of total vertical column ozone retrieval using UV-MFRSR include relatively low cost, computer-controlled operation, automated calibration stability checks, and minimal maintenance. It allows for the real-time measurement of total vertical column ozone. The UV-MFRSR is being used at 28 sites across the United States and 2 sites in Canada that form the U.S. Department of Agriculture UV-B Radiation Monitoring and Research Program. This constitutes a unique network of total vertical colunm ozone measurement.

Journal Article↗
PubMed2001

[Effect of endostatin gene transfer mediated by electric pulses into skeletal muscles on development of atherosclerotic plaques in mice].

OBJECTIVE: To investigate the effect of endostatin gene transfer mediated by electric pulses into skeletal muscles of mice upon the develpment of atherosclerotic plaques. METHODS: Eukaryotic expression plasmid of mouse endostatin was injected into the muscles of 2 groups of ApoE-deficient mice, group A at the age of 24 weeks, and group B at the age of 36 weeks (named therapy group as a whole). Gene transfer was mediated by electric pulses for ten times. Empty plasmid was used to mice at the same ages as controls. Twenty weeks later, blood-lipid was tested, and the aortas of the experimental animals were taken out to examine the areas of atherosclerotic plaques and count the endothelial cells and microvessels in the plaques. RESULTS: In the 24-week-aged group, the stenosis rate of aorta 16% +/- 4% before the experiment. Twenty weeks later, the stenosis rate was 56% +/- 14% among the control mice, and was 34% +/- 8% among the treated ones with an improvement rate of 54%. In the 36-week-aged group, the stenosis rate of aorta was 30% +/- 6% before the experiment. Twenty weeks after the begining of experiment, the stenosis rate was 64% +/- 12% among the control mice, and was 49% +/- 10% among the treated ones with an improvement rate of 44%. Twenty weeks after the begining of experiment, the endothelial cell count and microvessel appearance rate were less among the therapy group than among the controls. There was no significant difference in blood-lipid between the therapy group and the control group. CONCLUSION: Endostatin gene transfer into skeletal muscle effectively inhibits the development of atherosclerotic plaques.

Animals↗
PubMed2001

[The study of beta-2 adrenergic receptors gene transferred into cardiomyocytes by adenovirus vectors contain different promoter].

OBJECTIVE: To observe human beta(2) adrenergic receptors (beta(2)-AR) gene expression in cardiomyocytes transfected by adenoviral vector contain cmv or mlc-2v promoter. METHODS: Two adenoviral vectors (Adcmv beta(2) AR, Admlc beta(2) AR) were constructed, in which beta(2)-AR gene is under control of either the ventricle-specific myosin light chain-2 (mlc-2v) or the cmv promoter. The cultured neonate rat ventricular myocytes were infected by two adenoviral vectors, and the beta(2)-AR expression of on cultured neonate rat ventricular myocytes and their ability to potentiate beta-adrenergic signaling were assessed. RESULTS: The presence of beta(2)-AR mRNA was detected by RT-PCR, and the expression of the beta(2)-AR gene was demonstrated by protein immunoblots. According to a ligand binding assay, the density of beta-AR in the cardiomyocytes infected by Admlc beta(2) AR and Adcmv beta(2) AR was greater than that in the control. Moreover, the latter was higher than the former (234 +/- 6.4 fmol/mg protein vs 153 +/- 5.2 fmol/mg protein) (P < 0.01). It was demonstrated that beta(2)-AR gene significantly increased isoproterenol stimulated cAMP in cardiomyocytes. CONCLUSION: The results above demonstrated that human beta(2)-AR gene was expressed in the cardiomyocytes infected by recombinant adenovirus contain cmv or mlc-2v promoter, but both is different.

Adenoviridae↗
PubMed2001

Donor-derived IP-10 initiates development of acute allograft rejection.

An allograft is often considered an immunologically inert playing field on which host leukocytes assemble and wreak havoc. However, we demonstrate that graft-specific physiologic responses to early injury initiate and promulgate destruction of vascularized grafts. Serial analysis of allografts showed that intragraft expression of the three chemokine ligands for the CXC chemo-kine receptor CXCR3 was induced in the order of interferon (IFN)-gamma-inducible protein of 10 kD (IP-10, or CXCL10), IFN-inducible T cell alpha-chemoattractant (I-TAC; CXCL11), and then monokine induced by IFN-gamma (Mig, CXCL9). Initial IP-10 production was localized to endothelial cells, and only IP-10 was induced by isografting. Anti-IP-10 monoclonal antibodies prolonged allograft survival, but surprisingly, IP-10-deficient (IP-10(-/-)) mice acutely rejected allografts. However, though allografts from IP-10(+/+) mice were rejected by day 7, hearts from IP-10(-/-) mice survived long term. Compared with IP-10(+/+) donors, use of IP-10(-/-) donors reduced intragraft expression of cytokines, chemokines and their receptors, and associated leukocyte infiltration and graft injury. Hence, tissue-specific generation of a single chemokine in response to initial ischemia/reperfusion can initiate progressive graft infiltration and amplification of multiple effector pathways, and targeting of this proximal chemokine can prevent acute rejection. These data emphasize the pivotal role of donor-derived IP-10 in initiating alloresponses, with implications for tissue engineering to decrease immunogenicity, and demonstrate that chemokine redundancy may not be operative in vivo.

Acute Disease↗
PubMed2001

Differential NF-kappaB and IkappaB gene expression during development of cardiac allograft rejection versus CD154 monoclonal antibody-induced tolerance.

BACKGROUND: The Rel/NF-kappaB transcription factor pathway, regulated by IkappaB proteins, is considered central to immune responses, although there are surprisingly few in vivo data concerning alloresponses. METHODS: We undertook analysis of NF-kappaB and IkappaB mRNA intracardiac allograft expression, and NF-kappaB nuclear translocation, during acute rejection versus CD154 monoclonal antibody (mAb)-induced tolerance induction in fully MHC-disparate mice. RESULTS: Intragraft expression of all nine NF-kappaB and IkappaB genes increased during development of rejection, and nuclear translocation of p50, p52, and p65 was detected. CD154 mAb therapy decreased mRNA levels of all nine NF-kappaB and IkappaB genes, and impaired nuclear translocation of p50, p52, and p65 NF-kappaB proteins. However, prolonged survival could not be induced by CD154 mAb in p50- or p52-deficient allograft recipients, indicating an absolute requirement for expression of these genes in CD154 mAb-induced tolerance. CONCLUSIONS: We conclude that, whereas blanket approaches to NF-kappaB suppression are unlikely to be effective strategies for tolerance induction, a better understanding of the roles of individual NF-kappaB and IkappaB genes may allow development of more precise and effective therapies.

Animals↗
PubMed2001

Detection of soluble urokinase receptor by immunoradiometric assay and its application in tumor patients.

It has recently been found that tumor cells express large amounts of urokinase receptor (uPAR) on their surface and that the blood soluble uPAR (suPAR) level in cancer patients is increased. However, the significance of suPAR in tumor progression is still unclear. To investigate the significance of suPAR in evaluating clinical status of solid tumor patients, an immunoradiometric assay (IRMA) based on using two monoclonal antibodies (McAbs) to different epitopes of uPAR was established to determine the serum levels of suPAR in normal individuals and solid tumor patients. The detectable range of this suPAR IRMA was 1.95-500 microg/l. The affinity constant was 4.75x10(9) l/mol. The mean rate of recovery was 101.3%, and the mean coefficients of variation for intra- and interassay were 6.40+/-2.57% (mean+/-S.D., n = 11) and 10.48+/-2.65% (n = 5), respectively. The serum suPAR levels were 2.71+/-1.12 microg/l in 62 normal individuals, 3.71+/-1.69 microg/l in 30 patients with benign tumors, and 5.82+/-2.27 microg/l in 124 patients with malignant tumors. The serum suPAR levels of these two types of tumor patients were increased in comparison with that of normal individuals (P values less than.01 and.001). The extent of their increase in malignant tumors was much greater than in benign tumors (P < .001). The serum suPAR levels of patients with malignant tumors were correlated with tumor invasion, metastasis, and surgical intervention. Our data suggest that IRMA for suPAR could be a sensitive and specific assay and that the serum suPAR level would be a valuable index for evaluating the condition and prognosis of tumor patients in clinic.

Adolescent↗
PubMed2001

Trypanosoma cruzi trans-sialidase potentiates T cell activation through antigen-presenting cells: role of IL-6 and Bruton's tyrosine kinase.

Polyclonal lymphocyte activation and hypergammaglobulinemia characterize the acute phase of Chagas' disease, a debilitating condition caused by Trypanosoma cruzi. Such pathogenic hyper-reactivities not only compromise specific host defense against the pathogen, but may also contribute to infection-induced chronic autoimmune responses. Recent studies showed that T. cruzi trans-sialidase (TS) directly stimulates the polyclonal proliferation and Ig secretion of normal murine B cells in a T-independent, Bruton's tyrosine kinase (Btk)-dependent manner. Related to this observation, we now show that parasite-derived and recombinant TS potentiate the proliferation and cytokine secretion of normal T cells triggered by antigen-specific and non-specific stimuli. TS potentiates T cell activation through stimulating B cells and macrophages, independent of CD40/CD40L and CD43 pathways. In contrast, optimal TS potentiation requires interleukin-6 (IL-6) and Btk, as it is significantly reduced in splenocytes from IL-6-/- and Btk-defective Xid mice. The results suggest that TS, directly and indirectly, activates both antigen-presenting cell and T cell compartments, and that TS-induced IL-6 may further amplify such activation. These observations open up the possibility that TS drives the polyclonal lymphocyte activation in acute T. cruzi infection, a phenomenon contributing to the pathogenesis of Chagas' disease.

Agammaglobulinaemia Tyrosine Kinase↗
PubMed2001

Blood lead levels among children aged 1 to 5 years in Wuxi City, China.

The objective of this study was to determine mean blood lead levels and prevalence of elevated blood lead levels among 1- to 5-year-old children in Wuxi City, China. By use of a representative cross-sectional survey that included measurements of capillary blood lead, 1117 children aged 1-5 years were examined from October through December, 1997. The geometric mean blood lead level for children 1-5 years of age in Wuxi City was 8.2 microg/dL (0.40 micromol/L); 27.3% had blood lead levels >or=10 microg/dL and 1.0% had blood lead levels >or=20 microg/dL. Blood lead levels were significantly higher for males and for those living in industrial areas, particularly the Beitang, Mashan, and Xinqu districts. Residence in these districts and in the Jiaoqu industrialized district also increased the likelihood of an elevated blood lead level, with odds ratios ranging from 2.59 to 4.53. In conclusion, blood lead levels among Wuxi City children are high enough to be of concern, particularly in industrial areas. Further studies are needed to better define the extent of lead exposure among children in China. In addition, national standards for blood lead collection and measurement methods should be applied in China.

Child, Preschool↗
PubMed2001

Report of the consensus conference on diagnostic criteria of ALI/ARDS at high altitudes in Western China.

China is a mountainous country. The Qing-Zang plateau, Yun-Gui plateau, and Yellow Land plateau, which are known as the world's ridge, are located in the west of China. The highland area over 3,000 m in height occupies one-sixth of the land area of China and half the highland area of the world. About 60-80 million people live in the regions where the elevation ranges from 1,500 m to 4,000 m. In the latter half of the last century, the influence of complex environmental factors on the human body, such as low oxygen pressure, cold climate, strong radiation, high wind speed, and super-evaporation, were studied in an extensive and profound way and formed an important field of altitude medicine. For a long time, many researchers have carried out investigations related to the systemic inflammatory response syndrome (SIRS), acute respiratory distress syndrome (ARDS), and multiple organ dysfunction syndrome (MODS) and its pathophysiological mechanism initiated by cytokines and mediators, regarding which many problems are still unclear. However, systematic research into the mechanism from SIRS to ARDS to MODS in the highlands remains blank. The diagnostic criteria of ALI/ARDS in the highlands are quite different from that in the plain, and thus was a central topic for discussion at this meeting.

Adaptation, Physiological↗
PubMed2001

Contamination of potable roof-collected rainwater in Auckland, New Zealand.

One-hundred and twenty-five domestic roof-collected rainwater supplies in four rural Auckland districts were investigated in a cross-sectional survey to determine water quality. Samples of cold faucet water were analysed for physico-chemical and microbiological determinands, including metals (zinc, copper and lead), bacterial indicator organisms--heterotrophic plate count (HPC), total coilforms (TC), faecal coliforms (FC), enterococci (ENT), bacterial pathogens including Salmonella spp., Legionella spp., Campylobacter spp., Aeromonas spp. and the protozoa, Cryptosporidium and Giardia. Twenty-two supplies (17.6%) exceeded one or more of the maximum acceptable values (MAV) or maximum guideline values for chemical determinands of the New Zealand Drinking Water Standards (NZDWS) and 70 (56.0%) supplies exceeded the microbiological criteria of < 1 FC/100 mL. Eighteen supplies (14.4%) exceeded the NZDWS MAV for lead of 0.01 mg/L and three (2.4%) exceeded that for copper, of 2 mg/L. Those supplies with lead or galvanised iron comprising part of the roof or collecting system were more likely to show lead contamination (p = 0.019) as were those supplies with a pH less than 7 (p = 0.013). The presence of the indicator organisms HPC, TC, FC and ENT were all significantly correlated with one another. Aeromonas spp. were identified in 20 (16.0%) supplies. There was a positive association between the presence of Aeromonas and the bacterial indicator organisms. Households reporting at least one member with gastrointestinal symptoms in the month prior to sampling, were more likely to have Aeromonas spp. identified in their water supply than those households without symptoms (odds ratio 3.22, 95% CI 1.15-9.01, p = 0.021). Salmonella typhimurium was detected in one of 115 (0.9%) supplies. Legionella spp. and Campylobacter spp. were not detected. There were 50 supplies sampled for protozoa (sampling criteria: > or = 30 FC or > or = 60 ENT). Cryptosporidium oocysts were detected in 2 (4%) of these. Giardia was not detected. This study demonstrates that roof-collected rainwater systems provide potable supplies of relatively poor physiochemical and microbiological quality in the Auckland area. Further research is required on Aeromonas spp. as potential indicators of both microbiological quality and health risk along with design and maintenance strategies to minimise contamination of potable roof-collected rainwater supplies.

Copper↗
PubMed2001

Fluoride release/uptake of conventional and resin-modified glass ionomers, and compomers.

OBJECTIVES: To assess the levels of fluoride ions released from a range of freshly-prepared aesthetic restorative materials, and then the effects of a topical acidulated phosphate fluoride (APF) gel. METHODS: Five specimens each of four conventional GICs, two resin-modified GICs, two compomers, and a resin composite (control) were assessed for their fluoride ion release over 6 weeks, before being exposed to 1.23% APF gel for 4 min and then measuring their fluoride ion levels for another 6 weeks. RESULTS: Following an initial brief, variable burst of fluoride ion release, the rates then fell quickly for most materials and, although high rates of fluoride ion release were measured immediately following the application of APF gel, these rates also fell quickly for most materials. After 12 weeks, the mean fluoride ion levels were much lower than immediately before gel application. The APF gel treatment caused surface damage to all materials, especially to the conventional GICs. CONCLUSION: The results of this study suggested that much of the increased fluoride ion release found following topical exposure of the fluoridated restorative materials to APF gel was caused by surface effects rather than by chemical recharging.

Acidulated Phosphate Fluoride↗