To investigate the remineralising effect and bacterial growth inhibition of 38% silver diamine fluoride (SDF) solution and 5% sodium fluoride (NaF) varnish on artificial dentine caries lesions.
...Demineralised dentine blocks were treated with SDF + NaF (Group 1), SDF (Group 2), NaF (Group 3) and water (Group 4) and subjected to a Streptococcus mutans biofilm challenge. Lesion depth, precipitates’ characteristics and matrix (collagen)-to-mineral ratio were evaluated by micro-computer tomography (micro-CT), X-ray diffraction (XRD) and Fourier transform infrared spectroscopy (FTIR), respectively. The biofilm kinetics, viability and topography were assessed by counts of colony forming units (CFUs), confocal laser scanning microscopy (CLSM) and scanning electron microscopy (SEM), respectively. Data were analysed by two-way ANOVA test.
The lesion depths of Groups 1–4 were 170 ± 28 μm, 160 ± 32 μm, 353 ± 38 μm and 449 ± 24 μm, respectively. The addition of NaF to SDF did not show better remineralisation than SDF (p = 0.491). Metallic silver and silver chloride were found in Groups 1 and 2. The amide I-to-hydrogen phosphate ratios of the four groups were 0.14 ± 0.02, 0.14 ± 0.01, 0.29 ± 0.05 and 0.49 ± 0.16, respectively, and the addition of NaF to SDF did not offer better protection against collagen exposure than SDF (p = 0.986). The Log10 CFUs of Groups 1–4 were 5.75 ± 0.56, 4.49 ± 0.57, 6.55 ± 0.39 and 6.40 ± 0.38, respectively. The presence of NaF reduced the antibacterial effect of SDF (p < 0.001). The SEM and CLSM images supported the findings.
Application of SDF with or without NaF reduced the demineralisation of dentine caries, but SDF exerted stronger inhibition of biofilm growth than SDF with NaF.
NaF varnish affects the antibacterialeffects of SDF, the adjunctive application of SDF solution and NaF varnish is not recommended to arrest dentine caries in clinic.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UL, UM, UPCLJ, UPUK, ZRSKP
In March 2020, mild signs and symptoms of coronavirus disease developed in a healthy 33-year-old man in Hong Kong. His first infection did not produce virus neutralizing antibodies. In August, he had ...asymptomatic reinfection, suggesting that persons without a robust neutralizing antibody response might be at risk for reinfection.
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DOBA, IZUM, KILJ, NUK, ODKLJ, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
Integrin-linked kinase (ILK) is a mediator of aggressive phenotype in pancreatic cancer. On the basis of our finding that knockdown of either KRAS or ILK has a reciprocal effect on the other's ...expression, we hypothesized the presence of an ILK-KRAS regulatory loop that enables pancreatic cancer cells to regulate KRAS expression. This study aimed to elucidate the mechanism by which this regulatory circuitry is regulated and to investigate the translational potential of targeting ILK to suppress oncogenic KRAS signaling in pancreatic cancer. Interplay between KRAS and ILK and the roles of E2F1, c-Myc and heterogeneous nuclear ribonucleoprotein as intermediary effectors in this feedback loop was interrogated by genetic manipulations through small interfering RNA/short hairpin RNA knockdown and ectopic expression, western blotting, PCR, promoter-luciferase reporter assays, chromatin immunoprecipitation and pull-down analyses. In vivo efficacy of ILK inhibition was evaluated in two murine xenograft models. Our data show that KRAS regulated the expression of ILK through E2F1-mediated transcriptional activation, which, in turn, controlled KRAS gene expression via hnRNPA1-mediated destabilization of the G-quadruplex on the KRAS promoter. Moreover, ILK inhibition blocked KRAS-driven epithelial-mesenchymal transition and growth factor-stimulated KRAS expression. The knockdown or pharmacological inhibition of ILK suppressed pancreatic tumor growth, in part, by suppressing KRAS signaling. These studies suggest that this KRAS-E2F1-ILK-hnRNPA1 regulatory loop enables pancreatic cancer cells to promote oncogenic KRAS signaling and to interact with the tumor microenvironment to promote aggressive phenotypes. This regulatory loop provides a mechanistic rationale for targeting ILK to suppress oncogenic KRAS signaling, which might foster new therapeutic strategies for pancreatic cancer.
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EMUNI, FIS, FZAB, GEOZS, GIS, IJS, IMTLJ, KILJ, KISLJ, MFDPS, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, SBMB, SBNM, UKNU, UL, UM, UPUK, VKSCE, ZAGLJ
Abstract Objective To study the inhibitory effect of various commercially available concentrations of silver diamine fluoride (SDF) solutions on matrix metalloproteinases (MMPs). Methods Three SDF ...solutions with concentrations at 38%, 30% and 12% were studied. Two sodium fluoride (NaF) solutions at 10% and 3% were prepared, and they had the same fluoride ion concentrations as 38% and 12% SDF, respectively. Two silver nitrate (AgNO3 ) solutions at 42% and 13% were also prepared, and they had the same silver ion concentrations as 38% and 12% SDF, respectively. Ten samples of each experimental solution were used to study their inhibitory effect on three MMPs, which were MMP-2 (gelatinase A), MMP-8 (neutrophil collagenase) and MMP-9 (gelatinase B) using MMP assay kits. Positive control containing assay buffer at pH 9 and MMPs dilution was used to calculate the percentage inhibition. Results The percentage inhibition of 38%, 30% and 12% SDF on MMP-2 were 79%, 60% and 17%, respectively ( p < 0.001); on MMP-8 were 94%, 85% and 77%, respectively ( p < 0.001); on MMP-9 were 82%, 65% and 60%, respectively ( p < 0.001). The percentage inhibition on MMP-2, MMP-8 and MMP-9 by 38% SDF was significantly higher than the corresponding percentage inhibition by 10% NaF and 42% AgNO3. Significance Greater inhibitory effect on MMPs was found with higher concentration of SDF solution. SDF had more inhibition on MMPs than solutions of NaF and AgNO3 containing equivalent concentration of fluoride and silver ions, respectively.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UL, UM, UPCLJ, UPUK
Great discrepancies exist in the reported prevalence of altered energy metabolism (hypo- or hypermetabolism) in cancer patients, which is likely due to the vast array of phenomena that can affect ...energy expenditure in these patients. The purpose of this review was to critically evaluate key determinants of energy expenditure in cancer and the relevance for clinical practice. Resting energy expenditure (REE) is the largest and most commonly measured component of total energy expenditure. In addition to the energetic demand of the tumor itself, REE may be increased due to changes in inflammation, body composition and brown adipose tissue activation. Energy expenditure from physical activity is often lower in cancer compared with healthy populations, and there is evidence to suggest that the thermic effect of food might also be blunted and affected by cancer therapy. Although accurate assessment of energy metabolism is a cornerstone of adequate nutritional therapy, prediction methods often do not capture the true energy expenditure of most cancer patients. In fact, limits of agreement of prediction equations may range from 40% below to 30% above measured REE. Such variability highlights the need for a more comprehensive understanding of energy expenditure in cancer and the value of accurately assessing the energy needs of these patients.
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DOBA, EMUNI, FIS, FZAB, GEOZS, GIS, IJS, IMTLJ, IZUM, KILJ, KISLJ, MFDPS, NLZOH, NUK, OILJ, PILJ, PNG, SAZU, SBCE, SBJE, SBMB, SBNM, SIK, UILJ, UKNU, UL, UM, UPUK, VKSCE, VSZLJ, ZAGLJ
ABSTRACT We perform two-dimensional hydrodynamic simulations for the thermonuclear explosion of Chandrasekhar-mass white dwarfs with dark matter (DM) cores in Newtonian gravity. We include a ...19-isotope nuclear reaction network and make use of the pure turbulent deflagration model as the explosion mechanism in our simulations. Our numerical results show that the general properties of the explosion depend quite sensitively on the mass of the DM core M DM: a larger M DM generally leads to a weaker explosion and a lower mass of synthesized iron-peaked elements. In particular, the total mass of 56 Ni produced can drop from about 0.3 to 0.03 M as M DM increases from 0.01 to 0.03 M . We have also constructed the bolometric light curves obtained from our simulations and found that our results match well with the observational data of sub-luminous Type Ia supernovae.
We have previously demonstrated that peroxisome proliferator-activated receptor (PPARγ) activation inhibits hepatocarcinogenesis. We aim to investigate the effect of PPARγ on hepatocellular carcinoma ...(HCC) metastatic potential and explore its underlying mechanisms.
Human HCC cells (MHCC97L, BEL-7404) were infected with adenovirus-expressing PPARγ (Ad-PPARγ) or Ad-lacZ and treated with or without PPARγ agonist (rosiglitazone). The effects of PPARγ on cell migration and invasive activity were determined by wound healing assay and Matrigel invasive model in vitro, and in an orthotopic liver tumour metastatic model in mice.
Pronounced expression of PPARγ was demonstrated in HCC cells (MHCC97L, BEL-7404) treated with Ad-PPARγ, rosiglitazone or Ad-PPARγ plus rosiglitazone, compared with control (Ad-LacZ). Such induction markedly suppressed HCC cell migration. Moreover, the invasiveness of MHCC97L and BEL-7404 cells infected with Ad-PPARγ, or treated with rosiglitazone was significantly diminished up to 60%. Combination of Ad-PPARγ and rosiglitazone showed an additive effect. Activation of PPARγ by rosiglitazone significantly reduced the incidence and severity of lung metastasis in an orthotopic HCC mouse model. Key mechanisms underlying the effect of PPARγ in HCC include upregulation of cell adhesion genes, E-cadherin and SYK (spleen tyrosine kinase), extracellular matrix regulator tissue inhibitors of metalloproteinase (TIMP) 3, tumour suppressor gene retinoblastoma 1, and downregulation of pro-metastatic genes MMP9 (matrix metallopeptidase 9), MMP13, HPSE (heparanase), and Hepatocyte growth factor (HGF). Direct transcriptional regulation of TIMP3, MMP9, MMP13, and HPSE by PPARγ was shown by ChIP-PCR.
Peroxisome proliferator-activated receptor-gamma exerts an inhibitory effect on the invasive and metastatic potential of HCC in vitro and in vivo, and is thus, a target for the prevention and treatment of HCC metastases.
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DOBA, EMUNI, FIS, FZAB, GEOZS, GIS, IJS, IMTLJ, IZUM, KILJ, KISLJ, MFDPS, NLZOH, NUK, OILJ, PILJ, PNG, SAZU, SBCE, SBJE, SBMB, SBNM, SIK, UILJ, UKNU, UL, UM, UPUK, VKSCE, ZAGLJ
In high endemic areas of hepatitis B virus (HBV) infection, the vast majority of infection is acquired perinatally or during early childhood. The age of the patient is, therefore, almost equivalent ...to the duration of HBV infection. The natural history of chronic HBV infection consists of three chronological phases: immune tolerance, immune clearance and low replicative phases. The prevalence of hepatitis B e antigen (HBeAg) in asymptomatic HBV carriers is around 90% before 15 years of age, and decreases remarkably to less than 10% after 40 years of age. The immune clearance phase is characterized by a series of hepatitis flares and remissions. These will be followed eventually by HBeAg seroconversion, which is usually accompanied by remission of liver disease and confers favourable outcome. However, patients with persistent HBeAg seropositivity over 40 years of age are associated with a significantly higher risk for progression to cirrhosis than those with HBeAg seroconversion before 40 years of age, and thus should be considered as patients with ‘delayed’ HBeAg seroconversion. Antiviral or immunomodulatory therapy should be considered seriously for these patients.
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BFBNIB, DOBA, FZAB, GIS, IJS, IZUM, KILJ, NLZOH, NUK, OILJ, PILJ, PNG, SAZU, SBCE, SBMB, SIK, UILJ, UKNU, UL, UM, UPUK
While carbon dots (C‐dots) have been extensively investigated pertaining to their fluorescent, phosphorescent, electrochemiluminescent, optoelectronic, and catalytic features, their inherent chemical ...exchange saturation transfer magnetic resonance imaging (CEST MRI) properties are unknown. By virtue of their hydrophilicity and abundant exchangeable protons of hydroxyl, amine, and amide anchored on the surface, we report here that C‐dots can be adapted as effective diamagnetic CEST (diaCEST) MRI contrast agents. As a proof‐of‐concept demonstration, human glioma cells were labeled with liposomes with or without encapsulated C‐dots and implanted in mouse brain. In vivo CEST MRI was able to clearly differentiate labeled cells from non‐labeled cells. The present findings may encourage new applications of C‐dots for in vivo imaging in deep tissues, which is currently not possible using conventional fluorescent (near‐infrared) C‐dots.
Think differently: Metal‐free carbon dots (C‐dots) can be used as magnetic resonance imaging (MRI) agents owing to the chemical exchange of surface‐anchored protons with water. This inherent chemical exchange saturation transfer (CEST) magnetic resonance property of C‐dots enables them to be visualized in vivo in deep tissues.
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BFBNIB, FZAB, GIS, IJS, KILJ, NLZOH, NUK, OILJ, SBCE, SBMB, UL, UM, UPUK
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