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Biomedical subjects

C Shen

Publications and source records attributed to C Shen.

At least 19 recordsLinked to original sources
PubMed2007

Differences of bone mass and bone structure in osteopenic rat models caused by spinal cord injury and ovariectomy.

UNLABELLED: Both spinal cord injury and ovariectomy can result in ostepenia in rats. SCI induces more deterioration of cortical geometric structure and trabecular microstructure in the proximal tibial metaphysis than OVX. The proximal tibial metaphysis microstructure significantly correlates with its biomechanical properties. INTRODUCTION: The purpose of the present study was to compare the effects of spinal cord injury (SCI) and ovariectomy (OVX) on bone gain in young female rats. METHODS: Thirty young female Sprague-Dawley rats were randomized into three groups: age-matched intact control (CON), OVX and SCI. The tibiae were assessed for DXA and micro-CT analysis, biomechanical testing, the upper tibial epiphyseal plate height, and blood samples for biochemical analysis. RESULTS: SCI rats showed lower aBMD in the proximal tibiae as compared with OVX rats. Cortical geometric structural parameters of the tibial midshaft in SCI rats were significantly lower than OVX rats. SCI or OVX induced significant changes in all trabecular microstructural parameters in the proximal tibial metaphysis. The trabecular separation (Tb.Sp) and structure mode index (SMI) in SCI rats were significantly higher than in OVX rats. BV/TV explained 84% of the variation of ultimate load of the proximal tibial metaphysis. There was no difference of the upper tibial epiphyseal plate height between SCI and OVX rats. Serum NTX level in SCI rats was significantly higher than in OVX rats. CONCLUSIONS: SCI induces more deterioration of cortical bone geometric structure and trabecular microstructure in the proximal tibial metaphysis than OVX.

Absorptiometry, Photon↗
PubMed2006

Influence of pH and oxygen-inhibited layer on fluoride release properties of fluoride sealant.

OBJECTIVES: This study tested the hypothesis that the oxygen-inhibited layer on a light-cured methacrylate based resin and the pH of the storage medium would increase significantly the initial fluoride release and long-term release rate from fluoride dental sealant. METHODS: Forty-eight discs (16-mm diameter x 1-mm thick) were made from FluroShield (<5 wt% NaF) and Helioseal F (<30 wt% fluorosilicate glass) sealants. For each sealant, 24 discs were cured through a Mylar strip that covered the surface and the remaining 24 discs were cured in air allowing formation of the oxygen-inhibited surface. Each specimen in the 24-disc groups was stored individually in 25-mL vials, and divided into four six-vial groups to receive 10 mL of pH4-pH7 (designation of pH 4-7) lactate buffer solutions. The buffer solutions were replaced periodically up to 121 days. The cumulative fluoride release over time was used to determine the coefficients for short-term and long-term release. RESULTS: Two-way ANOVA showed that the mean coefficient values for either sealant were significantly influenced by the curing condition (p<0.0001) and pH (p<0.0001), except for short-term release from NaF sealant. The duration of short-term release was much longer for the fluorosilicate glass sealant. CONCLUSIONS: Both pH and the source of fluoride source incorporated in the sealant play significant roles in fluoride release.

Bisphenol A-Glycidyl Methacrylate↗
PubMed2006

Requirement for pre-existing of p21 to prevent doxorubicin-induced apoptosis through inhibition of caspase-3 activation.

Doxorubicin (DOX)-induced apoptosis is suppressed by p21 (waf1/cip1/sdi1), a cyclin dependent kinase (CDK) inhibitor. Here we show that exogenous expression of p21 before, but not after, the DOX-treatment protected p21-deficient human colorectal cancer cell line DLD1 from DOX-induced apoptosis. In previous work, we demonstrated that p21 inhibits DOX-induced apoptosis via its CDK-binding and CDK-inhibitory activity. Here we report that pre-existing p21 can associate with pro-caspase-3 and inhibit caspase-3 activation in the cells, which was at least in part responsible for enhancing survival of DOX-treated cells. Furthermore, the N-terminal domain of p21 was found to interact with pro-caspase-3 in DLD1 cells. Thus, we propose that pre-existing p21 is required to prevent DOX-induced apoptosis.

Antibiotics, Antineoplastic↗
PubMed2006

Spontaneous-emission rate in microcavities: application to two-dimensional photonic crystals.

We present a simple, efficient procedure to compute the spontaneous-emission rate from short-time finite-difference time-domain (FDTD) data of the electromagnetic field energy in microcavities of arbitrary geometry. As an illustration, we apply this procedure to two-dimensional photonic crystals. For comparison, we calculate the local radiative density of states employing an unconditionally stable FDTD method, that is without solving the eigenvalue problem and integrating over the (first) Brillouin zone. We demonstrate that both methods yield the same predictions about the enhancement or suppression of the spontaneous-emission rate by photonic crystals.

Journal Article↗
PubMed2006

Involvement of 4-1BB (CD137)-4-1BBligand interaction in the modulation of CD4 T cell-mediated inflammatory colitis.

4-1BB ligand (4-1BBL) expressed on antigen-presenting cells interacts with 4-1BB on activated T cells (especially CD8+ cells) and co-stimulates the latter to secrete cytokines and to proliferate. The role of 4-1BB-4-1BBL interaction was studied here in a model of colitis based on naive CD4+ T cell transfer to SCID mice, a disease model in which CD8 cells do not take part. We found that CD4+ T cells from 4-1BB-deficient mice, after transfer in SCID mice, proliferated more rapidly compared to wild-type CD4+ T cells. Mice reconstituted with naive CD4+ T cells from 4-1BB-deficient mice developed colitis, however, with a mixed Th1/Th2 response, in contrast to the Th1-type response in mice reconstituted with wild-type naive CD4+ T cells. Importantly, this altered cytokine response did not temper colitis severity. Although it has been reported previously that 4-1BB co-stimulation may contribute to regulatory T cell functioning, we found that CD4+CD25+ regulatory T cells from 4-1BB-deficient mice were perfectly able to prevent naive CD4+ T cell-induced colitis. In conclusion, our data provide evidence that 4-1BB-4-1BBL interaction modulates the effector CD4+ T cell-driven immune response and cytokine production in experimental colitis without affecting regulatory T cell function.

4-1BB Ligand↗
PubMed2006

Controlled release of chlorhexidine from UDMA-TEGDMA resin.

Chlorhexidine salts are available in various formulations for dental applications. This study tested the hypothesis that the release of chlorhexidine from a urethane dimethacrylate and triethylene glycol dimethacrylate resin system can be effectively controlled by the chlorhexidine diacetate content and pH. The filler concentrations were 9.1, 23.1, or 33.3 wt%, and the filled resins were exposed to pH 4 and pH 6 acetate buffers. The results showed that Fickian diffusion was the dominant release mechanism. The rates of release were significantly higher in pH 4 buffer, which was attributed to the increase of chlorhexidine diacetate solubility at lower pH. The higher level of filler loading reduced the degree of polymerization, leading to a greater loss of organic components and higher chlorhexidine release rates.

Chlorhexidine↗
PubMed2005

Alcohol consumption and cognitive function in late life: a longitudinal community study.

OBJECTIVE: To examine the association between alcohol use and cognitive decline in a longitudinal study of a representative elderly community sample free of dementia at baseline. METHODS: Cognitive functions and self-reported drinking habits were assessed at 2-year intervals over an average of 7 years of follow-up. Cognitive measures, grouped into composites, were examined in association with alcohol consumption. Trajectory analyses identified latent homogeneous groups with respect to alcohol use frequency over time, and their association with average decline over the same period in each cognitive domain. Models controlled for age, sex, education, depression, smoking, general mental status (Mini-Mental State Examination [MMSE]), performance on the given test at baseline, and subsequent new-onset dementia during follow-up. RESULTS: The authors found three homogeneous trajectories that they characterized as no drinking, minimal drinking, and moderate drinking. Few heavy drinkers were identified in this elderly cohort. Compared to no drinking, both minimal and moderate drinking were associated with lesser decline on the MMSE and Trailmaking tests. Minimal drinking was also associated with lesser decline on tests of learning and naming. These associations were more pronounced when comparing current drinkers to former drinkers (quitters) than to lifelong abstainers. CONCLUSION: In a representative elderly cohort over an average of 7 years, a pattern of mild-to-moderate drinking, compared to not drinking, was associated with lesser average decline in cognitive domains over the same period.

Age Factors↗
PubMed2005

Adalimumab induces apoptosis of human monocytes: a comparative study with infliximab and etanercept.

BACKGROUND: Adalimumab, a fully human monoclonal antibody to tumour necrosis factor, was recently introduced for therapy of Crohn's disease. AIM: Since induction of apoptosis of inflammatory cells is thought to be an important mechanism of action of the antitumour necrosis factor monoclonal antibody infliximab, we studied the induction of apoptosis of activated peripheral blood monocytes by adalimumab. METHOD: Apoptosis was analysed at the levels of the cell membrane, mitochondria and DNA by flow cytometry. RESULTS: We found that both adalimumab and infliximab induced apoptosis in cultured monocytes, while etanercept did not. Apoptosis induction was caspase-dependent and detectable already after 2 h. The production of interleukin-10 and interleukin-12 by monocytes was down-regulated significantly by adalimumab and infliximab but not by etanercept, while levels of soluble tumour necrosis factor in monocyte cultures were down-regulated by all three reagents. CONCLUSIONS: These data show that both adalimumab and infliximab affect monocyte cytokine production and induce apoptosis of activated monocytes. Our findings will have to be further correlated to therapeutic efficacy of these antitumour necrosis factor reagents.

Adalimumab↗
PubMed2005

Effect of flame cleaning of ceramic surface on the bond strength of composite to ceramic.

This study tested the hypothesis that flame cleaning of ceramic surface would increase the bond strength of composite to ceramic than pressure-vaporized steam cleaning. Eris and IPS-Empress ceramic blocks were fabricated, polished (control), airborne-particle abraded with 50-microm alumina particle (A), etched with 5% hydrofluoric acid gel for 2 min (E), or treated with a combination of A and E (AE). They were subjected to either steam cleaning for 20 s or flame cleaning over a gas burner for 2 s. Followed by an application of an adhesive resin, a composite was built-up. Twenty micro-tensile test specimens (approximately 0.9 x 0.9 x 16 mm) were obtained from each group and loaded to failure under tensile force using a universal testing machine at a crosshead speed of 0.5 mm min(-1). anova showed statistically significant differences in the mean bond strength by ceramic, surface roughness, and cleaning method (P < 0.0001). The groupings of the mean bond strength were as follows: flame-cleaned > steam-cleaned; IPS-Empress > Eris; and AE > E > A for IPS-Empress and AE > E approximately A for Eris (Duncan's multiple analysis; alpha = 0.05). This in vitro study suggests that mechanical bond of composite to ceramic can be improved with flame cleaning of ceramic surface.

Aluminum Silicates↗
PubMed2005

Human defensin 5 expression in intestinal metaplasia of the upper gastrointestinal tract.

BACKGROUND: Upper gastrointestinal tract intestinal metaplasia (IM) is termed Barrett's oesophagus (BO) or gastric intestinal metaplasia (GIM), depending on its location. BO and GIM are associated with chemical exposure resulting from gastro-oesophageal reflux and chronic Helicobacter pylori infection, respectively. Paneth cells (PCs), characterised by cytoplasmic eosinophilic granules, are found in a subset of IM at these sites, but histology may not accurately detect them. AIM: To determine human defensin 5 (HD5; an antimicrobial peptide produced by PCs) expression in BO and GIM, and to investigate its association with H pylori infection. METHODS: Endoscopic biopsies from 33 patients with BO and 51 with GIM, and control tissues, were examined by routine histology and for H pylori infection and HD5 mRNA and protein expression. RESULTS: In normal tissues, HD5 expression was specific for PCs in the small intestine. Five patients with BE and 42 with GIM expressed HD5, but few HD5 expressing cells in IM had the characteristic histological features of PCs. Most HD5 positive specimens were H pylori infected and most HD5 negative specimens were not infected. CONCLUSIONS: HD5 immunohistochemistry was often positive in IM when PCs were absent by conventional histology. Thus, HD5 immunohistochemistry may be superior to histology for identifying metaplastic PCs and distinguishing GIM from BO. The higher frequency of HD5 expression in GIM than in BO is associated with a higher frequency of H pylori infection, suggesting that in IM PCs may form part of the mucosal antibacterial response.

Adult↗
PubMed2005

Effect of CaF2 content on rate of fluoride release from filled resins.

Information on the time-dependent release of fluoride from filled resins containing fluoride particles as a function of particle content and solution pH is limited. This study characterized the fluoride ion release from filled resins containing CaF2 particles as a function of filler content and pH. Urethane dimethacrylate and triethylene glycol dimethacrylate resins were used to make filled-resin disks containing 9.09, 23.08, or 33.33 mass% CaF2 filler. Fluoride ion release for the 9.09 mass% concentration was independent of pH. Increasing the filler content from 9.09 to 33.33 mass% increased the fluoride release rate in pH 4.0 buffer solution, because of greater surface degradation. Fluoride ion release from disks stored in pH 6.0 buffer solutions occurred mainly by diffusion from disk surfaces, while fluoride release from disks in pH 4.0 buffers was controlled by diffusion from disk surfaces and degeneration of the resin matrix, which exposed more CaF2 particle surface area.

Calcium Fluoride↗
PubMed2004

Involvement of interleukin 18 in Crohn's disease: evidence from in vitro analysis of human gut inflammatory cells and from experimental colitis models.

An imbalance of immunoregulatory factors and/or cells contributes to uncontrolled mucosal T cell activation and inflammation in Crohn's disease (CD). Bioactive interleukin (IL)-18 has been shown to be produced by macrophages in CD lesions. We report here that T cells freshly isolated from inflamed tissue of CD patients (and not T cells from control intestinal tissue) were responsive to IL-18. In the presence of IL-18, these T cells produced more interferon (IFN)-gamma and less IL-10. To analyse further the role of IL-18 in this disease, an acute and a chronic model of murine colitis were used. IL-18 mRNA was significantly enhanced in trinitrobenzene sulphonic acid (TNBS) induced colitis, and treatment with IL-18 binding protein (IL-18BPa), which neutralizes IL-18 bioactivity, significantly reduced the severity of colitis. However, IL-18BPa did not affect the course of chronic colitis in CD45RBhighCD4+ T cell reconstituted SCID mice. Production of IFN-gamma in lamina propria mononuclear cell cultures from IL-18BPa-treated SCID mice was decreased, but at the same time fewer lamina propria CD4+ T cells harvested from IL-18BPa-treated mice compared to non-treated mice were in apoptosis. We conclude that IL-18 clearly has a modulatory role in the inflammatory cascade of CD and experimental colitis by affecting IFN-gamma and IL-10 production, and apoptosis. In view of the divergent effects of IL-18 neutralization in the two different murine colitis models, it is unlikely that IL-18 is at the top of this cascade.

Adult↗
PubMed2003

Carbon monoxide concentrations in paediatric sepsis syndrome.

Plasma carbon monoxide (CO) concentrations were measured in 12 patients with sepsis syndrome. CO concentrations were found to be significantly increased in patients compared with those in 30 normal controls. Patients with septic shock had significantly higher plasma CO concentrations than those without shock. Results suggest that CO might play an important role in paediatric sepsis syndrome.

Carbon Monoxide↗
PubMed2002

Repeated treatment with antidepressants differentially alters 5-HT1A agonist-stimulated [35S]GTP gamma S binding in rat brain regions.

Electrophysiological studies have led to the proposal that the neurobiological mechanism(s) underlying drug therapy of anxiety and depression involve(s) regionally specific adaptations in 5-HT(1A) receptor sensitivity. Depending on the drug utilized, a decrease in sensitivity of inhibitory somatodendritic autoreceptors, an increase in sensitivity of postsynaptic receptors, or both alterations, occur after several weeks of treatment. This hypothesis was tested using N,N-dipropyl-5-carboxamidotryptamine-stimulated guanosine-5'-O-(3-thio)triphosphate ([(35)S]GTPgammaS) binding assessed by autoradiography. Rats were treated for 21 days with one of four different anxiolytic/antidepressant drugs (in mg/kg): fluoxetine (10), imipramine (10), clorgyline (1), ipsapirone (2 x 20) or saline. Three brain regions rich in 5-HT(1A) receptors were examined: the dorsal raphe (somatodendritic), the dorsal hippocampus (postsynaptic) and the lateral septum (postsynaptic). Only imipramine (+17%) and fluoxetine (+54%) significantly increased agonist-stimulated binding in the dorsal hippocampus; all drugs except imipramine significantly decreased binding in the dorsal raphe (-19 to -41%). These results generally support the concept of a net enhancement of hippocampal 5-HT neurotransmission via one or more 5-HT receptor subtypes. The most consistent effect, however, was a significant decrease in stimulated [(35)S]GTPgammaS binding in the lateral septum after all four treatments (-14 to -23%), suggesting that this may be a heretofore unrecognized common outcome of antidepressant treatment deserving further study.

Animals↗
PubMed2001

Triplex forming oligonucleotide targeted to 3'UTR downregulates the expression of the bcl-2 proto-oncogene in HeLa cells.

The bcl-2 proto-oncogene is overexpressed in a variety of human cancers and plays an important role in programmed cell death. Recent reports implied that the 3'-untranslated region (3'UTR) functions effectively in the regulation of gene expression. Here, we attempt to assay the ability of triplex forming oligonucleotides (TFOs) to inhibit expression of a target gene in vivo and to examine the potential of the 3'UTR of the bcl-2 proto-oncogene in the regulation of bcl-2 gene expression. To do this, we have developed a novel cellular system that involves transfection of a Doxycyclin inducible expression plasmid containing the bcl-2 ORF and the 3'UTR together with a TFO targeted to the 3'UTR of the bcl-2 proto-oncogene. Phosphorothioate-modified TFO targeted to the 3'UTR of the bcl-2 gene significantly downregulated the expression of the bcl-2 gene in HeLa cells as demonstrated by western blotting. Our results indicate that blocking the functions of the 3'UTR using the TFO can downregulate the expression of the targeted gene, and suggest that triplex strategy is a promising approach for oligonucleotide-based gene therapy. In addition, triplex-based sequence targeting may provide a useful tool for studying the regulation of gene expression.

3' Untranslated Regions↗
PubMed2001

Prolonged vigabatrin treatment modifies developmental changes of GABA(A)-receptor binding in young children with epilepsy.

PURPOSE: To determine whether prolonged treatment with vigabatrin (VGB), an antiepileptic drug (AED) that acts by elevating brain gamma-aminobutyric acid (GABA) levels, interferes with age-related changes of in vivo GABA(A)-receptor binding in children with epilepsy. METHODS: Using [11C]flumazenil (FMZ)-positron emission tomography (PET) imaging, 15 children (aged 1-8 years) with medically intractable epilepsy were studied. Seven of these children were treated with VGB (1,000-2,500 mg/day) for > or =3 months before the FMZ-PET study. The remaining eight patients were medicated with other drugs that are known not to act directly on the GABAergic system. Absolute quantification of PET data was performed by using the volume of distribution (VD) of FMZ in brain tissue representing FMZ ligand binding. RESULTS: After controlling for age, hemispheric FMZ VD values were significantly lower in children treated with VGB as compared with the non-VGB group (p = 0.012). Regional FMZ VD values of the VGB-treated patients were significantly lower in all cortical regions and the cerebellum, whereas the difference was not significant in the thalamus and basal ganglia. No significant drug effect or drug-by-region interaction could be determined when the patients were separated according to treatment with carbamazepine (p = 0.97) or valproate (p = 0.55). CONCLUSIONS: VGB induces a decrease in GABA(A)-receptor binding in the cortex and cerebellum of the developing epileptic brain. A similar effect of other drugs and substances of abuse targeting the GABAergic system may be hypothesized. Because of the important role of the GABAergic system in developmental plasticity, the reversibility and functional consequences of this age-specific drug effect should be further studied.

Age Factors↗
PubMed2001

Ki-67 immunostaining in pancreatic cancer and chronic active pancreatitis: does in vivo FDG uptake correlate with proliferative activity?

UNLABELLED: PET with 18F-FDG has been shown to be useful in the detection and staging of pancreatic cancer. However, whether FDG uptake is dependent on proliferative activity is still unclear. The aim of this prospective study was to evaluate a probable correlation between FDG uptake and proliferative activity in benign and malignant pancreatic tumors. METHODS: Our series consisted of 23 patients with pancreatic cancer and 9 patients with chronic active pancreatitis (CAP). FDG PET was performed within 2 wk before surgery, and standardized uptake values (SUVs) were calculated for benign and malignant pancreatic tumors. Patients were selected when focally increased FDG uptake in previously known pancreatic tumors was present. Proliferation fraction was measured in tissue specimens using the anti-Ki-67 antibody MIB-1. A computer-assisted imaging system was used for quantification of nuclear Ki-67 immunostaining. Immunohistochemical findings were correlated to SUVS: RESULTS: Pancreatic cancer showed both intense nuclear staining of Ki-67 (39% +/- 16%) and high FDG uptake (SUV = 3.6 +/- 1.6). However, no significant correlation was found between in vivo FDG uptake and Ki-67 immunoreactivity (P = 0.65). By contrast, Ki-67 nuclear staining was significantly lower (3.8% +/- 2.7%, P < 0.05) in CAP, whereas FDG uptake was in the same range as for pancreatic cancer (SUV = 3.5 +/- 1.8). CONCLUSION: FDG uptake did not correlate with proliferative activity in pancreatic cancer. Proliferative activity was tenfold higher in malignant pancreatic tumors than in benign tumors associated with CAP, whereas FDG uptake in vivo did not differ significantly. Thus, a PET tracer indicating cellular proliferation should better differentiate between cancer and inflammatory lesions than do metabolic markers such as FDG.

Adenocarcinoma↗