Pseudo-cerebrospinal fluid rhinorrhea following traumatic cerebrospinal fluid rhinorrhea surgery: a case report.
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Biomedical subjects
Publications and source records attributed to S Sun.
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OBJECTIVE: To provide reliable information concerning the presence or the absence of Histoplasma capsulatum (H. capsulatum) infection in China, and data concerning this respect. METHODS: Three hundred normal people and 435 hospitalized patients, who lived in Hunan and Jiangsu provinces, and the Xinjiang Autonomous Region, were tested with yeast-phase histoplasmin (ALK/Berkerley Biologicals Laboratories, USA) and human pure protein derivative of tuberculin (PPD) on the volar surface of the forearm. Any reaction to the antigens over 5.0 mm in diameter of induration at 48-72 hours was considered positive. RESULTS: A total of 138 subjects (18.8%) in 735 patients reacted to histoplasmin with 5.0-45.0 (9.1 +/- 4.3) mm indurations. Significant differences of positive skin reaction rates in normal subjects were found in Hunan, Jiangsu and Xinjiang (8.9% vs 15.1% vs 2.1%). The overall positive rate of patients was 25.5%. Patients with tuberculosis [31.7% (78/246)] had a significantly higher positive skin reaction rate in comparison with those suffering from pneumonia [17.7% (11/62)], lung cancer [20.9% (9/43)], chronic obstructive pulmonary disease [17.3% (9/52)] and other diseases [12.5% (4/32)] (P < 0.01). Of 562 cases, 292 cases (52.0%) reacted to PPD with indurations of 5-50 (13.7 +/- 4.9) mm in diameter, 63 cases (11.2%) reacted to both histoplasmin and PPD, while 38 cases (6.9%) reacted to histoplasmin but not to PPD. CONCLUSIONS: The data suggest that there is H. capsulatum herd infection in China. The infection rate in Southeast China is higher than that in the Northwest, and the infection rate of patients with pulmonary tuberculosis is higher than that of normal persons and other pneumonopathy patients.
OBJECTIVE: To identify Cortex Cinnamomi and its confused species "Yin Xiang". METHOD: FT-Raman spectroscopy was used. RESULTS: Both Cortex Cinnamoni and its confused species had spectral features, and they could be easily identified. CONCLLUSION: The method is rapid, accurate, simple and non-destructive.
OBJECTIVE: To improve the HPLC method for determining ferulic acid(FA) in the human serum and to research FA clinical pharmacokinetics. METHOD: Serum concentrations of FA were determined by HPLC using methanol-water-acetic acid (40:59.7:0.3, v/v) as the mobile phase and the column packed with ODS (150 mm x 4.6 mm, 5 microns) as a fixed phase and the flow rate was 1.0 ml/min. FA was detected at 320 nm wave length. The internal standard was coumarin. The serum samples were treated by the water-boiling method. Peak of FA in serum was recognized by photodiode-array detection. RESULT: FA and internal standard were separated completely under the condition described as above. FA was linear in the range of (40.16-8032 ng/ml) (r = 0.9975). The CV was less than 10%, the average recovery was 100.3%, and the limit concentration in serum was 25.1 ng/ml. PK was in accordance with open bicameral model. CONCLUSION: This method can be applied to clinical pharmacokinetic study of FA.
Self-assembled devices composed of periodic arrays of 10-nanometer-diameter cobalt nanocrystals display spin-dependent electron transport. Current-voltage characteristics are well described by single-electron tunneling in a uniform array. At temperatures below 20 kelvin, device magnetoresistance ratios are on the order of 10%, approaching the maximum predicted for ensembles of cobalt islands with randomly oriented preferred magnetic axes. Low-energy spin-flip scattering suppresses magnetoresistance with increasing temperature and bias-voltage.
Recent studies have shown that the G protein-coupled, extracellular calcium ([Ca(2+)](o))-sensing receptor (CaR) forms disulfide-linked dimers through cysteine residues within its extracellular domain and that dimerization of the CaR has functional implications. In this study, we have investigated which of these disulfide linkages are essential for dimerization of the CaR and whether they are required for these functional interactions. Our results confirm the key roles of Cys(129) and Cys(131) in CaR dimerization. However, utilizing cross-linking of the CaR or immunoprecipitation of a non-FLAG-tagged CaR with a FLAG-tagged CaR using anti-FLAG antibody, we demonstrate that CaRs with or without these two cysteines form dimers on the cell surface to a similar extent. In addition, reconstitution of CaR-mediated signaling by cotransfection of two individually inactive mutant CaRs is nearly identical in the presence or absence of both Cys(129) and Cys(131), showing that covalent linkage of CaR dimers is not needed for functional interactions between CaR monomers. These findings suggest that the CaR has at least two distinct types of motifs mediating dimerization and functional interactions, i.e. covalent interactions involving intermolecular disulfide bonds and noncovalent, possibly hydrophobic, interactions.
Insulin resistance can be induced in vivo by intravenous infusion of glucosamine or in cells by incubation with glucosamine. However, a publication (Hresko, R. C., et al. (1998) J. Biol. Chem. 273, 20658-20668) suggests a trivial explanation of glucosamine-induced insulin resistance whereby intracellular ATP pools are depleted presumably due to the phosphorylation of glucosamine to glucosamine 6-phosphate, a hexosamine pathway intermediate. The reduced ATP level impaired insulin receptor (IR) autophosphorylation and tyrosine kinase activity toward substrates. The present work describes the development and comparison of two methods for inducing insulin resistance, by treating 3T3-L1 adipocytes overnight using either 25 mM glucose/5 nM insulin or 2 mM glucosamine. Under these conditions basal glucose transport rates were comparable with controls. Insulin-stimulated 2-deoxyglucose uptake, however, was reduced by approximately 45% in response to both high glucose/insulin and glucosamine treatment, relative to control cells. The total relative amounts of the insulin-responsive glucose transporter, Glut4, remained constant under both treatment conditions. The relative phosphotyrosine (Tyr(P)) contents of the insulin receptor and its substrate 1 (IRS-1) were assessed in whole cell homogenates. With both methods to induce insulin resistance, IR/IRS-1 Tyr(P) levels were virtually indistinguishable from those in control cells. Insulin-stimulated phosphorylation of Akt on Ser(473) was not impaired in insulin-resistant cells. Furthermore, the relative Tyr(P) content of the PDGF receptor was comparable in high glucose/insulin- or glucosamine-treated 3T3-L1 adipocytes upon subsequent challenge with PDGF. Finally, the relative amounts of glutamine:fructose-6-phosphate amidotransferase and O-linked N-acetylglucosamine transferase, two important hexosamine pathway enzymes, were similar in both treatments when compared with controls. Thus, 3T3-L1 adipocytes can be used as a model system for studying insulin resistance induced by increased influx of glucose. Under appropriate experimental conditions, glucosamine treatment can mimic the effects of increased glucose flux without impairment of tyrosine phosphorylation-based signaling.
Immune/inflammatory responses of arterial vessel wall constituents to lipid metabolic disturbances have been postulated to contribute to the pathogenesis of atherosclerosis. Mycophenolate mofetil (MMF), an antiproliferative agent used in clinical transplantation, has been shown to inhibit smooth muscle cell (SMC) proliferation and decrease the recruitment of monocytes into sites of chronic inflammation. This study was conducted to determine the effect of MMF on atherosclerotic plaque development after cholesterol-induced injury. New Zealand white rabbits were fed a high-cholesterol diet containing 0.5% cholesterol and 8% peanut oil. The experimental group (n = 10) was given MMF (80 mg/kg/day subcutaneously); the control group (n = 10) received placebo injections. The aortas were harvested at 12 weeks for immunohistochemical analyses. SMCs were identified by reactivity with a monoclonal antibody (mAb) to alpha smooth muscle actin. Monocytes/macrophages were detected with mAb RAM 11. Cross-sectional areas of the media and neointima were measured using computer-assisted image analysis. The density of SMCs and macrophage/foam cells within the neointima was calculated by dividing the number of cells by the area of the plaque. Total cholesterol, triglyceride, high density lipoprotein, and low density lipoprotein were significantly increased compared with levels before the initiation of a high-cholesterol diet, but there were no significant differences between the MMF-treated and untreated groups. Neointimal area in aortic tissue sections of the MMF-treated group (0.586 +/- 0.602 mm(2)) was significantly lower when compared with that in control animals (1.082 +/- 0.621 mm(2)) (P < 0.05). The densities of neointimal SMCs and monocytes/macrophages in the control group were 778 +/- 293 and 341 +/- 90 cells/mm(2), respectively. MMF treatment significantly reduced the number of neointimal SMCs (506 +/- 185 cells/mm(2)) (P < 0.05). The number of monocytes/macrophages was also reduced after MMF treatment (260 +/- 124 cells/mm(2)) but not significantly. Our results demonstrate that the administration of MMF significantly reduced neointimal SMC accumulation and plaque development in a hypercholesterolemic model of atherosclerosis.
The relation between trace element levels in drinking water and cognitive function was investigated in a population-based study of elderly residents (n = 1,016) in rural China in 1996-1997. Cognitive function was measured using a Chinese translation of the Community Screening Interview for Dementia. A mixed effects model was used to evaluate the effect of each of the elements on cognitive function while adjusting for age, sex, and educational level. Several of the elements examined had a significant effect on cognitive function when they were assessed in a univariate context. However, after adjustment for other elements, many of these results were not significant. There was a significant quadratic effect for calcium and a significant zinc-cadmium interaction. Cognitive function increased with calcium level up to a certain point and then decreased as calcium continued to increase. Zinc showed a positive relation with cognitive function at low cadmium levels but a negative relation at high levels.
Wang resin-bound intermediates derived from Fmoc-L-phenylalaninal and Fmoc-L-valinal, and a resin supported Horner-Wadsworth-Emmons reaction, were treated with cinnamaldehyde derivatives, acetic acid, and borohydride to give secondary amines which were subsequently benzoylated to afford various derivatives of 3. Heating 3 at 95 degrees C induced cycloaddition reactions and produced 4 as the major product. Compounds 3 which were derived from 4-methoxycinnamaldehyde were more reactive, but did not give 4 and 4-7g. The direct cleavage of 3b using TFA led to the isolation of cycloaddition-demethylation product 10. The derivative of 3, which contained an electron-withdrawing nitro group on the phenyl ring, produced a single diastereomer of 4. The Diels-Alder cycloaddition between two electron-deficient counterparts showed similar reactivity to that of the reactions which have a normal complementary electron-demand.
This paper describes the design, synthesis, and evaluation of transition metal complexes capable of recognizing flexible histidine-containing peptides in aqueous medium (25 mM HEPES buffer, pH = 7.0, 25 degrees C). When the pattern of metal ions on a complex matches with the pattern of histidine moieties on the peptide, strong interaction (K = 1.2 x 10(6) M-1) can be achieved. The complex was highly selective (> 200:1) in discriminating similar flexible peptides differing only by one glycine unit.
Unlike typical naive T cells, T cells with an activated (CD44hi) memory phenotype show a rapid rate of proliferation in vivo. The turnover of memory-phenotype CD8+ T cells can be considerably augmented by injecting mice with various compounds, including polyinosinic polycytidylic acid, lipopolysaccharide and immunostimulatory DNA (CpG DNA). Certain cytokines, notably type I (alpha, beta) interferons (IFN-I), have a similar effect. These agents appear to induce proliferation of CD44hi CD8+ cells in vivo by an indirect process involving production of effector cytokines, possibly interleukin-15, by antigen-presenting cells. Although none of the agents tested induces proliferation of naive-phenotype T cells, IFN-I has the capacity to cause upregulation of surface markers on purified naive T cells. Depending upon the experimental conditions used, IFN-I can either inhibit or enhance primary responses of naive T cells to specific antigen.
Synthesis of monodisperse iron-platinum (FePt) nanoparticles by reduction of platinum acetylacetonate and decomposition of iron pentacarbonyl in the presence of oleic acid and oleyl amine stabilizers is reported. The FePt particle composition is readily controlled, and the size is tunable from 3- to 10-nanometer diameter with a standard deviation of less than 5%. These nanoparticles self-assemble into three-dimensional superlattices. Thermal annealing converts the internal particle structure from a chemically disordered face-centered cubic phase to the chemically ordered face-centered tetragonal phase and transforms the nanoparticle superlattices into ferromagnetic nanocrystal assemblies. These assemblies are chemically and mechanically robust and can support high-density magnetization reversal transitions.
1. Unitary inhibitory postsynaptic currents (uIPSCs) were recorded in synaptically coupled pairs of CA1 hippocampal interneurons and pyramidal neurons in rat brain slices by using dual patch-clamp techniques. Paired-pulse modulation of uIPSCs at individual GABAergic synapses was tested. 2. GABAergic synapses could be divided into two subgroups, high and low failure, depending on their failure rate. 3. The external Ca2+ levels modulate the failure rate of uIPSCs. In 0.51 mM Ca2+, low-failure pairs had a high-failure characteristic, whereas high-failure pairs had a low-failure characteristic in 8 mM Ca2+. The results suggest that uIPSC failures result from the Ca2+-dependent release mechanism rather than axon propagation failures. 4. Paired-pulse facilitation (PPF) occurred in high-failure pairs when the interspike interval was 20 ms. Paired-pulse depression (PPD) was not predominant in high-failure pairs. 5. Potency of uIPSCs, the average amplitude of non-failure events, was enhanced by PPF, suggesting that multiple synapses connect each pair. Differing numbers of activated synapses contributed to the variable amplitude of uIPSCs from a given pair. 6. PPD occurred in low-failure pairs at the tested range of interspike intervals (20-200 ms). The uIPSC2 after a large uIPSC1 was smaller than the uIPSC2 after a small uIPSC1, suggesting that PPD is use dependent and due to a decrease in the quantal content (m) after the first release. 7. In 8 mM Ca2+, PPD occurred in high-failure pairs and was larger in low-failure pairs, suggesting that the occurrence of PPF or PPD depends on the baseline release probability. 8. The GABAB receptor antagonist CGP 55845A (5 microM) decreased the baseline release probability of inhibitory synapses and attenuated PPD indirectly, rather than by blocking presynaptic GABAB autoreceptors.
Mature T cells can be classified on the basis of cell surface markers into naïve- and memory-phenotype cells. These phenotypically-defined subsets exhibit distinct kinetic behaviour in vivo. Thus, naïve-phenotype T cells persist long-term in a non-dividing state, while memory-phenotype T cells include cycling cells and have a more rapid rate of turnover. We have investigated the possibility that the different kinetic behaviour of naïve- and memory-phenotype T cells reflects a differential responsiveness to cytokines. It was discovered that memory-, but not naïve-, phenotype T cells were stimulated to proliferate by a variety of infection-induced cytokines. These results suggest that cytokines contribute to the high background rate of turnover exhibited by memory T cells.
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BACKGROUND: Chronic sinus inflammation may be determined partly by a balance of proinflammatory and counterregulatory cytokines and other mediators in the sinus. However, their mechanistic roles in chronic rhinosinusitis (CRS) are not well understood. OBJECTIVE: To evaluate production of proinflammatory (interferon gamma [IFN-gamma] and interleukin [IL] 12) and counterregulatory cytokines (IL-10 and IL-4) by sinus lavage (SL), bronchial lavage (BL), and peripheral blood mononuclear (PBMN) cells in patients with CRS. METHODS: We analyzed SL, BL, and PB samples obtained at surgery from 26 patients with CRS. Cytokine production was determined by culturing cells with or without stimuli. The results were evaluated in comparison with other inflammatory variables (cytologic findings, total protein, IgG, and lactose dehydrogenase), bacterial cultures, and clinical features. RESULTS: Production of IFN-gamma by SL cells was variable and did not correlate with other inflammatory variables, microbes grown, IL-10/IL-12p40 production by SL cells, or IFN-gamma production by BL or PBMN cells. Production of IL-4 by lavage cells was undetectable. None of 10 patients with elevated IFN-gamma production (>800 pg/10(6) SL cells with mitogen stimuli) had allergic rhinitis, whereas 12 of 16 patients with low IFN-gamma production (<500 pg/10(6) SL cells) had allergic rhinitis with positive reactivity to common aeoroallergens. There was no significant difference in other variables measured between low and high IFN-gamma production groups. CONCLUSIONS: Elevated IFN-gamma production by SL cells may indicate much less possibility of allergic rhinitis in patients with CRS, but other variables measured did not differ in patients with high or low IFN-gamma production by SL cells.
BACKGROUND: Previously, we found minimal bacterial dissemination and no evidence of systemic inflammation in a rabbit sinusitis model in which the left maxillary sinus was inflamed by Bacteroides inoculation with the ostium closed. However, we observed an increase in anti-Bacteroides IgG antibodies in the contralateral sinus, lower airway, and middle ear, with an apparent increase in interferon gamma (IFN-gamma) messenger RNA expression in the ear and sinus mucosa. OBJECTIVE: To evaluate how IFN-gamma production in the upper and lower airway is associated with localized bacterial sinusitis. DESIGN: Interferon gamma levels were measured in lavage solutions from the sinus, airway, and middle ear and in serum at 1, 2, 3, and 4 weeks following bacterial inoculation. SUBJECTS: The subjects were 6 rabbits at each time point. The controls were untreated (n = 5) and sham-operated (n = 4-5) rabbits at 2 and 4 weeks. INTERVENTION: Bacteroides fragilis (10(8) plaque-forming units) was inoculated into the left maxillary sinus. RESULTS: Interferon gamma levels in the ear and sinus were less than 0.2 microg/g protein in controls. Following bacterial inoculation into the left sinus, IFN-gamma levels increased up to 10-fold in both sinuses and even more in the middle ear at 3 weeks, independent of bacterial dissemination. Mean +/- SD IFN-gamma levels in the airway (0.3+/-0.28 microg/g protein in controls) were not altered by bacterial inoculation into the sinus. Serum IFN-gamma levels were very low (<0.05 microg/g protein) in most rabbits and were unchanged by bacterial inoculation. CONCLUSIONS: Interferon gamma levels increase in the ear and contralateral sinus in response to localized sinus inflammation, indicating concerted mucosal proinflammatory immune responses in the upper airway. Such responses may lead to the aseptic middle ear inflammation often observed in patients with chronic sinusitis.