[A case of facioliasis hepatica].
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Biomedical subjects
Publications and source records attributed to Ying Zhao.
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Supramolecular complexes of PEI(OA)x show a lamellar structure, and reversible crystal phase transition of the side alkyl chains in the complex can be observed by temperature-variable FT-IR spectroscopy.
A novel bicyclic ketolide derivative, 10,11-didehydro-11-deoxy-3-O-descladinosyl-6-O-methyl-3-oxo-8,9-anhydroerythromycin 9,12-hemiacetal(6) was obtained from 3-O-descladinosyl-6-O-methylerythromycin 2'-acetate. The structure and stereochemistry of this novel compound were elucidated and established by NMR and X-ray crystallography.
The RNA recognition motif (RRM), one of the most common RNA binding domains, contains three highly conserved aromatic amino acids that participate in stacking interactions with RNA bases. We have investigated the contribution of these highly conserved aromatic amino acids to the affinity of the complex formed between the N-terminal RRM of the U1A protein and stem loop 2 of U1 snRNA. Previously, we found that substitution of one of these conserved aromatic amino acids, Phe56, with Ala resulted in a large destabilization of the complex. Here, we have modified A6, the base in stem loop 2 RNA that stacks with Phe56, to compensate for a portion of the destabilization caused by the Phe56Ala mutation. We have designed two modified adenosines, A-3CPh and A-4CPh, in which a phenyl group is linked to the adenosine such that it may replace the phenyl group that is eliminated by the Phe56Ala mutation in the complex. We have found that incorporation of A-3CPh into stem loop 2 RNA stabilizes the complex formed with Phe56Ala by 0.6 kcal/mol, while incorporation of A-4CPh into stem loop 2 RNA stabilizes this complex by 1.8 kcal/mol. Either base modification destabilizes the wild-type complex by 0.8-0.9 kcal/mol. Experiments with other U1A mutant proteins suggest that the stabilization of the complex between the Phe56Ala U1A protein and stem loop 2 RNA is due to a specific interaction between the Phe56Ala U1A protein and A6-4CPh stem loop 2 RNA.
Little is known about the interactions between Helicobacter pylori, which specializes in colonizing the mucin layer that covers the gastric mucosa, and primary gastric epithelial cells. The expression pattern of Toll-like receptors (TLRs) in primary gastric epithelial cells and cell lines was compared. Primary cells did not express TLR4, whereas all cell lines expressed a nonsignaling form of TLR4. Because other cells within the mucosa expressed TLR4, it was next investigated whether H. pylori can be recognized by TLR4--they cannot. Moreover, H. pylori infection of primary cells induced a regulated production of interleukin (IL)-6, IL-8, and tumor necrosis factor-alpha, whereas infection of cell lines only resulted in IL-8 production. The cytokine production in all cell types was strictly cag dependent. These findings indicate that, although the epithelium is important in directing the immune response against H. pylori infections, the response is independent of TLR4.
Angiotensin II (Ang II) induces changes in vessel structure by its capacity to activate genes that are coupled to signaling pathways such as extracellular signal-regulated kinase (ERK), p38, and phosphatidylinositol 3-kinase (PI3K). Using a DNA microarray containing 5088 genes and expressed sequence tags, we initially established a database of replicated experiments (n=4) to define the variances in mRNA expression in response to Ang II versus vehicle treatment. We observed a wide range of values for the coefficients of variation in a gene-specific manner. Guided by power calculations, we used statistical inference on a sufficient number of experimental replicates to minimize the number of false-negatives and define a subset of Ang II-responsive genes (P<0.05). To further characterize the molecular circuitry that couples Ang II stimulation with mRNA expression, we assessed expression profiles in the presence and absence of inhibitors of ERK, p38, and PI3K. Using two different methods of computational cluster analysis, we identified a subset of six matricellular proteins (eg, osteopontin and plasminogen activator inhibitor-1) that are coordinately upregulated by Ang II via an ERK/p38-dependent pathway. In addition, these cluster analyses identified calpactins I and II as novel Ang II-responsive genes. Given that Ang II promotes vascular lesion formation, we examined whether this matricellular gene cluster was also coordinately regulated in vivo. Indeed, we demonstrate that both calpactin I and osteopontin are upregulated in response to vascular injury. Taken together, the combined use of DNA microarrays, statistical inference, and cluster analysis identified novel, coordinately regulated Ang II-responsive genes that may mediate vascular lesion formation.
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To investigate early infant feeding practices in Jinan, China, a cross-sectional study was carried out in April-May 2000. Data were collected through structured interviews among nearly all the mother-infant pairs (247) in four communities in the city with infants under seven months of age. All but one was born in a hospital and rooming-in (infant sleeping in same room as mother) was widely practiced. Breastfeeding was practiced universally, but first contact with the new-born was delayed one or more hours for 51% of subjects. Colostrum was given to 94% of the infants, yet during the first three days, all but 34% were given water, artificial baby milk, glucose or other prelacteal feeds. Among infants under 4 months of age, 35% were currently exclusively breastfeeding, but at two months only 40% were, and only half that many had received nothing but breast-milk since birth. Exclusive breastfeeding has probably increased in China, but further promotion is still needed in this area.
OBJECTIVE: To investigate the relationship between the changes of upper airway and genioglossus muscle activity after the treatment with Snoreguard. METHODS: 31 patients with OSAS or snoring were treated with Snoreguard Cephalometric analysis was carried out to compare the changes of the upper airway before and after the treatment. The relationship between the change in morphology and that of genioglossus muscle activity among 22 patients was investigated. RESULTS: (1) The size of upper airway decreased significantly with Snoreguard. SPP-SPPW increased from (9.14 +/- 3.79) mm to (12.36 +/- 3.74) mm and TB-TPPW increased from (10.63 +/- 3.71) mm to (11.90 +/- 4.33) mm. UC-LC decreased from (21.96 +/- 11.06) mm to (10.48 +/- 8.55) mm and H-MP decreased from (20.60 +/- 6.65) mm to (11.01 +/- 6.84) mm. (2) The size of upper airway in part of the patients decreased with Snoreguard, but good treatment efficiency remained. CONCLUSION: The mechanism of Snoreguard is caused by the mechanical enlargement of upper airway.
OBJECTIVE: To observe the significance of ricin (RT) with chemical nidification to reduce the hepatotoxicity in mice and its anticancer effect. METHODS: Mice were exposed to RT and RT-PDP [ricin chemically modified by N-succinimidyl 3-(2-pyridyldithio)-propionate, (SPDP)] respectively, and their serum activity of glutathione-S-transferase (GST) and liver glutathione (GSH) content were determined. The ultramicro-structure under electron microscope was also observed. RESULTS: The GST activity increased with doses, and the increase in ricin group was higher than that in RT-PDP group; the activities of GST in RT group at 12.5, 15.0 micro g/kg [(93.65 +/- 12.30), (153.71 +/- 26.64) IU/L respectively] were higher than those in RT-PDP group [(62.97 +/- 11.22), (78.20 +/- 15.71) IU/L] (P < 0.05). The contents of GSH were decreased with doses; but the contents of GSH in RT-PDP group at 2.5, 5.0, 7.5, 10.0, 15.0 micro g/kg [(6.34 +/- 1.43), (4.14 +/- 1.82), (3.54 +/- 0.64), (2.73 +/- 1.82), (1.82 +/- 0.62) micro mol/L respectively] were still higher than those in RT group [(3.53 +/- 0.95), (2.12 +/- 0.54), (1.82 +/- 0.71), (1.52 +/- 0.34), (0.81 +/- 0.36) micro mol/L] (P < 0.01). Electron microscopic examination showed that the injury of liver cells in RT group was more severe than that in RT-PDP group. CONCLUSION: The hepatotoxicity of ricin in mice may be reduced by chemical modification.
Beta-catenin and T cell factor (Tcf) are distal components of the highly conserved Wnt pathway that govern cell fate and proliferation in lower organisms. Thus, we hypothesized that the regulation of beta-catenin and Tcf played a critical role in vascular remodeling. The first objective was to define beta-catenin expression in vascular smooth muscle cells (VSMCs) after balloon injury. Indeed, beta-catenin mRNA and protein were significantly elevated 7 days after balloon injury in the rat carotid artery. We hypothesized that beta-catenin accumulation in response to vascular injury inhibited VSMC apoptosis. In line with our hypothesis, transfection of a degradation-resistant beta-catenin transgene into rat VSMCs significantly inhibited apoptosis. Accumulation of beta-catenin also resulted in a 10-fold increase in the activation of Tcf. To test if Tcf was necessary to confer beta-catenin-induced survival, loss of function studies were carried out with a dominant negative Tcf-4 transgene lacking the beta-catenin binding domain, Tcf4(N31). Indeed, loss of Tcf-4 activity abolished beta-catenin-induced survival. We further postulated that beta-catenin and Tcf promoted cell cycle progression by activating cyclin D1, a target gene of Tcf-4. Beta-catenin activated cyclin D1, and this activation was partially blocked with loss of Tcf-4. In parallel, blockade of Tcf-4 resulted in inhibition of [3H]thymidine incorporation and partial blockade of the G1-S phase transition. In conclusion, beta-catenin and Tcf-4 play a dual role in vascular remodeling by inhibiting VSMC apoptosis and promoting proliferation.
New lanthanide luminescence materials were prepared. The main component lanthanide chelates generally need a relatively high content of rare earth. Inorganic luminescence materials only need low rare earth concentration using doped method. Similarly, lanthanide chelates can be added to complex matrix by doped method. In this way, low rare earth concentration emission was successful in the lanthanide chelates system as well. The influence of europium ion concentration on luminescence intensities was discussed. When the europium ion weight in the complex is only about 0.6%, the sample exhibits good luminescence properties. The fluorescence, Fourier transform infrared spectra, micro-Raman and electron spin resonance spectra of the samples were measured. And a possible luminescence mechanism was suggested by the inorganic doped mechanism and the luminescence of lanthanide complexes together.
Asthma is characterized by airway inflammation, bronchial hyperresponsiveness, and airway obstruction by bronchospasm and bronchial wall thickening due to smooth muscle hypertrophy. A rise in cytosolic free Ca2+ concentration ([Ca2+]cyt) may serve as a shared signal transduction element that causes bronchial constriction and bronchial wall thickening in asthma. In this study, we examined whether capacitative Ca2+ entry (CCE) induced by depletion of intracellular Ca2+ stores was involved in agonist-mediated bronchial constriction and bronchial smooth muscle cell (BSMC) proliferation. In isolated bronchial rings, acetylcholine (ACh) induced a transient contraction in the absence of extracellular Ca2+ because of Ca2+ release from intracellular Ca2+ stores. Restoration of extracellular Ca2+ in the presence of atropine, an M-receptor blocker, induced a further contraction that was apparently caused by a rise in [Ca2+]cyt due to CCE. In single BSMC, amplitudes of the store depletion-activated currents (I(SOC)) and CCE were both enhanced when the cells proliferate, whereas chelation of extracellular Ca2+ with EGTA significantly inhibited the cell growth in the presence of serum. Furthermore, the mRNA expression of TRPC1, a transient receptor potential channel gene, was much greater in proliferating BSMC than in growth-arrested cells. Blockade of the store-operated Ca2+ channels by Ni2+ decreased I(SOC) and CCE and markedly attenuated BSMC proliferation. These results suggest that upregulated TRPC1 expression, increased I(SOC), enhanced CCE, and elevated [Ca2+]cyt may play important roles in mediating bronchial constriction and BSMC proliferation.
OBJECTIVE: To observe the effects of respiratory support with high frequency jet ventilation (HFJV) in severely burned patients with inhalation injury during early postburn stage. METHODS: Twenty severely burned patients with TBSA of 79.6 +/- 29.3% and inhalation injury were enrolled in the study. Nineteen cases received tracheostomy after admission and only one received nasal intubation. All the patients underwent HFJV to correct hypoxia. The changes in blood gas analysis, respiratory rate and pulse were recorded before and 11 days after the ventilation. RESULTS: Tracheostomy was performed on 2.7 +/- 2.4 postburn days (PBDs), and HFJV was given during 4.4 +/- 2.9 PBDs. PaO(2) was evidently higher during 1 - 3 days after HFJV than that before the ventilation (P < 0.01) and remained at high level for 1 week after HFJV. There was no change in PaCO(2), respiratory rate and pulse during the ventilation. CONCLUSION: HFJV was beneficial in improving oxygenation and without any obvious side effects during the early management of severely burned patients with inhalation injury. This might be an optimal respiratory support pattern.
The research of air-adjustment storing ginseng shows that when the concentration of CO2 is above 50% and the concentration of O2 is under 5%, all adults will die in four days; all eggs and larvas will die in fifteen days. During the year of using this method air-adjustment, no vermins and mould have been found.
AIM:To observe the effects of ricin (RT) with and without chemical modification on both hepatotoxicity of mice and activity against hepatocellular cancer (HCC), and evaluate the possibility to improve RT anticancer activity via chemical modification.METHODS:RT was modified with N-succinimidyl3(2-pyridyldithio) propionate (SPDP),a heterobifunctional cross-linker, and SPDP derivative of RT (PDP-R) was obtained.The serum glutathione-s-transferase (SGST) activity,as an index of liver damage, was determined in mice intoxicated with RT and PDP-R,at various doses and time.The tissue damage of HCC in the nude mice ip injected with PDP-R was compared with that with RT at the same dose by immunohistochemical method, the relative content of both RT and PDP-R in the HCC tissues was measured by computerized image-analysis. RESULTS:The SGST activities increased with doses or/and time intoxicated with both RT and PDP-R, and the increase in the value of RT group was more significant than that in the PDP-R group; the SGST activity of RT group was 2.8-fold (P < 0.01) of PDP-R group at a dose of 12.5&mgr;g/kg for 42h, showing the much lower toxicity of R-PDP than that of RT. Under an optical microscope, hemolysis and necrosis of massive cells in the HCC tissues of PDP-R group were observed and the ratio of necrosis mounted to 90.5% while the corresponding value of RT group only to 62.5%.With computerized image-analysis, the average relative content of RT and PDP-R in the HCC tissues,represented as greyness, was 140.06 plus minus 3.43 and 169.10 plus minus 2.74, respectively. There was significant difference between the two (P< 0.05), indicating the higher content of PDP-R in the HCC tissue than that of RT.CONCLUSION:The hepatotoxicity of PDP-R to mice may be reduced by chemical modification with SPDP, but both the affinity of PDP-R to the HCC tissues and ability to kill it may be stronger than that of RT. So this might be a valuable attempt to improve the anticancer activity of RT.