Thrombosis of the galenic system veins in the adult.
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Biomedical subjects
Publications and source records attributed to Y Luo.
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We studied six cases of spongy degeneration of the CNS in infancy among Chinese. The main clinical features were cyclical vomiting and wailing, blindness, megalocephaly, convulsions, lethargy, and coma. Chief findings from light microscopic studies were spongiform change, moderate outfall of neurons, and marked astrocytosis, with formation of Alzheimer's cells type 2. Demyelination was only slight, if present. Electron microscopic studies revealed membrane-bound vacuoles, often containing membranous fragments or blisters and electron-dense granules.
Four cases of spinal muscular atrophy (SMA) are reported, 3 with detailed autopsy findings. These are compared with 2 cases of typical amyotrophic lateral sclerosis (ALS) with neuropathological data. The 3 autopsy cases of SMA only showed decreased numbers of anterior horn cells in the spinal cord, with no change in the cortical pyramidal cells, including the Betz cells, and no degeneration of the pyramidal tracts, while the ALS cases showed loss both of lower and upper motor neurons and degeneration of the pyramidal tracts. In our opinion, the infantile, juvenile, adult, and late-life forms of SMA are really a single disease entity that occurs at varying ages and is separate from ALS. The term lower motor neuron disease would be preferable because the lesions are not limited to the spinal cord, but also occur in the brain stem.
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The long-sleep (LS) and short-sleep (SS) mouse lines were selectively bred for differential sensitivity to the anesthetic actions of ethanol, but they also differ in sensitivity to nicotine. A recent study suggested that the LS mice develop more tolerance to ethanol and cross-tolerance to nicotine than do the SS following chronic ethanol treatment. The studies reported here expand on these previous studies by assessing potential tolerance to ethanol and cross-tolerance to nicotine using additional behavioral and physiological measures. In addition, the effects of chronic ethanol treatment on ethanol and nicotine metabolism were measured. The LS mice developed tolerance to ethanol as measured by effects on open-field activity, body temperature, and sleep time, whereas the SS mice did not develop consistent tolerance to ethanol's effects on any of these measures. Cross-tolerance to nicotine's effects on open-field activity and body temperature developed, but only in the LS mice. The ethanol tolerance is likely due to changes in CNS sensitivity to ethanol, but altered elimination of nicotine may explain much of the cross-tolerance to nicotine seen in chronic ethanol-treated LS mice.
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A novel artificial glutathione peroxidase mimic consisting of a selenocystine-di-beta-cyclodextrin conjugate (selenium-bridged-6, 6'-amino-selenocystine-6,6'-deoxy-di-beta-cyclodextrin), in which selenocystine is bound to the primary side of beta-cyclodextrin through the two amino nitrogen groups of selenocystine, was synthesized. The glutathione peroxidase activities of the mimic-catalyzed reduction of H(2)O(2), tert-butylhydroperoxide, and cumene hydroperoxide by glutathione are 4.1, 2.11, and 5.82 units/micromol, respectively. The first activity was 82 and 4.2 times as much as that of selenocysteine and ebselen, respectively. Studies on the effect of substrate binding on the glutathione peroxidase activity suggest that it is important to consider substrate binding in designing glutathione peroxidase mimics. The detailed steady-state kinetic studies showed that the mimic-catalyzed reduction of H(2)O(2) by glutathione followed a ping-pong mechanism, which was similar to that of the native glutathione peroxidase.
Hyaluronic acid (HA) is an abundant nonsulfated glycosaminoglycan component of synovial fluid and the extracellular matrix. HA is an important building block for biocompatible and biointeractive materials with applications in drug delivery, tissue engineering, wound repair, and viscosupplementation. Herein we describe the synthesis and characterization of HA-N-succinimide, an activated ester of the glucuronic acid moiety. This HA-active ester intermediate is a precursor for fluorescent probes, drug-polymer conjugates, and cross-linked hydrogels. As a demonstration, we used HA-NHS to prepare HA-BODIPY by coupling with the hydrazide derivative of the fluor. Intracellular uptake of HA-BODIPY into human ovarian cancer cells, which overexpress cell-surface HA receptors, was visualized using confocal microscopy.
A cell-targeted prodrug was developed for the anti-cancer drug Taxol, using hyaluronic acid (HA) as the drug carrier. HA-Taxol bioconjugates were synthesized by linking the Taxol 2'-OH via a succinate ester to adipic dihydrazide-modified HA (HA-ADH). The coupling of Taxol-NHS ester and HA-ADH provided several HA bioconjugates with different levels of ADH modification and different Taxol loadings. A fluorescent BODIPY-HA was also synthesized to illustrate cell targeting and uptake of chemically modified HA using confocal microscopy. HA-Taxol conjugates showed selective toxicity toward the human cancer cell lines (breast, colon, and ovarian) that are known to overexpress HA receptors, while no toxicity was observed toward a mouse fibroblast cell line at the same concentrations used with the cancer cells. The drug carrier HA-ADH was completely nontoxic. The selective cytotoxicity is consistent with the results from confocal microscopy, which demonstrated that BODIPY-HA only entered the cancer cell lines.
The serine/threonine kinases, Akt1/PKBalpha, Akt2/PKBbeta, and Akt3/PKBgamma, play a critical role in preventing cancer cells from undergoing apoptosis. However, the function of individual Akt isoforms in the tumorigenicity of cancer cells is still not well defined. In the current study, we used an Akt1 antisense oligonucleotide (AS) to specifically downregulate Akt1 protein in both cancer and normal cells. Our data indicate that Akt1 AS treatment inhibits the ability of MiaPaCa-2, H460, HCT-15, and HT1080 cells to grow in soft agar. The treatment also induces apoptosis in these cancer cells as demonstrated by FACS analysis and a caspase activity assay. Conversely, Akt1 AS treatment has little effect on the cell growth and survival of normal human cells including normal human fibroblast (NHF), fibroblast from muscle (FBM), and mammary gland epithelial 184B5 cells. In addition, Akt1 AS specifically sensitizes cancer cells to typical chemotherapeutic agents. Thus, Akt1 is indispensable for maintaining the tumorigenicity of cancer cells. Inhibition of Akt1 may provide a powerful sensitization agent for chemotherapy specifically in cancer cells.
Checkpoint kinase 1 (Chk1) is a checkpoint gene that is activated after DNA damage. It phosphorylates and inactivates the Cdc2 activating phosphatase Cdc25C. This in turn inactivates Cdc2, which leads to G2/M arrest. We report that blocking Chk1 expression by antisense or ribozymes in mammalian cells induces apoptosis and interferes with the G2/M arrest induced by adriamycin. The Chk1 inhibitor UCN-01 also blocks the G2 arrest after DNA damage and renders cells more susceptible to adriamycin. These results indicate that Chk1 is an essential gene for the checkpoint mechanism during normal cell proliferation as well as in the DNA damage response.
One day in July 1991, 78 people became victims of accidental alimentary intoxication in a factory in Hebei Province, China. Related samples, including rodenticide bait, the artificial carbonic kidneys used for the treatment of the victims, and the victims' blood, were analyzed by GC/MS. Tetramine [80-12-6], a highly toxic rodenticide, was identified as the toxicant. The effectiveness of artificial carbonic kidneys was evaluated. The analytical results revealed that detoxification of the patients was effective 48 hours after intoxication by percolating their blood through artificial carbonic kidneys.
During our evaluation of ion-mobility spectrometry (IMS) screening for the abuse of the beta-agonist clenbuterol during fattening in cattle, we found that clenbuterol could not be detected with the instrument in extracts obtained by solid-phase extraction or ion-pair extraction, although the recovery for these procedures was at least 85%. Several experiments showed that the signal loss occurred mainly during the evaporation of the organic solvent. Again, it could be shown that no clenbuterol was lost during this step. On further investigation, we found that so-called solvent residues, which are left after the evaporation of the organic solvent, caused a significant reduction of the clenbuterol signal. Other reagents used in our sample pretreatment procedures were also found to reduce the signal. For example, the signal reductions caused by the different reagents used for the ion-pair extraction of clenbuterol from human urine were determined. We think that IMS is only useful for our purpose if a chromatographic preseparation is performed.
In the present paper, disk extraction was evaluated for the rapid isolation of clenbuterol from human and calf urine, followed by high-performance liquid chromatography analysis with UV detection. A method was developed for the extraction with standard density C8 disks. The disks could be washed with 25% methanol in 0.01M sodium hydroxide without significant losses of clenbuterol. The recovery of denbuterol was about 85%, and the extracts were clean. The detection limit was about 10 ng/mL. The main advantages of these disks were the saving of time and the reduced amounts of organic solvents needed.
In this study, we developed and assessed an artificial anal sphincter driven by an shape memory alloy actuator (AS-SMA). The performance characteristics of the device were analyzed with a measurement system. Assessment showed that the AS-SMA could generate a pressure of 55 mm Hg at an atmospheric temperature of 36 degrees C, and displacement of the SMA actuator was 7.5 mm when the temperature of the SMA plate was 55 degrees C. To evaluate opening and closing, we studied a piglet colostomy model, in which the AS-SMA was implanted around the colostomy in the extraperitoneal space. Flow control tests using living porcine intestine revealed that the AS-SMA could maintain fecal continence against an intestinal pressure of 75 mm Hg. The high pressure zone corresponding to the location of the device was demonstrated in a manometric examination. For 6 days after surgery, we activated the AS-SMA twice a day and observed the bowel movements. The animal experiment indicated that the AS-SMA is able to control the bowel movements of patients with fecal incontinence if several problems, such as burning of tissue around the device and compression injury of the intestine, are resolved.