Biomedical subjects
Publications and source records attributed to H Yeo.
A new triterpene lactone named patrinolide A (1) has been isolated from the roots of Patrinia scabiosaefolia (Valerianaceae). Its structure was determined to be 11beta,21beta-dihydroxy-3-oxooleanan-28,13beta-olide on the basis of spectral analysis, including 2D-NMR techniques. Key words: Patrinia scabiosaefolia, Valerianaceae, Lactone, Patrinolide, 11beta,21beta-dihydroxy-3-oxooleanan-28,13beta-olide.
Oxidative stress has been implicated as a primary cause of neuronal death in certain neurodegenerative disorders and in aging brains. Natural products have been used in Asian societies for centuries for treating such neurodegenerative disorders as senile dementia. In an effort to identify active neuroprotective compounds from these products, we have employed cultures of rat cortical neurons as our screening system. A methanolic extract from dried roots of Cynanchum wilfordii Hemsley (Asclepiadaceae) significantly mitigated the neurotoxicity induced by H2O2 in this screening system. Activity-guided fractionation using several chromatographic techniques resulted in the isolation of the neuroprotective compound, cynandione A, a biacetophenone. At a concentration of 50 microM, cynandione A significantly reduced neurotoxicity induced by H2O2. Cynandione A significantly attenuated decreases in levels of glutathione, superoxide dismutase, and other enzymes that participate in the cellular defense against oxidative stress. Furthermore, cynandione A alleviated neurotoxicity induced by the excitotoxic neurotransmitter, L-glutamate, the neurotoxicity induced by kainate, but not that mediated by N-methyl-D-aspartate. Cynandione A was demonstrated to be a natural antioxidant as it facilitated the breakdown of hydrogen peroxide in vitro; however, no mechanism was uncovered to explain its neuroprotectant effects against glutamate and kainate. Therefore, cynandione A may be efficacious in protecting neurons from oxidative stress mediated via activation of alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate/kainate receptors since it exerted significant neuroprotective effects on cultured cortical neurons.
To identify hepatoprotective agents from plant sources we use primary cultures of rat hepatocytes injured by CCl4. The hepatoprotective agents are the compounds that mitigate the injury caused by CCl4. Using this system we have investigated the biochemical mechanisms involved in the hepatoprotective activity of cynandione A, a biacetopherone, isolated from the roots of Cynanchum wilfordii Hemsley (Asclepiadaceae). Cynandione A (50 microM) significantly reduced (approximately 50%) the release into the culture medium of glutamic pyruvic transaminase and sorbitol dehydrogenase from the primary cultures of rat hepatocytes exposed to CCl4. Glutathione, superoxide dismutase, catalase and glutathione reductase play important roles in the cellular defence against oxidative stress. Cynandione A appeared to protect primary cultured rat hepatocytes exposed to CCl4 from significant drops in the levels of each of these four specific markers. Cynandione A also ameliorated lipid peroxidation by up to 50% as demonstrated by a reduction in the production of malondialdehyde. These results suggest that cynandione A protected the hepatocytes from CCl4-injury by maintaining the level of glutathione and by inhibiting the production of malondialdehyde, due to its radical scavenging properties.
Bioactivity-guided fractionation of the CHCl3 extract from hooks of Uncaria rhynchophylla led to the isolation of two triterpene esters, namely uncarinic acids A (1) and B (2). Their structures were established by spectroscopic and chemical methods. These compounds inhibited phospholipase Cgamma1 with IC50 values of 35.66 and 44.55 microM, respectively.
The oxidative dimerization of ferulic acid has been carried out using horse-radish peroxidase as catalyst to give a dihydrobenzofuran neolignan (1), the structure of which was elucidated as (2SR,3RS)-2,3-dihydro-2-(4-hydroxy-3-methoxyphenyl)-3-n-buto xycarbonyl-5-(2E-carboxyethenyl)-7-methoxybenzofuran by spectroscopic analyses. This compound showed more potent cytotoxicity against several tumor cell lines than the starting material.
Three new steroidal glycosides named cynascyrosides A-C were isolated from the roots of Cynanchum ascyrifolium. The structures of these compounds were determined on the basis of spectroscopic and chemical evidence as cynajapogenin A 3-O-alpha-D-oleandropyranosyl-(1-->4)-beta-L-cymaropyranosyl -(1-->4)-beta-D- digitoxopyranoside; cynajapogenin A 3-O-beta-D-glucopyranosyl-(1-->4)-alpha-L-cymaropyranosyl- (1-->4)-beta-L-cymaropyranosyl-(1-->4)-beta-L-cymaropyranoside+ ++; cynajapogenin A 3-O-beta-D-glucopyranosyl-(1-->4)-alpha-L-cymaropyranosyl- (1-->4)-beta-D-digitoxopyranosyl-(1-->4)-beta-L-cymaropyranosid e.
We compared the radiological appearances and survival of four methods of fixation of a femoral stem in 538 hips after follow-up for five or ten years. The fixation groups were: 1) press-fit shot-blasted smooth Ti-A1-V stem; 2) press-fit shot-blasted proximally ridged stem; 3) proximal hydroxyapatite (HA) coating; and 4) cementing. Survival analysis at five to ten years showed better results in the HA-coated (100% at five to six years) and cemented stems (100% at 5 to 6 years) than in the two press-fit groups. There was a higher mean rate of migration in the smooth and ridged Ti-A1-V shot-blasted press-fit groups (0.8 mm/year and 0.6 mm/year, respectively) when compared with the HA-coated and cemented prostheses (both 0.3 mm/year). More radiolucent lines and osteolytic lesions were seen in the press-fit groups than in either the HA-coated or cemented implants, with a trend for a lower incidence of both in the HA compared with the cemented group. Proximal osteopenia increased in the press-fit and cemented prostheses with time, but did not do so in the HA group. There was a higher incidence of resorption of the femoral neck with time in the cemented group than in the other three. We conclude that the HA and the cemented interfaces both provide secure fixation with a trend in favour of HA. The cemented prosthesis meets the suggested National Institutes of Health definition of 'efficacious' at ten years.
DNA damage produces a series of oxidation products including 8-oxo-2'-deoxyguanosine and 8-oxoguanine, whose urinary excretion have been used to estimate in vivo oxidative injury. A monoclonal antibody to 8-oxoguanine was used to measure these adducts in urine taken from ill infants. In the process of this investigation we observed a large chromatographic peak that did not correspond to any of the known 8-oxoguanine adducts. A combination of liquid chromatography with electrochemical detection and gas chromatography/mass spectrometry allowed isolation and identification of the previously undescribed oxidation product, N2-methyl-8-oxoguanine. The excretion of this compound is increased in ill and growing infants but is also found in the urine of adult rats and humans. Experiments with allopurinol, a xanthine oxidase inhibitor, show that in humans, N2-methyl-8-oxoguanine is formed from the tRNA modified base N2-methylguanine. This is in contrast to the nonmethylated bases, which are converted to 8-oxo derivatives as a result of oxidative damage to nucleic acids and do not appear to be substrates for xanthine oxidase.
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Exomphalos carries a 67% chance of other serious defects, 37% of which are life-threatening. Diagnosis in utero means parents can be counselled and offered choices of treatment. Parents need long-term support if their baby has a syndrome or other abnormalities. Babies that survive do well and most lead normal lives.
After observations of cloudiness in the perfusion circuit at open intracardiac operations, laboratory experiments showed a precipitate in a Hartmann's solution (compound sodium lactate solution, Ringer-lactate) and sodium bicarbonate based priming fluid used for cardiopulmonary bypass. The precipitate was found to consist of calcium carbonate crystals. The crystals were not dissolved by adding plasma proteins, nor were they sufficiently cleared from the extracorporeal circuit by a 40 microns filter in the arterial line. The crystals may embolise in microvascular beds and thus be a cause of postoperative morbidity. The practice of adding sodium bicarbonate to the pump prime may be unnecessary.