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Biomedical subjects

S G Chen

Publications and source records attributed to S G Chen.

At least 55 records · Page 3Linked to original sources

[Protective effects of Angelica sinensis injection on myocardial ischemia/reperfusion injury in rabbits].

The injection of aqueous extract of Angelica sinensis (AS), 50 mg/kg, 30 ml, were administered intravenously at a rate of 0.4 ml/min by an infusion pump 10 min before the left anterior descending coronary artery of rabbit was ligated, the LVP and +/- dp/dtmax of the rabbit heart injured by ischemia/reperfusion in vivo, were significantly higher than those in the control group (N.S. group, P < 0.05-0.01), and the level of malon-dialdehyde (MDA) and the activity of creatine phosphokinase (CPK) in the blood plasma were lower than those in the control group remarkably (P < 0.05-0.01). These results showed that AS exerted obvious protective effects on myocardial dysfunction and myocardial injury induced by ischemia/reperfusion.

Animals↗

Fatal familial insomnia and familial Creutzfeldt-Jakob disease: different prion proteins determined by a DNA polymorphism.

Fatal familial insomnia and a subtype of Creutzfeldt-Jakob disease, two clinically and pathologically distinct diseases, are linked to the same mutation at codon 178 (Asp-178-->Asn) but segregate with different genotypes determined by this mutation and the methionine-valine polymorphism at codon 129 of the prion protein gene. The abnormal isoforms of the prion protein in these two diseases were found to differ both in the relative abundance of glycosylated forms and in the size of the protease-resistant fragments. The size difference was consistent with a different protease cleavage site, suggesting a different conformation of the protease-resistant prion protein present in the two diseases. These differences are likely to be responsible for the type and location of the lesions that characterize these two diseases. Therefore, the combination of the mutation at codon 178 and the polymorphism at codon 129 determines the disease phenotype by producing two altered conformations of the prion protein.

Codon↗

[Treacher-Collin's syndrome and translaryngeal guided intubation--case report].

Treacher-Collin's (T-C) syndrome, a first-arch congenital defect, that often manifests with severe facial deformity. Though a rare condition, it offers challenges to an anesthesiologist especially during plastic surgical procedure. These challenges are: (1) difficulty in maintaining a patent airway and (2) difficulty in intubation during induction of general anesthesia. We would like to report a case using transtracheal passage of a retrograde guide wire into the oropharynx prior to laryngeal endotracheal intubation. The technique can, by no means, solve all airway problems. However, proper utilization of this technique may sometimes be life-saving.

Adult↗

[Infected common iliac aneurysm due to Salmonella: a case report].

A 62-year-old male, presenting with chills and fever and RLQ abdominal pain, was found to have an infected aneurysm of the right common iliac artery infected by Salmonella group C1. CT scan of abdomen and arteriography definitely identified the lesions. Antibiotic treatment and surgical intervention with aneurysmectomy and suprapubic crossover femoro-femoral artery graft resulted in a good recovery and outcome.

Humans↗

Inhibition of brain protein kinase C subtypes by lead.

Protein kinase C (PKC) is an important enzyme in mediating cellular signal transduction and neuronal plasticity. Extremely low concentrations (picomolar range) of Pb++ have been reported to activate partially purified PKC from rat brain (Markovac and Goldstein, 1988). However, the lead activation of PKC at such low concentrations is still a matter of discussion (Simons, 1989). To clarify this point, we have examined the lead effect on highly purified PKC subtypes. Pb++ was found to be a potent inhibitor for all three PKC subtypes (types I, II and III) with IC50 of 2 to 10 microM. Characterization of this lead inhibition of PKC suggests that 1) the inhibition is not due to the competition with Ca++, 2) the site of action of lead is on the catalytic domain of PKC, 3) the inhibition is not dependent on the mode of activation (phosphatidylserine/diacylglycerol vs. cis-unsaturated fatty acid) and 4) the inhibition is totally reversible.

Animals↗

Phosphatidylcholine-dependent protein kinase C activation. Effects of cis-fatty acid and diacylglycerol on synergism, autophosphorylation and Ca(2+)-dependency.

A long-chain neutral phospholipid, dioleoylphosphatidylcholine, was found to support protein kinase C activation by cis-fatty acid and diacylglycerol (DAG). This effect of phosphatidylcholine (PC) is totally dependent on the presence of cis-fatty acid; PC greatly stimulates the cis-fatty acid-induced protein kinase C activity, but it does not activate protein kinase C at all, even in the presence of DAG, if cis-fatty acid is absent. DAG, however, plays a modulatory role in the presence of Ca2+; it further enhances the PC-potentiated cis-fatty acid activation of protein kinase C. Although the activities of all three protein kinase C subtypes tested (types I, II and III) are supported by this PC mechanism, type III is most sensitive to the DAG effect, and it is activated synergistically by cis-fatty acid and DAG. The potency of PC to support the synergistic activation of this subtype is equivalent to that of phosphatidylserine (PS). There are several differences, however, between PC- and PS-supported synergism observed in type III protein kinase C: (1) Ca(2+)-sensitivity is different; PC requires higher concentrations of Ca2+ (10-20 microM-Ca2+) than those required for PS (micromolar Ca2+); (2) PC/cis-fatty acid/DAG-induced autophosphorylation of protein kinase C subtypes (types I, II and III) is very weak, whereas PS/cis-fatty acid/DAG strongly stimulate autophosphorylation of these subtypes under the conditions at which both PC and PS systems fully activate the protein kinase C in terms of histone phosphorylation. These observations suggest that a neutral phospholipid such as PC may also participate in the activation and differential regulation of protein kinase C.

Animals↗

Synergistic activation of type III protein kinase C by cis-fatty acid and diacylglycerol.

Micromolar concentrations of cis-fatty acid synergistically activate type III protein kinase C with diacylglycerol. This synergistic effect occurs at low concentrations of cis-fatty acid and diacylglycerol, and it is capable of inducing almost full activation of this protein kinase C subtype at a physiologically relevant Ca2+ concentration (2 microM). The synergistic activation mode can be observed even in the absence of Ca2+, but micromolar Ca2+ significantly enhances the type III protein kinase C activation. cis-Fatty acid also augments the diacylglycerol-induced activation of other subtypes (type I and II), although the effect is smaller than that observed in type III. Neither the diacylglycerol- nor the cis-fatty acid-dependent mode of activation can fully activate any of these subtypes at a physiological concentration of Ca2+ (2 microM). Our results suggest that the generation of three second messengers, i.e. the increase in intracellular Ca2+ concentration and the generation of both cis-fatty acid and diacylglycerol in the cell, may be necessary signals for protein kinase C activation, particularly for type III protein kinase C.

Animals↗

Mechanisms of protective effects of berbamine on ischemia/reperfusion injury in isolated rat heart.

Isolated perfused rat heart model was used to observe the protective effects of berbamine on myocardial ischemia/reperfusion injury. The hearts were significantly injured by 40 min global ischemia followed by 20 min reperfusion. Berbamine could significantly improve heart function, prevent ventricular fibrillation, reduce CK release, preserve Na,K-ATPase activity, and reduce Na+ gain and K+ loss during ischemia and Ca2+ overload during reperfusion. With the use of low temperature ESR technique, in hearts subjected to 40 min ischemia and 15 sec reperfusion, oxygen-centered free radical signals became much more intense. In the presence of berbamine, these signals decreased. Results showed that berbamine could alleviate myocardial ischemia/reperfusion injury. This effect might be due to: 1) preserved myocardial Na,K-ATPase activity and inhibition of sodium overload at the end of ischemia, which might further lead to attenuation of reperfusion-induced calcium overload, and 2) reduction of oxygen free radical generation during reperfusion.

Alkaloids↗

Protective effects of an adenosine deaminase inhibitor on ischemia-reperfusion injury in isolated perfused rat heart.

We tested the effect of the adenosine deaminase inhibitor erythro-9-(2-hydroxy-3-nonyl)adenosine (EHNA) on ischemia-reperfusion injury in isolated perfused rat heart. In the ischemia-reperfusion group (n = 10), ventricular fibrillation occurred within 3 min of reperfusion after the 40-min ischemic period. The incidence of ventricular fibrillation was 90% with a mean duration of 3.15 +/- 0.97 (SE) min. Resting tension increased significantly. By contrast, the incidence of ventricular fibrillation after reperfusion in the EHNA-treated (5 microM) group (n = 10) was 20% (P less than 0.01), and the duration was 0.30 +/- 0.21 min (P less than 0.01). Resting tension was significantly lower and around the normal level in the EHNA-treated group (P less than 0.01). Contraction amplitude and heart rate recovered to nearly normal compared with the ischemia-reperfusion group (P less than 0.01). Coronary flow was greater in the EHNA-treated group (P less than 0.01). It is concluded that EHNA protects the heart, possibly by accumulation of adenosine that benefits the hearts and by blocking the xanthine oxidase pathway for free radical generation.

Adenine↗

The pattern of delivery and distribution of coronary venous retroinfusate in canine hearts.

The delivery and distribution of retroinfusate premixed with radionuclide microspheres (15 microns) in the coronary venous system of canine hearts was studied in in vitro and in vivo experiments. Results showed that about 51-85% of the retroinfusate was shunted directly by vessels greater than 15 microns in diameter to the right heart in cases of isolated heart study, while the remaining 21-42% passed through intramyocardial capillaries with obvious nutritional effects. In the closed-chest experiments, 95% of the retroinfusate was bypassed to the right heart; less than 5% went through the intramyocardial microcirculation system. Intramyocardial distribution pattern of the retroinfusate indicated a predominant supply to the left ventricular free wall. There was a preferential distribution of the retroinfusate to the ischemic area with a subendo subepi blood flow ratio of up to 1.79 +/- 0.21 post-LAD occlusion.

Animals↗

Fragmentation of DNA and chromatin during senescence in barley leaves.

DNA or chromatin from young (7 day) first seedling leaves of barley showed only one component which migrated little into 1% agarose gels on electrophoresis. However, DNA or chromatin from senescent (17-, 19-, and 23-day-old) leaves showed additional dispersed components migrating throughout the length of the gel which increased with age. These low molecular weight components increased even more on autodigestion of chromatin from senescent leaves by its associated DNase or by digestion of DNA from senescent leaves with partially purified chromatin DNase. DNA or chromatin from young leaves also produced gel pattern similar to old leaves on digestion with partially purified chromatin DNase from old barley leaves. Thus, fragmentation of DNA and chromatin by chromatin associated DNase, previously shown to increase 4000% on aging, occurs during senescence in barley leaves.

Aging↗