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G Y Ma

Publications and source records attributed to G Y Ma.

At least 19 recordsLinked to original sources
PubMed2006

Efficacy assessment of phenobarbital in epilepsy: a large community-based intervention trial in rural China.

BACKGROUND: Many people with epilepsy need not experience further seizures if the diagnosis and treatment are correct. Most epilepsy patients have convulsions, which are usually fairly easy to diagnose. This study tested a model for treatment of people with convulsive forms of epilepsy at primary health-care level in rural areas of China. METHODS: Patients with convulsive epilepsy were identified at primary care level and provided with phenobarbital monotherapy. Local physicians, who were provided with special training, carried out screening, treatment, and follow-up. A local neurologist confirmed the diagnoses. Efficacy was assessed from the percentage reduction in seizure frequency from baseline and the retention of patients on treatment. FINDINGS: The study enrolled 2455 patients. In 68% of patients who completed 12 months' treatment, seizure frequency was decreased by at least 50%, and a third of patients were seizure free. 72% of patients who completed 24 months' treatment had reduction of seizure frequency of at least 50% and a quarter of patients remained seizure free. Probability of retention was 0.84 at 1 year, and 0.76 at 2 years. Medication was well tolerated and reported adverse events were mild; only 32 patients (1%) discontinued medication because of side-effects. INTERPRETATION: This pragmatic study confirmed that this simple protocol was suitable for the treatment of convulsive forms of epilepsy in rural areas of China. Physicians with basic training could treat epilepsy patients with phenobarbital, with beneficial effects for most patients with convulsive seizures. Few cognitive or behavioural adverse events were noted, but formal psychometric testing was not done.

Adolescent↗
PubMed2001

The first product of phospholipid N-methylation, phosphatidylmonomethylethanolamine, is a lipid mediator for progesterone action at the amphibian oocyte plasma membrane.

Progesterone has been shown to act at plasma membrane receptors on the amphibian oocyte to trigger a cascade of changes in membrane phospholipids and to initiate the G(2)/M transition of the first meiotic division. The earliest event (0-1 min) is the transient N-methylation of phosphatidylethanolamine (PE) to form phosphatidylmonomethylethanolamine (PME), demonstrated using [(3)H]glycerol to prelabel oocyte plasma membrane PE. [(3)H]Glycerol-labeled PME rises 10-fold within the 1-2 min after exposure to progesterone and accounts for conversion of about 50% of the [3H]Glycerol-labeled PE. [(3)H]PME levels slowly decline over the following 10-30 min. [(3)H] or [(14)C] labeled fatty acid experiments showed that newly formed PME is enriched in linoleic or palmitic, but not in arachidonic acid, indicating that specific PE pools undergo progesterone-induced N-methylation. Two plasma membrane changes: activation of serine protease, and Ca(2+) release from the oocyte surface coincide with PME formation; both are prevented by pretreatment of oocytes with the N-methylation inhibitor, 2-methylaminoethane. Media containing PME micelles release both protease and Ca(2+) from intact oocytes within the first 1-2 min. The immediate downstream metabolites of PME, PDE and PC, do not induce serine protease activity or Ca(2+) release. We conclude that progesterone initially activates N-methyltransferase in the oocyte plasma membrane, and that the first product, PME, is responsible for activation of serine protease in the plasma membrane and the release of Ca(2+) from the oocyte surface.

Animals↗
PubMed1998

Mg2+ modulates membrane sphingolipid and lipid second messenger levels in vascular smooth muscle cells.

In vitro studies with smooth muscle cells from rat aorta and dog cerebral blood vessels indicate that variation in free Mg2+, within the pathophysiological range of Mg2+ concentrations, found in human serum, causes sustained changes in membrane phospholipids and lipid second messengers. Incorporation of [3H]palmitic acid into phosphatidylcholine (PC) and sphingomyelin (SM) was altered within 15-30 min after modifying the extracellular Mg2+ ion level ([Mg2+]o). Decreased Mg2+ produced a fall in both [3H]SM and [3H]PC over the first 2 h. After an 18-h incubation, the [3H]PC/[3H]SM ratio changed from about 20:1 to about 50:1. Increased [Mg2+]o resulted in a 2- to 3-fold increase in [3H]SM compared to only a small increase in [3H]PC over the same period. There was a reciprocal relationship between [3H]ceramide and [3H]1,2-DAG levels with highest [3H]ceramide and lowest [3H]-1,2-DAG levels seen at lowest [Mg2+]o. The results indicate that a fall in extracellular ionized Mg2+ concentration produces a rapid and sustained decrease in membrane sphingomyelin and a moderate rise in intracellular ceramide. A major effect of lowering [Mg2+]o appears to be a down-regulation of SM synthase. The increased membrane SM content and a concomitant decrease in cell ceramide, in the presence of elevated [Mg2+]o, may be relevant to the apparent protective role of adequate Mg intake on vascular function in humans.

Animals↗
PubMed1997

Mg2+ modulates membrane lipids in vascular smooth muscle: a link to atherogenesis.

Epidemiological studies associate low dietary magnesium intake with an increased incidence of ischemic heart disease and sudden cardiac death. We have used proton-magnetic resonance (1H-NMR) techniques and Mg2+-selective electrodes to monitor changes in lipid extracts of aortic and cerebrovascular smooth muscle as extracellular ionized magnesium ion concentration ([Mg2+]o) is lowered. We have found that, within the pathophysiological range of Mg2+ concentrations, fatty acid chain length and double bond content are progressively reduced as [Mg2+]o is lowered. In contrast, the plasmalogen content is progressively increased. A concomitant decrease in fatty acid chain length and double bonds indicates oxidation of double bonds resulting in truncation of the fatty acids. A decrease in lipid oxidation in the presence of elevated Mg2+ could contribute to the apparent protective role of increased Mg2+ intake on vascular function in humans.

Animals↗
PubMed1997

Progesterone binding to plasma membrane and cytosol receptors in the amphibian oocyte.

We have found a single class of progesterone binding sites at the amphibian oocyte plasma membrane, whereas two progesterone receptor forms, similar to those in chick and human, are present in the cytosol. In this study both plasma membranes and 105,000 x g cytosol from Rana pipiens oocytes were photoaffinity labeled with the synthetic progestin [3H]R5020. SDS-polyacrylamide gel electrophoresis of the photolabeled proteins in the oocyte cytosol indicate that the two forms have molecular weights essentially identical to that found for human breast tissue and chick oviduct, i.e., 80 and 110 kDa, and that the forms were present in approximately equimolar ratios. In contrast, the plasma membrane form is present as a single 110 kDa species and accounts for at least 50% of the total 110 kDa species. The presence of large amounts of the 110 kDa protein in both membrane and cytosol suggests that the plasma membrane receptor may not be unique, and that the 110 kDa form may function both in membrane and cytosol and/or that part of the cytosolic 110 kDa form represents progesterone receptor in the process of being transported to or from the plasma membrane.

Animals↗
PubMed1997

Inhibitory effects of copper-aspirin complex on platelet aggregation.

AIM: To study the inhibitory effects of copper-aspirin complex (CuAsp) on platelet aggregation. METHODS: With adenosine diphosphate the effects of CuAsp on platelet aggregation in vitro or in vivo were investigated. Radioimmunoassay and fluorophotometry were used to measure thromboxane B2 (TXB2) generation from platelets, the levels of TXB2 and of 6-keto-PGF1 alpha in plasma and the platelet serotonin release reaction. RESULTS: In vitro, CuAsp inhibited arachidonic acid (AA)-induced aggregation (IC50 = 17 mumol.L-1, 95% confidence limits: 9-33 mumol.L-1), the release of 5-HT (IC50 = 19 mumol.L-1, 95% confidence limits: 10-30 mumol.L-1), and TXB2 generation from platelets (P < 0.05). CuAsp 10 mg.kg-1 i.g. selectively inhibited AA-induced aggregation, and increased the 6-keto-PGF1 alpha concentration in plasma while decreased that of TXB2. CONCLUSION: CuAsp, in vitro or in vivo, shows more potent inhibitory effects on AA-induced aggregation than aspirin (Asp), related to the inhibition of platelet cyclooxygenase and the release of active substances from platelets.

6-Ketoprostaglandin F1 alpha↗
PubMed1996

Progesterone triggers the rapid activation of phospholipase D in the amphibian oocyte plasma membrane when initiating the G2/M transition.

Previous reports indicate that, in the Rana pipiens oocyte, progesterone triggers a rapid rise in 1,2-diacylglycerol (DAG) derived from phosphatidylcholine (PC) in the plasma membranes. This DAG transient, which appears and is terminated within 60-90 s, is derived both from a phospholipase which we assumed to be phospholipase C and from sphingomyelin (SM) synthase. We now find that progesterone stimulates PC and DAG turnover primarily via the phospholipase D (PLD) and phosphatidic acid phosphohydrolase (PAP) pathways as well as via the SM-ceramide pathway. Rana oocytes were prelabeled with [3H]choline chloride under conditions in which about 70% is incorporated into PC of the plasma membrane of the intact oocyte or with [3H]lysoplatelet activating factor (1-O-octadecyl-sn-glycero-3-phosphocholine, lysoPAF) which is selectively incorporated into plasma membrane PC. Progesterone induced the release of [3H]choline from intact oocytes into the medium within 60-90 s. This choline release was dose-dependent and was not inhibited by a putative PC-specific phospholipase C inhibitor, D609. Progesterone also induced a transient rise in [3H]lysoPAF-derived [3H]DAG within 1-2 min followed by a rise in [3H]PA. In the presence of 20 mM ethanol, progesterone stimulated formation of [3H]lysoPAF-derived phosphatidylethanol, indicating progesterone activation of PC-specific PLD and concomitant formation of PA. A DGK inhibitor (D102) reduced the level of [3H]PA, produced a sustained rise in [3H]DAG and was a weak inducer of meiosis in oocytes not exposed to progesterone. A PA phosphohydrolase inhibitor (propranolol) elevated [3H]PA and completely inhibited the progesterone-induced rise in DAG. Progesterone thus acts at oocyte plasma membrane receptors to release PC-derived DAG via both SM synthase and PC-PLD. The duration of the DAG signal is regulated by the coordinate action of DGK and PAP.

Animals↗
PubMed1994

Progesterone-induced phospholipid N-methylation and sphingomyelin synthesis in the amphibian oocyte plasma membrane: a second source of the 1,2-diacylglycerol second messenger associated with the G2/M transition.

The effects of progesterone and GTP gamma S on phospholipid N-methylation and sphingomyelin synthesis were studied in plasma-vitelline membranes isolated from amphibian (Rana pipiens) oocytes. Plasma-vitelline membranes were preincubated with S-adenosyl-L-[methyl-3H]methionine for 2 min at 20 degrees C and total phospholipids extracted at 0, 15, 30 and 60 s after addition of progesterone and/or GTP gamma S. Progesterone levels (3 microM) that induce meiosis in the intact oocyte stimulated [3H-methyl]incorporation into phosphatidylmonomethylethanolamine (PME) 9-10-fold over the first 60 s, with smaller increases in phosphatidyldimethylethanolamine (PDE) and phosphatidylcholine (PC). [methyl-3H] labeling of sphingomyelin (SM) rises after 30 s, approaching that of [methyl-3H]PME by 60 s. 17 beta-Estradiol, a noninducer of meiosis, was inactive. When oocytes were prelabeled with [3H]palmitic acid, it was found that a fall in [3H]ceramide coincides with the transient increase in [3H]SM, indicating that the end product of N-methylation (PC) undergoes a transfer reaction with ceramide to form SM and 1,2-DG. GTP gamma S levels previously reported to stimulate PC-specific phospholipase C activity in oocyte plasma membranes (5 microM) also stimulated both [methyl-3H]PME and [methyl-3H]SM formation. An inhibitor of phospholipid N-methylation, 2-(methyl-amino)ethanol, blocked stimulation of [methyl-3H]SM synthesis by both progesterone and GTP gamma S as well as induction of meiosis by progesterone. Progesterone thus acts at the oocyte plasma membrane to stimulate PE N-methyltransferase and SM synthase. The finding that GTP gamma S mimics progesterone suggests that N-methyltransferase is mediated by G-protein(s). The transient increase in 1,2-DG which we had previously reported to occur within 1-2 min following progesterone stimulation of the Rana oocyte appears to arise from PC by two different pathways: SM synthesis and hydrolysis of PC by phospholipase C.

Animals↗
PubMed1994

[Effect of protopine on rabbit platelet function].

Protopine (Pro) inhibited dose-dependently rabbit platelet aggregation induced by ADP, arachidonic acid (AA), collagen, or aggregoserpentin of Trimeresurus mucrosquamatus venom (TMVA) in vitro. Their IC50 were 25.3, 30.5, 46.9, 33.4 mumol.L-1, respectively. Pro 10, 20 mg.kg-1 iv also inhibited the platelet aggregation induced by these inducers. The effects (maximal at 5 min) lasted 1 h. By using fluorophotometry and RIA, it was seen that Pro suppressed the release of 5-HT from platelets during aggregation induced by collagen, AA, or TMVM in vitro. Pro did not block the formation of thromboxane A2 during aggregation induced by AA and did not increase the content of cAMP in rabbit platelet, but increased the content of cGMP in rabbit platelets. The antiplatelet effect of Pro may be related to an increase cGMP in rabbit platelets and the suppression of the release of the active substances from platelets.

Alkaloids↗
PubMed1993

Prevalence, infectivity, and risk factor analysis of hepatitis C virus infection in prostitutes.

A population of 622 prostitutes in Taiwan was tested for antibodies to the hepatitis C virus (anti-HCV) using a synthetic peptide assay composed of representative determinants from capsid and nonstructural (NS) viral proteins. Seventy-four (12%) were positive and the remaining 548 (88%) were negative. Seventy-nine samples were retested by a second-generation anti-HCV assay composed of recombinant capsid and NS proteins of HCV. Both assays had a nearly perfect agreement (Kappa value = 0.91). Of the positive cases, 31% were positive for reactivity to capsid only. Most (60/74, 81%) of the cases positive for synthetic peptide assay were HCV RNA positive, indicating potential infectivity. On the basis of the results of synthetic peptide assay, univariate analysis showed that history of paid sex for longer than 6 months, blood transfusion, acupuncture, intravenous drug abuse, and age over 20 years were significant risk factors of HCV infection (P < 0.01). Elevated alanine aminotransferase levels (> 40 U/L) were positively associated with anti-HCV, while the presence of serum hepatitis B surface antigen was a negatively associated factor. Multivariate analysis revealed that history of paid sex for longer than 6 months and blood transfusion were positively associated with anti-HCV (P < 0.001). The latter only accounted for less than one fifth of the HCV-infected prostitutes. This study indicates strongly that sexual transmission is an important route for HCV infection in prostitutes. This risk group may spread HCV to other populations as a sexually transmitted disease.

Adolescent↗
PubMed1993

Steroid action at the plasma membrane: progesterone stimulation of phosphatidylcholine-specific phospholipase C following release of the prophase block in amphibian oocytes.

Progesterone, acting at the amphibian oocyte plasma membrane, triggers the progression of the prophase oocyte nucleus through the first meiotic metaphase. We previously reported a transient increase in 1,2-diacylglycerol (1,2-DG) within the first 1-2 min after exposure of Rana pipiens oocytes to progesterone. We have now investigated the source of the 1,2-DG, using this highly synchronous oocyte population. Phospholipid pools of intact prophase-arrested oocytes were labeled with [3H]glycerol, [methyl-3H]choline chloride or 1-O-[3H]octadecyl-sn-glycero-3-phosphocholine (lyso platelet activating factor, lysoPAF). [3H]LysoPAF is selectively taken up into the plasma membrane of the intact oocyte and esterified to form the [3H]alkyl-analogue of phosphatidylcholine (PC). Intact oocytes and/or isolated plasma membranes were then stimulated with progesterone and the changes in [3H]DG, [methyl-3H]phosphocholine and [3H]phospholipids were monitored as a function of time. Progesterone induced a transient increase in [3H]glycerol-derived DG, [methyl-3H]phosphocholine and [3H]alkyl-2-acylglycerol from [3H]alkyl-PC within the first 2 min, indicating activation of a PC-specific phospholipase C. Different pulse-labeling conditions indicate a biphasic rise in [3H]DG from [3H]glycerol-labeled oocytes; the first rise (1-2 min) when phospholipid labeling in the plasma membrane is enriched followed by an approximately 3-fold larger rise at 5-15 min when phospholipids of intracellular membranes are preferentially labeled. An early transient increase in [3H]DG or [3H]alkyl-2-acylglycerol was also seen when progesterone and/or guanosine 5'-O-(3-thiotriphosphate) (GTP-gamma-S) were added to isolated plasma-vitelline membranes prepared from oocytes prelabeled with either [3H]glycerol or [3H]lysoPAF. Progesterone thus appears to activate a G-protein-linked PC-specific phospholipase C in the oocyte plasma membrane which is followed by much larger DG release from intracellular membranes. The transient character of the hydrolysis suggests that this may represent a mechanism for transducing a membrane event into a meiotic signal.

Animals↗
PubMed1979

Catabolic effects of adrenaline and angiotensin II in the perfused liver of normal and genetically obese (ob/ob) mice.

1. Rapid effects of hormones on the metabolism of glycogen and fatty acids were studied in the perfused liver of normal and genetically obese (ob/ob) mice. 2. In livers from normal and obese mice adrenaline and angiotensin II stimulated glycogenolysis. 3. These hormones inhibited the synthesis de novo of long-chain fatty acids in livers from normal mice, but not in livers from obese mice. 4. The proportion of acetyl-CoA carboxylase in the active form was decreased by adrenaline but not by angiotensin II in livers from obese mice. 5. The potency of hormone effects on liver suggests that they could occur in the intact animal. 6. The results add to the evidence that hepatic fatty acid synthesis in genetically obese (ob/ob) mice is irreversibly resistant to inhibition by a range of hormones. Such resistance could be of primary significance in the pathogenesis of the obesity.

Acetyl-CoA Carboxylase↗
PubMed1978

Effects of glucagon and insulin on fatty acid synthesis and glycogen degradation in the perfused liver of normal and genetically obese (ob/ob) mice.

1. Rapid effects of hormones on glycogen metabolism and fatty acid synthesis in the perfused liver of the mouse were studied. 2. In perfusions lasting 2h, of livers from normal mice, glucagon in successive doses, each producing concentrations of 10(-10) or 10(-9)M, inhibited fatty acid and cholesterol synthesis. In perfusions lasting 40--50 min, in which medium was not recycled, inhibition of fatty acid synthesis was only observed with glucagon at concentrations greater than 10(-9)M. This concentration was about two orders of magnitude higher than that required for the stimulation of glycogen breakdown. Glucagon did not inhibit the activity of acetyl-CoA carboxylase, assayed 10 or 20 min after addition of glucagon (10(-9) or 10(-10)M). It is proposed that the action of glucagon on hepatic fatty acid biosynthesis could be secondary in time to depletion of glycogen. Insulin prevented the effect of glucagon (10(-10)M) on glycogenolysis, but not that of vasopressin. 3. Livers of genetically obese (ob/ob) mice did not show significant inhibition of lipid biosynthesis in response to glucagon, although there was normal acceleration of glycogen breakdown. This resistance to glucagon action was not reversed by food deprivation. Livers of obese mice exhibited resistance to the counteraction by insulin of glucagon-stimulated glycogenolysis, which was reversible by partial food deprivation.

Acetyl-CoA Carboxylase↗
PubMed1976

Resistance to hepatic action of vasopressin in genetically obese (ob/ob) mice.

1. Fatty acid synthesis, measured in the perfused liver of genetically obese (ob/ob) mice with 3H2O or [14C]actate, did not show the inhibition by [8-arginine]vasopressin (antidiuretic hormone) that is observed in livers from normal mice. 2. Hepatic glycogen breakdown in obese mice was stimuulated by vasopressin, but not as extensively as in lean mice. 3. If obese mice received a restricted amount of food, then fatty acid synthesis still did not respond to vasopressin, but glycogen breakdown was fully stimulated. 4. Cholesterol synthesis was not inhibited by vasopressin in livers from obese mice. 5. Vasopressin inhibited fatty acid synthesis in intact lean mice, but not in obese animals. 6. These results suggest that genetic obesity could be due to an inborn error within the mechanisms (other than adenylate cyclase) which mediate responses to extracellular effectors.

Animals↗