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X Y Ma

Publications and source records attributed to X Y Ma.

At least 19 recordsLinked to original sources

Observation of two new N* peaks in J/psi-->ppi-n and ppi+n decays.

The decay J/psi-->NNpi provides an effective isospin 1/2 filter for the piN system due to isospin conservation. Using 58x10(6) J/psi decays collected with the Beijing Electromagnetic Spectrometer at the Beijing Electron Positron Collider, more than 100 thousand J/psi-->ppi-n+c.c. events are obtained. Besides the two well-known N* peaks at around 1500 MeV/c2 and 1670 MeV/c2, there are two new, clear N* peaks in the ppi invariant mass spectrum around 1360 MeV/c2 and 2030 MeV/c2 with statistical significance of 11sigma and 13sigma, respectively. We identify these as the first direct observation of the N*(1440) peak and a long-sought missing N* peak above 2 GeV/c2 in the piN invariant mass spectrum.

Journal Article↗

Observation of a threshold enhancement in the plambda invariant-mass spectrum.

An enhancement near the m(p)+M(Lambda) mass threshold is observed in the combined pLambda and pLambda invariant-mass spectrum from J/psi-->pK(-)Lambda;+c.c. decays. It can be fit with an S-wave Breit-Wigner resonance with a mass m=2075+/-12(stat)+/-5(syst) MeV and a width of Gamma=90+/-35(stat)+/-9(syst) MeV; it can also be fit with a P-wave Breit-Wigner resonance. Evidence for a similar enhancement is also observed in psi(')-->pK(-)Lambda;+c.c. decays. The analysis is based on samples of 5.8x10(7)J/psi and 1.4x10(7)psi(') decays accumulated in the BES II detector at the Beijing Electron-Positron Collider.

Journal Article↗

Observation of the decay psi(2S)-->K0SK0L.

The decay psi(2S)-->K(0)(S)K(0)(L) is observed using psi(2S) data collected with the Beijing Spectrometer at the Beijing Electron-Positron Collider; the branching fraction is determined to be B(psi(2S)-->K(0)(S)K(0)(L))=(5.24+/-0.47+/-0.48)x10(-5). Compared with J/psi-->K(0)(S)K(0)(L), the psi(2S) branching fraction is enhanced relative to the prediction of the perturbative QCD "12%" rule. The result, together with the branching fractions of psi(2S) decays to other pseudoscalar meson pairs (pi(+)pi(-) and K+K-), is used to investigate the relative phase between the three-gluon and the one-photon annihilation amplitudes of psi(2S) decays.

Journal Article↗

The increase in levels of interferon-inducible proteins p202a and p202b and RNA-dependent protein kinase (PKR) during myoblast differentiation is due to transactivation by MyoD: their tissue distribution in uninfected mice does not depend on interferons.

The murine 200 family proteins p202a, p202b, and p204, and also RNA-dependent protein kinase (PKR) are inducible by interferons (IFNs). p202a, p202b, and p204 modulate the activity of a large variety of transcription factors and also are involved in muscle differentiation. PKR is a multifunctional serine/threonine kinase, which is involved in antiviral defense and cell growth control and in the response to various stress signals. We reported earlier that the level of p204 increases during cultured C2C12 myoblast differentiation to myotubes in consequence of transactivation by the skeletal muscle-specific MyoD protein. The levels of p202a, p202b, and PKR also increase during the differentiation. We report here that these increased protein levels also are due to the transactivation of their genes by MyoD. This is made possible by the occurrence in each of these genes of at least six E boxes, which are recognition sites for MyoD. We also show that the distribution of the p204, p202a, p202b, and PKR proteins in five tissues of adult C129 mice is the same in wild-type mice and mice lacking the IFN-alpha, IFN-beta, and IFN-gamma receptors. This indicates that the synthesis and distribution of these proteins in uninfected adult mice are not affected by endogenous IFNs.

Animals↗

Superoxide-mediated early oxidation and activation of ASK1 are important for initiating methylglyoxal-induced apoptosis process.

Methylglyoxal (MG) is a physiological metabolite, but it is known to be toxic, inducing stress and causing apoptosis. Our previous studies demonstrated that MG induced apoptosis in Jurkat cells by activating the c-Jun N-terminal kinase (JNK) signal transduction pathway, which induced an obvious decrease in mitochondrial membrane potential, followed by caspase-3 activation. Here, we observed that MG-induced apoptosis was associated with both rapid production of superoxide anion (O(2)(-)) followed by a marked increase in ROS and striking and temporal activation of ASK1. Overexpression of wild-type ASK1 could enhance the rate of apoptosis induced by MG, whereas the expression of the kinase-inactive form of ASK1 notably prevented cells from MG-induced death. NAC and PDTC blocked the activation of ASK1 and MG-induced apoptosis completely. Moreover, nonthiol antioxidants SOD-mimic MnTBAP and catalase together obviously inhibited MG-induced ASK1 activation and apoptosis induction. Correspondingly, MG-mediated ASK1 activation was enhanced by diethyldithiocarbamate (DDC). Addition of antioxidant into the culture of cells at a later stage (4-8 h after the initial MG treatment) failed to prevent their death. These results suggest that activating ASK1 at the early stage linking to production of O(2)(-) is crucial for subsequent progression of apoptosis in MG-treated Jurkat cells.

Acetylcysteine↗

Effects of human tissue plasminogen gene transfer on allograft coronary atherosclerosis.

BACKGROUND: Transplant coronary atherosclerosis is a major limiting factor to successful long-term cardiac transplantation. The depletion of tissue plasminogen activator (tPA) in the arteriolar smooth muscle cells has been associated with a higher incidence of accelerated graft atherosclerosis. In vivo overexpression of tPA may inhibit accelerated graft atherosclerosis and improve the long-term results of heart transplantation. We evaluated the feasibility, distribution, and effects of intracoronary transfer of the human tPA (htPA) gene in a rabbit heterotopic cardiac transplant model, using a novel cationic liposome compound designed for improved delivery to vascular endothelium. METHODS: Human tPA cDNA under the control of the SV40 promoter (100 microg) was complexed with the novel cationic liposome (+/-)-N-(3-aminopropyl)-N,N-dimethyl-2,3-bis(dodecyloxy)-1-propanaminium bromide (GAP: DLRIE) (50 microg), and delivered ex vivo to the donor heart by slow intracoronary infusion. Control hearts received an "empty" liposome preparation. Grafts were then implanted into recipient rabbits in the heterotopic cervical position. For the analysis of gene expression, beating donor hearts were collected at 4 days. To examine the effects of htPA expression on graft atherosclerosis, animals received a 0.5% cholesterol diet for 30 days posttransplant, as well as 10 mg/kg cyclosporine A daily. Beating hearts were collected at 30 days posttransplant and analyzed for the development of transplant atherosclerosis by image analysis. RESULTS: Northern blot analysis for the htPA messenger RNA (mRNA) transcripts showed significantly higher counts in hearts receiving the htPA gene as compared to controls. The distribution of these transcripts favored the left ventricle (LV) and septal regions over the right ventricle (RV). Scintillation analysis of specimens stained by immunoflourescence showed expression of htPA throughout the perivascular myocardium that was significantly higher in grafts transduced with the htPA gene than in control or native hearts. Expression in the vascular wall was also significantly enhanced. Scintillation counts per x 200 field were 262 +/- 145 in htPA-transduced hearts and 20 +/- 27 in controls (p = 0.001), and mean luminescence was 83.7 +/- 12.5 in htPA-transduced hearts and 62.9 +/- 12.8 in controls (p = 0.01). Intimal hyperplasia was assessed by mean percent luminal stenosis in small- and medium-sized arteries and was 31.12 +/- 23.5% in htPA-transduced hearts and 86.59 +/- 17.5% in control hearts (p < 0.0001). These results demonstrate that expression of the htPA gene can be induced by ex vivo intracoronary gene transfer at the time of allograft preservation. Liposome-mediated delivery of the htPA gene at the time of transplantation results in significant early transgene expression, and significantly inhibits the development of graft coronary atherosclerosis.

Animals↗

[The influence of interleukin-1 on nerve growth factor secretion in newborn rat astrocytes in vitro].

OBJECTIVE: To study the nerve growth factor (NGF) expression and the influence of IL-1 alpha or IL-1 beta on NGF secretion in newborn rat astrocytes. METHODS: Astrocytes obtained from the brain cortex of newborn rats were cultured and purified, and they were divided into three groups, experimental, control and blank groups. IL-1 alpha or IL-1 beta were added into the experimental group with 25, 50 and 100 U/ml, each group was cultured for 24, 48 or 72 hours, and then the NGF contents in cultured astrocytes suspension media were measured by a two-cite enzymelinked immunoserbent assay (ELISA). RESULTS: Astrocytes could secret NGF by themselves and each concentration of IL-1 alpha or IL-1 beta media at any testing time could enhance NGF secreting in newborn rat astrocytes in certain degrees. The effects of IL-1 beta were stronger than IL-1 alpha, the strongest effect in the unit time was observed in IL-1 beta with 50 U/ml for 24 hours. CONCLUSION: Astrocytes can express NGF, and IL-1 alpha or IL-1 beta can enhance the NGF expression in newborn rat astrocytes.

Animals↗

Experimental studies on small hooks preceding large hooks in the growth and development of Taenia solium metacestodes.

In the present study, we have determined the growth and development pattern of rostellar hooklets of Taenia solium cysticerci (Zhengzhou and Harbin strains) in three pigs (1 SEM and 2 L-SEM strains) 89-196 days post experimental infection. A total of 3,675 cysticerci were collected from 3 pigs, 3,007 (82%) of 3,675 cysticerci were evaginated by enzyme method. 439 (15%) evaginated cysticerci were carefully examined and measured after dehydration, staining, and mounting on microscopic slides. Among 439 cysticerci, 234 (53%) had pair rostellar hooks, 88 (20%) with unpair hooks, 60 (14%) only small (outer row) hooks, and 57 (13%) no hooks including 34 hooks were completely dropped and 23 no hooks developed. The number ranged from 10 to 17 pairs for pair hooks and 1 to 29 for unpair ones. The length and width of rostallar hooks on the scolex of cysticerci were usually larger in the pig with longer infection time. Moreover, cysticerci with pair and unpair rostellar hooks had only small hooks and no hooks were present on their scolices. However, cysticerci with only large (inner row) hooks were not found. These findings indicate that the growth and development of small hooks precedes that of the large hooks in the formation of the two-row pattern rostellar hook in Cysticercus cellulosae.

Animals↗

Studies on abnormality of metacestodes and adult worms of Taenia solium and Taenia saginata asiatica in rodents and pigs.

Abnormalities are not uncommon in Taenia saginata and T. solium. After examining 328 mature proglottids from 2 adult worms from two experimentally infected hamsters, 13 (4.0%) were found to have no genital pore but with numerous testes and several vas efferents; 1 (0.3%) one genital pore with one reproductive system; 12 (3.7%) one on each side with two sets of reproductive system; 17 (5.2%) two on one side with 2 sets of reproductive system; 8 (2.4%) one on one side and two on the other side with 3 sets of reproductive system; 2 (0.6%) two on each side with 4 sets of reproductive system; 4 (1.2%) three on one side with 3 sets of reproductive system, and 4 one on one side and three on the other side with 4 sets of reproductive system. Nine evaginated abnormal cysticerci of T. s. asiatica from three experimentally infected SCID mice each had two protoscoleces and a big bladder. From two experimentally infected pigs, one abnormal cysticercus was observed to have two invaginated canals each in one end. Another one had a neck-band behind the scolex and a big bladder. This paper is not only the first report of abnormality of T. solium from hamster but also the first one of abnormal cysticerci of T. s. asiatica from pigs and mice.

Animals↗

The interferon- and differentiation-inducible p202a protein inhibits the transcriptional activity of c-Myc by blocking its association with Max.

p202a is a murine protein that is induced during the fusion of myoblasts to myotubes and can also be induced by interferon. Even 2-3-fold overexpression of p202a in cells retards proliferation. p202a was shown to modulate transcription by binding, and inhibiting the activity of several transcription factors including c-Fos, c-Jun, AP-2, E2F1, E2F4, NF-kappaB, MyoD, and myogenin. Here we report that p202a also bound the c-Myc protein in vitro and in vivo; the C-terminal p202a b segment bound the C-terminal basic region helix-loop-helix-leucine zipper (bHLHLZ) region of c-Myc. The transfection of a p202a expression plasmid inhibited the c-Myc-dependent expression of reporter plasmids in transient assays; moreover, overexpression of p202a in stable cell lines decreased the endogenous levels of mRNAs whose expression is driven by c-Myc. These effects of p202a are consistent with our finding that the binding of p202a to c-Myc inhibited the binding of c-Myc to Max in vitro and in vivo. p202a also inhibited the c-Myc-induced anchorage-independent growth and apoptosis of Rat-1 cells. The inhibition of c-Myc-dependent transcription, proliferation, and apoptosis by p202a is in line with the involvement of p202a in differentiation.

Animals↗

Preliminary study of oral polylactide microcapsulated insulin in vitro and in vivo.

AIM: Although the oral route for insulin delivery is the most convenient, directly administered oral insulin is degraded by proteolytic enzymes in the gastrointestinal (GI) tract. Polylactide was prepared in order to microcapsulate the insulin to avoid the enzymes in the GI. The physical characteristics and therapeutic possibilities of polylactide microcapsulated insulin (PLA-MCI) were studied in vivo and in vitro. METHODS: PLA-MCI was prepared by the two-step method of emulsion and solvent extraction. Its morphologic character was observed by scanning electron microscopy (SEM). The insulin release profile was determined in vitro by insulin measurement and in vivo by blood glucose measurement after the force-feeding of 66 diabetic rats. RESULTS: When the microcapsule was spherical in shape (diameter 1.5-2.0 microm) the entrapment efficiency of insulin was 90% and the loading rate was 10% (W/W). The PLA-MCI (which contained 3.0 units of insulin/mg of PLA) had peak release rates of 65-74% over 6-8 h in phosphate buffer. The same dose of PLA-MCI (insulin 2.5 mg) led to decreased responses (from 28% to 68% of control blood glucose levels) in the level of blood glucose in 32 rats which had not fasted after they had been force-fed. When 1.2, 1.8, 2.2 and 3.0 mg of insulin + PLA-MCI was administered to eight diabetic rats, their blood glucose levels decreased by 28%, 36%, 54% and 78%, respectively. CONCLUSIONS: PLA microcapsules are capable of protecting insulin from degradation by the proteolytic enzymes in the GI and of alleviating hyperglycaemia for a prolonged period of time in diabetic rats. It may therefore be considered as a new carrier for oral insulin.

Administration, Oral↗

Antagonistic effect of 3,6-dimethamidodibenzopyriodonium gluconate on lipid peroxidation in cerebral cortical neuronal cultures and rat brains during focal cerebral ischemia reperfusion.

AIM: To study 3,6-dimethamidodibenzopyriodonium gluconate (I-93) antagonistic effects on lipid peroxidation in cerebral cortical neuronal cultures and rat brains during focal cerebral ischemia-reperfusion. METHODS: Cerebral cortical neurons were cultured and rat focal cerebral ischemia-reperfusion model was established by reversible middle cerebral artery occlusion (MCAO) without craniectomy. The efflux of lactate dehydrogenase (LDH) from neurons, content of malondialdehyde (MDA) in neurons and brain homogenate, activity of superoxide dismutase (SOD) in brain homogenate, and index of cerebral edema as well as brain morphology were investigated. RESULTS: I-93 10-40 mumol.L-1 concentration-dependently inhibited efflux of LDH and elevated levels of MDA induced by addition of H2O2(10 mumol.L-1) in vitro. I-93 0.5 mg.kg-1 improved the cerebral morphology, reduced brain edema, decreased MDA content, and enhanced SOD activity in brain homogenate. CONCLUSION: I-93 protects neurons from H2O2-induced neurotoxicity and ischemia-reperfusion mediated damage by increasing the activity of antioxidant enzymes and suppressing the generation of lipid peroxides.

Animals↗

[Effects of intraventricular injection of adenosine on renal sympathetic nerve activity].

The effects of intraventricular injection of adenosine and its analogues on renal sympathetic nerve activity (RSNA) were examined in sinoaortic denervated and vagotomized anesthetized rats. In response to intraventricular bolus injection of adenosine, RSNA was increased by 41.9 +/- 6.08% (P < 0.001), mean arterial pressure (MAP) was initially increased by 1.39 +/- 0.19 kPa (P < 0.001) and subsequently decreased by 3.74 +/- 0.64 kPa (P < 0.001), and heart rate (HR) was reduced by 95 +/- 14 bpm (P < 0.001). To determine the adenosine-receptor subtype which mediates the response of RSNA to adenosine, we used selective A1-receptor agonist (R-PIA) and A2-receptor agonist (NECA) and found that MAP and HR were reduced by R-PIA and NECA. The effects lasted significantly longer than those of adenosine. R-PIA induced an increase in RSNA by 31.6 +/- 5.21% (P < 0.001), while NECA showed no effect on RSNA. The renal sympathoexcitatory response to intraventricular injection of adenosine was completely inhibited by pretreatment with a selective A1-receptor antagonist (DPCPX). Following the bilateral stellate ganglionectomy, intraventricular injection of adenosine failed to induce the increase in RSNA. The results indicate that adenosine may activate cardiac sympathetic afferents through A1-receptor, resulting in a reflex augmentation of RSNA.

Adenosine↗

[Expression of c-fos in spinal cord, medulla oblongata and thalamus following epicardial application of adenosine].

Effects of epicardial application of adenosine on the expression of c-fos proto-oncogene in spinal cord, medulla oblongata and thalamus were examined in 12 sinoaortic denervated and vagotomized anesthetized rats. The results showed that following epicardial application of adenosine the Fos-like protein immunoreactive (FLI) neurons were remarkably increased in the dorsal horn of T3 spinal segment, nucleus paragigantocellularis lateralis (PGL) of medulla oblongata, ventral postero-lateral thalamic nucleus (VPL), posterior thalamic nucleus (Po), parafascicular thalamic nucleus (PF) and centrolateral thalamic nucleus (CL), while the blood pressure and heart rate were not affected. Only a few FLI neurons were found in the vehicle-control rats. The results indicate that epicardial application of adenosine may activate the pain-related neurons in spinal cord, medulla oblongata and thalamus.

Adenosine↗

[Effects of intraventricular and epicardial application of adenosine on electrical activity of medullary PGL neurons].

The effects of intraventricular injection and epicardial application of adenosine on spontaneous electrical activity of nucleus paragigantocellularis lateralis (PGL) neurons in rostral ventrolateral medulla (RVLM) were examined in 35 anesthetized rats with sinoaortic denervation and vagotomy. The results obtained were as follows: (1) The spontaneous discharge of 121 PGL neurons (mean discharge rate: 22.5 +/- 1.9 spikes/s) were recorded in 35 rats. (2) In response to intraventricular injection of adenosine (0.5 mumol/kg), mean arterial pressure (MAP) was initially increased by 1.7 +/- 0.2 kPa(P < 0.001) and subsequently decreased by 4.6 +/- 0.5 kPa(P < 0.001), while the heart rate (HR) was decreased by 126.5 +/- 12.3 bpm (P < 0.001). Of 35 PGL spontaneous discharge units responsive to intraventricular injection of adenosine, 30 showed an average increase from 21.9 +/- 2.6 to 29.2 +/- 3.4 spikes/s (P < 0.001), 3 with no change, while 2 with a decrease. (3) Following epicardial application of 20 mmol/L adenosine, the BP and HR were not significantly changed, while the spontaneous discharge of 22 PGL neurons were increased from 18.8 +/- 1.9 to 26.9 +/- 2.8 spikes/s (P < 0.001), and that of 3 neurons was not changed. (4) The excitatory response of PGL neurons to intraventricular injection or epicardial application of adenosine was completely inhibited by pretreatment with selective adenosine A1-receptor antagonist 8-cyclopentyl-1, 3-dipropylxanthine (DPCPX, 500 micrograms/kg). (5) Following epicardial application of phenol or bilateral stellate ganglionectomy, adenosine failed to affect the activity of PGL neurons. The results obtained indicate that adenosine may stimulate cardiac sympathetic afferents through adenosine A1-receptor, thereby resulting in the activation of PGL neurons.

Action Potentials↗

Effects of vitamin E on the blastogenic response of splenocytes and lipofuscin contents in the hearts and brains of aged mice.

Semipurified diets containing 30 or 500 ppm of dl-alpha-tocopherol (VE) were fed for 12 weeks to young (3-month-old) and old (20-month-old) Swiss mice. We measured the blastogenic response of splenocytes, the serum VE, and the lipofuscin levels in brains and hearts. We found that old mice fed with 500 ppm VE diet had a significantly higher serum VE level and blastogenic response of splenocytes to concanavalin-A (ConA) and lipopolysaccharide (LPS) than those fed with 30 ppm VE diet (p < 0.01). However, the lipofuscin level in the brains and hearts of aged mice declined substantially with the VE supplementation (heart: p < 0.001, brain: p < 0.05). Furthermore, the effects of dietary VE on the serum VE and tissue lipofuscin content in aged mice were much more obvious than in the young animals.

Aging↗