Biomedical subjects

W Gai

Publications and source records attributed to W Gai.

14 recordsLinked to original sources

PubMed2004

Observation of multipactor in an alumina-based dielectric-loaded accelerating structure.

We report a new regime of single-surface multipactor that was observed during high-power testing of an 11.424-GHz alumina-based dielectric-loaded accelerating structure. Previous experimental observations of single-surface multipactor on a dielectric occurred in cases for which the rf electric field was tangential and the rf power flow was normal to the dielectric surface (such as on rf windows) and found that the fraction of power absorbed at saturation is approximately 1%, independent of the incident power. In this new regime, in which strong normal and tangential rf electric fields are present and the power flow is parallel to the surface, the fraction of power absorbed at saturation is an increasing function of the incident power, and more than half of the incident power can be absorbed. A simple model is presented to explain the experimental results.

Journal Article↗

PubMed2004

Differential target molecules for toxicity induced by streptozotocin and alloxan in pancreatic islets of mice in vitro.

Streptozotocin (STZ) and alloxan (ALX) are potent diabetogens in different species of laboratory animals. Here, we describe differential in vitro effects of STZ and ALX on beta-cell molecules that are essential for glucose transport and metabolism, the glucose transporter 2 (GLUT2) and glucokinase (GK), respectively. Incubation of isolated pancreatic islets of C57 BL/6 mice with STZ or ALX for 30 min resulted in a concentration-dependent gradual loss of beta-cell function as determined by basal and D-glucose (D-G)-stimulated insulin release. ALX concentration-dependently reduced the mRNA expression of GLUT2 and GK and the effect on GLUT2 was more marked. STZ, in contrast, did not affect the mRNA expression of GLUT2 and GK, but concentration-dependently reduced the GLUT2 protein expression. Both STZ and ALX failed to affect the mRNA expression of proinsulin and of beta-actin. The deleterious effects of STZ and ALX were not due to beta-cell loss, because the total RNA yields and protein contents as well as the proinsulin mRNA expression in isolated islets of the differentially treated islets did not differ significantly from controls. Furthermore, islets that had been exposed to STZ or ALX responded to the non-glucose secretagogue arginine in a pattern comparable to that of solvent-treated cultures. When preincubating islet cultures with either D-G or its chemically closely related analogue 5-thio-D-glucose (5-T-G), different effects were obtained after treatment with either ALX or STZ. Thus, preincubation with 5-T-G protected the cultures from STZ-induced GLUT2 protein reduction, whereas D-G failed to do so. Preincubation with D-G, however, protected the cultures from ALX-induced reduction of GLUT2 and GK mRNA expression, whereas 5-T-G, at best, exerted a modest protection against ALX at a concentration of 1 mmol/l. Apparently, in vitro, GLUT2 protein is a key target molecule for STZ, while GLUT2 mRNA and GK mRNA are target molecules for ALX.

Alloxan↗

PubMed2001

Proteasomal activation mediates down-regulation of inositol 1,4,5-trisphosphate receptor and calcium mobilization in rat pancreatic islets.

Inositol 1,4,5-trisphosphate receptor (IP3R) protein levels in isolated rat pancreatic islets were investigated in response to carbachol (CCh) and sulfated cholecystokinin 26-33 amide stimulation. Within 2 h, CCh reduced IP3R-I protein levels by 22% and IP3R-II and -III levels to 65% or more below basal. Sulfated cholecystokinin 26-33 amide decreased the levels of IP3R-I, -II, and -III by 34%, 60%, and 66% below basal, respectively. The effect of CCh was concentration- and time-dependent, with a persistent decline in IP3R levels for up to 6 h after the onset of stimulation. CCh-pretreated islets also showed an inhibition of glucose-stimulated insulin secretion. Proteasome inhibition completely blocked the down-regulatory effects of CCh on IP3Rs and significantly increased the insulin secretory response to glucose stimulation in the presence of CCH: Islet stimulation by glucose, alpha-ketoisocaproic acid, and tolbutamide completely protected IP3Rs against the down-regulatory effects of CCH: 2-deoxyglucose and 3-O-methyl glucose failed to affect CCh-induced IP3R down-regulation. The protective effects of glucose on IP3R down-regulation were completely inhibited by the Ca(2+) channel-blocking agent nimodipine. Intracellular Ca(2+) ([Ca(2+)](i)) levels in Fura-2 (fluorescent Ca(2+) indicator)-loaded islets, in the absence of extracellular Ca(2+), increased in response to glucose stimulation; but in islets pretreated with CCh, glucose did not increase [Ca(2+)](i) above basal levels. However, in islets pretreated with CCh and the proteasomal inhibitor MG-132 (carbobenzoxyl-leucinyl-leucinyl-leucinyl-H), the glucose-stimulated increase in [Ca(2+)](i) was significantly higher than the change observed for glucose-stimulated [Ca(2+)](i) in the absence of MG-132. The results suggest that muscarinic receptor stimulation modulates IP3R protein levels in islets through a proteasomal activation pathway, and that down-regulation of IP3Rs has a profound effect on Ca(2+) mobilization in islets that may relate to insulin secretory responsiveness.

Animals↗

PubMed2000

Radio-frequency measurements of coherent transition and cherenkov radiation: implications for high-energy neutrino detection

We report on measurements of (11-18)-cm wavelength radio emission from interactions of 15.2 MeV pulsed electron bunches at the Argonne Wakefield Accelerator. The electrons were observed both in a configuration where they produced primarily transition radiation from an aluminum foil, and in a configuration designed for the electrons to produce Cherenkov radiation in a silica sand target. Our aim was to emulate the large electron excess expected to develop during an electromagnetic cascade initiated by an ultrahigh-energy particle. Such charge asymmetries are predicted to produce strong coherent radio pulses, which are the basis for several experiments to detect high-energy neutrinos from the showers they induce in Antarctic ice and in the lunar regolith. We detected coherent emission which we attribute both to transition and possibly Cherenkov radiation at different levels depending on the experimental conditions. We discuss implications for experiments relying on radio emission for detection of electromagnetic cascades produced by ultrahigh-energy neutrinos.

Journal Article↗

PubMed1999

Extensive axonal Lewy neurites in Parkinson's disease: a novel pathological feature revealed by alpha-synuclein immunocytochemistry.

Lewy bodies and coarse Lewy neurites are the pathological hallmarks of degenerating neurons in the brains of patients suffering from Parkinson's disease (PD). Recently, the presynaptic protein alpha-synuclein was shown to be a major component of Lewy bodies and Lewy neurites. This study demonstrates for the first time that extensive and thin alpha-synuclein-immunoreactive inclusions are present in the axonal processes of neurons.

Axons↗

PubMed1999

Interaction between terminal complement proteins C5b-7 and anionic phospholipids.

We have recently shown that C5b-6 binds to the erythrocyte membrane via an ionic interaction with sialic acid before the addition of C7 and subsequent membrane insertion. In this study we assessed the role of anionic lipids in the binding of the terminal complement proteins to the membrane and the efficiency of subsequent hemolysis. Human erythrocytes were modified by insertion of dipalmitoyl phosphatidylcholine (DPPC), dipalmitoyl phosphatidylserine (DPPS), dipalmitoyl phosphatidylethanolamine (DPPE), or dipalmitoyl phosphatidic acid (DPPA). Lipid incorporation and the hemolytic assays were done in the presence of 100 micromol/L sodium orthovanadate to prevent enzymatic redistribution of lipid. We found that the neutral lipids, DPPC and DPPE, did not affect C5b-7 uptake or hemolysis by C5b-9. In contrast, the two acidic phospholipids, DPPS and DPPA, caused a dose-dependent increase in both lysis and C5b-7 uptake. We conclude that the presence of anionic lipids on the exterior face of the membrane increases C5b-7 uptake and subsequent hemolysis. It is known that sickle cell erythrocytes have increased exposure of phosphatidylserine on their external face and are abnormally sensitive to lysis by C5b-9. The data presented here provide a plausible mechanism for this increased sensitivity.

1,2-Dipalmitoylphosphatidylcholine↗

PubMed1999

Wakefield excitation in multimode structures by a train of electron bunches.

We discuss wakefield excitation and propagation in dielectric structures, particularly concentrating on the case of multiple drive beam excitation in multimoded structures. We emphasize calculations of the energy loss of the drive beam train, the amplitude of the wakefield, and the relationship between power flow and stored energy in the dielectric wakefield device. We show that for a collinear multimode structure the amplitude of the wakefield generated by a bunch train is less than or equal to the wakefield generated by a single bunch of the same total charge. Furthermore, the transformer ratio R is shown to be always less than 2, even in the multiple drive beam case.

Journal Article↗

PubMed1996

Trk receptor alterations in Alzheimer's disease.

The expression of trk receptors in postmortem normal, Huntington's disease and Alzheimer's disease human brains was investigated using immunohistochemistry, in-situ hybridisation and Western blotting. Alzheimer's disease hippocampi displayed an increase in trkA receptor levels in astrocytes in the CA1 region, some of which were associated with beta-amyloid-positive plaques. Truncated trkB receptors were found in high levels in senile plaques, while the full-length receptor was expressed in glial-like cells in the hippocampus of Alzheimer's disease brains. In-situ hybridisation studies indicated that trk receptor mRNA was also elevated in Alzheimer's. The appearance of trkA and trkB receptors in astrocytes and plaques in Alzheimer's disease might be related to beta-amyloid deposition and could be implicated in the development of Alzheimer's disease.

Adult↗

PubMed1995