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M Ge

Publications and source records attributed to M Ge.

32 records · Page 2Linked to original sources
PubMed1993

An electron spin resonance study of interactions between gramicidin A' and phosphatidylcholine bilayers.

The model of microscopic order and macroscopic disorder was used to stimulate electron spin resonance spectra of spin-labeled lipids, 5-PC, 10-PC, and 16-PC in multilamellar vesicles of dipalmitoylphosphatidylcholine (DPPC) containing gramicidin A' (GA) at temperatures above the gel-to-liquid crystal transition of DPPC. The simulations show that at a lower concentration of GA (i.e., molar ratios of DPPC/GA greater than 3), GA has only a slight effect on the acyl chain dynamics. The rotational diffusion rate around the axis parallel to the long hydrocarbon chain remains unchanged or increases slightly, while the rate around the perpendicular axes decreases slightly. These spectra from DPPC/GA mixtures could only be fit successfully with two or more components consistent with the well-known concept of "boundary lipids," that is, the peptide induces structural inhomogeneity in lipid bilayers. However, the spectra were significantly better fit with additional components that exhibit increased local ordering, implying decreased amplitude of rotational motion, rather than immobilized components with sharply a reduced rotational rate. The largest relative effects occur at the end of the acyl chains, where the average local order parameter St of 16-PC increases from 0.06 for pure lipid to 0.66 for 1:1 DPPC/GA. The inhomogeneity in ordering in DPPC bilayers due to GA decreases with increasing temperature. The hyperfine tensor component Azz increases for 10-PC and 16-PC when GA is incorporated into DPPC bilayers, indicating that water has deeply penetrated into the DPPC bilayers. Simulations of published electron spin resonance spectra of 14-PC in dimyristoylphosphatidylcholine/cytochrome oxidase complexes were also better fit by additional components that were more ordered, rather than immobilized. The average local order parameter in this case is found to increase from 0.11 for pure dimyristoylphosphatidylcholine to 0.61 for a lipid/protein ratio of 50. These spectra and their simulations are similar to the results obtained with 16-PC in the DPPC/GA mixtures. The relevance to studies of lipid-protein interactions for other proteins is briefly discussed.

1,2-Dipalmitoylphosphatidylcholine↗
PubMed1992

Fibrinogen degradation product fragment D induces endothelial cell detachment by activation of cell-mediated fibrinolysis.

We studied the effects of fibrinogen degradation product (FDP) fragment D on endothelial monolayer integrity and the mechanisms of fragment D-induced endothelial cell detachment from the substratum. Incubation of bovine pulmonary artery endothelial cells (BPAEC) with fragment D caused concentration- and time-dependent cell detachment from the substratum. The optimal response occurred at fragment D concentrations of 2 microM and required an incubation time of 24 h. BPAEC challenged with fragment D increased the concentration and activity of urokinase-type plasminogen activator (uPA) in the conditioned medium within 2 to 4 h of incubation. Fragment D also induced the release of tissue-type plasminogen activator, but to a lesser extent than uPA. Fragment D concurrently increased plasminogen activator (PA) activity in a concentration-dependent manner. Increased PA activity was followed by augmentation of cell-associated plasmin activity and subsequent increase in the degradation of 125I-fibrinogen and 125I-vitronectin precoated in the subendothelial matrix. Pretreatment of BPAEC with anti-uPA antibody, and inhibitors of uPA (dansyl-GGACK) and plasmin (aprotinin) prevented approximately 60% of the fragment D-induced endothelial cell detachment. We conclude that FDP fragment D increases secretion of endothelial PAs and enhances the generation of plasmin, thereby contributing to proteolysis of extracellular matrix and endothelial cell detachment. Fragment D may be a critical mediator linking activation of fibrinolysis to vascular endothelial injury in inflammatory disorders.

Amino Acid Sequence↗
PubMed1991

Role of ICAM-1 in neutrophil-mediated lung vascular injury after occlusion and reperfusion.

We examined the role of intracellular adhesion molecule 1 (ICAM-1 or CD54) in the development of pulmonary edema in rabbits after pulmonary artery occlusion and reperfusion using a monoclonal antibody (MAb) RR1/1 directed against ICAM-1, a ligand for the CD18 leukocyte adhesion glycoprotein complex. A vascular clamp was placed around the left pulmonary artery for 24 h and then released to allow reperfusion for 2 h. Lungs subjected to 24 h of unilateral pulmonary artery occlusion showed increased binding of 125I-labeled RR1/1 and immunocytochemical evidence of ICAM-1 expression in pulmonary vascular endothelial cells compared with the contralateral lung. MAbs RR1/1 (0.5 mg/kg) or IB4 (1.0 mg/kg) (MAb directed against an epitope on the CD18 adhesion glycoprotein) was infused 45-60 min before the start of reperfusion to assess the roles of ICAM-1 and CD18 in the response. After reperfusion, the lungs were removed, suspended from one end of a weighing balance, and perfused with Ringer-albumin (0.5 g/100 ml), and the changes in lung weight were monitored for 60 min. Lung tissue myeloperoxidase (MPO) content (a marker of neutrophil sequestration) was determined after reperfusion. The increases in lung weight gain in the RR1/1- and IB4-treated groups of 960 +/- 100 and 865 +/- 110 mg, respectively, were less (P less than 0.05) than in untreated controls (3,550 +/- 725 mg).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Fibrinogen degradation product fragment D increases endothelial monolayer permeability.

We assessed the effects of the two primary high-molecular-weight fibrinogen degradation products (FDP), fragments D and E, on the pulmonary vascular endothelial barrier function. Fragments D and E were purified to homogeneity by QAE Sephadex chromatography followed by gel filtration. Incubation of bovine pulmonary artery endothelial monolayers with 0.5-2.0 microM fragment D for 2 h caused a doubling of transendothelial 125I-albumin clearance rate (a measure of 125I-albumin permeability). Fragment E only produced a 0.6-fold increase in 125I-albumin clearance rate at concentration of 4.0 microM. Both FDP remained active in incubating media with serum. The permeability-increasing effect of fragment D was reversible and was not due to cell detachment or lysis. The fragment-D effect was time dependent and was associated with redistribution of endothelial F-actin microfilaments. The effect was independent of the carboxy-terminal sequence on gamma-chain of fragment D. Fragments D and E binding to pulmonary artery endothelial cells was specific and reversible, but fragment D binding was three-fold greater than fragment E, which may account for the greater permeability increase mediated by fragment D. The results indicate that FDP, especially fragment D, increase endothelial permeability to albumin. The response involves specific binding of fragment D to endothelial cells and redistribution of intracellular actin.

Actins↗
PubMed1988

Endogenous GABA released into the fourth ventricle of the rat brain in vivo is enhanced by noxious stimuli.

In vivo release of endogenous gamma-aminobutyric acid (GABA) and glutamic acid into the 4th ventricle of the rat brain in response to noxious stimuli was examined. Both these compounds were dansylated and the concentrations determined, using high-performance liquid chromatography (HPLC) combined with an UV detector. Following noxious stimuli (subcutaneous injection of diluted formalin into the hind-paw or noxious pinch of the hind-paws), there was a remarkable release of GABA, but not of glutamic acid. Basal on our heretofore obtained data that bicuculline methiodide, a GABAA antagonist, produces a potent analgesia in mice, the present results suggest that the GABAergic system in the brain stem may promote nociceptive transmission in rats.

Animals↗
PubMed1987

Presynaptic opioid kappa-receptor and regulation of the release of Met-enkephalin in the rat brainstem.

Opioid kappa-agonists had much more potent inhibitory effects on the high K+-evoked Met-enkephalin release from rat brain slices than did the mu- or delta-agonists. The opioid kappa- antagonist, MR2266 enhanced the evoked release of Met-enkephalin to a greater extent than did mu- or delta-antagonists in vitro and had a potent analgesia in mice in vivo. These findings suggest that the release of Met-enkephalin may be regulated in vitro and in vivo, mainly by presynaptic kappa-receptor-mediated mechanisms.

Action Potentials↗
PubMed1987

Subconvulsive doses of intracisternal bicuculline methiodide, a GABAA receptor antagonist, produce potent analgesia as measured in the tail pinch test in mice.

Bicuculline methiodide, a GABAA antagonist produced potent analgesia in the tail pinch test when it was given intracisternally (i.c.) but not intrathecally (i.t.). The ED50 was 5 ng/mouse. This analgesia was antagonized by i.c. muscimol, a GABAA agonist. On the contrary, muscimol (i.t.) produced bicuculline-reversible analgesia. These findings suggest that brain GABA may transmit the nociceptive information while GABA in the spinal cord may inhibit it.

Analgesics↗
PubMed1986

Low doses of naloxone produce analgesia in the mouse brain by blocking presynaptic autoinhibition of enkephalin release.

The involvement of presynaptic autoinhibition of Met-enkephalin release in naloxone-induced analgesia was studied. In both acetic acid writhing and tail-flick tests in mice, naloxone produced biphasic effects, analgesia at very low doses (1 microgram/kg s.c. or 1 ng intracisternal) and hyperalgesia at higher doses (100 micrograms/kg s.c. or 100 ng intracisternal). Morphine at 10(-6) to 10(-5)M depressed the high K+-evoked release of Met-enkephalin from slices of the rat brainstem by 12.5-55.9% of control, while naloxone at 10(-6)M significantly enhanced the release by 80.6%. These findings strongly suggest that in the mouse brain a very low dose of naloxone produces analgesia by blocking autoinhibition of enkephalin release.

Analgesia↗
PubMed1982

Silica fragments from millet bran in mucosa surrounding oesophageal tumours in patients in northern China.

Millet bran is a component of the diet in the area of highest oesophageal cancer incidence in northern China. Millet bran was found to contain up to 20% by weight of silica; some of this silica occurs as friable sheets or sharply-pointed fibres. These types of silica in millet bran are the most likely source of an unusual contamination with fragments of silica found in the oesophageal mucosa surrounding tumours in patients in northern China. A group of mucosal samples analysed together contained over 5,000 particles/g (100 parts per million by weight), ten times as many as were found in tissue from normal controls taken at necropsy in London. The modal diameter was 10 microgram (1-70 microgram). The particles were in the body of the mucosa and were not simply a surface contaminant. Silica fragments and fibres of similar size originating from other plant species occur in the diet in the two other regions of greatest incidence of oesophageal cancer, the Transkei and Iran. If such fragments enter the mucosa, they must cause some degree of trauma, and they may also be able to stimulate proliferation by providing anchorage. These findings suggest the possibility that silica particles might be involved in the aetiology of oesophageal cancer.

Adult↗
PubMedDate not supplied

Non-opioid analgesia of the neuropeptide, neo-kyotorphin and possible mediation by inhibition of GABA release in the mouse brain.

The novel neuropeptide, neo-kyotorphin, produced a naloxone-resistant analgesia in the tail pinch test when given (IC) to mice. Pretreatments with implantation of a morphine pellet or with phentolamine (10 micrograms IT) or with reserpine (10 mg/kg SC) did not attenuate this analgesia, yet the analgesia was antagonized by GABA mimetics, such as muscimol (0.1 microgram IC), nipecotic acid (100 mg/kg IP). Neo-kyotorphin inhibited the Ca2+-dependent and depolarization-evoked release of 3H-GABA, from crude synaptosomes of the lower brain stem of rats. These findings suggest that inhibition of GABA in the brain may in part be involved in neo-kyotorphin-induced analgesia.

Analgesics↗
PubMedDate not supplied

Technical note: reference values of haematocrit in young people and relationship with altitude.

The purpose of this paper is to provide scientific basis for a unified standard reference value of haematocrit in young people in China. The reference values of haematocrit levels in healthy young people have been collected according to the Wintrobe methods; the relationship between the reference values of haematocrit in young people and altitude has been tested in this paper. It has been found that the reference value of haematocrit in young people increases when the altitude gradually increases, and such relationship is quite significant, The method of mathematical univariate regression analysis is used to deduce two regression equations: Y1 = 44.3 + 0.00357X +/- 3.7, and Y2 = 39.7+0.00318X +/- 2.6. If the altitude value of a s known, the particular area of China is known, the reference value of haematocrit in young people there can be calculated by means of the regression equations. Furhermore depending on the altitude, China can be divided into three districts: Qingzang District, Central District and Eastern District.

Adolescent↗