UMLS:C0026916 - FACTA Search

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Query: UMLS:C0026916 (MAC)
5,226 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The routine use of nitrous oxide as a component of the carrier gas has been unanimously called into question in recent surveys, in fact, its use is now recommended in indicated cases only. Whereas a lot of contraindications are listed in the surveys, precise definitions of justified indications are not given. In clinical routine practice, there are absolutely no problems in carrying out inhalational anaesthesia without nitrous oxide. The missing analgetic effect can be compensated for by moderately increasing the additively used amount of opioids, while the missing hypnotic effect can be achieved by raising the expired concentration of the inhalational anaesthetic by not more than 0.2-0.25 x MAC. Thus, when isoflurane is used, an expired concentration of 1.2 vol% is desired, in the case of sevoflurane of 2.2 vol% and with desflurane of 5.0 vol%. In addition, doing without nitrous oxide facilitates the performance of low flow anaesthetic techniques considerably. Since the patient only inhales oxygen and the volatile anaesthetic, the total gas uptake is reduced significantly. Washing out nitrogen is no longer necessary. This means that the initial phase of low flow anaesthesia, during which high fresh gas flows have to be used, can be kept short. Its duration is now determined by the wash-in of the volatile anaesthetic. Since there is no uptake of nitrous oxide, a considerably greater volume of gas is circulating within the breathing system, minimizing the possibility of accidental gas volume deficiency. Thus, if anaesthesia machines with highly gas-tight breathing systems are used, even the performance of non-quantitative closed system anaesthesia becomes possible in routine clinical practice. The carrier gas flow can be reduced to just that amount of oxygen which is really taken up by the patient. This oxygen volume can be roughly calculated by applying the Brody's formula. Using fresh gas flows as low as 0.25 l/min, however, will result in a significant decrease of the output of conventional vaporizers outside the circuit. Thus, it becomes nearly impossible to maintain an expired isoflurane concentration of 1.2 vol%. With respect to their pharmcokinetic properties, the newer low soluble volatile agents sevoflurane and desflurane are better suited for use with flows corresponding to the basal oxygen uptake. Our own clinical experience, gained in the last six months from a trial involving over 1,800 patients, shows that the increase in opioid consumption resulted in additional costs of about 0.25-0.50 DM per patient. The increased concentration of inhalational agents brought additional costs of 3.00 to 5.00 DM for a two-hour anaesthesia. On the other hand, doing without nitrous oxide saved 2.61 DM per one-hour anaesthesia, whereby our consumption of nitrous oxide is extremely low as minimal flow anaesthesia is performed consistently. Furthermore, these calculations disregard the cost of the technical maintenance fo the central gas piping system and of the regular measurement of workplace contamination with nitrous oxide by a certified institute, which in Germany, ad least, is obligatory. The additional costs of nitrous oxide-free inhalational anaesthesia seem to be balanced by the savings. Given the numerous justified arguments against the routine use of nitrous oxide, the lack of precisely-defined indications and the clinical experience showing that doing without nitrous oxide is uncomplicated, self-financing and ecologically beneficial, the use of nitrous oxide should be given up completely.
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PMID:[Nitrous oxide free low-flow anesthesia]. 1092 Apr 82

The purpose of the present study was to elucidate the role of oestrogen in the pathogenesis of Mycobacterium avium complex (MAC) pulmonary disease, which occurs most frequently in postmenopausal women. The study was carried out in a murine infectious model using ovariectomized DBA/2 female mice. Infection with MAC was established by intratracheal administration of bacilli. In some experiments, ovariectomized mice were treated with exogenous 17 beta-estradiol (E2). The number of bacilli in the lungs of infected mice which received ovariectomy was significantly larger than that in the lungs of sham-operated control mice, and treatment of ovariectomized mice with exogenous E2 restored the burden of bacilli to the same level as that in the sham-operated control mice. We next examined the effect of E2 in vitro using bone marrow-derived macrophages obtained from DBA/2 female mice. The macrophages showed bacteriostatic activity against MAC after treatment with interferon-gamma (IFN-gamma) and this activity was further enhanced by the exogenous addition of E2 to the culture medium. In parallel with these findings, E2 augmented the production of reactive nitrogen intermediates (RNI) by macrophages pretreated with IFN-gamma and stimulated with MAC, as shown by evaluating nitrite production and inducible nitric oxide synthase mRNA expression. These findings taken together suggest that absence of endogenous oestrogen appears to be responsible for the development of MAC pulmonary disease in this mouse model and that the enhancement by E2 of anti-MAC activity of murine macrophages induced through increased RNI production may play some role in resistance to MAC infection.
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PMID:Effect of oestrogen on Mycobacterium avium complex pulmonary infection in mice. 1129 30

Although viscosity (mu) is a crucial factor in measurements of flow with a pneumotachograph, and density (rho) also plays a role in the presence of turbulent flow, these material constants are not available for the volatile anaesthetic agents commonly administered in clinical practice. Thus, we determined experimentally mu and rho of pure volatile anaesthetic agents. Input impedance of a rigid-wall polyethylene tube (Zt) was measured when the tube was filled with various mixtures of carrier gases (air, 100% oxygen, 50% oxygen+50% nitrogen) to which different concentrations of volatile anaesthetic inhalation agents (halothane, isoflurane, sevoflurane, and desflurane) had been added. Mu and rho were calculated from real and imaginary portions of Zt, respectively, using the appropriate physical equations. Multiple linear regression was applied to estimate mu and rho of pure volatile agents. Viscosity values of pure volatile agents were markedly lower than those for oxygen or nitrogen. Clinically applied concentrations, however, did not markedly affect the viscosity of the gas mixture (maximum of 3.5% decrease in mu for 2 MAC desflurane). In contrast, all of the volatile agents significantly affected rho even at routinely used concentrations. Our results suggest that the composition of the carrier gas has a greater impact on viscosity than the amount and nature of the volatile anaesthetic agent whereas density is more influenced by volatile agent concentrations. Thus, the need for a correction factor in flow measurements with a pneumotachograph depends far more on the carrier gas than the concentration of volatile agent administered, although the latter may play a role in particular experimental or clinical settings.
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PMID:Viscosity and density of common anaesthetic gases: implications for flow measurements. 1187 31

Abundance and distribution of plant cell surface proteins of the hydroxyproline-rich glycoprotein (HRGP) class were studied in the pea-Rhizobium symbiosis using immunoblot analysis. The MAC 265-epitope was especially abundant in pea root nodules containing nitrogen-fixing Rhizobium bacteria. A 180-kDa MAC 265-HRGP dominated in pea shoot plasma membranes, while almost no MAC 265-HRGP was detected in root plasma membranes. We show here that a major difference between the plant-derived peribacteroid membrane of the symbiosomes and the root plasma membrane was the presence of a 100-kDa MAC 265-HRGP in the former. Arabinogalactan proteins (AGPs), as recognized by the monoclonal antibodies MAC 207 and JIM 8, were not detected in the peribacteroid membrane, while two isoforms (100 and 220 kDa) were detected in shoot and root plasma membranes. Specific MAC 265-HRGP isoforms were found in the peribacteroid space fraction of the symbiosomes and thus as soluble proteins in the interface between the symbionts. The abundance of the MAC 265-epitope was much reduced in non-nitrogen-fixing nodules when this phenotype resulted from a dicarboxylate transport mutation in Rhizobium. There was no reduction in the abundance of the MAC 265-epitope in non-fixing phenotypes resulting from a mutation in the plant. The results suggest that bacterial signals related to the bacterial ability to fix nitrogen, might be responsible for the regulation of HRGP expression in root nodules.
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PMID:Rhizobium colonization induced changes in membrane-bound and soluble hydroxyproline-rich glycoprotein composition in pea. 1197 41

The profiles of the interaction of antimycobacterial drugs with macrophage (MPhi) antimicrobial mechanisms have yet to be elucidated in detail. We examined the effects of various antimycobacterial drugs on the anti-Mycobacterium avium complex (MAC) antimicrobial activity of reactive oxygen intermediates (ROIs), especially of an H(2)O(2)-halogen (H(2)O(2)-Fe(2+)-NaI)-mediated bactericidal system, reactive nitrogen intermediates (RNIs), and free fatty acids (FFAs), which are known as central antimicrobial effectors of host MPhis against mycobacterial pathogens. We have found that certain drugs, such as rifampin (RIF), rifabutin (RFB), isoniazid (INH), clofazimine (CLO), and some fluoroquinolones, strongly or moderately reduced the anti-MAC activity of the H(2)O(2)-Fe(2+)-NaI system, primarily by inhibiting the generation of hypohalite ions and in part by interfering with the halogenation reaction of bacterial cell components due to the H(2)O(2)-Fe(2+)-NaI system. This phenomenon is specific to the H(2)O(2)-Fe(2+)-NaI system, since these drugs did not reduce the anti-MAC activity of RNIs and FFAs. From the perspective of the chemotherapy of MAC infections, the present findings indicate an important possibility that certain antimycobacterial drugs, such as rifamycins (RIF and RFB), INH, CLO, and also some types of fluoroquinolones, may interfere with the ROI-mediated antimicrobial mechanisms of host MPhis against intracellular MAC organisms.
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PMID:Interaction of antimycobacterial drugs with the anti-Mycobacterium avium complex effects of antimicrobial effectors, reactive oxygen intermediates, reactive nitrogen intermediates, and free fatty acids produced by macrophages. 1515 11

The suppressor activity of splenic macrophages induced by Mycobacterium intracellulare infection (MI-M phi s) against T cell concanavalin A (Con A) mitogenesis is mediated by MI-M phi's mediators, such as reactive nitrogen intermediates (RNIs), phosphatidylserine, free fatty acids, prostaglandin E(2) and to a minor extent TGF-beta. Here, we have compared the roles of RNIs and TGF-beta in the expression of MI-M phi's suppressor activity against Con A mitogenesis and anti-CD3 monoclonal antibody (mAb)- and anti-CD28 mAb-induced mitogenesis (TCR signal-induced mitogenesis) of the target T cells, and have found the following. First, N(G)-monomethyl-L-arginine (NMMA) inhibited MI-M phi's suppressor activity against TCR signal-induced mitogenesis as well as Con A mitogenesis. Second, anti-TGF-beta mAb weakly restored the MI-M phi-mediated suppression only in the case of Con A mitogenesis, under limited conditions, such as very low cell densities of MI-M phi s. Third, the blocking effects of NMMA plus anti-TGF-beta mAb were somewhat more prominent in the case of Con A mitogenesis than in the case of TCR signal-induced mitogenesis. Fourth, Con A- or TCR signal-stimulated MI-M phi s secreted significant amounts of the latent TGF-beta but not the active one. These findings indicate that RNIs, but not TGF-beta, play important roles in the MI-M phi-mediated suppression of TCR signal-induced mitogenesis, as well as Con A mitogenesis, of the target T cells.
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PMID:Roles of reactive nitrogen intermediates and transforming growth factor-beta produced by immunosuppressive macrophages in the expression of suppressor activity against T cell proliferation induced by TCR stimulation. 1578 7

It has been suggested that N2O may alter the sensitivity of the brain to ischemia. To test this hypothesis. we examined the effects of N2O on the development of left-right hemispheric asymmetry in the electroencephalogram (EEG) during hemorrhagic hypotension in rats subjected to unilateral carotid occlusion. Rats were anesthetized with halothane/O2/air, and ventilated to normocarbia (PaCO2 approximately 40 mm Hg). Catheters were placed in the femoral artery and vein, and both common carotid arteries (CCA) were exposed. Bilateral fronto-occipital screws were then placed to record left and right hemispheric EEGs, which were processed by computer and stored on disc. Animals were then randomly assigned to one of three treatment groups (n = 8 each): group 1, 0.5 MAC (0.5%) halothane + 0.5 MAC (70%) N2O; group 2, 1 MAC (1.0%) halothane + 70% nitrogen; and group 3, 1 MAC halothane + 70% N2O. After stabilization, the left CCA were occluded. Animals with EEG changes at this point were discarded. Beginning 5 min later, venous blood withdrawal was started at a rate of 0.25 ml/min, while mean arterial blood pressure (MAP) and EEG were continuously recorded. After exsanguination was complete, EEG data (raw and processed) were re-examined by an individual who was unaware of the anesthetics administered to determine the MAP at which any evidence of EEG asymmetry appeared. There were no intergroup differences in weight, PaO2, PaCO2, pHa, blood glucose. hematocrit, or starting (prebleed) MAP. The earliest change in the EEG was typically a decrease in total amplitude over the hemisphere ipsilateral to the carotid occlusion. Adding 70% N2O to a 1 MAC halothane background (group 2 vs. group 3) had no effect on the MAP at which this EEG asymmetry appeared (54 +/- 13 vs. 53 +/- 10 mm Hg). However, this MAP was significantly higher in animals breathing 0.5 MAC halothane + 0.5 MAC N2O (group 1, 78 +/- 17 mm Hg, p = 0.0019 by ANOVA). We conclude that 70% N2O had no direct effects on the MAP at which EEG abnormalities appear (group 2 vs. 3), and that the observed differences are more closely related to the concentration of volatile agent. Whether these differences are related to anesthetic-induced differences in the brain's tolerance to reduced CBF or whether there are differences in cerebral blood flow (CBF) autoregulation are unknown.
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PMID:EEG changes during carotid occlusion and hypotension in the rat: the effects of nitrous oxide. 1581 50

Picolinic acid (PA) potentiates macrophage (MPhi) antimicrobial activity against intracellular Mycobacterium avium complex (MAC). Here, we studied the mechanisms of this phenomenon using human THP-1 MPhis. First, when PA-treated MAC-infected MPhis were cultured in the presence or absence of reactive oxygen intermediate (ROI) scavengers, nitric oxide synthase (NOS) inhibitors or phospholipase A(2) (PLA(2)) inhibitors, none of these agents blocked the activity of PA in potentiating MPhi anti-MAC activity. Second, when PA was added to the in vitro anti-MAC bactericidal system consisting of either ROIs, reactive nitrogen intermediates (RNIs) or free fatty acid (FFA) molecules, which are the major MPhi antimicrobial effectors, PA inhibited the activity of ROIs and conversely potentiated the activity of RNIs; PA did not affect the activity of FFAs. Third, PA reduced mRNA expression of NADPH oxidase and beta-defensin-1 by MAC-infected MPhis, whilst neither cytosolic PLA(2) nor CAP37 mRNA expression was affected. Notably, inducible NOS and secretory PLA(2) mRNA expression was not detected for MAC-infected MPhis even when given PA treatment. These findings suggest that ROIs, RNIs, FFAs and beta-defensin-1 do not play important roles in the PA-induced potentiation of MPhi anti-MAC activity.
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PMID:Effects of picolinic acid on the antimicrobial functions of host macrophages against Mycobacterium avium complex. 1729 87

A new carrier matrix for nanoemulsion drug delivery was synthesized from glycine as the raw material, using mesoporous/microporous electron rich carbon-silica composite surface (MAC(800)). MAC(800) was prepared from rice husk in two-stage carbonization. The surface area, pore volume, and pore size distribution of MAC(800) were measured, using nitrogen adsorption isotherms at 77K. The unpaired electron density of MAC(800) was measured in electron spin resonance spectroscopy (ESR), using TEMPOL (4-hydroxy-2,2,6,6-tetramethyl piperidine-1-oxyl) as the reference spin probe. Glycine was converted into ketene at the surface of MAC(800), which further underwent radical polymerization to form a low molecular weight ketene polymer (LMKP) of ester structure. The structure and the properties of LMKP were confirmed through (13)C, (1)H and DEPT nuclear magnetic resonance (NMR) spectroscopy, attenuated total reflectance-Fourier transform infrared spectroscopy (ATR-FTIR) and size exclusion chromatography (SEC). The two hydrophilic drugs namely ciprofloxacin hydrochloride (CPH) and gentamicin sulphate (GS) were chosen for the nanoemulsion preparation and characterization. They were characterized for morphology, interaction of drugs with the polymer and their crystallinity, using HR-TEM, DSC and XRD, respectively. The encapsulation efficiency of the LMKP towards the drugs ciprofloxacin hydrochloride and gentamicin sulphate were 26% and 12%, respectively. The dissolution studies of the nanoemulsion were carried out for the pH 6.5, 7.4 and 8.0. The cytocompatibility studies were done for LMKP as well as nanoemulsion using Hep2 epithelial cells.
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PMID:Nanoemulsion drug delivery by ketene based polyester synthesized using electron rich carbon/silica composite surface. 1856 42

Macrophages (M(phi)s) play a central role as anti-microbial effector cells in the expression of host resistance to mycobacterial infections. With respect to antimicrobial effector molecules of host M(phi) against mycobacterial pathogens, recent studies suggest the possibility that the reactive nitrogen intermediates (RNI)--and reactive oxygen intermediates-independent antimycobacterial mechanism(s) may be crucial for the antimycobacterial function of host M(phi). In this context, we previously found that free fatty acids (FFAs) such as arachidonic acid (AA) and linolenic acid exhibited potent antimicrobial activity against mycobacterial organisms, including Mycobacterium tuberculosis (MTB) and Mycobacterium avium complex (MAC). In addition, FFAs in combination with RNI played critical roles in manifestation of the activity of M(phi) against mycobacterial organisms. Moreover, our recent studies have shown the following findings. First, anti-MTB activity of IFN-gamma-activated M(phi)s was specifically blocked by arachidonyl trifluoromethylketone (aTFMK), an inhibitor of cytosolic phospholipase A2 (cPLA2). Second, ATP potentiated the anti-MAC bactericidal activity of M(phi)s cultivated in the presence of clarithromycin and rifamycin. This effect of ATP was closely related to intracellular Ca2+ mobilization and was specifically blocked by aTFMK. Third, intramacrophage translocation of membranous AA molecules to MAC-containing phagosomes was also specifically blocked by aTFMK. In the confocal microscopic observation of MAC-infected M(phi)s, ATP enhanced the intracellular translocation of cPLA2 into MAC-containing phagosomes. These findings suggest that FFAs (especially AA) produced by the enzymatic action of cPLA2 play important roles as antimycobacterial effectors in the expression of M(phi) antimicrobial activity against mycobacterial pathogens.
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PMID:[Novel type of antimicrobial mechanism in host macrophages against mycobacterial infections]. 1980 80

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