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PubMed2001

Diffusion time dependence of the apparent diffusion tensor in healthy human brain and white matter disease.

The diffusion time dependence of the brain water diffusion tensor provides information regarding diffusion restriction and hindrance but has received little attention, primarily due to limitations in gradient amplitude available on clinical MRI systems, required to achieve short diffusion times. Using new, more powerful gradient hardware, the diffusion time dependence of tensor-derived metrics were studied in human brain in the range 8-80 ms, which encompasses the shortest diffusion times studied to date. There was no evidence for a change in mean diffusivity, fractional anisotropy, or in the eigenvalues with diffusion time in healthy human brain. The findings are consistent with a model of unrestricted, but hindered water diffusion with semipermeable membranes, likely originating from the extracellular space in which the average extracellular separation is less than 7 microns. Similar findings in two multiple sclerosis plaques indicated that the size of the water diffusion space in the lesion did not exceed this dimension.

Anisotropy↗
PubMed2004

Defining pathways of loss and secretion of chemical messengers from astrocytes.

It is becoming evident that glia, and astrocytes in particular, are intimately involved in neuronal signaling. Astrocytic modulation of signaling in neurons appears to be mediated by the release of neuroactive compounds such as the excitatory amino acid glutamate. Release of these transmitters appears to be driven by two different processes: (1) a volume regulatory response triggered by hypo-osmotic conditions that leads to the release of osmotically active solutes from the cytoplasm into the extracellular space, and (2) intracellular calcium-dependent vesicle-mediated excytotic release. The regulatory volume decrease may be mediated by any of several different pathways that increase membrane permeability, thus allowing osmolytes to travel down their concentration gradient into the extracellular space. Such pathways include anion channels, hemichannels, P2X receptor channels, and transporters or multidrug resistance proteins. The excytotic release process may use calcium triggered synaptic like vesicle fusion or alterations in constitutive vesicle trafficking to the membrane. Determining the contribution of any of these release mechanisms requires agents that can be used to specifically block pathways of interest. Currently, many of the pharmacological compounds being used exhibit a great deal of cross-reactivity between several of these pathways. For example, the popular anion channel inhibitor 5-nitro-2-(3-phenyl-propylamino)benzoic acid (NPPB) is an efficient blocker of both hemichannels and vesicle loading. This demonstrates the need to more fully characterize the activities of the agents currently available and to choose pathway blockers carefully when designing experiments.

Animals↗
PubMed1994

Ultrastructure of quick-frozen secretory ameloblasts of the rat molar tooth.

Ameloblasts in molar tooth germs from 4 to 12-day-old neonatal rats were quick-frozen and then freeze-substituted in acetone-tannic acid and acetone-osmium tetroxide. Following quick freezing and freeze-substitution, the preservation of ameloblasts was principally the same as seen in conventionally-fixed ones. Several differences, however, became apparent between two methods. Concerning enamel formation, the quick-freezing procedure greatly improved the preservation including that of the extrusion of secretory granules into the extracellular space. The exocytosis is a type of merocrine secretion. The precursor stippled material was demonstrated at the front of Tomes' processes and in the intercellular space of the distal terminal junction. In the more advanced stage, the stippled material tended to decrease gradually in amount. Prior to the formation of the typical Tomes' process, large secretory granules fused directly with the distal plasma membrane, which plays a role in the formation of prismless enamel. After the typical Tomes' process had formed, secretory granules containing electron-dense material instead of the large secretory granules accumulated in the distal portion of the Tomes' process. These latter secretory granules had two different destinations; i.e. the granules discharged their contents into the infoldings of the distal part of Tomes' process and into the infoldings of the lateral cell membrane. These types of secretion seem to have a functional role in the rod or inter-rod enamel formation. The ultrastructure of the stippled material consisted of 3-dimensionally interconnected strands after quick freezing, which is different from the appearance of granules embedded in amorphous material after conventional fixation. The stippled material was seen in the intercrystal space among the newly formed crystals. Also, an extensive tubulo-vesicular structure was preserved in both the cell body and Tomes' process. The present data suggest that the membrane of this structure showed a smooth contour opening to the extracellular space, and also an intimate relationship with the secretory granules.

Ameloblasts↗
PubMed1996

Up-regulation of cystatin C by microglia in the rat facial nucleus following axotomy.

Cystatin C, a cysteine proteinase inhibitor, is expressed in the central nervous system (CNS) as well as many other organs of mammals. However, little is known concerning whether its expression is regulated under pathological conditions of the CNS and what types of cells are responsible for this regulation. We performed differential hybridization screening of cDNA libraries derived from the rat facial nucleus and found a cDNA of rat cystatin C to be up-regulated following facial nerve axotomy. In situ hybridization using an RNA probe for rat cystatin C revealed that cystatin C mRNA in the facial nucleus was markedly increased in amount by day 7 after axotomy and was then decreased to the normal level by day 50. The intense signal for cystatin C mRNA in the damaged facial nucleus was localized in the glial cells which had the morphological characteristics of microglia. Light and electron microscopic immunohistochemistry using a rabbit antibody specific for cystatin C confirmed that microglia in the damaged facial nucleus were strongly positive for cystatin C. The immunoreactivity was also found in the extracellular space, consistent with the fact that cells producing cystatin C generally secrete this protein. These results demonstrate that cystatin C is markedly up-regulated by microglia in response to axotomy and is probably secreted by these cells into the extracellular space, suggesting that this proteinase inhibitor has (a) significant function(s) in the processes of neuronal degeneration, regeneration, and/or repair subsequent to axotomy.

Animals↗
PubMed2003

[Ultrastructural observation of rat thymus tissue with coronavirus infection].

OBJECTIVE: To investigate the ultrastructure of rat thymus tissues with rat coronavirus (RCV) infection for clarifying the mechanism responsible for the morphological changes of the cells infected by RCV. METHODS: Routine electron microscopy was performed for observing RCV-infected rat thymus tissues. RESULTS: Following RCV infection, endoplasmic reticulum (ER) pools of different dimensions were observed in the cytoplasm of the thymic epithelial reticular cells, merging subsequently with each other into larger ER lakes filled with particles of mature RCV, or viral inclusion bodies. After germination on the ER membrane, the viruses entered the matrix of the ER lake to mature and were eventually excreted to the extracellular space. The RCV particles were spherical in shape with a diameter of 100-130 nm and two distinct membranes, the outer one being the envelope and the inner one the nuclear capsid to enclose the viroplasm. Between the envelop and nuclear capsid was a electron-lucent middle layer comprising one to two thin membranous structures. Large quantity of short spike-like projections starting from the nucleus capsid penetrated the middle layer and the envelop to reach the glycoprotein coat and formed a corona-like structure. Mature RCV particles were distributed around the ER pools, cytoplasm, and intercellular space, and the RCVs in the endosome/lysosome were devoid of the envelop and nuclear capsid. CONCLUSION: The ER lakes are involved in the maturation of the viruses, and the envelop and nuclear capsid of the virus entering the cells from extracellular space are removed and degraded in the endosome/lysosome. Replications of virus occurs in plasma of the thymic epithelial reticular cells, and no RCV can be detected in the thymocytes.

Animals↗
PubMed2006

Extracellular heat shock protein 72 is a marker of the stress protein response in acute lung injury.

Previous studies have shown that heat shock protein 72 (Hsp72) is found in the extracellular space (eHsp72) and that eHsp72 has potent immunomodulatory effects. However, whether eHsp72 is present in the distal air spaces and whether eHsp72 could modulate removal of alveolar edema is unknown. The first objective was to determine whether Hsp72 is released within air spaces and whether Hsp72 levels in pulmonary edema fluid would correlate with the capacity of the alveolar epithelium to remove alveolar edema fluid in patients with ALI/ARDS. Patients with hydrostatic edema served as controls. The second objective was to determine whether activation of the stress protein response (SPR) caused the release of Hsp72 into the extracellular space in vivo and in vitro and to determine whether SPR activation and/or eHsp72 itself would prevent the IL-1beta-mediated inhibition of the vectorial fluid transport across alveolar type II cells. We found that eHsp72 was present in plasma and pulmonary edema fluid of ALI patients and that eHsp72 was significantly higher in pulmonary edema fluid from patients with preserved alveolar epithelial fluid clearance. Furthermore, SPR activation in vivo in mice and in vitro in lung endothelial, epithelial, and macrophage cells caused intracellular expression and extracellular release of Hsp72. Finally, SPR activation, but not eHsp72 itself, prevented the decrease in alveolar epithelial ion transport induced by exposure to IL-1beta. Thus SPR may protect the alveolar epithelium against oxidative stress associated with experimental ALI, and eHsp72 may serve as a marker of SPR activation in the distal air spaces of patients with ALI.

Adult↗
PubMed2004

Neuronal, glial and synaptic remodeling in the adult hypothalamus: functional consequences and role of cell surface and extracellular matrix adhesion molecules.

The adult hypothalamo-neurohypophysial system (HNS) undergoes activity-dependent morphological plasticity which modifies astrocytic coverage of its oxytocinergic neurons and their synaptic inputs. Thus, during physiological conditions that enhance central and peripheral release of oxytocin (OT), adjacent somata and dendrites of OT neurons become extensively juxtaposed, without intervening astrocytic processes and receive an increased number of synapses. The morphological changes occur within a few hours and are reversible with termination of stimulation. The reduced astrocytic coverage has direct functional consequences since it modifies extracellular ionic homeostasis, synaptic transmission, and the size and geometry of the extracellular space. It also contributes indirectly to neuronal function by permitting formation of synapses on neuronal surfaces freed of astrocytic processes. Overall, such remodeling is expected to potentiate activated neuronal firing, especially in clusters of tightly packed neurons, an anatomical arrangement characterizing OT neurons. This plasticity connotes dynamic cell interactions that must bring into play cell surface and extracellular matrix adhesive proteins like those intervening in developing neuronal systems undergoing neuronal-glial and synaptogenic transformations. It is worth noting, therefore, that adult HNS neurons and glia continue to express such molecules, including polysialic acid (PSA)-enriched neural cell adhesion molecule (PSA-NCAM) and the glycoprotein, tenascin-C. PSA is a large, complex sugar on the extracellular domain of NCAM considered a negative regulator of adhesion; it occurs in large amounts on the surfaces of HNS neurons and astrocytes. Tenascin-C, on the other hand, possesses adhesive and repulsive properties; it is secreted by HNS astrocytes and occurs in extracellular spaces and on cell surfaces after interaction with appropriate ligands. These molecules have been considered permissive factors for morphological plasticity. However, because of their localization and inherent properties, they may also serve to modulate the extracellular environment and in consequence, synaptic and volume transmission in a system in which the extracellular compartment is constantly being modified.

Animals↗
PubMed1984

Elastin: relation of protein and gene structure to disease.

The elastic properties of many tissues such as the lung, dermis, and large blood vessels are due to the presence of elastic fibers in the extracellular space. These fibers have been shown by biochemical and ultrastructural analysis to be comprised of two distinct components, a more abundant amorphous component and the microfibrillar component. The microfibrillar component is found in 10- to 12-nm fibrils which are located primarily around the periphery of the amorphous component but, to some extent, interspersed within it. The protein, elastin, makes up the highly insoluble amorphous component and is responsible for the elastic properties. Elastin is found throughout the vertebrate kingdom except for very primitive fish and possesses an unusual chemical composition consonant with its characteristic physical properties. Elastin is composed largely of glycine, proline, and other hydrophobic residues and contains multiple lysine-derived cross-links, such as the desmosines, which link the individual polypeptide chains into a rubber-like network. The intervening, hydrophobic regions of the polypeptide chains between the cross-links are highly mobile, and the elastic properties of the fibers can be described in terms of the theory of rubber elasticity. Recent application of recombinant DNA techniques has led to further understanding of the structure of elastin. Analyses of the bovine and human elastin genes have demonstrated that the hydrophobic and cross-linking domains are encoded in separate exons. These exons tend to be small, varying from 27 to 114 base pairs, and are separated by large intervening sequences. Furthermore, DNA sequence analysis has demonstrated that the elastin molecule contains two cysteine residues which were not previously identified near the carboxy terminus and which may be important in the interaction of elastin with other extracellular matrix proteins. Further DNA sequencing should determine the complete amino acid sequence of elastin. Biosynthetic studies and in vitro translation of elastin mRNA have demonstrated that a 72,000-dalton polypeptide, designated tropoelastin, is the initial translation product. Analysis of several developing systems has demonstrated that elastin synthesis is controlled by the level of elastin mRNA. After packaging into membrane-bound vesicles in the Golgi apparatus, tropoelastin is secreted by exocytosis into the extracellular space where it is cross-linked by a copper-requiring extracellular enzyme, lysyl oxidase. Elastin can be solubilized only by proteases that have consequently been designated elastases, although these are general, powerful proteases that can hydrolyze numerous proteins.(ABSTRACT TRUNCATED AT 400 WORDS)

Amino Acid Sequence↗
PubMed1992

Calcium antagonism and norepinephrine release in myocardial ischemia.

In myocardial infarction, adrenergic stimulation of the heart is thought to cause cell damage and malignant arrhythmias. In rat hearts as well as in human cardiac tissue, ischemia induces norepinephrine (NE) release, which results in micromolar catecholamine concentrations in the interstitial space of the ischemic myocardium. It has been found that local metabolic, rather than centrally evoked NE release, plays the crucial role in excess adrenergic activation of the ischemic myocardium. NE release in ischemia is nonexocytotic and has been characterized as a two-step process. (a) Induced by energy deficiency, NE escapes from its storage vesicles and accumulates in the axoplasm. (b) NE is transported across the plasma membrane into the extracellular space via the neuronal NE carrier (uptake1), which has reversed its normal transport direction because of increased intracellular sodium concentration. NE release induced by ischemia is independent of the presence of calcium in the extracellular space and is not altered by blockade of N-type (neuronal) calcium channels. Furthermore, modulation of protein kinase C does not interfere with NE liberation in the ischemic myocardium. This independence of extracellular calcium, calcium entry into the neuron, and protein kinase C activity is in contrast to the strong calcium dependence of exocytotic transmitter release, which is found under physiological conditions. On the basis of these findings, it was unexpected that calcium antagonists such as gallopamil, verapamil, diltiazem, felodipine, and nifedipine suppress ischemia-induced NE release. The most potent effect was found for gallopamil with a concentration of 50% inhibition (IC50) of 300 nmol/L.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1981

Ultrastructure of a cerebral white matter lesion in a 41-year-old man with Leigh's encephalomyelopathy (LEM).

A brain biopsy taken from a 41-year-old man with Leigh's encephalomyelopathy (LEM) was studied under the electron microscope. The sample of cerebral white matter revealed degenerated oligodendrocytes, reactive astrocytes and scavenger cells filled with miscellaneous debris. Myelin underwent splitting and vacuole formation as well as lamellar and vesicular dissolution. Degenerative and reactive changes were prominent in the axons, many of which were calcified. There was marked fibrous gliosis of the tissue and the extracellular space was enlarged. The small vessels were notably involved; evidence of capillary growth was also found. In sum, the overall picture was one of loss of tissue continuity, loss of axons and loss of myelin, opposite to which stood expansion of the extracellular space, accumulation of filament-filled astroglial process, hypertrophy and hyperplasia of the capillaries and increase of the tissue cellularity. The study has confirmed and defined at the ultrastructural level the well-known histological features of LEM. However, the formal, let alone the causal pathogenesis of the disease remains as obscure as ever.

Adult↗
PubMed1979

Correlation between response to norepinephrine and removal of 45Ca from high-affinity binding sites by extracellular EDTA in rabbit aortic smooth muscle.

Divalent ion chelators (EDTA, EGTA) were found to remove 45Ca from high-affinity binding sites in isolated rabbit aortic smooth muscle in a concentration-dependent manner. Measurement of 14C-labeled EDTA uptake (10 to 60-min incubation periods) yielded tissue/medium ratios equivalent to the extracellular space [14C]-sucrose tissue/medium ratio). Addition of high EDTA concentrations (0.5--1.5 mM) elicits large but reversible increases in 45Ca efflux, rapidly removes virtually all 45Ca from muscles previously incubated with 45Ca for as short a time as 7 min (filling of extracellular and superficial sites) or as long as 180 min (more complete equilibration of 45Ca), and blocks the norepinephrine-induced contractile response (this response is only partially inhibited by 0.05 mM EDTA, a concentration too low to remove most of the 45Ca present). Furthermore, phosphatidyl serine, a compound known to decrease exchangeability of 45Ca in this tissue, inhibits the EDTA-induced increase in 45Ca loss. Thus, those slowly depleted Ca++ stores that are important for the contractile action of norepinephrine are removed by EDTA even though this chelator is confined to the extracellular space. Possibly, release or removal of high-affinity Ca++ is regulated by EDTA-accessible Ca++ bound at relatively superficial membrane sites.

Animals↗
PubMed1989

Morphologic features of the aqueous humor drainage pathways in horses.

The iridocorneal angle of the horse was anteriorly lined by a pectinate ligament, consisting of several layers of vertically oriented collagenous beams, that were interrupted by a network of extracellular spaces. The anterior chamber angle consisted mostly of a large uveal trabecular meshwork that was composed of widely-spaced, thick trabeculae. These trabeculae were attached in part posteriorly to extensions of the ciliary body musculature and anteriorly inserted into the prominent pectinate ligament. The corneoscleral trabecular meshwork was shaped hemiobovately and formed the external boundary of the iridocorneal angle. The extracellular spaces were smaller and more evenly spaced than those in the uveal trabecular meshwork. Uveal and corneoscleral trabecular meshwork beams were mostly composed of cores of collagen and elastin surrounded by several layers of basement membrane-like material and, in turn, were entirely enveloped by trabecular cells. An anterior narrow zone of broad corneoscleral trabeculae was composed of elastin-collagen cores surrounded by circular bundles of long-spacing collagen. The angular aqueous plexus was extensive, forming much of the external border of the outer corneoscleral trabecular meshwork. A dense zone was associated with the angular aqueous plexus, completely encompassing these aqueous outflow vessels. Posteriorly, the iridocorneal angle was confluent with a well-defined band of trabeculae that was situated between the ciliary body musculature and subjacent sclera and extended posteriorly to the anterior-most region of the choroid where these trabeculae tapered and ended. This region is referred to as the supraciliary trabecular meshwork and indicates a potentially extensive route for outflow of aqueous humor in the equine eye.

Animals↗
PubMed2007

Fusion of the genes for AHL-lactonase and S-layer protein in Bacillus thuringiensis increases its ability to inhibit soft rot caused by Erwinia carotovora.

Two genes, ctc and ctc2, responsible for surface layer (S-layer) protein synthesis in Bacillus thuringiensis CTC, were mutated and resulted in B. thuringiensis Tr5. To synthesize and express the N-acyl-homoserine lactonase (AHL-lactonase) in the extracellular space of B. thuringiensis, the aiiA ( 4Q7 ) gene (an AHL-lactonase gene from B. thuringiensis 4Q7), which confers the ability to inhibit plant soft rot disease in B. thuringiensis 4Q7, was fused with the upstream sequence of the ctc gene, which in turn is essential for S-layer protein secretion and anchoring on the cell surface. The resulting fusion gene, slh-aiiA, was expressed in B. thuringiensis Tr5 to avoid competition for the extracellular space with the native S-layer protein. Our results indicate that B. thuringiensis Tr5 containing the fusion gene slh-aiiA displayed high extracellular AHL-degrading activity. When compared with wild-type B. thuringiensis strains, the ability of the constructed strain to inhibit soft rot disease caused by Erwinia carotovora SCG1 was markedly increased. These findings provide evidence for a significant advance in our ability to inhibit soft rot disease caused by E. carotovora.

Antibiosis↗
PubMed1995

Extracellular and intracellular degradation of collagen by trophoblast giant cells in acute fasted mice examined by electron microscopy.

The fine structure of trophoblast giant cells and their interaction with collagen at the antimesometrial region on the 9th day of pregnancy was examined in fed and acute fasted mice. Collagen fibrils and filamentous aggregates (disintegrating collagen fibrils) were observed in the extracellular space. Three types of intracellular vacuoles containing collagen fibrils were present: vacuole type A exhibited typical cross-banded collagen immersed in finely granular electron-translucent material; and vacuoles type B and C showed electron-opaque granular material containing, respectively, faint cross-banded collagen and narrow clear stripes often with faint periodicity. In fed animals vacuoles type B were absent and the others were less evident. Only fasted animals showed extracellular acid phosphatase activity on collagen fibrils, filamentous aggregates and confined regions of the extracellular space. Intracellular acid phosphatase activity was observed in vacuoles type B and in lysosomes. The results indicate that trophoblast giant cells are capable of breaking down extracellular collagen and also of internalizing collagen for intracellular degradation. It is likely that these events are part of the process of invasion of the uterine wall. However, in fasted mice, collagen breakdown is more pronounced, and it may therefore contribute to the provision of amino acids and other nutrients for the undernourished fetus.

Acid Phosphatase↗
PubMed2002

Diffusion parameters in the striatum of rats with 6-hydroxydopamine-induced lesions and with fetal mesencephalic grafts.

Functional recovery after transplantation of dopaminergic cells into the lesioned striatum is dependent on widespread diffusion of the transmitter released by the graft. In the present study, we investigated the diffusion parameters of the extracellular space in the striatum of control, 6-hydroxydopamine-lesioned, intrastriatally grafted, and sham-grafted rats in vivo. We used two types of grafts-single macrografts or multiple micrografts. The real-time iontophoretic tetramethylammonium method enabled us to extract three extracellular space diffusion parameters: volume fraction, alpha, tortuosity, lambda, and nonspecific uptake of tetramethylammonium, k'. Compared with controls (alpha = 0.19, lambda = 1.59), in lesioned animals both alpha and lambda were lower (alpha = 0.14, lambda = 1.50). alpha and lambda were increased inside macro-and micrografts, where alpha = 0.24 and lambda = 1.80, and in sham-grafted areas, where alpha = 0.24 and lambda = 1.72. In regions outside the grafts (alpha = 0.15, lambda = 1.51) or in sham grafts (alpha = 0.14, lambda = 1.49), the values of alpha and lambda were similar to the values observed in lesioned striatum. Nonspecific uptake (k') did not differ among the groups. Our results show that, compared with control, alpha and lambda were decreased in dopamine-depleted areas and increased in areas with grafts. Multiple but smaller graft deposits, in contrast to their enlarged capability for dopaminergic reinnervation, impair the conditions for diffusion and extrasynaptic transmission in a larger area of the striatum than do single macrografts, presumably because of more extensive tissue damage, cell loss, and astrogliosis.

Animals↗
PubMed1997

Age-dependent changes of presynaptic neuromodulation via A1-adenosine receptors in rat hippocampal slices.

The presynaptic neuromodulation of stimulation-evoked release of [3H]-acetylcholine by endogenous adenosine, via A1-adenosine receptors, was studied in superfused hippocampal slices taken from 4-, 12- and 24-month-old rats. 8-Cyclopentyl-1,3-dimethylxanthine (0.25 microM), a selective A1-receptor antagonist, increased significantly the electrical field stimulation-induced release of [3H]-acetylcholine in slices prepared from 4- and 12-month-old rats, showing a tonic inhibitory action of endogenous adenosine via stimulation of presynaptic A1-adenosine receptors. In contrast, 8-cyclopentyl-1,3-dimethylxanthine had no effect in 24-month-old rats. 2-Chloroadenosine (10 microM), an adenosine receptor agonist decreased the release of [3H]-acetylcholine in slices taken from 4- and 12-month-old rats, and no significant change was observed in slices taken from 24-month-old rats. In order to show whether the number/or affinity of the A1-receptors was affected in aged rats, [3H]-8-cyclopentyl-1,3-dimethylxanthine binding was studied in hippocampal membranes prepared from rats of different ages. Whereas the Bmax value was significantly lower in 2-year-old rats than in younger counterparts, the dissociation constant (Kd) was not affected by aging, indicating that the density rather than the affinity of adenosine receptors was altered. Endogenous adenosine levels present in the extracellular space were also measured in the superfusate by high performance liquid chromatography (HPLC) coupled with ultraviolet detection, and an age-related increase in the adenosine level was found. In summary, our results indicate that during aging the level of adenosine in the extracellular fluid is increased in the hippocampus. There is a downregulation and reduced responsiveness of presynaptic adenosine A1-receptors, and it seems likely that these changes are due to the enhanced adenosine level in the extracellular space.

Acetylcholine↗
PubMed2002

A tobacco S-like RNase inhibits hyphal elongation of plant pathogens.

Ribonuclease (RNase) NE gene expression is induced in tobacco leaves in response to Phytophthora parasitica. Using antibodies directed against RNase NE, we demonstrate that RNase NE is extracellular at the early steps of the interaction, while the fungal tip growth is initiated in the apoplastic compartment. After production in Pichia pastoris and biochemical purification, we show that the S-like RNase NE inhibits hyphal growth from P. parasitica zoospores and from Fusarium oxysporum conidia in vitro. Conversion into an enzymatically inactive form after mutagenesis of the active site-histidine 97 residue to phenylalanine leads to the suppression of this activity, suggesting that RNase NE inhibits the elongation of germ tubes by degradation of microbial RNAs. Exogenous application of RNase NE in the extracellular space of leaves inhibits the development of P. parasitica. Based on its induction by inoculation, its localization, and its activity against two plant pathogens, we propose that RNase NE participates in tobacco defense mechanisms by a direct action on hyphal development in the extracellular space. The RNase activity-dependent antimicrobial activity of the S-like RNase NE shares similarities with the only other biological activity demonstrated for plant RNases, the inhibition of elongation of pollen tubes by the S-RNase in gametophytic self-incompatibility, suggesting a functional link between self and nonself interactions in plants.

Amino Acid Substitution↗
PubMed1987

Body composition after 'very-little-stomach' biliopancreatic bypass.

The nutritional status prior to and 3 months and 1 year after biliopancreatic bypass surgery was evaluated. The common nutritional indexes (serum albumin and transferin concentrations, daily urinary creatinine excretion and delayed hypersensitivity) were determined. The body compartments were derived from total body water (TBW) and total body sodium (TBNa), measured by dilutional technique, and total body potassium (TBK), calculated from TBW, TBNa, and the ratio of the sodium plus potassium content divided by the water content in a sample of whole blood. Before surgery, obese patients showed a dilatation of both fat an lean compartments with a normal lean body mass (LBM) qualitative composition, as indicated by TBNa/TBW, and TBNa/TBK ratios not greater than those measured in controls. Three months following very-little-stomach biliopancreatic bypass (VLS BPB), a consistent reduction of body weight and body fat were observed. The body cell mass value fell and reached a level closely similar to that found in lean control subjects. LBM showed only a slight decrease. A sharp increase of TBNa/TBW and TBNa/TBK ratios demonstrated a dilatation of the extracellular space. This malnutritional status was not detected by the usual nutritional parameters. One year after VLS BPB surgery, the patients' body composition became very similar to that of lean subjects, though a TBNa greater than that of controls suggested that a slightly expanded extracellular space was still present.

Adult↗