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Infections with mycobacteria other than tubercle bacilli are responsible for a variable percentage of cross-reactions to tuberculin. Two major suggestions for circumventing this problem have been made: the first, development of a quantitative tuberculin test, is based on the fact that most cross-reactions are smaller than those caused by true tuberculous infections; the second, preparation of purified skin test antigens from other mycobacteria, is based on the hope that greater specificity will be displayed by homologous sensitin. Effort so far has been focused on the culture filtrates as the source of antigen. This article describes the preparation of low molecular weight purified protoplasmic peptides (PPP) of specificity and sensitivity superior to purified protein derivatives.
The specificity of purified protein derivatives (PPD) prepared from the culture filtrates of Mycobacterium tuberculosis (PPD), M. kansasii (PPD-Y), M. intracellulare (PPD-B), and M. scrofulaceum (PPD-G) were compared to comparable protoplasmic extracts (PPP) of the same organisms by gel diffusion and delayed hypersensitivity reactions in sensitized guinea pigs. PPD and, to a lesser degree, PPD-Y demonstrated specificities sufficient to enable identification of homologously sensitized guinea pigs in the above group of four mycobacteria. PPD-B and PPD-G did not always elicit the largest reaction in homologously sensitized animals. The PPP sensitins from M. tuberculosis and M. kansasii produced as good skin reactions at 24 and at 48 hr as did their PPD counterparts. The PPP from M. scrofulaceum and M. intracellulare were more specific and more reactive than corresponding PPD, regardless of the time of comparison. Although based on different immunological mechanisms, the specificity of these two groups of sensitins, as demonstrated by delayed hypersensitivity, correlated well with serological comparisons in the gel diffusion test. The low degree of specificity of PPD-B and PPD-G in contrast to that of corresponding PPP was reflected in the precipitin bands in agar gel.
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The behavior of the cell depends to a large extent on the permeability of the outer non-aqueous surface layer of the protoplasm. This layer is immiscible with water but may be quite permeable to it. It seems possible that a reversible increase or decrease in permeability may be due to a corresponding increase or decrease in the water content of the non-aqueous surface layer. Irreversible increase in permeability need not be due primarily to increase in the water content of the surface layer but may be caused chiefly by changes in the protoplasm on which the surface layer rests. It may include desiccation, precipitation, and other alterations. An artificial cell is described in which the outer protoplasmic surface layer is represented by a layer of guaiacol on one side of which is a solution of KOH + KCl representing the external medium and on the other side is a solution of CO(2) representing the protoplasm. The K(+) unites with guaiacol and diffuses across to the artificial protoplasm where its concentration becomes higher than in the external solution. The guaiacol molecule thus acts as a carrier molecule which transports K(+) from the external medium across the protoplasmic surface. The outer part of the protoplasm may contain relatively few potassium ions so that the outwardly directed potential at the outer protoplasmic surface may be small but the inner part of the protoplasm may contain more potassium ions. This may happen when potassium enters in combination with carrier molecules which do not completely dissociate until they reach the vacuole. Injury and recovery from injury may be studied by measuring the movements of water into and out of the cell. Metabolism by producing CO(2) and other acids may lower the pH and cause local shrinkage of the protoplasm which may lead to protoplasmic motion. Antagonism between Na(+) and Ca(++) appears to be due to the fact that in solutions of NaCl the surface layer takes up an excessive amount of water and this may be prevented by the addition of suitable amounts of CaCl(2). In Nitella the outer non-aqueous surface layer may be rendered irreversibly permeable by sharply bending the cell without permanent damage to the inner non-aqueous surface layer surrounding the vacuole. The formation of contractile vacuoles may be imitated in non-living systems. An extract of the sperm of the marine worm Nereis which contains a highly surface-active substance can cause the egg to divide. It seems possible that this substance may affect the surface layer of the egg and cause it to take up water. A surface-active substance has been found in all the seminal fluids examined including those of trout, rooster, bull, and man. Duponol which is highly surface-active causes the protoplasm of Spirogyra to take up water and finally dissolve but it can be restored to the gel state by treatment with Lugol solution (KI + I). The transition from gel to sol and back again can be repeated many times in succession. The behavior of water in the surface layer of the protoplasm presents important problems which deserve careful examination.
Freezing behavior of wood tissue of red osier dogwood (Cornus sericea L.) cannot be explained by current concepts of freezing resistance. Previous studies indicated that water in wood tissue presumably froze extracellularly. However, it was observed that xylem ray parenchyma cells within these tissues could survive temperatures as low as -80[deg]C and the walls of these cells did not collapse during freezing (S.R. Malone and E.N. Ashworth [1991] Plant Physiol 95: 871-881). This observation was unexpected and is inconsistent with the current hypothesis of cell response during freezing. Hence, the objective of our study was to further examine the mechanism of freezing resistance of wood tissue of red osier dogwood. We studied freezing stress response of xylem ray parenchyma cells of red osier dogwood using freeze substitution and transmission electron microscopy. Wood samples were collected in winter, spring, and summer of 1992. Specimens were cooled from 0[deg]C to -60[deg]C at 5[deg]C/h. Freezing stress did not affect the structural organization of wood tissue. However, the xylem ray parenchyma cells showed two unique responses to a freezing stress: protoplasm contraction and protoplasm fragmentation. Protoplasm contraction was evident at all freezing temperatures and in tissues collected at different times of the year. Cells with fragmented protoplasm, however, were noticed only in tissues collected in spring and summer. Protoplasm contraction in winter tissue occurred without apparent damage to the protoplasm. In contrast, protoplasm contraction in spring and summer tissues was accompanied by substantial damage. No evidence of intracellular ice formation was observed in parenchyma cells exposed to freezing stress. Differences in protoplasm contraction and appearance of cells with fragmented protoplasm likely indicated seasonal changes in cold hardiness of the wood tissue of red osier dogwood. We speculate that the appearance of fragmented protoplasm may indicate that cells are being injured by an alternative mechanism in spring and summer.
The electric potential difference (1 to 15 mv.) between two loci of the slime mold connected with a strand of protoplasm changes rhythmically with the same period (60 to 180 seconds) as that of back and forth protoplasmic streaming along the strand. When atmospheric pressure at a part of the plasmodium is increased (about 10 cm. H(2)O), the electric potential at this part becomes positive (0 to 20 mv.) to another part with a time constant of 2 to 15 minutes. If the atmospheric pressure at a part of the plasmodium is changed (about 10 cm. H(2)O) periodically, the electric potential rhythm also changes with the same period as that of the applied pressure change, and the amplitude of the former grows to a new level (i.e., forced oscillation). The electric potential rhythm, in this case, is generally delayed about 90 degrees in phase angle from the external pressure change. The period of the electric potential rhythm which coincided with that of the pressure change is maintained for a while after stopping the application of the pressure change, if the period is not much different from the native flow rhythm. Such a pressure effect is brought about by the forced transport of protoplasm and is reversible as a rule. In the statistical analysis made by Kishimoto (1958) and in the rheological treatment made in the report, the rhythmic deformation of the contractile protein networks is supposed to be the cause of the protoplasmic flow along the strand and of the electric potential rhythm. The role of such submicroscopic networks in the protoplasm in various kinds of protoplasmic movement is emphasized.
SUMMARY: The generally accepted concept that astrocytes are highly resistant to hypoxic/ischemic conditions has been challenged by an increasing amount of data. Considering the differences in functional implications of protoplasmic versus fibrous astrocytes, the authors have investigated the possibility that those discrepancies come from specific behaviors of the two cell types. The reactivity and fate of protoplasmic and fibrous astrocytes were observed after permanent occlusion of the medial cerebral artery in mice. A specific loss of glial fibrillary acidic protein (GFAP) immunolabeling in protoplasmic astrocytes occurred within minutes in the area with total depletion of regional CBF (rCBF) levels, whereas "classical" astrogliosis was observed in areas with remaining rCBF. Severe disturbance of cell function, as suggested by decreased GFAP content and increased permeability of the blood-brain barrier to macromolecules, was rapidly followed by necrotic cell death, as assessed by ultrastructure and by the lack of activation of the apoptotic protease caspase-3. In contrast to the response of protoplasmic astrocytes, fibrous astrocytes located at the brain surface and in deep cortical layers displayed a transient and limited hypertrophy, with no conspicuous cell death. These results point to a differential sensitivity of protoplasmic versus fibrous cortical astrocytes to blood deprivation, with a rapid demise of the former, adding to the suggestion that protoplasmic astrocytes play a crucial role in the pathogenesis of ischemic injury.
In electron microscopic studies, protoplasmic anastomoses were found to occur between smooth muscle cells in the gastrointestinal tracts of rats. The protoplasmic connections are apparently cylindrical in form and contain cytoplasm having a density similar to that of the cellular regions connected. The membranes enclosing the cytoplasmic connections are continuous with the membranes of the connected cells. These connecting structures have been called intercellular bridges, which is adequately descriptive if emphasis is placed on the interpretation that they represent protoplasmic anastomoses. To emphasize this, the term may be modified; i.e., anastomotic intercellular bridges. In some cellular connections, transverse diffuse lines are seen. These may be interpreted as either disintegrating or reforming plasma membranes which is consistent with the concept that protoplasmic continuity is transitory. Since the animals were dissected under hypothermia, reduction of muscular activity by the chilling may have helped to preserve the structure of existing anastomotic intercellular bridges. The intercellular protoplasmic anastomoses may play a role in the conduction of action potentials from one smooth muscle cell to another.
We have studied semithin frozen sections of developing and adult rat central nervous system (CNS) by indirect immunofluorescence in order to determine the antigenic phenotype of protoplasmic and fibrous astrocytes. Using antibodies against glial fibrillary acidic protein (GFAP) to identify astrocytes, we show that the great majority of fibrous astrocytes in adult optic nerve are labeled by the monoclonal antibody A2B5, while the great majority of protoplasmic astrocytes in adult cerebral cortex are not. Astrocytes located at the periphery of the adult optic nerve that form the glial limiting membrane are more like protoplasmic astrocytes than fibrous astrocytes in that they strain relatively weakly with anti-GFAP antiserum and are A2B5-. In the developing rat optic nerve, protoplasmic-like astrocytes appear at least one week before the first fibrous astrocytes can be detected. Taken together with our previous observations on astrocytes in suspensions and cultures of developing rat optic nerve (Raff, M.C., E.R. Abney, J. Cohen, R. Lindsay, and M. Noble (1983) J. Neurosci. 3: 1289-1300; Raff, M.C., R.H. Miller, and M. Noble (1983) Nature 303: 390-396), these results suggest that protoplasmic and fibrous astrocytes are distinct classes of glial cells that differ in their antigenic phenotype and developmental history, as well as in their morphology and location within the CNS.
The prenatal developmental histories of layer I, fibrous (white matter), and protoplasmic (gray matter) astrocytes have been studied in the human neocortex by the rapid Golgi method. The developmental route followed by each of these astrocytes is a distinct process which evolves from a specific precursor, occurs at a different time, and is linked to a specific event. The differentiation of layer I astrocytes is linked to the neocortex external glial limiting membrane (EGLM), that of fibrous astrocytes to the early white matter vascularization and maturation, and that of protoplasmic astrocytes to the late gray matter ascending vascularization and maturation. At the start of development, three glial precursors are established in the neocortex: 1) original radial neuroectodermal cells with nuclei above the primordial plexiform layer (PPL) by losing their ependymal and retaining their pial attachments become early astrocytes of layer I and EGLM components; 2) neuroectodermal cells with nuclei below the PPL that retain their pial and ependymal attachments become type I radial glial cells which are committed to the guidance of neurons and the early EGLM maintenance; and, 3) neuroectodermal cells that lose their pial but retain their ependymal attachment are transformed into type II radial glial precursors. By progressively losing their ependymal attachment, type II radial glia precursors become freely migrating cells, establish vascular contacts, and differentiate into fibrous astrocytes (and into oligodendrocytes?) throughout the subplate, developing white matter, and paraventricular regions. After the formation of the gray matter, additional layer I astrocytes are needed for the EGLM late prenatal and postnatal maintenance because type I radial glia cells start to regress and to reabsorb their EGLM endfeet. A late ependyma-to-pia migration of glial precursors progressively repopulates layer I with additional astrocytes and establishes the ephemeral subpial granular layer (SGL) of Ranke. From the 15th week of gestation to the time of birth, late astrocytes of layer I lose their EGLM attachments, migrate freely into the maturing gray matter, establish vascular contacts, and differentiate into protoplasmic astrocytes. The protoplasmic astrocytes of the gray matter evolve from transformation of layer I astrocytes rather than from radial glia cells as is generally believed.
Adrenal grafting for Parkinson's disease has led to modest functional improvement despite poor graft survival. One explanation is a neurotrophic response within the traumatized striatum. This study was undertaken to investigate the time course of the astrocytic response in vivo and in vitro, and the expression of ciliary neurotrophic factor (CNTF) mRNA following striatal injury. Unilateral stereotaxic biopsy of the rat striatum was performed and gelatin sponge (gel-foam) was immediately placed into the biopsy cavity. Rats were sacrificed on days 1, 3, 5, 7, 14, and 28 post biopsy. Immunohistochemical staining of the traumatized striatum with antibodies to glial fibrillary acidic protein (GFAP) was carried out. The reactive astrocytes which appeared within 7 days after trauma were mostly protoplasmic on the basis of morphology, and maximal on day 7, being 30 times the level in the normal striatum. After day 7, fibrous astrocytes appeared and increased up to day 28, while protoplasmic astrocytes decreased. In addition, immunocytochemical double staining of short term cultured astrocytes from the traumatized striatum with anti-A2B5 and anti-GFAP antibodies revealed that 84% and 90% of astrocytes were type 1 astrocytes on days 3 and 7, respectively; however, by day 28 47% of astrocytes were type 2. Northern blot analysis revealed that CNTF mRNA expression was up-regulated and peaked on day 7, coincident with a predominance of protoplasmic astrocytes in vivo and type 1 astrocytes in vitro, respectively. These findings suggest that the expression of CNTF mRNA is part of the early astrocytic response to trauma, particularly associated with protoplasmic astrocytes in vivo and type 1 astrocytes in vitro.(ABSTRACT TRUNCATED AT 250 WORDS)
In Podospora anserina, protoplasmic incompatibility due to the combination of nonallelic genes is suppressed by the addition of a recessive mutation in the modA gene to a dominant mutation in the modB gene. The effect of the modA and modB mutations on several features of protoplasmic incompatibility was investigated. Results show that the modA mutation suppresses two of them: the shutoff of RNA synthesis and the inhibition of synthesis of normal proteins. The suppression of a third feature of protoplasmic incompatibility, i.e., the synthesis of specific proteins, involves both the modA and the modB mutations. Employing the dihydrostreptomycin sensitivity of the modA gene product, it is shown that the modA gene controls the synthesis of one of these proteins (laccase III) at a posttranscriptional level. Concerning the modB gene, its effect was studied by means of a thermosensitive recessive mutation in this gene. It is demonstrated that the presence of this mutation results in the occurrence, in the cell extract, of enzyme activities (laccase III and its associated activities) and polypeptides specific to protoplasmic incompatibility. Furthermore, it could be deduced that the modB gene operates on these syntheses at a posttranscriptional level.
The effect of noradrenaline and isoprenaline on cyclic AMP accumulation has been investigated in primary rat astrocytes which contain either (a) protoplasmic astrocytes alone or (b) both fibrous and protoplasmic astrocytes. Isoprenaline and noradrenaline stimulated cyclic AMP formation in both astrocyte culture preparations. Combinations of noradrenaline (1 microM) and isoprenaline (1 microM) produced a cyclic AMP response which was 58% and 26% of that produced by isoprenaline alone in protoplasmic and mixed fibrous/protoplasmic cultures, respectively. In both preparations this inhibitory effect of noradrenaline was antagonized by the alpha 2-adrenoceptor antagonist yohimbine (1 microM). A striking feature of the concentration-response curve for isoprenaline (EC50 = 0.8 microM) in mixed fibrous/protoplasmic cultures was that the cyclic AMP response decreased sharply at concentrations above 1 microM. This phenomenon was not seen in cultures containing protoplasmic astroglia alone. The fall in the isoprenaline concentration-response curve was not observed in the presence of the alpha-adrenoceptor antagonist phentolamine (1 microM), the dihydropyridine calcium antagonist isradipine (10 microM), the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (0.1 mM) or in nominally calcium-free medium. The effect of phentolamine was mimicked by the alpha 1-adrenoceptor antagonist prazosin (1 microM) but not by the alpha 2-antagonist yohimbine (1 microM). In conclusion, the data from this study suggest that two different populations of astrocytes in in vitro culture are able to raise intracellular cyclic AMP levels via beta-adrenoceptor activation and that there are differences in the extent of alpha-adrenoceptor (both alpha 1- and alpha 2-) mediated inhibition of cyclic AMP accumulation between the two primary astroglial cell preparations.
Laser light scattered from particles in the streaming protoplasm of a living cell is shifted in frequency by the Doppler effect. The spectrum of the scattered light can be measured and interpreted to infer details of the velocity distribution in the protoplasm. We have developed this approach to study the protoplasmic streaming in the fresh-water alga Nitella. Our results indicate a characteristic flow pattern to which diffusion makes a negligible contribution. No difference in the velocity of particles of different size is indicated. The streaming velocity linearly with temperature with a supraoptimal temperature of 34 degrees C, and the velocity distribution becomes narrower at high temperatures. The protoplasmic streaming can be inhibited by laser light, and this effect has been used to study the photoresponse of the algae. Using beam diameters of about 50 mum, we have shown that the inhibition is very local, becoming minimal at a displacement of about 200 mum in the upstream direction and 400 mum in the downstream direction. Prolonged exposure produces a bleached area free of chloroplasts, which is three orders of magnitude less sensitive to photoinhibition.
UNLABELLED: Protoplasmic astrocytomas, composed of process-poor astrocytic cells and a microcystic background, are rare variants of low grade astrocytoma. Three hundred eight low grade astrocytomas over a 23-year period were reviewed. Sixteen (5.2%) were classified as pure protoplasmic astrocytoma. Patients (12 males, 4 females) ranged in age from 2.5 to 41 years (mean, 20.7 years). All patients presented with seizures and three had headaches. Duration of symptoms ranged from 7 months to 28 years (mean, 6.6 years). Nine tumors (56%) were left-sided and seven right-sided (44%). Seven (44%) occurred in the temporal lobe, six (37%) in the frontal lobe, two (13%) in the parietal lobe, and one (6%) in the thalamus. Surgery consisted of partial lobectomy with total tumor resection in nine and biopsy alone in seven. Five patients received adjuvant therapy with no apparent effect on survival. At frozen section, protoplasmic astrocytoma was most confused with fibrillary low grade astrocytoma (n = 6). Follow-up revealed 10 patients with no evidence of disease 2 to 108 months postoperatively (mean, 41 months), 5 patients were alive with disease 10 to 84 months postoperatively (mean, 56 months) and 1 patient died with disease at 36 months. Of patients with total tumor resection, eight had no evidence of disease and one died with disease. IN CONCLUSION: (1) protoplasmic astrocytomas in this study were more frequently observed in males at a younger mean age than fibrillary low grade astrocytomas as reported in literature; (2) temporal and frontal lobes were the most likely site of origin; and (3) complete excision may be beneficial, whereas adjuvant therapy appeared to have no effect on outcome.