scholarly journals THE TRANSFORMATION OF PNEUMOCOCCAL TYPES

1930 ◽  
Vol 51 (1) ◽  
pp. 123-147 ◽  
Author(s):  
Martin H. Dawson
Keyword(s):  
Single Cell ◽  
Subcutaneous Injection ◽  
Intermediate Stage ◽  
Group Iv ◽  
Type I ◽  
Type Ii ◽  
Type Iii

1. Type-specific S pneumococci may be transformed from one specific S type into other specific S types through the intermediate stage of the R form. 2. R forms of pneumococi, derived from any specific S type, may be transformed into S organisms of other specific types by the following procedure:—The subcutaneous injection, in white mice, of small amounts of living R forms together with vaccines of heterologous S cultures. (i) S vaccines heated for 15' at temperatures between 60° and 80°C., are effective in causing R forms, derived from heterologous S types, to revert to the type of the vaccine. (ii) S vaccines heated for 15' at temperatures between 80° and 100°C., are not effective in causing R forms, derived from heterologous S types, to revert to the type of the vaccine. (iii) S vaccines heated for 15' at temperatures between 80° and 100°C., may cause 2 R and 3 R cultures to revert to their original S type. (iv) S vaccines of any type, including Type I, heated for 15' at temperatures between 80° and 100°C., are not effective in causing 1 R cultures to revert to their original S type. (v) S vaccines heated for periods as long as two hours at 60°C. are effective in causing R forms, derived from heterologous types, to revert to the type of the vaccine. 3. A single cell R strain, derived from a Type II S pneumococcus, has been successively transformed into a Type III S, a Type I S and a Group IV S culture. 4. Corresponding with the various degrees of "degradation" of the R form there are varying degrees of "development" of the S form. 5. The nature of the conditions responsible for alteration of type as induced by these procedures has been investigated and the causes responsible for the transformations are discussed. 6. All attempts to produce transformation of type in vitro have been unsuccessful. 7. The rô1e which the phenomenon of transformation of type may play in problems of infection and epidemiology is indicated.

417. In vivo and in vitro evidence for cancer stem cells in human endometrial cancer

2008 ◽  
Vol 20 (9) ◽  
pp. 97
Author(s):  
S. Hubbard ◽  
C. E. Gargett
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Single Cell ◽  
Type I ◽  
Type Ii ◽  
Cloning Efficiency ◽  
Isolated Cells ◽  
Vimentin Expression ◽  
Self Renewal

Cancer stem cells (CSCs) have been identified in solid human cancers, including breast, colon, and ovary. Recent evidence suggests that the highly regenerative human endometrium harbors rare populations of epithelial stem/progenitor cells1. We hypothesised that CSCs are responsible for the epithelial neoplasia associated with endometrial carcinoma (EC), the most common gynaecological malignancy in women. The aim of this study was to demonstrate that a rare population of EC cells posses CSC properties. Stem cell characteristics were assessed in 25 EC and 2 endometrial hyperplasia tissues obtained from women aged 62 ± 9 yrs. Samples were cultured at clonal densities (100–500 cells/cm2) for 3–5 wks to determine cloning efficiency. Individual clones were serially subcloned (<10 cells/cm2) every 2–4 wks to determine self renewal capacity. Isolated cells in serial dilution (103–106 cells) were placed under the kidney capsule of immunocompromised mice for 12–16 wks to examine for the presence of tumour initiating cells (TIC). Resulting tumours and original parent tumours were examined for markers by immunohistochemistry. Most samples (23/26) contained rare colony forming cells. The cloning efficiency was 0.23% ± 0.28% (n = 11) in G1, 0.78% ± 0.67% (n = 8) in G2, 0.22% ± 0.21% (n = 3) in G3, 0.03% (n = 2) in type II tumours, and 0.14% (n = 2) in hyperplasia samples, and did not differ significantly between grades or between type I EC and normal endometrial epithelial samples 1. Single cell derived clones subcloned 2.5 ± 1.4 (n = 11), 3.2 ± 0.4 (n = 5), 3.5 (n = 2), 3.0 ± 1.7 (n = 3), and 2.5 (n = 2) times in G1, G2, G3, type II tumours and hyperplasia samples respectively, indicating increasing self renewal capacity with increasing tumour grade. Transplanted EC single cell suspensions initiated tumour growth with similar morphology, ERα, PR, EpCAM, cytokeratin, and vimentin expression as the parent tumour, indicating the presence of TIC. This evidence suggests that rare cells possessing the CSC properties of clonogenicty, self renewal, and tumorigenicity, may be responsible for the initiation and progression of EC. (1) Chan RWS et al. (2004). Biology of Reproduction. 70:1738–1750

scholarly journals Transepithelial Migration of Toxoplasma gondii Is Linked to Parasite Motility and Virulence

2002 ◽  
Vol 195 (12) ◽  
pp. 1625-1633 ◽  
Author(s):  
Antonio Barragan ◽  
L. David Sibley
Keyword(s):  
Toxoplasma Gondii ◽  
Ex Vivo ◽  
Type I ◽  
Type Ii ◽  
Long Distance ◽  
Type Iii ◽  
Migratory Capacity ◽  
Virulent Type ◽  
Parasite Motility

After oral ingestion, Toxoplasma gondii crosses the intestinal epithelium, disseminates into the deep tissues, and traverses biological barriers such as the placenta and the blood-brain barrier to reach sites where it causes severe pathology. To examine the cellular basis of these processes, migration of T. gondii was studied in vitro using polarized host cell monolayers and extracellular matrix. Transmigration required active parasite motility and the highly virulent type I strains consistently exhibited a superior migratory capacity than the nonvirulent type II and type III strains. Type I strain parasites also demonstrated a greater capacity for transmigration across mouse intestine ex vivo, and directly penetrated into the lamina propria and vascular endothelium. A subpopulation of virulent type I parasites exhibited a long distance migration (LDM) phenotype in vitro, that was not expressed by nonvirulent type II and type III strains. Cloning of parasites expressing the LDM phenotype resulted in substantial increase of migratory capacity in vitro and in vivo. The potential to up-regulate migratory capacity in T. gondii likely plays an important role in establishing new infections and in dissemination upon reactivation of chronic infections.

Three Types of Hereditary Antiterombin III Deficiency

1979 ◽  
Author(s):  
I. Nagy ◽  
H. Losonczy
Keyword(s):  
Antithrombin Iii ◽  
Clinical Signs ◽  
Type I ◽  
Type Ii ◽  
Type Iii ◽  
Basic Activity ◽  
At Iii ◽  
And Function

The authors detected in the last seven years 15 patients with hereditary antithrombin III/AT III/ abnormality. All of them had typical clinical signs of recurrent arterious and venous thromboembolie. The abnormality inherited as an autosomal trait. Three types of the abnormality could be observed. In Type I both quantity and function of AT III were extremely decreased. In type II AT III is normal in quantity but abnormal in function. In Type III AT III is quantitatively normal and also its function seems normal as far as its basic activity is concerned /activity measured in absence of heparin/, but its abnormality becomes manifest in the presence of heparin in vitro/and also in vivo/. 5 of the patients belonged to Type I, 4 to Type II and 6 to Type III. In 60 examined family members of the 15 patients an abnormal AT III could be observed in 44, clinical signs in 23.The examination of AT III activity in the presence of a given amount of heparin ia of great importance in recognition of the different types of antithrombin III abnormalities.

scholarly journals Erythroid progenitors in adult chronic pure red cell aplasia: relationship of in vitro erythroid colonies to therapeutic response

Blood ◽  
1984 ◽  
Vol 64 (1) ◽  
pp. 71-77 ◽  
Author(s):  
C Lacombe ◽  
N Casadevall ◽  
O Muller ◽  
B Varet
Keyword(s):  
Myeloproliferative Disorders ◽  
Pure Red Cell Aplasia ◽  
Type I ◽  
Red Cell ◽  
Type Ii ◽  
Erythroid Progenitors ◽  
Chronic Myeloproliferative Disorders ◽  
Type Iii ◽  
Red Cell Aplasia

Twenty-two cases of idiopathic chronic pure red cell aplasia (PRCA) in adults have been studied to evaluate their erythroid progenitors in vitro using the plasma clot technique. Three types of culture growth patterns were observed and classified as follows. Type I: showing a normal number of autologous CFU-E; type II: CFU-E and BFU-E were detectable but constantly decreased; type III: CFU-E and BFU-E were undetectable. The results were reproducible when patients were studied on two or more occasions. A strong correlation was found between the in vitro growth of autologous erythroid colonies and the results of immunomodulating therapy in 18 evaluable patients. A constant response to immunomodulating treatment was observed in type I patients. A constant failure of treatment was observed in type III patients, whereas results of therapy were unpredictable in type II patients. Two patients with chronic PRCA associated with thymoma and three with chronic myeloproliferative disorders were also studied. Patients with PRCA and thymoma behaved in vitro like type I patients. Patients with chronic myeloproliferative disorders exhibited very low numbers or no CFU-E or BFU-E (type II or III). These data support the hypothesis that at least two mechanisms are responsible for PRCA--one immunologically mediated and the other resulting from a stem cell defect. Moreover, they suggest that the study of erythroid progenitors in vitro might be useful in predicting the immunosuppressive therapy effect in adult chronic PRCA.

Distinct localization and function of1,4,5IP3 receptor subtypes and the1,3,4,5IP4 receptor GAP1IP4BP in highly purified human platelet membranes

Blood ◽  
2000 ◽  
Vol 95 (11) ◽  
pp. 3412-3422 ◽  
Author(s):  
Samer S. El-Daher ◽  
Yatin Patel ◽  
Ashia Siddiqua ◽  
Sheila Hassock ◽  
Scott Edmunds ◽  
...  
Keyword(s):  
Inositol Phosphate ◽  
Adenosine Monophosphate ◽  
Human Platelets ◽  
Surface Proteins ◽  
Receptor Subtypes ◽  
Type I ◽  
Type Ii ◽  
Type Iii ◽  
Receptor Antibodies

Platelet activation is associated with an increase of cytosolic Ca++ levels. The 1,4,5IP3receptors [1,4,5IP3R] are known to mediate Ca++ release from intracellular stores of many cell types. Currently there are at least 3 distinct subtypes of1,4,5IP3R—type I, type II, and type III—with suggestions of distinct roles in Ca++ elevation. Specific receptors for 1,3,4,5IP4 belonging to the GAP1 family have also been described though their involvement with Ca++ regulation is controversial. In this study we report that platelets contain all 3 subtypes of1,4,5IP3R but in different amounts. Type I and type II receptors are predominant. In studies using highly purified platelet plasma (PM) and intracellular membranes (IM) we report a distinct localization of these receptors. The PM fractions were found to contain the type III 1,4,5IP3R and GAP1IP4BP in contrast to IM, which contained type I1,4,5IP3R. The type II receptor exhibited a dual distribution. In studies examining the labeling of surface proteins with biotin in intact platelets only the type III1,4,5IP3R was significantly labeled. Immunogold studies of ultracryosections of human platelets showed significantly more labeling of the PM with the type III receptor antibodies than with type I receptor antibodies. Ca++ flux studies were carried out with the PM to demonstrate in vitro function of inositol phosphate receptors. Ca++ release activities were present with both 1,4,5IP3 and1,3,4,5IP4 (EC50 = 1.3 and 0.8 μmol/L, respectively). Discrimination of the Ca++-releasing activities was demonstrated with cyclic adenosine monophosphate (cAMP)-dependent protein kinase (cAMP-PK) specifically inhibiting 1,4,5IP3 but not1,3,4,5IP4-induced Ca++ flux. In experiments with both PM and intact platelets, the1,4,5IP3Rs but not GAP1IP4BP were found to be substrates of cAMP-PK and cGMP-PK. Thus the Ca++ flux property of1,3,4,5IP4 is insensitive to cAMP-PK. These studies suggest distinct roles for the1,4,5IP3R subtypes in Ca++movements, with the type III receptor and GAP1IP4BPassociated with cation entry in human platelets and the type I receptor involved with Ca++ release from intracellular stores.

Distinct localization and function of1,4,5IP3 receptor subtypes and the1,3,4,5IP4 receptor GAP1IP4BP in highly purified human platelet membranes

Blood ◽  
2000 ◽  
Vol 95 (11) ◽  
pp. 3412-3422 ◽  
Author(s):  
Samer S. El-Daher ◽  
Yatin Patel ◽  
Ashia Siddiqua ◽  
Sheila Hassock ◽  
Scott Edmunds ◽  
...  
Keyword(s):  
Inositol Phosphate ◽  
Adenosine Monophosphate ◽  
Human Platelets ◽  
Surface Proteins ◽  
Receptor Subtypes ◽  
Type I ◽  
Type Ii ◽  
Type Iii ◽  
Receptor Antibodies

Abstract Platelet activation is associated with an increase of cytosolic Ca++ levels. The 1,4,5IP3receptors [1,4,5IP3R] are known to mediate Ca++ release from intracellular stores of many cell types. Currently there are at least 3 distinct subtypes of1,4,5IP3R—type I, type II, and type III—with suggestions of distinct roles in Ca++ elevation. Specific receptors for 1,3,4,5IP4 belonging to the GAP1 family have also been described though their involvement with Ca++ regulation is controversial. In this study we report that platelets contain all 3 subtypes of1,4,5IP3R but in different amounts. Type I and type II receptors are predominant. In studies using highly purified platelet plasma (PM) and intracellular membranes (IM) we report a distinct localization of these receptors. The PM fractions were found to contain the type III 1,4,5IP3R and GAP1IP4BP in contrast to IM, which contained type I1,4,5IP3R. The type II receptor exhibited a dual distribution. In studies examining the labeling of surface proteins with biotin in intact platelets only the type III1,4,5IP3R was significantly labeled. Immunogold studies of ultracryosections of human platelets showed significantly more labeling of the PM with the type III receptor antibodies than with type I receptor antibodies. Ca++ flux studies were carried out with the PM to demonstrate in vitro function of inositol phosphate receptors. Ca++ release activities were present with both 1,4,5IP3 and1,3,4,5IP4 (EC50 = 1.3 and 0.8 μmol/L, respectively). Discrimination of the Ca++-releasing activities was demonstrated with cyclic adenosine monophosphate (cAMP)-dependent protein kinase (cAMP-PK) specifically inhibiting 1,4,5IP3 but not1,3,4,5IP4-induced Ca++ flux. In experiments with both PM and intact platelets, the1,4,5IP3Rs but not GAP1IP4BP were found to be substrates of cAMP-PK and cGMP-PK. Thus the Ca++ flux property of1,3,4,5IP4 is insensitive to cAMP-PK. These studies suggest distinct roles for the1,4,5IP3R subtypes in Ca++movements, with the type III receptor and GAP1IP4BPassociated with cation entry in human platelets and the type I receptor involved with Ca++ release from intracellular stores.

scholarly journals Erythroid progenitors in adult chronic pure red cell aplasia: relationship of in vitro erythroid colonies to therapeutic response

Blood ◽  
1984 ◽  
Vol 64 (1) ◽  
pp. 71-77 ◽  
Author(s):  
C Lacombe ◽  
N Casadevall ◽  
O Muller ◽  
B Varet
Keyword(s):  
Myeloproliferative Disorders ◽  
Pure Red Cell Aplasia ◽  
Type I ◽  
Red Cell ◽  
Type Ii ◽  
Erythroid Progenitors ◽  
Chronic Myeloproliferative Disorders ◽  
Type Iii ◽  
Red Cell Aplasia

Abstract Twenty-two cases of idiopathic chronic pure red cell aplasia (PRCA) in adults have been studied to evaluate their erythroid progenitors in vitro using the plasma clot technique. Three types of culture growth patterns were observed and classified as follows. Type I: showing a normal number of autologous CFU-E; type II: CFU-E and BFU-E were detectable but constantly decreased; type III: CFU-E and BFU-E were undetectable. The results were reproducible when patients were studied on two or more occasions. A strong correlation was found between the in vitro growth of autologous erythroid colonies and the results of immunomodulating therapy in 18 evaluable patients. A constant response to immunomodulating treatment was observed in type I patients. A constant failure of treatment was observed in type III patients, whereas results of therapy were unpredictable in type II patients. Two patients with chronic PRCA associated with thymoma and three with chronic myeloproliferative disorders were also studied. Patients with PRCA and thymoma behaved in vitro like type I patients. Patients with chronic myeloproliferative disorders exhibited very low numbers or no CFU-E or BFU-E (type II or III). These data support the hypothesis that at least two mechanisms are responsible for PRCA--one immunologically mediated and the other resulting from a stem cell defect. Moreover, they suggest that the study of erythroid progenitors in vitro might be useful in predicting the immunosuppressive therapy effect in adult chronic PRCA.

scholarly journals The Toxoplasma gondii-Shuttling Function of Dendritic Cells Is Linked to the Parasite Genotype

2009 ◽  
Vol 77 (4) ◽  
pp. 1679-1688 ◽  
Author(s):  
Henrik Lambert ◽  
Polya P. Vutova ◽  
William C. Adams ◽  
Karin Loré ◽  
Antonio Barragan
Keyword(s):  
Dendritic Cells ◽  
Toxoplasma Gondii ◽  
Phenotypic Traits ◽  
Type I ◽  
Type Ii ◽  
Parasite Genotype ◽  
Type Iii ◽  
Parasite Motility

ABSTRACT Following intestinal invasion, the processes leading to systemic dissemination of the obligate intracellular protozoan Toxoplasma gondii remain poorly understood. Recently, tachyzoites representative of type I, II and III T. gondii populations were shown to differ with respect to their ability to transmigrate across cellular barriers. In this process of active parasite motility, type I strains exhibit a migratory capacity superior to those of the type II and type III strains. Data also suggest that tachyzoites rely on migrating dendritic cells (DC) as shuttling leukocytes to disseminate in tissue, e.g., the brain, where cysts develop. In this study, T. gondii tachyzoites sampled from the three populations were allowed to infect primary human blood DC, murine intestinal DC, or in vitro-derived DC and were compared for different phenotypic traits. All three archetypical lineages of T. gondii induced a hypermigratory phenotype in DC shortly after infection in vitro. Type II (and III) strains induced higher migratory frequency and intensity in DC than type I strains did. Additionally, adoptive transfer of infected DC favored the dissemination of type II and type III parasites over that of type I parasites in syngeneic mice. Type II parasites exhibited stronger intracellular association with both CD11c+ DC and other leukocytes in vivo than did type I parasites. Altogether, these findings suggest that infected DC contribute to parasite propagation in a strain type-specific manner and that the parasite genotype (type II) most frequently associated with toxoplasmosis in humans efficiently exploits DC migration for parasite dissemination.

scholarly journals THE TRANSFORMATION IN VITRO OF R PNEUMOCOCCI INTO S FORMS OF DIFFERENT SPECIFIC TYPES BY THE USE OF FILTERED PNEUMOCOCCUS EXTRACTS

1932 ◽  
Vol 55 (1) ◽  
pp. 91-99 ◽  
Author(s):  
J. Lionel Alloway
Keyword(s):  
Type I ◽  
Type Ii ◽  
Specific Nature ◽  
Type Iii ◽  
Capsular Material

1. Avirulent R pneumococci derived from S forms of a specific type may be changed by growth in broth containing anti-R serum and a heated, filtered extract of S pneumococci of a different type, into virulent S organisms identical in type with the bacteria extracted. This has been accomplished in the case of R strains derived from Type II pneumococci, employing extracts prepared from Type III and Type I S forms. 2. The constituents of the extract supply an activating stimulus of a specific nature in that the R pneumococci acquire the capacity of elaborating the capsular material peculiar to the organisms extracted.

Labelling of non-A, non-B hepatitis infected chimpanzee hepatocytes with nuclease-gold conjugates

1984 ◽  
Vol 42 ◽  
pp. 250-251
Author(s):  
G. D. Gagne ◽  
M. F. Miller ◽  
D. A. Peterson
Keyword(s):  
Endoplasmic Reticulum ◽  
Experimental Infection ◽  
Uranyl Acetate ◽  
Type I ◽  
Cellular Injury ◽  
Type Ii ◽  
Tubular Structures ◽  
Type Iii ◽  
Type Iv ◽  
Infected Chimpanzee

Experimental infection of chimpanzees with non-A, non-B hepatitis (NANB) or with delta agent hepatitis results in the appearance of characteristic cytoplasmic alterations in the hepatocytes. These alterations include spongelike inclusions (Type I), attached convoluted membranes (Type II), tubular structures (Type III), and microtubular aggregates (Type IV) (Fig. 1). Type I, II and III structures are, by association, believed to be derived from endoplasmic reticulum and may be morphogenetically related. Type IV structures are generally observed free in the cytoplasm but sometimes in the vicinity of type III structures. It is not known whether these structures are somehow involved in the replication and/or assembly of the putative NANB virus or whether they are simply nonspecific responses to cellular injury. When treated with uranyl acetate, type I, II and III structures stain intensely as if they might contain nucleic acids. If these structures do correspond to intermediates in the replication of a virus, one might expect them to contain DNA or RNA and the present study was undertaken to explore this possibility.

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