Connective-tissue component of the myocardium in the emergency stage of compensatory hyperfunction of the heart

1980 ◽  
Vol 89 (3) ◽  
pp. 371-373
Author(s):  
I. A. Chervova ◽  
T. V. Pistsova ◽  
E. V. Zamaraeva
Keyword(s):  
Connective Tissue ◽  
Tissue Component ◽  
Connective Tissue Component ◽  
Compensatory Hyperfunction

Tympanosclerosis

1980 ◽  
Vol 89 (4_suppl) ◽  
pp. 1-16 ◽  
Author(s):  
Maurice Schiff ◽  
Antonio Catanzaro ◽  
Jacques F. Poliquin ◽  
Allen F. Ryan
Keyword(s):  
Connective Tissue ◽  
Basement Membrane ◽  
Tympanic Membrane ◽  
Lamina Propria ◽  
Middle Ear ◽  
Immunofluorescent Staining ◽  
Ground Substance ◽  
Disease Entity ◽  
Tissue Component ◽  
Connective Tissue Component

Tympanosclerosis is a disease which affects the tympanic membrane (TM) and middle ear. The locus for the essential pathology is in the connective tissue component of the drum which is the lamina propria. In the middle ear, the pathology is in the basement membrane. In the early stages there is a minimal involvement of the mesenchymal component, usually seen as a small white macula, or scar, in the drum. In advanced disease, the hyalinization of the mesenchymal component together with the attraction of the calcium ion leads to a thick, dense, calcified scar. The theory of pathogenesis for this disease entity is that the connective tissue component of these structures is stimulated by infection, inflammation, or trauma involving some degree of local immunological hypersensitivity. With severe middle ear infection, the mucosa of the inner surface of the drum becomes permeable, and the ground substance of the lamina propria becomes edematous taking up water together with components of complement from the middle ear disease. The abnormal middle ear secretions contain the immunoglobulin components capable of participating in the process. If there is any damage to the connective tissue, the adsorption and repair permits the body to react immunologically against the destroyed tissue, thereby sensitizing this area. Experiments were performed with the guinea pig in which the tympanic membrane was removed and the lamina propria isolated and prepared as an immunological antigen. When this material was injected into the rabbits, a high, satisfactory antiguinea pig tympanic membrane antibody was formed (anti-GPTM). It was then possible to remove this anti-GPTM antibody from the serum. The tissue specificity was determined by immunofluorescent staining which showed it to be adsorbed onto the TM, middle ear mucosa, as well as the basement membrane of the respiratory tract. The guinea pigs which were passively sensitized with anti-GPTM antiserum demonstrated the binding of the antibodies on the tympanic membrane when subject to trauma, infection, or cautery. The manifestation was in the anatomical area related to the injury. Complement fixation was, likewise, demonstrated. Controlled animals which were not traumatized, or were not passively sensitized, included those which were injected with IgG from rabbits not sensitized against GPTM. They showed no fixation of antibody or complement in the TM. Following injury the antibody and complement bound to the TM provide the necessary elements for the subsequent immunopathologic disease entity known at tympanosclerosis.

Observations on the corpus luteum during pregnancy and lactation in the marsupials Isooson macrous and Perameles nasuta

1979 ◽  
Vol 27 (5) ◽  
pp. 881 ◽  
Author(s):  
AG Lyne ◽  
DE Hollis
Keyword(s):  
Connective Tissue ◽  
Maximum Size ◽  
Corpora Lutea ◽  
Lactation Period ◽  
Tissue Component ◽  
Luteal Cells ◽  
Connective Tissue Component ◽  
Pregnancy And Lactation ◽  
The Mean ◽  
Formed Structure

Ovaries from the bandicoots I. macrourus and P. nasuta, collected during pregnancy and lactation, were examined macroscopically and with the light microscope. The mean number of corpora lutea (CL) was greater in I. macrourus (5.13) than in P. nasuta (3.31). This difference in ovulation rate was reflected in the mean number of embryos and the mean number of pouch young respectively (I. macrourus 4.05, 3.07; P. nasuta 2.63, 2.65). During the first few days of pregnancy, the transformation of follicle granulosa cells into luteal cells was accompanied by the intrusion of the theca, which produced a network of blood vessels and connective tissue. A conspicuous feature of the developing CL was the presence of pools of blood between the luteal cells. By 5-6 days of pregnancy, the CL was a fully formed structure, the central cavity having been filled in by hypertrophy of the luteal cells and an increase in the connective tissue which formed a central core. The luteal cells had almost reached their maximum size and they contained numerous lipid droplets. Mitoses of luteal cells were not evident at any stage in the formation of the CL or later, though some of the luteal cells had two or more nuclei. The structure of the CL and the diameter of the luteal cells and their nuclei remained almost constant until regression occurred after the 45th day of the 60-day lactation period. Regression of the CL was characterized by a marked reduction in the size of the luteal cells and their nuclei as well as an increase in the connective tissue component. Diameters and volumes of the CL were similar in the two species, reaching maxima during the second half of pregnancy and changing very little until the 45th day of lactation, after which they decreased rapidly. This decline occurred whether or not the animals subsequently ovulated during the last quarter of the lactation period.

IgE alone stimulates mast cell adhesion to fibronectin via pathways similar to those used by IgE + antigen but distinct from those used by Steel factor

Blood ◽  
2003 ◽  
Vol 102 (4) ◽  
pp. 1405-1413 ◽  
Author(s):  
Vivian Lam ◽  
Janet Kalesnikoff ◽  
Corinna W. K. Lee ◽  
Valerie Hernandez-Hansen ◽  
Bridget S. Wilson ◽  
...  
Keyword(s):  
Mast Cells ◽  
Connective Tissue ◽  
Immunoglobulin E ◽  
Extracellular Calcium ◽  
Phosphatidylinositol 3 Kinase ◽  
Murine Bone Marrow ◽  
Steel Factor ◽  
Connective Tissue Component ◽  
Late Antigen ◽  
Extracellular Regulated Kinase

Abstract We recently demonstrated that immunoglobulin E (IgE), in the absence of cross-linking agents, activates signaling pathways in healthy murine bone marrow–derived mast cells (BMMCs) and that this activation enhances BMMC survival, at least in part, via secretion of autocrine-acting cytokines. We report herein that IgE alone also triggers the adhesion of both BMMCs and connective tissue mast cells (CTMCs) to the connective tissue component, fibronectin (FN). This adhesion occurs to the same extent as that triggered by optimal levels of Steel factor (SF) or IgE + antigen (IgE + Ag) and is mediated by an increased avidity of the integrin very late antigen 5 (VLA-5). Moreover, this IgE-induced adhesion, which is prolonged compared with that elicited by SF or IgE + Ag, requires phosphatidylinositol 3-kinase (PI3K), phospholipase C γ (PLCγ), and extracellular calcium but not extracellular-regulated kinase (Erk) or p38. Interestingly, we found, using the calcium channel blocker, 2-APB (2-aminoethoxydiphenyl borate) and Lyn–/– BMMCs that both IgE- and IgE + Ag-induced adhesion to FN require extracellular calcium entry, whereas SF does not. Furthermore, our data suggest that FN acts synergistically with IgE to prolong intracellular phosphorylation events and to enhance IgE-induced inflammatory cytokine production and BMMC survival.

Sign in / Sign up

Export Citation Format

Share Document