Testicular Leydig cells: differentiated cells responding to multiple hormonal control and producing varied products.
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This new replicative model here explained is the result of the fact that, even if replication and transcription are distinct events during the cell evolution, they are functionally correlated, being responsible both for the main features of the cell, and for hormones affinity, too. This model of replication suggests the spreading of replication, in both directions symmetrically from the origin site of each replicon, as well as a simultaneous replication of both DNA strands, despite the fact that one of them was until now called "lagging" strand. These two events are explained by initiation of each DNA catena with distinct RNA polymerase forms depending on the presence or absence of the sigma 70 recognition factor (or its beta gamma analogous eukaryotic factor). The arguments sustaining these events were gathered from many already known genetic studies, some of them being here supposed to new interpretations (for instance, the phi x 174, M13 phages replication models). The disposition of both DNA strands during replication allows the intervening of both RNA polymerase types only in RNA primer synthesis. However, other physical restrictive interactions suggested theoretically prevent the going on of RNA polymerases activity like they do during transcription. This is the main reason that determines the exposure of DNA conformational changes occurring in the replication. These explanations may bring a possible new light about the "mystery" of the phenomenon producing the "replicative eye" inside the double helical structure of DNA.
Heat production was measured in relation to cell differentiation and phagocytie function using cells of human monocyte-histiocyte cell line U937. U937 cells differentiated monocytic phagocytes when cultured with lymphokine. Heat production increased as result of differentiation and phagocytosis. An important finding was that the heat increase in differentiated cells and during phagocytosis was directly proportional to the concentration of lymphokine. This strongly suggested that heat production is a quantitative parameter not only for cell differentiation but also for phagocytic function. The measurement of heat produced by mammalian cells can therefore be used to quantitate the differentiation and function of cells.
Cell differentiation is the process by which genetic information is selectively expressed to produce cells with various morphologies and functions. The integrated changes necessary for this fundamentally important process have recently been the subject of intense study. This review will summarize data from several laboratories correlating differentiation with the activity of the enzyme ADP-ribosyl transferase and with changes in single-strand DNA breaks in various diverse eukaryotic systems. We will then discuss the implications of these observations for differentiation in general, including the possibility that rearrangement of genetic material is a widespread mechanism for controlling gene expression.
A general theory giving an explanation of microbial cell differentiation is presented. Based on experimental results, an unstable hyperoxidant state is postulated to trigger differentiation. Simple rules, involving the reduction of dioxygen and the isolation from dioxygen by diverse mechanisms, are proposed to govern transitions between the growth state and the differentiated states. With this view, common features of microbial differentiation processes, dimorphic growth, cell differentiation in dioxygen evolving phototrophs and in anaerobes are analyzed. The theory could have implications for understanding cell differentiation in higher organisms.
Cells in the neurogenic region of an insect ectoderm have two alternative fates, making neurons or epidermis. The fates seem to be determined through a laterally inhibitory interaction among cells. That is, initially homogeneous cells are all competent to differentiate into neuroblasts. Once a cell has differentiated as a neuroblast, it inhibits its immediate neighbors from following this pathway. The differentiation process is simulated by a digital computer in a planar array of polygonal domains similar to a cell pattern. We find that the number of cells differentiating as neuronal precursors in insect neurogenesis is that expected under the hypothesis of lateral inhibition of cell differentiation between immediate neighbors.
Cell surface glycolipid expression as well as total glycolipid content of various B cell lines, representative of different B cell stages, and normal B lymphocytes were examined. Glycolipids, made up of a carbohydrate chain attached to a lipid called ceramide, are classified in four main 'series'. These series are defined according to the identity and chemical bonding of the sugars closest to the ceramide moiety. The pre-B cell lines contained lacto-series type II chain-based glycolipids and II3-alpha-N-acetyl-neuraminosyllactosylceramide (GM3) ganglioside. Upon differentiation, the lacto-series synthesis was shut down whereas compounds of the globo-series appeared: resting lymphocytes and lymphoblastoid cell lines (LCL) expressed GM3, globotriaosylceramide (Gb3), and globoside (Gb4). At a later stage of B cell differentiation, biosynthesis of the ganglio-series was extended and myeloma cells expressed II3-alpha-N-acetyl-neuraminosylgangliotriosylceramide (GM2). At the cell surface, in addition to Gb3, that we previously described as specifically expressed on Burkitt's lymphoma cells and on a subset of germinal centre tonsillar B cells, two glycolipids seemed specific of certain B cell lines: Gb4 was strongly positive on six out of eight LCLs and on the low buoyant density fraction of tonsillar B lymphocytes, whereas GM2 ganglioside was only detected on the two myeloma cell lines. These results, demonstrating the stage-dependent expression of certain glycolipids, suggest that these carbohydrate molecules could play functional roles during B cell differentiation.
Cell lines derived from the lens generally fail to maintain synthesis of crystallins in long-term culture. Here we demonstrate that the N/N1003A line of undifferentiated lens epithelial cells, derived from a newborn rabbit, does not produce detectable levels of alpha-, beta- or gamma-crystallin transcripts, yet is capable of supporting the transient expression of the mouse gamma 2-crystallin promoter, a promoter which is active only in terminally differentiated lens fiber cells in vivo. Analysis of a set of deletion constructs suggested that sequences required for activity of the mouse promoter in N/N1003A cells are similar, but not identical, to those previously shown to be essential in primary chick embryo lens explants. Therefore, these results suggest that different transcriptional factors may be capable of supporting lens-specific activity of the mouse gamma 2 promoter. In addition, this cell line, N/N1003A, should be useful for investigations on the elements regulating gamma-crystallin gene expression.
The white blood cell count, the differential cell count, and morphological changes in leukocytes can provide valuable diagnostic information that can aid the physician in determining the cause of illness. These simple laboratory tests, all too frequently either abused or ignored, when employed with precision can supplement but not supplant clinical judgment.
The aim of the study was to determine the pulmonary 67-gallium uptake, bronchoalveolar lavage (BAL) cell differentiation and the activity of BAL cells, measured as release of superoxide anion (O2-), and to investigate the results whether there are relations. In 11 nonsmoking systemic scleroderma (SS) patients and 11 systemic lupus erythematosus (SLE) patients with lung involvement double-sided BAL were performed, mainly in regions with increased 67-gallium uptake. Release of O2- was measured by INT-assey. BAL cell differentiation was in SS and SLE pathological in 68.2% without side-difference. In contrast to SS, O2(-)-release in SLE depends on BAL cell differentiation and is most increased in normal BAL cell differentiation. There is no correlation between 67-gallium uptake and both BAL cell differentiation and O2(-)-release. The results suggest, that in contrast to SS, BAL cells in SLE with pathological differentiation are less activated than BAL cells with normal differentiation probable due to autoimmunological factors. Pulmonary 67-gallium scan and BAL seem to be independent from each other.
1. The variation in cellular glycogen content of differentiating cells derived from myxamoebae that initially contained a wide range of glycogen contents (0.047-5.56mg of glycogen/10(8) myxamoebae) has been studied. 2. Myxamoebae that initially contained 0.047-3.62mg of glycogen/10(8) myxamoebae all gave rise to fruiting bodies that contained similar amounts of glycogen (0.06-0.11mg of glycogen/10(8) cells) but myxamoebae that initially contained 5.56mg of glycogen formed fruiting bodies containing 0.5mg of glycogen/10(8) cells. 3. Despite the high net rate of glycogen disappearance (during cell differentiation) from cells that contained more than 2mg of glycogen/10(8) cells initially, there were still significant variations in the rate of glycogen synthesis. The rate of glycogen synthesis reached a peak at the aggregation stage. 4. Evidence is presented showing that the rate of this synthesis of glycogen is controlled by factors other than the intracellular concentration of glycogen synthetase. 5. Our results are discussed in the context of the theory that the rates of glycogen synthesis and degradation act as a control mechanism for cell differentiation. 6. Criteria are discussed for deciding whether a biochemical event is causally or secondarily related to morphogenesis.
As has been reported, doses of 12-O-tetradecanoylphorbol-13-acetate (TPA) as small as 1 to 100 ng/ml induced human promyelocytic leukemia HL-60 cells to differentiate terminally into macrophage-like cells rather than toward cells of the granulocytic series. This differentiation was accompanied by the appearance of monocyte/macrophage markers and by the disappearance of myeloid markers from the view point of enzyme cytochemistry. Contrasted to untreated HL-60 cells, TPA-treated cells increased in cell size and showed increased phagocytotic activities against opsonized sheep blood red cells and activated yeast. Nitroblue tetrazolium-positive cells increased rapidly after TPA exposure. The alterations of the cell cycle traverse of HL-60 cells by TPA were analyzed by [3H]thymidine autoradiography, flow microfluorimetry, and mitotic cell counting. TPA sequentially caused (a) inhibition of cells to move from G1 to S near G1/S boundary in G1; (b) temporary inhibition in G2; (c) growth arrest of most cells in G1 within 2 to 3 days after TPA exposure.
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