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M E Atkinson

Publications and source records attributed to M E Atkinson.

At least 37 records · Page 2Linked to original sources

Ultrastructural morphometry of blastogenesis. II. Stimulated lymphocytes, the progeny of blast cells induced in vivo with DNCB.

As a companion to an earlier study, the morphometric attributes of stimulated (blast-derived) lymphocytes in mouse axillary lymph nodes have been established using stereological and autoradiographic methods. Blast transformation was induced in vivo with dinitrochlorobenzene (DNCB) and stimulated cells were labelled with tritiated thymidine. Random samples of cells were taken for light and electron microscopic morphometry. In comparison to the unstimulated lymphocyte, the stimulated cell increased in size and possessed a greater plasma membrane surface area. Increase in cell size was the result of increases in the volumes of all measured subcellular compartments both in the nucleus and the cytoplasm. Heterogeneity of the stimulated cell population precludes firm conclusions regarding the significance of all these ultrastructural changes, though alterations in cell surface are discussed in the context of known biochemical differences accompanying blastogenesis.

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The surgical anatomy of the mandibular distribution of the facial nerve.

There are many controversies about the course of the mandibular nerve in the submandibular region. In an attempt to resolve these and improve the safety of submandibular approaches a study was undertaken based on anatomical dissection and measurement of 110 facial halves. In over half the specimens the mandibular nerves ran below the mandible and a significant proportion continued below the mandible distal to the facial vessels. The nerves lay in a plane between the platysma and the investing fascia. These findings influence the placement and depth of incisions in the submandibular region and the margins of safety attainable.

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The surgical anatomy of the cervical distribution of the facial nerve.

In an attempt to improve the safety of the submandibular approach to the mandible and submandibular anatomical dissections of 100 facial halves were undertaken. Observations were made on the course of the cervical branch of the facial nerve in relation to bony and soft tissue landmarks and fascial planes. The course of the nerve and its relation to the platysma muscle and investing fascia dictate the placement and depth of incision used for the submandibular approach.

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Ultrastructural morphometry of blastogenesis I: transformation of small lymphocytes stimulated in vivo with dinitrochlorobenzene.

Changes in the volumes and surfaces of subcellular compartments of unstimulated small lymphocytes and immunoblasts in mouse axillary lymph nodes have been established using stereological techniques. Blast transformation was induced in vivo with dinitrochlorobenzene (DNCB). Cell samples were obtained by random sampling regimes applied at light and electron microscopic levels. From electron micrographs the volume densities of euchromatin, heterochromatin, nucleoli, mitochondria, Golgi apparatus and rough endoplasmic reticulum were determined. Cell surface/volume ratios were also computed. By estimating mean nuclear volumes using light microscopy, it was possible to calculate absolute compartmental volumes and to evaluate the plasma membrane surface areas of average cells. Transformation in this model was characterized by a considerable cellular hypertrophy and a substantial increase in plasmalemma surface. Hypertrophy was the consequence of increases in the volumes of all measured intracellular compartments, notably euchromatin and "residual cytoplasm" (including ground cytoplasm and free ribosomes). These changes are discussed in the context of the altered metabolic status of cells.

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Changes in the plasma membrane surface of lymphocytes stimulated in vivo with DNCB.

Stereological principles have been used to evaluate ultrastructural changes which accompany the transformation of lymphocytes stimulated in vivo with dinitrochlorobenzene (DNCB). Whereas unstimulated lymphocytes and blast cells have slightly more than the minimal containing plasmalemmal surface for their volume, stimulated (blast-derived) lymphocytes have an excess surface area in the order of 30%. This observation is discussed in the context of altered cell function and the biosynthesis of additional membrane components.

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On the problem of counting and sizing mitochondria: a general reappraisal based on ultrastructural studies of mammalian lymphocytes.

The authors ask the question whether the parameters "numbers" and "volume" are suitable for the morphometric analysis of mitochondria. In several types of cell, irregularity of mitochondrial shape makes it technically difficult, if not impossible, to obtain reliable stereological estimates of mean organelle volume or number per unit volume. Of more fundamental concern is whether number of mitochondria per cell is of any real value as a structural correlate of respiratory potential and hence as a measure of cell function. Alternative parameters might serve better for this purpose. Though the problem is illustrated by reference to quantitative studies of lymphocytes, it is also pertinent to the investigation of many other cell types.

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An autoradiographic study of experimental odontogenic cyst formation in the mouse.

Proliferative populations of cells within the epithelial lining of developing experimental odontogenic cysts were identified by labeling with 3H-thymidine. Mouse molar teeth extracted from 10-day-old mice were transplanted subcutaneously and host animals were injected with 3H-thymidine 1 h prior to sacrifice. The cysts which developed around the crown of the transplanted teeth were prepared for autoradiographical examination. Labeling indices were high initially but decreased rapidly as the cysts enlarged. The pattern of labeling, however, bore no resemblance to the labeling of the reduced enamel epithelium from which the cysts developed. It was concluded that labeling activity reflects only the state of development and activity of the cyst and not the origin of the cyst.

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A histological study of odontogenic cysts formed following mouse molar tooth transplantation.

The enamel organs of subcutaneously transplanted mouse molar teeth undergo cyst formation and present a model for the study of the pathogenesis of development odontogenic cysts. Maxillary molars extracted from 10-day-old C57B1 mice were grafted subcutaneously into adult mice of the same strain. The grafts were recovered between 2 and 50 days after operation and routinely prepared for histological examination. After initial degeneration, the enamel organ took the form of a squamous epithelium in which after 5 to 6 days squamous hyperplasia took place. Cystic degeneration within the epithelium produced cavities lined with a thick parakeratotic stratified squamous epithelium which resembled the lining of an epidermoid implantation cyst. As the cysts enlarged the lining changed in appearance to a thin squamous non-keratinized epithelium. Similar features have been described in other experimentally produced cysts and in some odontogenic cysts in humans. Their different morphology may arise frominteraction betwen the surrounding connective tissue with epithelium at different stages of development.

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An autoradiographical study of [3H]thymidine incorporation into subcutaneously transplanted mouse molar teeth. Cell proliferation and migration in transplanted teeth.

Mice bearing either allografts or isografts of 10 day old molar teeth were injected with [3H]thymidine to identify proliferating and migrating cells within the graft and surrounding tissues. In isografts proliferating cells were found successively in the area underlying the cervix, in the cervical pulp and the coronal pulp. However, cells did not migrate from the cervical host tissue into the pulp, and it was concluded that donor cells are responsible for reparative processes in tooth isografts. Very few labelled cells were identified at any time in tooth allografts, which were not repaired. It is suggested that allografts are not repaired because allogeneic inhibition prevents the residual donor tissue from proliferating and differentiating. Inhibition of proliferation of residual cells may also account for the absence of a cell-mediated immune response to tooth allografts.

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