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Biomedical subjects

N I Walker

Publications and source records attributed to N I Walker.

47 records · Page 3Linked to original sources
PubMed1992

Undifferentiated (embryonal) sarcoma of the liver. Pathologic findings and long-term survival after complete surgical resection.

Undifferentiated (embryonal) sarcoma of liver is a rare tumor with a reputed poor prognosis. Four patients with this tumor are reported, of whom three were alive without recurrence 1.5, 2.5, and 12 years after initial complete surgical resection, and two of whom received no adjuvant therapy. The fourth patient, in whom complete surgical resection of tumor was not achieved, died with recurrent tumor at 13 months. The latter tumor differed histologically and consisted mainly of closely packed smaller undifferentiated cells with a higher mitotic and apoptotic rate. Eosinophilic globules, characteristic of embryonal sarcoma, were found in some cases to contain condensed nuclear chromatin, evidence of origin from tumor cells dying by apoptosis. One tumor mainly contained large cysts lined by biliary-type epithelium; this suggested an origin from a multipotent precursor cell able to differentiate along both stromal and epithelial lines.

Adolescent↗
PubMed1992

Ultrastructure of the rat pancreas after experimental duct ligation. II. Duct and stromal cell proliferation, differentiation, and deletion.

Ligation of the pancreas in rats was followed by rapid atrophy of the distal part of the gland, where deletion of the acinar cells by apoptosis and simultaneous extensive proliferation of duct cells resulted in the lobules being converted into groups of closely packed small ducts within 5 days. We found no ultrastructural evidence that cells lining these small ducts arose from acinar cells by a process of dedifferentiation, as has been suggested by some investigators. During the succeeding weeks, some of the ductal lining cells developed islet cell or partial acinar cell differentiation. The latter soon died by apoptosis, and some ductlike and islet cells were also deleted by this means. Most of the apoptotic bodies formed in the ducts were phagocytosed by intraepithelial macrophages. In the longer term, continuing apoptosis eventually resulted in the disappearance of many ducts, only their thickened basal laminae remaining. Differentiation of stromal fibroblasts into contractile myofibroblasts may have contributed to shrinkage of the duct-obstructed glandular tissue, and apoptosis of endothelial cells probably accounted for the associated reduction of the capillary bed.

Analysis of Variance↗
PubMed1989

Cell death by apoptosis during involution of the lactating breast in mice and rats.

The role of cell death in involution of lactating breast was investigated in mice and rats by light and electron microscopy. Apoptosis, recognized by sharply demarcated compaction of chromatin against the nuclear envelope and by shrinkage and budding of the whole cell to form membrane-bounded apoptotic bodies, was responsible for major loss of cells in both species. In the mouse, rapid involution during the first 2 days was associated with shedding of large numbers of apoptotic bodies derived from alveolar epithelial cells into alveolar lumens. This was followed by more gradual regression, during which the bodies were mostly phagocytosed by macrophages within the epithelium. In the rat, glandular involution was a more gradual and uniform process, with shedding of apoptotic epithelial cells into alveolar lumens being much less conspicuous. Apoptosis of myoepithelial cells was observed in mice, the resulting apoptotic bodies being phagocytosed by intraepithelial macrophages, but was not detected in rats. Apoptosis of capillary endothelial cells caused rapid regression of the capillary beds in both mice and rats. Intraepithelial macrophages increased in number during involution, developed cytoplasmic lipofuscin pigment, and either remained within the epithelium or migrated to the interstitium and regional nodes. Cell loss by apoptosis has been demonstrated during involution and atrophy of a variety of other glands. It characteristically results in shrinkage of a tissue without disruption of its basic architecture.

Animals↗
PubMed1989

Spontaneous rupture of the liver associated with amyloidosis.

Fatal spontaneous rupture of the liver is described in a 46-year-old women with hepatic amyloidosis diagnosed premortem by liver biopsy. An autopsy revealed systemic amyloidosis, with no evidence of an underlying chronic inflammatory condition, infection, or immunocyte dyscrasia. By computerized search, this is only the third reported case of spontaneous rupture of the liver complicating amyloidosis.

Amyloidosis↗
PubMed1988

Patterns of cell death.

Cell death takes two distinct forms, necrosis and apoptosis. Necrosis is a degenerative phenomenon that follows irreversible injury. Apoptosis, in contrast, appears to be an active process requiring protein synthesis for its execution; it is implicated in physiological regulation of tissue size, and, where it occurs pathologically, a homeostatic role for the death is often evident. Morphologically, apoptosis involves condensation of the nuclear chromatin and cytoplasm, fragmentation of the nucleus, and budding of the whole cell to produce membrane-bounded bodies in which organelles are initially intact. These bodies are disposed of by adjacent cells without inflammation. Biochemically, there is distinctive internucleosome cleavage of DNA in apoptosis, which is quite different from the random DNA degradation observed in necrosis.

Adult↗
PubMed1988

Melanosis coli. A consequence of anthraquinone-induced apoptosis of colonic epithelial cells.

A condition closely resembling human melanosis coli was induced in the guinea pig large intestine by daily oral administration of the anthraquinone danthron. Each treatment caused a transient, dose-related wave of apoptosis of the colonic surface epithelial cells. Most of the resulting apoptotic bodies were phagocytosed by intraepithelial macrophages and carried by them through fenestrae in the epithelial basement membrane to the lamina propria. Here, the apoptotic bodies were transformed into typical lipofuscin pigment in macrophage heterolysosomes. Continued danthron administration caused progressive accumulation of pigmented macrophages in the bowel wall, whereas ongoing migration of pigmented macrophages to regional lymph nodes resulted, after danthron was ceased, in sequential loss of the pigmented cells from the superficial and deep lamina propria. Examination of colonic biopsies from patients with melanosis coli shows increased numbers of apoptotic bodies in the surface epithelium and lamina propria, suggesting implication of the same cellular processes in the formation of the pigment in man.

Animals↗
PubMed1987

Cell death and cell proliferation during atrophy of the rat parotid gland induced by duct obstruction.

Rat parotid gland atrophy after unilateral duct ligation was studied by light and electron microscopy. Death of secretory acinar cells, which took the form of apoptosis, resulted in their complete disappearance within 5 days. The remnants of the dying cells were mostly phagocytosed and degraded by macrophages within the glandular epithelium; a few were taken up by adjoining epithelial cells. The acinar cell deletion was accompanied by increased mitosis of striated and intercalated duct epithelial cells. However, over many weeks, there was enhanced apoptosis of duct cells, which eventually led to marked shortening of intercalated ducts. Apoptosis of capillary endothelial cells was observed and may account for the reduction in the capillary bed known to accompany gland atrophy. The end-stage lesion comprised small numbers of ducts in a condensed stroma. Compensatory hyperplasia, involving proliferation of duct and acinar cells, was demonstrated in the contralateral glands.

Animals↗
PubMed1987

Ultrastructure of the rat pancreas after experimental duct ligation. I. The role of apoptosis and intraepithelial macrophages in acinar cell deletion.

After ligation of the rat pancreas, acinar cells disappeared from the distal gland within 5 days. Necrosis was responsible for minor cell loss during the first 24 hours, but most of the acinar cells were deleted by apoptosis. This distinctive form of cell death, which has been implicated in atrophy of other tissues, was characterized by cellular condensation followed by surface budding to produce membrane-bounded apoptotic bodies. Most of these were ingested and degraded by mononuclear phagocytes resident within the epithelium and a few by adjoining acinar cells. As atrophy progressed, the phagocytes increased in number through division and immigration of monocytes. The apoptotic deletion of acinar cells was characteristically effected without basement membrane disruption and was accompanied by simultaneous duct cell proliferation. The consequent rapid glandular remodeling resulted in reduction of the lobules to clusters of ductules in a collagenous stroma.

Animals↗
PubMed1983

An autoradiographic study of the cell proliferation during involution of the rat pancreas.

After ligation of the rat pancreas, DNA synthesis in centoacinar cells and cells of the intercalary ducts, proximal and distal to the ligature, was suppressed for about 18 hr. This preceded a large increase in thymidine labelling of the nuclei of these cells. The increase in the thymidine indices was much greater and more prolonged in the distal pancreas where duct-like structures were formed that replaced the acini. DNA synthesis in acinar cells proximal to the ligature was suppressed for 36 hr preceding an increase in the thymidine indices much smaller than that in the duct cells. DNA synthesis in acinar cells distal to the ligature ceased and the acinar cells progressively died. We propose that the pancreas is composed of proliferative units, each comprising acinar cells, centroacinar cells and intercalary ducts, which react as a whole when acinar cell loss occurs in pathological processes.

Animals↗
PubMed1981

Involution of the pancreas after ligation of the pancreatic ducts. I: a histological study.

A detailed histological study of pancreatic involution after ligation of the pancreatic duct is reported. Cytological evidence acinar cell damage is evident from the beginning and loss of zymogen granules occurs early. The acini diminish in size rapidly from the 36th hour to the 3rd day. The cell deletion appears to occur in 2 phases with apparently different characteristics. The first phase appears to be related to the initial cell damage. The letter phase is more general but of uncertain nature. Considerable proliferation of cells occurs in the ducts resulting, with the few remaining acinar cells, in duct-like structures which themselves undergo involution. The duct changes therefore are not passive but involve continued cell proliferation and cell death over a long period.

Animals↗