Cause Of Necrosis Research Articles

The Ecology and Evolutionary Biology of Cancer: A Review of Mathematical Models of Necrosis and Tumor Cell Diversity

Recent evidence elucidating the relationship between parenchyma cells and otherwise "healthy" cells in malignant neoplasms is forcing cancer biologists to expand beyond the genome-centered, "one-renegade-cell" theory of cancer. As it becomes more and more clear that malignant transformation is context dependent, the usefulness of an evolutionary ecology-based theory of malignant neoplasia becomes increasingly clear. This review attempts to synthesize various theoretical structures built by mathematical oncologists into potential explanations of necrosis and cellular diversity, including both total cell diversity within a tumor and cellular pleomorphism within the parenchyma. The role of natural selection in necrosis and pleomorphism is also examined. The major hypotheses suggested as explanations of these phenomena are outlined in the conclusions section of this review. In every case, mathematical oncologists have built potentially valuable models that yield insight into the causes of necrosis, cell diversity, and nearly every other aspect of malignancy; most make predictions ultimately testable in the lab or clinic. Unfortunately, these advances have gone largely unexploited by the empirical community. Possible reasons why are considered.

Canine gallbladder infarction: 12 cases (1993-2003).

A cohort of 12 dogs with severe transmural gallbladder necrosis is described. All dogs had cholecystectomies performed. In six dogs, perforation of the gallbladder was noted at surgery. Eight dogs survived the immediate postoperative period, and four dogs died. Histologically, inflammation was absent or minimal in all cases, suggesting that cholecystitis was not the cause of necrosis. Thrombi (n = 2) and atheromatous vascular changes (n = 1) represent possible vascular causes of this condition. The findings of coagulative necrosis in these 12 dogs are compatible with "gallbladder infarction," and the authors propose this term to describe the histopathologic appearance of the gallbladder.

Foci of eosinophil-related necrosis in the liver: imaging findings and correlation with eosinophilia.

The purpose of our study was to describe CT and sonographic findings of foci of eosinophil-related hepatic necrosis and to correlate those findings with eosinophil counts in the peripheral blood. We retrospectively reviewed 17 helical CT and 16 sonographic examinations (including follow-up examinations) in 10 patients with pathologically proven foci of eosinophil-related necrosis. Underlying causes were anisakiasis (n = 2), malignant neoplasms (n = 3), hypereosinophilic syndrome (n = 3), and idiopathic (n = 2). CT and sonographic images were reviewed by consensus by three radiologists, with an emphasis on the morphology and distribution of foci. Imaging findings were correlated with eosinophil counts in the peripheral blood. All foci of eosinophil-related necrosis were observed as focal hypoattenuating lesions on all phases of helical CT and as focal hypoechoic lesions on sonography. Foci varied in size and were round or oval. The number of these foci seemed to be in proportion to the percentage of eosinophils in the peripheral blood. Most foci showed interval regression on follow-up CT or sonography as peripheral blood eosinophil counts decreased. Foci of eosinophil-related necrosis cause focal hepatic lesions of varying size, shape, and number on helical CT and sonography. The number and extent of these foci were closely correlated to eosinophil counts in the peripheral blood.

Does avascular necrosis cause collapse of the dome of the talus in severe haemophilia?

Does avascular necrosis cause collapse of the dome of the talus in severe haemophilia?

Does avascular necrosis cause collapse of the dome of the talus in severe haemophilia?

Arthropathy of the ankle joint is commonly observed in people with severe haemophilia. A review of the radiological appearance of ankle arthropathy provides evidence that the changes in the talar bone of the ankle joint are probably due to avascular necrosis. This may arise due to impairment to the arterial supply, as it enters the talar neck, secondary to the increased pressure at the time of haemarthroses.

The causes of necrosis of arteriovenous flaps and its modification. (Chinese)

The causes of necrosis of arteriovenous flaps and its modification. (Chinese)

The role of cytokines in mediating the bystander effect using HSV-TK xenogeneic cells.

We have previously demonstrated that genetically modified syngeneic murine tumor cells (KBALB) expressing the herpes simplex virus thymidine kinase gene (HSV-STK) can kill nearby unmodified tumor cells in the presence of ganciclovir (GCV). The killing was mediated by a 'bystander effect' as evidenced by the prolonged animal survival when syngeneic HSV-TK gene-modified tumor cells were inoculated into mice with an intraperitoneal tumor. In this study we investigated whether irradiated xenogeneic HSV-TK gene-modified tumor cells, a human colon carcinoma cell line (HCT) transfected with the HSV-TK gene, can mediate the 'bystander effect' when used in vitro and in vivo. In vitro experiments indicate that irradiated HSV-TK gene-modified xenogeneic cells (HCT) can mediate a bystander effect on the adjacent cells when the tumor population consisted of as few as 10% of the HSV-TK expressing HCT tumor cells. In vivo, animal survival experiments demonstrate that the xenogeneic gene-modified tumor cells could generate the 'bystander effect' in mice with intraperitoneal tumors as evidenced by prolonged animal survival. In addition, histologic examination of the tumors from experimental animals showed extensive tumor necrosis 3 days post HSV-TK/GCV treatment in comparison to control animals. To evaluate the cause of necrosis in vivo, we assayed for cytokines, which may be involved in mediating this process, by performing RT-PCR and immunohistochemistry on tumor RNA and tumor cells, respectively. Production of IL-1 alpha and IL-6 mRNA within the experimental tumors was observed by RT-PCR. However, mRNA expression for other cytokines including IFN-gamma, IL-2 and IL-4 was not present. Immunohistochemical analysis for IL-1 alpha protein showed reactivity within the infiltrating mononuclear cells indicating the release of this soluble factor. These results indicate that the bystander effect can be generated using irradiated xenogeneic cells both, in vitro and in vivo. Furthermore, this process is mediated by the release of cytokines such as IL-1 alpha, IL-6 which enhances the bystander effect in vivo by immunostimulation.

Spectrum of renal cortical necrosis in acute renal failure in eastern India.

Renal cortical necrosis is an uncommon cause of acute renal failure. We report 23 cases of biopsy-proven renal cortical necrosis which constituted 6.3% (23/363) of all cases of acute renal failure studied over a period of seven years (1985-92). The patients were divided into two groups: obstetric and non-obstetric. Obstetric complications were responsible for renal cortical necrosis in 15 (65.2%) patients while non-obstetric conditions accounted for the remaining eight (34.8%) cases. The overall incidence of cortical necrosis in obstetric acute renal failure was 15/63 (23.8%) patients, the incidence being nearly equal in early (20.5%) and late (29%) pregnancy. Post-abortum renal failure was the sole cause of cortical necrosis in early pregnancy in the obstetric group. Haemolytic uraemic syndrome (three patients) and septicaemia (two patients) were the main cause of necrosis in the non-obstetric group. The cortical necrosis was diffuse and patchy in 17 and six patients, respectively. The disease had a fatal prognosis in 20 (87%) patients; mortality was due to uraemic complications and infections in the majority of patients. The high frequency of post-abortum renal cortical necrosis in our patients is similar to the experience of other Indian workers.

Joint oxygen-glucose deprivation as the cause of necrosis in a tumor analog.

The sandwich system was recently developed as an in vitro tumor analog. Like spheroids, sandwiches are organized, multicellular systems in which the interplay between diffusion and consumption leads to the formation of spatial gradients; a necrotic center and a viable cell border subsequently develop. Using sandwiches of the 9L and V79 cell lines, the effects of oxygen and glucose deprivation on the onset and formation of necrosis were investigated. The data indicate that in sandwiches necrosis is a result of a shortage of both substances. Complementary cell monolayer experiments to determine a number of consumption parameters were performed. On the basis of the data, we propose a joint oxygen-glucose deprivation model for V79 cell necrosis. It is assumed a cell dies when oxygen deprivation in conjunction with glucose deprivation lowers the cell's ATP production rate below a critical value. Interactions of the concentrations and consumptions of oxygen and glucose are analyzed theoretically; concentration profiles are obtained by numerically solving coupled non-linear integral equations arising from the diffusion equation. The predicted viable border widths are in good agreement with the observed values.

Microorganisms on Water Hyacinth in Eastern Australia: A Survey in Relation to Biological Control by Insects

Fungi were isolated from diseased and decaying water hyacinth, Eichhornia crassipes (Mart.) Solms-Laub. from twenty three sites in eastern Australia. Some of the fungi had not previously been recorded on this host, but the majority were species known on water hyacinth in America and Asia, including pathogens Acremonium zona tum (Sawada) Gams and Cercospora piaropi Tharp. Bacteria isolated were Pseudomonas fluorescens and a non-fluorescent pseudomonad unlike any published species description. A greater variety of fungi occurred on plants damaged by the insect biological control agents, Ncochetina eichhorniae Warner and Sameodes a/bigullalis (Warren) than on plants not attacked by these insects. Many of the species are ubiquitous on decaying plant material. No particular fungus could be recognised as the main cause of necrosis which is associated with damage by insect larvae to the petiole and rhizome, but microorganisms are considered to be important in achieving the overall biological control. In contrast to other infections of the lamina, the lethal effect of a leaf blight was linked to severe infection of the lamina of the younger leaves. In glasshouse pathogenicity tests, Fusarium spp., A. zona tum and C. piaropi caused more disease than any other microorganism tested. A. zona tum and C. piaropi are considered to have the greatest potential for development as mycoherbicides.

放射線治療による喉頭壊死の２症例 組織学的所見を中心に

Two cases with radiation necrosis of the larynx are reported. The first case, 77-year-old male, suffered from supraglottic carcinoma (T2N1). When he received 46 Gy irradiation, he complained of severe throat pain. Although antibiotics and steroid were given, he developed necrosis of the larynx and was laryngectomized. Histological examination showed typical changes of radiation effect: thickening of the wall of blood vessel, fibrous thickening of the perichondrium, and fibrosis and atrophy of the skeletal muscle. The second case, 62-year-old male, suffered from supraglottic carcinoma (T2N0). Four months after 60 Gy irradiation, he complained of increasing throat pain. His larynx was found to be necrotic and was excised. Destruction of the perichondrium by invasion of tumor cells was histologically observed. This change was considered to be a main cause of necrosis of the cartilage. Once necrosis of the cartilage occurs, a laryngectomy is required. Therefore, early diagnosis of perichondritis is necessary to prevent necrotic change of the cartilage by medical treatment. The laryngologist should also recognize that recurrent tumor may hide under significantly edematous mucosa which persists after completion of radiotherapy.

Vascular anatomy of the pectoralis major myocutaneous flap.

In a series of 43 pectoralis major myocutaneous flaps (PMMF), five (12%) developed partial or total necrosis. The cause of necrosis was speculative in each case. To evaluate the problem, we studied the vascular supply to the PMMF, specifically, the lateral thoracic artery (LTA) and the pectoral branch of the thoracoacromial artery (TAA-PB). Ten aortic arch angiograms and 35 cadaver dissections were analyzed. The LTA and TAA-PB provided pedicles of comparable size in most cases, and in several the LTA was significantly larger than the TAA-PB. In one angiogram the TAA-PB was totally occluded, probably by atheromatous plaque. Peripheral vascular disease can affect myocutaneous flaps. We postulate that the LTA can nourish the PMMF by itself and sustain flaps that might otherwise develop necrosis.

高血圧自然発症ラットの脳血管傷害の病理学的研究

Brains of spontaneously hypertensive rats (SHR) were histopathogically studied, and the effects of salt loading on the cerebrovascular diseases were investigated. Brains of SHR showed hemorrhage, necrosis and edema. As the morphological cause of hemorrhage, microaneurysms were observed in the hemorrhagic foci. Cellular hyperplasia of the pial arteries, hyaline degeneration, fibrinoid necrosis and thrombus formation of the intracerebral arterioles and small arteries were found as the cause of necrosis of the brains. In the study of vascular permeability using horse-radish peroxidase as a marker, an increased vascular permeability was demonstrated in the rats with very high blood pressure beyond 220 mmHg. For the development of fibrinoid necrosis, thrombus formation and an increased vascular permeability, endothelial injury due to hypertension seems to play an important role. Because the localization of increased cerebrovascular permeability corresponded well with that of cerebral necrosis, and there were transitional findings between brain edema and cyst formation in the brain, at least some necrotic foci were suggested to be caused by an increased cerebrovascular permeability. The incidence of cerebrovascular changes was high in stroke-prone substrains such as A 1-sb and A3. The effects of promoting hypertension by salt loading were especially severe in the above substrains.

Hypotension-induced post-traumatic necrosis of the right colon

Necrosis of the right colon developed after hemorrhagic shock in six young traumatized patients who did not have colon injury. The mean duration of hypotension was 112 minutes, and the mean resuscitation fluid volume required was 22 liters. Signs of right colon necrosis appeared 2 to 7 days after injury (median 2 days). All patients survived right colectomy and ileocolostomy or ileostomy and mucous fistula. The cause of necrosis of the right colon after hemorrhagic shock from major trauma is not clear. Anatomic abnormalities in blood supply to the right colon or a derangement in the physiologic processes of the microcirculation of the right colon must be considered.

Pathological anatomy of conifer needle necrosis

The pathological anatomy of pine needle necrosis caused by major environmental stresses was investigated to determine if histological responses could provide a diagnostic tool. All stresses studied caused a general hypertrophy of the epithelial tissue of the resin canals, occluding these ducts. Granulation of transfusion and mesophyll parenchyma cells was also a general response to stress. Hypertrophy of the phloem cells and transfusion parenchyma was caused by almost all stresses in some instances but was most consistent for necrosis caused by natural senescence, drought, or fluoride. Collapse of the mesophyll cells best characterized necrosis caused by ozone, sulfur dioxide, salt, or boron toxicity. The greatest value of microscopic examination of the tissues adjacent to the necrotic areas was found to lie in the elimination of certain pathogens, narrowing the possible causal agents. Histological examination could ascertain when certain air pollutants were not responsible for a particular injury; for instance, the absence of mesophyll collapse can definitely eliminate sulfur dioxide as a cause of necrosis. Conversely, though, presence of mesophyll cell collapse, because of its ubiquitous nature, could not establish etiology.

Left ventricular papillary muscles. Description of the normal and a survey of conditions causing them to be abnormal.

The left ventricular papillary muscles appear to be the last portions of the heart to be perfused by coronary arterial blood. As a consequence they are sensitive anatomic markers of myocardial ischemia. Foci of necrosis or fibrosis therefore are commonly seen in these structures, particularly the posteromedial papillary muscle, which has a poorer blood supply than does the anterolateral muscle. Coronary arterial luminal narrowing is the most common cause of necrosis or fibrosis of the left ventricular papillary muscles. Other conditions, all associated with inadequate cardiac output, which may produce these lesions include left ventricular outflow tract obstruction, especially that resulting from congenitally malformed aortic valves, acute valvular regurgitation (infective endocarditis), various cardiomyopathies, and primary endocardial fibroelastosis with or without anomalous origin of one or both coronary arteries from the pulmonary trunk. Various infiltrative diseases, including inflammation (Aschoff bodies, sarcoid, abscesses), amyloid, iron, and neoplasms, also may involve the papillary muscles. Their most common congenital malformation is the parachute or single papillary muscle. Fibrosis or necrosis of adjacent left ventricle free wall without involvement of the papillary muscles themselves may simulate clinically "papillary muscle dysfunction." The anterior papillary muscle of the right ventricle is frequently affected by conditions which also affect the left ventricular papillary muscles. Whether or not necrosis or fibrosis of the right ventricular papillary muscle causes tricuspid regurgitation, however, is unknown at present.

The pathology of thirty-nine fatal cases of epidemic hemorrhagic fever

The pathologic changes observed in thirtynine fatal cases of hemorrhagic fever in 1952 have been studied in the light of the significant clinical data. The cases have been grouped according to the clinical phase in which death occurred in an attempt to determine the sequential development of the pathologic changes and to evaluate the role of shock in their pathogenesis. Several conclusions resulting from this correlation of clinical and pathologic data seem clearly evident. The almost constant occurrence of hemorrhage in the right atrium of the heart, of severe congestion of the renal medulla, and of congestion and infarct-like necrosis in the anterior lobe of the pituitary gland, in association with the pattern of the vascular changes, supports the contention proposed in the Japanese literature and by Steer and Hullinghorst 1,2 that capillary damage is the basic process. Retroperitoneal edema, observed only once in secondary shock, is the striking pathologic feature when the patient dies during shock in early phases of the disease. It is rarely encountered after the eighth day when the initial shock usually terminates, suggesting that vascular damage has subsided. Recurrent shock in the later phases of the disease is due to other contributing factors. The abrupt increase in incidence of pulmonary edema in the oliguric phase, particularly after the eighth day of the disease when retroperitoneal edema is rare, supports the clinically suspected role of redistribution of fluid and electrolytes coincident with resorption of the abnormal interstitial fluid. The frequent coexistence of pulmonary edema and bronchopneumonia in the oliguric and diuretic groups and the high incidence of pulmonary abscess formation support the concept of Moon that pulmonary edema of the albuminous type is conducive to the development of pulmonary infections. The almost constant presence of necrosis of the anterior lobe of the pituitary gland in cases of more than nine days' duration, irrespective of occurrence, type or duration of preceding shock, strongly suggests that shock is not the only major factor in the pathogenesis of pituitary necrosis in hemorrhagic fever. Anoxemia from severe congestion and stasis resulting from vascular damage is also an important factor and probably is the major cause of necrosis in the absence of shock.