Cellular hyperplasia

CNS Copper deposits affect the whole CNS. Degeneration and tissue loss as well as atrophy of the lenticular nucleus prevail. Occasionally, there are also small necrotic foci with a diffuse spot-like distribution. Micro-cavernous lesions occur due to the destruction of nerve cells. Myelinized fibres and oligodendrocytes are present, but there is also cellular hyperplasia and hypertrophy of astrocytes rich in protoplasm. The cerebral changes detectable in CT scanning do not correlate with the degree of severity of the functional disturbances (320, 335) however, there is a close correlation between the lesions detected by MRI and certain neurological findings. (350, 366, 376, 388) (s. p. 615)... 

M (increases in nasal cell Wilmer et al. 1987 turnover rates squamous metaplasia with cellular hyperplasia)... 

M (increased cell turnover rates thinning disarrangement of the nasal epithelium squamous metaplasia with cellular hyperplasia minimal to moderate rhinitis)... 

Skin defects or diseases can be provoked by solvents which cause irritation, cellular hyperplasia and swelling, or removal of hpids. Skin defects are provoked mainly by fi e-quent use of solvents thus enhancing flieir absorption. 

Ornithine decarboxylase is a pyridoxal dependent enzyme. In its catalytic cycle, it normally converts ornithine (7) to putrisine by decarboxylation. If it starts the process with eflornithine instead, the key imine anion (11) produced by decarboxylation can either alkylate the enzyme directly by displacement of either fluorine atom or it can eject a fluorine atom to produce viny-logue 12 which can alkylate the enzyme by conjugate addidon. In either case, 13 results in which the active site of the enzyme is alkylated and unable to continue processing substrate. The net result is a downturn in the synthesis of cellular polyamine production and a decrease in growth rate. Eflornithine is described as being useful in the treatment of benign prostatic hyperplasia, as an antiprotozoal or an antineoplastic substance [3,4]. 

Kang S, Duell EA, Fisher GJ, et al (1995) Application of retinol to human skin in vivo induces epidermal hyperplasia and cellular retinoid binding proteins characteristic of retinoic acid but without measurable retinoic acid levels or irritation. J Invest Dermatol 105 549-556... 

Precancerous cells have cellular changes that are abnormal but not yet malignant and may be described as hyperplastic or dysplastic. Hyperplasia occurs when a stimulus is introduced and reverses when the stimulus is removed. Dysplasia is an abnormal change in the size, shape, or organization of cells or tissues. 

Papules are small, solid, elevated lesions that are usually less than 1 cm in diameter. They may result from metabolic deposits in the dermis, from localized dermal cellular infiltrates, or from localized hyperplasia of cellular elements in the dermis and epidermis. 

The effects of pure antiestrogens in the uterus have also been extensively studied, since it is an estrogen-dependent organ and the target of the main side effects of tamoxifen therapy, such as endometrial hyperplasia, hypertrophy of glandular epithelium, or even focal cellular atypia (Sourla et al. 1997). 

Animal data suggest that renal and liver effects may occur in humans exposed to high doses of hexachloroethane. Kidney and liver effects are not specific to hexachloroethane. Lesions of the kidney (nephropathy, linear mineralization, and hyperplasia) were reported at 10 mg/kg/day or greater in male rats (NTP 1989). Urinalysis also revealed granular and cellular casts in rats exposed to hexachloroethane (47 mg/kg/day or greater) for 13 weeks (NTP 1989). Because other compounds cause similar effects and because some of these effects are unique to male rats, they are not valuable as biomarkers for human hexachloroethane exposure. 

Inflammation, cellular infiltration, pneumonia, bronchitis, endothelial hyperplasia, and capillary thrombosis occurred in guinea pigs exposed by inhalation to 26-52 ppm phenol for 41 days (Deichmann... 

Decreases in the relative weights of the lymph nodes and thymus were noted in male mice following daily dermal exposures for 1 week to 0.1 mL kerosene (Upreti et al. 1989). In addition, thymocyte counts, bone marrow nucleated cell counts, thymic cortical lymphocytes, and the cellularity of the thymic lobules were decreased. Increases in the cellular populations of the popliteal lymph nodes and the axial lymph nodes were also present. This study is limited because females were not tested. Chronic exposure to 500 mg/kg/day JP-5 induced granulocytic hyperplasia in the bone marrow in male and female mice and hyperplasia in the lymph nodes of female mice (NTP/NIH 1986). Plasmacytosis of the lymph nodes was found to be secondary to dermatitis in mice chronically exposed to 250 and 500 mg/kg/day of marine diesel fuel. 

TCE carcinogenesis may require exposure to high doses sufficient to cause cellular necrosis. Repeated cycles of necrosis and regeneration would occur with the emergence of hyperplasia and then neoplasia. Low exposures commonly encountered in human studies are not sufficient to initiate the carcinogenic process. 

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