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Pathology
Published in John A Plumb, Health Maintenance Of Cultured Fishes, 1994
Hyperplasia refers to an increase in the size of a body part or organ due to an increase in the number of cells present. One form of hyperplasia is characterized by an increased thickness of gill lamellae epithelium due to infection or exposure to a continuous mild irritation. Hyperplasia can result from water pollutants as well as from some fish viruses that cause formation of hyperplastic lesions, particularly of the integument. (Enlargement of a thyroid gland to form a goiter in humans is an example of hyperplasia.) Numerous examples of hyperplastic growth on the head, mouth, skin, and fins of fish have been documented.
Animal models and mechanisms of tobacco smoke-induced chronic obstructive pulmonary disease (COPD)
Published in Journal of Toxicology and Environmental Health, Part B, 2023
Priya Upadhyay, Ching-Wen Wu, Alexa Pham, Amir A. Zeki, Christopher M. Royer, Urmila P. Kodavanti, Minoru Takeuchi, Hasan Bayram, Kent E. Pinkerton
In a more recent examination of heavy smoking approximating 4 packs per day, female macaques (average age = 11 years) were exposed in chambers over the course of 4 or 12 weeks to determine TS-induced pathological processes in the model (Polverino et al. 2015). Inflammation, mucus metaplasia, glandular hypertrophy/hyperplasia, and peribronchial fibrosis were evident. A “pre-emphysematous” profile was indicated by elevated MMP, apoptosis of alveolar septal cells, and oxidative stress in lung tissue. After 12 weeks, pulmonary function changes were minimal relative to sham exposure. These included a trend toward reduced forced expiratory volume in one second, and an approximately 20% increase in quasistatic compliance versus a 7% decrease in sham-exposed controls. Further studies in this model showed that a combination of TS and influenza infection enhanced connective tissue growth factor expression in bronchial epithelial cells which might accelerate cell senescence (Jang et al. 2017).
Development of updated RfD and RfC values for medium carbon range aromatic and aliphatic total petroleum hydrocarbon fractions
Published in Journal of the Air & Waste Management Association, 2021
Chad M. Thompson, Virunya S. Bhat, Gregory P. Brorby, Laurie C. Haws
The NTP study authors characterized nasal goblet cell hypertrophy as “larger and more abundant goblet cells covering the nasal septum in Level I and surrounding the vomeronasal organ in Level II” (NTP 2004). The NTP Nonneoplastic Lesion Atlas describes goblet cell hyperplasia as “goblet cells are increased in number in the epithelium lining …, ” and “[t]he goblet cells may be enlarged or hypertrophied, but goblet cell hypertrophy should not be concurrently diagnosed; rather, the hypertrophy should be described in the pathology narrative.” (Miller and Cesta 2014). In short, the nasal goblet cell hypertrophy in the NTP (2004) study would currently be diagnosed as goblet cell hyperplasia. In this regard, Miller and Cesta (2014) state Goblet (mucous) cell hyperplasia … is seen after exposure to some irritants and may be the only change noted in response to short-term exposure to a mild irritant. It is most often seen in areas of the nasal cavity that are lined by transitional and respiratory epithelium (levels I and II) … Goblet cell hyperplasia has been seen in both short- and long-term studies. It is thought to be an adaptive response to irritant exposure and is not considered a preneoplastic change.
Effects of continuous and pulsatile flows generated by ventricular assist devices on renal function and pathology
Published in Expert Review of Medical Devices, 2018
Takuma Miyamoto, Jamshid H. Karimov, Kiyotaka Fukamachi
In summary, CF support seemed to have some effect on SMCs in arteries, but affected areas and their histological appearance were not consistent (Table 1). Most studies showed increased number of SMCs, but this arose from hyperplasia, not hypertrophy. Nishimura et al. [9] and Ohnishi et al. [10] noticed a phenotype change in the SMCs. Thyberg et al. [14] described the SMC phenotype in their review. Cells in a contractile state have a muscle-like appearance and contract in response to chemical and mechanical stimuli. Such contractile cells predominate in the vessels of adults and are primarily involved in the control of blood pressure and flow. However, these cells are able to return to a synthetic phenotype. The authors described two phenotypes: (1) the contractile phenotype, cells with a heterochromatic nucleus and cytoplasm dominated by bundles of myofilaments coalescing in dense bodies and abundant mitochondria; and (2) the synthetic phenotype, cells with cytoplasm dominated by cisternae of rough endoplasmic reticulum and a large juxtanuclear Golgi complex. These studies showed that CF LVAD support led to SMC proliferation and phenotypic change from contractile to synthetic cell types, owing to decreased pulsatility. Our group [13] and that of Kihara et al. [12] found inflammatory cell infiltration around the periarterial area. This condition could be associated with activation of the renin-angiotensin-aldosterone (RAA) system (discussed below).