When comparisons are made between the bizygomatic diameter of different subjects, or when measurements made on the living are compared with those on skulls, the thickness of the soft tissue overlying the zygions is of considerable importance.The thickness of these tissues over each of 208 zygions of cadavera has been studied and has been found to differ considerably. The range was from 1.4 mm to 21.4 mm, and the thickness was related to the general body-build -fat, medium or thin. Statements in the literature assume that 6 m m is a suitable estimate of the total thickness of the soft tissues over both zygions. However the present findings indicate that these assumptions are not justified, for in 92% of these specimens the thickness exceeded 6 mm.
The human pathogen Helicobacter pylori causes inflammation in the stomach of infected hosts, leading in some cases to the development of gastric cancer. Several mouse models have been developed to study Helicobacter-induced carcinogenesis with similarities to gastric adenocarcinoma and mucosa-associated lymphoid tissue lymphoma (MALToma) in humans. These models require chronic infection of animals with mouse-colonizing isolates of H. pylori or with related gastric Helicobacter spp., such as the canine/feline species Helicobacter felis. Furthermore, consistent with the known influence of host and environmental factors in human gastric cancer, it is possible to manipulate the type and severity of gastric lesions in mouse Helicobacter infection models through the use of different mouse genetic backgrounds and/or by the administration of known cocarcinogens, such as alkylating agents (e.g., N-nitroso-N-methylurea), or even elevated quantities of dietary salt. Here, we describe protocols for the inoculation of mice with gastric Helicobacter spp. and the administration of these cocarcinogens. Furthermore, we will describe the various methodologies used to study gastric inflammation and carcinogenesis in Helicobacter-infected animals.
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