Testing the hypothesis that crypt cell hyperplasia inhibits lactase expression by mouse jejunal enterocytes. 1988

M W Smith, and S Lloyd, and P S James
Department of Cell Biology, AFRC Institute of Animal Physiology, Babraham, Cambridge.

Lactase activity and crypt cell proliferation both increased significantly in mouse jejunal villi in the presence of the intestinal parasite Nematospiroides dubius. Comparisons are made between this result and others showing lactase activity to decline whenever crypt cell proliferation is increased.

UI MeSH Term Description Entries
D006965 Hyperplasia An increase in the number of cells in a tissue or organ without tumor formation. It differs from HYPERTROPHY, which is an increase in bulk without an increase in the number of cells. Hyperplasias
D007583 Jejunum The middle portion of the SMALL INTESTINE, between DUODENUM and ILEUM. It represents about 2/5 of the remaining portion of the small intestine below duodenum. Jejunums
D008807 Mice, Inbred BALB C An inbred strain of mouse that is widely used in IMMUNOLOGY studies and cancer research. BALB C Mice, Inbred,BALB C Mouse, Inbred,Inbred BALB C Mice,Inbred BALB C Mouse,Mice, BALB C,Mouse, BALB C,Mouse, Inbred BALB C,BALB C Mice,BALB C Mouse
D009349 Nematode Infections Infections by nematodes, general or unspecified. Infections, Nematode,Infection, Nematode,Nematode Infection
D009351 Nematospiroides dubius A species of intestinal nematode parasites which occur most commonly in mice. Infection is by ingesting larvae. This particular species is used extensively in immunological research. Heligmosomoides polygyrus
D012016 Reference Values The range or frequency distribution of a measurement in a population (of organisms, organs or things) that has not been selected for the presence of disease or abnormality. Normal Range,Normal Values,Reference Ranges,Normal Ranges,Normal Value,Range, Normal,Range, Reference,Ranges, Normal,Ranges, Reference,Reference Range,Reference Value,Value, Normal,Value, Reference,Values, Normal,Values, Reference
D005696 Galactosidases A family of galactoside hydrolases that hydrolyze compounds with an O-galactosyl linkage. EC 3.2.1.-. Galactosidase
D006801 Humans Members of the species Homo sapiens. Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man
D000818 Animals Unicellular or multicellular, heterotrophic organisms, that have sensation and the power of voluntary movement. Under the older five kingdom paradigm, Animalia was one of the kingdoms. Under the modern three domain model, Animalia represents one of the many groups in the domain EUKARYOTA. Animal,Metazoa,Animalia
D001616 beta-Galactosidase A group of enzymes that catalyzes the hydrolysis of terminal, non-reducing beta-D-galactose residues in beta-galactosides. Deficiency of beta-Galactosidase A1 may cause GANGLIOSIDOSIS, GM1. Lactases,Dairyaid,Lactaid,Lactogest,Lactrase,beta-D-Galactosidase,beta-Galactosidase A1,beta-Galactosidase A2,beta-Galactosidase A3,beta-Galactosidases,lac Z Protein,Protein, lac Z,beta D Galactosidase,beta Galactosidase,beta Galactosidase A1,beta Galactosidase A2,beta Galactosidase A3,beta Galactosidases

Related Publications

M W Smith, and S Lloyd, and P S James
January 1990, Biochimica et biophysica acta,
M W Smith, and S Lloyd, and P S James
January 1990, Experimental physiology,
M W Smith, and S Lloyd, and P S James
November 1986, Biochemical pharmacology,
M W Smith, and S Lloyd, and P S James
July 1975, Virchows Archiv. B, Cell pathology,
M W Smith, and S Lloyd, and P S James
July 1986, The Journal of physiology,
M W Smith, and S Lloyd, and P S James
March 1991, Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology,
M W Smith, and S Lloyd, and P S James
August 1986, Clinical science (London, England : 1979),
M W Smith, and S Lloyd, and P S James
August 1985, Journal of cellular physiology,
M W Smith, and S Lloyd, and P S James
January 1996, The Anatomical record,
M W Smith, and S Lloyd, and P S James
January 1991, Comparative biochemistry and physiology. A, Comparative physiology,
Copied contents to your clipboard!