| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
The histologic appearance of the mammary gland in sexually mature male and female rats shows distinct sex-dependent differences which are not present in mice, dogs or humans. The mammary gland in the female rat has a tubuloalveolar morphology with frequent ducts, fewer alveoli and a single layer of low cuboidal epithelium lining the ducts and alveoli. In contrast, a lobuloalveolar morphology is present in mammary glands of male rats, and the ducts and alveoli are lined by several layers of large cuboidal or columnar cells. The recognition of these differences can be important when investigating compounds that affect trophic hormones, as highlighted in a recent study by Rudman et al. The investigators administered the selective estrogen receptor modulator (SERM) compound LY2066948 hydrochloride to female rats and noted that the mammary glands developed a phenotype very similar to that of male rats. The SERM was responsible for androgen-dependent virilism of the female mammary gland, and this effect was blocked by administration of the androgen receptor antagonist flutamide. Importantly, female mice did not develop mammary gland virilism upon administration of LY2066948 hydrochloride. The authors advise that the morphologic alterations seen in the female rats should not be interpreted as atypical hyperplasia, and propose that the term "glandular virilization" be used instead.
Rudmann DG, Cohen IR, Robbins MR, Coutant DE, Henck JW. Androgen dependent mammary gland virilism in rats given the selective estrogen receptor modulator LY2066948 hydrocholoride. Toxicol Pathol 33:(6): 711–719, 2005[Medline]
Tissue microarrays (TMAs) prepared from paraffin blocks are becoming widely used for histologic and immunohistochemical studies and allow the analysis of up to several hundred tissue sections on a single slide. Depending on the design of the TMA, each specimen may be represented by three or four cores. Liu and colleagues have developed a novel tool called TMA-Combiner to aid in the analysis and retrieval of immunohistochemical data from replicate cores on a TMA. Immunohistochemical staining may vary between cores, resulting in different scores for the same tissue. Using a series of "combination rules," the TMA-Combiner software consolidates the immunohistochemistry data into a single score and allows the investigator to record and extract data from multiple TMAs. The software is freely available on the authors' website and is designed to interface with their other TMA analysis tools such as TMA-Deconvoluter.
Liu CL, Montgomery KD, Natkunam Y, West RB, Nielsen TO, Cheang MCU, Turbin DA, Marinelli RJ, van de Rijn M, Higgins JPT. TMA-Combiner, a simple software tool to permit analysis of replicate cores on tissue microarrays. Mod Pathol 18:(12): 1641–1618, 2005[ISI][Medline]
Hypertrophic cardiomyopathy (HCM) is characterized by increased left ventricular wall thickness and myofiber disarray. It is the most common cardiac disease in domestic cats and a common cause of sudden death in young adults. The condition is often familial, and causative mutations in several genes have been identified in humans. Meurs et al investigated HCM in a colony of Maine Coon cats with familial HCM and identified a mutation in the sarcomeric myosin binding protein C gene (MYBPC3). The single base pair mutation in exon three changes a conserved alanine to proline and is postulated to alter the protein structure by reducing alpha helix formation with a concurrent increase in random coils. This represents the first known spontaneous cause of familial HCM in a non-human species.
Meurs KM, Sanchez X, David RM, Bowles NE, Towbin JA, Reiser PJ, Kittleson JA, Munro MJ, Dryburgh K, MacDonald KA, Kittleson MD. A cardiac myosin binding protein C mutation in the Maine Coon cat with familial hypertrophic cardiomyopathy. Hum Mol Genet 14:(23): 3587–3593, 2005
High plasma levels of C-reactive protein (CRP), an acute phase reactant protein, are considered a risk factor for human cardiovascular disease. CRP is often found within atherosclerotic lesions of the arterial intima, but it is unclear whether CRP is deposited directly from the plasma or it if is synthesized by arterial cells and/or intralesional macrophages. To clarify this issue, Sun et al studied CRP production in two rabbit models—Watanabe heritable hyperlipidemic rabbits and cholesterol-fed rabbits. They found that CRP levels were significantly higher in hypercholesterolemic rabbits than normal rabbits. Furthermore, CRP levels were correlated with the degree of hypercholesterolemia and the severity of the atherosclerotic lesions. CRP was present in both early and late atherosclerotic lesions and appeared to co-localize with apolipoprotein B. Intralesional macrophages were infrequently positive for CRP mRNA or protein, supporting the notion that the CRP in atherosclerotic lesions is derived from the circulation and not synthesized by intimal cells or macrophages.
Sun H, Koike T, Ichikawa T, Hatakeyama K, Shiomi M, Zhang B, Kitajima S, Morimoto M, Watanabe T, Asada Y, Chen YE, Fan J. C-reactive protein in atherosclerotic lesions: its origin and pathophysiological significance. Am J Pathol 167:(4): 1139–1148, 2005
Pneumonic plague, caused by the bacterium Yersinia pestis, is almost always fatal. Although the histopathologic lesions of the pulmonary disease have been investigated in a number of animal species, the underlying pathogenesis is largely unknown. Lathem et al investigated the molecular and cellular events in mouse lung tissue following intranasal infection with Y. pestis. The agent elicited an initial anti-inflammatory response which was followed by a pro-inflammatory response and death within 3–4 days. Similar to humans, the mice developed a severe, multifocal, purulent bronchopneumonia with large aggregates of extracellular bacteria. The extracellular organisms were used for microarray analysis to identify bacterial virulence factors. Some of the molecules up-regulated during infection included those of the ypo-ysc type III secretion system and genes contained within the chromosomal pigmentation locus.
Lathem WW, Crosby SD, Miller VL, Goldman WE. Progression of primary pneumonic plague: a mouse model of infection, pathology, and bacterial transcriptional activity. Proc Natl Acad Sci USA Epub Nov 23, 2005
| ||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
