Much of the cell surface on the ciliate Tetrahymena thermophila is covered by a polarized lattice of cytoskeletal structures that are associated with basal bodies of the ciliary rows. Unique structural landmarks, including an oral apparatus and contractile vacuole pores, develop before cell division in localized domains located, respectively, posterior and anterior to the transverse fission zone. All of these structures can be visualized by specific monoclonal antibodies. A single-locus recessive mutation, disorganized-A (disA), primarily affects the striated rootlets of the ciliary-row basal bodies and brings about a severe disorganization in the positioning and orientation of these basal bodies and associated cytoskeletal elements. Nonetheless, the new oral apparatus, contractile vacuole pores, and other unique structures appeared at or near their normal sites along the anteroposterior axis of disA cells, indicating that the positioning of these localized structures is not dependent on the integrity of the ciliary rows. Abnormalities were present in the details of construction of some of the localized structures and in aspects of cell shape that may be influenced by these details. In the main, however, analysis of disA mutant cells indicates that intracellular domains near the cell poles develop independently of the vectorial polarity of the ciliary rows.

Transformation of Tetrahymena pyriformis to a rapid-swimming (presumably dispersal) form can be induced by washing cells and suspending them in distilled H2O, Dryl's solution or 10 mM Tris. Transformation is possible with high efficiency in mass cultures of axenically grown cells within approximately 5 h at 30 C. The radically different phenotype produced during transformation is characterized by a more elongate body form, increased numbers of somatic basal bodies and cilia, a long caudal cilium and oral membranelles positioned beneath the cell surface. DNA quantities characteristic of G1, S, and G2 cells are found in these transformed ciliates, suggesting that achievement of a particular stage in the DNA-division cycle is not a prerequisite for transformation. Preliminary observations on cells belonging to syngens 2-12 indicate that they also have a capacity to form a caudal cilium, but that the amicronucleate strain GL-C does not. Possible relevance of the transformed phenotype for taxonomy of Tetrahymena is discussed.

The sequence of formation and ciliation of basal bodies and the subsequent organization of compound ciliary structures of the oral apparatus of Tetrahymena thermophila was reanalyzed with the aid of scanning electron microscopy of cells in which the epiplasmic layer was exposed, as well as by light microscopy of protargol-impregnated specimens. This combination of methods allowed the delineation of numerous steps in the patterning of the oral ciliature, some of which have received little or no previous attention. Highlights include: the initial formation of "strings" of nonciliated new basal bodies in juxtaposition to relatively few basal bodies of the stomatogenic kinety; generation of basal body pairs, roughly oriented along the anteroposterior axis of the cell, that later align side-by-side to assemble promembranelles; condensation and reorientation of promembranelles simultaneous with addition of a third row of basal bodies anterior to the original two rows; production of a very short fourth row of basal bodies at the anterior right end of each developing mernbranelle; generation of the outer basal body row of the undulating membrane (UM) after alignment of the inner row, with transient ciliation of the inner row preceding permanent ciliation of the outer row; limited basal body resorption at the ends of membranelles; and sculpturing of the right ends of membranelles by a movement of basal bodies associated with formation of the ribbed wall adjacent to the UM. In the old anterior oral apparatus a repetition of the processes of generation of a new outer UM row and sculpturing of right ends of membranelles takes place in synchrony with the corresponding events in the oral primordium, following prior shedding of the old outer UM row and loss of the sculptured pattern in association with temporary regression of the ribbed wall microtubules. Oral development is complex, with different processes involved in the assembly of the mernbranelles and the UM, and with

Background & Aims Increased waist circumference and visceral fat are associated with increased risk of Barrett's esophagus (BE) and esophageal adenocarcinoma (EAC). This association might be mediated by mechanical and endocrine mechanisms. We investigated the distribution of fat in subjects with BE and its association with esophageal inflammation and dysplasia. Methods We collected data from 50 BE cases and 50 controls (matched for age and sex, identified from a radiology trauma database) seen at the Mayo Clinic in 2009. Abdominal (subcutaneous and visceral) and gastroesophageal junction (GEJ) fat area was measured using computed tomography with standard techniques. Esophageal inflammation (based on a histological score) and dysplasia grade were assessed from esophageal biopsies of BE cases by a gastrointestinal pathologist. Conditional logistic regression was used to assess the association of body fat depot area with BE status, esophageal inflammation and dysplasia. Results All BE subjects had controlled reflux symptoms without esophagitis, based on endoscopy. GEJ fat area (odds ratio [OR], 6.0; 95% confidence interval [CI], 1.3–27.7; P=.02), visceral fat area (OR, 4.9; 95% CI, 1.0–22.8; P=.04) and abdominal circumference (OR=9.1; 95% CI, 1.4–57.2; P=0.02) were associated with BE, independent of BMI. Subcutaneous fat area was not associated with BE. Visceral and GEJ fat were significantly greater in BE subjects with esophageal inflammation (compared to those without, P=.02) and high-grade dysplasia (HGD) (compared to those without, P=.01), independent of BMI. Conclusions GEJ and visceral fat are associated with BE, and with increased esophageal inflammation and HGD in BE subjects, independent of BMI. Visceral fat might therefore promote esophageal metaplasia and dysplasia.

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