Biomedical subjects

J C Cheville

Publications and source records attributed to J C Cheville.

57 records · Page 4Linked to original sources

PubMed1989

Uptake and excretion of Brucella abortus in tissues of the face fly (Musca autumnalis).

To determine their capacity to host Brucella abortus, face flies were examined 1 to 120 hours after feeding on broth containing bacteria and bovine erythrocytes. Brucella abortus was cultured in large numbers from whole flies for 12 hours after feeding, but not after 72 hours. Histologic analysis showed that brucellae were rapidly taken into the midgut, sequestered from erythrocytes, transiently stored, and shed in the feces; there was no evidence of bacterial replication within epithelial cells. Immunoperoxidase and immunogold techniques revealed that most brucellae in the gut were confined to the lumen by the peritrophic membrane, that brucellae were degraded in secondary lysosomes of midgut epithelial cells, and that intact brucellae passed into connective tissues surrounding the midgut. Bacterial excretion without midgut replication is consistent with transient, but not long-term, insect transmission in nature.

Animals↗

PubMedDate not supplied

Evaluation of Ki-67 (MIB-1) in placentas with hydropic change and partial and complete hydatidiform mole.

The separation of complete from partial hydatidiform mole and of partial mole from placentas with hydropic change on gross and microscopic evaluation can be difficult, and ploidy provides important diagnostic information. We applied an immunohistochemical marker of proliferation, Ki-67 (MIB-1), to 10 complete moles, 11 partial moles, and 8 placentas with hydropic change to determine whether growth fraction differs in these three placentas and can aid in diagnosis. Ploidy was confirmed using flow cytometry and fluorescence in situ hybridization with probes to chromosomes 7 and 2. The Ki-67-determined growth fractions (number of positive cells/total number of cells) for villous stromal cells, cytotrophoblast, and proliferating trophoblast were evaluated separately by counting 200 cells of each population. Growth fraction on stroma did not differ among the three entities. Mean percent growth fraction for cytotrophoblast was 13.3% for hydropic change, 14.6% in partial moles and 38.7% in complete moles (P = .004 hydropic change to complete moles, P = .003 partial moles to complete moles). There was no significant difference between hydropic change and partial mole. Mean percent growth fraction for proliferating trophoblast was 38.5% in hydropic change, 25.9% in partial moles, and 67.1% in complete moles (P = .08 hydropic change to complete moles, P = .004 partial moles to complete moles). Again, no significant difference was identified between hydropic change and partial moles. Ploidy analysis using fluorescence in situ hybridization and flow cytometry confirmed diploidy in hydropic change and complete moles and triploidy in partial moles. Ki-67 may be useful in separating complete moles from partial moles but not partial moles from hydropic change.

Cell Division↗

PubMedDate not supplied

Focal microsatellite mutations in relatives with prostatic adenocarcinoma.

Instability of short tandem repeat sequences, microsatellite instability (MI), has been reported to play an important role in the tumorigenesis of various adenocarcinomas, including prostatic adenocarcinoma. Although prostate cancer is not widely recognized as a heriditary cancer, familial clustering is well known. To investigate the frequency of microsatellite instability in familial prostatic adenocarcinomas we analyzed archival tumor tissue from seven paired first degree relatives with prostatic adenocarcinoma. Twelve dinucleotide, nine trinucleotide, six tetranucleotide repeats and the CAG repeat of the androgen receptor gene were screened for MI. Solitary mutations were observed in four separate cases (28.6%) and widespread somatic alterations were not identified. No statistical correlation to pathological characteristics was determined. Our data indicate that microsatellite instability is an uncommon phenomenon in prostatic adenocarcinoma within first degree relatives. Those changes present appear to manifest as focal mutations in contrast to the more global changes seen in MI.

Adenocarcinoma↗