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Biomedical subjects

F Qian

Publications and source records attributed to F Qian.

60 records · Page 4Linked to original sources
PubMedDate not supplied

Co-assembly of polycystin-1 and -2 produces unique cation-permeable currents.

The human kidney is composed of roughly 1.2-million renal tubules that must maintain their tubular structure to function properly. In autosomal dominant polycystic kidney disease (ADPKD) cysts develop from renal tubules and enlarge independently, in a process that ultimately causes renal failure in 50% of affected individuals. Mutations in either PKD1 or PKD2 are associated with ADPKD but the function of these genes is unknown. PKD1 is thought to encode a membrane protein, polycystin-1, involved in cell-cell or cell-matrix interactions, whereas the PKD2 gene product, polycystin-2, is thought to be a channel protein. Here we show that polycystin-1 and -2 interact to produce new calcium-permeable non-selective cation currents. Neither polycystin-1 nor -2 alone is capable of producing currents. Moreover, disease-associated mutant forms of either polycystin protein that are incapable of heterodimerization do not result in new channel activity. We also show that polycystin-2 is localized in the cell in the absence of polycystin-1, but is translocated to the plasma membrane in its presence. Thus, polycystin-1 and -2 co-assemble at the plasma membrane to produce a new channel and to regulate renal tubular morphology and function.

Animals↗
PubMedDate not supplied

Resin-dentin interfacial ultrastructure and microtensile dentin bond strength after five-year water storage.

OBJECTIVE: To evaluate a total-etch three-step adhesive system's resin-dentin interfacial ultrastructure and microtensile dentin bond strength (microTBS) after multi-year storage in water. METHODS: Resin composite crowns were formed on 600 grit SiC flattened extracted human molars using a total-etch three-step adhesive system (Optibond FL, Kerr) and a hybrid resin composite (Prodigy, Kerr). microTBS specimens were fabricated and placed in water with 0.5% chloramine T at 37 degrees C until respective static load to failure testing at one-month, six-months and five-year storage. Failure modes were determined by scanning electron microscopy. The interfacial ultrastructure of the resin-dentin interface was analyzed by transmission electron microscopy (TEM) at 48-hours and 44-months storage. microTBS was modeled with Weibull distribution for survival analysis and failure curve distributions were analyzed by the Wald chi-square statistic for significant differences at alpha=0.05. RESULTS: The characteristic tensile strength (sigma omicron) at one-month, six-months and five-year storage was 52.63, 14.77 and 23.57 Mpa, with a Weibull modulus of 3.04, 1.56 and 1.28, respectively. Failure distributions for all groups were significantly different (p<0.0001) with one-month > five-year > six-months. TEM interfacial morphology demonstrated hydrolytic degradation of hybrid layer components at 44-months storage. SIGNIFICANCE: The decrease in tensile strength and changes in ultrastructure may be caused by water sorption and resultant hydrolytic degradation of the adhesive joint.

Absorption↗
PubMedDate not supplied

Characterization of multiple cathepsin B mRNAs in murine B16a melanoma.

We have previously shown that the highly metastatic murine B16a melanoma expresses a high level of cathepsin B mRNA which is associated with three transcripts of 2.2, 4.0 and 5.0 kb, while in contrast only a single 2.2 kb cathepsin B RNA was detected in normal murine tissues. Using recombinant DNA techniques, cDNAs corresponding to these three transcripts have been isolated from a B16a melanoma cDNA library. Sequence analysis indicates that all three mRNA transcripts contain identical coding sequences for normal preprocathepsin B. However, the 4.0 and 5.0 kb transcripts contain unusually long extended 3' untranslated regions. These results suggest that the post-transcriptional processing pathway of the cathepsin B gene is modified in B16 melanomas. The results also indicate that the increased extracellular secretion of larger forms of cathepsin B by tumors is most likely due to post-translational mechanisms and does not involve alternative splicing or a coding mutation in the gene.

Amino Acid Sequence↗