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Biomedical subjects

Shihe Li

Publications and source records attributed to Shihe Li.

5 recordsLinked to original sources
PubMed2005

Cytoplasmic dynein's mitotic spindle pole localization requires a functional anaphase-promoting complex, gamma-tubulin, and NUDF/LIS1 in Aspergillus nidulans.

In Aspergillus nidulans, cytoplasmic dynein and NUDF/LIS1 are found at the spindle poles during mitosis, but they seem to be targeted to this location via different mechanisms. The spindle pole localization of cytoplasmic dynein requires the function of the anaphase-promoting complex (APC), whereas that of NUDF does not. Moreover, although NUDF's localization to the spindle poles does not require a fully functional dynein motor, the function of NUDF is important for cytoplasmic dynein's targeting to the spindle poles. Interestingly, a gamma-tubulin mutation, mipAR63, nearly eliminates the localization of cytoplasmic dynein to the spindle poles, but it has no apparent effect on NUDF's spindle pole localization. Live cell analysis of the mipAR63 mutant revealed a defect in chromosome separation accompanied by unscheduled spindle elongation before the completion of anaphase A, suggesting that gamma-tubulin may recruit regulatory proteins to the spindle poles for mitotic progression. In A. nidulans, dynein is not apparently required for mitotic progression. In the presence of a low amount of benomyl, a microtubule-depolymerizing agent, however, a dynein mutant diploid strain exhibits a more pronounced chromosome loss phenotype than the control, indicating that cytoplasmic dynein plays a role in chromosome segregation.

Anaphase↗
PubMed2005

[Study on the effect of composite of basic fibroblast growth factor and partially deproteinized bone on the repair of femoral head defects].

OBJECTIVE: To evaluate the effect of composite (bFGF/PDPB) of basic fibroblast growth factor (bFGF) and partially deproteinized bone (PDPB) on the repair of femoral head defect. METHODS: Forty-eight femoral heads with defect derived from 24 New Zealand rabbits were divided into 3 groups at random, which were implanted with bFGF/PDPB (group A), PDPB (group B) and nothing (group C) respectively. The rabbits were sacrificed at 2, 4, and 8 weeks after operation, and then the femoral heads were obtained. The specimens injected with Chinese ink were created. Then X-ray examination, histopathological and morphological examination of blood vessel, and image analysis were made. RESULTS: The bone defects healed completely 8 weeks after operation in group A. The implants in the repaired tissue were not substituted completely in group B. The bone defects did not heal completely in group C. Two weeks after operation, affluent newly formed vessels were seen in repaired areas in group A. No significant difference between group A and group B was observed 8 weeks after operation. In group C, newly formed vessels were scarce 2, 4, and 8 weeks after operation. There were 3 sides rated excellent, 2 good and 1 fair in group A; 1 excellent, 2 good, 2 fair and 1 poor in group B; and 1 fair and 5 poor in group C according to the X-ray evaluation 8 weeks after operation. Eight weeks after operation, the volume fraction of bone trabecula in repaired tissue was higher in group A than that in group B (P < 0.05), and the fraction in group C was the lowest among the 3 groups (P < 0.05). CONCLUSION: The composite of bFGF and PDPB can effectively promote the repair of femoral head defect of rabbit.

Animals↗
PubMed2005

[Experimental study on repairing segmental bone defects with three bio-bone derived materials].

OBJECTIVE: To evaluate the osteogenesis of three bio-bone derived materials in repairing segmental bone defects. METHODS: Sixty Japanese rabbits were made 10 mm radius segmental defects and divided into 5 groups (groups A, B, C, D and E, n=12). Composite fully deproteinised bone (CFDB, group A), partially deproteinised bone (PDPB, group B), partially decalcified bone (PDCB, group C), autogenous iliac bone graft (group D) and no implant (group E) were implanted into the radius segmental bone defects of rabbits. The specimens were examined after 4, 8, 12 and 24 weeks; the osteogenesis was evaluated through X-ray radiograph and undecalcified solid tissue histological examination. RESULTS: The border between the material and host's bone was distinct after 4 weeks and blurred after 8 weeks; the density of partial edge of the material was similar to that of radii after 12 weeks. The medullary cavity of bone reopened in group B; the density of most defect area was similar to that of the host bone and there was a few high density shadow in group C; the density of most defect area was higher than that of host bone in group A after 24 weeks. There was no significant difference in radiograph scoring between groups A, B and C after 4 weeks and 8 weeks (P>0.05); the scores of group B and C were higher than that of group A after 12 weeks (P<0.05); and the scores were arranged as follow: group D > group B > group C > group A after 24 weeks (P<0.05). Bone callus grew toward defect area and new bone adhered to the material after 4 weeks and 8 weeks; more new bone formed, and the materials were absorbed and degraded with time. The quantity of bone formation was more in group D than in group B and in group B than in group C and in group C than in group A after 24 weeks (P<0.05). CONCLUSION: PDPB had good osteogenesis in repairing the segmental bone defect, PDCB was inferior to it, both PDPB and PDCB are fit to repair segmental bone defect. Both of them were inferior to autogenous bone.

Animals↗
PubMed2003

Accumulation of cytoplasmic dynein and dynactin at microtubule plus ends in Aspergillus nidulans is kinesin dependent.

The mechanism(s) by which microtubule plus-end tracking proteins are targeted is unknown. In the filamentous fungus Aspergillus nidulans, both cytoplasmic dynein and NUDF, the homolog of the LIS1 protein, localize to microtubule plus ends as comet-like structures. Herein, we show that NUDM, the p150 subunit of dynactin, also forms dynamic comet-like structures at microtubule plus ends. By examining proteins tagged with green fluorescent protein in different loss-of-function mutants, we demonstrate that dynactin and cytoplasmic dynein require each other for microtubule plus-end accumulation, and the presence of cytoplasmic dynein is also important for NUDF's plus-end accumulation. Interestingly, deletion of NUDF increases the overall accumulation of dynein and dynactin at plus ends, suggesting that NUDF may facilitate minus-end-directed dynein movement. Finally, we demonstrate that a conventional kinesin, KINA, is required for the microtubule plus-end accumulation of cytoplasmic dynein and dynactin, but not of NUDF.

Aspergillus nidulans↗