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Biomedical subjects

Y Gu

Publications and source records attributed to Y Gu.

At least 307 records · Page 17Linked to original sources

[Experimental study on transplantation inside and outside tendon sheath].

The range of motion of PIP and morphological changes of tendon grafts were studied after inside outside tendon sheath grafting in rabbits. It was found that the inside tendon sheath grafting together with early postoperative mobilization healed without adhesion, and most of the cells remained viable. After outside tendon sheath grafting, the tendon cells proliferated with extensive adhesions. The range of PIP motion was greater after inside tendon sheath grafting than that after outside tendon sheath grafting. The results suggest that tendon grafting is donor-tissue-specific and the synovial layer of inside tendon sheath plays an important role in preventing adhesion formation.

Animals↗

[Experimental study of sodium hyaluronate products on prevention of tendon adhesion].

In an experiment sodium hyaluronate product (SHP) was used to observe its effects on healing and preventing adhesion of rabbit muscle tendon. Several methods were used such as gross and histopathological observation, imaging analysis, anti-tension strength measurement. The results confirmed that SHP could reduce collagen contents in peri-tendon tissues and fibroblasts after surgery and decrease the formation of scars in peri-tendon tissues. Therefore, it is effective in preventing muscle tendon adhesion and improving slide function of muscle tendon. Besides, it does not hinder muscle tendon healing.

Animals↗

[Flexor tendon repair: timing of surgery and sheath management].

Effect of timing of repair and management of sheath on functions of injuried tendons was evaluated in a clinical relevant model using 60 white leghorn chickens. The flexor digitorum profundus (FDP) tendons of the long toes were cut and were repaired at 1, 4, 8, 14 and 20 days after injury. The sheath on the left foot was closed and that on the right excised. The tendon excursion, toe motion, morphology of the sheath and tendon healing were studied 6 weeks after tendon repair. Tendon functions were the best in primary repair, and they got worse as the delay became longer. Repair in the late stage produced significantly worse tendon functions. Sheath closure with remarkable tension worsened tendon healing. We conclude that the optimal timing for tendon repair is at the primary stage. Delayed tendon repair can be performed within 3 weeks to one month after injury, but the repair is preferably done in initial several days of delay. Direct sheath closure is not advocated in tendon repair in the delayed period.

Animals↗

[A morphological study of degenerative mechanism of articular cartilage by abnormal high stress].

The articular cartilage from the right knee of 87 rats whose left calcaneal tendons had been transected was examined under transmission and scanning electron microscopes, and light microscope. Morphological observation showed a few small focal areas of cartilage surface disruption, pit and collagen fibrillation at 2 weeks after operation. After 1 month, many clusters of chondrocytes could be found, showing hyperactive synthetic and secretary activity. The cartilage degenerated progressively. The initial lesion in high stress side was at the matrix of cartilage, the collagen network was disrupted, then proteoglycan become degraded. The microenvironment of chondrocytes was changed with degradation of matrix. The chondrocytes became degenerative. The degeneration of chondrocytes influence the matrix again. A vicious cycle was thus formed. At the early stage of the degeneration of the cartilage induced by high-stress, som chondrocytes proliferate and have hyperactive synthetic and secretive functional activity. But soon, most of the chondrocytes degenerate. That is because of the chondrocytes have got repaired in response to initial matrix lesion and the normal microenvironment had degraded with aggravation of matrix lesion. These chondrocytes again became degenerative quickly.

Animals↗

Bis-catechol-substituted redox-reactive analogues of hexamethonium and decamethonium: stimulated affinity-dependent reactivity through iron peroxide catalysis.

Symmetrically bis-catechol-substituted analogues (1 and 2, respectively) of hexamethonium and decamethonium were synthesized and investigated as redox-activated affinity reagents toward the neurotoxin-binding sites of the nicotinic acetylcholine receptor (nAcChR), purified from Torpedo californica electroplax. These reagents bound to nAcChR with Kd = 1.8 x 10(-8) and 2.3 x 10(-7) M for 1 and 2, respectively. In the presence of a metal, Fe(II)/Fe(III), and peroxide, both reagents produced a rapid and efficient half-of-sites inactivation of neurotoxin-binding sites in the nAcChR in a concentration-dependent manner, which paralleled the extent of receptor binding of the reagents. In the absence of Fe(II)/Fe(III) peroxide, redox-dependent inactivation occurred for both 1 and 2 more slowly and only at concentrations much higher (10(3)-10(4) times) than those necessary to produce significant binding to nAcChR. However, receptor inactivation in the absence of added metal peroxide was still more efficient for 1 and 2 than observed previously for [(trimethylammonio)methyl]catechol (3), the prototypic redox-dependent affinity reagent after which 1 and 2 were patterned. Thus, the new reagents reported are expected to provide more efficient and selective conditions for redox-dependent inactivation at nAcChR and other macromolecular sites to which such reagents may be directed.

Animals↗

Leucine-zipper dimerization motif encoded by the AF17 gene fused to ALL-1 (MLL) in acute leukemia.

Chromosome region 11q23 is involved in reciprocal chromosome translocations associated with human acute leukemias. These aberrations fuse the ALL-1 gene located at 11q23 to a series of partner genes positioned on a variety of human chromosomes. The fused genes encode chimeric proteins. Here we report the cloning and characterization of the ALL-1 partner at 17q21, the AF17 gene. The AF17 gene encodes a protein of 1093 amino acids, containing a leucine-zipper dimerization motif located 3' of the fusion point and a cysteine-rich domain at the N terminus. The latter can be arranged in three zinc fingers and shows homology to a domain within the protein Br140 (peregrin). AF17 contains stretches of amino acids previously associated with domains involved in transcriptional repression or activation. Based on features of AF17 and of the proteins encoded by the other partner genes analyzed and in conjunction with other recent studies, we propose a model in which ALL-1 rearrangements result in loss of function of the gene. In this model, the partner polypeptide plays an accessory role either by repressing activity of the truncated ALL-1 protein or by blocking the function of the normal protein presumably present in the leukemic cells.

Amino Acid Sequence↗

ALL-1 tandem duplication in acute myeloid leukemia with a normal karyotype involves homologous recombination between Alu elements.

Rearrangements of the ALL-1 gene by reciprocal translocations involving chromosome band 11q23 are frequently associated with human acute leukemia. We have previously reported the detection of ALL-1 gene rearrangements in adult patients with acute myeloid leukemia lacking cytogenetic evidence of 11q23 translocations. These included 2 of 19 patients with normal karyotypes as well as 3 of 4 patients with trisomy 11 as a sole cytogenetic abnormality. Rearrangement of the ALL-1 genes in two of the patients with trisomy 11 was shown to result from a direct tandem duplication of a portion of the gene spanning exons 2-6. Here we report the characterization of the ALL-1 gene rearrangement in one of the previously reported acute myeloid leukemia patients with a normal karyotype. ALL-1 rearrangement in this patient results from a direct tandem duplication of a portion of the gene spanning exons 2-8. RNA polymerase chain reaction and DNA sequence analysis show that the partially duplicated ALL-1 gene is transcribed into mRNA capable of encoding a partially duplicated protein. Sequence analysis of the genomic fusion region provides evidence for Alu-mediated homologous recombination as a mechanism for partial duplication of the ALL-1 gene.

Acute Disease↗

Mechanism of action of the redox affinity reagent [(trimethylammonio)methyl]catechol.

The synthesis of 4- and 5-hydroxy-3-[(trimethylammonio)methyl]catechol (4- and 5-HTMC) was carried out to examine their proposed involvement as intermediates in the spontaneous redox-dependent half-of-sites inactivation of neurotoxin binding sites in the nicotinic acetylcholine receptor (nAcChR) mediated by the parent compound 3-[(trimethylammonio)methyl]catechol (TMC) [Nickoloff et al. (1985) Biochemistry 24, 999-1007]. Oxidation of 4- and 5-HTMC occurred with sodium periodate with facile conversion to the corresponding p-quinones which were intercepted with thiols and cyclopentadiene. Both 4- and 5-HTMC inactivated neurotoxin binding in the nAcChR in a time course and over a concentration range consistent with their involvement as intermediates in the TMC redox-dependent inactivation of neurotoxin ([125I]-alpha-bungarotoxin) binding sites. Rapid concentration-dependent inactivation of neurotoxin sites occurred over a 10-1000 microM range and was resistant to further inactivation after 50% loss of available toxin binding sites on the nAcChR. Both 4- and 5-HTMC inactivated nAcChR neurotoxin sites much more rapidly and efficiently than was observed previously with TMC. The apparent binding constants for 4- and 5-HTMC with the nAcChR, calculated from their concentration-dependent inactivation behavior toward toxin binding sites, were Kd = 224 +/- 98 and 39 +/- 17 microM, respectively. The observed results and the redox potentials (vs Ag/AgCl reference electrode) measured by cyclic voltammetry at pH 1.8 for TMC (719 mV) and the 4- and 5-HTMC derivatives (519 and 443 mV, respectively) supported the previously proposed mechanism for inactivation of the nAcChR by TMC.(ABSTRACT TRUNCATED AT 250 WORDS)

Benzalkonium Compounds↗

ALL-1 partial duplication in acute leukemia.

The ALL-1 gene, located on chromosome band 11q23, is fused to a variety of other genes by reciprocal chromosomal translocations present in 5-10% of human acute leukemias. We have recently reported the detection by Southern blot of ALL-1 gene rearrangements in adult patients with acute myeloid leukemia lacking cytogenetic evidence of 11q23 translocations. These include 2 of 19 patients with normal karyotypes as well as 3 of 4 patients with trisomy 11. To characterize the abnormal ALL-1 genes, we cloned the ALL-1 rearrangements from two patients with trisomy 11. Characterization of the clones, together with Southern blot analysis, indicates that the ALL-1 rearrangement in both patients is the result of a direct tandem duplication of a portion of the ALL-1 gene spanning exons 2-6. The partial ALL-1 duplication is also detected by Southern blot analysis in a patient with a normal karyotype. RNA PCR and DNA sequence analysis show that the partially duplicated ALL-1 gene is transcribed into mRNA capable of encoding a partially duplicated protein. Partial duplication of ALL-1, in which a portion of a putative protooncogene is fused with itself, represents an additional genetic mechanism for leukemogenesis. Our findings suggest that the presence of trisomy in malignancy may sometimes indicate the partial duplication of a cellular protooncogene.

Acute Disease↗

Sequence analysis of the breakpoint cluster region in the ALL-1 gene involved in acute leukemia.

DNA rearrangements caused by chromosome translocations between band 11q23 and various chromosomes can be detected by a single probe, B859, an 859-base pair complementary DNA fragment derived from the human ALL-1 gene. To try to understand why band 11q23 becomes a frequent target of the translocations, we have sequenced the entire breakpoint cluster region, a 8342-base pair BamHI genomic fragment delineated by B859. We found eight Alu repeats located within this region in the same orientation as the ALL-1 gene. We have also analyzed the sequences of the breakpoints in 10 patients with 6 different types of 11q23 aberration. In five patients the breaks coincided with Alu sequences on chromosome 11, but not on the partner chromosomes. Also, seven of the breaks occurred in the region delineated by exons 6 and 7, which is composed mainly of Alu sequences. In three patients topoisomerase II recognition site-like sequences, at different stringency levels, were identified at the breakpoints on chromosome 11. We conclude that while there is no specific sequence element present at all the breakpoints, the high density of Alu sequences in the breakpoint cluster region possibly makes the latter more prone to recombination events.

Acute Disease↗

An approach for treating the uncertainties in the impact of climate change.

Past accumulated data supported by the predictions of climate models suggest that our world is getting warmer. Scientists are trying to construct mathematical models of both climate and crop systems to identify what types of climate changes could constitute a significant risk or benefit for agriculture. However, due to the many uncertainties regarding these models, it is impossible to make unequivocal predictions. At present, almost all the research in this area is carried out without considering the uncertain nature of the problem. The approach outlined here attempts to find a way to deal with the above uncertainty problem. Artificial intelligence techniques are being developed with the aim of performing inferences based on uncertain information. In our method, causal graphs are used for explicit representation of the relationships between climatic factors and yield. Probabilities are used to express the uncertainties associated with these links, and Bayes' theorem is applied to deal with uncertainty reasonings. This approach has the additional advantage of allowing the prediction to be readily updated as results from improved climate and crop models become available. These opportunities are being evaluated initially by using the model for potato growth developed at the Scottish Crop Research Institute.

Journal Article↗

Borrelia burgdorferi antigens that are targeted by antibody-dependent, complement-mediated killing in the rhesus monkey.

We identified surface antigens of Borrelia burgdorferi that are targeted by antibody-dependent, complement-mediated killing (ADCK) in the rhesus monkey. For this purpose, we had available serum samples from three animals infected with B. burgdorferi JD1 by needle inoculation and from two monkeys that were infected with the same B. burgdorferi strain by Ixodes scapularis tick bite. Sera from monkeys from the first group contained antibodies to OspA and OspB detectable by Western blot (immunoblot) using whole B. burgdorferi antigens, whereas serum samples from animals in the second group did not. The targeting of OspA and OspB by functional antibodies was demonstrated directly by showing that ADCK was partially inhibited when antibodies were preincubated with an excess of soluble recombinant OspA or OspB. Simultaneous addition of OspA and OspB did not result in an additive inhibitory effect on ADCK, a result that suggests that the epitopes on OspA and that on OspB targeted by antibody in this mechanism are the same, or at least cross-reacting. The targeting of non-OspA, non-OspB surface antigens was inferred from the fact that sera from tick-inoculated animals, which did not contain detectable anti-OspA or anti-OspB antibodies, were able to effect ADCK. This killing effect was not inhibitable by the addition of recombinant OspA or OspB or both proteins together. We also showed that both immunoglobulin G and M antibodies participate in the ADCK mechanism in the rhesus monkey. Rhesus complement does not kill B. burgdorferi in vitro in the absence of antibody, and antibody alone is effective in killing only at serum dilutions lower than 1:15. However, such "complement-independent" antibodies were not present in all bleeds. Two main conclusions may be drawn from the analysis of our results. First, both OspA and OspB are targeted by the ADCK mechanism in the rhesus monkey. Second, one or more B. burgdorferi surface antigens that are neither OspA nor OspB also participate in ADCK.

Animals↗

Apoptosis in decidual tissue regression and reorganization.

During blastocyst implantation, cellular degeneration of decidual tissue spreads from the antimesometrial region to the mesometrial region to accommodate the developing conceptus. To identify the mechanism of decidual regression and its tissue localization, decidual formation was induced in either intact pseudopregnant rats or ovariectomized rats treated with steroids. Antimesometrial and mesometrial cells were separated by elutriation and cultured for 48 h before DNA analysis. Nucleosomal DNA fragmentation was observed in antimesometrial cells, whereas DNA fragmentation was less marked in mesometrial cells. To determine whether a similar pattern of apoptosis occurred during decidual development in vivo, decidua tissues from antimesometrial and mesometrial regions were obtained on days 8-14. Nucleosomal DNA fragmentation was first detected on day 10 in the antimesometrial region, with fragmentation in the mesometrial region delayed by at least 24 h. DNA fragmentation increased in both tissues with time, but was always more pronounced in antimesometrial cells. Sulfated glycoprotein-2 (SGP-2) has been associated with apoptosis, and its expression was examined by Northern analysis. Levels of SGP-2 messenger RNA (mRNA) were detected in the antimesometrial region on day 9 and increased markedly by day 10; mesometrial expression was delayed 24 h. Levels of SGP-2 mRNA in both regions decreased before the onset of DNA fragmentation. In contrast, cathepsin-D expression, detected by immunohistochemistry, was localized to few mesometrial and antimesometrial cells between days 9-12, with all cells showing extensive staining by day 14. To determine whether changes in progesterone control mechanisms initiated decidual apoptosis, plasma progesterone levels were measured by RIA, and progesterone receptor mRNA levels in decidual tissues were examined by reverse transcription-polymerase chain reaction. Both parameters remained unchanged during decidual growth and regression. These results provide biochemical evidence that decidual regression occurs by apoptosis initiated in the antimesometrial region and with progression to the mesometrial region. Apoptotic cell death occurs despite high levels of plasma progesterone and high levels of progesterone receptor message in decidual tissue.

Animals↗

Expression of decidual prolactin-related protein in the rat decidua.

It is well established that rat decidual tissue produces a PRL-like hormone(s) that binds to the PRL receptor on both the corpus luteum and the decidual cells and initiates profound changes in the endocrine milieu required for the establishment of pregnancy. The recent cloning of a decidual PRL-related protein (dPRP) prompted us 1) to determine whether the expression of this gene is triggered by decidualization of the endometrial stromal cells, 2) to examine the temporal and cell-specific pattern of its expression, and 3) to examine the role of both decidual signals and PRL on levels of its messenger RNA (mRNA). Total RNA was isolated from uteri of either nonpseudopregnant rats or pseudopregnant rats with or without decidual tissue. A 1-kilobase mRNA species hybridizing strongly with the dPRP probe was present in decidualized uteri. No dPRP mRNA could be detected in uteri not subjected to decidualization. Developmental studies indicated a constant high level of dPRP mRNA in the decidual tissue until day 12 of pseudopregnancy, followed by a marked decline at a time when extensive cell death occurs in the decidua, suggesting that dPRP is constitutively expressed in this tissue. To examine the cell-specific expression of dPRP, antimesometrial decidua was separated from mesometrial decidua, and the large antimesometrial cell population was separated from the small mesometrial cells by elutriation. The results of Northern analysis revealed clearly that dPRP is abundantly and solely expressed in the large antimesometrial cells. No dPRP mRNA could be detected in the mesometrial cells and in numerous other endocrine and nonendocrine tissues. A faint signal was observed, however, in the trophoblast. Despite the very strong paracrine regulation between the antimesometrial and mesometrial cells and the high levels of PRL receptor expression in these cells, both in vivo and coculture experiments revealed no regulation of dPRP gene expression by either PRL or mesometrial cell signal, adding further support to the possibility that once induced, dPRP remains constitutively expressed. In summary, the results of this investigation revealed that the expression of dPRP in endometrial stromal cells is triggered by the induction of decidualization and that this gene is selectively and abundantly expressed in a defined cell population located in the anti-mesometrial region of the uterus. Thus, dPRP is not only a useful indicator of decidualization, but is also an excellent marker for the differentiated antimesometrial cells.

Animals↗

[Clinical application of neurovascular island flap in the hand].

From 1962 to 1992, four kinds of neurovascular island flaps of the hand were used for the treatment of skin defects in the hand in 72 cases. Of these flaps, 38 were pulp flaps of the finger, 24 were based on the first dorsal metacarpal artery, 7 were from second dorsal metacarpal artery and 3 were from hypothenar area. All the flaps survived except 1. Postoperative follow-up showed excellent or good results in 94.4%. The indications of the operation, flap design and surgical procedure are described. The anatomical feature, the advantages and disadvantages of the flap are discussed.

Adolescent↗