PubMed Health⌕ Search

Biomedical subjects

H Qi

Publications and source records attributed to H Qi.

At least 55 records · Page 3Linked to original sources
PubMed1999

Droloxifene does not blunt bone anabolic effects of prostaglandin E2, but maintains prostaglandin E2-restored bone in aged, ovariectomized rats.

Droloxifene (DRO) is a selective estrogen receptor modulator that prevents bone loss by inhibition of bone turnover associated with estrogen deficiency in both growing and aged female rats. The purposes of this study were to test: (a) whether DRO can maintain prostaglandin E2 (PGE2)-restored bone after discontinuation of PGE2 in aged, ovariectomized (ovx) rats; (b) if an inhibition of bone turnover by DRO reduces bone anabolic effects of PGE2; and (c) whether bone mass restored by PGE2 plus DRO can be maintained after discontinuation of both agents. Female rats at 12 months of age were sham-operated (sham) or ovx. Three months postsurgery, ovx rats were treated with either PGE2 (3 mg/kg per day, subcutaneously [s.c.]) alone, or PGE2 plus DRO (10 mg/kg per day, per os [p.o.]) for 2 months. Thereafter, the PGE2 or PGE2 plus DRO treatment was withdrawn and the rats were then treated with either vehicle or DRO for another 1.5 months. Using dual-energy X-ray absorptiometry (DXA), total lumbar vertebral bone mineral density (LV-BMD) was determined in vivo at months 0, 3, 5, and 6.5. At the end of the study, the rats were autopsied, and BMD of total femur, femoral shaft, distal femoral metaphysis, and proximal femur was determined ex vivo by DXA. Standard static and dynamic bone histomorphometric parameters were determined on the fourth lumbar vertebral body (L-4). At 3, 5, or 6.5 months postsurgery, LV-BMD decreased significantly (-15%, -19%, and -19%, respectively) in the vehicle-treated ovx rats compared with sham. Beginning at 3 months post-ovx, PGE2 alone or in combination with DRO for 2 months completely restored LV-BMD back to the sham level. There was no difference in LV-BMD in PGE2 alone or PGE2 plus DRO. Upon cessation of PGE2 treatment, a significant decrease in LV-BMD was observed in the PGE2-alone group (-12%). On the other hand, when DRO treatment was given after discontinuation of PGE2, the PGE2-restored LV-BMD was completely maintained. In the PGE2 plus DRO group, no loss in LV-BMD was observed after cessation of either PGE2 alone or both PGE2 and DRO. However, treatment with DRO following 2 months of PGE2 plus DRO further increased LV-BMD (+10%). At the end of the study, ex vivo femoral BMD data confirmed the observation in lumbar vertebrae. Histomorphometric results of L-4 indicated that loss in bone mass after cessation of PGE2 in PGE2 alone group was associated with increased bone turnover. Treatment with DRO in the maintenance phase inhibited bone turnover and prevented bone loss induced by withdrawal of PGE2. Trabecular bone mass was maintained in the PGE2 plus DRO followed by vehicle group and further increased in the PGE2 plus DRO followed by DRO groups. We found that: (a) DRO is efficacious in maintaining PGE2-restored bone after discontinuation of PGE2; (b) DRO did not blunt the anabolic effects of PGE2; (c) bone loss occurred after cessation of treatment in the PGE2-alone group, whereas it was maintained after cessation of treatment in PGE2 plus DRO group; and (d) an additional anabolic effect was found in ovx rats treated with PGE2 plus DRO followed by DRO.

Absorptiometry, Photon↗
PubMed1999

Neurofuzzy adaptive controlling of selective stimulation for FES: a case study.

A controller was designed for the selective stimulation of the sciatic nerve with a multiple contact cuff electrode to generate a desired torque in the ankle joint of cat. The design integrates three approaches, artificial neural network (ANN) modeling, fuzzy logical adaptation, and geometrical mapping. The geometrical mapping refers to the vector transformation from the joint coordinates to the virtual muscle coordinates which have been conceptually developed to represent the major recruitment features of contact-based functional units in the physical plant. This method reduces the complexity of generating a data set for training the neural network in the feedforward path and implementing the on-line learning algorithm embedded in the feedback loop. The controller was evaluated by computer simulation with the experimental data obtained from the torque generation in five acute cats. The results show that the ANN-based feedforward is capable of predicting 65% of a given desired isometric torque, and the fuzzy logical machine is able to provide suitable gains for feedback modulation to reduce the error from 35 to 8.5% and produce a robust control.

Animals↗
PubMed1999

The relationship between interleukin-8 and airway hyperresponsiveness in guinea pigs.

OBJECTIVE: To explore the relationship between interleukin-8 (IL-8) and airway hyper-responsiveness (AHR) of asthma in guinea pigs. METHODS: IL-8 at a dose of 0.5 microgram/kg or 5.0 micrograms/kg was administered intranasally to guinea pigs twice a week for 3 weeks. 24 hours after the last administration, airway responsiveness was measured as an overall index of airway response to the increasing concentrations of histamine inhaled (25, 50, 100 and 200 micrograms/ml), and the numbers of different inflammatory cells in bronchoalveolar lavage fluid (BALF) were counted. RESULTS: The IL-8 treatment significantly enhanced airway responsiveness to histamine in a dose-dependent manner (P < 0.05 or P < 0.01) and induced a significant influx of neutrophils in BALF (P < 0.01), and a great number of neutrophils were seen within the airway wall, but not within the control animals treated with phosphate buffered saline (PBS). CONCLUSION: The IL-8 could produce neutrophil inflammation of the airways and induce AHR, which suggested that IL-8 may play an important role in asthma, especially in the development of AHR.

Animals↗
PubMed1999

[The model of piggyback orthotopic liver transplantation in pigs].

To establish the pig model of piggyback orthotopic liver transplantation(PBOLT), twelve cases of pig PBOLT were performed. The result showed that ten pigs were survived after operation, and the operative successful rate was 83%. The mean operation time and mean anhepatic-phase time were 7 hours and 34 minutes, respectively. The mean bleeding amount was 1200 ml. The appearance and tissue structure of liver in every stage under optic microscope were normal. The results indicate that the pig model of PBOLT is feasible and that it is important to decrease the anhepatic-phase time for a successful liver transplantation.

Animals↗
PubMed1999

[Piggyback allogenic orthotopic liver transplantation: one case report].

Piggyback allogenic orthotopic liver transplantation was performed successfully on one patient with primary liver carcinoma. The operation took 11 h and 30 min. The resection of the liver in the patient was initiated by the ligation and transection of the veins within the third hepatic portal. The hepatic venous system was reconstructed with the end of the superhepatic inferior vena cava anastomosed to the side of the inferior vena cava at the angle of 30 degrees-45 degrees in the recipient. The hemodynamics was steadfast intraoperatively, without extracorporeal venous bypass. The patient had a good post-operative recovery. The patient died of respiratory failure caused by metastasis.

Adult↗
PubMed1999

[Light and electron microscope observations of heart and vascular tissues in animals acutely infected with tubercle bacilli].

The objective of this study was to observe the heart and vascular pathological lesions of some animals acutely infected with H37Rv tubercle bacilli. C57 BL/6N mice and rabbits were used for the establishment of the models. Light sections were stained with HE, Z-N, MCT and BCGS-P. Ultrathin sections were stained with uranyl and lead citrate and examined by electron microscope. The results showed that tubercle bacilli were present in heart and vascular tissues. Myocardial fibre, pericardium and vascular tissues had various degrees of lesions. The lesions of myocardial fibre and pericardium were more serious than that of the vascular tissues. These findings suggest that the toxin of the tubercle bacilli can damage the tissues of the infected animals, and the excessive reproduction can be also a factor detrimental to the infected tissues.

Acute Disease↗
PubMed1998

Caspase-2 (Nedd-2) processing and death of trophic factor-deprived PC12 cells and sympathetic neurons occur independently of caspase-3 (CPP32)-like activity.

We have previously shown that caspase-2 (Nedd-2) is required for apoptosis induced by withdrawal of trophic support from PC12 cells and sympathetic neurons. Here, we examine the relationship of caspase-2 processing and cell death to induction of caspase-3 (CPP32)-like activity in PC12 cells. Caspase-2 processing, at a site tentatively identified as D333, led to the formation of an N-terminal 37 kDa product. This processing correlated temporally with induction of caspase-3-like activity. Agents previously shown to inhibit caspase-3-like activation, such as bcl-2 and the Cdk inhibitor flavopiridol, also acted upstream of caspase-2 processing. The general caspase inhibitors BAF and zVAD-FMK inhibited N-terminal caspase-2 processing. In contrast, the more selective caspase inhibitor DEVD-FMK inhibited the induction of caspase-3-like activity but did not affect caspase-2 processing or significantly suppress death in PC12 cells or sympathetic neurons. This indicates that caspase-3-like activity is not required for either caspase-2 processing or apoptosis in this paradigm. An antisense oligonucleotide to caspase-2 inhibited cell death but did not affect caspase-3-like activity, indicating that caspase-2 is not upstream of this activity and that activation of caspase-3-like caspases is not sufficient for death. Thus, in our paradigm, caspase-2 processing and caspase-3-like activity are induced independently of each other. Moreover, although death requires caspase-2, caspase-3-like activity is neither necessary nor sufficient for death.

Amino Acid Chloromethyl Ketones↗
PubMed1998

The protozoan parasite Toxoplasma gondii targets proteins to dense granules and the vacuolar space using both conserved and unusual mechanisms.

All known proteins that accumulate in the vacuolar space surrounding the obligate intracellular protozoan parasite Toxoplasma gondii are derived from parasite dense granules. To determine if constitutive secretory vesicles could also mediate delivery to the vacuolar space, T. gondii was stably transfected with soluble Escherichia coli alkaline phosphatase and E. coli beta-lactamase. Surprisingly, both foreign secretory reporters were delivered quantitatively into parasite dense granules and efficiently secreted into the vacuolar space. Addition of a glycosylphosphatidylinositol membrane anchor rerouted alkaline phosphatase to the parasite surface. Alkaline phosphatase fused to the transmembrane domain and cytoplasmic tail from the endogenous dense granule protein GRA4 localized to dense granules. The protein was secreted into a tuboreticular network in the vacuolar space, in a fashion dependent upon the cytoplasmic tail, but not upon a tyrosine-based motif within the tail. Alkaline phosphatase fused to the vesicular stomatitis virus G protein transmembrane domain and cytoplasmic tail localized primarily to the Golgi, although staining of dense granules and the intravacuolar network was also detected; truncating the cytoplasmic tail decreased Golgi staining and increased delivery to dense granules but blocked delivery to the intravacuolar network. Targeting of secreted proteins to T. gondii dense granules and the plasma membrane uses general mechanisms identified in higher eukaryotic cells but is simplified and exaggerated in scope, while targeting of secreted proteins beyond the boundaries of the parasite involves unusual sorting events.

Alkaline Phosphatase↗
PubMed1998

Cloning and characterization of a novel member of the transforming growth factor-beta/bone morphogenetic protein family.

Members of the transforming growth factor-beta (TGF-beta) superfamily of growth and differentiation factors have been identified in a wide variety of organisms, ranging from invertebrates to mammals. Bone morphogenetic proteins (BMPs) constitute a subgroup of proteins belonging to the TGF-beta superfamily. BMPs were initially identified by their ability to induce endochondral bone formation at ectopic sites, suggesting a critical role for this family in development and regeneration of the skeleton. They are also expressed at a variety of nonskeletal sites during development, suggesting possible extraskeletal roles for these proteins. We cloned a novel member of the BMP family that is expressed at high levels in the placenta and the prostate and that we have designated as prostate-derived factor (PDF). Based on cDNA sequence analysis, the predicted PDF protein contains two cysteines in addition to the seven conserved cysteines that are the hallmark of the members of the TGF-beta superfamily. In addition, Northern blot hybridization to poly(A)+ RNA showed low levels of expression in the kidney and pancreas. We further characterized the expression of this member of the BMP family by in situ hybridization and immunohistochemistry. These results show high expression in the terminal villae of the placenta. The expression of the protein as visualized by immunohistochemistry shows an expression pattern identical to that of the message in the terminal villae of the placenta. In day 18 rat embryos, protein expression was also seen in the skin and in the cartilaginous tissue of developing skeleton. Orchidectomy and dihydrotestosterone treatment of rats revealed that PDF expression is regulated by androgens in the prostate. In addition, subcutaneous implantation of recombinant PDF induced cartilage formation and the early stages of endochondral bone formation. These data indicate that PDF has a functional relationship to the BMPs.

Amino Acid Sequence↗
PubMed1998

Induced activation of the Toxoplasma gondii nucleoside triphosphate hydrolase leads to depletion of host cell ATP levels and rapid exit of intracellular parasites from infected cells.

The nucleoside triphosphate hydrolase of Toxoplasma gondii is a potent apyrase. The protein is synthesized in large amounts and transported through the secretory pathway of the parasite and into the vacuolar space in an oxidized and thereby enzymatically inactive form. Complete activation of the purified enzyme is known to require dithiols (e.g. DTT); subcellular fractionation demonstrates that little if any (<5%) of the enzyme in the vacuolar space is active in the absence of DTT. Both native and epitope-tagged nucleoside triphosphate hydrolase (NTPase) were partially activated during immunoprecipitation, precluding precise assessment of enzyme activity in the vacuolar space but suggesting that protein-protein interactions may trigger activation. When infected cells were treated with DTT, the NTPase was activated in a dose-response fashion, as assessed by migration on SDS-polyacrylamide gel electrophoresis and by an increase in enzymatic activity. After activation, enzyme activity decreased with time in the presence of DTT; this inactivation was slowed by the presence of excess ATP. A rapid fall in host cell ATP was accompanied by an abrupt exit of parasites from cells. These results demonstrate that the oxidation/reduction status of the NTPase, the only parasite dense granule protein that contains disulfide bonds, is tightly controlled within the vacuolar space and may influence parasite exit from cells.

Acid Anhydride Hydrolases↗
PubMed1998

Immature teratoma of the pineal gland with isochromosome 12p.

An immature teratoma arising in the pineal gland in a 27-year-old male was shown to present an isochromosome 12p as evidenced by cytogenetic and fluorescence in situ hybridization analysis. As i(12p) is characteristic of gonadal germ cell tumors, this case indicates that similar genetic pathways may operate in gonadal and intracranial teratomas.

Adult↗
PubMed1998

Iron measures in coronary angiography patients.

Excess iron has been postulated as a risk factor for coronary artery disease (CAD) because of its presence in atherosclerotic lesions, its ability to oxidize low density lipoprotein cholesterol (LDLc), and its promotion of oxygen reperfusion damage after an ischemic event. Whether iron, indirectly measured by its storage protein ferritin and its transport protein transferrin, is related to CAD was examined in a consecutive series of white male (n = 457) and female (n = 114) cardiac patients. Atherosclerosis measures were analyzed in patients grouped by tertiles of ferritin. A similar analysis was done with tertiles of transferrin. Contrary to expectations, men in the third tertile of ferritin had a smaller mean number of stenoses than men in the two lower tertiles (4.9 versus 5.6 and 5.9; P = 0.027); otherwise, there were no statistically significant differences in either number of lesions or extent of arterial narrowing based on tertiles of either measure. Separate multiple logistic regression models with age, fibrinogen, LDLc and triglycerides as covariates provided no evidence that ferritin (odds ratio = 0.88 with 95% C.I. = 0.72-1.07 for men and odds ratio = 0.79 with 95% C.I. = 0.54-1.16 for women) or transferrin (odds ratio = 0.60 with 95% C.I. = 0.31-1.16 for men and odds ratio = 1.33 with 95% C.I. 0.52-3.42 for women) were important correlates of the presence of atherosclerosis in this study.

Coronary Angiography↗
PubMed1998

Prostaglandin E2 increases bone strength in intact rats and in ovariectomized rats with established osteopenia.

It is well documented that prostaglandin E2 (PGE2) has the ability to stimulate bone formation, improve bone structure, and increase bone mass in intact or osteopenic rat models. However, the effects of PGE2 on the mechanical properties of bone have not been investigated previously. The purpose of our study was to determine the effects of PGE2 on the mechanical strength of bones in rapidly growing, adult, and ovariectomized rat models. In study I, PGE2 at 3 mg/kg per day, or vehicle, was given by daily subcutaneous injections for 30 days to rapidly growing (3-month-old) intact male rats. Compared with controls, PGE2 significantly increased initial maximal load and stiffness of cancellous bone at the distal femoral metaphysis (DFM) as determined by an indentation test. As determined by a compression test, rats treated with PGE2 showed a significant increase in maximal load, and a nonsignificant increase in stiffness in the fifth lumbar vertebral body (L5) when compared with controls. In study II, PGE2 at 3 mg/kg per day, or vehicle, was given by daily subcutaneous injection for 30 days to mature (10-month-old) intact male rats. PGE2 treatment significantly increased initial maximal load and stiffness of the DFM and L5. PGE2 induced a significant increase in maximal load, but not stiffness, in the femoral neck (FN), as determined by a cantilever compression test. There was an increase in maximal load in a three-point bending test at the femoral shaft (FS) although the increase did not achieve statistical significance. No change in stiffness in the FS was found after PGE2 treatment. In study III, 3-month-old female rats were sham-operated or ovariectomized (ovx) for 30 days. Thereafter, PGE, at 1 or 3 mg/kg, or vehicle, were given by daily subcutaneous injection to these rats for 30 days. After 30 and 60 days, ovx induced a significant decrease in initial maximal load and stiffness of cancellous bone at the DFM as compared with sham controls. In ovx rats with established osteopenia, PGE2 at 1 mg/kg per day nonsignificantly increased the initial maximal load and stiffness, whereas, at 3 mg/kg per day, PGE2 completely restored the initial maximal load and stiffness of DFM to sham control levels. Similarly, maximal load and stiffness of L5 decreased significantly in ovx rats compared with sham controls at 30 days postsurgery. PGE2 at 1 mg/kg per day partially restored the maximal load, whereas, at 3 mg/kg per day, it completely restored the maximal load and stiffness of L5 in the established osteopenia, ovx rats. At the FS, PGE2 at 3 mg/kg per day nonsignificantly increased maximal load (+11%) and significantly increased stiffness (+25%) compared with ovx controls. Neither ovx nor PGE2 treatment caused a significant change in the maximal load and stiffness of the FN in this study. These results reveal that PGE2 significantly increased the mechanical strength at various skeletal sites in rapidly growing and mature male rats, although the increase in femoral shafts was not statistically different. Furthermore, PGE2 completely restored mechanical strength to the cancellous bone in ovx rats with established osteopenia.

Animals↗
PubMed1998

Effects of CP-336,156, a new, nonsteroidal estrogen agonist/antagonist, on bone, serum cholesterol, uterus and body composition in rat models.

We have discovered a new, nonsteroidal, potent estrogen agonist/antagonist, CP-336,156. CP-336,156 binds selectively and with high affinity to the human estrogen receptor-alpha with a half-inhibition concentration of 1.5 nM, which is similar to that seen with estradiol (4.8 nM). When given orally to immature (3-week-old) female Sprague-Dawley rats for 3 days at doses of 0.1, 1.0, 10, or 100 microg/kg x day, unlike 17alpha-ethynyl estradiol, CP-336,156 had no effect on uterine wet or dry weight. Similarly, no uterine hypertrophy was observed in aged (17-month-old) female rats treated (p.o.) with CP-336,156 at 10 or 100 microg/kg x day for 28 days. We also found that CP-336,156 decreased total serum cholesterol and fat body mass and had no effect on lean body mass in these aged female rats. In 5-month-old ovariectomized (OVX) Sprague-Dawley female rats, CP-336,156 completely prevented OVX-induced increases in body weight gain, total serum cholesterol, and serum osteocalcin at doses between 10 and 1000 microg/kg x day after 4 weeks. At these doses, CP-336,156 completely prevented OVX-induced bone loss and inhibited the increased bone turnover associated with estrogen deficiency in lumbar vertebrae, proximal tibiae, and distal femora. Similar to estrogen, CP-336,156 induced apoptosis and p53 expression with a concomitant decrease in the number of tartrate-resistant acid phosphatase-positive multinuclear cells in rat bone marrow cell cultures in vitro, suggesting that the induction of apoptosis may be a mechanism for the estrogenic activities of CP-336,156 in bone. In summary, CP-336,156 is a new, orally active, nonsteroidal, potent estrogen agonist/antagonist that has similar effects in bone as estradiol but without the uterine-stimulating effects associated with estradiol in rats.

Adipose Tissue↗
PubMed1998

Ovarian development in mice bearing homozygous or heterozygous null mutations in zona pellucida glycoprotein gene mZP3.

The plasma membrane of all mammalian eggs is surrounded by a thick extracellular coat, the zona pellucida (ZP), whose paramount function is to regulate species-specific fertilization. The mouse egg ZP is composed of only three glycoproteins, mZP1-3, that are synthesized and secreted exclusively by oocytes during their 2-3 week growth phase. Disruption of the mZP3 gene by targeted mutagenesis in embryonic stem (ES) cells yields mice heterozygous (mZP3 +/-) or homozygous (mZP3-/-) for the null mutation. As expected, male mice bearing the null mutation are indistinguishable from wild-type males with respect to viability and fertility. Female mZP3 +/- mice are as fertile as wild-type animals, but their eggs have a thin ZP (approximately 2.7 microns thick) as compared to the ZP (approximately 6.2 microns thick) of eggs from wild-type animals. On the other hand, female mZP3-/- mice are infertile and their eggs lack a ZP. The infertility apparently is due to the lack of a sufficient number of eggs in oviducts of superovulated mZP3-/- females. Light micrographs reveal that development of ovarian follicles is often retarded in mZP3-/- mice as compared to wild-type animals. This is manifested as reduced ovarian weights, reduced numbers of Graafian follicles, and reduced numbers of fully-grown oocytes in mZP3-/- females. It seems likely that the pleiotropic effects of the homozygous null mutation on ovarian development may be due, at least in part, to disruption of intercellular communication between growing oocytes and their surrounding follicle cells.

Animals↗