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Biomedical subjects

H Qi

Publications and source records attributed to H Qi.

At least 109 records · Page 6Linked to original sources

The patterns of control signals underlying elbow joint movements in humans.

Position, velocity, flexor and extensor electromyographic (EMG) activity of fast, moderate and slow elbow movements to a target were recorded and simulated using a model in which reciprocal and co-activation central commands, proprioceptive feedback and mechanical properties of muscles were considered. Two hypotheses concerning the pattern of shift in the equilibrium point (EP) underlying the movements were tested. First, the nervous system specifies a constant rate of EP shift to produce movement and encodes displacement by the duration of the shift (ramp-shaped pattern). Second, in fast movements, the EP rapidly shifts towards the future final position but then shifts back and forth eventually reaching the final EP (N-shaped pattern). The ramp pattern was consistent with kinematic and EMG experimental data regardless of movement speed. In contrast, the N-shaped pattern was incompatible with the kinematic characteristics of fast movements.

Elbow Joint↗

The cytoplasmic raf oncogene induces a neuronal phenotype in PC12 cells: a potential role for cellular raf kinases in neuronal growth factor signal transduction.

The neuron-like differentiation of PC12 cells is induced by nerve growth factor (NGF) through stimulation of a membrane-bound protooncoprotein signaling pathway containing the NGF receptor Trk, the tyrosine kinase Src, and the GTP-binding protein Ras. The Raf-1 and B-raf protooncogenes encode cytoplasmic serine/threonine kinases that are stimulated by NGF in a Ras-dependent manner. To investigate the possible roles of cytoplasmic Raf kinases in eliciting neuronal differentiation, we have expressed the activated Raf-1 oncogene in PC12 cells. Expression of the raf oncogene results in the elaboration of a neuron-like phenotype, including neurite growth and the induction of the NGF-responsive genes NGFI-A and transin. The actions of activated Raf-1 and NGF are not additive. Furthermore, activated Raf-1 oncoprotein can prime cells for transcription-independent neurite growth by NGF and can elicit rapid neurite growth from NGF-primed cells. Our data indicate that the pathways utilized by NGF and activated raf to effect PC12 differentiation overlap and lead to the suggestion that cellular raf kinase activities play significant roles in transducing the differentiating signals of neuronal growth factors.

Animals↗

Skeletal effects of withdrawal of estrogen and diphosphonate treatment in ovariectomized rats.

The study was designed to determine the skeletal effects of withdrawal of estrogen and diphosphonate treatment in the estrogen-deplete state. Groups of ovariectomized (OVX) rats were treated with vehicle alone, estrogen, or the diphosphonates etidronate or risedronate for a 180-day period. A group of sham-operated control rats was treated for 180 days with vehicle alone. All treatments were then terminated, followed by sequential sacrifice of rats at 0, 35, 90, 180, and 360 days after withdrawal of treatment. The proximal tibia from each animal was processed undecalcified for quantitative bone histomorphometry. At the end of the treatment period, vehicle-treated OVX rats were characterized by cancellous osteopenia and increased bone turnover relative to vehicle-treated control rats. Treatment of OVX rats with estrogen or diphosphonates depressed bone turnover and protected against cancellous osteopenia. During the withdrawal period, OVX rats previously treated with estrogen exhibited rapid bone loss associated with increased bone turnover. The bone protective effect of the hormone in OVX rats was nearly completely lost by 90 days of withdrawal. In contrast, OVX rats maintained low levels of bone turnover and normal cancellous bone mass at 180 days of withdrawal from diphosphonate treatment. The results suggest that estrogen-deplete women who are withdrawn from estrogen replacement are at high risk for subsequent bone loss. They further suggest that widely spaced periods of intermittent diphosphonate treatment may be sufficient to prevent the development of osteopenia in postmenopausal and oophorectomized women.

Animals↗

Parathyroid hormone is more effective than estrogen or bisphosphonates for restoration of lost bone mass in ovariectomized rats.

The study was designed to compare the therapeutic efficacy of estrogen, the bisphosphonate risedronate (NE-58095), and PTH for restoration of lost bone mass in osteopenic, ovariectomized (OVX) rats. In addition, the skeletal effects of these single treatments were compared to those of concurrent treatments with PTH + estrogen or PTH + NE-58095. OVX rats were untreated for the first 4 weeks postovariectomy to allow for the development of moderate tibial osteopenia. These animals were then subjected to the various treatments for periods of 5, 10, and 15 weeks. Their proximal tibiae were processed undecalcified for quantitative bone histomorphometry. Treatment of osteopenic OVX rats with estrogen or NE-58095 alone depressed bone turnover and prevented additional cancellous bone loss from occurring during the treatment period. However, these therapeutic agents failed to restore lost bone in OVX rats to control levels. In contrast, OVX rats treated with PTH alone exhibited a marked stimulation of bone formation which resulted in augmentation of cancellous bone mass to a level 2-fold greater than that of vehicle-treated control rats. Concurrent treatment of OVX rats with PTH + estrogen as well as PTH + NE-58095 also effectively reversed cancellous osteopenia in OVX rats, but did not appear to be more beneficial to the estrogen-deplete skeleton than treatment with PTH alone. The results indicate that PTH is a powerful stimulator of bone formation and completely restores lost cancellous bone in osteopenic OVX rats. Furthermore, the bone anabolic effects of PTH are much more pronounced than those of estrogen or bisphosphonates. These findings in an animal model of estrogen depletion provide support for PTH as a potentially effective treatment for oophorectomized and postmenopausal women with established osteoporosis.

Animals↗

[Influence of 11 ginsenoside monomers on action potentials of myocardiocytes].

Eleven ginsenoside monomers were added to cultured myocardiocytes of neonatal Wistar rats in a concentration of 20 micrograms.ml-1. And the action potentials (AP) were led with microelectrodes. Rb1, Rb2, Rb3, Rc, Rg1, Rg2, Re, and Rh1 inhibited AP, decreasing APA by 20%, 13%, 5%, 18%, 30%, 37%, 28%, and 23%, respectively. The potency of the most effective monomer Rg2 20 micrograms.ml-1 was similar to that of the calcium channel blocker nimodipine 1.25 micrograms.ml-1. Rd, Rf, and Ro had no significant influence on AP. The average potency of the panaxatriol saponin (PTS) monomers were greater than that of the panaxadiol saponin (PDS) monomers. The above demonstrate the reason why the calcium channel blockade action of PTS is stronger than that of PDS results from the summation of monomer drug effects.

Action Potentials↗

[Antioxidative action of soyasaponin monomers I, A1, A2, and their inhibitory effects on action potential and beating of myocardiocytes in culture].

Ventricular myocardiocytes from newborn Wistar rats were cultured. Soyasaponin monomers I, A1, A2 2 micrograms.ml-1 added to the culture medium, like nimodipine 1.25 microgram.ml-1, decreased the number of spontaneously beating clusters and the action potential parameters of myocardiocytes, which restored after washing out and were reversed by Ca2+ 80 micrograms.ml-1 or epinephrine 10 micrograms.ml-1, indicating the Ca2+ channel blockade action of the saponin monomers. Adding xanthine 0.42 mmol.L-1 and xanthine oxidase 5.4 nmol.L-1 into culture medium led to the increase of free radical content of the myocardiocytes and the decrease of action potential parameters, which were reversed by I 2 micrograms.ml-1, indicating the antioxidative action of saponin monomer I.

Action Potentials↗

[Sodium channel blocking effect of scorpion venom on cultured mouse myocardiocytes].

Myocardiocytes of mice were cultured. Action potentials were recorded with microelectrodes inside the cells. Scorpion venom from Buthus martensii Karsch 3.75 or 7.5 micrograms.ml-1 decreased the duration of action potential and all of the depolarization concerned parameters of myocardiocytes. The Vmax, TP, APA behaved apparently in a dosage-dependent way. Restoration happened after washing out. Tetrodotoxin 2.5 micrograms.ml-1 acted in a similar way. Nimodipine 3.0 micrograms.ml-1 led to a decrease in action potential duration. BaCl2 0.1 mmol.L-1 elongated the action potential duration, while decreased the parameters concerned with depolarization. These results indicate that the scorpion venom has Na+ channel blocking action.

Action Potentials↗

Preservation of hippocampal brain slices with in vivo or in vitro hypothermia.

Hippocampal brain slices show CA1 injury similar to that seen after global ischemia in vivo. Cooling rats to 31 degrees C prior to sacrifice or cooling slices to 21 degrees C for 45 min increased the percentage of normal CA1 pyramidal cells after 5 h in vitro from 30% to over 80%. Brain slices also show a unique, consistent injury in dentate which is lessened by transient cooling to 21 degrees C but not by cooling the animal.

Analysis of Variance↗

[Effects of semen Ziziphis Spinosae oil and Ziziphis Spinosae extract on the decrease of serum lipoprotein and inhibiton of platelet aggregation].

Our experiments have shown that oral administration of Semen Ziziphis Spinosae oil(SZSO) or Ziziphis Spinosae extract (ZSE) given to quails for 53 days can significantly reduce their TC, LDL and TG and markedly subdue the fatty degeneration in their livers. Also, SZSO pressed into the stomach of rats for five days can conspicuously inhibit their platelet aggregation, while ZSE cannot.

Animals↗

[Effects of tetrandrine on platelet aggregation, platelet adhesion and coagulation].

We examined the effect of tetrandrine on platelet aggregation, platelet adhesion and coagulation in vitro. The results showed that tetrandrine markedly inhibited the platelet aggregation induced by ADP or collagen. Tetrandrine also markedly inhibited platelet adhesion and thrombosis, but didn't change thrombin coagulation time and plasma coagulation time obviously.

Alkaloids↗

Effects of dextran on hippocampal brain slice water, extracellular space, calcium kinetics and histology.

Hippocampal brain slices are valuable models for studying brain function but are compromised by several artifacts, including significant water gain and histologic injury, which occur under certain incubation conditions. Addition of colloid to Krebs-Ringer buffer (K-R) has been shown to eliminate water gain but has not achieved widespread acceptance. We confirm prior observations that dextran and PEG lessen the increase in slice mass during incubation in a dose-dependent manner with no water gain occurring at 4% concentrations. However, we also observe that addition of colloid to standard K-R induces severe neuronal pyknosis. Fortunately, the pyknosis can be eliminated by reduction in buffer osmolarity through adjustment of NaCl, producing markedly improved slice histology in dextran buffer, especially in the CA3 and CA4 regions of the hippocampus which are severely injured when incubated submerged in K-R at 37 degrees C. Extracellular space markers are not affected by either colloid. The volume of distribution for 45Ca is much larger in dextran buffers than in K-R and variability of 45Ca kinetics is also reduced. In the presence of dextran, hypoxia induces significant slice water gain, a relatively selective histologic injury and an alteration of tissue Ca2+ kinetics. Use of dextran buffers may eliminate many troubling brain slice artifacts.

Animals↗