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Biomedical subjects

Yi Zhang

Publications and source records attributed to Yi Zhang.

At least 235 records · Page 13Linked to original sources

Effects of synchronous or asynchronous electroacupuncture stimulation with low versus high frequency on spinal opioid release and tail flick nociception.

Electroacupuncture stimulation (EAS) is known to change brain neurotransmitter release. In the present study, we investigated the effects of synchronous or asynchronous electroacupuncture stimulation with low versus high frequency on spinal opioid release and tail flick nociception. Rats were given "2/100 Hz" EAS, which stands for an asynchronous mode of stimulation, in which 2 Hz was alternated with 100 Hz, each lasting for 3 s, or "(2 + 100) Hz" EAS, a mode of stimulation in which 2 Hz stimulation was applied to the left hind leg simultaneously with 100 Hz stimulation on the right hind leg. The rats were subjected to the same total number of electrical stimulations in these two modes. Results were as follows: (1) 2/100 Hz EAS was 40% more potent than (2 + 100) Hz EAS (P < 0.01) in producing an anti-nociceptive effect. (2) Intrathecal (i.t.) injection of the mu-opioid receptor antagonist D-Phe-Cys-Tyr-D-Trp-Orn-Thr-Pen-Thr amide (CTOP) blocked in a dose-dependent manner the anti-nociceptive effect produced by 2/100 Hz EAS but not by (2 + 100) Hz EAS, whereas i.t. injection of the kappa-opioid receptor antagonist norbinaltorphimide (Nor-BNI) blocked the anti-nociceptive effect induced by both modes of EAS. (3) I.t. injection of endomorphin-2 antiserum blocked in a dose-dependent manner the anti-nociceptive effect of 2/100 Hz EAS but not that of (2 + 100) Hz EAS, whereas i.t. injection of dynorphin antiserum blocked the anti-nociceptive effect induced by both modes of stimulation. (4) 2/100 Hz EAS increased the release of both endomorphin-2 and dynorphin, whereas (2 + 100) Hz EAS increased the release of dynorphin but not of endmorphin-2. We conclude that the more potent anti-nociceptive effect induced by 2/100 Hz EAS, as compared with that of (2 + 100) Hz EAS, was due, at least partly, to the synergistic interaction of endomorphin-2 and dynorphin in rat spinal cord.

Afferent Pathways↗

Effect of hypothermia on transthoracic defibrillation in a swine model.

BACKGROUND: Induced hypothermia (H) appears a promising intervention to protect the heart and brain after resuscitation from cardiac arrest. However, the influence of H on transthoracic defibrillation energy requirements is not well documented. METHODS: In 39 swine (21.4+/-1.3(S.E.) kg) hypothermia was induced by surrounding the head, thorax and abdomen with ice. The swine were divided into four groups: (1) normothermia (N) followed by severe H (30 degrees C) (n=10), (2) severe H followed by N (n=10), (3) N followed by moderate H (33 degrees C) (n=10) and (4) moderate H followed by N (n=9). After 30s of electrically induced ventricular fibrillation (VF), the swine were defibrillated (biphasic waveform) at energies of 20J, 30J, 50J and 100J in random order in both N and H conditions. RESULTS: For pigs in Group 1 (N followed by severe H), shock success in terminating VF was higher during hypothermia (odds ratio 4.09 (95% CI: 2.21, 5.58; p<0.0001), despite the fact that impedance rose from 39+/-3Omega (N) to 42+/-3Omega (H) (p<0.001) and current fell from 22+/-8 (N) to 21+/-7A (H) (p<0.001). There were no significant differences in the shock success between N and H for the other groups. Post-defibrillation ventricular asystole occurred less often during hypothermia compared to normothermia (p=0.0002). CONCLUSION: Severe H facilitated transthoracic defibrillation in this swine model. Since impedance rose and current fell during H, the improved shock success must be due to a hypothermia-induced change in the mechanical or electrophysiologic properties of the myocardium. Moderate hypothermia did not alter the energy requirement for defibrillation.

Animals↗

Macrophage ablation attenuates adenoviral vector-induced pancreatitis.

BACKGROUND: The objective of these studies is to determine the effects of macrophage ablation on the course of acute viral pancreatitis. Macrophages secrete proinflammatory cytokines triggering local pancreatic and systemic inflammation in the acute phase of virus-induced pancreatitis. We hypothesized that ablation of macrophages should attenuate the host inflammatory response in a mouse model of adenovirus-induced pancreatitis. METHODS: Liposome-encapsulated dichloromethylene-diphosphonate, a macrophage-depleting agent, was used before direct pancreatic injection of a recombinant adenovirus expressing a marker gene in C57Bl/6 and IL-6 knockout (KO) mice. RESULTS: C57Bl/6 mice depleted of macrophages had diminished pancreatic inflammation in the first 24 hours after vector administration. IL-6 KO mice depleted of macrophages had more severe inflammation than similarly treated C57Bl/6 mice. C57Bl/6 mice depleted of macrophages, and IL-6 KO mice had prolonged transgene expression and diminished cytotoxic T lymphocyte responses to adenoviral vector. Mortality was highest in IL-6 KO mice depleted of macrophages. Depletion of macrophages also prevented detectable serum IL-6, IL-10, or IL-12 levels in C57Bl/6 mice. CONCLUSIONS: The data suggest that macrophages play a role in the acute inflammatory response to viral vector-induced pancreatitis and that IL-6 may be protective. Understanding of the mechanisms that initiate the host immune cascade will allow more effective use of adenoviral vector-based pancreatic gene delivery.

Acute Disease↗

Integrated semiconductor nanocrystal and epitaxical nanostructure systems: structural and optical behavior.

Integration of semiconductor epitaxical nanostructures and nanocrystals into two classes of quantum structures, uncovered adsorbed nanocrystals or buried via epitaxical overgrowth, is successfully demonstrated through structural and optical studies. The combination InGaAs/GaAs epitaxical structures and InAs nanocrystals is employed as a vehicle with the functional aim of exploiting the well developed optoelectronic communication technology based on the former with the biochemical and biomedical applications for which the latter are well suited.

Arsenicals↗

Terpenoids from the roots and rhizomes of Nardostachys chinensis.

A new diterpene, 10-isopropyl-2,2,6-trimethyl-2,3,4,5-tetrahydronaphtha[1,8-bc]oxocine-5,11-diol (1), and a new monoterpene, 6-hydroxy-7-(hydroxymethyl)-4-methylenehexahydrocyclopenta[c]pyran-1(3H)-one, together with four known sesquiterpenes, delta1(10)-aristolene-9beta-ol, debilon, nardosinone, and kanshone A, were isolated from the roots of Nardostachys chinensis. The structures of the new compounds were established on the basis of their spectroscopic data, and the structure of 1 was confirmed by X-ray crystallographic analysis.

Diterpenes↗

The diverse functions of histone lysine methylation.

Covalent modifications of histone tails have fundamental roles in chromatin structure and function. One such modification, lysine methylation, has important functions in many biological processes that include heterochromatin formation, X-chromosome inactivation and transcriptional regulation. Here, we summarize recent advances in our understanding of how lysine methylation functions in these diverse biological processes, and raise questions that need to be addressed in the future.

Animals↗

Mesenchymal stem cells derived from human placenta suppress allogeneic umbilical cord blood lymphocyte proliferation.

Human placenta-derived mononuclear cells (MNC) were isolated by a Percoll density gradient and cultured in mesenchymal stem cell (MSC) maintenance medium. The homogenous layer of adherent cells exhibited a typical fibroblast-like morphology, a large expansive potential, and cell cycle characteristics including a subset of quiescent cells. In vitro differentiation assays showed the tripotential differentiation capacity of these cells toward adipogenic, osteogenic and chondrogenic lineages. Flow cytometry analyses and immunocytochemistry stain showed that placental MSC was a homogeneous cell population devoid of hematopoietic cells, which uniformly expressed CD29, CD44, CD73, CD105, CD166, laminin, fibronectin and vimentin while being negative for expression of CD31, CD34, CD45 and alpha-smooth muscle actin. Most importantly, immuno-phenotypic analyses demonstrated that these cells expressed class I major histocompatibility complex (MHC-I), but they did not express MHC-II molecules. Additionally these cells could suppress umbilical cord blood (UCB) lymphocytes proliferation induced by cellular or nonspecific mitogenic stimuli. This strongly implies that they may have potential application in allograft transplantation. Since placenta and UCB are homogeneous, the MSC derived from human placenta can be transplanted combined with hematopoietic stem cells (HSC) from UCB to reduce the potential graft-versus-host disease (GVHD) in recipients.

Adipocytes↗

Decrease of transthyretin synthesis at the blood-cerebrospinal fluid barrier of old sheep.

Transthyretin (TTR), synthesized by the choroid plexus (CP) and secreted into cerebrospinal fluid (CSF), is involved in thyroxine (T4) transport and chelation of beta-amyloid peptide, attenuating neurotoxicity. To characterize age-related changes in TTR synthesis, CSF and CPs were collected from young adult (1-2 years) and old (>8 years) sheep anesthetized with thiopentone sodium. TTR in old sheep CSF was low compared to young (n = 4 each); however, CP messenger RNA (mRNA) for TTR did not change. CPs were perfused with Ringer containing 14C-leucine to assess de novo protein synthesis, or with 125I-T4 to assess T4 transport. Protein synthesis, including TTR, was reduced in old sheep CP and in newly secreted CSF. 125I-T4 Vmax and Kd (but not Km) were reduced in old sheep CP. These age-related changes suggest reduced capacity of CP to maintain CSF T4 homeostasis and could also reduce chelation of beta-amyloid and be an added risk for Alzheimer's disease.

Aging↗

Rapacuronium preferentially antagonizes the function of M2 versus M3 muscarinic receptors in guinea pig airway smooth muscle.

BACKGROUND: Rapacuronium, a nondepolarizing muscle relaxant that was proposed as a replacement for succinylcholine for rapid intubation, was withdrawn from clinical use as a result of fatal bronchospasm, but the mechanism of this effect is not known. Preferential antagonism of presynaptic M2 muscarinic receptors versus postsynpatic M3 muscarinic receptors can facilitate bronchoconstriction. The authors questioned whether rapacuronium preferentially antagonized M2 versus M3 muscarinic receptors in intact airway. METHODS: Guinea pig tracheal rings were suspended in organ baths and muscle relaxants' antagonism of prejunctional M2 muscarinic autoreceptors was evaluated by augmentation of muscle contraction elicited by electrical field stimulation. Muscle relaxants' antagonism of postjunctional M3 muscarinic receptors was assessed by attenuation of muscle contraction elicited by acetylcholine. RESULTS: Rapacuronium displayed a 50-fold higher affinity for antagonism of the M2 versus M3 muscarinic receptor. Moreover, its affinity for the M2 but not the M3 receptor was within concentrations achieved clinically. In addition, rapacuronium caused an increase in baseline tone of airway smooth muscle that was antagonized by atropine but not by previous depletion of nonadrenergic noncholinergic neurotransmitters or by inhibitors of histamine receptors, tachykinin receptors, leukotriene receptors, or calcium channels. CONCLUSION: These findings are consistent with the hypothesis that rapacuronium may precipitate bronchoconstriction by selective antagonism of the M2 muscarinic receptor on parasympathetic nerves, enhancing acetylcholine release to act upon unopposed M3 muscarinic receptors on airway muscle. An additional mechanism of rapacuronium-induced bronchoconstriction is suggested by increases in baseline muscle tension.

Animals↗

Rapacuronium augments acetylcholine-induced bronchoconstriction via positive allosteric interactions at the M3 muscarinic receptor.

BACKGROUND: Neuromuscular blocking agents' detrimental airway effects may occur as a result of interactions with muscarinic receptors, allergic reactions, or histamine release. Rapacuronium, a nondepolarizing muscle relaxant, was withdrawn from clinical use because of its association with fatal bronchospasm. Despite its withdrawal from clinical use, it is imperative that the mechanism by which bronchospasm occurred is understood so that new muscle relaxants introduced to clinical practice do not share these same detrimental airway effects. METHODS: Airway smooth muscle force was measured in guinea pig tracheal rings in organ baths exposed to muscle relaxants with or without subthreshold concentrations of acetylcholine. Antagonism of muscarinic, histamine, neurokinin, leukotriene receptors, or blockade of L-type calcium channels or depletion of nonadrenergic, noncholinergic neurotransmitters was performed. Muscle relaxants' potentiation of acetylcholine-stimulated inositol phosphate synthesis and allosteric interactions on the kinetics of atropine-induced [3H]N-methylscopolamine dissociation were measured in cells expressing recombinant human M3 muscarinic receptors. RESULTS: Rapacuronium, within clinically achieved concentrations, contracted tracheal rings in the presence but not in the absence of subthreshold concentrations of acetylcholine. This effect was prevented or reversed only by atropine. The allosteric action of rapacuronium was demonstrated by the slowing of atropine-induced dissociation of [3H]N-methylscopolamine, and positive cooperativity was demonstrated by potentiation of acetylcholine-induced inositol phosphate synthesis. CONCLUSION: Many muscle relaxants have allosteric properties at muscarinic receptors; however, positive cooperativity at the M3 muscarinic receptor within clinically relevant concentrations is unique to rapacuronium. These findings establish novel parameters that should be considered in the evaluation of airway safety of any newly synthesized neuromuscular blocking agents considered for clinical practice.

Acetylcholine↗

Maxillary reconstruction with the free fibula flap.

BACKGROUND: The objective of this study was to evaluate the outcomes of using the free fibula flap in the reconstruction of maxillary defects. METHODS: Thirty-four consecutive cases of maxillary reconstruction with the free fibula flap were reviewed. All clinical data were analyzed, including primary diseases, types of maxillary defect, free fibula flap design, perioperative complications, and follow-up results. The main postoperative functional indices, including oral diet, speech, type of dental restoration, and aesthetic results, were evaluated. RESULTS: Of the 34 patients who underwent maxillary reconstruction with the free fibula flap, the primary diseases were malignant tumor in 20 patients, benign tumor in 11 patients, and trauma in three patients. Free fibula flap transfer was successful in all cases. Postoperative complications occurred in five patients. Recipient-site wound infection occurred in two patients and donor-site wound dehiscence occurred in three patients. One patient with donor-site wound dehiscence had postoperative lameness. The oral and nasal cavities were separated well by the flap in all patients. The patients were able to take food orally and had no problems with speech intelligibility. Osseointegrated implants were placed in four patients, and complete conventional prostheses were applied in 19 patients. Excellent cosmetic results were obtained in 22 patients. CONCLUSIONS: Alveolar arch defects can be reconstructed successfully using free fibula flaps. This procedure also allows for dental implant rehabilitation, which can improve the patient's appearance and oral function and enhance the overall quality of life. The fibula free flap transfer has a high success rate and low perioperative complication rate, making it an ideal choice for maxillary defect reconstruction.

Adult↗

A self-learning call admission control scheme for CDMA cellular networks.

In the present paper, a call admission control scheme that can learn from the network environment and user behavior is developed for code division multiple access (CDMA) cellular networks that handle both voice and data services. The idea is built upon a novel learning control architecture with only a single module instead of two or three modules in adaptive critic designs (ACDs). The use of adaptive critic approach for call admission control in wireless cellular networks is new. The call admission controller can perform learning in real-time as well as in offline environments and the controller improves its performance as it gains more experience. Another important contribution in the present work is the choice of utility function for the present self-learning control approach which makes the present learning process much more efficient than existing learning control methods. The performance of our algorithm will be shown through computer simulation and compared with existing algorithms.

Algorithms↗

Osteopontin expression correlates with melanoma invasion.

Melanoma is one of the most aggressive cancers affecting humans. Although early melanomas are curable with surgical excision, metastatic melanomas are associated with high mortality. The mechanism of melanoma development, progression, and metastasis is largely unknown. In order to uncover genes unique to melanoma cells, we used high-density DNA microarrays to examine the gene expression profiles of metastatic melanoma nodules using benign nevi as controls. Over 190 genes were significantly overexpressed in metastatic melanomas compared with normal nevi by at least 2-fold. One of the most abundantly expressed genes in metastatic melanoma nodules is osteopontin (OPN). Immunohistochemistry staining on tissue microarrays and individual skin biopsies representing different stages of melanoma progression revealed that OPN expression is first acquired at the step of melanoma tissue invasion. In addition, blocking of OPN expression by RNA interference reduced melanoma cell numbers in vitro. Our observations suggest that OPN may be acquired early in melanoma development and progression, and may enhance tumor cell growth in invasive melanoma.

Adult↗

Nanodissection of single- and double-stranded DNA by atomic force microscopy.

Nanodissection of single-stranded DNA (ssDNA) and double-stranded DNA (dsDNA) has been investigated by atomic force microscopy (AFM). It is found that both ss- and dsDNA can be repeatedly dissected by an AFM tip. However, a comparison study indicates that ssDNA is a little bit more easily broken by the AFM tip than dsDNA. This is supported by the fact that the time requested to break ssDNA is shorter than that of dsDNA in the same dissection procedure under the same load. Our experiment also shows that dissection of the DNA strand is very sensitive to the load applied, and a small change of the load lead to different results.

DNA↗

Activation of the mitochondrial apoptotic pathway in a rat model of central retinal artery occlusion.

PURPOSE: Apoptosis is known to play a role in cell death in transient retinal ischemia. Little is known about the specific molecular pathways involved. The purpose of the current study was to evaluate a rat model of central retinal artery occlusion (CRAO) that simulates the clinical features of CRAO in humans and to elucidate whether the mitochondrial apoptotic pathway is involved. METHODS: CRAO was induced in the central retinal artery by intravenous injection of rose bengal and green laser irradiation of the artery. CRAO was documented at 1, 3, 6, and 24 hours after laser irradiation. Changes in Bax (proapoptotic Bcl-2-associated X protein), cytochrome c, and caspase-9 cleavage in the cytosolic and mitochondrial fractions of neural retinal tissues were measured by Western blot analysis. Apoptosis within the retina was examined by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL). RESULTS: Complete CRAO was induced; however, occlusion became incomplete with spontaneous reperfusion of branch arteries, starting at 3 hours after laser irradiation. Only one or two branch arteries remained occluded at the 24-hour time point. Time-dependent, apoptotic changes were observed in inner and outer retinal cell layers. Western blot analysis revealed mitochondrial translocation of Bax from the cytoplasm, starting at 3 hours and peaking at 6 hours after laser irradiation. This translocation was accompanied by cytosolic accumulation of cytochrome c and cleavage of caspase-9. CONCLUSIONS: This model is highly relevant to clinical manifestations of CRAO and is an ideal animal model for research. These findings indicate the activation of the mitochondrial pathway in ischemic retina induced by CRAO. The model provides a better understanding of ischemia-induced retinal apoptosis. Antiapoptosis therapy directly targeting the mitochondrial pathway in CRAO or other retinal ischemic diseases may be beneficial.

Amacrine Cells↗

Thiopental produces immobility primarily by supraspinal actions in rats.

The spinal cord mediates most of the immobilizing action of inhaled anesthetics. In the present study we investigated whether spinal or supraspinal sites mediate the immobilizing action of thiopental in rats. Thiopental was administered IV, intrathecally (IT), intracerebroventricularly (ICV), or simultaneously IT and ICV. Only the IV infusion produced anesthesia, defined as immobility in response to application of a tail clamp (i.e., the equivalent of minimum alveolar concentration, MAC). Consequently, the MAC-sparing effect (for isoflurane) of thiopental was used to assess the immobilizing contribution of IT and ICV infusions of thiopental. Thiopental concentrations were determined in whole brain, spinal cord, and a slice of cerebral cortex distant from the infusion sites. These concentrations were correlated with the MAC-sparing effect of the thiopental infusions in a multiple regression model. To assess the rate at which thiopental penetrates the cord, rat spinal cords were equilibrated in a bath of thiopental ex vivo and the concentration of thiopental in the cord was measured as a function of equilibration time. This was repeated in vivo with IT infusions of thiopental spanning the time of the behavioral studies. We found that IT or ICV infusion of thiopental 25 microg/min decreased isoflurane MAC <25%. The associated thiopental concentrations in the spinal cord after IT infusion, and in the whole brain after ICV infusion of 25 microg/min thiopental, exceeded by 500% and 680%, respectively, the concentrations found in the spinal cord and in the whole brain after IV infusion of thiopental in a dose that produced anesthesia in the absence of isoflurane. The percentage decrease in the MAC of isoflurane correlated primarily with the concentration of thiopental found in cerebral tissue not in contact with the cerebral ventricles. The spinal cord infusion produced an approximately 20% decrease in MAC. Ex vivo IT thiopental readily diffused into the spinal cord, with a time constant of approximately 1 h. We conclude that, unlike inhaled anesthetics, the immobilizing action of thiopental is largely supraspinal. Centers in the brain other than those near the third and fourth ventricles produce the greatest effect.

Anesthetics, Inhalation↗

Administration of epinephrine does not increase learning of fear to tone in rats anesthetized with isoflurane or desflurane.

Previous reports suggest that the administration of epinephrine increases learning during deep barbiturate-chloral hydrate anesthesia in rats but not during anesthesia with 0.4% isoflurane in rabbits. We revisited this issue, using fear conditioning to a tone in rats as our experimental model for learning and memory and isoflurane and desflurane as our anesthetics. Expressed as a fraction of the minimum alveolar anesthetic concentration (MAC) preventing movement in 50% of rats, the amnestic 50% effective dose (ED(50)) for fear to tone in control rats inhaling isoflurane and injected with saline intraperitoneally (i.p.) was 0.32 +/- 0.03 MAC (mean +/- se) compared with 0.37 +/- 0.06 MAC in rats injected with 0.01 mg/kg of epinephrine i.p. and 0.38 +/- 0.03 MAC in rats injected with 0.1 mg/kg of epinephrine i.p. For desflurane, the amnestic ED(50) were 0.32 +/- 0.05 MAC in control rats receiving a saline injection i.p. versus 0.36 +/- 0.04 MAC in rats injected with 0.1 mg/kg of epinephrine i.p. We conclude that exogenous epinephrine does not decrease amnesia produced by inhaled isoflurane or desflurane, as assessed by fear conditioning to a tone in rats.

Anesthesia, Inhalation↗

Integration of the hepatitis B virus X fragment in hepatocellular carcinoma and its effects on the expression of multiple molecules: a key to the cell cycle and apoptosis.

We investigated hepatitis B virus (HBV) DNA integration and expression of several proteins involved in the cell cycle and apoptosis, including cyclin A, retinoblastoma protein (pRB), Fas-associated death domain protein (FADD), tumor necrosis factor receptor-associated death domain protein (TRADD), and nuclear factor kappaB (NF-kappaB) in HBV-associated hepatocellular carcinoma (HCC) and liver cirrhosis (LC). Archival HCC and LC specimens were obtained from 35 patients each with HBV infection; 5 normal liver specimens used as controls were also obtained. Polymerase chain reaction and Southern blot hybridization were used to detect the integration of HBV DNA in the HCC and LC specimens. The protein levels were determined by Western blot assay. The difference in HBV DNA integration between HCC and LC and correlation between HBV-encoded X protein (Hbx) integration and protein expression were analyzed statistically. HBV DNA was detected in 33 (94%) of the HCC and LC specimens. HBx integration differed in the HCC [24 (69%)] and LC [14 (40%)] specimens (p=0.015). Sixty percent of the HCC specimens and 6% of the LC specimens had increased cyclin A expression. Also, 34, 37, 69, and 77% of the HCC specimens were positive for pRB, FADD, TRADD, and NF-kappaB expression, whereas 80, 60, 100, and 100% of the LC specimens were positive for pRB, FADD, TRADD, and NF-kappaB expression. Significant correlations between HBx integration and the level of expression of cyclin A (r=0.452; p=0.006), pRB (r=-0.419; p=0.012), and TRADD (r=0.470; p=0.004) were discovered. Therefore, integration of HBV DNA occurred frequently in HCC and LC cases with chronic HBV infection, whereas HBx integration occurred more often in HCC than in LC cases (p=0.015). HBx integration and altered expression of genes is a key to apoptosis and may play important roles in HBV-induced hepatocarcinogenesis.

Apoptosis↗