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Biomedical subjects

X H Liu

Publications and source records attributed to X H Liu.

At least 19 recordsLinked to original sources
PubMed2003

Morphine alleviates early stages of apoptosis in cultured CEM x174 cells infected with simian immunodeficiency virus.

The reduction in apoptosis caused by short-term exposure of CEM x174 cells infected with SIVmac239 to morphine was investigated. Eeffects of morphine on the viability of normal and infected CEM x174 cells were determined by MTS assay. Apoptosis induced by SIVmac239 and the effects of morphine were analyzed by flow cytometry. cAMP levels, PKA activity, and the resulting histone H3 phosphorylation levels were measured. The results show a pronounced decrease in numbers of infected SIVmac239 cells compared to controls. Morphine elevated cell viability in the infected groups. Annexin V binding assays showed that 1 microM l(-1) morphine increased the percentage of viable cells and decreased apoptotic cells. Morphine also downregulated cAMP and PKA activity in both groups, but more markedly in the infected group. Histone H3 phosphorylation was elevated after virus infection and decreased in the presence of morphine. The results indicate that the cAMP-PKA signal transduction cascade is involved in morphine regulation of early SIVmac239-induced apoptosis.

Apoptosis↗
PubMed2003

Myocardial extracellular signal regulatory kinases are activated by laser treatment.

AIM: Transmyocardial laser revascularization (TMR) and percutaneous transluminal myocardial laser revascularization (PTMR) have anti-anginal effects on certain groups of patients with ischemic heart disease, possibly by inducing myocardial neoangiogenesis through the mechanical injury. Here we examine the effects of TMR and PTMR on extracellular signal regulatory kinases (ERKs), which have been implicated in the control of neoangiogenesis in vitro. METHODS: Eight pigs were anesthetized with ketamine and fentanyl. In five pigs TMR was performed in the left ventricular anterior wall and PTMR in the posterior wall. Biopsies were taken either after 2 hours, 3, 7, 14, and 30 days. Three pigs served as controls and provided samples for baseline values and time-matched controls at 2 hours and 3 days. ERKs activity was determined by increased phosphorylation of myelin basic protein. Total ERKs protein abundance was determined by Western blot with an antibody against ERK1 and ERK2. RESULTS: It was found that ERKs activity was higher in all samples from the laser treated myocardium than in the control sample at baseline (TMR: >or=1878 pmol Pi x min(-1) mg pr(-1) vs 104 pmol Pi x min(-1) mg pr(-1), respectively, p<0.05. PTMR: >or=346 pmol Pi x min(-1) mg pr(-1) vs 136 pmol Pi min(-1) mg pr(-1), respectively, p<0.05). The time-matched samples showed increased activities of ERKs after laser treatment. The protein level of ERKs in myocardium treated with TMR and PTMR parallelled the data on ERKs activity. CONCLUSIONS: Our data suggest that the ERKs system is activated in the porcine heart by the mechanical injury of TMR and PTMR.

Angioplasty, Balloon, Coronary↗
PubMed2001

Inhibition of axotomy-induced neuronal apoptosis by extracellular delivery of a Bcl-XL fusion protein.

Bcl-2 and Bcl-XL prevent neuronal apoptosis during development, neurodegenerative disease, and trauma. To test a new anti-apoptosis strategy for neuroprotection, we engineered nontoxic components of anthrax toxin into a Bcl-XL delivery system. Delivery of Bcl-XL by this system prevented apoptosis of cultured rat cerebellar granule cells and macrophages, and the prevention depended on both the Bcl-XL and the anthrax toxin receptor binding/translocation moieties. Furthermore, neuronal death in vivo in a retinal ganglion cell model of axotomy-induced apoptosis was inhibited by administration of this fusion protein. Thus, Bcl-XL protein can be delivered into cells from the medium or interstitial space, offering a new way to block apoptosis upstream of many caspases and the mitochondria dysfunction phase of apoptosis.

Animals↗
PubMed2001

Differential scanning calorimetry studies of intraembryonic freezing and cryoprotectant penetration in zebrafish (Danio rerio) embryos.

Nucleation temperatures of intraembryonic water and cryoprotectant penetration in zebrafish embryos were studied using differential scanning calorimetry. The effects of embryo developmental stage, dechorionation, partial removal of yolk, cooling rate, and cryoprotectant treatment on the temperatures of intraembryonic freezing were investigated. Embryo stages were found to have a significant effect on the nucleation temperatures of intact embryos. Freeze onset temperatures of -11.9 +/- 1.5, -15.6 +/- 0.3, and -20.5 +/- 0.1 degrees C were obtained for intact embryos at 6-somite, prim-6, and high-pec stages, respectively. After dechorionation, the freeze onset temperatures of intraembryonic water shifted to significantly lower temperatures, being -23.5 +/- 0.8, -18.7 +/- 0.7, -24.9 +/- 0.8 degrees C for 6-somite, prim-6, and high-pec stages, respectively. Yolk-reduced high-pec stage embryos showed significantly lower nucleation temperatures with an average onset at -27.9 +/- 0.4 degrees C. The effect of cryoprotectant treatment on the nucleation temperatures of intraembryonic water varies among different embryo stages and different cryoprotectants. Thirty-minute treatment with 2 M methanol significantly decreased the nucleation temperatures of dechorionated 6-somite embryos whilst no temperature decrease was observed for prim-6 or yolk-reduced high-pec embryos. Thirty-minute exposure to 1 M propylene glycol did not significantly affect the nucleation temperatures of dechorionated 6-somite, prim-6, or yolk-reduced high-pec embryos. In order to increase the permeability of embryos to cryoprotectants, the yolk sacs of dechorionated embryos at 6-somite or prim-6 embryos were punctured with a sharp micro-needle before exposure to cryoprotectants. The punctured prim-6 embryos showed significantly lower temperatures of intraembryonic freezing after 30 min of exposure to 2 M methanol following the multi-punctures. The nucleation temperatures of punctured 6-somite or prim-6 embryos were also decreased significantly after exposure to 1 M propylene glycol for 30 min. These results suggested that in intact embryos, intraembryonic freezing appeared to be seeded by the external ice in the perivitelline fluid and that in dechorionated embryos (in the absence of external water) intraembryonic freezing was more likely a consequence of heterogeneous nucleation. Methanol was demonstrated to show a limited degree of penetration into prim-6 stage embryos, but it did not penetrate later-stage embryos such as prim-6 and yolk-reduced high-pec. No propylene glycol permeation was observed for embryos at all stages. However, multi-punctures of yolk resulted in the permeation of both cryoprotectants into prim-6 embryos and propylene glycol permeation into 6-somite embryos. These findings may have important implications in overcoming the problem associated with the low membrane permeability of zebrafish embryos to cryoprotectants.

Adaptation, Physiological↗
PubMed2001

Effect of cooling rate and partial removal of yolk on the chilling injury in zebrafish (Danio rerio) embryos.

High chilling sensitivity is one of the main obstacles to successful cryopreservation of zebrafish embryos. So far the nature of the chilling injury in fish embryos has not been clear. The aim of this study is to investigate the effect of cooling rate and partial removal of yolk on chilling injury in zebrafish embryos. Zebrafish embryos at 64-cell, 50%-epiboly, 6-somite and prim-6 stages were cooled to either 0 degrees C or -5 degrees C at three different cooling rates: slow (0.3 degrees C/min or 1 degree C/min), moderate (30 degrees C/min), and rapid (approximately 300 degrees C/min). After chilling, embryos were warmed in a 26 degrees C water bath, followed by 3-day culturing in EM at 26 +/- 1 degrees C for survival assessment. When embryos were cooled to 0 degrees C for up to 30 min, 64-cell embryos had higher survival after rapid cooling than when they were cooled at a slower rate. When 64-cell embryos were held at -5 degrees C for 1 min, their survival decreased greatly after both slow and rapid cooling. The effect of cooling rate on the survival of 50%-epiboly and 6-somite embryos was not significant after 1 h exposure at 0 degrees C and 1 min exposure at -5 degrees C. However, rapid cooling resulted in significantly lower embryo survival than a cooling rate of 30 degrees C/min or 1 degree C/min after 1 h exposure to 0 degrees C for prim-6 stage or 1 h exposure to -5 degrees C for all stages. Chilling injury in 64-cell embryos appears to be a consequence of exposure time at low temperatures rather than a consequence of rapid cooling. Results also indicate that chilling injury in later stage embryos (50%-epiboly, 6-somite and prim-6) is a consequence of the combination of rapid cooling and exposure time at low temperatures. Dechorionated prim-6 embryos were punctured and about half of yolk was removed. After 24 h culture at 26 +/- 1 degrees C after removal of yolk, the yolk-reduced embryos showed higher embryo survival than did control embryos after rapid cooling to -5 degrees C for 10 to 60 min. Results suggest that cold shock injury after rapid cooling can be mitigated after partial removal of yolk at the prim-6 stage. These findings help us to understand the nature of chilling sensitivity of fish embryos and to develop protocols for their cryopreservation.

Animals↗
PubMed2001

Transmission disequilibrium analysis of HLA class II DRB1, DQA1, DQB1 and DPB1 polymorphisms in schizophrenia using family trios from a Han Chinese population.

Our goal was to evaluate the role of HLA in the risk of developing schizophrenia, in a Han Chinese population. In several Japanese studies, there is evidence of association with DR1 and schizophrenia. A variety of other associations have been reported in other populations, including negative associations with DQbeta(*)0602 and positive associations with DR1(*)0101. Using sequence specific oligonucleotides, we genotyped four HLA markers (DRB1, DQA1, DQB1 and DPB1) in 165 family trios, consisting of Han Chinese schizophrenic subjects and their parents. Individual markers were analysed for transmission distortion in the trios using the transmission disequilibrium test. Multiple haplotype transmission was performed using the program TRANSMIT v2.5. The four markers were in strong linkage disequilibrium with each other (P value from 0.002 to 0). There was no evidence of overall transmission disequilibrium for each of the four loci. For DRB1, we did not find transmission distortion for the DRB1(*)04 and DRB1(*)08 alleles, as reported previously, but the DRB1(*)03 allele was preferentially not transmitted (P=0.009), and the DRB1(*)13 allele was preferentially transmitted from parents to schizophrenic offspring (P=0.041). Using haplotypes of pairs of markers, a significant global P value of 0.019 was achieved when using DRB1 and DQA1, mainly as a result of the excess transmission of DRB1(*)13-DQA1(*)01 (P=0.012) and a deficit in transmission of DRB1(*)03-DQA1(*)05 (P=0.002). In summary, we did not confirm any of the specific HLA allelic associations reported previously in Japanese or other populations. However, our results are compatible with the view that this region of HLA might contain a susceptibility gene which is in linkage disequilibrium with DRB1 and DQA1 genes.

Adolescent↗
PubMed2001

Pathogenesis of Shiga toxin-induced hemolytic uremic syndrome.

The term hemolytic uremic syndrome (HUS) was first introduced to describe a heterogeneous group of diseases characterized by microangiopathic hemolytic anemia, thrombocytopenia, and acute renal failure. Substantial progress has been made in our understanding of the etiology and pathogenesis of HUS. This article reviews some of the classic and new concepts related to the pathogenesis of Shiga toxin (Stx)-HUS and discusses their clinical relevance for the diagnosis and treatment of this syndrome. Infection with Stx-producing bacteria can induce HUS after a prodromal illness with or without diarrhea. Stx-induced renal endothelial injury is the primary pathogenic event. However, Stx also damages mesangial cells, as well as glomerular and renal tubular epithelial cells. Young children are at greatest risk for Stx-HUS because they express high levels of Stx receptors in renal glomeruli. Older children and adults express lower levels of glomerular Stx receptors and may develop Stx-HUS whenever the combined effects of lipopolysaccharide and cytokines upregulate the expression of Stx receptors and sensitize glomerular endothelial cells to Stx-induced injury, activate the coagulation-fibrinolytic system, and induce endothelial injury. Chemokine receptors and cytokines released by inflammatory cells (i.e., monocyte chemoattractant protein-1, interleukin-6, interleukin-8,) or injured endothelial cells (i.e., basic fibrobast growth factor) may play roles in this process. Measurement of the activity of a von Willebrand factor protease in plasma may help distinguish patients with thrombotic thrombocytopenic purpura from those with Stx-HUS.

Aging↗
PubMed2001

Up-regulation of a fibroblast growth factor binding protein in children with renal diseases.

BACKGROUND: Basic fibroblast growth factor (bFGF) is an angiogenic growth factor that is involved in renal growth and the pathogenesis of renal diseases. We have detected high levels of bFGF accumulated in the kidney of HIV-transgenic mice and in children with HIV-associated renal diseases and the hemolytic uremic syndrome (HUS). However, the mechanism modulating the activity of bFGF under these circumstances is poorly understood. We carried out experiments to determine whether a secreted binding protein (FGF-BP) that modulates the activity of bFGF during the process of tumor growth was expressed in pediatric kidneys and to define whether the expression of FGF-BP was altered in pediatric renal diseases associated with high levels of bFGF. METHODS: Immunohistochemistry and in situ hybridization studies were done in 41 renal sections from children with HIV nephropathies, HUS, other pediatric renal diseases, controls, and fetal kidneys. Western blots and reverse transcriptase-polymerase chain reaction studies were done in selected urine samples and cultured renal cells. Recombinant FGF-BP was produced to study the mitogenic activity of FGF-BP in cultured human renal proximal tubular epithelial cells (RPTEcs). RESULTS: The expression of FGF-BP was up-regulated predominately in renal tubular epithelial cells in children with renal tubular injury, HIV-associated nephropathy (HIVAN), and HUS, and FGF-BP was secreted in the urine of these patients. FGF-BP was also abundantly expressed in developing fetal renal tubules. Recombinant FGF-BP enhanced the mitogenic effects of bFGF in cultured human RPTEcs. CONCLUSIONS: The localization of FGF-BP in renal tubular epithelial cells could provide a mechanism by which the activity of bFGF is modulated in developing and regenerating renal tubules of children.

AIDS-Associated Nephropathy↗
PubMed2001

Chronic potassium depletion induces renal injury, salt sensitivity, and hypertension in young rats.

BACKGROUND: Chronic hypokalemia has been associated with renal hypertrophy, interstitial disease, and hypertension in both adult animals and humans. However, the effects of potassium (K(+)) depletion on the rapidly growing infant have not been well studied. The purpose of this study was to determine the effects of severe chronic dietary K(+) depletion on blood pressure (BP) and renal structural changes in young rats. METHODS: Sprague-Dawley rats (50 +/- 5 g) were fed either a control or a potassium-deficient diet (<0.05% K(+)) for 14 to 21 days. At the end of this period, the blood pressure (BP) was measured in all rats, and six rats in each group were sacrificed to determine changes in renal histology and renin-angiotensin system (RAS) activity. The remaining rats in each group were then switched to a high-salt (6% NaCl)--normal-K(+) (0.5%) diet or were continued on their respective control or K(+)-deficient diet for an additional six days. Blood pressure measurements were done every three days until the end of the study. RESULTS: K(+)-depleted animals had significant growth retardation and increased RAS activity, manifested by high plasma renin activity, recruitment of renin-producing cells along the afferent arterioles, and down-regulation of angiotensin II receptors in renal glomeruli and ascending vasa rectae. K(+)-depleted kidneys also showed tubulointerstitial injury with tubular cell proliferation, osteopontin expression, macrophage infiltration, and early fibrosis. At week 2, K(+)-depleted rats had higher systolic BP than control rats. Switching to a high-salt (6% NaCl)--normal-K(+) diet resulted in further elevation of systolic BP in K(+)-depleted rats, which persisted even after the serum K(+) was normalized. CONCLUSION: Dietary potassium deficiency per se increases the BP in young rats and induces salt sensitivity that may involve at least two different pathogenic pathways: increased RAS activity and induction of tubulointerstitial injury.

Animals↗
PubMed2001

Ultrasonic destruction of chloroform and carbon tetrachloride in aqueous solution.

The sonochemical destruction of binary mixtures of chloroform and carbon tetrachloride in aqueous solution at 30 kHz has been studied. The influences of initial concentration, bicarbonate/chloride, and acoustical intensity on the destruction rates have been observed. It was found that the destruction of the two compounds appeared to follow pseudo-first-order reaction kinetics with the current experimental concentration range. The rate constant of chloroform for initial concentration as high as 100.4 mg/L decreased compared to initial concentration 36.13 micrograms/L, when the rate constants of carbon tetrachloride hardly changed. However, their destruction rates increased with increasing acoustical intensity and were independent of addition of bicarbonate or chloride. The resulting yield of ionic product (Cl-) for chloroform was determined.

Carbon Tetrachloride↗
PubMed2001

Attenuation of ischemia-induced mouse brain injury by SAG, a redox-inducible antioxidant protein.

Cerebral ischemia resulting from a disruption of blood flow to the brain initiates a cascade of events that causes neuron death and leads to neurologic dysfunction. Reactive oxygen species are thought, at least in part, to mediate this disease process. The authors recently cloned and characterized an antioxidant protein, SAG (sensitive to apoptosis gene), that is redox inducible and protects cells from apoptosis induced by redox agents in a number of in vitro cell model systems. This study reports a neuroprotective role of SAG in ischemia/reperfusion-induced brain injury in an in vivo mouse model. SAG was expressed at a low level in brain tissue and was inducible after middle cerebral artery occlusion with peak expression at 6 to 12 hours. At the cellular level, SAG was mainly expressed in the cytoplasm of neurons and astrocytes, revealed by double immunofluorescence. An injection of recombinant adenoviral vector carrying human SAG into mouse brain produced an overexpression of SAG protein in the injected areas. Transduction of AdCMVSAG (wild-type), but not AdCMVmSAG (mutant), nor the AdCMVlacZ control, protected brain cells from ischemic brain injury, as evidenced by significant reduction of the infarct areas where SAG was highly expressed. The result suggests a rather specific protective role of SAG in the current in vivo model. Mechanistically, SAG overexpression decreased reactive oxygen species production and reduced the number of apoptotic cells in the ischemic areas. Thus, antioxidant SAG appears to protect against reactive oxygen species-induced brain damage in mice. Identification of SAG as a neuroprotective molecule could lead to potential stroke therapies.

Adenoviridae↗
PubMed2001

Platelet-activating factor antagonist BN 50730 attenuates hypoxic-ischemic brain injury in neonatal rats.

Platelet-activating factor (PAF) is a lipid derived from breakdown of cell membranes that is postulated to be a mediator of cerebral ischemic injury. PAF regulates CNS gene transcription via intracellular binding sites. To test the hypothesis that PAF mediates CNS injury in part by modulating gene transcription, we evaluated the neuroprotective efficacy of the drug BN 50730, an antagonist of the intracellular (microsomal) CNS PAF binding site, in the neonatal rat model of unilateral cerebral hypoxia-ischemia. Seven-day-old rats underwent right carotid ligation followed by a 2.5-h exposure to 8% O(2), and were then treated with BN 50730 (2.5 or 25 mg/kg per dose) or vehicle, at 0 and 2 h after the end of hypoxia. Ipsilateral cortical, striatal, and hippocampal damage was quantitated either 5 d later, or at 5 wk after the insult. Treatment with BN 50730 resulted in approximately 60- 80% reduction in ipsilateral tissue loss at both times. Learning and memory were evaluated 5 wk after insult using the Morris Watermaze place navigation task. Severity of cortical and striatal damage correlated significantly with learning and memory deficits. These results support the hypothesis that PAF is a pathogenetic mediator of hypoxic-ischemic damage in the immature brain. Accumulating evidence suggests that PAF mediates its deleterious effects in the immature CNS via multiple mechanisms.

Animals↗
PubMed2001

Orexin a preferentially excites glucose-sensitive neurons in the lateral hypothalamus of the rat in vitro.

Falls in blood glucose induce hunger and initiate feeding. The lateral hypothalamic area (LHA) contains glucose-sensitive neurons (GSNs) and orexin neurons, both of which are stimulated by falling blood glucose and are implicated in hypoglycemia-induced feeding. We combined intracellular electrophysiological recording with fluorescein labeling of GSNs to determine their neuroanatomic and functional relationships with orexin neurons. Orexin A (1 micromol/l) caused a 500% increase (P < 0.01) in spontaneous firing rate and rapid and lasting depolarization that was tetrodotoxin-resistant and thus a direct postsynaptic effect. Orexin A altered the intrinsic neuronal properties of GSNs, consistent with increased excitability. Confocal microscopy showed that GSNs were intimately related to orexin neurons: orexin-immunoreactive axons were frequently entwined around GSN dendrites, establishing close and putatively synaptic contacts. Orexin-cell axons also passed in close proximity to glucose-responsive neurons, which are inhibited by low glucose, but orexin A caused smaller depolarization than on GSNs and only a 200% increase in spontaneous firing rate (P < 0.05 vs. GSN). We conclude that GSNs are specific target neurons for orexin A and suggest that they may mediate, at least in part, the acute appetite-stimulating effect of orexin A. Orexin neurons may regulate GSNs so as to control the onset and termination of hypoglycemia-induced feeding.

Animals↗
PubMed2001

Predicting octanol/water partition coefficient using solvation free energy and solvent-accessible surface area.

The regression model for octanol/water partition coefficients (Kow), is founded with only two molecular descriptors available through quantum chemical calculations: solvation free energy (delta Gs), and solvent-accessible surface area (SASA). For the properties of 47 organic compounds from 17 types, the model gives a correction coefficient (adjusted for degrees of freedom) of 0.959 and a standard error of 0.277 log unit. It is a suitable way to predict the partition properties that are related to solute-solvent interactions in the water phase.

Kinetics↗
PubMed2001

Gene construction, expression, and characterization of double-copy truncated form of human insulin-like growth factor I.

AIM: To increase the production of recombinant truncated form of insulin-like growth factor I [des(1-3)IGF-I], purify the expressed product, and compare its bioactivity with that of standard IGF-I. METHODS: The second copy of des(1-3)IGF-I gene was inserted into the previously constructed pExSec1/IGF-I to form a pExSec1/2(IGF-I) expression plasmid, then the plasmid was transformed into a protease-deficient E coli strain BL21(DE3). The engineered bacteria were cultured and induced by IPTG at 12 degrees C. The expressed product was purified through ultrafiltration and Sephadex G-50 gelfiltration. The bioactivity of the preliminarily purified protein was tested by MTT method and compared with standard IGF-I. RESULTS: The amount of des(1-3)IGF-I expressed by pExSec1/2(IGF-I) reached up to 20 % of the total soluble bacterial protein, which was higher than the amount (12 %) expressed by a single copy of pExSec1/IGF-I gene. The purity of recombinant des(1-3)IGF-I reached 49 % and 82 % after ultrafiltration and gelfiltration. The bioactivity of des(1-3)IGF-I after gelfiltration was about 77 % of standard IGF-I at the same concentration. CONCLUSION: The yield of recombinant des(1-3)IGF-I was increased about 8 % by construction of expression plasmid with two copies of des(1-3)IGF-I gene compared with only one copy of gene, and preliminarily purified des(1-3)IGF-I showed about 77 % bioactivity compared with standard IGF-I.

3T3 Cells↗
PubMed2001

[Study on allele-specific diagnostic PCR of the traditional Chinese medicines of the deers].

AIM: To develop a convenient and accurate method of DNA molecular marker for the identification of traditional Chinese medicines made of deers, consisting of pilose antler, penis and testis, tendon and foetus. METHODS: Based on the analysis of DNA sequence of mitochondrial Cyt b gene from original animals of both genuine crude drugs, Cervus nippon and Cervus elaphus, and adulterants, a pair of allele-specific primers named as ILu01-L and ILu01-H were designed for distinguishing geniune crude drugs of deers from their adulterants. RESULTS: The results of diagnostic PCR annealing at 64 degrees C for original animals showed that a 365 bp fragment was only amplified from DNA templates of Cervus nippon and Cervus elaphus. For the identification of medicinal materials total of 43 samples from 6 packages were tested under the same reaction conditions except for DNA templates extracted from these crude drugs. Only 9 samples mentioned above was shown to generate positive amplificon. The result indicate that of 8 samples from 1 package of pilose antler and only 1 sample of deer tendon was genuine crude drug. After that, 3 amplified fragments selected randomly were performed with sequencing analysis with the purpose of verifying the results from diagnostic PCR. Data from sequencing confirmed the reliability of diagnostic PCR identification. CONCLUSION: The diagnostic primers designed in the present study were highly specific for Cervus nippon and Cervus elaphus, and they could be used for the authentication of traditional Chinese medicines made from the deer. The quality of the crude drugs of the deer in the current market is a problem and more effective quality control for these traditional Chinese medicines is urgently needed.

Alleles↗