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Biomedical subjects

F Xiao

Publications and source records attributed to F Xiao.

At least 37 records · Page 2Linked to original sources
PubMed2001

Expression of 35S::Pto globally activates defense-related genes in tomato plants.

The tomato (Lycopersicon esculentum) resistance gene Pto confers resistance to the bacterial pathogen Pseudomonas syringae pv tomato carrying the avirulent gene avrPto. Overexpressing Pto under the control of the cauliflower mosaic virus 35S promoter constitutively activates defense responses in the absence of pathogen infection and nonspecifically enhances disease resistance. To elucidate the mechanisms underlying this resistance, we isolated cDNAs corresponding to transcripts that accumulated in 35S::Pto plants. By using suppression subtractive hybridization, we isolated 82 unique cDNA clones, most of which corresponded to differentially expressed transcripts. Most of the genes examined were also induced by pathogen inoculation. Sequence analysis showed that a large number of genes encode defense-related proteins, and most had not been previously isolated from tomato. The isolated cDNAs also include those with a putative role in the oxidative burst, proteolysis, the hypersensitive response, signal transduction, and a number of genes with unknown functions. The isolation of these cDNAs of diverse functions will assist in the characterization of defense pathways activated during disease resistance.

Bacterial Proteins↗
PubMed2001

Skin reflectance in the Han Chinese and Tibetan populations.

Genetic and environmental factors are involved in the determination of skin pigmentation in humans. With the recent development of statistical and genetic tools in mapping complex traits in humans, it is becoming feasible to utilize such methods in identifying genes involved in skin pigmentation. Furthermore, the use of new portable reflectance spectroscopy instruments such as the Photovolt ColorWalk colorimeter allows researchers to measure skin reflectance of a large number of subjects with ease and accuracy. We used a new portable instrument (Photovolt ColorWalk) to study the skin reflectance of 372 Han Chinese and 274 Tibetan individuals to establish background reflectance measurements of unexposed skin of the inner upper arm in these two populations. In addition, we explored the effect of various factors such as age and gender on skin reflectance.

Adolescent↗
PubMed2001

[A study on pathological changes of closed diffuse brain injury in rats with H.E., esterification-silver stain and albumin immunohistochemical stain].

OBJECTIVE: To observed the pathological changes of closed diffuse brain injury in the rats died immediately and 15 min to 5 days after the injury. METHODS: H.E. staind and esterification-silver stain were applied to investigate the closed diffuse brain injury. RESULTS: In rats died immediately after the concussive injury, a number of shrunken neurons(type I change), distended neurons(type II change) and wave-like nerve fibers were identified in the brain tissue, especially in brain-stem. At 2 h and 8 h after injury, brain edema and axonal swelling appeared clearly in the cortex and white matter, especially in brain-stem. At post-traumatic 8 h and 24 h, the axonal retraction balls began to appear. The amount of neurons undergoing type I and II changes and constraction balls increased along with the survivor time. After 4 days and 5 days, brain edema alleviated, but the retraction balls and axonal swelling still existed. With Esterifica-tion silver stain, the above changes of neurons and nerve fibers were more obvious. With ABC stain, the distribution of albumin(Al) was extended from the perio-vascular area to diffuse distribution. Al positive staining were more obvious in injuried neurons and nerve fibers. CONCLUSION: The distribution of the concussive damage in the brain are coup, contra-coup and centripental.

Albumins↗
PubMed2000

Reduced nitric oxide is involved in prenatal ischemia-induced tolerance to neonatal hypoxic-ischemic brain injury in rats.

To explore the role of nitric oxide (NO) in the hypoxic-ischemic (HI) tolerance phenomenon, NO production and brain injury following neonatal hypoxia-ischemia (induced by unilateral common carotid artery ligation followed by hypoxic exposure) were assessed in rat pups with or without HI preconditioning. A previously demonstrated prenatal HI rat model of preconditioning was used in this study. On G17, rat fetuses were subjected to either HI in utero (PreHI) for 30 min or a sham operation (SH). The PreHI treatment provided significant protection against neonatal HI-induced brain injury, as indicated by decreased ipsilateral brain weight reduction, less severe tissue damage, and decreased activation of caspase-3. Concomitant with the protective effect of prenatal HI preconditioning, elevation of nitrite/nitrate content in the ipsilateral cortex of the brain, as an indirect measure of NO production, was significantly lower in the PreHI group than in the SH group following neonatal HI. The protective effect of prenatal HI preconditioning could be reversed by sodium nitroprusside (SNP), a spontaneous NO donor, while SNP had no effect on neonatal HI-induced brain injury in the SH group. Intraperitoneal administration of SNP to pups from the PreHI group (2 mg/kg, 24 and 1.5 h before neonatal HI) increased neonatal HI-induced brain injury similar to that observed in the SH group. On the other hand, L-N(G)-nitro-arginine (2 mg/kg, i.p., 1.5 h before the hypoxic exposure), an NO synthase inhibitor, significantly attenuated neonatal HI-induced brain injury in the SH group. The overall results indicate that reduced NO production in the preconditioned rat brain contributes to prenatal HI-induced tolerance to neonatal HI brain injury.

Animals↗
PubMed2000

Thiopental combination treatments for cerebral resuscitation after prolonged cardiac arrest in dogs. Exploratory outcome study.

We postulate that mitigating the multifactorial pathogenesis of postischemic encephalopathy requires multifaceted treatments. In preparation for expensive definitive studies, we are reporting here the results of small exploratory series, compared with historic controls with the same model. We hypothesized that the brain damage mitigating effect of mild hypothermia after cardiac arrest can be enhanced with thiopental loading, and even more so with the further addition of phenytoin and methylprednisolone. Twenty-four dogs (four groups of six dogs each) received VF 12.5 min no-flow, reversed with brief cardiopulmonary bypass (CPB), controlled ventilation to 20 h, and intensive care to 96 h. Group 1 with normothermia throughout and randomized group 2 with mild hypothermia (from reperfusion to 2 h) were controls. Then, group 3 received in addition, thiopental 90 mg/kg i.v. over the first 6 h. Then, group 4 received, in addition to group 2 treatment, thiopental 30 mg/kg i.v. over the first 90 min (because the larger dose had produced cardiopulmonary complications), plus phenytoin 15 mg/kg i.v. at 15 min after reperfusion, and methylprednisolone 130 mg/kg i.v. over 20 h. All dogs survived. Best overall performance categories (OPC) achieved (OPC 1 = normal, OPC 5 = brain death) were better in group 2 than group 1 (< 0.05) and numerically better in groups 3 or 4 than in groups 1 or 2. Good cerebral outcome (OPC 1 or 2) was achieved by all six dogs only in group 4 (P < 0.05 group 4 vs. 2). Best NDS were 44 +/- 3% in group 1; 20 +/- 14% in group 2 (P = 0.002); 21 +/- 15% in group 3 (NS vs. group 2); and 7 +/- 8% in group 4 (P = 0.08 vs. group 2). Total brain histologic damage scores (HDS) at 96 h were 156 +/- 38 in group 1; 81 +/- 12 in group 2 (P < 0.001 vs. group 1); 53 +/- 25 in group 3 (P = 0.02 vs. group 2); and 48 +/- 5 in group 4 (P = 0.02 vs. group 2). We conclude that after prolonged cardiac arrest, the already established brain damage mitigating effect of mild immediate postarrest hypothermia might be enhanced by thiopental, and perhaps then further enhanced by adding phenytoin and methylprednisolone.

Animals↗
PubMed2000

Immunotherapy of tumors with xenogeneic endothelial cells as a vaccine.

The breaking of immune tolerance against autologous angiogenic endothelial cells should be a useful approach for cancer therapy. Here we show that immunotherapy of tumors using fixed xenogeneic whole endothelial cells as a vaccine was effective in affording protection from tumor growth, inducing regression of established tumors and prolonging survival of tumor-bearing mice. Furthermore, autoreactive immunity targeting to microvessels in solid tumors was induced and was probably responsible for the anti-tumor activity. These observations may provide a new vaccine strategy for cancer therapy through the induction of an autoimmune response against the tumor endothelium in a cross-reaction.

Amino Acid Sequence↗
PubMed2000

Cure of refractory duodenal ulcer and infection caused by Helicobacter pylori by high doses of omeprazole and amoxicillin in a homozygous CYP2C19 extensive metabolizer patient.

A 53-year old female patient with duodenal ulcer and Helicobacter pylori infection was treated three times with a proton pump inhibitor-based triple therapy, such as lansoprazole-clarithromycin-amoxicillin (INN, amoxicilline) and lansoprazole-minocycline-cefaclor. However, the H pylori infection was not cured. A culture test revealed that her infection was a clarithromycin-resistant but amoxicillin-sensitive strain of H pylori. Moreover, a polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) analysis revealed that she was a homozygous extensive metabolizer of cytochrome P450 (CYP) 2C19 (wt/wt). The usual dose of the proton pump inhibitor was therefore assumed to be insufficient for her and then she was treated with a high dose of omeprazole (120 mg/day) and amoxicillin (2,250 mg/day) for 2 weeks. The H pylori infection and the ulcer lesion were then cured. One of the factors associated with success or failure of cure of H pylori infection by the proton pump inhibitor-based triple therapy appeared to be CYP2C19 genotype status. Dual treatment with a sufficient dose of a proton pump inhibitor plus amoxicillin could cure H pylori infection even after the failure to cure H pylori infection by a usual proton pump inhibitor-based triple therapy in patients with the wt/wt homozygous extensive metabolizer genotype of CYP2C19.

Amoxicillin↗
PubMed2000

Relationships between a roller and a dynamic pressure distribution in circular hydraulic jumps

We investigated numerically the relation between a roller and the pressure distribution to clarify the dynamics of the roller in circular hydraulic jumps. We found that a roller which characterizes a type II jump is associated with two high pressure regions after the jump, while a type I jump (without the roller) is associated with only one high pressure region. Our numerical results show that building up an appropriate pressure field is essential for a roller.

Journal Article↗
PubMed2000

The expression of renin and the formation of angiotensin II in bovine aortic endothelial cells.

One controversy in the field of vascular angiotensin generation has surrounded the nature and particularly the source of vascular renin. This study investigated the expression of renin protein and its mRNA in aortic endothelial cells using immunocytochemistry, Western blotting, in situ hybridization and reverse transcription PCR (RT-PCR). Using a monoclonal antibody against human renin, immunocytochemical analysis revealed positive immunoreactivity in the cytoplasm of cultured bovine aortic endothelial cells. Immunoblotting of solubilized proteins separated by SDS-PAGE from cultured aortic endothelial cells identified two immunoreactive species with molecular masses of approximately 37-40 kDa. In situ hybridization showed that renin mRNA was localized in the cytoplasm of these cells. Using RT-PCR of RNA extracted from bovine aortic endothelial cells with primers specific for human renin, a clear single band was detected, which had the predicted size of 142 bp for (pro)renin. Angiotensin II (Ang II) was assayed in conditioned medium (CM) from cultured bovine aortic endothelial cells, and in addition, the effects of Ang II and CM on the proliferation of aorta smooth muscle cells (ASMC) were also studied. The results showed that CM contained Ang II equivalent to 15.05+/-4.67 pg/10(6) cells. Assay of smooth muscle cell proliferation by cell number, and by tritiated thymidine uptake, showed that proliferative responses in the presence of Ang II at a concentration of 10(-6)M were evident within 1 day of subculture, and cell numbers were nearly twice those of controls after 2 days. Thymidine incorporation into ASMC was also increased by Ang II in a dose-dependent manner and by endothelial cell CM. In both cases, stimulated proliferation was inhibited by the Ang II type 1 (AT1) receptor selective antagonist, losartan. These findings suggest that these vascular endothelial cells are a source of locally synthesized renin that may thus be involved in vascular Ang II generation. They also suggest that Ang II produced by the endothelial cells may be secreted and stimulate ASMC proliferation via the AT1 receptor.

Angiotensin II↗
PubMed2000

Aldosterone mediates angiotensin II-stimulated rat vascular smooth muscle cell proliferation.

Aldosterone, possibly locally generated, has been suggested to have a role in potentiating angiotensin II (AII)-stimulated hypertrophy of cultured vascular smooth muscle cells. To examine the possibility that aldosterone may mediate the proliferative actions of AII, rat aortic smooth muscle cells (RASMCs) in culture were treated with AII in the presence and absence of the specific AII type 1 receptor (AT1) antagonist, losartan, and aldosterone was assayed in culture medium extracts by radioimmunoassay. AII significantly enhanced aldosterone formation (at 10(-8) M: 123.8+/-14.85 vs control 71. 28+/- 8.71 fmol/10(5) cells, P<0.05; at 10(-7) M: 172.38+/-33.44, P<0.05), but not in the presence of losartan (at 10(-8) M: 53. 71+/-18.73, P>0.05; at 10(-7) M: 89.68+/-25.05, P>0.05). In other studies, the reverse transcriptase-polymerase chain reaction, performed on RNA extracted from RASMCs using aldosterone synthase (CYP11B2) specific primers, gave a single band of about 268 bp, consistent with that expected for the enzyme. Finally, using [(3)H]methylthymidine uptake as an index of cellular proliferation, tritium incorporation was increased in the AII-treated group at concentrations greater than 10(-10) M. The aldosterone antagonist, spironolactone (10(-5) M), inhibited the incorporation of [(3)H]thymidine into RASMCs stimulated by AII. These results suggest that locally generated aldosterone may mediate the effects of AII, acting via the AT1 receptor, in stimulating RASMC proliferation.

Aldosterone↗
PubMed1999

Protection of neonatal rat brain from hypoxic-ischemic injury by LY379268, a Group II metabotropic glutamate receptor agonist.

Neuroprotective effects of a Group II metabotropic glutamate receptor agonist, LY379268, were examined in a neonatal rat model of hypoxia-ischemia (unilateral common carotid artery ligation followed by hypoxic exposure for 1.5h in 7-day-old rat pups). LY379268 administered 5 min after hypoxic exposure (2, 5, or 10 mg/kg, i.p.) significantly reduced brain injury as measured by reductions in the ipsilateral brain weight and in CA1 hippocampal neuron density. The significant neuroprotective effects were also observed when this compound (5 mg/kg) was administered 30 min, but not 60 min, after hypoxic exposure. The neonatal hypoxia-ischemia (HI) procedure significantly increased caspase-3 activity and induced DNA fragmentation in the ipsilateral cortex compared with that in the contralateral cortex 24 and 72h after the insult, respectively. LY379268 did not prevent this increase in caspase-3 activity and DNA fragmentation in the ipsilateral cortex. These results suggest that activation of Group II metabotropic glutamate receptors may provide neuroprotection against HI brain injury. However, blockade of caspase-3 activation and the apoptotic pathway appears not to be involved in the neuroprotective effects of LY379268 observed in the neonatal rat model of HI.

Amino Acids↗
PubMed1999

Prenatal hypoxia-ischemia alters expression and activity of nitric oxide synthase in the young rat brain and causes learning deficits.

Inhibition of nitric oxide synthase (NOS) is known to possibly impair learning and memory. Our previous studies have demonstrated that prenatal hypoxia-ischemia (HI) decreases NOS expression and NOS activity in the neonatal rat brain. To investigate whether effects of prenatal HI on NOS expression continue and whether prenatal HI affects learning and memory in young rats, NOS expression and NOS activity were determined in the hippocampus of rat brains at 28 days of age following a prenatal HI insult on G17. Performances in the passive avoidance test and the Morris water maze test were also studied in these young rats prior to sampling. Rat fetuses were subjected to either a 30-min prenatal HI insult or a sham operation (SH) on gestation day 17 and rat pups were delivered naturally. Increased locomotor activity was observed in the prenatal HI rats as compared to the SH rats on postnatal days 13 and 15, but not on postnatal days 20 and 30. Prenatal HI affected learning ability in these young rats at 28 days of age, as indicated by a delayed acquisition of passive avoidance and by longer escape latency in the Morris water maze test as compared to the SH group. Prenatal HI did not affect retention of passive avoidance and spatial memory. Concomitant with these learning deficits, expression of neuronal NOS and endothelial NOS mRNAs as well as Ca2(+)-dependent NOS activity in the hippocampus of the prenatal HI rat brain were significantly decreased as compared to the SH group. These results suggest that a 30-min prenatal HI insult on gestation day 17 in rats has long-lasting effects on NOS expression and NOS activity in the offspring brain and on learning ability of these young rats. The learning deficit in offspring is possibly associated with the reduction in expression of NOS mRNA and NOS activity in the hippocampus of these animals.

Animals↗
PubMed1999

In vivo activity of leflunomide: pharmacokinetic analyses and mechanism of immunosuppression.

BACKGROUND: Leflunomide is an experimental drug with demonstrated ability to prevent and reverse acute allograft and xenograft rejection. The two biochemical activities reported for the active metabolite of leflunomide, A77 1726, are inhibition of tyrosine phosphorylation and inhibition of dihydroorotate dehydrogenase, an enzyme necessary for de novo pyrimidine synthesis. These activities can be distinctly separated in vitro by the use of uridine, which reverses the anti-proliferative effects of A77 1726 caused by inhibition of de novo pyrimidine synthesis. We report the effect of uridine on the in vivo immunosuppressive activities of leflunomide. METHODS: We first quantified the serum levels of A77 1726, the active metabolite of leflunomide, after a single treatment of leflunomide (5, 15, and 35 mg/kg). Additionally, we quantified the levels of serum uridine and of nucleotide triphosphates in the liver, spleen, and lymph nodes of Lewis rats after the administration of a single dose of uridine (500 mg/kg; i.p.). Lewis rats heterotopically transplanted with brown Norway or Golden Syrian hamster hearts were treated for 50 or 75 days with leflunomide (5, 15, and 35 mg/kg/day; gavage) alone or in combination with uridine (500 mg/ kg/day; i.p.). Hematocrits were determined and the levels of alloreactive or xenoreactive immunoglobulin (Ig)M and IgG were determined by flow cytometric analysis. The allograft and xenografts, small bowel, liver, kidney, and spleen were subjected to pathological examination. RESULTS: A linear relationship was observed between the serum A77 1726 concentrations in Lewis rats and the dose of leflunomide administered. Peak A77 1726 concentrations were 20.9, 71.8 and 129.3 mg/l (77.5, 266.1 and 478.8 microM) for the 5, 15, and 35 mg/kg doses of leflunomide, respectively. The concentration of uridine in the serum of normal Lewis rats is 6.5 microM; after i.p. administration of 500 mg/kg uridine, the serum uridine concentrations peaked at 384.1 microM in 15-30 min. The rapid elimination of uridine was not reflected in the lymphoid compartments, and the pharmacokinetics of pyrimidine nucleotides in the spleen resembled that of A77 1726. This dose of uridine, when administered daily (500 mg/kg/day, i.p.), weakly antagonized the immunosuppressive activities of leflunomide (5, 15, and 35 mg/kg/day) in the allotransplantation model. In contrast, in the xenotransplantation model, the same concentration of uridine completely antagonized the immunosuppressive activities of low-dose leflunomide (15 mg/kg/day) and partially antagonized the immunosuppressive activities of high-dose leflunomide (35 mg/kg/day). Toxicities associated with high-dose leflunomide (35 mg/kg/day) were anemia, diarrhea, and pathological changes in the small bowel and liver. These toxicities were significantly reduced by uridine co-administration. CONCLUSION: These studies reveal that the blood levels of A77 1726 in Lewis rats satisfy in vitro requirements for both inhibition of de novo pyrimidine synthesis and protein tyrosine kinase activity. Our data also illustrate that the in vivo mechanism of immunosuppression by leflunomide is complex and is affected by at least the following four factors: type and vigor of the immune response, availability of uridine for salvage by proliferating lymphocytes, species being investigated, and concentration of serum A77 1726.

Aniline Compounds↗
PubMed1999

Attention-sensitive visual event-related potentials elicited by kinetic forms.

Previous event-related potential (ERP) studies have shown that selectively attending to a relevant stimulus feature was associated with selection negativity (SN) components. The present study aimed at investigating the ERP indices of attentional selection based on forms defined by motion (kinetic forms). ERPs were recorded from subjects who attended selectively to sequentially presented kinetic forms of bars in one visual field and detected occasional tilted bar targets. Two kinds of kinetic forms were used as the visual stimuli in separate experiments. The main findings were that spatial attention enhanced the amplitude of early ERP components 1 and N1 as well as the late component N2. Topographic maps of voltage and low resolution electromagnetic tomography (LORETA) of the dN2 wave (difference waveform between N2 under attended condition and N2 under unattended condition) suggested an origin in the right occipitotemporal cortex. According to its timing and morphology, the dN2 wave was considered to be an endogenous ERP (like the SN) and was interpreted as reflecting attentional facilitation of the processing of forms defined by motion primarily involving the right occipitotemporal areas.

Adult↗
PubMed1999

H+/K+-adenosine triphosphatase mRNA in gastric fundic gland mucosa in patients infected with Helicobacter pylori.

BACKGROUND: How Helicobacter pylori infection affects gastric acid secretion has not been made clear. This study aimed to elucidate the effects of H. pylori infection on H+/K+-adenosine triphosphatase (ATPase) mRNA in gastric fundic gland mucosa. METHODS: Twenty patients with chronic gastritis and H. pylori infection were treated with lansoprazole and antibiotics. Before and 1 month after treatment gastroduodenoscopy was performed, and changes in the amount of H+/K+-ATPase mRNA in the fundic gland mucosa, gastric juice pH, and serum gastrin levels were determined. RESULTS: The amount of H+/ K+-ATPase mRNA in the fundic gland mucosa was increased in patients with eradication of H. pylori, in whom significant decreases in gastric juice pH and serum gastrin levels were observed. No significant changes were observed in patients without eradication of H. pylori. CONCLUSIONS: These results suggest that one of the mechanisms by which H. pylori infection suppresses acid secretion is by the inhibition of proton pump synthesis in parietal cells.

DNA Primers↗
PubMed1999

Aspiration of activated charcoal elicits an increase in lung microvascular permeability.

BACKGROUND: Gastric decontamination with orally administered activated charcoal is the recommended treatment for many poisonings. However, ingestion of central nervous system depressants resulting in loss of protective airway reflexes may result in pulmonary aspiration of activated charcoal. Although activated charcoal has been reported to be an inert substance, evidence suggests that pulmonary aspiration of charcoal is associated with lung edema formation and pulmonary compromise. This study tested the hypothesis that intratracheal instillation of activated charcoal disrupts the integrity of the lung microvascular barrier. METHODS: The capillary filtration coefficient (Kf,c), a sensitive measure of lung microvascular permeability, was determined isogravimetrically prior to and after intratracheal instillation of activated charcoal 0.04 g/kg (12% weight/vol solution, pH 7.4) or an equal volume of sterile water in isolated, perfused rat lungs. Arterial blood gas analysis was determined prior to and after tracheal instillation of activated charcoal or sterile water in a separate group of animals. RESULTS: Intratracheal instillation of activated charcoal resulted in a significant increase in pulmonary microvascular permeability compared to lungs treated with sterile water or control lungs (delta Kf,c = +0.21 +/- 0.076; -0.014 +/- 0.04; and -0.041 +/- 0.02 mL/min/cm H2O/100 g lung tissue, respectively, p < 0.05 ANOVA). There was no significant difference in baseline blood gases in the 3 experimental groups. There was a significant decrease in arterial Po2, bicarbonate, and pH in animals administered activated charcoal compared to time-matched controls and animals administered sterile water. CONCLUSIONS: Intratracheal instillation of activated charcoal is associated with a significant increase in lung microvascular permeability and arterial blood gas derangements. The effects of activated charcoal on pulmonary microvascular barrier integrity may contribute to the lung edema formation and pulmonary compromise observed following clinical aspiration of activated charcoal.

Animals↗
PubMed1999

[The SEM observation of brain tissues and vascular corrosion cast of closed diffuse brain injuries].

The morphologic changes of the closed injured brain of rats were observed by SEM. The rats either died immediately after conclusive injuries or were killed after 5 minutes to 5 days after injuries. The main changes were as follows: the diffuse disorder, twist, wave-like distortion and break of neuron fibers; axonal swelling; formation of axonal retraction balls; stripping and denotation of myelin sheath The ball-like swelling of neuron, break of neuron membrane and vascular wall, and microthrombus formations were also observed. These damages worsened with prolongation of surviving time of the rats. The axonal retraction ball appeared 8 hours after the injury and was approximately 3-5 cm in diameter, and developed to 7-8 cm after 3-5 days. It is observed that frontal lobe, cerebellum and brain stem were severely damaged.

Animals↗