Biomedical subjects

H Yao

Publications and source records attributed to H Yao.

At least 37 records · Page 2Linked to original sources

PubMed2003

[Prosthetic valve endocarditis after aortic valve replacement with freestyle stentless xenograft].

A 52-year-old man underwent aortic valve replacement with freestyle stentless xenograft, using subcoronary technique for active infective endocarditis in June, 2001. Eighteen month later he had late prosthetic valve endocarditis associated with aortic annular abscess due to Staphylococcus epidermidis infection. The abscess was debrided and gelatin-resorcin-formalin glue (GRF glue) was injected into the abscess cavity. Abscess cavity was closed with continuous running suture of 3-0 polypropylene stitches. Finally the aortic valve was replaced with ATS mechanical valve (20 mmAP). After administration of vancomycin and gentamicin for 4 weeks, he discharged on 57th postoperative day in good condition. We strongly suggest that GRF glue is essential to close the aortic annular abscess of combined with aortic regurgitation due to active infective endocarditis.

Aortic Valve↗

PubMed2003

[Surgical treatment for left ventricular false aneurysm caused by infective endocarditis; report of a case].

A 24-year-old man who had left ventricular (LV) false aneurysm, which is caused by mitral valve infective endocarditis, underwent aneurysmectomy, direct closure of aneurysmal mouth and concomitant mitral valve replacement. Post-operative course was uneventful. It has been reported that the etiology of this false aneurysm was due to the vegetations' friction, which could have caused an initial endocardial ulceration that progressively expanded into the myocardium. The false aneurysmal wall should be completely removed in order to eliminate the possibility of recurrence of the infective endocarditis. We believe that the surgical treatment should be carried out as soon as possible after completion of diagnosis because the aneurysmal wall is usually quite thin and could rupture easily.

Adult↗

PubMed2002

Quantitative MRI findings and cognitive impairment among community dwelling elderly subjects.

OBJECTIVES: To study the factors which influence cognitive impairment among elderly subjects living in a local community, based on both MRI and clinical findings, to further elucidate the causes of dementia, and also to help develop strategies for its prevention. METHODS: Cranial MRI and other medical examinations were performed on non-demented elderly subjects who resided in one rural community. A total of 254 subjects aged from 60 to 91 years of age, with a mean age of 73.9 (SD 6.8) were examined. The mini mental state examination (MMSE) was used to identify cognitive impairment. White matter lesions and cerebral atrophy on MR images were measured quantitatively. A multivariate analysis was also performed with the existence of cognitive impairment as the dependent variable, and the MRI findings and clinical observations were used as the independent variables. RESULTS: Cognitive impairment was present in 46 subjects (18.1%). They were older, had a lower educational level, and more frequent hypertension compared with those without cognitive impairment. The packed cell volume was lower in the impaired group. In addition, their MRI findings showed significantly larger quantities of white matter lesions and cerebral atrophy, as well as more infarcts. A logistic regression analysis demonstrated a significant relation among such factors as white matter lesions (odds ratio (OR) 1.575, 95% confidence interval (95% CI) 1.123-2.208), cerebral atrophy (OR 0.761, 95%CI 0.587-0.987), and lower education (OR 0.682, 95%CI 0.544-0.855) for subjects with a cognitive impairment. CONCLUSIONS: White matter lesions and cerebral atrophy are factors which induce a cognitive impairment in community dwelling elderly subjects without dementia. It is important to carefully watch for any abnormalities in these factors, and to perform cohort studies to check for the above risk factors, to both prevent and make an early diagnosis of dementia.

Aged↗

PubMed2001

Inhibition of Na+/H+ exchanger reduces infarct volume of focal cerebral ischemia in rats.

Activation of Na+/H+ exchanger (NHE) may have an important role in ischemic cell death by means of intracellular overload of Na(+) and Ca(2+). Recent evidence has suggested that inhibitors of NHE have protective effects on myocardial ischemia both in vivo and in vitro. In this study, we tested the hypothesis that FR183998, an inhibitor of NHE, reduces infarct volume produced by focal cerebral ischemia in rats. We used 20 male spontaneously hypertensive rats. Either FR183998 (1 mg/kg; n=10), or vehicle (n=10) was given intravenously to the rats and the distal middle cerebral artery of each animal was occluded using a photothrombotic technique. We measured regional cerebral blood flow using laser-Doppler flowmetry throughout the experiments. After 3 days, infarct volume was measured in each animal group. To estimate the brain edema, we also calculated the cortical volume in both hemispheres. The infarct volume in the FR183998-treated group (82+/-8 mm(3), mean+/-S.E.M.) was significantly smaller than that in the control group (115+/-12 mm(3)) (P=0.034). The cortical volume of the occluded side in the FR183998-treated group (359+/-7 mm(3)) tended to be smaller than that in the control group (378+/-9 mm(3)) (P=0.116). The regional cerebral blood flow and physiological variables during ischemia were not significantly different between the two groups throughout the experiments. These results suggest that inhibition of NHE by FR183998 may have beneficial effects in reducing infarct volume and brain edema during cerebral ischemia. Thus, NHE may play an important role in the development of neuronal damage during acute cerebral ischemia.

Animals↗

PubMed2001

Stimulus timing-dependent plasticity in cortical processing of orientation.

The relative timing of presynaptic and postsynaptic spikes plays a critical role in activity-induced synaptic modification. Here we examined whether plasticity of orientation selectivity in the visual cortex depends on stimulus timing. Repetitive pairing of visual stimuli at two orientations induced a shift in orientation tuning of cat cortical neurons, with the direction of the shift depending on the temporal order of the pair. Induction of a significant shift required that the interval between the pair fall within +/-40 ms, reminiscent of the temporal window for spike timing-dependent synaptic plasticity. Mirroring the plasticity found in cat visual cortex, similar conditioning also induced a shift in perceived orientation by human subjects, further suggesting functional relevance of this phenomenon. Thus, relative timing of visual stimuli can play a critical role in dynamic modulation of adult cortical function, perhaps through spike timing-dependent synaptic plasticity.

Animals↗

PubMed2001

Synthesis and evaluation of hydroxylated polyamine analogues as antiproliferatives.

A new means of accessing N(1)-cyclopropylmethyl-N(11)-ethylnorspermine (CPMENSPM) and the first synthesis of (2R,10S)-N(1)-cyclopropylmethyl-2,10-dihydroxy-N(11)-ethylnorspermine [(2R,10S)-(HO)(2)CPMENSPM] are described. Both of these polyamine analogues are shown to be more active against L1210 murine leukemia cell growth than either N(1),N(11)-diethylnorspermine (DENSPM) or (2R,10R)-N(1),N(11)-diethyl-2,10-dihydroxynorspermine [(2R,10R)-(HO)(2)DENSPM] after 96 h of treatment; the activity was comparable to that of (2S,10S)-N(1),N(11)-diethyl-2,10-dihydroxynorspermine [(2S,10S)-(HO)(2)DENSPM] at 96 h. Both cyclopropyl compounds reduced putrescine and spermidine pools, but less effectively than did DENSPM and its derivatives. Only CPMENSPM, and not (2R,10S)-(HO)(2)CPMENSPM, lowered spermine pools. As with DENSPM and (2R,10R)-(HO)(2)DENSPM, both cyclopropyl analogues diminished ornithine decarboxylase and S-adenosylmethionine decarboxylase activity. Unlike the hydroxylated DENSPM compounds, both cyclopropyl norspermines substantially upregulated spermidine/spermine N(1)-acetyltransferase. The most interesting effect of hydroxylating CPMENSPM is the profound reduction in toxicity compared with that of the parent drug. The same phenomenon had been observed for the DENSPM/(2R,10R)-(HO)(2)DENSPM pair. Thus, hydroxylation of norspermine analogues appears to be a way to maintain the compounds' antiproliferative activity while reducing their toxicity.

Acetyltransferases↗

PubMed2001

DNA fragmentation in ischemic core and penumbra in focal cerebral ischemia in rats.

Although apoptotic cell death has been suggested to be involved in ischemic injury of the brain, the precise mechanisms of ischemic neuronal cell death are unknown. Here, we examined the biochemical feature of apoptosis (i.e. DNA fragmentation) in male spontaneously hypertensive rats (5-7 months old) subjected to photothrombotic distal middle cerebral artery (MCA) occlusion. After MCA occlusion, the brain was cut in a cryostat to produce a standard coronal block and samples were dissected from the regions corresponding to the ischemic core, penumbra and contralateral control areas. Changes in cerebral blood flow (CBF) were monitored at 1 mm posterior and 2-4 mm lateral to the bregma by means of a laser-Doppler flowmetry. After MCA occlusion, CBF was decreased to 72+/-18 (+/-S.D.), 50+/-14, and 35+/-11% of the control values at 2, 3, and 4 mm from the midline, respectively. DNA fragmentation characteristics of apoptosis were examined in these samples by conventional and pulse-field gel electrophoresis. On the conventional gel electrophoresis, nucleosomal DNA fragmentation was detected in the penumbral zone at 6 h after MCA occlusion. Large DNA fragments of 50 and 20 kbp were detected in the penumbral zone and also in the ischemic core region at 3 h after distal MCA occlusion. The large DNA fragments seen on the pulse-field gel elecrophoresis were further degraded to small DNA fragments at 6 h after MCA occlusion in the penumbral zone but not in the core regions. The evolving DNA fragmentation was observed between 3 and 6 h after the onset of brain ischemia in the penumbra, suggesting that apoptosis may contribute to the development of ischemic infarction.

Animals↗

PubMed2001

Mechanism of sulfide oxidations by peroxymonocarbonate.

A detailed mechanism for the oxidation of aryl sulfides by peroxymonocarbonate ion in cosolvent/water media is described. Kinetic studies were performed to characterize the transition state, including a Hammett correlation and variation of solvent composition. The results are consistent with a charge-separated transition state relative to the reactants, with an increase of positive charge on the sulfur following nucleophilic attack of the sulfide at the electrophilic oxygen of peroxymonocarbonate. In addition, an average solvent isotope effect of 1.5 +/- 0.2 for most aryl sulfide oxidations is consistent with proton transfer in the transition state of the rate-determining step. Activation parameters for oxidation of ethyl phenyl sulfide in tert-butyl alcohol/water are reported. From the pH dependence of oxidation rates and (13)C NMR equilibrium experiments, the estimated pK(a) of peroxymonocarbonate was found to be approximately 10.6.

Journal Article↗

PubMed2001

Transcription and temporal cascade in Chilo iridescent virus infected cells.

Chilo iridescent virus (CIV) is the type species for genus Iridovirus, and belongs to the family Iridoviridae. Members of this family are large, isometric, cytoplasmic DNA viruses. Our laboratory has established that CIV replicates productively in the cotton boll weevil, Anthonomus grandis. Given the economic importance of this host and the dearth of knowledge on this virus, we have initiated host-virus interaction and molecular studies on CIV. This report focuses on regulation of transcription in CIV infections. We carried out northern analyses on total cellular RNA from infections of IPRI-CF-124T cells, using a complete genomic library of CIV and several putative gene-specific probes. Our data show a temporal cascade based on analysis of 137 detectable transcripts comprising 38 immediate-early (IE), 34 delayed-early (DE), and 65 late (L) transcripts. Analysis with gene-specific probes supported the cascade pattern. Both helicase and RNA polymerase were immediate-early; major capsid protein was late. The CIV gene expression cascade appears to operate primarily at the transcriptional level. Temporal classes observed are consistent with earlier studies at the polypeptide level and with transcriptional patterns in frog virus 3, genus Ranavirus in the Iridoviridae. Our results provide an important basis for understanding mechanisms driving the CIV temporal cascade.

Aphidicolin↗

PubMed2001

Prevention and detection of spinal cord injury during thoracic and thoracoabdominal aortic repairs.

BACKGROUND: Spinal cord injury is a most dreaded and unpredictable complication. In this study, based on our experimental results in dogs and early clinical results, we reviewed the incidence of paraplegia and the detection of spinal cord injury. METHODS: Eighty-two patients who underwent elective surgical repair of the descending thoracic and thoracoabdominal aorta over 17 years were subjects for this study. Sixty-two patients were male and 20 were female. Their mean age was 61.6 years (range, 17 to 81 years). Monitoring somatosensory evoked potentials (SEP) and measurement of mean distal aortic pressure and cerebrospinal fluid pressure were performed perioperatively. RESULTS: Sixty patients had no ischemic change in SEP. In 17 patients with significant ischemic changes of SEP, SEP recovered by increasing spinal cord perfusion pressure to more than 40 mm Hg. Two patients with complete loss of SEP experienced paraplegia. One patient had delayed paraplegia. CONCLUSIONS: These results strongly suggest that SEP, mean distal aortic pressure, cerebrospinal fluid pressure should be monitored during aortic cross-clamping. Maintaining spinal cord perfusion pressure at more than 40 mm Hg by increasing mean distal aortic pressure or withdrawal of cerebrospinal fluid is valuable for preventing paraplegia.

Adolescent↗

PubMed2001

IFN-gamma gene therapy by intrasplenic hepatocyte transplantation: a novel strategy for reversing hepatic fibrosis in Schistosoma japonicum-infected mice.

Liver-targeted gene therapy using hepatocyte as recipient cells has recently been documented to be effective in treatment of numerous hepatic diseases, such as metabolic diseases and liver carcinoma. IFN-gamma elicits antipreliferative and antifibrogenic activity in a variety of mesenchymal cells, including hepatic satellite cells. To investigate the antifibrogenic response of liver gene therapy mediated by intrasplenic transplantation of gene-modified hepatocytes, normal mouse liver cell line BNL CL.2 cells were transfected with murine IFN-gamma gene (BNL.IFN-gamma) in vitro, and transplanted intrasplenically into Schistosoma japonicum-infected mice. The amounts and distribution of IFN-gamma (which inhibits collagen synthesis), TGF-beta (which stimulates collagen synthesis) and extracellular matrix, including type I and III collagen, were detected. In mice infected with S. japonicum and then treated with BNL.IFN-gamma, an increase of IFN-gamma and decrease of TGF-beta1 were detected at 20 weeks postinfection compared to untreated S. japonicum-infected mice. Immunohistochemical analysis showed that S. japonicum infection induced a marked increase of type I and III collagen synthesis. Whereas, 4 weeks after treatment with BNL.IFN-gamma, net synthesis rates of type I and III collagen were markedly decreased in the liver of infected mice. In addition, a decreased expression of TGF-beta1 and its receptor TGF-betaRII in the liver of BNL.IFN-gamma-treated mice was also observed. Moreover, the decrease in TGF-beta1 and TGF-betaRII protein approximately paralleled the decrease in their mRNA expression, which was detected by RNA dot blotting. The data indicate that intrasplenic transplantation of IFN-gamma gene-modified hepatocyte can be a candidate approach to treat hepatic fibrosis.

Animals↗

PubMed2001

Arginine induced acute pancreatitis alters the actin cytoskeleton and increases heat shock protein expression in rat pancreatic acinar cells.

Arginine induced acute pancreatitis was evaluated as a novel and distinct form of experimental pancreatitis with particular attention to the actin cytoskeleton and expression of heat shock or stress proteins. Arginine induced a dose related necrotising pancreatitis in rats, as shown by histological evaluation, and an increase in serum amylase. Severe pancreatitis induced by 4.5 g/kg arginine was accompanied by dramatic changes in the actin cytoskeleton, as visualised with rhodamine phallodin. Intermediate filaments were also disrupted, as visualised by cytokeratin 8/18 immunocytochemistry. Arginine pancreatitis was accompanied by a stress response with a large increase in the small heat shock protein HSP27, as well as HSP70, peaking at 24 hours and localised to acinar cells. There was a lower increase in HSP60 and HSP90 and no effect on GRP78. HSP27 was also shifted to phosphorylated forms during pancreatitis. A lower dose of arginine (3.0 g/kg) induced less pancreatitis but a larger increase in HSP70 and HSP27 expression and phosphorylation of HSP27. Thus HSP expression can be overwhelmed by severe damage. The present work in conjunction with earlier work on caerulein induced pancreatitis indicates that changes in the actin cytoskeleton are an early component in experimental pancreatitis.

Actin Cytoskeleton↗

PubMed2001

Increased neuronal excitability and seizures in the Na(+)/H(+) exchanger null mutant mouse.

Mice lacking the Na(+)/H(+) exchanger isoform 1 (NHE1) manifest neurological diseases that include ataxia, motor deficits, and a seizure disorder. The molecular basis for the phenotype has not been clear, and it has not been determined how the lack of NHE1 leads, in particular, to the seizure disorder. We have shown in this work that hippocampal CA1 neurons in mutant mice have a much higher excitability than in wild-type mice. This higher excitability is partly based on an upregulation of the Na(+) current density (608.2 +/- 123.2 pA/pF in NHE1 mutant vs. 334.7 +/- 63.7 pA/pF in wild type in HCO/CO(2)). Alterations in Na(+) channel characteristics, including steady-state inactivation (shift of 18 mV in the depolarization direction in the mutant), recovery from inactivation (tau(h) = 5.22 +/- 0.49 ms in wild-type neurons and 2.20 +/- 0.20 ms in mutant neurons), and deactivation (at -100 mV, tau(d) = 1.75 +/- 0.53 ms in mutant and 0.21 +/- 0.05 ms in wild-type neurons) further enhance the differences in excitability between mutant and wild-type mice. Our investigation demonstrates the existence of an important functional interaction between the NHE1 protein and the voltage-sensitive Na(+) channel. We hypothesize that the increased neuronal excitability and possibly the seizure disorder in mice lacking the NHE1 is due, at least in part, to changes in Na(+) channel expression and/or regulation.

Action Potentials↗

PubMed2001

Role of Na(+)/H(+) exchanger during O(2) deprivation in mouse CA1 neurons.

To determine the role of membrane transporters in intracellular pH (pH(i)) regulation under conditions of low microenvironmental O(2), we monitored pH(i) in isolated single CA1 neurons using the fluorescent indicator carboxyseminaphthorhodafluor-1 and confocal microscopy. After total O(2) deprivation or anoxia (PO(2) approximately equal to 0 Torr), a large increase in pH(i) was seen in CA1 neurons in HEPES buffer, but a drop in pH(i), albeit small, was observed in the presence of HCO(3)(-). Ionic substitution and pharmacological experiments showed that the large anoxia-induced pH(i) increase in HEPES buffer was totally Na(+) dependent and was blocked by HOE-694, strongly suggesting the activation of the Na(+)/H(+) exchanger (NHE). Also, this pH(i) increase in HEPES buffer was significantly smaller in Na(+)/H(+) exchanger isoform 1 (NHE1) null mutant CA1 neurons than in wild-type neurons, demonstrating that NHE1 is responsible for part of the pH(i) increase following anoxia. Both chelerythrine and H-89 partly blocked, and H-7 totally eliminated, this anoxia-induced pH(i) increase in the absence of HCO. We conclude that 1) O(2) deprivation activates Na(+)/H(+) exchange by enhancing protein kinase activity and 2) membrane proteins, such as NHE, actively participate in regulating pH(i) during low-O(2) states in neurons.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗

PubMed2001

Adenovirus-mediated gene transfer to ischemic brain: ischemic flow threshold for transgene expression.

BACKGROUND AND PURPOSE: Gene therapy may be a promising approach for treatment of brain ischemia, although protein synthesis is generally inhibited in ischemic conditions. Our goal in this study was to examine effects of brain ischemia on transgene expression of adenovirus-mediated gene transfer to ischemic brain. METHODS: Brain ischemia was produced by photochemical occlusion of the distal middle cerebral artery of spontaneously hypertensive rats (n=15). Ninety minutes after ischemia, adenoviral vectors encoding bacterial beta-galactosidase were injected into ipsilateral (nonischemic [I-n], peri-ischemic [I-p], and ischemic core [I-c] areas) and contralateral parietal (C) cortices. Cerebral blood flow before and during ischemia at each injected area was measured by laser-Doppler flowmetry. Expression of transgene was detected by histochemistry for semiquantitative scoring or by biochemical assay for quantitative analysis. RESULTS: Blood flow to the cortex decreased to 72+/-10% (mean+/-SEM) at I-n, 41+/-6% at I-p, and 23+/-3% at I-c after 10 minutes of ischemia. Expression of the reporter gene was consistently detected at C and I-n at each survival period. The semiquantitative score for transgene expression decreased according to severity of ischemia (C, 2.3; I-n, 2.6; I-p, 1.1; I-c, 0.3; mean values). beta-Galactosidase activity detected by chemiluminescent assay revealed that the values (mean+/-SEM) in the ischemic area (I-p, 15.9+/-9.2 mU/mg protein; I-c, 1.3+/-0.5) were significantly smaller than that of the nonischemic area (C, 45.4+/-6.9). Analysis of cerebral blood flow at I-p revealed that cerebral blood flow threshold for transgene expression was approximately 40% of the resting value. CONCLUSIONS: Adenovirus-mediated gene transfer into the ischemic brain provided effective expression of transgene at the nonischemic and peri-ischemic areas. Gene transfer to the ischemic brain may be a promising approach for treatment of ischemic penumbra.

Adenoviridae↗

PubMed2001

Elevated plasma homocysteine levels and risk of silent brain infarction in elderly people.

BACKGROUND AND PURPOSE: Silent brain infarction (SBI) on MRI is common in elderly people, and recent studies have demonstrated that SBI increases the risk of progression to clinically apparent stroke and cognitive decline. Therefore, an early and accurate detection of SBI and a search for potential treatable risk factors may have a significant impact on public health. METHODS: Community-dwelling elderly people aged >/=66 years who participated in the present study (n=153) underwent brain MRI and standardized physical and neuropsychological examinations as well as blood biochemistry determinations, including total plasma homocysteine (pHcy), renal function, vitamin status, and polymorphisms of the methylenetetrahydrofolate reductase gene. RESULTS: SBI was found in 24.8% of the participants. In the univariate analysis, the pHcy levels in subjects with SBI (13.6+/-4.1 micromol/L) were significantly higher (P=0.0004) than those in subjects without SBI (11.0+/-3.3 micromol/L). When pHcy levels were stratified into high (>/=15.1 mmol/L), moderate (11.6 to 15.0 mmol/L), and low (</=11.5 mmol/L) groups, age (P<0.0001), male sex (P<0.0001), the habits of cigarette smoking (P<0.0001) and of alcohol consumption (P=0.0002), and folate levels (P=0.01) were significantly associated with an elevation of pHcy levels. The elevated pHcy levels were significantly associated with SBI after individual adjustment for age, sex, hypertension, renal function, and the habits of smoking and alcohol consumption. CONCLUSIONS: pHcy level is associated with age and nutritional and other lifestyle factors, and it contributes to a risk for SBI.

Age Distribution↗

PubMed2001

Cerebral blood flow and metabolism in silent brain infarction and related cerebrovascular disorders.

The appropriate management of silent stroke requires better understanding of the haemodynamic status in the brain. However, only a few studies have examined cerebral blood flow and metabolism in subjects with silent stroke. Positron emission tomography demonstrated a slight decrease in cortical blood flow with an increase in oxygen extraction fraction (ie misery perfusion) in subjects with silent brain infarction, whereas both cerebral blood flow and oxygen metabolism decreased in patients with symptomatic brain infarction (matched hypoperfusion). These findings confirm that brain circulation is haemodynamically compromised in subjects with silent stroke. Another important point is that subcortical silent stroke may induce a reduction in cortical blood flow and metabolism by a disconnection mechanism (ie diaschisis) between the cortex and the subcortical structures. Silent infarction is not innocuous in terms of compromised cerebral circulation, which may lead to cognitive decline or subsequent clinical stroke. In the future, further developments in functional imaging will permit a more sophisticated analysis of brain circulation and metabolism in silent stroke.

Brain↗

PubMed2001

[Toxicokinetics of terephthalic acid].

In order to study the toxicokinetics of terephthalic acid(TPA) in rats, and provide scientific basis for its biological exposed index (BEI), the concentrations of urine TPA in rats after single oral administration in dose of 100 mg/kg BW were determined by high pressure liquid chromatography. The toxicokinetic parameters were computed by using 3P97 program. The results showed that the first-order kinetics and two-compartment model were noted on the elimination of TPA. The main toxicokinetic parameters were as follows: Ka = 0.51/h, T1/2ka = 0.488 h, T1/2 alpha = 2.446 h, Tpeak = 2.160 h, Ku = 0.143/h, T1/2 beta = 31.551 h, Xu(max) = 10.00 mg. The excretion rates of TPA in urine were about 50%, 52% and 53% in 0-24 h, 0-48 h and 0-72 h respectively after administration. TPA is well absorbed when given orally and rapidly eliminated via urine. Urine TPA at the end of work shift should be considered as a biomarker of exposure for the occupational workers.

Animals↗