Biomedical subjects

H Yao

Publications and source records attributed to H Yao.

At least 19 recordsLinked to original sources

PubMed2006

Appearance of a liquid crystalline nematic-isotropic critical point in a mixture system of rod- and bent-shaped molecules.

Heat capacity measurements have been made on a liquid-crystal mixture system formed from bent-shaped molecule 1,3-phenylene bis[4-(4-8-alkoxyphenyliminomethyl)benzoates] (P-8-O-PIMB) and rod-shaped molecule n-pentyl-cyanobiphenyl (5CB). The obtained results can be understood assuming that the addition of P-8-O-PIMB molecules to the 5CB system affects as a field conjugate to the nematic order parameter. The B(X)-B(4) transition can be viewed as the nematic-isotropic transition of 5CB, which is embedded in a framework of the B(4) structure of P-8-O-PIMB molecules. The present mixture system offers a rare example of the nematic-isotropic critical point, whose critical behavior has not been studied yet in detail.

Journal Article↗

PubMed2006

The intra-arterial injection of microglia protects hippocampal CA1 neurons against global ischemia-induced functional deficits in rats.

In the present study, we have attempted to elucidate the effects of the intra-arterial injection of microglia on the global ischemia-induced functional and morphological deficits of hippocampal CA1 neurons. When PKH26-labeled immortalized microglial cells, GMIR1, were injected into the subclavian artery, these exogenous microglia were found to accumulate in the hippocampus at 24 h after ischemia. In hippocampal slices prepared from medium-injected rats subjected to ischemia 48 h earlier, synaptic dysfunctions including a significant reduction of synaptic responses and a marked reduction of long-term potentiation (LTP) of the CA3-CA1 Schaffer collateral synapses were observed. At this stage, however, neither significant neuronal degeneration nor gliosis was observed in the hippocampus. At 96 h after ischemia, there was a total loss of the synaptic activity and a marked neuronal death in the CA1 subfield. In contrast, the basal synaptic transmission and LTP of the CA3-CA1 synapses were well preserved after ischemia in the slices prepared from the microglia-injected animals. We also found the microglial-conditioned medium (MCM) to significantly increase the frequency of the spontaneous postsynaptic currents of CA1 neurons without affecting the amplitude, thus indicating that MCM increased the provability of the neurotransmitter release. The protective effect of the intra-arterial injected microglia against the ischemia-induced neuronal degeneration in the hippocampus was substantiated by immunohistochemical and immunoblot analyses. Furthermore, the arterial-injected microglia prevented the ischemia-induced decline of the brain-derived neurotrophic factor (BDNF) levels in CA1 neurons. These observations strongly suggest that the arterial-injection of microglia protected CA1 neurons against the ischemia-induced neuronal degeneration. The restoration of the ischemia-induced synaptic deficits and the resultant reduction of the BDNF levels in CA1 neurons, possibly by the release of diffusible factor(s), might thus contribute to the protective effect of the arterial-injection of microglia against ischemia-induced neuronal degeneration.

Animals↗

PubMed2006

Convection and diffusion in charged hydrated soft tissues: a mixture theory approach.

The extracellular matrix of cartilage is a charged porous fibrous material. Transport phenomena in such a medium are very complex. In this study, solute diffusive flux and convective flux in porous fibrous media were investigated using a continuum mixture theory approach. The intrinsic diffusion coefficient of solute in the mixture was defined and its relation to drag coefficients was presented. The effect of mechanical loading on solute diffusion in cartilage under unconfined compression with a frictionless boundary condition was analyzed numerically using the model developed. Both strain-dependent hydraulic permeability and diffusivity were considered. Analyses and results show that (1) In porous media, the convective velocity for each solute phase is different. (2) The solute convection in tissue is governed by the relative convective velocity (i.e., relative to solid velocity). (3) Under the assumption that all the frictional interactions among solutes are negligible, the relative convective velocity for alpha-solute phase is equal to the relative solvent velocity multiplied by its convective coefficient (H (alpha)) which is also known as the hindrance factor in the literature. The relationship between the convective coefficient and the relative diffusivity of solute is presented. (4) Solute concentration profile within the cartilage sample depends on the phase of dynamic compression.

Compressive Strength↗

PubMed2006

RhoC GTPase is required for PC-3 prostate cancer cell invasion but not motility.

It is projected that in 2005, approximately 220 900 men will be newly diagnosed with carcinoma of the prostate (CaP). Men who are diagnosed with locally advanced or metastatic disease undergo androgen ablation therapy and most will relapse and progress within 18 months. Metastasis to bone is the major clinical concern during CaP progression, as it is associated with intractable pain, bone fracture and paralysis resulting from spinal cord compression. Therefore, an understanding of the key mechanisms involved in CaP cell bone metastasis is vital to development of novel treatments. The Rho GTPases are molecular switches involved in cell survival, motility and invasion. Increased expression of RhoC GTPase is linked to enhanced metastatic potential in multiple cancers; however, the role of RhoC GTPase in CaP metastasis has not been addressed. In the current study, we demonstrate that RhoC GTPase is expressed and active in PC-3 CaP cells. RhoC inhibition, either pharmacologically with C3 exotransferase or molecularly through expression of a dominant-negative RhoC, promotes IGF-I stimulated random motility but decreases in vitro invasion and experimental metastases. Inhibition of RhoC activity results in drastic morphologic changes and alterations in the expression and distribution of focal adhesion-related proteins. These data suggest that RhoC inhibition leads to activation of other GTPases involved in nondirected motility and that expression of active RhoC is required for the invasive phenotype of PC-3 cells.

ADP Ribose Transferases↗

PubMed2006

The placentas of patients with severe acute respiratory syndrome: a pathophysiological evaluation.

AIMS: The pathology of the placentas delivered from pregnant women who had severe acute respiratory syndrome (SARS) in Hong Kong was studied. METHODS: The pathology of the placentas was retrospectively studied in detail and compared with control sets. The clinical data of the women and neonates were also reviewed. RESULTS: A total of seven placentas were studied. The placentas from two women convalescent from SARS in the first trimester were normal. In three placentas delivered in the acute stage of SARS, there were increases in intervillous or subchorionic fibrin which might be related to disturbances in maternal placental blood flow due to the hypoxic respiratory disease. Extensive fetal thrombotic vasculopathy (FTV) with sharply demarcated zones of avascular fibrotic villi was noted in the placentas of two patients convalescent from SARS in the third trimester. Both pregnancies had intrauterine growth retardation, oligohydramnios and newborns small for gestation. The aetiology of the FTV might be related to thrombotic tendency due to SARS or placental hypoxia. CONCLUSIONS: This report highlights placental pathology that was probably the result of pathophysiological alteration of the maternal fetal unit during SARS. Further studies are required to delineate the relationship between severe maternal respiratory disease, placental pathology and pregnancy outcome.

Adult↗

PubMed2005

FK506 enhances triptolide-induced down-regulation of cyclooxygenase-2, inducible nitric oxide synthase as well as their products PGE2 and NO in TNF-alpha-stimulated synovial fibroblasts from rheumatoid arthritic patients.

OBJECTIVE: To explore the effects of FK506 on the inhibition of cell proliferation and the expression of cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS) and their products PGE subset2 and NO in TNF-alpha-stimulated human rheumatoid arthritis synovial fibroblasts (RASF) treated with triptolide (TP), and to study the mechanisms involved when combining FK506 and TP in RA therapy. MATERIALS AND METHODS: RASF used in the experiments were obtained from the synovial tissue of patients with RA before being cultured. RASF were pretreated with FK506 (10 approximately 1000 nM) for 2 hours before being stimulated with TNF-alpha (20 ng/ml) in the presence or absence of TP (10 ng/ml) . RASF proliferation was determined by [3 supersetH]-TdR incorporation. Production of PGE subset2 and NO in culture supernatants of RASF was detected by competitive ELISA and enzymatic reduction of nitrate, respectively. Expressions of COX-2 and iNOS mRNA in RASF were analyzed by semi-quantitative RT-PCR. Expressions of COX-2 and iNOS protein were estimated by Western-blot and a cellular enzyme immunoassay. NFkappaB activity in whole-cell extract of treated RASF was also measured using an ELISA-based method. RESULTS: Neither FK506 nor TP at a lower concentration (10 ng/ml) affected TNF-alpha-induced COX-2 and iNOS expressions or PGE subset2 and NO productions in synovial cells. Combined treatment of FK506 and a lower concentration of TP (10 ng/ml) reduced both COX-2 and iNOS mRNA and protein expression, and correspondingly reduced PGE subset2 and NO produced by synovial fibroblasts. This effect was highly correlated with FK506 concentration (10 approximately 1000 nM). NFkappaB activity in TNF-alpha-stimulated synovial cells was suppressed more profoundly by FK506 plus TP (10 ng/ml) than by TP (10 ng/ml) alone. However, no change was observed regarding the inhibition of synovial cell proliferation after combined treatment of FK506 and TP. CONCLUSION: FK506 enhanced TP-mediated down-regulation of COX-2 and iNOS as well as their products PGE subset2 and NO in human TNF-alpha-stimulated RASF by more profoundly suppressing the activity of NFkappaB.

Arthritis, Rheumatoid↗

PubMed2005

Association of RANTES with the replication of severe acute respiratory syndrome coronavirus in THP-1 cells.

BACKGROUND: Severe acute respiratory syndrome (SARS) is a novel infectious disease which is characterized by an overaggressive immune response. Chemokines are important inflammatory mediators and regulate disease due to viral infection. In previous study, we found that SARS-CoV has the ability to replicate in mononuclear cells. In present work, we sought to characterize the replication of SARS-CoV at the presence of RANTES in THP-1 cells. METHODS: To determine whether RANTES play an role in the process of SARS, THP-1 cells were incubated with heat-inactivated SARS-CoV and ELISA was used to test RANTES levels in the supernatants; Then the effect of dexamethasone on the induced secretion was evaluated. Real-time PCR was used to investigate the effort of RANTES on the replication of SARS-CoV in vitro. Macrophages, induced by THP-1 cells, were used as cell model. FINDINGS: Inactive SARS-CoV could induce THP-1 cells secret RANTES and this increase effect could not be suppressed by DXM. RANTES itself could inhibit the replication of SARS-CoV in THP-1 cells when it was added into the culture before or at the same time with the virus; No inhibition effect was shown when RANTES were added into the culture after SARS-CoV infected the cells.

Animals↗

PubMed2005

Calorimetric investigations of liquid-crystal compounds exhibiting almost no layer-shrinkage behavior through the smectic-A-smectic- C* transition.

Heat-capacity measurements have been made on liquid-crystal compounds exhibiting almost no layer-shrinkage (NLS) behavior through the Sm-A-Sm- C(*) phase transition. The transition was found to be second order for two of the substances studied. It was found that the heat-capacity anomaly accompanying a second-order Sm-A-Sm- C(*) transition with NLS behavior is quite similar to that observed for typical antiferroelectric liquid crystals of the 4-(1-methylheptyloxycarbonyl)phenyl 4'-octyloxybiphenyl-4-carboxylate (MHPOBC) group, showing three-dimensional (3D) XY behavior in the vicinity of the transition. On the other hand, for one compound which shows a weakly first-order transition, the anomaly is almost symmetric above and below T(c) , with a significant fluctuation effect in the Sm-A phase. For this compound, the critical behavior of the heat-capacity anomaly is almost tricritical in the immediate vicinity of T(c) , while away from T(c) the behavior can be explained with the 3D XY model. This suggests that the underlying transition with the 3D XY critical behavior is driven to almost being tricritical but remaining weakly first order. No indication of low-dimensional character in the critical behavior was found in both cases.

Journal Article↗

PubMed2005

Postischemic gene transfer of midkine, a neurotrophic factor, protects against focal brain ischemia.

Gene therapy may be a promising approach for treatment of brain ischemia. In this study, we examined the effect of postischemic gene transfer of midkine, a heparin-binding neurotrophic factor, using a focal brain ischemia model with the photothrombotic occlusion method. At 90 min after induction of brain ischemia in spontaneously hypertensive rats, a replication-deficient recombinant adenovirus encoding mouse midkine (AdMK, n=7) or a control vector encoding beta-galactosidase (Adbetagal, n=7) was injected into the lateral ventricle ipsilateral to ischemia. At 2 days after ischemia, we determined infarct volume by 2,3,5-triphenyltetrazolium chloride staining. There were no significant differences in cerebral blood flow 1 h after ischemia between AdMK and Adbetagal groups. Infarct volume of AdMK group was 51+/-27 mm3, which was significantly smaller than that of Adbetagal group (86+/-27 mm3, P<0.05). TUNEL-positive and cleaved caspase-3-positive cells in the periischemic area of AdMK-treated rats were significantly fewer than those in Adbetagal-treated rats, suggesting that the reduction of infarct volume by midkine was partly mediated by its antiapoptotic action. Thus, gene transfer of midkine to the ischemic brain may be effective in the treatment of brain ischemia.

Adenoviridae↗

PubMed2005

The tumor suppressor adenomatous polyposis coli gene is associated with susceptibility to schizophrenia.

The etiology of schizophrenia is unclear, although family, twin, and linkage studies implicate genetic factors. Here, we identified adenomatous polyposis coli (APC), a tumor suppressor gene, as a risk factor for schizophrenia. We compared leukocytic gene expression patterns of six pairs of patients with schizophrenia and healthy controls by microarray. APC expression levels were significantly increased in all patients compared to healthy controls. To confirm the findings of microarray analysis, we measured expression levels of APC in the leukocytes from 30 relapse patients taking antipsychotic medication, 29 first-episode drug-naïve patients, and 30 healthy controls using real-time quantitative reverse transcription (RT)-polymerase chain reaction (PCR). APC expression levels were significantly increased in leukocytes of schizophrenics both taking and not taking antipsychotic medication and hence the increase of APC expression was not due to antipsychotic medication. APC is located at 5q21-22, which has been previously reported to be linked with schizophrenia. Further, we performed the transmission disequilibrium test (TDT) and TDT based on haplotypes to search for the association between schizophrenia and APC by examining 163 parent-offspring trios of Chinese descent. We analyzed three single-nucleotide polymorphisms (SNPs) (rs2229992, rs42427, rs465899) at the exon region of APC. TDT showed that the three SNPs are significantly associated with schizophrenia (TDT chi(2)=4.23, P<0.05; 4.15, P<0.05; 8.49 P<0.01, respectively; HHRRchi(2)=5.54, P<0.05; 4.40, P<0.05; 9.79, P<0.01, respectively). We found a significant association between the APC haplotypes from rs2229992-rs42427-rs465899 and schizophrenia (Global chi(2)=44.376,df=7, P<0.001). The C-A-T haplotype has a frequency of more than 57% and has a strong association with schizophrenia (chi(2)=15.04, P<0.001). These results indicate that the APC may be a candidate gene conferring susceptibility to schizophrenia and also may be associated with reduced vulnerability to cancer in schizophrenia.

Adenomatous Polyposis Coli Protein↗

PubMed2005

[Aortic valve replacement presence of anti-Jr(a) antibody].

A 65-year-old female with a heart murmur developed progressive symptom of chest oppression. She was diagnosed severe aortic valve stenosis with echocardiogram. Antibody screening revealed anti-Jr(a) antibody. Preoperatively, erythropoietin was administered. Over 14 days, a total 1,000 ml of her blood was drawn and stored for autologous transfusion. The aortic valve was replaced with ATS mechanical valve [18 mm advanced performance (AP)]. Following surgery, her stored blood was administered to him. But her HCT was 17% on the 1st postoperative day. Frozen thawed red cells were transferred 7th postoperative day.

Aged↗

PubMed2004

Expression of FAP-1 by human colon adenocarcinoma: implication for resistance against Fas-mediated apoptosis in cancer.

Although colon carcinoma cells express Fas receptors, they are resistant to Fas-mediated apoptosis. Defects within the intracellular Fas signal transduction may be responsible. We investigated whether the Fas-associated phosphatase-1 (FAP-1), an inhibitor of Fas signal transduction, contributed to this resistance in colon carcinomas. In vivo, apoptosis of cancer cells was detected in situ using terminal deoxynucleotidyltransferase-mediated dUTP nick-end labelling (TUNEL). FAP-1, FasR, and Fas ligand (FasL) were detected using immunohistochemistry. In vitro, colon carcinoma cells were primarily cultured, and their sensitivity to Fas-mediated apoptosis was evaluated by treatment with agonistic anti-FasR CH11 IgM monoclonal antibody in the presence or absence of synthetic Ac-SLV (serine-leucine-valine) tripeptide. Fas-associated phosphatase-1 expression was detected in 20 out of 28 colon adenocarcinomas. In vivo, a positive correlation between the percentage of apoptotic tumour cells and the number of FasL-positive tumour infiltrating lymphocytes was observed in FAP-1 negative cancers, but not in FAP-1-positive ones. Primarily cultured colon cancer cells, which were refractory to CH-11-induced apoptosis, had higher expression of FAP-1 on protein and mRNA levels than the sensitive group. Resistance to Fas-mediated apoptosis in tumour cells could be abolished by Ac-SLV tripetides. Fas-associated phosphatase-1 expression protects colon cancer cells from Fas-mediated apoptosis, and blockade of FAP-1 and FasR interaction sensitises tumour cells to Fas-dependent apoptosis.

Adenocarcinoma↗

PubMed2004

Experimental investigations of one liquid-crystal compound exhibiting the no-layer-shrinkage effect near the Sm-A-Sm- C(*) transition.

Three experimental probes have been employed to investigate the nature of the smectic- A -smectic- C ( Sm-A-Sm- C(*) ) phase transition of one liquid-crystal compound showing almost no layer-shrinkage effect through the transition. Results from both x-ray diffraction and optical studies indicate that the compound exhibits a crossover behavior of different molecular packing arrangements within the bulk Sm-A phase window. The calorimetry results show a significant critical anomaly near the Sm-A-Sm- C(*) transition, although it was found to be weakly first order.

Journal Article↗

PubMed2003

Combining inference from evolution and geometric probability in protein structure evaluation.

Starting from the hypothesis that evolutionarily important residues form a spatially limited cluster in a protein's native fold, we discuss the possibility of detecting a non-native structure based on the absence of such clustering. The relevant residues are determined using the Evolutionary Trace method. We propose a quantity to measure clustering of the selected residues on the structure and show that the exact values for its average and variance over several ensembles of interest can be found. This enables us to study the behavior of the associated z-scores. Since our approach rests on an analytic result, it proves to be general, customizable, and computationally fast. We find that clustering is indeed detectable in a large representative protein set. Furthermore, we show that non-native structures tend to achieve lower residue-clustering z-scores than those attained by the native folds. The most important conclusion that we draw from this work is that consistency between structural and evolutionary information, manifested in clustering of key residues, imposes powerful constraints on the conformational space of a protein.

Evolution, Molecular↗

PubMed2003

New insight into deformation-dependent hydraulic permeability of gels and cartilage, and dynamic behavior of agarose gels in confined compression.

Equilibrium, creep, and dynamic behaviors of agarose gels (2.0-14.8%) in confined compression were investigated in this study. The hydraulic permeabilities of gels were determined by curve-fitting creep data to the biphasic model (J. Biomech. Eng. 102 (1980) 73) and found to be similar in value to those published in the literature (AIChE J. 42 (1996) 1220). A new relationship between intrinsic permeability and volume fraction of water was found for agarose gel, capable of predicting deformation-dependent permeabilities of bovine articular cartilage and 2% agarose gel published in literature. This relationship is accurate for gels and cartilage over a wide range of permeabilities (four orders of magnitude variation). The dynamic stiffness of the gels increases with gel concentration and loading frequency (0.01-1.0Hz). The increase in dynamic stiffness with loading frequency is less pronounced for gels with higher concentrations. The results of this study provide a new insight into deformation-dependent permeability behavior of agarose gel and cartilage, and are important for understanding biological responses of cells to interstitial fluid flow in gel or in cartilage under dynamic mechanical loading.

Cartilage, Articular↗

PubMed2003

The role of HCO3(-)-dependent mechanisms in pHi regulation during O2 deprivation.

We have reported in our previous work that, in the absence of HCO(3)(-), Na(+)/H(+) exchanger is responsible for an anoxia-induced alkalinization in hippocampal CA1 neurons. HCO(3)(-)-dependent mechanisms have been reported to play a key role in pH(i) regulation in nerve cells, but how their function is affected by O(2) deprivation has not been well studied. In this work, pH(i) measurements (obtained from dissociated neurons loaded with carboxy-seminaphthorhodafluor-1 and using confocal microscopy) and whole-cell patch clamp recording techniques were used to investigate the role of HCO(3)(-)-dependent membrane exchangers on CA1 neurons during O(2) deprivation. Anoxia (5 min) induced a small acidification in neurons in the presence of HCO(3)(-) and this acidification was changed to a significant alkalinization when neurons were bathed with Hepes buffer or when 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid was applied in a HCO(3)(-) solution, indicating that HCO(3)(-)-dependent mechanisms were involved. A marked anoxia-induced acidification (0.33+/-0.11 pH unit) was seen when the Na(+)/H(+) exchange was blocked with 3-(methylsulfonyl-4-piperidino-benzoyl)-guanidine methanesulfonate in the presence of HCO(3)(-), but the same anoxia did not cause a significant pH(i) change in a Na(+) free, HCO(3)(-) solution, suggesting that the anoxia-induced acidification in the presence of 3-(methylsulfonyl-4-piperidino-benzoyl)-guanidine methanesulfonate is dependent on both Na(+) and HCO(3)(-). Furthermore, anoxia did not cause a significant pH(i) change when both 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid and 3-(methylsulfonyl-4-piperidino-benzoyl)-guanidine methanesulfonate were present. Current clamp recordings showed a significant membrane depolarization following anoxia in HCO(3)(-) solution but not in Hepes buffer. Our data suggest that, in hippocampal neurons: a) pH(i) regulation during O(2) deprivation is affected not only by metabolism but also by membrane exchangers, and b) besides the activation of Na(+)/H(+) exchange, anoxia activates a 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid-sensitive, Na(+)-dependent acid loader (possibly electrogenic).

Animals↗

PubMed2003

Genetic analysis on HLA loci in Japanese patients with abdominal aortic aneurysm.

PURPOSE: autoimmunity has been proposed as one of the pathogenesis of abdominal aortic aneurysm (AAA). There is also a likelihood that when aorto-iliac occlusive disease (AIOD) coexists with AAA, some other occlusive atherosclerotic diseases, such as ischemic heart disease and cerebrovascular disease, may develop, leading to a very poor long-term prognosis. Previous studies using serological HLA typing showed that HLA-DR15 was a risk factor for AAA. In this study, we performed HLA-DNA typing by PCR to clarify the relationship between AAA and HLA genotypes in Japanese patients with AAA. In addition, we analyzed whether HLA genotypes are involved in the pathogenesis of AIOD. RESULTS: we examined 78 HLA genotypes of class I (HLA-A and -B) and class II (HLA-DR) and found that 60.4 and 30.4% of 49 AAA patients had HLA-A2 and HLA-B61, respectively. These frequencies were significantly higher than those in control individuals (HLA-A2, p < 0.05; HLA-B61, p < 0.005). We also found that 55.6% of nine AAA patients with AIOD had both HLA-B52 and HLA-DR B1*1502. In contrast, only 10.0% each of 40 AAA patients without AIOD showed HLA-B53 or HLA-DR B1*1502. CONCLUSIONS: this study showed that HLA A-2 and HLA B-61, but not HLA DR-15, were important genetic risk factors for the development of AAA among the Japanese population. We also found high frequencies of HLA-B52 and HLA-DR B1*1502 in the AAA patients with AIOD than in those without, although this must be confirmed using a larger number of AAA patients with AIOD.

Aged↗

PubMed2003

[Thymic carcinoma (mixed small cell undifferentiated squamous cell carcinoma); report of a case].

A 52-year-old man was admitted to our hospital on October, 1997 with complains of left anterior chest pain. A chest X-ray and computed tomography on admission showed evidence of a mass in the left anterior mediastinum. The patient was treated with combination chemotherapy [cisplatin (CDDP), etoposide (VP-16)] and radiation therapy (2 gray x 25 days), preoperatively. Median sternotomy revealed a tumor invading into the left anterior chest wall, the pericardium, and partial pleura. The tumor was extirpated with combined resection of invaded organs. Microscopically and immunohistochemically, the tumor was diagnosed mixed small cell and undifferentiated squamous cell carcinoma documented by Snover et al. The patient was discharge on March 1998, but 2 years later after operation, he was dead by recurrent. We reported a rare case of thymic carcinoma.

Aged↗