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Biomedical subjects

J Hao

Publications and source records attributed to J Hao.

At least 55 records · Page 3Linked to original sources

Critical loads of acidity for surface waters in China.

For further control of acid rain and sulphur dioxide pollution, the Chinese government has designated the Acid Rain Control Zone and the Sulphur Dioxide Pollution Control Zone for those areas that are, or could become, affected by acid deposition or ambient sulphur dioxide concentrations. One of the most important principles for designating the Acid Rain Control Zone is that the critical load is exceeded by the sulphur deposition. Through the steady-state water chemistry method (SSWC), critical loads of acidity for surface waters were mapped based on available data. Results show that surface waters sensitive to acid deposition, i.e. surface waters with low critical loads, are mainly found in north-east China, on the Tibetan Plateau, and in north-west China. Compared with the critical loads of soils, critical loads of surface waters are usually higher in almost all areas in China. The reason for very low critical loads of surface waters in some regions dominated by soils geologically not sensitive to acid deposition may be attributed to the low temperature, high altitude and low runoff. In contrast, surface waters in south China are not susceptible to acid deposition, and so far acidification of surface water has not been found in spite of the heavy acid rain. As can be seen from the critical load exceedance map, nearly 10% of the surface waters are subject to risk of acidification in 1995.

Acid Rain↗

The effect of coriaria lactone on NMDA receptor mediated currents in rat hippocampal CA1 neurons.

To investigate the exact mechanism of epileptogenesis induced by coriaria lactone (CL), the effect of CL on NMDA receptor mediated current (IAsp) in rat hippocampal CA1 neurons was investigated by using nystatin perforated whole-cell patch clamp. 10(-6)-10(-4) mol/L Asp acted on NMDA receptors and elicited an inward current (IAsp) at a holding potential (VH) of -40 mV in presence of 10(-6) mol/L glycine and absence of Mg2+ extracellularly. CL enhanced NMDA receptor mediated current induced by Asp, but had no effect on threshold concentration, EC50, Hill coefficient as well as maximal-effect concentration and reversal potential of IAsp. The effect had no relationship with holding potential. These results showed that CL could enhance NMDA receptor mediated current to increase [Ca2+]i of neurons by acting on Gly site, thereby inducing epilepsy.

Animals↗

Screening of novel epilepsy-related genes and isolation and identification of cDNAs.

Twenty cDNA differential fragments were isolated from the hippocampus of rats in epileptic state using mRNA differential display technique. Four fragments were sequenced and compared with the known sequences in the Genebank, which showed that ERG8, ERG11, ERG12 had no significant identity to any known sequences; ERG14 had 64%-69% identity to microtubulin-associated protein of the rat. Because the differential expression of these genes was caused by epilepsy inducer coriaria lactone (CL) and anti-epilepsy drug MK-801 and ERG8 might be a novel candidate epilepsy gene; ERG11 and ERG12 might be novel candidate anti-epilepsy genes. Since the microtubulin-associated protein is closely associated with the collateral sprouting of mossy fibers in the hippocampus of seizured rat, the high expression of ERG14 in the early stage of epilepsy might predict the growth of axon and formation of synapse.

Animals↗

Increased interleukin-8 (IL-8) expression is related to aseptic loosening of total hip replacement.

Aseptic loosening is an increasing problem in total hip replacement (THR). Chronic inflammatory reaction against implant wear particle results in collageno- and osteolysis, leading to loosening of the implant. Cytokines are known to play a major role in this particular inflammatory process. The aim of the present study was to examine interleukin-8 (IL-8) in the synovial-like interface membrane (SLIM) and pseudocapsular tissue of THRs and to compare it to normal knee synovial membrane. Eleven patients suffering from aseptically loosened THRs were included. All the SLIM and pseudocapsular tissue samples were obtained during revision operations. Ten control samples of normal synovium were collected per arthroscopy from the superior recessus of the knee. For immunohistochemical IL-8 detection, polyclonal mouse anti-human immunoglobulin (Ig)G1 IL-8-primary antibody was used with the alkaline phosphatase anti-alkaline phosphatase (APAAP) method. Results were quantitated using the Vidas image analysis system. The highest count levels (mean +/- SEM) were detected in SLIM tissue (386+/-82 cells/mm2). The difference was statistically significant compared with pseudocapsular tissue (193+/-36 cells/mm2) and control samples (18+/-5 cells/mm2). Count levels in control tissue were on average 5% of the SLIM tissues values. The present study determines for the first time the cellular origin of IL-8 in aseptically loosened THRs and also quantitates the IL-8-producing cells in the periprosthetic tissue. The results reveal a high rise in IL-8 concentration in SLIM and in synovial tissues. This finding moves us one step forward in solving the complex network of multiple factors affecting loosening of hip implants.

Adult↗

Effect of chronic AT(1) receptor blockade on cardiac Smad overexpression in hereditary cardiomyopathic hamsters.

OBJECTIVE: As the pharmacological suppression of angiotensin has been associated with cardioprotective effects in cardiomyopathy, our primary aim was to determine whether the expression of Smad protein components of the cardiac TGF-beta signaling cascade is modulated by chronic AT(1) receptor blockade. Furthermore, we examined the relationship between cardiac Smad protein expression and altered collagen turnover in the cardiomyopathic heart. METHODS: Male UM-X7. 1 cardiomyopathic (CMP) Syrian hamsters at early (65 days) and late (200 days) stages of cardiomyopathy were subjected to 4 week losartan (15 mg/kg/day) treatment. Expression of left ventricular (LV) receptor-activated (Smad 2) and common-mediator (Smad 4) Smads from control (F1-beta strain) hamsters, non-treated cardiomyopathic (CMP), and losartan-treated CMP animals was assessed. Collagen turnover, including fibrillar collagen synthesis/accretion and cardiac MMP activity was assessed. RESULTS: Elevated mRNA abundance of fibrillar collagens and ANF were present in cardiomyopathic hearts and these trends were normalized in the early stage losartan-treated group. 4-Hydroxyproline and zymographic assays confirmed fibrosis and elevated MMP-1 and -2 activities in CMP hearts. Losartan treatment was associated with a modest reduction of cardiac 4-hydroxyproline concentration, and a significant reduction of both MMP-1 and MMP-2 activities. While TGF-beta(1) mRNAs were elevated in both CMP groups vs. controls, total TGF-beta protein content was not different in CMP vs. controls. In LV preparations containing nuclear extract, elevated Smad 2 and Smad 4 protein expression was noted in cardiomyopathic hearts vs. controls. Losartan treatment of late-stage CMP hamsters was associated with a significant reduction in Smad 2 and a modest reduction of Smad 4 protein expression vs. untreated CMP samples. CONCLUSIONS: Altered cardiac Smad expression, present in both early and late stage cardiomyopathy, is positively correlated with the occurrence of cardiac fibrosis and elevated collagen turnover in failing CMP hearts. Four week AT(1) blockade is associated with normalized expression of cardiac Smad 2 proteins, and these changes occur in parallel with some aspects of collagen turnover in failing cardiomyopathic hearts.

Analysis of Variance↗

Nociceptin/orphanin FQ in spinal nociceptive mechanisms under normal and pathological conditions.

Nociceptin and its receptor are present in dorsal spinal cord, indicating a possible role for this peptide in pain transmission. The majority of functional studies using behavioral and electrophysiological studies have shown that nociceptin applied at spinal level produces antinociception through pre- and post-synaptic mechanisms. The spinal inhibitory effect of nociceptin is not sensitive to antagonists of opioid receptors such as naloxone. Thus, nociceptin-induced antinociception is mediated by a novel mechanism independent of activation of classic opioid receptors. This has raised the possibility that agonists of the nociceptin receptor may represent a novel class of analgesics. Supporting this hypothesis, several groups have shown that intrathecal nociceptin alleviated hyperalgesic and allodynic responses in rats after inflammation or partial peripheral nerve injury. Electrophysiological studies have also indicated that the antinociceptive potency of spinal nociceptin is maintained or enhanced after nerve injury. It is concluded that the predominant action of nociceptin in the spinal cord appears to be inhibitory. The physiological role of nociceptin in spinal nociceptive mechanisms remains to be defined. Moreover, further evaluation of nociceptin as a new analgesic calls the development of non-peptide brain penetrating agents.

Analgesics↗

Interaction between angiotensin II and Smad proteins in fibroblasts in failing heart and in vitro.

Angiotensin II (angiotensin) and transforming growth factor (TGF)-beta(1) play an important role in cardiac fibrosis. We examined Smad proteins in 8-wk post-myocardial infarction (MI) rat hearts. AT(1) blockade (losartan) attenuated the activation of TGF-beta(1) in target tissues. Losartan administration (8 wk, 15 mg. kg(-1). day(-1)) normalized total Smad 2 overexpression in infarct scar and remnant heart tissue and normalized Smad 4 in infarct scar. Phosphorylated Smad 2 (P-Smad 2) staining decreased in cytosol from failing heart vs. the control, which was normalized by losartan, suggesting augmented P-Smad 2 movement into nuclei in untreated failing hearts. Using adult primary rat fibroblasts treated with angiotensin (10(-6) M), we noted rapid translocation (15 min) of P-Smad 2 into the nuclei from the cytosol. Nuclear P-Smad 2 protein level increased with angiotensin treatment, which was blocked by losartan. We conclude that angiotensin may influence total Smad 2 and 4 expression in post-MI heart failure and that angiotensin treatment is associated with rapid P-Smad 2 nuclear translocation in isolated fibroblasts. This study suggests that cross talk between angiotensin and Smad signaling is associated with fibrotic events in post-MI hearts.

Active Transport, Cell Nucleus↗

Modeling traffic-related air pollution in street canyons of Beijing.

It is important to develop a general model to accurately simulate the air pollution in urban street areas. In this paper, the Operational Street Pollution Model (OSPM) initially developed in Denmark is tested with measured data from a relatively wide and open street in Beijing. Major factors influencing the dispersion, such as emission factors, stationary source emissions, and solar radiation, are analyzed. Results show that the model can reflect the basic dispersion pattern in the street but gives systematically higher concentrations. After modifications to estimate street-level wind speed in the model, performance is obviously improved.

Air Movements↗

Actions of bovine plasma fibronectin on cultured human dental pulp cells.

OBJECTIVE: Fibronectin (FN) has been shown to play a crucial role in odontoblast differentiation, and it is involved in the repair of dentine and pulp. The responsiveness of human dental pulp (HDP) cells to bovine plasma FN was investigated. MATERIALS AND METHODS: After isolation and selection noncarious freshly extracted third molars in vitro, HDP cells were incubated for 72 hours one of four concentrations (10, 20, 40, 80 micrograms/ml) of bovine plasma FN with Dulbecco's modified eagle medium (DMEM) containing 1% fetal calf serum (FCS). We examined cell proliferation (using an MTT assay), DNA synthesis (using incorporation of [3H]-thymidine), the cell area, and alkaline phosphatase (ALPase) activity of the culture supernatant. The expression of FN, types I and III collagens, binding of lectins concanavalin(ConA), or wheat germ agglutinin (WGA) in vitro was examined by means of immunocytochemistry. The expression degree and the cell area were analyzed semi-quantitatively with an image processing and analysis system. RESULTS: After 72 hours, HDP cells appeared contracted and smaller in the absence of FN when compared to cells incubated with FN. HDP cells were in spread state with all four concentrations of FN. FN (20, 40 micrograms/ml) stimulated cell proliferation, promoted incorporation of [3H]-thymidine, and increased the levels of ALPase activity in supernatant. The binding of ConA, the expression of type I collagen, and FN were significantly increased, while the binding of WGA, and the expression of type III collagen were significantly decreased in the FN (40, 80 micrograms/ml) groups when compared to the FN (10, 20 micrograms/ml) groups. CONCLUSION: These findings suggest that HDP cells utilize FN for attachment and subsequent spreading. FN might have mitogenic activity and some role in the regulation of differentiation of pulp cells into odontoblasts.

Alkaline Phosphatase↗

[Modified total cavopulmonary connection for treating patients with functional single ventricle].

OBJECTIVE: To modify the classic procedure for better surgical results of total cavopulmonary connection (TCPC). METHODS: Modified TCPC was performed in 13 patients with functional single ventricle. In the modified TCPC procedure, the distal end of the superior vena cava (SVC) was connected with the upper edge of the right pulmonary artery (RPA) with the anastomosis orifice near the left side, and the proximal end with the lower edge of RPA with the anastomosis orifice near the right side. Among them, intra-atrial tunnel was established with a partial tube of PTFE using the lateral tunnel technique in 8 patients, and the distal end of the inferior vena cava (IVC) was directly connected with the lower edge of RPA using extracardiac conduit in the beating heart in 5. RESULTS: One patient (7.7%) died early. Twelve patients survived and had the SatO(2) (94.6 +/- 1.2)% postoperatively while inspiring air. Angiography showed that most blood from IVC enters the right lung and most blood from SVC the left lung. No late mortality was seen during the follow up for 6 months to 2 years and 2 months. NYHA class I was noted in 10 patients and class II in 2. Echocardiography showed that left ventricular volume reduced significantly and ventricular function was normal. CONCLUSIONS: Modified TCPC produces optimal blood flow between the two lungs, elevates postoperative Sat O(2) effectively, decreases ventricular volume load and improves ventricular functions.

Adolescent↗

[Surgical correction of complete atrioventricular septal defect with tetralogy of Fallot].

OBJECTIVE: To report the surgical correction of complete atrioventricular septal defect with tetralogy of Fallot (AVSD-TOF). METHODS: Six consecutive patients aged 3 - 9 years underwent correction of complete AVSD-TOF. The two-patch technique for atrioventricular septal defect was used. The ventricular septal defect was closed through a right ventriculotomy and right atriotomy in each case. The commissure between the superior and inferior bridging leaflets of the left portion of the common atrioventricular valve was closed in each patient. RVOT obstruction was relieved by a transannular autologous pericardium with monocuspid valve. RESULTS: Postoperative complications included respiratory failure in 1 patient, low cardiac output syndrome in 1, and MOF in 1. There was one mortality because of MOF in the early postoperative period. Five survivors were followed up from 6 months to 5.5 years (mean 2.3 years). There was no late mortality and only one patient had mild left atrioventricular valve regurgitation. NYHA cardiac function was class I in 4 patients and class II in 1. CONCLUSIONS: AVSD-TOF can be corrected using the two-patch technique and closure of the ventricular septal defect through a combined approach using a right ventriculotomy and right atriotomy. Routine closure of the commissure of the left portion of the atrioventricular valve results in a low incidence of regurgitation. Good functional result can be achieved in most patients postoperatively.

Cardiac Surgical Procedures↗

[Effect on keratocyte-mediated collagen degradation by Pseudomonas aeruginosa].

OBJECTIVE: To study the pathogenesis of cornea melting (ulceration) by pseudomona (P) aeruginosa for instruction of clinical treatment. METHODS: Type I collagen gels with or without suspended keratocytes were incubated for 24 hours under medium containing sterile P. aeruginosa culture broth. Native collagen fibrils were removed from the media by ultrafiltration. The ultrafiltrates were then hydrolyzed, and the amount of hydroxyproline was measured spectrophotometrically. The effect of a synthetic matrix metalloproteinase (MMP) inhibitor, Galardin, on collagen degradation was also examined. RESULTS: P. aeruginosa broth induced type I collagen gel degradation directly. In the presence of keratocytes, degradation by P. aeruginosa broth was enhanced. Galardin significantly reduced the amount of collagen degraded by P. aeruginosa culture broth, no matter keratocytes were present or not. CONCLUSION: P. aeruginosa culture broth directly degrades type I collagen and also increases keratocyte-mediated collagen degradation. The result is helpful to the clinical treatment of cornea melting caused by P. aeruginosa, and the mechanism should be further studied.

Animals↗

[Induction of skin immune tolerance of mouse to rat xenogeneic transplantation].

OBJECTIVE: To explore a moderate and effective project which will be clinically suitable to induce donor-specific tolerance across xenogeneic barriers. METHODS: 4 x 10(7) Lewis rat bone marrow cells were infused to 300 rad total body irradiated (TBI) C57BL/6 (B6) mice, combined with intraperitoneal administration of cyclophosphamide (CTX) and intravenous injection of anti-mouse CD4 monoclonal antibody. Recipient B6 mice were characterized for the tolerance status with donor Lewis rat skin graft, mixed lymphocyte reaction (MLR), and delayed-type hypersensitivity (DTH) assays after 30 days. Adoptive transfer and the effect of IL-2 on MLR were detected to further explore the tolerance mechanism. RESULTS: Survival time of donor rat skin grafts was specifically prolonged in the tolerant B6 mice. The results of MLR and DTH assays showed donor-specific hyporeactivity, while the tolerant B6 mice were still immunocompetent to MHC-disparate third party BALB/c mouse or DA rat stimulator cells. CONCLUSIONS: A reliable xenogeneic transplantation tolerance of mouse to rat was achieved by this project of tolerance induction. The result of in vitro and in vivo adoptive transfer of spleen cells from tolerant B6 mice demonstrated that the suppressor cells were unlikely to exert effect in the tolerance. The inhibition of specific MLR could be reversed by adding IL-2, indicating that clonal anergy instead of clonal deletion is responsible for the tolerant maintenance.

Animals↗

Genetic studies on a family with acute myelogenous leukemia.

Seven cases of myelogenous leukemia--two acute erythroleukemia (AEL), four acute myelogenous leukemia (AML), and one acute myelomonocytic leukemia (AMMoL)--were found in 22 members of three consecutive generations of a family in the past 16 years (1973-1989). By using cytogenetic, hematologic, and biochemical analyses of those surviving in this family, we also found four members who might develop leukemia in the future. Southern blot analysis of one of the four members and her father (an acute leukemia patient) with a v-ERBB probe showed that the gene abnormalities consisted of a c-ERBB rearrangement (hereditary) and a rearrangement/amplification of the same gene.

Blotting, Southern↗

Elevation of expression of Smads 2, 3, and 4, decorin and TGF-beta in the chronic phase of myocardial infarct scar healing.

We have previously shown that non-myocytes present in healed 8-week infarct scar overexpress transduction proteins required for initiating the elevated deposition of structural matrix proteins in this tissue. Other work suggests that TGF-beta 1 may be involved in cardiac fibrosis and myocyte hypertrophy. However, the significance of the altered TGF-beta signaling in heart failure in the chronic phase of post-myocardial infarction (MI), particularly in the ongoing remodeling of the infarct scar, remains unexplored. Patterns of cardiac TGF beta 1 and Smad 2, 3, and 4 protein expression were investigated 8 weeks after MI and were compared to relative collagen deposition in border tissues (containing remnent myocytes) and the infarct scar (non-myocytes). Both TGF-beta 1 mRNA abundance and protein levels were significantly increased in the infarct scar v control values, and this trend was positively correlated to increased collagen type I expression. Cardiac Smad 2, 3, and 4 proteins were significantly increased in border and scar tissues v control values. Immunofluorescent studies indicated that Smad proteins localized proximal to the cellular nuclei present in the infarct scar. Decorin mRNA abundance was elevated in border and infarct scar, and the pattern of decorin immunostaining was markedly altered in remote remnant heart and scar v staining patterns of control sections. Expression of T beta RI (53 kDa) protein was significantly reduced in the scar, while the 75 kDa and 110 kDa isoforms of T beta RII were unchanged and significantly increased in scar, respectively. These results indicate that TGF-beta/Smad signaling may be involved in the remodeling of the infarct scar after the completion of wound healing per se, via ongoing stimulation of matrix deposition.

Activin Receptors, Type I↗

Coexistence of immune-neuro-endocrine substances in the rat central neurons.

To investigate the expression of interleukin-2 (IL-2), metabotropic glutamate receptor subunit 1 (mGluR1) and estrogen receptor (ER) in neurons of the rat central nervous system (CNS) and identify the coexistence possibility of these immune-neuro-endocrine substances in the central neurons, the tri-labeling immunocytochemical technique with different species-specific primary antibodies (goat anti-IL-2 antibody, rabbit anti-mGluR1 antibody and mouse anti-ER antibody) were used to incubate two serial neighbor sections (one for demonstrating IL-2, another for mGluR1 and ER) of the cerebral cortex, medulla oblongata and spinal cord. There were IL-2-, mGluR1- and ER-immunoreactivity (IR)-positive labeled neurons in the above-mentioned central areas. The IL-2-IR production showed brown color, located in the cytoplasm; In the neighbor serial section, the mGluR1-IR, production showed blue-black color, located on the cell membrane; the ER-IR production also showed brown color, located in the cytoplasm and nuclei. There were mGluR1/ER double-labeled cells in the same section, which accounted for about 50%-60% of the total single and double labeled neurons. It was identified by projection check of serial neighbor sections that had mGluR1/ER/IL-2 tri-labeled cells, which accounted for about 30% of total mGluR1/ER double-labeled neurons. The results indicate that mGluR1, ER and Il-2 can coexist in the same rat central neurons, therefore, providing morphological basis for the theory about immune-neuro-endocrine network at the cellular level for the first time.

Animals↗

Expression of Gi-2 alpha and Gs alpha in myofibroblasts localized to the infarct scar in heart failure due to myocardial infarction.

OBJECTIVE: Patients surviving large transmural myocardial infarction (MI) are at risk for congestive heart failure with attendant alteration of ventricular geometry and scar remodeling. Altered Gi-2 alpha and Gs alpha protein expression may be involved in cardiac remodeling associated with heart failure, however their expression in scar tissue remains unclear. METHODS: MI was produced in Sprague-Dawley rats by ligation of the left coronary artery. Gi-2 alpha and Gs alpha protein concentration, localization and mRNA abundance were noted in surviving left ventricle remote to the infarct, in border and in scar tissues from 8 week post-MI hearts with moderate heart failure. RESULTS: We observed a 4.5- and 5.0-fold increase in immunoreactive Gi-2 alpha protein concentration occurs in the border and scar regions vs. control values, respectively, in 8-week post-MI rat hearts. Similarly, immunoreactive Gs alpha protein concentration was increased 3.4- and 8.2-fold, respectively, in these tissues vs. controls. Double-fluorescence labeling and phenotyping studies revealed that both Gi-2 alpha and Gs alpha proteins were localized to myofibroblasts in the infarct scar and to viable myocytes bordering the scar. Northern analysis revealed that the Gi-2 alpha/GAPDH ratio was increased in both viable and scar regions (1.24- and 1.85-fold respectively) from experimental hearts when compared to sham-operated control values when compared to noninfarcted left ventricle, the value of this ratio in scar tissue was elevated approximately 1.5 fold. The Gs alpha/GAPDH ratio was significantly increased (1.28-fold) only in the scar region vs. control. CONCLUSION: Our results indicate a marked increase in the expression of Gi-2 alpha and Gs alpha from myofibroblasts of the infarct scar as well as remnant myocytes bordering the scar in 8-week post-MI rat hearts. We suggest that these changes may be associated with ongoing remodeling in the infarct scar in chronic post-MI phase of this experimental model.

Analysis of Variance↗