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Biomedical subjects

Y H Li

Publications and source records attributed to Y H Li.

At least 73 records · Page 4Linked to original sources

Liposomal antioxidants provide prolonged protection against acute respiratory distress syndrome.

BACKGROUND: We have previously shown that N-acetylcysteine (NAC), an antioxidant, in the resuscitation fluid after shock prevents lung injury in response to lipopolysaccharide (LPS) by inhibiting chemokine generation by alveolar macrophages in the lung. However, the protection was short-lived. We hypothesized that liposomal (Lip) NAC delivered intratracheally might be delivered directly to the target cells and exert prolonged effect. METHODS: Sprague-Dawley rats were bled to a blood pressure of 40 mm Hg for 1 hour and resuscitated with shed blood and equal volume of Ringer's lactate. In some studies 500 mg/kg NAC was included in the resuscitation fluid. Thirty minutes later, 150 microl LipNAC (9.4 mg/kg NAC) was given intratracheally. One hour and 18 hours after resuscitation, LPS (30 microg/kg) or saline was given intratracheally. Lung injury was assessed by permeability to (125)I-albumin, bronchoalveolar lavage neutrophils and lung myeloperoxidase. The cytokine-induced neutrophil chemoattractant (CINC) expression in the lung was assessed by Northern blot. RESULTS: At the early time point, both NAC and LipNAC protected the lung with the effects in significantly reducing the increases in transpulmonary albumin flux, neutrophil influx and myeloperoxidase in the lungs of shock/LPS rats. However, by the late time point, only LipNAC retained its salutary effect. This correlated well with persistent ability to prevent CINC increase. In addition, Lipalpha-tocopherol (alpha-T) and LipNAC/alpha-T were tested and determined to be effective to protect the lung. CONCLUSIONS: Liposomal encapsulation of antioxidants at low dose provides long lasting protection against acute respiratory distress syndrome after shock. This may represent a novel treatment approach.

Acetylcysteine↗

Epidemiological and nutritional research on prevention of cardiovascular disease in China.

Anthropological evidence suggests that regional differences in eating practices may be characterized by sub-ethnicity. Hakka is one sub-ethnicity who still retain a unique way of life in China. A field survey on diet and health among the Hakka people was undertaken in 1994. Approximately 200 participants were interviewed for their medical history, life-style and food habits. Blood pressure, body mass index, blood sample, 24 h urine and electrocardiogram were collected. The food samples taken from one tenth of the participants were analyzed for the ingredients in their daily meals. From this survey the prevalence of hypertension in Hakka was approximately 10 %. The sodium/potassium ratio was lower than that in Guangzhou and comparable with that in Okinawa, the island of longevity in Japan. For men, taurine level was found to be close to that in Mediterranean countries, where there is low mortality from cardiovascular diseases. For women, the taurine level was even higher, approximating that of Japanese women, who show the greatest longevity and lowest cardiac mortality worldwide. Less obesity was found in Hakka people than that in the US, Canada or Japan. These findings suggest that the following are the major reasons for these positive findings: the Hakka people maintain traditional food habits and maintain active awareness of their health; the major foods are rice, fish, vegetables and fruits; wide use of soybeans; extensive consumption of visceral organs which have rich source of trace elements. These eating practices and nutritional patterns may be beneficial factors for preventing atherosclerosis and hypertension.

Adult↗

Downregulatory cytokines in tracheobronchial aspirate fluid from infants with chronic lung disease of prematurity.

UNLABELLED: Chronic lung disease of prematurity (CLD) is associated with an inflammatory response in the preterm lung and increased levels of proinflammatory cytokines in tracheobronchial aspirate fluid (TAF). We investigated TAF levels of transforming growth factor-beta1 (TGF-beta1), interleukin-10 (IL-10), interleukin-4 (IL-4) and interleukin-12 (IL-12) cytokines possibly important in downregulating the proinflammatory response and/or inducing lung fibrosis in infants with developing and established CLD. Infants with CLD (n = 24) were compared with preterm infants with RDS that resolved (n = 22) and postoperative infants without lung disease (n = 23). TAF levels of TGF-beta1, IL-10, IL-4 and IL-12 were studied by quantitative enzyme immunoassay. Levels of TGF-beta1 were significantly higher during the first week of life in infants who developed CLD, remained high at 2 wk and past 4 wk of age. TAF levels of TGF-beta1 did not decrease significantly in six infants with CLD after treatment with steroids. TAF IL-10 was detected in 12/46 (26%) preterm infants. Infants with CLD or RDS were more likely to have measurable TAF levels of IL-10, compared with the postoperative infants without lung disease (p < 0.02 and 0.04, respectively). TAF levels of IL-4 or IL-12 were below the detection limits in all samples. CONCLUSIONS: We have demonstrated a sustained increase of TGF-beta1 levels in TAF from preterm infants who develop CLD, suggesting an important role for TGF-beta1 in the fibrotic response in the CLD lung. The elevated TGF-beta1 levels, combined with an absent or irregular secretion of IL-4, IL-10 and IL-12, can have importance for the increased tendency for the development of CLD in preterm infants.

Age Factors↗

Two new gene cassettes, dfr17 (for trimethoprim resistance) and aadA4 (for spectinomycin/streptomycin resistance), inserted in an Escherichia coli class 1 integron.

Two new gene cassettes, dfr17 and aadA4, inserted in a class 1 integron of Escherichia coli EC107, are described here. The dfr17 cassette encodes trimethoprim resistance and has 91% identity with the dfrVII dihydrofolate reductase gene. The aadA4 cassette confers resistance to spectinomycin and streptomycin and shows 94% identity with the aadA3 gene. The integron carrying the dfr17 and aadA4 cassettes was located on a conjugative plasmid, pEC1072.

DNA Transposable Elements↗

In vivo and in vitro modulation of intercellular adhesion molecule (ICAM)-1 expression by hypertonicity.

Hepatic ischemia-reperfusion (I/R) is an important cause of organ dysfunction in the critically ill. With reperfusion, Kupffer cells release pro-inflammatory cytokines that promote endothelial cell (EC) expression of adhesion molecules such as intercellular adhesion molecule (ICAM)-1, facilitating neutrophil (PMN) infiltration. Studies suggest hypertonic saline (HTS) might exert beneficial effects on development of organ injury following shock on the basis of reduced PMN-EC interactions. We hypothesized that HTS alters expression of EC ICAM-1 and thus minimizes PMN-mediated injury. To test our hypothesis, we used an in vivo model of hepatic I/R and an in vitro model of activated EC. Rats underwent 30 min of hepatic ischemia after pretreatment with HTS (7.5% NaCl, 4cc/kg ia) or normal saline (NS). At 4 h reperfusion, plasma was taken for aspartate aminotransferase (AST) and liver tissue was harvested for assessment of hepatic ICAM-1 mRNA by Northern blot analysis. Human umbilical vein endothelial cells (HUVECs) were activated by lipopolysaccharide (LPS) and exposed to hypertonic medium (350-500 mOsM). HUVEC ICAM-1 protein was measured by cell ELISA and ICAM-1 mRNA by Northern blot analysis. HTS prevented hepatic I/R injury as measured by AST. AST of shams was 282.6+/-38.1 IU/L. I/R following NS pretreatment caused significant injury (AST 973.8+/-110.9 IU/L) compared to sham (SM) (P < 0.001). Pretreatment with HTS exerted significant protection following I/R with an AST of 450.9+/-56.3 IU/L (P < 0.05). There was no significant difference in AST levels between SM and HTS groups. Reduced hepatic injury after HTS and I/R was accompanied by inhibition of I/R-induced hepatic ICAM-1 mRNA expression compared to NS treated animals (P < 0.01). Similarly, hypertonicity inhibited HUVEC LPS-induced ICAM-1 protein (LPS: 1.86+/-0.19 absorbance units; 400 mOsM +/- LPS: 1.45+/-0.14 absorbance units; 450 mOsM + LPS: 1.02+/-0.19 absorbance units, P < 0.001) and mRNA expression. Thus, hypertonicity modulates endothelial ICAM-1 expression as one possible protective mechanism against I/R injury.

Animals↗

Activation of nuclear factor kappaB and induction of inducible nitric oxide synthase by Ureaplasma urealyticum in macrophages.

Chronic lung disease (CLD) of prematurity is an inflammatory disease with a multifactorial etiology. The importance of Ureaplasma urealyticum in the development of CLD is debated, and steroids produce some improvement in neonates with this disease. In the present study, the capability of U. urealyticum to stimulate rat alveolar macrophages to produce nitric oxide (NO), express inducible nitric oxide synthase (iNOS), and activate nuclear factor kappaB (NF-kappaB) in vitro was characterized. The effect of NO on the growth of U. urealyticum was also investigated. In addition, the impact of dexamethasone and budesonide on these processes was examined. We found that U. urealyticum antigen (> or =4 x 10(7) color-changing units/ml) stimulated alveolar macrophages to produce NO in a dose- and time-dependent manner (P<0.05). This effect was further enhanced by gamma interferon (100 IU/ml; P<0.05) but was attenuated by budesonide and dexamethasone (10(-4) to 10(-6) M) (P<0.05). The mRNA and protein levels of iNOS were also induced in response to U. urealyticum and inhibited by steroids. U. urealyticum antigen triggered NF-kappaB activation, a possible mechanism for the induced iNOS expression, which also was inhibited by steroids. NO induced by U. urealyticum caused a sixfold reduction of its own growth after infection for 10 h. Our findings imply that U. urealyticum may be an important factor in the development of CLD. The host defense response against U. urealyticum infection may also be influenced by NO. The down-regulatory effect of steroids on NF-kappaB activation, iNOS expression, and NO production might partly explain the beneficial effect of steroids in neonates with CLD.

Animals↗

Priming for enhanced alveolar fibrin deposition after hemorrhagic shock: role of tumor necrosis factor.

Hemorrhagic shock due to major trauma predisposes to the development of acute respiratory distress syndrome. Because lung fibrin deposition is one of the hallmarks of this syndrome, we hypothesized that resuscitated shock might predispose to the development of a net procoagulant state in the lung. A rodent model of shock/resuscitation followed by low-dose intratracheal lipopolysaccharide (LPS), a clinically relevant "two-hit" model, was used to test this hypothesis. Resuscitated shock primed the lungs for an increased tissue factor and plasminogen activator (PA) inhibitor-1 gene expression in response to LPS, while the fibrinolytic PA was reduced. These alterations were recapitulated in isolated alveolar macrophages, suggesting their role in the process. LPS-induced tumor necrosis factor (TNF) was also augmented in animals after antecedent shock/resuscitation, and studies using anti-TNF antibodies revealed that TNF expression was critical to the induction of the procoagulant molecules and the reduction in PA. By contrast, TNF did not appear to play an important role in neutrophil sequestration in this model, inasmuch as anti-TNF had no effect on lung neutrophil accumulation or chemokine expression. However, treatment prevented albumin leak by preventing alveolar neutrophil activation. The inclusion of the antioxidant N-acetyl-cysteine in the resuscitation fluid resulted in prevention of both the development of the net procoagulant state and lung neutrophil sequestration, suggesting a role for upstream oxidant effects in the priming process. These studies provide a cellular and molecular basis for lung fibrin deposition after resuscitated shock and demonstrate a divergence of pathways responsible for fibrin generation and neutrophil accumulation.

Acetylcysteine↗

Ureaplasma urealyticum-induced production of proinflammatory cytokines by macrophages.

Ureaplasma urealyticum is relatively common in the respiratory tract of very low birth weight infants and has been hypothesized to be involved in the development of chronic lung disease. The purpose of this study was to investigate whether U. urealyticum could stimulate macrophages to produce proinflammatory cytokines in vitro, which are early pathologic changes in the lung during the development of chronic lung disease. A human monocytic cell line (THP-1) differentiated to macrophages, a rat alveolar macrophage cell line (Nr8383), and human lung macrophages from tracheobronchial aspirate fluid in preterm infants were exposed to U. urealyticum antigen for 24 h. The protein levels of human IL-6, tumor necrosis factor-alpha (TNF-alpha), and rat TNF-alpha were measured with ELISA. Rat IL-6 was analyzed with a specific bioassay. The mRNA levels of these cytokines were detected by reverse transcriptase-PCR. The production of TNF-alpha and IL-6 increased after stimulation with U. urealyticum in both the human and rat macrophage cell lines. In tracheobronchial aspirate fluid macrophages, U. urealyticum increased the production of TNF-alpha from 14 to 84% and IL-6 from 46 to 268% above control levels. U. urealyticum also induced gene expression of TNF-alpha and IL-6. In conclusion, U. urealyticum could be an important factor in the development of chronic lung disease because of its ability to induce alveolar macrophage proinflammatory cytokine production.

Animals↗

The Sofield-Millar operation in osteogenesis imperfecta. A modified technique.

We have reviewed the results of the Sofield-Millar operation on 58 long bones in ten patients. If more than three osteotomies were undertaken the time to union of the bone was significantly prolonged (p < 0.001) with significant thinning of the bone (p < 0.02). We have used a modified technique in order to minimise surgical trauma and devascularisation of the bone. The rod is introduced under the control of an image-intensifier. Small surgical exposures are made only at the sites of corrective wedge osteotomies. The number of osteotomies is kept to the minimum.

Bone Resorption↗

Effect of atrial fibrillation on pulmonary venous flow patterns assessed by Doppler transesophageal echocardiography.

STUDY OBJECTIVES: To investigate the effect of atrial fibrillation (AF) on pulmonary venous flow (PVF) patterns in a cohort with nonrheumatic AF. DESIGN AND SETTINGS: A prospective and controlled study undertaken at a tertiary referral medical center. PATIENTS AND MEASUREMENTS: The echocardiographic parameters of left superior PVF as assessed by Doppler transesophageal echocardiography in 40 patients with chronic AF (group 1) were compared to those of 33 volunteers with sinus rhythm (group 2) and well-matched baseline characteristics. RESULTS: : All group 1 patients presented with single systolic forward flow (SFF) patterns. In contrast, single and double SFF patterns were found equally in group 2. With regard to reverse flow (RF), most group 1 patients (33 of 40) had an early systolic RF and none had atrial RF; however, most group 2 subjects (29 of 33) had an atrial RF. Some of the group 1 patients (17%) had a late systolic RF in the absence of significant mitral regurgitation. In group 1, the SFF appeared later and disappeared earlier than in group 2. The mean systolic peak velocity and time-velocity integral (TVI) of the SFF were significantly lower in group 1 compared to group 2. The diastolic peak velocity and TVI were not significantly different between groups. CONCLUSIONS: : Our data indicate that AF independently and significantly affects the PVF and leads to characteristic flow patterns different from sinus rhythm. The presence of AF reduces SFF in addition to the absence of atrial RF. These changes in the flow patterns should be taken into account while interpreting the implications of PVF in the presence of AF.

Aged↗

[Investigation on the stimulation effect of polypyrrole film on rat hepatic cells].

Poypyrrole(PPy) films were prepared at 1 x 10(-3) mA/cm2 electropolymerization current density on indium-tin oxide(ITO)substrate. The PPy films were well-distributed, translucent, stable and insoluble. Moreover, they can be sterilized by steam disinfection. Rat hepatic cells were cultured on these films. The results show that PPy films have good biocompatibility and they can accelerate cell growth under electrical stimulation. The cells on PPy films reach the largest cell density earlier than the cells on tissue culture polystyrene(TCPS). Furthermore, rat hepatic cells can generate on PPy films. The cells on PPy films grow faster and enter logarithmic growth phase earlier than those on TCPS.

Animals↗

Sick sinus syndrome in a patient with single coronary artery anomaly.

Single coronary artery anomaly is very rare. The reported manifestations include angina pectoris and congestive heart failure. Here we describe a case of single coronary artery anomaly presenting as sick sinus syndrome, which has no literature precedence. A 47-year-old woman had complained of intermittent dizziness for years. A Holter electrocardiogram showed sinus bradycardia and junctional or ventricular rhythm with a maximal ventricular pause of up to 3.2 seconds. Electrophysiologic study revealed prolonged corrected sinus nodal recovery time. Coronary angiography showed that the left anterior descending artery had a long course with a side branch originating from the proximal part and coursing anteriorly to the territory of the proximal portion of the right coronary artery. The sinus node is usually supplied by the sinoatrial branch via the right coronary artery. Aortography showed that the right coronary artery ostium was absent. A permanent pacemaker was implanted and the patient was discharged in good condition. The present case suggests that coronary artery anomaly may lead to compromised blood supply to the sinus node, and hence sick sinus syndrome.

Coronary Vessel Anomalies↗

[AFLP markers of restoring genes of the wild-abortive hybrid rice].

Fertile and sterile pools were set up by bulked segregant analysis (BSA) based on the selection for the highly fertile and highly sterile plants of Shanyou 63 F2 population. The AFLP analysis of the two pools indicated that 64 primer combinations amplified 3,477 stable and clear bands. Exception of the combination E-AGC/M-CAA, all primer combinations had not detected polymorphism between the two pools. It was proved by investigation of two parents, individuals of F2 segregant population, backbone sterile lines and restorer lines that the polymorphic fragment AP1 generated from the primer E-AGC/M-CAA was associated with the restoring gene. AP1 was a single copy detected by Southern blot hybridization. The distance between AP1 and the restoring gene was 4.76 cM.

Genes, Plant↗

[The effect of heat shock before rat partial hepatectomy on HSC70/HSP68 expression and phosphatase activities].

The contribution and content of the continuous heat shock protein 70/induced heat shock protein 68 (HSC70/HSP68), the contribution, variety and activity of acid phosphatases (ACP) and alkaline phosphatases (AKP) had been analysed qualitatively and quantitatively during the liver regeneration after 2/3 hepatectomy (PH) and HS (heat shock at 46 degrees C for 30 min, recovery for 8 h), which were compared with the results only by HS and only by PH. It was shown that the three kinds of treatment all can increase the activity of ACP, AKP and the expression of HSC70/HSP68, but with different change pattern. A further analysis show that after HS-PH the enhanced activity of ACP is related with that of 140 kD phosphatases, the enhanced activity of AKP is associated with that of 140 kD and 160-180 kD phosphatases. It can be reckoned from the results that ACP, AKP and HSC70/HSP68 all act on the heat shock response of hepatocyte and liver regeneration, and may take part in signal transduction in these processes, but ACP may play a dominant role in the start of hepatocyte multiplication, AKP and HSC70/HSP68 may play a dominant role in cytokineses.

Acid Phosphatase↗

Role of the monocarboxylic acid transport system in the intestinal absorption of an orally active beta-lactam prodrug: carindacillin as a model.

Transport of carbenicillin (CBPC) and its orally active prodrug (carindacillin, CIPC) was studied with rat intestinal brush border membrane vesicles (BBMV). CIPC was transported uphill into BBMV in the presence of a H(+) gradient, indicating that CIPC absorption is carrier-mediated. Indeed, CIPC was predominantly transported by the monocarboxylic acid transport system, although it might be possible that CIPC possesses some affinity to the oligopeptide transporter. In contrast, CBPC exhibited no affinity to either the oligopeptide or the monocarboxylic acid transport system. Apparent uptake clearance of CIPC was approximately 70-fold greater than that of CBPC. It was clarified that the modification of the chemical structure of CBPC (a dicarboxylic acid) to CIPC (a monocarboxylic acid) by ester formation may have resulted in the increased affinity to the monocarboxylic acid transport system, which, in turn, led to improved absorption of the prodrug.

Algorithms↗

Prevalence of TT virus DNA in eastern Taiwan aborigines.

We studied the prevalence of TT virus (TTV) DNA in the general population of the eastern Taiwan aborigine villages, about 11% (34 of 317). There is no association between the presence of HBsAg and TTV DNA or between the presence of HCV RNA and TTV DNA. Therefore, the infection of HBV or HCV and the presence of TTV DNA appear to be independent from each other. The association between the presence of TTV DNA and the elevated alanine aminotransferase (and/or aspartate aminotransferase) activity was also investigated. The presence of TTV DNA was not found to be correlated with abnormal liver function (P = 0.574) when age, gender, and the presence of HBsAg, HCV RNA, and HGV RNA were all considered in the assay. The sequence homology of TTV DNA fragments between different isolates from Taiwan and N22 (the clone obtained from the original prototype strain) from Japan ranged from 84 to 97%. The recombinant protein encoded by the TTV DNA fragment corresponding to the open reading frame of N22 was expressed in E. coli successfully. However, no serum response against the recombinant protein was detected.

Adolescent↗

Decreased left atrial appendage function is an important predictor of elevated left ventricular filling pressure in patients with congestive heart failure.

OBJECTIVE: The aim of this study was to investigate whether left atrial (LA) appendage function, as indicated by LA appendage blood flow velocities and its ejection fraction, could identify elevated left ventricular filling pressure in patients with chronic congestive heart failure. METHODS: Using transesophageal echocardiography, adequate pulsed Doppler LA appendage active emptying and filling velocities could be recorded in 25 consecutive patients (16 men and 9 women, aged 57+/-10 years) with chronic congestive heart failure (symptom duration > or =1 year). LA appendage ejection fraction calculated as (LA appendage maximal area)-(LA appendage minimal area)/(LA appendage maximal area) x 100 was also determined in these patients. Left ventricular end-diastolic pressure was recorded during cardiac catheterization performed within 24 h of echocardiographic study. RESULTS: Left ventricular end-diastolic pressure was 2 to 47 mm Hg. There were close negative correlations of LA appendage emptying velocity (r=-0.508; P<0.01), filling velocity (r=-0.429; P<0.05) and LA appendage ejection fraction (r=-0.523; P<0.005) with left ventricular end-diastolic pressure. LA appendage active emptying velocity <30 cm/s predicted left ventricular end-diastolic pressure >25 mm Hg with a sensitivity of 72.7%, a specificity of 92.9% and a positive and negative predictive value of 88.9 and 81.3%. CONCLUSIONS: The findings suggest that measurement of LA appendage blood flow velocities and contractile function by transesophageal echocardiography can be used to predict elevated left ventricular filling pressure in patients with congestive heart failure.

Atrial Function, Left↗