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Biomedical subjects

Y Yang

Publications and source records attributed to Y Yang.

At least 91 records · Page 5Linked to original sources
PubMed2004

Efficacy of mycophenolate mofetil versus azathioprine after renal transplantation: a systematic review.

INTRODUCTION: Our objective was to evaluate the efficacy of mycophenolate acid (MMF) versus azathioprine (AZA) after renal transplantation. MATERIALS AND METHODS: The following electronic databases were searched: Medline, Embase, Cochrane library, and Chinese Biomedicine database (CBM). Randomized controlled trials (RCTs) were subjected to Revman 4.11 for statistical analyses. RESULTS: Twenty-three RCTs were identified to compare MMF and AZA for antirejection, prophylaxis after renal transplantation. The data showed that MMF (2 g/d) was more beneficial than AZA to improve graft and long-term patient survivals, but there was no statistical differences between MMF (3 g/d) and AZA. Whether at 6 months or at 1 year after renal transplantation, the use of MMF (2 g/d) or MMF (3 g/d) markedly reduced the incidence of biopsy-proven rejection. CONCLUSION: Compared with AZA, MMF is a more potent immunosuppressive drug, that is more efficient in reducing the incidence of acute rejection episodes after renal transplantation. MMF can improve the graft and patient survival rate. The 2 g per day dosage is more acceptable.

Azathioprine↗
PubMed2004

Torsional vibrational modes of tryptophan studied by terahertz time-domain spectroscopy.

The low-frequency torsional modes, index of refraction, and absorption of a tryptophan film and pressed powders from 0.2 to 2.0 THz (6.6-66 cm(-1)) were measured by terahertz time-domain spectroscopy at room temperature. It was found that there were two dominated torsional vibrational modes at around 1.435 and 1.842 THz. The associated relaxation lifetimes ( approximately 1 ps) for these modes of the tryptophan molecule were measured. Using a density-functional calculation, the origins of the observed torsional vibrations were assigned to the chain and ring of the tryptophan molecule.

Coated Materials, Biocompatible↗
PubMed2004

Current problems and potential techniques in in vivo glucose monitoring.

Accurate in vivo monitoring of glucose concentration would be a valuable asset, particularly for management of diabetes and preterm infants during critical care. In vivo glucose monitoring devices can be divided into two categories: implanted and non-invasive. Extensive research into in vivo glucose monitoring over recent decades has not resulted in the widespread use of clinically reliable monitoring systems. For implanted devices, poor biocompatibility of the materials used for fabrication remains a major challenge, whilst progress in the commercial development of non-invasive devices is hampered by the problem of multiple interference between the detected signals and the biological components. In this review, the methods available for in in-vivo glucose monitoring are described and the associated problems are discussed.

Biosensing Techniques↗
PubMed2004

Outcomes of autologous stem cell transplantation in patients with multiple myeloma who received dexamethasone-based nonmyelosuppressive induction therapy.

High-dose chemotherapy (HDC) followed by autologous stem cell transplantation (ASCT) improves survival in myeloma (MM). The role of induction therapy on outcomes of ASCT in MM has not been systematically studied. Nonmyelosuppressive (NMS) steroid-based induction can be used in MM, with the potential of reducing neutropenias and other toxic effects prior to ASCT. NMS induction however could be associated with poorer outcomes if disease control or stem cell collection were inadequate. We studied outcomes of 136 MM patients who underwent HDC and ASCT as part of their initial therapy between March 1998 and December 2000. Of these, 46 received HDC and ASCT without any exposure to myelosuppressive agents, 39 received myelosuppressive therapy for disease control and/or stem cell collection, and 51 received alkylating agent-based initial treatment. We compared OS and EFS rates, stem cell collectability, and contamination of the grafts with monoclonal plasma cells. After a median of 33 months, response rates, EFS and OS rates were comparable in the three groups of patients. Adequacy of stem cell collection and plasma cell contamination were similar. Our data support the hypothesis that NMS induction for patients with MM is safe and effective and does not compromise the results of HDC.

Dexamethasone↗
PubMed2004

Reduction of ascites mortality in broilers by coenzyme Q10.

Effects of coenzyme Q10 (CoQ10) supplementation on growth performance and ascites were studied in broilers. One hundred eighty 1-d-old Arbor Acre male broiler chicks were randomly allocated into 3 groups with 6 replicates each. From d 8, the diets were supplemented with CoQ10 at levels of 0, 20, and 40 mg/kg, respectively. From d 15 to 21, all the chicks were exposed to low ambient temperature (15 to 18 degrees C) to induce ascites. Average feed intake, BW gain, and feed conversion ratio of the broilers during 0 to 3 wk, 3 to 6 wk, and 0 to 6 wk were measured. The results showed that there were no influences observed on broilers' growth performance, but the mortality due to ascites was reduced by CoQ10 supplementation (P < or = 0.05). Erythrocyte osmotic fragility (EOF) was significantly decreased by 40 mg/kg CoQ10 compared with the control, but no significant changes were observed on blood packed cell volume (PCV) among the treatments. Pulmonary arterial diastolic pressure was significantly decreased on d 36, but no significant changes were observed on right ventricular pressure (RVP), pulmonary arterial systolic pressure, and the maximum change ratio of right intraventricular pressure (+/- dp/ dtmax). Ascites heart index (AHI) was significantly decreased by 40 mg/kg CoQ10 supplementation (P < or = 0.05). The results of this study suggested that CoQ10 has a beneficial effect in reducing ascites mortality in broilers, and 40 mg/kg CoQ10 seems to be more effective than 20 mg/ kg CoQ10.

Animal Feed↗
PubMed2004

High-fat diet alters K+-currents in porcine coronary arteries and adenosine sensitivity during metabolic inhibition.

Coronary arteries from animals on normal diets (ND) exhibit well-maintained responses to dilators under ischemic conditions. The reported altered metabolic requirements and K+-currents in blood vessels from hypercholesterolemic animals fed high-fat diets (HF) led us to hypothesize that under metabolically depressed conditions (N2/2-deoxyglucose) coronary arteries from pigs would exhibit significantly decreased responses to adenosine (ADO) as compared with pigs given ND. Diet had no major effect on responses of coronary rings to ET-1, nor on the sensitivity to ADO or 2-chloroadenosine (2-CAD) relaxation under metabolically supported conditions. During metabolic inhibition the response curves for both ADO and 2-CAD were shifted to the right (P < 0.05), with the HF group shifted about 4-fold more than ND (P < 0.05). To determine the involvement of K+-channels, ADO responses were measured in the presence of 4-aminopyridine (4-AP, 1 mM) or glybenclamide (GLYB, 10 microM). The larger shift in the HF group during metabolic inhibition was not affected by GLYB, but disappeared in the presence of 4-AP with ND now behaving similarly to HF. These results indicate that HF diet may have a 4-AP-like effect on voltage-dependent K+-channels (KV). Patch-clamp measures of whole cell K- currents showed the HF cells to have reduced 4-AP sensitive currents (P < 0.02). The 4-AP insensitive currents were similar in both groups. Thus, reduced KV channel activity may play a role in the depressed ADO relaxation associated with metabolic inhibition of HF coronary arteries. These factors may place the coronary circulation of HF at increased risk during an ischemic episode.

Adenosine↗
PubMed2004

DNA-based prenatal diagnosis in a Chinese family with xeroderma pigmentosum group A.

BACKGROUND: Xeroderma pigmentosum (XP) is a group of autosomal recessive diseases characterized by hypersensitivity to ultraviolet rays. Among its eight complementation groups, XP group A (XPA) is the most severe type. The XPAC gene has been identified as the defective gene in XPA patients. OBJECTIVES: To examine genomic DNA from a Chinese family with XPA, to determine the XPAC mutation and, after genetic counselling, to undertake DNA-based prenatal diagnosis in a subsequent pregnancy. METHODS: Fetal DNA was extracted from amniotic fluid and used to amplify exon 5 of XPAC containing the potential mutation. Direct sequencing and restriction endonuclease digestion were used for prenatal diagnosis. RESULTS: We identified a homozygous nonsense XPAC mutation of 631C-->T, which results in an R211X mutation in XPA protein, in the proband. Both her parents are heterozygous. Prenatal diagnosis demonstrated a heterozygous sequence predicting an unaffected child, and a healthy girl was born. CONCLUSIONS: These data provide the first example of a DNA-based prenatal test for genodermatosis in China.

Child, Preschool↗
PubMed2004

A new keratin 5 mutation (K199T) in a family with Weber-Cockayne epidermolysis bullosa simplex.

A new missense mutation in the keratin 5 gene (KRT5) in a Chinese family with Weber-Cockayne type epidermolysis bullosa simplex is reported. Direct sequencing identified a heterozygous A --> C substitution at nucleotide 596 altering codon 199 of KRT5 from lysine to threonine in all affected family members, but not in the unaffected family members or in 50 unrelated control samples. The mutation is designated K199T. This mutated lysine residue is sited within the 1A domain of keratin 5 and is highly conserved among all type II keratins. The mutation may perturb the alignment of tonofilaments and, as a consequence, result in skin fragility and blistering.

Adult↗
PubMed2004

Increased hepatic platelet activating factor (PAF) and PAF receptors in carbon tetrachloride induced liver cirrhosis.

BACKGROUND AND AIMS: The liver is a major site for the synthesis and actions of platelet activating factor (PAF), a potent hepatic vasoconstrictor and systemic vasodilator. As PAF is implicated in portal hypertension and hyperdynamic circulation associated with liver cirrhosis, we characterised changes in the hepatic PAF system in experimental cirrhosis. METHODS: In rats made cirrhotic by carbon tetrachloride (CCl(4)) administration for eight weeks, we determined hepatic levels of PAF and its cognate receptor, and the effects of PAF and PAF antagonist (BN52021) on portal and arterial pressure. RESULTS: Compared with control rats, cirrhotic rats had higher hepatic PAF levels, higher apparent hepatic efflux of PAF, and higher PAF levels in arterial blood (p<0.01, p<0.01, p<0.05, respectively). Relative to controls, cirrhotic livers had elevated hepatic PAF receptors (by mRNA and protein levels and [(3)H]PAF binding), higher (p<0.01) baseline hepatic portal pressure, and an augmented (p = 0.03) portal pressure response to PAF infusion (1 microg/kg). Portal infusion of BN52021 (5 mg/kg) showed that elevated endogenous PAF was responsible for 23% of the cirrhotic portal pressure increase but made no contribution to systemic hypotension. Finally, increased PAF receptor density was observed in the contractile perisinusoidal stellate cells isolated from cirrhotic livers relative to those from control livers. CONCLUSIONS: In cirrhosis, increased hepatic release of PAF elevates systemic PAF; in combination with upregulated hepatic PAF receptors in stellate cells, this contributes to portal hypertension.

Animals↗
PubMed2004

Endothelin receptor antagonist TAK-044 arrests and reverses the development of carbon tetrachloride induced cirrhosis in rats.

BACKGROUND AND AIMS: Hepatic concentrations of the powerful vasoconstrictor and fibrogen endothelin 1 (ET-1) and its receptors increase in human and experimental cirrhosis, suggesting a major role for ET-1 in the pathology of chronic liver disease. We investigated whether ET-1 receptor antagonism, after the development of fibrosis and cirrhosis, arrests/reverses the progression of chronic liver disease. METHODS: Chronic liver injury was induced in rats by carbon tetrachloride (CCl(4)) treatment (0.15 ml/kg intraperitoneally twice a week) in conjunction with phenobarbital in drinking water (0.4 g/l) for four (group 1: fibrosis) and eight (group 2: cirrhosis) weeks. Rat were then treated concurrently with the ET-1 receptor antagonist TAK-044 (10 mg/kg/day) and CCl(4)/phenobarbital for a further four weeks. RESULTS: Histopathological examination revealed significant arrest of progression to cirrhosis in group 1 and reversal of cirrhosis in group 2 rats. TAK-044 treatment caused significant amelioration of portal hypertension, systemic hypotension, and liver injury (reduced activities of serum aspartate aminotransferase, alanine aminotransferase, and lactate dehydrogenase), and improved hepatic synthetic capacity (increased serum albumin concentration) in both groups of rats relative to vehicle treated rats. TAK-044 treatment reduced collagen synthesis, as evidenced by decreased hepatic hydroxyproline content, mRNA expression of collagen-alpha type I, and tissue inhibitors of matrix metalloproteinases 1 and 2, and mRNA and protein expression of a potent fibrogenic cytokine, transforming growth factor beta1. CONCLUSIONS: The results emphasise the role of ET-1 in the development of cirrhosis and strongly suggest that blockade of its actions can be a rational therapy for chronic liver disease and its complications.

Animals↗
PubMed2004

Aberrant epithelial expression of trefoil family factor 2 and mucin 6 in Helicobacter pylori infected gastric antrum, incisura, and body and its association with antralisation.

AIMS: To determine gastric expression of trefoil family factor 2 (TFF2) and MUC6 in Helicobacter pylori positive and negative subjects, and its association with antralisation at the gastric incisura. METHODS: Gastric biopsies from the antrum, incisura, and body of 76 dyspeptic patients without ulcers were used for the determination of H. pylori infection, histological changes, and epithelial TFF2 and MUC6 expression. RESULTS: In the foveola, the rates of TFF2 and MUC6 immunostaining were greater in H. pylori infected (n = 27) than in uninfected patients (n = 49) at the antrum (59.3% v 4.1% for TFF2 and 63.0% v 4.1% for MUC6; both p < 0.001) and incisura (44.4% v 2.0% for TFF2 and 48.1% v 0% for MUC6; both p < 0.001). In the deeper glands, the rates were also greater in H. pylori infected than in uninfected patients at the incisura (85.2% v 22.4% for both TFF2 and MUC6; p < 0.001). Antral-type mucosa was present at the incisura in 28 of the 76 patients. TFF2 and MUC6 expression in the foveola and deeper glands was significantly associated with antral-type mucosa, independent of H. pylori status. CONCLUSIONS: Helicobacter pylori infection increases the expression of TFF2 and MUC6 in the gastric epithelium. Aberrant TFF2 and MUC6 expression is associated with antralisation of gastric incisura.

Adult↗
PubMed2004

Mutations in SCN9A, encoding a sodium channel alpha subunit, in patients with primary erythermalgia.

Primary erythermalgia is a rare autosomal dominant disease characterised by intermittent burning pain with redness and heat in the extremities. A previous study established the linkage of primary erythermalgia to a 7.94 cM interval on chromosome 2q, but the causative gene was not identified. We performed linkage analysis in a Chinese family with primary erythermalgia, and screened the mutations in the two candidate genes, SCN9A and GCA, in the family and a sporadic patient. Linkage analysis yielded a maximum lod score of 2.11 for both markers D2S2370 and D2S2330. Based on critical recombination events in two patients in the family, we further limited the genetic region to 5.98 cM between D2S2370 and D2S2345. We then identified two missense mutations in SCN9A in the family (T2573A) and the sporadic patient (T2543C). Our data suggest that mutations in SCN9A cause primary erythermalgia. SCN9A, encoding a voltage-gated sodium channel alpha subunit predominantly expressed in sensory and sympathetic neurones, may play an important role in nociception and vasomotor regulation.

Base Sequence↗
PubMed2004

Regulation of interleukin-1beta and interleukin-1beta inhibitor release by human airway epithelial cells.

In asthma, human airway epithelial cells (HAECs) regulate the intensity of mucosal inflammation, in part, by releasing the pro-inflammatory cytokine interleukin (IL)-1beta. However, the IL-1beta inhibitors, IL-1 receptor antagonist (IL-1RA) and soluble IL-1 receptor type II (sIL-1RII), regulate IL-1beta bioactivity. In order to better understand the control of IL-1beta activity in the airway mucosa, the role(s) of tumour necrosis factor (TNF)-alpha, cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP) in the release of IL-1beta and its inhibitors by cultured HAECs were examined. HAECs were treated with TNF-alpha (2-200 ng.mL(-1)), dibutyryl cAMP (0.01-1 mM), 8-bromo-cGMP (0.01-1 mM) or vehicle for 24 h, and cytokine levels in the HAEC-conditioned medium were measured by enzyme-linked immunosorbent assay. HAECs produced IL-1beta, IL-1RA and sIL-1RII constitutively, but the inhibitor concentrations greatly exceeded that of IL-1beta (by approximately 100- and approximately 550-fold, respectively). TNF-alpha dose-dependently increased the levels of all IL-1beta cytokine family members. However, over the range of TNF-alpha concentrations studied, IL-1beta concentration increased more than those of its inhibitors. cAMP increased constitutive and TNF-alpha-stimulated IL-1beta release but reduced that of sIL-1RII. In contrast, cGMP had no effect on IL-1beta but reduced IL-1RA and sIL-1RII release. Under basal conditions, the disproportionate release of inhibitors relative to interleukin-1beta by human airway epithelial cells probably prevents interleukin-1beta-mediated biological effects. Tumour necrosis factor-alpha, cyclic adenosine monophosphate and cyclic guanosine monophosphate may potentiate mucosal inflammation by increasing interleukin-1beta levels relative to those of its inhibitors in the airway mucosa.

Asthma↗
PubMed2004

NO-1886 decreases ectopic lipid deposition and protects pancreatic beta cells in diet-induced diabetic swine.

The synthetic compound NO-1886 (ibrolipim) is a lipoprotein lipase activator that has been proven to be highly effective in lowering plasma triglycerides. Recently, we found that NO-1886 also reduced plasma free fatty acids and glucose in high-fat/high-sucrose diet-induced diabetic rabbits. In the current study, we investigated the effects of NO-1886 treatment on ectopic lipid deposition and the islet pathology in miniature swine fed a high-fat/high-sucrose diet. Our results showed that feeding this diet to miniature swine caused insulin resistance, increased lipid deposition in non-adipose tissue, such as in the heart, skeletal muscle, liver and pancreas, and also caused pancreatic beta cell damage. However, supplementing 1% NO-1886 (200 mg/kg per day) into the high-fat/high-sucrose diet decreased ectopic lipid deposition, improved insulin resistance, and alleviated the beta cell damage. These results suggest that improvement of lipid disorder, non-adipose tissue steatosis and insulin resistance may be very important for the protection of beta cell damage. Therefore, NO-1886 is potentially beneficial for the treatment of insulin-resistance syndrome.

Animals↗
PubMed2004

Salivary immunoglobulin A and lysozyme in patients with psoriasis.

INTRODUCTION: We compared the salivary immunoglobulin A (IgA) and lysozyme concentration and secretion rates among mild and severe psoriasis patients and controls in Singapore. MATERIALS AND METHODS: Fifty-one psoriasis patients and 24 controls participated in the study. None of the patients were on immunosuppressive therapy. The Psoriasis Area and Severity Index (PASI) was used to assess the severity of psoriasis. Patients were divided into mild and severe groups by the median PASI score. Each subject contributed a 5-minute unstimulated salivary sample. Enzyme-linked immunosorbent assay method was used to determine the salivary IgA and lysozyme levels. RESULTS: Psoriasis patients had lower concentration and secretion rate of IgA (geometric mean [GM], 97.5 micro g/mL and 32.3 micro g/min) and lysozyme (GM, 127.6 micro g/mL and 42.1 micro g/min) than controls (IgA GM 256.3 micro g/mL, 79.1 micro g/min; lysozyme GM 180.9 micro g/mL, 55.8 micro g/min) [P = 0.000 (IgA concentration), P = 0.000 (IgA secretion rate), P = 0.015 (lysozyme concentration) and P = 0.150 (lysozyme secretion rate)]. However, no significant differences were observed between mild and severe patients for both IgA and lysozyme concentrations and secretion rates. PASI score showed negative, but non-significant, correlations with either log salivary IgA (r = -0.22, P = 0.13) or log lysozyme (r = -0.09, P = 0.53) secretion rates. CONCLUSION: Psoriasis patients had lower concentrations and secretion rates of salivary IgA and lysozyme compared to controls. However, among patients, the salivary IgA and lysozyme levels are variable and not related to severity of psoriasis.

Adult↗
PubMed2003

Dissecting autoimmune diabetes through genetic manipulation of non-obese diabetic mice.

Type 1 diabetes results from a genetically and immunologically complex autoimmune process that is specifically directed against the pancreatic beta cells. Non-obese diabetic mice spontaneously develop a form of autoimmune diabetes closely resembling the disease in humans. This happens because, like human diabetic patients, non-obese diabetic mice have an unfortunate combination of apparently normal alleles at numerous loci associated with Type 1 diabetes. In isolation, each of these allelic variants affords a small degree of susceptibility to diabetes. In combination, however, they set in motion a series of immunological events that lead to islet inflammation and overt diabetes. Type 1 diabetes is associated with defects in self-tolerance and immunoregulation. It involves presentation of beta cell antigens to autoreactive T lymphocytes by professional antigen-presenting cells, the recruitment of antigen-activated T cells into pancreatic islets, and the differentiation of these antigen-activated lymphocytes into beta cell killers. Understanding the precise sequence of events in the pathogenesis of Type 1 diabetes has been, and remains, a challenging task. Much of our understanding of the immunology of the disease stems from studies of genetically engineered, non-obese diabetic mice. These mice provide reductionist systems, with which the contribution of individual cellular elements, molecules or genes to the disease process can be dissected. This review focuses on the lessons that have been learned through studies of these mice.

Animals↗
PubMed2003

Maturation-dependent changes of angiotensin receptor expression in fowl.

An angiotensin (ANG) receptor homologous to the type 1 receptor (AT1) has been cloned in chickens (cAT1). We investigated whether cAT1 expression in various tissues shows maturation/age-dependent changes. cAT1 mRNA levels detected in renal glomeruli [in situ hybridization (ISH)] and kidney extract (RT-PCR) are significantly (P < 0.01) higher in 19-day embryos (EB) than in chicks (CH, 2-3 wk) and pullets/cockerels (PL/CK, 14-16 wk). The levels in adrenal glands (concentrated in subcapsular regions) are high in EB and further increased in CH and PL/CK. cAT1 mRNA is also detectable in smooth muscle (SM)/adventitia of EB and CH aorta and in the adventitia, but not SM, from PL/CK aortas. The endothelia from small arteries and arterioles, but not from aorta, express cAT1 mRNA (ISH). In all age groups, ANG II induces profound endothelium-dependent relaxation of abdominal aorta, partly (37-47%) inhibitable (P < 0.01) by Nomega-nitro-l-arginine methyl ester (l-NAME, 10(-4) M), suggesting the presence of ANG receptor in endothelium. l-NAME-resistant ANG II relaxation, examined in a limited number of EB or CH aortas, was reduced by 125 mM K+ or apamin plus charybdotoxin. The results suggest that 1) cAT1 is present in kidney, adrenal gland, and vascular endothelium (heterogeneity exists among arteries) of EB, CH, and PL/CK, and in aortic SM/adventitia of EB/CH but only in adventitia of PL/CK; 2) levels of cAT1 gene expression change during maturation in a tissue-specific manner; and 3) ANG II-induced relaxation may be partly attributable to nitric oxide and potassium channel activation.

Adrenal Glands↗