Search PubMed⌕ Search

Biomedical subjects

L Du

Publications and source records attributed to L Du.

At least 55 records · Page 3Linked to original sources
PubMed2000

Effect of protein denaturation on void fraction in foam separation column.

Foam fractionation is a cost-effective process that uses air to extract protein from a liquid (in this case "crude" dilute egg-albumin solution). This article deals with how the void fraction (fraction of air in the aerated solution) of foam is affected by heat denaturation of the protein. A 2-mm glass tube was used to sample the foam-liquid interface fluid in a 35-mm-diameter column in order to detect small changes in void fraction and foam production, which are not easily detected directly from the bulk foam. The main control variable in this study was the protein solution preheating time. As the preheating time increased, the initial void fraction in the column decreased. The initial void fraction of the undenatured solution ranged from about 0.73 to 0.80, and the void fraction for significant preheating times of 5 min ranged from approx 0.68 to 0.72. Furthermore, the period of foam production increased from 5 to 7 min for undenatured proteins in solution to as long 15 min for 5-min preheated solutions. Side-port sampling through a small capillary tube has the potential to be used as a rapid and inexpensive way to determine the level of protein denaturation by directly determining the void fraction and then estimating the effect of denaturation from a protein denaturation calibration curve of the void fraction.

Biotechnology↗
PubMed2000

Naloxone protects rat dopaminergic neurons against inflammatory damage through inhibition of microglia activation and superoxide generation.

Degeneration of dopaminergicrgic neurons in the substantia nigra of the brain is a hallmark of Parkinson's disease and inflammation and oxidative stress are closely associated with the pathogenesis of degenerative neurological disorders. Treatment of rat mesencephalic mixed neuron-glia cultures with lipopolysaccharide (LPS)-activated microglia, resident immune cells of the brain, to release proinflammatory and neurotoxic factors tumor necrosis factor-alpha, interleukin-1beta, nitric oxide, and superoxide and subsequently caused damage to midbrain neurons, including dopaminergic neurons. The LPS-induced degeneration of the midbrain neurons was significantly reduced by cotreatment with naloxone, an opioid receptor antagonist. This study focused on understanding the mechanism of action for the protective effect of naloxone on dopaminergic neurons because of relevance to Parkinson's disease. Both naloxone and its opioid receptor inactive stereoisomer (+)-naloxone protected the dopaminergic neurons with equal potency. Naloxone inhibited LPS-induced activation of microglia and release of proinflammatory factors, and inhibition of microglia generation of superoxide free radical best correlated with the neuroprotective effect of naloxone isomers. To further delineate the site of action, naloxone was found to partially inhibit the binding of [(3)H]LPS to cell membranes, whereas it failed to prevent damage to dopaminergic neurons by peroxynitrite, a product of nitric oxide and superoxide. These results suggest that naloxone at least in part interferes with the binding of LPS to cell membranes to inhibit microglia activation and protect dopaminergic neurons as well as other neurons in the midbrain cultures from inflammatory damage.

Animals↗
PubMed2000

Systemic infusion of naloxone reduces degeneration of rat substantia nigral dopaminergic neurons induced by intranigral injection of lipopolysaccharide.

A massive degeneration of dopamine-containing neurons in the substantia nigra (SN) in the midbrain is characteristic of Parkinson's disease. Inflammation in the brain has long been speculated to play a role in the pathogenesis of this neurological disorder. Recently, we reported that treatment of primary rat mesencephalic mixed neuron-glia cultures with lipopolysaccharide (LPS) led to the activation of microglia, resident immune cells of the brain, and subsequent death of dopaminergic neurons. The LPS-induced degeneration of dopaminergic neurons was significantly attenuated by the opiate receptor antagonist (-)-naloxone and its inactive isomer (+)-naloxone, with equal potency, through an inhibition of microglial activation and their production of neurotoxic factors. In this study, injection of LPS into the rat SN led to the activation of microglia and degeneration of dopaminergic neurons: microglial activation was observed as early as 6 h and loss of dopaminergic neurons was detected 3 days after the LPS injection. Furthermore, the LPS-induced loss of dopaminergic neurons in the SN was time- and LPS concentration-dependent. Systemic infusion of either (-)-naloxone or (+)-naloxone inhibited the LPS-induced activation of microglia and significantly reduced the LPS-induced loss of dopaminergic neurons in the SN. These in vivo results combined with our cell culture observations confirmed that naloxone protects dopaminergic neurons against inflammation-mediated degeneration through inhibition of microglial activation and suggest that naloxone would have therapeutic efficacy in the treatment of inflammation-related neurological disorders. In addition, the inflammation-mediated degeneration of dopaminergic neurons in the rat SN resulting from the targeted injection of LPS may serve as a useful model to gain further insights into the pathogenesis of Parkinson's disease.

Animals↗
PubMed2000

Progress in the molecular genetic research of multinodular goiter.

Multinodular goiter is a worldwide-distributed disease, but yet its pathology and genetic etiology are not clear. At present, most researches have been restrained to traditional epidemiological survey and the disease has been rarely studied at the level of molecular genetics. The pathogenesis of multinodular goiter, as is generally accepted by most researchers, can be attributed to many factors such as hormones, growth factors and the inherent functional heterogeneity of thyroid follicles. Since hormone and iodine metabolization are widely recognized as a major mechanism in determining the formation of multinodular goiter, some reports in literature are mainly focused on such genes that are responsible for hormone synthesis and iodine metabolization. Mapping experimental data were available to support location of multinodular goiter gene(s) onto chromosome 14q by whole genome scanning in a large pedigree analysis. Additional data, particularly those extracted from large scaled marker-assisted mapping experiments, are important so as to confirm the gene location, to improve resolution of the location, and finally to dissect the genes underlying the disease at molecular level.

Chromosome Mapping↗
PubMed2000

[Endoluminal stent-graft repair of aortic aneurysms].

OBJECTIVE: To study the clinical value of the treatment of aortic aneurysms with endovascular stent-graft prosthesis. METHODS: After a unilateral surgical arteriotomy, Talent, Vanguard and Chinese stent-graft were advanced through the femoral arteries and placed in the proper position of the aneurysm sac under X-ray fluoroscopic guidance. RESULTS: Four patients with descending aneurysm, 1 patient with abdominal aortic aneurysm (AAA) involving the renal artery, superior mesenteric artery and celiac artery, and 1 patient with right common iliac artery aneurysm received straight stent-grafts. Five patients with infrarenal AAA received bifurcated stent-grafts. CT and MRA were performed during a follow-up of 3 - 19 months. Aortic aneurysms were completely excluded from the circulation. Five patients prolonged fever was noted and 1 patient was found to have a leakage 3 months later, and hemiplegia in 1 after procedure. CONCLUSIONS: Endovascular treatment of aortic aneurysm is technically feasible and can effectively exclude aortic aneurysms from the circulation. Endoluminal repair may serve as an interventional strategy to treat aneurysm, especially in patients at high surgical risk, but long term effect needs further study.

Adult↗
PubMed2000

[Abdominal aortic aneurysm treated by endovascular stent-graft and conventional surgical repair: a comparison].

OBJECTIVE: To evaluate the feasibility of abdominal aortic aneurysm (AAA) treated by endovascular stent-graft. METHODS: The clinical data of 52 patients with AAA treated by endovascular stent-graft (n = 20) and conventional surgical repair (n = 32) were analysed retrospectively. Patients conditions, operative hours, blood loss, function recovery and complications were compared. RESULTS: No significant difference was observed in sex, age, other disease, anesthesia risk category, aneurysm type, aneurysm diameter, technical success rate, and mortality rate between the groups (P > 0.05). The patients who underwent intraluminal treatment had significant reductions in operative time, blood loss, intensive care unit and hospitalization. But there was a high complication rate in the endovascular stent-graft group. All complications were connected with the interventional technique; endo-leak was the chief complication after operation. CONCLUSIONS: Endovascular treatment has marked merits such as reduced trauma, short hospitalization stays, and early functional recovery. It is suitable for the patients who can't undergo open surgical repair. But the complications caused by this technique needs further study.

Aged↗
PubMed2000

[Study on the effect of several antioxidants on the stability of oils].

The stability of oils is very important for ensuring the sanitation and quality of oils and the foods containing oils and fats. In this study, BHT, TBHQ and micro-capsule antioxidants (mixed antioxidants) were tested for their properties of antioxidation in oils under different temperatures. The results showed that the mixed antioxidant used in oils was more effective than the single antioxidant, especially under high temperature. It was concluded that microcapsule antioxidant was effective, economical and relatively safe when it was used in oils for frying foods.

Antioxidants↗
PubMed1999

Norepinephrine transporter gene polymorphism is not associated with susceptibility to major depression.

The monoamine neurotransmitters serotonin, norepinephrine and dopamine have been implicated in the pathogenesis of depression, schizophrenia and mood disorders. The mechanism of action of certain antidepressant drugs, particularly the tricyclics and the newly available norepinephrine and serotonin reuptake inhibitors (NSRIs) drugs, venlafaxine and nefazodone, suggest that the norepinephrine transporter, which is a target for these antidepressant drugs, and its malfunction may be involved in major depression. In this association study, we tested the hypothesis that variants of the human norepinephrine transporter (NET) gene confer susceptibility to major depression. One hundred and five patients with major depression and 74 unrelated matched controls were analyzed for a silent 1287G/A polymorphism (NET-8) in exon 9 of the NET gene. No significant differences in genotype or allele frequencies were found between controls and patients, nor between subgroups of depressed patients classified by suicidal ideation. In addition, 60 controls and 60 patients were genotyped for a missense substitution Thr99Ile in exon 2 of the NET gene (NET-1), but only one control was heterozygous for this variant. These results suggest that the NET gene is unlikely to be involved in the susceptibility to major depression.

Adult↗
PubMed1999

Frequency of long allele in serotonin transporter gene is increased in depressed suicide victims.

BACKGROUND: There is evidence indicating that serotonin uptake and density of 5-HT2A receptors are altered in brain regions of depressed suicide victims and in platelets of depressed suicidal subjects. The present investigation tested the hypothesis that these changes in the serotonergic system in depressed suicide victims are trait rather than state markers and associated with a polymorphism in respective candidate genes. METHODS: Two polymorphic variants (102T/C polymorphism and His452Tyr functional polymorphism) of the 5-HT2A receptor gene and a functional polymorphism in the 5' regulatory region of the 5-HT transporter gene, have been determined in genomic DNA obtained from postmortem brain samples of 24 depressed suicide victims and 31 control subjects of the same ethnic background. In a subset of subjects, density (Bmax) of 5-HT uptake sites (labeled with 3H-paroxetine) and of 5-HT2A receptors (labeled with 3H-ketanserin) was also determined in prefrontal cortex samples. RESULTS: The major finding of this study was a significantly higher frequency of the 5-HT transporter gene long (L) allele (chi 2 = 3.9, df = 1; p = .048) in depressed suicides. No significant differences between suicides and controls were observed for the 102T/C polymorphism and His452Tyr polymorphism of 5-HT2A receptor gene. The density of 3H-paroxetine binding sites tended to be higher in subjects expressing the short (S) allele of 5-HT transporter gene. Furthermore, there was a significant difference in serotonin transporter binding sites between the genotype S/S and combined genotypes S/L and L/L. CONCLUSIONS: Our finding provides the first evidence suggesting that a functional polymorphism in the regulatory region of serotonin transporter gene may be associated with suicide in depressed subjects.

Adult↗
PubMed1999

Tentative novel mechanism of the bystander effect in glioma gene therapy with HSV-TK/GCV system.

Although many works support gap junctional intercellular communication (GJIC) having a close relation to bystander cell killing in herpes simplex virus thymidine kinase (HSV-TK) gene and ganciclovir (GCV) treatment, our previous work suggested that other factors involved in bystander effect besides GJIC exist. To confirm our primary work, we evaluated the mode of the bystander cell (C6) co-cultured with TK-positive cells (TF10.2) in our designed "insert plates" in which two cell lines could be separated but share the same medium. Another method that we used was adding the supernatant from the medium of GCV-treated TF10.2 cells to the wild type C6. Growth inhibition of the bystander cells was observed despite the absence of GJIC. In addition, apoptotic cell death of TK+ cells and bystander cells was obvious. These studies suggested that other pathways besides cell-cell contacts may play a role in bystander cell killing; the factors released from TK-positive cells could induce apoptosis of bystander cells.

Apoptosis↗
PubMed1999

Relationship between central and peripheral serotonin 5-HT2A receptors: a positron emission tomography study in healthy individuals.

5-HT2A receptors on platelet membranes are often measured as indirect markers of the central 5-HT2A receptors. However, the 5-HT2A receptors on the platelets and those in the brain have never been assessed simultaneously in humans. The purpose of this study was to evaluate the relationship between platelet membrane and neocortical 5-HT2A receptors measured simultaneously in normal healthy volunteers. Twelve healthy volunteers had the 5-HT2A receptors on their platelet membranes assessed in vitro using [3H]lysergic acid diethylamide ([3H]LSD) and their central 5-HT2A receptors measured in vivo using [18F]setoperone and positron emission tomography (PET) imaging. We find no significant correlation between the binding potential (Bmax/Kd) of 5-HT2A receptors on platelets and in brain in the same individual (F1,10 = 0.7, P = 0.42). The study was limited by a small sample and the fact the two different ligands were used (i.e. LSD for platelets and setoperone for brain); nonetheless, the findings suggest that changes in platelet 5-HT2A receptors may not indicate similar changes in central 5-HT2A receptors.

Adult↗
PubMed1999

Familiarity leads to female mate preference for novel males in the guppy, Poecilia reticulata.

Guppies are a model vertebrate for studies of sexual selection and life history evolution. None the less, there have been few investigations of the factors responsible for maintaining extreme within-population genetic variation in male coloration. In a laboratory study, we tested the hypothesis that frequency-dependent mate choice contributes to the maintenance of this variation. We attempted to avoid biases inherent in earlier studies of the 'rare male effect' by familiarizing females to males bearing a particular colour pattern and later presenting them with alternate male types, in equal numbers. Females were significantly more likely to mate with males having novel colour patterns than with males having a colour pattern with which they were familiar. This result is consistent with the hypothesis that mate choice is frequency dependent. Other factors such as male and female size were unrelated to mate preference. Implications of the results for theories of sexual selection and the maintenance of variation are discussed. Copyright 1999 The Association for the Study of Animal Behaviour.

Journal Article↗
PubMed1999

Evidence for Phex haploinsufficiency in murine X-linked hypophosphatemia.

Mutations in the PHEX gene (phosphate-regulating gene with homology to endopeptidases on the X-chromosome) are responsible for X-linked hypophosphatemia (HYP). We previously reported the full-length coding sequence of murine Phex cDNA and provided evidence of Phex expression in bone and tooth. Here, we report the cloning of the entire 3.5-kb 3'UTR of the Phex gene, yielding a total of 6248 bp for the Phex transcript. Southern blot and RT-PCR analyses revealed that the 3' end of the coding sequence and the 3'UTR of the Phex gene, spanning exons 16 to 22, are deleted in Hyp, the mouse model for HYP. Northern blot analysis of bone revealed lack of expression of stable Phex mRNA from the mutant allele and expression of Phex transcripts from the wild-type allele in Hyp heterozygous females. Expression of the Phex protein in heterozygotes was confirmed by Western analysis with antibodies raised against a COOH-terminal peptide of the mouse Phex protein. Taken together, these results indicate that the dominant pattern of Hyp inheritance in mice is due to Phex haploinsufficiency.

3' Untranslated Regions↗
PubMed1999

Personality correlates of auditory augmenting response to clicks repeated around 2Hz.

Eighty-three subjects (47 women and 36 men) were submitted to Plutchik-van Praag's (PVP) depression inventory, Zuckerman's sensation seeking scales and Zuckerman-Kuhlman's personality inventory, and underwent auditory evoked potential studies using clicks at 4 different intensities of 70, 80, 90 and 100 dB. The clicks were delivered at an interstimulus interval varying randomly around 0.5s, which can elicit an obligatory subcomponent of N1. The P2 latency was significantly prolonged at the highest intensity. The intensity dependence of peak-to-peak N1-P2 and of baseline-to-peak N1 and P2 components was pronounced and the majority of subjects were augmenters. The N1 latency elicited at 70 dB was positively correlated with the thrill and adventure seeking, which then correlated the activity. The correlation suggests that a lower level of arousal, as indicated by prolonged N1 latency, would lead one to seek higher stimulation, such as the augmented response, the increased desire of physical thrill and adventure and elevated activity. This study, therefore, supports Zuckerman's theory that a sensation seeking personality is related to cortical arousal level.

Acoustic Stimulation↗
PubMed1999

Identification and characterization of a type II peptidyl carrier protein from the bleomycin producer Streptomyces verticillus ATCC 15003.

BACKGROUND: Nonribosomal peptide synthetases (NRPSs) catalyze the assembly of a structurally diverse group of peptides by the multiple-carrier thiotemplate mechanism. All NRPSs known to date are exclusively type I modular enzymes that consist of domains, such as adenylation (A), peptidyl carrier protein (PCP) and condensation (C) domains, for individual enzyme activities. Although several A and PCP domains have been demonstrated to function independently, aminoacylation in trans has been successful only between PCPs and their cognate A domains. RESULTS: We have identified within the bleomycin-biosynthesis gene cluster from Streptomyces verticillus ATCC15003 the blmI gene that encodes a discrete PCP protein. We overexpressed the blmI gene in Escherichia coli, purified the BlmI protein, and demonstrated that apo-BlmI can be efficiently modified into holo-BlmI either in vivo or in vitro by PCP-specific 4'-phosphopantetheine transferases (PPTases). Unlike the PCP domains in type I NRPSs, BlmI lacks its cognate A domain and can be aminoacylated by Val-A, an A domain from a completely unrelated type I NRPS. CONCLUSIONS: BlmI represents the first characterized type II PCP. The BlmI type II PCP, like the PCP domains of type I NRPSs, can be 4'-phospho-pantetheinylated by PCP-specific PPTases but is biochemically distinct in that it can be aminoacylated by an A domain from a completely unrelated type I NRPS. Our results provide for the first time the genetic and biochemical evidence to support the existence of a type II NRPS, which might be useful in the combinatorial manipulation of NRPS proteins to generate novel peptides.

Adenine↗
PubMed1999

Childhood blindness.

PURPOSE: The objective of this study was to summarize available data regarding pediatric blinding diseases worldwide and to present the most up-to-date information on childhood blindness in the United States. METHODS: We obtained data from a complete search of the world literature and from direct contact with each of the schools for the blind in the United States. RESULTS: Five percent of worldwide blindness involves children younger than 15 years of age; in developing countries 50% of the population is in this age group. By World Health Organization criteria, there are 1.5 million children worldwide who are blind: 1.0 million in Asia, 0.3 million in Africa, 0.1 million in Latin America, and 0.1 million in the rest of the world. There are marked differences in the causes of pediatric blindness in different regions, apparently based on socioeconomic factors. In developing countries, 30% to 72% of such blindness is avoidable, 9% to 58% is preventable, and 14% to 31% is treatable. The leading cause is corneal opacification caused by a combination of measles, xerophthalmia, and the use of traditional eye medicine. There is no national registry of the blind in the United States, and most of the schools for the blind do not keep data regarding the cause of blindness in their students. From those schools that do have this information, the top 3 causes are cortical visual impairment, retinopathy of prematurity, and optic nerve hypoplasia. There has been a significant increase in both cortical vision loss and retinopathy of prematurity in the past 10 years. CONCLUSIONS: There are marked regional differences in the prevalence and causes of pediatric blindness, apparently based on socioeconomic factors that limit prevention and treatment schemes. In the United States the 3 leading causes of pediatric blindness are cortical visual impairment, retinopathy of prematurity, and optic nerve hypoplasia. There is a need for more complete and more uniform data based on the established World Health Organization reporting format.

Adolescent↗