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Biomedical subjects

L C Lu

Publications and source records attributed to L C Lu.

16 recordsLinked to original sources
PubMed1998

Elevated amniotic fluid levels of leukemia inhibitory factor, interleukin 6, and interleukin 8 in intra-amniotic infection.

OBJECTIVE: The study's objective was to determine and correlate amniotic fluid levels of leukemia inhibitory factor, interleukin 6, and interleukin 8 in patients with and without intra-amniotic infection. STUDY DESIGN: Amniocentesis was performed on 41 pregnant women with preterm contractions, labor, or premature rupture of membranes. Intra-amniotic infection was defined as the presence of a positive amniotic fluid culture result. Amniotic fluid tests for Gram stain, glucose, leukocyte counts, creatinine level, pH, and specific gravity were performed. Amniotic fluid levels of leukemia inhibitory factor, interleukin 6, and interleukin 8 were measured by an enzyme-linked immunoassay. Unlike in previous reports, cytokines were normalized by amniotic fluid creatinine levels. RESULTS: Fifteen patients had intra-amniotic infection and 26 did not. Amniotic fluid median levels of leukemia inhibitory factor, interleukin 6, and interleukin 8 were significantly higher in pregnant women with intra-amniotic infection than in those without intra-amniotic infection (leukemia inhibitory factor median 3912 pg/mg creatinine, range 0.0-199314, vs 56 pg/mg creatinine, range 0. 0-12148, P =.01; interleukin 6 median 2005 ng/mg creatinine, range 27-4071, vs 990 ng/mg creatinine, range 7.5-3409, P =.005; interleukin 8: median 4933 ng/mg creatinine, range 0.0-55058, vs 61 ng/mg creatinine, range 0.0-2399, P =.005). Amniotic fluid levels of leukemia inhibitory factor, interleukin 6, and interleukin 8 were positively correlated. CONCLUSIONS: The data indicate that leukemia inhibitory factor plays an important role in the pathogenesis of intra-amniotic infection. In addition, significant elevations of and correlations among amniotic fluid levels of leukemia inhibitory factor, interleukin 6, and interleukin 8 suggest that measurements of these cytokines in amniotic fluid may be of diagnostic and prognostic importance.

Adolescent↗
PubMed1998

Immunohistochemical localization of inducible nitric oxide synthase on human fetal amnion in intra-amniotic infection.

OBJECTIVES: Amniotic fluid levels of nitric oxide metabolites are significantly elevated in intra-amniotic infection. We hypothesized that fetal amnion is a possible site for the production of nitric oxide. Because inducible nitric oxide synthase is the key enzyme responsible for the generation of nitric oxide in patients with intra-amniotic infection, we used immunohistochemistry to localize it on human fetal amnion. STUDY DESIGN: Human fetal amnions were obtained from patients with and without intra-amniotic infection (n = 5, respectively). Intra-amniotic infection was diagnosed by positive amniotic fluid cultures and placental pathologic features. Human fetal amniotic membranes were processed into tissue blocks and embedded in paraffin. A rabbit polyclonal antibody against human inducible nitric oxide synthase was used as the primary antibody, followed by avidin-biotin immunoperoxidase localization. Normal rabbit serum was used as a negative control and ovarian carcinoma cells were used as the positive control. RESULTS: Anti-inducible nitric oxide synthase labeling of human fetal amniotic membranes in patients with intra-amniotic infection showed positive immunostaining of epithelial cells, specifically in the cytoplasm of the perinuclear area. In contrast, no anti-inducible nitric oxide synthase immunostaining on human fetal amniotic membranes could be identified in patients without intra-amniotic infection. CONCLUSIONS: Our data provide important evidence that inducible nitric oxide synthase can be induced on human fetal amnion in intra-amniotic infection. These findings strongly support our hypothesis that human fetal amnion may be a possible site for the synthesis of nitric oxide after inducible nitric oxide synthase is induced in response to infectious products in intra-amniotic infection.

Amnion↗
PubMed1998

Lipopolysaccharide enhances neurogenic plasma exudation in guinea-pig airways.

1. Lipopolysaccharide (LPS) is implicated in many pulmonary and airway inflammatory diseases. Tachykinins released from nerve endings increase vascular permeability. In this study, we have assessed the enhancement by LPS of tachykinin-mediated plasma exudation in guinea-pig airways, and examined the role of oxidants as well as leukocyte adherence. 2. LPS (100 microg kg(-1), i.v.) was administered 0-3 h before bilateral electrical stimulation of the cervical vagus nerves in animals anaesthetized with urethane and ventilated. Vagal stimulation increased vascular permeability in the airways. LPS enhanced the vagally-mediated plasma exudation with the peak effect at 1 h after LPS administration. LPS alone induced no significant plasma exudation. LPS also enhanced exogenous substance P (10(-8) mol kg(-1), i.v.)-induced plasma exudation. 3. The NK-1 receptor antagonist L-732,138 abolished vagally-induced plasma exudation and significantly inhibited the enhancement by LPS. Pretreatment with superoxide dismutase (SOD, 5000 U kg(-1), i.p.) did not affect the vagally-induced plasma exudation, but inhibited the LPS-enhanced neurogenic plasma leakage. The LPS-enhanced vagally-induced plasma exudation was not completely inhibited by either L-732,138 or SOD pretreatment alone, but was blocked by the combination of both pretreatments. 4. Neutrophil depletion by cyclophosphamide alone did not influence vagally-induced plasma exudation, but significantly inhibited the LPS-enhanced response. 5. In conclusion, we have demonstrated LPS enhanced neurogenic plasma exudation by augmenting the response to tachykinins, partly through NK-1 receptors, to directly increase vascular permeability or to enhance leukocyte adhesion-mediated endothelial cell injury. Tachykinins released from nerve endings may contribute to endotoxin-related airway inflammatory responses.

Animals↗
PubMed1998

[The density and larval habitats of dengue vectors in Chungho city].

A survey was conducted to understand larval habitats and density of dengue vectors in Chungho city during the period of August 12 to September 13, 1996. Most villages (41 in the total of 93) were found to have the density figures of three for Aedes albopictus Skuse. The second common density figures were found at 2nd and 4th levels. The most common breeding containers found were less than 5 cm in water depth and less than 100 cm2 in water area. The number of breeding containers reduced when the water depth and size increased. The common breeding containers in villages were flower vases (30%) and water buckets (18%). In the mountains, water buckets (34%) and kitchen tools (11%) were common. In parks, water buckets (29%) and tires (15%) were commonly found. In cemeteries, the common breeding containers were flower vases (57%) and earthenware pots (17%). The average (2.05 containers per man-hour) of positive water containers in the mountains was significantly higher than that in parks (0.62). However, the average in cemeteries (1.29) was not significantly different from those collected in mountains and parks.

Aedes↗
PubMed1997

Effect of endogenous nitric oxide on tumour necrosis factor-alpha-induced leukosequestration and IL-8 release in guinea-pigs airways in vivo.

1. Tumour necrosis factor-alpha (TNF-alpha) is implicated in the pathogenesis of many pulmonary and airway diseases. TNF-alpha stimulation may release interleukin-8 (IL-8) in airways mediated via an increase in intracellular oxidant stress. In the present study, we have assessed leukosequestration and IL-8 release in the airways in response to intratracheal administration of human recombinant TNF-alpha, and examined the modulatory role of endogenous NO by pretreatment with a NO synthase inhibitor N(omega)-nitro-L-arginine methyl ester (L-NAME). 2. TNF-alpha (10(2)-10(-4) u) was administered intratracheally in male guinea-pigs which were anaesthetized with urethane and were ventilated artificially. TNF-alpha induced a time- and dose-related increase in neutrophil numbers and a concomitant increase in human IL-8 equivalent level retrieved from bronchoalveolar lavage (BAL) with the peak effect at 10(3) u at 6 h of TNF-alpha injection (late phase). Intratracheal administration of recombinant human (rh)IL-8 (0.025, 0.25, 2.5 ng) producing a similar range of human IL-8 equivalent levels in BAL as measured in our results induced neutrophil recovery in BAL fluid to a similar extent. Administration of anti-IL-8 antibody prevented the late phase of neutrophil recruitment induced by TNF-alpha or rhIL-8. 3. Pretreatment with L-NAME significantly enhanced the TNF-alpha (10(3) u)-induced neutrophil recruitment and human IL-8 equivalents production at 6 h, but not at 1 h of TNF-alpha administration (early phase). L-Arginine reversed the responses to L-NAME. Pretreatment with 0.2% DMSO (i.v.) significantly inhibited TNF-alpha-induced neutrophil recruitment and human IL-8 equivalents release both in the early and late phase of the responses. Pretreatment with DMSO also inhibited the enhancement effect of L-NAME on the late phase of TNF-alpha-induced responses. DMSO failed to modify exogenous rhIL-8-induced neutrophil recruitment. Neither L-NAME nor DMSO alone induced any significant change in neutrophil numbers or human IL-8 equivalent level in BAL fluid. 4. Neutrophil depletion by cyclophosphamide pretreatment failed to modify TNF-alpha-induced human IL-8 equivalent release. 5. The expression of beta 2-integrin, CD11b/CD18 on neutrophils was increased only in the late but not early phase of TNF-alpha stimulation. L-NAME failed to modify these responses. 6. In conclusion, we demonstrated that NO may be an important endogenous inhibitor of TNF-alpha-induced leukocyte chemotaxis via inhibition of IL-8 production. Thus, the production of NO in airway inflammatory diseases may play a negative feedback role in self-limiting the magnitude of inflammatory responses.

Animals↗
PubMed1995

Sensory neuropeptides modulate cigarette smoke-induced decrease in neutral endopeptidase activity in guinea pig airways.

Cigarette smoke (CS) inhalation stimulates C-fibers to release sensory neuropeptides which mediate airway reflex responses to prevent irritants from entering the lower airways. When CS is inhaled via the upper airways, these airway defense responses may modulate the effect of CS on airway NEP activity and related airway hyperresponsiveness. To examine this possibility, we exposed guinea pigs to 1:10 diluted mid-tar cigarette smoke 100 puffs per day for 7 days and recorded pulmonary resistance of cumulative doses of neurokinin A (NKA, 10(-12)-10(-8) mol/kg, i.v.) or methacholine (Mch, 1-50 micrograms/kg, i.v.). NEP activity in the tracheobronchi was measured using fluorometric assay. Exposure of CS alone failed to alter the dose-response to NKA or Mch compared with air control. NEP activity in the airways after CS exposure was slightly but significantly lower than that of air control. Capsaicin pretreatment 1 week before CS exposure significantly shifted the dose-response curves of NKA, but not Mch, to the left and decreased NEP activity in the airways to a greater extent compared with CS exposure alone group. Capsaicin pretreatment alone failed to alter the responsiveness to NKA or NEP activity. CS also induced a significant increase in neutrophil counts in airways. Capsaicin pretreatment enhanced the effect of CS on neutrophil recruitment. We conclude that sensory neuropeptides may have a protective role in modulation of airways NEP activity downregulation induced by CS, probably by preventing CS from entering the lower airways or the chronic release of sensory neuropeptides induced by CS providing increased amount of substrata for NEP upregulation, and therefore modify the direct effect of CS on NEP activity and related airway hyperresponsiveness.

Airway Resistance↗
PubMed1989

Experimental vertical transmission of Japanese encephalitis virus by Culex tritaeniorhynchus and other mosquitoes.

Vertical transmission of Japanese encephalitis virus to the F1 adult stage was demonstrated in Culex tritaeniorhynchus, Cx. annulus, Cx. quinquefasciatus, and Armigeres subalbatus. Transmission to the F1 larval stage was demonstrated in Cx. pipiens, Aedes vexans, Ae. alcasidi, and A. flavus. In Cx. tritaeniorhynchus, vertical transmission rates (the percentage of parent females transmitting to progeny) varied (12-100%). Filial infection rates (the percentage of progeny infected) for a given mosquito virus combination were markedly affected by the interval of time between parental infection and oviposition, suggesting that vertical infection was not transovarial in nature but occurred at oviposition. Filial infection rates for Cx. tritaeniorhynchus also varied widely by family and, as measured in F1 larvae, rates in excess of 20% were observed in a family. Filial infection rates in Cx. tritaeniorhynchus F1 adults were about 4 times lower than those in larvae. Japanese encephalitis virus was sexually transmitted from male to female Cx. tritaeniorhynchus.

Animals↗
PubMed1989

A longitudinal study of the prevalence of Japanese encephalitis virus in adult and larval Culex tritaeniorhynchus mosquitoes in northern Taiwan.

Adult females and larvae of Culex tritaeniorhynchus were collected year-round for 3 1/2 years at a site near Taipei, Taiwan. One hundred sixty-four isolates of Japanese encephalitis (JE) virus were obtained from approximately 142,000 adult females and 1 isolate of the virus was obtained from approximately 382,000 larvae. Virus was recovered from adult females every year, except the first, beginning in May. The single larval isolate was from specimens collected in June. The vertical transmission of JE virus in Cx. tritaeniorhynchus as a possible inter-epidemic viral survival mechanism is examined.

Animals↗
PubMed1989

The relation between Campylobacter pylori and inflammatory cell infiltration of antral mucosa in patients with dyspepsia.

In order to understand the relation between the prevalence of Campylobacter pylori and the severity of gastritis, we conducted a survey of 166 randomly selected dyspeptic patients. The presence of C. pylori on the antral mucosa was aseptically determined by both urease and bacterial culture tests. Specimens of antral mucosa were obtained for pathologic gradings of inflammation: active gastritis, mononuclear cell infiltration C0 (nil) to C3 (lymphoid follicle); presence or absence of intestinal metaplasia. Pathologically, chronic gastritis was invariably present in almost all patients with dyspepsia: three-fourths of them showed evidence of active gastritis, one-third showed intestinal metaplasia. Half of the dyspeptic individuals had C. pylori colonization. The results suggest that the prevalence of C. pylori was closely related to the different grades of active gastritis; neither the different grades of chronic gastritis nor intestinal metaplasia affected the prevalence of C. pylori on gastric mucosa. We conclude from this study that C. pylori is closely related to active chronic gastritis because of the common presence of chronic gastritis in patients with dyspepsia.

Adult↗
PubMedDate not supplied

The bite of a wolf: systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is a chronic inflammatory disease of unknown etiology that occurs in people who have an aberrant immune system; it affects most major organ systems. People with SLE vacillate between periods of remission and exacerbation, with symptoms of fatigue and chronic pain, and experience disturbances in self-concept. SLE no longer has the high mortality rate of past years due to improved diagnostic tests that allow for earlier detection and treatment. SLE is a complex disease that affects the individual and the family. Rehabilitation nurses should use a holistic approach to treat altered functional ability and help individuals adjust to lifestyle changes associated with chronic illness and/or disability. Nurses with specialized rehabilitation knowledge and skill can help individuals with SLE realize and reach their optimal level of functioning, and thus improve their quality of life.

Female↗
PubMedDate not supplied

Elevated amniotic fluid nitric oxide metabolites and interleukin-6 in intra-amniotic infection.

OBJECTIVE: To compare amniotic fluid nitric oxide metabolites and interleukin-6 (IL-6) concentrations in patients with and without intra-amniotic infection. METHODS: Amniotic fluid nitric oxide metabolites, IL-6, Gram stains, glucose, leukocyte counts, leukocyte esterase activity, creatinine, pH, and specific gravity were determined in 14 patients with intra-amniotic infection and 26 patients without intra-amniotic infection. Intra-amniotic infection was defined as the presence of a positive amniotic fluid culture. The nitric oxide metabolites, nitrate and nitrite (NOx), were measured using Greiss reagent after reduction of nitrate to nitrite with aspergillus nitrate reductase. Interleukin-6 was measured by a two-site, enzyme-linked immunosorbent assay. Amniotic fluid nitric oxide metabolites and IL-6 concentrations were normalized by amniotic fluid creatinine levels. The Mann-Whitney U test, contingency table method, and Spearman's rank correlation test were used for statistical analyses. RESULTS: Amniotic fluid NOx and IL-6 levels were significantly higher in patients with intra-amniotic infection than in those without intra-amniotic infection (NOx: median = 2.06 mumol/mg creatinine, range = 0.74-6.81 versus 1.35 mumol/mg creatinine, range = 0.99-1.60, P = .01, IL-6: median = 2.00 micrograms/mg creatinine, range = 0.026-4.07 versus median = 0.04 micrograms/mg creatinine, range = 0.004-3.210, P = .0009, respectively). Patients with intra-amniotic infection had significantly elevated leukocyte counts, leukocyte esterase activity, Gram positive stains, and significantly lower amniotic fluid glucose levels compared with those without intra-amniotic infection. There were no differences in gestational age, maternal age, parity, race, pH, or specific gravity between the two groups. Amniotic fluid NOx was significantly correlated with IL-6 (r = .4, P = .02). Both amniotic fluid NOx and IL-6 were also positively correlated with amniotic fluid leukocyte counts, leukocyte esterase activity and Gram stains, and negatively correlated with glucose levels. CONCLUSIONS: Amniotic fluid NOx and IL-6 are significantly elevated and positively correlated during intra-amniotic infection. Both increased amniotic fluid IL-6 and nitric oxide may exert cytotoxic and cytostatic effects on the target cells. We suggest that measurements of amniotic fluid NOx and IL-6 may serve as useful clinical markers in patients with intra-amniotic infection.

Adolescent↗
PubMedDate not supplied

Medical treatment of duodenal ulcer: acid inhibition or Helicobacter pylori eradication?

To ascertain whether acid inhibition or Helicobacter pylori (HP) colonization is the decisive factor in the healing of duodenal ulcer, we treated 54 patients with famotidine and carried out long-term follow-up. Helicobacter pylori colonization was found in 70.4% of patients before treatment. There were no differences in the pre-treatment characteristics between patients with HP positive or HP negative ulcers. The 4-week and 8-week healing rates after famotidine treatment were 72.5% and 82.4% respectively. No difference in HP colonization was found between patients with ulcer healed and those with ulcer not healed (78.4% vs 64.3% at 4th week and 77.3% vs 71.4% at 8th week, P greater than 0.05). In patients with ulcer healed at 4th week, the intragastric pH was raised significantly and the antral acute inflammation was less severe than those with ulcer not healed. Ulcer recurrence was found in 76.9% of patients within 1 year, but there was no difference in ulcer recurrence between the patients with positive or negative HP colonization at the time of ulcer healing. Our results suggest that duodenal ulcer healing and recurrence are closely related to acid inhibition rather than to HP colonization.

Duodenal Ulcer↗