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Biomedical subjects

T C Sim

Publications and source records attributed to T C Sim.

At least 19 recordsLinked to original sources
PubMed1998

Effect of nimodipine on memory after cerebral infarction.

OBJECTIVES: Epidemiological studies indicate widespread memory impairment in patients with stroke in the early post-ictal stage. Nimodipine may have psychopharmacological properties and may improve memory. We conducted a single-blind randomized controlled trial to determine whether nimodipine given 7-14 days after cerebral infarction improved memory. MATERIAL AND METHODS: One hundred patients with acute cerebral infarction were consecutively enrolled between D7 to D14. After stratification, patients were randomized to receive oral nimodipine 90 mg daily for 12 weeks, or no drug. Independent assessors administered Mini-Mental State Examination (MMSE) and Fuld Object-Memory Evaluation (FOME) at baseline, 6 weeks, and 12 weeks. RESULTS: Patients receiving nimodipine showed greater improvement in FOME mean scores at 12 weeks (P=0.0334), and also in FOME score change across time (P=0.0283). Patients with severe disability who received nimodipine also showed greater MMSE score change across time (P=0.0495). CONCLUSION: Nimodipine given 7-14 days after cerebral infarction for 3 months results in memory improvement.

Aged↗
PubMed1997

Outcome after stroke rehabilitation in Hong Kong.

OBJECTIVE: To determine the outcome of patients discharged to the community after stroke rehabilitation. METHODS: One hundred and eighty-five consecutive patients discharged after stroke rehabilitation were enrolled for follow-up 12 months after discharge from a hospital in Hong Kong. A telephone interview to determine disability and place of residence was conducted. Disability was assessed by the Barthel Index and ratings of activities of daily living and mobility on a 4-point scale. RESULTS: One hundred and thirty-one patients or their carers were contacted (70.1%). This comprised 19 patients (10.3%) who died and 112 patients or their carers (60.5%) who were interviewed. Fifty-four patients (29.2%) were lost to follow-up. Comparison of the patients contacted and those lost to follow-up did not detect membership bias. Median Barthel Index of the surviving patients who were contacted rose from 90.0 (interquartile range 78.75-100.0) at discharge to 100.0 (interquartile range 85.0-100.0) at 12 months. Ratings of activities of daily living and mobility were maintained, with significant improvement in toileting. After rehabilitation 77.3% of the patients were discharged home and there was no significant change in residence at 12 months. Elderly patients (> or = 70 years old) had higher rates of institutionalization after hospital discharge and more disability although they achieved similar gains in Barthel Index and had similar lengths of hospital stay compared to younger patients. CONCLUSIONS: These results suggest that stroke patients were able to maintain their gains achieved during inpatient rehabilitation up to one year after discharge from hospital.

Activities of Daily Living↗
PubMed1996

The production of macrophage inflammatory protein-1 alpha by human basophils.

Macrophage inflammatory protein-1alpha (MIP-1alpha) has previously been shown to be produced by mononuclear cells, eosinophils, and neutrophils. Its production by basophils has not been investigated. The objective of this study was to investigate the production of MIP-1alpha by basophils. Peripheral blood basophils were separated by Percoll gradient centrifugation, cultured overnight, and processed for double immunocytochemistry using Abs against MIP-1alpha and FcepsilonRIalpha (alpha subunit of IgE receptor type 1). We demonstrated that basophils expressed immunoreactive MIP-1alpha upon stimulation with anti-IgE. Less than 5% of the basophils stained for MIP-1alpha without stimulation. The secretion of MIP-1alpha by basophils was studied by ELISA. In these experiments, basophils were further enriched to 65 to 99% (median, 86%) by a negative selection method. Basophils released MIP-1alpha when stimulated by Abs against IgE and FCepsilonRIalpha as well as IL-3 and the calcium ionophore, A23187. In parallel experiments, PBMC, eosinophils, and neutrophils did not produce MIP-1alpha in response to anti-IgE, but they did so in response to A23187. No MIP-1alpha release was detected in platelet preparations. Preincubation with IL-3 (15 min or 18 h) augmented anti-IgE-included basophil MIP-1alpha production. The secretion of MIP-1alpha by basophils was detectable shortly after stimulation and gradually increased over 24 h. Since MIP-1alpha has potent inflammatory and histamine-releasing activities, its production by basophils may indicate a positive feedback mechanism for allergic inflammation.

Antibodies, Anti-Idiotypic↗
PubMed1996

IL-13 released by and localized in human basophils.

We and others have shown that human basophils can synthesize and release IL-4. However, IL-13, a cytokine that closely resembles IL-4, has not hitherto been described as a basophil product. The production of IL-13 by basophils was demonstrated by immunocytochemistry. Approximately 70% of basophils stimulated with anti-FcepsilonRIalpha (antibody to the alpha subunit of IgE receptor type I) stained for IL-13. Under similar experimental conditions, mononuclear cells failed to stain for IL-13. The cytokine was localized to basophilic granules by electron microscopic examination of immunogold staining. The secretion of IL-13 into the culture supernatant was assayed by ELISA. Kinetic studies showed detectable IL-13 release at 3 h, which steadily increased up to 24 h. This is significantly different from the kinetics of basophil histamine and IL-4 release. IL-13 production was also observed upon stimulation with anti-IgE, anti-FcepsilonRIalpha, IL-3, and A23187 in a dose-dependent manner. PBMC, neutrophils, and eosinophils isolated from the same donors did not release IL-13 after anti-IgE stimulation. The anti-IgE-induced basophil IL-13 synthesis could be enhanced by IL-3 preincubation (with and without IL-3 preincubation, anti-IgE-induced IL-13 production was 227 +/- 99 and 42 +/- 13 pg/10(6) basophils, respectively). PBMC produced a significant amount of IL-1 3 upon stimulation with PHA, but a low level of IL-13 in response to A23187 and/or PMA. Eosinophils and neutrophils did not produce IL-13 when cultured with A23187, IL-5, and anti-FcepsilonRIalpha. This is the first demonstration of IL-1 3 production by basophils. Our data suggest that basophils, in addition to secreting mediators, can represent an important source of proallergic cytokines.

Basophils↗
PubMed1996

Intranasal fluticasone propionate inhibits recovery of chemokines and other cytokines in nasal secretions in allergen-induced rhinitis.

BACKGROUND: Allergen-induced nasal responses are associated with the recovery of proinflammatory mediators and cytokines. In recent years, a distinct group of chemotactic cytokines, chemokines, has been the focus of intense investigation as to their possible role in the pathogenesis of allergic diseases. Although corticosteroids have been known to be effective in the treatment of allergic diseases, their mechanism(s) of action has not been fully elucidated. OBJECTIVES: To study the effect of topical fluticasone on the recovery of chemokines (IL-8, MIP-1 alpha, and RANTES) and other cytokines (IL-1 beta, IL-6, and GM-CSF) from nasal mucosa following allergen challenge. To correlate the improvement of rhinitis symptoms with cytokine levels during early-phase and late-phase allergic responses. METHODS: A randomized, double-blind, placebo-controlled crossover study of fluticasone propionate, 200 micrograms q d, was performed in ten subjects with allergic rhinitis. Allergen challenge was administered after 1 week of treatment. Nasal secretions were collected immediately after challenge and during the late-phase reactions; symptom scores were recorded simultaneously. Nasal cytokines were assayed by specific ELISA. RESULTS: The allergen challenge caused early-phase and late-phase allergic reactions and increased recovery of IL-1 beta, IL-6, IL-8, RANTES, MIP-1 alpha, and GM-CSF from the nasal mucosa. Intranasal fluticasone inhibited the allergen-induced increase in nasal symptoms. This was associated with decreases in cytokine recovery. A significant correlation was observed between decreases in cytokine levels and in symptom scores after treatment. CONCLUSION: Our results suggest that treatment with topical fluticasone propionate inhibits allergen-induced nasal responses and the associated increase in the production/secretion of chemokines and other proinflammatory cytokines.

Administration, Topical↗
PubMed1995

Secretion of chemokines and other cytokines in allergen-induced nasal responses: inhibition by topical steroid treatment.

We have demonstrated the detection of proallergic cytokines in the nasal secretions after antigen challenges. Our aim was to determine the secretion kinetics of chemokines (interleukin [IL]-8, macrophage inflammatory protein-1 alpha [MIP-1 alpha], and RANTES) and other cytokines (IL-1 beta and granulocyte/macrophage colony-stimulating factor [GM-CSF] after allergen challenges and their inhibition by steroid therapy. Ten allergic patients were given either beclomethasone dipropionate (BDP) or placebo in a double-blind, randomized, crossover manner. Allergen challenges were performed after 1 wk of treatment. Nasal secretions were collected serially for 11 h after allergen challenge by a matrix method. Subjects maintained symptom scores at each time point of nasal secretion recovery. Cytokines were measured by specific enzyme-linked immunosorbent assays. The mean peak values for each cytokine and total symptom scores during the early (ER) and/or late-phase reactions (LPR) were significantly reduced during the BDP treatment period (p < 0.05). The levels of cytokine correlated (p < 0.05) with corresponding total symptom scores during ER (IL-1 beta and MIP-1 alpha) and LPR (all cytokines). Our findings document local elevations of IL-1 beta, GM-CSF, and chemokines in the nasal secretions after allergen challenges and their inhibition by steroids. We speculate that the inhibition of cytokine production and secretion in the nasal mucosa may contribute to the clinical efficacy of topical steroids.

Beclomethasone↗
PubMed1995

Interleukin-1 alpha mediates the enhanced expression of intercellular adhesion molecule-1 in pulmonary epithelial cells infected with respiratory syncytial virus.

The mechanisms of virus-induced enhancement of intercellular adhesion molecule-1 (ICAM-1) expression in epithelial cells are unknown. In the present study, the effect of respiratory syncytial virus (RSV) infection on the expression of ICAM-1 in human pulmonary type II-like epithelial (A549) cells was evaluated. Conditioned RSV media (cRSV) produced from growth of RSV in A549 cells induced a significant increase in the expression of ICAM-1. Treatment of the cells with noninfectious cRSV prepared by ultraviolet (UV) irradiation (UV-cRSV) or ribavirin treatment resulted in the expression of ICAM-1 to a similar extent as infectious cRSV. These results suggested that RSV induces the synthesis of a soluble mediator(s) that regulates the expression of ICAM-1. Cytokine analysis by immunoassay and polymerase chain reaction showed that RSV induces the synthesis of interleukin (IL)-1 alpha and -beta, and tumor necrosis factor alpha (TNF-alpha). Preincubation of UV-cRSV with soluble IL-1 receptor (sIL-1r) almost completely blocked the enhancement of ICAM-1 expression. Furthermore, simultaneous incubation of infectious purified RSV with sIL-1r resulted in a significant reduction in enhancement of ICAM-1 expression. Preincubation with neutralizing antibodies to IL-1 alpha and -beta, and TNF-alpha showed that the predominant ICAM-1 enhancing soluble mediator in UV-cRSV was IL-1 alpha. These experiments provide direct evidence for an autocrine mechanism of enhanced ICAM-1 expression in RSV-infected epithelial cells that is mediated primarily by IL-1 alpha. Pulmonary epithelial cells may play an important immunoregulatory role in the microenvironment of the lower respiratory tract infected with RSV.

Cell Adhesion↗
PubMed1995

The burgeoning problem of latex sensitivity. Surgical gloves are only the beginning.

Awareness of latex sensitization is increasing in both the medical and the general community. Nonimmunologic irritant contact dermatitis, often found on the hands of healthcare workers who wear latex gloves, is the most common feature of sensitivity. The exact latex antigen(s) to blame have not been clearly delineated, but risk factors have been established that can be used to identify persons susceptible to a hypersensitivity reaction. The severity of a reaction depends on the route of exposure; mucosal and visceral exposure poses the greatest risk of reaction. Thus, patients requiring multiple operations and procedures, such as those with spina bifida or congenital urinary tract anomalies, are at high risk. Persons in high-risk groups should be referred for appropriate evaluation and testing, advised to avoid exposure to latex-derived products, and told to carry self-injectable epinephrine.

Dermatitis, Occupational↗
PubMed1994

Proinflammatory cytokines in nasal secretions of allergic subjects after antigen challenge.

To study the role of cytokines in allergic late-phase reactions (LPR), we measured cytokines (interleukins [IL]-1 beta, IL-2, IL-4, IL-5, IL-6, and granulocyte-macrophage colony-stimulating factor [GM-CSF]) in nasal secretions (NS) of eight allergic subjects following antigen or saline provocation. NS were collected hourly for 10 h after challenge by a newly developed matrix method. All subjects recorded hourly symptom scores. Cytokines were measured using specific enzyme-linked immunosorbent assays (ELISA). Compared with prechallenge values, significant levels of IL-1 beta were detected in all subjects during the immediate reaction (peak, 51.0 +/- 22.4 pg/ml) and LPR (peak, 78.5 +/- 22.6 pg/ml) after antigen challenges (p < 0.01) but not saline challenges. In contrast, GM-CSF and IL-6 showed a delayed rise (peak, 26.4 +/- 1.3 pg/ml and 33.8 +/- 10.0 pg/ml, respectively) at hour 4 in the antigen-challenge period (p < 0.01 versus saline). NS from 4 donors also showed detectable IL-5 (7.6 to 155 pg/ml) during the immediate reaction and LPR after allergen challenges (versus saline, p < 0.01). The levels of cytokine correlated (p < 0.05) with corresponding total symptom scores during the immediate reaction (IL-1 beta) and LPR (IL-1 beta, GM-CSF, and IL-6). IL-2 and IL-4 were not detected in any sample. Thus, IL-1 beta, IL-5, IL-6, and GM-CSF are present in the LPR of allergic rhinitis, and their correlation with clinical responses may suggest their role in allergic inflammation.

Enzyme-Linked Immunosorbent Assay↗
PubMed1994

Interleukin-1 receptor antagonist protein inhibits the synthesis of IgE and proinflammatory cytokines by allergen-stimulated mononuclear cells.

The ability of interleukin-1 (IL-1) to activate diverse cell populations supports its role as a preeminent cytokine in the pathogenesis of chronic inflammation. In this study, we investigated the role of Il-1 and IL-1 receptor antagonist protein (IRAP) in the regulation of allergen-induced synthesis of IgE and proinflammatory cytokines. The temporal expression of IL-1 beta and IRAP during 5-day allergen-activated peripheral mononuclear cell (PMNC) cultures suggested differential production of the two cytokines. To determine the influence of IRAP on IL-1-mediated cellular responses, we cultured PMNC from allergic donors with specific allergens in the presence or absence of IRAP pretreatment. Culture supernatants were assayed for IgE and cytokines using specific enzyme-linked immunosorbent assay. IRAP at concentrations 0.01, 0.1, and 1 microgram/ml decreased the allergen-stimulated IgE synthesis by 33 +/- 7%, 50 +/- 7%, and 66 +/- 5%, respectively (P < 0.05). Increasing the concentration of allergen did not affect the reduction in IgE synthesis observed in the presence of IRAP. Lipopolysaccharide-stimulated IgE synthesis was also significantly inhibited by IRAP (P < 0.05). In parallel experiments, anti-IL-1 beta monoclonal antibody showed a comparable inhibitory pattern on IgE synthesis (P < 0.05). IRAP inhibited the synthesis of interleukin-6, tumor necrosis factor-alpha, and granulocyte/macrophage colony-stimulating factor in a dose-dependent manner (P < 0.05); the mean inhibition was 31 +/- 4%, 75 +/- 5%, and 88 +/- 2%, respectively, at 1 microgram/ml of IRAP.(ABSTRACT TRUNCATED AT 250 WORDS)

Allergens↗
PubMed1993

Sodium metabisulfite and SO2 release: an under-recognized hazard among shrimp fishermen.

Since the introduction of sodium metabisulfite as a food preservative, it has been associated with several idiosyncratic reactions (eg, bronchospasm, oculonasal symptoms, and urticaria/angioedema) in sulfite-sensitive individuals. The pathogenic mechanism of these reactions is not yet understood. We report the case of two crewmen on a shrimp trawler who were found dead in the ship's hold. Their deaths had occurred while they were applying dry sodium metabisulfite, referred to as "shrimp dip" in the shrimping industry. Postmortem examinations showed diffuse pulmonary edema consistent with death secondary to asphyxia. Associated findings were visceral congestion. Although it is possible to measure death from sodium metabisulfite with available records, its potential morbidity cannot be estimated. It is known that sodium metabisulfite can react with acids and water, releasing toxic sulfur dioxide (SO2) gas. In addition, SO2 gas reacts with respiratory tissue forming sulfureous acid, and inducing a pulmonary reaction causing hypoxemia. Furthermore, sodium metabisulfite, compared with sodium bisulfite, has a much greater propensity to release SO2 gas. We conclude that there is a need for improved education regarding the potential side effects of sodium metabisulfite, thus eliminating needless occupational morbidity and mortality.

Animals↗
PubMed1992

Development of a new technique for recovery of cytokines from inflammatory sites in situ.

We attempted to recover cytokines from nasal mucosal surface following allergen challenge. Repeated lavage of nasal mucosa of seven allergic patients was done, but we failed to detect IL-1 beta in the lavage samples even in ten-fold concentrated materials. Therefore, we developed a new technique to recover cytokines using filter strips. Small filter strips were placed on nasal turbinates for 10 min at different time points after allergen challenge. The strips were air-dried, and stored. For recovery of cytokines individual strips were washed with small volumes of Hepes buffer containing 0.3% human serum albumin. Eluates were assayed for the presence of IL-1 beta and GM-CSF using commercially available ELISA. We were able to detect IL-1 beta and GM-CSF in eluates. Both cytokines were consistently detectable in the late phase allergic reaction peaking at 5 h. Nasal challenge with saline failed to detect any cytokine during the 7 h observation period. In standardization experiments known quantities of IL-1 beta and GM-CSF were applied to filter strips and the recovery ranged from 67 to 89%. Thus, we developed a simple technique of recovery of cytokines from inflammatory mucosa in situ.

Allergens↗
PubMed1992

Measurement of histamine-releasing factor activity in individual nasal washings: relationship with atopy, basophil response, and membrane-bound IgE.

We collected individual pools of nasal washings (NWs) from 15 allergic and 15 nonallergic subjects to determine histamine-releasing factor (HRF) activity and to ascertain the relationship of these cytokines with atopic status, basophil releasability, and cell membrane-bound IgE. NWs were concentrated, dialyzed, and assayed with basophils from a single donor. Samples from 12 of 15 allergic subjects and from all the nonallergic subjects revealed greater than or equal to 15% histamine release (HR), 33.5% +/- 21.3% (mean +/- SD) and 38.6% +/- 19.6%, respectively (p greater than 0.05). When we assayed the same samples with autologous basophils, the allergic group demonstrated higher HR than the nonallergic group (31.9% +/- 19.7% versus 4.8% +/- 4.3%; p less than 0.001). A standard lot of mononuclear cell-derived HRFs was also screened with basophils from both groups. Means for HR from basophils of allergic and nonallergic subjects were 51.9% +/- 16.7% versus 26.3% +/- 8.2%, respectively (p less than 0.001). Pretreatment of basophils with lactic acid led to abrogation of sensitivity to HRF. Acid-stripped cells incubated with sera from patients with asthma regained their capacity to release histamine. We found that HRF activity can be detected in NWs of most donors, and there is no difference among allergic and nonallergic subjects. Our results suggest that the capacity of these cytokines to induce HR depends on several factors: atopic status, basophil releasability, and membrane-bound IgE.

Basophils↗
PubMed1992

Comparison of the sensitivity and precision of four skin test devices.

Twenty volunteers were skin tested with seven concentrations of histamine phosphate and a glycerosaline control to determine the relative sensitivity and precision of four skin test devices: Greer Pen (GP), Greer DermaPIK (DP), Center Multi-Test (MT), and Morrow Brown needle (MB). The end points of the study were (1) wheal and flare response of each device, with a dose-response curve, (2) the time required to apply each set of eight tests, and (3) the volunteers' subjective assessment of each device. On a different day, 10 of the volunteers were tested to determine the precision of each device. Dose-response curves for half-log dilutions of histamine phosphate were produced with a glycerosaline control. The DP and GP induced wheal and flare responses discernible from that of the glycerosaline control at a lower concentration of histamine phosphate than the MB and MT. The DP took a shorter time to apply eight samples than any other device. The MB was preferred by the most volunteers, but any device tested on the upper half of the back was usually preferred over that tested on the lower half. When 5 mg/ml histamine phosphate was used, coefficients of variation for each device demonstrated that for wheals the precision of the DP, GP, and MT was similar (mean, 21.1%, 23.1%, and 24.5%, respectively). The MB was larger (mean, 59.9%). For flares, the precision of GP and DP was similar (mean, 22.0% and 23.5%, respectively), with the MT and MB larger (mean, 35.5% and 58.2%, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Anaphylaxis. How to manage and prevent this medical emergency.

Anaphylaxis is a dramatic, major medical emergency. Understanding of the pathogenesis, emergency treatment, and subsequent prophylaxis can reduce both morbidity and mortality. Treatment of anaphylaxis should begin with a high degree of suspicion. Taking a wait-and-see attitude in hopes that the reaction will be mild may have serious results.

Anaphylaxis↗
PubMed1992

Effect of topical corticosteroids on the recovery of histamine releasing factors in nasal washings of patients with allergic rhinitis. A double-blind, randomized, placebo-controlled study.

Nasal washings (NW) have been used by many investigators as a readily available biologic fluid for studying the mechanism of allergic reactions. These fluids have been analyzed for the presence of various mediators, including cytokines. Recently, histamine releasing factors (HRF) have been detected in the NW. The objective of this study was to investigate the effect of treatment with topical corticosteroids on the recovery of these cytokines from the NW obtained from patients with allergic rhinitis. A group of 30 patients with ragweed pollen allergy were given either beclomethasone dipropionate (BDP) or placebo for 1 wk in a double-blind randomized manner. NW were performed twice before the start of the treatment period and were repeated twice at the end of the study. HRF activity was measured in the NW. Patients maintained a daily symptom score. The activity of HRF decreased significantly (mean +/- SD, pre = 37.2 +/- 21.3% versus post = 23.8 +/- 20.1%; p less than 0.01) in the BDP group, as did the mean symptom score (5.1 +/- 1.4 versus 1.5 +/- 1.5, p less than 0.01) at the end of the treatment period. In contrast, there was no significant change in HRF recovery (32.8 +/- 25.6% versus 33.8 +/- 25.3%; p less than 0.05) or symptom score (4.8 +/- 1.8 versus 5.4 +/- 1.9; p greater than 0.05) in the placebo group. There was a significant correlation between the net changes in symptom scores and the net differences in HRF activity. We speculate that the reduction in HRF in the nasal mucosa may contribute to the clinical efficacy of topical corticosteroids.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Hereditary angioedema: its diagnostic and management perspectives.

Although hereditary angioedema accounts for only a small fraction of all cases of angioedema, it is the most common genetically linked clinical disorder caused by the deficiency of a protein associated with complement activation. Attacks may be complicated by incapacitating cutaneous swelling, life-threatening upper airway impediment, and severe gastrointestinal colic. Recent physicochemical and genetic studies have contributed significantly to our understanding of the structure of the inhibitor protein. Measurement of serum C4 titer is an efficacious screening test. Normal levels during symptomatic periods rule out the diagnosis, whereas decreased levels warrant determination of C1 esterase inhibitor titer by immunoassay or functional assay. The functional assay is necessary to ascertain the genetic variant form. The importance of making the correct diagnosis cannot be overemphasized. It can avert potentially fatal consequences, such as upper airway obstruction and unnecessary abdominal surgery. The application of short-term preventive measures can avoid complications associated with trauma. Finally, abatement or elimination of symptoms in patients with incessant and disabling attacks can be attained by long-term therapy with currently available attenuated androgens.

Angioedema↗