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Biomedical subjects

S Ting

Publications and source records attributed to S Ting.

At least 19 recordsLinked to original sources
PubMed1998

A national survey of emergency department chest pain centers in the United States.

Although chest pain centers are promoted as improving emergency cardiac care, no data exist on their structure and processes. This national study determines the 1995 prevalence rate for emergency department (ED)-based chest pain centers in the United States and compares organizational differences of EDs with and without such centers. A mail survey was directed to 476 EDs randomly selected from the American Hospital Association's database of metropolitan hospitals (n = 2,309); the response rate was 63%. The prevalence of chest pain centers was 22.5% (95% confidence interval 18% to 27%), which yielded a projection of 520 centers in the United States in 1995. EDs with centers had higher overall patient volumes, greater use of high-technology testing, lower treatment times for thrombolytic therapy, and more advertising (all p <0.05). Hospitals with centers had greater market competition and more beds per annual admissions, cardiac catheterization, and open heart surgery capability (all p <0.05). Logistic regression identified open heart surgery, high-admission volumes, and nonprofit status as independent predictors of hospitals having chest pain centers. Thus, chest pain centers have a moderate prevalence, offer more services and marketing efforts than standard EDs, and tend to be hosted by large nonprofit hospitals.

Angina Pectoris↗
PubMed1998

Regulation of in vitro phosphorylation of the casein kinase II sites in B-50 (GAP-43).

Casein kinase II (CKII) phosphorylates the rat neuronal growth-associated protein B-50 (GAP-43) at serines 191/192 and threonines 88, 89 and/or 95 both in vitro and in neuronal growth cones. Since little is known concerning regulation of the phosphorylation of these sites, these studies were undertaken to characterize the factors which determine the degree of B-50 phosphorylation by CKII in vitro. Phosphorylation of rat B-50 on serine and threonine residues by recombinant human CKII is stimulated by polylysine. Maximal stimulation occurs at 10 microg/ml of polylysine, a concentration which has no effect on protein kinase C (PKC)-mediated phosphorylation of B-50. Digestion with Staphylococcus aureus V8 protease demonstrates CKII-mediated phosphorylation of B-501-132 and the C-terminal fragment S3/S4. Phosphorylation of B-50 by either CKII or PKC is inhibited by the N-terminal monoclonal antibody NM2, while the C-terminal antibody NM6 has no effect on phosphorylation by either protein kinase. Protein phosphatase 2A dephosphorylates both the CKII and PKC sites, while protein phosphatases 2B and 1 are more selective for the PKC site. These results indicate that the phosphorylations of B-50 by CKII and PKC are determined by distinct regulatory signals in vivo.

Animals↗
PubMed1989

Genetic regulation of macrophage production in response to surface components of Listeria monocytogenes.

Resistance to murine listeriosis requires humoral factors which alter production or delivery of monocytes to infective foci. Production of such factors is under genetic control and may be modulated by bacterial components. Two components from Listeria monocytogenes, monocytosis producing activity (MPA) and immunosuppressive activity (ISA) were used to study monocytopoiesis in mice with known abnormalities in microphage-related functions. Listeria-sensitive A/J mice fail to produce or respond to MPA or an endogenous mediator of monocytosis (EF). These studies provided evidence that a second humoral factor, decreases monocytopoiesis. Sera from A/J mice are more active in this respect and MPA treatment increases the amount of inhibitory factor in A/J mice. A polyclonal B cell activator, ISA, which induces suppressor splenic macrophages, suppresses the anti-SRBC response in resistant B10. A mice but not in A/J mice. ISA induced no change in prostaglandin E2 production by spleen cells of either strain. One interpretation of these findings is that A/J mice after stimulation by ISA or MPA, produce a substance which inhibits development of mononuclear phagocytes.

Animals↗
PubMed1989

Inhibition of dermographia, histamine, and dextromethorphan skin tests by ketotifen. A possible effect on cutaneous vascular response to mediators.

Forty-one subjects with dermographia were studied for a 4-week period. Twenty subjects received ketotifen therapy, the other 21 received chlorpheniramine (H1) for 2 weeks, and then chlorpheniramine plus cimetidine (H1 + H2). Both groups had significant suppression of dermographia and skin wheals caused by dextromethorphan and histamine after 2 weeks. The inhibition by ketotifen of dermographia, histamine wheal, and the dextromethorphan wheal increased from week 2 to week 4. During the first 2 weeks, ketotifen's activity was comparable to chlorpheniramine. Ketotifen's activity increased during the second 2 study weeks to match the additional chlorpheniramine. These results suggest that ketotifen may have additional pharmacologic activities besides H1 antagonism, including possible inhibition of mast cell mediator release. As a consequence, cutaneous vascular hyperresponsiveness may decrease. Ketotifen appears promising as treatment for allergic skin disorders.

Adult↗
PubMed1988

Ethanol-induced urticaria: a case report.

Urticaria, after ingesting ethanol, is rare. A 36-year-old Caucasian male developed multiple, generalized, pruritic urticarial lesions 5 to 15 minutes after drinking alcoholic beverages of any type. A blinded challenge with 5 mL of chemically pure 95% ethanol in concentrated grape juice caused urticaria and an elevation of plasma histamine. Pure grape juice alone was unreactive. Prick skin tests with Brewers' yeast, ethanol, acetaldehyde, and acetic acid were negative. Hydroxyzine (25 mg, p.o., q.i.d.), given for three days prior to challenge, inhibited skin response and histamine release. Biopsy of the urticarial lesions caused by ethanol ingestion showed mast cell degranulation. In this subject, ethanol appeared to directly affect mast cell mediator release by non-IgE mechanisms.

Adult↗
PubMed1986

Analysis of plasma histamine: a modification of the enzymatic isotopic assay.

The enzymatic isotopic analysis of histamine requires extraction and concentration of [3H]-1-methylhistamine from the reaction mixture. The assay was modified to include enzymatic reaction at 0 degrees C to reduce blank values and direct application of protein-free reaction mixture to a thin-layer chromatography plate for isolating of the product. The analysis was quantitative down to 100 pg/ml of histamine, adequate for monitoring plasma histamine content.

Histamine↗
PubMed1986

The development of subsensitivity to nebulized atropine sulfate.

Ten adult asthmatic subjects were tested for response to inhaled atropine sulfate before and after 3 weeks of inhaled atropine therapy. Four of the ten initial responders no longer responded after the 3 weeks. The mean FEV1 increase was 0.49 L before treatment and 0.30 L after treatment (P = .025). Subsensitivity to the effects of atropine develops, but may be limited to a subset of patients.

Adult↗
PubMed1985

Inhibitory effect of hydroxyzine on antigen-induced histamine release in vivo.

By use of a modified heat-suction, skin blister technique, we found that oral hydroxyzine, 25 mg four times a day, inhibits antigen-induced ultrastructural changes of mast cells and in vivo histamine release in the skin of ragweed-sensitive individuals. To our knowledge this is the first demonstration that an orally active antihistamine can inhibit in vivo cutaneous anaphylactic reactions.

Administration, Oral↗
PubMed1985

Orthostatic proteinuria and milk ingestion.

An adolescent, contemplating a military career, was found to have orthostatic proteinuria. A thorough evaluation failed to reveal any renal abnormalities. He was tested on a milk-free diet at the request of the parents. The proteinuria cleared, but recurred on an initial open challenge; it did not recur subsequently on a blinded challenge. This experience suggests that patients with orthostatic proteinuria should be evaluated with an elimination diet trial.

Adolescent↗
PubMed1985

Failure of Verapamil in inhibiting allergen-induced histamine release in vivo.

In order to evaluate the effect of Verapamil on human cutaneous anaphylactic responses, ragweed-sensitive individuals were skin tested with ragweed, ragweed plus Verapamil, and Verapamil alone. In addition, using a skin chamber technique, the effect of Verapamil on antigen-induced histamine release in vivo was investigated. The results suggest that Verapamil, applied locally in non-irritant doses, does not affect Type I hypersensitivity skin reactions.

Allergens↗
PubMed1985

Metered dose inhaler induced bronchospasm in asthmatic patients.

Beta-adrenergic agonists in metered dose inhalers (MDIs) are used extensively in the treatment of asthma. Previously we reported that 23 of 1450 (1.6%) of our asthmatic patients experienced immediate bronchoconstriction after using MDI-albuterol. In this study we investigated immediate bronchoconstriction after use of MDI-metaproterenol and after placebo-inhaler with "inert ingredients" only. Results suggest that those patients who complained of chest tightness or lack of relief following the use of MDI beta-adrenergic agonists are having true bronchoconstriction. The bronchoconstrictive response is most likely caused by the propellants or the other inert ingredients contained in these MDIs.

Administration, Intranasal↗
PubMed1985

Food allergy and adult migraine: double-blind and mediator confirmation of an allergic etiology.

Foods as a cause for migraine attacks were evaluated in 43 adults with recurrent migraine. Skin testing, elimination diets, double-blind challenges, and measurements of plasma histamine were performed. Thirteen subjects experienced 66% or greater reduction in headache frequency during a diet trial. Six subjects became headache free. Eleven of 16 skin test-positive patients responded to diet manipulation, while only two of 27 skin test-negatives did (P less than .005). Seven subjects agreed to double-blind challenges. In five of seven, at least one food provoked migraine. Placebo challenges did not provoke migraine. In three subjects, plasma histamine rose during migraine provoking challenges. The relationship between food ingestion and migraine is based in part on allergic mechanism. Tests for IgE-specific food allergy appear helpful in selecting patients likely to benefit from diet therapy.

Adolescent↗