Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P15088 (mast cell)
 14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute copper deficiency produces disturbances in the microcirculation and structure of extracellular matrix proteins, causes an increase in mast cell population, which is followed by an increased content of their degranulation products, produces disturbances in histamine metabolism and decreases the activity of some antioxidant enzymes. These pathogenic mechanisms are similar to the processes underlying stress ulcer formation. The histamine H2-receptor antagonist ranitidine, a drug with the highest application for stress ulcer prophylaxis, has the ability to helate the copper ion and to influence its tissue distribution and the processes of generation and neutralization of reactive oxygen species (ROS). In order to determine the interrelation between the disturbances of copper homeostasis, stress ulcers and ranitidine, we investigated the impact of a short-term diet with powdered milk in combination with cold-restraint stress with or without ranitidine on the severity of acute gastric mucosal lesions, copper content, lipid peroxidation and the activity of superoxide dismutase and catalase in the stomachs of rats.
 ...
PMID:Influence of acute copper deficiency, cold-restraint stress and the H2 blocker ranitidine on the severity of acute gastric mucosal lesions and lipid peroxidation in rats. 1177 55

Anaphylaxis represents the maximal variant of an immediate-type allergic reaction involving the whole organism with manifestations in different organ systems. IgE-mediated mast cell and basophil activation is the major pathomechanism; however, immune complex and pseudo-allergic reactions also may lead to the same symptomatology. The most common elicitors are drugs, additives, occupational substances, animal venoms, aeroallergens, and contact urticariogens but also physical factors (cold, heat, ultraviolet light, exercise). When no eliciting factors can be detected, the term "idiopathic anaphylaxis" is used. The diagnosis of idiopathic anaphylaxis is, therefore, a diagnosis of exclusion and may be made only after careful allergy history taking and diagnosis involving in vitro tests. Possible mechanisms underlying the pathophysiology of idiopathic anaphylaxis include undetected diseases (eg, mastocytosis occulta), concomitant anaphylaxis-enhancing medication (b-blockers), secretion of histamine-releasing factor from T lymphocytes, autoantibodies against IgE or IgE receptors, and angiotensin II deficiency. One of the many differential diagnoses of anaphylaxis may have been overlooked. The treatment of idiopathic anaphylaxis follows the rules of antianaphylactic therapy.
 ...
PMID:Idiopathic anaphylaxis. 1189 24

Long-term management of asthma includes identification and avoidance of precipitating factors of asthma, pharmacotherapy and home management plan. Common precipitating factors include viral upper respiratory infections, exposure to smoke, dust, cold food and cold air. Avoidance of common precipitating factors has been shown to help in better control of asthma. Pharmacotherapy is the main stay of treatment of asthma. Commonly used drugs for better control of asthma are long and short acting bronchodilators, mast cell stabilizers, inhaled steroids, theophylline and steroid sparing agents. After assessment of severity most appropriate medications are selected. For mild episodic asthma the medications are short acting beta agonists as and when required. For mild persistent asthma: as and when required bronchodilators along with a daily maintenance treatment in form of low dose inhaled steroids or cromolyn or oral theophylline or ketotifen are required. Moderate persistent asthma should be treated with inhaled steroids along with long acting beta agonists for symptom control. For severe persistent asthma the recommended treatment includes inhaled steroids, long acting beta agonists with or without theophylline. If symptoms are not well controlled, a minimal dose of oral prednisolone preferably on alternate days may be needed in few patients. Newer drugs like leukotriene antagonists may find a place in control of exercise-induced bronchoconstriction and mild and moderate persistent asthma. Patients should be followed up every 8-12 weeks. On each follow up visit patients should be examined by a doctor, compliance to medications should be checked and actual inhalation technique is observed. Depending on the assessment, medications may be decreased or stepped up. For exercise induced bronchoconstriction: cromolyn, short or long acting beta agonists may be used. In children with seasonal asthma, maintenance treatment according to assessed severity should be started 2 weeks in advance and continued throughout the season. These patients should be reassessed after discontinuing the treatment. Parents should be given a written plan for management of acute exacerbation at home.
 ...
PMID:Long-term management of asthma. 1198 Apr 67

Long-term management of asthma includes identification and avoidance of precipitating factors of asthma, pharmacotherapy and home management plan. Common precipitating factors include viral upper respiratory infections, exposure to smoke, dust, cold food and cold air. Avoidance of common precipitating factors has been shown to help in better control of asthma. Pharmacotherapy is the main stay of treatment of asthma. Commonly used drugs for better control of asthma are long and short acting bronchodilators, mast cell stabilizers, inhaled steroids, theophylline and steroid sparing agents. After assessment of severity most appropriate medications are selected. For mild episodic asthma the medications are short acting beta agonists as and when required. For mild persistent asthma: as and when required bronchodilators along with a daily maintenance treatment in form of low dose inhaled steroids or cromolyn or oral theophylline or leukotriene antagonists are required. Moderate persistent asthma should be treated with inhaled steroids along with long acting beta agonists for symptom control. For severe persistent asthma the recommended treatment includes inhaled steroids, long acting beta agonists with or without theophylline. If symptoms are not well controlled, a minimal dose of oral prednisolone preferably on alternate days may be needed in few patients. Patients should be followed up every 8-12 weeks. On each follow up visit patients should be examined by a doctor, compliance to medications should be checked and actual inhalation technique is observed. Depending on the assessment, medications may be decreased or stepped up. For exercise induced bronchoconstriction: cromolyn, short or long acting beta agonists or leukotriene antagonists may be used. In children with seasonal asthma, maintenance treatment according to assessed severity should be started 2 weeks in advance and continued throughout the season. These patients should be reassessed after discontinuing the treatment. Parents should be given a written plan for management of acute exacerbation at home.
 ...
PMID:Long-term management of asthma. 1261 55

Ten percent of chronic urticarias are physical urticarias. Patients suffering from physical urticaria all have a suggestive history with specific eliciting stimuli (cold, heat, water, sun.) and wheals in the areas where the stimulus acts. The involved pathomechanisms are not well known. An unknown allergen (related to a cold or a heat injury, a polar molecule contained in the stratum corneum and soluble into water, a photoallergen) could induce a mast cell mediator release, followed by an infiltration by eosinophil then neutrophils polymorphonuclears. T-cells are not highly involved. Dermographism, the most frequent can be cured by anti-H1. In diagnosing cholinergic urticaria physical exercise has to be done by the patient (jogging, running, riding), anti-H1 are efficient. In other physical urticarias (delayed-pressure, cold, solar, heat, vibratory urticarias) as to be managed as follows: (1) to perform specific tests with respectively (weights; ice cube; UVA, UVB and visible light exposure; hot water contained in a tube; a vortex mixer); (2) to avoid eliciting stimuli; (3) to treat the associated diseases e.g. in secondary cold urticaria; (4) to try to induce a physical tolerance, a review is enclosed concerning cold, solar, heat and aquagenic urticarias; (5) to associate or not non sedative 2(nd) generation antihistamines. All the other alternative treatments are discussed but none of them has been evaluated.
 ...
PMID:[Physical urticarias]. 1284 5

Peptic ulcer is a common disorder of gastrointestinal system and its pathogenesis is multifactorial, where smoking and nicotine have significant adverse effects. Smoking and chronic nicotine treatment stimulate basal acid output which is more pronounced in the smokers having duodenal ulcer. This increased gastric acid secretion is mediated through the stimulation of H2-receptor by histamine released after mast cell degranulation and due to the increase of the functional parietal cell volume or secretory capacity in smokers. Smoking and nicotine stimulate pepsinogen secretion also by increasing chief cell number or with an enhancement of their secretory capacity. Long-term nicotine treatment in rats also significantly decreases total mucus neck cell population and neck-cell mucus volume. Smoking also increases bile salt reflux rate and gastric bile salt concentration thereby increasing duodenogastric reflux that raises the risk of gastric ulcer in smokers. Smoking and nicotine not only induce ulceration, but they also potentiate ulceration caused by H. pylori, alcohol, nonsteroidal anti-inflammatory drugs or cold restrain stress. Polymorphonuclear neutrophils (PMN) play an important role in ulcerogenesis through oxidative damage of the mucosa by increasing the generation of reactive oxygen intermediates (ROI), which is potentiated by nicotine and smoking. Nicotine by a cAMP-protein kinase A signaling system elevates the endogenous vasopressin level, which plays an aggressive role in the development of gastroduodenal lesions. Smoking increases production of platelet activating factor (PAF) and endothelin, which are potent gastric ulcerogens. Cigarette smoking and nicotine reduce the level of circulating epidermal growth factor (EGF) and decrease the secretion of EGF from the salivary gland, which are necessary for gastric mucosal cell renewal. Nicotine also decreases prostaglandin generation in the gastric mucosa of smokers, thereby making the mucosa susceptible to ulceration. ROI generation and ROI-mediated gastric mucosal cell apoptosis are also considered to be important mechanism for aggravation of ulcer by cigarette smoke or nicotine. Both smoking and nicotine reduce angiogenesis in the gastric mucosa through inhibition of nitric oxide synthesis thereby arresting cell renewal process. Smoking or smoke extract impairs both spontaneous and drug-induced healing of ulcer. Smoke extract also inhibits gastric mucosal cell proliferation by reducing ornithine decarboxylase activity, which synthesises growth-promoting polyamines. It is concluded that gastric mucosal integrity is maintained by an interplay of some aggressive and defensive factors controlling apoptotic cell death and cell proliferation and smoking potentiates ulcer by disturbing this balance.
 ...
PMID:Smoking and the pathogenesis of gastroduodenal ulcer--recent mechanistic update. 1461 84

Coculture of mouse bone marrow-derived immature mast cells (BMMC) with Swiss 3T3 fibroblasts in the presence of stem cell factor (SCF) promotes morphological and functional maturation toward a connective tissue mast cell (CTMC)-like phenotype, which is accompanied by increased expression of several unique genes. Here we report the molecular identification of one of them, mast cell maturation-associated inducible gene (MMIG)-1. The MMIG-1 cDNA encodes a 117-kDa cytosolic protein that comprises an N-terminal PYRIN domain, a central nucleotide-binding domain, and nine C-terminal leucine-rich repeats. MMIG-1 shows >85% sequence similarity to human cryopyrin/PYPAF1, a causal gene for familial cold urticaria and Muckle-Wells syndrome. MMIG-1 was distributed in the cytosol of CTMC-like differentiated BMMC. MMIG-1 underwent alternative splicing in the leucine-rich repeats and each variant was induced differently in BMMC during coculture. Moreover, its expression was increased in the ears of mice with experimental atopic dermatitis. Thus, MMIG-1, a likely mouse PYPAF1 ortholog, may play a role in mast cell-directed inflammatory diseases.
 ...
PMID:Induction of PYPAF1 during in vitro maturation of mouse mast cells. 1468 36

Ocular allergy is a common condition that usually affects the conjunctiva of the eye and is therefore often referred to as allergic conjunctivitis. The severity of the disease can range from mild itching and redness, as seen in seasonal allergic conjunctivitis, to the more serious vision threatening forms of ocular allergy which affect the cornea, such as atopic keratoconjunctivitis. The pathogenesis of allergic conjunctivitis involves a complex mechanism which centers around IgE-mediated mast cell degranulation and release of multiple preformed and newly formed inflammatory mediators. The diagnosis of allergic conjunctivitis is usually a clinical one which can be made based on a thorough history and careful examination. Treatment of ocular allergy should begin with conservative measures including allergen avoidance, environmental control, ocular irrigation and cold compresses. Pharmacotherapy of allergic conjunctivitis consists of several classes of drugs. Antihistamines are widely used to treat mild conditions such as seasonal and perennial conjunctivitis and potent new agents such as levocabastine and emedastine are now available. Mast cell stabilizers such as sodium cromoglycate are both safe and effective and are commonly used in ocular allergy. More effective mast cell stabilizers such as nedocromil, lodoxamide and olopatadine are now being used. Nonsteroidal antiinflammatory drugs have demonstrated only limited efficacy and, as such, are not widely used. Topical steroids are very effective in treating signs and symptoms but are reserved for only refractory cases due to their serious side effects. Loteprednol and rimexelone are newer corticosteroids which reportedly have less of an effect on intraocular pressure. Cyclosporine has recently been shown to be highly effective in cases of vernal keratoconjunctivitis and atopic keratoconjunctivitis while producing no adverse effects.
 ...
PMID:Ocular allergic disease. 1474 64

The Harderian glands of rodents are large intraorbital exocrine glands with histologic organization that varies among mammalian species. Here we describe some ultrastructural and biochemical features of the Harderian gland in the Mexican volcano mouse Neotomodon alstoni alstoni, a species of restricted habitat. The Harderian glands from male and female adult mice were dissected, processed and embedded in Epon 812 for light and electron microscopy studies. Porphyrin and total lipids were biochemically determined. The macroscopic appearance of the Harderian gland is similar in the male and female. The gland is a bilobulate structure, situated in the orbit towards the posterior side of the eyeball, of whitish color and is surrounded by a connective tissue capsule. The male gland is slightly heavier (127 mg) than that of the female (113 mg). The Harderian gland shows a tubulo-alveolar organization and is composed exclusively of one type of secretory cells. No branched duct system within the gland was found. Adrenergic nerves endings and mast cell were observed in the interstices of the alveoli. Male and female glands produce similar levels of porphyrins. Triglyceride levels were significantly higher (P < 0.05) in the female compared to the male. Abundance of lipids could induce corneal lubrication of the Harderian gland which may confer a protective and adaptative function to the volcano mouse in its natural habitat during the dry and cold seasons.
 ...
PMID:The Harderian gland of the Mexican volcano mouse Neotomodon alstoni alstoni (Merriam 1898): a morphological and biochemical approach. 1561 8

The present study evaluated the effect of chronic cold stress on intestinal epithelial cell proliferation and inflammation. Male Wistar rats were subjected to cold exposure for three weeks. At the end of the cold exposure, intestinal cell proliferation, luminal nitrite and protein levels, intestinal myeloperoxidase activity and mast cell numbers were evaluated. Severely compromised proliferation rate of the crypt-base cells was observed under chronic stress conditions. Cells isolated from stressed rats showed a decreased DNA content in villus and lower villus cell fractions and an increased DNA content in the crypt cells, as compared to controls. Chronic cold stress resulted in increased luminal nitrite, luminal protein levels, and intestinal myeloperoxidase activity. The number of mast cells was significantly elevated under chronic stress conditions. Chronic cold stress resulted in a compromised intestinal epithelial cell proliferation rate and induced inflammation in the rat small intestine, through the combined action of nitric oxide, neutrophils and mast cells.
 ...
PMID:Effect of chronic cold stress on intestinal epithelial cell proliferation and inflammation in rats. 1623 23


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>