Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.4.15.1 (ACE)
18,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The adjuvant properties of a polydispersed beta-(1,4)-linked acetylated mannan, acemannan (ACE-M), were evaluated. Day-old broiler chicks were randomly selected and allocated to four flocks (Vac 1-4). The Vac 1 flock was sham vaccinated with saline. The Vac 2 flock was vaccinated with an oil-based vaccine (Breedervac III; Newcastle disease virus (NDV), infectious bursal disease virus (IBDV) and infectious bronchitis virus). The Vac 3 flock was vaccinated with a vaccine-ACE-M mixture, and the Vac 4 flock was vaccinated with vaccine and ACE-M at separate anatomical sites. ELISA titres to NDV and IBDV were determined. The immune response to NDV at 21 days postvaccination (PV) was significantly enhanced (P less than or equal to 0.05) by the addition of ACE-M to the vaccine, compared with vaccination without ACE-M. Subsequently, the vaccine-ACE-M mixture appeared to suppress the immune response to NDV. However, at day 35 PV, 95% of the Vac 3 chicks compared with 90% of the Vac 2 and 89% of the Vac 4 chicks exhibited protective titres. The response to IBDV differed from that to NDV. At day 21 PV the immune response to IBDV was essentially the same for all flocks that received vaccine, i.e. addition of ACE-M to the vaccine did not significantly enhance the immune response; however, it did significantly (P less than or equal to 0.05) sustain the immune response at days 28 and 35. In addition to the observed effect on titres to NDV and IBDV, ACE-M also had an effect on flock immunity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Antigen dependent adjuvant activity of a polydispersed beta-(1,4)-linked acetylated mannan (acemannan). 132 Mar 8

The lungs have an important role in the synthesis of ACE. In BAL fluid and serum the ACE activity was determined in 18 patients with sarcoidosis (11 with high intensity and 7 with low intensity alveolitis), 25 patients with atopic bronchial asthma and 17 with acute bronchitis. The activity of ACE was examined by a reagent set produced by Boehringer Mannheim Biochemica Test-Combination ACE cat. no. 789 011. In the high intensity alveolitis group of sarcoidosis patients the ACE activity was significantly increased in BAL fluid and serum in comparison to other observed patients. On the other hand, in patients with atopic bronchial asthma the ACE activity was also increased in comparison to acute bronchitis and referred norms. These findings suggest a role of atopic processes or administered therapy in ACE secretion in the airways.
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PMID:Activity of angiotensin I converting enzyme in sarcoidosis, atopic bronchial asthma and acute bronchitis. 217 61

The relationship between angiotensin converting enzyme inhibitors (ACE inhibitors) and the development of cough was studied in 80 patients. Cough developed in 25 (31%). Seventeen patients had detailed respiratory investigations of whom 12 developed a new cough. Five of the 12 patients had a remission on placebo and recurrence on rechallenge. Cough does occur with ACE inhibitors but there are other possible causes of cough such as asthma, bronchitis, smoking and heart failure. The true incidence of new cough with ACE inhibitors is uncertain at present.
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PMID:Angiotensin converting enzyme inhibitors and cough. 283 99

In serum of 530 patients with various lung diseases and in 70 healthy control subjects, kininase I (E.C. 3.4.17.3) and kininase II (E.C. 3.4.15.1) were measured spectrophotometrically using hippuryl-L-arginine for estimation of kininase Ia (KIa), hippuryl-L-lysine for kininase Ib (KIb) and hippuryl-L-histidyl-L-leucine for kininase II (KII). KIa and KIb were significantly elevated (p less than 0.02) in lung cancer and sarcoidosis, compared to tuberculosis and healthy controls. There was an increase (p less than 0.05) in lung cancer in relation to sarcoidosis, chronic obstructive bronchitis, tuberculosis, pulmonary fibrosis and healthy control subjects. KII was significantly elevated in sarcoidosis (p less than 0.0001). According to the histological types of lung cancer, no differences of KIa, KIb and KII have been found. The ratio KIa/KIb X KII was 2.3 in lung cancer and 6.7 in the group with sarcoidosis. These results show that the determination of kininases can be used for diagnosis of lung diseases.
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PMID:Kininase I and II activities in serum of patients with lung diseases. 302 81

As a symptom of an underlying condition, cough is one of the most common reasons patients see physicians. To the majority, a cough means that 'something is wrong' and it causes exhaustion and/or self-consciousness. Patients find these reasons as well as effects on lifestyle, fear of cancer and/or AIDS or tuberculosis to be the most troublesome concerns for which they seek medical attention. The treatment of cough can be divided into two main categories: (a) therapy that controls, prevents or eliminates cough (i.e. antitussive); and (b) therapy that makes cough more effective (i.e. protussive). Antitussive therapy can be either specific or nonspecific. Definitive or specific antitussive therapy depends on determining the aetiology or operant pathophysiological mechanism, and then initiating specific treatment. Since the cause of chronic cough can almost always be determined, it is possible to prescribe specific therapy that can be almost uniformly successful. Non-specific antitussive therapy is directed at the symptom; it is indicated when definitive therapy cannot be given. Practically speaking, the efficacy of nonspecific therapy must be evaluated in double-blind, placebo-controlled, randomised studies of pathological cough in humans. Such studies have demonstrated the efficacy of dextromethorphan, codeine and ipratropium bromide aerosol in patients with chronic bronchitis. While the preferred treatment for patients with cough due to angiotensin converting enzyme (ACE) inhibitor therapy is withdrawal of the offending drugs, it may be possible to ameliorate the cough by adding nifedipine, sulindac or indomethacin to the treatment regimen. The efficacy of protussive therapy has not been well documented. Although hypertonic saline aerosol and erdosteine in patients with bronchitis, and amiloride aerosol in patients with cystic fibrosis have been shown to improve mucus clearance, their clinical utility has not been adequately studied.
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PMID:Appropriate use of antitussives and protussives. A practical review. 769 10

Base on their own experience with isradipine and results of a multicentric study with amplodipine in the Slovak Republic, as well as based on data in the literature the authors conclude that: 1. In the treatment of arterial hypertension associated in the syndrome of insulin resistance (syndrome X and 5H resp.) with type 2 diabetes, hyperlipiproteinaemia and hyperinsulinism drugs of first choice include ACE-inhibitors and Ca antagonist of the second generation, dihydropiridine type, such as amplodipine, isradipine, fellodipine, nirtendipine etc. ACE inhibitors and Ca antagonist of the dihydropyridine type with prolonged effect have a good tolerance, few undesirable effect, a favourable effect on the decline of BP, regression of hypertrophy of the left ventricle and vascular wall; they do not cause deterioration of insulin resistance and thus do not interfere with compensation of diabetes and associated hyperlipoproteinaemia. 2. ACE inhibitors moreover reduce glomerular filtration and albuminuria and thus retard along with the effect on BP the progression of diabetic nephropathy. 3. In pre-existing hyporeninemic hypoaldosteronism (cca in 18% diabetic subjects) they can however cause dangerous hyperkalinaemia by further inhibition of the damaged renin-angiotensin-aldosterone system. In instances Ca inhibitors are indicated. The latter activate RAAS and do not have an impact on albuminuria. By their effect on the vas deferens they can increase glomerular filtration. 4. Diuretics are not suitable for the treatment of hypertension in X syndrome and the use of beta-blocking agents even with ISA and beta-1-selective preparations in restricted in particular when insulin is administered or other numerous contraindications are present (cardiac failure, bradyarrythmias, bronchitis etc.). Perhaps a combination of ACE-inhibitors and Ca antagonists of the 2nd generation with an alpha-blocking agent or hybrid alpha-beta-blocking agent is a suitable solution.
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PMID:[The role of calcium inhibitors in the treatment of arterial hypertension]. 924 72

Cough is probably the most frequent symptom in chest diseases. Hence, a rational and economical diagnostic procedure is essential to prevent unnecessary costs to the health services, i.e. acute bronchitis, a self-limiting disease, which is the most frequent cause for cough should not involve extensive per case costs. History, physical examination, chest X-ray and lung function testing--which constitute both the first and second, i.e. the basic level of a stepwise approach--allows to diagnose causes in most patients with cough. Without evidence of the cause after completing this basic diagnostic procedure patients with acute cough may require blood gases analysis, electrocardiography, echocardiography, lung perfusion study, spiral CT angiography, bronchoscopy or laboratory examinations for diagnosis of pulmonary embolism, aspiration or (seldom) pleuritis sicca. Chronic persistent cough (CPC) is diagnosed if the basic standard approach to chronic cough fails to lead to final diagnosis. Patients will then need further subtle diagnostic management, i.e. bronchial provocation testing, 24 hour pH probe, ENT- or neurological examination, high resolution CT of the thorax and bronchoscopy. We present two algorithms for the rational diagnostic approach to acute (figure 1) and chronic (figure 2) cough. Each algorithm considers spectrum and frequency of causes on the one hand, the positive predictive value, costs and patient discomfort due to the examination on the other. Nonetheless, despite extensive examination up to 20% of patients suffering from CPC the cause remains unclear [11]. Frequently, the capsaicin cough challenge test can reveal an idiopathic upregulation of the cough reflex as the hypothesised underlying condition. Psychogenic cough however, a rare condition in adults should not coincide with hypersensitivity of the cough reflex. Inconsistency and low reproducibility of results of the capsaicin challenge in patients with psychogenic cough preclude his routine clinical use. In conclusion, the very common acute bronchitis and the ACE inhibitor-induced cough do not require any other diagnostic procedure except patient history and physical examination. A simple basic diagnostic approach will usually allow to evaluate acute and chronic cough. In the remaining cases the proposed algorithm should be used for best results and to prevent excessive costs.
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PMID:[Proposals for a rationale and for rational diagnosis of coughs]. 1078 50

In non-smokers the underlying causes for chronic persistent cough (CPC) e.g. chronic cough without diagnostic chest X-ray or pulmonary function test--are usually as follows: several common upper airways diseases, bronchial (cough type) asthma, gastrooesophageal reflux or treatment with an ACE (angiotensin converting enzyme)--inhibitor. In 10% of CPC however the cause remains uncertain. We report a 30 year old non-smoker with severe coughing and repeated vomiting for two months. No laboratory or technical data could be collected suggestive of a common cause of CPC: Upper airways disease, bronchial flow limitation or hyperresponsiveness, ACE inhibitor medication, B. pertussis infection, gastrooesophageal reflux disease (by 24 hours pH-probe) were ruled out. Fiberbronchoscopic findings remained unremarkable, except for the bronchial biopsy specimen, which showed moderate eosinophilic inflammation of the mucosa and marked thickening of the subepithelial layer. Since the cough was non-productive, sputum induction with 3 ml nebulised 3% NaCl solution was performed. 28% of the granulocytes were eosinophil stained. A low quality morning sputum (< 1 ml) showed 21% eosinophilia. Thus, the diagnosis of eosinophilic bronchitis was established. 400 micrograms budesonide dry powder inhalations b.i.d. for one week resolved the cough, treatment was stopped after three weeks. No recurrence was seen two months later. Both the cough type asthma and the eosinophilic bronchitis could represent a form fruste of classical bronchial asthma beyond wheezing or dyspnoea, but with the common main symptom: cough. Since hyperresponsiveness and cough are phenotypic hallmarks of cough variant asthma, in eosinophilic bronchitis--beside cough--another two features of asthma are present: eosinophilic inflammation of the mucosa along with sputum eosinophilia and subepithelial layer thickening. Not surprisingly, eosinophilic bronchial inflammation could be shown in patients with cough variant asthma as well, who--up to 56% during a four year-period--develop classic asthma. The long-term outcome of eosinophilic bronchitis is not known, however. Thus, asthma, cough variant asthma and cough due to eosinophilic bronchitis can mirror different phenotypes or phases of the same entity. CPC due to either the cough type asthma or the eosinophilic bronchitis is like asthma fast responding to inhalative steroids. (Induced) sputum staining should be added to the diagnostic armamentarium of CPC.
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PMID:[Eosinophilic bronchitis without asthma--an additional rare cause for chronic persistent cough (CPC)? A 30-year old patient with severe CPC due to eosinophilic bronchitis without asthma or hyperreactivity]. 1144 11

This case presented the scenario of a patient who had severe bronchospasm from an unknown etiology. Further, she had difficulty speaking and denied any past medical history, which made a diagnosis more difficult. Prehospital providers were challenged with determining the differential diagnosis for bronchospasm and hypoxemia. Was the patient experiencing an anaphylactic reaction, acute asthmatic attack or something else? The key here, once again, is conducting a thorough assessment and patient history. Remember, all that wheezes is not asthma; therefore, providers in this case had to determine if the patient was suffering something such as anaphylaxis, asthma, bronchitis, pneumonia or even congestive heart failure (CHF). Typically, anaphylaxis and asthma affect ventilation, not oxygenation, so until the late stages of anaphylaxis or asthma, the patient will have difficulty moving air, but will be oxygenating OK. We understand that many respiratory conditions can cause wheezing, but CHF? Yes: As left ventricular function diminishes and leads to increased pulmonary pressure, serum begins to leak out of the pulmonary vessels and into the interstitial space. As the interstitial pressure increases, it causes narrowing of the bronchioles, and air traveling through the narrowed bronchioles causes the wheezing sound. Fluid may also be leaking out of the pulmonary capillaries and occupying space in the alveolar sacs. When the interstitial pressure is high and the bronchioles continue to narrow, providers may initially hear only the wheezing and not the crackles from the smaller airways. In these conditions, oxygen is not exchanged adequately into the blood, and the patient becomes hypoxemic. Good assessment and patient history will guide the EMS provider to the cause of bronchospasm. For example, does the patient have a history of asthma? If yes, asthma is likely to be the cause. Does the patient have any rash, hives or swelling? If yes, anaphylaxis is likely the cause. Is the patient elderly, and does he/she show pedal edema, JVD, hypoxemia and/or distended neck veins? If yes, CHF may be the cause. [table: see text] There are questions regarding the use of bronchodilators in patients suffering CHF. If a CHF patient is wheezing (bronchospasm), then a beta-2 selective breathing treatment may be appropriate, along with nitrates and diuretics. Oxygenation is the critical problem in CHF, and hypoxemia will continue to worsen cardiac function. Remember, both bronchoconstriction and alveolar sacs filling with fluid will impair oxygenation of the RBCs and ultimately the vital organs. Focused prehospital management of CHF is aggressive in restoring oxygenation. For example, many agencies are now using oxygen, nitrates, ACE inhibitors and CPAP. By better understanding the pathophysiology of respiratory emergencies and their differential diagnosis, we will improve patient outcomes.
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PMID:Breathless. 1196 14

Chronic cough is defined as persistence of the symptom for longer than one month. It is a common reason for consultation. A systematic diagnostic approach based on the history, clinical examination and a number of investigations (chest x-ray, lung function tests, oesophageal pH monitoring and sinus x-rays) reveals the cause in most cases. The main aetiologies are post-nasal drip, gastro-oesophageal reflex, asthma, chronic bronchitis, and the use of angiotensin converting enzyme inhibitors. Nevertheless, in some cases, the cause is not found. In this situation it is necessary to search for less common pathologies where cough is just a symptom of systemic disease, such as connective tissue disorder (Sjogren's syndrome, atrophic polychondritis), vasculitis (Wegener's granulomatosis), Horton's syndrome (cluster headaches), amyloidosis and inflammatory bowel disease. It may also be a matter of local pathology of the tracheo-bronchial tree, such as tracheo-bronchomegaly, tracheopathia osteoplastica, rare or unrecognized infections (whooping cough, post-viral cough, bronchial tuberculosis), reactive bronchial dysfunction, eosinophilic bronchitis or radiologically occult bronchial carcinoma. Il is also necessary to consider vocal cord dysfunction and cough due to medication before accepting a diagnosis of psychogenic cough.
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PMID:[Unrecognized causes of chronic cough]. 1204 Mar 21


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