ライフサイエンスコーパス: antimuscarinic

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1 e, disease severity, apathy, and exposure to antimuscarinics.

2 [1.09-2.43]), and more frequent exposure to antimuscarinics (3.07 [1.35-6.97]) (logistic regression)

3 ting T-cell subsets, and characterization of antimuscarinic acetylcholine receptor type 3 autoantibod

4 antinicotinic agent mecamylamine (MECA) and antimuscarinic agent scopolamine (SCOP) and were tested

5 movements are reduced significantly with an antimuscarinic agent used clinically, and we identify ch

6 h an inhaled corticosteroid or a long-acting antimuscarinic agent.

7 Studies have included a number of antimuscarinic agents (tolterodine, oxybutynin, propiver

8 Recent evidence suggests that newer antimuscarinic agents are not only superior to placebo,

9 The use of selective antimuscarinic agents in patients with moderate-to-sever

10 symptoms may not respond to monotherapy with antimuscarinic agents or alpha-receptor antagonists.

11 ls have received FDA approval; these are the antimuscarinic and anticholinergic/direct smooth muscle

12 ower urinary tract symptoms, combinations of antimuscarinics and alpha1-adrenoceptor blockers have pr

13 of these phenotypes to inhaled beta-agonist, antimuscarinic, and corticosteroid therapy.

14 In patients resistant to antimuscarinics, botulinum toxin may be an alternative--

15 rbations compared with the single longacting antimuscarinic bronchodilator glycopyrronium, with conco

16 ine, a Food and Drug Administration-approved antimuscarinic compound that has been shown to enhance m

17 hesis, we orally administered clemastine, an antimuscarinic compound that has been shown to enhance o

18 active molecules, we identified a cluster of antimuscarinic compounds that enhance oligodendrocyte di

19 severity following the administration of the antimuscarinic drug scopolamine hydrobromide (4 microg/k

20 The long duration of action of the antimuscarinic drug tiotropium and its kinetic subtype s

21 Antimuscarinic drugs affect bladder sensory symptoms suc

22 mized controlled trials have shown that both antimuscarinic drugs and alpha1-adrenoceptor blockers ca

23 As a variety of antimuscarinic drugs are approved for clinical use again

24 These antimuscarinic drugs prevented or reversed indices of pe

25 Antimuscarinic drugs remain the first-line treatment of

26 Pretreatment with the antimuscarinic drugs scopolamine and atropine was able t

27 ture review confirms the rationale for using antimuscarinic drugs, and that the currently used drugs

28 catheterisation, and storage dysfunction by antimuscarinic drugs.

29 A new generation of bladder-selective antimuscarinics has graduated through phase-III randomiz

30 review will provide an update on the use of antimuscarinics, in combination with an alpha-blocker, i

31 e than 2.5-fold higher in cases treated with antimuscarinic medication in the long term compared with

32 inary incontinence are commonly treated with antimuscarinic medications, but many discontinue therapy

33 ergistic bronchodilation over either inhaled antimuscarinic or beta2-agonist monotherapy.

34 apid, robust antidepressant responses to the antimuscarinic scopolamine occurred in currently depress

35 optimizing dopaminergic therapy and avoiding antimuscarinics should be considered.

36 Monotherapy with an antimuscarinic therapy alone in this patient group has p

37 py with an alpha-blocker, the addition of an antimuscarinic therapy is worth considering.

38 ty to sham treatment and benefits similar to antimuscarinic therapy may be observed.

39 provements can be achieved by addition of an antimuscarinic therapy to an alpha-blocker.

40 olume should be measured prior to commencing antimuscarinic therapy to rule out baseline retention su

41 nce is more homologous to antinicotinic than antimuscarinic toxins, but it lacks three almost invaria

42 I and III scores (r = -0.50; P < .01) and no antimuscarinic use (r = -0.21; P < .01).

43 younger ones with less severe disease and no antimuscarinic use.

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