Nowa wersja platformy, zawierająca wyłącznie zasoby pełnotekstowe, jest już dostępna.
Przejdź na https://bibliotekanauki.pl
Ograniczanie wyników
Czasopisma help
Lata help
Autorzy help
Preferencje help
Widoczny [Schowaj] Abstrakt
Liczba wyników

Znaleziono wyników: 56

Liczba wyników na stronie
first rewind previous Strona / 3 next fast forward last
Wyniki wyszukiwania
Wyszukiwano:
w słowach kluczowych:  aspirin
help Sortuj według:

help Ogranicz wyniki do:
first rewind previous Strona / 3 next fast forward last
EN
A simple, precise, and accurate HPTLC method has been established for simultaneous quantification of aspirin, atorvastatin calcium and clopidogrel bisulphate in the bulk drug and in a capsule dosage form. Chromatographic separation of the drugs was performed on aluminium foil plates precoated with silica gel 60 F 254 , with toluene-methanol-formic acid 6.5:3.5:0.1 ( v / v ) as mobile phase. Densitometric evaluation of the separated zones was performed at 254 nm. The three drugs were satisfactorily resolved with R F ± SD values 0.26 ± 0.01, 0.47 ± 0.01, and 0.78 ± 0.01 for aspirin, atorvastatin calcium, and clopidogrel bisulphate, respectively. The method was validated for linearity, specificity, accuracy, precision, and robustness, in accordance with ICH guidelines. Results from recovery studies indicated acceptable recovery of the drugs from the capsule dosage form. The intra-day and inter-day relative standard deviations were in the ranges 0.17–0.73% and 0.46–1.03% for aspirin, 0.36–0.87% and 0.44–0.62% for atorvastatin calcium, and 0.25–0.69% and 0.35–0.94% for clopidogrel bisulphate. The method proved to be a rapid and cost-effective quality-control tool for routine simultaneous analysis of aspirin, atorvastatin calcium, and clopidogrel bisulphate in the bulk drug and in a capsule formulation.
EN
Introduction and aim. Kawasaki disease (KD) is an acute vasculitis with unknown etiology, usually occurring in children under 5 years old. This article will summarize the three consensuses formulated in China about KD. Material and methods. English databases for consensus search include UpToDate, BMJ Clinical Evidence, National Guideline Clearinghouse, Joanna Briggs Institute Library, Cochrane Library, and PubMed, etc.; Chinese databases include China Biomedical Literature Service, China Knowledge Network, Wanfang database, etc. All literature searches ended on February 28, 2022. Analysis of the literature. KD is a common acquired heart disease in children and can lead to severe complications such as coronary injury. However, intravenous immunoglobulin (IVIG) combined with oral aspirin (Asp) is currently recognized as the most effective treatment in KD acute stage and the first-line treatment to prevent cardiovascular complications. Glucocorticoid (GC) is mainly used for KD patients with a high risk of coronary artery aneurysm (CAA), no immunoglobulin response, and confirmed CAA. There are already consensus guidelines on diagnosing and treating KD in different countries. This article summarizes the relevant expert consensus on aspirin, glucocorticoids and IVIG for the treatment of Kawasaki disease in China. Conclusion. Still, there are inconsistent opinions in the literature on the mechanism, optimal timing, and dosage of medication for KD.
EN
An isocratic reversed-phase liquid chromatograpic assay method was developed for the quantitative determination of atorvastatin and aspirin (ASP) in combined dosage form. A Phenomenex Gemini C-18, 5-μm column with mobile phase containing 0.02 M potassium dihydrogen phosphate-acetonitrile-methanol (30:30:40, v/v/v) adjusted to pH 3 using o-phosphoric acid was used. The flow rate was 1.0 mL min -1 and effluents were monitored at 240 nm. The retention times (RTs) of atorvastatin calcium (ATV) and ASP were 10.5 and 3.8 min, respectively. ATV and ASP stock solutions were subjected to acid and alkali hydrolysis, chemical oxidation, and dry heat degradation. The degraded product peaks were well resolved from the pure drug peak with significant difference in their RT values. Stressed samples were assayed using developed LC method. The proposed method was validated with respect to linearity, accuracy, precision, and robustness. The method was successfully applied to the estimation of ATV and ASP in combined capsule dosage forms.
EN
A simple, sensitive, specific, and cost effective method for simultaneous determination of Aspirin and Rosuvastatin calcium was developed and validated in single dosage formulation. The sample solution of ASP and RSTC was prepared using methanol as a solvent. Separation of ASP and RSTC was achieved with a mobile phase consisting of 20 mM KH2PO4 : Methanol (30:70 v/v) at a flow rate of 1.0 ml/min. Separations were performed on Merck hibar 250-4.6 RP18 (5 μm) column (150 mm X 3.0 mm), using a Shimadzu Prominence HPLC system equipped with a Shimadzu SPD-20A detector, Rhenodyne 7725i injector with 20 μL loop, LC-20 AD pump, CBM-20 Alite controller and LC Solution software. Retention times of ASP and RSTC were 3.747 and 5.969 minutes respectively. Absolute recovery of ASP and RSTC was 100.3 and 100.03 % respectively. The lower limit of quantification (LLOQ) of ASP and RSTC was 0.3097 and 0.1063 ppm and lower limit of detection (LLOD) of ASP and RSTC was 0.01535 and 0.01358 ppm respectively. Linearity was established for the range of concentrations 15.00-90.0 μg/ml and 2.0-12.0 μg/ml for ASP and RSTC respectively with the coefficient of determination (R2) of 0.994 and 0.999 for both the compounds. The inter- and intra-day precision in the measurement of ASP quality control (QC) sample 75 μg/ml, were in the range 0.1-0.2 % relative standard deviation (R.S.D.) and 0.2-0.3 % R.S.D., respectively. The inter- and intra-day precision in the measurement of RST quality control (QC) sample 10 μg/ml, were in the range 0.1-0.2 % R.S.D., and 0.0-0.3 % R.S.D., respectively. The developed method would be applicable for routine quality control of ASP And RSTC in bulk as well as in pharmaceutical formulations.
5
Content available Kwas acetylosalicylowy: wczoraj, dziś, jutro
75%
EN
Clinical utility of aspirin (acetylsalicylic acid, ASA) is one of the more important issues in the primary and secondary prevention of cardiovascular disease. The present paper provides analysis of aspirin history, mechanisms of its antiplatelet activity, and expediency of the use of low- and high-dose aspirin in the groups including patients after myocardial revascularization, and requiring secondary prevention of stroke. Also gender-specific aspirin properties were mentioned, highlighting the especially important role of aspirin in women at the age of >65 years, and its utility in all women, irrespectively of age, and those who are at high risk of cardiovascular disease, including atherosclerosis-related cardiovascular disease. Moreover, the mechanisms of aspirin resistance, characterized by inability of aspirin to prevent thromboembolic complications or inadequate platelet inhibition showed in laboratory results, were mentioned. Prevalence of resistance in aspirin-treated patients is estimated to be between 1 and 68%. Stress was also put on the aspirin safety, associated with prophylaxis of peptic ulcer disease, which can be achieved i.e. by the use of the enteric-coated aspirin. This form of aspirin is associated with lower risk of gastrointestinal mucosae damage and bleeding from the gastrointestinal tract. At the end of the article, the importance of the adherence to therapeutic guidelines of aspirin use, including assessment of variation in aspirin bioavailability associated with improper dosing and altered absorption in the gastrointestinal tract, was stressed.
PL
Zastosowanie kwasu acetylosalicylowego we wspołczesnej praktyce klinicznej jest jednym z podstawowych założeń pierwotnej i wtornej prewencji chorob układu sercowo-naczyniowego. W artykule przeanalizowano historię problemu, mechanizm efektywności przeciwpłytkowej kwasu acetylosalicylowego, celowość zastosowania jego wysokich i niskich dawek, a także wykorzystanie u pacjentow z nadciśnieniem tętniczym, po zabiegach rewaskularyzacji mięśnia sercowego oraz w profilaktyce udaru mozgu. Odniesiono się rownież do właściwości kwasu acetylosalicylowego zależnych od płci, podkreślając szczegolnie istotny wpływ u kobiet w wieku powyżej 65 lat oraz podając zalecenie stosowania u kobiet w każdym wieku, w tym u młodych, z podwyższonym ryzykiem rozwoju chorob układu sercowo-naczyniowego, m.in. Związanych z procesem miażdżycowym. Przeanalizowano także kwestię oporności na kwas acetylosalicylowy, ktora charakteryzuje się zarowno jego niezdolnością do zapobiegania rozwojowi powikłań zakrzepowych, jak i do adekwatnego tłumienia funkcji płytek krwi ocenianego w badaniach laboratoryjnych. Częstość ujawniania oporności na kwas acetylosalicylowy u chorych, ktorzy go stosują, waha się w zakresie 1–68%. Zwrocono uwagę na profilaktykę powikłań stosowania kwasu acetylosalicylowego związanych z rozwojem choroby wrzodowej – możliwe jest np. przyjmowanie postaci dojelitowej leku, ktora nieco zmniejsza ryzyko uszkodzeń śluzowki żołądka i krwotokow żołądkowo-jelitowych. Duże znaczenie ma przestrzeganie zaleceń terapeutycznych dotyczących kwasu acetylosalicylowego, tzn. należy uwzględniać możliwość obniżenia jego biodostępności w wyniku nieprzestrzegania zaleceń terapeutycznych, nieodpowiedniego sposobu dozowania albo zaburzeń jego wchłaniania w przewodzie pokarmowym.
PL
Niesteroidowe leki przeciwzapalne (NLPZ) pomimo licznych działań niepożądanych w dalszym ciągu pozostają najczęściej stosowaną grupą leków, które można nabyć bez recepty. Mechanizm ich działania polega na hamowaniu aktywności cyklooksygenaz (COX 1; COX 2), enzymów uczestniczących w jednym ze szlaków przemian kwasu arachidonowego, którego końcowymi produktami są prostaglandyny (PGE2 oraz PGI2-prostacykliny) oraz tromboksany. Zahamowanie aktywności cyklooksygenazy (COX) nieuchronnie prowadzi po wystąpienia działań niepożądanych. Do najczęściej występujących skutków ubocznych związanych ze stosowaniem niesteroidowych leków przeciwzapalnych należą objawy ze strony przewodu pokarmowego. Rzadziej z nadmiernym stosowaniem NLPZ wiąże się oddziaływanie nefrotoksyczne, hepatotoksyczne, negatywny wpływ na działanie układu oddechowego oraz stosunkowo niedawno potwierdzone działanie kardiotoksyczne. Należy więc wszelkimi możliwymi sposobami dążyć do zmniejszenia dostępności niesteroidowych leków przeciwzapalnych oraz monitorować stosowanie tych leków głównie u osób szczególnie narażonych na wystąpienie skutków ubocznych (ludzi starszych, z niewydolnością krążenia, nadciśnieniem tętniczym, chorobami nerek i przewodu pokarmowego).
EN
Non-steroidal anti-inflammatory drugs (NSAIDs), despite numerous adverse effects, still remain the most commonly used group of medicines that can be obtained without a prescription. The mechanism of their action consists in inhibiting the activity of cyclooxygenases (COX 1; COX 2); these are enzymes that participate in one of the routes of transformation of arachidonic acid, whose end products are prostaglandins (PGE2 and PGI2-prostacyclins) and thromboxanes. Inhibition of cyclooxygenase (COX) activity inevitably leads to adverse reactions. The most common side effects associated with the use of non-steroidal anti-inflammatory drugs include gastrointestinal symptoms. More rarely associated with the excessive use of NSAIDs are nephrotoxic, hepatotoxic, and negative effects on the respiratory system and the relatively recently confirmed cardiotoxicity. Therefore, all possible ways should be tried to reduce the availability of non-steroidal anti-inflammatory drugs and to monitor their use, mainly in people who are particularly exposed to side effects (the elderly, people with heart failure, hypertension, kidney and gastrointestinal diseases).
7
Content available Aspiryna – 115 lat po odkryciu
75%
EN
Aspirin has been known as a commercial drug for over a century, however, a much deeper understanding of its mechanism of action as an inhibitor of cyclooxygenase (COX) activity and thus, of prostanoid synthesis, is still lacking. Recent advances in understanding the central role of platelets in the pathophysiology of cardiovascular diseases and the identification of novel lipid mediators synthesized in the presence of aspirin have increased research upon the mechanisms of aspirin action.
PL
Aspiryna jest lekiem dostępnym komercyjnie od ponad stu lat, chociaż wciąż brakuje głębszego zrozumienia mechanizmu jej działania jako inhibitora aktywności cyklooksygenazy i syntezy prostanoidów. Niedawne odkrycia dotyczące centralnej roli płytek krwi w patofizjologii chorób układu sercowo-naczyniowego oraz identyfikacja nowych mediatorów lipidowych syntetyzowanych w obecności aspiryny nasiliły badania nad mechanizmami działania aspiryny.
EN
Melatonin (MT) and its precursor L-tryptophan (Trp) are implicated in the protection of gastric mucosa against noxious agents. However, the role of MT and Trp on the gastric mucosal injury induced by aspirin (ASA) in human has not been investigated. Studies in animals showed that both MT and Trp given intragastrically prevents the formation of gastric mucosal lesions induced by ASA. The aim of the present study was to determine the influence of MT and Trp given orally to healthy humans on gastric mucosal lesions induced by ASA. The present study included 21 healthy, Hp-negative male volunteers with intact gastro-duodenal mucosa aging 20-50 yr. They were divided in 3 groups; group1: 7 volunteers receiving daily 2 x 1g ASA (Polfa, Rzeszow) during 11 days; group 2: 7 healthy volunteers receiving 2x1g ASA and MT (Lekam, Zakroczyn) (5 mg 30 min prior to ASA) during 11 days and group 3: 7 healthy volunteers receiving 2x1g ASA and Trp (Ardeytropin, Germany) (0.5 g 30 min prior to ASA) during 11 days. Mucosal damage was evaluated at 3rd, 7th and 11th days of ASA administration by endoscopy using Lanza score. Plasma melatonin was measured using RIA and gastric mucosal generation of PGE2 was assessed also by RIA. ASA caused marked mucosal injury at all days of its administration except day 11th when only moderate lesions were evident. Pre-treatment with MT or Trp alone was accompanied by a significant decrease in gastric mucosal lesion score. Gastric mucosal generation of PGE2 was suppressed by about 90% in subjects treated with ASA without or with MT or Trp. We concluded that: MT and its precursor Trp significantly attenuate gastric mucosal lesions induced by aspirin. The action of Trp may be be mediated by MT produced in gastrointestinal tract from Trp. The gastroprotective action of MT and Trp is independent on gastric mucosal PGE2 generation.
|
|
tom 57
|
nr 12
15-24
EN
Expression of cyclooxygenase-2 (COX-2) is involved in the chronic inflammation-related development of Barrett’s adenocarcinoma and the use of selective COX-2 inhibitors (coxibs) might provide new chemoprevention strategy for Barrett’s adenocarcinoma (BA). Despite an excellent gastrointestinal (GI) safety profile of coxibs, their use is limited because of the possible cardiovascular complications. The coupling of NSAIDs with a NO-donating moiety has led to the birth of a new class of anti-inflammatory drugs, called the COX-inhibiting nitric oxide donators (CINODs). The member of this group, NO-aspirin (NO-ASA) retains the anti-inflammatory properties of traditional aspirin (ASA), but the release of NO accounts for anti-thromboembolic effect and better GI safety profile. The role of NO-ASA in the prevention of Barrett’s adenocarcinoma (BA) has not been studied so far. Therefore, the aim of the present study was: 1) to analyse the expression of COX-2 in the biopsies obtained from BE; 2) to compare the effect of NO-ASA with that of ASA on proliferation rate in Barrett’s adenocarcinoma cell line (OE-33 cells); 3) to determine the effect of both compounds on the apoptosis rate using FACS analysis and expression of 32-kDa procaspase-3 and active proapoptotic 20-kDa caspase-3 in OE-33 cell line. The expression of COX-2 was assessed in biopsies obtained from the Barrett’s mucosa and normal squamous epithelial esophageal mucosa from 20 BE patients by RT-PCR and Western blot analysis, respectively. The BA cell line (OE-33) was incubated with NO-ASA or ASA (10-1000µM). The cell proliferation and apoptosis rate was measured by BrdU and FACS-analysis, respectively. The expression of caspase-3 (active and inactive form) was analyzed by Western blot. In Barrett’s mucosa a significant up-regulation of COX-2 was observed. Compared with traditional ASA, NO-ASA caused a significantly stronger induction of apoptosis (dose-dependently). Inhibition of cell proliferation in OE-33 cells observed under NO-ASA treatment was due to the apoptosis induction. The increase in apoptotic rate was accompanied by the upregulation of active 20-kDa caspase-3. At the highest concentration (1000µM), a necrotic death of OE-33 cells was observed under NO-ASA treatment. We conclude that: NO-ASA caused induction of apoptosis in BA cell line and slight growth inhibition. These results indicate that this compound may represent a promising chemopreventive agent for Barrett’s adenocarcinoma.
|
|
tom 57
|
nr 5
125-136
EN
Aspirin (ASA) represents an important risk factor for gastric mucosal injury. Recently, vitamin C releasing aspirin (ASA-VitC) has been shown to reduce gastric toxicity of ASA in animal model of gastric injury. The aim of the present study was to compare the effect of ASA and ASA-VitC on the gastric mucosal damage before and after Helicobacter pylori (Hp) eradication in 10 young healthy Hp-positive volunteers. All subjects underwent endoscopy at day 0 (before ASA or ASA-VitC treatment) and at day 3 following treatment (1.6 g ASA/day or 1.6 g ASA + 0.96 g Vit C/day). In addition, in vitro experiments were performed in which gastric mucosal cell line (MKN-45 cells) was incubated with ASA or ASA-VitC alone or in combination with H.pylori. Expression of constitutive and inducible NO synthase (cNOS, iNOS) was analyzed by Western blot. Moreover, COX-2 expression was analyzed in gastric biopsies at mRNA and protein level by RT-PCR and Western blot, repectively. In humans, treatment with ASA-VitC induced significantly less gastric mucosal lesions than plain ASA. Furthermore, in comparision to plain ASA, ASA-VitC caused stronger inhibition of cNOS and increase in iNOS expression in the gastric mucosa. in vitro studies demonstrated a significant increase in iNOS expression in MKN-45 cells incubated with Hp. This effect was aggravated by the addition of ASA, but not ASA-VitC, to MKN-45 cells incubated with H.pylori. Both ASA and ASA-VitC stimulated the COX-2 expression in the gastric mucosa. We conclude that ASA-VitC in comparison with ASA induces less gastric mucosal damage and this protective effect may be due to its inhibitory effect on iNOS expression.
first rewind previous Strona / 3 next fast forward last
JavaScript jest wyłączony w Twojej przeglądarce internetowej. Włącz go, a następnie odśwież stronę, aby móc w pełni z niej korzystać.