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Pharmaceuticals, Volume 5, Issue 4 (April 2012), Pages 339-404

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Research

Jump to: Review

Open AccessArticle Oral Administration of Shark Type II Collagen Suppresses Complete Freund’s Adjuvant-Induced Rheumatoid Arthritis in Rats
Pharmaceuticals 2012, 5(4), 339-352; doi:10.3390/ph5040339
Received: 7 November 2011 / Revised: 12 February 2012 / Accepted: 21 March 2012 / Published: 28 March 2012
Cited by 9 | PDF Full-text (329 KB) | HTML Full-text | XML Full-text
Abstract
Objective: Shark type II collagen (SCII) is extracted as a glycoprotein from the cartilage of blue shark (Prionace glauca). We aim to confirm the effects of oral tolerance of SCII on inflammatory and immune responses to the ankle joint of [...] Read more.
Objective: Shark type II collagen (SCII) is extracted as a glycoprotein from the cartilage of blue shark (Prionace glauca). We aim to confirm the effects of oral tolerance of SCII on inflammatory and immune responses to the ankle joint of rheumatoid-arthritis rats induced by Complete Freund’s Adjuvant (CFA). Materials and Methods: The onset of rheumatoid arthritis (RA) was observed 14 ± x days after injection of CFA. Rats in the control group were treated with acetic acid by oral administration (0.05 mmol kg−1d−1, days 14–28), while rats in experimental groups were treated by oral administration with SCII (1 or 3 mg kg−1d−1, days 14–28), Tripterygium wilfordii polyglycosidium (TWP) (10 mg kg−1d−1, days 14–28), and bovine type II collagen from US (US-CII) (1 mg kg−1d−1, days 14–28), respectively. The severity of arthritis was evaluated by the articular swelling. The immunological indexes observed included delayed type hypersensitivity (DTH) reaction, the level of interleukins 10 (IL-10) in rat blood serum and morphological characterization. Mixed lymphocyte culture (MLC) was performed to investigate the relationship between T cell apoptosis and specific immune tolerance induced by SCII. Results: Treatment with SCII for 2 weeks significantly attenuated the acute inflammation. The rats orally administrated with SCII at the level of 3 mg kg−1d−1 (SCII 3) and US-CII had decreased DTH reaction compared with rats in control group. Rats treated with SCII 3 had the highest level of IL-10 with 102 pg/mL. SCII with concentration of 10 μg/L could help to significantly enhance level of Fas/Apo-1 in T cell in vitro. The result of histological staining indicated that the recovery of the articular membranes of ankle joint in SCII 3 group was greatly enhanced. Conclusions: Our results suggest that appropriate dose of SCII can not only ameliorate symptoms but also modify the disease process of Complete-Freunds-Adjuvant-induced arthritis. Oral administration of SCII might be a potential candidate as a novel drug for further investigation. Full article
(This article belongs to the Special Issue Immunosuppressant Drugs)
Open AccessArticle Ivabradine Prevents Heart Rate Acceleration in Patients with Chronic Obstructive Pulmonary Disease and Coronary Heart Disease after Salbutamol Inhalation
Pharmaceuticals 2012, 5(4), 398-404; doi:10.3390/ph5040398
Received: 8 February 2012 / Revised: 25 March 2012 / Accepted: 5 April 2012 / Published: 16 April 2012
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Abstract
Accelerated sinus rhythm is an important side effect of inhaled salbutamol which is especially harmful in patients with chronic obstructive pulmonary disease (COPD) and coronary heart disease (CHD). Cross-over, randomized, open label study design. 20 patients (18 males and two females) with COPD stage II–IV and comorbide CHD NYHA class I–III were included. Spirometry with 400 mg salbutamol inhalation was performed at two consecutive days of the study. Patients in group I were prescribed 5 mg ivabradine per os 3 h before salbutamol inhalation solely on the first day of the study and patients of group II received 5 mg ivabradine only on the second day of the study. Salbutamol caused a significant increase of HR by 5.5 bpm (95% CI 0.8; 10.2, p < 0.03). After ivabradine ingestion salbutamol did not change HR significantly by −2.4 bpm (−7.0; 2.3, p = 0.33). The attenuation of HR elevation by ivabradine was significant, p < 0.01. Salbutamol alone increased FEV1 by 6.0% (2.7; 9.3, p < 0.01). This effect was not impaired by ivabradine (FEV1 increase by 7.7% (2.8; 12.6, p < 0.01 versus baseline, p = 0.5 versus no ivabradine). Ivabradine 5 mg per os prevents heart rate acceleration after inhalation of 400 mg salbutamol. Ivabradine has no impact on lung function in patients with moderate-to-very-severe COPD and CHD comorbidity. Full article
(This article belongs to the Special Issue Ivabradine)

Review

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Open AccessReview On the Regulatory Approval Pathway of Biosimilar Products
Pharmaceuticals 2012, 5(4), 353-368; doi:10.3390/ph5040353
Received: 20 February 2012 / Revised: 20 March 2012 / Accepted: 28 March 2012 / Published: 30 March 2012
Cited by 22 | PDF Full-text (97 KB) | HTML Full-text | XML Full-text
Abstract
Biosimilars (or follow-on biologics) are a new class of medicine which enters the market subsequent to a previously approved version. They have demonstrated similarity to innovator biologic products in terms of quality, safety, and efficacy. The EMA has taken the lead in [...] Read more.
Biosimilars (or follow-on biologics) are a new class of medicine which enters the market subsequent to a previously approved version. They have demonstrated similarity to innovator biologic products in terms of quality, safety, and efficacy. The EMA has taken the lead in the regulatory approval framework for biosimilar products, and WHO has published guidelines on the evaluation of biosimilars in order to facilitate the global harmonization. Based on EMA and WHO guidelines, many other countries such as Canada, Japan and Korea have also issued their own guidance for evaluating follow-on biologics. The US FDA was authorized to approve follow-on biologics by the BPCI Act passed by the US Congress on March 23, 2010, and has just issued a draft guidance in early 2012. The basic concepts and main principles of approving biosimilars are similar among various nations, notwithstanding some differences in regard to the scope, the choice of reference product, and the data requirement. This article reviews the regulatory approval pathway of biosimilar products in different regions. Full article
(This article belongs to the Special Issue Biologics)
Open AccessReview Epigenetic Mechanisms and Therapeutic Perspectives for Neurodevelopmental Disorders
Pharmaceuticals 2012, 5(4), 369-383; doi:10.3390/ph5040369
Received: 29 February 2012 / Revised: 23 March 2012 / Accepted: 27 March 2012 / Published: 5 April 2012
Cited by 7 | PDF Full-text (211 KB) | HTML Full-text | XML Full-text
Abstract
The number of children with mild neurodevelopmental disorders, such as autism, has been recently increasing in advanced countries. This increase is probably caused by environmental factors rather than genetic factors, because it is unlikely that genetic mutation rates suddenly increased within a [...] Read more.
The number of children with mild neurodevelopmental disorders, such as autism, has been recently increasing in advanced countries. This increase is probably caused by environmental factors rather than genetic factors, because it is unlikely that genetic mutation rates suddenly increased within a short period. Epigenetics is a mechanism that regulates gene expression, depending not on the underlying DNA sequence but on the chemical modifications of DNA and histone proteins. Because mental stress can alter the epigenetic status in neuronal cells, environmental factors may alter brain function through epigenetic changes. However, one advantage of epigenetic changes is their reversibility. Therefore, diseases due to abnormal epigenetic regulation are theoretically treatable. In fact, several drugs for treating mental diseases are known to have restoring effects on aberrant epigenetic statuses, and a novel therapeutic strategy targeting gene has been developed. In this review, we discuss epigenetic mechanisms of congenital and acquired neurodevelopmental disorders, drugs with epigenetic effects, novel therapeutic strategies for epigenetic diseases, and future perspectives in epigenetic medicine. Full article
(This article belongs to the Special Issue Epigenetic Therapies and Biomarkers)
Open AccessReview Stroke Prevention in Atrial Fibrillation: Latest Clinical Trials and Guidelines
Pharmaceuticals 2012, 5(4), 384-397; doi:10.3390/ph5040384
Received: 15 March 2012 / Revised: 16 March 2012 / Accepted: 28 March 2012 / Published: 5 April 2012
PDF Full-text (139 KB) | HTML Full-text | XML Full-text
Abstract
Atrial Fibrillation (AF) is the most common sustained arrhythmia and 1/6 strokes is attributed to AF. The cornerstone of treatment remains maintaining sinus rhythm or appropriate ventricular rate control in addition to prevention of stroke. Oral anticoagulation therapy (OAC) with vitamin K [...] Read more.
Atrial Fibrillation (AF) is the most common sustained arrhythmia and 1/6 strokes is attributed to AF. The cornerstone of treatment remains maintaining sinus rhythm or appropriate ventricular rate control in addition to prevention of stroke. Oral anticoagulation therapy (OAC) with vitamin K antagonists (VKAs) has been the gold standard for almost 50 years and a significant reduction in the risk of stroke in patients with AF has been demonstrated. Nonetheless, only 50% of patients with guideline recommendations for OAC treatment actually receive VKAs and half of these will discontinue therapy within 3 to 5 years with only another half achieving therapeutic ranges more than 50% of the time. The aforementioned limitations in addition with frequent blood monitoring have prompted the development of a series of new OAC therapies. The present review focuses on the current pharmacological management for stroke prevention in patients with AF based on current and emerging evidence. Full article
(This article belongs to the Special Issue Anticoagulants)

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