Database : MEDLINE
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PMID:28394286
Author:Li SJ; Ou CY; He SN; Huang XW; Luo HL; Meng HY; Lu GD; Jiang YM; Vieira Peres T; Luo YN; Deng XF
Address:Department of Toxicology, School of Public Health, Guangxi Medical University, Nanning 530021, China. lishaojun0613@163.com.
Title:Sodium p-Aminosalicylic Acid Reverses Sub-Chronic Manganese-Induced Impairments of Spatial Learning and Memory Abilities in Rats, but Fails to Restore γ-Aminobutyric Acid Levels.
Source:Int J Environ Res Public Health; 14(4), 2017 Apr 10.
ISSN:1660-4601
Country of publication:Switzerland
Language:eng
Abstract:Excessive manganese (Mn) exposure is not only a health risk for occupational workers, but also for the general population. Sodium para-aminosalicylic acid (PAS-Na) has been successfully used in the treatment of manganism, but the involved molecular mechanisms have yet to be determined. The present study aimed to investigate the effects of PAS-Na on sub-chronic Mn exposure-induced impairments of spatial learning and memory, and determine the possible involvements of γ-aminobutyric acid (GABA) metabolism in vivo. Sprague-Dawley male rats received daily intraperitoneal injections MnCl2 (as 6.55 mg/kg Mn body weight, five days per week for 12 weeks), followed by daily subcutaneous injections of 100, 200, or 300 mg/kg PAS-Na for an additional six weeks. Mn exposure significantly impaired spatial learning and memory ability, as noted in the Morris water maze test, and the following PAS-Na treatment successfully restored these adverse effects to levels indistinguishable from controls. Unexpectedly, PAS-Na failed to recover the Mn-induced decrease in the overall GABA levels, although PAS-Na treatment reversed Mn-induced alterations in the enzyme activities directly responsible for the synthesis and degradation of GABA (glutamate decarboxylase and GABA-transaminase, respectively). Moreover, Mn exposure caused an increase of GABA transporter 1 (GAT-1) and decrease of GABA A receptor (GABA ) in transcriptional levels, which could be reverted by the highest dose of 300 mg/kg PAS-Na treatment. In conclusion, the GABA metabolism was interrupted by sub-chronic Mn exposure. However, the PAS-Na treatment mediated protection from sub-chronic Mn exposure-induced neurotoxicity, which may not be dependent on the GABA metabolism.
Publication type:JOURNAL ARTICLE
Name of substance:42Z2K6ZL8P (Manganese); 56-12-2 (gamma-Aminobutyric Acid); 5B2658E0N2 (Aminosalicylic Acid)


  2 / 535 MEDLINE  
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PMID:28292983
Author:Kerantzas CA; Jacobs WR
Address:Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, New York, USA.
Title:Origins of Combination Therapy for Tuberculosis: Lessons for Future Antimicrobial Development and Application.
Source:MBio; 8(2), 2017 Mar 14.
ISSN:2150-7511
Country of publication:United States
Language:eng
Abstract:Tuberculosis is a global health problem that causes the death of approximately 1.5 million people worldwide each year (WHO, p. 1-126, , 2015). Treatment of drug-susceptible tuberculosis requires combination antimicrobial therapy with a minimum of four antimicrobial agents applied over the course of 6 months. The first instance of combination antimicrobial therapy applied to tuberculosis was the joint use of streptomycin and -aminosalicylic acid as documented by the Medical Research Council of the United Kingdom in 1950. These antimicrobial drugs were the product of many decades of investigation into both organism-derived antibiotics and synthetic chemotherapy and were the first agents in those respective categories to show substantial clinical efficacy and widespread use for tuberculosis. The events leading to the discovery and application of these two agents demonstrate that investments in all aspects of research, from basic science to clinical application, are necessary for the continued success of science in finding treatments for human disease. This observation is especially worth considering given the expanded role that combination therapy may play in combating the current rise in resistance to antimicrobial drugs.
Publication type:HISTORICAL ARTICLE; JOURNAL ARTICLE; REVIEW
Name of substance:0 (Antitubercular Agents); 5B2658E0N2 (Aminosalicylic Acid); Y45QSO73OB (Streptomycin)


  3 / 535 MEDLINE  
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PMID:28161290
Author:Biancone L; Annese V; Ardizzone S; Armuzzi A; Calabrese E; Caprioli F; Castiglione F; Comberlato M; Cottone M; Danese S; Daperno M; D'Incà R; Frieri G; Fries W; Gionchetti P; Kohn A; Latella G; Milla M; Orlando A; Papi C; Petruzziello C; Riegler G; Rizzello F; Saibeni S; Scribano ML; Vecchi M; Vernia P; Meucci G; Italian Group for the Study of Inflammatory Bowel Disease (IG-IBD)
Address:Gastroenterology Unit, University of Rome "Tor Vergata", Department of Systems Medicine, Rome, Italy. Electronic address: biancone@med.uniroma2.it.
Title:Safety of treatments for inflammatory bowel disease: Clinical practice guidelines of the Italian Group for the Study of Inflammatory Bowel Disease (IG-IBD).
Source:Dig Liver Dis; 49(4):338-358, 2017 04.
ISSN:1878-3562
Country of publication:Netherlands
Language:eng
Abstract:Inflammatory bowel diseases are chronic conditions of unknown etiology, showing a growing incidence and prevalence in several countries, including Italy. Although the etiology of Crohn's disease and ulcerative colitis is unknown, due to the current knowledge regarding their pathogenesis, effective treatment strategies have been developed. Several guidelines are available regarding the efficacy and safety of available drug treatments for inflammatory bowel diseases. Nevertheless, national guidelines provide additional information adapted to local feasibility, costs and legal issues related to the use of the same drugs. These observations prompted the Italian Group for the Study of Inflammatory Bowel Disease (IG-IBD) to establish Italian guidelines on the safety of currently available treatments for Crohn's disease and ulcerative colitis. These guidelines discuss the use of aminosalicylates, systemic and low bioavailability corticosteroids, antibiotics (metronidazole, ciprofloxacin, rifaximin), thiopurines, methotrexate, cyclosporine A, TNFα antagonists, vedolizumab, and combination therapies. These guidelines are based on current knowledge derived from evidence-based medicine coupled with clinical experience of a national working group.
Publication type:JOURNAL ARTICLE; PRACTICE GUIDELINE
Name of substance:0 (Adrenal Cortex Hormones); 0 (Anti-Bacterial Agents); 0 (Antibodies, Monoclonal, Humanized); 0 (Tumor Necrosis Factor-alpha); 5B2658E0N2 (Aminosalicylic Acid); 83HN0GTJ6D (Cyclosporine); 9RV78Q2002 (vedolizumab); E7WED276I5 (Mercaptopurine); YL5FZ2Y5U1 (Methotrexate)


  4 / 535 MEDLINE  
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PMID:28147380
Author:Kruis W; Nguyen PG; Morgenstern J
Address:Evangelisches Krankenhaus Kalk, University of Cologne, Cologne, Germany.
Title:Promises and Dangers of Combination Therapy.
Source:Dig Dis; 35(1-2):56-60, 2017.
ISSN:1421-9875
Country of publication:Switzerland
Language:eng
Abstract:The efficiency of the existing methods of treating inflammatory bowel disease (IBD) is limited. There are 2 ways to address this problem - either create new treatment modalities or optimize current therapies. Optimisation may be accomplished by using combinations of established therapeutic strategies. With regard to topically acting compounds such as 5-aminosalicylic acid, combining oral and rectal preparations is a commonly used method. Another commonly used combination is anti-tumor necrosis factor (TNF)-α antibody modalities together with immunosuppressants (thiopurines, methotrexate). Several aspects favour those combinations such as increased effectivity, prevention of immunogenicity and perhaps less adverse events. Currently, discussion on directly additive therapeutic effects is in progress, which have been demonstrated in some clinical trials. As on date, the combination of infliximab with azathioprine is most likely the most effective treatment of Crohn's disease. On the other hand, a combination therapy with both compounds affecting the immune system has, of course, risks. For sure, the frequency with which serious infectious complications are arising is increasing. Furthermore, the number of patients experiencing malignancies such as hepato-splenic lymphoma or melanoma is strongly suspected to be on the rise. In summary, combinations of current treatments for IBD are widely established. Various strategies have been studied and significant improvements of therapeutic effects have been demonstrated. Unfortunately, some of those proven combinations increase therapeutic risks, for example, increase the frequency of serious infections and also of some malignancies. Therefore, great caution has to be exercised when applying combination therapies.
Publication type:JOURNAL ARTICLE; REVIEW
Name of substance:0 (Antibodies); 0 (Tumor Necrosis Factor-alpha); 5B2658E0N2 (Aminosalicylic Acid); MRK240IY2L (Azathioprine)


  5 / 535 MEDLINE  
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PMID:28074051
Author:Li K; Wang XD; Yang SS; Gu J; Deng JY; Zhang XE
Address:Key Laboratory of Agricultural and Environmental Microbiology, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan, China.
Title:Anti-folates potentiate bactericidal effects of other antimicrobial agents.
Source:J Antibiot (Tokyo); 70(3):285-291, 2017 Mar.
ISSN:0021-8820
Country of publication:Japan
Language:eng
Abstract:Synergies between sulfonamides and other antimicrobial agents have long been reported, but the reason still remains unclear. Previously, Vilchèze et al. found that, sulfamethoxazole (SMX) could potentiate the bacterialcidal activity of isoniazid (INH) and rifampin (RIF) in Mycobacterium tuberculosis. To test if this was also the case in other bacteria, the ability to potentiate bactericidal effect of RIF by SMX was evaluated in Escherichia coli, Staphylococcus aureus, Salmonella typhimurium and Mycobacterium smegmatis. And the ability to potentiate bactericidal effect of streptomycin (SM) by SMX was also evaluated in E. coli and M. Smegmatis. Susceptibility tests and drug exposure experiments were performed for RIF and SM in the presence of sub-ICs of SMX. In drug exposure experiments, 10 mg l of 7,8-dihydropteroic acid (DHP) was used to reverse the effect of SMX. In the presence of sub-ICs of SMX, MIC of RIF for E. coli and M. smegmatis decreased 2 and 16 fold, respectively. In the drug exposure experiments, addition of sub-ICs of SMX suppressed the growth of RIF and SM resistant population in a pool of susceptible bacteria, and the effects of SMX could be reversed by DHP. Besides, we also found that, sub-ICs of para-aminosalicylic acid (PAS) could bactericidal effects of INH, RIF and SM in M. tuberculosis. Taken together, our data suggest that, sub-ICs of anti-folates can potentiate bactericidal effects of other antimicrobial agents in various bacteria.
Publication type:JOURNAL ARTICLE
Name of substance:0 (Anti-Bacterial Agents); 0 (Anti-Infective Agents); 0 (Antitubercular Agents); 0 (Folic Acid Antagonists); 5B2658E0N2 (Aminosalicylic Acid); JE42381TNV (Sulfamethoxazole); V83O1VOZ8L (Isoniazid); VJT6J7R4TR (Rifampin)


  6 / 535 MEDLINE  
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PMID:28028696
Author:Abdu-Allah HH; Youssif BG; Abdelrahman MH; Abdel-Hamid MK; Reshma RS; Yogeeswari P; Aboul-Fadl T; Sriram D
Address:Pharmaceutical Organic Chemistry Department, Faculty of Pharmacy, Assiut University, Assiut, 71526, Egypt. hagag.abdallah@pharm.au.edu.eg.
Title:Synthesis and anti-mycobacterial activity of 4-(4-phenyl-1H-1,2,3-triazol-1-yl)salicylhydrazones: revitalizing an old drug.
Source:Arch Pharm Res; 40(2):168-179, 2017 Feb.
ISSN:0253-6269
Country of publication:Korea (South)
Language:eng
Abstract:The antitubercular drug; para-aminosalicylic acid (PAS) was used as the core scaffold for the design of a series of 1H-1,2,3-triazolylsalicylhydrazones upon coupling with triazole and arylhydrazone moietis to furnish a single molecular architecture. The obtained derivatives were screened against Mycobacterium tuberculosis H37Rv revealing good to high activity for the active compounds (MIC values of 0.39-1.5 µg/mL) compared to the marketed drugs isoniazid, rifampicin and ethambutol. Moreover, the most active analogue N-(1-(4-chlorobenzyl)-2-oxoindolin-3-ylidene)-2-hydroxy-4-(4-phenyl-1H-1,2,3-triazol-1-yl)-benzohydrazide (20) was found to be ten-fold more potent than PAS and equipotent to rifampicin (MIC 0.39 µg/mL), while exhibiting low cytotoxicity with a selectivity index of >128. In addition, this compound was shown to be active against persistent forms of mycobacteria comparable to standard drugs in nutrient starvation model. Accordingly, we introduce compound 20 as a valuable lead for further development. A 3D-QSAR study was also conducted to help in explaining the observed activity and to serve as a tool for further development.
Publication type:JOURNAL ARTICLE
Name of substance:0 (Antitubercular Agents); 0 (Hydrazones); 0 (Triazoles); 5B2658E0N2 (Aminosalicylic Acid); 8G167061QZ (Ethambutol); V83O1VOZ8L (Isoniazid); VJT6J7R4TR (Rifampin)


  7 / 535 MEDLINE  
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PMID:28011126
Author:Drozd KV; Manin AN; Churakov AV; Perlovich GL
Address:G.A. Krestov Institute of Solution Chemistry of the Russian Academy of Sciences, 1, Akademicheskaya St., 153045 Ivanovo, Russia.
Title:Drug-drug cocrystals of antituberculous 4-aminosalicylic acid: Screening, crystal structures, thermochemical and solubility studies.
Source:Eur J Pharm Sci; 99:228-239, 2017 Mar 01.
ISSN:1879-0720
Country of publication:Netherlands
Language:eng
Abstract:Experimental multistage cocrystal screening of the antituberculous drug 4-aminosalicylic acid (PASA) has been conducted with a number of coformers (pyrazinamide (PYR), nicotinamide (NAM), isonicotinamide (iNAM), isoniazid (INH), caffeine (CAF) and theophylline (TPH)). The crystal structures of 4-aminosalicylic acid cocrystals with isonicotinamide ([PASA+iNAM] (2:1)) and methanol solvate with caffeine ([PASA+CAF+MeOH] (1:1:1)) have been determined by single X-ray diffraction experiments. For the first time for PASA cocrystals it has been found that the structural unit of the [PASA+iNAM] cocrystal (2:1) is formed by 2 types of heterosynthons: acid-pyridine and acid-amide. The desolvation study of the [PASA+CAF+MeOH] cocrystal solvate (1:1:1) has been conducted. The correlation models linking the melting points of the cocrystals with the melting points of the coformers used in this paper have been developed. The thermochemical and solubility properties for all the obtained cocrystals have been studied. Cocrystallization has been shown to lead not only to PASA solubility improving but also to its higher stability against the chemical decomposition.
Publication type:JOURNAL ARTICLE
Name of substance:0 (Antitubercular Agents); 25X51I8RD4 (Niacinamide); 2KNI5N06TI (Pyrazinamide); 3G6A5W338E (Caffeine); 4H3BH6YX9Q (isonicotinamide); 5B2658E0N2 (Aminosalicylic Acid); C137DTR5RG (Theophylline); V83O1VOZ8L (Isoniazid)


  8 / 535 MEDLINE  
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PMID:27862714
Author:Fernandes MA; Braun HJ; Evason K; Rhee S; Perito ER
Address:Division of Pediatric Gastroenterology, Hepatology, and Nutrition, Department of Pediatrics, Benioff Children's Hospital San Francisco, University of California San Francisco, San Francisco, CA, USA.
Title:De novo inflammatory bowel disease after pediatric kidney or liver transplant.
Source:Pediatr Transplant; 21(1), 2017 Feb.
ISSN:1399-3046
Country of publication:Denmark
Language:eng
Abstract:A subset of children who receive a liver and/or kidney transplant develop de novo inflammatory bowel disease-like chronic intestinal inflammation, not explained by infection or medications, following transplant. We have conducted a single-center, retrospective case series describing the unique clinical and histologic features of this IBD-like chronic intestinal inflammation following solid organ transplant. At our center, nine of 327 kidney or liver recipients developed de novo IBD following transplant (six liver, two kidney, one liver-kidney). Most children presented with prolonged hematochezia and diarrhea and were treated with aminosalicylates. At time of diagnosis, five were not currently using mycophenolate mofetil for transplant immunosuppression. Histologic and endoscopic findings at IBD diagnosis included inflammation, ulcerations, granulomas, and chronic colitis. Since diagnosis, no patients have required surgical intervention, or escalation to biologic therapy, nor developed stricturing or perianal disease. In this case series, de novo post-transplant IBD developed in 4% of pediatric liver and/or kidney recipients; however, it often does not fit the classic patterns of Crohn's disease or ulcerative colitis.
Publication type:JOURNAL ARTICLE
Name of substance:0 (Immunosuppressive Agents); 5B2658E0N2 (Aminosalicylic Acid)


  9 / 535 MEDLINE  
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PMID:27491492
Author:Ou CY; Luo YN; He SN; Deng XF; Luo HL; Yuan ZX; Meng HY; Mo YH; Li SJ; Jiang YM
Address:Department of Toxicology, School of Public Health, Guangxi Medical University, 22 Shuang-yong Rd, Nanning, Guangxi, 530021, China.
Title:Sodium P-Aminosalicylic Acid Improved Manganese-Induced Learning and Memory Dysfunction via Restoring the Ultrastructural Alterations and γ-Aminobutyric Acid Metabolism Imbalance in the Basal Ganglia.
Source:Biol Trace Elem Res; 176(1):143-153, 2017 Mar.
ISSN:1559-0720
Country of publication:United States
Language:eng
Abstract:Excessive intake of manganese (Mn) may cause neurotoxicity. Sodium para-aminosalicylic acid (PAS-Na) has been used successfully in the treatment of Mn-induced neurotoxicity. The γ-aminobutyric acid (GABA) is related with learning and memory abilities. However, the mechanism of PAS-Na on improving Mn-induced behavioral deficits is unclear. The current study was aimed to investigate the effects of PAS-Na on Mn-induced behavioral deficits and the involvement of ultrastructural alterations and γ-aminobutyric acid (GABA) metabolism in the basal ganglia of rats. Sprague-Dawley rats received daily intraperitoneally injections of 15 mg/kg MnCl .4H O, 5d/week for 4 weeks, followed by a daily back subcutaneously (sc.) dose of PAS-Na (100 and 200 mg/kg), 5 days/week for another 3 or 6 weeks. Mn exposure for 4 weeks and then ceased Mn exposure for 3 or 6 weeks impaired spatial learning and memory abilities, and these effects were long-lasting. Moreover, Mn exposure caused ultrastructural alterations in the basal ganglia expressed as swollen neuronal with increasing the electron density in the protrusions structure and fuzzed the interval of neuropil, together with swollen, focal hyperplasia, and hypertrophy of astrocytes. Additionally, the results also indicated that Mn exposure increased Glu/GABA values as by feedback loops controlling GAT-1, GABA mRNA and GABA protein expression through decreasing GABA transporter 1(GAT-1) and GABA A receptor (GABA ) mRNA expression, and increasing GABA protein expression in the basal ganglia. But Mn exposure had no effects on GAT-1 protein expression. PAS-Na treatment for 3 or 6 weeks effectively restored the above-mentioned adverse effects induced by Mn. In conclusion, these findings suggest the involvement of GABA metabolism and ultrastructural alterations of basal ganglia in PAS-Na's protective effects on the spatial learning and memory abilities.
Publication type:JOURNAL ARTICLE
Name of substance:0 (GABA Plasma Membrane Transport Proteins); 0 (Slc6a1 protein, rat); 3KX376GY7L (Glutamic Acid); 42Z2K6ZL8P (Manganese); 56-12-2 (gamma-Aminobutyric Acid); 5B2658E0N2 (Aminosalicylic Acid)


  10 / 535 MEDLINE  
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PMID:27688654
Author:Ray G
Address:Gautam Ray, Gastroenterology Unit, Department of Medicine, B.R.Singh Hospital, Kolkata 700014, West Bengal, India.
Title:Inflammatory bowel disease in India - Past, present and future.
Source:World J Gastroenterol; 22(36):8123-36, 2016 Sep 28.
ISSN:2219-2840
Country of publication:United States
Language:eng
Abstract:There is rising incidence and prevalence of inflammatory bowel disease (IBD) in India topping the Southeast Asian (SEA) countries. The common genes implicated in disease pathogenesis in the West are not causal in Indian patients and the role of "hygiene hypothesis" is unclear. There appears to be a North-South divide with more ulcerative colitis (UC) in north and Crohn's disease (CD) in south India. IBD in second generation Indian migrants to the West takes the early onset and more severe form of the West whereas it retains the nature of its country of origin in migrants to SEA countries. The clinical presentation is much like other SEA countries (similar age and sex profile, low positive family history and effect of smoking, roughly similar disease location, use of aminosalicylates for CD, low use of biologics and similar surgical rates) with some differences (higher incidence of inflammatory CD, lower perianal disease, higher use of aminosalicylates and azathioprine and lower current use of corticosteroids). UC presents more with extensive disease not paralleled in severity clinically or histologically, follows benign course with easy medical control and low incidence of fulminant disease, cancer, complications, and surgery. UC related colorectal cancer develop in an unpredictable manner with respect to disease duration and site questioning the validity of strict screening protocol. About a third of CD patients get antituberculosis drugs and a significant number presents with small intestinal bleed which is predominantly afflicted by aggressive inflammation. Biomarkers have inadequate diagnostic sensitivity and specificity for both. Pediatric IBD tends to be more severe than adult. Population based studies are needed to address the lacunae in epidemiology and definition of etiological factors. Newer biomarkers and advanced diagnostic techniques (in the field of gastrointestinal endoscopy, molecular pathology and genetics) needs to be developed for proper disease definition and treatment.
Publication type:HISTORICAL ARTICLE; JOURNAL ARTICLE; REVIEW
Name of substance:0 (Antitubercular Agents); 0 (Biological Products); 0 (Biomarkers); 5B2658E0N2 (Aminosalicylic Acid); MRK240IY2L (Azathioprine)



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