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A drug delivery system based on physically cross-linked poly vinyl alcohol (PVA)/chitosan blend hydrogels for the release of sparfloxacin antibiotic as a model for drugs was described. Eco-synthesis in current work is based on synthesizing a hydrogel without using chemical crosslinking agents like in the conventional method. In addition all materials are used are non- toxic, safe, non-carcinogenic and can be accepted by the human body without danger. The swelling behavior was tested to be dependent on pH as temperature as well as time and number of freezing thawing cycles. The physical properties of the hydrogels, such as swelling percent, dissolution percent, gel fraction and mechanical properties was assessed. The antimicrobial activity of hydrogels having different compositions was evaluated for both gram positive and gram negative bacteria. Furthermore, the release of antibiotic from hydrogels prepared using the freeze—thawed process was studied. Results obtained disclose that the swelling percent of the hydrogels is pH- dependent and increases by increasing the chitosan percent and decreases with increasing the time and number of freezing cycle. With respect to the antimicrobial activity of the prepared hydrogels, display a positive effect for both gram positive and gram negative bacteria. Freeze-thawed hydrogels could serve as drug delivery system to release sparfloxacin in acidic medium. Indeed, the release percent of sparfloxacin relies on both pH and temperature.

Uniformly sized silver/chitosan- O -methoxy polyethylene glycol (chitosan- O -MPEG) core shell nanoparticles with different degree of substitution were synthesized. Thus, N -phthaloyl chitosan is reacted with polyethylene glycol monomethyl ether iodide in the presence of silver oxide by the following steps. At first, amino groups of chitosan are protected by fourfold excess of phthalic anhydride. Then N -phthaloyl chitosan is reacted with an appropriate amount of monomethyl ether iodide in the presence of silver oxide and lastly N -phthaloyl groups are removed to yield silver/chitosan- O -MPEG core shell nanoparticles. Structure of prepared silver/chitosan- O -MPEG core shell nanoparticles have been characterized by UV/Vis spectroscopy, transmission electron microscopy (TEM), Fourier transform infrared (FT-IR), X-ray diffraction, and scan electron microscopy (SEM-EDX). Experimental results revealed that the prepared silver core particles had the size 18 ± 2 nm. Core shell structure with chitosan- O -MPEG-coating had the size 40 ± 2 nm.

Multifunctioalization of cotton fabrics was developed by a novel finishing formulation. The method is based on chitosan- N -polyethylene glycol graft copolymer along with citric acid and sodium hypophosphite (SHP) as catalysts. Treatment of the cotton fabric resulted in the chemical attachment of the copolymer to the cotton fabric via bridging-based esterification where the latter involves reaction of one molecule of the polycarboxylic acid (citric acid) with both the amino group of the copolymer and the hydroxyl groups of cotton. Inclusion of the copolymer in the crosslinked structure of cotton as well as by hydrogen bonding and van der Waals forces are additionally possible. Synthesis of the copolymer was raised out by the reaction of chitosan with methoxy polyethylene glycol (MPEG) aldehyde followed by the reduction with sodium borohydride. MPEG was prepared by oxidation of PEG with acetic anhydride in dimethyl sulphoxide at room temperature. Methoxypolyethylene glycol- N -chitosan graft copolymer (MPEG- N -CTS) structure was confirmed by IR, NMR, X-RD and TGA techniques. The copolymer is soluble in water. The pad dry-cure method was used for the cotton fabrics treatment with aqueous solution of prepared copolymer along with citric acid and SHP. The so treated fabrics were monitored for copolymer content (expressed as N%), crease recovery, tensile strength, elongation at break, air permeability, water permeability, roughness, bursting strength and antibacterial activity. Fabric performances based on the outputs of these measurements advocate these multifunctionalized fabrics for use as medical textile.

The synthetic catecholamine isoprenaline (ISO) has been used as an inductor in the acute myocardial infarction model for more than a half century. Despite the fact that many articles were published on this topic, precise early haemodynamic pathology remains unknown. Acute haemodynamic changes were measured in rats; first, in preliminary experiments by the thermodilution method; and second, in main experiments continuously for 2 h using a Millar catheter. Animals received saline or ISO in the cardiotoxic dose (100 mg/kg, subcutaneously). Also, additional experiments were performed with salbutamol in order to evaluate the role of β2-receptors. ISO caused a rapid, within 1 min, approximately 40% decrease in arterial blood pressures, 30% increase in the heart rate, and 30% decrease in the stroke volume. Within the first 2 min, the changes were followed by decreases in afterload (−40%), preload (−10%), diastolic relaxation (−50%), diastolic filling (−40%), and a marked, but short-term, increase in the left ventricle contractility (+100%). Ejection fraction did not significantly change, suggesting diastolic dysfunction. Salbutamol, with the exception of diastolic pressure and afterload, did not substantially influence other parameters. In conclusion, this study demonstrated that diastolic dysfunction precedes systolic dysfunction and β2-receptor stimulation alone is not sufficient for an early induction of diastolic dysfunction.

1. The occurrence of IGF-I was investigated in rabbits with experimentally daunorubicin-induced cardiomyopathy. IGF-I was measured in the heart, serum, liver and skeletal muscle. 2. A significant increase in the IGF-I was found in the left heart ventricle in daunorubicin cardiomyopathy (152.9 +/- 10.0 ng/g vs 95.1 +/- 4.2 ng/g in the control group). This site of increased IGF-I activity corresponded well with the maximum of morphological changes (dispersed cytolysis of cardiomyocytes mostly without developed subsequent interstitial myofibrosis). 3. The highest levels of IGF-I were present in right and left cardiac atrium (but without significant differences between the groups). Furthermore, in skeletal muscle, the levels of IGF-I in the daunorubicin group (839.0 +/- 142.1 ng/g) were significantly higher in comparison with the control group (482.5 +/- 83.1 ng/g). 4. The level of IGF-I in the left ventricle in the daunorubicin group (but not in the control group) was significantly higher than that in the liver. There were no correlations observed between the levels of IGF-I in the heart and in the serum. 5. The increase in IGF-I concentrations in the left heart ventricle after the administration of daunorubicin may thus reflect possible autocrine/paracrine role of IGF-I in cardiomyopathy.

1 The occurrence of IGF-I was investigated in rabbits with experimentally daunorubicin-induced cardiomyopathy. IGF-I was measured in the heart, serum, liver and skeletal muscle. 2 A significant increase in the IGF-I was found in the left heart ventricle in daunorubicin cardiomyopathy (152.9±10.0 ng/g vs 95.1±4.2 ng/g in the control group). This site of increased IGF-I activity corresponded well with the maximum of morphological changes (dispersed cytolysis of cardiomyocytes mostly without developed subsequent interstitial myofibrosis). 3 The highest levels of IGF-I were present in right and left cardiac atrium (but without significant differences between the groups). Furthermore, in skeletal muscle, the levels of IGF-I in the daunorubicin group (839.0±142.1 ng/g) were significantly higher in comparison with the control group (482.5±83.1 ng/g). 4 The level of IGF-I in the left ventricle in the daunorubicin group (but not in the control group) was significantly higher than that in the liver. There were no correlations observed between the levels of IGF-I in the heart and in the serum. 5 The increase in IGF-I concentrations in the left heart ventricle after the administration of daunorubicin may thus reflect possible autocrine/paracrine role of IGF-I in cardiomyopathy.

1. A dithiol chelating agent--2,3-dimercapto-1-propanesulphonate (DMPS)--may be administered in acute or chronic intoxication with certain heavy metals (e.g. cadmium, cobalt, lead) that may cause cardiotoxicity. 2. DMPS can act as a depleter of physiologically important elements (e.g. potassium, magnesium, calcium) in various tissues including cardiac one. The possibility of subsequent alteration in cardiac function cannot be excluded. 3. Changes in the myocardial concentration of the above mentioned elements at the end of the experiment and cardiac function were studied during repeated i.v. administration of DMPS as single doses of 50 mg/kg/ week for 10 weeks in rabbits. Biochemical, haematological and histological examinations were also performed. 4. Most of the measured parameters were not affected by the repeated administration of DMPS. A significant decrease in magnesium and a near significant decrease in calcium in cardiac muscle was not accompanied by functional or morphological changes. It is still suggested, however, that care should be taken in using DMPS for treating patients with cardiotoxicity as a result of poisoning with heavy metals.

Cardiotoxicity represents the main drawback of clinical usefulness of anthracycline antineoplastic drugs. In this study, a content of selected elements (Ca, Mg, K, Se, Fe) in the post-mortem removed samples of the myocardial tissue was studied in three groups of rabbits: 1) control group (i.v. saline; n = 10); 2) daunorubicin-receiving animals (DAU; 3 mg/kg, i.v; n = 11); 3) animals receiving cardioprotective iron-chelating agent dexrazoxane (DEX; 60 mg/kg, i.p.; n = 5) prior to DAU. Drugs were administered once weekly for 10 weeks. 5-7 days after the last administration, cardiac left ventricular contractility (dP/dtmax) was significantly decreased in DAU-treated animals (745 +/- 69 versus 1245 +/- 86 kPa/s in the control group; P < 0.05), while in the DEX + DAU group it was insignificantly increased (1411 +/- 77 kPa/s). Of the myocardial elements' content studied, a significant increase in total Ca against control (16.2 +/- 2.4 versus 10.6 +/- 0.9 microg/g of dry tissue; P < 0.05) was determined in the DAU-group, which was accompanied with significant decreases in Mg and K. In the heart tissue of DEX-pretreated animals, no significant changes of elements' content were found as compared to controls, while the Ca content was in these animals significantly lower than in the DAU group (9.1 +/- 0.4 versus 16.2 +/- 2.4 microg/g; P < 0.05). Hence, in this study we show that systolic heart failure induced by chronic DAU administration is primarily accompanied by persistent calcium overload of cardiac tissue and the protective action of DEX is associated with the restoration of normal myocardial Ca content.

This study compares the chronic toxicity of two anthracyclines–daunorubicin and doxorubicin, commonly used for induction of anthracycline cardiomyopathy in the rabbit model. Such a comparative study has not been published until now. Both drugs were administered intravenously to male Chinchilla rabbits in doses at 3 mg/ kg (50 mg/m2) once weekly for 10 weeks. Selected biochemical, haematological and cardiovascular parameters and body weights were regularly monitored; additionally, a histological evaluation of heart, kidney and liver was performed at the end of the experiment. In the daunorubicin group, there were marked signs of the progressive development of heart failure, like the significant increases of the pre-ejection period/left ventricular ejection time index values (up to 134%)–and histological changes within the myocardium were also observed. On the other hand, the 10-week doxorubicin administration did not cause these changes that are typical for heart injury. Haematotoxicity, manifested particularly by aplastic anaemia, was apparent in both the experimental groups. Significant body weight loss (by 45.2%) and high premature mortality (100% versus 36.4%) reflected a greater general toxicity, especially nephrotoxicity of doxorubicin in comparison with daunorubicin. Further studies are necessary to find a possible explanation for these findings.

Cardiac troponin T (cTnT) plasma concentration is considered a useful marker of anthracycline-induced cardiomyopathy. In this study we used daunorubicin-treated Chinchilla rabbits as a model to investigate the relationship between left ventricular contractility and cTnT plasma concentrations. Two groups of animals were used: a control group (n=8) received i.v. saline, and an experimental group (n=11) received daunorubicin (3 mg/kg, i.v.). The substances were administered once weekly for 10 weeks, and 5-7 days after the last administration, left ventricular cardiac contractility (dP/dtmax) was invasively measured as a contractility index and blood was sampled for cTnT concentration determination (Elecsys Troponin T STAT immunoassay). Cardiac contractility was significantly lower in seven surviving daunorubicin-treated animals than in control animals (745.7+/-69.3 vs 1393.4+/-25.5 kPa/s; P<0.001), while cTnT plasma concentrations were significantly increased (medians 0.278 vs 0.000 ng/ml; P<0.001). When the dP/dtmax values of individual daunorubicin-treated animals were plotted against the corresponding cTnT plasma concentrations, a close negative linear correlation was found (R=-0.910; P<0.005; regression equation: dP/dtmax=-1861*cTnT+1234). This study suggests that determination of cTnT plasma levels, which is simple and inexpensive, could be used in anthracycline-treated patients for left ventricular systolic function assessment and contractility estimation.